Columbia (MnitJersd'tp intlieCitpotlrttigork College of $f)p)$ictan£( anli ^urseonsi Hibrarp Digitized by tine Internet Arciiive in 2010 witii funding from Open Knowledge Commons http://www.archive.org/details/diseasesofhearta1 91 Obabc DISEASES OF THE HEART AND ARTERIAL SYSTEM DESIGNED TO BE A PRACTICAL PRESENTATION OF THE SUBJECT FOR THE USE OF STUDENTS AND PRACTITIONERS OF MEDICINE BY ROBERT H. BABCOCK, A.M., M.D. Former Professor of Clinical Medicine and Diseases of the Chest, College of Physicians and Sur- geons (Medical Department of the Illinois State University), Chicago; Consulting Physician to Cook County Hospital, Passavant Hospital, Mary Thompson Hospital, Hospital of St. Anthony de Padua, and of Marion-Sims Sanitarium ; Member of the Association of American Physicians, American Climatological Associa- tion, American Medical Association, National Association for the Study and Prevention of Tuberculosis; Corresponding Mem- ber of Medico-Chirurgical Society of Edinburgh, etc. WITH THREE COLOURED PLATES AND ONE HUNDRED AND THIRTY-NINE ILLUSTRATIONS THIRD EDITION, REVISED NEW YORK AND LONDON D. APPLETON AND COMPANY 1910 6// Copyright. 1903, 1905, 1909, By D. APPLETON AND COMPANY rUINTKO AT THK APIT.KTON PKKSS, NKW YORK, U. K. A. PREFACE TO THE THIRD EDITION The changes in tins third edition are not numerons, but arc such as were needed to bring certain portions of this work up to date. Accordingly, the article upon Stokes-Adams disease has been entirely rewritten so as to conform with our recently acquired knowledge concerning heart-block and its relation to the Stokes- Adams syndrome. An addition has been made also to the original contribution by Dr. Otto Schmidt upon Gaertner's tonometer and its use in clinical medicine. These additional pages will be found under the caption of The SjDhygmomanometer, since instruments known by this generic appellation have supplanted the tonometer of Gaertner and the instrument of von Basch in the United States. Finally, a few foot-notes and corrections have been made which it is believed increase the value of the text. R. H. B. PEEFACE TO THE SECOND EDITION The changes made in this second edition while' not numerous and not affecting the work as a whole are yet important. In the main they concern that form of insufficiency of the auriclo-ven- tricular valves which depends not ujx)n endocarditis but upon alterations of the myocardium, and in the former edition was regarded as always relative. In this one the author believes he has given due recognition to that variety of mitral and tricuspid incompetence termed muscular. Hence a portion of Chapter XXII has been entirely rewritten, while allusions to muscular insufficiency have been introduced here and there in other chap- ters. The work has been enhanced in value thereby and has been brought strictly up to date. R. n. B. PREFACE In the preparation of this work the author has endeavoured to present the subject in a simjDle, practical fashion that would suit the needs of the student and practitioner of medicine. The- ories and speculations have been omitted or given but scanty consideration, in the belief that they tend to confuse the student. The anatomy and physiology of the circulatory organs have re- ceived only such notice as was thought necessary to a better un- derstanding of the matter in hand, since an extended consideration of them was believed out of place in a work devoted to diseased conditions. Although aware that physical signs are properly a part of the symptomatology of disease and should be considered under that head, still the author has thought it best to consider them separately, for the sake of facilitating the knowledge of that most difficult subject, the diagnosis of cardiac disease. Special attention has been paid to treatment, and this part of the subject will, be found far more detailed than is the case in most books dealing with diseases of the heart. It was hoped that by so doing the work might be given a more practical value to the general practitioner, although of course the author realized that he would lay himself open to adverse criticism, and could do but little more than lay down principles for management. The j)hraseology has been kept simple and free from needless technicalities, while in the terminology an attempt has been made to employ the terms which are in most familiar use among American and English physicians. jSTo claim is laid to originality, as is apparent from iv DISEASES OF THE HEART the numerous references to authors from whose works valnable suggestions and information have been derived. To all such authors, grateful acknowledgment is made. In conclusion the writer desires to express particular thanks to the following gentlemen : l)rs. O. L. Schmidt, for the article on Gaertner's Tonometer ; Edward F. Wells, for that on the Sphyg- mograph; Gustav Fiitterer, for anatomical specimens and jDhoto- graphs; W. A. Evans, for post-mortem examinations and other aid ; and Milton W. Hall, for preparing the illustrations. Finally, the author wishes to publicly express his indebtedness to his wife, for her encouragement to undertake this work, for her perusal of his manuscript, and suggestions, without which many passages might have been obscure, and for her invaluable aid in the revi- sion of proof. ROBEKT H. BaBCOCK. 103 State Street, Cuicago, III. CONTENTS GENERAL CONSIDERATIONS PERTAINING TO THE ANAT- OMY, PHYSIOLOGY, AND EXAMINATION OP THE HEART PAGE Introductory 1 Location of the heart ............ 1 The relations of the heart to the anterior thoracic wall 2 Position of' the great vessels and valves 3 Cardiac percussion . ' . . . . 5 Auscultatory or stethoscopic percussion 8 Palpato7'y percussion 10 Auscultation of the heart 12 Normal heart-sounds . . . 13 Meduplieation of the heart-sounds 16 Reduplication of the first sound 18 Gallop or canter rhythm 18 Murmurs . 21 Endocardial murmurs of organic origin 21 Cardiac areas 25 Accidefital murmurs • .26 Musical murmurs 29 Accidental musical murmurs „ . . 32 The differential diagnosis of accidental heart murmur 34 Exocardial murmurs . 36 SECTION I DISEASES OF THE PERICARDIUM CHAPTER I ACUTE PERICARDITIS Morbid anatomy " 37 Etiology 41 DRY PERICARDITIS Symptoms , c . c . 48 Course and termination . ..o ....... 56 V vi DISEASES OF THE HEART PAGE Physical signs. Inspection , c . 56 Palpation 57 Percussion , ... 57 Auscultation 57 LocatioJi of the jyericnrdial friction-sound . . , . . . .58 Rlnjthni of the friction-sound .......... 58 Intensity of the friction-sound 59 (Quality of the friction-sound 59 Effect of pressure on the pericardial uiunuur 59 Diagnosis 60 Differential diagnosis . 60 Prognosis 61 PERICARDITIS WITH EFFUSION Symptoms 65 Course and termination 73 Physical signs. Inspection 74 Palpation .75 Percussion . 76 Atiscultation 79 Secondary i)hysical siyns referable to the lu)igs 80 Diagnosis 81 Differential diagnosis 82 Prognosis 84 Treatment 86 Treatment in the stage of effusion 90 CHAPTER II CHRONIC PERICARDITIS Morbid anatomy 100 Etiology . " 103 Symptoms 104 Course and termination 117 Physical signs. Inspection 118 Palpation 120 Percussion 121 Auscultation 121 Diagnosis 122 Prognosis 123 Treatment 124 CHAPTER III I. HYDBOPERICARDIUM Morbid anatomy 127 Etiology 128 Symptoms 128 Physical signs. Inspection 128 Paljjation 128 Percussion . AtoscuUation Diagnosis Prognosis Treatment . CONTENTS vii 120 129 129 129 130 II. H^MOPERICARDIUM Morbid anatomy 130 Etiology 130 Symptoms 131 Physical signs . 131 Diagnosis 131 Prognosis . 131 Treatment 131 III. PNEUMOPERICARDIUM Morbid anatomy 132 Etiology 132 Symptoms 133 Physical signs. Inspection 134 Percussion 134 AuscuUcdio?i 134 Diagnosis 135 Prognosis 135 Treatment 135 IV. TUBERCULOSIS OF THE PERICARDIUM Morbid anatomy 136 Etiology 137 Symptoms 138 Physical signs 138 Diagnosis 138 Prognosis 138 Treatment . 138 V. SYPHILIS OF THE PERICARDIUM Morbid anatomy 139 Etiology 140 Symptoms 140 Physical signs 140 Diagnosis 141 Prognosis 141 Treatment 141 VI. CARCINOMA AND SARCOMA OF THE PERICARDIUM Morbid anatomy 141 Etiology 142 Symptoms 142 Physical signs 142 Diagnosis 142 Prognosis and treatment .....<,. o.o . 142 Vlll DISEASES OP THE HEART SECTION II DISEASES OF THE ENDOCARDIUM CHAPTER IV ACUTE ENDOCARDITIS PAGE Morbid anatomy 144 Etiology 150 Simple endocarditis 152 Ulcerative endocarditis 155 Syni|itoms 157 Acute simple endocarditis 157 Diagnosis 163 Course and termination 163 Ulcerative endocarditis . 163 Course and termination 172 Physical signs. Inspection 176 Palpation 176 Percussion 177 Auscultation 177 Diagnosis 178 Diagnosis ot ulcerative endocarditis 179 Prognosis 183 Treatment 187 Treatment of acute ulcerative endocardilis ....... 191 CHAPTER V chronic endocarditis Morbid anatomy Etiology Symptoms . 199 201 205 CHAPTER VI MITRAL regurgitation Morbid anatomy . Etiology Symptouis . Physical signs. InsjKction I'alpntion Percussion . Auscultation Diagnosis Prognosis Mode and causes of death 216 221 223 239 239 240 242 245 246 247 CHAPTER VII mitral stenosis Mf)rbid anatomy Etiology 249 252 CONTENTS IX PACK Symptoms 255 Pliysical signs. Inspection 258 Pidpation 259 Percussion 260 Auscultation 261 Diagnosis 268 Prognosis 269 Mode and causes of death 270 CHAPTER VIII AORTIC REGURGITATION Morbid anatomy 278 Etiology 280 Symptoms 282 Physical signs. Insjjection 297 Palpation 298 Percussion 801 Diagnosis 305 Prognosis 306 Mode and causes of death 307 CHAPTER IX AORTIC STENOSIS Morbid anatomy 319 Etiology 322 Symptoms 323 Physical signs. Inspection 335 Palpation 335 Percussion 336 Auscultation 337 Diagnosis 338 Prognosis 339 Mode and causes of death 340 CHAPTER X TRICUSPID REGURGITATION Morbid anatomy 344 Etiology 345 Symptoms 347 Physical signs. Inspection 349 Palpation 350 Percussion 351 Diagnosis 353 Prognosis 354 Mode and causes of death 354 CHAPTER XI TRICUSPID STENOSIS Morbid anatomy 355 Etiology 356 X DISEASES OF THE HEART PAGE Symptoms ^">7 Physical signs. Inspection 361 Percussion 362 AuscitUation 362 Diagnosis 363 Prognosis 364 Mode and causes of death 364 CHAPTER XII PULMONARY REGURGITATION Morbid anatomy 365 Etiology 366 Symptoms 367 Physical signs 370 Inspection 371 Palpation 371 Percussion 371 Auscultation 372 Diagnosis 373 Pi'ognosis . 374 Mode and causes of death 374 CHAPTER XIII PULMONARY STENOSIS Morbid anatomy 376 Etiology 380 Symptoms 380 Physical signs. Inspection 385 Palpation 386 Percussion 386 Auscultation 386 Diagnosis 387 Prognosis 387 Mode and causes of death 388 Summary of physical signs of valve lesions of the right heart .... 389 CHAPTER XIV COMBINED VALVULAR LESIONS Combined mitral stenosis and regurgitation Symptoms. Diagnosis . Prognosis . Mitral stenosis anij Symptoms. Diagnosis . Prognosis . AORTIC STENOSIS 390 391 391 392 392 392 392 393 CONTENTS XI PAGE Mitral stenosis and aoiitic regurgitation <,..,„,. 393 Symploins 393 Diagnosis 394 Inspection . . . . 395 Palpation , 395 Percussion 395 Auscultation 395 Prognosis 396 Mitral regurgitation and aortic stenosis ....... 396 Symptoms 396 Diagnosis , . . 396 Prognosis 396 Aortic regurgitation and mitral regurgitation . . ... . 397 Symptoms 397 Diagnosis 397 Prognosis 398 Aortic stenosis and aortic regurgitation . . , . . . . 398 Symptoms 398 Physical signs . . . ... 399 Diagnosis 399 Prognosis 400 CHAPTER XV the prognosis of valvular heart-disease in general Complications 405 Rheumatic diathesis 406 Digestive and bronchial disorders 407 Age 407 Temperament 408 Sex 409 Occupation 409 Habits . ' 410 Home surroundings 410 The probable effect on the patient of the knowledge of his lesion . . . 411 The effect of digitalis on the patient 411 The relation of prognosis to life insurance 412 CHAPTER XVI the treatment op valvular heart-disease Compensation being still perfect Exercise . Occupation Habits Marriage Clothing Baths Food, ninesses Use of drugs Change of climate, with. special reference to high altitude 414 414 419 430 422 425 427 428 429 430 433 xii DISEASES OF THE HEART CHAPTER XVII THE TREATMENT OF VALVULAR HEART-DISEASE {continued) ^^^^ II. Compensation being imperfect 435 Medicinal agents 444 Rest ...,., 448 Exercise 454 Resistance exercise 455 Naiiiieim baths 464 Diet 470 Clothing, habits, occupation 476 CHAPTER XVIII THE TREATMENT OE VALVULAR HEART DISEASE {conclilded) III. Compensation lost 478 The treatment of dropsy 489 Cathartics 492 The use of digitalis 494 Accessory heart tonics 499 Hypnotics 500 Rest 503 Exercise 502 Baths 503 Receiving visitors 503 Diet 503 SECTION III DISEASES OP THE MYOCARDIUM CHAPTER XIX ACUTE MYOCARUITIS Morbid anatomy 506 Etiology , ... 508 Symptoms 510 Physical signs. Inspection . .014 Pdlpation 514 Percussion 514 Auscultation 514 Diagnosis 514 Prognosis 515 Treatment 515 CHAPTER XX CHRONIC MYOCARDITIS Morbid anatomy 519 Etiology 522 ' CONTENTS Xlll PAGE Symptoms ' . „ . . . , 520 Physical signs. Inspection 543 Palpation 543 Percussion 544 A^iscultation 545 Diagnosis _ , . 547 Prognosis 540 Treatment 551 Commencing loss of heart-potver 553 Cardiac incompetency pronounced 555 CHAPTER XXI HYPERTROPHY OF TEE HEART Morbid anatomy 565 Etiology ■ 568 Symptoms 570 Physical signs. Inspection 571 Palpation 571 Percussion 571 Auscxdtation 572 Diagnosis 572 Prognosis 574 Treatment 575 CHAPTER XXII DILATATION OF THE HEART — RELATIVE AND MUSCULAR MITRAL INSUFFICIENCY I. DILATATION OF THE HEART Morbid anatomy Etiology Symptoms . Physical signs. Inspection Palpation Percussion . Auscultation Diagnosis Prognosis Treatment . (1) Bloodlettitig (2) Naulieim baths (3) Resistance exercises II. RELATIVE AND Pathology . Etiology Symptoms . Physical signs Diagnosis Prognosis . . Treatment . MUSCULAR MITRAL INSUFFICIENCY 576 577 580 585 585 585 586 586 587 590 591 592 592 595 596 597 597 597 598 598 xiv DISEASES OF THE HEART CHAPTER XXIII FATTY UliART — CARDIAC INADEQUACY OF TUE CORPULENT p^^.^. Morbid anatomy . . 599 Pathology 599 Etiology 600 Symptoms 602 Physical signs. Inspection 604 Palpation 604 Percussion 604 Auscultation 605 Diagnosis 605 Prognosis 606 Treatment 606 CHAPTER XXIV CARDIAC ASTHMA — CUEYNE-STOKES RESPIRATION — BRADYCARDIA — STOKES-ADAMS SYNDROME I. Cardiac asthma 613 II. Cheyne-Stokes respiration 615 Diseases in which Cheyjie-Stokes breathing is observed .... 617 Theories to explain Cheyne-Stokes respiration 617 Prognosis 622 Treatment 623 III. Bradycardia 624 IV. Stokes- Adams syndrome 627 Etiology and pathology 027 Symptoms 629 Prognosis • . . . . 635 Treatment 635 CHAPTER XXV ANGINA PECTORIS Definition 637 History 637 Pathology and etiology 640 Clinical history and features of an attack 649 Diagnosis 654 Prognosis 657 Treatment 658 CHAPTER XXVI SYPHILIS OF THE MYOCARDIUM — NEW GROWTHS IN THE MYOCARDIUM — ATROPHY OF THE HEART — SEGMENTATION AND FRAGMENTATION OF THE MYOCARDIUM I. Syphilis of the myocardium M(M-ljid anatomy Etiology .... Syin|)ti)ms . . . Diagnosis .... 663 663 663 664 664 CONTENTS XV PAGE Prognosis . . . , = 665 Treatment '...., 665 II. New growths in the myocardium 666 III. Atrophy of the heart 667 Morbid anatomy . . . 667 Etiology 667 Symptoms 668 Diagnosis 668 Prognosis 668 Treatment 668 IV. Segmentation and fragmentation of the myocardium .... 668 CHAPTER XXVII PEDUNCULATED AND BALL THROMBI OF THE HEART Pathogenesis and etiology 674 Symptoms 675 Diagnosis , 677 Prognosis 678 Treatment 678 Bibliography of cases of ball thrombi ........ 680 CHAPTER XXVIII DEXTROCARDIA Congenital dextrocardia . 681 Symptoms. 681 Diagnosis .....' 682 Acquired dextrocardia . . . . , 682 Morbid anatomy 682 Etiology .683 Symptoms 684 Diagnosis .^ 684 Inspection and 2Ml2}ation 684 Percussion 684 Auscultation 684 Prognosis 685 Treatment 685 CHAPTER XXIX CONGENITAL DISEASES OF THE HEART Morbid anatomy . . . . . . 686 Etiology 689 Symptoms 690 Physical signs. Insjjection 695 Palpation 696 Perctission 697 Diagnosis 701 Prognosis 701 Treatment 702 2 xvi DISEASES OF THE HEART SECTION IV CARDIAC NEUROSES Syn. : Functional Disorders of the Heart CHAPTER XXX PALPITATION, TACHYCARDIA, CARDIAC PAIN, PSEUDO-ANGINA PECTORIS PAGE Pathology '^'03 Symptoms • 'J'04 Palpitation '^04 Tachycardia 715 Cardiac pain ' • • • 718 Pseudo-angina pectoris 719 Etiology 722 Diagnosis 724 Prognosis 726 Treatment 727 Treatment of the attack 727 Palpitation 727 The attack of pain 728 CHAPTER XXXI ESSENTIAL PAROXYSMAL TACHYCARDIA Pathology 731 Etiology 732 Features of the paroxysm 732 Diagnosis 734 Prognosis 735 Treatment 735 SECTION V DISEASES OF THE ARTERIAL SYSTEM CHAPTER XXXII Arteriosclerosis 738 Morbid anatomy 739 Etiology 741 Symptoms 745 Physical signs 750 Diagnosis 751 Prognosis 754 Treatment 754 CONTENTS xvii CHAPTER XXXIII ACUTE AORTITIS — ACUTE ARTERITIS — SYPHILITIC ARTERITIS — ENDARTERITIS OBLITERANS — PERIARTERITIS NODOSA — STENOSIS OF THE AORTA AND PULMONARY ARTERY — CONGENITAL SMALLNESS OF THE ARTERIES I. ACUTE AORTITIS p^^^. Morbid anatomy 759 Etiology 760 Symptoms 760 Physical signs 761 Inspection 761 Palpation 761 Percussion .' 761 Auscultation 762 Diagnosis 763 Prognosis 762 Treatment 762 II. ACUTE ARTERITIS Morbid anatomy 762 Symptoms 763 Physical signs. Inspection — Palpation 763 Diagnosis 763 Prognosis , 763 Treatment 764 III. SYPHILITIC ARTERITIS Morbid anatomy 764 Etiology 765 Symptoms 765 Diagnosis 766 Prognosis 766 Treatment . . , . . , ' 766 IV. ENDARTERITIS OBLITERANS Morbid anatomy 766 Etiology 767 Symptoms 767 Diagnosis ' . . 768 Prognosis and treatment 769 V. PERIARTERITIS NODOSA Syn. : Congenital Aneurysm Morbid anatomy 769 Etiology 769 Symptoms 769 Diagnosis 770 Prognosis and treatment 770 xviii DISEASES OF THE HEART VI, STENOSIS OF THE AORTA AND PULMONARY ARTERY ^^^^ Stenosis of the aorta, congenital and acquired 770 Symptoms 771 Diagnosis '''71 Prognosis and treatment 772 Stenosis of the pulmonary artery 772 Symptoms 772 Diagnosis 772 Prognosis and treatment 773 VII. CONGENITAL SMALLNESS OF THE ARTERIES Symptoms 773 Diagnosis '74 Prognosis and treatment ■ . . . 774 CHAPTER XXXIV ANEURYSM OF THE THORACIC AORTA Morbid anatomy 775 Etiology . 777 Symptoms 781 Pain 782 Dyspnoea 783 Cough 784 Expectoration 784 Physical signs. Inspection 800 Palpation 801 Percussion °02 Auscultation 8Q2 Diagnosis 804 Prognosis 808 Modes and causes of death 808 Treatment 809 APPENDIX Mechanical devices as aids to determining cardiac disease . . . 815 The X-ray 815 The sphygmograph 818 Gaertner's tonometer . . . . • 8-o The sphygmomanometer ""^^ LIST OF PLATES AND ILLUSTRATIONS PLATE I. Anatomical relations of thoracic and abdominal viscera . . . . II. Aortic regurgitation with calcified vegetation that swung in blood cur- rent, causing atheroma of endocardium and of intima of aorta . III. Exterior of heart of Fig. 42, showing hypertrophy and dilatation of both ventricles ......... FACINO PAGE 576 unds are most distinctly Jieard cusps and Cardiac valve areas, showing ivTiere so Normal deep-seated cardiac dulness Auscultatory percussion Hein's palpatory percussion Ebstein's palpatory percussion . Maguire's palpatory percussion . Normal cardiac cycle . Cardiac valve areas, indicating sounds produced at various valves Interior of left ventricle, shoiving fihrous land connecting aortic responsible for musical murmur Heart of a buffalo calf, shoiving aberrant chordce tendince in left ventricle Cor villosum of acute plastic pericarditis .... Usual location of pericardial friction sound and fremitus Absolute dulness in ease of acute pericarditis . Case of pericarditis in which the sac contained 3^ pounds of fluid (Bramwell) Absolute dulness in ease of pericarditis with effusion Roteh's sign of beginning effusion .... Pins and Ewart's signs of pericardial effusion . Apex-beat and area of cardiac dulness in case of pericarditis with effusion The various sites for puncture in paracentesis pericardii . Cardiac dulness and location of border of liver in special cases Verrucose endocarditis of aortic and mitral valves . Verrucose endocarditis Malignant verrucose endocarditis of mitral valve Malignant verrucose endocarditis of aortic valve, with perforation of a cusp Apex-beat and relative dulness in case of acute endocarditis Apex-beat and absolute dulness later in same case . Apex-beat and relative cardiac dulness ; special case Area of maximum audibility and transmission of murmur ; special Chart T. Temperature in case of acute endocarditis Chart II. Temperature in case of acute endocarditis Diminution of relative cardiac dulness in one week under treatment Relative dulness in case of chronic endocarditis Condition of mitral valve causing regurgitation and obstruction 108 PAGE 4 6 8,9 0, 11 11 12 14 25 31 38 39 58 63 65 71 78 80 93 94 115 145 146 147 149 159 161 165 165 167 173 186 203 217 XX DISEASES OP THE HEART PAQE Diagram showing effects of a mitral leak on the circulation .... 2/JO Relative dulness in case of mitral insufficiency 237 Apex-beat and relative dulness in mitral regurgitation 230 Sphygmogram, showing irregular pulse in case of mitral regurgitation . . 240 Relative dulness in a typical case of mitral regurgitation .... 241 Point of maximum audibility and area of transmission of mitral regurgitant mui'mur 242 Time of mitral regurgitant murmur 243 Interior of left ventricle, showing buttonhole slit 250 Case of mitral stenosis, showing ascites and clubbing of finger-tips , . 258 Sphygmogram, from case of mitral stenosis 260 Location of apex-beat and area of deep-seated dulness in mitral stenosis . 260 Rhythm of characteristic murmur of mitral stenosis, " auricular systolic " . 261 Area of audibility of the presystolic murmur of mitral stenosis . . . 262 Rhythm of occasional variety of mitral stenotic murmur through entire ven- tricular diastole 264 " Interrupted modified presystolic " murmur of mitral stenosis . . . 265 Location of apex and relative dulness in case of mitral stenosis . . . 271 Location of apex and relative dulness in case of mitral stenosis and regurgi- tation 273 Location of apex and relative dulness in case of mitral stenosis . . . 276 Location of apex and relative dulness in case of aortic regurgitation . . 285 Sphygmogram of aortic regurgitation 299 Sphygmogram of pulsus bisferiens 300 Type of relative dulness in well-compensated aortic regurgitation . . . 302 Type of relative dulness in poorly compensated aortic regurgitation . . 302 Spot of maximum intensity and area of transmission of typical aortic regurgitant murmur 303 Rhythm of aortic regurgitant murmur 303 Relative dulness in case of aortic regurgitation oil Skiagram of chest in case of aortic regurgitation 312 Relative dulness and lower border of liver shortly before death . . . 316 Heart of aortic stenosis with adherent cusps and also acute endocarditis . 320 Heart of aortic stenosis showing calcified vegetations in sinuses of Valsalva . 321 Sphygmogram from case of aortic stenosis 329 Sphygmogram of uncomplicated aortic stenosis 336 Typical relative dulness in case of well-compensated aortic stenosis . . 336 Rhythm of aortic obstructive murmur 337 Place of maximum intensity and propagation of aortic stenotic murmur . 337 Relative dulness in case of primary tricuspid regurgitation .... 351 Relative dulness in ease of tricuspid regurgitation secondary to dilatation of right ventricle 3.52 Place of maximum audibility and area of propagation of tricuspid regurgi- tant murmur 352 Location of thrill and murmur in a typical case of tricuspid stenosis . . 361 Relative cardiac dulness in typical case of tricuspid stenosis .... 362 Area of deep-seated cardiac dulness in case of pulmonary regurgitation . . 368 Area of maximum intensity and of propagation of murmur in case of pul- monary regurgitation 360 The rhythm of murmur in typical case of puhnonary regurgitation . . :'.73 Heart of a boy, showing congenital stenosis of the pulmonary orifice . . 379 INTRODUCTORY 3 ity of this triangular area is filled by the pulmonary artery and the tip of the left auricular appendix as it curves around the outer border of the left ventricle to appear in front to and terminate near the trunk of the great artery. It is obvious, therefore, that only the upper third of the right auricle lies behind the sternum, while its lower two thirds are to the right of this bone. The left auricle is situated behind, being completely invested by the left lung and entirely obscured from view from the front. The same is the case also with the left ventricle, excepting a narrow strip which forms the left border of the heart and is visible anteriorly.' It is the inferior extremity of this narrow strip which, propelled against the wall of the thorax, occasions the apex-beat. Conse- quently it is a portion of the right ventricle only which is exposed to view after removal of the breastbone and adjacent costal car- tilages. The remainder of the heart, even that which lies ante- riorly, is covered from view by the lungs. The anterior lung borders are in apposition behind the middle of the sternum from the level of the second to that of the fourth costal cartilages. At this latter situation they diverge, the border of the right lung passing on downward to the level of the fifth right costal cartilage, where it turns off to the right to unite with the inferior margin of the same lung. The anterior margin of the left lung diverges abruptly at the level of the fourth cartilage, passing outward along the lower edge of this cartilage as far as its union with its rib. It then turns downward, and, after curving slightly inward and then outward, unites with the inferior border at the level of the sixth costal cartilage near its point of articu- lation with its rib. In consequence of this peculiar arrangement of the left lung a portion of the anterior surface of the right ven- tricle comes into immediate contact with the chest-wall, and, being uncovered by lung, forms the area of superficial cardiac dulness. By many this area is considered of great importance in the deter- mination of the size of the heart by percussion, as will be shown in dealing with the subject of cardiac percussion. Position of the Great Vessels and Valves. — The pulmonary artery lies about half an inch to the left of the breastbone and extends from the level of the centre of the third left interspace upward to the level of the second costal cartilage, where it divides into its two main branches. The position and course of the as- DISEASES OF THE HEART cending aorta inav be represented by a line drawn from the third left chondro-sternal articulation ni)ward across the breastbone to the junction of the right edge of that bone with the second right costal cartilage, which, therefore, is sometimes spoken of as the aortic cartilage, because at this point the aortic valve-sounds are most distinctly heard. The superior vena cava passes downward along the right cardiac border from the level of the second costal cartilage to a point opposite the middle of the third right inter- space. The four sets of valves are bunched closely together not far from the junction of the third left costal x;artilage with the border of the sternum, the pulmonary being most superficial, the mi- tral most internal, the tricuspid most inferior, and the aortic the most central. They cannot, - '^ therefore, be auscultated in the region of their anatomic seat .1 p^if one is to differentiate their individual sounds. For this reason we take advantage of the laws governing the conduc- tion of their sounds and aus- cultate them in certain areas named after the respective valves. Thus the mitral area is situated at the apex-beat and includes a limited district im- mediately roundabout. The tricuspid area includes the lower end of the sternum and a portion of the surrounding region. The pulmonic area is located in the second left intercostal space close to the edge of the breastbone, while the aortic area lies in the corresponding situation on the opposite side. It must not be supposed that the valve-sounds and murmurs are heard only in these situations — they are widely propagated iiiid blend witli one another, and in particular endo- cardial murmurs are often so widely conducted as to he distinctly audible in other areas than those to which they properly belong. Fio. 1.— Cardiac Valve Akeas. Sounds produced at various valves indicated : p, pulmonary : a, aortic ; <, tricuspid ; ^u, mitral. INTRODUCTORY 5 Leaving further consideration of this subject at this time, we now pass on to the discussion of the methods by which the size of the heart is ascertained during life (Fig, 1). Cardiac Percussion. — In employing this means of examination we aim to determine, first, the boundaries of the area of superficial dulness, and second, the limits of deep-seated dulness. To accom- plish the former, percussion must be made lightly, whereas the latter requires a firm, heavy percussion-stroke. The area of superficial or absolute cardiac dulness correspond- ing with the portion of the right ventricle uncovered by lung during inspiration, extends vertically from the upj)er edge of the fourth left costal cartilage to the sixth, and transversely from the left border of the sternum to a point midway between the parasternal and mamillary lines. As its outer or left boundary is irregular, and, roughly speaking, passes obliquely downward towards the left, this area is broader at its lower than at its upper margin. Enlargement of the heart crowds the lung-borders aside, and hence generally increases the dimensions of superficial dulness, especially to the right in cases of hypertrophy and dila- tation of the right ventricle. But a variety of conditions outside of the heart may increase or diminish the extent of superficial dulness, and hence render this not always a trustworthy indication of the actual size of the heart. Thus the lung-borders may be re- tracted by pleuritic adhesions and expose an abnormally large portion of the right ventricle, or being distended by pulmonary emphysema, they may diminish or entirely obliterate this area. Consequently it is preferable to rely upon deep rather than superficial percussion in endeavouring to ascertain the size of the heart, since when the limits of deep-seated or relative cardiac dulness are found increased we know it is due to increase in the size of the organ itself. Vierordt objects to this latter method because of its greater difficulty and uncertainty, since pulmonary resonance shades so gradually into the relative dulness overlying the heart that two observers of apparently equal skill may not agree in their results. Doubtless individual judgment depends very largely upon practice and delicacy of hearing, and doubtless emphysema, inelasticity of the ribs, great thickness of the parietes, etc., often make it impossible to accurately determine deep cardiac limits. ^Nevertheless the cases in which relative dulness is possi- DISEASES OF THE HEART ble of detection are so numerous that I prefer to rely upon it rather than on superficial dulness, and always urge students to make use of this method. The Deep Boundaries of the Heart (Fig. 2). — It is well known that all hearts are not of the same size even in health, the male heart being larger than the female, and that of a child relatively larger than that of an adult. Moreover, the right auricle measures more during diastole than during systole. Consequently measure- ments cannot be given that are invariable. Yet the following figures taken from Yierordt may be stated as the average. The adult heart '' extends from about 8 or 9 centimetres to the left of the median line (apex of the heart) to about 4 or 5 cen- timetres to the right of the same, i. e., about one and a half finger-breadths to the right of the right border of the ster- num (right auricle)." Busse, who employed Ebstein's palpa- tory percussion, found the left l)order of the heart in health never passed outside the mam- illary line, while Ilornkohl determined the average in adults to be 7.3 centimetres from the left sternal margin. On the right side the heart ex- tended a variable distance beyond the sternum, depending on the stature of the man, being 2.0 centimetres for one 130 centi- metres tall, and 3.0 centimetres for a male of 190 centimetres in height. In women those figures are slightly less, while in children the area of the heart measures relatively more than in adults. Tf the median line is taken as the landmark from which to measure, Ilondcohrs figures must be increased by 1 to 1.5 centi- metre, which, according to Ebstein, is half the M'idth of the ster- num. Consecjuently it is found that Vierordt's and Hornkolil's estimates are not so much at variance as they at first appear. Three methods of percussion are in use, and mentioned in the Fio. 2. — NoKMAL Deep-seated Cahdiac Dulness. PP. parasternal line; MM, inaniillary line. INTllODUCTORY T order of their popularity are: (1) plessimetric, (2) auscultatory, (3) palpatory percussion. I do not propose to discuss the advan- tages or disadvantages of employing a pleximeter and hammer, but merely to express my very positive preference for the use of the fingers, for the reason that thereby one is enabled to obtain valuable information from the sense of resistance. In ascertaining the area of absolute dulness light strokes are essential, while the reverse is the case as regards deep-seated dul- ness. Moreover, in outlining the area of relative dulness the pleximeter finger should be pressed firmly against the chest-vi^all, to exclude so far as possible the vibrations of the bony structures. This is the " ahgeddmpfte " percussion of the Germans. The finger is placed firml}^ at right angle to the ribs at a point well outside the cardiac area, and percussion is made with considerable force at ever decreasing distances from the sternum until a slight rise in pitch and increase of resistance indicate that the airless organ (the heart) has been reached. In this manner one is to percuss from above downward along the left parasternal line, beginning in the first intercostal space and ceasing when the upper border of the liver is reached. At the sides, percussion is to be performed first in an oblique direc- tion from above downward and inward, and next on a transverse line from without towards the centre. If, wherever comparative dulness is perceived, a mark is made with a dermographic pencil, these marks can subsequently be united, and will then represent the probable limits and shape of deep-seated cardiac dulness. If one prefers he can, instead of placing his finger across the ribs, press it strongly into the intercostal space parallel with the ribs, and if his finger is slender can thus convey his percussion-strokes more directly to the heart without eliciting so much vibration from the elastic structures intervening. Sansom makes use of a narrow pleximeter, which is of such small size as to fit well down into the intercostal space, and claims remarkably accurate results, more precise indeed than in any other way. It may be well to here remark that, when in women accurate percussion of the heart is impossible on account of the large size of the mammae, fairly trustworthy information concerning the size of the heart may be gained by careful palpation of the apex- 8 DISEASES OF THE HEART beat. Since the mamillary line is not a trustworthy guide in females, it is better to measure the site of the apex impulse from the mid-sternal line or from the mid-clavicular line, it being in the fifth interspace, an inch within the latter. Two statements should also be made regarding percussion of the heart in children. In the first place, the area of superficial dulness is said by Hornkohl to be somewhat more extensive than in adults, particularly above, where it is asserted to reach up into the thirtl intercostal space, while its outer margin passes some- what further beyond the left parasternal line, i. e., to a point a lit- tle nearer the mamillary than the })arasternal line. In the sec- ond place, it is important to bear in mind the great elasticity of the child's chest, and hence to percuss with far more delicacy than is advisable in grown people. Otherwise the note of pulmonary resonance and the vibrations of underlying structures will assur- edly prevent accurate and trustworthy results. For these reasons it is far preferable to rely on the other modes of j)ercussion now to be described. 3. — AUSCCLTATOKV pERCrssluN. Auscultatory or Stethoscopic Percussion. — This is a combina- tion of auscultation Jind percussion, and is based on the princijtle that when the stroke is iiiade over a solid organ its note is higher, INTRODUCTORY Fig. 4. — Auscultatory PEKCusiioN. sharper, and more clearly defined tlian when over an air-contain- ing organ. It is found, moreover, that there is a distinct differ- ence in the character of the note of two viscera of similar struc- ture. This is, of course, the same jDrinciple that underlies plessimetric percussion, but the auscultatory method enables one to appreciate more delicate shadings of tone and to define more precisely the deeply situ- ated borders of an organ or solid thoracic tumour. It even enables one to distinguish be- tween the dulness of pleuritic or pericardial effusion and that of a contiguous pulmonary con- solidation. It is practised in either of two ways : The examiner may with one hand hold the bell of his binaural stethoscope against the centre of the cardiac area, while with the tip of a finger of the disengaged hand he taps the chest-wall lightly from without inward and on a line with his stethoscope (Fig. 3), or he may have his instrument held by an assistant while he performs percussion in the ordi- nary manner (Fig. 4). The former mode is preferable, because more delicate. Such astonishing and incredible accuracy is claimed for auscultatory percussion, notably by Bezly Thorne, that Broadbent and others have been led to test it, and have come to the conclusion that it possesses no advantages over plessimetric percussion. I have employed it a great deal, and, although recog- nising its liability to error and its limitations, still I believe it is in certain cases with thin-walled elastic chests and when practised carefully a very accurate means of outlining the heart. I have repeatedly compared its findings with those of the two other meth- ods, especially plessimetric, and find it satisfactory and trust- worthy. One occasionally encounters chests in which for one rea- son or another it is next to impossible to determine the deep limits of the heart in the ordinary fashion. It is well in such cases to 10 DISEASES OP THE HEART try the method under discussion, since it will often help one out of his dilemnia. I should not recommend its employment to the exclusion of the plessimetric method, but merely as an adjunct thereto. Palpatory Percussion. — By this term is meant a method of using- both palpation and percussion at the same time. In other words, it is a method of ascertaining the heart's resistance, and thereby of ascertaining its outline and dimensions. It makes use of the feeling of resistance rather than of the auditory ])erception of ditl'ercnces in sound. Auenbruggcr and Lacnnec percussed the chest-wall immediately — that is, without the intervention of a ples- simeter ; the former, by striking with the tip of his finger, and the latter w^ith the end of his stethoscope. It is needless to say this mode of performing ])ercussion is more or less painful to the pa- tient. In 1S77 Ebstein proposed pal})ation of the heart and other solid viscera, as the liver, as a means of appreciating their size by their resistance, and at the International Medical Congress at Rome in 1S94 he read an elaborate paper in which he discussed and explained his method at considerable length. In this paper he called attention to a method employed by J. Ilein, which consists in palpating the heart with one finger while per- cussing with the other in the following manner: The palmar surface of the terminal phalanx of the outstretched middle fin- ger is placed upon the chest, wliile a light tap is made on the chest with the tip of the bent forefinger (Figs. 5 and (!). Then wliilo the extremity of the first finger rests against the wall of the thorax ho gives a light blow to the chest with tlie pad of llic middle finger. In each instance the fingers are allowed to rcmaiii foe an iiistaiit in contact with the part percussed, so as the better to perceive the sensation of resistance imparted. In this way, by alternately tapping with the b'm. ;■). — IIein'h I'Ai.rATuUY I'kkci ssmN. First position. INTRODUCTORY 11 two fingers, the entire area is traversed. This is said to yield very accurate results, but is by Ebstein considered inferior to his method, because not altogether devoid of pain to the patient. Ebstein, therefore, makes use of a small glass pleximeter, upon which he gives a gentle prejssing stroke with the tip of one fin- ger, which, flexed at its meta- carpal articulation, is held slightly and rigidly curved as the stroke is given (Fig. 7). The blow is not made with a quick rebound (staccato), but with a firm pushing movement (legato). The stroke is given in a line perpendicular to the surface thus percussed and the pleximeter is held firmly in position. Ebstein' s pleximeter of glass is ^ an inch (1.3 centi- metre) in width. If inch (4.0 centimetres) in length, and sur- mounted by a small handle f of an inch (1.5 centimetre) in height. With such a pleximeter Ebstein asserts the method is not only gratifyingly precise, as he has repeatedly proved on the cadaver by means of needles, but is easily acquired, which is an opin- ion contrary to that expressed by Vierordt. More- over, it possesses the additional advantage of en- abling the ex- aminer to avail himself of his perception of the sound and pitch of the note pro- duced, as well as of the sense of resistance. In this way two impressions are received simultaneously which serve to control Fig. 6.- -Hein's Palpatoby Percussion. Second position. Ebstein's Palpatory Percussion. 12 DISEASES OF THE HEART -.Maolike's Method of Pali-atouy Pekclssion. each other. Ebstein dechires also that by his method one can obtain satisfactory results in .cases of emphysema and in persons with a thick ])annic\ihis of fat or large mammary glands, all of which nsually preclude accu- rate percussion after the ordi- nary .method. Robert Maguire, of Eng- land, advocates palpator}^ per- cussion by tapping lightly with the soft palmar cushion of the terminal phalanx of one finger, and claims equally accurate re- sults (Fig. S). lie expressly states that the stroke must be not short and quick, but long and ])ressing, as if one were feeling or palpating with the finger. It is applicable, he says, not only to all solid or- gans, spleen and kidneys, as well as heart and liver, but also to collections of fluid in thoracic and peritoneal cavities. In cases which are at all obscure it is well to verify the con- clusions derived by any one method — plessimetric, auscultatory, or palpatory — by each of the others. For my part I value the aus- cultatory method the least highly, because so liable to error in exactly those cases ^\■llicll oflVr the greatest difficulty to ordinary percussion — that is, ('iii])]iyscuiatous, fat, and rigid chests. Auscultation of the Heart is another and indispensable means of making cardiac examinations, and by the inexperienced is apt to be relied upon, if not exclusively, at least to a degree out of pro- portion to its inij)()rtance as comjiared with ])ercussion. Neither can be comjiletc without the other. I desire also to emphasize the folly of iittcinpting to do accurate work without the use of a stothoscoj)e. Whatever form or kind of instrument enables one to liear tlu? most distinctly is, in my opinion, the best for him, re- gardless of the arguments advanced in favour of certain sorts. I make; use of a simple biiumi-al and of a inoiiaui'al stctlioscojx', em- ploying the laftci- when INTRODUCTORY 21 eachexiaj, which induce profound cardiac asthenia and consequent want of tonicity. According to French authors, it sometimes occurs over the riglit ventricle in cases of gastric disease, and Johnson says it may be produced by puhnonary emphysema. Fraentzel mentions it as occurring in other hmg affections, leading to dilatation and hyper- trophy of this right chamber, with marked cachexia. I once ob- served a true gallop-rhythm in the fourth and fifth right inter- spaces close to the sternum, for a brief time, during which there was very obvious overdistention of the right cavities secondary to a rheumatic mitral regurgitation. The very unusual situation of the rhythm in this instance is only explicable by the supposi- tion that in consequence of the enormous distention of the right ventricle the auriculo-ventricular sseptum had become pushed so far towards the right that the wall of the ventricle extended to the fourth and fifth right interspaces. It disappeared so soon as treatment had unloaded the cardiac chambers. Murmurs. — This is a comprehensive term, which includes all those adventitious acoustic phenomena connected in some way with the heart's action and not resembling in tone the normal car- diac sounds. They may be primarily divided into endocardial and exocardial. The endocardial are subdivided into organic or struc- tural and inorganic or accidental, called also functional, anaemic, hiemic, and dynamic. Exocardial are divisible into pericardial, pleuropericardial, and cardio-pulmonary. By organic murmurs are meant such as owe their origin for the most part to structural defect or alteration of the cardiac ori- fices or valves — in other words, to definite pathological changes of the structures recognisable after death. Accidental murmurs can- not, on the other hand, be ascribed to definite pathological lesions, and therefore have received a variety of appellations in accord- ance with the various theories offered in explanation of the phe- nomena. Endocardial Murmurs of Organic Origin. — Tliese were once thought to be caused by friction of the blood in its passage over the roughened inner surface of the heart. This theory was shown to be untenable as long ago as 1847, when it was replaced by the one now generally accepted — namely, that currents or eddies are produced in the stream of blood, the same as in any other fluid, 22 DISEASES OP THE HEART whenever it passes a point of constriction in its channel or flows suddenly into a portion of the containing-tube, Avhicli is wider than that directly above. These eddies and currents in their turn generate vibrations which are audible. These secondary currents are the fluid veins first demonstrated by Savart, but applied by Chauveau to the explanation of vascular and cardiac murmurs. Some of the conditions governing their production in the vas- cular system are the following : Constriction of the coats of a ves- sel by external pressure ; projection into its lumen of calcareous plates or masses capable of turning the blood-stream from its direct course ; aneurysmal sacs or vascular dilatations into which the blood-stream may swirl ; and in the heart itself, all pathological changes by which orifices are narrowed and valves rendered in- competent. In addition, murnmrs can be produced by vibration of thin membranes and bands as the l)lood-current sweeps over them. In Virchow's Archives, Band cxl, is one of a series of sug- gestive papers, by Kichard Geigel, wherein he takes exception to the prevailing notion concerning the causation of endocardial and vascular bruits. By a series of nuithematical formula' Geigel en- deavours to prove that if murmurs of tlie })itch of those usually heard were produced by vibrations in the blood-stream these would have to be of a length that would be physically impossible within the cardiac cavities. He therefore states tliat the origin of bruits in eddies and currents is utterly impossible, and declares them due to transverse vibrations of the walls of the structures inclosing the blood-stream. His line of reasoning is ingenious, and to my mind has much to commend it, since the generally accepted theory is not altogether satisfactory. It is this consideration which makes me venture to dwell for a few numients on tlic ex])hinatiou of murmurs ofi^ered by David- son, of Edinljurgh. According to liis tlicory, murmurs are due to vibrations set up in the valves by the impact of the blood-stream at an oblique angle. By niuuerous experiments he claims to have demonstrated that when a stream of fluid was injected into a rubber balloon or a portion of the small intestine, one end of which was tied securely a})out the nozzle of tlic syringe while the other was tightly ligatured, tlu; fluid veins and eddies thus generated at the end of the nozzle witliin tlie elastic receptacle did not pro- INTRODUCTORY 23 (luce more than a very faint murmur, audible by means of a binau- ral stethoscope. When, however, the fluid was made to strike the inner surface obliquely a distinct clear sound was generated, the intensity of which depended upon the force of impact. By re- ducing the rapidity and force of the stream Davidson was able to produce murmurs of varying loudness and roughness. By another set of experiments he was able in the same manner to generate an aortic systolic bruit. The conditions which favour the generation of organic vas- cular and cardiac murmurs are multiform, and hence such adven- titious sounds vary in respect to intensity, pitch, quality, and duration. They also obey the laws of conduction and are propa- gated in different directions, according to the seat and time of their production. Moreover, two murmurs of independent rhythm may be generated at the same orifice, or two or more may be pro- duced simultaneously at different locations. So that if one is to differentiate endocardial murmurs, and correctly interpret their significance, he must be familiar with these various character- istics. The intensity of a murmur bears a direct ratio to the ampli- tude of vibrations in the blood-stream, and therefore to the force of cardiac contractions, and is not at all a criterion of the gravity of a lesion. The forcible escape of blood through a small fenes- tration in a valve-segment, in itself a comparatively trifling regur- gitation, may be declared by a very loud murmur that is audible to the patient, or even to a bystander a number of feet distant. Thus Miller and Gibbs narrate the instance of a girl who pre- sented a murmur of such intensity that it could be plainly heard 12 feet away when the listener was in the same room and patient fully dressed, and 3 feet distant when separated from the patient by a closed door. On the other hand, a very grave valvular affection may, if cardiac power is feeble, occasion a scarcely audi- ble murmur or even none at all. It is well known, for example, that a presystolic murmur of mitral stenosis, intense while the heart is strong, may fade away to complete inaudibility when the heart becomes feeble. Conversely, a murmur scarcely audible during a period of car- diac asthenia may grow in intensity as heart-power is regained. This is the case particularly in aortic regurgitation. In the ex- 24 DISEASES OP THE HEART aniiiiation of a patient \vc therefore avail ourselves of the knowl- edge that forcible cardiac action intensiiies a luurniur l)v having him jnnip about or otherwise excite his heart to bring out an otherwise faint or inaudible murmur. Posture also influences the loudness of these sounds, some being more plainly, others less distinctly, heard in the recumbent position. Those of stenosis are more intense in the erect posture, while those of regurgitation are so in the recumbent. The reasons for such variations in intensity are based on the influence of the force of gravity, which is greater in some than in other positions (Gibson). Mitral systolic murmurs are nevertheless often louder in the upright than the supine posture, an effect to be attributed to the greater vigour of ventricular contraction when the patient stands. There are so many exceptions to the effect ordinarily exerted by position that a patient should always be examined sitting, standing, and reclining. The pitch depends upon the rapidity of the vibrations pro- ducing the murmur. Therefore, some murmurs are low-])itched, while others are high. The union of overtones with the funda- mental tone determines quality, and as pitch and quality go hand in hand, low-pitched murmurs are apt to be rumbling, growling, rasping, etc., while shrill ones are often musical, whistling, filing, sawing, twanging, and the like. Finally, the duration of murmurs is variable, depending on the length of time the vibrations endure. Other things being equal, it requires more time for the blood-stream to pass through a nar- rowed orifice than it does for it to regurgitate tlirough wider os- tium whose valve is defective, and therefore direct murmurs, as those of stenosis are called, are generally of greater duration than are the indirect ones of valvular insufiiciency. Tt may be stated as a general proposition, therefore, that the murmurs of ob- struction are less intense, lower in pitch, less musical in (juality, and of longer duration than are those of regurgitation, which, for the sake of emphasis, may be conversely stated to be higher, louder, more musical, and shorter. There are, however, excep- tions to this law. Fortunately, murmurs generated synchronously yet at different ostia are never identical in these four character- istics, and hence are usually distinguishable fi-oui ciK-h other. It is also of the utmost importance to note the rhythra of mur- INTRODUCTORY 25 murs, since in this way alone can be determined in what period of the cardiac cycle they are produced. They are either systolic or diastolic. Even the murmur of mitral and tricuspid stenosis is diastolic, since it occurs during the pause ; yet, as it is generated at the time of auricular contraction — that is, immediately prior to ventricular systole — it is commonly designated as presystolic, or, as proposed by Gairdner, as auricular systolic. The transmission of a murmur is along the surrounding solid media, and in the general direction in which the stream producing it flows. It is also governed largely by the intensity of the mur- mur. Fortunately for diagnosis, it is this law of conduction which aids in the tracing of a murmur to its seat of production. As already stated, the anatomical locations of the four orifices with their valves are so closely related within a circumscribed area that if the sounds, of whatever nature, were not propagated to certain regions where they can be heard with maximum intensity, their correct interpretation would be vastly more difficult. Every exam- iner of experience has realized the truth of this in the not very infrequent cases in which mur- murs are widely conducted and yet not most distinct in their own areas. Cardiac Areas. — These are four in number, corresponding to the ostia, and are definitely located in circumscribed regions on the chest-wall, where the re- spective valve-sounds and mur- murs are heard most clearly (Fig. 10). Thus the aortic area is located at the junction of the second right interspace and cor- Fig. lO.— Cardiac Valve Areas. responding costal cartilage with Sounds produced at various valves indicated : , , 1 T c , 1 , rrn P^ pulmonary : a, aortic ; /, tricuspid ; m, the border oi the sternum, ihe mitral. sounds, whether normal or adventitious, which are here the loudest, are generated at the aortic opening. The pulmonary area lies in the corresponding situation at the opposite or left edge of the breastbone. The 4 20 DISEASES OF THE HEART pulmonic sounds and nmrniiirs are heard with maximnni intensity in this area, although other bruits may be transmitted thither more often perhaps than to the aortic. The tricuspid area is located at the lower end of the sternum and corresponds quite accurately to the anatomic seat of the right auriculo-ventricular orifice — i. e., between the fourth left chondro-sternal articulation and the junc- tion of the fifth right costal cartilage with the sternum. Aortic^ diastolic, and mitral systolic murmurs are frequently very distinct in this area, while tricuspid bruits may often have their greatest intensity at a short distance therefrom, at either side or below. The mitral area is located at the situation of the apex-beat, but is not confined to this. Aortic regurgitant bruits are often trans- mitted, though feebly, into this region, and mitral systolic mur- murs are sometimes even more audible at some point above and to the inner or outer side of the nipple than directly at the apex. Details regarding the conduction of the various mur- murs may be found in the respective chapters on valvular affec- tions. Before leaving the subject of organic murmurs, although still more applicable to accidental ones about to be considered, I wish to caution against the error of relying upon these abnormal sounds in the diagnosis of heart-disease to the exclusion or subordination of other physical signs. In a sense, murmurs are only guide- posts which point out the way one is to look. They are highly valuable signs, but the information they furnish should be con- firmed by secondary physical signs, if it is to be taken to indicate valvular disease. A murmur may mislead one because accidental, and the failure to hear a bruit may do the same, but secondary signs will not, because they are founded on changes in the heart and circulation brought abo\it l)y the valvular defect. The reader will find more on this topic in the section devoted to valvular lesions. Accidental Murim/rs. — These are adventitious sounds heard in cardiac neuroses and certain blood-states, as chlorosis and various forms of anfcmia. Numerous terms are employed to designate this class of mur- murs, as functional, inorganic, hiiemic, anaemic, spanajmic, and dynamic. The first two imply that there is no structural cardiac affection, and that the murmurs are in some way dependent upon INTRODUCTORY 27 perversion of the heart's function. ILcmic, anipmic, and spanse- mic connnit one to the proposition of an altered blood-state being responsible for the murnmrs. The appellation dynamic carries with it the assmnption that the acoustic phenomena depend upon vibrations set up by powerful, perhaps irregular and faulty, action of the heart-muscle. The term accidental sufficiently declares its own meaning, and implies nothing more than that the murmur is a chance result of cardiac action. Theories to account for these murmurs are many and various, and so long as the condition or conditions governing their produc- tion are not definitely ascertained there can be no term that is not open to objection. These abnormal sounds may be heard in any situation over the organ, but are most frequent in the pul- monic and mitral areas. They are systolic and have a blowing or bellows-like character. Such competent and intelligent observers have advanced diverse theories in explanation of these murmurs that it seems to me the part of wisdom to assume that no one hypothesis is applicable to all cases. May they not have their origin in a variety of conditions, some within and some without the heart ? I shall describe briefly only the more important theories. I^aunyn explained the systolic murmur heard in the pulmo- nary area in cases of chlorosis and other depraved blood-states as being in reality due to mitral regurgitation, and assumed that, instead of obeying the law usually governing its propagation, it is conducted along the left auricular appendix to the tip, which, as we have seen, lies directly beneath the chest-wall in front, some- times overlapping the base of the pulmonary artery. This theory was warmly supported by Balfour, but appears now to meet with general disapproval. Russell proposed two theories, of which one attributed the murmur to narrowing of the pulmonary artery by pressure upon it of the dilated left auricle. In other cases he be- lieved a murmur of tricuspid insuf-ficiency was transmitted into the conus arteriosus, which, in consequence of dilatation of the right ventricle, became displaced outward in the second left inter- space. Hanford claims that the phenomenon, which is either heard only or intensified in the dorsal decubitus, results from the pressure upon the artery of a flabby and dilated heart. Foxwell agrees with Russell as regards pressure in some cases of the dilated 28 ' DISEASES OF THE HEART left auricle upon the artery, but explains other cases as due to a displacement upward of the pulmonary artery and a change in its axis and that of the right ventricle, in consequence of which its normal curve is increased and it is flattened somewhat against the wall of the chest. Bramwell attributes the murmur to the sudden discharge of a large wave of blood of abnormal composi- tion into the probably dilated artery. Sansom thinks that in a condition of right- ventricle weakness toiling to overcome increased resistance in the pulmonic system fibrillar tremors can be initi- ated at the overstrained portion of the right ventricle — i. e., the conns just below the valves — and in this way the murmur in ques- tion can be induced. Gibson holds that auricular or cardiac dila- tation cannot be assumed in these eases because the murmur oc- curs long before such dilatation takes place ; also that the experi- ments on which Foxwell's view is based were faulty ; also that if Sansom's theory is correct, then the murmur ought to exist more often than it does, and therefore advocates the view that it is the murmur of tricuspid insufficiency propagated into the pulmonary area. Quincke, cited by Balfour, concluded, as a result of obser- vations in 6 cases of healthy hearts and arteries, but with retrac- tion of the lung-borders, that a systolic basic murmur can be pro- duced by pressure by the heart of the pulmonary artery against the chest-wall. Vierordt agrees with Sahli that in many cases venous mur- murs are transmitted from the great intrathoracic veins to the heart. Potain urges the cardio-pulmonary origin of accidental murmurs, maintaining they are generated by the impulse of the heart's apex against the lung, an hypothesis that appears sup- ported by an observation of Fran(;ois-Franck's, Avho, during an operation upon a dog, detected a systolic mnrnnir in the region of the apex which disappeared so soon as the processus lingualis was lifted away from contact with the heart, and returned when this portion of pulmonary tissue was allowed to again rest against the surface of the organ. Such cardio-pulmonary origin is especially claimed for the murmurs of ana'uiia. Winckler, on the other hand, believes he has discovered the origin of accidental apex- bruits in a defective action of the p;i])illarv muscles or a faulty insertion of the valve-muscles, which |)ermits of regurgitation. Finally, it has been urged that these murmurs may have a INTRODUCTORY 29 ha?mic origin in eases of pernicious and other grave secondary anaemias, while opponents of this view urge the clinical observation that in such blood-states murmurs are not always present, and, on the other hand, occur when anaemia does not exist. Bearing on this objection are the experiments of Thalma, who found that par- tial exsanguination of dogs did not give rise to accidental mur- murs. A condition of overfulness of the vessels caused by the injection of a warm saline solution into the femoral vein was foUov/ed by their appearance. The number and diversity of the foregoing theories serve but to emphasize the sad fact that in medicine there are still many phenomena which have to be accepted as facts, without a satisfac- tory explanation. In respect to the origin of accidental murmurs, therefore, we can but place ourselves in a judicial attitude and await further proofs. Musical Murmurs. — These are here introduced because I pro- pose to classify them, not according to their acoustic characters or rhythm, but as organic and accidental, depending upon the ana- tomical conditions underlying them. First, organic musical mur- murs are those not infrequently heard in clearly demonstrable cardiac affections, usually valvular. In their time they may be systolic or diastolic, and in pitch and timbre they are variable. Thus they are described as sawing, filing, buzzing, whistling, etc. Their intensity may be such that the patient is annoyed by the murmur, and it is audible several feet distant, or it may require close attention for its detection. Regurgitant musical murmurs are, as a rule, more intense than direct ones. Yet I recall an elderly gentleman who presented a systolic aortic bruit of a strik- ingly sawing quality so loud as to be almost painful to the ear. In the case of a negro observed in my dispensary service some years ago there was an aortic diastolic murmur which was audible a short distance from the chest and had aroused the wonder of its possessor. It was not constant, and when present wholly obscured a soft diastolic murmur that was appreciable when the musical one was silent. Each time the sawing sound was present it was accompanied by a thrill in the third left interspace near the sternum of such intensity that it tickled the palm of the palpating hand. This bruit disappeared some weeks prior to death, and at the autopsy no cause for its peculiar quality could be discovered 30 DISEASES OF THE HEART other than the sclerotic and incompetent semihniar valves. In another man, with a bruit of almost identical characters, except- ing that it was constant, the necropsy revealed sclerotic aortic valves, one of the cusps being fenestrated, and there being two thin fibrous bands stretched between the edges of two of the curtains. This patient was a pauper at the Cook County Poorhouse, and before the autopsy could be made his body was confided to the tender mercies of one of the medical colleges. It was there found, and the heart secured after a lapse of three weeks. The heart was injured by the preserving fluid, pale and softened, so that during the examination of the delicate fibrous bands they were ruptured. Before the photograph was taken two threads of sew- ing cotton were passed through the edges of the valves in rep- resentation of the bands. The examination and preparation of this heart, shown in Fig. 11, were made by Dr. W, A. Evans. In this instance the fenestration permitted reflux of the blood-stream and the regurgitant wave set the bands to vibrating, and thus occa- sioned the murmur and accompanying thrill over the body of the heart, Engel has reported a similar case, in which a fibrous band was stretched across the aortic orifice to a pocket of one of the cusps. The Russian, who under the name of Lewis travels from one medical school to another to exhibit himself to the students, is the proud possessor of a " musical heart." In his case the singing bruit is systolic and of maximum intensity over the right ventri- cle, and by some observers has been thought to indicate tricusjnd insufiiciency and to be generated in the right ventricle at the auriculo-ventricuhir orifice during the reflux. In addition to fibrous bands or cords, some of the conditions causing a murmur to have a musical quality are said to be vibra- tions imparted to the thin, stiflened edge of a cusp or fenestra- tion, or to a delicate atheromatous plaque by the blood-stream as it passes over them. In a case of aortic stenosis with a loud systolic musical murmur reported by Mayne, two fibrous bands were found stretched across the cavity of the ventricle just below the greatly narrowed orifice. In another case of mitral insuffi- ciency, which during life had exhibited a musical murmur at the base and a systolic niui-mur at the apex, Potain discovered post mortem a cord wjiich passed to the wall of the ventricle from the INTRODUCTORY 31 edge of the anterior mitral valve just below the aortic orifice. Demange reported a case of tricuspid regurgitation in which the musical murmur was evidently due to a fibrous band stretched across the interior of the ventricle close to the tricuspid ring. Schroetter has suggested that a musical murmur may be generated Fig. 11. — IxTERioR of Left Vextkicle. Showing fibrous band connecting aortic cusps and responsible for musical murmur. by the vibration of a tendinous cord swinging free in the ventricle, or by one that, as a result of endocarditis, had been ruptured and subsequently attached in an abnormal situation. It is needless to remark that the musical quality of these murmurs possesses a pathological interest, but scarcely a diagnostic significance. At the most we cannot do more than conjecture their mode of 32 DISEASES OF THE HEART causation during life until the true condition is revealed by the autopsy. Accidental musical murmurs are rare, and yet that they da occur is attested by the following case : Miss V. was referred to me by Dr. Charles True, of Kankakee, in the spring of 1897, be- cause of attacks of intense nervousness and agitation accompanied by palpitation and pra?cordial pain, for which no adequate cause in the heart had been discovered. The patient was a farmer's daughter, nineteen years of age, tall and slender, and gave no his- tory of articular rheumatism or any other infection that would have led to inflammation of the cardiac structures. Family his- tory was also negative. The girl was extremely excitable and unable to give a very lucid or intelligent description of her symp- toms further than that she often became frightened, at wdiat was not at all clear, apprehended some imaginary danger to herself or family, and had rapid beating of the heart. During my ex- amination she was much agitated, and the heart action was greatly accelerated, about 120, but perfectly regular. The area of cardiac dulness, both superficial and deep, was not increased, but there was a blowing systolic murmur at the apex, the heart-sounds being sharp and ringing. She was moderately anaemic, and there was a slight enteroptosis. Aside from a not very troublesome fermenta- tive indigestion and constipation, her functions appeared to be normal and the urine was negative. The case was considered one of cardiac neurosis, the murmur accidental, and treatment con- sisted of haematics, laxatives, and remedies designed to lessen the indigestion. The patient was seen by me at rather infrequent intervals, and each time appeared to be somewhat improving. Re- peated examinations of the heart failed to elicit anything more than at her first visit, and the murmur subsequently disappeared. On one occasion, however, she seemed more than ordinarily per- turbed, and her pulse was more rapid than I had ever seen it. During my examination of the heart, which was always made as a matter of routine, I was astonished to hear over the body of the right ventricle a distinct, short, exquisitely twanging murmur of very high ])itch and pleasing quality. It seemed, as well as the tachycardia would allow me to judge, of a systolic rhythm. The action of the heart at the time was extremely rapid and violent. This interesting, and to me exceptional, phenomenon lasted for INTRODUCTORY 33 several minutes, indeed so long as the rapidity of cardiac action endured. When at length her pulse grew more quiet the musical murmur became inaudible and did not reappear. This patient was seen by me in Septe^nber, 1900, after a lapse of more than a year from her last visit, and although I diligently sought for the twanging sound and any signs of cardiac disease, I failed to detect any abnormality. The patient reported herself as in much better health and less excitable, being but rarely annoyed by her former symptoms, and indeed appeared not the least disturbed by the examination. Fig. 12. — Heart of a Buffalo Calf. Showing aberrant chordfe tendinee in left ventricle. The only explanation that has seemed to account for this re- markable phenomenon is that the musical murmur was due to the vibration of one of the so-called aberrant cords (Fig. 12) or mod- 34 DISEASES OF THE HEART ernlor hands, desoribcJ l)v H. F. Lewis. These cords are thin librons bands ruiming along the inner aspect of the wall, or stretched across the upper part of the cavity, or from a })apillary muscle to the sa^ptum. They have nothing to do with the chordne tendina?, and unless care is taken, may be cut in the opening of the ventricle and thus escape detection. Although most frequent in the left, they have been found in the right ventricle, and there are instances of such a band passing from the valve of the fora- men ovale into the cavity of the left ventricle and attached to a leaf of the mitral valve. It is supposed that the function of these moderator bands is to strengthen the cardiac walls in times of overstrain.* In the case narrated it is assumable that owing to the tachycardia the cardiac chambers became overfilled and an aberrant cord was thus put on the stretcli. In this state of ten- sion it was set to vibrating by the energetic and rapid cardiac con- tractions, thus generating the twanging murmur, like that of a violin-string twitched by the finger of the musician. Lewis says it is these al)errant cords which are responsible for the systolic, sometimes diastolic, musical murmur heard before death. Several of the musical murmurs observed in connection with valvular de- fVets have apparently been due to alierrant fibrous l)ands, so situ- ated as to linve been thrown into vibration by the ])lood-stream. The Diflferential Diagnosis of Accidental Heart Murmurs. — Un- osed, from the fact that the latter is so frequently observed in the course of acute infec- ACUT^E PERICARDITIS 45 tious diseases, but may apj^ear during the progress of any one of the chronic forms of kidney disease. Indeed, it is said to be a specially frequent complication of the small red kidney. Ursemia seems to particularly predispose to acute pericarditis, while the supervention of the latter contributes largely to the fatal termina- tion of the primary affection. Most authors content themselves with a statement of the fact and make no attempt to explain the well-known etiological connection between acute or chronic in- flammation of the kidney and inflammation of the pericardium. Two explanations may be given, however. By some the blood of nephritic patients is thought to contain some noxious substance, possibly of chemical nature, possibly of catabolic origin, which results from renal disease, and which in consequence of renal inadequacy is not excreted.* This noxa is an irritant, and gain- ing access to the pericardial cavity, there sets up an irritative in- flammation. Givadinovitch expresses the opinion that acute peri- carditis in Bright's disease is of true toxic nature. It is mostly fibrinous, but may be haemorrhagic and very rarely sero-fibrin- ous, and always occurs in an advanced stage of the renal dis- ease. According to the other less conservative explanation, peri- carditis is a true secondary infection, caused by the conveyance to the pericardium of germs circulating in the blood, and re- sponsible for the acute or chronic pericarditis. In cases of the small red kidney, it is assumed that invasion of the pericardium by bacteria takes place either because the renal disease has im- paired the germicidal action of the blood, or because it interferes with the proper elimination of the micro-organisms. Apropos of the statement that infection frequently occurs in Bright's disease, Flexner's observations may again be quoted. Of 32 cases of chronic nephritis occurring alone, in which there was general infection, micro-organisms were positively identified in * Chatin has reported four cases of pericarditis in patients suffering from nephritis. In three cases with effusion bacteriologic examination showed the fluid to be sterile. In these three cases the serum was hypertoxic. The toxic elements supposed to be responsible for the inflammation of the pericardium have been found neither in the circulating blood nor in the effusion ; and the existence of aseptic and amicrobie pericarditis in certain cases of Bright's disease is well established. The pericarditis of nephritis may sometimes develop as a complica- tion of an ordinary infection, and is usually aseptic or sterile. — Revue de medecine, July 10, 1900. 46 DISEASES OF THE HEART 29. It is worthy of note, however, that in none of these cases was pericarditis present. On the dflier hand, pericarditis was found 23 times in cases of chronic nephritis in which there was local infection, whether the nephritis existed alone or in combina- tion with some other chronic disease, as of the heart or liver. It would seem, therefore, that although a general infection may occur in the course of chronic nephritis, pericarditis does not take place unless there be some other local infection. In the majority of cases of pericarditis in the course of chronic nephritis there was pneumonia, either croupous or lobular. It may be queried, there- fore, whether the pericardial inflammation is not secondary to the local infection rather than to the nephritis itself. Acule Pneumonia. — This infection should certainly be given a place only subordinate to articular rheumatism in the etiology of acute pericarditis. The frequency of this association has been recognised by authors, but has been brought out with special clear- ness by Preble, who found pericarditis in 92.4 per cent of 79 cases of fatal pneumonia collected from the post-mortem records of Cook C^ounty Hospital. Preble came to the conclusion that the danger of pericarditis bears a direct relation to the extent of lung involvement, and is also relatively more frequent in left-sided than right-sided pneumonias. The inflammation of the pericar- dium may result from direct extension through the lymphatics or may occur independently, and is due to the pneumococcus, which has been frequently identified in the exudate. Scarlatina. — This is sometimes complicated by the occurrence of acute pericarditis, and in some cases this has taken place dur- ing the stage of desquamation. As the scarlatinal organism has not been identified in the pericardial effusions, this latter is prob- ably to be regarded as a mixed infection due to streptococci or staphylococci. Bauer observed a post-scarlatinal pericarditis co- incident with rheumatic manifestations, and was therefore inclined to attribute it to the affection of the joints; but inasmuch as pus germs are often responsible for the rheumatic affection, the peri- carditis, as well as the rheumatism in that case, may very well have been an instance of mixed infection following the scarlatina. Other Infections. — Other diseases in the course of whicli acute pericarditis has occasionally been observed are erysipelas, small- pox, tyjjhoid fever, measles, cholera, and even diphtheria. It ACUTE PERICARDITIS 4Y must also be remembered that Flexner found as foci of infection bronchitis, leg ulcer, sloughing myoma, cancer of the stomach, and even tonsillitis and disease of the peritoneum. In some it was probably a secondary event, in others a true mixed infection. When pericarditis complicates acute pleuritis it is generally stated to be by extension. It is, in fact, either a secondary event due to the one and the same cause, or it is a mixed infection. Acute inflammation of the pericardium has been associated with varying diseases of neighbouring parts — e. g., enlarged glands or tumours in the mediastinum, abscess, or caries of a rib, and has resulted from a rupture into the sac of an empyema, from perforation from an ulcer of the OBSophagus or stomach, and even from intraperitoneal abscess. When caused by such conditions the pericarditis is usually purulent. One very remarkable case has been narrated of perforation and inflammation of the pericar- dium by a set of false teeth which had been accidentally swal- lowed and had lodged in the oesophagus, where it caused ulceration. Acute pericarditis is sometimes occasioned by aneurysm of the aorta and by new growths in the pericardial sac — e. g., tubercles. These are capable of setting up an acute inflammatory process of the pericardium, but as a rule the inflammation is subacute or chronic, which probably explains why it so frequently escapes clinical observation. It is doubtful whether gummata ever in- duce acute pericarditis. Haemorrhagic pericarditis occurs as a secondary infection in the course of scurvy, purpura hasmorrhagica, and haemophilia. Some writers also assert that cancer and tuberculosis induce the haem- orrhagic variety. Ebstein has reported two cases of hiemorrhagic pericarditis, and stated that pericarditis was specially likely to be haemorrhagic in the chronic or recurring form, and also in the aged and in the haemorrhagic diathesis. In this condition, he thinks, there is a toxic or infectious cause that creates a tendency to haemorrhagic exudates. Such changes are at least as important as the mechanical ones. The pericarditis secondary to scorbutus may be regarded as a type of this class. It may also occur in alcoholism, which induces the haemorrhagic diathesis. In most cases of traumatic pericarditis the blood found in the sac comes from the bleeding wound. Cases of traumatic origin in which the pericardium is not perforated are harder to understand. 48 DISEASES OF THE HEART Valvular Defects. — Chronic valvular disease seems undoubt- edly to predispose to pericardial inflammation ; tins is said to be particularly the case with aortic insufficiency. Why valvular le- sions should thus tend to the production of pericarditis is a mat- ter for conjecture. By the advocates of the doctrine of the infec- tious origin of all inflammations, it would probably be explained as an instance of secondary or mixed infection, in consequence of the very close anatomical and physiological connection existing between the endocardium and pericardium. Trauma. — Finally, acute pericarditis is sometimes the result of direct injury, as gunshot or stab wounds, blows' upon the chest- wall and laceration by fractured ribs. Under such circumstances micro-organisms are usually introduced into the pericardium, and there set up an acute inflammatory process which, if the cocci be pyogenic, will prove to be suppurative. DRY PERICARDITIS SvN. : Fibrinous, Plastic, Adhesive Pericarditis The pathology and etiology of this form have already been consi(l(n-(Ml, and therefore I shall pass at once to Symptoms. — This disease usually arises during the course of some already existing infectious process, and therefore its inva- sion, and even its subsequent progress, are likely to be masked for a time by the clinical phenomena of the primary affection. In- deed, some authors go so far as to state that there are so few subjective symptoms attending dry pericarditis that it may be said to be a latent afi^ection. In many instances this is probably correct, but I believe the existence or absence of subjective phe- nomena is determined by the degree of intensity and extent of the pericardiiil inflammation. If in the course of acute articular rheumatism there is a sud- den elevation of temperature which cannot ])e explained by the fresh involvement of other joints, or if (Icliriiiin or pronounced disturbance of the nervous system suddenly takes place, especially in children, it is suspicious of some of the lieart-structures having become invaded by the inflannnatory ])rocess. This organ, there- fore, should at once be carefully examined, and if necessary re- peatedly examined, for, according to the fig\ires already quoted DRY PERICARDITIS 49 from Poynton, the pericardium in children is a specially frequent seat of inflammation. If, as thought by Roberts, the opinion appears to be quite prevalent among general practitioners that acute fibrinous pericarditis is not very frequent among children, and not apt to leave serious consequences behind, it certainly would seem to be in place to again call attention to Poynton's figures. Out of 150 fatal cases of rheumatic heart-disease in chil- dren, there was evidence of more or less acute plastic pericarditis in all but 9. In 113 the pericardium was more or less adherent, while in 11 the adhesion was complete. Moreover, the pericarditis appeared to contribute more to the fatal issue than did the endo- carditis, for the reason that the inflammatory process extended from the pericardium to the myocardium and led to dangerous dilatation. Pain. — This is an early and fairly constant symptom, although in some cases it appears to be more like a vague sense of distress than actual pain. It is generally felt in the cardiac region, but may be located in the epigastrium, while in some cases it radiates over the front or side of the chest, even along the course of the brachial plexus into the arm. In a case of this kind described by Sibson there was also endocarditis. Occasionally it is experienced between the shoulders, and is then held to indicate inflammation of the posterior portion of the sac. Baumler has described pain and sensitiveness on the side of the larynx. In some instances there is associated with the pain such a hypersesthesia of the skin of the pra^cordia as to make percussion of the heart almost impos- sible. Painful deglutition has been frequently reported, and is not difiicult to understand when we remember that the pericar- dium is attached to the oesophagus and would be pressed upon by the ingesta in their passage down the gullet. Patients have also been known to complain of the heart hurting them with each contraction, and it may well be that when the covering of the heart is inflamed pain can be felt every time the organ changes in form during systole. In character and severity this symptom differs much in differ- ent cases. It may be sharp and cutting or dull and heavy. In a case observed recently the patient was only able to describe his pain as a steady dull ache over the heart. Usually the anguish is continuous, although in some cases it is intermittent, coming and 60 DISEASES OP THE HEART going like a veritable neuralgia. In others again it assumes a paroxysmal character. The countenance generally betrays suffer- ing by an expression of pain or distress, and the patient not infre- quently keeps his hand upon his heart. Although this symptom, pain, is doubtless due, in large part at least, to the friction pro- duced by the rubbing together of the inflamed pericardial sur- faces, still its intensity depends also upon the sensitiveness of the patient, it being well known that some persons never feel pain so acutely as do others of a less phlegmatic temperament. The pain of pericarditis persists so long as the inflamed surfaces continue to rub against each other, and hence when these become separated by effused fluid this symptom abates or disappears. Therefore, if pain suddenly ceases while the continuance of pyrexia points to continuance of the active inflammation, it may be taken to indi- cate beginning effusion into the sac. Cough may or may not be present, but when present is usually dry and frequent, and when conjoined with pain may give rise to the suspicion of pleurisy. In a fourteen-year-old girl seen not long ago and in whom the inflamed pericardium had led to great car- diac dilatation, with consequent pressure on the left lung, the attending physician at first mistook the case for one of pneu- monia. This case is so instructive that I will briefly rej^ort its salient features. On a certain Friday this girl complained of slight pain and stiffness of one of her legs, but was not prevented there])y from going to school as usual. The following Monday she felt several slight chills, which were attributed to the coldness of the room in which she was at the time. For several days follow- ing she showed signs of malaise, and in other respects did not seem well, yet did not give up and go to bed. Friday night, a whole week from her initial rheumatic attack^ she spent at a friend's house, but when the next morning came was unmistakably ill, and the family doctor was sent for. He found her with a dry cough, hurried respirations, rapid pulse, considerable fever, and a sharp pain in the left side above the heart. Examining tlie lungs, and discovering some dulness and bronchial breathing at the left posterior base, lie pronounced the case ])neumonia — an error that could have been avoided by a proper examination of the heart. Three days later another physician saw the patient, and at once recognised the true character of the disease. When on the ensu- DRY PERICARDITIS 51 ing afternoon I was called in consultation, the cardiac dulness presented the characteristic triangular outline and a systolic apex- murmur was audible, but the friction-sound had disappeared. The case was one of acute pericarditis, as shown a few days subse- quently by the results of aspiration. The amount of effusion was small, however, and the marked increase in the area of cardiac dulness was due chiefly to the dilatation the heart had undergone. It was impossible to say whether the mitral systolic murmur indi- cated a valvular lesion or was relative in consequence of the dila- tation. But as there was a history of some sort of illness three years before, at which time she had " heart trouble," it was feared that the valves were defective and were perhaps sharing in the present inflammation. In this case the pericarditis had probably begun almost a week before she was obliged to give up, so that it is not strange that the process should have induced signs of pres- sure by the end of the first week. This patient ultimately made a good recovery. ^ The pulse in these cases is accelerated, running sometimes as high as 130, or even 140 to the minute, and is usualy compres- sible and regular in the early stage before the myocardium has become much affected. The respirations are usually rapid and often shallow, either because the patient shrinks from taking a deep breath, lest the pain be intensified, or because an actual sense of dyspnoea is ex- perienced. Temperature. — An elevation of body-temperature probably at- tends most cases of acute pericarditis, but is often masked or modi- fied by the fever due to the primary affection. As a rule, the degree of pyrexia is not great, averaging perhaps 102° to 103° F., and being generally continuous or mildly remittent. When it occurs in the course of chronic nephritis, or when it is associated with chronic myocardial or endocardial lesions and independent of rheumatism, the pericarditis frequently runs its course with- out fever, or at all events with so slight a pyrexia as to be over- looked. The duration of the temperature is somewhat variable, depending on the intensity of the infection, but may be said to average two to three weeks. Loss of appetite and other derangements of the digestive tract, as flatulence and constipation, are usually present, the same as in 52 DISEASES OF THE HEART other febrile and acute infectious processes, while the uriiie is scanty and high-coloured. If it contains albumin, this is due to an associated nephritis or depends either upon a primary affection or upon a long-standing visceral engorgement resulting from ante- cedent cardiac disease and is not due to the pericarditis itself. Sleep is disturbed or prevented altogether by the pain and nervousness cai;sed by the inflammation. C/hildren are often fret- ful and restless. The countenance is pale and anxious or expres- sive of suffering. In the spring of 11)01 I treated a gentleman of fifty-five for symptoms of failing heart, the result of chronic myo- carditis and associated vascular and renal changes. He was tak- ing a course of Xauheim baths and seemed to be getting on very well, when I left town for a few days. Upon my return I re- ceived word that he v.^as very ill and in much pain. I found Mr. H. sitting in a chair looking pale and drawn, and when he spoke it was with a hollow, feeble tone of voice. This was Thursday afternoon. He stated that on the Tuesday morning preceding he had been seized with a dull, heavy pain over the heart, which had not left him for a moment since. He had not slept for two nights, and could not lie down on account of his great shortness of breath. The pulse was 106, weak, inclined to be thready, yet regular. His breathing was not noticeably disturbed so long as he was quiet, but his temperature in tlie mouth was 101.2° F. Suspect- ing pericarditis, I yet purposely reserved my investigation of the heart for the last and Avent over the lungs carefully, finding noth- ing more than rides of hypostatic congestion at the posterior bases. Coming to the heart I could detect no change over what had been discovered at my last visit, the Saturday previous, excepting that the tones were much more feeble. The area of dulness did not a])])(>ar increased. I was about to give up, in doubt of the nature of tlio troul)le, when I chanced to catch in a circumscribed location over the roots of the great vessels at the left of the sternum a soft brush- ing iimi'imii- tliat had not been there at any of my exaiiiiiintioiis before. This murmur was systolic and short, not at all like a pericardial rub in rhythm, but u])on ])ressing firmly with the stethoscope I discovered tliat the imirniur entirely disappeared. This convinced me tliat the case was one of acute pericarditis, and, knowing the feebleness of the degenerated heart, I believed DRY PERICARDITIS 53 the attack would prove speedily fatal. A mustard-plaster, fol- lowed by hot fomentations, was ordered, and a nurse was at once secured. At my next visit, four hours later, the pain was miti- gated somewhat, but the patient's condition was manifestly worse. Strychnine, ^\, was ordered hypodermically every two hours, and in addition ^ of morphine with atropine was injected. I left him, feeling that the night was to prove a critical one, and at mid- night I received a telephone message that Mr. H. was failing rap- idly, his breathing being very laboured, and his pulse at the wrist too rapid and thready to be counted. A physician living close by the patient was sent at once and began the administration of stimulants, but with no apparent effect, as the patient died two hours later. It was subsequently stated to me that as his condi- tion grew worse the pain became less. Consciousness was re- tained to the last. J^o autopsy was held, but I believe that effu- sion began to take place, which relieved the pain by separating the inflamed surfaces, and at the same time overpowered by its pressure the degenerated myocardium, which led to rapid asystolism. The insidiousness of onset yet intensity of subsequent sjanp- toms are well shown by the case of Mrs. B., a ISTorwegian, aged twenty-eight, who consulted me in April, 188 Y, " for heart trou- ble." Her mother had died of rheumatic heart-disease under my care, and her younger sister had mitral regurgitation, also of rheu- matic origin. Six years previously, after the birth of her only child, the patient had articular rheumatism and was ailing for a year, yet had not had symptoms of heart-disease afterward. In December, 1886, she had rheumatism in right knee, both elbows, and left shoulder. Three weeks before coming to me she had begun to suffer from prcecordial pains, dyspnoea, and palpitation, each heart-beat accompanied by pain, which was increased by deep breathing and lying down. Percussion occasioned pain, the pain being most marked over the sternum and adjacent left intercostal spaces, from the second to the sixth, particularly in the third and fourth. The patient's face was dusky, the eyes dull, and a systolic pulsation was visible and palpable in the pulmonic area. There was slight epigastric pulsation, and the pulse was regular and feeble. The apex-beat was in the fifth left interspace, somewhat too far to the left, quick, 54 DISEASES OP THE HEART and accompanied by a feeble thrill. Cardiac dulness was in- creased in all directions, and in the mitral area there was a loud, harsh systolic murmur transmitted to the back. All the sounds, especially the pidmonic second, were sharj^ly accentuated, and over the base of the heart was a triple murmur that by its rhythm and other characters was plainly a pericardial friction-rub. Excepting retraction of their anterior margins the lungs were negative. Her temperature and urine were normal. The diagno- sis was mitral insufficiency of rheumatic origin, and acute peri- carditis, probably plastic, and also rheumatic. Patient was sent home to bed and a blister was applied to the pra^cordium. At first, after rest in bed, local applications and salicylate of soda, the j^atient's condition improved, and she was allowed to get up at the end of ten days. In a few days, however, she again took to her bed, and from this time forward her symp- toms steadily grew worse. Cough became very troublesome, with difficult mucous or muco-sanguineous expectoration, and there were anorexia and constipation. The pulse always remained at 120, and as it failed to be slowed by digitalis, the drug was discontin- ued. June 2d there was a sudden attack of acute rheumatism in the left hand and wrist with substernal pain, and temperature rose to 102° F. Salicylate of soda gave prompt relief to pain, and as the urine was scanty and acid, the salicylate was discontinued for the bicarbonate of potash, which was administered until the urine became alkaline. June 6th, at 2 a. m., there was a sudden exacer- bation of substernal jDain and distress. A pericardial friction- sound now developed over the body of the right ventricle, chiefly below and to the left of the ensiform ap2:)endix. There was great epigastric tenderness and interscapular pain. The anterior mar- gin of the left lung became somewhat more retracted, and the apex- beat now moved nearer to the left anterior axillary line. The patient complained much of pain across the front of the chest, along the lines of the diaphragm, from the right inframamillary to the left infra-axillary region. She complained bitterly of pain in the ])it of the stomach, and suffered with nausea and vomiting. June 8th found ])atient much distressed for breath and unable to retain food. Epigastric pain diminished, but condition of the heart very much as before. Fever was 102° F. at 8 r. m. Stimu- lants and food in small amounts were ordered. At 11 i*. m. there DRY PERICARDITIS 55 were sudden defervescence, and profuse perspiration for the rest of the night. June 9th patient orthopnccic, pulse 138, unequal, and weak ; pain abated ; but patient restless. Examination re- vealed dulness of left base, as high as lower angle of scapula. Ex- pectoration scanty ; cough almost impossible ; passed a very bad night; opiates given freely. June 10th, summoned hastily at noon to see patient. Abdomen very distended with gas ; breath very short ; heart very feeble ; carminatives, stimulants, and enemata ordered, but very little relief obtained. Death at Y.30 r. M. Treatment throughout tonic, supporting, sedative, and anti- rheumatic. Autopsy by Dr. Elbert Wing nineteen hours after death. The inner surface of the pericardium was covered here and there with loose fibrous threads, which presented the appearance of cor villo- sum, while upon both the anterior and posterior surfaces of the heart was an area of recent pericarditis. The sac contained a small amount of serous effusion. The myocardium showed changes of chronic myocarditis, probably dating from the time of the previous attack of pericarditis. The mitral valves gave evi- dence of chronic endocarditis that had led to their insufficiency, and showed also the effects of recent endocarditis. There was acute circumscribed pleuritis of the left side with about 8 ounces of sero-fibrinous effusion. In the right pleural cavity were old pleuritic adhesions. The lungs were hypersemic and (Edema- tous. There was subacute diaphragmatic peritonitis, also sub- acute splenitis, and passive congestion of the liver. Kidneys and other organs were negative. In some patients, particularly children suffering from acute articular rheumatism, there may be marked symptoms pointing to profound disturbance of the nervous system. These are jactita- tions, subsultus tendinum, cerebral excitement and restlessness, and low muttering delirium. It must not be supposed that all the foregoing symptoms are of a necessity present in any one case of acute fibrinous pericar- ditis, or that they always have the gravity just described. In one patient pain is the chief complaint, another may be annoyed by persistent palpitations, others may manifest no particular disturbance either of the heart or nervous system. Unless the pericarditis is associated with inflammation of the endocardium, 56 DISEASES OF THE HEART dyspnopa is not likely to be marked iiulil the acute inflammatory process gives place to extensive etfusion. Respiration may be accelerated, but there is not actual air-hunger. In many instances, as previously stated, this affection remains so latent that if the physican were to rely for its detection upon subjective manifestations, the disease would surely be overlooked. For this reason the medical attendant should make daily examina- tions of the heart as a matter of routine practice, in all cases of rheunuitic fever or other infectious diseases capable of lighting uj) ])eri('ardial inflannnation. Course and Termination. — If an acute dry pericarditis is circumscribed, the plastic exudate not involving the whole sac, the activity of the process may speedily subside, and all evidence of its existence disappear in the course of a few days or a week. If, on the other hand, the inflammation is intense, and involves the myocardium, or if the plastic exudate is poured out over the entire organ, the course of the disease may extend over several weeks. In such cases, particularly in children with already existing valvu- lar disease, death is not unlikely, or if the patient recovers, he is likely to be left with a damaged heart. Acute cardiac dilatation is not infrequent, as shown by Poyn- ton's statistics. Indeed, all clinical observers of much experience with pericarditis in children have come to look upon dilatation of the heart as a quite general result, and to regard its occurrence with considerable apprehension. The extension of the inflamma- tion to the myocardium is a matter of grave danger, and one that is likely to result fatally. If flbrin be deposited in a thick layer over the entire surface of the dilated organ, it may act as a me- chanical hindrance to the subsequent return of the heart to normal size. This extensive fibrinous exudation results, furthermore, in an adherent pericardium, which will be described in a subsequent cha])ter. Physical Signs. — T nspeciion. — From the very nature of acute fibrinous pericarditis it is evident that no information of more than a merely negative kind can be derived from an ocular examination of the patient. The countenance may express anxiety or suffering, and inspection of the chest may note some disturb- ance of respiration or an exaggerated and rapid heart-beat; but if there be evidence of deranged circulation this will probably DRY PERICARDITIS 57 be found due to associated cardiac disease, as acute endocarditis, myocarditis, cardiac dilatation, or a chronic valvular defect. Palpation. — In some cases the hand, or, as preferred by Rob- erts, the tips of the fingers, laid gently on the prgecordium, detects a vibration or fremitus, which is the tactile impression produced by those conditions that give rise to the pericardial friction-sounds subsequently to be described. If felt at all, this fremitus is de- tected over the body of the heart, usually in the second or third intercostal space, not far from the left sternal margin. It may, however, in rare instances be detected at different points through- out the pra^cordium. Unfortunately this sign is not often present, but when it exists, it conveys the impression of a rubbing or grat- ing of two rough surfaces, a sort of " to-and-f ro " or back-and-forth rub, which is not strictly synchronous with cardiac systole and -diastole. It is this peculiar gliding character of the friction- fremitus which readily enables one to distinguish it from an endo- cardial thrill. Pressure may modify the intensity of this fremi- tus: moderate pressure increasing, forcible pressure diminishing -or obliterating it altogether. Percussion. — In this form of pericardial inflammation the out- line of cardiac dulness may only be affected in so far as this dis- •ease leads to dilatation of the heart ; in other words, percussion reveals nothing characteristic of plastic pericarditis, or that will be of material service in arriving at a diagnosis. Auscultation. — In the early stage of acute pericarditis of whatever form, and it may be throughout the entire course of •dry pericarditis, auscultation furnishes for the most part our only means of diagnosis. ISTormally, the two pericardial surfaces glide over each other without friction and noiselessly. But when one or both of them have become roughened by fibrinous exudation more or less friction of movement is occasioned, and this is de- clared by the so-called pericardial friction-sound. Before describing this in detail, it may be well to state that .a pericardial friction-sound has also been detected independently of pericarditis. It may be produced by the milk-spots usually found on the inferior surface of the right ventricle, also by con- -cretions (Bauer) ; by dryness of the serous surfaces (Collin and Walsh) ; and by viscosity of the pericardium during an at- tack of cholera (Pleischl), Nevertheless, such facts do not viti- 6 58 DISEASES OF THE HEART ate the truth of the statement that in the recognition of the peri- cardial friction-sound lies onr best and usually our onlv reliable means of arriving at a djagnosis. Location of the Pericardial Frictioiruiurniur. — As this exo- cardial murmur, as it is called in contradistinction to endocardial murmurs of valvular disease, is often very circumscribed, it is important to know where it is most frequently and best heard. This is generally over the body of the heart at the origin of the great arteries upon which the peri- cardium is reflected, or in some cases upon the anterior surface of the right ventricle, very rarely at the aj^ex of the heart. Consequently this friction-sound is audible at the left of the sternum in the sec- ond, third, and fourth left in- tercostal spaces in the same locality as that in which friction-fremitus is commonly felt (Fig. 14). In some instances of extensive pericarditis it is heard at scattered points or throughout the pra^cordium. Rhythm of the Friction-sound. — This is the most important feature of the pericarditic rul), and the one upon which depend- ence is chiefly placed in the interpretation of its nature. It is very variable, but whatever its peculiarity in any given case, it is as a rule not limited to systole and diastole, as are endocardial murmurs. Instead of being synchronous with either the first or second heart-sound, or bearing a definite relation to these tones, the pericardial rub seems to overlap them or to occur at a time that is wholly independent of them. Thus, according to Skodr. it may accompany, precede, or follow the heart-sounds in what seems to be a sort of hit-or-miss fashion. The rhythm is very difficult to describe, but when (nice heard in a typical case is again easily recognised. In most instances the friction-murmur is composed of either two or tliree parts, and when of but two, has a to-and-fro i4. — L'.-LAi. l^.MAIl't.N "Ir i'tlill AlilllAL Friction Sound and Fkemitvs. DRY PERICARDITIS 59 or back-and-fortli rhythm, after the manner of a double aortic bruit, but distinguishable from this by its time and quality. The variability in the rhythm of this sound is owing to the fact that the roughened pericardial surfaces are made to rub against each other either during contraction or relaxation of the auricles or during the corresponding phases of the ventricles. Therefore, when this friction-murmur is made up of three parts, one is pre- systolic, produced by the systole of the auricles, and the other two, of longer duration, fall in the systole and diastole of the ventricles. Very infrequently, according to Bauer, each side of the heart can produce a systolic and a diastolic rub of different duration, so that each heart-beat may be accompanied by four murmurs. Very rarely also a friction-murmur is synchronous with either one or the other heart-sounds, and when this is the case its duration is greater than that of the tone it accompanies, a circumstance by which its true character can generally be recognised. If in such a case one is in doubt as to whether the murmur is exocardial or endocardial, he can generally ascertain its nature by noting the effect of pressure, since this exerts little if any influence upon valvular murmurs. Finally, it should be remembered that a fric- tion-sound may disappear for hours together and then again be- come audible. Intensity of the Friction-sound. — This depends upon two con- ditions : ( 1 ) the nature of the exudate, ( 2 ) the force of cardiac contractions. If the deposit is fresh and semifluid and the car- diac action feeble, the sound of the rub is likely to be indistinct. If, on the other hand, the fibrin is dry and uneven and the heart is beating forcibly, the friction-sound is likely to be loud. Quality, of the Friction-sound. — This differs in different cases, depending probably upon the dryness and viscosity of the fibrin. It may be grating, creaking like leather, crackling like parchment or like the crunching of dry snow beneath the heel, etc., but in my experience is most often of a soft brushing quality, very dis- similar to the timbre of valvular bruits. The Effect of Pressure on the Pericardial Murmur. — It is usually found that pressure with the stethoscope modifies this friction-sound in its intensity if not its quality. Gentle pressure by bringing the roughened surfaces closer together intensifies it, while firm pressure diminishes or obliterates it entirely. It is 60 DISEASES OP THE HEART sometimes found also that the intensity of the murmur is affected in one way or another by the patient's position, being louder in the erect, weaker in the recumbent posture or the reverse. In some cases also the intensity is affected by respiration, being louder when by forced inspiration the pericardial layers are brought into lirmer apposition, and contrariwise enfeebled when separated by expiration. The reverse of this has been observed, however. There is nothing in acute pericarditis per se to cause abnor- mal alteration of the heart-sounds. As stated by Roberts, either tone may be obscured by an unusually loud and harsh friction- murmur, but in general they are heard through the murmur in those cases in which they happen to l)e synchronous. When the inflammatory process has invaded the myocardium or has weak- ened it through dangerous dilatation, the cardiac sounds are likely to become feeble, and the first at the apex may be more or less toneless, but there is nothing in this peculiar to pericarditis. Stasis in the pulmonary system is evinced among other things by undue accentuation of the ])ulmonic second tone, while in conse- quence of the feeble discharging power of the left ventricle the aortic second sound becomes enfeebled. Diagnosis. — The diagnosis of dry pericarditis is not as a rule attended Avith insuperable difficulty. In cases in which it is latent or its symptoms are masked l)y those of the primary affection it may be easily overlooked. In most instances its presence is declared by the history of an antecedent or associated rheumatism, by prsecordial pain, etc., and by the character- istic rubbing thrill and murnuir. When the anamnesis and symp- tomatology are negative, reliance must be placed upon the auscul- tatory phenomena, and these failing, a correct diagnosis is hardly possible. Differential Diagnosis. — This concerns acute endocarditis, pleurisy, and pneumonia. The diagnosis of acute endocarditis is hardly possible unless valvuhir murmurs and other definite changes in the sound that the exudate was fibrinous, or if united with serum, the proportion of the latter was not large. The ex- tensive dilatation present was attributed in part to the mitral lesion, and in part to the dilating influence of the pericarditis, Avhether associated with acute myocarditis or not. The symptoms in this case were not distinctly those of pres- sure ; respiration was greatly accelerated, to be sure, but there was no cyanosis, no downward displacement of the liver, and no orthopncea; in short, the symjitoms pointed more to disturbance of the nervous system, with consequent rapidity of breathing, than to circulatory embarrassment. The very considerable hepatic en- gorgement could be very reasonably referred to the free mitral leak and the greatly overstrained right ventricle. This patient ultimately made a good recovery. On the same day on which I saw the preceding patient. Dr. Jo- sephson asked me to visit a little girl of six, who was also suffer- ing from acute pericarditis. She had ])assed through an attack of scarlatina in the Jnly preceding, and for the past three or four weeks had been suffering from acute articular rheumatism, which PERICARDITIS WITH EFFUSION 71 was still present when slie came nnder the doctor's charge eight days before my visit. lie had at once recognised an acute inflam- matory affection of the heart. Her somewhat fluctuating tempera- ture had averaged about 102° F. The child's condition when I saw her was as follows: She was sitting in bed, not even venturing to rest against the pillows, breathing 60 or more times to the minute, and during the forenoon of that day her respirations had actually been 90 to the minute. The pulse was very rapid, small, and dicrotic, but perfectly regu- lar. The expression one of patient sufi^ering. Upon removal of the clothing the skin was found hot, dry, and scaly, yet broke out into a perspiration a few minutes afterward upon the child There was every evidence of capillary The making a little exertion and venous congestion. abdomen M'as distended and hard, particularly about the waist-line ; the thorax was evi- dently distended to its utmost capacity, the entire front of the chest bulging, and the in- tercostal spaces more or less smoothed out. The apex-beat was feebly palpable below and a little to the left of the nip- ple, and there was diffused systolic shock over the body of the organ. Absolute cardiac flatness (Fig. 17) began at the right nipple, passed upward to the first interspace, then downward and outward into the left axillary region, well outside of the visible and palpable apex-beat. Its lower boundary reached at least to the eighth costal cartilage, and the distended sac could be felt in the epigastrium. A rough, blowing systolic murmur was very loud in the mitral area to the left, while the heart-sounds were loud over the base of the organ, the pulmonic second being very banging and slightly split. From the middle of the sternum down- ward to the ensiform was a grating pericardial friction-sound, which had a simple to-and-fro rhythm not synchronous with either 17. — Absiiute Dii.m;--. i ase of Pericarditis with Effusion. T2 DISEASES OF THE HEART systole or diastole. At the left base, posteriorly, was a dull patch corresponding with Ewart's dull patch in outline, but the harsh, very hurried breath-sounds were everywhere audible. In front, resonance was impaired beneath both clavicles, and the sense of resistance imparted to the finger upon percussion of the prsscor- dium was remarkably intense. In this case the diagnosis was also acute pericarditis, but, unlike the foregoing, there was a massive exudate, occasioning very grave pressure-signs. There was also present the same valvu- lar lesion, mitral regurgitation, but there was very strong suspi- cion of the existence of acute endocarditis, since from the history of scarlet fever in July, with more or less rheumatism subse- quently, with no other previous etiological factor, it was not likely that the mitral disease dated back more than six months. Deglutition gave this little sufferer so much distress that she would hesitate for minutes together before making up her mind to take the proffered medicine or nourishment. In this case the urgency of the symptoms arose from pressure. Dyspnoea was so great that the little thing begged to be allowed to stand up, evi- dently to relieve the thoracic organs, already much compressed, from still greater pressure by the abdominal viscera forced upward against the diaphragm in the sitting position. The contrast presented by these two cases was most instructive. In this latter case paracentesis pericardii was advised without delay. It would have been cruel, if not useless, to postpone the operation until trial had been made of cathartics and diuretics. Far better tap first, and administer these afterward. Suppurative pericarditis generally occasions ])honomena of sepsis, but chills, fever, and sweating are sometimes said to be absent (Koberts). When present they are an indication of sepsis, and as such may be a part of the symptomatology of the primary affection as well as of the pericarditis. When the effusion is foetid, as rarely happens, septic symptoms are most marked, and pros- tration comes on early and is extreme. In some cases there is nothing in the nature of the sym]>toms whoreby one may deter- mine the purulent character of the exudate. The symptomatology of hwrnorrliagic ])(M-ioarditis depends upon the rapidity with wliicli the eftiision takes ])lacc, rather than upon its nature. A lia-iiKirrhngic cff'usion into the pericardial sac PERICARDITIS WITH EFFUSION 73 during the course of scorbutus, for example, may take place so suddenly that symptoms of pressure aud of anaemia rapidly de- velop. In other cases the effusion is slowly produced, and symp- toms manifest themselves gradually or are entirely absent. In Ebstein's two cases the symptoms were those of pressure, cyanosis, dyspnoea, cough, and pain, but in one the condition was thought to be extreme cardiac dilatation, and its true nature was not recognised until at the autopsy. Although in the second case pericardial effusion was recognised during life, there was nothing in the symptoms to point to the h?emorrhagic character of the exudate. Course and Termination. — There is no uniformity in the clinical history of pericarditis with effusion. Cases vary widely from each other in the mode of onset, in the course they pursue, and in their mode of termination. An ordinary case occurring during a rheumatic attack may be expected to terminate by absorp- tion in two to four weeks ; this happy event may very rarely take place within a few days, the disease having passed through the suc- cessive stages of inflammation, effusion, and absorption in less than a week. In other instances the affection manifests a strong tendency to become either subacute or chronic. While in others, again, the disease is characterized by phases of partial absorption and improvement, which are each in turn followed by a recurrence of inflammation and increased effusion (Bauer), until at length the patient is worn out by the persistent and obstinate nature of the disease. These variations depend, no doubt, upon the activity of the etiological agent, and are not at all surprising, for, as every one knows, no disease presents uniformity in its clinical phenomena. Other conditions besides the activity of the pathogenic agent also determine the course and severity of an acute pericarditis. Its occurrence with or as a sequel to pleurisy or pneumonia is also likely to influence its course and termination, in accordance with the intensity of these latter processes and the degree to which they have undermined the patient's resistance. When pericarditis is the result of chronic nephritis it is very likely to run a slow and latent course. In children with inflammatory rheumatism the disease is apt to prove persistent, and if it does not destroy life by invading the myocardium, terminates in complete or partial synechia pericardii. 74 DISEASES OF THE HEART Suppurative pericarditis is a very serioiTS affection, manifest- ing but little tendency to spontaneous recovery. It is stated, how- ever, that if the pyogenic bacteria be not very virulent, and if life be prolonged for a considerable time beyond the stage of active inflammation, absorption of the more liquid portion of the exu- date may take place, the residue becoming cheesy and in time in- filtrated with lime-salts. They are eventually transformed into calcareous plates, which may even be so extensive as to inclose the heart in a case of bone-like hardness. I have observed two such cases ; in one a calcareous plate the size of a silver dollar was found on the anterior surface of the left ventricle, while in the other, masses of lime completely surrounded the organ. This latter case will be described in the article on Adherent Pericar- dium. Most cases of purulent pericarditis, unless relieved by sur- gical interference, pursue a rapid course, and jDatients succumb more or less speedily to the etTects of py?emia, resulting either from the pericardial or primary affection. In the form of ha?morrhagic pericarditis, which occurs in the course of scurvy and is observed in the maritime provinces of Russia, the effusion often takes place with great rapidity and destroys life in one or two days. In these cases death seems due in no small measure to the rapidly induced anaemia. Finally, the course of acute pericarditis with effusion is deter- mined not alone by the intensity of the inflammation, but by the amount of the exudation. If this is sufficient to greatly distend the sac, its absorption is hindered by the tension thus occasioned. In some instances, no doubt, a pericardial exudation is absorbed, and no permanent ill effects remain. Physical Signs. — Inspection. — The degree of information afforded by insj)cction depends upon the amount of effusion and the conditions residing in the chest-walls. In a child of tender age or a person with a yielding chest-wall a comparatively small pericardial effusion may occasion perceptible prominence of the praecordium, while if the thorax is voluminous, and the costal car- tilages have become hard and inelastic from age, it is possible for even an enormously distended sac to produce no visible bulging of the cardiac area. As a rule, however, more or less prominence in this region is observed, wliilo the intercostal spaces look filled out, and the skin covering them appears tense and shiny. The apex- PERICARDITIS WITH EFFUSION Y5 beat is not visible, or but faintly so, and cardiac impulse is feebly diffused or wanting. The apex-beat, moreover, if visible, may be situated lower than normal when the liver is depressed by a mas- sive effusion, and in such a case there may be bulging of the epi- gastrium. Cyanosis and distended veins give evidence of circulatory dis- turbance, while respiratory embarrassment is evinced by hurried breathing and restricted movements of the chest. If copious effu- sion occasions great ]3ressure, and particularly if this has formed rapidly, the attitude of the patient and the expression of his coun- tenance betray suffering and it may be oppression. Inspection is an aid to diagnosis, but cannot solely be relied upon, since precordial bulging in children may be the result of cardiac enlargement without pericarditis. Palpation. — In great effusion the roughened pericardial sur- faces are removed from each other, and hence the hand no longer detects the peculiar fremitus present in the beginning of the pro- cess, when the exudate is fibrinous and not serous. Otherwise paljDation serves chiefly to corroborate the result of inspection. The prsecordial area may impart a sense of increased resistance from internal pressure, and the normal intercostal de- pressions are found obliterated. Rarely there is fluctuation. In- creased resistance and tension may also be detected in the epigas- trium. Older writers were accustomed to attach great importance to an elevation of the apex-beat, which they explained by lifting of the apex of the heart by the effused liquid. Roberts, Ewart, and others regard this as erroneous, believing that w^hat was thought to be the apex-beat is, in fact, the impulse of the body of the heart as it is thrown against the anterior chest-wall by the collection of fluid behind, the apex of the organ being at the same time moved backward and to the left. In cases of extreme effu- sion the depression of the diaphragTn, occasioned by the heavy sac, leads to an actual lowering of the apex-beat (Bauer). The peri- cardial fremitus present during the inflammatory stage disappears with the occurrence of effusion. In some cases the head of the left clavicle is said by Ewart to be elevated so that the first rib can be felt all the way to the sternum (" first-rib sign "). The most striking character of the pulse is its want of tension. It is rapid and may be regular or irregular, even intermittent. In 76 DISEASES OF THE HEART some instances pulsus paradoxus is present. This is an inversion of what is usually observed during the two acts of inspiration and expiration. Instead of becoming stronger and fuller at the end of inspiration and the beginning of expiration the pulse becomes small and weak, or may even disappear during deep inspiration, becoming again stronger and fuller toward the end of expiration and the beginning of the next ensuing inspiration. Pulsus para- doxus is inconstant and is not pathognomonic when present, and possesses therefore only a negative value. Percussion. — This method of investigation furnishes the only reliable sign of pericardial effusion, since by this means one is often able to determine the presence of so small an amount as 100 cubic centimetres (Bauer), 150 to ^00 cubic centimetres (Aparti and Figaroli). That one may understand why so much reliance is to be placed upon percussion, I will consider for a few moments in what way pericardial effusion alters the normal relation of the parts and modifies the area of cardiac dulness. The pericardium is a closed sac, which is thrown around the heart, being wrapped about the origin of the great vessels above, and attached to the central tendon of the diaphragm below. When fluid is effused into this closed cavity it sinks to the most depend- ent part, and then creeping upward distends the sac in all direc- tions, pushing aside the anteri(U' borders of the overlapping lungs. The area of absolute cardiac dulness now becomes altered in a striking manner (Fig. 17), and to an extent commensurate with the amount of effusion. Some authorities consider that this alter- ation of cardiac dulness corresponds in shape with that of the dis- tended sac (Bauer, Sibson), while others attribute it chiefly to the crowding aside of the lung-nuirgins (Duchex, Rotch). My own opinion is that the configuration of this area depends largely upon the anatomical arrangement of the lung-borders overlapping the heart, since when they become retracted by adhesions and in cardiac dilatation, the shape of the resulting dulness is essentially the same, though less extensive, as in pericarditis with effusion. Probably both factors, the sha])e of the sac and the arrangement of the lung-l)orders, are responsible for the peculiar outline of the area of dulness observed. This area of absolute dulness or flat- ness is variously described as triangular, pyramidal, pear-shaped, or pyriform, that of a truncated cone, or '' that of a bag of fluid PERICARDITIS WITH EFFUSION 77 spreading out at the base"' (Ewart). Its broad base rests upon the diaphragm, while its rounded apex occupies the upper sternal region. A glance at Fig. 17 shows that the direction of the two side-lines is not the same, being rather more vertical at the right. The right arm of this irregular triangle is shorter and straighter, while the upper or left boundary presents an indentation or con- cavity soon after leaving the apex, and, sloping gradually down- ward, joins the base-line at a rounded somewhat obtuse angle. The shape of this area is by most authors considered very char- acteristic, although Shattuck is of the opinion that the peculiar feature is not the form, but the fact that the dulness spreads out in all directions. Rosenbach lays stress on the increase or movabil- ity of dulness to the right when the patient lies on his right side. Although Bauer agrees in the statement that the flat area of pericardial effusion may be recognised by its characteristic pear- shaped outline^ he nevertheless expresses the opinion that more importance should be attached to the surrounding zone of relative dulness, " since, indeed, the absolute cardiac dulness not uncom- monly in cases of well-marked effusion show^s little or no altera- tion." In cases of extreme pericardial effusion the base of this flat area may extend nearly across the anterior surface of the chest, from within, or in some cases even outside the right mamillary line, to a variable distance outside the left mamillary or to the left anterior axillary line. In consequence of the depression of the left lobe of the liver caused by the weight of the distended sac, the inferior margin of this area may reach as low^ as the sixth, or in extreme cases even the seventh left intercostal space, while its broad conical apex may extend as high as the level of the second costal cartilage or the first interspace. When this flat area has attained such proportions it is usually not difficult to determine the nature of the case. Yet, since a greatly dilated heart may also crowd aside the lungs and occasion a similar extension of the area of cardiac dulness, error can only be avoided by attention to the following points: (1) When the pericardial sac is distended by fluid its left latero-inferior bound- ary extends beyond the situation of the apex-beat, and hence this latter, as determined by auscultation, is found situated within and above the extreme left lower angle of cardiac dulness. In dilata- 78 DISEASES OF THE HEART tion of the heart, on the other hand, it is the organ itself which determines the dulness, and therefore the apex-beat corresponds with the onter and lower limit of cardiac dulness. Leube lays great stress on this point in the differential diagnosis of these two conditions. (2) In cases of pericardial effusion the line of de- marcation between the area of flatness and surrounding pulmo- nary resonance is very abrupt, while in cardiac dilatation the transition from flatness to resonance is much less pronounced. Bauer and Sansom both attach great importance to the abruptness of this transition in cases of pericardial effusion. At the same time one should not forget the fact that occasionally the distended sac may be overlapped by the lungs, and therefore absolute dulness may shade off through a surrounding zone of comparative dulness into full pulmonary resonance. When pericardial effusion takes place the first change notice- able upon percussion is the development of a small triangular area of dulness in the fifth right in- tercartilaginous space, or, as the Germans term it, in the cardio-hepatic angle (Fig. 18). This sign, first described by Rotch, and sometimes called Botch's sign, is due to the fact that when eft'usion collects it first distends the sac at its lower right corner, occupying the space between the curved inferior margin of the heart and the upper line of hepatic dulness immediately to the right of the lower end of the sternum. Ewart and Ebstein have also directed attention to the occurrence of this small triangular dull patch. Xormally, the outer bound- ary of cardiac dulness over the right auricle presents a curved line, passing from the level of the third costal cartilage downward and outward, and, after crossing the fourth cartilage, passes in- ili.. i^. i;tedly they should be employed, their utility is open to doubt. I pass, therefore, to the considera- tion of the second object of treatment. In some cases effusion takes place with such rapidity and in- PERICARDITIS WITH EFFUSION 91 duces such urgent pressure-symptoms that surgical interference has to be resorted to without delay. More often, however, indi- cations of pressure appear slowly, and time is afforded for a trial of medicinal treatment. Absolute rest is now imperative, and the patient, if old enough, must be advised of the necessity of refraining from any sudden movement, lest it occasion fatal syncope. He should be supported in a semi-recumbent posture by a bed-rest or pillows, and he must not be allowed to sit up to take nourishment or medicine. He should be disturbed as little as possible for the purpose of examin- ing the heart. The state of the circulation, as shown by pulse and venous engorgement, is to be carefully watched, and so long as the quality and rate of the pulse remain good, strychnine may be the only heart-tonic required. So soon, however, as the pulse shows dicro- tism or irregularity in force, size, and frequency, tincture of fat- free digitalis must be ordered in doses suitable to the age of the patient — to an adult 10 drops every four to six hours. The daily quantity of urine should be accurately noted, and in these cases a pronounced falling off of its amount is an indication for digitalis, even though the pulse remains fairly good. Careful examination of the liver will always detect more or less engorgement of this organ. Palpation of the liver is often painful or unsatisfactory by reason of abdominal distention, but we know by experience and deduction that stasis within the por- tal system is taking place, and hence hydragogue cathartics form an important, nay an indispensable, part of our therapeutic meas- ures in this stage. By depleting the portal system catharsis aids in maintaining the venous circulation. Instead of weakening the patient, it adds materially to his comfort by lessening epigastric pain and relieving abdominal pressure. Sleep should be induced by a hypnotic, for nothing will more surely tend to exhaust the nervous system than insomnia. I have sometimes foimd that the addition of a :^ or ^ grain of codeine to a sulphonal powder insures the action of the latter. At this stage morphine or a preparation of opium is to be given with very great caution. It may be indicated by dyspnoea or restlessness, but actual danger attends the administration of the drug, through its depression of the respiratory centres. If it be given to allay the 92 DISEASES OF THE HEART dyspnoea, atropia should always be added to the morphine, because of its well-known effect in deepening respiration. The passive congestion within the abdominal cavity impairs digestion and lessens absorption, yet nourishment is imperatively demanded, both by the nerve-centres and heart-muscle. Only such food should be given as can be easily assimilated, and as but a small amount should be taken at a time, it should be concentrated and highly nutritious. Some of the prepared foods will now be found to be of great service. When by the subsidence of the pyrexia, if that has existed, it is judged that the active inflammatory process has ceased, or when repeated examinations of the heart indicate that the amount of effusion is stationary, the query naturally arises. What means are to be employed for its removal \ Shall an attempt be made to promote this by absorption, or shall paracentesis pericardii be per- formed? This brings up the question, is absorption of the effu- sion possible ? Clinical experience certainly gives an affirmative answer. Theoretically, absorption of the exudation may be hin- dered or prevented by an abundant coating of fibrin over the surface of the pericardium whereby the fluid cannot reach the Ijmiphatic spaces, or in consequence of great venous stasis the lym])hatic vessels may be surcharged, and the flow in them be too sluggish to promote active absorption. Xevertheless, particu- larly in rheumatic cases, experience affords abundant proof of the frequent, even rapid, absorption of extensive jiericardial effusion. Therefore, I believe the physician is culpable who refuses to make the atteni])t at least to carry off the fluid ])y a resort to diuretic and cathartic remedies. xV great degree of venous stasis often neutralizes the effect of diuretics until congestion within the renal veins has been relieved by resort to hydragogue cathartics. The two classes of remedies should be conjoined therefore. In my opinion, the infusion of digiiaJifi affords the best means of estab- lishing free diuresis. A tal)les]K)onful to begin with may be ad- ministered to ail ailult every four iioiiis. wliilo tlie patient also receives daily some unirritating cathartic, ca])able of inducing a number of copious watery stools. I have seen truly astonishing results follow such a plan of treatment. This is well illustrated by the case of a boy of seven years with mitral regurgitation of PERICARDITIS WITH EFFUSION 93 rheumatic origin, in a state of perfect compensation, who had been under occasional observation for a year. On May 9, 1899, he developed what appeared to be a mild case of follicular tonsillitis, for which he received appropriate treat- ment. Three days later he Avas reported not so v^^ell, and at my visit that same day he was found to have a temperature of 101° F. He comjDlained of vague pains in the knees, which were not red- dened or swollen, but showed an erythema. As the attack was un- doubtedly rheumatic, salicylate of soda was ordered, and as the boy lived in a suburb he was put in charge of a local physician. May 28th I was asked to see him again, when a prsecordial fremitus, which disappeared upon pressure, and a soft to-and-fro murmur, quite different from his endocardial one, with which I was so familiar, left no doubt of the existence of an acute pericarditis. The attending ph^^sician stated that these friction-murmurs had developed a few days previ- ously. By June 5th the actual increase in the area of cardiac dulness gave evidence of the occurrence of effusion, though the cardiac impulse and fric- tion-sounds still persisted over the body of the organ. Py- rexia was moderate, pulse 120, of good quality, and respira- tions were accelerated. An ice-bag had been worn most of the time since May 28th, although pain had at no time been a very marked feature. From now on the exudation increased steadily in amount until, by June 28th, the ex- treme limits of cardiac dulness reached from just within the right nipple, quite to the left axillary line, far outside the easily located apex-beat (see Fig. 20). The persistence of the pericardial rub, somewhat less intense, to be sure, together with palpable cardiac impulse over the body of the heart, and the distinctness of the heart-sounds and of the Fig. 20. — Apex-beat and Akea of Cardiac Dulness in Case of Pericarditis with Effusion. 94 DISEASES OF THE HEART mitral regurgitant inuriiuir, were thought to indicate the existence of adhesions on the anterior surface of the organ and to have prevented the eifused fluid from covering over the heart. That the effusion was considerable was evinced by the great distention of the sac laterally and downward, by great pressure upon the lungs, and pronounced circulatory embarrassment. There were marked cyanosis, distention of the superficial veins, great enlarge- ment and tenderness of the liver, and slight ankle oedema. Respi- rations were 48, pulse 146, small, and dicrotic, but still regular. Salicylate of soda had been discontinued upon appearance of the effusion, lest it might too greatly depress the heart, and as the scanty urine was highly acid, bicarbonate of soda and citrate of potash had been substituted. As digitalis and mild cathartics had failed to appreciably diminish the amount of effusion, surgical interference was decided upon. The selection of the site of puncture was left to me, and, be- lieving that in consequence of adhesions over the front of the heart the exudation could be most surely reached at some lateral point, I selected the fifth left interspace, between the apex- impulse and the outer margin of flatness (Fig. 21). Accord- ingly the surgeon introduced his trocar in that situation and obtained fluid. This was dis- tinctly bloody in appearance and so surprised the operator that after ixn-mitting an ounce or two to flow he withdrew his cannula for the purpose of dis- cussing the significance of the blood. We concluded it was a hu'morrhagic effusion, and ad- vised a fresh tapi)iiig. This was now objected to by the ])are)its on the ground that once at a time was enough, and a repetition of the |)rocedure was deferred. It was never repeated, however, and because of the following considerations: 'Jl. — 'I'lIK VAIilors SiTi;- I'.i: I'l \. II i;l' IV Paisacentesis Pekicardii. Dotted line indicates course of interniil main mary artery. PERICARDITIS WITH EFFUSION 95 The great obstacle to absorption was believed to lie in the enor- mous congestion within the portal system, and the boy's dis- tress was due not so much to pressure from the effusion as to the extreme stasis within the abdomen. Tapping the pericar- dium might relieve the heart, but with all the conditions pres- ent in the mitral regurgitation for the maintenance of hepatic engorgement it could not materially improve the state of things in the portal system. Consequently, with the heart-muscle show- ing no very threatening signs of failure, it was thought best to make one last vigorous onslaught on the stasis within the hepatic vessels. Accordingly a drachm of the saturated solution of Epsom salts was ordered hourly until it began to exert effect. At the same time a drachm of the fresh infusions of digitalis made from English leaves was prescribed every four hours. The results were astonishing. Several doses of the magnesia sul- phate were taken next morning without any very marked effects upon the bowels, but instead the kidneys began to act, and in the next twenty-four hours diuresis amounted to something like 8 quarts. Islot only did the patient's dyspnoea lessen, but the area of cardiac dulness began promptly to diminish in size, the liver became softer and less tender, and the patient's improvement was clearly noticeable even to his parents. The salts were con- tinued daily, though with gradually diminishing amounts. After two or three days sirup of squills was added to the infusion of digitalis, and the progress towards recovery continued without in- terruption. This little patient lived nearly three years, and then died from a fresh pericarditis, with signs of dilatation, but not effusion. Some are sceptical concerning the efficacy of medicinal treat- ment in promoting absorption, basing their objections on the fact that absorption sometimes sets in spontaneously, even after the pericardial effusion has remained stationary for some time. Nevertheless, in this case, the change for the better began so soon after the administration of the magnesium-salt that I believe it can be justly regarded as an instance of propter hoc, not post hoc. Unfortunately, the result of therapeutic measures is not always so brilliant as was this. The effusion persists in spite of hydragogue cathartics and diuretics, or the exudation takes place so rapidly and copiously that it threatens to overpower the heart before time 96 DISEASES OF THE HEART is allowed for remedies to exert their effect. In either event the pericardium ought to be tapped, and it is best not to delay. It seems to me there can be no question concerning the indication for paracentesis in such cases, but early in the disease I see no call for surgical interference so long as alarming pressure-symp- toms do not supervene. Sites for Puncture. — Properly performed, this operation is safe, and as it is likely to afford prompt relief, one should always stand ready to tap whenever such intervention is indicated. The indications are not always found in dyspnoea, cyanosis, and rapid- ity of the pulse; these symptoms are present in all cases of peri- cardial effusion of considerable amount, but indications are present whenever the heart shows evidence of dangerous weakness by syn- copal attacks and intermittence, or when sufficient time having been given for spontaneous recovery, or for absorption through medicinal treatment, these do not take place. Paracentesis being decided on, it only remains to select a suitable point for punc- ture. Various sites (see Fig. :21) are recommended, and all aim at reaching the fluid most readily without fear of w^ounding the heart, internal mammary artery, or other structures. The point most usually recommended is in the fifth left inter- costal space at a safe distance from the internal mammary artery. As this passes downward from 7 to ^ inch from the edge of the sternum, the needle may be introduced either very close to the sternal border, so as to be between it and the vessel, or at the outer side of the artery 1 inch or more from the bone. Potch pre- fers the fifth right interspace close to the sternum, since at this point the sac is sure to be distended, even should the amount of fluid prove smaller than is anticipated. Shattuck has ])unctured in the fifth left S])ace, 1 to 2 inches outside the ni]iple-line, just witliin the left lateral border of cardiac dulness, where, as a mat- ter of fact, I advised ta])ping in the case narrated, although at the time I was not aware of Shattuck's recommendation. The objec- tion urged against this site is the possibility of wounding the pleura at this point. Tliis is, of course, a cogent reason, yet if the sac is greatly distended it will have ])ushed the border of the left lung well aside, and the pericardium will occupy the region normally filled by the lung. In my case fluid was readily reached, and the surgeon was confident he did not touch the pleura. An- PERICARDITIS WITH EFFUSION 97 other point at which the sac can often be safely pierced in cases of extensive effusion is in the angle between the left margin of the xiphoid cartilage and the adjacent costal cartilages. The fluid tends to gravitate to the bottom of the sac, and consequently weighs down the diaphragm and left lobe of the liver, so that if the needle is thrust upw^ard and backward there is very little danger of wounding the diaphragm. For additional particulars concerning paracentesis, as well as incision of the pericardium, the reader is referred to works on surgery. Whether all the effusion possible is to be withdrawn, or whether only a portion, sufficient to lessen the pressure and favour subsequent absorption of the remainder, is a matter that must oe left to the judgment of the operator. Personally, I advocate the removal of the whole or of as much as can be taken without danger of the heart coming in contact with the point of the needle. Theoretical considerations suggest the expediency of following the operation by the administration of diuretics and heart-tonics. The latter include digitalis and its congeners, which sustain and strengthen the heart-muscle while at the same time they increase pressure in the renal artery, and thus re-enforce any other diu- retic remedies. The emplojanent of such agents serves to deplete visceral congestion and to thus enhance the benefit derived from the withdrawal of the fluid which is the original cause of the stasis. The treatment of purulent effusion should be surgical. Should the nature of the primary infection and symptoms of more or less pronounced septicaemia suggest that the pericarditis is suppura- tive, the character of the exudate should be determined by explora- tory puncture, and if this prove to be pus, it should be evacuted without delay in accordance with proper surgical methods. Lil- ienthal, of l^ew York, reported before the JSTew York Academy of Medicine a case of suppurative pericarditis, occurring in a lad who was recovering from pneumonia, affecting three lobes. Eight- een ounces of pus w^ere withdrawn at the time of the exploratory puncture, and 40 more at the time the sac was cut down upon and opened. The pus contained numerous pneumococci. The tem- perature had been irregularly intermittent. Complete recovery followed the operation. Eucaine was used as a local anaesthetic. Hcemorrhagic effusion is to be managed according to the prin- ciples governing the treatment of the sero-fibrinous form, no spe- 98 DISEASES OF THE HEART cial indication for treatment being presented bj the bloody charac- ter of the effusion. Xo great effect is to be expected, however, from either medical or surgical treatment in those cases in which the affection is associated with a serious blood-state or djscrasia, and measures should be directed to the removal of these latter. The subsequent management of a patient convalescing from acute pericarditis consists in such measures as will rapidly restore the general health and heart-tone in the hope that the organ may not be left seriously damaged. We possess no means of either preventing adhesions or promoting the absorption of fibrinous deposits. CHAPTER II CHRONIC PERICARDITIS Syn. : Adherent Pericardmm, Synechia Pericardii, Concretio Pericardii sen Concretio Cordis Chronic pericarditis may be divided into two great groups: (1) That in which it involves only the two layers of the sac, peri- carditis interna chronica, and (2) that in which the process in- volves both the pericardium and mediastinum, pericarditis in- terna et externa chronica. In both of these forms inflammation results in the formation of fibrous tissue, which binds the parts more or less closely and extensively together. There is still an- other much rarer form in which the chronic inflammation is asso- ciated with serous distention of the sac, and is termed therefore chronic pericarditis with effusion. Adherent pericardium is the term most commonly applied by English writers to the first form, while the second is known as chronic adhesive {s. fihroiis, s. indurative) niediastinopericarditis. Adherent pericardium has long been recognised by pathologists, but, owing to the difficulty of its diagnosis, escaped clinical recog- nition, although it is a comparatively frequent post-mortem find- ing. Out of 86 cases of heart-disease examined after death at St. Mary's Hospital from 1890 to 1893, there were, according to John Broadbent, 31 instances of adherent pericardium. Although, according to Roberts, Sir Samuel Wilks had fre- quently called attention both pathologically and clinically to the existence of chronic fibrous thickening within the mediastinum and involving the pericardium, chronic indurative mediastino- pericarditis was first systematically described by Kussmaul in 1873. In 1894 Harris, of Manchester, added another valuable contribution to the subject and collected all the published cases. Eor much of what will be said in the following pages I wish to 99 100 DISEASES OP THE HEART express acknowledgnieiiT to Harris's monogra])h, and to thank- fully acknowledge the stininliis derived therefrom. It has en- abled me to give more intelligent and discriminating study to the cases which have come to my notice. I now systematically look for indications of chronic mediastinopericarditis, and discover them many times when otherwise I should probably have over- looked them. Unfortunately, ante-mortem observations of several pronounced cases have been nuide in which post-mortem corrobora- tion of the diagnosis has been denied. Several instructive and typical instances will be narrated in these pages. I wish also to express my indebtedness to John Broadbent's monograph on this subject, as well as to Friedel Pick's paper, Pericarditic Pseudo- cirrhosis of the Liver, in which is particularly discussed the effects on the liver and the production of ascites. Morbid Anatomy. — The morbid anatomical changes found in chronic j^ericarditis are almost always the result of previous acute inflammation. The more common form is the result of the organization of the fibrinous exudate of an ordinary silastic peri- carditis. This process nuiy begin as early as the third or fourth day of the acute inflammation. It is essentially a conservative process, tending to make good the damage wrought by the inflam- mation. This is brought about by the conversion of the inflam- matory exudate into a granulation-tissue, and finally into fibrous cicatrical tissue. The deeper layers of the exudate are first invaded by newly forming blood-vessels and connective-tissue cells with many leuco- cytes, which form the granulation-tissue. This gradually grows into and replaces the entire exudate, and in the course of time the development of intercellular substance converts it into the glisten- ing, white cicatrix. If during this process the two layers of the pericardiuiji arc in contact, union takes })lace and the cicatriza- tion produces firm adhesion between the opposing surfaces. These adhesions mux be general or local, varying with the extent of the original process, and with the conditions obtaining at the time of organization of the exudate. When the adhesion is circumscribed it is most frequently found in tlie parts of the sac where the motion is the least, most frequently, then, at the base of the heart, about the great vessels, less often at the a])ex oi- at the l)orders of the organ. When adhe- CHRONIC PERICARDITIS 101 sion does not occur, the formation of scar-tissue produces glisten- ing white areas on the surface of the heart, which show where the previous inflammation existed. These are the so-called milk- spots or inaculcE tendinice. An intermediate condition between this and the synechia peri- cardii, or completely adherent pericardium, is that shown when slight circumscribed adhesions have been partially or completely torn apart by the motion of the heart, producing string-like pro- cesses of fibrous tissue that may connect the two surfaces, or may, in rare cases, hang loose in the pericardial sac. When the layers are not adherent, in rare cases fluid is found in the sac. The layers of the pericardium may be adherent with but slight thickening, but it is the rule to find considerable increase in fibrous tissue, especially in the chronic tuberculous form, where it may become extreme. Calcification may occur, especially following a purulent peri- carditis, the pus becoming first inspissated, and then impregnated with lime-salts. Such calcareous plates may be isolated, or may form a complete investment for the heart, resembling a coat of mail (Ziegler). In this case the motion of the heart is permitted by cracks and fissures in the calcareous mass. Chronic pericarditis is often associated with chronic endocar- ditis, for the reason that they both often have the same rheumatic origin. Moreover, chronic valvular disease seems to predispose to pericardial inflammation. Secondary to the pericarditis are usually found more or less hypertrophy and dilatation of the heart, with degeneration of the myocardium, which probably are the result of the mechanical hin- drance to the heart's action, and also of the visceral changes that are always the result of long-standing circulatory disturbance. Also associated with the chronic pericarditis may be an indura- tive mediastinitis. It may exist alone, but its more frequent oc- currence in combination with indurative pericarditis renders it appropriate to consider it here. It consists of a more or less ex- tensive hyperplasia of the connective tissue of the mediastinum, which binds together the structures contained therein, and is often associated with adhesion of the two' layers of the pericardium. This development of fibrous tissue results either from an extension of a chronic pericarditis through the parietal layer of the peri- 102 DISEASES OF THE HEART cardium, or from a chronic proliferative inflammation of the me- diastinum itself, either alone or associated with pericarditis. Ex- tensive fibrons adhesions may bind the heart-sac inseparably to the diaphragm, or the sac may be united to the anterior chest-wall,, to the pleura', (jesophagus, spinal column, or to all these structures. In some instances the contents of the mediastinum are so matted together by dense fibrous tissue that they cannot be separated without laceration of the organs. When such extensive adhesions exist they may be found to form but a part of a chronic inflammatory or proliferative process which has led to extensive or general adhesions between the two layers of the pleura, or between the lungs and the diaphragm. In exceptional cases fibrous adhesions have formed only at the roots of the great vessels, and have led to partial or complete oblit- eration of the superior vena cava, either alone (Roberts), or in. combination with involvement of the main trunk of the pulmo- nary artery, or the ascending aorta (Kussmaul). At the present writing I have under observation a female patient, in whom, to judge from physical signs, chronic mediastinopericardial adhe- sions have led to such i-etraetion of the borders of the lungs that the entire anterior surface of the heart is uncovered. The apex- beat is held immovably fixed in the seventh intercostal space, anterior axillary line. The normal excursion movements of the diaphragm in front are entirely abolished, and the respiration is of purely costal type. The secondary effects of this form of the disease are not lim- ited to the heart, as in the simple adherent pericardium. As the disease is usually combined wath chronic valvular disease, it is difficult to say how much importance is to be attached to this, and how much to the fixation of the pericardium in the production of the great hypertrophy and dilatation found in these cases. The changes in the lungs of chronic broncliitis and brown induration are due partly to the passive hypeni'mia secondary to the cardiac disease, and partly to the retraction and immobility of the lungs incident to the pleuro-pericardial or associated pleuritic adhesions. Cirrhosis of the liver is generally present, and is largely re- sponsible for the ascites so frequently observed as a terminal event. There may be also thickening and contraction of the capsule of the liver and spleen, and more or less evidence within the abdom- CHRONIC PERICARDITIS 103 inal cavity of what appears to have been a general serositis or pro- liferative inflammation of the serous membranes. Chronic Pericarditis ivith Effusion. — This form of pericardial disease is but rarely encountered; when, however, it does exist, it may be considered to have originated in one of two ways: (1) It may start as an acute attackj which, instead of undergoing complete subsidence, suffers repeated exacerbations, and finally merges into a chronic inflammatory process. (2) In consequence of the mildness of the infection the pericarditis assumes a slowly progressive character from the beginning, at no time manifesting a tendency to undergo arrest. In the former class the exudation fluctuates in amount from time to time, according as the intensity of the inflammation abates, and partial absorption occurs, or ac- cording as fresh infection occurs the inflammatory process again rekindles. In the second class, chronic from the outset, effusion accumulates slowly, and either remains stationary, after having reached a certain degree, or tends to gradually increase. This form of chronic pericarditis is said to be observed chiefly in elderly or aged individuals, and to be associated with chronic nephritis. Roberts expresses the opinion that such cases can be differentiated only Avith great difiiculty from instances of hydro- pericardium, and that it is quite jDossible, indeed, that the chronic pericarditis originated in a simple serous transudation. This, it seems to me, is quite unlikely unless the originally serous effusion becomes infected by pus-cocci, in which event it would likely be transformed into pyopericardium. Etiology. — Chronic pericarditis is in most instances of either rheumatic or tuberculous origin, the inflammation having been slowly progressive from the start. In other cases an acute process passes into a chronic one, which exhibits no tendency to abate- ment, but persists for years with repeated exacerbations of the inflammation. This is the case particularly with the form which, starting in the sac, spreads to the mediastinum, and ultimately becomes a chronic fibrous mediastinopericarditis. In some cases a mediastinitis is first set up and subsequently invades the pericardium. This last form may originate as either a chronic or acute mediastinitis, which is set up by disease of the bronchial or mediastinal glands, malignant tumours, tuberculosis of the lungs, pleura or glands, pneumonia, or by trauma. 104 DISEASES OF THE HEART The disease is most frequently observed in young adults and in children. Of 22 cases collected by Harris in which autopsy was held, only 2 occurred in persons past thirty, while 9 were under eighteen years of age. Several instances have been re- ported of its post-mortem discovery in infants. According to Har- ris, chronic indurative mediastinopericarditis is much more fre- quent in males than females, 20 out of 25 cases having belonged to the former sex. Symptoms. — Many cases of adherent pericardium run an absolutely latent course, and are only discovered on the autopsy table. In other cases the symptoms are those of circulatory and respiratory embarrassment, and are attributed to dilatation or to an associated valvular disease. In a third series of cases the synechia pericardii is overlooked owing to the development of ascites and other symptoms of hepatic cirrhosis. For the most part the last-mentioned class of cases belongs to what has been described as chronic adhesive mediastinopericarditis. The explanation of these clinical differences is not always clear, but probably depends upon several factors. If the pericar- dial adhesions are of limited extent they may produce no appre- ciable secondary effects on the heart or circulation, but if they lead to total obliteration of the sac, and particularly if this latter is also bound to some of the surrounding structures, cardiac hyper- trophy is likely to result, which, if slight, is not recognised clinic- ally and does not occasion symptoms of embarrassed circula- tion. If, however, the heart is dilated as well as hypertrophied, it is very apt to be more or less inadequate with resulting respira- tory and circulatory symptoms. The enlargement of the organ may be recognised, but not its cause, and the condition is perhaps considered cardiac myasthenia or even chronic myocarditis. Sir William Broadbent is of the opinion that pericardial adhe- sions load most frequently to enlargement of the right heart in conseciueiice of the relative thinness of its wall, Avhile others main- tain that tlie entire lieart is hyix-i'trophied. The mode of produc- tion of hyj)ertrophy in cases of adherent pericardium is difficult of satisfactory explanation, but is due in some way to the hampering of the heart's work. In most instances conditions are prescMit which easily account for the cardiac hypertroj)liy. Chronic valvnhir disease and adher- CHRONIC PERICARDITIS 105 ent pericardium coexist, or the heart is restricted in its function by adhesions between it and surrounding parts (chronic adhesive mediastinopericarditis). In still other instances the effects of a valve lesion are intensified by mediastinopericardial adhesions. In any case the pericarditis either prevents the establishment of adequate compensation or occasions premature loss of such com- pensation as may have been attained. When symptoms eventually appear they may be such as are seen in uncomplicated but uncompensated valvular defects ; ve- nous stasis, hepatic and other visceral engorgement, oedema, as- cites, dyspnoea, and cough with or without expectoration, which may be simply catarrhal or bloody, according to the degree of pul- monary congestion. In some cases wdthout coexisting valvular disease the earli- est symptoms are palpitation, either with or without dyspnoea, called forth by effort or excitement, and occasion much discom- fort and alarm. In such the pulse is apt to be habitually rapid, while cardiac impulse is exaggerated in force and extent. In other cases, again, circulatory disturbance is shown by digestive disorders, lasting for many years and attributed to simple dys- pepsia or chronic gastritis, but never traced to their proper source because of its obscurity or impossible diagnosis of the peri- cardial adhesions. In all such cases there is nothing to distin- guish them from ordinary instances of cardiac incompetence due to dilatation or mitral disease. Physical examination usually discloses hepatic enlargement, and if signs of heart-disease are not apparent the condition is thought to be cirrhosis of the liver, either hypertrophic or atro- phic, according to the degree of enlargement and density or smoothness of the organ. In cases of adherent pericardium displaying pronounced en- gorgement of the liver, I have been impressed by its peculiar ob- stinacy to treatment. The hepatic congestion is most difficult of reduction by ordinary methods, and displays a striking tendency to recur so soon as treatment is abandoned. For several years I have had in charge a patient whose mitral valve leaks and whose enormously enlarged heart is apparently completely incased in fibrous tissue that binds down the organ on all sides, so that no amount of rest in bed or digitalis seems to 106 DISEASES OF THE HEART reduce its size in the least. The liver has always been greatly engorged, extending for a long time nearly to the crest of the ileum, and requiring the daily use of saline laxatives to relieve the patient from pain and discomfort. For the past year the organ has been gradually diminishing somewhat in size and in- creasing in thinness and hardness. The patient has experienced remarkably little dyspnoea on effort, but is greatly annoyed by the pounding and tumultuous action of the heart, this sensation being specially noticeable in the epigastrium. Of late, she has had a great deal of cough, difficult mucous expectoration, and upon several occasions slight haemoptysis. She has to be extremely careful in her diet, and her urine and menses have become scanty. Another female patient with pronounced mitral insufficiency has pericardial adhesions that bind down the left side and base of the heart, fixing the apex-beat immovably in place, far to the left and downward, but the border of the right heart is apparently free from adhesions. Whereas the left ventricle never varies in size under any conditions, the right heart, as shown by the area of cardiac dulness, becomes dilated with the greatest ease and rapidity. The liver, which is ])ersistently enlarged, fluctuates somewhat in size in accordance with the state of the right heart, but even when at its smallest always extends from 2 to 3 inches below the inferior costal margin, no matter how vigorous may be the onslaughts upon it by means of Epsom salts. This patient's symptoms are not of the digestive organs, but are those of short- ness of breath and a rapid pounding action of the heart and gen- eral weakness. The urine remains fairly abundant, and the menses are too profuse and protracted. She is always promptly benefited by absolute rest in bed, a milk diet, cathartics, and digi- talis, although this last-named agent never materially slows the heart. The most interesting class of cases are tliose whose clinical fea- tures closely resemble a case of atrophic cirrhosis of the liver. These cases, usually of chronic fibrous mediastinopericarditis, generally pursue a latent course for many years, and often, even after symptoms have set in, are not recognised as adherent peri- cardium until they come to autopsy. Not only is there a chronic engorgement of the liver, l)iit there is a perihepatitis with increase CHRONIC PERICARDITIS 107 of the interstitial connective tissue. In time this fibrous tissue, undergoing contraction, causes a reduction in size and marked increase in the hardness of the liver, which, extending below the costal arch to a variable distance, feels thin, dense, and regular, the notch being intensified, and often one lobe disproportionately- larger than the other. It is now, when the organ has shrunken and grown dense, that symptoms begin. The patient's attention is first attracted by an increase in the size and firmness of his abdomen. In some instances icterus accompanies or even pre- cedes this increase of girth. At length driven to seek medical advice, he is discovered to have slight icterus and ascites, usually without oedema of the lower extremities. The physican examines the heart and urine, detects no heart-disease and discovers no albumin, but perhaps some bile. The case is put down as one of hepatic cirrhosis. The following is an illustrative case : A man of fifty-five, who had been intensely jaundiced for near- ly two years, and in August, 1900, was tapped for ascites, called me in consultation a short time ago. The ascites, which had for a time been reduced by apocynum cannabinum, only to speedily recur, had been again drawn off the morning of the day I saw him. He had had articular rheumatism eighteen years before, but had suffered no shortness of breath or other discomfort since. The thin-bordered, dense, slightly granular-feeling liver extended in the median line nearly to the umbilicus and from one costal arch to the other, being lost beneath the right ribs, just outside the right mamillary line. Owing to the recent paracentesis, the peri- toneal cavity was free from fluid, and there was no cedema. The cardiac area was somewhat increased to the right and downward, the sounds were clear and strong and free from murmurs. The rather tapping apex-beat was in the fifth left interspace inside the vertical nipple-line, and there was a distinct though feeble pulsa- tion in the epigastrium. In the fifth and sixth interspaces, be- tween the apex-beat and sternum, and also in the sulcus between the ensiform appendix and adjacent costal cartilages, a systolic re- traction could be perceived both by palpation and inspection. Furthermore, when the patient was instructed to take a slow, deep breath, the right external jugular could be seen to bulge out during the inspiratory effort. This distention was also palpable. Pulsus 108 DISEASES OF THE HEART paradoxus could not be detennined. I had no hesitation in mak- ing a diagnosis of pseudo-atrophic cirrhosis of the liver secondary to an adherent pericardium. This patient died a few weeks later. One of the most typical cases, and by the way the first of the kind I ever saw, was seen in 1801 with Dr. Christophe. The patient was a male, aged fifty-two, had always enjoyed good health until an attack of the grip in February, 1880, after Avhich his health failed progressively. Six weeks prior to my visit he took to the house with dropsy and ascites. The former yielded to caf- feine and digitalis, but the latter persisted until drawn off by tap- ping the day before I saw him. The patient was in bed, of medi- um height, considerably emaciated, and complained of dyspncea, dry cough, anorexia, flatu- lence, constipation, scanty non- albuminous urine, pain in the hepatic region, and insomnia. The lungs were negative, but on examining the heart the apex-beat was found to be a weak tap in the fifth left in- terspace on the nipple-line and to be followed by a distinct diastolic rebound or shock, while there was in addition an unmistakable systolic reces- sion of the fifth interspace, from the border of the ster- num to a point outside of the apex-impulse. Cardiac dul- ness extended from the right sternal border to ^ an inch outside the left nipple, and in the mitral area was a harsh systolic mur- mur that was transmitted to mid-axillary line (Fig. '22). Both heart-sounds were audible, and the socoiid at the apex was followed by a short diastolic murmur. The inferior hepatic border was palpable 2 inches below the costal arch, and was thin, hard, and somewhat irregular. The ])ulse was slow, tense, and regular, and there was no icterus. The diagnosis was jdainly that of mitral regurgitation and Location of Border of Liver. CHRONIC PERICARDITIS 109 adherent pericardium with secondary cirrhosis of the liver and ascites. The chronicity of such a case is attested by the fact that after repeated tappings and prolonged confinement to the house this patient again appeared in public, and was accidentally encoun- tered by me in the fall of 1895. He admitted that he was not very well, and that he still had his ascites. He died a few months sub- sequently. In this interesting case cardiac symptoms did not as- sert themselves, and the clinical history was essentially that of atrophic cirrhosis of the liver, and would ordinarily pass for such. The following case is narrated because of its interesting clini- cal course and instructive pathological findings: ]\Irs. M., aged forty-five, consulted me in February, 1S93, because of an obsti- nate cough which had developed the J^ovember previous and re- sisted treatment. She gave a history of scarlatina at the age of seven, and of a pain, probably rheumatic, in the right hip almost continually betw^een her tenth and thirteenth years. She stated, also, that at that time she suffered from shortness of breath upon attempting to run or go upstairs, and at such times had an inclina- tion to faint. She thought her pulse had always been irregular, since whenever she had had occasion to require the services of a physican comment was made upon its irregularity. She was mar- ried at the age of twenty-one, and two years later gave birth to her only child, both the pregnancy and labour having been uneventful, excepting for a mild " milk leg." Fourteen years subsequently she became a widow. She had considered herself well except for nervousness and attacks of neuralgia. In the fall of 1892 was treated for pain and swelling of right leg, between ankle and knee, and for " fulness and tightness " about the waist. In iSTo- vember had contracted a bronchitis, and since then had not been free from cough, although under treatment for same. Her only symptoms at the time she consulted me were fre- quent paroxysmal cough, with scanty mucous expectoration, pain across the chest, in consequence of the cough, and moderate short- ness of breath on exertion. Digestion, bowel movements, and mic- turition seemed normal. She had passed the menopause several months before. She was 5 feet 1 inch in height and weighed 145 pounds. The pulse was 103, somewhat irregular, not intermittent, small, 110 DISEASES OF THE HEART and weak. The lungs were resonant throughout, and the breath- sounds vesicular ; no rales except line inspiratory crepitus at the extreme right base, close to the spinal column, and at the extreme lower limit of the left lung, from the anterior axillary to the pos- terior scapular line. These rales were thought to indicate old pleuritic adhesions. The apex-beat was in the fifth left space 2 inches from the sternum, broad, strong, and at times thumping. There was slight epigastric pulsation, and cardiac dulness was increased somewhat to the right. The pulmonic second sound was accentuatedj while the first at the apex was at times split and thumping, at times preceded by a short, rough presystolic murmur. A systolic apex-murmur was not very distinct. Xo signs of adherent pericardium were noted at that time either because overlooked, or because the chronic me- diastinitis did not develop until a year or two subsequently. The lower border of the liver, firm and rounded, was palpable nearly at the level of the umbilicus. There was no oedema. The diagnosis was made of mitral stenosis in a fair state of compensation, secondary hepatic engorgement, and chronic bron- chitis, probably secondary also to the mitral disease. Under appropriate treatment, directed mainly to relieving stasis in the pulmonic and general venous systems, cough gradu- ally disappeared, and the patient considered herself in fair health during the summer. In May it was noted that the pulse was 100, not intermittent, but slightly irregular in force. The following October, after I had returned from Bad Xauheim, and instituted the balneological treatment of heart-disease in my practice, the patient decided to try a course of baths. For a time they seemed to benefit her, but after about three weeks she said she began to notice increase in the size of her abdomen at its lowest part. I at once examined her, and to my surprise detected unmistakable signs of moderate ascites. The baths were discontinued in the belief that inasmuch as they had not prevented the development of ascites, they would not cause its removal. From that time onward ascites gradually increased until in June, 1894, paracentesis was performed for the first time. From this time to the date of her death, a period of three years, the fluid was drawn off 32 times, the longest interval between the tap- pings being seven weeks and the shortest six days. In addition CHRONIC PERICARDITIS 111 she took elaterin in large doses and various diuretic remedies. Palpation of the liver now showed that it had become thin, very hard, and deeply notched. About two years before her death she began to suffer from what appeared to be attacks of subacute bronchitis. At such times there was mild continuous pyrexia and the cough was most harassing, often effectually preventing sleep and requiring large doses of codeine phosphate. All known expectorants in various combinations were tried with apparently no more effect than to facilitate expectoration. The only treatment that seemed of ma- terial benefit was truly heroic catharsis, since the withdrawal of the ascites seemed only to remove pressure on the diaphragm, but not to lessen the great venous engorgement. These attacks grew more frequent, the intervals between them shorter, until at last cough became chronic and persisted to the end. During these months I saw her but rarely, as her son, who was a physician, devoted himself to her care. At one of my visits, a year or more before her death, I discovered fine crackling rales all around the base of the right lung, particularly in front, which were brought out distinctly by deep inspiration, and were un- changed by cough. These rales eventually spread so as to be heard nearly to the clavicle, while as time went on similar crepitant sounds became audible more or less extensively at the base of the left lung. They did not seem to have the characters of pleuritic friction, and I was at a loss to explain them. It may here be stated, however, that the autopsy subsequently showed them to have been due to wide-spread pleuritic adhesions. A year before her death her son first detected systolic reces- sion of the intercostal space, close to the site of the apex-beat, and pulsus paradoxus. Bacilli were never discovered in the spu- tum, and repeated examinations of the urine showed nothing more than the usual changes due to passive congestion. The last months of life were spent in a continual struggle to keep within reasonable limits the ever-present and never-conquerable venous engorgement. (Edema of the lower extremities supervened many weeks before the end, which finally took place in May, 1897, with symptoms closely resembling but not identical with uraemia. Thanks to the intelligent study of the case by her son, the ante- 112 DISEASES OF THE HEART mortem diagnosis was made of chronic indurative mediastino- pericarditis. !Xo other signs ever developed than the few men- tioned above, pulsus paradoxus and a visible s;v'stolic recession in immediate proximity to the apex. The autopsy was made by Dr. W. A. Evans twenty-seven hours after death, and was briefly as follows : The abdomen contained a small amount of fluid, and the omentum was adherent to the ab- dominal wall above the umbilicus and along the linea alba, adhe- sions being so firm that they could not be separated without tear- ing the omentum. The uterus was larger than normal, the right tube very firmly adherent to rectum and posterior part of the uterus, right ovary being normal ; left tube also firmly adher- ent to the left side of the rectum and side of pelvis and posterior wall of the uterus, completely covering the left ovary, which was also normal. There was an exudate upon the anterior surface of the left broad ligament. The liver was adherent to the abdominal wall over both right and left lobes, the ])arietal layer of the peri- tona'um being thickened and its visceral layer showing evidence of old inflammation. The organ measured 9 by 5 inches, its right lobe 4 inches vertically, and its left lobe 2 inches in its antero- posterior diameter. The surface of the liver was markedly irregu- lar and divided by scars into large areas, its lower border being so notched that it was practically impossible to make out the lobes. Its capsule was irregularly thickened, presenting the ap- pearance of lace-work. The substance of the organ was firm, cut- ting with resistance, and the lobules, very irregular in size, stood out prominently, and the connective tissue of the capsule could be traced into the underlying liver substance^ — in short, it was in a state of advanced Glissonian cirrhosis. The right kidney, 5] inches long and 2^ wide and 2 thick, showed increase in the thickness of its capsule, some parenchym- atous degeneration and interstitial overgrowth. The left kid- ney, 5 by 3 by If inches, with capsule firmly adherent in places and thickened, showed other changes the same as in right kidney. The spleen showed marked tliickening and some interstitial splenitis. The gastro-intestinal tract showed no especial changes, except that the peritoneal covering was thickened. The appendix was firmly bound down to the right iliac fossa CHRONIC PERICARDITIS 113 by a solid mass of adhesions behind the caecum, and was less than 1 inch in length. The right pleural cavity was the seat of very extensive adhe- sions, which were most firm anteriorly and more abundant at the apex than at the base. There was considerable fluid in this cavity, and the lung was firmly attached to the diaphragm. The pulmo- nary pleura was thickened, and on section the surface of the lung showed considerable anaiimia, no tuberculous nodules, and no in- flammation. The left lung was adherent at base anteriorly and also poste- riorly, adhesions to diaphragm being very solid. At apex was a superficial calcareous mass attached to the visceral pleura, and in other respects the left lung was of the same appearance and con- dition as the right lung. The pericardium w^as attached to the pleurae and chest-wall, and m situ felt like a solid bony shield, reaching to the sixth rib and ^ an inch within the left mammary line. Upon removal of the heart it was found that the organ was completely incased by several calcareous plates, which were closely in apposition with yet separated from each other, so that the lines of separation had allowed the heart to undergo contraction and relaxation. These plates of lime united the two pericardial layers firmly. The walls of the several chambers were hypertrophied, particularly the left auricle and right ventricle. With exception of the left ventricle the cavities were all moderately dilated. The heart-muscle had the appearance of brown atrophy. All valves excepting the mitral were healthy, these being thickened, stiffened, adherent along their edges, and projected into the cavity of the ventricle like a cone or funnel. The mitral orifice was moderately thickened with old sclerotic tissue and admitted one finger. To me it is very interesting and quite remarkable that the pa- tient was never able to give any history of an attack of pericar- ditis, which the necropsy showed must have been very extensive. It probably occurred at so early a period in childhood, perhaps subsequent to the scarlatina, that it failed to be impressed on her memory, or was not discovered at the time. If it was secondary to the scarlet fever, forty-one years elapsed before it finally led to the patient's death. The post-mortem findings, furthermore, revealed in a striking manner the extent to which chronic pro- 114 DISEASES OF THE HEART liferative inflammation may involve other structures, notably the liver, and may lead ultimately to the clinical features of hepatic cirrhosis with ascites. The adhesive inflammation of the pleurae probably occurred at the time when the j)atient manifested a low grade of fever with cough, and fine, dry crepitus over the front and base of the right lung, and subsequently also of the left. This case also illustrates the chronicity of some of these cases, and the fact that death is the result not so much of cardiac asthenia as of the effect on the system of the associated conditions. That etio- logical data in such cases are frequently wanting, and that there- fore the primary cause of the symptoms may be unsuspected to the end, is shown by tlie following case : Mrs. D., a physician's wife, aged forty-six, was first seen by me December 24, 1894, because of .increasing symptoms of cardiac disease. Her statements were positive that with the exception of measles and whooping-cough in childhood she had never been ill before the onset of her present trouble. She had been a school- teacher up to her marriage three years before. Her husband stated that he at first noticed tachycardia shortly after marriage, but no other symptoms had been observed until May, 1894. She then developed dyspnoea on exertion, and occasionally oedema of the lower extremities and face. During the summer of 1894 she took sulphate of strychnine, digitalis, strophanthus " off and on " without apparent benefit, but had recently shown some im- provement on iodide of potash and belladonna. Her menses were absent since July ; the only symptoms complained of were slight, dry cough, a not very marked breathlessness on exertion, a feeling of weakness, and occasional puffiness of the lower extremities. She was of medium height and well nourished. Examination discovered signs of fluid in the right pleural cavity, reaching to the lower angle of the scapula, and some fine crackling nlles at the extreme posterior left base that grew more abundant after cough. Otherwise tlie lungs were negative. The pulse was small, weak, regular, and moderately accelerated. The apex-beat was in the fifth left interspace, just outside the nipple-line, diffused and weak. There was no epigastric pulsation, but at the level of the fourth costal cartilage deep-seated cardiac dulness reached from 1 CHRONIC PERICARDITIS 115 inch to the right of the sternum to fully midway between the left nipple and the anterior axillary line (i'ig. 23). There were no murmurs, but the first sound at the apex was weak and the second at the base reduplicated, the pulmonic second being accentuated. 'No signs of adherent pericarditis were noticed. The lower hepatic border was palpable at the level of the umbilicus, and was thin and hard. The spleen was not enlarged, and there was no ascites. The case was considered one of general cardiac dilata- tion supervening upon a previ- ous hypertrophy of the left ventricle and upon the in- creased pulmonary blood-pres- sure occasioned by the fluid in the right pleural cavity. How much of the increase in heart's dulness to the left was attributable to dilatation, and how much to transposi- tion of the organ from pres- sure by the intrapleural fluid, was left an open question. In the absence of a definite his- tory of pleurisy and of other signs of dropsy, the nature of the liquid in the pleural cavity, whether an exudate or transudate, was a matter of doubt. The liver was evidently cirrhotic. Exam- ination of the urine was negative. In spite of physical rest, digitalis, diuretics, and cathartics, the amount of intrapleural fluid remained stationary for the next three weeks. Paracentesis was then performed, and the fluid rap- idly reaccumulating, the operation was repeated within a Aveek. After the second aspiration the fluid mounted to the upper level of the third rib and symptoms of pressure increased. It was then decided to try the efficacy of baths (Bad Xauheim). These were endured so badly, however, that they were discontinued after four days. By February 6tli the actual embarrassment had become so pronounced that this fact, together with the failure of paracen- tesis to permanently reduce the amount of pleural effusion, led the Fig. 23. — Showing Apex-beat, Cakdiac Dulness, and Liver Border in Case (p. 114). 116 DISEASES OP THE HEART consulting surgeon to advise resection of a rib in the hope that jDermanent drainage would afford time and opportunity for the heart to regain its former vigour. The proposal having been laid before the patient and her husband, and their consent obtained, the operation was done the next day. Everything seemed to pro- gress favourably for a few days, when suddenly symptoms of pro- nounced fibrinous pleuritis developed in that side. Temperature rose to 102° F., strength waned rapidly, and the patient died ten days after the operation. I may say here that the infection was subsequently proved to be a pneumococcus one. The autopsy was made by Dr. Hektoen twenty-four hours after death, and the findings may be briefly stated to have been a totally adherent pericardium, with several plates of lime-salts upon the surface of the ventricles, the largest lamina being about the size of a silver half dollar. The sac was also bound by adhesions to the left pulmonary pleura, but not to the chest-wall. The valves and myocardium seemed normal, there was evidence of recent right- sided pleurisy with collapse of the lung, and acute oedema of the left lung with some fresh diaphragmatic pleurisy on that side. The liver was cirrhotic, but not atrophied. Kidneys were healthy, and there were evidences of perihepatitis and peri- splenitis. The necropsy seemed to make it evident that the condition within the right pleural cavity had been a hydrothorax, while the pericardial adherence explained why medical treatment had been unavailing. Had this patient lived, and time been afforded for shrinkage of the liver to take place, ascites would undoubtedly have developed, and the case have presented the clinical features of what Pick terms pericarditic pseudocirrhosis of the liver, the same as did the others. In explanation of ascites in such cases Heideman lays down the four following propositions: (1) In these cases there is chronic inflammation of all the serous membranes. (2) The stag- nation occasioned by degeneration of the cardiac muscle leads to ascites, because on account of the chronic peritonitis the peritoneal vessels offer a locus minoris resistentice. (3) The cirrhotic pro- cess in the liver so often observed under these circumstances is oc- casioned by extension of the inflammatory irritation from the capsule of the liver as well as by the chronic hyperaemia. (4) CHRONIC PERICARDITIS 117 Bv the growth and contraction of this connective tissue in and about the liver the stagnation and transudation in the abdominal cavity are increased. Course and Termination.- — The course of chronic adhesive pericarditis varies much, depending upon the extent of the adhe- sions and the coexistence or not of other diseases, as chronic valvular lesions. If the process is confined to obliteration of the sac the condition may last for many years, and the patient subse- quently die from some independent affection. Usually, however^ the same as when mediastinopericarditis leads to extensive union with the surrounding parts, the disease, after having persisted for a long time without symptoms, is likely to bring about those cir- culatory and respiratory disturbances already described, and so well illustrated by the foregoing cases. If adherent pericardium is associated with valvular disease it affects the latter injuriously, and its more rapid course is inseparably connected with that of the endocardial lesion. In such a case cardiac breakdown is inevita- ble, and not likely to be long postponed. Xevertheless, even here much depends upon the treatment and upon the patient's intelli- gent appreciation of his condition. In the case of the young lady whose mitral insufficiency is sadly complicated by adhesion of the left side of the heart and apex to the retracted lung-border and chest-wall, symptoms of right ventricle failure came on only three years after her first attack of rheumatism, and were undoubtedly hastened by the pericardial adhesions (see page 106). It is now nearly eighteen months since her symptoms became alarming, and the fact that her overburdened right ventricle is to-day actually doing better work than a year ago is due to the persistent use of appropriate remedies and to her having learned that so soon as the first signal of danger is perceived she must take to her bed until the right heart recovers its tone. The manner in which many cases of this affection terminate has already been made apparent. Either the symptoms are those of atrophic cirrhosis of the liver or they are indicative of cardiac insufficiency of mitral disease. Either stasis in the systemic veins and viscera increases until the patient succumbs to general exhaus- tion, or in another set of cases he is worn out after months or years by the ever-recurring ascites, the heart not evincing special weak- ness. According to Kussmaul, pulmonary infarcts are particu- 118 DISEASES OF THE HEART larly frequent in cases of chronic mediastinopericarditis, and these may prove the cause of death. Physical Signs. — Inspection. — The ease and certainty with which adherent ])cricardiuni can be recognised clinically depend upon the situation and extent of the adhesions. If the sac is bound down to the heart, but not to surrounding parts, the condi- tion does not of a necessity produce recognisable physical signs, and this fact explains why sinechia pericardii is so often first de- tected on the post-mortem table. In the cases in which an adher- ent pericardium is diagnosed there are generally adhesions be- tween the sac and some of the surrounding structures, as the ante- rior thoracic wall, the pulmonary pleura on either side, and the diaphragm. Accordingly, it is in cases of chronic indurative mediastinoperi- carditis that the diagnosis is most easily and frequently made. This is owing to the fact that the existence of adhesions interferes witb the change in form and position of the heart normally occasioned by ventricular systole. During this phase in its contractions the heart becomes depressed at its base, and assuming a more rounded shape thrusts its point forward, upward, and towards the left, and thus produces the impulse against the chest-wall known as the apex-beat. It is evident that if adhesions restrict these movements the heart will of a necessity pull on the part to which it is bound. This pulling action is exerted during ventricular s3'stole, and con- sequently the most obvious and the most frequently observed sign of adherent pericardium is a I'isihlc systolic recession of the chest- wall. It may be perceived in various situations, but most com- monly in the neighbourhood of the apex-beat. Only a very lim- ited area may be thus drawn inward, but in most instances a systolic sinking takes i)lace in several of the interspaces near the apex and even in the e])igastrium, the extent and location of the adhesions determining tlie extent and position of this sign. It is best observed by placing the patient in a strong light, and then looking at the bared chest from above downward or from one side to the other. It is well to have the ])atient suspend respiration for a mo- ment wliilc inspection is being iiiadc, that tlie observer may not be deceived or confused by sinking of the soft parts incident to move- CHRONIC PERICARDITIS 119 ments of the diaphragm. Ordinarily, there is but slight difficulty in detecting this systolic indrawing in question. One should be careful, however, not to mistake for a sign of pericardial adhesions the systolic depression that sometimes takes place in the third and fourth interspaces close to the left border of the sternum in cases of great cardiac hypertrophy, and which is due to atmospheric pressure as the base and body of the heart recede from the chest- wall during systole. As might be expected, it is the yielding soft parts that display systolic retraction most readily, and as it is possible that even near the apex this may be owing to atmospheric jDressure, this sign is not jDathognomonic. The value of the sign is far greater, therefore, when the ribs and end of the sternum are drawn inw^ard together with the intersi3aces. I have not observed this, but it is said to sometimes occur. Sir William Broadbent first described a systolic retraction of the tenth and eleventh interspaces below the inferior angle of the left scapula in cases of adherent pericardium, and hence it is often spoken of as Broadhenfs sign. It is occasionally perceived on the right side also. It is ascribed to the drawing on the diaphragm of a hypertrophied and powerfully contracting heart, and when pres- ent is considered indicative of extensive adhesions between the sac and the diaphragm. Gibson very justly attaches great importance to fixation or im- mobility of the apex. J^ormally the heart, and hence its apex, gravitates towards the dependent side whenever the patient as- sumes either lateral decubitus. When he lies on the left side the point of the heart strikes the chest-wall a couple of inches farther to the left than when he is on his back, while in the right lateral position the impulse is nearly or quite behind the sternum, and hence imperceptible. Consequently in any case in which this mo- bility of the apex is not observed, it is suggestive, nay indicative, of its fixation by external adhesions. The position of the heart's apex should also become lowered during the inspiratory descent of the diaphragm, striking behind the sixth costal cartilage, or even the sixth interspace. The existence of adhesions may pre- vent this, and accordingly fixation of the apex during the two res- piratory acts is likewise a sign of adherent pericardium. The other phenomena perceived by inspection in some cases 120 DISEASES OF THE HEART are connected with the external jugular veins, and are (1) in- spiratory swelling of the veins, known as KussmauVs sign, and (2) diastolic collapse of the veins, known as Friedreich's sign. In my experience these signs are not as frequently met with as is the drawing inward of the interspaces, and I do not recall an in- stance of diastolic collapse of the veins. Kussmaul's sign is pres- ent when i^ericardial adhesions prevent the dilatation of the right auricle that normally takes place during inspiration. Instead of the inspiratory act exerting an aspirating effect upon the contents of the veins, and thus collapsing them, the opposite effect is pro- duced, and the jugulars become visibly distended. Diastolic col- lapse does not appear to l)e limited necessarily to the jugulars, since Broadbent has observed it in the superficial veins on the front of the chest, and says it was due to traction of fibrous bands on the coats of the internal mammary vein uniting this vessel to the peri- cardium, and causing its sudden dilatation during ventricular re- laxation. In the case of the cervical veins their diastolic collapse is probably to be explained by the aspiratory force exerted by the sudden diastolic rebound of the right auricle, pulled upon as it is by adhesions between it and surrounding parts. Two other physi- cal signs that remain to be considered are best perceived by the hand, and are therefore described under palpation. Palpation. — In some exceptional instances the hand laid over the apex perceives a distinct sudden shock not synchronous with systole, but with diastole. It is spoken of, therefore, as the dias- tolic shock or rebound. It is caused by the pulling of fibrous adhe- sions which, put on the stretch during systole, pull the heart sud- denly back against the chest-wall after systole has ended. Such a rebound can scarcely be occasioned by any other condition than ex- ternal pericardial adhesions, and therefore by some is considered pathognomonic of the disease under discussion. I have observed it but twice, once in the patient whose case I have reported, and the other time in a man at Cook County Hospital who had, in addition, aortic insufficiency. The second ])lienomenon observable 1)V palpation is tlio pulsus paradoxus. Normally the pulse l)ecomes fuller and stronger to- wards the end of inspiration, smaller and weaker towards the end of expiration. In the paradoxic pulse, on the contrary, the re- verse obtains, strong ins]>iration causing a diminution in the force CHRONIC PERICARDITIS 121 and volume, it may be even an intermission of the pulse, while towards the close of expiration the pulse regains its usual strength and fulness. This peculiarity may sometimes be perceived in pericarditis with effusion, and therefore, while its presence serves to corroborate other signs of adherent pericardium, it in nowise can be looked upon as pathognomonic. Aside from enabling one ■ to appreciate the two signs just mentioned, palpation is of service in determining the mobility or fixation of the apex and the degree of enlargement and density of the liver — conditions I deem of con- siderable importance in doubtful cases. Percussion. — This is of great value in all cases of suspected or known heart-disease. In adherent pericardium cardiac hyper- trophy or dilatation is very apt to exist, and hence one should in every suspected case attempt by percussion to ascertain the limits of deep-seated dulness, since in the absence of any other etiological factor to account for enlargement, this condition would point to the likelihood of adhesions. It is not uncommon in cases of suspected adhesions for the area of absolute cardiac dulness to be increased in all directions, particularly upward and to the left. This may be due to a simple crowding aside of the anterior lung-margins by a hypertrophied heart, yet the borders may be retracted and fixed by pleuropericar- dial adhesions. In this latter condition the line of demarcation between pulmonary resonance and cardiac dulness is unaffected by respiratory movements. Therefore, percussion is of service in enabling one to determine whether or not the lung-borders are bound down by adhesions. Auscultation. — For the most part this is of negative value, particularly if the synechia pericardii is not associated with me- diastinopericarditis. In the latter condition auscultation some- times detects fine friction-rales along the margins of the lungs where they join the area of superficial cardiac dulness ; and if such parchment-like crackling sounds persist during the cessation of respiratory movements, they furnish strong proof of the existence of pleuropericardial adhesions. Roberts quotes Perez as authority for the statement that in some instances of chronic mediastinopericarditis a creaking sound upon the body of the sternum is audible during up and down movements of the arms. I have tested this in several of my pa- 10 122 DISEASES OF THE HEART tients, and in two I detected this creaking friction-sound described by Perez. As in these cases other positive signs of adherent peri- cardium were present, this sign of Perez possessed considerable interest, if not material importance. Diagnosis. — From the foregoing description of the physi- cal signs it is apparent that in some cases the diagnosis of peri- cardial adhesions can be made almost at a glance, while in others the most skilful diagnostician may not be able to decide whether the pericardium is adherent or not. The difficulty is found in cases in which the two layers of the sac are united without adhesions to the surrounding parts. In such, one must observe critically the jugular veins and the radial pulse in the hope of detecting some of the anomalies that have been described. The size of the heart should also be mapped out by percussion, and the liver should be examined as to its size, density, and outline, since synechia pericardii may declare itself by no other signs than by its eifect on these organs. In cases of chronic indurative mediastinopericarditis the mat- ter of diagnosis is usually far less difficult. Indeed there may be a conjunction of several physical signs. Thus in one of my pa- tients the apex is firmly fixed far below and to the left of the nipple. There is systolic retraction of the soft parts between tlie apex and the epigastrium, and of the intercostal spaces below the left scapula. The anterior margins of both lungs are drawn aside and immovable, causing nearly the whole heart to be uncovered, as shown by the great area of superficial dulness. The liver ex- tends nearly to the iliac crest and is hard and deeply notched, while owing to the enormous size of the heart and liver the front of the chest looks distended and smooth, and when the patient stands the abdomen appears disproportionately large and pendu- lous. Pulsus paradoxus and inspiratory swelling of the cervical veins are also present. Lastly, one should always be suspicious of an adherent peri- cardium in every case of rheumatic valvular disease, and if in such a case the liver resembles in thickness and density the organ in atrophic cirrhosis, yet is not so contracted, if ascites develops without apparent cause, or takes place prior to or out of propor- tion to anasarca, there is good reason to suspect the complication of an adherent pericardium. CHRONIC PERICARDITIS 123 The differential diagnosis between Laennec's atrophic cirrhosis of the liver and the pericarditic psendocirrhosis just considered is often the most difficult. Aid may be obtained by attention to the following points: (1) In Laennec's cirrhosis there is often a history of alcoholism, malaria, or syphilis, while in the other form there may be a history of previous pericarditis, a rheumatic at- tack in childhood, or. of some acute illness with prsccordial pain and other symptoms suspicious of pericarditis. (2) In Laennec's cirrhosis ascites develops prior to anasarca, whereas in the variety now considered it may sometimes follow more or less oedema of the lower extremities (Pick). (3) In the former there are no signs of heart-disease, while in the latter careful examination usually detects enlargement of the heart either alone or in combination with valvular disease. (4) In the pseudo-atrophic form there may be some of the signs of adherent pericardium. Finally, before leaving the subject of diagnosis of chronic peri- carditis, it is necessary to say a few words concerning the recogni- tion of that rare form in which the chronic inflammation is shown by fluid distention of the sac. In this variety there are apt to be pressure-effects, but if the effusion takes place insidiously such effects may not declare themselves. In such an event the effusion is usually detected accidentally, or if discovered its true nature may not be suspected. Roberts cites a case reported by Samuel West of the existence of a supposed cyst which was repeatedly tapped during life, yet which after death was found to be a chronic peri- cardial effusion. Unless this condition is observed to have origi- nated acutely its diagnosis must depend upon percussion and aus- cultation evidences of distention of the sac in accordance with the rules laid down for the diagnosis of acute pericarditis with effusion. Prognosis. — If pericardial adhesions occur independently of other disease, and if not so firm or extensive as to materially ham- per the heart's action, they may in nowise affect life prospects. If, on the contrary, pericardial synechia is complicated by a chronic valve-lesion, the prognosis is unfavourable as to great length of life. If the heart is bound down more or less completely to the surrounding parts, it is only a question of time when serious inadequacy will develop. In some cases the adhesive process is stationary, while in chronic indurative mediastinopericarditis the 124 DISEASES OP THE HEART tendency to subsequent adhesive inflammation of other serous membranes and to the spreading of the adhesive process within the mediastinum furnishes an exceedingly grave outlook for the future. When ascites, anasarca, and other symptoms of the final breakdown appear there is small prospect of a restoration of compensation. Under such conditions the duration of life is likely to be bounded by a few months or even a few weeks. Although, as in the cases narrated, the struggle may be extended over a number of years, the patient is a chronic invalid at the best, and can only with great difficulty postpone the fatal event. The absence of all subjective and objective symptoms furnishes presumptive evi- dence that the adhesions are not extensive. If, on the contrary, symptoms of engorgement within the lesser and greater circula- tion are never wholly absent, they aflPord the basis for unfavourable prognosis. The greater the secondary cardiac hypertrophy and dilatation, particularly in children, in whom chest capacity is small, the slighter the prospect of the long retention of adequate compensation. When the last stage of the journey is reached it is likely to be a short one. The prognosis of chronic pericardial effusion depends upon its etiology and the length of time during which it has existed. It also depends upon its association or not with some other disease, as chronic nephritis, and upon its amenability to treatment. Treatment. — It goes without saying that we possess no means of breaking up the pericardial adhesions ; at the most we can only strive to lessen their ill effects and to prevent. an exten- sion of the process. In our endeavour to accom]>lish the latter, any rlieumatic attack or acute illness, no matter how trifling, should be promptly and energetically combated by appropriate means. The patient should be at once confined to the house, and if possi- ble to the bed, in order to relieve the heart of any unnecessary work, and tlicreby if possible pi-event fresh pericardial inflamma- tion or restrain the activity of the process, sliouhl the pericardium again become attacked. Salicyhites, counter-irritants, or other mild antiphlogistic measures are in order. The chief aim of management should be to preserve compen- satory hypertrophy, and so far as possible to minimize the ill ef- fects produced by the; cai'diac disorder. In my opinion, the first essential is that the patient be not left in absolute ignorance of CHRONIC PERICARDITIS 125 his condition, lest lie fail to grasp the full importance of the rules laid down for his guidance. Most individuals are greatly alarmed by being told they have heart-disease, and therefore great judg- ment and tact are required in imparting such information. If the patient has no suspicion of anything being wrong with his heart, and is of a nervous, excitable temperament, he would better be told only a part of the truth. It may be stated that his heart is not strong, and that if he will prevent the development of serious trou- ble he must obey certain injunctions, the careful observance of which will i^reserve his health. In other instances the whole truth may be told plainly, but in a manner not calculated to create alarm. Only in this way can we expect our patients, ignorant of physiol- ogy and pathology, to avoid harmful efforts, and to correct injuri- ous habits. In a word, a heart handicapped by extensive adhesions, and perhaps also by serious valve-disease, must not be given more work to perform than it is capable of without strain. Inasmuch as what will be said on this subject in the chapters devoted to the treat- ment of Valvular Disease in General is applicable to the aifection now under consideration, the reader is referred to those chapters for the details of this part of the management. The injurious secondary effects of adherent pericardium are not limited to the heart, but are also felt by the organs of diges- tion and elimination. Congestion within the portal system must be diminished from time to time by the administration of a brisk cathartic. The patient, and even the physician, often rest con- tent with the fact that the bowels move regularly every day, and lose sight of the benefit derived in these cases from periodically unloading the liver. ISTothing is better to this end than a blue pill or a grain or two of calomel, followed the next morning by a glass of some saline aperient water. The patient should remain under the regular, though perhaps not very frequent, supervision of a physician, who, detecting early indications of cardiac strain, may promptly meet the danger by ordering an appropriate heart-tonic. Digitalis and strychnine should not be given as a routine practice, but should be reserved for times of emergency. As a rule the symptoms pointing to overstrain on the part of the heart can be allayed by regulation of the diet, restricting the amount of work or exercise, and it may be by insisting upon rest 126 DISEASES OP THE HEART in the house for a time. The food should be relatively rich in proteids, moderate in quantity, and taken at regular intervals. If the individual is inclined to corpulence, or suffers from fermenta- tive indigestion, carbohydrates and fats should be allowed spar- ingly. Unrestrained consumption of fluids is objectionable, since it is a very easy matter for the intake of liquids to greatly exceed the needs of the system and the eliminating power of the excretory organs. When the breakdown of compensation at length comes, with all its attendant manifestations, the case is to be managed in ac- cordance with the principles governing the treatment of the same condition in any other form of cardiac disease. It has been my experience that one cannot expect or achieve as brilliant results from the employment of digitalis in these cases as in valvular affections unfettered by adhesions. It is not so much a question of whipping on the jaded heart as it is of relieving it of as much of its load as possible. Physical rest must be strictly enforced therefore, and catharsis must be brisk. Digitalis must be given for the purpose of invigorating rather than greatly slowing the heart, and with a view of obtaining its diuretic effect. Diuretin and other diuretic remedies are also in order. It is now that strychnine is of particular service, and to produce its most bene- ficial effects it should be administered hypodermically. Pain, cough, insomnia, and other distressing symptoms are to be relieved as they arise. One should not hesitate to remove ascites by aspi- ration whenever it accumulates to the extent of seriously embar- rassing the heart and respiratory organs. If the anasarca does not yield to appropriate remedies, it may be drained off by the use of Southey's tubes or by incising the ankles, always under strict aseptic precautions. CHAPTEE III HYDROPERICARDIUM — H^^MOPERICARDIUM — PNEU- MOPERICARDIUM-TUBERCULOSIS OF THE PERI- CARDIUM-SYPHILIS OF THE PERICARDIUM-CAR- CINOMA AND SARCOMA OF THE PERICARDIUM I. HYDROPERICARDIUM By this term is meant a transudation of serum into the peri- cardial sac. It is a non-inflammatory process, and the analogue of what takes place under similar conditions in other serous cavi- ties. The presence in the pericardium of 1 or 2 drachms of serum may be regarded as physiological ; the condition is pathological only when the transudate reaches such an amount as to constitute a veritable dropsy (hydrops pericardii). Although the condition is the counterpart of transudation into other serous cavities, it does not occur with anything like so great frequency as hydro- thorax and ascites. Morbid Anatomy. — Upon the chest being open the pericar- dial sac is found more or less distended and fluctuating, the same as in pericarditis with effusion ; a great difference is discovered, however, when the sac is opened. Instead of fibrin-masses and other evidences of inflammation, together with a serous exudate, the sac contains a clear, straw-coloured fluid, poor in albumin, and containing very little if any fibrin. Because of its relative defi- ciency in albumin the specific gravity of the transudate is lower than that of a sero-fibrinous effusion, ranging from 1.008 to 1.015. The pericardial tissues may look more or less (Edematous; but aside from this appearance and being filled with serum, the sac presents nothing worthy of note. In addition, there are associated changes in other tissues and organs — such as oedema, depending upon the same cause as the hydropericardium ; as chronic diseases of the heart or kidneys, or both, which have served to bring about 137 128 DISEASES OF THE HEART the serous transiKlation into the sac. The transudation into the pericardium varies in amount from a few ounces to several pints. Etiology. — Ilydropericardium is a dropsy, and therefore is prodiu't'd in the same manner and depends upon the same variety of causes as dropsical fluid in other situations. The causes may be divided therefore into general and local. The general include chronic cardiac disease, nephritis, both acute and chronic, and ca- chexias. By local causes are meant those diseases, such as tumours, Avhich, sitmitcd within the thorax, exert pressure on neighbouring blood-vessels, and thus bring about stasis in the veins and capil- laries of the pericardium. Chronic heart-disease leads to dropsy in the same way, but the stasis within the pericardial vessels is only a ])art of a general condition. Symptoms. — These are likely to be overshadowed by those of dropsical accumulation in the pleural cavity and general venous congestion. If by chance hydropericardium exists alone, a very rare event, or forms the leading pathological condition, the syni])- toms are those resulting from pressure, and consist of the same phenomena of circulatory and respiratory embarrassment as are observed in cases of extensive sero-fibrinous pericarditis. Dysp- noea is more or less marked, and may even amount to orthopnoea ; cyanosis and venous congestion are also present, and the pulse is small, feeble, rapid, and it nuiy be irregular. The more rapidly the hydropericardium supervenes the more ])ronounced the symp- toms. As dropsical distention of the sac, when it develops in the course of chronic cardiac or renal disease, is one of the terminal events, it (h've]o])s so slowly that sym])tonis ai'c likely to be latent, and tlierefore e>ca))C notice. Physical Signs. — Inspect ion. ^Thia affords but little if any information, owing to the fact that in most eases distention of the chest has already been produced by associated hydrothorax or the heart and lungs have been crowded ujiward by ascites. Should some local disease have occasioncul the hydropericardium, and the thoracic ])arietes l)e sniiicieiit ly yieldiui:, tliei-e will be more or less I)ra'Cordial bulging, togetlier with absence of cardiac impulse. Paljmlioii. — Wluit has been said regarding inspection applies also to palpation. The chief, and perhaps the only thing noted, i? absence of cardutc impulse, and possibly a sense of increased prai- HYDROPERICARDIUM 129 cordial resistance. The pulse presents nothing characteristic, since the changes observed in it are also produced by the primary cardiac affection. Percussion. — This affords us our chief means of diagnosis, the same as in pericardial effusion; for particulars the reader is re- ferred to what has already been said under that head. Owing to the probable association of hydropericardium with hydrothorax, the characteristic shape of praBcordial dulness is likely to be modi- fied by and merge into that of the latter affection. Under such circumstances, it would only be at the upper part of the sternum that percussion might be of any special value as regards the detec- tion of the hydropericardium. If the area of cardiac flatness extends high up towards the suprasternal notch, with a bluntly rounded apex, well above the area of dulness due to the hydro- thorax, this fact might, theoretically at least, be of aid in deter- mining the existence of transudation into the pericardium. Auscultation. — Owing to the intervention of fluid between the heart and the chest-wall, cardiac sounds are feeble and distant, and they may indeed be almost inaudible. If murmurs, due to some pre-existing valvular disease, are also present, these are likewise enfeebled. Diagnosis. — From the foregoing considerations it is evident that the diagnosis of hydro23ericardimn is not only difiicult, but may be actually impossible. In those extremely rare cases of pericardial dropsy due to local causes the diagnosis is governed by the same principles as in mass- ive pericardial exudation. The differential diagnosis between these two conditions is to be made by the history, symptoms, associated diseases, and pres- ence or absence of pericardial friction. In effusion there is his- tory of rheumatism or some acute infectious disease, of pyrexia, prsecordial pain, palpitation, etc. Even in distention of the sac pericardial friction-sounds may be retained. In hydropericar- dium, on the other hand, there is history or evidence of some chronic valvular or renal disease, and all symptoms of acute in- flammation are wanting, and there is no pericardial rub. Prognosis. — This is unfavourable, both because of the nature of the primary disorder to which the hydropericardium is second- ary, and because the distention of the sac is likely to hasten car- 130 DISEASES OF THE HEART diac failure. The prognosis is also influenced by the amenability to treatment of the cause of the dropsy. Treatment. — This resolves itself essentially into the treat- ment of the primary disorder, since with the removal of the gen- eral dropsy the fluid within the pericardium is absorbed. Unless the symptoms be exceedingly threatening, surgical treatment, if not actually unwise, affords only a very temporary relief. In other words, the treatment of hydropericardium is unavailing un- less its cause can be remoyed. The management of dropsy when associated with chronic cardiac disease, will be found fully nar- rated in subsequent chapters. II. n^MOPERICARDIUM By this term is not meant hai'morrhagic pericarditis, but an extravasation of blood into the pericardium independent of any inflammatory process. It is fortunately a rather rare condition, and yet occurs many more times than it is recognised. It requires but very brief consideration. Morbid Anatomy. — As with serous transudation or effu- sion, the escape of blood into the pericardium causes a distention of the sac proportionate to the amount of the extravasated blood. If the fia^morrhage takes place rapidly the amount discovered post mortem is usually not large, because it has speedily occasioned the death of the patient. If, on the other hand, it takes place slowly, the sac may be greatly distended. The blood may be wholly fluid or have undergone more or less coagulation. After the evacuation of the pericardial contents, careful scrutiny discovers evidence of some one of the causes of the haemorrhage. Etiology. — Blood may be effused into the pericardium in consc(pience of external injury, as by gunshot or stab wounds, laceration of the sac by the sharp edge of a fractured rib, etc. It also follows rupture of the heart-muscle, the bursting of an aortic aneurysm, or in rare instances, of one of the coronary arteries. It is stated that sacculated aneurysms of the ascending arch fre quently rupture into the pericardium. Of 953 cases of aortic aneurysm analyzed by Hare and Holder, death took place from rupture 289 times, and of these, 75 cases ru]itured into the peri- cardium. Rupture of the heart occurs from degeneration of the myocardium, and is fortunately a comparatively infrequent event. H^MOPERICARDIUM 131 Laceration of the heart-wall has occasionally been observed to fol- low a crushing injury to the chest. Symptoms. — As would naturally be expected, hicmorrhage into the pericardial sac occasions the very gravest symptoms. If this takes place slowly through a minute slip in the wall of the heart or aorta, symptoms come on gradually, and are those of acute aniTcmia, together with slowly induced and progressive heart-fail- ure. These are a sense of precordial distress, anxiety, weakness and prostration, dyspnoea, pallor with cyanosis, a weak, rapid, perhaps irregular, pulse, coldness of the extremities, and clammy perspiration. Death takes place within a few hours, or perhaps a day or two. Should the haemorrhage be free, and the sac become rapidly distended, the symptoms are those of sudden and profound shock, the patient passing quickly into a state of collapse, and dying in a few minutes. If the rupture does not occasion appreciable pain there may be nothing in the symptoms to direct attention to the pericardium. In most instances the course is rapid, leading to a speedily fatal termination. Physical Signs. — These are the signs of fluid distention of the sac, and hence do not require repetition. In the majority of instances death is too rapidly induced or the distention of the pericardium too small to occasion appreciable physical signs. Diagnosis. — If the life of the patient is sufficiently prolonged, and if the sac is sufficiently filled, it is possible for the trije nature of the difficulty to be recognised by examination of the prsecor- dium. If the presence of fluid in the pericardium is made out, the history of its sudden appearance and the symptoms of shock and collapse will probably enable one to surmise at least the true na- ture of the malady and to differentiate it from hydropericardium. Diagnosis may also be facilitated by history of some antecedent affection as aneurysm, likely to lead to haemorrhage. Prognosis. — If ha^mopericardium results from trauma, the prognosis depends upon whether or not the injury is amenable to surgical treatment. In cases due to aortic or cardiac rupture the prognosis is absolutely unfavourable, and death is the inevitable, it may be the immediate, result. Treatment. — This in traumatic cases is surgical, and is best left to text-books on surgery. In the other class of cases there 132 DISEASES OP THE HEART is no treatinciit, oxce]it possiblv in those raro instanco.=! of trau- matic laceration of the lieart, when the surgeon should promptly lay open the sac, evaeutc the hlood, in the hope of discovering the source of the luemorrliage, and of being able to repair the injury by suturing the heart-muscle. Medicinal treatment is limited to stimulation of the heart and an attempt to support the powers of life. In most instances the physician arrives on the scene too late to do more than witness the death-struggle or sign the death-certificate. III. PNEUMOPERICARDIUM This is so extremely rare an affection that but few have been so fortunate as to observe an instance of the kind. By this term is meant a collection of air or gas within the pericardial sac, and hence it is the counterpart of the condition known as pneumo- thorax. Morbid Anatomy. — Pneumopericardium is usually associ- ated with collection of fluid, most commonly of pus, wdthin the sac. The amount of contained air or gas is variable, but is sufii- cient, together with the exudation, to occasion great distention. If the gas is not absorbed, and the pericardium be opened post mortem, the gas escapes with a hissing noise and often possesses a fd'tid odour. In some instances its avenue of entrance can be easily ascertained, while in others there is no discoverable open- ing into the pericardium, either because, if such have existed, it has become closed, or because the gas has been generated in loco. There are usually present also evidences of acute peri- carditis. Etiology. — Pneumopericardium may be produced in any one of tlirec ways: (1) Perforation of the sac from without may allow of the entrance of atmospheric air; (2) communication may be established between the sac and some portion of tlie digest- ive tract, thus permitting the ingress of the gases normally exist- ing in the latter; or (3) gas may be generated within the peri- cardium without solution of its continuity. The entrance of atmospheric :iir into the sac usually takes place through a ])erfo- rating wound, as from a bullet or some stabbing instrument. In rare instances air may enter the pericardium thi'ough tlie lung in consequence of laceration l)y the shai-p edge of the fractured star- PNEUMOPERICARDIUM 133 nnm or rib, or by rupture of a pulmonary cavity situated in im- mediate contiguity to the sac. When a communication is established between the pericardium and oesoj)hagus, air is forced into the former with each act of swal- lowing. Walshe has narrated an interesting case of perforation of the pericardium, and resulting pneumopericardium, during an attempt by a juggler to swallow a short sword. When gas is admitted to the sac from some one of the hollow viscera it is usually in consequence of the extension of a previ- ously existing ulcerative process. The most frequent communi- cation formed in this way is with the stomach, by reason of an ulcer, when situated on its posterior wall. Of 28 cases of perfora- tion of the diaphragm by gastric ulcers collected by Ludwig Pick, only 10 were cases in which the ulceration had perforated the pericardium. CoUingwood Fenwick records a very interesting- case which occurred in his practice, in which a gastric ulcer had perforated the pericardium with an immediately fatal result, and yet no previous symptoms had occurred to point to the presence of the gastric ulcer. In 4 of the 10 cases collected by Pick the two surfaces of the pericardium had become adherent before the ulceration had perforated, so that the ulcerative process involved the substance of the heart itself. Ulceration into the sac may also take place from the oesophagus, but, as already stated, atmos- pheric air is then admitted, instead of stomach or intestinal gases. In the minds of some, the spontaneous development of pneumo- pericardium is a matter of doubt. Gibson is of the opinion that in some of the cases supposed to be of this origin the pneumoperi- cardium was in reality the result of an opening into the sac, which, however, became so quickly and perfectly closed that no trace of such opening could be discovered. IsTevertheless, the discovery of gas-forming bacilli renders intelligible and possible the spontaneous development of pneumopericardium, and may ex- plain some cases that would be difficult or impossible to account for on any other hypothesis. This mode of production is exceed- ingly infrequent, to say the least. Such a pneumopericardium is preceded or accompanied by acute suppurative or hsemorrhagic pericarditis. Symptoms.- — Subjective manifestations are essentially those of sudden distention of the sac from any other cause. They are 134: DISEASES OF THE HEART symptoms of pressure ; but inasmuch as the entrance of gas takes place suddenly, symptoms develop rapidly and are extreme. In some instances there are symptoms of shock; a weak, irregular pulse, a pale, anxious countenance, the skin covered with cold sweat, which, together with orthopnooa, produces a picture of mor- tal agony. The physician's attention is at once directed to the heart, the examination of which reveals a most singular group of objective symptoms. Physical Signs.- — Insijection and Palpation. — These afford evidence of pericardial distention but not of the .nature of the dis- ease, and are of minor importance since the diagnosis is readily established by other means of exploration at our disposal. Percussion. — The phenomena perceived by percussion are unique ; instead of cardiac dulness, encroached upon and sur- rounded by pulmonary resonance, the pra?cordiuni is found to be tympanitic, either throughout or at its upper portion. If the peri- cardium contains fluid, as well as air or gas, there is dulness over the dependent part and high-pitched tympany above. Gas being lighter than the exudate, change in the patient's position from the recumbent to the upright, and from side to side, causes the gas to move about, so as to be always above the level of the fluid; hence there is change in the location of dulness and tympany ac- cording to the posture of the i)atient. In the erect position dul- ness occupies the bottom and tympany the apex of the sac. If the patient lies on his left side the fluid gravitates in that direction, with corresponding dulness surmounted by tympany ; and, on the other hand, the assumption of the right lateral decubitus causes a corresponding alteration in the relative position of the gas and liquid, with resulting transposition of tympany and dulness. Moreover, the larger the amount of exudate the smaller the space allotted to the gas, and hence the higher the pitch of the tym- panitic note. Stokes claimed in one case to have detected " cracked-pot " resonance. AuscuUation. — Perhaps the most striking features are the peculiar sounds ol)served on auscultation. The movements of the heart cause an agitation of the gas and li(|uid contents of the sac, and hence a true succussion-sound or splaslhin.g. This is variously described as churning, splashing, or like that produced by a water- wheel. These are sometimes accompanied by that musical sound PNEUMOPERICARDIUM 135 known as the metallic tinkle, likened to the dropping of water. This pericardial splashing is of precisely the same character as the hypocratic succussion-sound elicited by shaking a patient with pneumohydrothorax. In some instances these metallic sounds are audible at a distance from the patient's chest. Diagnosis. — This combination of a clear ringing tympanitic percussion-note with sjDlashing in the cardiac area is so unique that an erroneous diagnosis can scarcely be made. It seems to me, therefore, far afield to discuss the differential diagnosis between this affection and dilatation of the stomach or pulmonary vomica in immediate proximity to the heart, which are conditions said by some authors to render a mistake in diagnosis possible. Finally, the confounding of this disease with the presence of air and fluid within the pleural cavity is scarcely likely, if one will bear in mind that in pneumothorax the succussion-sound is only obtained when the patient's body is agitated, while in the affection under discussion the peculiar sound is present even when the patient is at rest. Prognosis. — This is always serious, yet in traumatic cases there is hope of cure through surgical interference, while the same may be said regarding cases associated with purulent pericarditis. Should gas gain entrance to the pericardium, and be not followed by infection of the sac and inflammation, there is a possibility of its ultimate absorption. Moreover, the prognosis depends upon the suddenness of the formation of pneumopericardium. If this is sufficiently rapid to occasion symptoms of shock, there is strong likelihood that the patient will succumb. If, on the other hand, the condition develops slowly, symptoms may not be very urgent, and time may be allowed for surgical intervention. Treatment. — It goes without saying, that in most cases if sur- gical skill cannot remove the cause, other treatment, no matter how energetic, will be found unavailing. The same principles govern the therapeutic management as in other forms of pericardial dis- ease. Supporting and stimulating measures are aways indicated, and may even enable the patient to rally from the initial shock. Pain and distress should be relieved by a dose of morphine admin- istered hypodermically. Heat should be applied to the extremi- ties. Camphor, ammonia, ether, and brandy are useful stimu- lants, and should be given freely. The physician should not for- 13G DISEASES OP THE HEART get the great value of stryeliniue and digitalis in su])])ortiiig the heart; the former should be administered under the skin. IV. TUBEK( TLOSIS OF THE PEKICAKDIUM Morbid Anatomy. — Tuberculosis produces in the pericar- dium all of the characteristic lesions to which it may give rise in other regions of the body. The process may be acute or chronic in course, and either exudative, productive, or destructive in nature. The acute process is not often to be distinguished from an ordinary acute pericarditis except by microscopic and bacterio- logical methods. The exudate may be fibrinous, sero-fibrinous, or jnirulent, but tuberculous pericarditis shares with the inflamma- tion of malignant disease the distinction of being the most fre- quent cause of lux'morrliagic exudation in the pericardium. Tuber- cles may not be demonstrable post mortem, and when found are often exceedingly small, even microscopic. They are usually found on the parietal layer of the sac, owing to the frequency with which the infection extends from neighbouring viscera. The mil- iary tubercles may be covered by the fibrinous exudate, and are then to be discovered by detaching tlu; fibrin. They uuiv, however, be easily seen, and when collected in groups give rise to areas of caseation. These caseous areas may invade the myocardium, and in one instance a cheesy mass had perforated the wall of an auri- cle and projected into its cavity, being covered by a thrombus where it was in contact with the blood. Again, when the production of granulation tissue is the pre- dominating feature of the ])rocess, the two layers of the pericar- dium are bound together by a bluish translucent mass of new- formed tissue. This of course becomes white as it grows older, and the condition of adherent pericardiimi is produced. Only rarely is the caseous mass calcified after the cessation of the active process — calcification being more comiiioii in the inspissated re- mains of })urulent exudates. Acute pericarditis is probaI)ly tuberculous in a larger propor- tion of cases than has been supposed, and indeed cannot be con- sidered a rare condition. Of 1,048 autospies on adults dead from all eauses, Wells found this condition in 10 cases, or nearly 1 per cent; and since in 128 cases the pericardium was actively involved, TUBERCULOSIS OP THE PERICARDIUM 137 the 10 cases ainoiint to about 8 per cent. Osier reports 7 per cent from his series of cases. Chronic tuberculous pericarditis may follow an acute attack, and in this case the post-mortem findings are those of an ordinary chronic j)ericarditis, with the addition at times of grayish tuber- cles, or of areas undergoing caseous degeneration. It is the excep- tion, however, rather than the rule, to find distinct evidences of tuberculous origin, even in cases in which the clinical history almost conclusively proves this. Indeed, in spite of the large number of cases of acute pericarditis that are tubercular, and which pass on into the chronic form, it is very exceptional to dis- cover any conclusive post-mortem evidence of tuberculosis in cases of chronic pericarditis. The findings include thickening of the membrane and more or less complete adhesions of the two layers, the translucent bluish granulation tissue of the acute stage having been replaced by firm, white cicatricial tissue. Pericardial tuberculosis may be chronic from the outset, in which event the lesions are more apt to be of a distinctly tuber- culous nature, tubercles and caseating areas being common. Etiology. — Authors distinguish a primary as well as a sec- ondary form of pericardial tuberculosis. According to Osier, the primary form may be " associated only with caseation of the bron- chial or, ^particularly, the anterior mediastinal glands." In other cases there are no such associated lesions, and in these the tuber- culous affection of the pericardium is mipossible to explain. The secondary form is the one generally encountered, and de- pends upon previously existing tuberculous disease elsewhere in the body. This may be caries of a vertebra, a rib, or the sternum, caseous bronchial or mediastinal glands, tuberculosis of the lung, pleura, or retroperitoneal lymph-glands, or tuberculous peritonitis. Occasionally miliary tubercles within the pericardium are a part of a general miliary infection. This form of pericardial disease is most common between the ages of fifteen and thirty, yet has been seen in individuals at either extreme of life. Osier met with a case in a child of five, Duck- worth in an infant of only five months, and Lajard in a woman of eighty-eight. A patient of mine who died of pulmonary con- sumption, with acquired dextrocardia, and in whose adherent pericardium tubercles existed, was a j'Oung man of eighteen. The 11 / 138 DISEASES OP THE HEART disease affects both sexes, but for some strange reason appears to be rather more common in males. Other predisposing causes are all those conditions that render an individual susceptible to this form of infection. Symptoms. — In most cases the disease is wholly latent, and is only discovered on the autopsy table. This is due to the fact that the disease is generally subacute or chronic, and arises insidiously. If it gives rise to ac\ite inflammation with effusion the symptoms arc those of acute pericarditis from other causes — pain, palpita- tion, fever, friction-sounds, and, upon distention of the sac, the pressure-effects already considered. Even an exudative pericar- ditis of this origin nuiy in some instances pursue a chronic course. Physical Signs. — Objective manifestations of the disease are wanting unless the affection is declared as an acute process. When such is the case there are the fremitus, pericardial friction- sound, and, with filling of the sac by exudation, the evidence of fluid distention — i. e., triangular area of dulness and disappear- ance of the cardiac impulse, etc. ; in short, the signs already de- scribed in the chapter on Acute Pericarditis. Diagnosis. — Owing to the insidious onset and latent naturb of this disease it is rarely diagnosticated during life. If in the course of pulmonary tuberculosis or of pleuritis in a tuberculous subject the physical signs of pericardial involvement should make their appearance, one might with confidence make the diagnosis of pericardial tuberculosis ; but without such favouring conditions it is not at all likely that the disease would be discovered. Prognosis. — This is not always serious so far as it affects the duration of life, yet it undoubtedly contributes its share to the unfavourable termination of the general tuberculous disease. Its remote effects are an adherent pericardium and cardiac insuffi- ciency. The appearance of a tuberculous pericardial effusion in the late stages of pulmonary tuberculosis, the patient being al- ready rnflu'C'tio, would undoubtedly hasten the fatal issue. Treatment. — This is to be conducted on the lines already laid down for the management of other forms of acute pericarditis. V. SYPHILIS OF THE PERICARDIUM Invasion of the pericardium by sy])liilis is so rare an affection that most text-books on diseases of tlic Iicnrt citlier do not con- SYPHILIS OF THE PERICARDIUM 139 sider it at all or give it the very briefest possible mention. Eich- horst, for example, simply states that gaimmata in this situation have been described by Lancereaux and Orth. In Allbutt's Sys- tem of Medicine I fail to find any mention of syphilis under dis- eases of the pericardium, and the same may be said of Hayden , and Walslie in their classical works on the heart. Gibson, whose remarks on this subject are more voluminous, devotes but a single page to it, and would seem to have been largely indebted to Mra- cek's jDaper, which has likewise furnished the inspiration for the following brief consideration: Morbid Anatomy. — Syphilis of the pericardium is always a very rare affection, and is almost never met with unassociated with syphilitic changes in the heart-muscle. When present, the disease is limited to the visceral layer and manifests itself either as gummata or circumscribed thickenings. Although cases have been described as syphilitic pericarditis with sero-fibrinous exu- dation, Mracek is of the opinion that their syphilitic nature is open to doubt. Of the two forms in which pericardial syphilis declares itself, fibrinous thickening is much the more common. At the time Mracek's monograph appeared only 3 authenticated cases of gumma within the pericardium had been described — one each by Lancereaux, Orth, and Mracek. The portions of the epicardium that appear thickened and fibrous are usually found to overlie and be intimately connected with areas of proi;ounced myocardial fibrosis or a gumma situated within the heart-muscle. The development of connective tissue usually begins in the immediate neighbourhood of the blood-ves- sels, and then extends more or less widely into the surrounding parts. In the second case of Mracek's series, in which the epicardium was thickened and elevated in a circumscribed zone, immediately overlying a small gumma, the microscope revealed signs of recent inflammation of the adipose tissue. This tissue was thickly infil- trated with cells, particularly in those parts next to the muscle- substance and around the borders of the gummy tumour. Imme- diately above the gumma there was, in addition to cellular infiltra- tion, a pronounced hyperaemia of the veins and capillaries. On the overlying surface of the epicardium the fibrous tissue was old and firm. 140 DISEASES OF THE HEART In the course of time the blood-vessels suppl^'ing the newly formed connective tissue undergo obliteration, and the latter be- comes transformed into firm cicatricial tissue. Thickening of the serous membrane is not necessarily associated with a deposit of fibrin, and consequently pericardial adhesions are not always ob- served. In some instances, however, the two layers are found loosely united in the areas in which the connective tissue has undergone hyperplasia. Total obliteration of the sac is almost never encountered. Syphilitic pericarditis is a very chronic process, much more so than is tuberculous pericarditis; and Mracek affirms that in those cases in which it is difficult to determine whether the process is tuberculous or syphilitic, the presence of a sero-fibrinous or ha?morrhagic exudation tells in favour of its tuberculous origin. In cases of exudative pericarditis syphilis is the last thing to be thought of. In some instances the sac may be found to contain a small amount of clear serum, but when present this is a transuda- tion due to compression of the blood-vessels by the products of sy})liilitic disease. Very rarely lupmopericardium may also be produced, as in one case by a rupture of a small cardiac aneurysm, itself the result of syphilitic fibrous myocarditis. Etiology. — Syphilitic disease in this situation is a late mani- festation of the infection. There are no known factors which determine its invasion of the pericardial sac, but, as it is a consti- tutional disease, it is only singular that it is not more frequently 2)resent in this location. Symptoms. — Syphilis of the pericardium either occasions no syinj)tiiiiis, or these arc obscured by those of syphilitic disease in other ])arts of tlie body or in tlie heart-muscle. luasniucli as pericardial clianges of this nature are almost always found in con- nection with luetic disease of the myocardium or endocardium, it is impossible to say how much, if any, of the symptomatology is to be attributed to the pericardial disease. It is liighly probable, however, that the chief role in this res])ect is ])layed by the myo- cardial (h'geueration or the sclerotic endocarditis, as the case may be. The cardiac niaiiifcstations will be fully described in the cliii|)tcr on Heart Sy])liilis. Physical Signs. — l^lx<'c|)t in the rare cases in which the pericardial changes lead to tli(; development of a friction-sound CARCINOMA AND SARCOMA OP THE PERICARDIUM 141 or to dropsical distention of the sac, there are no distinctive ob- jective signs of the local disease. Diagnosis. — Even in a luetic patient with distinct cardiac symiDtoms, they are far more likely to be due to syphilis of the myocardium than of the pericardium, and hence one should be very guarded in making the diagnosis of the latter condition. The intra-vitam recognition of pericardial syphilis is on the whole, therefore, very unlikely. Prognosis. — Per se pericardial syphilis cannot be regarded as a dangerous affection; the adhesions it induces are usually so circumscribed and loose that they probably exert little if any in- jurious influence in the way of cardiac hypertrophy and dilata- tion. In general it may be stated that the prognosis is that of syphilitic disease of the heart-muscle, which, as experience shows, is very amenable to proper management. Treatment. — This consists of the vigorous employment of mercury and the iodides, and need not here be discussed. VI. CARCINOMA AND SARCOMA OP THE PERICARDIUM Malignant disease, like syphilis, attacks the pericardium with such infrequency as to merit but brief consideration. Morbid Anatomy. — Owing to the extreme rarity of pri- mary tumours of the sac, but little can be said concerning them. Williams and Miller have reported a case of sarcoma of the peri- cardium in a boy of thirteen. The tumour was a diffuse, small- celled sarcoma of the parietal layer, which had produced uniform thickening, but had not invaded the epicardium. There was no dis- coverable involvement of the lymph-nodes in any other part of the body, and for this and other reasons the authors concluded that the growth had originated in the lymphatic structures of the sac itself. Of secondary tumours, those most commonly invading the sac are lymphosarcoma from the mediastinal nodes, and carcinoma from the stomach or oesophagus. The new growth may uniformly infiltrate the parietal layer of the sac, or single nodules may pro- ject into its interior. There is always more or less fluid in the sac, either of inflammatory or of dropsical nature. The inflam- mation due to cancerous disease of the pericardium is particularly apt to produce a ha?morrhagic exudate — being in this regard like the tuberculous disease. 142 DISEASES OF THE HEART Etiology. — Primary malignant disease of the pericardium is so rare that, according to Gibson, the only authentic case on record was the one observed by Koester. Sir William Broadbent has, however, reported an instance of sarcoma, which was thought to be primary, and I have mentioned above the case reported by Williams and Miller. In the vast majority of cases this affection of the sac is secondary to new growths in other situations, as in the (psopliagus, lungs, pleura, mediastinal glands, liver, etc. Symptoms. — As a rule this disease of the pericardium is latent or the clinical picture is that of the primary tumour. Physical Signs. — So far as known, there are no distinctive physical signs of malignant invasion of the pericardium. If such are produced, they are those of secondary inflammation or of drop- sical distention of the sac, and require no repetition. Diagnosis. — This is rarely if ever possible, and would natu- rally depend on objective manifestations of pericardial disease, which, as just stated, are very uncertain. Prognosis and Treatment. — The former is hopeless, since the disease is not amenable to surgical interference, and the lat- ter must be confined to measures calculated to relieve suffering and promote euthanasia. SECTION II DISEASES OF THE ENDOOAEDIUM CHAPTEE IV ACUTE ENDOCARDITIS This is an inflammation of the lining membrane of the heart, which it has long been customary to divide into two forms, for rea- sons apparent in the various adjectives applied to them. Thus one is called simple or benign, because it does not often destroy life directly, but permits the patient to recover, although with valvular lesion. The terms vegetative and verrucose are also ap-' plied to this variety, particularly by the Germans, on account of the nature of the inflammatory changes induced. Simple and benign refer to its clinical manifestations, verrucose and vegeta- tive to its anatomical characters. The other form, fortunately much less frequent than the pre- ceding, is spoken of as malignant, to designate its usually fatal ending ; and infectious or infective, in allusion to certain etiological and clinical characteristics. Its anatomical features, on the other hand, are shown by its other names — ulcerative, dij^htheritic, mycotic. Diphtheritic was applied to it by Virchow, and mycotic by Winge, who was the first to describe microbes in the valves. In conformity with the plan of this work, which is to desig- nate diseases by their most familiar and generally employed names, these two affections will be spoken of as acute simple and acute ulcerative endocarditis. In accordance with custom, more- over, they will be considered as distinct clinical entities, although I am not unmindful of the fact that a sharp dividing line cannot always be drawn between them either clinically or anatomically. The endocardium may become inflamed during foetal as well as extra-uterine life; but the two halves of the heart are affected 143 14-i DISEASES OF THE HEART with different degrees of frequency during these two periods of existence. After birth it is the lining membrane of the left side that is generally attacked by inflammation, as is so well shown by Sperling's oft-cited statistics of 300 cases at the Berlin Pathologi- cal Institute. Of these, the left side alone was found affected 268 times, right heart alone 31 times, both together 29 times. Of the cases affecting the left side, the mitral valves were involved 255 times, the aortic but 129 times. Morbid Anatomy. — The endocardium is the lining mem- brane of the heart, and is continuous with the intinia of the blood- vessels through the various openings in the auricles and ventricles. It consists of two lamina:^ — a fibrous, very thin in most portions, and an endothelial, the latter consisting of a single layer of flat- tened cells, which are in contact with the blood. The valves of the heart are folds of the endocardium, the fibrous layer being increased to give them greater strength. The valves contain no muscular tissue, and are avascular, with excep- tion of the attached margins of the mitral and tricuspid leaflets, which contain a few very small vessels. These are the only por- tions of the endocardium that contain blood-vessels, as the mural endocardium, as well as the remaining portions of the valves, de- rives its nutriment from the blood passing over it. Lymphatics are, however, numerous. Anatomically, it is exceedingly difficult to draw any sharp dis- tinction between the benign and malignant forms, as all inter- mediate grades are found and the differences seem to be only those of intensity of the process. These differences are doubtless de- ])endent on infection by different organisms, of which a large num- ber have been described by different investigators. In the simple form the first change visible to the unaided eye is a cloudiness or opacity of the membrane. This is probably in all cases preceded by the lodgment of micro-organisms on the sur- face, which had been rendered vulnerable by some previous injury. Wyssokowitch, Prudden, and others have shown by animal experi- ments that cultures of pathogenic bacteria, injected into the cir- culation, })roduce the lesions of endocarditis only when the endo- cardium has been previously injured, as by passing a probe doAvn the carotid artery or jugular vein. This probably explains the fact that the lesions are most often found on the valvular endoear- ACUTE ENDOCARDITIS 145 (linm, as these portions are most liable to injury. In intra-uterine life endocarditis is most common in the right heart, and more often on the tricuspid than on the pulmonary valves. In extra-uterine life the lesions are most common on the mitral valve, next on the aortic, and only very rarely on the valves of the right side. Furthermore, the lesions are usually found, not Fig. 24. — Verrucose Endocarditis of Aortic and Mitral Valves. Specimen in collection of Dr. Gustav Fiitterer. on the free margins of the valve-cusps, but along a line correspond- ing to the point of maximum contact when the valves close (Fig. 24). In the case of the auriculo-ventricular valves this is on the auricular surface, while on the semilunar A^alves it is on the ven- tricular surface. From these facts it is evident that the work that the valve has to do and the strain to which it is subjected are fac- tors in the determination of the location of the process. 146 DISEASES OF THE HEART Following the appearance of cloudiness, the membrane becomes thickened and adematoiis, while the straining and pounding to which the seg-ments are subjected are very apt to produce erosions ilP'li Fio. 25. — Verrucose Endocarditis of Mitral Valve. Specimen in collection of Dr. Gustav Fiitterer. or lacerations. These naturally occur at the points weakened by the invasion of micro-organisms, and if tlu^ eroded surface is not at once covered l)y the deposit of tibiin from the blood, a consid- erable loss of substance may take place. This is far more common, however, in the malignant form, although it has been observed in simple endocarditis comi)licating rheunuitism. !More commonly the eroded surface, necrotic fi-om the action of bacteria, is at once covered by a de]X)sit of fibrin from the blood. This fibrin forms a firm warty mass of a yellowish or reddish colour, which rises above the surface of the membrane, and hence has received the name ACUTE ENDOCARDITIS 147 of vegetation. The name is, however, not very appropriate, as the so-called vegetation is in its formation and composition a throm- bus, and may contain all the elements of a thrombus, fibrin, red and white blood-corpuscles, and blood-platelets. By the time that the vegetation has reached such a size as to be noticeable to the unaided eye, the process of repair has begun at its base. 'J'his is accomplished by the ingrowth of young con- FiG. 26. — Malignant Vebbucose Endocarditis of Mitral VAL^•E. Specimen in collection of Dr. Gustav Fiitterer. nective-tissue cells and the formation of a granulation tissue which finally replaces the entire mass of adherent fibrin, and in time becomes covered by the endothelium from the neighbouring 148 DISEASES OF THE HEART mt'iiibraiie. The growth can now he more i)ro])crly terniod a vege- tation, as it is essentially an outgrowth from the snbjacent tissue, and some authors limit the term to this form. The accumulation of fibrin over such an afFeetcd area may be very large, but the average vegetation is about 8 millimetres in length. When of the irregular form described, the endocarditis is spoken of as the warty or verrucose variety (Figs. 24-27). The vegetation may be large and polypoid in shape or long and string-like, attached at one end so as to swing in the blood- stream. The disease is then spoken of as of the polypoid or vil- lous variety respectively. The vegetation may be too large for complete organization, and may soften and redissolve in the blood-stream, or portions may break off and be carried in the blood until they reach a vessel of too small calibre to permit their passage, when they plug the vessel and cut off the circulation of the parts sujjplied by it. The infarcts thus produced by the emboli of simple endocarditis are usually of a non-infective nature. The further repaii- of these lesions and the changes in the valves consequent to them are dealt with under the head of Chronic Endocarditis. The malignant form of the disease is nuiinly characterized by the intensity of the infection, and the fact that embolic phenomena are more common than in the sim])le, and are almost always of a sei)tic nature. The local lesions may be vegetative, suppurative, or ulcerative, depending on the nature and violence of the infec- tion. In all cases the necrosis of the affected areas is more marked than in the simple form, and ultimately leads to loss of substance, the portions sloughed off passing into the circulation as septic emboli. The valve-cusp thus ulcerated is naturally weakened, and fre- quently gives way before the pressure of the blood, forming small pouches in the valve, the so-called vahuhii- aneurysms, or giving way completely perforate the valves. Acute Viilvulai' insufficiency can thus be ])roduced (Fig. 27). A valve-lea lid may become partially detached, and the free end swing in the blood-stream. Ulceration of the ]i;i])illai-y muscles or tlie eliordie tendina' nuiy produce stretching or I'ujjture of the cords, or :i tlii'()ud)us covering the affected area nuiy mat them closely together. When the lesions are situated on the mural endocardium, per- ACUTE ENDOCAKDITIS 149 foration is possible, and the interventricular sseptum has been found perforated, or communication has been established between auricle and ventricle, or betAveen the right auricle and the aorta. When the disease is produced bv bacteria of suppuration, abscess Tig. 27. — Malignant Verrucose Enducaeditis of Aortic Valve, with Perforation OF A Cusp. Specimen in colleetion of Di'. Gustav Fiitterer. of the myocardium may result, and, discharging, empty its con- tents into the circulation. (Septic Emboli.) Associated with acute endocarditis are found the anatomical changes produced by the disease to which the endocarditis is sec- ondary, since it is extremely rare to find it as an independent dis- 150 DISEASES OF THE HEART ease. It is very often associated with the chronic form of endo- carditis. The secondary changes in the simple form are trifling, and as a rnle produce no symptoms. It is only in the conrse of time, when the disease passes into the chronic form, that serious damage is done. Secondary to the malignant form, on the contrary, are circulatory disturbances consequent on the ulceration or perfora- tion of the valves, and more important still, the metastatic foci of disease set up all over the body by means of septic emboli. The spleen and kidney are especially apt to suffer in this way. The infarcts so produced may be few, or innumerable muiide foci of suppuration may be scattered over the whole body. It is to these septic emboli that this form of the disease owes its malignant character. Etiology. — It may be stated as a general proposition, that the bacterial origin of acute endocarditis, both simple and ulcerative, has been established. Heiberg's discovery in 1872 of micrococci in the thrombotic masses of the malignant form has led to an unbroken series of researches and experiments by the most bril- liant pathologists in Europe and this country, with the result that the cloud of doubt and speculation once enveloping this sub- ject has at length been cleared away. Special activity in this work was displayed during the years immediately following 1885, and prominently figuring in this line of investigation are the names of Virchow, Klebs, Birch-Hirschfeld, Koester, Weichsel- baum, Fraenkel and Saenger, Ilosenbach and T^etter in Germany; Gilbert and Lion, Cornil and Babes, Ivoux, Josseraut, ^nd Dessy, in France; Dreschfeld, Cayley, Purser, in England; Osier, Flex- ner, and Prudden in this country. It is manifestly .impossible within the limits of this work to give a detailed account of the nature of the researches made by these eminent workers, and it must suffice to state the facts that have been established. Micro-organisms have been quite generally found in cases of malignant endocai^ditis, some of them being the same as those found in other infectious diseases, a few being specific to endo- carditis. Occasionally two or more varieties have existed in the same case. The bacteria most usually discovered have been strep- tococcus pyogenes, ])articularly of erysipelas; staphylococcus pyogenes, aureus, and albus, and the micrococcus lanceolatus. ACUTE ENDOCARDITIS 151 The gonococcus, the bacilhis of typhoid fever, of diphtheria, of in- fluenza, and of tuberculosis have also been found, although much less frequently. Weichselbaum identified certain bacteria, which, because they appear to occur only in endocarditis, he named bacillus endocar- ditidis griseus and capsulatus and micrococcus endocarditidis rugatus. The bacillus immobilis et fostidus was also found by Fraenkel and Saenger. That these various bacteria are capable of inducing endocarditis has been shown by experimentation on ani- mals. A number of investigators injected pure cultures of micro- organisms obtained from infected valves into the jugular veins of dogs and rabbits, and afterward found these cocci, often in masses, both on the surface and in the deeper layers of both aortic and mitral valves, the valves themselves showing characteristic inflam- matory changes. By some experimenters it was asserted that endocarditis could be only thus produced after the valves had suf- fered trauma by chemical or mechanical irritation. Others, on the contrary, claimed to have produced endocarditis by injection of microbes into animals without previous injury of the endo- cardium. In numerous instances the bacteria found on the affected valves have also been identified in the septic emboli thro^vn off during the course of the disease, while in a few instances the blood of patients suffering from infective endocarditis has been found to contain septic organisms. The bacteria found in the lesions of ulcerative endocarditis occurring as a complication of typhoid fever and diphtheria are usually pyogenic. This is also true of most cases of gonorrhoeal endocarditis, although the gonococcus has been definitely identi- fied in the endocarditic lesions. . The pneumococcus of Fraenkel has been frequently found in endocarditis, both simple and ulcera- tive, but, according to Osier, more frequently in the latter variety. It appears well established that a primary endocarditis of bac- terial origin is occasionally, although rarely, met with. Most in- stances of endocarditis are secondary to some general or local in- fection. There has been considerable speculation, and for a time there was a heated discussion, particularly between Klebs and Koester, over the route by which microbes are carried to the infected valves. 152 DISEASES OP THE HEART Klebs and \'ircliow inaiiitaiiied they were (l('])ositod on the surface of the cvisps ont of the blood, while Koester declared they were carried thither in the niinnte capillaries situated in the deeper layers of the valves. He maintained that the masses of cocci caused embolic plugging of the vessels, which was followed by rup- ture, thus setting free the bacteria and allowing them to reach the surface. x\gainst this explanation was urged the scarcity of blood- vessels in the valves, as well as the fact that the earliest evidence of inflammatory change is along the line of contact of the cusps. It is now held that both contentions are correct, but Virchow's view is accepted by the majority of observers. The adherents of Virchow's opinion believe that the pressure of the blood forces the micro-organisms between the endothelial cells of the endocardium — a theory that probably accounts for the develoi)ment of endocar- ditis in the left heart after birth and in the right side during fa3tal existence. As is well known, blood-pressure is greater in the right ventricle before and in the left ventricle after birth. Another explanation for the localization of endocarditis is that inasmuch as oxygen is necessary to the growth and activity of most bacteria, these organisms are most active in blood relatively rich in oxygen, a condition obtaining in the right cardiac chambers in the foetus and in the left during extra-uterine existence, A most interesting question relates to those conditions that de- termine whether the endocarditis is to be simple or ulcerative, since both forms are of microbic origin, and . some of the same organisms have been found in the endocarditic vegetations of both varieties, What are the factors that determine the malignancy or benignity of the affection ? It has been suggested that this de- pends upon the number of bacteria present. It is more probable, however, that when healthy valves are attacked the nature of the endocarditis depends upon th(; virulence of ihv infecting organ- isms. Other factors are of influence, however, aside from the nature or virulence of the bacteria, and these will now be con- sidered. Simple Endocarditis. — Articular rheumatism is the disease par excellence in which acute; sim])l(! endocarditis is most frequently observed. Why this is, is not as yet satisfactorily established, but there appears to be a growing belief among pathologists in the bacterial ACUTE ENDOCARDITIS 153 origin of rheumatism, as opposed to the once prevalent notion of its dependence upon lactic acid in the blood. The relative fre- quency with which these two affections are associated is variously estimated. Of 32 cases of inflammatory rheumatism that termi- nated fatally, Fagg found the valves affected in all but 12. Ac- cording to Hayden, Peacock found endocarditis in 16 per cent of his cases of rheumatism, while Fagg puts the ratio as high as 40 or 50 per cent. French as well as English observers put the propor- tion much higher than do the Germans; thus Bouillaud, 55 per cent ; Budd, 48 per cent ; Fuller, 23 per cent ; while Wunder- lich and Lebert give it as 23 per cent, and Bamberger 20 per cent. These differences probably depend upon the severity of the rheu- matic attack, since all observers agree in the statement that the valves are far more likely to become inflamed in acute than in sub- acute or chronic forms of articular rheumatism. Endocarditis is especially liable to occur in a first attack of arthritis, particularly when this is severe and several joints are involved. There is no doubt, however, of its development as a result of subacute or chronic rheumatic manifestations. Hayden is of the opinion that in rare instances endocarditis may be the only manifestation of the rheumatic poison. The period in the course of acute rheumatism at which endocarditis may occur is given by Hayden from the sixth to the ninth day, and by Fuller as from the sixth to the twentieth day. The earlier the time of life at which acute rheu- matism develops, the greater is its liability to set up acute endo- carditis. The next most frequent predisposing cause of this form of en- docardial inflammation is generally stated to be chorea. Endo- carditis of this origin is numerically less frequent than the rheu- matic, whereas the relative frequency of chorea and endocarditis is thought by some observers to be greater ; thus, of 16 cases of fatal chorea occurring at Guy's Hospital during twenty years, Fagg found post-mortem evidence of endocarditis in 14. Here, again, there has been much speculation concerning the reason of the asso- ciation between chorea and endocarditis. By some the latter is attributed to acute articular rheumatism, which is now recognised to be frequently associated with chcrea. Thus in 40 cases of the latter affection manifesting organic heart-disease, Gowers found in all a trustworthy history of associated rheumatism. There are 12 154 DISEASES OF THE HEART some observers, on the other liand, who hold that chorea is capable of causing endocarditis independently of associated or antecedent arthritis. Since girls are undeniably more subject to chorea than are boys, endocarditis of this origin is observed more frequently in the former sex. Scarlatina and measles are also accredited with the causation of endocardial inflammation. This may be either a secondary re- sult, or the endocarditis may be due to a mixed infection. Inas- much, however, as scarlet fever is not infrequently followed by rheumatic manifestations, the endocarditis is held by some to be referable to the latter and not to the former affection. Other irruptive diseases, particularly enteric fever and small- pox, are also capable of setting up endocarditis, but as subse- quently stated, this is more likely to be malignant than merely simple. Although gonorrha^a is more likely to cause the ulcerative form, vegetative endocarditis undoubtedly occurs as a result of gonococcus or perhaps a mixed infection, a conclusion that would seem justified by the entire absence of any other etiological factor in certain cases of valvular disease. As previously stated, there is both clinical and pathological evidence of the occurrence of acute endocarditis in the course of croupous pneumonia or in consequence of pneumoeoecus infection. Although such an endocarditis is more likely to be ulcerative, it may nevertheless be benign. In a fatal case of pneumonia, which had exhibited no evidences of endocarditis during life, Haushalter found a colony of pneumococci in the interior of one of the mitral cusps, while the otlior showed an almost invisible swelling of the endothelium near the point of insertion of the valve. From this he concluded that not only is acute endocarditis a probable se- quence of pneumonia, but also endocarditic changes of a slow sclerotic type may be ultimately set up. His conclusions were as follows: (1) The absence of murmurs during life or of naked eye changes post mortem does not j)rove the integrity of the valve, since during the course of the pneumonia the pathogenic organ- isms may be carried into the interior of the valve, and thus prove the starting-point of future valvular mischief. (2) The possi- bility of such an endocarditis should be remembered, since a latent period may exist between the primary disease and the develop- ACUTE ENDOCARDITIS 155 ment of the endocarditis. (3) The possibility of such an occur- rence renders it advisable for the physician to keep a patient under prolonged observation after recovery from pneumonia, and to make repeated examinations of the heart, that he may thereby detect the earliest manifestations of a valvular lesion. Injury of the valves through strain is generally recognised as one of the conditions predisposing to the occurrence of acute endo- carditis. By some it is contended, however, that strain alone is not sufficient, but must be united with some previously existing defect. Strain is probably capable of setting up fresh inflamma- tion of a valve, already the subject of a former though slight endo- carditis. Rupture of a cusp may undoubtedly prove a starting- point of acute inflammatory change. Age is an undoubted predisposing factor, acting in most cases, however, in the way of rendering individuals susceptible to articu- lar rheumatism, the exanthemata or other diseases, themselves capable of bringing about endocarditis. Supporting this view or interpretation of the influence of age is the statement that rheu- matism is more likely to occasion endocarditis in childhood than in the later periods of life. Both sexes are liable to endocarditis, yet according to some this affection is more frequent among fe- males, although males are said to be more subject to articular rheumatism. To my mind there is nothing in sex, per se, render- ing the endocardium more vulnerable in females than it is in males. Females are more subject to chorea and, by reason of their sex, to puerperal septicaemia and infections from pelvic disease, and hence it may well be that they furnish a greater numerical proportion of cases of acute endocarditis, benign as well as ulcera- tive. With increasing experience, I find myself growing in the conviction that hereditary influence plays a not unimportant role in the development of endocardial disease. Cardiac, and particu- larly valvular lesions, as such, cannot be inherited, but it seems to me that in some families whose members evince pronounced rheu- matic diathesis, there is an inherent vulnerability, possibly heredi- tary, of the endocardium in the presence of rheumatism. Ulcerative Endocarditis. — It is a well-known fact, established both by clinical and post-mortem observation, that the malignant form is particularly prone to .develop as the result of fresh bacte- 156 DISEASES OF THE HEART rial invasion in valves already the seat of chronic endocarditis or sclerotic change. This is particidarly trne of the aortic-valve apparatus. Infections endocarditis is also specially liable to attack indi- viduals suffering from exhausting diseases or cachexiie, chronic alcoholism, cirrhosis of the liver, hepatic abscess, cancer, etc. General infection, as pyannia, puerperal septicaemia, influenza, diphtheria, variola, and localized septic processes or abscesses, predispose to malignant rather than to simple endocarditis. Flex- ner found stai)hylococcus aureus in a case of endocarditis in which the atrium of infection was leg ulcer; in another, staphylococcus, the point of entrance being the intestine ; in still another, strepto- coccus and staphylococcus, the atrium being hepatic abscess. This form of acute endocarditis has been particularly frequent in asso- ciation with puerperal septictemia due to infection either of the uterus or its adnexa. It has been known to follow tonsillitis, and even so apparently trivial a local process as a furuncle. Croupous pneumonia or a pneumococcus meningitis has not infrequently been found as the prinuiry infection in cases of ulcer- ative endocarditis. Although the pneumococcus may occasionally give rise to the simple form, it is much more frequently respon- sible for ulcerative inflammation of the valves. This malignant form is also stated by Dreschfeld to have been associated with 7 cases of gall-stones " with or without suppuration of the biliary passages." Dreschfeld thinks that the discovery of the bacterium coli commune in diseases of the biliary passages may explain their connection with acute endocarditis. In this connection it is inter- esting to note that Flexner, in one case of endocarditis associated with carcinoma of the pylorus, identified the bacillus coli, together with the bacillus pyocyaueus ; and Ilasenfeld has reported arti- ficially produced endocarditis in animals infected with the bacillus pyocyaneus. Of further interest is the fact that, despite the severe infectious process, distinct hy])ertro])hy of the heart was observed to develop in so sliort a time as a week. Finally, this form of endocarditis, although much less fre- quently than the siiiii)l(', nuiy exist in connection with articular rheumatism, as mentioned by Osier and others. Its dependence upon the di])htheria bacillus, though rare, is undoubted. Howard has rej)orted a case in which a bacillus was ACUTE ENDOCARDITIS 157 discovered identical in all respects with tlie Klebs-Loeffler bacillus. It is now generaly recognised that septic endocarditis, although capable of being set up by pathogenic organisms, is most fre- quently caused by streptococci and staphylococci. Symptoms. — Just as it is sometimes difficult from a patho- logical standpoint to say whether the soft, easily detached thrombi belong to the vegetative or infective variety, so a sharp dividing line cannot always be drawn clinically between the two forms of endocarditis. Nevertheless, I think it will conduce to clearness if, as is usually done, they are described separately. Acute Simple Endocarditis. — As this process frequently occurs in the course of articular rheumatism, of which it may be regarded as a manifestation, and not a convplication, its symptoms are often masked by those of the arthritis. If the endocarditis be of a mild type, it may pursue a latent course, and only be detected by its results when years subsequently the individual is found to have a valvular lesion, probably dating back to some almost forgotten rheumatic attack. Such a possibility should always be borne in mind by any physician attending a case of articular rheumatism, however mild, and should incite him to a daily examination of the heart, since many times acute endocarditis is only recognisable by such means. If in the course of rheumatic fever, especially towards the end of the first week, the temperature unexpectedly rises, and can- not be accounted for, by involvement of a fresh joint or some com- plication, attention should be at once fastened upon the heart. If the endocardium has become inflamed, with or without implica- tion of the pericardium, the fact will eventually declare itself by the physical signs subsequently to be described, even though sub- jective symptoms are wanting. In some cases subjective symptoms become manifest from the start, and are then due probably either to the severity of the endo- carditis or to associated myocarditis or pericarditis. These symp- toms are pr^ecordial pain more or less pronounced, or an ill-de- fined sense of oppression and discomfort in the cardiac region, pal- pitation, the heart-action in some cases being quite tumultuous, and particularly a subjective sense of dyspnoea. By this term is meant a sensation on the part of the patient of air-hunger, which may not be evinced by laboured or hurried respiration, but which 158 DISEASES OF THE HEART is usually greater than can be accounted for upon examination of the chest. I cannot now recall a single case of acute endocarditis, recognised as such, in which this symptom was not present. In some instances this feeling of breathlessness actually amounts to orthopna-a ; in others dyspnoea is paroxysmal, compelling the pa- tient to sit up in bed during the continuance of the paroxysm. In mild cases the pyrexia is likely to be mild, and possesses no pecu- liar character. In other instances the disease produces profound constitutional disturbances, with fluctuating fever and profuse perspiration, plainly suggesting infection, and with a pulse so empty, irregular, and perhaps accelerated, as to at once direct the physician's atten- tion to the heart. These are the eases difficult, if not impossible, of differentiation from the malignant form. Embolic phenomena are less frequent in the benign than in the malignant form, yet when embolisms occur the symptoms they induce are referable to mechanical interference with the circula- tion, rather than to a local or general septic process. The most usual seat of infarcts is in the kidney, intestines, and brain. They undoubtedly occur many times without giving rise to recognisable symptoms ; yet when such are produced, they are a sudden, sharp pain in the affected part or organ, chill more or less pronounced, and pyrexia. If the embolus lodge in a kidney the urine is likely to contain blood, albumin, and even i)us. Hemiplegia and aphasia, the result of cerebral embolism, may in rare instances furnish the first, or perhaps the conclusive, evidence of the existence of acute endocarditis. The following case is instructive: W. J. M., male, aged forty-eight years, height six feet, weight 176 pounds, first consulted me November 9, 1896, not, he said, because he thought himself in poor health, but because, having some heart-trouble, a friend advised him to get my opinion. Family history was un- important in its bearings upon the patient's condition, but it was stated that one sister had died of consumption, another of insanity, and a third, then living, had heart-disease. Patient declared that he had not been ill since his twelfth year, but had had syphilis at the age of twenty. After his death, it was stated by his wife that the patient had known for seven years of the existence of some sort of heart-disease. Symptoms such as dyspnoea and palpitations were denied, but the patient, when questioned ACUTE ENDOCARDITIS 159 regarding pain, said, " Once in a while a little, down near the heart." The pnlse was noted as 89, not distinctly collapsing, the left seeming slightly smaller. Carotids and subclavians throbbed stronglj^ Apex-beat in sixth left intercostal space, 3f inches from the sternum, and the cardiac impulse was heaving ; diffused from the fifth to the seventh, but maximum in the sixth interspace. Absolute cardiac dulness was practically normal, but the relative was increased to the left, extending 5| inches to the left of the breastbone, downward to the seventh rib, •and but 1 inch to the right of the sternum (Fig. 28). The first sound at apex was muiSed and the second was wanting; throughout the pr?ecordium the sounds were obscured by murmurs, both systolic and diastolic, which were audible over the entire cardiac area, but were of maximum inten- sity in the aortic area and on the body of the sternum. A snapping systolic tone was audible in the femoral artery. In the aortic area bimanual palpation with slight pressure brought out a, systolic shock and thrill. Examination of abdomen and urine was negative. The diagnosis lay between aneurysm of the ascending aorta and insufficiency of the aortic valves, but the lesion was subse- quently decided to be a valvular one of sclerotic, possibly syphilitic origin. For the next few months the patient was seen at rather iiifre- quent intervals until the last of March, 1897. In February of that same year patient was knocked down by a runaway horse, but did not think he sustained special injury. Towards end of March he began to complain of insomnia, great nervousness, and restlessness. The heart was rapid and pounding, and there was Fig. 28. — Apex-beat and Relative Dul- ness, Case of Acute Endocarditis (p. 158). 160 DISEASES OF THE HEART dyspnoea, even in repose, which increased paroxysmallv without cause. Urine analysis showed pus, blood, and albumin. Patient was ordered to keep to the house and confine himself to milk diet, with potassium citrate and tincture of digitalis in small doses, with saline cathartics daily. After about two months the urine lost all traces of blood and albumin, but patient's gen- eral condition grew worse, and he was ordered to keep his bed. Heart's action was still rapid and pounding, but regidar, and dysp- noea with paroxysmal exacerbations very marked. Patient sweated profusely, but the thermometer never showed fever. One night complained of pain in right hypochondrium below ribs, embolism was suspected, but subsequently doubted. Liver reached 3 fingers below costal arch, was moderately tender, firm, and with rounded border. The condition was thought to be pass- ive congestion without infarction. About the last of May patient developed mental symptoms, as shown by ugliness of temper, espe- cially towards wife; it appeared to be a mild acute mania, and the wife stated that the mother as well as a sister had died insane. Hyoscine hydrobromate w^as ordered, supplemented subsequently by valerianate of ammonia, with improvement, the delirium being- only occasional and ugliness less. June 2, 1897, examination showed the following: Radial pulse distinctly collapsing, venous pulsation in forearm, but external jugulars not turgid and without pulsation. Apex-beat in sixth left interspace, anterior axillary line, systolic impulse in second and third right interspaces near sternum, followed by diastolic thrill, also a more feeble pulsation in fourth, fifth, and sixth right interspaces, slight systolic shock in second left interspace near sternum. Absolute dulness, patient in dorsal decubitus, reached 6 centimetres to right of median line, and from second to sixth costal cartilage, the note being flat, with marked resistance from second rib to fourth interspace, and slightly less dull below this point. Dulness also reached 10.5 centimetres to left of median line (Fig. 29). Auscultation showed first sound at apex, dull and muffled, but no distinct murmur, a double tone audible below left clavicle and down along left axillary line; a systolic tone and soft diastolic murmur in second left interspace and outward li inch from ster- num. Tlicrc wiis also a faint second sound in the ])nlmonary area^ ACUTE ENDOCARDITIS 161 and when the patient took a Jeep inspiration and held his breath the second sound seemed to be changed into a soft murmur. The soft diastolic murmur at left of sternum was transmitted faintly downward. A painfully loud and harsh diastolic and systolic murmur was heard in second and third right interspaces, and transmitted more feebly into fifth, out to nipple and up to neck. The condition was interpreted as follows : Acute endocarditis ingrafted on a chronic endocarditis, affecting aortic valves and aorta, and producing dilatation of this vessel. jSTo evidence could be found of inflammation of other valves, and yet the great extent of dulness to right of sternum was thought due, in addition to aortic dilatation, to dilata- tion of the right auricle, sec- ondary ito mitral insufiiciency. Cough was at no time a marked symptom, except two or three paroxysms a few hours before death, when patient seemed to have pain in left lung. During the last few weeks of life there was moderate cedema of ankles and shins, also puffiness, but no pain, in left wrist and hand. Forty-eight to sixty hours be- fore death patient became comatose, with cold extremi- ties, very rapid, feeble, and irregular pulse, and. the trunk and lower extremities became studded with small brownish-red spots, that had all the characters of cutaneous embolisms. Death, which took place June 24th, seemed to be the result of gradual cardiac asthenia. The autopsy, made by Dr. W. A. Evans thirteen hours after death, was briefly as follows: Very large numbers of petechia? over abdomen, chest, and legs, about the size of a pea. Some inter- stitial splenitis and perisplenitis and zones of connective-tissue growths representing old infarcts. These were generally subcap- sular. Fig. 29. — Apex-beat and Absolute Dul- ness Later in Same Case as Fig. 28. 162 DISEASES OP THE HEART Liver. — Fatty infiltration — nutmeg. Large numbers of small islands of connective-tissue increase, quite generally distributed in subcapsular zone. A small mass of calcareous material in lower portion of right lobe, superficial. In left lobe a small fresh in- farct about 6 millimetres in diameter. Left Kidney. — Slight parenchymatous nephritis. Right Kidney. — In the cortex an old infarct 1 centimetre in diameter, over this the surface of the kidney depressed. This in- farct, fatty in appearance, reddish, surrounded by a reddish zone. It was this infarct which in March had occasioned the bloody and albuminous urine. Left Pleural Cavity. — ^o fluid, no adhesions except to dia- phragm. Left Lung. — Congested and oedematous. In anterior edge of inferior lobe an apoplectic focus about 1 centimetre in diameter, quite recent. Right Pleural Cavity. — Extensive old, firm, fibrous adhesions quite general. Right Lung. — Congested and (edematous, single ha?morrhagic infarct 2 centimetres in diameter. Pericardium. — I^o effusion, uniform adhesions between peri- cardial layers. They strip easily, appear gelatinous or mucoid. Aorta. — Tubular dilatation of aorta in its first portion. The lumen is somewhat ovoid, measuring 9 by 8 centimetres. The aortic ostium dilated with compensatory stretching of the aortic cusps. The aortic cusps, measured along their free edge, show a length of 5 centimetres, 4^ centimetres, and 3^ centimetres re- spectively. All of the cusps show ridges of atheroma, with con- siderable thickening and stiffening. At the base of the largest cusp, a calcareous plate. Thickening, redness, and some deposit of fibrin on each of the cusps, especially towards the free edge. The valves not competent. Aorta atheromatous. Areas of calcification, atheromatous ulcers, and some vegetations around these losses of substance. The left ventricle enormously dilated, its wall .J centimetres in thickness at its thickest portion. Myo- cardium is not especially fatty. Mitral valves show multiple foci of acute endocarditis, consisting of small, round red masses, the size of a pin-head. Left auricle very much dilated, right heart otherwise normal. ACUTE ENDOCARDITIS 163 Oultiires made from the vegetations give no growth of micro- -organisms. Diagnosis. — Tubular aneurysm first portion of aorta ; ather- oma of aorta and aortic cusps ; hypertrophy and dilatation of the left heart ; acute endocarditis and endaortitis, vegetative in char- acter. Recent infarcts in liver and lungs. This case illustrates the proneness of acute inflammation to attack valves that have undergone sclerotic changes. It is prob- able that the aortic regurgitation diagnosed in the fall of 1896 was due partly to incompetence of the cusps from stiffening and rigidity and partly to stretching of the ring consecutive to the dila- tation of the ascending aorta, the valves not being able to ade- quately close the ostium in spite of their compensatory stretching. With the exception of the lack of febrile temperature the symp- toms strongly suggested ulcerative endocarditis, and show how difficult and unwise it is to attempt a sharp clinical distinction between the two forms of endocarditis. The anatomical changes were those of the vegetative variety, and yet in its rapid course and fatal termination the process may be said to have been ma- lignant. Course and Termination. — As already stated, in some ■cases rheumatic endocarditis of a mild type may be easily distin- guished from infective endocarditis, while other cases seem to ■occupy intermediate ground, and clinically, at least, cannot be classed with either one or the other type. It is plain, therefore, that the course and termination are equally variable. Simple rheumatic endocarditis may pursue a favourable 'Course, and terminate in the recovery of the patient, nay, may even subside without serious impairment of the affected valve. In the majority of cases, however, the patient is usually left with a •chronic valvular lesion. Ulcerative Endocarditis. — Under this head are reckoned those •cases of inflammation of the endocardium which manifest more or less pronounced symptoms of general sepsis, whether the ter- mination is in death, by far the more frequent occurrence, or in recovery, of which instances are now and then reported. As might be expected from a consideration of the etiology and mor- bid anatomy of this class of cases, the clinical picture varies much, according as the local — that is, cardiac — or the general symptoms 164 DISEASES OF THE HEART predominate. In the majority of cases the symptoms are those of general sepsis, with very subordinate, or it may be with no mani- festations on the part of the heart. In such cases the inflamma- tory chaniies in the endocardium are to be regarded as merely an incident of the general infection, and therefore Rosenbach classi- fies these cases as merely local manifestations of a general infec- tion. The endocarditis is but one of the many possible local ex- pressions of the infection, in consequence of the profound disturb- ance of nutrition there induced. In this class of cases the conspicuous features are phenomena characteristic of pyaemia, an irregularly continuous pyrexia, with few if any rigors, sweatings, great prostration, anannia, emacia- tion, anorexia, diarrhoea, a dry, brownish tongue, abdominal dis- tention, stupor or low muttering delirium, persistent dorsal decu- bitus, and enlargement of the spleen. The pulse is only moder- ately accelerated, in most instances impressing one as being chiefly remarkable for its feebleness and want of tension, Avhile the heart may display absolutely no evidence of disease, or may be slightly __— — — 3- -- *" —-\ — .^^ A- - "^ '^^---^ T-W J 'A ■ jS aujuinj) | | { | -=^"' lO ^, ""^ _| "^ L. -_ _j __. — ■ -# . " J =Y- -L,_^ ^■"T 1 . ~^ m __ . — -^ 1 '^—j . J ■ — —-—1 _ 1 ^^ OJ ^•^ ^ '^^1^ XX jS 911 [inf) ^_ —■^~~ 1 = \ i \~\ 1 1 1 1 -U L_ I 1 ■ 1 _ .— — i "^ o — "" — — . AX- ^aS ail U t\f) ^ "^ OS f^' r — ■— AX- Ls axil uinf) 00 i __- — ' — ~~ ■ — — -____ " ■ — L i_ V i> . \ \ ■» XX -;sj- aau raaif) ^^ 05 — ] - — . __^ 1 ~ la — — ^ _ A ■~~ ■ — - ' 1^- -^ •31 ^ - — "H ~" — ^~. — ^- 1 " M y-" 1 — — ___^ ~1 ^~ 1 ______!- 1 (N _ — ■ 1 — 1 ' — ^ ] — L _ , — ^— ■ AX- . ! _l 1 1 1 1 's s °iyi CO i^ 168 DISEASES OF THE HEART without quinine, his temperature was 102.2° F., on the 9th a degree lower, while 5 grains t. i. d. on the 10th kept fever down to 100.2° F. The results thus obtained convinced nie that the quinine acted as an antipyretic, but that, in spite of doses sufficient to exert a more lasting influence in case the symptoms were due to malaria, the fever reasserting itself so soon as the drug was stopped, there was some other cause at work. The urine was now tested again for peptone, and with positive results. I therefore became satis- fied that the case was one of pyaemia. It should also be stated that the blood had been tested for the Widal reaction, and this proved to be absent. As the gall bladder had been found enlarged at the first ex- amination, and was still palpable, it was thought highly probable that there might be an empyema of this receptacle as the source of the infection. Accordingly the patient was seen by Dr. Bayard Holmes, who corroborated the gall-bladder enlargement and con- curred in the opinion of a probalde empyema. This seemed all the more likely to be the focus of infection from the fact that no disease could be discovered in the rectum or elsewhere. A few days subsequently Dr. Holmes operated on the gall bladder, but although it was enormously distended with fluid, this was not purulent, the condition being a catarrh and not an empyema. jSTo ill effect followed the operation, but the wound healed very slowly. For a day or two the temperature fell somewhat, but then resumed its former characters, bei)ig down nearly or quite to normal in the early part of the day and rising in the afternoon or evening to between 101° and 102° F. Rigors were never manifested,' and repeated queries concerning chilly sensations al- ways elicited a positive denial of them. Perspirations were also absent, or at the most amounted to no more than a scarcely per- ceptible moistness of the skin M^here covered. Week by week the patient lost in strength and flesh, and grew more ana'mic in appearance, although his ability to take consider- able nourishiiK'iit jxii-sistcd. lie also displayed slight apathy, lying flat in bed, and changing position but seldom. Pain was not com- plained of, and in vain was a daily search kept up for signs of embolism. During these weeks the pulse slowly and gradually became a little more accelerated, reaching 11 G or thereabout. Its ACUTE ENDOCARDITIS 169 striking feature was its feebleness. This want of tension, together with the growing weakness of tlie heart-sounds, induced nie to administer strychnine in doses of -gV of a grain 4 times daily, along with 5, and afterward 7 drops of tincture of strophanthus thrice daily. He was also given moderate doses of wine and whisky. It was always difficult, owing to the rigidity of the chest-wall and the voluminousness of the lungs, to satisfactorily map out deep-seated cardiac dulness, but I became convinced that the heart gradually increased somewhat in size, though no more than could be attributed to myasthenia. Pari passu with the increas- ing feebleness of the heart-sounds the systolic apex-murmur aug- mented in intensity and extent of audibility until at length it spread throughout the entire prsecordium. It remained to the last a- rather harsh blowing murmur, and no new bruits ever devel- oped. IsTeither did oedema become more than a Very slight pitting over the tibise, and I could not make out any increase in the size of the liver or more than a trifling increase in the area of splenic dulness, the organ not being distinctly palpable. In brief, the entire clinical history was that of an ever-growing anaemia, or better, marasmus with moderate intermittent pyrexia. In this respect I should think it a fair example of the type of cases described by Komberg as antemic rather than markedly sep- tic, and yet there was no doubt of the existence of a mild pyaemia. Peptone was repeatedly found in the urine, and thus, with the in- creased leucocytosis, confirmed the conclusion drawn from the tem- perature record. This is well shown by the annexed chart. Death occurred the middle of September, about eight weeks after he came under observation, ]^o autopsy was had, but I believe this Avas a pyemia, with implication of the endocardium as a secondary and not a primary event. In still other cases of ulcerative endocarditis there are rigors, sudden high elevations of temperature, and profuse sweating, fol- lowed by sharp decline of the pyrexia, the picture not unlike the paroxysms of malaria, excepting that the septic phenomena lack the periodicity of malarial infection. Murchison has narrated an instance of this kind that lasted three months, and was so sug- gestive of malaria to the friends that in deference to their wishes quinine was freely administered, but without appreciable effect on 13 170 DISEASES OF THE HEART the disease. In his case, however, there was physical evidence of an aortic valvuhir lesion. There are other cases, again, in which the temperature pursues a still more erratic course, rising and falling abruptly for days, and then suddenly sinking to normal, or it may be to below normal. Remaining thus for days or even weeks, it again assumes its for- mer irregularly intermittent type. During the apyrexial period the pulse still remains conspicuously feeble, and the patient fails to regain strength, so that by these symptoms it becomes manifest that actual improvement is not taking place. Thus, whatever the various manifestations, they are in them- selves indicative of sepsis, and there is nothing to show that the heart has become affected. Occasionally, on the other hand, the involvement of the endocardium is evinced by the appearance of cutaneous infarcts or by phenomena of embolic plugging of vessels in the intestinal organs. The lodgment of emboli in the skin is shown by the appearance on the extremities or trunk, still more rarely upon the neck and face, of reddish spots of variable size, from that of a pin's head to a pea, or somewhat larger. These petechia) may be few and scattered irregularly, or they may come in showers and at irregular intervals. Septic infarcts in the liver, spleen, kidneys, etc., are productive of abscesses, which may be miliary and escape detection during life or be of recognisable size. In some instances the clinical picture is dominated by these embolic phenomena. I recall a case in which it was the detection of a splenic abscess which seemed to justify the diagnosis of septic endocarditis. I was asked by Dr. Haskin, of Highland Park, to see a gentleman of about sixty who had been having irregular chills, fever, and sweatings suggestive of malaria. His illness had begun six weeks before with malaise, and had speedily developed the symptoms of sepsis. Three days prior to my visit he had suddenly com- plained of sharp pain in the left liypochondrium with tenderness. 1 found him unconscious, and lying turned to the left side, with his thighs flexed, skin hot and moist, pulse moderately rapid, but notably weak and soft. There was a distinct blowing systolic murmur in tlie mitral area. Splenic dulness was greatly in- creased, and although palpation evidently caused pain and was resisted, a rather soft tumour having the form of the spleen could ACUTE ENDOCARDITIS 171 be felt extending well down below the left costal margin. The case was thought to be an instance of abscess of the spleen, prob- ably secondary to acute ulcerative endocarditis. Death took place a day or two later, and, although an autopsy could not be ob- tained, permission was granted to make an abdominal incision for the purpose of verifying the existence of the abscess. The abdo- men was opened accordingly, and so soon as the doctor's finger pressed ui^on the spleen the organ burst and pus welled up over his finger. In this case no etiological factor could be obtained, and yet it seemed plainly one of septic endocarditis with infective infarct in the spleen. When emboli of this character lodge in the kidney, they are declared by albumin, pus, and blood, with casts in the urine. There is a class of cases characterized by Romberg as atypical which run their course with all appearance of an acute ha?mor- rhagic nephritis, albuminuria, pus, blood in varying amounts, casts, renal epithelium, and cylindroids. This condition of the urine persists throughout, but with re- missions and exacerbations. A mildly irregular, continuous fever accompanies the nephritis, and the patient displays pronounced and increasing anaemia. It is this feature, together with the per- sistent pyrexia out of proportion to the temperature usually ob- served in nephritis, which throws light on the nature of the case. The discovery of an old-standing valvular lesion contributes great- ly to the establishment of the diagnosis. Lastly, cases are encountered which display such manifest car- diac symptoms that by some clinicians they are classed in a special group. These are such as either develop upon a chronic valve- lesion or occasion such rapid ulceration and destruction of the valves that objective cardiac phenomena become apparent. Symp- toms of general sepsis may not be marked, or if pronounced, de- pend largely upon infective emboli. The pulse is peculiarly soft, regular or irregular, and more or less accelerated out of propor- tion to the degree of fever. The patient usually manifests djsj)- noea, and it may be cyanosis. Both liver and spleen are enlarged from congestion or infarcts. Exceptionally one may upon re- peated examinations of the heart detect some evidence of changes going on, such as increasing feebleness of impulse, slight increase in the area of dulness, and perchance a soft murmur where previ- 172 DISEASES OP THE HEART oiislj none existed, or an alteration of one already present. ]More often such examinations are futile, and the diagnosis is largely conjectural or has to be made from the symptom-complex. Course and Termination. — The duration of acute ulcera- tive endocarditis is exceedingly variable. The disease may run its course to a fatal termination within a few days from its com- ing under observation, or its course may be dragged out over a period of weeks and even months. Some cases progress steadily to a fatal issue, while others show periods of seeming improve- ment, followed by exacerbations and more rapid decline. When death is the result it occurs either in consequence of local changes in the heart and cardiac asthenia, or as a result of acute pulmo- nary oedema or pulmonary infarcts. In other cases the patient is worn out by prolonged sepsis, or death is directly attributable to the effects of embolism in the brain, kidneys, spleen^ etc. A gentleman of about forty, who had a perfectly compensated mitral regurgitation of rheumatic origin, became ill in the fore part of February with what, from the history, appears to have been an acute follicular tonsillitis. It subsided in a few days, but the man did not regain his accustomed health. lie felt weak and slightly feverish, had vague pains, dull headache, and lost appe- tite. Thinking his liver was at fault, he went to French Lick Springs, Indiana, and there drank the waters, took a course of baths, and exercised, but without improvement. While there he was annoyed by tenderness and ])ain in the ends of his fingers, and observed that at such times there was a faint reddish colour of the skin immediately above the roots of the nails. He was told it was rheumatic. At lengtli, failing to regain health, he returned home, and towards the end of A])ril sought my o])inion, partly on account of a frequent dry cough that had recently develo])ed. I had known liiiii in liciilth, and had previously examined his heart. The change in his appearance and general condition shocked me. Ilis voice was weak and tremulous, his hands shook, his face was pale and sallow. His eyes were not perfectly clear, the skin of his arms and trunk was flabby, faintly yellow, and altliough at first dry, became bedewed with nK)isture upon the exertion of undress- ing. Ilis temperature in the mouth was 90.8° F., and the pulse of 105 was weak and small, but regular. I was struck by the fact ACUTE ENDOCARDITIS 173 that its rate did not fall appreciably, even while he was resting on the lounge after my exami- nation. The heart did not seem to be enlarged, but the apex-beat was feeble and preceded by a short, scarcely percepti- ble thrill. The old mitral sys- tolic murmur was pres- ent, but in addition the first sound had a sugges- tion of a presystolic bruit, and the second sound was feeble. The lungs were negative, the liver barely j)alpable, and urine contained a trace of albumin with granular and hyaline casts. From the history of tonsillitis and the symp- toms, I at once suspected endocarditis, and sent him home to bed. His temperature, which was carefully recorded four times daily, showed a fairly continuous py- rexia, from about 100° F. to 101° F. and a frac- tion (Chart II). His pulse remained persist- ently in the neighbour- hood of 105, and the heart-findings were un- changed. He was given ;3 - - ^ ~^ > o < o »- < > CO •< :^ > in ' kC >• -H ~. ^ ;;::: " CO - PC >■ Si < I:: =■ 3 rH 3 c: — =•' 55 — cui si s =3 ' 1 »- § — ' §3 ~ - S5 •< :CI L_ 3: =- CO «= CT - S =r - - ?, "■ - >. CO - _, i= - -= ■^ r± - ot ■^ ;:: >- s => ■ 2 ■^ :::i - oo < - » t- " y ~: > CO - >=. "P u >o < J-. ^ = - -f ' ;:> 00 *c P» a :* ;^ 1= p= »- o ~ =z ;;> o < ■ < \ -PCOC? 1-IOG5 GOt'CO ooo oooi a oi a 174 DISEASES OF THE HEART strychnine and jeast-nnclein in full doses. The diet was as hearty as his feeble digestion would pennit. He felt so com- fortable that he Avas kept in bed with difficulty. Things remained in this condition for two weeks, when he one day complained of localized pain and stiffness in the calf of the left leg, but with no objective phenomena. His cough was so persistent that repeated examinations of the lungs were made, at first with negative results. At length I dis- covered moderate dulness of the right upper lobe with ill-defined bronchial breathing, but no rales. About this same time enlarge- ment of the spleen became demonstrable. At a loss to account for the changes at the right apex, I requested Dr. Arthur R. Edwards to see the patient. He agreed in the view that there was probably septicaemia with endocarditis, but could not give a satisfactory ex- planation of the pathological condition in the lung. The pain in the left leg he thought was due to embolism. The faint blush at the root of the nails with tenderness, pain, and moderate clubbing was also observed by him, but without special comment. Coincidently with the appearance of distinct signs in the right apex the fever rose a degree or two, headache was complained of, and cough without expectoration became troublesome. This con- dition, which I now believe was a pneumonia of the same bacterial origin as the general sepsis, persisted for about two weeks, and then gradually disappeared, the lung clearing up, and the patient's general condition returning to what it was before this attack. For the next month or six weeks the clinical picture remained nearly in statu quo. Occasionally he spoke of sudden pains in the shoulder or elsewhere, which lasted for a few days and then vanished. Once he complained of pain and tenderness of the liver, and the organ became slightly more enlarged. This condition per- sisted for perhaps a week, and then disappeared slowly. All this time there was the same relentless pyrexia, which at times fluc- tuated rather more than before — but with exception of its becom- ing somewhat weaker in action and sounds, the heart showed no distinct change. The character of the temperature is shown in the annexed chart. Crede's ointment was rubbed into the skin freely for two weeks, and was then succeeded by daily injections beneath the in- tegument of an old antistreptococcus serum in doses of 10 cubic ACUTE ENDOCARDITIS 175 centimetres. Although kej)t up for more than a week this treat- ment produced no results, unless perhaps a feeling of somewhat greater strength and a slight reduction of temperature. At length, near the middle of July, the patient, who all the time declared he did not feel very ill, suddenly experienced an excruciating j)ain in the third finger of the left hand. The finger became cold, pale, and exquisitely sensitive to touch, as well as so painful that it prevented sleep. Examination made it apparent that an embolus had lodged in the artery near the middle of the third phalanx. Plugging was so complete and the patient's suf- fering so intense that it became necessary to amputate the finger on the fourth day. It was now apparent that he was failing stead- ily, although slowly. The heart-rate increased to 120, the apex- impulse less defined, the first sound inaudible, but the murmur not appreciably more distinct, indeed rather less intense, and the fever increased, but without rigors or sweatings. Indeed, throughout the illness these had been conspicuous by their absence. I saw him for the last time on the afternoon of July 2 2d, at which time he declared he felt so comfortable and happy that he believed he was going to get well. His countenance was slightly suffused, and as he had not emaciated greatly, his friends could not realize how ill he in reality was. - During the forenoon of the 2-ith he was suddenly seized with pain in the lungs, which was followed by violent coughing and the expectoration of blood. Evi- dently pulmonary infarcts had taken place and betokened the near approach of the end. The cough grew so incessant as to require considerable doses of morphine hypodermically for its control. These were followed by unconsciousness, in which condition he lingered until the afternoon of Julv 25th, when he suddenlv expired. The course of this undoubted case of septic endocarditis occu- pied five months from the attack of tonsillitis. It was plainly one of sepsis from the date of his visit to my office, yet without the occurrence of embolisms there was little to direct one's attention to the heart. I was familiar with the previous condition of the heart, and hence able to detect slight alteration in the physical signs which might have been otherwise unrecognised. Yet the thina; that riveted mv attention from the start was the almost un- swerving persistence of the pulse at very nearly the same rate, 176 DISEASES OP THE HEART 105, in spite of rest in bed, until near the termination of the case, when it rose to 120. A highly interesting feature also was the condition of the ter- minal phalanges of the fingers. The faint redness, pain, and, it seemed to me, slight increase of heat, were due to capillary dilata- tion, which caused the ends of the fingers to become distinctly bulbous in the course of a few months. During the preceding winter I had observed this same phenomenon, only to a much more marked extent, in a young woman who was in the ward at Cook County Hospital suffering from mitral disease, and, judging from the symptoms, from endocarditis. She subsequently left the hospital, so that I cannot state the cardiac condition definitely. In her case the finger-ends became distinctly red and unmistak- ably bulbous. In both these instances there was pyrexia associ- ated with cardiac disease. May not this phenomenon in the finger- tips point to something more than mere capillary paresis, perhaps to such a disturbance of the cardio-vascular apparatus as may sug- gest involvement of the heart as well as general infection ? It is a matter of profound regret that an autopsy could not be obtained in the case which has been narrated at such length. Physical Signs. — Inspection is of very negative value, since although it may enable one to detect signs of circulatory disturb- ance, it does not furnish proof of such disturbance being due to endocarditis. Besides, valvulitis is so often masked by the symp- toms and physical signs of the primary affection that inspection of the patient reveals only such changes in the patient's appear- ance as belong to the rheumatism or other original disease. Palpaiion is likewise of minor aid in \]u) detection of acute endocarditis. It may assist in the recognition of some old-stand- ing valvular lesion, or in determining the presence of abnormal pulsations, variations in the force, position, and extent of the apex-boat, the possible development of tlirills in the course of the affection, enlargement or not of the liver, etc., all findings that bear in certain cases on the condition of the heart, but, lik(^ inspec- tion, it cannot furnish direct evidence of tlie existence of acute endocarditis. Its chief value is in the diidy of the pulse, which in all suspected cases should be carefully studied, changes in its tension being often of greater value than alterations of rate or rhytvlmi. ACUTE ENDOCARDITIS 177 Percussion. — This is indispensable if one will correctly appre- ciate the significance of anscnltatory phenomena, since the condi- tion which occasions an organic murmur also leads to dilatation or hypertrophy, and therefore to a corresponding alteration in the area of cardiac dulness. If endocarditis occasions mitral incom- petence, it will also eventually occasion secondary enlargement of the right ventricle. Consequently daily percussion over this cham- ber should be made in order to detect the earliest ej^^idence of any alteration in the outline of the right and lower cardiac border. On the other hand, aortic disease produces increase of dulness on the left side with gradual alteration in the position of the apex- beat. Accordingly percussion is of very great value, since without the information derived from it a careful diagnostician would scarcely venture on an opinion concerning the nature of an endo- cardial murmur, especially an apex-murmur, which, as is well known, is of frequent occurrence in febrile affections without inflammatory changes in the valves. Auscultation. — Even this furnishes only exceptionally a trust- worthy means of recognising endocarditis, for, as will be sho^vn later on, a murmur is not always to be accepted as an indication of valvulitis. It is not so much the detection of an actual murmur that is significant, as it is the recognition of changes in the character and relative intensity of the cardiac tones. Daily careful study of the sounds must be made therefore. The earliest evidence that all is not right at the mitral orifice (the seat of inflammation in 50 per cent of cases) is said by English observers, who it must be acknowledged have given close attention to this subject, to be not a murmur, but a muffling or indistinctness of the first sound at the apex. A blowing murmur, which is purely accidental, may ac- company the first sound in a given case, and hence the occur- rence of a murmur with the sound is not so significant as an alter- ation in the sound itself, since it is reasonable to assimie that if the production of the soimd is interfered with it may be by inflam- matory changes. Such alteration of the second sound at the base is likewise suspicious of endocarditis affecting the semilunar valves. If in a case impurity of any of the tones is observed, it is very likely to grow into a more or less distinct murmur in the course 178 DISEASES OF THE HEART of time, Avliile there will also develop the secondary changes in the heart approi)riate to the lesion, whatever it may be. A diastolic murmur developing in the aortic area may be set down as not accidental, and therefore indicative of inflammation at this ostium. If this inflammation seriously impair the integrity of the valve, it will be shown in time by the occurrence of the secondary cardiac and vascular signs, which are described at length in the chapter on Aortic Regurgitation. A presystolic murmur rarely develops as a result of acute endo- carditis unless the process is ingrafted upon an old-standing mitral regurgitation. Inflammation attacking previously healthy valves usually produces incompetence of these, or this combined with a minor degree of obstruction. Therefore, the murmur is apt to be purely systolic, or systolic with a very short, scarcely recognisable presystolic one. When, however, an old endocarditis affecting the mitral valve becomes rekindled, as not infrequently happens, then a presystolic bruit may develop, and so developing it furnishes almost indubitable proof of endocarditis being present. This cir- cumstance has more than once enabled me to diagnosticate correctly the occurrence of endocarditis, as proved by subsequent events. A systolic murmur in any of the cardiac areas must always be regarded with doubt until its true significance is shown by the development of secondary physical signs. This is true of such a murmur even in the aortic notch, for experience has taught that even here a murmur may be accidental. It is, however, in the case of an apex systolic murmur ])articularly that caution must be exercised. (1) Because accidental bruits are most often mitral, or mitral and pulmonic. (2) Because such a mitral systolic mur- mur may be the result of a previously existing regurgitation, and not at all due to the rheumatism in the course of which it may happen to be discovered. (3) Because, as shown by a case re- ported by James W. Walker, of this city, an endocarditis nuiy exist without its giving rise to any murmur whatever. In his case the anterior and left posterior aortic cusps presented on their surface large masses of soft, friable, nodular vegetations, which had filled the ostium, and yet repeated and careful examinations during life liad utterly failed to detect any murmur. Diagnosis. — These three considerations make very plain the fallacy of depending upon the 2)resence or absence of a murmur ACUTE ENDOCARDITIS 179 in making a diagnosis of acute endocarditis. Inasmuch, therefore, as acute simple endocarditis may escape detection entirely or may be only suspected, one is frequently compelled to leave its diag- nosis an open question until after it has occasioned sufficient structural change to produce secondary physical signs. One must . therefore depend upon the history and symptoms even more than on distinctive objective signs. Even the pyrexia, acceleration of the pulse and respiration, prjipcordial pain, nervousness, and restlessness may all be attribu- table to the rheumatism. When the endocarditis is mural — i. e., confined to the lining membrane of the cavities — the valves escap- ing altogether, a positive diagnosis cannot be made without the occurrence of embolic phenomena. Differential Diagnosis. — Acute pericarditis is scarcely likely to be mistaken for acute simple endocarditis, and yet it is con- ceivable that such might be the case when the friction-murmur happens to coincide with one of the heart-sounds, and hence simu- late an endocardial bruit. In such a case the greater pain and the subsequent development of signs of effusion ought to set one right. Should an inexperienced auscultator mistake a to-and-fro pericardial rub over the base of the aorta for the double murmur of aortic insufficiency of recent origin, he may be able to correctly interpret the rub by noting the absence of the secondary cardiac and vascular signs of an aortic valve-lesion. Pernicious ancemia may under some circumstances very closely simulate acute endocarditis without embolic phenomena. I have seen such a case, in which the systolic apex-murmur of ever-in- creasing intensity, the low irregular pyrexia, great prostration, pain in the hepatic region, with nausea and vomiting, were, to- gether with a history of infection of the forefinger and lymphan- gitis four months earlier, highly suggestive of a low grade of en- docardial inflammation, particularly as the patient gave additional history of rheumatism. The blood-examination and ultimate au- topsy findings established the correct diagnosis. The Diagnosis of Ulcerative Endocarditis may in some cases be easy, in others only a matter of conjecture. What has been said concerning the physical signs of the simple applies equally well to the malignant form. In some instances the entire clinical pic- ture is that of general sepsis, and there are no findings to betray 180 DISEASES OF THE HEART its localization in the heart. Tii otlicrs characteristic signs of valvular insufficiency develop or the tokens of an old lesion un- dergo modification, or indications of a new lesion become added to those of a pre-existing defect. For these reasons repeated and minute examinations of the lieart are necessary. The detection of a murmur is in itself of small moment sometimes, Lut the dis- covery of changes in the rhythm of one already existing, as by a presystolic being prefixed to a systolic bruit, or an alteration in its timbre, a previously soft one becoming harsh or musical, or the addition of a diastolic murmur to a systolic one, all such modifica- tions are of great significance, and sh(»uld be carefully noted. The most reliable aid in the diagnosis of malignant endocar- ditis is found, however, in the history and symptoms. One must always seek for an efficient etiological factor. For example, it was not a great while ago that I was asked to see in consultation a young woman who was running an irregular course of fever, was emaciating, losing strength, and had a cardiac murmur. It was evident at a glance that she was suffering from pronounced sep- tica-mia, but the question that the physician wanted cleared up was whether the cardiac findings indicated septic endocarditis. There was history of an old rheumatic mitral disease. It did not require very long search to find evidences of cutaneous infarcts, and when in response to inquiry concerning a vaginal discharge, the nurse stated that there had been an extremely ofi^ensive one earlier in the illness^ and when a vaginal examination disclosed cervical laceration, the chain of testimony was complete. An abor- tion had led to uterine infection, this to septicaemia, and this lat- ter to an ulcerative process within the heart, which was predis- posed to iullaiimuition by its old-standiug mitral l(>si(m. Symptoms of })ya'mia — i. e., chills, fever, and sweating — in- dicate general sepsis, but do not warrant the inference that the endocardium is involved. This can only be assumed when embolic phenomena are discovered or there are some cardiac findings as well as symptoms of general sepsis. It is very necessary, there- fore, to make (htily cxaniination of the skin, spleen, and urine for detection of the changes already mciitioiicd as forming an essen- tial part of the symptomatology of this form of endocarditis. In the very obscure cases in which end)olic phenomena are not present and there are no cardiac findings to exjdain the pyrexia ACUTE ENDOCARDITIS 181 and other features that point to infection, yet in which the feeble- ness of pulse and heart-sounds suggest the possibility of a primary focus of infection in the endocardium, information is likely to be obtained from examination of the blood. Usually in infections there is pronounced leucocytosis, but in a few cases Neusser found an absence of increase, and he consequently concluded that when in a given case of septicaania there is either an absence or possi- bly a decrease of leucocytosis, it points to the likelihood of ma- lignant endocarditis. Bacteriological examination of the blood in a suspected case is not often productive of results, and yet should be made when all other means of arriving at a diagno- sis fail. Differential Diagnosis. — It is not sufficient to merely make a diagnosis of acute endocarditis ; one must also determine its na- ture. Therefore in making a differential diagnosis the following points may be of assistance: (1) The possible etiological factor; in the simple form, articular rheumatism, chorea, scarlatina, or some other generally recognised cause of benign endocarditis ; in the ulcerative, some antecedent pus infection or focus of suppura- tion, croupous pneumonia, gonorrhcea, rectal abscess, otitis media, quinsy, trauma, furuncle, carbuncle, leg ulcer, etc. (2) The char- acter of the temperature. In simple endocarditis fever may be absent or due to the primary disease, subsiding with the disap- pearance of the rheumatism, etc., or it may pursue a mild con- tinuous course. In the ulcerative form the temperature-curve is that of pus-infection of the characters that were described in the symptoms. (3) Blood changes and bacteriological examination of the blood are negative in the simple form, while in the malignant there may be pronoimced leucocytosis. The occurrence of septic phenomena without such increase points to septic endocarditis. (4) Urinary findings. The discovery of albumin, pus, and blood with casts is in favour of mycotic endocarditis, since hsemorrhagic nephritis is not a part of the clinical history of the simple form. (5) Hgemorrhages into the skin or from the mucous membranes may occur in the ulcerative, but not in the benign variety of endo- carditis. (6) Embolic phenomena, although occasionally observed in the simple, are yet generally found in the malignant endocar- ditis. (7) Enlargement of the spleen is in favour of the mycotic as against the simple form. (8) Eecovery is the rule in simple 182 DISEASES OF THE HEART and the exception in ulcerative endocarditis, although its course to a fatal issue may be slow. Typhoid fever is the disease above all others for which ulcer- ative endocarditis is likely to be mistaken. As a matter of fact, most cases of the latter affection are diagnosed as enteric fever, and so regarded until in the dead-house they are found otherwise. The points of difference are the following: (1) In typhoid fever the temperature is not so erratic, and in the first week often dis- play's the characteristic gradiuilly ascending curve. (2) The pulse in this disease is usually slow, out of proportion to the degree of temperature. In its want of tension during the height of the malady it may be like that of endocarditis. (3) Splenic enlarge- ment comes at an earlier period in enteric fever, and is more con- siderable. (4) Rose-spots usually appear between the eighth and twelfth day, are apt to be in crops upon the trunk, disappear temporarily on pressure, are of a nearly uniform size, and have a darker centre, fading out towards the periphery. Cutaneous em- bolisms, on the contrary, appear most often upon the extremities, are irregularly distributed, of variable size, do not fade on pres- sure, and have a necrotic pale centre, becoming of a deeper colour towards the edge. (5) The stools of abdominal typhus are often, though by no means always, diarrhcfal, have the pea-soup appear- ance, and contain the Ebertli bacillus. (6) Typhoid-fever pa- tients are very apt to manifest signs of bronchitis. (7) Except- ing epistaxis early in its course and possible haimorrhage from the bowel during the middle or latter portion, lumnorrhages are not common in typhoid fever. (8) In the Widal agglutination test we now possess a reliable means of differentiating enteric fever from malignant endocarditis, and it should invariably be made in every doubtful case.* The value of this differential test was shown in a case under my care a few months ago. A young man with extreme aortic regurgitation of rheumatic origin was under treatment for attacks of pni'cordial pain, and as there were symptoms pointing to a rup- ture of compensation he was put to bed. A few days thereafter he began to manifest a low grade of irregular temperature, but without any other symptoms. His ])ulso remained disproportion- * According to MacFarland, there was in 4,000 cases only 4 per cent of error. ACUTE ENDOCARDITIS 183 ately slow, and I at once suspected typhoid fever, although not unmindful of the possibility of endocarditis. Rose-spots were never discovered, notwithstanding repeated daily inspection of the trunk, and splenic enlargement could never be satisfactorily made out either by palpation or percussion. There was no diar- rhoea at any time, the bowels being rather confined. The Widal test was resorted to at the end of the first week, and settled the diagnosis as one of enteric fever. Had this means of differential diagnosis not been available I should have felt exceedingly uneasy as to the nature of the case and its possible outcome. As it was, I felt no more anxiety than would be natural in such a severe valvular lesion, complicated by the occurrence of the abdominal typhus, and a possible infection of the chronic endocarditis in con- sequence. The error of mistaking ulcerative endocarditis for malarial infection is so easily avoidable nowadays by the discovery of the Plasmodia that it ought never to be committed, and is inexcusable. Prognosis. — This depends not only upon the nature of the endocarditis, whether benign or ulcerative, but also upon certain modifying conditions, as the extent and seat of the inflammation, the concurrence or not of acute pericarditis or myocarditis, whether it is a first attack or has been ingrafted upon a chronic endocarditis, and lastly upon the presence or absence of septic in- farcts. If the inflammation expend its energies in a local deform- ing process through the development of new connective tissue within the valves, or the formation of vegetations upon their sur- face, or that of the contiguous orifice, the endocarditis does not usually destroy life directl}'^, but leaves the individual with a per- manent valvular defect. This statement must be modified, how- ever, in accordance with the seat of the inflammation. If this is confined to the left auriculo-ventricular opening, which fortu- nately is the case in at least one-half of the instances, the imme- diate prognosis is much less grave than when the endocarditis attacks the aortic valves, rendering them incompetent. Rapidly induced insufficiency occasions dilatation of that chamber into which the blood regurgitates. The secondary effect of endocarditis of the mitral cusps is dilatation of the left auricle, of the aortic cusps, dilatation of the left ventricle, and there is abundant proof, both clinical and other- 184 DISEASES OP THE HEART wise, that dilatation of the auricle is less dangerous to life than dilatation of the ventricle. Moreover, in mitral regurgitation, the resistance offered by the walls of the left auricle is re-enforced by the column of blood in the pulmonary vessels and by the right ventricle, while in insufficiency of the aortic valve there is not only danger of paralysis of the left ventricle from overdistention, but if in consequence of stretching of this cavity and of the left au- riculo-ventricular ring the mitral valves become relatively incom- petent, the evils and dangers of mitral are added to those of aortic regurgitation. If the inflammatory process extend also to the myocardium or pericardium the prognosis becomes far more serious, since the myocarditis favours a rapid dilatation of the organ. Sturges directed attention to the liability in children to inflammation of all of these structures, giving it the name " acute carditis," and pointed out the extremely serious nature of this condition. The gravity of the prognosis in these cases is attested by the following figures, to which reference has already been made in the chapter on Acute Pericarditis: Of 150 cases of fatal rheumatic endocar- ditis in children, Poynton found the pericardium healthy in only 9, while in 34 the myocardium showed changes of one kind or an- other. Death was thought attributable to the condition of the myocardium rather than to that of the endocardium. If an acute endocarditis becomes ingrafted upon the chronic process, or attacks valves already the seat of sclerotic changes, the prognosis becomes very doubtful, since it is a well-known fact that under such circumstances the inflammatory process is very likely to prove septic. Moreover, even if the endocarditis should not be malignant, it is certain to intensify the changes already existing, either by causing still greater destruction of the valves or by trans- forming a predominating insufficiency into a stenosis through the development of thrombi about the edges of the opening. Thus a lesion which was compensated may be converted into one of such gravity that compensation is never again possible. 1'he occurrence of embolisms renders the prognosis exceed- ingly serious, both as tf» the immediate and remote effects. Even in simple rheumatic endocarditis an eiid)olus may be carried into the brain, the left middle cerebral artery being the one most fre- quently plugged, and occasion hemiplegia. In the case of endo- ACUTE ENDOCARDITIS 185 carditis of the rigiit heart, pnhnonary infarcts frequently con- tribute to the fatal termination. Should the emboli be septic, more than a mechanical effect is produced. Single or multiple abscesses in the spleen, liver, kidneys, or even scattered throughout the body, set up symptoms of general infection. These are the cases properly classed under the category of malignant endocarditis, since in them death is the inevitable result. Should the urine at any time display the characters of ha^morrhagic nephritis, it is to be regarded as an omen of evil import. The very interesting and practical question arises. Can acute rheumatic endocarditis subside, leaving the valves uninjured ? This query has been answered in the affirmative by some writers, their belief being based upon the disappearance of a systolic apex- murmur that had been observed to develop during an acute rheu- matic attack. My experience has been too limited to warrant miy forming an opinion upon the subject, yet I frankly state I would be loath to accept any other than post-mortem evidence of the cor- rectness of such a belief. Under the influence of infection and pyrexia, weakening of the myocardium and papillary muscles may very readily occasion dilatation, and a systolic murmur in the mitral area be developed. With returning health these may re- gain their tone, and the dilatation and murmur disappear. Can any one assert therefore, without fear of contradiction, that the appearance and subsequent disappearance of such physical signs indicate recovery from acute endocarditis, and not from cardiac dilatation ? The following case observed during convalescence from pneumonia is one in point : A healthy young married man of twenty-seven passed through a pneumonia of the right lower lobe in the fall of 1899. About a week after the crisis, when convalescence was progressing finely, he arose from bed early one morning and walked into the adjoining bath-room to pass his urine. He sud- denly became weak and dizzy, and upon returning to his bed- chamber his pulse was observed to be 135 to the minute and weak. Whenever during that day he attempted to walk about the room his pulse immediately arose in frequency and became correspond- ingly diminished in strength. I was asked to see him that same evening, and found him reclining on the sofa, his pulse about 100, regular, but compressible, the apex-beat feeble, in the fifth left interspace slightly outside the nipple-line. 14 186 DISEASES OF THE HEART Relative cardiac dulness was increased transversely, particu- larly to the left, reaching 12.5 centimetres to the left of the medi- an line. The temperature was normal, respirations tranquil, and the patient had no sense of dyspnoea. Cardiac sounds were every- where audible, but the aortic second w^as weak, and accompany- ing the first sound at the ajiex was a faint systolic blowing mur- mur. There was no history of previous attacks of rheumatism, and until the date of his pneumonia the patient had indulged in much athletic exercise without shortness of breath or palpitation. Realizing the possibility of an acute endocarditis of pneumococ- cus origin, I insisted upon absolute physical repose, ordered light diet, and a gentle saline aperient. On the following day, the condition being essentially the same, ^ of a grain of strychnine sulphate three times a day was or- dered. As the temperature remained normal and the murmur had not increased, two days later tincture of digitalis was cau- tiously administered. Within twenty-four hours the left ventricle had come down 0.5 centimetres, and upon the digitalis being increased, the next twenty- four hours wit- nessed a still further diminu- tion in the extent of relative cardiac dulness to the left. In the course of the next week or ten days the heart meas- ured but 10 centimetres to the left of the median line, and w\is normal at the right (Fig. 32). Two months subsequently, after the patient had been without medicine for several weeks, and liiid ri'turned to liis usual mode of life, the left ven- tricle measured but J> centimetres, a reduction of more than 3 centimetres since the date of my first examination. Was this case to be regarded as one of acute endocarditis following croupous pneumonia? Certaiidy not. It was one of simple acute dilata- ¥m. '62. — DlMlNU'i'lON <.>F litLATlVK CaKUIAO Dulness in One Week, under Tkeat- MENT. Case (p. 185;. ACUTE ENDOCARDITIS 187 tion, chiefly of the left ventricle, res^^lting primarily from asthe- nia of the heart-muscle in consequence of the effect of the toxins of the pneumococcus. Treatment. — Clinical experience the world over accords w^ith the conclusion naturally drawn from a consideration of the pathol- ogy and morbid anatomy of acute endocarditis — viz., that when the process has once become established, we possess no means of causing absorption of inflammatory product or restoring the endo- cardium to a healthy state. It should be our aim, therefore, to prevent where we cannot cure. Our first duty is to study the effi- cacy of prophylactic measures. Our efforts in this direction should not be restricted to prevention of endocarditis, but should first be directed against that disease, articular rheumatism, which is so largely responsible for inflammation of the cardiac structures. Proper sanitation and attention to the diet, clothing, habits, and occupation of patients may do much to this end. Of special value are all measures calculated to maintain a high standard of nutrition, and persons of distinct rheumatic diathesis should be impressed with the danger of exposure to wet and cold. Children in whom rheumatic manifestations are obscure, should be carefully examined whenever ailing, for possible evidence of rheu- matic infection, and if this be discovered, should promptly be given some preparation of a salicylic acid. Much has been written concerning the prevention of cardiac involvement during rheumatic attacks; and when the salicylic- acid treatment of rheumatism came into use, strong hope was entertained of its ability to prevent endocarditis. Even now there are those who believe that by diminishing the severity of, or even cutting short, the rheumatic attack, this treatment lessens the lia- bility to cardiac inflammation. The same also may be said of the alkaline treatment, or of the combinations of the alkalies and salicylates. For the most part, observers of long experience have come to the conclusion that whereas the salicylate-treatment does not assure the prevention of endocarditis it would better be per- severed with, since if properly administered it is not likely to do harm. For my part I do not believe in the prophylactic power of this drug over the cardiac manifestations of articular rheu- matism. Given a case of this disease in which salicylate of soda is em- 188 DISEASES OF THE HEART ployed, and acute endocarditis or pericarditis does not develop, can any one assert it would have occurred had the remedy not been administered ? Are there any statistics to show that endocarditis has been less frequent than before the use of the salicylates ? Even if one or more series of rheumatic cases treated with this remedy show a smaller percentage of endocarditis than others not so treated, how can one be sure that the difference in results is not purely accidental, since all rheumatic attacks do not inevitably lead to cardiac inflammation ? By all means during a rheumatic attack resort to salicylic acid, or one of its salts, to potash or soda, local applications to the affected joints, to regulation of the diet, and any other approved means of antirheumatic treatment. But do not be too confident that endocarditis will not develop. Should it not, consider your- self and the patient fortunate. I confess to the same scepticism concerning the efficacy of local treatment of the prtccordium, as leeches, blisters, and cold ap- plications, in preventing acute endocardial inflammation. The only prophylactic measure that appeals to me as rational is the pro- curement of as much rest to the heart as possible, by keeping the patient quiet during his attack of rheumatism, that the valves may not suffer trauma by reason of strain. Fortunately, in an acute attack of severity the urgency of the symptoms compels the patient to remain at rest ; but in eases of subacute rheumatism, particu- larly if an old valvular defect already exists, the patient should be urged to remain at rest, so as to lessen the tension of the valves and the possibility of having inflammation rekindled in them. This is often irksome to the patient, but if he has the reason ex- plained to him he is likely to acquiesce, although perhaps with no very good grace. Even after all the rheumatic syni})toms have disappeared the patient should be cautioned against violent exer- cise, and should be kept under rather frequent observation, that the earliest evidence of endocarditis, sliouM such arise, may not be overlooked. Upon the occurrence of acute endocarditis, or of subjective or objective symjjtoms sus])i('ious of such an inflammation, tlie pa- tient should prom])tly l)e juit to bed, if not there already, and kept there as quiet as possible, both mentally and physically. The ob- ject of this is apparent ; bodily exertion as well as mental excite- ACUTE ENDOCARDITIS 189 ment augments the frequency of cardiac contractions and subjects the valve-curtains to increased strain. The same principles should apply to the treatment of inflamed valves as to that of inflamed joints. The use of the latter not only causes pain, but intensifies the inflammation. Unfortunately, the heart cannot be put at en- tire rest, but by slowing its contractions its diastole or period of rest is lengthened and its contractions are less violent. Theoret- ically, at least, the inflammatory process would thus be less active and the danger lessened of rupture of the inflamed and tender cusps, or of dislodgment of a soft, not firmly seated thrombus, and the formation of embolism. If the heart's action is violent or too rapid, attempt should be made to quiet it by placing ice-bag to the prseeordium or by the administration of bromides. Digitalis is very commonly administered for this purpose, but it cannot be stated too emphatically that this drug is inadmissible in the treatment of acute endocarditis. It not only does no good, but is positively harmful. Although capable of slowing the heart, digitalis at the same time increases the strength of systole, and thereby subjects the valves to more than ordinary strain. The benefit to be derived from a slowing of the contractions is offset by the injury to the valves and by other dangers possible from this more forcible closure, as already explained. It is better to let the heart keep its own gait than attempt to control it by possi- bly injurious means. Aconite or veratrum viride are likewise injurious, but in a different way. They are depressors to the myocardium ; and if this be inflamed or weakened by serous infiltration, there is danger of these drugs causing serious dilatation. The same objection can- not be urged against the local employment of cold, and as a matter of fact this therapeutic agent is highly praised by those who have given it an extended trial. As stated in the chapter on Acute Pericarditis, the ice-bag is preferable to cloths wrung out in ice- water, since they do not subject the patient to the danger of taking cold by wetting the clothing, and for the same reason are more comfortable. The ice-bag should not be applied directly to the bare skin, but a dry, light cloth should be interposed. Should the heart and circulation have become very feeble, cold had better not be resorted to, because cardiac depressors are no longer indi- cated. 190 DISEASES OP THE HEART Hot applications to the piwcordiiim are then more serviceable on account of the stimulating effect they produce. Vesication of the prsecordium, either in the form of one large blister, or of re- peated small blisters, is a treatment that once met with much favour, but is objectionable, since it occasions more nervous irri- tation than it is likely to do good. The application of mustard or the tincture of iodine or of a turpentine stupe are less objec- tionable because less severe, and are sometimes capable of alleviat- ing pain. Mercurials and tartar emetics are now known to exercise no restraining influence over the inflammatory process, and are there- fore no longer used by the best authorities. Moderate doses of iodide of potash have been recommended, in the hope of restricting the formation or promoting the absorption of the inflammatory products. It is, however, doubtful if this remedy possesses any such influence in the course of acute endocarditis. When medicines are powerless to cut short an attack, or even probably to diminish its severity, we are left to a purely symp- tomatic treatment. Pain and restlessness should be alleviated by the use of opium, and in the case of adults morphine hypoder- mically is the best mode of administration. In children great care must be exercised in its use, and it is always well to first try the efficacy of bromides in conjunction with cold applications and soothing liniments. Antipyrine, phenacetiiie, and other remedies of this class are capable of exerting depression, and if employed at all should be in small doses and with strychnine or some stimu- lant. The pyrexia of acute simple endocarditis is usually not high, and therefore such anti})yretics are not likely to be needed for the reduction of temperature. If this should become necessary, it would be best attempted by judicious sponging. Insomnia may be prevented by bromide, paraldehyde, sulphonal, or trional, or, best of all, by some preparation of opium. So soon as the endocardium is found to be the seat of acute inflammation the physician should constantly bear in mind the possibility of the heart finally succumbing tlirough weakness, if not structural change of the myocardium. The organ should be sustained, therefore, by that best of all heart-tonics, strychnine. Opium is also a heart-tonic, and wliilo being given for the relief ACUTE ENDOCARDITIS 191 of j^ain, also supports the heart, provided it be not administered with greater frequency or in larger doses than are required to alleviate the symptoms. Sulphate of strychnine is, hov^ever, the remedy on which chief reliance should be placed. Given in mod- erate doses, at first -gV of a grain to an adult three times a day, it may be increased to -sq, or even to -^-q, if signs of myocardial weakness supervene. Should the disease assume a grave charac- ter, and attacks of threatening asystolism make their appearance, by cyanosis, feeble and irregular pulse, paroxysms of dyspnoea, or signs of pulmonary oedema, the heart should be promptly stimu- lated by ammonia, camphor, ether, brandy, and the like. Inhala- tions of oxygen may also be resorted to, and are likely to prove temporarily, if not permanently, beneficial. The patient's general strength should likewise be sustained by nutritious, though light, diet. Milk, beef juice, an occasional raAv egg, soup, broth, and wine jelly are all serviceable. A cup of soup (prepared from Mosquera's beef jelly), tropon and somatose, form admirable adjuvants to the dietary. The nourishment should be given frequently, every two to three hours, and in small amounts, care being taken to avoid all articles of diet which occa- sion gaseous distention of the stomach and intestines. Constipa- tion should not be permitted, and even if the action of the bowels is regular, benefit is likely to accrue from the occasional adminis- tration of a blue pill or small dose of calomel, followed by a gentle saline aperient. The urine should be watched, and if it become bloody or albuminous the diet should be restricted to milk, and the patient urged to drink freely of pure water. Acute Ulcerative Endocarditis. — Fortunately there are grada- tions in the severity of this type of the affection; were it not so the physician would be but a helpless spectator of the ravages of this dreadful malady. Indeed, such is his attitude in severe cases, or in those that have made considerable progress before recog- nition of their true nature. The first duty of the medical attend- ant is to search for the cause — that is, the source of the primary in- fection — and, if this is discovered and can be removed by surgical interference, to promptly resort to such treatment. This, alas! is not generally possible ; but if, as Sir Douglas Powell thinks, un- sanitary environment and exposure to sewer-gas emanations are ■capable of setting up fresh infection in a case of old-standing valvu- 192 DISEASES OF THE HEART lar disease, tlien the patient should be promptly removed to a healthful location. The next indication is to resort to ever}- means which affords any hope of re-enforcing tissue resistance, as a nutritious and easily assimilated diet. The lines of treatment already laid down for the sustaining of the heart and protecting it against the injury resulting from unnecessary work in the simple form are equally applicable to the ulcerative. Indeed, they are still more urgently required; for not only is inflammation more destructive and likely to invade the myocardium, but even when this escapes ulceration or abscess formation the heart-muscle is likely to suffer from the enfeebling effect of the toxaemia. In severe cases the prostration of the patient generally calls for the administration of small, frequently repeated doses of brandy or ammonia. The use of alcohol in conditions of sepsis is very generally ennDloyed, and, in the opinion of many clinicians, is highly useful. Some indeed advocate whisky in large and fre- quently administered amounts. Strychnine should be given in full doses, and will yield the best results if administered hypodermic- ally. Quinine was formerly exhibited in doses of 15, 20, or more grains for the control of the fever; but with a clearer knowledge of the etiology and pathology of this affection, we now know that this remedy can exert no controlling influence over its course. Iron and arsenic have also been employed, and Powell speaks highly of the latter, not as a curative agent, but simply as a car- diac and general tonic. Attempts have been nuide to introduce into the system antisep- tics in sufficient quantity to exert at least a modifying influence upon the sepsis. The one deserving special mention is sulpho- carbolate of soda, which has been thought in mild cases to exert a favourable influence. Sansom has reported one case in which dui'iug its use such iiii])rovcment took ]dace that the patient left the hospital ; she returned, however, and succumbed to a fresh attack or accession at the end of ten months, " At the autopsy the diagnosis of septic endocarditis was confirmed, the mitral, tricuspid, and aortic valves being diseased and infiltrated with micrococci." Drechfeld, in speaking of this remedy in 4-drachm doses, men- tions a case reported by Sansom (probably the one just quoted) ACUTE ENDOCARDITIS 193 in which, when death took place at a later period, " distinct cica- tricial tissue was found at the site of the old ulcerations." If this or any other antiseptic remedy, as salol and salophen, is to do good, it must be in very large, frequently repeated doses, so as to rapidly bring the system under their influence, and should then be continued for a considerable time. These latter remedies recommend themselves in cases with a rheumatic element, because composed of salicylic as well as carbolic acid; but the depressing effect of the former upon the myocardium must not be forgotten. For my part I am inclined to attribute whatever benefit has seemed to follow such treatment to their local antiseptic action upon the intestinal tract. Fermentative processes and diarrhoea, as shown by foetor of the discharges, are very common within the digestive tube of patients suffering from sepsis. Such a condition may not only intensify the pyrexia and other symptoms of infec- tion, by itself setting up an infection of intestinal origin, but it prevents the proper digestion and assimilation of nourishment. If now this putrefactive fermentation can be prevented by intes- tinal antisepsis, the patient's nutrition will improve and his tissue resistance be augmented. It is possible, perhaps, by having this additional enemy thus removed, the system may be able to cope successfully with the primary invader. At all events, the physi- cian should employ these and every other means that afford possi- ble chance of improvement in dealing with so formidable an ad- versary. The universal success of the antitoxin treatment of diphtheria, and the encouraging reports that have come from the use of anti- streptococcus serum in some cases of pyaemia and puerperal sej)- ticsemia, indicate the dawn of a new era in theraj)eutics. It is to be hoped that in the not very distant future we shall possess a serum potent against each kind of pus-producing microbe. At present we are limited to the serum just mentioned; and inasmuch as the streptococcus is the agent frequently at work in cases of septicaemia, and the judicious employment of this serum appears not to be injurious, we are certainl}^ warranted in giving it a trial in cases of septic endocarditis. This has already been done, although to what extent I am not able to say, nor have I been able to find how many cases of this disease treated in this manner have appeared in the literature to date. 194 DISEASES OF THE HEART Douglas Powell has tabulated 14 cases of ulcerative endocar- ditis in which antistreptococcns serum has been employed in Lon- don. The results are as follows: Three recoveries, 9 deaths, and 2 in which no favourable result ensued. Powell is of the opinion that these results appear more discouraging- than they really are, from the fact that the serum was employed in the late stages of the disease, owing to a natural hesitancy to try a new remedy, and after " large embolic detachments had set up fresh centres of cultivation in many positions," He concludes therefore: " It may be laid down as a principle, governing treatment by this particular serum, that the more distinct the history of a previous endocardial lesion and a subsequent exposure to an infection through a suppu- rative medium, or a sewer-gas sepsis, the more appropriate the case for the treatment. This rule would discourage its employ- ment in cases in which the pneumococcus, gonococcus, or some other microbes divergent in character from the streptococci and staphylococci were concerned ; and if with the recognition of this principle, and its earlier and bolder carrying out, more encourag- ing results are obtained, it will certainly follow that analogous measures will be found for the circumvention of the other forms of microbic action." If the primary source of infection, an abscess for instance, be not discovered, and therefore not removed by the surgeon, or if fresh emboli laden with pus cocci repeatedly discharge into vari- ous parts of the system, to maintain the already existing sepsis or set up fresh centres of infection, then assuredly antistreptococcns serum will prove of little or no beneiit. If, on the contrary, the patient is suffering from pyaemia, the original portal of infection having been closed, and no fresh intoxi- cation having taken place, then this serum would be of service, even though the streptococcus be not the only microbe concerned in the process. With this formidable streptococcus disposed of, the system ought, theoretically at least, to be able to cope success- fully with the other kind of bacteria. Of course, hope of recov- ery or even improvement can only be entertained in comparatively mild cases, or when, as Powell says, the disease is recognised and treatment begun early. A process with a pronounced destructive tendency cannot probably be checked, but there are cases of septic endocarditis which are shown by the clinical history to be not thus ACUTE ENDOCARDITIS 195 rapidly destructive or malignant. Since no one can foresee how virulent the endocarditis is to prove, the patient should be given the benefit of a doubt, and the serum tried. Gibson suggests that in every case an examination of the blood should be made for possible detection by culture, inoculation, experiment, or other- wise of the nature of the infective agent; but their detection, it must be remembered, is extremely unlikely. Endocardial inflammation following pneumonia, or in which the pneumococcus has been identified, promises no hope of im- provement from this treatment. It is to be hoped that we shall possess some day an eflicient antipneumococcus serum, and indeed the researches of the Klemperer brothers and others afford some promise of this being attained. Personally I have had but little experience with antistrepto- coccus serum in acute endocarditis. The wife of a physician had suffered for years from an aortic regurgitation of rheumatic origin. At the time I saw her she had been ill for several weeks with moderate fever of a remittent type that fluctuated between about 100° and 102° F., or a little more. She complained much of prtecordial distress and paroxysms of pain, also of pain in the lower extremities about the joints, although the latter were not appre- ciably swollen or tender. The usual antirheumatic remedies — sal- icylates, alkalies, etc. — did not appear to exert any influence over the affection, and as I believed she was suffering from fresh endo- carditis, possibly of a septic type, I advised a trial of antistrepto- coccus serum. This was obtained from St. Louis, and was given in two doses of 10 cubic centimetres each. Her husband subse- quently sent me a report, from which the following has been extracted: " Mrs. B. had been very sick about one month when you saw her. The attack set in with a spell of tachycardia, lasting be- tween three and four days, pulse-rate near 200 during all that period. The joints were only slightly inflamed, temperature about 102° F., with but slight variation. I gave two doses of antistrepto- coccus serum three days apart, as you directed, without immediate effect on temperature or symptoms. At end of two weeks, how- ever, temperature subsided nearly to normal. A very heavy ery- thematous rash followed the use of the serum. She gradually crept from her perilous condition, dropsy disappeared, appetite 196 DISEASES OF THE HEART returned with a fair degree of strength. She had a good deal of bronchitis, and was much worse after you saw her than she was then. No one who saw her at her worst thought she could possibly recover." The nature of this ease was very doubtful, and from Dr. B.'s report the serum appears to have been of doubtful utility. Yet I recall distinctly having subsequently met another practitioner,, who had been present at the time of my examination, and who stated in no unequivocal terms that in his opinion the serum had been of benefit. About a year ago I saw in consultation with Dr. Lovewell a man of about forty who had been ill for a number of weeks with an intermittent fever, rigors, and sweatings, symptoms of cardiac disease, and distinct evidence of an aortic valve-affection, which had not existed before his illness. The origin of the infection could not be ascertained. There were well-marked signs of aortic insufficiency, which from the general septic phenomena and albu- minuria could not have been other than a malignant endocarditis. As everything in the line of antiseptics had been tried to no pur- pose, I advised the use of anti streptococcus seriim. The patient survived a number of weeks longer, but died suddenly as a result apparently of emotional excitement. I did not see the patient again, but had news of his condition from Dr. Lovewell, who stated more than once that under the use of the serum the tem- perature became lower, less irregular, and the other indications of sepsis less pronounced. In fact, the general condition im- proved so much that tlie doctor at one time began to entertain the hope of his patient's ultiniato recovery. It will be remembered that in the case reported of my patient of forty, who died of pulmonary infarcts, this serum was likewise employed. It failed to exert any other effect than to slightly re- duce temperature and produce a feeling of somewhat greater strength. In this instance it was not used until late in tlie illness and after embolic phenomena had more than once aj^jpeared, I regret that the treatment with the serum was not begun earlier^ although I am very doubtful if it would have materially affected the ultimate result. These experiences are too limited to be of value in forming an estimate of the utility of the serum, but inasmucli as its use was not attended by unpleasant effects ACUTE ENDOCARDITIS 197 I shall certainly continue to give it a trial whenever this seems indicated. Such cases are so desperate, and the prospect of recovery so slight, that I believe one is justified in resorting to whatever affords even a chance of benefit ; and if an old preparation is em- ployed, there is not much danger of producing erythema or articu- lar inflammation, and the remedy cannot prove more harmful than the disease itself, unchecked. J. Michell Clarke has reported a case of a woman of twenty- two who had had an attack of rheumatism at eighteen, followed by left-sided pleurisy with effusion. She complained of weakness, dyspncjea, pra^cordial pain, and oedema of the ankles. While under treatment for these symptoms she had a sudden chill, followed by a temperature of 103° F. After remaining high for four days the temperature fell to normal, and after so remaining for about a week, again rose, and prevailed for nine days with a very irregu- lar course. There was a systolic apex-murmur, another loud sys- tolic murmur in the pulmonary area, and a faint diastolic one at the right base. Bacteriologic examination of the blood from a vein was negative. A diagnosis of ulcerative endocarditis was made, and treatment with antistreptococcus serum was instituted. In- jections were given from December 31, 1899, to February 9, 1900, sometimes daily, at other times every other day, and once five days intervened between injections. The doses varied from 10 cubic centimetres to 20 cubic centimetres, though as a rule 15 cubic centimetres were given. The patient recovered, and exami- nation revealed the apex in the fifth interspace nipple-line with a loud, blowing murmur throughout the prtecordium and posterior- ly, but loudest in the aortic area. Douglas Powell speaks of the administration of yeast, and re- ports a case in which recovery appeared to be due to this remedy. It is probable that the efficacy of yeast is due to the nuclein of the yeast-cell, therefore in Vaughan's yeast-nuclein we possess a preparation more efficient than a solution of yeast. This may be administered either by the mouth or rectum, a solution, ISTo. 2, being specially prepared for this purpose, or solution No. 1 may be injected under the skin up to 60 or 80 minims in the course of the day. ISTuclein or nucleinic acid acts by increasing the number of the polynuclear leucocytes, which are the forms chiefly in- 198 DISEASES OF THE HEART creased in the leiicocytosis observed in infection, and by the in- crease of which the germicidal action of the blood is avigmented. Many encouraging reports have been made of the favourable effects of yeast-nuclein in cases of pus-infection and cryptogenetic infection. I employed it in one case of acute endocarditis super- vening upon an old valvular lesion, which followed a follicular ton- sillitis, that may have been rheumatic, but if so was the only mani- festation of rheumatism. The remedy was administered by the rectum, owing to the patient's dread of hypodermic injections. Under its influence, or at least during its administration, the mild pyrexia which liad existed for about ten days, without showing indication of subsiding, gradually sank to normal. The patient subsequently died. From the foregoing it is evident that the most the physician can do in the treatment of acute endocarditis is to aid nature by helping to maintain the vital powers and by removing obstacles that lie in nature's way. CHAPTER V CHRONIC ENDOCARDITIS Morbid Anatomy. — Two forms of chronic endocarditis are fonnd, one the result of the proliferative processes following an acute inflammation, and the other a part of a general fibroid trans- formation of the vascular system, arteriosclerosis. In the form following the acute disease the development of fibrous tissue begins with the organization of the vegetations and thrombi that have formed in the earlier stages. As a rule the vegetations are for the most part absorbed, but the process of or- ganization leaves a slight nodular thickening on the surface of the endocardium. The formation of new connective tissue goes much further than the mere repair of the acute lesions, however, for what reason we cannot say, and the entire substance of the valve is infiltrated by fibrous tissue, which in the course of time undergoes contraction that causes a thickening and deformity of the valve-cusps. This process, then, though initially of an in- flammatory nature, eventuates in a sclerosis. The second form is of sclerotic origin from the beginning, and is usually associated with a similar process in the blood-vessels, particularly the arteries. In this process the aortic valve is the one most frequently involved, and the process seems to be often a direct extension of the disease from the aorta. It is, however, by no means rare to find the mitral valve involved, and often both are affected together. The stiffening and deformity of the valve-leaflets leads to dis- turbance of their function in two ways : The segments may be retracted or their edges curled in such a way as to permit the pas- sage of blood in the wrong direction (Regurgitation). The con- dition is then spoken of as insufiiciency, incompetence, or regurgi- tation. If, however, the deformity of the valve is of such a nature 199 200 DISEASES OF THE HEART as to cause a narrowing of the orifice, the condition is known as stenosis. . Stenosis may be brought about by thickening and rigidity of the valve-segments so that they cannot open perfectly for the passage of the blood, or the remains of vegetations or thrombi, which have undergone organization or calcification, may encroach on the opening. The special ways in which these lesions are pro- duced will be considered in detail under the head of the individual valvular diseases. It should be noted here, however, that stenosis of an ostium and incompetency of the corresponding valve are usually associated conditions, though as a rule one or the other predominates and gives its character to the lesion. Fibroid thickening of the mural endocardium is not uncom- mon in connection with chronic valvulitis, especially of the sclero- tic type. It may also occur as a part of an interstitial myocar- ditis. The membrane is thickened and of an opaque whitish or yellowish colour — the latter when fatty change is prominent. Mural endocarditis is often associated with dilatation of a heart- cavity, and is then probably due to the stretcliing of the membrane. The secondary changes in chronic valvulitis are mainly those due to the circulatory disturbance occasioned by the stenosis or in- competence, as the case may be. If a valve is incompetent it per- mits regurgitation into the chamber behind during its diastole, and this cluunbor then receives blood from two sources, the normal one, and tlirough the iiieouijx'tent valve. Sucli an oversupply of blood leads to an overdistention of the chamber, and to an in- creased efi"ort in order to completely empty itself. The continu- ance of these conditions leads to a permanent increase in the capa- city of the chamber, while the increased work thrown on the musculature of the wall causes an increase in its strength and 1 1 1 ick ness ( Hypertrophy ) . If the deforming process results in stenosis, the chamber heliind the defect e.x])criences increased ditHculty in expelling its contents, and develops hypertrophy of the kind known as concentric, because associated with little or no dilatation. The chamber in front of a stenosed orifice, on the otiier hand, is ajit to become atro]>hied and reduced in size, since it receives a diminished supply of blood, and its work is corres|)oii(liiigly lessened. The (listiii'l):ni('('s of circulation secondary to valvular disease CHRONIC ENDOCARDITIS 201 are by no means limited to the heart itself, but affect the various oi'gans and tissues of the body. The blood-supply to the arteries is lessened, obstruction to discharge of blood from the veins exists, and thus is induced passive congestion, which affects not only the organs drained by the veins, but in vi^ell-marked cases also the arterial system which supplies them. In the course of time this congestion reacts injuriously on the heart in a manner to be fur- ther elaborated under the head of the respective valve-lesions. Acute endocarditis is often found associated with the chronic, and indeed the latter predisposes markedly to the former. Changes in the myocardium are also frequent, usually in consequence of nutritional disturbance, which is secondary to the dilatation and hypertrophy, or to associated atheroma of the coronary arteries. Pericarditis is also not infrequently associated with chronic endo- carditis, and is generally of the adhesive variety. This is, of course, due to the two diseases having had the same remote origin. Etiology. — The strictly sclerotic form of endocarditis is not of microbic origin, but is either an expression of nutritional change incident to age, gout, renal and vascular disease, or is the result of strain. That some individuals evince a family tendency to sclerotic changes in the entire circulatory apparatus, as well as in the kidneys, appears proved by the frequent observation of atheromatous valvular disease in two or more members of the same family. Age is thought to be a factor in the causation of this form of chronic valvular disease; and yet the occurrence of the disease in some individuals at a comparatively early age indicates that. there is some other influence at work besides senility. Chronic endocarditis is so frequently observed in persons of a distinctly arthritic habit that gout has come to be regarded as an important etiological element. With respect to such gouty influ- ence, it seems to me that it is rather the entire manner of living which has to be taken into account. For example, I recently ex- amined a physician's father, whose case illustrates what I mean very well. Dr. W., from the interior of Illinois, brought his father to me with the following history : The patient Avas a German, sixty- nine years of age, who had enjoyed robust health up to two years 15 202 DISEASES OF THE HEART before, at which time he developed redness and swelling, with some pain of the great-toe joints. This was regarded as gouty, and nnder appropriate therapeutic and dietetic management dis- appeared. Six months before his visit to me he began to complain of shortness of breath upon exertion, whereupon his son made an examination of the lieart and detected a murmur. The routine treatment w^ith digitalis, strychnine, nitroglycerine, and cathartics had failed to produce appreciable benefit, and twice there had been expectoration of bloody sputum. During the previous two weeks he liad had two nocturnal attacks of dyspnoea that came on in the small hours, while still a third took place after an evening meal. The son furthermore stated what was of special interest from an etiological standpoint — viz., that his father had always led a seden- tary life, getting exercise by driving instead of walking, had always eaten heartily of rich food, indulged freely in beer and other alcoholic beverages, after the German custom, and had been a heavy smoker, lie had never had inflammatory rheumatism or any other illness. The patient was a man of i)Owerful physique, and in spite of his gray hair did not look at all like an old man. Plis normal weight was 207, but at date of examination was 190 pounds, while his height was G feet. His chest was broad and deep^ his bones large and strong, the muscular system well developed, abdo- men not corpulent, and subcutaneous fat not excessive. The nails were moderately ridged, the radial arteries stiff but not beady, the temporal and carotid arteries not stiffened, and the subclavians did not stand out prominently nor throb strongly, as they often do in old men. There was a ])rononnced, visible, and palpable epigastric pulsation reaching at least 2 inches below the xyphoid^ cartilage, but the apex-beat could not be made out. In the aortic area was a systolic thrill, palpable upon moderate pressure during expiration. The thoracic parietes were so hard and resisting that ])ercussion was difficult, but the lungs were everywhere resonant and respiratory sounds were faint and vesicular. Absolute car- diac dulness was not increased, but by resort to palpatory, aus- cultatory, and ordinary plessimetric percussion, relative dulness was found greatly increased upward, to the left, and downward, but not notably to the right. The left border reached an inch outside of the left nipple, in all 5 inches from the left edge of CHRONIC ENDOCARDITIS 203 the sternum (Fig. 33). With exception of the pubnonic second sound, itself feeble, the heart-tones could not be heard. There was, however, a loud systolic murmur of distinct sawing quality audible throughout the pra?cordia and for a distance beyond the left nipple into the axillar}^ region. Upon careful study of this murmur it was found to have two areas of maximum intensity, one in the second right interspace near the sternum, the other in the vicinity of the left nipple. Moreover, in these two areas the pitch Avas slightly yet distinctly different, being lower and harsher in the aortic and more musical in the mitral area. The heart's rate was 90, and its rhythm regular. The liver was pal- pable. The audible pulmonarv second tone and hj^pertrophic dilatation of the right ventri- cle confirmed the evidence obtained from the mitral mur- mur and established the ex- istence of mitral regurgita- tion. The aortic systolic bruit and loss of the aortic second sound, together with the sys- tolic thrill, gave evidence of stiffness, and perhaps steno- FiG. 33. — Kelative Uulness, Case of Cheonic Endocaeditis (p. 201). sis of the aortic valves. The absence of a rheumatic history, the patient's age, the late development of symptoms, the moderate arteriosclerosis, and lastly, the heart findings, all seemed to war- rant the opinion that the valvular changes were due to sclerotic endocarditis. The condition of the kidneys was not ascertained at that time, as the son had not examined the urine, but inasmuch as there was nocturnal micturition, renal cirrhosis was thought probable, and it was advised to have the urine collected for twenty- four hours and examined. In this case I believe the cause lay in the strain to which the valves of the left heart had been subjected for man}- years in con- sequence of the abnormal blood-pressure brought about by his ex- cessive consumption of food and alcoholic liquids without suffi- 204 DISEASES OF THE HEART cient physical exercise. How much, if any, influence can be attrib- uted to tobacco and waste products I cannot say. The influence of strain has long been recognised in the produc- tion of the sclerotic changes now being considered. High blood- pressure, lasting for years, is a cause of yalvular as well as of yascular strain, but inasmuch as the indiyiduals in whom such in- jurious blood-pressure is obseryed generally lead inactive lives, dine well, and often suffer from indigestion and constipation, it is likely that the products of defective metabolism circulating in the blood act as chemical irritants, and play a not unimportant part in the development of sclerotic changes. Disease of the aortic valves is frequently observed in men who pursue laborious occupations, as smiths, carpenters, etc., and hence arduous physical exertion is also accredited with the pro- duction of valvular and vascular strain and consequent sclerosis. It is in this class of workers that rupture of an aortic cusp is most frequently observed, with its disastrous sequels. It has always seemed to me not an easy thing to correctly estimate the influence of physical strain in working people, since they are so often given to the immoderate use of alcohol and tobacco, and frequently be- come victims of syphilis. We should probably consider that in these people all these factors are at work, and attribute their chronic endocarditis to their mode of life in general, without at- tempting to isolate any one etiological factor. Syphilis is un- doubtedly capable of setting up sclerotic deformity of the valves, although endocardial changes follow luetic disease far less often than do myocardial and vascular degeneration. Of that form of chronic endocarditis which is met with in the young, and which is of true inflammatory origin, the one gl'eat cause is rheinnatism. Although these valvular lesions may un- doubtedly begin in an acute vegetative endocarditis, which merges gradually into a chronic process, it is often a low grade of sub- acute inflammation from the beginning that brings about this form of chronic endocarditis. This inflammation may originate in an acute rheumatic attack, and be recognised clinically at the time, or it may develop so slowly and insidiously as to create no Bvmptoms, and remain undetected for years. Indeed, it is not at all uncommon for valvular diseases originating in this manner to be first diagnosed after compensation has begun to wane. This CHRONIC ENDOCARDITIS 205 slowly forming endocarditis gives rise chiefly to stenosis, and, in accordance with the law of numerical frequency, to stenosis of the left auriculo-ventricular orihce. Physicians sometimes fall into the loose manner of speech of the laity and call the pains of myalgia and an intractable or oft- recurring neuralgia, rheumatic. They should remember, however, that these so-called rheumatic pains are etiologically and patho- logically very different from the articular rheumatism that sets up endocarditis. When a student in Munich, I questioned Prof. Joseph Batier on this subject, and received the emphatic reply that " muscular rheumatism never produces valvular disease." For further discussion of the etiology of endocarditis the reader is referred to the chapter upon Acute Endocarditis and those deal- ing with the individual valve-lesions. Symptoms. — The reader of the following chapters will doubtless be impressed by the fact that the different forms of valvular disease present considerable similarity as regards those derangements of circulation of a mechanical nature and those dis- turbances of visceral function which give rise to subjective symp- toms. Such differences as exist are not so much differences in kind as in degree. Any one of the valvular defects may, so long as it is perfectly compensated, exist for years without revealing its existence to the consciousness of the patient, but when compensa- tory hypertrophy is no longer adequate, conditions result whicli must of a necessity force themselves upon the notice of the patient with greater or less prominence. In mitral disease the sensations are mainly due to passive congestion, while in lesions at the aortic orifice they are the result of a diminished or defectively sustained supply of arterial blood; yet in both it would be inaccurate to draw such a strict divi- sion. In mitral disease there is defective arterial circulation as well as venous stasis, and when in aortic valve defects compensa- tion fails, there is more or less passive engorgement added to the imperfect arterial flow. Consequently, the clinical picture takes its colouring from both conditions, but in varying proportions, and hence in all forms of valvular disease there comes a time in the stage of destroyed compensation Avhen whatever individual features each affection may have once possessed become blende'd into the symptom-complex of cardiac inadequacy in its broad 206 DISEASES OF THE HEART sense. Some of these eharaeteristies are plainly recognised as the effects of mechanical pressure in the venous system, as the dull, tense pain of hepatic congestion, the scanty albuminous urine, the hsemorrhoidal congestion and fluxes, and, in large part at least, the serous transudations and the digestive disorders. Other symptoms are probably owing to the incomplete elimi- nation of the normal products of metabolism; or to the nmnufac- ture and accumulation in the system of abnormal products which result from perverted function on the part of the stomach, liver, and other chylopoietic viscera; or there is a combination of these various toxins, with a lessened supi)ly of oxygen and other neces- sary nutritive principles, that may explain some of the subjective phenomena, such as the dull, oppressive headache, the insomnia, nervousness, and in some instances the low, muttering, or even ac- tive delirium occasionally observed in the terminal stage. The dyspnoea of advanced heart-disease is probably a manifes- tation of both mechanical pressure in the pulmonary vessels and upon the lungs by the dilated heart and by hydrothorax, but also of deficient oxygenation through sluggish blood-flow and from bron- chial obstruction by mucus and serum. Since, then, so many factors enter into the production of the nmnifold symptoms com- plained of or manifested by sufferers from valvular heart-disease, it is not possible to satisfactorily account for them all or to explain why some are present in one and absent in another case. We have also to reckon with individual tendencies, neuroses, intercurrent affections, complications, etc., all of which serve to modify the legitimate clinical picture. For example, I recall a certain young woman who first came under my care for an un- compensated mitral regurgitation of rhenmatic origin in 1803, and who during the ensuing five years presented some highly in- teresting and puzzling phenomena. At the beginning hers was an urdinarv case of mitral insuffi- ciency with slight a?dema. which readily yielded to treatment, and she was lost sight of for two years. She then rea]>iieared, having shortly before had a recurrence of rheumatism, and had thereafter Iteen married, both of which occurrences were unfortunate for her. ( 'om])ensation was .so defective, probably in consequence of a fresh endocarditis whicli had passed beyond its acute stage, and which coidd be recognised as having existed oidy by its effects, or in CHRONIC ENDOCARDITIS 207 consequence of a pericarditis that had led to adhesion between the sac and anterior chest-wall, that the patient manifested both ascites and anasarca. Besides this very obvious disturbance of circulation she suf- fered greatly from insomnia and a degree of emotional instability that could reasonably be considered hysterical and made her ex- tremely hard to control. But the particular feature that puzzled me for a time was the fact that the secretion of urine, scanty at all times, became almost suppressed whenever for the sake of sparing the overburdened heart she was subjected to rest in bed. Whether or not this was due to the abolition of those accessory aids to venous How residing in muscular movements of the lower extremities and in deepened inspiration incident to gentle exercise about her apartment I could not decide, but this seemed probable from the subsequent fact that the enormous hepatic engorgement and ascites did not disappear until she was given a course of re- sistance exercises. Pari passu with this removal of the mechanical hindrance to circulation the insomnia vanished and her normal mental state re- turned. Compensation was at length regained and retained for a number of months. Six months later, however, she suddenly de- veloped an excruciating and obstinate neuralgia in the course of the right brachial plexus, for which I could discover no adequate cause, and which resisted all treatment. It was accompanied by cough with scanty mucous expectoration, of which repeated care- ful examinations of the heart and lungs failed to detect any cause aside from the old-standing valvular lesion. At length, discour- aged by her failure to obtain relief, she returned to her home in the country, where during the next few weeks she expectorated masses of tenacious sputum, which were said when put in water to spread out and look like the branches of a tree. Whether this was an instance of fibrinous bronchitis or not I cannot say, but certain it is, that when finally her bronchitis subsided her neural- gia also disappeared. I have always believed this was a manifes- tation of infection, since, as we know, cardiac patients are particu- larly prone to obscure infections, and that the neuralgia could not be regarded as anywise a symptom directly attributable to her heart-disease. The next event in this patient's series of experiences occurred 208 DISEASES OF THE HEART about a year later. She had again been suffering from rheuma- tism, as I was told, when, according to her sister's statement, she suffered one night from severe pain in the region of the heart, for which hot cloths were being applied. Suddenly the sufferer exclaimed, " There ! something has broken, and the pain has all gone." She then seemed to sink away, her pulse becoming too weak and rapid to be counted, her extremities cold, and her coun- tenance blue. Stimulants revived her, but all night she continued to have sinking spells, which necessitated the administration of restoratives. The explanation of this attack has never been clear to me. Whether a tendinous cord snapped, or a pericardial adhesion gave way, or whether the pain may not have been due to a muscular cramp, I cannot say. Under the influence of heat the muscle may have suddenly relaxed, and thus caused a sensation, which to the suffering and highly nervous apprehensive girl was naturally at- tributed to the heart, and threw her into a condition of mental shock which reacted on the weakened heart. At all events, the attack was fraught with no less alarm to the friends than to the patient, and an explanation was sought, which could not be given. Six weeks subsequently the patient was again brought to the city in a truly deplorable condition. There were marked evi- dences of cardiac asthenia and consequent circulatory embarrass- ment, pronounced icterus, oedema of the ankles, ascites, enormous hepatic congestion, o'denia of the left but not the right arm, and in the heart signs of double mitral disease, relative tricuspid in- sufficiency, and adherent pericardium. The feature of chief interest, however, was connected with the dropsy of the left upper extremity. This was strictly local- ized, extending from the fingers up to and ceasing with the shoul- der. Palpation of the axilla disclosed that the axillary vein had been converted by thrombosis into a firm cord. To what distance the thrombosis extended down the arm could not be determined, but it did not involve the jugular veins. The " swelling," it was stated, had made its appearance a week earlier, but aside from the annoyance did not api)oar to occasion pain or distress. This highly interesting and coin])ai-atively rare condition was an instance of venous thrombosis occurring in some cases of valvu- lar disease. It has formed the subject of an instructive paper CHRONIC ENDOCARDITIS 209 by Dr. William Welch, which was read at the session of the Asso- ciation of American Physicians in 1900. Welch was able to col- lect but 28 recorded instances, including his own, although, as stated by him, the condition probably occurs more often than it is recognised. Of these 28 cases, all but 4 involved the veins of the upper extremities and neck, a fact which lends to it addi- tional interest and importance. Twent^'-two cases showed throm- bosis of the left side alone 15 times, bilaterally 8 times, while only twice was it confined to the right. Welch found that the thrombosis might be limited to the veins of the arm, to those of the neck, or might involve all the veins — that is, the superior vena cava, the innominate, both internal and external jugular, sub- clavian, axillary and brachial, and even, as in one case, the supe- rior thyroid. Although thrombosis uiay and does sometimes occur in indi- viduals suffering from chronic arteriosclerosis and nephritis, yet in Welch's 28 cases there was in every instance valvular disease as follows : Mitral regurgitation 9 times, mitral stenosis alone 6 times, mitral stenosis with insufficiency 6 times, and aortic regur- gitation with relative mitral incompetence once. In 10 instances there was associated aortic and mitral disease. The thrombus was either red or reddish-gray, and although in some instances it was softened at its centre, it for the most part was firm through- out, and occluded the vessel excepting at its extremities. In one case it was a " wall thrombus." It is also interesting to note that the thrombosis appeared to have begun at the lower end of the in- ternal jugular in those instances in which it involved the cervical veins. This fact led Welch to conclude that the formation of the thrombus was favoured by the peculiar anatomical arrangement of the cervical veins on the left side, together with the conditions governing the blood-flow in them. As pointed out by Ilanot, the left innominate vein is longer and more oblique than the right, which, together with the right- angle junction of the left internal jugular with the subclavian and the bulbous expansion of the internal jugular, favours, in Welch's opinion, the formation of eddies or whirling currents at that point, and thus furthers the development of thrombosis. Moreover, he thinks there is probable pressure upon the sub- clavian vein by the dilated left auricle and dilated pulmonary 210 DISEASES OF THE HEART veins, so that circulation in the cervical and arm veins becomes extremely sluggish, and thus provides another favouring factor. Finally, in one of his cases Welch was able by cultures to identify the streptococcus pyogenes, which, he thinks, warrants the hypoth- esis that in these cases there is an infectious origin for the throm- bosis, a conclusion which is strengthened by recent observations going to show that in all cases of venous thrombosis there is an infection. In my case there is good reason to believe that the patient was still suffering from some infection, for she had but a few weeks earlier gone through with what was called rheumatism by her home physician, yet which may very well have been a strepto- coccus infection, which so often presents the appearances of artic- ular rheumatism. Moreover, there were three small, distinctly in- durated lymphatic glands situated just above the left clavicle, near the outer border of the left sterno-cleido-mastoid muscle, while the patient displayed a slight elevation of temperature. In other re- spects my case conformed with the most of Welch's requirements — namely, she was a female, of but twenty-three years of age, and was a sufferer from mitral disease. Her symptoms too were char- acteristic in the localization of the oedema to the affected arm below the location of the thrombosis. She did not, however, suffer pain, at least not at the time the interesting condition was de- tected, the occluded vein was not tender, and I failed to discover any enlargement and tenderness of the lymphatics of the arm, as is often present. If such existed, they were hidden from observa- tion by the oedematous condition of the extremity. Welch states, finally, that in at least one of the cases collected by him there was mild delirium, which was attributed to the cerebral oedema discov- ered at the autopsy. In the matter of the diagnosis of this form of venous tlirom- bosis there is no difficulty, ])rovided the thrombosed vein can be felt, and even wlien not, strictly localized dropsy in one arm or one side of the neck renders the existence of thrombosis very likely. Nevertheless, according to ITanot, the greater length and obliquity of the left innominate vein may sometimes cause unilateral and circumscribed a'dema even when venous thrombosis is not present. The prognosis is unfavoural^le to recovery from the dropsy if the veins are extensively plugged. If the thrombosis is not com- CHRONIC ENDOCARDITIS 211 plete, or is of limited extent, it is possible for collateral circulation to become established and absorption to take place. Finally, the condition is likely to occur in the terminal stage of the valvular disease, and if very extensive it may contribute to the patient's death. It is not common for patients witn chronic valvular disease to suffer from embolism, and yet such a possibility should always be borne in mind. It is stated that such an occurrence is more fre- quent in mitral than aortic disease; and I have under observa- tion a female patient with mitral insufficiency who has perma- nent contracture of the fingers of the left hand and but partial use of the arm as a result of an embolus that was thrown off pre- sumably from her mitral valve nearly six years ago. The symp- toms of embolism are usually said to be pain in the part where the plug lodges, nausea, and even vomiting, a chill, and rise of temperature. To judge from cases of embolism observed in acute endocarditis and from pulmonary infarcts, I should say that pain in the affected part is the most constant symptom. The splenic artery is a frequent seat of embolism, and it may well be that the transient pain from which cardiac patients not infrequently complain in the region of the spleen may be of this origin. It is unsafe to make such a diagnosis, however, unless one can detect enlargement and tenderness of this organ following the pain. This is emphasized by the fact that these patients are very prone to sudden and sharp pains of a neuralgic character in various situations, particularly in the abdomen. I recall an instance that was narrated to me by an ophthal- mologist of sudden blindness of one eye resulting from the plug- ging of the retinal artery, and as the lady possessed a blowing sys- tolic apex-murmur, the embolus was thought to have been a minute vegetation from her mitral valves. I have also been informed of a young lady with valvular disease who, upon awakening one morn- ing, was found to have lost during the night all recollection of certain members of her own family. This peculiar lapse of mem- ory was attributed by her medical attendant to embolism. Pulmonary infarcts are not at all uncommon in cases of ad- vanced valvular disease, and are evinced by sudden acute pain in the affected lung, together with frequent cough and the spitting of clear blood. These cases must not be confounded with instances 212 DISEASES OP THE HEART of ha?moptYsis due to sudden increase of pnlnionarv congestion, as not seldom occurs in mitral patients who have overtaxed their hearts. In these cases the history of some exertion and the ab- sence of sudden, sharp jiain will usually aid in the differential diagnosis. Embolism of tlie middle cerebral artery is attended by such manifest symptoms that there is usually but little difficulty in determining the cause of the phenomena. In a single instance I have observed the conjunction of true epilepsy with valvular disease. The patient was a man of about forty who presented well-marked signs of mitral stenosis. His valvular lesion was of rheumatic origin, and his convulsions ante- dated his cardiac disease by some years. There was every reason to conclude that the association of these two affections was purely accidental as regards their etiology. The fits were usually excited by indiscretions in diet, and required bromides for their control. Although never assuming any causative relation between the two, I yet believed they exerted a deleterious influence upon each other. I am very certain that the epilepsy affected his mitral disease unfavourably by serving to maintain and aggravate the dilatation of the cardiac chambers. Such cases as this are not to be regarded as instances of cardiac epilepsy, which term has been employed to designate attacks of pra'cordial pain accompanied by loss of con- sciousness and succeeded by twitchings of the muscles of the face. The association of epilepsy and heart-disease in my case serves to emphasize the fact that valvular diseases may be complicated and have their clinical picture modified by other affections. I speak of this because inexperienced jjhysicians are apt, when treat- ing patients with valvular disease, to attribute all symptoms to the cardiac complaint. Cardio])aths frequently become anaemic and neurotic, hysteri- cal or neurasthenic, and then complain of all sorts of sensations, which it is clearly impossible to attribute to their valvular affection. The French describe what they term " cardiac cachexia " in distinction froin cardiac asthenia, and wliich is analogous to the cachexias of malignant or tuberculous disease. They ascribe it to some chemical change in the blood. It is not at all uncommon to see cardiac ])atients who, while presenting no very marked S}Tnp- toms of cardiac inanber, which has "econ- hjpemopto ^^_^^^.^^^ ^^.^ force an unnatural amount of Wood Cyanosis of face Cyanosis, and clubbing of fingers Congestion and cedema of lungs Engorgement of portal system Congestion and (i-dema of lower limbs. Fio. 35.— Diagram si V..■,rrT^ ON THE ClUCVLATIO N UK A MlTllAI. LkaK. MITRAL REGURGITATION 221 cavity is in a state of diastole wlien it receives this inrush, and, being relaxed, becomes after a time dilated. At the same time it is forced to handle a larger volume of blood, which it can only- do by nndergoing hypertrophy, and thns at last this ventricle comes in its turn to feel the secondary effects of the circulatory disturbance. In time, moreover, when stasis has become everywhere aj^par- ent, the left ventricle undergoes still further dilatation, for which it has become prepared by certain structural changes within its inyocardiuin. Its myocardium is flabby and of a brown instead of the normal beefy red colour, while its fibres are found micro- scopically to be reduced in size and to contain granules of brown pigment, especially near the nucleus. This increased dilatation of the ventricle at this time is explained by some as due to the high blood-pressure in the arterial system secondary to stasis in the veins, which abnormal arterial blood-pressure interferes with the easy emptying of the ventricle. This is a defective explanation, however, since physiologically the abnormal blood-pressure in the venous system leads to lowered instead of heightened blood-pres- sure in the arteries. The dilatation of the left ventricle is now due to the weakness of its own wall, which does not permit it to completely empty its cavity with each systole. Thus is estab- lished a residue which augments the amount of blood received from the auricle with the next diastole, while at the same time its wall is powerless to withstand the dilating force of this stream that pours into it. Thus is at length set up a vicious circle in consequence of wdiich the effect of the original valvular incom- petence intensifies the regurgitation. The typical heart, then, of mitral insufficiency is enlarged. The enlargement is mostly of the right ventricle, and the organ has in consequence a rounded apex. The tricuspid orifice, and often the pulmonary, is found to be wider than usual, owing to the dilatation of the right ventricle. The left ventricle is mod- erately and the left auricle greatly enlarged, while the mitral valve shows the structural changes already described, which have been the cause of the whole trouble. Etiology. — What has already been said concerning the causa- tion of chronic endocarditis applies equally to mitral insufficiency, since this is but one of the manifestations of that affection. I shall 222 DISEASES OF THE HEART therefore only add a few general considerations bearing on the localization of the deforming process at the mitral orifice. Incompetence of the left auriculo-ventricular valve is a verv frequent cardiac affection — is indeed the most frequent of all vahadar defects. This is particularly the case in children and young adults, forming in this period of life the counterpart in point of frequency of the sclerotic changes at the aortic orifice in persons, chiefly men, past middle age. The influence of childhood and youth in the generation of mitral regurgitation lies doubtless, not in the fact of the age, per se, but in the prevalence in the young of those diseases, inflammatory rheumatism, chorea, and the exanthemata, which set up endocarditis. The greater liability of the mitral than of the aortic valves to suffer from endocardial inflammation in the earlier decades of life is probably owing to their being exposed to relatively greater strain, which their more delicate structure fits them less well to endure. As regards sex, it is generally stated that mitral regurgita- tion is more fre(pient among males than females, but in analyzing m}'' case-records I find no predominance of either sex. After throwing out all cases that from the history, age, or symptoms cannot be safely considered as organic, there remain 126 cases in which regurgitation was due to structural alteration of the valves. These were divided equally between the two sexes. Classifying these 126 cases according to decades, there were 6 boys and 6 girls between one and ten years of age, 12 males and 16 females be- tween ten and twenty, 18 of each sex between twenty and thirty, 14 each between thirty and forty, and 15 males and 7 females over forty. Examined with reference to rheumatism and other diseases, it was found that 32 males and 28 females gave a history of rheumatism alone, 4 males and 6 females of scarlatina alone, 5 males and 4 females of measles alone, 1 female of chorea alone, while of more than one disease 1 male and 8 females had had rhcuiiiatism and scarlatina, 4 each had had rheumatism and mea- sles, and 4 each rheumatism, scarlatina, and measles, 2 males and 5 females scarlatina and measles, 2 females measles and pertussis, and 1 f'ciiialc all four diseases, 2 males and 5 females chorea, in combination with some of the other diseases mentioned. Two males gave a history of venereal disease. Of the remaining cases, in which no definite history of previous disease could be elicited, MITRAL REGURGITATION 223 the organic nature of the lesion was rendered probable either bv the existence of arteriosclerosis or by the youthful age of the pa- tient and the absence of anaemia or other factors pointing to a rela- tive mitral insufficiency. Symptoms. — The presence or absence of distinctively cardiac symptoms dejDends upon the degree of the leak and of the com- pensatory hypertrophy that has been established. Consequently we have to distinguish cases in which subjective manifestations of circulatorv disturbance are wanting from those in which there is more or less evidence of cardiac inadequacy. In the former class such symptoms as are complained of are probably referable indirectly to the valvular defect, but are nevertheless such as we encounter in persons without disease of the heart. In some in- stances they direct the experienced physician's attention to the possibility of mitral disease, while in others they seem to point rather to disorders of other organs, and the discovery of the re- gurgitation is accidental. In such cases the individual first learns of his malady on applying for life insurance, or upon subjecting himself to physical examination prej)aratory to athletic training, or wpon consulting his physican for some trifling ailment. The dam- age to the valve is slight and compensatory hypertrophy is perfect. It would in some instances be better for such persons not to be informed of their defect, since although they are able to endure games of skill and considerable exertion, as tennis, without con- scious symptoms, they are likely after learning of their lesion, par- ticularly if of a nervous, excitable temperament, to be alarmed by palpitation, which prior to their knowledge did not attract their attention. In other instances regurgitation is free, yet there is a truly re- markable absence of subjective consciousness of its existence. This is generally due to the completeness of the compensatory hypertrophy on the part of the right ventricle and the left auricle. Yet I have known individuals of a not very impressionable tem- perament who, in spite of rather inadequate compensation, were unconscious of symptoms referable directly to their mitral dis- ease. Some excitable neurotic persons, like those first alluded to, consult physicians for symptoms referable to the digestive tract, or nervous system, rather than to the heart itself. These are anorexia, or discomfort after food, constipation, or an irregular 224 DISEASES OF THE HEART State of the bowels, distressing pra?cordial pains, which either set up or are accompanied by palpitation, and which greatly alarm the patient and friends. In a multitude of such cases there is no objective evidence of loss of compensation, and the patients are able to enjoy outdoor sports or to participate in feats of endurance without subjective symptoms. Again, cases occur in which the only symptoms are such as are usually classed under the head of lithiemia, or the irregular mani- festations of gout, and occurring in persons of sedentary habits^ are removed by regular outdoor exercise. In other cases the most that can be said is they appear to have an unstable nervous system, and their symptoms in nowise differ from those of other individuals of the same category whose hearts are healthy. In all such the valvular lesion does not appear to be directly responsible for the manifestations, and yet it may well be that these can be referred to defective nutrition and elimination in consequence of the circulatory disturbance. It is not uncommon for females with organic mitral insuffi- ciency to present evidence of simple secondary anaemia or of chlo- rosis without symptoms of cardiac inadequacy. If in such cases there is shortness of breath u])on unusual exertif>n, it is no greater than may reasonably be attributed to the blood-state. I recall a remarkably interesting and instructive instance of this kind. In March, 1901, a young married lady of twenty- four sought my opinion because of " a grating sound in the heart," which first attracted her notice in the fifth month of her pregnancy, and which still annoyed her at times of unwonted physical effort, as during- rapid walking. Aside from this symptom, there was nothing that made her conscious of her heart. She admitted getting a little out of breath, but this was so slight she had not given it any attention. Both her parents had died of ])ulm(»nary tuberculosis, but of her brothers and sisters, seven in all, none had shown signs of the dis- ease. She had had pneumonia when but a year old, scarlatina at eight, measles and ])ertussis in childhood, but never rheunmtism, and up to the time of her marriage, at twenty-two years of age, she had considered herself well, Ix'iug able to romp and play like other children without trouble. With exception of the " grating sound " jnentioned, her pregnancy and confinement had been uneventful, and she could not recall having suff'ered from more dyspnoea than MITRAL REGURGITATION 225 do other women towards the later months of pregnancy. She had nursed her baby for nine months, and during that period lost 29 pounds, of which seven had been regained in the seven months fol- lowing the weaning of her infant. Her appetite was poor, bowels were irregular, and she was aj^t to suffer from sour stomach and eructations. The menses were regular but scanty. Hands and feet were generally cold, and she said she had grown nervous, being easily excited. Pain of any kind was trifling, forming a marked contrast to most of the cases I encounter. In all this history and description of symptoms there was nothing to point to the heart outside of her declaration that she sometimes heard a queer sound, which she wanted to learn the meaning of. The pulse was 85, equal, regular, but too small and weak. The broad, strong apex-beat was in the normal situation, and no increase of either superficial or deep cardiac dulness could be made out. However, the first sound was partly obscured by a loud, rasping murmur that was audible throughout the cardiac area and transmitted around the left side to the lower angle of the scapula. The pulmonary second sound was accentuated, and in the dorsal decubitus a softer blowing systolic murmur could be heard in the pulmonary area. Thinking this last might be a chlorotic murmur, I had the blood examined, and found that the haemoglobin was reduced to 65 per cent, red and white cells being normal in number. In spite of the absence of a rheumatic history and despite chlorosis, there seemed no good reason to doubt the existence of a mitral regurgitation of endocarditic origin, but as compensation was preserved, the patient was reassured as to the harmlessness of the sound she had noticed. In fact, she was given to understand that the more serious conditions were the blood-state and loss of weight, which in the light of her family history certainly required attention. She was given a little strychnine and a few drops of digitalis to improve the strength of her pulse, but main attention was bestowed upon the matter of nutrition. Milk, raw eggs, and fresh air were insisted upon. The patient obeyed instructions to the letter, and soon was disposing admirably of two quarts of milk and ten raw eggs daily in addition to three good meals. Her colour, weight, and general condition improved steadily, until at the end of two months she looked the picture of health. ISTevertheless, the 226 DISEASES OF THE HEART murmur persisted, and once in a while she heard that same endo- cardial soimd. It no longer worried her, however^ and she never complained of any other symptoms referable to the heart or dis- ordered circulation. In this case it would be difficult to say how much the mitral regurgitation was responsible for her condition. I believe the leak was so slight that it did not materially affect the chylopoietic and blood-making organs, but that the state of her general health was attributable to her child-bearing and lactation, which in a woman with hereditary predisposition to pulmonary tuberculosis proved too great a draught on her vitality. Had she been allowed to go on in her reduced condition she would in time have devel- oped symptoms either of cardiac inadequacy or of tuberculosis. As it is, she is now likely to remain free from symptoms of valvu- lar disease for an indefinite time. I have notes of the case of a young man who, because of a mitral regurgitant murmur and not very severe symptoms of car- diac strain, was ordered to bed by his physician, and there re- mained for two years. When I saw him he had mitral insuffi- ciency sure enough, but his prolonged rest had established perfect compensation, the heart being not demonstrably enlarged and the liver of normal size. Yet he declared he could not get up or stand, much less walk. I compelled him to get on to his legs, and little by little to walk about, with the result that he found he could exercise without harm or symptoms of heart-weakness. He was easily frightened about himself for two or three years, but did not manifest dyspncr'a or other cardiac symptoms even when riding his wheel over hilly and sandy roads. The last time he was seen by me, now several years ago, he was as well as nine-tenths of the young men who, like him, are school-teachers. At the most he had to be careful of his stomach and guard against constipation. A medical student, age the sclerotic form of this valvular lesion, and in such it is probably but a manifestation of a general tendency to fibrosis. The association of mitral stenosis with renal disease is shown by Goodhart's statistics, who found it })resent in al)out 1.4 of 102 cases of chronic nephritis that came tu autopsy, while Pitt, in the MITKAL STENOSIS 255 post-mortem records of Guy's Hospital, found mitral stenosis and granular kidney three times as frequently as stenosis without this form of renal disease. It is a striking fact, on which all writers comment, that mitral stenosis is encountered far more frequently in the female than in the male sex. This is especially true of the disease in persons below the age of forty, in whom it is probably of inflammatory origin, while the sclerotic form of the lesion does not appear to predominate greatly in either sex. Of 42 cases of pure mitral stenosis of which I have records, 28 occurred in females and 14 in males, and of the entire number but 20 gave a clear history of rheumatism. It is thus seen that of my cases females numbered twice as many as males, bearing out the statement that mitral obstruction is par excellence a disease of the gentler sex. Symptoms. — Inasmuch as the effects of mitral regurgitation and mitral stenosis on the circulation are practically the same, there is a close similarity in the symptoms of the two affections. Therefore, much of what was said under the head of mitral regur- gitation also applies to mitral stenosis. Undoubtedly this affec- tion may remain latent for years, but it is less likely to do so than is regurgitation. Xevertheless, hard and fast lines in this regard cannot be drawn, for the manifest reason that the degree of the effect stands in direct proportion to the gravity of the lesion. If compensation is adequate, symptoms referable to the heart, or that call the attention of the patient to his heart, may be entirely ab- sent; and yet a patient with any considerable degree of stenosis is not likely to be robust, or to possess much physical endurance. Children are likely to be more or less stunted in development, both mentally and bodily ; while in the case of adult females I have been impressed by the frequency with which they are tall and thin, with evidence of anaemia. Their circulation, as might be expected, is defective, as shown by coldness of the hands and feet and great sensitiveness to low temperature. Even when not suf- fering from symptoms referable to pulmonary congestion, as dysp- noea, they are apt to complain of digestive and menstrual disor- ders, sour stomach and scanty menstruation being particularly common. They are generally constipated and their urine is diminished in amount, of correspondingly high specific gravity, and loaded with urates. 256 DISEASES OF THE HEART Patients with mitral stenosis are also very prone to attacks of bronchitis, -which ultimately run into chronic bronchial catarrh. They are also particularly liable to acute pulmonary oedema upon extra exertion, and in such instances the cough and haemoptysis or frothy, perhaps blood-tinged, sputum often give rise to the fear of pulmonary tuberculosis. I have this very day seen a well- marked instance of the kind. In other cases there is persistent dry cough due to bronchial congestion, which may attract attention from the heart to the lungs. I well remember the case of a lady who, consulted me for an obstinate dry cough, which was found due to a mitral stenosis, the existence of which had not been suspected. Indeed, I myself had examined her about a year previously during an attack of tachycardia, and at that time was unable to detect any implica- tion of the valves. As a rule breathlessness on exertion is an early symptom with patients suffering from pronounced mitral constriction, even though in all other respects compensation seems good. When the narrowing of the orifice is extreme, when the heart-muscle begins to fail from degeneration or preponderating dilatation, dyspnoea becomes an exceedingly distressing symptom, and may be present, though in a less degree, even when the patient is at rest. Palpi- tations may also be an annoying feature, and there may be sharp or dull pnecordial pains with areas sensitive to pressure, the same as in mitral regurgitation. I am unable to recall a single instance in which there was typical angina pectoris. In other cases there is a sense of pra'cordial fulness or dis- tention, particularly upon exertion. More or less vertigo declares itself \\])im the patient suddenly assuming the erect position, or he is annoyed by a feeling of fulness or confusion in the head. This, which is a symptom of passive cerebral congestion, often amounts to actual headache. Insomnia, disturbing dreams, and other effects of venous congestion become more and more pronounced, and the patient passes into the stage of completely destroyed com- pensation. Gi!dema, which is at first confined to the ankles and tends to disappear over night, creeps upward into the thighs, rendering locomotion difficult and painful. Owing to the feeble, rapid, and arrhythmic action of the overdistended heart, the pulse is thready, MITRAL STENOSIS 25T perhaps unequal in the two wrists, intermittent, and often ex- tremely difficult to count. This intermittence may be due to cardiac intermissions, or to such an inequality in the force of the heart's contractions that some of the blood-waves fail to reach the wrist. The hands and forearms may be cold, and the superficial veins stand out prominently in striking contrast to the emptiness of the arteries. Pulmonary congestion declares itself by increased dyspnoea that may even amount to orthopnoea, by cough and sero-mucous or sero-sanguinolent sputum, dulness at the bases of the lungs, par- ticularly behind, and by copious, moist rales. If the tricuspid valve gives way, permitting regurgitation into the auricle, the turgid jugulars pulsate. The liver, already swollen, perhaps ten- der, grows still more engorged, and likewise pulsates synchro- nously with the epigastric throbbing of the dilated right ventricle and the so-called positive pulse in the cervical veins. The taking of food is attended with formation of gas that distends the stom- ach and bowels, adding greatly to the patient's distress, and ren- dering adequate nourishment difficult. The sufferer frequently complains of dull or burning pain in the pit of the stomach, and is tormented by an intolerable thirst. Congestion of the head is shown by duskiness of the countenance, swimming of the head, or headache, and insomnia. In some cases there is a condition of somnolence, and the sufferer falls into short, unrefreshing naps, which are disturbed by dreams, and from which he awakes with a start. The skin is not infrequently bedewed by a cold sweat, which about the head and neck may be so copious as to run off in trickling streams. Stasis within the renal veins leads to scantiness of the urine, which is dark in colour, loaded with urates, and often contains albumin and casts. The action of the bowel becomes irregular and constipated, or as the dropsy invades the abdominal structures the patient may be annoyed by frequent scanty, liquid stools. Con- gestion of the hsemorrhoidal veins sometimes gives rise to addi- tional distress. Disorders of the pelvic viscera are common at this time in the female ; the catamenia are apt to be scanty and irregular, and leucorrho-a is not uncommon. Day by day the dis- tress of the patient increases ; during his waking hours he longs for the relief of sleep at night, and by night his discomfort makes him 25S DISEASES OF THE HEART long in turn for the days. Days drag on into weeks, and not infre- quently weeks into months, with ever-augmenting dropsy, which at length invades the serous cavities (Fig. 43). Ascites and tumefaction of the abdominal walls intensify pressure upon the diaphragm and abdominal vessels, rendering breath- ing still more la- boured. The pres- sure thus occa- sioned still further impedes the re- turn flow from the veins of the low- er extremities, and causes an increase of anasarca. If hydrothorax now sets in, the pa- tient's shortness of breath becomes ex- treme, and he is obliged to support his body by resting his arms on a table in front of him. I Fig. 43. — Case of Mitkal Stenosis, showing Ascites and i i r have known a sut- ferer from mitral disease in this stage to remain thus for several weeks, not venturing to leave her chair. Fortunately for these patients, nature is not able long to maintain the unequal struggle, and unless treatment brings relief, death does so ere long. Occasionally in this extreme stage the end comes through sud- den stoppage of the licart, but as a rule it is the result of some one of the causes that will be narrated in the part of this subject de- voted to the mode of death. Physical Signs. — Inspection is apt to detect more or less cyanosis, and in pronounced cases there may be distinct blueness Clibbixg of Finger-tips. Areas of superficial and deep-seated dulness are indicated. MITRAL STENOSIS 259 of the lips and finger-tips. Patients, particularly children, who have had the disease for years usually display clubbing of the terminal phalanges. Often there is bulging of the prsecordium, particularly at the lower end of the sternum, as well as visible epi- gastric pulsation. If compensatory hypertrophy is great, and lung-borders are retracted, the eye may discern a systolic pulsation over the body of the heart and a short diastolic shock in the pul- monary area the same as in regurgitation. The apex-beat is usu- ally feeble, and not likely to be outside of the nipple or below its usual situation. Palpation confirms the impression received by the eye, but in addition detects a thrill at the apex, which, preceding the ventricu- lar impulse, is known as presystolic. This thrill resembles the purring of a cat, and hence is called " fremissement cataire." It may be short and soft, or rough, and extend throughout the greater part of diastole. In some instances a shorter, feebler thrill fol- lows the second sound, occupying the forepart of the diastolic period. The presystolic thrill is found to lead up to, and termi- nate in a short, sharp systolic shock or " thumping " apex-beat. This thrill is often so short as to convey the impression of the apex-beat being split, the second of the two impulses being the sharper and stronger. A sharp stroke, imparted by the sudden closure of the pulmonic valve, is sometimes felt distinctly in the second left interspace, close to the sternum. Epigastric pulsation is generally pronounced, and gives the impression of a 230werfully contracting right ventricle. In compensated cases of stenosis the pulse is small, feeble, and regular, and less rapid than in mitral regurgitation. There has been much controversy, chiefly among the English, as to whether the pulse of mitral obstruction or of insufficiency is the more likely to be irregular. This, in my opinion, is a matter of slight practical importance, and yet in my experience I have found the pulse to be more often irregular in regurgitation than in stenosis. The annexed sphygmographic tracing (Fig. 44) is from a case of pronounced mitral stenosis in a female, and shows the pulse small, of high tension, and regular. When pulse-tension is pro- nounced, it is due to capillary resistance and not to the energy of left ventricular contraction. Concerning the irregularity of the 260 DISEASES OF THE HEART Fig. 44. — Sphygmogram from Case of Mitral Stenosis. (Personal observation.) pulse in mitral disease, it may be again stated that observations of Kadizewsky appear to prove that the character of the pulse in this respect depends upon the state of the myocardium of the au- ricles. When this is healthy, the pulse is regular ; when degenerated, either fibroid or fatty, the pulse becomes irreg- ular, even arrhythmic. Popoff has called attention to the occasional occurrence of a pulsus differens in this disease, by which term is meant an ine- quality in the two radial pulses, the left being the smaller. As this is observed when compensation is destroyed, and may dis- appear with restoration of cardiac energy, Popoff attributes the inequality to pressure of the greatly dilated left auricle on the left subclavian artery. Preble has also noticed its occurrence in some of his cases. As pulsus diiferens may also be produced by aneu- rysm, embolism, thrombosis, arteriosclerosis, etc., it is important that all such causes be ex- cluded before the phenomenon is attributed to extreme dila- tation of the auricle, a matter that may be of some moment in ]>rognosis. Percussion shows a simi- lar change in absolute and relative cardiac dulness as de- scribed in the article on mi- tral regurgitation — viz., an increase of cardiac dulness towards ilie right side and downward (Fig. 45). This increase bears a direct rela- tion to the degree of stenosis. According to Leiibe, percus- sion sliows a more pronounced enlargement of the right heart in this form of mitral disease than in insufficiency, a point he regards as of importance in the differ- ential diagnosis between these two affections. Fig. 45. — Locaiion ok ApfcxiitAT and Area of Deep-seated Dulne.ss in Mi- tral Stenosis. MITRAL STENOSIS 261 Another difference lies in the fact that, owing to atrophy in- stead of hypertrophy of the left ventricle, dulness is not likely to be much if at all increased to the left. Auscultation. — In pronounced cases of mitral stenosis, auscul- tation at the apex of the heart detects a murmur of such intensity and distinctive character that it at once fastens the attention of the examiner. In most instances it is a long-drawn, rough bruit, which, beginning after the second sound, runs up to and termi- FiG. 46.- -Khythm of Chaeacteristic Mukmue of Mitral Stenosis, " Auricular-Systolic." nates abruptly in a clear, sharply accented first sound. The mur- mur is spoken of, therefore, as presystolic, and in this respect cor- responds exactly to the thrill already described. When well marked, this presystolic murmur is so striking as to be almost pathognomonic of mitral obstruction (Fig. 46). The rhythm of this bruit, by which is meant the time of its occurrence, has been the subject of considerable controversy, for the reason that some observers have declared it to be in reality systolic and only seemingly presystolic. The generation of the first sound, say they, is delayed in consequence of the rigidity of the mitral valve, and hence, although the murmur begins with the contraction of the ventricle, its occurrence prior to the first tone gives it the appearance of preceding ventricular systole. The arguments in support of this opinion have never convinced me of 262 DISEASES OF THE HEART its correctness, and consequently I regard the brnit as truly pre- systolic. When we reflect on the physiology of cardiac action we see that a murmur which is audible before ventricular systole is generated during diastole, and that therefore the murmur of mitral stenosis is diastolic. This is not all, however ; the bruit in most cases is plainly heard to begin in the latter portion of the long pause — i. e., the diastolic interval — and to end exactly with the first tone. It is synchronous, therefore, with the contraction of the left auri- cle, which, as we know, takes place immediately before that of the ventricle. For the reason, then, that the murmur is generated dur- ing auricular systole, Gairdner long ago proposed the name for it of the " auricular systolic " murmur. This term is too restricted, however; since, as is well known, the bruit in some cases commences before the contraction of the auricle, in fact immediately after the second sound, and lasts throughout the long pause. It is consequently a •liastolic and not always an auricular systolic murmur, and as such is in contrast to the systolic one of mitral re- gurgitation. It has also been c-alled the " mitral direct " murmur, because transmitted in the direction of the blood- stream — i. e., from the mitral opening directly to the apex of the left venti"icle. Indeed, it may be stated en passant, that all bruits of stenosis are called direct and those of re- gurgitation indirect iiniiimirs. Considering, then, the des-igna- tions that have been given to thf murmur in question, the best is the one in most general use, which is presystolic. The murnuir is heard most distinctly close to the apex-beat, not directly at the seat of impulse, but slightly within and above, at the point, in fact, where the thrill is felt most plainly (Fig. Fui. 47. — Akea of AruiHiLiTV ok tiik I'he- SySTOLIC MUKMUR OF MiTRAL StENOSIS. It is frequently limited to this area. MITRAL STENOSIS 263 47). Its area of audibility is sometimes very limited, being con- fined to the immediate proximity of the apex, but I have known the murmur to be audible for a considerable distance in all direc- tions, although even then it is not transmitted so widely outside of as inside of and above the apex-beat. The quality or timbre of the bruit is exceedingly rough and harsh, so that it is frequently described as rolling, blubbering, spluttering, etc. Balfour happily describes it in some instances as sounding like V-o-o-t or the sound produced by the attempt to roll out the letters R-r-b, or when still more prolonged R-r-r-b. The final consonant of these combinations is supposed to represent the short, sharp first sound that terminates the bruit. The mur- mur never possesses the soft, blowing quality of the mitral regur- gitant murmur, since obstructive bruits are always rougher than those of regurgitation. The length and intensity of a presystolic murmur are influ- enced by posture and the rate of cardiac action. Thus a bruit, which is short and rather indistinct when the heart is beating rapidly, or when the patient is standing,, is very likely to increase appreciably in duration and to display its true character more dis- tinctly after the individual has lain down and the heart's action has become slower. In other instances the reverse obtains, the bruit being most distinct in the erect posture. One should aus- cultate in all positions and under varying conditions of cardiac action. Another peculiarity of the mitral direct murmur is its change- ability, by which is meant that it is not always the same in dis- tinctness at different times. I recall vividly a woman in whom on several occasions I felt certain of the existence of a mitral presys- tolic murmur. On one occasion, however, after an absence from observation of several months, her heart presented no such mur- mur as I had heard before, but instead a feeble first sound accom- panied by a faint systolic whiff. Some weeks subsequently, after having taken digitalis and strengthened the contractions of the left auricle, the old-time presystolic murmur reappeared. Broad- bent regards this changeability as of great significance in the dif- ferential diagnosis between stenosis and regurgitation. The foregoing description applies to most cases of mitral ob- struction, but not to all, and as it is the exceptions that are every 26i DISEASES OF THE HEART now and then encountered, they will now be described. In some instances the bruit is so short that it is scarcely recognisable as separate from and preceding the first sound. I have generally noted in such cases, however, that the first sound is short and thumping, and appears to have prefixed to it a short thrill, which causes the impulse to convey to the hand the impression of its having slidden up to its maximum instead of having given a clean thrust, as does the healthy heart. Difficult as it is to recognise this indistinct or abortive murmur, it is extremely important to be able to do so, since it is in the detection of obscure signs of disease that the skilled physician differs from his unskilled colleague. The reverse of this short, scarcely recognisable bruit is the long-drawn murmur, which Traube first described and designated the " modified presystolic murmur." This is the murmur which, commencing directly at the close of systole — i. e., immediately after the second sound — extends through the long pause of dias- tole, and ends with the next first sound (Fig. 48). A not at all infrequent auscultatory finding is a short murmur occurring after the second sound and known as early diastolic, and which is Fio. 48. — Rhythm of Occasional Variety of Mitual Stenotic Murmur, thkouoh Entire Ventrioixak Diastole. tlien succeeded l)y a short period of silence, and then a character- istic presystolic murmur (Fig. 49). 1'his anomaly is therefore a breaking in two, as it were, of the long murmur, and by Fraentzel MITRAL STENOSIS 265 was called the " interrupted modified presystolic murmur." It is very diagnostic, but may easily mislead an inexperienced auscul- tator. Should such difficulty of interpretation arise, error may be Fig. 49. — " Interrupted Modified Presystolic " Murmur of Mitral Stenosis. avoided by due attention to the associated secondary physical signs and to the modifications of the heart-sounds soon to be described. Another departure from what is usually heard in mitral ste- nosis is the retention of the presystolic bruit and of the first sound without a second sound, or of the murmur alone ivithout either of the cardiac tones. Attention is directed to these anomalies by Broadbent, who states that under such circumstances it is possible for the murmur to be mistaken for a systolic one followed by a second sound, or for the bruit to be considered systolic, and to have replaced the sound altogether. Care should be taken to avoid such an error, since a systolic murmur means regurgitation, and for sake of prognosis as well as treatment stenosis should be recog- nised as such whenever it exists. A mistake can probably be avoided by palpation of the carotid pulse, when it will be found that this is preceded by the murmur. Such comparison of the time of the murmur with that of the carotid pulse is likewise valuable when, as stated by Fraentzel, the presystolic murmur disappears in the last weeks of life, or be- comes merged into a systolic one. The various modifications in rhythm and intensity of the 19 266 DISEASES OF THE HEART mitral obstructive nmrnnir are due to differences in the rapidity and force with which the blood flows through the narrowed orifice. It is conceivable — e. g., that during the fore part of diastole blood flows too gently into the relaxed ventricle to produce sonorous eddies and vibrations. When, however, it is energetically pro- pelled by auricular contraction, eddies or currents are generated of sufiieient force to give rise to the presystolic murmur. In the same manner a diastolic murmur following the second tone owes its production to sonorous eddies generated as the blood gushes out of the auricle into the ventricle. Then as blood-pressure in the ventricle is raised, vibratory, and hence audible currents cease for a time, until auricular systole again throws the blood-stream into sound-producing currents and eddies. Xarrowing and rough- ening of the mitral orifice furnish all the conditions essential for the generation of eddying or whirling currents in the blood-stream as it passes the ostium. Yet if the blood-flow is languid the eddies within it may fail to set up vibrations of sufficient force to be con- ducted to the ear or hand of the examiner. This explains why shortly before death or during times of great cardiac feebleness the presystolic murmur may disappear, and why it reappears as heart-power is restored. Heart-sounds. — The recognition of the characteristic murmur of mitral obstruction is not enough ; it is necessary to also study and recognise peculiarities in the heart-sounds. In well-marked cases the first tone at the apex is short and valvular, or, as is said, *' thumping." This quality is so peculiar and striking as to be quite distinctive and of itself sufficient many times for an experi- enced auscultator to make a diagnosis on it alone. It is the audi- tory impression of the sharp, quick tap that forms the apex-beat in this disease. The second sound at the apex may be distinct, but in most cases it is indistinct. At the base of the heart it is sometimes split or reduplicated in consequence of the pulmonic valve being closed a fraction of a second later than the aortic, according to the law tliat the valve closure is delayed in that artery in which blood- pressure is the higher. In ;(<1dition also the ])uliii()nic second sound is accentuated. The phenomenon, liowcvcr, which is of greatest interest in many ways is what is tei-med the simulated or apparent doubling MITRAL STENOSIS 267 of the second sound. This is to be distinguished from the split- ting of the second soimd at the base. It is limited strictly to the mitral area, sometimes to the very site of the apex-thrust, and con- sists in the occurrence of a third tone, which immediately follows the normal second sound. English clinicians have given much study to this apparent doubling of the second sound, and have offered a variety of explanations for its occurrence. The most reasonable theory is, as suggested by Sansom, that it is. in some way a sound of valve-tension being produced as the blood gushes forci- bly out of the auricle into the ventricle. This seems borne out by the observation that this sound sometimes becomes changed into, or replaced by an early diastolic murmur. Sansom states also that this double sound is heard at some time or other in all cases of mitral stenosis, and indeed may in some instances be the only indi- cation of the lesion. When this auscultatory phenomenon is present, together with a presystolic murmur, it forms a very striking assemblage of sounds that cannot possibly be mistaken for any other condition than mitral stenosis. I have known this doubling of the second sound to be inappre- ciable when the heart was not strong, and to come out clearly and beautifully as treatment restored cardiac power. When the heart beats slowly and regularlj^ it is a matter of no difficulty to differ- entiate the several sounds and murmurs heard in mitral stenosis. When, on the contrary, the rhythm of the heart is disturbed, the impression may be received of an indistinguishable jumble of sounds, both normal and adventitious. Thus, I have a male pa- tient with a rheumatic mitral narrowing combined with a slight degree of insufficiency who presents such a jumble. When, as now and then happens, his heart's action is tolerabl}^ slow and regular I hear the following: A rough pres^'^stolic murmur ending in a thumping first sound, then an exceedingly brief pause, followed by a doubled, or apparently doubled, second sound, which in its turn is succeeded by a short, early diastolic murmur and a short silence preceding the next presystolic bruit. At times a short sys- tolic murmur accompanies the first sound, and as this heart is gen- erally very irregular in rhythm it can better be imagined than de- scribed what an unintelligible mixture is made by its sounds and murmurs. 268 DISEASES OF THE HEART Diagnosis. — The diagnosis of mitral stenosis is usually a comparatively sim2)le matter. It may, however, be difficult and next to impossible to say whether it or insufficiency is present. Such a differentiation is important, however, from the standpoint of prognosis and treatment, and should be made when possible. As aids in this direction are the following: (1) Sex, stenosis being more common in females, regurgitation in males. (2) The short, sharp apex-beat preceded by a thrill of longer or shorter duration. (3) The greater extent of dulness over the right heart in stenosis with stronger and more distinct epigastric pulsation. (4) A rougher lower pitched murmur occurring in some portion of the diastole, usually presystolic, but often also early diastolic. (5) Doubling of the second soimd, limited strictly to the mitral area or to the apex. (6) The likelihood in stenosis of more pro- nounced secondary effects in other organs than the heart. (7) The greater smallness and feebleness of the pulse in stenosis, and the greater likelihood of arrhythmia in regurgitation. As a matter of fact differential diagnosis is not likely to be difficult except in the stage of lost compensation, and then less de- pendence must be placed on the auscultatory findings than on the evidences of greater secondary effects in stenosis. In all cases the question of ascertaining the exact nature of the lesion is not all of diagnosis. One has also, or in addition, to decide the degree of the lesion and the severity of its effects, and whether or not the findings account for the symptoms complained of. The degree must be determined by careful consideration of the murmurs, sounds, and secondary effects. The longer the pre- systolic murmur, the more thumping the first sound and apex-beat, the greater the enlargement of the right and the smaller the left ventricle, the feebler and smaller the pulse, the more pronounced the evidences of secondary effects on the liver — then the more pro- nounced will be the degree of narrowing. The association of a mitral regurgitant bruit points to a medium degree of stenosis, and so, according to Sansom, does the simulated doubling of the second sound at the apex. Dyspna-a on even sliglit exertion, as slow walking, great prone- ness to cough, and other signs of bronchial congestion, a feeling of weakness and fatigue out of proportion to the effort occasioning it, scantiness of urine, (■iii])tiii<'ss of the arterial system — are all symp- MITRAL STENOSIS 269 toms indicative of serious circulatory embarrassment, and attribu- table to the valvular disease. On the other hand, neuralgic pains in the pra^cordia and a feeling of fulness or uneasiness in the cardiac region, coldness and numbness of one hand and not the other, or of the hands and not the feet, headache, and prolonged vertigo, the patient being quiet and the pulse not feebler than usual, a feeling of nervousness and restlessness — may all be neurotic manifestations depending on de- fective nutrition or elimination, and in such cases are apt to be out of proportion to the degree of the lesion and to symptoms dis- tinctive of cardiac disease. Prognosis. — In general, this is less favourable than that of mitral incompetence, and for two reasons: (1) Obstruction is con- stant and tends to greater stasis in the pulmonic vessels, in conse- quence of which the left auricle and right ventricle are subjected to greater strain. They are likely, therefore, to break in their com- pensation at an earlier period. (2) Mitral stenosis is a progress- ive lesion, and may under the influence of repeated attacks of sub- acute rheumatism become at length so extreme that life cannot be maintained. When the narrowing is pronounced there is but a small vol- ume of blood ejected into the arterial system, general nutrition is correspondingly poor, complications on the part of the lungs are more likely, outdoor exercise is difficult if not impossible, normal metabolic processes are interfered with, and general nutrition becomes very defective. In a word, even when uncomplicated and apparently well com- pensated, mitral stenosis offers an exceedingly grave prognosis. By some authorities the average length of life is set down as not far from ten years. It stands next to aortic regurgitation in point of gravity. The following figures are of interest as showing the average age at which death took place in several series of cases. Of San- som's 61 cases death occurred at 32.7 years. In Hayden's 42 cases death took place at 37.8 years. Of Broadbent's 53 cases it oc- curred at 33 years for males, and 37 to 38 for females. Samways found that at Guy's Hospital during a period of ten years the average length of life for both sexes was 38.33 years; in less pro- nounced forms, 43.6 years; more extreme cases, 33.6 years. 270 DISEASES OF THE HEART The influence of age, habits, occuijations, environment, etc., will be considered in the chn]iter devoted to Prognosis in General. Mode and Causes of Death.. — Death in eases of mitral stenosis results most commonly from increase of cardiac asthenia, the same as in mitral regurgitation, or from the overpowering effects on the heart and lungs of hydrothorax and stasis in the pul- monary system. Pulmonary infarcts are particularly liable to occur, and nre then the immediate cause of death. Sudden death is possible, but is not likely except in the terminal stage^ when sudden exertion may bring about diastolic arrest of the already overburdeued heart. Even when compensation is fairly good the patient may at any time succumb to an attack of acute bronchitis or pneumonia. A lad of sixteen, whose compensation allowed him to occasionally enjoy a hunting trip, contracted a cold on such a trip, and died two days thereafter of what was thought by his physician to be extreme pulmonary congestion. An attack of acute pulmonary oedema is also a possible cause of death the same as in mitral re- gurgitation. In one case coming under my knowledge obstinate vomiting contributed largely to the fatal result by preventing retention of food and remedies. The end appeared to come as much through general as cardiac exhaustion. Death may be preceded by mild delirium, or consciousness may be retained to the last. Of 24 cases analyzed by Hustedt with reference to causes of death, he found heart-weakness in 8 cases, pulmonary infarct in 1, pneumonia in 4, pulmonary collapse in 1, emphysema in 2, apo- plexy in .3, bronchitis in 1, pleurisy in 1, meningitis in 1, perito- nitis in 1, and delirium in 1. The following cases illustrate so well many of the features that have been dwelt on in the foregoing pages that they are here appended : ^Nfrs. (A, Irish-American, aged thirty-four, was admitted to St. Anthony's Hospital, November 20, 1900, com])laining of breath- lessness on exertion, cough, and frothy white sputum. IJoth par- ents had died of heart-disease, but three sisters and one brother were living and healthy. The patient had had measles and pertussis in childhood, l)ut no rheumatism. She had been married thirteen years, had six children, of which the youngest was three, and had MITRAL STENOSIS 271 had six abortions, all of which she had herself induced, and which had not been followed by chill or fever. During the first pregnancy she had had cedema of the left leg, passed no urine for two days, and had come near '' smothering," Her physician declared she had " water around her heart," and had tapped her, but she could not say whether water had been obtained or not. She had been troubled with dyspna?a on exertion for a number of years, and this had always been particularly bad during her pregnancies! Examination showed a woman of medium height, weighing 114 pounds, slight cyanosis about lips, cold, moist extremities, and pulsation of the external jugu- lars, tongue having a whitish coat and indented by the teeth. The pulse was 134, compres- sible, and irregular in force and volume, but there was no pitting of the skin over the ankles or elsewhere. The apex-beat was in the sixth in- terspace, 4^ inches to left of the midsternal line, of the character of a faint tap in an area of diffused impulse (Fig. 50). A presystolic thrill ran up to and ended with this faint, sharp tap, and there was marked epigastric pulsa- tion. Relative dulness was in- creased in all diameters, from third interspace to sixth, and from 2 inches to right of median line to 5 inches to left of the same. The first sound was thumping, heard throughout prtecordia, and followed quickly by a scarcely perceptible second sound, the aortic second being weak and the pulmonic second markedly accentuated. A harsh murmur of greatest intensity in the mitral area began im- mediately after the second, ran up to and ended with the next ensuing first sound, and was not transmitted into the axillary re- gion. The lungs revealed impaired resonance at the posterior bases, with some moist rales. The liver was palpable two finger- breadths below the inferior costal margin, but the spleen was not Fig. 50. — Location of Apex and Eelative Dulness in Case of Mitral Stenosis (p. 270). 272 DISEASES OF THE HEART palpable, and there was no evidence of free fluid in the abdomen. The urine was scanty, dark-coloured, and contained a trace of albu- min. The temperature was 98.6° F. and respirations 28. Her stomach was very irritable, and for several days she had not been able to retain nourishment. Four hours after her admission her pulse had increased in rapidity and feebleness, and so few of the pulse-waves reached the wrist that the heart-rate had to be counted with the stethoscope. It was beating 180 per minute. Cyanosis had deepened, cough and dyspnoea were very bad, rales had grown more numerous, and the liver had increased in size. Her condition was so critical that she was given a hypodermic injection of -| of a grain of morphine with ■gi^ of atropine, nitroglycerin y^^, and -gJ^ of sulphate of strych- nine, this latter to be repeated every two hours during the night. An ounce of sulphate of magnesia was also administered, and a few hours subsequently she was put upon 10-minini doses of tinc- ture of digitalis every four hours. By the next day her condition had improved materially, the pulse coming down to 134, and being rather more regular, but the strychnine, digitalis, and a daily dose of salts were continued. Without detailing all the fluctuations of this patient for the ensuing ten days, it may be said that the pulse showed ever-recurring vagaries, being at one time fairly regular, all waves reaching the wrist, and at others being rapid, irregular, and intermittent. The liver also varied in size, dimin- ishing and increasing according to the persistence and regularity with which the salts were administered. The cough, however, gradually grew less, expectoration diminished, pain left the epi- gastrium, she retained nourishment, and as a rule got several hours' good sleep each night. As the condition improved, the strychnine was lessened in frequency of administration, but the digitalis was continued. At one time indeed its action was sup- plemented by strophanthus. At length, by November 30th, her pulse-rate averaged 84, and it was recorded that all the waves reached the wrist. Dulness and rfdes had left the lungs, but the liver still remained palpable, although smaller in size. The pa- tient then left the hos])ital abruptly. Two months subsequently she again re-entered, complaining as before of cough and expec- toration, but showing no dropsy. Treatment again benefited her, and she again withdrew from observation. I am indebted for MITRAL STENOSIS 273 the notes of this case to Dr. J, R. Yung, one of the internes at the time. This case illustrates fairly well the symptoms and amenabil- ity to treatment of a case of mitral stenosis in which compensa- tion was broken, but not irreparably so, and in which, with signs of stasis amounting even to a relative incompetence of the tricus- pid valve, there was no oedema. In fact, the brunt of the dis- turbance was borne mainly by the lungs, the dulness and rales, the dyspnoea, cough, and frothy expectoration being the result of the great pulmonary engorgement. It is hard to explain why in such a case oedema is absent, whereas in other individuals with apparently no greater stasis, dropsy will be a marked and dis- tressing feature. It certainly seems to corroborate the view that dropsy depends upon the state of the blood and nutrition of the capillaries, as well as upon the degree of capillary and venous engorgement. This patient subsequently succumbed to a third attack in the hospital. Mr. B., aged twenty-nine, tailor, consulted me January 9, 1900, on account of great breathlessness upon the slightest effort. He gave a history of rheuma- tism four years previous, since which time he had suffered with subacute articular pains. Gonorrhoea six years ago, with stricture at present time. With the exception of a ^^ bad eye," nature unknown, at six years of age, has had no other illness. Heart began to trou- ble him one year after the rheumatic attack, but was not treated for heart-disease until the summer of 1899. His symptoms were great dys- pnoea on effort, cough once in a while at morning and evening, vertigo upon exercise, some pain between the shoulders, and poor appetite, but sleep good. His pulse while sitting was weak, small, regular, and 90. The Fig. 51. — Location uf Ai'Ex axu Relative DuLNzss IN Case of Mitral Stenosis AND Kegdrgitation (p. 273). 274 DISEASES OF THE HEART examination of the heart discovered the weak apex-beat at the fifth interspace, nipple-line, Sf inches from median line, and preceded by a short thrill (Fig. 51). The apex-beat was not thumping, but there was marked epigastric pulsation. Abso- lute dulness was increased from right border of sternum, at fourth costal cartilage, to left of parasternal line. Relative dulness from lower border of third costal cartilage above to junction of sixth and seventh costal cartilages below, If inch to right of median line and to f of an inch outside of nipple. The pulmonic second sound was found accentuated. Second sound was not doubled at base, but limited to area of the apex-beat was an apparent doubling of the second sound, the second element at times having the character of a short murmur, and separated from the following presystolic murmur. At lower inner edge of the apex-beat the first sound was also doubled at times. A short, rough presystolic murmur was found just within, and a blowing systolic at the apex. The murmurs and sounds made a rolling, tumbling rhythm. In dorsal decubitus the appar- ent doubling of second sound was very marked at inner edge of apex. As the heart occasionally slowed, the first sound was found also doubled, the first element replacing the presystolic murmur. The systolic murmur became plain and whistling with a very pro- nounced blow 2 inches to left of nipple. The liver was palpable a finger-breadth below the costal arch. The diagnosis made was mitral stenosis and insufficiency, with secondary cardiac hyj)ertrophy and dilatation. Mrs. A., aged thirty-three years, weight 115 pounds, height medium, American, was examined March 29, 1901. Her father was living, but had cough, while a maternal uncle and a maternal aunt had died of consumption. At eighteen she had suffered from a severe attack of inflammatory rheumatism, and had had more or less joint pains for three or four years subsequently. Of chil- dren's diseases, she had had a mild attack of scarlatina when a child, and thought that during her childhood she had also had pleurisy. She had had a .second pleuritis a year prior to her examination by me. Her present illness dated back to 1891, when she first began to have a cough, but her symptoms had grown much worse for the last year, and she had grown percep- tibly paler. In the way of symptoms, she complained chiefly of MITRAL STENOSIS 275 chronic cough, which was most troublesome at night, and of con- siderable yellowish sputum, in which tubercle bacilli were said to have been discovered. She noticed shortness of breath in walk- ing and ascending stairs. The appetite was poor and the diges- tion weak, although bowel movements were regular, as also were the menses. Sleep was disturbed by the cough, and there was slight pain in the right hip and the left side of the chest near the shoulder. The voice was husky, but it may be said in passing that laryngoscopic inspection revealed no infiltration of the larynx. Examination. — The pulse was 105, small, regular, and of no- ticeably low tension. The temperature taken at 12 m. was 99° F. Respirations were shallow, but not hurried. The chest was mod- erately emaciated, very shallow in its antero-posterior diameter, and flattened both above and below the right clavicle. Vocal frem- itus was increased at both apices, particularly the right. Upon the right side, dulness extended from the apex to the third inter- space in front and to the middle of the scapula behind, shading off to impaired resonance as far as the tip of the scapula and below this point, becoming again more pronounced towards the posterior axillary line. In the right infraclavicular region there were bronchial breath-sounds, moist rales of varying size, and the voice-sounds were so concentrated and hollow as to strongly suggest a cavity. Posteriorly, respiratory sounds were also bron- chial, and the act of coughing developed numerous fine and coarse crackling rales as far down as the inferior scapula angle. At the left apex there was impaired resonance both front and back to the level of the second rib, and over this area breath-sounds were broncho-vesicular, and cough produced crumpling rales that ex- tended below the limits of slight dulness. The apex-beat was situated in the fifth left interspace slightly within the liipple-line, was feeble, and of the character of a quick thump, and was preceded by a short yet distinct thrill that ended with the cardiac impulse. Relative heart's dulness was somewhat increased towards the right and downward, but did not reach beyond the vertical nipple-line at the left (Fig. 52). Upon aus- cultation the first sound at the apex was short, sharp, and thump- ing, the second sound was not doubled, and the pulmonic second tone was markedly accentuated. A rather short, rough, distinctly 276 DISEASES OF THE HEART presystolic murmnr ran up to and ended abruptly with the sharp first sound, and was of greatest intensity in the standing position. A high-pitched systolic whiff accompanied the systole in the mitral area, but was not trans- mitted to any appreciable dis- tance outside this area. The abdomen was flat and thin, the lower hepatic border distinctly palpable and tender to pressure, and hepatic dul- ness reached from the upper margin of the sixth rib in the mamillary line to slightly be- low the inferior costal arch. The diagnosis was clearly chronic pulmonary tuberculo- sis with softening and vomica in the right lung, incipient disease of the left upper lobe, mitral stenosis of first degree, with probably some regurgitation, the valvular lesion being of rheumatic origin and in good com- pensation. This case is interesting because of the rather rare association of pulmonary tuberculosis and mitral stenosis, and would seem to corroborate the view that this valvular lesion is sometimes of tuberculous origin, were it not for the very definite history of inflammatory rheumatism at the age of eighteen. It likewise shows the fallacy of Rokitansky's statements concerning the an- tagonism between mitral stenosis and consumption. It is worthy of note, however, that in this case the narrowing was not extreme and was combined with regurgitation, a form of mitral disease which is not so infrequently associated with pulmonary tubercu- losis as was once thought. Furthermore, this case raises the very interesting query if this stenosis may not have exerted a retarding influence upon the progress of tho lung affection, although in this connection it should be stated that her residence has been in southwestern Kan- sas, where the air is dry and the altitude not far from 2,000 feet. Fig. 52. — Location of Apex and Kelative DuLNESs IN Case of Mitral Stenosis (p. 274). MITRAL STENOSIS 277 For my part I am much more inclined to attribute the slow ad- vance of the pulmonary affection in this case to other factors, possibly to climatic influences, possibly to inherent mildness of the tuberculous infection itself, rather than to the mitral obstruc- tion, since, as suggested by Sansom, it is reasonable to assume that a valvular lesion would have a tendency to impair the resistance of the organism, particularly in one inheriting a predisposition to tuberculous disease. CHAPTER VIII AORTIC REGURGITATION In .this form of valvular disease a portion of the blood dis- charged into the aorta with each ventricular systole leaks back into the left ventricle during its diastole. xVlthough relative in- competence may be produced by dilatation of the aortic ostium, the disease in question is in the vast majority of cases due to structural defect of the valve itself. Morbid Anatomy. — Defects in the aortic valve leading to regurgitation are as nearly analogous to those found in mitral re- gurgitation as the anatomy of the valve will allow. They may follow acute endocarditis, or may be the result of a non-inflamma- tory sclerosis. The latter is more often the case here than at the mitral orifice because the aortic valve has to bear the brunt of the increased blood-pressure due to muscular exertion. The leaflets, one or all, may be retracted, curled, or shrivelled, so as to permit a free regurgitation. Old vegetations on the ven- tricular surface may interfere with their complete apposition. In short, the conditions parallel those found in mitral insiifiiciency, with exception of the influence of contraction of the chordae ten- dinese and papillary muscles. Acute incompetence may occur during ulcerative endocarditis by the perforation of one of the valve-cusps. Very rarely a cusp may rupture during violent muscular exercise. The aortic semi- lunar valve is one of the most delicate structures in the body, and yet one of the strongest, sustaining as it does the Avhole blood- pressure of the systemic circulation. It is hence extremely un- likely that muscular exertion could be severe enough to raise blood-prcBsure to a height sufficient to rupture a healthy valve. Probably in such cases the valve has been weakened either by de- generation or inflammation. As in mitral disease, regurgitation is often combined with 278 AORTIC REGUEGITATION, WITH CALCIFIED VEGETATION THAT SWUNG IN BLOOD CURRENT. CAUSING ATHEROMA OF ENDOCARDIUM AND OF INTIMA OF AORTA. AORTIC REGURGITATION 279 some degree of stenosis, but regurgitation may occur without nar- rowing, and occasionally, in consequence of dilatation of the ven- tricle, even with stretching, of the aortic ring. That such en- largement of the ring, leading to relative insufficiency, could take place, was long doubted, owing to the great strength of the annulus iibrosus, but so many instances of the kind have been observed that there is no longer any room for doubt. The first effect on the heart is dilatation of the left ventricle. This is due to the impact on its inner surface of the regurgitant stream, 'which in very free regurgitation re-enters with nearly the force with which it was driven out of the ventricle. Such lesions, however, are of gradual development, and the increasing work leads to a corresponding hypertrophy of the wall of the ventricle, which enables it not only to withstand the strain of the regurgita- tion, but to expel the greatly increased volume of blood present in the chamber at the beginning of its systole. This hypertrophy in aortic insufficiency is of early development and often becomes so extreme that some of the largest hearts on record are those show- ing this defect. The wall of the hypertrophied ventricle may be as thick as 4 centimetres (If inch). - The apex of the left ventricle projects far beyond that of its fellow, and the interventricular sseptum is displaced, encroaching largely on the cavity of the right chamber. As long as the mitral valve remains intact the effects of aortic regurgitation upon the heart are limited to the left ventricle. If, however, the mitral is incompetent, either from disease of the valve or relatively from the enlargement of the ventricle, the phe- nomena described as the results of mitral incompetency are added to those of the aortic lesion. In such an event, of course, the right heart is also enlarged, and the largest hearts have been those show- ing this combination of lesions. Such a heart may weigh as much as 3 or 4 pounds. Indeed, von Ziemssen has reported 6 pounds as the weight of a specimen obtained from one of the great Stokes's patients. On account of its size such a heart is spoken of as cor hovinum. The heart presented to me by Dr. C. C. O'Byrne weighs 2| pounds, and in it the regurgitation could not have been extreme (Plate II). The point of interest in this specimen is the swinging vegetation, 3 centimetres long, and containing calcareous nodules, which evidently swung in the blood-stream, now in the 280 DISEASES OF THE HEART ventricle, and again in the aorta, for on the intima of the aorta and on the mural endocardium of the ventricle, at the points where the vegetation must have struck, are marked atheroma- tous patches. There is said to have been a musical murmur during life. The greatly increased force with which such a ventricle pro- pels the blood into the aorta throws great strain on the walls of that vessel, and hence atheromatous changes are often found not only in the aorta, but in the whole arterial system. That such change is due to this valvular disease is indicated by the fact of its occurrence in young and otherwise healthy individuals, in whom it would not be expected to exist. When this valvular disease is the result of a general sclerosis, the myocardium is apt to be so degenerated as a result of coronary involvement that hypertrophy is not great. It is when the disease develops in young and healthy individuals as a result of endocar- ditis that the enormous heart is usually found. Etiology. — Endocarditis affecting the semilunar valve may have the same origin as that of the left auriculo-ventricular valve, and hence the discussion of its causes does not need to be repeated. Aortic regurgitation may be met with in persons of both sexes and of all ages. It is a striking fact, however, that this lesion, even when due to rheumatic endocarditis, is far more com- mon in males than in females. When developed at or after mid- dle age, it is usually due to those conditions which bring about sclerosis, and which are fully considered in other chapters (pages 201 and 741). This sclerotic form is also undoubtedly met with more frequently in males than in females, and for the reason that arterial degeneration is more common in the former — and there- fore the etiological factors leading to sclerotic change in the aortic cusps are essentially those of arteriosclerosis. In a considerable portion of males suffering from aortic re- gurgitation there is a history of syphilis and the abuse of alco- hol. In a most typical case of this lesion recently seen in a man of thirty-nine, syphilis and whisky were the only two causative factors to be elicited. Gout and bodily toil, particularly if com- bined with alcoholic excess, also seem to be causative agents of considerable importance. As already stated incidentally in Morbid Anatomy, severe AORTIC REGURGITATION 281 strain may bring about acute incompetence of one of the aortic cusps through rupture at some point that had been previously weakened by inflammation or atheromatous degeneration. There is a form of aortic insufficiency which, although not due to valvular defect, yet presents the same clinical features as the organic form, and is so frequently encountered that it may here be briefly dwelt upon. This is a relative incompetence of the semi- lunar valve, and its causes are found in conditions that predis- pose to stretching of the ventricular wall and of the basal ring of the aorta. They are therefore (1) degenerative changes in the myocardium, (2) diseases of the aorta that greatly narrow its lumen, or, per contra, lead to its dilatation, and (3) mediasti- nal tumours, which by pressure diminish the calibre of the aorta. The most frequent cause of this relative insufficiency is aneurysm affecting the ascending arch, or a general dilatation of the aorta secondary to sclerosis. In one instance of the latter kind coming under my notice it was associated with mitral regurgitation, also of atheromatous type, but which had existed for years. During the later weeks of life in this case aortic incompetence developed, and after death was found due to extensive atheromatous degen- eration and dilatation of the aorta, reaching from its origin to the beginning of the descending portion of the vessel. In another case in which regurgitation through the aortic valve had run its course to a fatal termination within a few months, post-mortem examination disclosed stenosis of the ascend- ing aorta, about I an inch above the insertion of the valve, so pronounced that the lumen was diminished by at least a half. This narrowing was caused by a growth of fibrous tissue which completely encircled the aorta, and from the history appeared to have originated in acute inflammation a year and a half pre- viously. As already stated, relative aortic incompetence may be the ultimate effect of chronic myocarditis, which is associated with sclerosis of the aorta, and which so seriously impairs the resist- ing power of the ring that it gradually yields to the distending force of the blood-wave as it recoils against the closed valve. I have seen more than one instance of the kind as disclosed by the necropsy, although during life (he regurgitation had been attrib- uted to structural defect of the valve-segments. 20 282 DISEASES OP THE HEART Of 53 cases of aortic regurgitation of wliicli I have records, 46 occurred in the male and only 7 in the female sex. Seventeen of the males and -i of the females were below the age of forty. Eleven of the former who were less than forty years of age gave a history of rheumatism or scarlatina, while 10 over forty also had had one or the other of these diseases. Of the females, 2 below forty and 1 over that age, gave a history of rheumatism or scarla- tina. Of the total number of cases, therefore, 24 were probably due to endocarditis. It may also be stated that of the 29 males and 3 females over forty there were 19 males and 2 females in whom the lesion, owing to the absence of probable endocarditis, could be reasonably attributed to atheroma. In whatever way these figures are looked at they exhibit the striking preponder- ance of men over women afflicted with this particular valve-defect. Symptoms. — It goes without saying that in this as in other valvular diseases it is the degree of compensation which deter- mines the presence or absence of distinctively cardiac symptoms. In other words, if the lesion is of inflammatory origin, and if the state of the myocardium has permitted the development of great hypertrophy, the disease may remain entirely latent for many years. Arduous occupations requiring great physical effort, feats of endurance and skill, mountain-climbing, running, boat-racing, football playing, tennis, etc., are often endured without discom- fort. I recall an attorney with pronounced aortic insufficiency of rheumatic origin who consulted me soon after his return from a six-weeks' vacation in Colorado. He had ridden his wheel at an altitude of 6,000 feet with no more discomfort than he would have experienced in Chicago. The only time he had suffered any inconvenience was when he had taken the train up Pike's Peak. Upon reaching the summit, 13,000 feet, he fainted away, yet upon returning to the foot of the mountain he got on his wheel and rode away as if nothing had happened. Dyspnoea is not experienced in this stage, and aside from vio- lent action of the heart, patients are totally unconscious that the organ is anywise different from that of their fellows. If any dis- turbance of bodily function exists, it is not such as arises from venous congestion, for so long as the mitral valve remains com- petent stasis back of the left ventricle is impossible. The state of the circulation is one of intermittent anaemia on AORTIC REGURGITATION 283 the part of the arterial system. At each systole the arteries are flushed, and with each diastole they are relatively depleted. The tendency, therefore, is to a lack of nutrition of the various organs and tissues throughout the body. This is not specially manifest in some persons, while in others there is more or less pallor and delicacy of body. The muscular system in particular is weak, and some children show inability for sustained mental effort, yet as a rule young persons with aortic regurgitation show nothing either in appearance or deportment to indicate the existence of their lesion. A well-compensated aortic insufficiency is not likely to inca- pacitate an otherwise healthy young adult for the active and even the arduous duties of professional or mercantile pursuits. Many a hard- worked medical man with this lesion is able to sustain the severe mental and physical strain of a large general practice with- out more fatigue than his more fortunate confreres. The only symptoms experienced by some patients are palpitation or slight vertigo, or both, and yet trivial as they may seem to be they are sometimes the earliest announcement of faltering energy on the part of the left ventricle. In one instance, more than twenty years before the patient's death, any effort or excitement beyond a certain moderate degree, brought on attacks of such violent pal- pitation as to necessitate absolute repose for hours in the recum- bent posture. These attacks were also produced by even small doses of digitalis, and as they were allayed by aconite they were thought due to extreme hypertrophy. In most cases such violent cardiac action is an expression of weakness rather than of ex- cessive strength, as sometimes supposed. When dizziness is expe- rienced, it is usually, though by no means always, induced by sudden exertion, and in such cases it is generally found that the regurgitation is very free. The cerebral arteries are flushed w^ith each systole, but in consequence of the regurgitation blood-pressure wdthin them is not sustained, and when for any reason the reflux into the ven- tricle is intensified, transient anaemia of the brain results and vertigo is felt. In some cases dizziness is produced by intermit- tence in the heart's contractions, and it is then a mild manifesta- tion of what in other cases becomes a syncopal attack. Indeed, fainting is an occasional symptom in this disease, in consequence 284 DISEASES OF THE HEART of the fact that the state of the cerebral circulation is the opposite of what obtains in mitral stenosis. This explains, I think, why it is that aortic patients are able to lie low in bed, whereas those suffering from mitral disease usually prefer to sleep with their head and shoulders propped up on two pillows. In the former there is an unconscious attempt to overcome the force of gravita- tion upon the cerebral circulation, while the latter class of patients seek to aid venous flow out of the head by that same force of gravi- tation. Disorders of digestion are not so common in aOrtic as in mitral patients, and when present are referable not to interference with the circulation, as has been explained is the case in lesions at the auriculo-ventricular orifice, but they are due in most instances to errors in diet or whatever deranges gastro-intestinal function in individuals who have no heart-disease. The comparative immunity from symptoms enjoyed for years, it may be, by persons whose disease is the result of endocarditis, is not the fortunate lot of those in whom the aortic valves have become incompetent in consequence of sclerosis, and in whom the myocardium is incapable of maintaining adequate compensatory hypertrophy. In persons, therefore, whose signs of aortic regurgi- tation develop during middle age, symptoms are apt to appear early and to be pronounced. These do not differ essentially from those experienced by patients of the other class, and are palpita- tion, vertigo of more or less intensity and frequency, a feeling of general weakness, uncomfortable pr?ecordial oppression, more or less pain that may be distinctly anginal or of an anginoid char- acter, and in particular distressing attacks of dyspnoea. When these symptoms arise a fatal termination is not far distant. With Dr. G. W. Webster, October 13, 1900, I saw an Irishman who presented a very striking picture of the distress often experi- enced in the terminal stage of aortic incom])etence. There was no history of inflammatory rheumatism, but of syphilis and the im- moderate use of alcohol. Three weeks prior to my visit he had been in the country, and while there had overexerted himself, become greatly fatigued, and had begnn to suffer from attacks of sudden weakness with a feeling of suffocation. Upon his admission to the hospital he was suffering from frequent attacks that seemed to portend speedy dissolution. llis hurried and somewhat AORTIC REGURGITATION 285 laboured respirations would suddenly become so augmented in severity that he would spring into the upright position gasping for breath, coughing and raising frothy mucus, while cyanosis became marked, and the pulse grew rather more rapid, irregular, and extremely feeble. The face became anxious, and, in a word, the whole appearance of the man was one of direst distress. The examination on admission disclosed aortic regurgitation and a secondarily leaking mitral, with very swollen and tender liver. Hypodermics of morphine relieved these attacks in a measure, and under the free use of cathartics, digitalis and iodide of soda, the condition so much improved that the mitral no longer leaked. I found a rather spare man of medium stature who looked much older than he really was. He was semi-recumbent, and although comfortable was yet breathing with apparent difficulty and greater than normal rapidity. There was no oedema, and signs of stasis were not notice- able. The temporal and cervi- cal arteries throbbed strongly, the pulse was quick and of the character known as bis- feriens, and the radial arteries were stiff. The lower border of the liver was palpable a short distance below the costal arch, but the organ was not hard or tender. Cardiac im- pulse was diffused and weak, the indistinct broad apex-beat being in the sixth interspace, midway between the left mamillary and anterior axil- fig. 53— Location of Apex and Kelative lary lines. Percussion showed Durness, Case of Aortic Insufficiency slight increase 01 cardiac dulness to the right of the sternum and downward, but very great extension of dulness towards the left and downward. The outer border was broadly rounded, after the manner often de- scribed as indicative of preponderating dilatation of the left ven- tricle in cases of aortic insufficiency with broken compensation (Fig. 53). When hypertrophy predominates, the outline of the 286 DISEASES OF THE HEART left Yentricle is long and pointed with a rather sharp apex. Upon ansciiltation there was at once detected a systolic and diastolic murnuir of the usual character in aortic regurgitation, but with the exception of the accentuated pulmonic second tone the heart- sounds were scarcely audible. Indeed, the aortic second was quite wanting, and in the neck was replaced by the feeble dis- tant diastolic bruit. At the seat of the apex the ear perceived a dull or toneless thud rather than the normal first sound, and the diastolic murmur was faintly distinguishable. In the femoral artery, pressure elicited the double murmur of Duroziez. The diagnosis was easy enough. It was an aortic regurgita- tion of atheromatous origin in the stage of ruptured compensa- tion that had led to venous stasis. The congestion of the lungs was shown by the frequent cough and sero-mucous sputum, and the stasis in the general system by the hepatic enlargement and scanty urine. The patient was unable to sleep, and the taking of food was followed by the formation of gas, which contributed its quota to the already existing dyspnoea. The prognosis was of the worst, for it was only too evident that the left ventricle could not withstand the impact of the regur- gitating stream. That this was free was shown by the absence of the aortic second sound^ which had become wholly replaced by the diastolic murmur. The attacks of increased dyspna^a and cardiac feebleness were the manifestation of left ventricle failure or asys- tolism and portended grave danger. In fact, although as vigor- ous and skilful treatment was maintained as could be devised, it exercised no appreciable effect on the patient's condition, and after lingering another five days he expired in one of his attacks. There is a twofold reason why aortic regurgitation of the sclerotic type is particularly serious. Xot only has more or less myocardial degeneration preceded the development of the valvu- lar defect, but the reflux of a portion of the contents of the aorta into the left ventricle augments the cardiac ischa'mia resulting from the aortic and often coexisting coronary sclerosis. I will not discuss the much-debated question whether the coronary arter- ies are fluslied during systole or diastole, since this is amply set forth in works on physiology, but only state that the weight of evidence is in favour of tlie svstolic flushinc of the heart-muscle. AORTIC REGURGITATION 287 It is sufficient to emphasize tlie fact that in aortic regurgitation blood-pressure is not sustained within the coronary any more than in other arteries, and hence cardiac nutrition cannot be good. There comes at length a limit in all cases to cardiac hyper- trophy because the heart-muscle becomes more or less degenerated, and therefore incapable of maintaining the circulation and of withstanding the dilating force of the regurgitant stream. Its flagging energy is shown by more rapid and perhaps less regular contractions, even, it may be, by occasional intermissions. Therefore, the earliest and most reliable indications of failing compensation are generally sho^vn in the pulse. Even before sub- jective symptoms bring the patient to his medical adviser the pulse-waves are no longer of uniform frequency, force, and vol- ume. The radial pulse is accelerated, but it does not strike the j)alpating finger with its old-timed suddenness and vigour, the artery not being so powerfully and quickly distended as when the ventricle contracts with energy. Consequently the physician may not so readily distinguish the peculiar characters of the aortic re- gurgitant pulse. At irregular intervals the pulse seems to falter a little, or a small, weak beat follows its predecessor more quickly than usual, and is followed by others of normal strength. This is the expression of an accessory or extra systole, intro- duced now and then into the regular series of contractions for the purpose of re-enforcement (pulsus intercurrens), or it is the result of the ventricle giving a hurried, incomplete contraction, in consequence of fatigue. As muscular incompetence increases, the pulse grows more irregular, or indeed becomes permanently intermittent. It increases in frequency, and its distinctive collaps- ing character, to be subsequently described, grows less apparent. Subjective symptoms annoy or even alarm the patient, who begins to notice an unwonted breathlessness. Attacks of vertigo or even syncope supervene. If the patient does not now die sud- denly and unexpectedly, he is likely to suffer from irregularly re- curring attacks that are of grave danger because indicating immi- nent cardiac paralysis. These are a more or less sudden feeling of great weakness or prostration, with cyanosis, a feeble, irregu- lar, perhaps accelerated and empty pulse, dyspnoea, and an inde- scribable feeling of impending dissolution. In addition, he may suffer from cough with frothy, it may be bloody, expectoration 288 DISEASES OP THE HEART and other symptoms indicative of stasis in the jmlmonarv vessels and general venous system. If the mitral valve has become rela- tively incompetent, regurgitation through the auriculo-ventricu- lar opening is added to that already present at the aortic orifice, and the sjanptoms become the same as those of the last stages of mitral disease. Early in my practice I was called to attend a middle-aged woman, whom I found intensely dropsical^ ortliopnocic, and pre- senting unmistakable evidence of aortic and relative mitral insuf- ficiency. Rest in bed, infusion of digitalis and catharsis speedily removed the anasarca, closed up the mitral valves, and, in short, so greatly improved her condition that she thought herself fully re- stored. Despite my warning, and contrary to my strict orders, she insisted upon leaving her bed and sitting dressed in the family living room. Only a day or two thereafter, while alone in her apartment, she lieard a rap on the door, arose quickly to answer the knock, opened the door, and almost immediately fell to the floor and died. In this case I believe life might have been prolonged had the mitral valves continued to leak, and thus acted as a safety-valve for the left ventricle. I am led to this opinion by my observation of a case with Dr. Lowrence at Chebanse, 111. The patient was an old man, who was suffering from albuminuria, dropsy, congested liver, and orthop- noea. Upon examination, there were the usual signs of stiffened arteries and aortic regurgitation, but, in addition, a mitral regur- gitant murmur, pulsation of the external jugulars, and a murmur characteristic of tricuspid insufficiency. I'he outlook seemed very bad, and but small hope for improvement was held out. Never- theless, upon the daily moderate use of cathartics and nitro- glycerin, tlio replacement of digitalis by strophanthus, and the hypodermic administration of small tonic doses of morphine, this patient actually improved beyond all expectation, and several months subsequently was reported by the doctor as still alive and in tolerable comfort, being able to drive out in pleasant weather, although, needless to say, compensation was never re- stored. I believe in this instance the leakage of the mitral and tricuspid valves relieved the two ventricles from dangerous strain and threw the brunt of the trouble back upon the liver and general venous system. The stasis thus resulting, of course, produced res- AORTIC REGURGITATION 289 piratory embarrassment and functional derangement of the ab- dominal viscera, but actually served to prolong life. In my care in the wards of Cook County Hospital there are at the present writing two men with aortic regurgitation in whom mitral incompetence has become added. Both present evidence of venous stasis in a moderate degree, chiefly hepatic and pulmo- nary. One complains of weakness and but little else, the other of insomnia ; yet in both patients things are growing slowly worse in spite of rest in bed and the usual heart-tonics. To all intents and purposes they have become converted into cases of mitral disease, the most frequent sequel of events in aortic regurgitation. The chief difference, however, lies in the refractoriness to treatment and in the liability, one might almost say certainty, of a sudden death. In June, 1899, I saw with Dr. Houston a powerfully built Irishman, weighing over 200 pounds, Avho was suffering from dyspnoea, which had suddenly developed six weeks previously. His personal history was negative with exception of swelling of one knee some six or eight years before. This may have been a monarticular rheumatism^ and if so, it may have been responsible for the man's valvular disease. It was not followed by any symp- toms, for with exception of a fall that occasioned pain near the heart for a day he had been perfectly well up to his present ill- ness. No history of overexertion or any other exciting cause for his dyspnoea could be elicited. His shortness of breath had set in abruptly while he was attending his duties as engineer, and at first had been more severe than it was when I saw him, the im- provement being due to treatment, l^evertheless he was incapaci- tated for work, and counsel was sought in the hope of obtaining some suggestion for his further improvement. The pulse was arrhythmic and rapid, displaying feebly the usual characters of aortic insufficiency, and the vessels did not feel thickened and stiff. The broad, heaving apex-impulse was displaced downward into the sixth interspace and outward to the anterior axillary line. There was epigastric pulsation and a sys- tolic thrill in the aortic area. The heart-tones were everywhere audible, though feebly, and there was a loud, rough systolic mur- mur at the base to right of sternum, followed by a very feeble diastolic bruit. At the apex could be made out a softer systolic 290 DISEASES OF THE HEART murmur possessing the characters of a mitral regurgitant one, which, together with evidences of enlargement of the right heart, convinced me that the mitral as well as the aortic valves were leaking. The liver was palpahle and tender, and the urine con- tained a small amout of albumin. I looked upon the mitral insuf- ficiency as relative and secondary to the aortic disease. The prognosis was very unfavourable, notwithstanding the degree of improvement that had already attended treatment, be- cause when compensation is once lost in this form of valvular disease it is rarely possible to restore the dilated and perhaps de- generated left ventricle to its former vigour. The patient was informed of his grave state, and was advised to keep his room for as long a time as was thought best, the dura- tion to be determined by results. In addition to rest, the treat- ment was to consist of strychnine, digitalis, and nitroglycerin ; food was to be light but sustaining, and cathartics were to be employed daily, but not enough to weaken him. The purpose of the last-named remedies was chiefly to prevent the patient from being obliged to strain at stool, as might be the case were he to become at all constipated. It is well known that effort of this kind is particularly bad, even dangerous, for persons whose left ventricle is in a state of dilatation. In aortic regurgitation the sudden constriction of the arteries incident to straining is liable to cause sudden and fatal diastolic arrest of the heart. In October I saw the patient again, and was not surprised, although disappointed, to find that in spite of treatment the dila- tation of the left ventricle and resulting insufficiency of the mitral valves had increased. The action of the heart was more regular, but in other respects things had grown rather more ominous. lie was now ordered to keep his bed strictly, and was put on larger doses of digitalis. Improvement did not follow, and he began to suffer much from sudden paroxysms of dyspna3a, which were very alarming to him and his friends. His liver also became greatly engorged, and his whole condition grew steadily more threatening. Strychnine and nitroglycerin were increased, and he was given daily injections of morphine, -J of a grain, with atropine to lessen dypsnoea, quiet his nervousness, and sustain his heart. It was decided to persevere in the use of digitalis, interrupt- AORTIC REGURGITATION 291 ing it from time to time and substituting therefor tincture of strophantlius, to prevent the possible cumulative action of the fox- glove. This was carried out until at length a singular mental state developed, characterized by delusions closely resembling a mild mania. As Dr. Houston had observed a similar mental state once before in a patient whom I had turned over to his charge, and in that instance had discovered it was caused by digitalis, he concluded it was of the same nature and origin in this case and promptly stopped the drug. As in the other case, so also in this, the delusions and other maniacal manifestations lasted about twenty-four hours, and then disappeared entirely; This rare effect of the prolonged administration of this agent will be spoken of in the chapter on Treatment of Valvular Diseases. Patient was seen again in January. He was still in bed, where he had remained since the fore part of October, was quite recumbent, and breathing tranquilly, although he stated he had occasional paroxysms of dyspnoea that compelled him to spring up for breath. These spells of difficult breathing had returned upon him about the 1st of January after a period of constipa- tion. His physician stated that as a result of vigorous purgation, digitalis, strychnine, and morphine hypodermically, and restricted diet, which was kept up for nearly two months, his condition had by late autumn improved wonderfully. The enlarged liver had re- turned nearly to normal, his colour had grown quite natural, and his pulse stronger, of better volume, and regular, the heart-sounds stronger, and the apex-beat fairly well defined. Recently, how- ever, the patient had become intolerant of the cathartics and pro- longed rest in bed, and had implored to be allowed to sit up. I found the pulse about 70, with two intermissions in a min- ute and a half, but very compressible, and its collapsing character not well marked. The liver was palpable, particularly the left lobe, which was very tender in the epigastrium. There was no oedema, although the feet were a little puffy. Cardiac impulse was wanting except for an occasional vague apex-beat consider- ably outside the left nipple in the sixth interspace. Heart's dul- ness was pronounced, presenting in this regard a marked contrast to its condition in October, when it was obscured by pulmonary resonance. It was of triangular outline, reaching to the third interspace, and from 2 inches to right of sternum across nearly 292 DISEASES OF THE HEART to the left anterior axillary line, well outside of the occasionally ])alpable impulse. The lungs were eyerywhere resonant. The heart-sounds were audible though faint, the aortic second being particularly feeble, and the pulmonic second accentuated. A loud, harsh murmur was present throughout the pra^cordium, which was systolic, but could not be traced to any particular area. Oyer the body of the organ it disappeared on firm pressure, permitting other more distant and persistent murmurs to be distinguished. These were found to be a harsh aortic systolic, a soft mitral systolic transmitted to the back, and a feeble diastolic, which was of aortic origin, as shown by its area of intensity and direction of propa- gation. The diagnosis was apparent; added to his old-standing aortic insuificiency with relatiye mitral regurgitation there was a peri- carditis with moderate effusion. The liyer was both congested and displaced downward. The prognosis was most unfavourable, for in addition to the cardiac dilatation depending largely on myocardial degeneration, a pericarditic effusion had taken place. As is well known, this sometimes superyenes upon a chronic valvular disease, particu- larly aortic insufficiency, and is then apt to be a terminal event. It was stated to the family that sudden death was not improbable. In the way of treatment, compound cathartic pills were or- dered, the patient objecting to elaterium and disagreeable saline waters ; digitalis in considerable doses, a grain of codeine thrice daily to promote quiet and to lessen the paroxysms of dyspncea, and restricted diet. Morphine was not prescribed because of its constipating and other objectionable effects. In spite of the greatest possible care this ])atient did not im- prove, and one month later died suddenly and quietly M'hile rest- ing in bod, as usual. This case not only portrays the clinical pic- ture often seen in aortic regurgitation, but also illustrates the powerlessness of our art in attempting to stay the progress of the disease. In this and Dr. Webster's case there was one symptom com- mon to both — i. e., paroxysmal dyspnd'a. In the one case it seemed due to sudden threatening asystolism of the left ventricle, as shown by feebleness, rapidity, and irregularity of the pulse, and pulmonary congestion, manifested by cough and frothy expectora- AORTIC REGURGITATION 293 tion. In the other there was also threatening weakness of the heart's action, but the striking concomitant was the intense anx- iety amounting to fear, so that the patient would spring up in bed gasping for breath and looking wild and terrified. In both these instances, moreover, the symptoms of cardiac breakdown de- veloped suddenly, and were never again wholly lost, in this re- spect differing markedly from the gradual onset of compensatory failure seen in mitral affections. In both cases mitral regurgita- tion Avas superadded, but instead of the end coming with pro- nounced dropsy death was sudden, before venous stasis progressed to that degree. In my experience young persons who have contracted their aortic insufficiency in consequence of endocarditis rarely suffer from cardiac pain, while, on the other hand, I have observed numerous instances of angina pectoris in individuals whose aortic lesion had resulted from degenerative changes. In 1891 I began to treat a married woman of about thirty who was afflicted with aortic incompetence and attacks of precordial pain. She was quite stout, and this made examination of the heart difficult. The radial pulse was collapsing, though not as full and quick as in typical cases, and she had an aortic regurgitant murmur. The apex-beat could not be distinctly made out, and the large breast prevented my determining the boundary of deep-seated dulness at the left. The absence of manifest cardiac hypertrophy rather puzzled me, but eventually led me to conclude that the leak was not very free, and consequently that there was not much hyper- trophic dilatation of the left ventricle. After she had been under treatment for a time she called attention to a pulsation in the neck. This was found to be just behind and above the right sterno-cla- vicular articulation in the location of the innominate artery. It was attributed to aneurysm of the arch of the aorta, which thus brought the innominate prominently into view. The patient was taken to several diagnosticians for opinion, and among others to the late Dr. Christian Fenger, by whom my diagnosis was con- firmed. This discovery of a probable aneurysm changed my views concerning the etiology and pathology of the case. Whereas the history had led me to regard the aortic regurgitation as of rheu- matic origin, I now considered it secondary to aortic aneurysm, a view that seemed to account for the attacks of angina. 294 DISEASES OF THE HEART The patient then left Chicago, and I did not see her for sev- eral years. At length I was one day nnexpectedly summoned to visit her at one of the hotels to which she had betaken herself immediately upon her return from Europe the day before. She was in a truly pitiable plight. The attacks of agonizing pain had become so frequent and severe that she literally could not walk across the room without one being evoked, and she was taking large doses of nitroglycerin and whisky, though with but slight eifect. The circumference of the neck was greater than normal, although the evident congestion had not produced a-dema. The old-time pulsation was still in evidence. It did not appear to have increased in area, and the only alteration I could detect in the heart-findings was greater rapidity and feebleness of action. She was given injections of morphine sufficient to somewhat blunt her sensibility to pain, but aside from this there was nothing that could be done. She dragged out a miserable existence for a few weeks longer, and then in one of her attacks death mercifully ended her sufferings. At the autopsy, which was performed by Dr. Frank S. John- son, who had also seen the case, the aortic valves were found very incompetent and sclerotic, but whether the process had originally been of endocarditic origin or not it was difficult to decide. There was a moderate degree of enlargement of the left ventricle, the walls of which were fatty. The two most interesting features, however, were (1) occlusion of the mouths of the coronary arter- ies by deposits of lime-salts, so that they with difficulty admitted the point of a fine probe, and (2) the size of the aorta. Xo aneu- rysm could be detected, but careful measurement showed that the ascending portion of the arch was uniformly increased in diam- eter by about 1 centimetre, while its walls were possibly a trifle thinner than normal. It seemed probable, therefore, that when distended by the abnormally large blood-wave it became stretched sufficiently to amount to a considerable dilatation, which had caused some pressure on the great veins, hence the congestion of the base of the neck, and the prominence of the innominate artery. It was now easy to understand the frequency and intensity of her angina. The heart-muscle simply could not be flushed with blood through the extremely narrowed coronary ostia. Whenever physical exertion called for more 1)1o(k1 witliiu the coronary arter- AORTIC REGURGITATION 295 ies it was hot forthcoming, and cardiac ischsemia was manifested by a cry of agony. From the foregoing, it is plain that cases of aortic regurgita- tion can be divided into two classes. In the one, the lesion is the result of endocarditis, contracted during a period of life when the myocardium and arterial walls are still young and healthy — great compensatory hypertrophy is possible, and the disease may endure for many years without giving rise to symptoms. These appear at length only after the heart-muscle can no longer be sustained by the coronary circulation, or the breakdown occurs as the result of fresh endocarditis ingrafted on the old process in the course of acute articular rheumatism. In my care, five years ago, was a viva- cious young lady of eighteen, who presented the typical signs of free aortic regurgitation, a quick, collapsing pulse, a broad, heav- ing apex-beat., situated far below and to the left of its normal situation, and a loud diastolic murmur. She consulted me because of having noticed that she could no longer run upstairs, dance, ride a wheel, or do other things which before were unattended with consciousness of the heart's action. She did not get out of breath, but was annoyed by forcible pounding of the heart and by the occasional sensation as if it " gave a flop." She had some flatulent indigestion and was constipated. The pulse was now and then intermittent, and for the purpose of cor- recting this intermittence she was given small doses of tincture of digitalis, 5 drops 3 times a day. When she next returned, after a few days, she stated that the pounding of the heart was worse instead of better. The digitalis was reduced, but still intensified her symptoms, and was discontinued. Thinking that the inter- missions might be due to gastro-intestinal derangement, she was given remedies to correct the constipation and improve digestion. There was some improvement, but still the heart did not become entirely regular. One day she complained of dull frontal head- ache, some pains and stiffness of the muscles, which seemed to me a muscular rheumatism, possibly of uric-acid origin. Accord- ingly, she was put upon potash and salicylate of soda, and or- dered to drink freely of water. This was a happy hit, for she lost the intermittence of the pulse, and was no longer annoyed by the heart's pounding. A year later, believing I had discovered evidence of a tendency 296 DISEASES OF THE HEART to growing dilatation of the left ventricle, I gave her a course of ]Sraulieini baths, which agreed with her, and she felt so well that I lost track of her for some months. Indeed, with one exception, after the baths were finished, I never saw her again. But one day, encountering her mother in the cars, I learned that in Au- gust, eight months subsequent to her last visit at mj office, she developed what appeared to be a mild attack of articular rheu- matism. As I was out of the city, a neighbouring physician was given charge of the case, and he very properly confined her to bed. After about a week the rheumatic manifestations had sub- sided, and she was thought to be getting on finely. One morn- ing she awoke in excellent spirits and seemed nowise in imme- diate danger. Nevertheless, during the forenoon, when she sat up in bed to drink a glass of water, she suddenly, without warn- ing, fell back upon her pillow and expired. No autopsy was held, and I have no means of knowing the exact condition, but I be- lieve that probably the heart had become weakened by fresh endo- carditis attending the mild rheumatic attack, and under such cir- cumstances the exertion of sitting up occasioned sudden diastolic arrest of the left ventricle. It simply illustrates the liability of these patients to sudden, unexpected death. In the second class belong patients whose valvular defect is the local manifestation of degenerative changes, which, if not due to syphilis, the gouty diathesis, strain, and the like, are associated with advancing age. In such persons compensatory hypertrophy rarely proves so enduring as in the young, and may fail early, because the myocardium is already degenerated, or because the state of the coronary arteries does not permit that degree of nour- ishment necessary to the maintenance of hypertrophy. In this second class should also be reckoned those cases in which the aortic insufficiency is the result of rupture. In this latter group, pain, praecordial distress, and other symptoms of cardiac incompetence are apt to appear promptly after the injury, and to persist without relief. Naturally, however, the ability of the heart to compensate the defect depends upon the extent of rupture — that is, the degree of regurgitation jx'nn itted — and ii]xin the state of the heart-mus- cle. Dilatation of the left ventricle usually develops rapidly, with little or no hypertrophy, and hence after a few weeks or months the heart succumbs. AORTIC REGURGITATION 297 In persons suffering from slowly induced degenerative •changes symptoms appear slowly, but are never so delayed in com- ing as in patients whose incompetence originate in endocarditis. In most instances the symptoms that initiate breaking compen- sation are such as may be referred either to cerebral anaemia — i. e., vertigo and syncopal attacks — or to cardiac fatigue and de- generation — i. e., irregularities of the pulse, palpitation, and angina pectoris. When, on the other hand, cardiac failure leads to stasis in the lesser circulation, or in the great veins of the general system^ the symi^toms gradually become those of the terminal stage of mitral disease — i. e., dyspnoea, cough, and frothy, or it may be sati- guineous expectoration, disturbed visceral functions in general, ■oedema, and attacks of threatening asystolism. When at last aortic regurgitation has reached this stage the struggle is less likely to be protracted, and death is usually more sudden than in defects at the left auriculo-ventricular orifice. Physical Signs. — Inspection. — In cases of pronounced ■aortic regurgitation the disease reveals its presence to the skilled eye by the throbbing of the temporal and carotid arteries. In contrast with the cyanosis of mitral disease the aspect of the pa- tient is apt to present more or less pallor, especially if the disease has developed in early life. Inspection of the chest usually de- tects strong pulsation of the cardiac area to the left of the ster- num, the degree and extent of this pulsation depending upon the thinness and flexibility of the chest-wall, as well as on the hyper- trophy of the heart. Occasionally a wave-like impulse is seen to pass from the base downward towards the apex-beat, while in some cases there may be slight systolic retraction of the third and fourth interspaces to the left of the sternum, in consequence of atmospheric pressure, as the hypertrophied heart recedes from the chest-wall. The apex-beat is displaced outward and downward, in some ■cases even as far as the seventh or eighth left intercostal space, close to the left anterior axillary line. It is broad and heaving, at once conveying the impression of a large and powerful organ. In the young, with broad intercostal spaces, the dimensions of the left ventricle may be almost as accurately delineated by the vis- ible impulse as by percussion. 21 298 DISEASES OF THE HEART In niicklle-aged individuals, on the contrary, particularly if the chest is capacious, the apex-beat may be scarcely perceptible. In some instances, no doubt, this is owing to the inability of the degenerated, heart to establish great compensatory hypertrophy. When very free regurgitation is compensated by great hyper- trophy, the eye sometimes discerns visible pulsation in the periph- eral arteries, as the radial or the dorsalis pedis. This phenom- enon, which is brought out with special distinctness by extension of the hand or foot, is the ocular manifestation of that peculiar- ity of the pulse about to be described under palpation as the pulsus altus et celer. Quincke has described a visible pulsation of the retinal artery, which may be more or less tortuous and elongated with each pulsation. Capillary and venous pulse will be considered later on. Palpation. — The hand laid upon the praccordium detects pow- erful cardiac impulse, and over the apex-beat sometimes perceives a short presystolic thrill, or rather receives an impression as if the tip of the heart slid up to its maximum impulse. The impact of the apex resembles the striking of a huge fist against the chest- wall, and if the patient be slight, the whole chest may seem to quiver with the shock. Systolic thrill is sometimes felt in the aortic area. Under some circumstances a diastolic thrill is also manifest. The most remarkable feature in this part of the examination is presented by the pulse. Its characteristics are so distinctive that a diagnosis is often possible from it alone. First carefully stud- ied and accurately described by Sir Dominick Corrigan, it is often called Corrigan pulse, while other terms applied to it are the collapsing pulse, the water-hammer pulse, the locomotive pulse^ and the pulsus alius et celer. In well-marked cases the finger laid upon the radial artery, or upon any other readily accessible artery for that matter, is suddenly lifted by a large, powerful pulse-wave, which, advancing swiftly along the vessel, strikes the finger like a shot or ball, and then instantly recedes. The vessel, in other words, after Ix-iiig (piickly distended as quickly collapses, hence the name colla])siiig pulse. It is well shown in the accom- panying tracing (Fig. 54). This characteristic of the pulse is intensified by raising the AORTIC REGURGITATION 299 jDatient's hand to a level higher than that of the heart, and thus allowing the force of gravity to hasten the quick recession of the pulse-wave. The quickness of the pulse-wave has thus been dwelt upon for the purpose of emphasizing the difference between the speed with which it travels along the artery, and the frequency with which Fig. 54. — Sphygmogram of Aoetic Eegurgitation. Tracing by Dr. Edward F. Wells. the individual pulse-waves follow each other. Consequently, a frequent pulse is a rapid or accelerated pulse, whereas a quick pulse is one that strikes the finger suddenly and is not sustained. A pulse may be both frequent and quick, as in fever, but a quick pulse does not necessarily have to be also a rapid one. In aortic regurgitation, however, the pulse is both sudden and accelerated. In some cases when the arteries have become more or less sclerotic and tortuoiTS the bounding pulse-wave , seems to lift the vessel from its bed, and hence some writers have spoken of it as the locomotive pulse. To make the raison d'etre of this collaps- ing character understood, it is necessary to describe how the valvu- lar disease under consideration modifies pulse-tension. Under normal conditions blood-pressure within the arterial system is maintained at a uniform height by the periodic dis- charge of blood into the aorta and by the elastic recoil of the arterial walls aided by the tightly closed semilunar valves. The blood-stream driven against the valve by the recoiling aortic walls is intercepted and forced onward through the arterial system. If the aortic valves, incompetent by disease, are unable to check the backward flow of the blood a portion of it regurgitates into the left ventricle, and blood-pressure in the arterial system is corre- spondingly lowered instead of being maintained at a uniform level. Accordingly, the Avave of blood constituting the pulse- wave quickly recedes and allows the arterial walls to collapse, as it were. .The hypertrophied left ventricle, made more than nor- 300 DISEASES OF THE HEART nially capacious by dilatation, discharges its contents with a de- gree of energy proportionate to its hypertrophy; and as its con- tents are angmented oyer the normal by the amount that has the moment before regurgitated, the aorta becomes powerfully dis- tended by this abnormally large mass of blood. In consequence of the partial emptiness of the arteries caused by the regurgita- tion the large blood-waye meets with but little resistance, and trayelling rapidly towards the periphery, distends the arteries in its course. Hence the greater the compensatory hypertrophy of the left ventricle, the fuller, stronger, and quicker will be the pulse. The freer the regurgitation the more marked will be the collapse of the yessel-walls. The degree of difference, therefore, between the distention and collapse of the artery is a measure not only of the degree of the regurgitation, but also of the resulting compensatory hypertrophy, for when the left yentricle begins to fail, this pecul- iar collapsing quality of the pulse grows less pronounced, although the regurgitation is no whit less free. Very exceptionally the pulse is said to exhibit the character knoAvn as bisferiens and represented in Fig. 55. If the finger is pressed lightly on the artery it receiyes a sensation as if the pulse-waye were divided into two portions, of which Fig. 55.— p. bisferiens. the sccoud is the Stronger. Allbutt's Syst. of Med., vol. V, p.9.31. rT^^ ^ , 1 he lormor represents the sudden distention of the artery, and the latter is the palpable ex- pression of the pra-dicrotic or tidal wave. Pulsus bisferiens is usu- ally stated to be found in aortic obstruction, but according to Graham Stecll, cited by Clifford Allbutt, undoubtedly occurs in some cases of regurgitation associated with little if any stenosis. In one of Steell's instances this peculiarity was not equally con- stant or pronounced on both sides of the body. Its production is therefore difficult of explanation, as well as inconstant. I have never obtained a tracing showing a bisferiens pulse in aortic insuf- ficiency, but T have certainly felt pulses in some cases which, to my finger, seemed plainly of this character. Not infrequently, pulsation is so pronounced in the arterioles that the fingers of the patient throb appreciably when grasped AORTIC REGURGITATION 301 and the diagnosis of his malady can be made while in the act of shaking his hand. Two other phenomena, the capillary pulse and visible venous pulse, should properly have been described under inspection, but have been reserved until now for the reason that they will be bet- ter understood after what has just been said concerning the pecu- liarities of the pulse. In cases in which arterial tension is very low in consequence of free regurgitation, the capillaries are dis- tended by the blood-wave instead of being kept uniformly filled, and hence display what is known as the capillary pulse (Quincke's sign). This may be well seen in the palm and beneath the nails when the hand is warm, or it may be evoked by friction of the skin — e. g., of the forehead — until an area of hypersemia is pro- duced. If the periphery of such a red zone is closely watched, its edge will be seen to alternately advance with each systole and recede with each diastole of the heart. Capillary pulsation is also sometimes plainly visible on the soft palate. By venous pulse is, meant a visible pulsation in the superficial veins. This is sometimes well marked in the subcutaneous veins of the back of the hand and the forearm when the extremity is al- lowed to hang down until the vessels become turgid. This venous pulse is a slow undulatory wave which, as Broadbent suggests, may be best noticed by laying a filament of sealing wax across the sur- face of the vein. Venous pulsation is specially pronounced when arterial tension has been still further reduced by fever. Neither of these last two phenomena is peculiar to aortic regurgitation, for they may be observed in severe anaemia which has sufficiently lowered pulse-tension. They are, however, most distinct and typ- ical in aortic incompetence. Finally, when regurgitation is very free, a distinct thrill may be felt in the cervical arteries and even in the brachials. This was well felt in a man of about thirty-five, who died suddenly a few weeks subsequently. In this case the thrill was palpable when the finger was laid ever so lightly on the vessel, and seemed to bo but the palpable expression of vibrations imparted to the arterial coats by the suddenness and violence of the impact of the blood- stream. Percussion. — As in other cases of valvular disease, percussion affords our best means of noting to what extent and in what direc- 302 DISEASES OF THE HEART tion the heart has suffered enlargement. It is particularly valu- able in cases in which the size of the chest or the feebleness of cardiac impulse prevents us from judging- of the size of the heart by inspection and palpation. In compensated cases cardiac dulness is in- creased only to the left and downward, and the outline of the left ventricle is rather pointed (Fig. 56). As dila- tation comes on, the left car- diac border becomes more rounded and the apex is blunt and broad, so that one should always strive to percuss out the shape of the left ventricle Fiii. i)ii. — T vfE uF KtLATivi. Dllness in Well- compensated Aortic Eegi'rgitation. from 57). and is es de- as well as its distance the median line (Fig. Increased dulness to the right is present only secondarily, a measure of back pressure important to determine. Auscultation. — Regurgitation through the aortic valv clares itself by a murmur syn- chronous with the second heart sound and therefore diastolic in time, which is heard with greatest intensity over the l^ase of the heart any- where between the second right costo-sternal articulation and the junction of the fifth left costal cartilage with the l)reastbone (Figs. 58 and 59). Its most usual scat of maxi- mum loudness is on the body of the sternum at the level o1 the third costal cartilage, and . • • . •. Fkj. 57. — Tvi'i'. UK Relative Dulnems in vet in some instances it mav ;. . '- • I'ooKLV (. omi'ensatei) Aoutio Kequiwi- be heard most j da inly or heard tation. AORTIC REGURGITATION 503 only in the fourth left interspace, close to the breastbone. It is generally most distinct in the erect position or when the heart's action is excited. ISTeverthe- less I have certainly observed cases in which the murmur be- came more distinct and easily recognised when the patient was recumbent. This murmur is transmitted downward to- wards the ensiform appendix, and in some instances also towards the left, even as far as the apex. When audible, with more than usual inten- sity at the apex, the murmur is thought by some to indicate incompetence of the left pos- terior flap. As previously remarked with reference to the mitral reffurgitant murmur, the intensitv and the extent of conduction of this aortic diastolic murmur furnish no criterion of the gravity of Fia. 58. — Spot of Maximum Intensity (small ciecle) and Area of Transmis- sion OF Typical Aortic Keglrgitant Murmur. Fig. 59. — Khythm of Aortic Regurgitant Murmur. the lesion. Indeed, numerous instances have been recorded in which no bruit at all was audible for a variable time immediately 304 DISEASES OP THE HEART prior to death. This is probably owing to a want of sufficient force and rapidity in the regurgitant stream to generate sonifer- ous vibrations. The duration of this murmur is usually short, and its quality is soft rather than harsh, and is unlike that of any other murmur excepting the bruit of pulmonary regurgitation. In exceptional cases the diastolic aortic murmur may have a true musical tone. I Avell recall the case of a coloured man, in whom the intra-vitam diagnosis of aortic regurgitation was sub- stantiated post mortem, and who presented this musical quality in a most marked degree, but not with every ventricular diastole. At irregular intervals the soft diastolic bruit was associated with^ or replaced by a musical murmur so intense that it was heard by the patient, and imparted a distinct thrill to the hand laid upon the heart to the left of the sternum. A few days before death this musical murmur entirely subsided, and at the post-mortem examination no condition that could explain its production could be discovered, although diligently sought for. The valves pre- sented the appearance ordinarily found in cases of endocarditic insufficiency. The heart-sounds usually present more or less modification. The first sound at the apex is apt to be mufiled or toneless, while the second sound is enfeebled. In the aortic area the second sound may be entirely wanting, being replaced by the diastolic murmur, or there may be a faint rudimentary second sound. The aortic first sound may be audible or replaced by a rough, more or less intense, systolic murmur. This bruit is usually interpreted as signifying an associated stenosis. This conclusion, however, is not always justifiable, since such a systolic murmur may be due either to roughness without narrowing of the orifice, or to sclero- sis of the aortic intima. When both a systolic and diastolic mur- mur are heard, they are often spoken of as a " to and fro " mur- mur, and such a combination is very frequent. There are also certain auscultatory phenomena connected with the peripheral arteries which furnish valuable secondary signs of this valvular lesion. Over the carotid and subclavian arteries a faint systolic murmur is often found to replace the first sound, while if the regurgitation is free the normal second tone is ab- sent. When one auscultates the fomorals, he hears a sharp snap, which is synchronous with ventricular systole and is the audible AORTIC REGURGITATION 305 expression of the sudden tension into which the arterial coats are thrown as they are distended by the large sudden pulse-wave. If rather more pressure is exerted upon the vessel by means of the stethoscope, this snapping tone disappears and becomes replaced by a distinct murmur, the murmur of constriction, which can be elicited over any artery of sufficient size when no valvular disease exists. When regurgitation is free, it is usually possible by trying different degrees of pressure to at length bring out more or less clearly not only this systolic murmur, but also a diastolic one, so that one becomes conscious of a double murmur, of which, in my experience, the systolic is usually the louder. This double femoral bruit was first described by Duroziez, and hence is often spoken of as Duroziez's sign. It is considered pathognomonic of aortic regurgitation, since in no other disease are the conditions pre- sented for its production. The explanation of this phenomenon is as follows: Constriction of the artery throws the blood-stream into audi- ble vibrations as it passes the point of pressure, and, normally, this is all; but in aortic insufficiency the blood-wave recedes during diastole and passes again this point of constriction, with the result that it is a second time thrown into vibrations, and a diastolic murmur is generated. In most cases these acoustic phenomena are elicited only over arteries of large calibre, but when the lesion is very pronounced and the left ventricle is powerful, both the sys- tolic snap and the double bruit may be heard in small vessels, as the radial and even the dorsalis pedis. Diagnosis. — Ordinarily the recognition of aortic insufficiency is not difficult. In some instances it may be detected at a glance, but when the individual is past middle age, with sclerotic arteries and a voluminous thorax, the collapsing character of the pulse and a powerful cardiac impulse may not be pronounced, and care is requisite to determine that the condition is not an aortic aneu- rysm that has led to regurgitation. In all doubtful or indistinct cases particular study should be given to the vascular signs, since they are conclusive, and a diastolic bruit is not. Indeed it is to be remembered that when in the last stages the heart has become very weak, the murmur previously present may entirely disappear. Moreover, the diagnosis of this lesion may be rendered not easy by the association of relative mitral incompetence, or of other organic 306 DISEASES OF THE HEART defects. In all such cases one must minutely investigate the vas- cular system and rely on its disclosures rather than on cardiac findings, although even here valuable information may be obtained if attention is paid to the secondary changes instead of the auscul^ tatory findings. Before leaving the subject of the diagnosis of this disease, I desire to dwell for a few moments on a subject which has given rise to much controversy. Many years ago the late Austin Flint, one of the most careful clinical observers this country has pro- duced, directed attention to tho presence of a presystolic apex- murmur in some cases of aortic regurgitation, and declared it was an accidental murmur which did not necessarily denote the co- existence of mitral stenosis. He was vehemently attacked by Bal- four, who declared a functional presystolic murmur an impossi- bility. But corroboration of Flint's ol)servation has come from so many sources that there can no longer be any doubt of the cor- rectness of his statements. His explanation of the mode of its production is, however, probably not correct in the light of more recent physiological knowledge concerning the closure of the mitral valves. The mur- mur is now thought due to vibrations of the mitral curtains as they are caught between the regurgitant stream on the one hand, and that pouring out of the left auricle on the other. It is quite pos- sible for mitral constriction and aortic regurgitation to coexist, and in any instance of this latter disease in which a mitral presys- tolic murmur is recognised its correct interpretation is made pos- sible by giving due consideration to the presence or absence of secondary changes in the right ventricle, and the smallness yet colljijising cliaracter of the radial pulse. Prognosis. — A proper estimation of the prognosis of aortic regurgitation requires a sharp distinction between the forms due to endocarditis and those of degenerative origin. Furthermore, in each group and in each individual instance, the jM'ognosis is in direct relation to the degree of compensatory hypertrophy, the same as in any other valvular defect. If, in the first class — that is, of endocarditic origin — compensation becomes once well estab- lished, it is possible for the disease to be borne for many years. Mr. W., the description of whose sudden death will be narrated, was known to have aortic regurgitation of severe type for at least AORTIC REGURGITATION 307 twenty-eight years, and perhaps longer. When, however, com- pensation begins to fail, the prognosis is very grave, for it cannot be so readily restored as in mitral disease. Indeed, some authors are of the oj)inion that compensation can never be reinstated; at the most there being hope only of retarding the downward progress. When in the second category of cases, those of degenerative nature, compensation becomes established, it is at the best only for a comparatively limited period, owing to the probable presence of chronic myocarditis, and when this compensation once breaks, it is irretrievably gone. Henceforth the progress of the malady is for the most part steadily downward. In all cases the prospect of even partial recovery is slight, and of restoration to a life of ac- tivity and freedom from symptoms is nil. It is stated that very rarely a regurgitation may be converted into a predominating stenosis by the growth on the valves and ring of vegetations, in consequence of fresh endocarditis; and whenever this occurs the prognosis becomes more favourable, pro- vided, of course, there be no myocarditis or other complications. This possibility is too remote to be ordinarily taken into considera- tion. Mode and Causes of Death. — ISTo other valvular disease so often terminates abruptly. The suddenness of the death is due to paralysis of the left ventricle in diastole. In most cases, no doubt, warning has been given of the pending catastrophe by ir- regularities of the pulse, vertigo, or other symptoms which failed at the time to attract the patient's attention, or were too insig- nificant to impress him with their gravity. Death follows some sudden effort, as assuming the erect from the recumbent position, springing out of a chair to leave the room, jumping on to a moving street-car, and the like. The muscular effort incident to such sud- den movements abruptly raises blood-pressure within the vessels supplying the groups of contracted muscles, and drives the blood into the left ventricle during its period of relaxation with a degree of force which the ventricle is unable to resist. It fails to respond by a subsequent systole, and the patient falls to the ground in an attack of fatal syncope. Fortunately for the patient, as well as for the peace of mind of his friends, assurance can be given that sudden death in the way 308 DISEASES OF THE HEART just described is not usual. Indeed, it occurs in the minority of cases of aortic regurgitation. According to Broadbent, it occurred in 10 out of 38 cases taken from the records of St. Mary's Hos- pital. Sudden death occurs by far the most frequently as result of fibroid and fatty degeneration of the myocardium, and, there- fore, we should look for it in individuals whose aortic valves are incompetent in consequence of degenerative changes rather than in the young, whose valvular lesion is of endocarditic origin. This does not apply, however, when the heart is freshly attacked by an acute endocarditis. The case of the young lady of eighteen illus- trates that under such circumstances the end may come unex- pectedly and without warning. We have seen in most cases of aortic regurgitation that the symptoms showing complete loss of compensation become those of pronounced venous stasis, the same as in the last stage of mitral disease. It is to be expected, therefore, that exitus lethalis should take place in the same manner, and in fact such is the case — i. e., from gradual cardiac asthenia or acute pulmonary oedema. Striimpell directs attention to the not infrequent occurrence of pericarditis in aortic insufficiency, particularly when the valves have been attacked by fresh inflammation, and in such the peri- carditis is very apt to lead to the death of the patient. Of 24 cases analyzed by Hustedt, the causes of death were as follows : Heart-weakness, 8 ; pulmonary infarct, 9 ; pneumonia, 2 ; oedema of the lungs, 3 ; apoplexy, 1 ; and pleuritis, 1. The suddenness of death is illustrated by the case of ^fr. W., aged forty-five, who had had aortic insufliciency dating from chorea and rheumatism in boyhood, and had shown symptoms of failing compensation for at least two years. These consisted in feebleness and irregularity of the pulse, and attacks of weakness and faintness of such severity that they compelled him to seek aid of the nearest physician, Notwithstanding the extreme degree of fatigue and exhaustion occasioned by his duties, he persisted in the daily attendance at his oflice. The day of his death he left home as usual and proceeded to his place of business. While in the act of stooping over a table, he sank to the floor, and ex- flaimed, " I am dying! " His clerk, who was standing near, lifted him into a chair, and asked if he should run for a doctor. The sufl'erer looked up, smiled, and shook his head, as much as to say, AORTIC REGURGITATION 309 *^ No, it is of no use," and a few moments thereafter he quietly expired. That this patient was fully aware of his being in daily — yes, hourly — danger of death was shown by the fact that he had given explicit directions to his clerk what to do in the event of such a fatality. Reflecting upon this case, one cannot help won- dering by what knowledge this patient recognised the significance of his final attack, and refused to have a medical man summoned, when in previous attacks he had always sought the services of the most accessible physician. The following case is appended because it emphasizes in an imjDressive way several points with respect to aortic regurgitation. In the first place it illustrates the important part played by heart- strain; in the second, how hopeless is the prognosis in these cases; thirdly, the futility of treatment; and, lastly, the manner of death in a considerable proportion of them. I recently witnessed the death of a gentleman of forty-two who had sought medical advice three months before on the sup- position that his distress was due to some form of stomach trouble. Excepting scarlatina at the age of six, he had never known a day's illness, and his habits had been exemplary with the one exception that he had been accustomed to take about two drinks a day of whisky before meals. He had always been devoted to hunting and £shing, and had spent much time each year in the woods, at which times he had always shouldered his pack and tramped along with his guides, having many a time, as he said, " Done them up and come in at night fresh as a daisy, while they were beat out." He had thought nothing of carrying 60 pounds on his back all day through the woods, and had paddled and portaged with the best of them. When not out hunting or fishing he had been untiring in his devotion to business, and for the previous seven years had worked with colossal energy in building up vast interests in the North. In addition to tireless work with his brain in his office, he had endured and indeed revelled in efforts connected with his business schemes, requiring and displaying extraordinary physical endurance, so that he was the marvel of his friends. On one occa- sion, in December, 1900, this robust man of medium stature and weight, without an ounce of superfluous fat, all muscle and sinew, started with a crew of men up his railroad to inspect some work, and, as the engine was forced to " buck snowdrifts " and make a 310 DISEASES OF THE HEART way for itself, the engineer suddenly discovered that, having neglected to fill his tank afresh, it was out of water. The weather was intensely cold, and this meant that the fire would have to be dumped and the locomotive be allowed to freeze up, or that in some way a supply of water must be obtained. They were near a river, and this indomitable man of whom I write started on a dead run through the deep snow for a camp of his men a mile and a half distant, where he knew he could obtain some pails. He went himself because he knew he could get there in quicker time than any of his men, and, too, would have the authority to take the buckets. Arriving there, he shouldered a package of half a dozen iron buckets and started back, running all the way through the snow with his load of 75 pounds. He arrived in time to save the engine, but completely exhausted. Xevertheless he recovered in the course of the day, and thought nothing more of it, going about his herculean daily work in and out of the office as before. But outraged ]S"ature was to have her revenge yet. In April fol- lowing his almost superhuman effort, this man of affairs took a hard, fast horseback ride of ten miles over a very rough road, and before he reached his destination he became seized with a severe pain in the epigastrium, which, however, ceased to trouble him greatly after he had dismounted. From that time on until I saw him the next October, he had grown steadily less and less able to endure exertion without this epigastric distress, to which dyspnoea finally became added. In June following his ride, he had climbed down and up a ladder into and out of a mine several hundred feet in depth, and on reaching the surface again had noticed that he was very much winded, and from this time forward he was obliged to walk slowly if he did not wish to suffer from his pain and short- ness of breath. The night previous to his arrival in Chicago, and on several other occasions, he had been awakened in the small hours by a feeling of oppression which compelled him to sit up on the edge of his bed and breathe hard. On this particular occa- sion he had attributed his attack to the closeness of the sleeping- car, had taken a drink of whisky, experienced speedy relief, and, lying down, had gone to sleep. Such in l)riof was his history, as full of interest as a romance. From his recital I expected to find a case of simple cardiac dila- tation from overstrain, such a case as I had shortly before finished AORTIC REGURGITATION 511 treating. Imagine my surprise, therefore, when I discovered a collapsing but not large pulse of about .110, a diffused, rather indefinite apex-beat way below and outside the left nipple, percus- sion evidence of a greatly hypertrophied and dilated left ven- tricle (Fig. 60), feeble heart-sounds, and everywhere a loud dou- ble murmur plainly aortic in origin. Duroziez's sign and capillary pulse were present, and the liver was palpable and tender a couple of inches below the inferior costal margin. The left lobe was specially swollen and sensitive to pressure. The urine was and always remained negative. Here, then, was an aortic regurgitation, but what was its eti- ology ? Was it possible that there had been a valvulitis years before and that the compensation had been broken down by his prodigious exertions, or had the heart - muscle been not quite healthy and had that run started a stretching of the aortic ring which had been increased by succeeding ef- forts, or had the strain led to an aortitis or aneurysm, and this to insufficiency of the valves ? Rupture of a cusp was out of the question, be- cause of the absence of serious symptoms in the weeks imme- diately succeeding his run. A previous valvulitis was not impossible, for it is well known that the enormous secondary hypertrophy of the left ven- tricle sometimes developed in cases of rheumatic incompetence of the aortic valves, is capable of enduring an extraordinary degree of strain for years, as witness some of the cases treated by the great Stokes. In this instance there was no history of anything to lead to endocarditis except the scarlatina, and that occurred thirty- six years before, and if that had led to valvular insufficiency its presence had never been suspected or betrayed by a symptom. Moreover, thirty-six years is a very long time for an aortic regur- FiG. 60. — Relative Dulness ix Case of Aortic Eeguegitation (p. 309). First examination. 312 DISEASES OF THE HEART gitation to exist without discoverv. I therefore considered this explanation as less likely than one of the others. Regarding aneu- rysm as cause of aortic ineonn)etenee, I had already observed a case in which such was the condition, not a very unusual one, but for the greater part of a year there had been no symptom to point ■■ ■ ■ ^K^B^HBsl^^^^^lwf^ ^^^^^^^^^^^1 ^^^^H ^H HRRHSn^ ^^^^1 ^H n m 1 1 I 1 ^^^^^^1 ^^^^i^^^^ \ ¥ui. 01. — Skiaouam ok (."iiK.-fT in Tase of Aoijtic Reourgitation. to aneurysm, and it was not discovered until three months prior to death from pressure on the left lung. C'onscciuently I now had a Roentgen-ray ])icture taken for the 00 feet. Even there she was not able to walk without considerable dyspncea. After the death of the young man this lady went abroad, and in Europe sought medical advice. She was advised to take a course of baths under Dr. Schott, at Bad Xauheim, and while there had her first violent attack of angina pectoris. This folloAved one of her baths. ]^o special benefit was produced by the balneological treatment, and she returned to America. During the winter of 1897 and 1898 she passed through an attack of acute nephritis, but wdien she consulted me the urine showed no albumin or other ab- normal findings. The heart was greatly enlarged, but compensa- tion was still fair. That summer she had a violent attack of angina following a fatiguing walk across a very uneven meadow, and thereafter was never again well. When I saw her in the fall I considered it necessary to confine her to bed for a number of weeks, and when at length she was per- mitted to get up she was still obliged to remain on one floor and to move about with great slowness. The action of the heart did not quicken much under exertion^ but the pulse grew very feeble, the veins of the neck swelled, and she breathed with evident difficulty. She had several severe anginal seizures, which will be described in the article on Angina Pectoris. Strength was gained with great slowness, and she was rarely free from more or less cardiac distress. This took the form chiefly of breathlessness, distention of the ab- domen by flatus, and hepatic congestion. There was never any oedema, but the ankles often felt swollen and stiff. She passed the summer of 1899 at the seashore under the care of my friend, Dr. Edward O. Otis, of Boston, and in the autumn returned no worse but apparently no better as regarded her heart. All these months she had been kept on approved cardiac tonics and was frequently obliged to resort to hydragogue cathar- tics because of the relief they afforded. The ensuing winter was a hard one for her, as she was most of the time confined to her apartments in the care of a trained nurse. This was necessary by reason of the possibility of an anginal paroxysm and because at 332 DISEASES OF THE HEART night she would sometimes awake deathly cold, in a drenching sweat, and feeling extremely faint. The pulse at these times was small and feeble, and the coun- tenance was blue. Prompt stimulation relieved her, but not al- ways speedily, for it seemed as if absorption from the stomach was slow, and hence resort was had to hypodermics of y^„ of nitro- glycerin, followed at once by heat to the surface and diffusible stimulants. During that winter, and indeed I may say most of the time for nearly three years, the pulse-rate did not vary much from 96, sinking as low as 90 when she was at her best, and when at her worst rising to 105. I believe that on a few occasions I noted a few beats less than 90, usually regular. As a general thing the pulse was tense, and exacerbation of symptoms was invariably preceded by a noticeable increase in its hardness. This patient was much distressed by frightful dreams, from which she awoke with a start and a feeling of faintness. She was also easily startled by unexpected noises, although she appeared to have her nerves under good control. Insomnia was very dis- tressing, and yielded to nothing so well as to hypnotism. She had to be extremely careful in diet, for at times everything seemed to create gaseous distention of the stomach and bowels with imme- diate aggravation of her dyspnoea. During that winter relative incompetence of the mitral valve became constant, and every now and then tricuspid regurgitation was added. Even without actual leakage of the tricuspid valve the cervical veins remained much distended and at times caused pain by their pressure. I have since noted painful swelling of the jugulars in another patient, but as a rule have not known patients to complain of actual pain from this cause. Whenever an attempt was made to invigorate the circulation by considerable doses of digitalis or other cardiac tonics, this pa- tient became annoyed by a feeling in the heart, which she charac- terized as " pounding," so that the treatment finally settled down to an attempt to keep down pulse tension and stasis by moans of nitroglycerin and cathartics, with strychnine and caffeine in small four-hourly doses, and careful feeding. Thus weeks dragged into months, spring came and passed, the heated term was at hand, with its thunder-storms, for which she possessed an uncontrollable ])h()bia, and she was again sent down AORTIC STENOSIS 333 to Dr. Otis, at Rye Beach. B}- fall her condition grew so threat- ening from cardiac dilatation and visceral congestion that she was not able to return to Chicago until Thanksgiving. When at last she was able to make the journey and reached home I found her in a deplorable state. Both auriculo-ventricular valves were leak- ing, and the liver was enormously increased in size. The lungs were so congested that she was harassed by a frequent cough, which completely exhausted her, made the face actually purple, and caused her to gasp for breath for many minutes. The difficult sputum was often bloody, or if not actually san- guineous was made up of thick, tough brownish mucus. The bases of the lungs were dull, and everywhere were copious moist and dry rales. Heroin, strychnine hypodermically, energetic catharsis, and apomorphine in -g-grain doses at last pulled her out of her desperate condition, and by Christmas she was reasonably com- fortable. She was obliged to remain in bed, however, or to ex- change this for an invalid's chair. A^Tienever she made this eifort her pulse grew weak, the veins distended, and she was unable to speak for a minute or two on account of shortness of breath. The excitement and fatigue of the holidays nearly used her up. Her cough returned with increased visceral hypersemia and be- came so frequent and distressing that it could only be controlled by hypodermic administration of hydrochlorate of heroin -^^ of a grain. This, however, after a day or two produced nausea and vomiting, and then I actually feared the strain of emesis would make her heart stop beating altogether. As it was, after each vomiting spell she sank back on her pillows, blue in the face, gasp- ing for breath and too exhausted to speak, while the perspiration simply poured oif of her. At length, however, things mended somewhat, and if not rea- sonably comfortable, she was at least not miserable. Then albu- min and casts appeared in the urine in large amounts, and this patient sufferer began to fail slowly but steadily. By the middle of January it became necessary to resort to stimulating injections of morphine and atropine to keep off the horrible sensation of fainting which took possession of her. Strychnine was increased to the limit of toleration, and in addition hypodermics of a grain of valerianate of caffeine were also given every two hours. Stasis became so distressing, although oedema was never a very 334 DISEASES OP THE HEART marked feature, that cathartics became a daily necessity. I recog- nised that the morphine was a two-edged sword, increasing the danger, of urannia and upsetting the stomach, while at the same time affording her relief from positive misery, and therefore it was not withheld. At length, towards the end of February, this boon became so necessary that more than a grain a day was administered. This sufferer's craving for stimulation be- came most urgent and distressing — so much so that whenever the effect of the stimulants passed off she at once felt a ter- rible sensation of dying. Of course this could not be kept up for long, and finally, five days before her death, the stomach gave out. Whether owing to the morphine,' to the gastric hypera?mia, to irritation of the nerve-centres, or urjcmia, I am not able to say, the vomiting became incessant except when she was under the influence of large doses of morphine, as often as every five bours. There actually seemed to be no circulation at times, as judged by the state of the venous system, and yet that poor heart kept right on, beating 105 times a minute, and for the most part regu- larly. It seemed as if the end must come at any moment through diastolic arrest of the organ, and yet merciful death was withheld for five weary days. At length, forty hours before the struggle ceased, I stopped all medication, except what morphine was actu- ally required to prevent unnecessary suffering, in the hope that by so doing the end might be hastened. Still that heart went on, although gradually growing weaker and weaker. Twenty hours prior to death she sank into coma — merciful coma — and at five o'clock in the morning the sufferer suddenly gave a little gasp, there came a gush of blood to her lips, and all was over. Death was probably due to pulmonary apoplexy, in consequence of sudden nrrest of the left ventricle nn instant before that of the riglit. No excuses are offered for the detailed narration of this case, since I believe it is highly instructive. Two years and a half elapsed between the time this patient first took to her bed and her death, and during all these thirty months it was one uujceasing fight against the inevitable. The original defect at the aortic ori- fice became converted, so far as symptoms wore concerned, into a mitral and tricuspid regurgitation ; l)uf with this difference, that AORTIC STENOSIS 335 the aortic narrowing absolutely precluded all possibility of over- coming the dilatation of the left ventricle and the closing of the mitral valves. Every now and again treatment closed up the tricuspids, but nothing could restore adequate arterial circula- tion. The more one tries in such cases to force the left ventricle to contract energetically the more is its dilatation likely to be increased. In this case there was another element that had to be reckoned with — namely, the angina pectoris and the probable degeneration of the myocardium resulting from the cardiac ischnemia that led to the angina. From the start I foresaw the inevitable result, and we only put up as good a fight as we could. Physical Signs. — Inspection. — In most cases of aortic steno- sis there is nothing in the patient's appearance to attract attention unless it be some degree of pallor. Cyanosis is not present so long as compensation is preserved, and therefore when observed it is indicative either of some associated lesion or of cardiac inade- quacy that has led to stasis. The chief value of inspection lies in the fact that it enables one to detect the location of the apex-beat. This, in consequence of the hypertrophy of the left ventricle, is seen displaced downward and outward, the extent of displace- ment depending upon the degree of hypertrophy. In thin individuals with broad intercostal spaces there is sometimes a diffused lifting of that portion of the chest-wall, overlying the left ventricle, but this is rarely so pronounced as in aortic regur- gitation. Palpation. — Tlie hand laid upon the priecordia perceives a slow, broad, heaving impulse, and at once receives the impression of a powerfully contracting organ. Palpation is consequently a valuable means of examination by enabling one to judge of the contractile energy of the left ventricle. In corpulent persons the thickness of the thoracic parietes may conceal the real force of the apex-beat, but as a rule feebleness of the impact, even when the apex is displaced, is a token that dilatation of the ventricle is weakening its systoles. Furthermore, in many cases of aortic narrowing careful palpation of the base of the heart detects a thrill or fremissement at some point along the course of the ascending aorta. This is generally in the second right inter- space close to the edge of the sternum, but it may be on the 336 DISEASES OF THE HEART Fig. 66. — Sphtgmogram of Uncomplicated Aortic Stenosis. Personal observation. breastbone or in the third interspace, immediately adjoining the left sternal border. The intensity of this thrill is variable, bnt its rhythm is always systolic. It is needless to remind the reader that this vibration is the palpable expression of eddies or currents in the blood-stream after it has passed the point of con- striction. The pnlse of aortic stenosis is small and usually weak in con- sequence of the diminution in the amount of blood ejected from the ventricle. Its size there- ^^^^^^^^^^^^^^^^^^^^ fore furnishes indication I^^Sl^^SI^^SI^^S^H the So IHI^K^^IH^^IH^^I^I long as the myocardium is healthy and compensatory hy- pertrophy is maintained the pulse is regular, and in rate is generally somewhat below the nor- mal. Accordingly, an undue acceleration, or an irregularity, or intermittence of the pulse is a sign of weakness. If aortic incom- petence is associated the pulse is likely to be modified in accord- ance with the characters of that lesion. The sphygmographic tracing of aortic stenosis shows rather distinctive char- acters. The amplitude is not great, the line of ascent is oblique, the summit rounded, the descent gradual, and the secondary waves indistinct. These characters are shown in Fig. 6G, Avhich is the copy of a tracing obtained from one of my patients who presented the signs of pure and uncom- plicated narrowing of the ostium, tliere being no dias- tolic murmur of regurgita- tion, and the left ventricle hypertro])hied with very little dilatation. Percussion. — So long as compensation is preserved, deep- seated cardiac dulness is increased towards the left and downward Fii.. 67. — Tvi'ii;al Kelative J)ri.NKss i\ Case of WEi.L-coMPEXfATEi) Aortic Stenosis. AORTIC STENOSIS m to an extent commensurate with the degree of left ventricle hyper- trophy (Fig. 67). It is only when failing compensation has led to pulmonary congestion, or when aortic stenosis is united with a Fig. 68. — Khythm of Aortic Obstructive Murmur. mitral defect, that percussion detects any increase of absolute and relative cardiac dulness to the right. Auscultation. — The first sound at the apex is apt to be dull and muffled in conse- quence of the preponderance of its muscular element, while the second tone is likely to be enfeebled. Over the base of the heart in the aortic area the ear perceives a murmur which is synchronous with the first sound, and is therefore systolic (Figs. 68 and 69). In pure stenosis there is only this one bruit, but not infre- quently there is also a dias- tolic murmur due to accom- panying aortic regurgitation. rpi . T T1 j-l,^ Fig. 69. — Place of Maximum Intensity 1 he systolic murmur, like the , . x. ^ .„ ^ . ^^ "J ' _ (small circle) and Propagation of thrill, is of variable intensity, Aortic Stenotic Mu-rmur. 338 DISEASES OF THE HEART but as a rule it is heard with great distinctness, and is of a harsh or grating quality. Its direction of propagation is with the blood-stream upward into the neck, and it is not rare for the bruit to be audible in the left interscapular region along the course of the descending aorta. In exceptional instances when very intense it is heard throughout the praecordia, particularly upon and down the sternum, being sometimes most distinct in the left third interspace over the anatomic seat of the aortic valves. The murmur generally replaces the first tone at the base, and when the valves are too stiff and thick to close, the second tone in the aortic area and in the cervical arteries is wanting or so enfeebled as to be merely a rudimentary click. Consequently, in those cases in which the aortic second sound is retained in its normal intensity and clearness, this fact suggests the possibility that the obstruc- tion is situated in the conus arteriosus or at the ostium, the valves themselves lieing but slightly affected. Diagnosis. — As a general thing there is but little difficulty in diagnosticating the disease in question. The conjunction of signs of left ventricle hypertrophy with a systolic murmur in the aortic area and enfeeblemcnt of the second tone at the right of the ster- num, is as a rule sufficient evidence for its diagnosis, particularly if the person is under forty, and furnishes a history of a previous attack of rheumatism. There are three conditions, however, that must be differentiated : (1) sclerosis of the aorta or its valves with- out obstruction, (2) aortic aneurysm, and (3) an accidental mur- mur, often called anamiic. In favour of arteriosclerosis are the following: ^Middle or ad- vanced age, stiffened peripheral arteries, accentuation and ringing quality of the aortic second sound. The left ventricle alone may be hypertrophied, but in most cases the whole heart is enlarged. A history of syphilis as against inflammatory rheumatism also makes strongly for sclerosis instead of stenosis. The difficulty is still further increased by the consideration that degenerative changes may lead to narrowing of the orifice in one way or an- other. Consequently, a precise differential diagnosis between these two diseases cannot always l)e made. As regards an aortic aneurysm — every one knows that when this is small it is often impossilile of detection, yet the following differential points may be stated : The patient's age, being forty AORTIC STENOSIS 339 or more, a history of syphilis or of injury or strain, stiff arteries, symptoms of pressure, as pain, dyspnoea,- and cough, inequality in the size of the pulses of the neck and upper extremities, displace- ment rather than hypertrophy of the heart, pulsation, particularly if expansile and combined with bulging in the aortic area, circum- scribed dulness over the manubrium sterni or at either side, and in addition to the systolic aortic murmur, a booming second tone that is not quite pure or is accompanied by a faint bruit. If doubt is still entertained, resort should always be had to the X- ray. Indeed, if this means of diagnosis is accessible, it should be appealed to for confirmation in all cases. Mediastinal tumours pressing on the aorta are so rare that they will not be considered. If all the signs of aneurysm just mentioned were present in every case a differential diagnosis would not be difficult, but un- fortunately such is seldom the case. I recall a patient in the wards of Cook County Hospital who presented a conjunction of signs that rendered the condition of his aortic orifice a subject of much controversy, and owing to his departure from the hospital were never cleared up. In this case there was a history of syn- copal attacks, and this fact, it was argued by some, made strongly for stenosis. On the other hand, I felt quite certain of a circum- scribed area of deep-seated dulness in the first interspace close to the right sternal margin, and therefore believed the condition was more likely an aneurysm. Lastly, an accidental murmur in the aortic area may, when occurring in the young, give rise to the suspicion of a stenosis. The error can be avoided by attention to the following points : The absence, it may be, of a rheumatic history, the sex (the patient being most frequently a female, in whom aortic stenosis is compara- tively rare), the absence of left ventricle hypertrophy, retention of the aortic second sound, the presence of other accidental mur- murs in other areas, as pulmonary and mitral, the softer quality of the murmur, greater frequency of the radial pulse, and the detection of ana?mia in some instances. Prognosis. — This depends upon the etiology of the affection and the degree of compensation that has been established. If ste- nosis has resulted from degenerative changes in the valves, there are likely to be associated defects in the aortic walls, and it may be in the coronary arteries, which seriously affect the blood-supply 340 DISEASES OF THE HEART to the heart, and hence prognosis is correspondingly unfavourable. Under such conditions compensatory hypertrophy cannot be main- tained for long, even if it has been developed. For the same rea- son there can be but slight hope of its reinstatement after it has once shown indications of breaking. In these unpromising cases the assurance cannot safely be given that sudden death will not take place. In this respect it presents a similarity to aortic regur- gitation. When the stenosis has been produced by endocarditis in the young, the life-prospect stands in direct relation to the degree of narrowing and the perfection of compensation. Cases of moderate severity may exist many years without symptoms, and the patient may be likely to die of some intercurrent disease. This is substan- tiated by the frequency with which aortic obstruction is discov- ered post mortem in cases in which its existence was not known or in nowise contributed to the individual's death. When, however, compensation has once begun to break down, even though the heart-muscle is not greatly degenerated, the prog- nosis becomes most serious. The loss of compensation is due to initiation or increase of dilatation in consequence of the resistance having become disproportionate to the strength of the ventricle. In most instances, to be sure, the myocardium of the ventricle has suffered degeneration of its contractile elements, in consequence of the small supply of blood sent to the coronary arteries; yet by reason of the progressive nature of the valvular defect the ostium may at length become so reduced in size that even a healthy ven- tricular wall cannot carry on adequate coronary circulation. In either contingency it is out of the question for the ventricle to again develop predominating and adequate hypertrophy. Accord- ingly, the prognosis is very different from that of failing compen- sation in mitral regurgitation, in which, if not too badly lost, it may be repeatedly restored. Mode and Causes of Death. — Stenosis of the aortic ori- fice randy LennuuUes in Hudden death. Certainly it possesses no inherent tendency to such an end, as aortic regurgitation may be said to possess. In obstruction tlio failing ventricle tends to grad- ual, not sudden dilatation, and hence the fatal issue is likely to come through the effects of progressing stasis, the same as in mitral defects. In some cases increasing weakness of the heart AORTIC STENOSIS 341 ends in fatal exhaustion before oedema and transudation into the serous cavities become marked. The last -weeks, or even months, of life may accordingly be highly distressing to both patient and friends, and death be welcomed as a deliverer. Of 20 cases of aortic stenosis Hustedt found the following causes of death : Cardiac asthenia 2, pulmonary phthisis 7, pneu- monia 3, marasmus 2, pulmonary oedema, apoplexy, nephritis, bronchitis, emphysema, carcinoma, and ana?mia, each 1. It is noteworthy that but 2, or 0.9 per cent, were attributable directly to the heart, while the remaining 20 were due to intercurrent dis- eases. It is also interesting to note that in 7 cases death was due to pulmonary tuberculosis, and that therefore aortic stenosis may be said to predispose to this disease, probably in consequence of the general malnutrition, which is favoured by obstruction at the aortic orifice. This finds further corroboration in the fact that 2 died of marasmus and 1 of anaemia. 342 DISEASES OF THE HEART 'fe' '^ si 5!J e a ii fe ^ *— ^ , to S; -s « c M .2 '5 F-S S « eS O) OJ Qj '^ fc* ■5 c _* bb E c "3 bo 'to a. to *J .-'S ^ Ui 1 0;^ "3 CO ^ J. -= tS (D -g "« X E . tC O. = 3 J2 5i .i i ^ OJ QJ t fe '^ « OS c ^1 G . bO 3 to c "3 to Q, s § § C QJ .^ -=< to 'S s 8 t; g § 1 S S 13 boiS s g 3 0) "= 05 a- 3 . S s' .be 'm to i C > -0 _ QJ . -rz ■■" ns ® to Is %1 3 03 -1^ s r- i~ CO a 3 J2 [Sd QJ 5 3 ■d -H ^ ii S "2 d 2-2 2 eS S c bo-^ s S ® % 1 9^ 1 :5 2 s t- h 1 -^ 1; -3 2 t; V C B 1 •- '"' >T< ^ -*i) to ^ » '2 to «i is S :c ;S -^ fcO^ -3 to -^ rQ *i le QJ bo g jS 3 P QJ "5 ^ bb^ ? to ^ 3 ut the pulnmnarv valves leaked slowly to the hydrostatic test. Looking into the j)iihiionarv artery from above, it appeared as if a nipple with a small opening at its apex projected into the vessel, and at one side near its base was a second small opening, which was closed in below by a thinner membrane (Fig. 81). The right ventricle was hypertrophied and dilated, and the right auri- cle was also enlarged. One cusp of the tricuspid valve showed a slight thickening ahmg its base. The mitral valves were negative except a slight thickening; aortic valves were thickened along base and margins, while small atheromatous phupies were found in the beginning of the aorta. The left ventricle appeared slightly dilated. The interven- tricular sa;'ptum was complete, but in the interauricular Sfcptum PULMONARY STENOSIS 383 there was a valve-like passage, which would not quite admit two matches, was perhaps 3 millimetres in diiimeter, and corresponded Fig. 81. — Heart from Case of Pulmonary Stenosis (p. 380). Line shows narrowed pulmonary orifice. in situation and shape to the foramen ovale (Fig. 82). Thus it was seen that the intra-vitam diagnosis was confirmed in its main features. A more careful inspection of the heart, made a year later after having been preserved in a formalin solution, showed that the cone which projected into the pulmonary artery, and rep- resented the semilunar valves, was made up of a uniform mem- brane, somewhat thicker than normal valves, and showed no lines or ridges that indicated the points of fusion of the cusps. The opening at the apex was oval, measuring 15 millimetres by 8 milli- metres at its broadest point. The edges of the cone were thick- ened, and the second minute opening at its side, near its base, was 384 DISEASES OF THE HEART found to be a saccular dilatation projecting into the Inmen of the cone. The diameter of the pnlnionarv artery was 22 millimetres, of the aorta 18, and of the foramen ovale 3 millimetres. From the foregoing description it is apparent with what imcer- taintv one can classify this case as congenital or acquired. There were no indications of endocarditis, as it ordinarily appears after Fi(i. !s'.i. — Same IIeakt as Fig. 81. Left iiuricle is laid open, und line indicates patent foramen ovale. birth. The pulmonary artery was not contracted, but rather dilated, the interventricular sa'ptum was complete, and the fora- men ovale was not more patent than it is in a considerable propor- tion of hearts without a suspicion of congenital disease. Never- theless, the appearance of the cone, which replaced the semilunar PULMONARY STENOSIS 385 valves, rendered it probable that this case was of congenital origin, and that intra-nterine endocarditis caused a fusion of the seg- ments at a period subsequent to the closure of the septa, and that the stenosis was not sufficient to prevent the closure of the foramen ovale after birth. Moreover, the volume of blood driven into the j^ulmonary artery could not have been very small, and must have been divided into fluid veins, which threw the stream against the arterial coats in such a way as to maintain ade- quate blood-pressure within the vessel. It is interesting to reflect that, although the lesion, according to the patient's history, gave rise to no subjective symptoms, it should yet ultimately have led to pulmonary tuberculosis, the usual sequence in such cases. Regarding physical signs in this case, it is also of interest to note the wide propagation of the murmur. This was more marked in the left lung, and as the left branch of the pulmonary artery was found to be rather larger than the right, there was probably direct connection between the size of the artery and the transmis- sion of the murmur ; for had the vessel been narrowed, the audi- ble vibrations could not have been transmitted to any great dis- tance. If a conclusion from a single case is justifiable, it is likely that the symptoms directly referable to pulmonary stenosis depend upon its degree and upon the association of other developmental defects even more than upon the obstruction itself. Physical Signs. — Inspection. — Cyanosis is not always pres- ent in congenital cases, and when present is not uniform thro.ugh- out the body. It is this bluish tint which led old writers to des- ignate the underlying abnormality by the generic term of Morbus Ceruleus. Cyanosis is most apparent on the cheeks, ears, fingers, elbows, and knees, and is intensified by coughing or physical exer- tion. As shown by my case, it is not so likely to be present when the stenosis has not led to or is not associated with defects, as, e. g., patency of the foramen ovale or of the interventricular sseptum. In the acquired form patients are more apt to show pallor of the countenance, and there may be turgescence of the superficial veins as a direct result of interference with the outflow of blood from the right heart. Inspection of the prsecordium detects bulg- ing over the situation of the right ventricle — i. e., at the lower end of the sternum and the parts immediately adjacent. Such a bulg- 386 DISEASES OF THE HEART ing is most marked in cases in which the valvular lesion is either congenital or has existed from very tender years. It is due to hypertrophy of the right ventricle, and hence there is associated pulsation in the epigastrium and over the prominent area. PaJpation. — This corroborates some of the information de- rived by inspection, and enables one still better to appreciate the extent and force of the cardiac impulse imparted by the hyper- trophied right ventricle. In addition, there is usually felt a sys- tolic purring vibration or thrill in the pulmonic area — i. e., in the second left intercostal space, close to the sternum. This fremisse- ment may be exceedingly delicate, as in the case observed by me, or it may be distinct and harsh. The pulse presents no distinctive characters aside from small- ness, feebleness, and increased frequency. Percussion. — By this means is revealed marked increase of both absolute and relative cardiac dulness, the increase being downward and to the right, over the situation of the right ventricle and corresponding auricle (Fig. 79). In my case this alteration of cardiac dulness was very pronounced, and aided materially in the diagnosis of the lesion by assuring me of the existence of right ventricle hypertrophy. Auscultation. — The conditions here are favourable to the gen- eration of a bruit, and as it is produced during the passage of the blood from the right ventricle into the pulmonary artery, the mur- mur is systolic (Fig. 83). Its seat of maximum intensity is over the base of the heart, at the left of the sternum, in the second and third intercostal spaces (Fig. 80). At first this bruit may be thought to be aortic in origin, but if its direction of propagation is studied this will be found to be upward and to the left towards the left clavicle rather than to the right and upward, as is the case with the murmur of aortic stenosis. Another point' of difference is that the pulmonic systolic murmur is not heard in the cervical arteries, where, on the contrary, the two cardiac tones are usually distinct. If intense, the murmur may be heard throughout the pra.'cordium, though in all instances its area of maximum intensity corresponds with the location of the systolic thrill. In my case the murmur was transmitted widely, but was more distinct in the left than in the right half of the thorax. In auscultating towards the apex and over the body of the right ventricle the murmur grows PULMONARY STENOSIS 387 less intense, while the two cardiac sounds become more distinct. The murmur maj- be rough and loud, or soft and faint. The pul- monic second sound is diminished in intensity, or may be absent altogether, while the two aortic sounds are distinct. Fig. 83. — Khythm of Typical Polmonaey Stenotic Murmur. Diagnosis. — The difficulty of diagnosis in this affection lies in its differentiation from aortic stenosis or possibly in deciding whether the bruit may not be accidental, since it is situated where such an accidental murmur is so often heard. If, however, proper attention is paid to the secondary physical signs as described above, in particular to the evidence of hypertrophy of the right, not of the left ventricle, one can scarcely fail to interpret the mur- mur correctly. If after such careful study of all the physical signs doubt is still entertained, the sphygmograph will be found of service in enabling one to differentiate between this lesion and aortic stenosis, for it goes without saying that pulmonary obstruc- tion can in nowise modify the characters of the radial pulse. Finally, the discovery of pulmonary tuberculosis and of cyanosis in cases in which the two halves of the heart communicate, fur- nishes a certain degree of evidence in favour of the existence of pulmonary obstruction. Prognosis. — Patients with pulmonary stenosis rarely live be- yond the third decade. Even when the disease does not directly destroy life, it does so indirectly by predisposing to pulmonary 388 DISEASES OF THE HEART tuberculosis. This has been so frequently observed that no doubt can be entertained concerning the intimate connection existing be- tween these two diseases. When phthisis has once supervened the prognosis becomes that of the secondary affection, and since the stenosis is irremovable there Ciin be no hope of the arrest of the tuberculosis. The influence of this cardiac defect upon the pro- duction of consumption is through the ana?mia of the lungs which the narrowing of the ostium occasions. Mode and Causes of Death. — In ITustedt's G cases of pul- monary stenosis death was caused in 1 case by heart w'eakness, in another by miliary tuberculosis, and in the 4 others by phthisis. PULMONARY STENOSIS 389 t^ >-. 4.3 , ^J i i o a •s s ■^ M . -^' . (E a, 03 O c 03 'IJ m ,a r^ £4 03 (I I *^ a .2 o '-^^ 3 "73 -Q G Id ^ 03 -, S-'^ 8 '0 s 2 g G CO ? o3 , =1-1 3 ;s OS O ^ CO 'S ^ 2^ fe o a> CO 03 W a5 CO a> S 13 . Oi Oh G -1-3 t^ CO c3 tZ2 g £ 4J P^ >> b =^ G 3 CO t>2 o3 to G ^ S CO If 3 a i g >> a 5 ^ . ra b^ ,S c q-l 111 be ^ ■^ CO _g 3 o t; o O CO q2 t; ns -w ts (1) «^ ^ "3 ^ s 0, ^ 3l 1 'S £ S o CO 4-3 OS 5 ^ ^ 'j:; &, p c3 CO G ? Is CO OJ CO 03 CO ^^ t- G 03 03 C G G 1— 1 '"' '"' '"' CO _^ o i: i " -^ ^ - > ^ cL a> t> CO 13 rt" S ^ oj '7^ S c3 ^ s i « be 4J a, ^ a. _bc s 3 °r 5*-t "ti^ XS 3 ^0. Oi H CO _3 1) XI ^ .2 1 (V O 1=1 o S5> ^ •' S 'C <= -= -^ -2 "S ??r,fe -« ^ o3 -►^ &C IS 4J > 5 'H ^ g be tn be 'Sh > CO ^ Is §^ ■;3 .Si 03 t- CO -w a G 03 k -kJ 'Sc !S) CO u W '2 3 ^ e 03 CO be CD '3 '3. 03 G 03 ■ , §1 2 c S .0 a •C -^ 'S 9 '-^ "3 H H eu ft^ CHAPTER XIV COMBINED VALVULAR LESIONS Cheonic valvular defects have been dealt with singly, since by so doing their distinctive individual features could be brought out more clearly and without danger of confusion. It would be a mistake, however, to consider these forms of heart-disease as always, or indeed as generally, occurring alone. As a matter of fact certain of them are usually combined, while it is possible for any two or three, or even for all of them to be united. The most common association is that of both stenosis and regurgitation at the same orifice. Tkus it is comparatively rare to find aortic obstruction without also some insufficiency, or the reverse, while in the same manner the two mitral lesions are usually combined in varying proportions. Indeed, a moment's reflection will convince one that the structural alterations set up by endocarditis are very prone to result in both incompetence of the valves and narrowing of the ostium, the clinical features of each case being determined by the predominant lesion. This is not all ; lesions at one orifice may be complicated by a defect situated at another. To be explicit, mitral stenosis may be combined with either aortic stenosis or regurgitation, or both, and the same way with mitral insufficiency, or a double mitral disease may be associated with either or both of the aortic defects. Let us now consider these various combinations in detail. COMBINED MITRAL STENOSIS AND REGURGITATION As already stated, the endocarditic changes that lead to mitral disease are very apt to cause both constriction and insufficiency. Extreme narrowing is more likely to exist alone than is free re- gurgitation, and yet even when there is a buttonhole mitral, it is possible for an insignificant leak to also occur, although the insuffi- ciency may not be declared by a systolic apex-murmur. On the nno COMBINED Valvular lesions 391 other hand, mitral segments that are too stiff to close are quite likely to depend in front of the opening in such a manner as to oppose some barrier to the free ingress of the blood from the auri- cle. In children the mitral curtains are not infrequently so shriv- elled as to form a mere fringe about the ring, and when such is the case stenosis is absent. In adults, particularly when the incom- petence is the result of atheroma, pure and unmixed regurgitation is the exception. The effects on the heart are essentially those of either form of mitral disease when existing alone, and yet the left ventricle and left auricle manifest certain modiiications depending upon the as- sociation of stenosis with incompetence. The ventricle is neither so dilated as in unmixed regurgitation, nor so atrophic as when there is extreme obstruction. Similarly, the left auricle is neither so hypertrophied as in predominating stenosis, nor so dilated as in free regurgitation. When conjoined, the two lesions, therefore, exert a somewhat restraining influence upon each other as regards the secondary effects on the cardiac cavities directly affected. The changes in the right heart are those incident to retarded pulmo- nary circulation, and their extent depends upon which of the two lesions predominates. Symptoms. — The symptoms depend upon the degree of com- pensation, and this on whether the stenosis or the regurgitation is the gre^lter. They have been described in considering the re- spective mitral defects, and do not need to be recapitulated. Diagnosis. — The diagnosis is as a rule not difficult, for the reason that the signs of the two diseases are combined with varying distinctness in different cases. The apex-beat is not so displaced nor so forcible as in uncomplicated regurgitation, nor, on the other hand, is it so distinctly thumping as in pure stenosis, but presents the characters of both affections. There is usually a presystolic thrill at the apex, but it is less long and less intense than in stenosis alone, being commonly only a short vibration, which seems to be merely a prolongation of the apex-shock. Car- diac dulness is increased transversely, but chiefly to the right, and the pulmonic second sound is accentuated. Auscultation detects a combination of both a presystolic and a systolic murmur, the latter being well marked as a rule, and the former long and relatively pronounced, or short and difficult of 392 DISEASES OF THE HEART recognition, according to the degree of narrowing. I have some- times found in these cases that the systolic bruit is the predomi- nant one in the erect position, while in the dorsal decubitus the presystolic murmur comes out more distinctly. This is the reverse of what has been stated as the rule regarding the influence of position upon the two mitral murmurs when uncombined. I have also observed that often, when only the presystolic bruit is audible directly at the apex, the systolic murmur can be detected further to the left and on the back. Prognosis. — The prognosis is, other things being equal, rather more favourable when these two conditions are united than when either exists alone, and I believe for the reason that they tend to check each other. MITRAL STENOSIS AND AORTIC STENOSIS This is an exceedingly serious combination, since at both of the left ostia there is a mechanical impediment to the passage of blood from the pulmonary into the aortic system. The left ventricle re- ceives and discharges an abnormally small volume of blood, de- pending on the degree of constriction, and hence is a thick-walled chamber of limited capacity, while in marked contrast are the greatly hypertroi)hiod and dilated left auricle and right ventricle. Symptoms. — Symptoms appear early, and are pronounced in consequence of the great stasis within the lungs and body gener- ally. Cyanosis and dyspnea are present, often in an extreme degree, while engorgement of the abdominal and pelvic organs is shown by all of its attendant phenomena, both subjective and objective. Diagnosis. — The pulse is small, weak, and slow or acceler- ated, according to the state of compensation. The apex-beat is weak and preceded by a presystolic thrill, unless indeed it be pro- duced by the impulse of the hypertrophied right ventricle, when it may be diffused and quite strong between the sternum and left nipple. Epigastric pulsation and a marked increase of absolute and relative cardiac dulness to the right evince the secondary enlarge- ment of the right heart. There are heard a rough, low-pitched presystolic murmur at or within the apex and an accentuated pul- monic second sound indicative of the mitral lesion, and in addi- combined' VALVULAR LESIONS 393 tion, a harsh systolic bruit in the aortic area with a feeble second tone, showing obstruction at this orifice." Prognosis. — The prognosis is of necessity very unfavourable, since compensation cannot long be preserved, and when broken can be restored, if at all, only with great difficulty. MITRAL STENOSIS AND AORTIC REGURGITATION This is also a serious combination, yet the degree of its gravity is determined by the extent and predominance of the lesions. The secondary effects on the heart are those produced by ob- structed outflow from the kings and left auricle, together with such as are usually caused by reflux into the left ventricle — namely, hypertrophy and dilatation of the left auricle and right ventricle, and in the case of the left ventricle, such a degree of hypertrophy and dilatation as would follow regurgitation of a diminished volume of blood from the aorta, diminished in conse- quence of the stenosed mitral opening. In one case the mitral lesion predominates, and the effects on the heart and circulation are essentially the same as in uncomplicated mitral narrowing. In another this defect is subordinate to the aortic lesion, and the secondary changes in the heart are chiefly such as are found in aortic insufficiency. Symptoms. — The symptoms are consequently determined by the predominating lesion. In all examples of this combination there is more or less dyspnoea of effort, but when the mitral sur- passes the aortic defect in gravity this symptom is more pro- nounced. Thus I have observed two female patients with this combina- tion. In one the aortic regurgitation was plainly the greater, and she was able to take a fair amount of exercise, even slow bicycle- riding, without special discomfort. If the effort became too severe it produced palpitation and breathlessness. The other woman in whom the mitral defect predominated, and was still further com- plicated by pericardial adhesions, showed great hepatic and con- siderable general venous engorgement and complained of weakness and decided shortness of breath upon even slight exertion. Both these patients broke down their compensation while under my ob- servation, ar.d in both this rupture proved irretrievable. The lat- ter was given a course of baths, after having been confined to bed 27 394 DISEASES OP THE HEART for a number of weeks. They failed utterly to reinstate the heart. Digitalis also proved powerless. Dropsy did not appear, but the circulation became extremely feeble, temperature remained per- sistently subnormal, falling on several occasions to 96° F., and once to 95° F., dyspntea grew greater, and death took place one week after she returned to her Dakota home, under what final appearances I have not been able to learn. The other patient considered herself in usual health until mid- summer of 1901. Then, apparently as a result of the intense heat, the fatigue of a short journey, and an attack of indigestion, follow- ing a too hearty supper that same day, she began to suffer from most annoying palpitation whenever she walked .about, no matter how slowly. Weakness also set in, and with the palpitation in- creased in spite of digitalis and other therapeutic measures. These symptoms at length obliged her to keep her bed, and even then her condition grew so much worse that she was brought back to Chicago. I found her in a deplorable plight. The pulse was extremely small and weak, about 100, and the right appreciably smaller than the left. The right arm and a portion of the right thoracic wall were cedematous, in consequence of thrombosis of the external jugular, subclavian, and axillary veins. The liver was palpable and hard, but there was no dropsy of the ankles. The bases of the lungs were dull with fine crackling rales, and she coughed up bloody sputum. The right heart was much dilated, and the sounds and murmurs were feeble. She complained much of exhaustion, slept pooi'ly, and passed a scanty amount of urine containing a trace of albumin. After a time dropsy of the legs set in, and towards the close of her illness thrombosis took place in the veins of the left side of the neck, with resulting a'dema of the corresponding arm. There was nothing to indicate acute endocai'ditis, and licnce the thrombosis was ])robably due to coagulation of the blood from pressure and stasis. This very interesting phenomenon — i, e., venous throm- bosis in cases of heart-disease — has been considered more fully under Syiii])toms of Chronic Endocarditis (]). 205). Diagnosis. — The diagnosis of combined mitral stenosis and aortic regurgitation is made by the discovery of the physical signs of both lesions modified and more or less obscured by each other. COMBINED yALVULAR L?]SIONS 395 Ins'pection shows the apex-beat displaced to the left and down- ward, as in aortic incompetence, but to a less extent. If the steno- sis is considerable, and has led to right-ventricle hypertrophy, there is epigastric pulsation, and there may also be visible engorge- jnent of the superficial veins. On palpation the displaced apex-beat is found to be less forci- ble and heaving than in pure aortic regurgitation, and there is a more or less distinct and prolonged presystolic thrill, depending on the degree of mitral constriction. The characters of the pulse are also found modified. By reason of the stenosis it is small and weak, while the aortic lesion gives it a collapsing character. In one of my patients mentioned above this was fairly well marked, while in the other it was not appreciable by the finger, the pulse being distinguished by smallness and lowness of tension. In cases in which the mitral obstruction is the dominant lesion palpation is also likely to detect more or less hepatic enlargement. Percussion discovers increased cardiac dulness in all diame- ters, and is of great aid in the determination of the coexistence of these two lesions. Mitral stenosis does not cause increase of dulness to the left of the nipple ; and, conversely, aortic regurgitation does not occasion increase of dulness to the right. Yet in this combined lesion dulness is increased in both these directions. Consequently, the results of percussion taken in connection with those of auscultation are of the greatest possible importance. Auscultation. — This also furnishes valuable information, al- though it should never be relied upon to the exclusion of the sec- ondary physical signs perceived by the other means of investiga- tion. The mitral disease is shown by a characteristic presystolic murmur at the apex and by accentuation of the pulmonic second sound, the aortic insufficiency by a diastolic bruit in the aortic area or upon the sternum, and transmitted downward and to the left, while the secoild tone in the second right interspace is enfee- bled or absent. If in doubt concerning the significance of this murmur, one should auscultate the femoral artery, since when aortic regurgitation is also present there is a sharp systolic snap, and it may be also a double murmur in this vessel. Extreme mitral stenosis in its late stages may occasion pulmonary incom- petence with a diastolic bruit, and therefore auscultation of the 396 DISEASES OF THE HEART feniorals is of greatest importance in the differentiation of this iusnfficiencv from aortic regnrgitation. Prognosis. — -The prognosis depends iqxtn the degree of the two lesions and u})on which predominates ; yet, on the whole, the conrse is likely to be that of mitral stenosis. MITRAL REGURGITATION AND AORTIC STENOSIS A moment's reflection wdll convince one of the exceeding seriousness of this combination. The obstruction to the outflow into the aorta serves to intensify the regurgitation into the auri- cle, because the blood flows in the direction of least resistance, which in this case is backward rather than forward. If the steno- sis is extreme, it leads to great stasis and exerts all the local and constitutional effects of a most pronounced regurgitation. The heart becomes enlarged in its entirety, but the hypertrophy of the left ventricle, instead of overcoming the obstruction, serves but to intensify the force of regurgitation. The work of maintaining the circulation falls chiefly on the right ventricle, and as this is a thin-walled chamber, capable of but limited compensatory hyper- tro])hy, it will not long be able to keep up the unequal struggle. Symptoms are those of mitral disease of an extreme degree, and do not need to be recapitulated. Diagnosis. — The pulse is small and feeble, while its rate and rhythm are determined by the state of compensation. The apex- beat is displaced downward and outward, and relative cardiac dulness is increased in all directions. Two systolic murmurs are audible, one in the mitral area, and one in the aortic, which are to be distinguished from each other by their different points of maximum intensity, by their propagation, and by their different quality. The former, blowing and softer, is transmitted to the left, while the aortic, lower pitched and rougher, is propagated upward into the arteries of the neck. There is intensification of the pulmonic second and diminution of the aortic second sound. The chief difficulty of diagnosis does not lie in recognising the presence of the mitral insufhciency, but in determining whether or not this is relative, in consequence of dilatation of the left ven- tricle scfoTidary to the long existing aortic stenosis. Prognosis. — Under the most favourable circumstances the prognosis is grave, since the compensation on the part of the right COMBINED VALVULAR LESIONS 307 ventricle is likely to be short lived, and when once ruptnred can- not possibly be restored. jMoreover, both pulmonary and tricuspid insufficiency are likely to result when compensation fails, and then render the prognosis hopeless, AORTIC REGURGITATION AND MITRAL REGURGITATION This combination is not infrequently encountered in the late stages of aortic insufficiency when dilatation of the ventricle has led to relative incompetence of the auriculo-ventricular valve. It may, however, be seen as a combined lesion when both defects are the result of structural alteration. The combination is a grave one, and yet, as stated by Bacelli, a double regurgitation of the kind under discussion does not begin to be so serious as obstruction at the aortic and leakage at the mitral ostium. Symptoms. — The influence of the mitral lesion is to lessen the effect of the aortic regurgitation on the general system, since a part of the blood intended for the aorta is diverted into the auri- cle, and the arterial system is not so violently distended by each blood-wave. Arterial tension does not present such a striking con- trast during systole and diastole as in uncomplicated insufficiency of the semilunar valve. Tor this very reason, however, the arte- rial blood-supply to the various organs and tissues is diminished, and there is marked arterial ansemia. In addition there are the symptoms of venous congestion, only limited by such capacity for compensatory hypertrophy as resides in the right ventricle. The heart is likely to attain enormous size, as shown by the position of the apex-beat far to the left of the nipple and downward, and by great increase of both relative and absolute cardiac dulness. Diagnosis. — This is not usually a matter of much difficulty. The pulse is small yet collapsing, and there is increased dulness both to left and right. Auscultation reveals both a basic diastolic and apex systolic bruit, with feebleness of the aortic second ac- centuation of the pulmonic second, and often absence of the sys- tolic sound at the apex. Inspection and palpation disclose passive congestion of the venous system and abdominal viscera. In ease the diastolic bruit is likely to be thought a mitral diastolic one, 398 DISEASES OF THE HEART its real nature may be ascertained l)_v auscultation of the femoral arteries. Prognosis. — When the combined defects are both primary, a fair degree of compensation may bo attained and preserved for a time. When, however, cardiac adequacy is once seriously im- paired, there is but small prospect of its restoration. If the mitral leak is secondary, it indicates such a grave loss of ventricular tone as to make practically h()i)eless the possibility of again closing up the mitral orifice by treatment, no matter how skilful and ener- getic it may be. This was shown by the history of the cases nar- rated in the cluipter on Aortic Regurgitation. AORTIC STENOSIS AND AORTIC REGURGITATION This combination is not very infrequent, but does not exist so often as the diagnosis is made. This holds true particularly with regard to cases of aortic incompetence. The rough systolic mur- mur so commonly heard in persons who present unequivocal signs of free regurgitation through the aortic ostium leads most inex- perienced auscultators to conclude that there must also be stenosis. This inference is erroneous, however, as shown by necro])sies. Vegetations about the orifice, the ragged and stiff leaflets, athero- matous patches on tlie surface of the aortic intima, are all capable of throwing the blood-stream into audible vibrations as it passes through the ring without in the least acting as an obstruction, an important fact in its bearing on the clinical features of the case. In predominating aortic stenosis, on the other hand, some de- gree of regurgitation is very likely to occur, as has been stated in the chapter dealing with obstruction at this orifice. The thicken- ing and rigidity of the valve flaps, wliich ])revent their being thrown widely open by the emerging stream, also intcn-fere with their complete closure as ventricular contraction ends. T Fence a ])(»rtion of the blood-wave finds its way l)ack into the ventricle. In other cases one of the cusps may be fenestrated, or for some other reason incompetent, Avhereas its fellows are not, being only incapa- ble of opening in a normal manner. Symptoms. — The -symptoms produced by combined aortic stenosis and regurgitation partake in cliaracter and gravity of the features which are special to the predominating lesion. If incom- petence is the greater, compensation is possible for years without COMBINED .VALVULAR LESIONS 399 the individual being made aware of its presence. If stenosis pre- dominates and is pronounced, the left ventricle is not likely to establish such a degree of hypertrophy as will maintain complete adequacy for very long. The reflux, even if slight, as measured by actual quantity, is yet sufficient to cause more or less dilatation of the chamber, and hence the driving force of its wall is impaired. Consequently, the patient is more apt to notice some breathlessness and perhaps palpitation under conditions that ought not to affect him were either stenosis alone or regurgitation alone the lesion. Physical Signs. — The physical signs are modified also by this combination, and display in varying proportion the characters of each defect. Thus the pulse is neither so large and collapsing as in pure aortic regurgitation, nor so small and slow as in uncompli- cated stenosis, but is collapsing and also small. Capillary pulsa- tion and Duroziez's double femoral bruit are either absent or very imperfectly obtained. The impulse of the heart against the chest-wall is not so forci- ble and extensive as in free regurgitation, and the apex-beat in size and displacement partakes rather of the character of stenosis. Hypertrophy of the left ventricle is more apparent than is its dila- tation, with thickening. The hand is very apt to perceive a systolic thrill in the aortic area, and percussion demonstrates that the heart is not so large as in uncombined aortic insufficiency. There are two murmurs, of which the systolic is likely to be intense and rasping, wdiile the diastolic is of inferior prominence in all respects. The sounds normally heard in the second right interspace and in the cervical arteries are likely to be absent and replaced by murmurs. Diagnosis. — The diagnosis of this combination is as a matter of fact very difficult, and it is often impossible to determine defi- nitely whether both conditions are united or not. This is emphat- ically true if the case is seen for the first time after compensation has failed. Relative mitral insufficiency or pronounced feeble- ness of the left ventricle may then modify the pulse, sounds, and murmurs in the manner just described. However, if the fem- oral artery is auscultated, and the left side of the heart is accu- rately outlined by percussion, Duroziez's sign will declare the freedom of the reflux, and percussion will demonstrate the enor- 400 DISEASES OP THE HEART mous enlargement of the left ventricle secondary to free regurgita- tion without obstruction. A moderately slow, small, yet collapsing pulse, a vigorous, rather circumscribed, not greatly displaced apex-impulse, a systolic aortic thrill and bruit without powerfulh' throbbing and thrilling cervical arteries, absence of double femoral souffle, and no de- monstrable capillary pulse — these signs, together with a regurgi- tant murmur, would justify the conclusion that stenosis and insuffi- ciency coexist, but that the former probably predominates. The sphygmograph ought to show the rounded summit and anacrotic notch of obstruction and the ill-sustained down stroke of regurgi- tation (see Figs. 54 and 66). Prognosis. — The prognosis of this double defect is certainly far from favourable, either as to length of life or as to restora- tion of heart-power, when this has once given way. This certainly applies to ju'onounced stenosis with regurgitation, whereas it is conceivable that a minor degree of narrowing might, by rendering regurgitation less free, serve to protect the wall of the left ventricle against the speedily damaging effects of free reflux through a widely patent orifice. CHAPTER XV THE PROGNOSIS OF VALVULAR HEART-DISEASE IN GENERAL Something has been said already on the subject of prognosis in the chapters devoted to the individual valve-lesions, and there- fore some repetition will be unavoidable. In attempting to fore- cast the course and termination of a given case one should con- sider (1) the special characters of the lesion, (2) the degree of the secondary effects in the heart and other organs, and (3) extraneous factors of age, temperament, environment, etc. The characters of valvular disease which influence prognosis are its nature, location, and degree, and these cannot always be considered separately. As a general proposition, it may be stated that stenosis is a more serious defect than is regurgitation, and yet its gravity depends largely on its location. Furthermore, the amount of disturbance to the circulation is determined so much by the degree of the local defect that this latter may render most serious a valvular disease, which from its nature and situation alone would ordinarily furnish a more favourable prognosis. In fact the forecast is so largely based on the conditions of each case that one would go far astray if he were to be guided by general principles alone. Although aortic insufficiency is to be ranked first as regards gravity, still a distinction should be made between cases originat- ing in the young in endocarditis, commonly rheumatic, and those of atheromatous origin, observed at or beyond middle age. In the former group great compensatory hypertrophy and a healthy heart-muscle may enable the organ to functionate adequately for many years, far longer indeed than do many cases of mitral dis- ease, although in itself this latter is considered a less serious lesion. On the other hand, when aortic incompetence is due to a sclerotic process, the myocardium is rarely healthy and compensa- 401 402 DISEASES OF THE HEART tion is short lived, or indeed is never perfect. In snch a case prog- nosis is grave from the start. It is in this particular lesion that sudden and unexpected death is likely to take place. Indeed, it is almost the only valvular disease which so terminates, since when death occurs unexpectedly in other defects it is very exceptionally instantaneous, and then is the result of some accident, such as em- bolism, or it terminates weary weeks or months of failing heart- power. In aortic regurgitation it is not very rare for patients to fall dead unexpectedly in the midst of apparently good health. When- ever compensation shows unmistakable signs of failure, sudden death in this disease is not a very remote possibility. Moreover, compensation may be broken at any time by a rheumatic attack, and once impaired it is rarely restored. Absence of the aortic second sound and dilatation of the left ventricle are therefore prognostically grave, since they indicate free reflux and feeble ventricular resistance. Stenosis of the aortic ring presents a less grave prognosis than does regurgitation at this orifice. The reason for this difference is to be found in the effect of the two lesions on the wall of the left ventricle. A narrowing of the outlet leads to hypertrophy with relatively little dilatation, unless of course the obstruction be so pronounced that the chamber is unable to empty itself during sys- tole, and stasis results behind the point of constriction. So long as the hypertrophied ventricle is able to discharge its contents with each contraction, and the effect of the lesion is limited to the ven- tricular wall, the prospect of a continuance of life for many years without distressing symptoms, and even of death at the end through some intercurrent affection, is good. When, however, compensa- tion in this disease is once destroyed, there is small likelihood of its repair, and the prognosis becomes very serious. Yet in this, as other lesions, it is its severity, even more than its nature and loca- tion, which determines the degree of its seriousness. An extreme stenosis as regards length of life is even worse than free regurgi- tation. When the two lesions are combined the prognosis is as a rule more unfavourable. Of the two mitral defects, it is generally conceded that stenosis is the more serious. One reason for this is that the disease is not stationary, but tends to grow more pronounced in consequence of PROGNOSIS OF VALVULAR* HEART -DISEASE IN GENERAL 403 contraction of the newly formed fibrous tissue and of the increase of fibrine deposited upon the vegetations. ^ Another reason, as we shall see later on, lies in the greater intensity of the secondary effects on the heart. Mitral regurgitation, on the other hand, is under ordinary circumstances the most favourable of the four lesions situated in the left heart. When the leak is not too free and there are no serious complications, such as aortic stenosis and ad- herent pericardium, the defect in question is not incompatible with long life and great mental and bodily vigour. It is possible, how- ever, for the regurgitation to be so free that this relatively benign disease is thereby converted into a very serious one, Leyden states that sudden death occurs in only 2 per cent of mitral disease. With the exception of relative tricuspid in^ifficiency, diseases of valves of the right heart are so infrequent that nothing needs to be added to what has been said already concerning their prognosis in the respective chapters. Incompetence of the right auriculo-ven- tricular valves secondary to other diseases is generally regarded as of serious import, not because it threatens life directly, having, as it is said, a safety-valve action, but because it indicates serious dis- proportion between the degree of the primary disease and the strength of the right ventricle. If it occurs with anything like the frequency claimed for it by Gibson, then one should not attach to it a very unfavourable prognosis. ]S[evertheless the degree of importance to be attributed to it depends much on the nature of the primary affection. If it be secondary to vesicular emphysema or to valvular disease of the left side of the heart, as pronounced mitral stenosis, the development of tricuspid regurgitation must be looked upon as an omen of impending disaster. This form of tricuspid disease cannot be regarded as a separate and independ- ent affection, and therefore should be classed among the secondary effects of valvular disease, which are now to be discussed in their bearing on prognosis. From the foregoing it is evident that although the nature and seat of valvular defects influence their prognosis, yet it is their intensity to which we must chiefly look when directing our attention to the heart. It has been distinctly stated in previous chapters that in estimating the extent of a valvular defect one must not rely upon the intensity of the murmur, but upon the evi- dences of disordered circulation. These are the secondary effects 404 DISEASES OF THE HEART or signs which are of such vahie oftentimes in making a diagnosis as Avell as in stating the prognosis. One reason for the grave outlook in cases of mitral stenosis is the fact that this defect occasions widespread stasis in the ves- sels of the pulmonary and venous systems, while the diminished supply of blood to the left ventricle leads to shrinkage in the size of this cavity. If the left auriculo-ventricular opening has become greatly reduced in diameter, no amount of vigour of the left auri- cle and right ventricle can maintain the equilibrium of the blood- stream. It is only a matter of time when the pulmonary system and right heart, systemic veins, and abdominal organs are bound to become engorged. In mitral incompetence, on the other hand, the left auricle and pulmonary veins may be able to bear the brunt of the regurgitat- ing stream for a long time. Moreover, the left ventricle undergoes hypertrophy, and forcibly ejects into the aorta all that portion of the blood that does not escape into the auricle. There is not so marked a tendency to disturbance of general nutrition. Yet, of two typical cases of mitral disease, the one constrictive and the other regurgitant, if the former with its natural tendency to greater stasis actually displays less pronounced secondary effects, it offers a better rather than a graver prognosis, because compensation is complete. The general venous stasis in the regurgitant case evinces either such a freedom of reflux that the parts behind could not long withstand it, and compensation was necessarily lost, or that compensation was not able to take place at all. Even if treatment should succeed in reinstating the circulation, still the fact of compensation having once been lost would render the prog- nosis worse than it would be in the case of stenosis in which com- pensation had never been impaired. Again, comi)are a case of perfectly compensated insufficiency of the aortic valves with one of extreme narrowing of that orifice in which dilatation of the left ventricle is beginning to outbalance the hypertrophy, and signs of stasis are appearing in the pulmo- nary and general venous systems. In one, secondary effects are limited to the licart and shown l)y tlic ad jusfiiu'iit of the left ven- tricle to the altered conditions. In the other they have jiassed beyond the heart and invaded the remainder of the circulatory apparatus. It is ]jlain tliat here the degree of the lesion has re- PROGNOSIS OF VALVULAR JIEART-DISEASE IN GENERAL 405 versed the usual order of things as respects the prognosis in these two valvuhir defects. The foregoing remarks show how unreliable would be a prog- nosis in valvular heart-disease, which was not based on a careful study of the extent, even more than the nature and location, of the particular defect, and that individual cardiac conditions deter- mine the relative gravity of each case. jSTevertheless, I must re- peat that my experience leads me to agree with Broadbent in the opinion that, generally speaking, aortic regurgitation is the most serious and mitral regurgitation the most favourable of the four valvular diseases of the left heart. The two stenoses occupy an intermediate position, and of these, mitral constriction is the graver. This subject is still further complicated by the consid- eration that there are still other factors that must be reckoned with. For the most part these are of minor importance, and yet some of them make strongly for or against an encouraging forecast. Complications. — The gravity of any valvular defect is neces- sarily enhanced by the existence of complications, although to what extent is determined in great measure by the nature of the complication. Intercurrent acute disorders, which act as compli- cations while they last, are considered by themselves. Here are discussed only such chronic local alterations and diseases of other viscera as must of a necessity unfavourably affect the course of valvular lesions. Pericardial adhesions, whether strictly internal or such as bind the heart to some of the surrounding parts, cer- tainly exercise a malign influence, since they interfere more or less seriously either with the establishment or the maintenance of ade- quate compensation. Their effect is specially detrimental if by fixation of a chamber in the state of dilatation they prevent its reduction and efficient hypertrophy. I have seen this more than once exhibited in a case of mitral incompetence in which fixation of the left heart threw extra strain upon the right ventricle, as evinced by its ready dilatability. When a chronic adhesive medi- astinitis holds the right heart adherent back-pressure on the two cav?e and liver is increased. The pseudo-cirrhosis of the liver leads in time to obstinate ascites, and patients succumb to the hepatic complication long before they would be likely to die from cardiac inadequacy alone. Moreover, an adherent pericardium •106 DISEASES OP THE HEART nut infrequently renders futile therapeutic efforts which prove highly efficacious in cases without such complication. The association of two or more valve-lesions affects prognosis, not by shortening life necessarily, although such is likely to be the effect, but by rendering impossible the development of perfect compensation and compelling extraordinary carefulness, lest what small measure of compensation already exists be broken down alto- gether. The reader will find more on this subject in the chapter on Combined Valvular Lesions, It goes without saying that chronic nephritis is a very grave complication, Not only does the renal act badly on the cardiac affection, but this latter, by lowering blood-pressure in the renal arteries, intensities the insufficiency of the kidneys. The evils of uraemia are then likely to be added to those of defective circula- tion. The chronic nephritis renders it unlikely that the patient will live out the term of years that would naturally be granted him by his valvular defect alone. The kidney complication also ren- ders less availing all attempts to remove dropsy whenever it appears. Pulmonary tuberculosis is not often seen in combination with valvular disease, excepting of course pulmonary stenosis. When it occurs, however, I believe it enhances the gravity of prognosis, for I cannot see how they can fail to react injuriously on each other. Anything which, like valvular disease, impairs nutrition must nec- essarily lessen the likelihood of successful resistance to tubercu- losis, while the destruction of hmg-tissue must seriously affect the already damaged heart. Harmful blood-states, as chlorosis and anoemia, affect progno- sis in proportion to their severity and their amenability to treat- ment. Rheumatic Diathesis — Some individuals display a marked tendency to rheinuatic attacks, either acute or subacute, and every now and then suffer from pains in shoulder, wrist, or other joints. In such the outlook is not bright, for the reason that any one or all of these mild attacks may be attended by fresh endocardial inflam- mation either of the same or other valves, or that pericarditis may develop. Even if an active endocarditis is not excited, the changes already set up in the valves may be rendered progressive. Conse- quently, a case furnishing favourable prognosis originally may be PROGNOSIS OP VALVULAR HEART-DISEASE IN GENERAL 407 converted into one of a most serious nature. In a word, therefore, recurrences of rheuniatisiii, n(^ matter how mihl, are to be regarded as affording a glo<»my prognosis in any case of valvular disease. Digestive and Bronchial Disorders. — These, like rheumatism, yet in a different way, are capable of unfavourably affecting prog- nosis. Disturbance of the digestive function is not infrequently observed in victims of valvular disease in whom careful examina- tion fails to detect signs of secondary effects in other organs. The chylopoietic viscera may have their function impaired by lack of arterial blood of good quality, cardiopaths being often anaemic, or in aortic cases by a defective flushing with arterial blood, or in mitral patients by passive congestion, this last being too slight to be recognised by ordinary means of examination. Whether the indigestion is owing to such causes or is the result of improper food or faulty habits in eating, it is likely to impair general, and hence cardiac nutrition, and thus render prognosis less encour- aging. A tendency to acute bronchial catarrhs in mitral patients not only evinces greater pulmonary congestion than is otherwise appar- ent, but also renders them liable to an attack of bronchitis, which may at any time severely strain compensation. In them, there- fore, prognosis cannot be looked upon as so favourable as if they were less sensitive to atmospheric changes and did not so easily get up a cough, for the severe expiratory effort of coughing sub- jects the right ventricle to added strain. Age. — The prognosis of valvular disease is more serious at either extreme of life and most favourable in young adults. In elderly individuals the myocardium is apt to be more or less degen- erated, and although, as Leyden believes, compensation is often as perfect as in the young, it is more easily destroyed. Further- more, the sclerotic process, which is usually responsible for the valvular defect, is progressive, and one possesses no means of fore- casting whether these changes will progress slowly or rapidly. I recall the instance of a gentleman of sixty- four in whom I detected signs of aortic sclerosis and probable coronary sclerosis in explana- tion of his attacks of angina without any evidence of valvular in- competence or of stenosis. Yet at his death, less than three years subsequently, the autopsy disclosed, I have been informed, well- marked insufficiency of the atheromatous aortic valves, signs of 408 DISEASES OF THE HEART the lesion having developed and been detected by his physician some months prior to his death. The gravity of the prognosis in childhood is attributable to a variety of canses. In the first place, the heart-muscle, although free from degenerations, is easily exhausted. The chest is small and affords scant room for the often enormous hearts observed in children with long-standing valvular disease. Any one who has seen much of valvular disease in children must have observed that they are strikingly unconscious of symptoms which in adults occa- sion complaint. They are highly sensitive to pain, yet appear to pay no attention to palpitation and shortness of breath during play ; although the onlooker may observe tumultuoTis action of the heart, hurried breathing, and cyanosis. Children are therefore very likely to overstrain their already damaged hearts ; and that this does not occur more frequently is quite remarkable. These little ones are excitable and emotional, and therefore unable to exert the self-control so often necessary for the preservation of compensation. They often display astonishingly vigorous appe- tites and overload their stomachs with the sweetmeats and dainties they crave, and are permitted by indulgent parents to have. These ferment with the formation of gas, which, distending the digestive organs, causes them to crowd upward upon and still further em- barrass the heart in its action. Lastly, rheumatism in childhood is so insidious and atypical that it is very frequently overlooked. Prompt and efficient treatment is not instituted, and this disease being frequent in early years of life excites fresh attacks of endo- carditis, lights up a pericarditis, or renders existing valve-lesions progressive. Mitral stenosis in young children is particularly un- favourable. It may be briefly stated that valvular disease at this period of life is very likely to end fatally before the patient reaches adult age either directly or tlirough complications. Temperament. — This possesses a not unimportant relation to the prognosis of the diseases now under consideration. The pa- tient who is impulsive, impetuous, and thoughtless is like a child unaccustomed to self-control, and if required to exercise self-re- straint frets and chafes in spirit. Such a person will be forever committing indiscreet acts, and will only acquire with difficulty that patience and equipoise of spirit whicli serve as ballast to damaged hearts. Individuals given to outbursts of anger, to PROGNOSIS OF VALVULAR HEART-DISEASE IN GENERAL 409 worry, to fretting over trifles, and who appear never to become reconciled to their physical disability, can never be expected to retain their compensation so avcII or so long as will those who always have themselves well in hand. Verily, all cardiopaths should bear in mind that Bible utterance, " He that ruleth his own spirit is greater than he that taketh a city." Sex. — Mitral disease, and in particular mitral stenosis, is more frequent in the fair sex, while men are more subject to aortic in- sufficiency. In a sense, therefore, sex may be said to exert a gen- eral influence upon prognosis. The inquiry that now concerns us is how does sex affect the prognosis of a given valvular lesion after it has once been established, without reference to its nature. In other words, what is the relative prognosis, ceteris 'paribus, of the same defect in the two sexes. This is a very difficult matter for decision, since it involves questions of habits, occupation, etc. Females are exposed to certain perils of pregnancy and child- bearing, while, on the other hand, men have to encounter even greater dangers incident to occupations that often produce cardiac overstrain. The reader will find these influences discussed at some length in the chapter on Treatment of Valvular Disease in Gen- eral. One respect wherein women usually furnish a more favour- able prognosis than do males is that of habits — that is, a greater freedom from the injurious efl^ects of excess in tobacco, alcohol, and venery. Women are generally held to be more emotional and excitable than men, yet in the matter of self-control they seem to me to possess an advantage over their brothers. The most marked instances I have ever seen of apprehension — nay, of alarm and nervous agitation — lest the examination result in the discovery of a heart-lesion, have been in young men. The female sex is more prone to anaemia and chlorosis, and the injurious influence of these blood-states is too well knowm to require more than this passing reference. In most other respects I think the question of sex re- solves itself into that of the individual. Occupation. — This exerts a powerful influence upon prognosis. The day labourer who earns his daily bread by the sweat of his brow cannot be expected to keep his compensation intact for so long as will he whose vocation does not subject his heart to the possibility of overstrain. All authors are agreed in the declaration that nothing in the daily life of these patients affects their hearts, 28 410 DISEASES OF THE HEART and hence the prognosis, more disastrously than does severe and prolonged or too oft-repeated physical exertion. This is particu- larly true of mitral narrowing, even in the stage of compensation. Patients with well-compensated insufficiency of the aortic valves may endure overstrain for a time without apparent injury ; but so soon as dilatation of the left ventricle has begun to gain the as- cendency over hypertrophy, a continuance of the strain will in- evitably result in a breakdown, and that too at no very distant date in most instances. Habits. — These are matters of utmost importance if the lives of patients with valvular disease are to be prolonged. They should be minutely inquired into, therefore, by the medical at- tendant. The daily life of these sufferers should be ordered on the principle of moderation in all things. Whatever is injurious to a healthy person is doubly so to one wdth an unsound heart. Consequently a prognosis which, as regards everything else, may be good, may be rendered very uncertain, if not actually bad, by the discovery of evil practices. By these are meant particularly excess in tobacco, alcohol, or other narcotics, and in sexual in- dulgence. But patients may also increase the gravity of prog- nosis by gluttony, loss of sleep, exciting novel reading, gaming, etc. — in short, by whatever promotes nervous and cardiac ex- citement. Home Surroundings. — These include all those n^atters of sanita- tion, as dampness, sunshine, ventilation, drainage, the ability to obtain suitable food and clothing, freedom or not from domestic worry and annoyances, opportiniity for recreation, etc. — in a word, the residential and social conditions which in all of us make for happy, contented lives. The prognosis in the case of the poor man cannot be expected to be as good as that of him w^ho is able to command everything that can minister to his comfort and well-being. If, e. g., a pa- tient with mitral stenosis or a failing aortic insufficiency is com- pelled by the exigencies of his purse or environment to labour or to ascend wearisome flights of stairs or steep acclivities upon re- turning to his home, no matter how often this may be, he can hardly be expected to keep this up without eventually suffering injury. These and many other matters may seem too obvious to require mention, and yet they are details which the physician PROGNOSIS OF VALVULAR HEART-DISEASE IN GENERAL 411 must take into consideration if he would, form a reliable prog- nosis. The Probable Effect on the Patient of the Knowledge of his Lesion. — This is a matter, in my opinion, having a decided bearing on prognosis, and which, therefore, should be discussed. Physi- cians and the laity generally believe a cardiopath must not be informed of the fact when he is found to have a cardiac defect, lest he be alarmed and become morbid and introspective. Doubtless there are many nervous, apprehensive persons who would be harm- fully affected by such knowledge. When such is the case I believe it renders prognosis less favourable, because if kept in ignorance of his true condition he is not prepared to avoid whatever may be harmful. If detrimental influences are to be shunned, patients must have explained to them how and why these are injurious to them, since the doctor's dictum in this regard is not enough for an intelligent person. Kept in ignorance or put off with an evasive answer, he may be set to pondering and conjecturing, and hence to fancying his condition is worse than it really is. I be- lieve, therefore, that it is a positive gain to a cardiopath to acquaint him wath at least a part if not all of the truth. Of course he does not need to be informed with brutal abruptness, but gently and in a manner calculated not to frighten him unduly. The individual who cannot bear even a part of the truth without detriment will assuredly furnish a less favourable prognosis than he who, know- ing the truth, accepts it philosophically, and determines to make the best of a bad bargain. The Effect of Digitalis on the Patient. — It goes without saying that when valvular disease has reached such a stage as to necessi- tate the administration of digitalis the prognosis is not good even at the best. Thus much any one knows, but only a few, if any, are able to prognosticate how much longer the heart is going to bear up, even sustained by such a prop. In such a case, as pointed out by Leyden, a certain degree of information may be derived from a study of the effect of the remedy. If the beneficial action of digitalis is quickly lost after its administration has been discontinued, and the heart manifest its need of this tonic by a speedy return of symptoms, the prognosis is serious, for it indicates myocardial inadequacy. It is a still more unfavourable indication if from time to time the dose of 412 DISEASES OP THE HEART digitalis has to be increased to maintain its effect, for it points to the not distant arrival of a time when the heart will cease to respond to the remedy, and the end will not be far to seek. The Relation of Prognosis to Life Insurance. — There was a time when an individual with valvular disease was rejected indiscrimi- nately by all insurance companies. In England, and by some com- panies now in this country, some of these patients are accepted as " defective risks,"' and therefore it is in order to discuss this sub- ject in this place. There are two classes of persons with valve- lesions whom I would reject except possibly for a very limited term of years, and only then at so high a premium as to make it almost prohibitive. These are cases of pronounced mitral steno- sis and insuthciency of the aortic leaflets. Even when the latter appears compensated there is always the possibility of sudden and unexpected death, which, as already stated, renders prognosis very uncertain. Stenosis of the left auriculo-ventricular orifice is pro- gressive, and how rapidly this tendency will declare itself no one can foresee. On the contrary, mitral regurgitation, and to a some- what less degree aortic stenosis, may sometimes be considered rea- sonably safe risks as defectives. It will be noted that I say some- times. This is because, no matter how excellently the lesion may be compensated, there are circumstances of individuality or en- vironment which determine prognosis adversely. Therefore the examiner should consider exhaustively and intelligently all those factors which have a bearing directly or remotely on the prospect of the patient living as long as the characters of his disease might be expected to allow. Laborious occupations and bad habits are, in my opinion, a bar to safe insurance of these risks. On the other hand, a robust young man who knows that his mitral valves leak, and who is determined to order his daily conduct in a manner cal- culated to afford his heart the very best chance of carrj'ing him through to midille or advanced age, may often ])rove a safer risk than many another sound man who banks on his fine health and splendid physique. CHAPTEE XVI THE TREATMENT OF VALVULAR HEART-DISEASE Feom a therapeutic standpoint, cases of valvular disease are to be divided into three classes, according to the state of compensa- tion: (1) Those in which the lesion is compensated, (2) in which compensation is incomplete, and (3) in which cardiac inade- quacy is so pronounced that compensation is wholly wanting. We call a valvular defect compensated when the cardiac pump, in spite of its defect, is able to maintain the circulation in nearly or quite its normal state, and there are no symptoms to make the patient aware of his malady. Under such circumstances laborious occuj^ations, athletic exercises, and games or outdoor sports re- quiring considerable strength and agility are endured without more breathlessness or palpitation than are usual with persons having sound hearts. In the second class, patients are still able to perform their daily duties and engage in some of the less severe sports, but it is with more or less distress and evident signs of heart- strain. There are different degrees of imperfect compensation in this class, and hence it is one of wide limits. In the third class, in which compensation is wholly lost, patients are not only inca- pacitated for physical exercise, but the circulatory disturbance is shown by stasis, generally by oedema, and by subjective symptoms that are present even when the patient is at rest. When compen- sation is perfect, examination of the heart discloses the existence of a lesion, but no secondary effects in the general circulation. In the second class signs of more or less visceral and venous conges- tion are detected, although subjective symptoms may be insignifi- cant, and in the third these reach their severest grade. It is evi- dent, therefore, that treatment appropriate to the last stage is not indicated in the first. ISTeither do patients whose compensation is still maintained intact require the same strict management as do those who are beginning to manifest failing heart-power. Conse- 413 414 DISEASES OP THE HEART qiieiitlv, ill dealing with the inanagemeiit of valvular heart-disease, I shall consider it with reference to the three divisions just made. I. COMPENSATION BEING STILL PERFECT The object of management in this stage is the maintenance of cardiac power. Occasionally a j)atient with valvular disease seeks medical advice for the purpose of learning how he can preserve his heart in statu quo. As a rule, however, such a compensated lesion is discovered accidentally by the physician, wdio is then confronted by the query whether in case the patient is ignorant of his heart- disease he should be informed of it or not. I hold that in such a case the answer must depend upon the circumstances of the case, such as the temperament of the individual, his habits, and the nature of his employment and manner of life. If the knowledge that he has heart-disease is likely to frighten him and render him introspective, then the knowledge would better be withheld, unless, of course, he is leading a kind of existence calculated to break down his compensation. Under such circumstances it may be nec- essary, and the part of wisdom, to inform him that his heart is not sound, and is likely to be damaged by his manner of living. In such an instance, however, the information should be imparted in a manner not calculated to create needless alarm. If the individ- ual is reasonable and cool-headed, particularly if his pursuits are active, I believe he should be jilaiiily told of the existence of his valvular defect, for, other things being equal, the knowledge by a person that he has a locus rninoris resistentltv is likely to make for a longer lease of life. Since, then, the aim of management in this stage is to preserve compensation, the physician must concern himself with the minut- est details of the patient's daily life. lie would take a narrow view of a case indeed who contented himself with the (piestion of medicinal treatment. Conipcnsdtcd valve-defects require not dr)i(js, hut instruction upon the following points: Exercise. — It may be laid down as a general pro])osition suit- able to all forms of compensated valve-defects that when any kind of exercis(! does not produce sym])toms of cardiac strain it may be l)ermitt('(l. Indexed, as will be seem later on, judicious exercise j)roiii(it('s conipensatory hyjx'i'lrophy in some forms of valvular dis- ease. I'here are other lesions, however, which by their very nature THE TREATMENT OF VaLVULAR HEART-DISEASE 415 are theoretically likely to and often actually do suffer injury in time from severe bodily exertion. This statement applies particu- larly to cases of mitral stenosis. If the left auriculo-ventricular opening is but slightly constricted, considerable, even severe physi- cal effort may be endured without symptoms, but as a rule some shortness of breath is experienced, and patients should be explic- itly warned against persisting in their exertion when dyspnoea is felt. The effect of muscular contraction and deepened respiration incident to exercise is acceleration of the flow of venous blood to the right heart and lungs. If the blood cannot readily pass the mitral ring, it becomes dammed back in the left auricle and pul- monic veins, engorging and overstraining the right ventricle. This may resist the stress for a time, but if the strain is too prolonged or too frequently repeated the cardiac walls finally yield and the hypertrophy, upon which adequate compensation depends, is su- perseded by dilatation. Therefore, patients with pronounced mitral stenosis, even when compensated, should be cautioned against violent, prolonged, or too oft-repeated exercise of a severe kind. Hurrying up stairs or hills, running, and even very rapid walking, fast bicycle-riding, sports and games that necessitate run- ning and springing without frequent pauses to permit recovery of breath — e. g., furious sparring, wrestling and fencing, lawn-tennis, basketball, and the like — are among the kinds of exercise particu- larly likely to harm patients with mitral stenosis, even when com- pensated. On the other hand, if they indulge moderately, they may enjoy rowing, paddling, and bowling. Billiards, golf, and croquet are specially suited to them, while some may be permitted to hunt, and nearly all to fish. When the constriction is not pro- nounced, gentle horseback riding, slow bicycling, and even the lighter kinds of gymnasium work are permissible. In specifying the kind of exercise and sport to be allowed, the physician should always bear in mind the personal equation. The degree of the lesion and the gravity of its secondary effects, even more than the nature of the lesion, determine the patient's ability to endure exer- cise without harm. The individual temperament, judgment, and power of self-restraint are also of great importance. The physi- cian must endeavour to inform himself as accurately as possible regarding the effect of any given kind of exercise on the particu- lar patient before coming to a decision. 416 DISEASES OF THE HEART What lias been said of mitral stenosis applies also to cases of aortic obstruction when this is pronounced. Slight narrowing of this orifice is often compatible with great muscular exertion and active exercise. When, however, compensation is once broken in these cases, it is repaired with difficulty, if indeed at all, and there- fore good judgment and careful study of each case are essential to a wise decision. In these cases exercise should not be carried to the production of palpitation, particularly prolonged palpitation. The wall of the left ventricle is susceptible of far greater hyper- trophy than is that of the right; besides the effect of an aortic stenosis is confined for a time at least to the ventricle, and does not embrace the thin-walled auricle, and consequently exercise is likely to be better endured than when the obstruction is at the mitral opening. The next in order on an ascending scale, as regards its ability to withstand the effects of exercise, is mitral regurgitation. In this disease, owing to the circumstance that during diastole there is no impediment to the filling of the ventricle, and notwithstanding that a portion of the blood gushes back during systole into the auri- cle, there is not the same degree of engorgement in the parts back of the seat of lesion as in mitral constriction. Of course the meas- ure of the heart's resistance is governed by the degree of the incom- petence and, as in all valve-lesions, by the state of the heart-muscle. If the leak is very free, compensation is not so apt to be complete as when the regurgitation is insignificant. In cases of well-com- pensated insufficiency of the mitral valve continued and severe exercise may often be indulged in without the production of an- noying symptoms. This statement applies to the rheumatic rather than the atheromatous form of the lesion. I know an attorney who, fifteen years ago, when a growing lad, had a pronounced though perfectly compensated mitral insufficiency, and who played lawn-tennis enthusiastically without any other discomfort on the part of his heart than the consciousness of rapid, strong beating of the organ. Despite frequent injunctions to the contrary, he con- tinued to indulge in this sport during several years, and is now reported to be so well that lie does not know he has a heart. An- other of my patients, a mercliant past thirty, with a mitral incom- petence in a state of admirable compensation, is much given to sparring and broadsword practice, which, he declares, never gave THE TREATMENT OP VALVULAR HEART-DISEASE 417 him any shortness of breath and only a rapid heart-action, that subsided so soon as the exertion ceased. " Such instances are not rare, and yet severe physical efforts are not without danger to these patients. Such as are fond of manly sports should be advised of the pos- sibility of cardiac overstrain, and told to desist when excessive palpitation or pronounced dyspna^a is experienced. They feel the better for a certain amount of outdoor exercise, and when young and vigorous in other respects their heart-muscle, like their skele- tal muscles, is likely to grow soft and weak if debarred from ath- letic sports altogether. Other things being equal, the state of the voluntary muscles is a fair index to the condition of the cardiac muscle. Of two individuals with well-compensated mitral leakage, one with well-knit muscles trained to exercise, the other unaccus- tomed to outdoor sports because of sedentary ^^ursuits, the latter may break down his compensation by some effort which would be no more than child's play to the former. It is probable that per- sons with mitral regurgitation would be more likely to suffer injury from long running than by games that necessitate intermit- tent and short spurts of speed or strength. Mountain-climbing, boat-racing, and other forms of contest or strength, which experi- ence has shown cause dilatation of healthy hearts, will bring about overstrain of diseased ones more readily and surely. As a general rule cases of aortic regurgitation should be placed at the top of the list as regards endurance of exercise without injury. This statement does not apply to persons who have ac- quired their aortic incompetence after the age of forty, and there- fore probably as a part or manifestation of a sclerotic process that may have invaded the myocardium also. In such, even when com- pensation is still maintained, exercise should always be moderate. The salvation of patients with this lesion depends on hypertrophy of the left ventricle. The great Stokes recognised this fact, and accordingly used to recommend active physical exercise to patients with this form of valve-disease. Von Ziemssen has stated that upon one occasion, when visiting Stokes in Dublin, the latter directed his attention to a man running along the street behind his wagon, and said that he was one of his patients with aortic insuffi- ciency who was carrying out this kind of exercise at his (Stokes's) advice, for the purpose of developing left ventricle hypertrophy. 418 DISEASES OF THE HEART Another of Stokes's patients with the same lesion was a farmer who was ahle to do a day's ploughing as well as if his heart were sound, and in fact declared he felt the better for the exercise. This patient died of acute pericarditis soon after von Ziemssen learned the facts of his case, and his heart was given to von Ziems- sen, who declared it weighed several pounds and was the most marked example of coi' bovlnum he had ever seen. A well-compensated aortic regurgitation will endure arduous physical labour and the most energetic kinds of exercise so long as the myocardium is healthy. Therefore it is young or compara- tively young patients whose aortic-valve disease is of rheumatic origin who are able to endure great physical exertion for many years without a breakdown. Such patients are far more likely to be unconscious of the existence of their cardiac mischief than are the subjects of mitral disease. In the former cardiac stress is manifested not so much by dyspnoea as by palpitation, and if their valve-defect dates from an attack of rheumatic endocarditis in childhood, as is often the case, they have grown up so accustomed to these palpitations that they are apt to speak of them as but a manifestation of strong action of the heart. While such patients can be quite safely permitted considerable latitude in the matter of exercise, they should nevertheless be closely watched for the first evidence of failing compensation. For so soon as the heart begins to waver in its work, bounds must be set to their activity. Whatever is the nature of the valvular disease, the physician should always remember that after the fourth decade of life arte- rial degeneration is frequent, and the myocardium is likely to have suffered changes depending thereon. Consequently, liberty in ex- ercise is more hazardous after than before this period of life, even in the case of old-standing lesions that have not previously inter- fered with active habits. From this time onward increasing cau- tion must be observed, and heed given to what may appear to be but trivial symptoms of heart-strain. Should a valve become de- fective at this period of life, either as a result of endocarditis or atheroma, severe exercise and incautious efforts of all sorts are to be forbidden, even though good compensation seems to have been established. Every physician of ex]M>rience is aware of the readi- ness with which compensation fails after middle age. Fortunately for such persons they have arrived at years of discretion, and find THE TREATMENT OP VALVULAR HEART-DISEASE 419 less difficulty in restraining their impulses to overdo than ig the case with the young. Exercise must now be had by walking, driv- ing, easy riding, billiards, and golf. Pulley weights, the Whitley exerciser, clubs, dumb-bells, etc., if permitted at all, are to be used under the supervision of the medical attendant or of a nurse capa- ble of detecting signs of danger. Moderation in all things must now be the motto of these patients. Occupation. — The principles underlying the matter of exercise should also determine the selection of a suitable occupation or the decision whether or not the patient's vocation is to be continued. The following employments are suitable for persons with mitral stenosis : Book-keeping, stenography, banking in any capacity, or other forms of desk-work, telegraphy, clerking, engraving, watch- making, tailoring, shoemaking, harness-making, saddlery, etc.^ and for females the various kinds of needlework, typewriting, stenography, and desk-w^ork. Employments that necessitate heavy lifting and the carrying of heavy parcels, as porterage^ running up and down stairs, swinging of heavy hammers, etc., are injuri- ous, since they put added strain on the right ventricle. Dusty occupations induce catarrhs and coughs, and in this respect favour bronchial congestion, to which mitral patients are predisposed already. For the same reason they should not follow occupations which expose them to vicissitudes of weather and sudden changes of temperature. Of the professions, journalism, dentistry, archi- tecture, designing, and the various branches of art work, are all suitable — while theology, law, and such other vocations as require public speaking put a strain on the right heart and are less eligi- ble. Teaching is not so bad, whereas the profession of medicine, especially a general practice, is too arduous and involves too much exposure for persons with pronounced although compensated mitral narrowing. A specialty permitting office practice is not so objectionable, and yet any one with this lesion should be discour- aged from studying medicine, or becoming a trained nurse or mas- seur. Work with light tools, as carpentering, joinery, house-paint- ing and decorating, and even light gardening, may answer for some cases of aortic disease, when not admissible for severe mitral ste- nosis. Most of the occupations followed by females are not too severe for mitral patients who have good compensation, excepting 420 DISEASES OP THE HEART such work as requires the carrying of trays heavily loaded with dishes and the frequent running upstairs. A general classification or division of occupations may he made as follows. Those that are indoors and require the use of the mental faculties rather than the muscles are suitable to mitral patients and persons with serious aortic lesions. Outdoor employments and work performed by the muscles rather than the brain may be endured by subjects with compensated aortic regurgitation and the slighter forms of aortic stenosis and some cases of mitral insufficiency. Finally, vocations attended with much excitement or nerve-strain, as locomotive driv- ing, operating on the stock-exchange, detective and police work (these last two for other reasons as well), sea-faring, and soldier- ing, are unsuited to any form of valve-disease, no matter how excel- lent the compensation. The medical attendant can do much good by directing the choice of occupations for the young, and in the case of those who have developed disease after their work in life has been fixed by pointing out how the evils of the occupation may be minimized. Habits. — It has already been stated that moderation should be the governing principle in the lives of cardiac patients. Excess of every kind, particularly in sexual indulgence, is to them most injurious. It not only occasions a harmful degree of cardiac ex- citement, but it saps the strength and lowers the tone of the nerv- ous system. The medical attendant who has charge of a young man with valvular disease neglects his duty if he does not instruct his patient concerning the evils of sexual excess. I have known young married people of both sexes have their compensation seri- ously threatened after a few months of unbridled license in this regard. Although males are the chief sufferers in this respect, women with valve-lesions are often made to suffer through the inconsiderate demands of their husbands. The tobacco habit has l)ocome so well-nigh universal, and youths are so often addictcnl to cigarette-smoking, that a few words regarding this habit are also indispensable. Young men who are just learning the seductive pleasures of tobacco should be strenuously urged not to form the ha])it, while those cardiac patients who are already addicted to smoking should be advised to discontinue it, or if unwilling to do that, to keep the use of tobacco well within the limits of lianiifiil excess. Just how many THE TREATMENT OF, VALVULAR IIEART-DISEASE 421 mild cigars or pipcfuls of mild tobacco a patient with compen- sated valvular disease may be safely allowed to smoke daily is a question impossible of general answer. The degree of indulgence permissible will vary in different cases, and must be determined by careful observation of the effect produced in each instance. The inhalation of tobacco smoke is most pernicious, particularly to individuals with mitral disease, since it will surely increase the already existing tendency to bronchial irritation. If it be true that smoking produces antemia, then those persons whose com- pensation depends upon adequate nourishment of the heart-muscle cannot afford to have their red blood-cells impaired. It is well known that the unmoderate use of tobacco occasions functional cardiac disorders, and, according to French authorities, raises arterial tension. Since, then, a healthy heart may suffer from tobacco intoxication, surely an unhealthy heart will experience the ill effects even more certainly and powerfully. When tobacco deranges digestion and causes insomnia, as it is well known to do in some individuals, its use should be peremptorily forbidden. I have heard it stated, with how much truth I know not, that Sir Morell Mackenzie was wont to say that the injurious effect of tobacco could be measured by its influence upon salivary secretion. In other words, when smoking causes salivation and frequent expectoration, it is an indication that the individual is too suscep- tible to its influence to safely persist in its use. As regards the liquor habit, I do not propose to enter into a discussion concerning the food value of alcohol and its effect on the animal economy. Whatever be our views respecting the mod- erate use of liquor in its various forms, we all agree as to the evils of its excessive employment. What has been said already regarding the baneful effect of cardiac excitation in cases of com- pensated valve-lesions applies with added force to the immoder- ate consumption of alcohol. It goes without saying, that the possi- bility of destroying compensation is always present when a pa- tient gives himself over to a debauch. I am a firm believer in the medicinal virtues of alcohol, but in the compensated stage of valvular disease the heart requires no medicinal treatment, and the only indication I can see for an alcoholic beverage is to pro- mote the appetite and improve digestion of those individuals who habitually take too little nourishment for the requirements of 422 DISEASES OF THE HEART their damaged hearts. The conclusion to which I have arrived, and which governs niv actions respecting the matter under dis- cussion, is that the young and vigorous with satisfactory compen- sation do not need alcohol in any form. Moreover, the danger of their becoming slaves to the habit is so real that the circumstances have to be very exceptional which make me incur the responsibil- ity of recommending the use of even beer or wine to such patients. If one has been accustomed to a stimulant with his dinner then I do not interfere with his habit, contenting myself with a caution against its immoderate use. The habit of taking a hot toddy before retiring for the night is certainly not a good one, since, as pointed out by Fothergill, it accelerates cardiac action, and thereby robs the heart of some of its rest that ought to be obtained through the slowing of its contractions during sleep. Marriage. — The baneful effects of one phase of married life have already been considered under the head of habits. There is another aspect of the subject which I propose to consider here. For the male who has been warned against and will avoid the dangers of a too ardent love, marriage is certainly advisable, since it conduces to regularity of living, and provides him with the comforts of a home that cannot be obtained in a boarding-house or hotel. In the case of a woman also it is better to be a happy wife with a comfortable home and a kind, considerate husband to minister to her needs than to be left alone, and possibly heart hungry. It is quite another thing if she is to become a domestic drudge, obliged to cook and wash for the family and to bear off- spring. It is as regards the dangers of pregnancy and child- bearing for women with valvular disease, even when compensated, that I wish to discuss marriage. Should a girl who has a valve- lesion become a wife ? is the question often asked of the medical attendant. It is a most serious one to answer, and puts an enor- mous responsibility on the medical adviser. There are many cases of even compensated valvular defects in which pregnancy and childbirth are fraught with considerable risk. Yet every physi- cian of experience can prol)ably recall numerous instances of mothers who have successfully carried th(Mv offspring through to Itirtli, in s])ite of serious lieart-disoase. Let us take up tlie valve- defects of the left heart separatel3\ Mitral disease, and of this mitral stenosis is the form most THE TREATMENT OP VALVULAR HEART-DISEASE 423 frequently met with in women. Theoreticallj^, this is the lesion which should be the most seriously affected during the latter months of pregnancy and the expulsive stage of labour. As the gravid uterus rises in the abdominal cavity and when in the last two months its fundus interferes with the proper descent of the diaphragm, and crowds the viscera aside, dysj^nusa and cyanosis appear, and walking often occasions serious distress. The right heart becomes embarrassed in consequence of mechanical interfer- ence with the circulation. The pregnant uterus impedes the de- scent of the diaphragm, so that the flow of blood out of the great veins and through the right heart into the lungs is deprived of the aid resulting from full and regular respiration. Moreover, the pressure upon the intra-abdominal veins ^retards the return flow from the inferior extremities, and blood-pressure in the capillaries is increased. This raises pulse-tension, and by thus increasing peripheral resistance throws greater work upon the left ventricle. Under the most favourable conditions this chamber discharges but a small volume of blood into the arterial system, and when its out- flow is still further impeded by abnormal peripheral resistance, it results in augmented stasis within the left auricle, pulmonary system, and right heart. The vicious circle already existing by reason of the mitral stenosis and the strain upon the right ven- tricle are intensified. If this is not too severe, the woman may be able to endure her pregnancy to full term. When at length labour comes on, and the expulsive stage is reached, there is imminent danger of the right ventricle giving way under the added stress of violent straining efforts. The same condition obtains in mitral regurgitation, but the enlargement of the left ventricle, which if compensation is pres- ent is hypertrophied as well as dilated, is a factor for good by enabling the heart to withstand increased peripheral resistance. The augmentation of arterial tension would by raising intra- cardiac blood-pressure increase the regurgitation into the left auri- cle were it not counteracted by the left-ventricle hypertrophy. The danger is that the ventricle may not be able to resist the strain, in which event the evils of the mitral incompetence become intensified, and the right ventricle at length suffers from over- strain. Even if the injurious tendencies of pregnancy are suc- cessfully withstood, the woman with mitral regurgitation is sub- 424 DISEASES OF THE HEART jected to the same danger during the second stage of labour as is one with stenosis. Whether the exi)hination just given is correct or not, the danger to mitral patients during this trying period lies in pulmonary engorgement and failure of the right ventricle. With this peril kept constantly in mind the attentive accoucheur can often conduct the pregnancy and gestation to a successful issue. Capillary and venous stasis are to be lessened by saline or other not drastic cathartics and by keeping the patient at rest. When the expulsive efforts of labour endanger the integrity of the right ventricle or when stasis in the lungs leads to pulmonary o'dema, instrumental delivery becomes impel'atively indicated, and must not be delayed. In these cases chloroform is not at- tended witli more than ordinary danger. In eases of aortic-valve disease the strain of childbearing is on the left ventricle. Regurgitation through the aortic orifice is likely to be increased, and in aortic stenosis the augmented peripheral resistance hinders the output from the left ventricle in the same manner as if the orifice were for the time being still further contracted. Nevertheless, if compensatory hypertrophy is suflicient, the left ventricle alone, or chiefly, bears the brunt of the struggle. Tlie patients as a matter of fact endure the ordeal of childbearing often without dangerous cardiac embarrassment and better than do mitral sufferers. According to Davis's state- ments, more than 50 ])er cent of mitral and 23 per cent of aortic cases succumb to the dangers of pregnancy and gestation. Only yesterday 1 saw a woman in the seventh month of preg- nancy who prior thereto presented well-marked evidence of mitral regurgitation with stenosis, considerable enlargement of the right ventricle, and dyspnci'a of effort. Except upon walking for a considerable distance and in ascending stairs, this patient yester- day evinced no ])ron()niiced signs of cardiac embarrassment, and declared she was not sjiccially inconvenienced by her pregnancy. Her pulse was only moderately accelerated, appreciably tense and strong, and the apex-beat was powerful, indicating adequate hypertrophy of the left ventricle. There was increased dulness to the right, but it was not excessive, and the right ventricle gave no sign of being dangerously overl)urdened. If this patient re- ceives proper management during the remaining two months, and THE TREATMENT OP VALVULAR HEART-DISEASE 425 is not permitted to overstrain herself during labour, I believe her heart will not suffer damage from this, her eighth pregnancy. Her husband, who is a physician, states that she had heart-disease at the time of her marriage, fourteen years ago. The following conclusions may be stated: (1) Pregnancy is a condition of gravity, but not necessarily of peril, to women with compensated valvular disease. (2) Labour is a time of real dan- ger, the extent of which depends upon the nature of the lesion and the degree of compensation, but is often endured without catastrophe. (3) Mitral disease is more liable to disastrous con- sequences from both pregnancy and gestation than are aortic de- fects. (4) Even in mitral disease the degree of danger depends upon the state of compensation, (5) Pregnant women with valv- ular disease require special watching as labour approaches, and during the expulsive stage should be delivered instrumentally at the earliest indication of dangerous heart-strain. (6) The perils of marriage should be clearly stated to both of the contracting parties, and when compensation is imperfect or is maintained with difficulty they should be advised not to wed. (7) Interfer- ence with pregnancy is justifiable only when the nature and sever- ity of the lesion render the maintenance of compensation impossi- ble or when serious symptoms have already supervened. Clothing. — The physician who would instruct his patient in matters of importance in maintaining compensation must have regard for what sometimes appear to be things of trifling moment. Among such details is to be included the clothing. All who have much experience in the management of cardiopathies come in time to realize the influence exerted by varying conditions of blood-pressure. The reason of one man's success, as contrasted with another's failure, in the treatment of heart-disease is often found in the close attention he pays to undue rise of blood-pres- sure. Take, for example, an ordinary case of mitral stenosis. Without any recognisable change in the cardiac condition or in his daily conduct, a patient will be conscious that his breathing becomes embarrassed by efforts usually put forth without any such effect. He consults his medical adviser, who, familiar with the case, discovers by studying the pulse and state of the venous circulation that there is unwonted tension in the arterial system. He finds, furthermore, that there is constipation perhaps, and 29 426 DISEASES OP THE HEART knowing the influence of this condition over blood-pressure through the splanchnics, he administers a mercurial pill ; tension within the abdomen and arterial system is lowered, and the patient's breathing returns to its nsual state. A tendency to pal- pitation in a case of aortic regurgitation may be Avholly due to increased capillary resistance and be relieved by the administra- tion of a vaso-dilator. It is because of the effect on blood-pressure produced by a patient's manner of dress that the matter of clothing becomes important, and may make for or against the establishment or preservation of compensation. Cardiac sufferers are often very sensitive to the cold and to sudden changes of weather, partly on account of a rheumatic diathesis and partly because of sluggish cutaneous circulation, as in mitral stenosis, or of relative arterial ana'mia in aortic disease. Wool should therefore be worn next to the skin, and during seasons of low temperature the hands and feet must be kept warm by heavy not too tightly fitting gloves and shoes. It is well to have the latter constructed with cork soles, and in very cold weather overshoes may be a necessity. Outer garments should not only be warm, but they must not be so heavy as to tire the wearer. It is very important that the clothing does not constrict the vessels. This applies to shoes, gloves, col- lars, belts, and waistbands in the case of males, and to garters, corsets, and tight dresses on the part of females. Constriction of the extremities tends to raise blood-pressure as well as to mechan- ically impede circulation, and should be corrected in every case of valvular disease. Harm is chiefly done, however, by garments that constrict the chest and abdomen. A woollen undervest that has become shrunken until uncomfortably tight, an overcoat that is outgrown, and can be buttoned only w^ith difficulty, is in a measure at least injurious in the same way as is a too tight corset. Xot only are respiratory movements hampered and venous circu- lation retarded in consequence, but the hypertrophied and there- fore compensated heart is more or less compressed and restricted in its movments; abdominal viscera are engorged and displaced; the play of the diaphragm is limited, and the evil consequences of the valvular lesion itself are intensified. These effects are evinced by increase of cyanosis and shortness of breath, both of which disappear or lessen when the clothing has been removed. THE TREATMENT OP VALVULAR HEART-DISEASE 427 Instead, therefore, of suspending the skirts from the hips, to effect which they have to be fastened snugly about the waist, it is preferable that women, particularly slender ones, wear gar- ments of one piece, so that the weight may be borne by the shoul- ders ; or they should replace the ordinary corset by a corset-waist, to which the skirts can be buttoned, thus avoiding constriction of the waist. 'Not many months ago I was consulted by a lady on account of attacks of dyspnoea and cyanosis, which at times amounted even to partial syncope. She presented signs of pro- nounced mitral stenosis with considerable secondary enlargement of the heart and hepatic congestion. She was inclined to cor- pulence, and to preserve her figaire wore a long, stiff corset, which, in response to my inquiry, she declared was loose and comfortable. jSTot convinced on the poifit, I measured her waist both on the bare skin and outside of the corset, and thus demonstrated that when her corset was hooked she actually measured 4 inches less than she did next to the skin. I then explained at some length the harm she was doing herself, and succeeded in getting her to re- form her mode of dressing, much to her relief, as she subsequently acknowledged. In this instance I am convinced that the symp- toms of cardiac stress under conditions of exercise were due largely to the additional impediment to circulation and respira- tion occasioned by the tightness of her clothing. Baths. — I have found in numerous instances that ladies with valvular disease were in the habit of taking a semiweekly hot bath, and some of them confessed to lying in the water for twenty minutes or more. Inquiry generally elicited the fact that the bath was followed by a feeling of languor, even amounting in some instances to prostration. It is well known that such hot baths are weakening to the heart and lower vascular tone. They should be forbidden therefore, and the patients advised to content themselves with a rapid sponge-bath daily if strength permits, and once a week a tub-bath of short duration, and of a temperature closely approximating that of the human body. Mitral patients endure bathing less well than do those with aortic lesions. Yet in all cases the degree of latitude permissible in the matter of baths is to be determined by their effect. If they are followed by a healthy reaction — that is, by warmth of the skin and a sense of rest or well-being — they are beneficial; but if a cardiac patient 428 DISEASES OP THE HEART finds his bath leaves him with cold extremities and a feeling of fatigue, and that the exertion of briskly rubbing his body into a glow occasions breathlessness or palpitation, frequent bathing is likely to do him harm. Swinnning, whether in salt or fresh water, is to be considered not alone with reference to the temperature of the water ; there is the shock of the sudden plunge or immersion, and also the exertion of proi)elling the body while at the same time sustaining the weight or pressure of the surrounding liquid. For these vari- ous reasons this form of bathing is apt to put a good deal of strain on the heart, and persons with mitral lesions, or those whose de- fects, of whatever nature, are maintaining compensation with difficulty, should either indulge in this sport not at all or only under great restriction, both of frequency and duration. It is probable that many of the cases of supposed death from cramp in the water are in reality instances of heart-failure or asystolism. The Turkish and Russian baths and the various modifications of the shower-bath or douche found at health-resorts affect the heart and vascular system powerfully, and should not be taken by cardiac sufferers without the advice of a physician who is familiar with their effects and competent to decide on the advisa- bility of such baths in each instance. The saline and carbonated baths employed for therapeutic purposes at Bad Xauheim may be left out of consideration at this time, since they are not indicated for individuals whose valvular defects are in the stage of compensation. Food. — Of all matters concerning our patients none is so essen- tial as that of nourishment, and yet there is nothing, I venture to say, about which physicians of more than average intelligence and experience are so unable to give precise and suitable instruc- tions. In works on diet are. to be found tables of various food- stuffs compiled with regard to the needs of the human organism under conditions of work and repose, and from which one may construct dietaries suitable to the requirements of cardiac patients. In this chapter I shall only make certain general statements that apply to the regimen of persons whose lesions have not greatly deranged circulatory e(iuii)oise. Adequate compensation in any given case implies, nay, neces- sitates, the supposition that the circulation of the digestive appa- THE TREATMENT 0^ VALVULAR HEART-DISEASE 429 ratus is not appreciably disturbed. The conclusion is warranted, therefore, that there is no digestive disorder secondary to the car- diac mischief and necessitating a corresponding modification of the diet. It is only essential that the food be of good quality, well- cooked, and sufficient. The proportion of proteids suitable to each case will be governed by the amount of exercise taken, the kind of work, and the tendency or not to obesity. The same consid- erations apply to the quantity as well as the quality. The proper preparation of the food is essential if digestive disorders are to be avoided. It is of importance also that meals be taken at regular hours ; gluttony is injurious, and the amount of fluids taken with meals should be definitely stated, 10 ounces being ordinarily sufficient. Patients who are anaemic must be given a liberal allow- ance of beef, eggs, milk, and such vegetables and fruits as are rich in iron-forming compounds; those who incline to constipa- tion are to get a dietary calculated to correct the tendency. Tea and coffee in moderation may be allowed. In a word, so long as compensation is complete there is no indication for special rules to govern the dietary further than what would be required for the preservation of health in the same individual were he not afflicted with an incurable malady. Illnesses. — Among so many items of importance in the preser- vation of compensation it is difficult to specify one as greater than another, and perhaps it is not wise to attempt to do so. Yet I wish to lay particular emphasis on this point — namely, no illness or indisposition, apparently trivial in itself, should ever be so regarded in a person who has suffered injury from endocarditis. This is specially true of children. In them rheumatism is so apt to be masked that an infection of the throat, a persistent pain in an extremity, a rise of temperature without obvious cause, should always receive careful medical attention. The intestinal tract affords so ready and frequent a portal of infection that no devia- tion from the standard of health is to be neglected as of no conse- quence. Far better is it to bear the imputation of being over- careful and fussy than to some day awake to the consciousness that your neglect has permitted injury to visit one of your pa- tients, whose compensated valvular lesion might otherwise have gone on years longer. Tell your patients emphatically and clearly that a tonsillitis, yes, or even an acute eoryza, is never to be neg- 430 DISEASES OP THE HEART lected. Ill a case of mitral disease, particularly of stenosis, an attack of simple bronchitis may break down utterly the integrity of the right ventricle. Be always suspicious of slight fevers, which to those living in a malarial region may appear to be of that nature; such a trivial yet persistent run of fever has only too often turned out to be an endocarditis. In cases of pneu- monia and other serious affections cardiac sufferers merit more than ordinary care and watchfulness, if they are to come through undamaged. This is particularly true of persons with mitral de- fects not only because of the possible lighting up of a fresh endo- carditis, but because the strain to wdiich the right ventricle is subjected by reason of the valvular mischief is. enormously aug- mented by the pneumonic consolidation — while at the same time cardiac endurance is impaired through the effect of the pneumonic toxines on the myocardium. If in such a case paralysis of the vaso-motor centres leads to cyanosis, the outlook is serious indeed. The gravity of pneumonia, la grippe, and other acute infections, gonorrha-a, diphtheria, scarlatina, measles, puerperal septica?mia, etc., in all cases of compensated valvular disease, is so obvious, particularly as respects the liabilit}^ to fresh endocarditis, that further comment is unnecessary. Considerations of prophy- laxis require, therefore, that our cardiopaths be properly in- structed on these points. If it be objected that this is likely to render them introspective, and even hypochondriac, or if the patients are children, then the requisite information may be imparted to the family, friends, or j)arents. No one need fear that his motives will be misunderstood. Indeed, I am convinced that the American public likes to be talked to by physicians as if they were intelligent and reasonable beings, and that nothing con- duces more to the establishment of confidence in the medical prac- titioner than frankness and ])laiii dealing in all matters that con- cern the hcallh of his patients. Use of Drugs. — It is an error to suppose that every individual presenting signs of valvular mischief requires medicinal treat- ment. Digitalis or some other heart-tonic is not to he ordered in every case in ivhich an endocardial murmur is heard. Inexpe- rienced practitioners fresh from a medical college are very apt to commit this mistake, and consequently the foregoing injunction is not out of ])lace. When a person willi valvular disease presents THE TREATMENT OP VALVULAR HEART-DISEASE 431 himself in your office, inquire minutely into the matter of symp- toms, and if he does not acknowledge any indicative of cardiac stress, remedies influencing the heart directly are not indicated. If you belong to that class who believe no person should be allowed to leave the physician's office without a prescription or a drug of some kind, lest forsooth the patient fancy he has not received his money's worth, then let it be a placebo. As a matter of fact, there are few persons who cannot be satisfied under such circumstances with an expression of opinion coupled with sound advice on the points under discussion in this chapter. Careful inquiry will usually bring out some pernicious habit, faulty digestion, consti- pation, some impairment of appetite, etc. ; or there may be more or less anaemia, bronchial irritation perhaps, monorrhagia, some deviation from perfect health, which permitted to go on, will in time exert malign influence on compensation. Any such condition calls for correction, and to this end medicinal treatment may be indicated. What medicaments are suitable in each instance is, of course, to be left to the judgment of the medical adviser. Although slight disturbances demanding attention are often dependent upon scarcely detectable disorders of circulation, they are not necessarily so in perfectly compensated cases, and hence these patients may generally be treated, so far as regards medi- cines, as they would be were they wholly free from endocardial defects. Two conditions likely to prove more injurious to individuals with a valve-lesion, although compensated, than would be the case if his valves had not been damaged, are constipation and flatulent distention of the bowel. In both there is splanchnic irritation and consequent alteration of blood-pressure, but in the latter the effect of mechanical encroachment upon the contents of the tho- racic cavity must be reckoned with. Uncorrected it may con- tribute materially to the destruction of heart adequacy, to say nothing about the patient's discomfort in the way of postprandial breathlessness in mitral and tendency to palpitation in aortic dis- ease. Both disorders of digestive function tend to impair the appetite, give rise to neuralgias, anaemia, coldness of the extrem- ities, and many other phenomena of auto-infection. Moreover, flatulent indigestion, probably through the absorption of toxines, is a frequent cause of deranged cardiac rhythm. This not only 432 DISEASES OF THE HEART annoys or even alarms the patient, bnt it may even lead to the development of dilatation. It is for the relief of such disturbing factors as these, therefore, that drugs find their legitimate use in the management of compensated cardiopathies. In most cases the speediest and surest relief is likely to be afforded by a mercurial, a grain of calomel in divided doses, or 5 grains of blue mass, fol- lowed next morning by a Seidlitz powder or a glassful of some laxative water. Cascara, aloes, rhubarb, podophyllum, etc., })an- creatin, ox-gall, nitrohydrochloric acid, subgallate of bismuth, salol or salophen, naphthol preparations, etc., alone or in various combinations and with which the reader is duly familiar, are serviceable, and will generally afford relief. Only when gastro-intestinal disorders occasion persistent de- rangement of cardiac action are digitalis, strophauthus, caffeine, convallaria, and sparteine to be prescribed in this class of cases; even then the remedy is to be withdrawn so soon as the arrhyth- mia or acceleration of the pulse has been corrected. Temporary palpitation or vertigo on the part. of aortic patients nuiy generally be removed by minute doses of glonoiu. ^wij ^<^ tttt '*1' ^ grain at intervals of two, three, or four hours, either alone or in conjunc- tion with 3 to 5 drops of digitalis. When compensation has been seriously threatened by cardiac overstrain or some other disturb- ing factor, digitalis and strychnine may be needed in addition to rest and restricted diet ; but in all such instances rest in bed for a few days is unquestionably the agency of greatest value, and should be rigidly enforced until the period of danger is past ; not until then is the patient to be permitted to resume his usual mode of life and to return to his wonted exercise. In this class of cases " eternal vigilance is the price of safety." Change of Climate, with Special Reference to High Altitude. — The question is so often asked whether a ])aticnt with heart-dis- ease should go to Colorado or make the journey over the moun- tains to California, that it seems best to discuss this subject here when foiisidering those conditions llint make for tlic ])resorvntiou of comjxMisation. It is quite generally the opinion among medi- cal men that the existence of a valvular lesion contra-indicates residence in elevated climates. This is too sweeping, as shown by clinical observation. My medical friends in Colorado assure me that their patients with valvular disease, of whatever kind, suffer THE TREATMENT OP VALVULAR HEART-DISEASE 433 no nioro inconvenience from their heart-lesions in Denver or Colorado Springs than do })ersons similarly affected at the sea level. Moreover, Kegnard, in an elaborate work on the effect of high altitude on the heart and circulation, expresses the opinion that cardiac lesions j^ei- se do not contra-indicate residence in the mountains when this is necessary, and that aside from the discom- fort of becoming accustomed to the high altitude individuals afflicted with heart-disease do not experience permanent harm. ^Nevertheless, he would not advise residence in such a climate for a cardiopath, since there is nothing in his disease calling for such a climatic treatment. This opinion impresses me as too broad, judging from the experience of some of my cardiac patients. I have known persons with mitral and aortic regurgitation to visit Colorado, and there, at an elevation of 6,000 feet, to take consid- erable exercise without discomfort, and apparently without harm. Others with vascular and cardiac degeneration have found the same to be true with them, and in fact one gentleman was actu- ally able to walk with more ease at 7,000 feet than in Chicago. On the other hand, my patients who were not able to endure high altitude were sufferers from mitral stenosis, aortic stenosis, and mitral incompetence, when complicated by pericardial or pleu- ritic adhesions. These cases were all reported and discussed by me in a paper before the American Climatological Association in 1899, and will be found in the Transactions of that year. Singu- larly enough, Dr. Sewall, of Denver, in discussing my paper, stated that at that very time he had under observation in Denver a female with pronounced mitral stenosis, who had formerly been under my care in Chicago, and who was able to endure the eleva- tion, not only of Denver, but also of Cripple Creek situated at an altitude of about 12,000 feet. She died a year subsequently, I understand, and I have often wondered if her residence at that elevation did not aid materially in shortening her life. As the discussion of theories is foreign to the spirit of this work, I shall not discuss at length the considerations which make me conclude that residence in high altitudes is likely to prove injurious to persons having stenosis or regurgitant lesions com- plicated by pericardial or pleural adhesions. Suffice it to say that the effect of a rarefied atmosphere is acceleration and small- ness of the pulse, together with increase in the depth and fre- 434 DISEASES OP THE HEART qiieucj of the respirations, the degree of this effect depending of course upon the degree of the altitude. The blood flows to the heart more rapidly, and if there is an obstruction at one of the orifices, this acts as a barrier to the rapid and easy passage of the blood, which tends to accumulate back of the hindrance. In mitral or aortic stenosis this would be in the lungs and right heart, and hence symptoms due to this engorgement are likely to result. If adhesions exist, they interfere more or less with the expansion of the thorax, which takes place in high climates, and consequently they ought to hinder that adjustment to altered conditions, which is essential if one is to become accustomed to a high altitude. Further reflection and observation since the publication of my paper on this subject have led me to the belief- that probably all or nearly all individuals with valvular diseases can endure an altitude of 6,000 to 10,000 feet without injury, provided they do not take much exercise. Until they have grown accustomed to the rarefied air they should not walk at all, but remain in bed. At least such is tlie opinion and advice I give when consulted on this important question. Finally, it is probable that much of the dyspnoea and palpitation complained of by some at high alti- tudes is due in part, perhaps largely, to the fact that in the moun- tains the walks are not level. Hill-climbing is trying for cardio- paths, even at the sea level, and at an elevation where the air is thin such an exertion could readily prove doubly injurious. The phenomena of mountain-sickness — that is, rush of blood to the head, with vertigo, and even nausea, or in extreme cases bleeding from the nose and ears — are liable to attack healthy persons at too higli an altitude, particularly during physical exertion. In their milder degrees they may affect cardiopaths in transit to and from the Pacific coast, but apart from these unpleasant symptoms patients who remain at rest in the car need not apprehend serious results even in passing the loftiest points. When vertigo or a tendency to syncope is experienced, relief usually follows the ad- ministration of a diffusible stimulant and the assumption of the rccundjcnt position. Nevertheless, caution would suggest the tak- ing of the less lofty routes. CIIAPTEK XVII THE TREATMENT OF VALVULAR HEART-DISEASE (CoriHrmed) II. COMPENSATION BEING IMPERFECT A WANT of perfect compensation may have either one of two explanations. It may have never been adequately developed after the subsidence of the acute process that led to the valvular mis- chief, or having been once established it may be destroyed in con- sequence of a variety of causes. In the first instance the develop- ment of complete compensation may be impossible, owing to the extent of the damage sustained by the valves, in consequence of de- generation of the myocardium, or of the coexistence of complica- tions or conditions residing in the patient's temperament, environ- ment, etc. In such a case the course of the disease is generally too short to admit of its being brought into the category of chronic valvular affections. For the same reasons a long-continued main- tenance of compensation may be impossible after it has once be- come established. In many cases, however, it is possible to arrest the do-wnward tendency and restore heart-power when the injuri- ous influences are discovered and removed. If these cannot be removed, then their baneful effects must be counteracted by all those therapeutic measures which are at our disposal. In the management of compensated valvular disease the physi- cian conducts a defensive campaign, so to speak, whereas when compensation has failed, he is called on to wage an active offensive warfare against all those forces that are striving to destroy his patient. His success depends not only upon the skill with which his therapeutic weapons are wielded, but also upon the precision of his orders, and the faithfulness with which these are executed. The treatment of valvular disease in this stage requires also atten- tion to details of daily life, no matter how trivial they may appear to be, and the recognition of complications. Moreover, there are 435 436 DISEASES OF THE HEART few patients in whose envirdiuiicnt inilucnccs do not exist which, if permitted to i;o on, will not act nnfavonrably and retard the restoration of adecpiate eonqjensation. For this reason these ninst be ascertained and removed so far as is possible. It is plain, therefore, that the proper management of these cases consists in mnch more than the mere administration of heart-tonics or other medicinal remedies. That highly gratifying results follow such strict and careful management is shown by the narration of the next three cases. Miss N., referred by Dr. Minor, of Asheville, N. C, was first seen by me in July, 1898. She had spent the preceding winter in Asheville, and had there sought medical advice in the early j)art of summer because of increasing difficulty of breathing in walking, the altitude being 2,200 feet and the nature of the ground hilly. The winter immediately previous had also been passed in Asheville, but without her having noticed the same shortness of breath. She gave a history of inflammatory rheu- matism three years before, and a year and a half before of an ill- ness which, judging from her account, must have been an inflam- mation of a serous membrane within the thorax. Her age was twenty-two. Her pulse was much accelerated, 120 or more, regu- lar, and equal. The ankles were edematous, and the abdomen was distended by the greatly engorged liver. The broad, fairly powerful apex-beat was found immovably fixed in the sixth inter- costal space, near the anterior axillary line, and superficial car- diac dulness extended somewhat beyond the right sternal margin, upward to the third costal cartilage and at the left, almost to the mamillary line. There was an intense blowing systolic apex-mur- mur transmitted to the left and accompanying, not replacing, the first sound, the pulmonic second sound being very accentuated. I |)(in auscultation, fine crackling rfdes were detected dui'ing in- spiration along the upper and left border of prspcordial dulness, and upon the arms being raised and lowered a creaking sound could be plainly heard at the superior boundary of dulness on the sternum. In tliis case it was manifestly not so mucli the mitral leak that was serious, as it was the fixation of the left ventricle that was preventing the maintenance of compensation. Moreover, it was foreseen that diuitalis aixl similar remedies could exercise but THE TREATMENT OP VALVULAR HEART-DISEASE 437 limited control over the heart, since only slight if any reduction in the dilatation of the left ventricle was possible by reason of the restraining adhesions. Efforts had to be directed, therefore, to lessening the resistance residing in the congested portal system and at strengthening the right ventricle. The former was to be accomplished by purgatives, tonic doses of digitalis, and the re- moval of all constricting clothing ; the latter by those same means, re-enforced by abstaining from too much physical exertion, and if need be by rest from all exercise. Accordingly the patient was told to give up her corset, which she did, to take an aperient water daily before breakfast, and thrice daily 15 drops of tincture of digitalis. Stair-climbing was forbidden. Directions regarding the quantity and kind of food and the amount of fluids were added. The degree of improvement was so insignificant during the next few weeks that at length absolute rest in bed was advised and acted upon. Then benefit became at once apparent in slowing of the pulse and diminution of dulness over the right heart. The liver also began to shrink, urine grew more abundant, and oedema disappeared. After five weeks of enforced rest the patient was permitted to gradually resume her ordinary mode of life, except- ing that she was not allowed to go out. All this time digitalis or strophanthus was continued in about the same dose (15 drops) of the one and 10 drops of the latter thrice daily, with excep- tion of every sixth day, when it was omitted. Apex-impulse grew somewhat stronger, but never altered its position in the least ; the marked change was in the right ventricle and liver. After a few weeks longer of such management it was decided to try the effect of a course of ]!Tauheim baths. They were given in her home and not at my rooms, as was then the rule with pa- tients whom I subjected to this treatment. Whether because I could not watch their effect as closely in this way, or on account of the hampering effect of the adhesions (I believe it was the latter), the baths did not produce a beneficial effect. Heart-rate increased and showed a tendency to unsteadiness, dulness to the right be- came increased, and the amount of urine diminished. They were discontinued, therefore, and no permanent harm resulted. Considerable difficulty was experienced in getting this patient to give up her candy and obey instructions as to diet ; but the habit of making her furnish me with an account of what she ate and 438 DISEASES OF THE HEART drank finally convinced lier that I was in earnest, and now her obedience to orders is all that can be desired. In this case men- struation is too profuse and somewhat irregular; so that she has been instructed to remain in bed during her menses, and hydras- tin hydrochlorate is sometimes administered. During the summer of 1899 her health was quite satisfactory, and she was able to enjoy a number of outings with friends without very irksome re- striction on her pleasures. She has been very subject to annoying pains in her shoulders, but especially in her chest beneath the ster- num, and upon several such occasions there has been a circum- scribed, faint, yet distinct friction directly above the superior line of cardiac dulness, which was taken to indicate a fresh lighting up of mediastinitis. These attacks have generally yielded to counter-irritation and antirheumatic remedies. Towards spring of 1900 her condition began to run down slowly but surely, and complaint of " rheumatic pains " was fre- quent ; the pulse quickened, and her flesh grew flabby and cold. She consented to enter a hospital, where her temperature could be carefully watched, as the possibility of endocarditis was enter- tained. Temperature remained subnormal, however, rather than febrile. Ilcr urine was collected and examined, with the follow- ing result : Total amount in twenty-four hours, GGO cubic centi- metres; specific gravity, 1.028; urea, 3 per cent; 2f per cent .of albumin ; numerous hyaline and granular casts. Animal food was withheld, copious draughts of water insisted upon, and citrate of potash was administered, together with moderate doses of fox- glove in tincture. A week later the urine amounted to 2,500 cubic centimetres, had a specific gravity of 1.013, urea 1.3 per cent, neither albumin nor casts. This must have been a mild nephritis and not merely congestion, since the kidneys responded so well to the free intake of fluids. As was to be expected, the patient's condition improved rapidly, the pulse-rate decreased strikingly ; and two weeks afterward she returned home. It is now four months later, and albumin has not again been found in the urine. She has been allowed animal food but sparingly, and has been required to driidc wat(n- freely between meals, with the result of her feeling iiiiusually well, and being able to enjoy a moderate amount of walking again, "^riiis lady is an invalid, to be sure, who has to lead a restricted existence; but she is able to THE TREATMENT OF VALVULAR HEART-DISEASE 439 attend matinees and social functions of a quiet kind, in fine, to get a good deal of enjoyment out of life. Slic cannot entertain the hope of becoming a wife and mother, and has been so informed. In this case digitalis has been taken most of the time, because it has been repeatedly prov'ed by trial that when discarded en- tirely its need is shown after a few days by increased breathless- ness and subjective as well as objective rapidity of the heart's action, to 120 or more. The tincture has generally been pre- scribed, sometimes 10 drops once daily, and at other times 5, 7, or 10 drops two or three times a day. Upon a few occasions scantiness of the urine and oedema, shown by pitting of the ankles, has necessitated the administration of the fresh infusion of English leaves, a tablespoonful three or four times daily. JSTow and then citrate of potassium has been added. Sulphate of strych- nine has also been taken much of the time, and whenever she has felt more than usual weakness she has profited much from the compound syrup of hypophosphites. She has been dependent on medicinal remedies, but no doubt a large part of her really good condition is owing to the excellent care she has taken of herself. She has dressed sensibly, wearing a loosely fitting corset- waist,- and so far as possible suspending her skirts from her shoulders. Walking has been done at a slow pace and for short distances, care being taken not to walk against a strong wind, and to stop for rest whenever shortness of breath or palpitation has been experienced. Ascending stairs has been avoided, or when that was impossible they have been mounted a few stairs at a time, with frequent pauses to let her heart quiet down or to recover breath. During stormy weather she has either remained indoors or has driven in a closed carriage to her destina- tion. Any indisposition, however trivial, has received prompt attention, and a day of unwonted fatigue or exertion has been generally followed by rest in bed or on a couch. Her dietary has been simple and nutritious, and she has not been permitted to be in the least constipated. On the contrary, she took an aperient water every morning for a year at least, with a dose of calomel whenever her liver showed more than ordinary congestion or she felt a sense of fulness about the waist. Latterly the laxative water has been taken only every other day. Finally, she has been required to see me at regular intervals, generally two or three 440 DISEASES OF THE HEART times a month, that thei'el)y t^hc mii;ht he kej)t inuler control. In her case certainly eternal vigilance has been the price of safety. Master W. B., aged eight, was examined by me in June, 1896, at request of Dr. John Streeter. He was a frail, undersized, pale boy, whose whole life had been one of many illnesses ; broncho- pneumonia five times in early childhood, innumerable attacks of fever, with coated tongue, pain in the right hypochondrium, nau- sea, and irritable stomach, which had generally yielded to calo- mel and milk diet, and had been considered " storms of uric acid." For a year prior to my visit patient had been under treat- ment by Dr. M. Allen Starr, of New York, who, it was stated, had administered bromide of soda every night during the year. The mother had tirst learned of her boy's heart-disease in April, 1890. Patient was very subject to attacks of acute tonsillitis, having but just recovered from one, and at the time of my examination had an acute coryza. He had the facial appearance indicative of adenoids, breathed through the mouth, and beneath the angle of the left inferior maxilla the neck was tumefied by enlarged cervical glands. His chest was long, narrow, sunken below the clavicles, prominent in the prtecordium, and expanded poorly on inspira- tion ; the finger-ends were noticeably bulbous, but there was no cyanosis. The heart was greatly enlarged, there was a loud, harsh systolic apex-murmur of wide propagation, and both liver and spleen were palpable with much corroborative increase of dulness. The little fellow suffered from dyspna'a and occasionally palpi- tation on ascending stairs or hurried walking. Urine was scanty and of high specific gravity, otherwise negative. His appetite was capricious, digestion weak, and bowel movements irregular. It w^as my opinion tliat, if much improvement was to be at- tained, three things would have to be done — the removal of the nasal obstruction, the development of the chest, and the improve- ment of the blood condition. The adenoids could have been safely removed under ether and even chloroform skilfully ad- ministered, and thus the first step taken towards proper ex})ansion of the chest. I have notes of a simihir condition in a boy of five or six, which was successfully oj^erated on without the slightest untoward effects as regarded his mitral insufiiciency and with ultimate benefit to the child. In \]n\ ])resent case the mother wanted the treatment of the nasal obstruction postj)oned, and I THE TREATMENT OF^ VALVULAR HEART-DISEASE 441 have never learned whether it lias been done or not. It was evi- dent that if the already enlarged heart was to have room in the thorax for further increase of its compensatory hypertrophy the capacity of the chest would have to be augmented. Accordingly, his attendant, an intelligent trained nurse, was instructed how to give resistance gymnastics and breathing exercises. These were intended not alone to strengthen his heart and develop his thorax, but also to facilitate blood-flow by better asj^iration up out of the congested liver and abdominal vessels. A highly gratifying expe- rience in other cases had already shown how effective and bene- ficial such exercises are in such a condition. In addition, improved nutrition was sought to be achieved through a dietary suited to his blood-state and to his feeble digest- ive and assimilative processes. Starches and sugars were greatly though not entirely cut off, such as were allowed being carefully selected — zwieback, toast, a little baked potato, etc. Meat and eggs were allowed in moderate amounts, and certain fresh vege- tables and fruits were added to the diet list. Such medicinal remedies as would aid digestion, keep down fermentation, and unload the portal vessels were prescribed. To the last end calo- mel was the drug selected, care being taken not to produce a too powerful purgative effect. Cardiac tonics, digitalis and strych- nine, were a minor part of the treatment, being administered in such doses only as would gradually tone up the heart. Some im- provement began to be apparent almost directly, but the family removed to the East before time was afforded to observe the ulti- mate results. Information came to me, however, some weeks sub- sequently that the plan of management detailed was bringing about improvement. I have not seen the patient since that time. W. H. W., aged thirty-nine years, male, physician, consulted me in August, 1896, on account of an attack of mild articular rheumatism, one week previously, in right knee and both hips. He gave a history of inflammatory rheumatism at age of nine or ten, at fifteen remembers he had shortness of breath, and thinks he had intermittence. In 1880 valvular disease was diagnosti- cated. During 1895 he had an afternoon temperature from 99° to 100° F., but the cause was not discovered. In December, 1895, had a fever of 103° F. that lasted three days, and yielded to rest in bed and milk diet. Afterward felt better than before. His 30 442 DISEASES OP THE HEART condition was good the following winter, and until his recent in- flammatory attack he has attended quite constantly to an exact- ing general practice. At the date of my examination there was slight dizziness on walking, temperature at 3 p. m. was 99,8° F., pulse was 98, sitting, falling to 94 on assuming the dorsal decu- bitus, and was collapsing ; capillary pulse was present, and there was a systolic snap in the femoral artery. The broad, strong apex-beat was in the sixth left interspace, 3^ inches to left of sternum, and there was a diffused systolic impulse over the body of heart to left of the breastbone. First sound at apex was pro- longed and impure, suggesting a presystolic murmur,- while the aortic second was muffled. In the aortic area was a soft, faint diastolic murmur, transmitted downward and to the left. The diagnosis was plainly an aortic insufficiency of rheumatic origin, and a still persisting mild rheumatism. He was advised to give up active exercise so long as any trace of joint inflammation persisted, and to take salicylate of ' soda with small not frequent doses of digitalis. The patient subse- quently reported his recovery and return to practice. During the ensuing three years he abandoned general practice and limited himself to ofiice work; he moved his residence a short distance out of the city, which necessitated travelling to and fro on an ele- vated road, and the ascending of long, steep stairs to the stations. He consulted me several times, and on one occasion reported an attack of hamioptysis following some exertion. After that attack I confined him to bcnl for a week or so, and put him on digitalis, strychnine, and a vaso-dilator. He quite frequently experienced intermittence of the pulse for days together, and as he had some digestive disturbance at those times, it was thought the intermis- sions were due to that cause. On one occasion, in the latter part of 1898 or the beginning of 1899, he was suddenly seized with partial syncope while at work over a patient in his office, which, however, was recovered from after a few days rest at home, with the use of digitalis and nitroglycerin. At length, in January, 1900, he entered my office one morning saying he had just had a quite profuse hiiemoptysis without the provocation of unusual physical effort. The heart was liurried and occasionally intermittent; its left border was much outside of the left nipple, its apex rather too rounded, and its impulse THE TREATMENT OP VALVULAR HEART-DISEASE 443 not well defined. It was also noted that a rough systolic murmur had developed in the aortic area, which had not existed a year or two previously. The condition was considered very threatening, as the haemoptysis pointed to pulmonary congestion in conse- quence of temporary inadequacy of the left ventricle. The em- phatic admonition was given him to return home at once and go to bed for an indefinite time, probably many months. The advice was acted on, and he began the regular employment of small, thrice daily, doses of tincture of digitalis, with 3 grains of potas- sium iodide t. i. d., and strychnine; glonoin was substituted now and then for the iodide. His dietary was light yet nutritious, and the bowels were kept free by calomel and other laxatives, as occasion required. For a short period he had a light run of fever, with vague joint pains, which yielded to salicylates. His cardiac action was invariably irregular after breakfast, but subsequently grew less annoying or disappeared entirely after his morning glass of milk was aban- doned, and his early meal was made more substantial. This patient remained in bed for four months, at the end of which time his heart was found to have retracted somewhat in size, gained in the force and concentration of its apex-beat, and had become noticeably steadier in action. He was then permitted to resume exercise very gradually, at first about his room, and thus by slow degrees to accustom himself to his ordinary habits of life. When at length he had grown able to get about as before his illness, he went into the country, and there, driving about with a medical friend, soon got to feeling as well as usual. Small doses of digitalis and strychnine were continued after he left his bed and resumed walking, for the purpose of maintaining what the heart had gained by the prolonged rest. Considering the age of this patient (now forty-three) and his history of repeated subacute rheumatism and probable aggravation of the endocarditic changes, the results secured were highly gratifying, and illustrate the immense value of physical inaction in the recumbent posture in cases of aortic regurgitation with breaking compensation. This patient has had no return of his symptoms, so far as I have learned, up to the present writing, l^evertheless, the prognosis is not encouraging, for unless the doctor is very careful a final and irretrievable breakdown is likely to occur at any time. iU DISEASES OF THE HEART Medicinal Agents. — From the narration of the foregoing cases it becomes apparent that the principle of management applicable to the stage of compensation does not obtain when heart-power shows signs of failure. In this stage digitalis or one of its con- geners is generally of great service, and is often indispensable for the remainder of the patient's life. Foxglove is incomparably superior to all cardiac tonics of its class, and should always be preferred so long as vascular changes are not present and when it does not disagree with the stomach. The former objection does not exist in the young and in some persons at or past middle age, "When the arteries are stiff and the vaso-constrictor effect of digi- talis is likely to occasion injurious rise of blood-pressure, this effect can be overcome by the administration of -j-^^ of nitroglyc- erin every two or three hours in the form of a tablet of required strengtii or a minim of the official solution. Two or three grains of an iodide salt are said to accomplish the same purpose, and may be administered three times a day. If strophanthus is em- ployed instead of digitalis, a vaso-dilator may or may not be neces- sary, according to the degree of vascular tension. The unpleasant effect of digitalis on the stomach is said to reside in a free-fat and certain narcotic principles, the irritating qualities of the drug in free acids, all of which can be removed without impairing its effi- ciency. The method of removing these objectionable constituents was announced in 1899 by Dr. England, the chemist of the Phila- delphia Hospital. Accordingly, such a fat-free tincture of digi- talis is now prepared by several manufacturers of pharmaceutical preparations, which has been found to possess equal if not greater potency than the tinctures ordinarily in use. In most cases of the kind now under consideration digitalis is needed for its tonic effect, not as a diuretic, and therefore the dose may be a moderate one — 5, 10, or 15 drops of the tincture once, twice, or thrice daily, as the case may be. The length of time during which digitalis is to be administered is also variable. Usually, hoAvever, it will be required for many weeks or even months; in grave cases it may even be coiilinucd for the rest of the patient's life. I am con- vinced that a digitalis-habit may be acquired, yet see no objec- tion to this .so long as the continued use of the remedy prevents a total loss of compensation. xlncther medicinal agent of generally recognised value as a THE TREATMENT OP VALVULAR HEART-DISEASE 445 cardiac tonic is strychnine. It stimulates the heart through its action on the cardiac motor ganglia. The slight retardation of the pulse-rate, which is produced by its stimulation of the inhibitory apparatus, is transient, and therefore not to be reckoned with in considering its therapeutic influence. The increase of arterial tension, said to result from its stimulation of the vaso-motor cen- tres, is so slight that opinions are at variance on this point. This effect is certainly too trifling to prove an objection to its employ- ment, even in cases showing pronounced vascular degeneration and consequent high and sustained pulse-tension. The question of prime importance is, In what dose is strychnine to be admin- istered ? Believing that if it stimulates cardiac contractions in small doses through its action on the motor ganglia, it ought to do this still more powerfully in large ones, I have been in the habit of ordering doses that to many seem dangerous — that is, I have many times prescribed g^j- of a grain hypodermically every three, and even every two, hours, until seven or even eight injections have been given in a day, and have continued these doses for days, and even weeks together without ill effects, so far as I could dis- cover. On the contrary, they have seemed to be of positive bene- fit. Indeed, I may say it never occurred to me that the remedy, even in these doses, could do more harm than occasion the primary phenomena of its physiological effect. As I have but rarely observed twitchings to result, and in these cases have promptly discontinued the drug; I have not thought to question its beneficial action. In a recent conversation with Dr. R. G. Curtin, of Phila- delphia, I was surprised to find that he strenuously objects to such large doses on the ground that it is likely to produce short and irritable systoles instead of long and strong contractions of the ventricle, such as are required to drive the blood onward ener- getically. He thinks that the neurility of the cardiac nerves and ganglia become exhausted. He stated, moreover, that he was gratified to find, during a recent visit abroad, that such experi- enced clinicians as Ernest Sansom and Lauder-Brunton do not exhibit the agent in large doses, contenting themselves in fact with -g^o of a grain three or four times daily. Such opinions are worthy of consideration, and are here given in the hope of stimulating original observation on this point. It is difficult to abandon notions that have dominated one for many years and 446 DISEASES OP THE HEART seem to have the support of favoiirable experience. I feel sure that under the influence of such large and frequently repeated doses I have seen a weak heart rally and evince signs of aug- mented power. I have certainly known a dying heart to be kept beating for hours and days by the combined use of strychnine and nitroglycerin after speedy death seemed inevitable. There can be no doubt of patients becoming so dependent upon this medi- cine, when taken for a long period, that they develop a strychnine habit, the same as a morphine habit. Only the former is not so harmful nor so difficult of abandonment. Whatever may be the answer to this question of large or small dosage in cases of dire urgency, I would not wish to be thought to advise them when cardiac power is only beginning to fail or cannot be said to be entirely competent. In the stage now con- sidered it would probably suffice to prescribe ^ or at most ^^ thrice daily. The length of time during which this agent is to be continued must depend upon the circumstances of each case, and therefore is to be left to the judgment of the medical attendant. The value of the nitrite compounds has already been stated in speaking of the vaso-constrictor effect of digitalis. It may be said in addition that these agents are often highly beneficial in the treatment of aortic regurgitation even when digitalis is not indi- cated. The earliest premonition of failing heart-power in these cases is sometimes shown by attacks of vertigo, and occasionally by syncope, in other instances by a " pounding action of the heart," to quote the language of the patients. These symptoms are an indication that arterial tension is outstripping the contract- ing force of the left ventricle, which is consequently unable to suc- cessfully cope with the heightened peripheral resistance. Digi- talis augments the vigour of cardiac systole, but it also still fur- ther raises arterial tension, and hence may increase rather than lessen the tendency to palpitation. It is better, therefore, to try the effect of ^iu) or it may be less of nitroglycerin three to four times daily for the removal or reduction of undue vascular ten- sion, in the hope that the symptoms will disappear without re- course to digitalis or strophanthus. Glonoin stimulates the heart only indirectly by causing vaso-dilatation, and thus removing ob- stacles in its path, so to s])eak. Exce])ting, therefore, as a vase- THE TREATMENT OF VALVULAR HEART-DISEASE 447 dilator, nitroglycerin is rarely to be employed in this stage of valvular affections. A perusal of the cases narrated in this chapter will impress the reader with the great benefit often derived from cathartic remedies, and the important role played by them in the manage- ment of patients. Their utility was first really impressed upon me by the writings of English authors, and to their teachings I owe much of my success in the management of cardiopathies. I shall have more to say on this subject farther on. It will suffice at this time to direct attention to the tendency of most valvular lesions, especially mitral and those of the right heart, to conges- tion of the veins of the abdominal viscera even before signs of compensatory disturbance grow pronounced. These congestions cannot be so surely and quickly relieved by any other means ; often they cannot be removed at all without recourse to purga- tives. If all that was needed was to increase the driving force of the left ventricle, and thus to push the venous blood onward, then digitalis would be the remedy par excellence. In these valvular diseases, however, there is an impediment to the flow of venous — i. e., of the return blood through the lungs and heart. Behind this impediment the circulation becomes dammed up. The surest mode of preventing an inundation is to provide an outlet, and this is done by carrying off some of the water of the blood through the intestines. When this has once been accomplished, then a heart-tonic or stimulant may be able to reinstate a satisfactory degree of circulatory equilibrium. In some cases it is impossible to do more, or even hope to do more, than keep the stasis within bounds and render the heart's labour somewhat easier. Aloes, cascara, etc., which unload the colon relieve constipation when it exists, but they do not occasion free watery stools, such as are needed to deplete the engorged portal and tributary veins. To this end, saline preparations or such other drugs as are not too drastic are required. Of these, nothing is more efficient than sulphate of magnesia in saturated solution or dissolved in hot water and taken half an hour before breakfast. Its taste is very objectionable to some persons, and it is sometimes rejected by a sensitive stomach. In such an event it is better tolerated if to it are added half a dozen minims of the ordinary essence of ginger 448 DISEASES OF THE HEART kept in every hoiiseliolJ. Four ounces of the compound infusion of senna, the familiar " black draught " of the English, make a very potent and not especially disagreeable hydragogue cathartic. Pulvis jalapi compositus is also highly efficient, and by me greatly esteemed. A teaspoonful may be taken by the average individ- ual, whose venous stasis is pronounced, without his being unduly weakened thereby. There are many other remedies having a simi- lar action, of which space forbids mention. Of all, however, there is nothing which will ordinarily pro- duce such happy results as calomel or blue pill. That they power- fully affect the circulation and promote excretion is shown by the diuresis they promote even before they ■ have emptied the bowel. It is generally well to administer the mercurial at bed- time, and have it followed next morning by a saline. The fre- quency with Avhieh such cathartic medication is to be employed will have to be determined by the degree of stasis and the diminu- tion that ensues. Patients with valvular disease are often ansemic, either be- cause the liver is unable to utilize nucleo-albumins in the manu- facture of iron, or in consequence of the destruction of haemo- globin by some ferment generated in the intestines. The so-called ha'matics, iron, arsenic, and the hypophosphites, w'ould appear to be indicated, therefore, and certainly do act as a tonic, but to my mind it is doubtful whether their beneficial effect is not due to their improving appetite and digestion rather than to their directly increasing the percentage of hemoglobin. Medicines that always appear to me to be of positive utility are all those that facilitate the better digestion of food and lessen the likelihood of gastro-intestinal fermentation. These are pep- sin, pancreatin, taka-diastase, dilute hydrochloric acid, the sim- ple bitters, and the various antiseptic remedies, salol, salophen, benzonaphthol, etc. The use of these agents, together with the improved function of the digestive organs incident to the re- lief of stasis by catharsis, has always seemed to me to do more towards the lessening of the spana^mia than do iron and arsenic. Rest. — Leaving now the consideration of medicinal remedies, we come to certain other factors that are of utmost importance in the restoration of compensation, and of these rest takes the first place. It is universally recognised by practitioners that for weak- THE TREATMENT OP VALVULAR HEART-DISEASE 440 ened hearts no measure is so beneficial as physical repose in the recumbent position. JNTot so with the laity, and patients fre- quently persevere with some form of exercise in the mistaken notion that thereby they will regain strength. So soon as a heart that is damaged by endocardial disease exhibits signs of being sorely overtaxed, physical exertion should be interdicted and the patient put at entire rest until conditions are improved. The rea- sons for this are not far to seek, being found in the mechanical effect on the circulation and in the resulting improvement to car- diac nutrition. When in valvular disease compensation is imperfect, absolute physical rest for several weeks seldom fails to prove highly benefi- cial. The heart is not compensating, because it is being overtaxed by having to receive and discharge more blood than it can handle easily. If in such a case the patient is put to rest, active muscular movements are abolished and respiration is less rapid and more shallow. Venous blood is delivered to the right auricle less rap- idly and the right ventricle is given less work to do. Cardiac contractions become less frequent, but more efficient, and its cham- bers are better able to empty themselves. Thus the decreased inflow and the increased outflow tend to diminish dilatation and promote the re-establishment of that preponderating hypertrophy essential to compensation. Improvement of circulation is shown by the better quality and rhythm of the pulse, by the reduction of signs of stasis, and by augmented excretion of urine. There is improved visceral function in general, and there is better nutri- tion of the whole body as well as of the heart-muscle. This latter, which is of great importance if cardiac power is to be maintained, also results directly from the fact that physical repose favours a better coronary circulation. With the slower action induced by physical inactivity the heart tends to gain in power, and the left ventricle to discharge a greater blood-wave into the aorta. The coronary arteries are bet- ter filled, and the heart-muscle receives a supply of blood more adequate to its needs. This, however, is but a part of the benefit to the heart proceeding from enforced rest, particularly in cases of mitral and aortic obstruction. It has been explained how this treatment lessens cardiac dilatation. It is the right heart chiefly that profits in this way, the ventricle emptying its contents more 450 DISEASES OF THE HEART completely, and stasis in the auricle being diminished. This now acts favourably on the circulation in the coronary veins. With lessened intra-auricular blood-pressure resistance to the outflow from them is less, owing to the fact that they empty into this auricle. Stasis within them tends to subside, and with a better circulation the products of cardiac metabolism are more fully removed. Let us now consider the benefit resulting from rest in the indi- vidual valve-lesions of the left heart. In mitral stenosis there is practically a dam built across the blood-stream at the point where the blood coming from the lungs is poured into the left ventricle. So long as compensation exists the hypertrophied left auricle and right ventricle arc a])le to discharge over this pathological dam — that is, through the narrowed mitral ojiening — so large a portion of the blood sent through the lungs that serious congestion within the pulmonary vessels does not take place. When compensation begins to fail, and cardiac contractions to grow more rapid, the diastolic pause, during which the left ventricle is expected to fill, is shortened, and time is not allowed for the left auricle to empty its contents. Stasis begins in the parts back of the stenosis, and grows ever greater with the progressing loss of compensation. Something must be done to diminish the rapidity and volume of the stream pouring into the left auricle. This is precisely what is accom- plished by rest. Diastoles are lengthened, more time is given for the filling of the left ventricle, which consequently throws a larger quantity of blood into the arterial system, and there is a tendency to restoration of the proper balance between the aortic and pul- monic systems, on the one hand, and the great arterial and venous systems on the other. In mitral incompetence there is a systolic reflux into the left auricle, and the stream entering this chamber from the lungs is momentarily checked, to be the next instant unimpeded as diastole succeds systole and the blood gushes into the ventricle. Yet, while there is a momentary checking of the flow in the ]uilmonic vessels and an in('vitid)l(^ tendency to back-i)ressure, the column of blood into the left auricle and ])ulnionary veins,, together with the walls of these vessels and of the auricle, serves to resist the regurgitant rush from the ventricle. So long, therefore, as this resistance is THE TREATMENT OP VaLVULAR HEART-DISEASE 451 effectual cardiac adequacy is uuimpaircd, and evidences of stasis are wanting. When tliis compensation begins to fail, it is necessary to re- lieve the walls of the left auricle, the pulmonary vessels, and the right ventricle from overstrain by lessening the frequency of re- gurgitation and by retarding the flow from the systemic veins into the heart and lungs. Rest accomplishes this, and thus proves a powerful factor in the resumption of heart-power and the removal of stasis. In the same way also as in mitral stenosis the coronary veins are better emptied and the coronary arteries are better flushed, nutrition of the heart-muscle is improved, the aortic system re- ceives more blood with each systole, and an improved general nutrition results. When in aortic obstruction compensatory hypertrophy of the left ventricle begins to yield to dilatation, the contents of the ven- tricle are no longer adequately driven through the stenosed orifice. Signs of stasis appear and increase in proportion to loss of com- pensation. _^Two things are now required if the threatening breakdown is to be averted : ( 1 ) More forcible contractions on the part of the left ventricle, and (2) the delivery of less blood to the ventricle. Rest slows the heart by lengthening its diastoles, and but little if at all its systoles ; while if it affects the vigour of the latter, it does so only indirectly by relieving it of strain and improving its nutri- tion. It can do very little, therefore, towards enabling the left ventricle to drive blood through the narrowed aortic orifice, and, moreover, experience has taught that when in this disease the left ventricle begins to weaken, it is an indication that the stenosis has overpowered the ventricle. All that is left is to spare this cham- ber as far as possible. It is by accomplishing this, or the second requirement mentioned above, that rest is of service in aortic ste- nosis. It serves to retard the flow of blood into the left ventricle, and thus to lessen the amount which this chamber is required to discharge past the point of constriction. Therefore, although this therapeutic measure is of service in conserving heart-power in this affection, it cannot accomplish such brilliant results as in mitral disease. In aortic regurgitation failing compensation means impaired 452 DISEASES OP THE HEART resistance on the part of the left ventricle to the distending force of the regurgitant stream, a still more imperfectly sustained blood-pressnre in the arterial system, and after a time secondary overfilling of the veins, right heart, and lungs. The danger lies in sudden diastolic arrest of the left ventricle while the mitral valve is still competent, or in such a dilatation of the ventricle that relative mitral insufficiency with all its consecutive evils is pro- duced. The yielding left ventricle must therefore be relieved of dangerous overstrain. Inasmuch as physical exertion and the erect position are thought to raise intra-aortic blood-pressure and intensify the regurgitation, the removal of these injurious, even dangerous, influences becomes imperative. This can only be ac- complished by a rigid, and often prolonged, confinement in the re- cumbent position. There are also two other reasons for insisting upon rest in these cases: (1) Physical inaction slows the flow of blood in the systemic veins, and thus tends to check the discharge into the ven- tricle from the left auricle. With this stream, as well as the re- gurgitant one reduced, the disabled ventricle is called on to handle less blood and finds its labours diminished. (2) Kest of body means also rest to the heart, since by slowing down its contractions its diastole or period of repose is lengthened, while the actual amount of work required of it is reduced. It may ])e argued that the lengthening of diastole favours a better filling of the ventricle, and therefore compels it to put forth greater effort in order to discharge this larger amount of blood. This would be so if the flow to the left auricle were not retarded ; but this latter being the ease, there is not so much likelihood of overfilling the ventricle as when the patient is up and active. This consideration, however, renders it probable that the chief benefit of rest lies in the rest to the heart-walls and in the less forcible reflux from the aorta. The mechanical conditions existing in this lesion, and the nature of the patludogical changes that take place in the myocar- dium, render prognosis exceedingly grave whenever a case of aortic incom])etence shows signs of failing compensation. The probability of restoring heart-power is so slight that any means, however unpromising, should be made the most of. Accordingly, rest of body and mind must be enforced with greatest rigour and THE TREATMENT OP VALVULAR HEART-DISEASE 453 for an indefinite length of time, not merely for weeks, but for many months. As a matter of fact, the prospect of regaining car- diac power in serious loss of compensation is poor, and rest is of service mainly in prolonging life. Since, then, rest is so valuable a means of treatment in our attempt to preserve or restore cardiac adequacy in uncompensated valvular disease, the physician must not content himself with par- tial obedience. If the case is urgent, he must see that his orders are carried out faithfully. When a patient is told that rest in bed is needed, he must be made to understand that by it is meant not rest for a few hours each day, but rest both day and night. Moreover, it does not mean that he can get up as often as he pleases to fetch some article he wants or to walk to the toilet, that is situated perhaps a short distance down the hall. It means that he is to remain in bed, and is to have the attention of a nurse who can spare him all avoidable effort. Patients suffering with aortic insufficiency require more rigid enforcement of absolute rest than do most persons with mitral disease. A single indiscreet effort may undo all that has been gained by weeks of inaction. Therefore, such a patient who is struggling to preserve his left ventricle from complete destruction must lie as quiet as possible, making use of the bed-pan and urinal bottle, and taking his meals in the dorsal decubitus. If this is impossible, as is sometimes the case with nervous individuals, then they may be lifted a little higher by the nurse, and, sup- ported by pillows, may take their meals in this position. Better yet is the adjustable bed, which permits every possible position, without the slightest exertion on the part of the patient. Of course each case has to be treated on its own merits and according to its own exigencies. One patient may be permitted partial rest, and yet do well, while another may require the strict- est enforcement of this principle of management. In some cases, also, the attempt to carry out rigid confinement to bed for months, no matter how important it may be, is sure to create such a spirit of restlessness and discontent as will counteract all that is gained by physical repose. It is evident, therefore, that judgment and tact are often required in the enforcement of this therapeutic agency. Finally, when asked, as he is sure to be, how long rest is neces- 454 DISEASES OF THE HEART sary, the physician should not bind himself to any definite time, but should let it be determined by results. Exercise. — When at length under the influence of enforced rest secondary congestions have been lessened or removed and the heart has regained a sufficient degree of strength, the patient may be permitted to gradually resume exercise. At first he may walk slowly and for a brief period about his room, care always being observed to avoid such a length of walk as causes fatigue, or such sudden efforts as produce shortness of breath and palpi- tation. By degrees the walks may be extended until the patient is able to leave the house and stroll leisurely in the open air. He must not, however, ascend stairs or hills until by proper exercise on the level his heart has grown equal to the effort. Apropos of hill-climbing, a word may be said of the Terrain Cure, or Oertel's plan of having patients with weak hearts develop cardiac power by ascending gentle acclivities. It consists in having a patient walk slowly up a gentle incline at such a pace as does not occasion dyspnoea or consciousness of a laboured and rapid action of the heart — infallible signs of cardiac strain. Then, when an ascent of a certain grade has been mastered, a slightly more diffi- cult slope is to be attempted and overcome in the same careful manner as before, and thus paths of greater and greater steepness are surmounted. It must always be enjoined upon the patient that he is to make these ascents with great deliberation, not per- mitting himself to talk during such efforts, and stopping to rest whenever his breatliing grows short or his heart begins to pound. It is possible in this manner for weakened hearts to attain much greater endurance, even to develop hypertrophy. Experience has demonstrated, however, that it is particularly suited to cases of myocardial weakness rather than of valvular disease. When a mechanical impediment to the circulation exists, as in stenosis or regurgitation, hill-climbing is dangerous, and patients are very apt to overdo. Furthermore, Oertel's method has to be very care- fully supervised if it is to bring about good and not ill results. Consequently, it is but little employed as compared with other modes of treatment, and for cases of uncompensated valvular lesions is rarely advocated. The one system involving ])hysical exertion which gives the best results, and is adapted even to most instances of uncompen- THE TREATMENT OP VALVULAR HEART-DISEASE 455 sated valvular disease, is that forming a part of ISTauheim treat- ment, and which will now be described. Resistance Exercises. — These consist of voluntary movements by the patient of flexion, extension, and rotation of the extremi- ties and trunk, which efforts are carefully resisted by an attendant trained to the work. Not only must the attendant understand how to resist the patient's movements without constricting the part to which he applies resistance, but he must so adjust his counter-pressure to the patient's strength as to not occasion res- piratory or circulatory embarrassment. He must therefore be suffi- ciently skilled • to detect signs of distress and to judge whether too great or too slight resistance is being offered. The indications of respiratory and circulatory embarrassment, for which the attendant is to watch, are dilatation of the nostrils and sighing or irregular breathing, increasing duskiness or pallor of the countenance, a drawn look about the mouth, yawning, per- spiration, and palpitation. So soon as any of these signs are de- tected the movement is to be stopped and the patient's extremity slowly allowed to assume a position of rest. Then, after a suffi- cient period for repose, the exercises may be resumed. Patients are very apt to hold the breath while executing these movements or to hold the body rigid, thus putting forth effort with more than the limb that is being resisted. The attendant should therefore remind the patient from time to time to continue breathing, and should see to it that his pose is easy and unconstrained. Atten- tion to these points will enable a patient to go through the series of movements without fatigue or strain. Furthermore, the same movement is never to he made twice in succession, and each one is to be followed by a brief pause. It is also well in some cases to allow the individual to sit and rest occasionally during the treat- ment. As his endurance grows, such precautions become less and less necessary, although the attendant must never allow himself to be thrown off his guard and forget to maintain close watch of the patient's.. condition. Many persons of considerable muscular strength a.^'s wclined to regard the exercises as too easy and to think no len th(t can accrue from such gentle exertions. They consequenStartiant to have more resistance offered ; but to all such requests the-lactendant must turn a deaf ear. The last injunction to be observed is to have the movements 456 DISEASES OF THE HEART made slowly and vnthont jerldness. Unsteadiness of movement is certain to be produced if a slow movement, particularly of the arms, is too strongly resisted. The object or purpose of these exercises is not to develop the muscles, but to influence the heart and circu- lation ; all of which is only accomplished when the various move- ments are executed slowly and steadily, and the counter-resistance is accurately adjusted to the patient's strength — that is, his car- diac not his muscular strength. Finally, the operator must not grasp the patient's arm, wrist, or leg, as the case may be, for this would hinder the free play of the muscles, but he is to exert counter-pressure or resistance by placing the palmar surface of his hand or fingers against that side of the patient's limb which looks in the direction towards which the extremity is to be moved. It often conduces to steadiness of movement for the assistant to place his other hand against some other part of the limb or trunk than that to which resistance is applied. The following descrip- tion gives the exercises in the order in which they are usually executed : (1) The arms are extended in front of the body on a level with the shoulders and with the ]ialms of the hands touching. They are then slowly and steadily moved outward until at a line with the front of the chest, while at the same time the attendant gently resists this horizontal movement. The attendant now changes his hands, so as to exert pressure against the palmar surface of the wrists,, i the patient slowly and steadily brings his arms back to the poa . i rhence the original movement started (Fig. 84). (2) The right arm hanging at the side, with tn , palm of the hand forward, the forearm is slowly flexed against counter-resist- Fio. 84. THE TREATMENT OF VALVULAR HEART-DISEASE 457 ance bj the attendant nntil the fingers touch the front of the shoulder. The attendant then changes his point of pressure to the back of the arm, and the extremity is slowly returned to its former position at the side (Fig. 85). (3) This consists of precisely the same movement, but exe- cuted by the left arm. (4) Both arms, depending at the side, are slowly raised lat- erally until the thumbs meet above the head, and are then brought down to their original position, these movements being carefully resisted throughout. (5) The patient clinches his hands in the form of a fist, but with the thumbs extended upon the ulnar surface of the index fingers. The tips of the thumbs are then gently pressed together in front of the abdomen, and, a proper degree of resistance being offered, they are thus slowly raised until the hands rest on the top of the head, after which they are slowly lowered to the original position (Figs. 86 and 87). (6) The arms, depending at the sides, are then elevated for- ward and upward without bend- ing them until they are held aloft on a line with the perpendicular axis of the body. They are next slowly allowed to resume their position at the side in the same careful manner in which they were raised. To properly resist this movement requires much practice and skill, for the reason that the hand of the attendant must be continually slipped around the patient's wrist to suit the changing attitude, first to the horizon- tal and then the vertical (Figs. 88 and 89). (7) Starting with the arms hanging at the side, the right arm is slowly rotated forward, upward, backward, and downward around the shoulder- joint as the pivot, and then in the reverse 31 Fig. 85. Fig. 86. Fig. 87. Fig. by. THE TREATMENT OF XALVULAR HEART-DISEASE 459 direction until the circle is completed, counter-pressure being all the time exerted by the attendant, (8) This consists of a similar movement, executed by the left arm. These two movements are difficult both for the patient and the attendant, and should not be given to patients who are very weak or whose hearts are incapable of withstanding much exer- cise. Resistance to this movement is likewise extremely difficult, for the reason that the attendant has to change hands during the progress of the movement, yet without causing jerkiness or too much interference. (9). The patient bends his body forward at the hips with- out flexing his knees, and then brings it back to the erect position, while the attendant, standing at his side, resists the forward movement by one hand against the ujDper part of the sternum and the other in the middle of the back, and the return movement of the trunk by one hand against the upper dorsal region and the other upon the epigastrium (Figs. 90 and 91). (10) Standing with the feet firmly planted upon the floor, the patient rotates his trunk around its vertical axis, at first to the left, next to the right, and then back, so as to face forward, as before starting. The attendant resists this movement by placing one hand against the advancing shoulder and the other in the opposite axilla, and then changing his hands as the body is rotated in the opposite direction (Fig. 92). (11) In this movement the trunk is bent laterally, first in one direction, then in the other, and lastly is brought at rest in the upright posture. To resist this flexion the attendant places one hand on the hip and the other against the side of the chest towards which the body is to be bent (Fig. 93). (12) Both arms hanging at the sides, with the palms facing towards the thighs, are simultaneously moved backward and upward as far as possible without bending the body, and are then brought down to the sides, resistance meanwhile being carefully exerted by the attendant (Fig. 94). (13) The patient supports himself by resting one hand on a chair, and then raises the opposite leg as far as possible in a lat- eral direction, while the attendant resists both the upward and the return movement (Figs. 95 and 96). Fit*. 90. Fii,. 'Jl. Fio. 'J2. Fio. 'J3. 460 Fig. 94. Fiii. H5 YiG. i)G. Fu.. u: 461 Fni. '.t'j I'lo. 101. THE TREATMENT OF VALVULAR HEART-DISEASE 463 (14) This is the same movement, but done with the opposite extremity. ^ (15) Resting one hand on a chair, as heforo, the patient extends his opposite leg and thigli, bnt without Ixmding his knee, as far forward and upward as possible, after which the extremity is slowly returned to its original position, resistance to both movements being offered by the attendant (Figs. 07 and 9S). (16) This is a similar effort put forth by the opposite ex- tremity. (17) Both hands supported on the back of a chair, one leg is flexed at ±he knee while re- sistance is offered by the attend- ant's hand placed at the heel. The return is resisted by the hand against the ankle just above the instep (Figs. 99 and 100). (15) This is a corresponding movement by the other leg, re- sisted in the same manner. (19) Supporting himself by the back of a chair the patient flexes his thigh at the hip, the leg hanging limp and flexed, wdiile the attendant resists first the upward and then the downward movement (Figs. 101 and 102). (20) This is a similar movement by the opposite thigh. If desired, additional movements of flexion, extension, and rotation of the hands and feet may be devised. In carrying out these exercises care should be taken that movements involving the use of the same groups of muscles do not succeed each other directly, but are interrupted by exercises made by different sets of muscles. The purpose of this precaution is the avoidance of undue muscular fatigue of weak patients. Given with requisite deliberation, and with sufficient pauses for rest between move- ments, such a series of resistance gymnastics ordinarily takes about Fig. 102. 464 DISEASES OP THE HEART half an hour. If after a rest of ten to fifteen niinntcs the i):iticnt does not feel or evince fatigue, he may then repeat the series. Tliey are generally given daily, an hour or more after a meal. Patients whose condition is fairly good may be allowed to per- form them twice a day — that is, in the forenoon and again in the afternoon. These exceedingly simple exercises are a powerful agent for good or a means of great harm, depending on the manner in which they are given and the condition of the heart. I do not believe they should be given to patients whose compensation is wholly gone. In this opinion I differ, I think, with Schott and Bezly Thorne, who have written so much in praise of them. If there is pronounced stenosis of an orifice, with great dilatation of the chambers back of the lesion, harm may follow their employment, the same as with digitalis incautiously given. This was sadly illustrated in one of my cases. First lessen the cardiac inade- quacy by rest and other treatment, and then these movements are likely to prove highl}^ beneficial. In more than one patient, whose enormously congested liver had refused to subside under the free and prolonged use of cathartics and heart-tonics, I have seen the organ diminish rapidly in size during the administration of re- sistance together with breathing exercises. It seemed as though they served to bring about an aspiration of the blood out of the engorged liver. They are far superior to massage, which seems to me to i)roduce just the opposite effect. Massage promotes a more rapid and ampler flow of blood to the heart, while resist- ance movements ai'c thought to exert their salutary effect by dilat- ing the arterioles, and thus unloading the overburdened heart. Nauheim Baths. — The balneological treatment of heart-disease has not received as much attention in this country as in Europe, and yet it has been growing in popularity even here. Large num- bers of wealthy Americans and Englishmen annually make pil- grimages to Germany for treatment at the little resort known as Bad Nauheim, where the employment of cool saline and efferves- cing baths was first introduced in this class of affections. Patients of moderate means cannot afford so expensive a journey, and must either forego this treatment altogether or content themselves with the use of artificially prepared waters. For tlie consolation of such it may be stated that amj)le experience all over the world, but THE TREATMENT OF VaLVCJLAR HEART-DISEASE 465 particularly in England, has shown that equally efficient results may be obtained in this way as at Bad Nauheim. I myself took a course of baths at that resort in the summer of 1893, and ever since my return have been employing this plan of treatment in suitable cases, and can justly claim priority in this regard over all others in this country. I have not desired to make a fad of this treatment, and therefore have not subjected as many patients to it as might have been done, but it is within bounds to say that considerably over one hundred have thus been treated by me. Some of my patients have taken the baths in Germany, generally after a course in Chicago, although one has just finished here who has previously treid the baths at Bad ISTauheim. All agree in the statement that the effects with artificial waters are the same as with the natural, the chief and perhaps striking difference consisting in the more powerful effervescence of the latter, par- ticularly in the form of the Sprudel-Strom-Bad (flowing effer- vescing bath). Another advantage in favour of the latter lies in the consideration that when a patient goes to Germany he leaves his cares behind him, and while there abandons himself to the one purpose of getting well. On the other hand, I have been assured that, owing to the immense number of invalids who frequent the place, patients are apt to miss the watchful care and oversight which many of them require and receive at home. The waters of Bad jSTauheim are impregnated with various chloride salts, the two to which particular virtue is attributed in their effect upon the circulation being the chlorides of sodium and calcium. In addition, the springs used for the j)reparation of the baths are highly charged with carbonic acid, which makes them very stimulating, particularly when used in the form of the flow- ing bath — that is, with a steady stream of effervescing water flowing over the body of the bather in the tub. This is compara- tively rarely prescribed, being considered too exhilarating for any except those in fairly robust health. It is the rule in the employment of this balneological treatment to begin with water of a temperature of 93° to 95° F., according to the ability of the patient to react, and with water containing 1 per cent of sodium chloride and ^ per cent of calcium chloride, but no carbonic acid, this latter being added at the end of the second week, or when a temperature of 91° to 90° F. has been attained. The duration of 466 DISEASES OF THE HEART the first bath is from five to eight minutes, depending upon the strength and reaction of the individual. One treatment is taken daily for two or three successive days, and then comes a day of rest. This is to prevent undue depression, as is likely to be expe- rienced when no interruption in the course of treatments occurs. The patient is required to rest, by preference lying down, after each bath, and if reaction is not good and prompt to take a warm drink of some kind and to cover up warmly. He is also required to see his medical attendant daily, or as often as the latter may elect, that the effect of the treatment may be judged of and the baths modified as his progress requires. The principle underlying the ordering of these is that the percentage of the ingredients is to be increased, the temperature lowered, and the duration length- ened until finally the chloride of sodium reaches 3 per cent, chlo- ride of calcium 1 per cent, the temperature 87° or 85° F., and the time twenty minutes. The rapidity with which this change can be effected depends upon . the degree of objective and subjective improvement ob- served, but as a rule this maximum is not attained under three or it may be four weeks. In the more serious cases, or such as ex- hibit considerable anaemia and sluggish reaction, it is not always wise to bring the temperature below 89° or even 90° F., although the maximum in strength and duration may be the same as when lower temperatures are prescribed. It is not well to reduce the temperature more than a degree at a time, and whenever this is done the proportion of the salts is usually increased. For the most part effervescing baths are ordered at the end of ten days or two weeks, or when the higher percentages of salts have been reached ; but if the patient is inclined to chilliness at a temperature that ought to produce at least a tolerable feeling of warmth, or if afterward the extremities are cold and the skin does not get into a good glow, it may be well to add the gas at an earlier period. The warmer saline baths, 95° to 92° F., are con- sidered soothing, while the cooler effervescing ones, 89° to 85° F., are stimulating, and hence are not applicable to very weak hearts. The direct effect of each bath should be to render the pulse slower, of better quality, and more regular if previously irregular. The area of deep-seated cardiac dulness diminishes and the heart- sounds grow stronger. Endocardial murmurs intensified by dila- THE TREATMENT OF VALVLTLAR HEART-DISEASE 467 tation may become less loud, or if weak from cardiac asthenia, may after the bath be found to be more intense. The degree of benefit is to be determined chiefly by the size of the heart and by the character of its action. As a rule, also, the patient is con- scious of a sense of well-being and of some lessening of whatever symptoms have annoyed him. If the treatment has been judiciously ordered and overseen, the heart is found to gain in strength week by week, visceral con- gestions diminish, as evinced by increased diuresis, the colour of the skin grows more like that of health, and the patient gradually gains in vigour and ability to exercise without discomfort. Just how this balneological treatment brings about improve- ment is still a matter of speculation and discussion, being by Schott explained on the hypothesis of increased tissue change together with a reflex stimulation of the heart Avhicli causes its slower and more powerful contractions, and with a physiological stimulation of the arterioles and capillaries by the passage of the gas and salts through the skin. By others, in particular Broad- bent, the beneficial action of the baths is attributed to dilatation of the cutaneous capillaries, in consequence of which resistance to the work of the left ventricle is lessened and the transfer of blood from the venous to the arterial system is promoted. The objection urged against this explanation is, that the rate of the pulse should be increased rather than decreased, so that there must be some additional influence at work. The following is the view of Medicinalrat Groedel of Bad jSTauheim : " The incon- testable success which our baths have on the heart's function and the entire circulation is only to be explained if we believe in a direct action by way of the end-organs of the cutaneous nerves on the central vascular and cardiac nervous system, both trophic and motor." It may also be stated that so far as concerns the demon- strable effect of the two means of treatment, the resistance gym- nastics and the baths, the results if not the action are identical in diminished size of the dilated heart and improved energy and steadiness of its contractions. Consequently it is customary at Bad ISlauheim to have the patient receive both forms of treatment each day. Finally, it is usual to send the patient away at the close of a course of baths for a rest of a month to six weeks, after which he returns for another course known as the after-cure. 468 DISEASES OF THE HEART Inasmuch as the effect on the heart and cirenhition of the arti- ficial and natural waters is identical, 1 will now describe how the former are prejiared. The ingredients required are common salt (chloride of sodium) and chloride of calcium, bicarbonate of so- dium, and compressed tablets of acid sulphate of lime. Instead of these latter, commercial hydrochloric acid may be used. The first is to be had as ordinary '' butter salt " of the trade, while the calcium salt comes in iron drums holding from 600 to 800 pounds. This latter is, moreover, deliquescent, and, being corro- sive, is most conveniently kept in a strong solution of definite strength. I have it kept on hand by one of the Chicago druggists, who dispenses it to my patients on my prescriptions. To begin with, the baths contain onl}^ these two ingredients, and are there- fore simple brine baths. It takes from 50 to 60 gallons of water in an ordinary-sized bath-tub to immerse a person of average size up to his neck when lying in a semi-recumbent position. When the amount of water is known it is an easy matter to determine tHe number of pounds of salt and the number of pints of calcium- chloride solution to be added. When at length the water is to be charged with carbonic acid in addition, it is done by dissolving bicarbonate of soda, 2 pounds to each bath, and the same number of ounces of commercial muriatic acid or the compressed tablets already mentioned. The acid is so corrosive and difficult to keep without its fumes injuring the furniture of the bath-room that I now order the packages of " effervescing bath salts " manufac- tured for the purpose by two firms in Kew York city, and which are likewise kept in stock by the Chicago druggists. Each pack- age contains 2 pounds of soda and 8 tablets and printed direc- tions for their use. One such package is required for a single bath. These effervescing tablets possess this additional advantage over the acid, that the evolution of gas is steady and continuous. They are also, however, corrosive, and the bottom of the tub should be protected by a rubber sheet. It is my custom to prescribe the baths in groups of three with the rest day between — that is, on every fourth day — and a course usually extends over a period of six weeks. In most cases the resistance exercises are also taken, l)ut some hours prior to or after the bath, that the effect on the heart may be maintained. I always strive to impress patients with the importance of living THE TREATMENT OF VALVULAR IIEART-DLSEASE 469 as quiet and routine a life as possible, and in particular to strenu- ously avoid undue cardiac strain that they may not destroy the benefit expected to be derived from the treatment, I can recall only 5 cases in which this plan of treatment seemed to do harm rather than good. Two were instances of chronic myocarditis, the hearts being very dilated and their action arrhythmic. One was a mitral lesion with oedema and other signs of rather a badly destroyed compensation ; but as this patient was compelled to journey some distance each day to get his bath, it may be that the exertion thus required, and not the treatment, was responsible for the want of improvement. The remaining two were cases of serious valvular disease complicated by pericardial adhesions. In both, the engorgement of the liver became mani- festly greater towards the termination than at the commencement of the course, and the treatment was discontinued. All other patients have exhibited more or less improvement, while in some instances this has been most gratifying both to the patient and myself. I am very positive in my belief that this treatment should not be given to persons whose compensation is wholly lost, or indeed seriously broken, and therefore the consideration of this measure has been introduced in this portion of the present chapter. I have just finished giving a course of 30 baths to a lady with a pure mitral stenosis who, when she began, gave indications of failing, or at least threatened, compensation. The second sound at the heart's apex was wanting, there being only a presystolic murmur and sharp first sound. She complained of much ill-defined dis- comfort at the heart, and the pulse was rapid and exceedingly feeble. Before the course was completed the second sound had returned at the apex, the area of cardiac dulness was distinctly smaller, and the pulse was slower and of greater volume. She declared she felt perfectly well. In this instance, as is often my habit, I ordered the frequent use of a laxative water, and for a time 5-drop doses of fat-free tincture of digitalis thrice, then twice, and at last but once daily. I do this because it has seemed to me that in this way I have secured more lasting results. Contra-indications to the employment of this balneological treatment are the following: Aortic aneurysm, pronounced and extensive arteriosclerosis, and, in my opinion, all cases manifest- 470 DISEASES OE THE HEART ing marked signs of cardiac inadequacy, such as ascites and con- siderable dropsy with a greatly distended and feeble heart, and cases complicated by extensive mediastinopericardial adhesions. Chronic renal disease does not contra-indicate the treatment unless, of course, it has led to too pronounced a degree of car- diac incompetence. Lastly, it may be stated that if the pulse does not grow of better quality after the bath, but, on the contrary, is observed to become less full and strong, the treatment will not produce beneficial results and would better be discontinued. Diet. — This is a matter requiring in this stage of valvular heart-disease very careful attention, yet concerning which notions are for the most part woefully vague and inaccurate. Physiologi- cal chemistry has not yet worked out the changes taking place in the digestive process as a result of disease. We know that the passive congestion of the abdominal organs produced by un- compensated cardiac disease leads to a chronic catarrh of the stonuich (Einhorn), with diminution and even disappearance of the hydrochloric acid (lliifler and Jorn), which, with its im- paired motility, may seriously derange its function. Reasoning by analogy, we may also assume that the pancreatic and hepatic secretions are likewise altered in quantity and quality, or that if not secreted in less amounts they are poured into the duodenum in diminished quantity in consequence of catarrhal obstruction to their outflow. Just what modification in the character of the pancreatic juice takes j^lace we do not know, yet clinical obser- vation seems to warrant the inference that the amylopsin and fat-splitting ferment are more unfavourably influenced than is the proteolytic ferment. Furthermore, in consequence of sluggish circulation in the veins that carry blood to the portal system, the bile is absorbed slowly from the intestine, and when secreted is watery and poor in mineral constituents. Although the secretion of bile is but a minor function of the liver, still a deterioration in its quality and diminution in its quantity must exert a baneful influence upon intestinal digestion. These theoretic considerations are borne out by clinical observations, for cardiac patients are very prone to gaseous distention of the stonuich and intestines and to eructa- tions and other indications of fonuentation of the ingesta. The fatty acids thus engendered occasion still further irritation of the THE TREATMENT OF VALVULAR HEART-DISEASE 471 stomach and establish a vicious circle which augments the evils primarily attributable to disturbed circulation. This is not the only aspect of the case. There is alteration in the metabolic processes incident to derangement in the blood-sup- ply to the digestive and other viscera, while toxines are locally developed which either must be destroyed in the engorged and functionally impaired liver or must pass through into the general blood-stream and exert their noxious effects upon the heart and nervous system. The investigations of Husche appear to show that the excretion of urea and uric acid is altered. The retention of the former is variable, while the excretion of the latter is hin- dered during disturbance of compensation and increased after this has been restored. It is not strange, in the light of the foregoing considerations, that some patients are greatly disturbed by fermentative indiges- tion after the taking of the simplest and most easily digested food. Dyspnoea is intensified or developed, or they are distressed by palpitation. Others are not conscious of local disturbance, but complain of pains and aches, muscular stiffness and cramps, nerv- ous symptoms, such as despondency, insomnia, and frightful dreams, fidgetiness of the legs, and sundry other sensations that are so commonly attributed to uric-acid retention. It may be re- marked here, however, that Dr. Wesener's researches appear to show that these constitutional symptoms, as well as many others, are due not to uric acid, but to indicamiria and oxaluria. One of my patients was greatly troubled by headache, insomnia, and other nervous phenomena, and Wesener's analysis of her urine col- lected at the time showed an enormous excess of indican and oxalic acid. Thereupon an attempt was made to stop proteids and administer carbohydrates in the hope of relieving her dis- tress. It was found, however, that at once she began to have so much flatulent distention of the stomach and bowels with aggrava- tion of her dyspnoea that the non-nitrogenous diet had to be aban- doned for a return to meats, etc., wdth all their evil consequences. The problem of how to pieet the food requirements of cardiac sufferers is a complex one and most difficult of solution when w^e have to do with the stage of imperfect compensation. It is quite generally agreed that in cases of heart-disease uncomplicated by renal lesions the myocardium should be supplied with a relatively 4Y2 DISEASES OP THE HEART large proportion of proteids. The main reason for this lies in the fact that the nitrogenous principles are tissne-forniing, and hence reparative elements of the dietary, and should be in excess when- ever there is a demand for increased muscular work, as is the case in cardiac affections, ^loreover, meats and other foods rich in proteids do not undergo the same sort of fermentation and gen- erate so much gas as do earholivdrates, and do not so injuriously distend the hollow abdominal viscera. They are not so bulky, and therefore, relatively to the quantity ingested, contain a far larger proportion of nutrient material. For obvious reasons persons with uncompensated valvular lesions should have their dietary definitely ordered and carefully supervised' by their medical attendants. It should be remembered that digestion and assimilation are both slow, and therefore the first rule to be laid down is that food is not to he taken at short intervals, but ample time allowed for the stomach to empty itself before fresh nourishment is adminis- tered. The fatty acids and other irritating products of fermenta- tion often occasion a feeling of faintness or gnawing at the epi- gastrium which is mistaken for hunger and thought to indicate a need for more food. In other cases appetite is poor and patients are unable to eat heartily at the regular meal-hours, and hence the friends and even the physician get the idea that the meals must be re-enforced by milk, egg-nog, etc., midway between. I have thus known nourishment to be administered every two or three hours. Sucli is undoubtedly a mistake. The congested and per- haps ocdematous walls of the stomach cannot by energetic peristal- sis empty the chyme into the duodenum as rapidly as normal, and the conditions for decomposition being favourable, the taking of additional food l)efore the stomach is ready for it results in serious disturbances. rurthermore, tliese patients are often tormented by thirst and are permitted to pour down liquids of all kinds into the already distended and irritated viscus at irregular intervals, so that ab- dominal distention, eructations, flatulence, and increased dysp- ncea add to the patient's distress. These considerations have in- duced me to set five or five and a half hours as the proper length of the interval that should elapse between the meals. I do not ])C'rmit milk to be taken between times, since by being curdled in THE TREATMENT OP VALVULAR HEART-DISEASE 473 the stomach it is practically the same as solid food. When in some cases the feeling of faintness and weakness makes some intermediate nourishment unavoidahlc; I order a clear broth or bouillon, or weak tea containing a little cream but no sugar, etc. So simple a restriction as this has often been found to work won- ders in removing the thirst and epigastric gnawing. A cupful of hot water drunk an hour previous to a meal seems to facilitate the expulsion of the stomach contents and to clear the way for the ingestion of fresh food. The next rule is the restriction of the quantity of fluids to be taken with meals. In severe cases liquids should be limited to 6 ounces, and even in mild ones 10 ounces should be the maximum. This does not mean only water in addition to any other fluids that may have been ordered, but includes all liquids combined and consumed in addition to solid ingesta. The purpose of this restriction is to prevent undue distention of the stomach in those cases in which such distention would be likely to occasion short- ness of breath or embarrassed cardiac action. The rule is that patients are to be restricted in the amount of their solid food, for it is not rarely observed that they manifest a veritable bulimia, and if permitted to do so will overload their stomach and sorely overtax their digestive and assimilative capa- city. A simple and usually sufficient guide as to the amount that may be safely consumed is to be found in the injunction that they finish each meal feeling they could eat more. A little, well digested, is worth far more than a good deal, poorly digested. This restriction not only lessens the danger of distending the atonic organs which it has been shown furthers decomposition, but it tends to prevent the cardiac embarrassment occasioned by repletion. Such a limitation of the patient's food must not be carried to the extent of starvation ; and yet if the quality of the nourishment is judiciously selected it will often be a matter for surprise how small a bulk will suffice — nay, how it will minister to the patient's comfort. In considering the articles of food suitable to this class of suf- ferers I think it best to deal with the subject in a general way rather than to attempt to make up appropriate menus. Tea and coffee should be weak and contain such an amount of sugar and cream as depends upon the degree of digestive disturbance. Cocoa 33 474 • DISEASES OP TEE HEART or Lroiiia is preferable to clioeolate because containing less fat, and when made with milk is nutritious. If wine or liquor is thought advisable, it should be freely diluted with water. But- termilk, kumjss, and malted milk make a valuable addition to the dietary, and generally agree well. Effervescing beverages are objectionable on account of the distention they occasion ; and for this and other reasons malt bev- erages are not advisable, unless in special cases when they are craved on account of their bitter taste or their stimulating the flagging appetite. Iced drinks and very hot fluids are not well borne, since medium temperatures are better for weak stomachs. The admissibility of soups and l)roths must be determined by the condition of the kidneys and the habits of the individual. When chronic ne])hritis exists, stock soups and meat extracts are to be forbidden, since animal extractives are irritating to the renal epithelium. It should be remembered that beef-tea and the like are stimulants and possess no real food value. Cream soups, or purees as they are called, are not open to the same objection and are highly nutritious. All these are fluids, however, and when taken in connection with solid food should be limited in amount, lest they blunt the appetite for what is to follow and create a feeling of repletion. Carbohydrates should be allowed but sparingly because of the following considerations: In the first place they readily undergo fermentation and occasion flatulent distention of the stomach and bowels; while in the second place they are so readily oxidized that they appropriate the oxygen necessary for the utilization of the nitrogenous principles of the dietary. Nevertheless, sugars and starches cannot be withheld entirely, and hence they must be in the least objectionable forms. To diminish their tendency to fermentation the latter should be so thoroughly subjected to heat in cooking that the starch granules become converted into grape-sugar. Toast, zwieback, light crack- ers, and " pulled bread " and muffins or tea biscuits made with baking-powder are preferable to bread which has been raised by means of yeast and is often imperfectly baked. If potatoes are allowed, they should l)e baked and mealy, and even cooked in this way they should not be taken in unlimited amounts. Rice when well boiled may be also permitted in restricted quantity, but sweet THE TREATMENT OF VALVULAR HEART-DISEASE 475 potatoes, cereals, and tlie multifarious combinations of flour, but- ter, and sugar, whether with or without eggs and milk, known as cake, griddle-cakes, etc., are inadmissible. Most desserts, and in particular sweetmeats, confections, pre- served and canned fruits, are to be allowed only to those patients who can dispose of such articles without annoying flatulence. Fruits are best in their natural state, and even then should be ripe and fresh. Apples are particularly good because of their rela- tively large percentage of nucleo-albumin, and when baked are often better tolerated than when uncooked. Pineapple has always seemed to me a particularly desirable fruit because containing a natural digestive ferment of great efficiency. As a general thing I regard it as better for cardiopaths to take fruits at the close rather than at the beginning of a meal, as they do not blunt the appetite nor create so much gas. Most of the fresh vegetables are valuable additions to the dietary, either because rich in proteids and other nutritive prin- ciples, or on account of their serving as relishes and containing various salts essential to the organism. Peas, lentils, string- beans, and spinach are said to be relatively rich in iron-forming principles. Tomatoes, cabbage, cauliflower, turnips, and kindred varieties are apt to disagree, but if well borne may be permitted. Asparagus, when not contra-indicated by renal disease, celery, let- tuce, greens of various kinds, and young onions are allowable, while cucumbers, tender radishes, and olives may be left to indi- vidual desire and ability to tolerate without distress. Mush- rooms are very rich in proteids, and for renal patients supply a form of nitrogenous food that is not open to objection as is animal food with its extractives. Beets are rich in sugar, as is corn, and are likely to occasion flatulence. Of foods rich in proteids beef and pork head the list, but perhaps are not so easily digested as are veal, lamb, and mutton, which are excellent when not too fat. All meats should be roasted, broiled, or stewed, not fried ; but however prepared, they should be as free from gravy as possible and ought to be so well done as to have destroyed the germs of decomposition through whose action during the time of hanging the meat becomes tender. Fowl and game-birds form a capital adjunct to the heavier meats, as also do fish and most kinds of shell-fish, particularly oysters when raw. 476 DISEASES OF THE HEART Some of the salted fish and meats when n.ot too rich provide appe- tizing and nutritions dishes. Canned sahnon, sausages, etc., are too rich in oil and fat, and are apt to cause eructations, whereas fresh tripe is said to be easy of digestion. Cheese is highly nutri- tious, and when known not to occasion constipation or distress may be allowed. This is especially the case with cottage and cream cheese. This article of food should not be taken when cooked. Eggs are very digestible and form a valuable addition to the dietary of this class of invalids. Years of experience in the feeding of cardiopaths has con- vinced me that their food should be plain and that where more than ordinary indigestion exists the menu should not be elaborate. It has seemed to me an excellent plan in some instances to sepa- rate the carbohydrates from the aninuil foods — that is, to give them by themselves. Then at the meals composed chiefly of ani- mal food only vegetables or relishes, such as asparagus, lettuce, or celery, are allowed in addition. In this manner has been pre- vented much of the putrefactive decomposition of meats which engender the distressing symptoms of indicanuria and oxaluria. In conclusion, a few words may not be amiss concerning an absolute milk diet in cases of cardiac inadequacy. It has been highly recommended in conjunction with absolute physical rest as an excellent means of restoring compensation when this is threat- ened. It acts probably by lowering arterial tension and lessening or removing the evils of the defective digestion of solid food, since milk alone acts as an intestinal antiseptic. Furthermore, by virtue of its sugar, milk often exerts a pronounced diuretic action, and thus aids in the removal of minor degrees of dropsy. When administered as the exclusive article of diet, it is best given blood- warm and in moderate amounts at regular intervals — e. g., a cuj)ful every two hours. It sometimes agrees best when diluted with an alkaline water, as Vichy or Seltzer water. Such a diet should not be maintained indefinitely, and in most instances pa- tients begin to plead for more substantial nourishment at the end of two or three days. It should be ])ersisted in, however, until the results aimed at liave Ijocu readuMl, when a gradual return to solid food is to be iikhIc. Clothing, Habits, Occupation. — What has been said in preced- ing pages under these heads applies with still greater force to THE TREATMENT OP VALVULAR HEART-DISEASE 477 subjects of valvular niiscliief Avlicn their compensation is imper- fect. The influence of these factors is subsidiary to those that have just been considered, and yet these matters are by no means unimportant. A too tight corset or waistcoat may so hamper thoracic movements and so impinge on the distended right or left ventricle as to frustrate all attempts to reinstate compensation by digitalis, resistance exercises, baths, etc. Constriction of the chest and abdomen is therefore to be sedulously guarded against. The immoderate use of tobacco will assuredly prove depress- ing to the heart-walls we are striving to strengthen. Alcoholic excess, even though intoxication does not result, injures an un- compensated heart by causing excitation and exhaustion of the cardiac muscle-fibres. Sexual excess, perhaps even very moderate indulgence of this kind, may maintain or increase the very dila- tation we are endeavouring to overcome. It should therefore be strictly forbidden until such time as the heart-power shall have been reinstated. Occupation of all kinds, particularly such as involve even the lightest possible physical effort, and exciting, long-continued brain work, must be laid aside while compensation is defective. Unfor- tunately, the circumstances of the patient do not always admit of a rigid enforcement of this injunction. When this is the case, the danger of injury from his occupation must be explicitly stated, that the work may be performed in the easiest possible manner. It is always w^ell to furnish such explanation, together with a warning, that in the event of damage resulting from a con- tinuance of the employment the physician may not be held respon- sible for the failure of treatment. Only by attention to details can the medical man hope to turn what threatens to prove a disas- trous defeat into a brilliant and it may even be an unexpected victory. It is precisely in this class of cases that modern cardio- therapy obtains its most signal and astonishing triumphs. There is no other class of cases which so amply rewards intelligent and painstaking management. CHAPTER XVIII THE TREATMENT OF VALVULAR HEART-DISEASE {Concluded) III. COMPENSATION LOST In some cases of valvular disease that have reached this stage, restoration of their compensation is impossible and the physician can do no more than mitigate the jDatient's suiferings or add a few weeks or months to his life. In other cases skilful management may so assist the heart in its struggle that it is able to overcome the obstacles in the way of the circulation and regain a measure of its former adequacy. The weapons with which to aid Nature are at the command of all, but the knowledge how to make them most effective is possessed by only a few. Digitalis is the weapon on which chief reliance is to be placed. It has its congeners, which are sometimes of greater service because of some differences in their action — e. g., strophanthus, which exerts less constricting effect on the arterioles. It is safe to say, however, that thera- peutists of greatest experience place more reliance on digitalis than any other remedy of its class, and that as a clinician grows in experience in the treatment of this group of lesions he generally comes to employ this drug more and more often, and strophanthus and similar remedies with decreasing fre(pieney. It is not alone necessary to have knowledge of its mode of action; one must also understand the indications and contra-in- dications for its use. The skilled hunter will procure more game with an expenditure of less ammunition than will an untrained sportsman. So likewise with this great remedy. The experi- en('('(l and skilled clinician will acconijilish more oftentimes with small doses than can he who is not trained to recognise the condi- ti(ms that do or do not call for its administration. Inexperienced ])ractitioners are apt to think they must order digitalis so soon as called on to treat a case of valvular disease willj ruj)tured cora- 478 THE TREATMENT OF VALVULAR HEART-DISEASE 479 pensation, no matter how great the visceral congestion or extensive the (Edema. Indeed, the presence of dropgy is generally consid- ered the indication for digitalis, and hence this drug is prescribed as the sovereign remedy ; when this fails, the case is considered hopeless. As a general proposition it is true; bnt in many cases the giving of digitalis at first is analogous to whipping a horse that cannot draw his load up hill. He fails, not because of lack of effort, but because his load is beyond his strength. Lighten his load, and the poor beast will surmount the hill without faltering. The crippled heart fails in its labours, as a rule, because its task has become too great, and not from weakness inherent in its myo- cardium. It has become like a jaded horse, exhausted yet willing still, which may respond for a time to whip and spur, but will die in the attempt. Overdilatation — that is, overdistention — of the cardiac cavities renders the heart incapable of responding to a drug which slows the organ by prolonging diastole and thus favouring a better fill- ing of its chambers. The heart is already filled to its utmost and fails to contract adequately because of abnormal endocardial blood-pressure. Even under the stimulus of digitalis its walls cannot cope successfully with its contents. As a matter of fact, the drug only intensifies its embarrassment. The stasis within the organ must first he relieved, after which digitalis may he adminis- tered with satisfactory results. This may be done by bloodletting or by catharsis; 12 to 16 ounces of blood may be drawn from the arm, or wet cups or leeches may be applied to the pracordia. I prefer, and have usually employed, hydragogue cathartics, because they lessen directly the hepatic stasis that coexists with the cardiac distention and forms another of the conditions acting as a barrier to the action of digitalis. The following is a case in point : April 17, 1895, I was asked to treat Miss T., aged forty-four, who had been ill with heart-disease for about six weeks and had been given up by a number of doctors as a hopeless case. In fact, the last physician had declared nothing could be done for her, had acted on this belief, prescribed only some codeine to relieve her cough, and had gone his way. The lady gave a history of articular rheumatism twenty-five years before, since which time she had been short of breath. Her present symptoms, however, dated from about six weeks back, yet could not be traced to any 480 DISEASES OP THE HEART sj^ecial exciting cause. A j)roiiomice(l aggravation of her condi- tion had followed the exertion on the previous Sunday of dress- ing and going downstairs to dinner. I found her sitting up in bed on account of dyspnoea and cough which had prevented sleep for several nights. Her colour was a peculiar bluish-yellow or slightly greenish hue, and anasarca was extreme, extending to the trunk, and including the upper extremi- ties. The radial pulses were so ilickering that the heart-rate had to be counted by auscultation. As nearly as I could determine, owing to the great arrhythmia, the heart was beating between 160 and 170 times a minute. There was no cardiac impulse percep- tible. Both absolute and relative dulness w^as enormously in- creased, the latter reaching from 1^ inch to the right of the right sternal margin very nearly to the left anterior axillary line. Heart-sounds were feeble, the first being partly obscured by a murmur that seemed to possess an indistinct presystolic portion ; the pulmonic sound was very accentuated and the corresponding aortic was weak. The bases of both lungs, jiarticularly the right, showed dulness that did not shift, and numerous fine moist rilles. The firm rounded border of the liver was palpable three finger- breadths below the costal arch, and the abdomen yielded signs of ascites. The urine showed nothing more than the usual changes of congestion. The patient's distress was pitiful, unable to eat or sleep, hold- ing herself upright in bed without even the support of pillows, labouring for air, coughing, and expectorating bloody, frothy mucus. The diagnosis was plain — mitral disease of rheumatic origin, which at last had broken down and led to this enormous dilatation of the heart, hypostatic pulmonary congestion, hepatic engorgement, tcdema, and ascites. There were no serious com- plications, and yet it Avas very questionable whether or not the heart-walls would ever recover from the enormous strain to which they were subjected. To the family I expressed a guarded opin- ion as to the result of treatment, yet encouraged the sufferer to ho]»o for recovery, that she might siniimon courage from hope to endure the vigorous onslanghts on her (rdema that would have to be made. It seemed to me useless to prescribe digitalis with the heai't in that state; so T resolved to sustain it with strychnine, which, owing to the fact that she could not afi'ord a nurse, was THE TREATMENT OP VALVULAR HEART-DISEASE 481 given by inoiitli, g^^ every three hours during the day, while each evening I injected the same dose hypodermically, together with -J of morphine and yj-^ of atropine, to induce sleep and lessen the cough. Then as a package of symphorol had been given me for trial, I decided to try its effect on the dropsy. A cathartic was also administered, but not a very powerful one. The diuretic failed absolutely, and Merck's diuretin was tried with the same want of success. Then without changing the strychnine and even- ing dose of morphine it was decided to make use of purgation — good, vigorous purgation of the old-fashioned sort. The patient's strength, by the way, had increased appreciably, although the oedema had only grown somewhat less hard. She was also able to take a little more nourishment, consisting of milk and eggs. Accordingly compound jalap powder in teaspoonful doses was administered until a large number of copious watery stools were secured. Indeed at one of my visits — the first, I be- lieve, after the powder had been ordered — she was found sitting on the night-stool, and in response to my queries concerning the effect of treatment, stated she had been sitting there for two hours, preferring that to the effort and fatigue of changing from bed to the stool and back again every few minutes. The influence on the heart and circulation was wonderful and gratifying. First her cough and dyspnoea subsided and the sputum lost its bloody char- acter ; the abdomen softened down, and the oedema left the arms and flanks; the pulse grew a trifle less rapid, but appreciably more waves reached the wrist ; cardiac dulness became rather less extensive also. Then I decided to let up a little on the purgation and to administer infusion of digitalis carefully prepared from English leaves, strychnine and morphine to be continued as be- fore. The results were almost magical; the heart quieted down and daily grew in regularity and strength; dropsy disappeared entirely, and the patient, free from cough, was able to lie down with ease and enjoy a comfortable night's sleep. The morphine was discontinued, but the strychnine was left undisturbed. May 1st the patient was turned over to Dr. Houston, who resided in the neighbourhood, and by him reports of her progress were made to me. The last time I saw the patient, about June 1st, she was sitting dressed on a sofa, without the faintest trace of oedema, the pulse 80, perfectly regular, the heart of nearly 482 DISEASES OF THE HEART normal size, and witli a loud systolic apex-murmur. Compensa- tion had become re-established for the time. A peculiar and inter- esting feature of this case now developed; the patient became quiet, morose, and melancholy, very unlike her cheerful, patient self during the height of her peril. This change of disposition Dr. Houston found was due to digitalis and disappeared with cessa- tion of the drug. This patient removed during that same summer to Moline, and there, her old symptoms of asystolism returning, she died in February, 1896. In this case the treatment, though successful, was severe, and under similar conditions I would now advise removing the ascites by aspiration, which, by more quickly relieving intra-abdominal pressure, would permit the earlier employment of digitalis. In most cases of the kind, moreover, diuretin accomplishes the re- moval of the dropsy. Its failure in this instance was owing prob- ably to the extreme renal stasis, which should first have been lessened. I have seen remarkable results follow its use in cases of cardiac dropsy in which stasis was less pronounced. A. C, a tall, slender girl of fourteen years, was seen in con- sultation with the late Dr. E. M. Hale, December 14, 1891, be- cause of heart-disease and increasing dropsy. There was a his- tory of chorea at eight years of age and again in August, 1891, since which latter attack she had not been well. Oedema had gradually appeared and increased in spite of treatment by her home physician ; hence she had been brought to Chicago and jjlaced in charge of Dr. Hale. A urine analysis of December 9th by Dr. C. Mitchell had shown a fourteen-hour quantity of 13 ounces, specific gravity 1.027, acid, urea stated as reduced to 75 per cent of normal, a small amount of albumin and hyaline and granular casts. The symptoms were the usual ones of dyspncca, weakness, and swelling of the lower extremities, anorexia, and constipation. The patient lay on a couch semi-recumbent, evincing plain signs of venous stasis. The lower extremities were moderately ocdematous, and the external jugulars were distended, but not ]))ilsating. There was noticeable prominence of the prjTCordium and great distention of the abdomen, which yielded signs of free fluid, the liver being palpable three finger-breadths below the cos- tal arch. The heart was greatly increased in size, the apex-beat THE TREATMENT OP VALVULAR HEART-DISEASE 483 being in the sixth left interspace outside the nipple, and there was a loud mitral systolic and short presystolic murmur. My notes do not state the pulse-rate, but mention that the pulse was regular, rapid, and small. Signs of the heart being immovably fixed in position were discovered at a much later period. In view of the fact that die-italis had been taken without favourably influencing the dropsy, it was decided to put her on 90 grains of diuretin in twenty-four hours and administer a moderate dose of calomel. Two days subsequently the urine was reported to be 81 ounces and to contain a trace of albumin but no casts. This wilful little miss then began to be so annoyed by the frequent micturition that she refused any longer to take diuretin, and this was stopped. It was replaced by heart-tonics, first digitalis, and then -^ grain of convallamarin thrice daily. Her improvement was so rapid that after about two weeks she was taken to her Iowa home in care of a trained nurse, by whom orders as to diet and exercise were strictly enforced. Uninterrupted gain was made until February, when the patient wearied of her restraint and my services were dispensed with. The following October I learned that she was riding horseback, playing lawn- tennis, and bicycling, but '' her lips looked blue." Five years now elapsed before I again saw" her, but I learned meanwhile that she had another breakdown similar to her first one, her recovery being very slow, and requiring severe purgation. My next examination of this patient was in the early fall of 1896, at which time she was attending a young ladies' school in one of our suburbs. The heart was very greatly enlarged; its apex-beat was immovable in the sixth left interspace well towards the anterior axillary line; and mitral regurgitation appeared to be the predominant lesion. Hepatic engorgement was consider- able and cardiac embarrassment was evident upon exertion. She was resorting occasionally to a few drops of strophanthus, but no cathartics. She was induced to take a laxative water at regular intervals, which speedily lessened the visceral congestion. She also con- sented to try the efficacy of a course of baths a la Nauheim sup- plemented by resistance gymnastics. The results were gratifying, the dilatation of the right heart being appreciably reduced and the cardiac tone in general being greatly improved for the next 484 DISEASES OP THE HEART two years, as she subsequently stated. She passed the winter of lS98-'i)9 at a young ladies' school near Philadelphia, and was in tolerable health until April, 1899, when she had an attack of acute rheumatism. This resulted in an acute pericarditis with effusion, which left her very feeble for the ensuing two months, much of that time being spent in a wheel-chair at Atlantic City. I had the opportunity of examining her in June, when the heart was found enormously enlarged, with an intense systolic apex-mur- mur, and also a loud diastolic one immediately following the sec- ond sound. This murmur was of nuiximum intensity at and about the apex, and was evidently mitral^ produced by the inrush of blood into the dilated left ventricle during the beginning of its diastole. The action of the heart was unsteady, the abdominal organs were much engorged, and the patient was pale and weak. She was put on strophanthus, strychnine, and iron, and went on to her home. Her condition improved during that summer, yet remembering the benefit obtained by the Nauheim treatment in 1896, she returned for another course in October, 1899. My notes record that the apex-impulse was broad and heaving in the sixth and seventh interspaces 5 inches to left of the ster- num ; absolute and relative dulness greatly increased, the latter ex- tending nearly to the left anterior axillary line, and at the right to 1^ inch to the right of the breastbone. The apex was fixed in position, and a double murmur was still present in the mitral area, both very intense. The external jugulars were full and the liver palpable. Signs of insufficiency of the aortic valves were diligently sought for, but in vain. The mitral valves alone were involved. The enormous hypertrophy and dilatation of the left ventricle were due to the exo-pericardial adhesions acting in con- junction with the mitral disease. Baths and exercises w^ere begun ()(!tober 19tli, and j^ovember 1st it was recorded that the left external juguhir was turgid. The ])ati('nt, conlrarv to instruc- tions, was ascending too many stairs and eating too heavily. Ca- tharsis and great care in the matter of exercising reduced the turgescence of the veins and liver for a while. On November 2'>d it was again recorded that the jugulars were full and the lips blue. This was attributed to her having hurried in dressing and having walked against a strong cold wind. The venous con- gestion again dimiiiislicd, althoiigli iml entirely. At the close of THE TREATMENT OP -VALVULAR HEART-DISEASE 485 the course of treatments, which had extended throngh six weeks, it was noted that the left heart had not diminished in size at alL The enlargement of the right heart was less, however, the action of the heart less easily disturbed, and the patient felt stronger, having lost the weakness, perspirations, and sensation as if the " heart was trembling," symptoms of which she spoke at the date of commencing the treatment. The winter following she felt better than ever before. Since the above was written this patient suffered a final break- down, and died under niy care in May, 1901. Her last symptoms have been described in the chapter on Mitral Regurgitation. March 18, 1896, I was requested to see Mrs. T., aged thirty- four years, who had been dropsical for several months. The patient had had inflammatory rheumatism at the age of twelve or thirteen and again at thirty, soon after the birth of her second child, but had not been aware of cardiac symptoms until Septem- ber 10, 1895. She had then been aroused in the night by a violent attack of palpitation ; and a few weeks subsequently had suddenly developed headache, paralysis of the right side of the face, and partial left hemiplegia. This had gradually improved, leaving behind a paralysis of the extensors of the left arm and contracture of the fourth and fifth fingers. After this attack dropsy had gradually come on, and had resisted treatment by several local homceopathic physicians. For six weeks prior to my seeing her she had been unable to lie down, and had only slept by sitting with her arms supported on a table in front of her. An enormous cedema extended as high as the waist and involved also the left or paralyzed arm. The greatly distended abdomen yielded fiuctua- tion and percussion evidence of free fluid. The liver was made out as greatly enlarged, and there were signs also of fluid in the right pleural cavity. The pulse in the right radial was very arrhythmic, small, and accelerated ; the left radial pulse was, and it may be remarked still is, smaller and feebler than the right. The external jugulars were a good deal distended but did not pulsate. The apex-beat was in the seventh and eighth intercostal spaces close to the left anterior axillary line. It was at first thought to be pushed over by the right-sided hydrothorax, as the fluid in the pleural cavity was thought to be. The first heart-sound was audi- ble in spite of a loud systolic murmur which was transmitted 486 DISEASES OF THE HEART around to the back; the puhnonic second sound was much inten- sified. With exception of the shifting dulness at the right base, the lungs Avere negative. The urine was scanty, but gave no evidence of renal disease apart from congestion. Tliis case was thought to be merely one of mitral regurgita- tion in the stage of destroyed compensation. A year later, how- ever, well-marked retraction of the tenth and eleventh left inter- costal spaces posteriorly was discovered, Broadbent's sign of ad- herent pericardium, and the apex was immovable. Early in April, after I took charge of the case, a quart of clear serum was withdrawn from the right pleural cavity, after which reso- nance and vesicular respiration returned to that side. This was after treatment had removed the dropsy, and hence this was concluded to be an old pleuritic effusion that had escaped previ- ous recognition. The preliminary treatment in this case, as in that of Miss T., was heroic purgation. It seemed useless to administer digitalis or diuretics until after the excessive stasis had been reduced by catharsis, and hence the patient was assured of relief if she would have the courage to bear some very severe treatment. Her re- sponse was to the effect that she would gladly endure anything that would relieve her of her suffering. Accordingly -^-^ of a grain of elaterin was prescribed hourly until it began to oi)erate. At my visit next day I learned she had taken ten of the elaterin granules and that she had vomited 11 times and purged 20. In- dications of improvement were already appreciable, and as she expressed herself as ready to stand another round, the granules were ordered repeated on the following day. Their effect was immense, after which the dropsy diminished still more. To sus- tain her during this ordeal she received full doses of strychnine by mouth, stimulants whenever necessary, and a concentrated nourishing diet consisting largely of eggs and strong broths. By the fifth day the circiihition had manifestly improved, but she felt and appeared very weak. The family was much concerned and thought the ])atient was never going to endure the treatment. 'J'he sufferer was uiidininted, however, and I was obliged on more than one occasion to censure certain members of the family se- verely for talking before the patient in a way to dishearten her. Digitalis was then ordered in tablespoonful doses of the fresh in- THE TREATMENT OF .VALVULAR HEART-DISEASE 487 fusion every four hours, and the vigour of the catharsis was abated, from 4 to 6 watery stools daily being still secured. It was not long- before the patient was able to rest in bed, a thing she had not been able to do for nearly two months. The sceptics in the family circle were now convinced and ready to assist in any therapeutic measure proposed. The (Dedema was stubborn, yet wholly subsided in about three weeks. When this had been ac- complished aspiration of the right pleural cavity was performed with the result previously stated. Digitalis was continued daily for a year, but in the form of the tincture and for the most part in doses of 15 drops three to four times a day. The change in the pulse was very gratifying, being in June, as given in my notes, only 65 and tolerably regular. The liver still remained greatly enlarged and kept showing such a tendency to increase in size and firmness whenever the bowels were not kept freely open that at length the patient was instructed to keep on hand a satu- rated solution of Epsom salts, and of this to take every morning such an amount as would secure several fluid evacuations. This order was strictly obeyed, and in conjunction with the cardiac tonics produced the happiest results. Before the summer was past she was walking about the house and enjoying drives. As- cending stairs was strictly forbidden, however, and was not even attempted for at least a year. Although this patient never lost her appetite and seldom expe- rienced indigestion, her dietary was made very simple and of a somewhat restricted quantity that there might be no chance of her overloading her stomach to the detriment of her still enor- mously hypertrophied and dilated heart. It consisted in the main of a small dish of cereal and cream, a soft-boiled egg, a little buttered toast, and a cup of cereal coffee for breakfast ; for dinner at midday a fair-sized piece of meat, green vegetables, little or no potatoes, some bread and butter, and a simple plain dessert, as plain pudding, or some fresh fruit, water in limited quantity being the beverage ; for the evening meal she generally took a little cold meat with bread and butter and cooked fruit of some kind. After a . considerable time, in consequence of the de- velopment of symptoms that seemed to indicate she was getting too much meat for the limited amount of exercise, I took away the animal food in the evening and she confined herself to her 488 DISEASES OF THE HEART favourite cereal at this incal. This patient oheyed instructions to the letter, and, owing largely to this circumstance, gained grad- ually in endurance and improved in colour until at the end of two years was said by friends to no longer look like an invalid. For the past four years she has taken very little medicine and has been able to attend to her household, even doing considerable work at different times. She has been allowed to go upstairs, provided she does not hurry, and has not been injured thereby. I have seen her on the average once every two weeks, yet have not always prescribed medicine, contenting myself with seeing that everything was progressing as well as could be expected. There has been verj' little time when she has not taken a little digitalis, usually a single daily dose of 5 or 10 drops, but now and then, when the heart has shown a disposition to greater arrhythmia or hurry, this amount has been exceeded. There have been periods of days or a few weeks when I have seen fit to order iron or strychnine, and at a few times, chara'cterized by unusual constriction of the pulse and scantiness of urine, she has been obliged to resort to nitroglycerin, usually to the relief of the condition. In the fall of 1899 this patient contracted a bron- chitis which was attended with such a degree of fever and conges- tion of the right lung that for a day or two I feared she would get a broncho-pneumonia. It finally ^nelded, however, to rest in bed, heroin and apomorphine hydrochlorate, the heart being sustained by some extra doses of strychnine and digitalis. This patient has never showni much dyspna\a, but did for a number of months suffer a good deal from fugitive pains in the left half of the thorax with areas of intercostal tenderness, while below the right scapula and passing through to the front was at times a wearing dull pain that was only mitigated by lying down. Her liver is still very large and growing, as the months go on, percep- tibly thinner at its border and harder. It drops down also, being readily pushed upward. I therefore attributed her right-sided pain to the pulling of the heavy liver on its supports. As the reader has observed, the foregoing cases are all in- stances of mitral disease, and two of them complicated by peri- cardial adhesions. They were consequently not the most promis- ing, yet responded to treatment in a highly gratifying manner. Such is not so with cases of aortic-valve disease, as proved by THE TREATMENT OP '^ALVULAR HEART-DISEASE 489 the cases detailed in the chapter devoted to Aortic Regurgitation. In 1894 I had in charge a young man -nineteen years of age afflicted with insufficiency of the aortic valves of rheumatic origin. Compensation was not badly ruptured to judge from his symp- toms. He displayed no oedema or marked venous stasis, almost his only subjective consciousness that all w^as not right being shortness of breath and palpitation upon exertion. Yet the heart was dilated and the pulse notably arrhythmic. It was hoped benefit would result from a course of therapeutic baths and exer- cises. As a matter of fact some degree of strength appeared to be imparted to the heart, for the impulse became more defined, the sounds more distinct, and his subjective sensations less pro- nounced. Nevertheless, not many weeks had elapsed after the course of treatment when he suddenly had an attack of partial syncope, on account of which he was confined to bed and cardiac tonics were administered. He did not improve, and a few days later died suddenly with manifestations that strongly suggested embolism of one of the main divisions of the pulmonary artery. An autopsy was not obtained. The Treatment of Dropsy. — When this supervenes in the down- ward course of valve-lesions, it is not to be regarded merely as an indication of cardiac inadequacy, but as evidence of obstruction to capillary circulation, plus ansemia and greater permeability of the capillary walls. The pressure of the transuded serum still further obstructs capillary flow and augments cardiac embarrass- ment. It must be removed, therefore, before the strength of the heart can be restored. In this stage of valvular disease the occur- rence of dropsy is very common, and its removal is the problem first requiring solution. In some instances this is easy and only necessitates for its accomplishment the invigoration of cardiac contractions by putting the patient at rest and by administering cathartics and digitalis. According to my experience, the infusion of digitalis exerts a more decided diuretic action than does any other preparation or any other remedy excepting diuretin. It should be freshly pre- pared from English leaves, as these are more reliable than the German, which are said to contain a considerable proportion of stems. The substitution of a fluid extract for the leaves in the preparation of the infusion is never to be tolerated. The addition 33 490 DISEASES OP THE HEART of squills or of a potassium salt, as the citrate or acetate, is thought by some to intensify the diuretic action of the infusion, but is objectionable. Squills is likely to occasion irritation of the gastro-intestinal tract and render the stomach intolerant of the digitalis. If potash is used in conjunction it is better alone, so that either of the drugs may be increased, decreased, or withdrawn without affecting the other. To procure its action on the kidneys the infusion should be given in full doses, ^ an ounce every four hours, and continued for several days or so long as it continues to augment the flow of urine. Its action should be closely watched, that the remedy may be stopped so soon as signs of its cumulative effect are detected. These are slowing of the heart's contractions to 60 or less, nausea, and a falling off in the amount of urine after this has first been increased. It should be remembered that some persons become nauseated by digitalis even before it has been taken long enough to produce its poisonous effects. The most trustworthy indication that the drug would best be discontinued is found in the excretion of urine. If this does not augment after digitalis has been exhib- ited for two or three days, even though the pulse-rate falls, there is nothing to be gained by further administration of the medicine at this time. If persevered in there is danger of cumulative action. Again, if after having been increased for a while the urine begins to diminish, digitalis is beginning to exert its toxic effect, and ought at once to be stopped. Even if these unfavour- able signs do not appear I make it a rule to withdraw the infu- sion at the end of five days, or after the 8 ounces comprised in the pharmacopoeial formula have been exhausted. The drug contin- ues to be eliminated for a day or so longer, and hence it is not usually necessary to follow it directly by any other similarly acting agent. It is not uncommon for digitalis to fail to remove dropsy, and when such is the case it is well to try diurctin — Knoll. This is often surprising in its action, as in one case in which after the failure of digitalis it increased the urine from a pint in twenty- four hours to 8 quarts. Even this remedy may fail, but if it is fresh and given in large doses of 90 to 120 grains a day it gener- ally proves a powerful diuretic. It is best given in solution, 15 grains every three or four hours, yet in conjunction with digitalis THE TREATMENT OP VALVULAR HEART-DISEASE 491 smaller doses are sometimes efficient. Diuretin has a disagreeable soapy taste, and after a time may occasion nausea and even vom- iting. It also loosens the bowels in some instances. Its taste and unpleasant effects may be counteracted by the addition to each dose of a drachm or two of essence of pepsin. For the knowledge of this valuable therapeutic fact I am indebted to the wife of a former patient who was compelled to take large doses of diuretin for a long time. I have tried numerous other highly vaunted diuretic reme- dies, but none aside from diuretin has ever fulfilled expectations. Sugar of milk and vegetable diuretics, as apocynum cannabinum and squills, have never yielded satisfactory results. Indeed, I do not see how they can be expected to overcome dropsy when this is due to cardiac inadequacy and renal congestion. The indications are to relieve stasis and to stimulate heart action, which they can- not do. I have not employed calomel as a diuretic since I have dreaded a possible ptyalism. When used for its effect on the kid- neys, it is in doses of 3 grains several times daily in conjunction with opium to restrain its action on the bowels. Administered in this manner it is said by the Germans to prove highly efficient in cases of cardiac dropsy uncomplicated by renal disease. It seems to me, however, that one is justified in resorting to so pow- erful an agent only when all other means have failed. If the dropsy is so extreme that serous transudation in the abdomen or other cavities intensifies the patient's distress, it is often found that digitalis, diuretin, or caffeine, even in heroic doses, fail to increase the urine. This is due to the impossibility of securing adequate blood-pressure in the renal arteries. Stasis in the renal veins must first be lessened if one is to induce pro- nounced kidney action. For this reason such enormous oedema must be diminished or removed through the skin, bowels, or by mechanical means. Profuse sweating is not advisable, since hot- air baths and pilocarpine are too depressing for heart patients. We are restricted consequently to catharsis and operative pro- cedures. The latter include punctures or incisions of the skin of the ankles to permit the serum to drain away. This is often an effi- cient mode of removing obstinate dropsy, but is likely to be ob- jected to by the patient or his friends. Great cleanliness is re- 4:92 DISEASES OF THE HEART quired to prevent inflammation of the integument. A most excel- lent means of securing such drainage, and one not open to the objection of possible infection, is in the use of Southey's tubes. These are tiny silver cannulas which by aid of a minute trocar can be inserted beneath the skin of the ankles, and are then secured in place by strips of adhesive plaster or by rubber bands. Hypo- dermic needles can be used in the same manner. The quantity of serum that will trickle away through these tubes is astonishing. Dropsical accumulation in the serous cavities may be with- drawn by tapping, a procedure which, if slowly done, is devoid of danger of collapse. It occasions pain, and patients generally shrink from being tai)ped on this account. They also often urge the additional objection that it Avill have to be repeated, and hence in private practice it is seldom resorted to. When consent to this proceeding can be secured, the physician should not content him- self merely with having thus removed the fluid. It will quickly rcaccumulatc unless the advantage thus gained can be held. Con- sequently the tapping should be followed by the administration of digitalis or diuretin, or both. It may be well also to administer an active purge, for by such measures recourse to aspiration more than once may perhaps be prevented. In the case of most private patients it will be found that they prefer active catharsis. They have had more or less experience with purgation in times past, it may be, and they naturally look upon it as less painful than being tapped. Cathartics. — Whenever it becomes necessary to remove serous accunmhitions through the intestinal tract, it should be remem- bered that it can only be accomplished by the production of many copious watery discharges daily. It is not sufficient that the de- jections are semifluid and number two or three daily; Nature often does this much by a pouring out of serum into the intestinal canal, in consequence of which the patient has several loose, even liquid, passages daily. In spite of Nature's treatment, the dropsy goes on increasing. JSTature thus furnishes the indication for treatment, and fortunately we are able to aid her by the adminis- tration of hydragogue cathartics. This procedure is sometimes objected to on the ground that the cardiac suiferer is too weak to endure the depletion. As a matter of fact the patient's weakness is due to his circulatory embarrassment, and experience teaches THE TREATMENT OF VALVULAR HEART-DISEASE 493 that instead of being enfeebled to the degree a healthy individual would be by the purgation, the cardiopatK actually finds he feels stronger so soon as the primary effect of the catharsis is past. This is particularly true of mitral patients to whom heroic purga- tion is specially beneficial. Although in the case of Mrs. F. elat- erin was highly successful, still it is so drastic that now^adays I generally order a less irritating remedy. The best hydragogue is a saturated solution of sulphate of magnesia, and of this I am accustomed to prescribe a tablespoonful hourly to an adult until it begins to exert its effect. I have known patients to take as much as 4 and even 6 ounces before getting appreciable results. The efficacy of the remedy is enhanced if the patient is not allowed to follow the medicine by more than a swallow of water — just enough to remove the bitter taste of the salts. If it is com- plained that the drug produces a bad feeling in the stomach, this can usually be counteracted by the addition to each dose of 5 to 10 drops of essence of Jamaica ginger, which is generally found in the house. Compound jalap powder is likewise very efficient and does not prove so drastic as is supposed. Of this, a heaping teaspoon- ful can be safely given to an adult daily. The old-fashioned " ten ten," which is 10 grains each of calomel and jalap, was much employed by our forefathers, and is not so severe as it is thought to be. It is better, however, to give 5 grains of calomel with soda, or a blue pill of 5 or 10 grains, either remedy to be followed after eight or ten hours by ^ an ounce of Epsom or Rochelle salts. Bitartrate of potassium is also a capital drug for the removal of dropsy, and by some patients is better tolerated than is sulphate of magnesia. Glauber's salts alone is too disa- greeable, but may sometimes be combined with Epsom salts to advantage. It is one of the ingredients of Carlsbad water, by the way. Carlsbad salts are often prescribed to cardiac patients, but, to be very efficient for the removal of oedema, has to be given in large doses dissolved in considerable hot water, being said to be more efficacious when administered warm. If copious watery stools are to be secured, it is best to prescribe rather concentrated remedies and not allow the intake of much water. In case such energetic catharsis is found to weaken the patient, his strength may be sustained by strychnine, aromatic spirits of ammonia, whisky, or some other stimulant. Furthermore, the 494 DISEASES OF THE HEART success of such treatment depends not alone upon its vigour, but also upon its persistent continuance, day after day, until the upper-hand has been gained over the dropsy. It recpiires judg- ment and courage on the part of the physician and fortitude and faith on the part of the patient. But if judiciously persevered with, it generally rewards the sufferer. The Use of Digitalis. — When at length venous stasis has been diminished, and the cardiac cavities have been relieved, digitalis may be prescribed, and will then be found to complete the good work begun by the cathartics. The beneficial action of this rem- edy is generally attributed to its increasing the force of cardiac systoles, in consequence of which the arterial system becomes bet- ter filled. But, as suggested by Broadbent, a part of its beneficial influence is to be found in the greater tonicity imparted to the vessels through its vaso-constricting action. With improved vas- cular tone, blood-flow is hastened, and with accelerated circula- tion in the capillaries and lymphatics absorption of transuded serum is promoted. In addition digitalis lengthens diastole, and thus favours the emptying of the pulmonic veins, right heart, and great systemic veins, and thus counteracts the impending stagna- tion of the circulation, Blood-flow in the renal vessels is im- proved, and forthwith there is a corresponding improvement in the renal function. Accordingly, as previously stated, it is aug- mented diuresis that furnishes the most reliable token of the bene- ficial action of digitalis. The occurrence of dropsy is a possibility in all four lesions of the left heart, but is far less often seen in destroyed compensation of disease of the semilunar than of the auriculo-ventricular valve. Wlien, however, oedema occurs in aortic-valve lesions, it is because dilatation of the ventricle has led to relative incompetence of the mitral leaflets with back pressure in the ])ulmonic system, disten- tion of the right heart, and the establishment of a condition iden- tical with that of uncompensated primary mitral disease. In cases, therefore, of aortic defects manifesting dropsy the indication is for the administration of cathartics and digitalis the same as in mitral disorders. I Ixdieve, however, that the latter should be administered witli judgnumt. There are some physi- cians who advocate the employment of large doses of digitalis in all cases of aortic regurgitation with br(jken compensation. My THE TREATMENT OP VALVULAR HEART-DISEASE 496 experience leads nie to agree with Broadbent when he says that a distinction should be made between cases of aortic insufficiency with ccdema and those without. When loss of compensation is shown by symptoms pointing to left-ventricle feebleness rather than by oedema and back pressure consequent upon relative mitral regurgitation, then I am emphatically of the opinion that digi- talis must be given with caution. It is quite possible in such cases for digitalis to increase peripheral resistance to a danger- ous degree through vascular constriction. Endoventricular blood- pressure is correspondingly raised, and if the ventricular wall is very feeble, unexpected death is not a very remote contingency. In such cases, therefore, digitalis should be given cautiously, and its effects should be attentively watched. When, on the other hand, droj)sy is present, the drug may be given more freely, although it is not likely to accomplish such brilliant results as in cases of mitral disease. Indeed, it has seemed to me that in some cases of aortic insufficiency with sec- ondary mitral leakage large doses of digitalis actually augmented pulmonary and right heart engorgement by driving more blood backward through the mitral than forward through the aortic ori- fice. Such certainly was the effect observed in the case narrated at the close of the chapter on Aortic Regurgitation. Qi^dema was not present, yet the state of the heart seemed to call for heroic doses of digitalis in the forlorn hope of lessening the dilatation of the left ventricle. Instead of doing this, however, the digitalis appeared to aggravate back pressure, and at last death came sud- denly and unexpectedly. When the mitral valve has given way in cases of aortic ob- struction there is still less prospect of reinstating the ventricle by large doses of digitalis. The impediment to outflow into the arterial system is likely to cause still freer reflux into the auricle if by large doses of digitalis the physician attempts to force the ventricle beyond a certain point. We now come to the consideration of the question whether digitalis is equally efficient in both forms of mitral disease. Broadbent is of the opinion that foxglove manifests its happiest results in mitral regurgitation, whereas in mitral constriction the medicine is not always well tolerated. This difference is due, he holds, to the fact that the narrowing of the oriflce interferes 496 DISEASES OF THE HEART with the aspiration of blood out of the lungs which follows the better emptying of the ventricle produced by digitalis. This argu- ment applies cogently, no doubt, to cases of extreme stenosis in which the orifice is reduced to a mere buttonhole slit, for it is evi- dent that in such an extreme condition no agent can drive or coax an adequate volume of blood past the barrier. Nevertheless, ex- perience teaches that even in such cases digitalis is useful if prop- erly given. This is in accord with the following consideration: Digitalis prolongs diastole, and thus affords more time for the stream pent up in the auricle to flow into the ventricle, and hence to be expelled with the next ensuing systole. Inasmuch, however, as the capacity of the left ventricle is reduced- in pronounced ste- nosis of the mitral ring, the blood-wave thrown into the aorta is of a necessity small, and mammoth doses of digitalis are not likely to accomplish more than moderate ones. If the beneficial influence of this remedy were limited to the left ventricle, the usefulness of the drug would bo limited indeed in these cases. But it acts also on the right ventricle and left auricle, and by strengthening the vigour of their contractions it enables these chambers to exert greater propulsive force. In the light of these considerations it would be a grave mistake to conclude that this remedy is of no value in mitral stenosis even when broken com- pensation has led to a3dema and other signs of serious stasis. The combined use of depleting measures and digitalis will some- times achieve gratifying results. Fortunately stenosis and regur- gitation are often conjoined at the mitral oritlce, and hence such cases are to be treated as if only insufficiency were present. When, therefore, digitalis is to be employed for the relief of dropsy due to ruptured compensation in mitral disease, it is to be given in large and, as Balfour says, " cumulating " doses. They must, however, be carefully watched, and the remedy must be stopped so soon as signs of its toxic action are perceived. It is my habit in such cases to administer ^ an ounce of the fresh infusion every four hours for four or five days. If it is employed in this maimer, and if it is witlidrawu so soon as the increased diu- resis first ])i'o(luced l)Ogins to be succeeded by a diminution in the amount of urine, there is ordinarily no danger of serious cumula- tive effects. If for some n^ason the drug does not exhibit its diuretic action, although slowing of the jnilse is obtained, then THE TREATMENT OF VALVULAR HEART DISEASE 497 the remedy should bo stopped for a day or two, after which it may again be given in smaller doses. There is no use in administering digitalis for the relief of oedema in small doses over a long time. I have frequently seen it fail when thus given, whereas subse- quently prescribed in large doses during several days it has suc- ceeded in accomplishing what it previously failed to do. Finally, I wish to again emphasize the statement that if this un- rivalled agent is to be employed for the removal of oedema it is best given as an infusion of the English leaves. The tincture, the fluid extract, or the powder, digitoxine,* and the various digitalins, whether French or German, will not prove so efficient. The tincture is preferable for prolonged administration in small tonic doses. It will undoubtedly augment the flow of urine by energizing cardiac contractions, but for the removal of oedema would have to be given in doses that would be dangerous in the hands of the average medi- cal man. This is particularly true of digitoxine and the French or crystallized digitalia. Excepting the latter, I have tried all forms of the drug, and I think I can safely assert that all can be accom- plished with the reliable tincture and properly prepared effusion that can be with the other less familiarly known preparations. I well remember my experience with digitoxine. In one case it pro- duced so powerful an effect in what was considered a safe dose, that I speedily discontinued it in alarm. In the second case, that of a middle-aged woman with mitral disease and an arrhythmic pulse, the remedy was administered cautiously and without appreciable effect one way or the other, when suddenly, almost without warning, the patient died. I could not say her death was due to the digitox- ine, and yet I have always had an uncomfortable s"_spicion that it was. Therefore I would urge inexperienced practitioners or such as practice in the country, where they cannot keep their patients under as close scrutiny as if they were near at hand — in a hos- pital, for instance — to content themselves with safer preparations. Strophanthus, convallaria majalis, adonis vernalis, erythro- jDhlein, and barium chloride belong to the digitalis group, and therefore possess diuretic properties, convallaria having been particularly lauded by the Kussians. ISTone of them is the equal * Since June, 1906, 1 have made frequent use of an imported solution of digitox- ine with highly gratifying results in both regulating the heart and increasing the amount of urine. 33 498 DISEASES OF THE HEART of digitalis, however, and in serious eases they are not likely to prove so reliable. I have used them as adjuncts or substitutes for foxglove when this had to be discontinued temporarily or could not be tolerated, but I have never ventured to rely on any one of them exclusively when dealing with a critical ease of cardiac in- competence from valvular disease. In the young with rheumatic endocardial lesions, or in older persons whose arteries are not aj^preciably stiff, one need not apprehend ill effects from the vaso- constrictor effect of digitalis, while if the remedy be given in ice-water, or if the fat-free tincture be used, it will rarely disa- gree seriously with the stomach. When the vessels are athero- matous its effect on the arteries must be reckoned with, and then strophanthus may have to be used instead or be combined with digitalis. In these cases the latter can generally be employed sucecssfully even for the treatment of oedema if nitroglycerin be given often enough to counteract the constriction of the arterioles. Before concluding the subject of the administration of digi- talis I wish to direct attention to the possibility of its occasioning mental symptoms that may be misunderstood and attributed to the disease instead of to its right cause. These are hallucinations and delirium. II. O. Hall has recently contributed a paper on this peculiar action of the drug, and quotes from an article thereon by Duroziez, who reported twenty instances of the kind. In this present work I have referred to the fact tliat in two pa- tients whom I attended in connection with Dr. Houston a peculiar mental and emotional state developed during the prolonged admin- istration of digitalis and disappeared after the discontinuance of the remedy. In Miss T., with mitral disease, there was a singular sort of sullen moroseness with taciturnity, while the other patient, a man with aortic insufficiency, manifested a mild delirimn of a harmless kind. Hall suggests that this effect may follow tlie ad- ministration of even moderate doses for a considerable ])eri()d, and very properly queries if it does not occur far oftener than is sus- pected. For my part I frankly confess that until my attention was directed to this singular effect of digitalis by Dr. Houston I had no suspicion of its possibility. Tliere may be no danger asso- ciated with this action, but it may iudiciite an unusual degree of susceptibility to its influence, and tliiif in such ])ersons one should be especially on his guard against the cnniulative action of the THE TREATMENT OP VALVULAR HEART-DISEASE 499 agent. This latter is no fancied one, and should always be kept in mind. It is probable that digitalis poisoning occurs far more fre- quently than is suspected. I am painfully certain that in one instance the sudden death of one of my patients was due to digi- talis, which was being administered in large doses. In this case, however, the patient disobeyed my emphatic injunction to remain absolutely quiet in bed, and fell dead while walking about, just as I had warned him he might do if he got up. Since that time it has been my custom to discontinue digitalis every fifth or sixth day in all cases in which it is being taken in considerable doses or wheu the patients are not under frequent observation. In this way time is allowed for the elimination of the drug. Lastly, it is said that there is less danger of a cumulative eifect if a daily cathartic is taken, since it may be largely eliminated through the bowels. Accessory Heart-tonics — Strychnine is a valuable heart-tonic at all times, and when compensation is lost is of great value. It should not be depended on alone, but prescribed as an adjuvant to the cardiac energizers already luentioned. Administered hypo- dermically it is undoubtedly more rapid and powerful than by the mouth, and would best be employed in that manner. Its bene- ficial action is not confined to the heart, for it is a respiratory stimulant as well, tending thereby to lessen the sense of dyspnoea. Through its powerful effect as a tonic to the nervous system it induces a feeling of strength and well-being very soothing to the tired, often irritable sufferer. It certainly helps a patient endure the insomnia that so often attends his loss of compensation. I have always been of the opinion that to display its kindly action strychnine should be given in full doses, care being had to avoid its physiological effects in toxic amounts. One thirtieth of a grain hypodermically may usually be administered every four, or in extreme cases every three hours. I have not hesitated to order that dose as often as every two hours, or even hourly in times of great peril. The objection to such doses have been previ- ously stated. (See page 44.5.) Another remedy of inestimable service when the heart threat- ens to fail altogether or the patient is tormented by dyspnoea, par- ticularly at night (cardiac asthma), is morphine. If adminis- 500 DISEASES OP THE HEART tcred hypodermically and in small doses this drug proves a pow- erful cardiac stimulant. An eighth or a tenth of a grain thrown under the skin will arouse a flagging heart, steadying its action and improving the quality of the pulse in a manner not equalled by any other agent of which I am aware. If -j^ of atropine is combined it serves to warm up the skin by flushing the capillaries, and by deepening the respirations relieves dyspnoea. Given at bedtime, morphine will generally carry the sufl"erer through the night without his wonted attack of dyspnoea and depression. In some instances it acts as a hyjmotic, but even when it fails of this action it allays restlessness and induces a sense of well-being that is most grateful. Larger doses are more or less depressing, and exhibited by the mouth the stimulating action of the remedy is not the same as by subcutaneous injection. I have known many a patient to tolerate morphine in this manner for weeks, and when it was at length withdrawn not to experience any special discom- fort. It is not to be resorted to indiscriminately, but only in those cases in which it is necessary either to tide over a period of crisis or to promote comfort of body and repose of spirit. Of course for the relief of pain larger doses are necessary, as is like- wise the ease when it is desired to produce sleep. Hypnotics. — The ultimate aim of treatment in the stage we are now considering is the restoration of circulatory equilibrium, and thereby of heart-power, and yet we should never forget that the accomplishment of our aim often depends almost as much upon attention to subordinate or accessory conditions as upon measures addressed to the heart directly. For instance, cardio- paths suffering from ruptured compensation are very apt to com- plain of actual insomnia or of fitful and unrefreshing sleep. This may be due to disturbed cerebral circulation, to retention of waste products, or to the generation of toxines, or to all these factors combined. So long as natural sleep is wanting, the invalid is de- j)rived of what Shakespeare has so fitly termed " Nature's sweet restorer," and the exhaustion of ilie nerve-centres . following pro- longed wakefidness may throw the balance against recovery. Moreover, the heart itself is robbed of the rest which comes from its slower action during sleep. It is most important, consequently, to combat this distressing condition by such means as will prove harmless. . THE TREATMENT OF VALVULAR HEART-DISEASE 501 In some cases sleep follows the measupes directed against vis- ceral congestion and oedema, or is directly induced by the hypo- dermics of morphine administered for relief of nocturnal dysp- noea. When such is not the case, recourse should be had to hyp- notic remedies as such. Chloral hydrate is too powerful a cardiac depressor to be safely employed in uncompensated valvular disease, or indeed in any case in which the pulse is not strong and tense. On the other hand, chloralamide-Bayer is said to exert no injurious effect on the circulatory apparatus. If it affects the pulse at all, it is by accel- erating it while at the same time augmenting its tension. The main draw^back to this agent is its liability to occasion headache next morning and its unpleasant acrid taste. To obviate the for- mer effect, therefore, an equal amount of potassium bromide may be added to each dose of chloralamide, while its disagreeable taste may be disguised by some palatable sirup. The remedy is per- fectly safe in doses of from 15 to 40 grains, and to prove efficient ought to be given in a single full dose. A good formula is the following: Chloralamide-B. 2 grammes, spiritus frumenti 15 cubic centimetres, potassii bromidium 2 grammes, and syrupus glycyrrhiza^, q. s., ad 30 cubic centimetres. M. et sig. This dose to be taken at bedtime. Chloralose is a hypnotic highly recommended by Balfour in his capital work The Senile Heart. Its dose is from 2 to 8 grains, best given in capsule, and is said to tend to slowing of the pulse while at the same time lowering its tension. I formerly pre- scribed it a good deal, but ultimately abandoned it because I found that when my lady patients took 5 grains at a single dose, or were obliged to repeat a capsule containing 2| to 3 grains, they were apt to complain of nervousness the next morning ; it is, how- ever, safe and usually produces sleep quickly. Sulphonal and tri- onal are both safe and efficient hypnotics for the class of cases now considered, since although they accelerate the pulse and somev\diat raise arterial tension, they do not depress the heart. Paraldehyde in full medicinal doses of a drachm acts similarly to chloral hj^drate as a soporific, but unlike the latter is perfectly safe even for weak hearts, being said to slow and strengthen the pulse. Its action is not so prolonged, however, and patients often object to it on account of its burning taste and persistent odour 502 DISEASES OF THE HEART in the breath. This does not by any means complete the list of available hypnotic remedies, but comprises those that are the most efficient for cardiac sufferers. Should these not occasion sleep, and in uncompensated valvular lesions insomnia is often most intractable, recourse would better be had to morphine or some preparation of opium, of the advantages of which as a heart-tonic I have already spoken. Rest. — Having dwelt at some length on the medicinal manage- ment of this stage of valvular heart-disease, 1 now desire to add a few remarks concerning the great importance of physical repose. Nothing is more essential when compensation has failed than the strict enforcement of absolute rest. There is no greater mistake, and nothing that will more surely render futile all attempts to re- move dropsy, than to permit the patient to walk about. Even the moderate exertion of visiting the closet in an adjoining room will often.be sufficient to maintain the venous congestion and a'dema. The patient should be required to remain absolutely in bed or on a couch, and he should make use of a bed-pan. Only in those instances in which ])aticnts find it impossible to so empty the bowel or bladder should this rule find an exception. When such is the case, they may be permitted to leave their bed and sit upon a night-stool placed close at hand, or better still use an adjustable bed. The effort of raising themselves in bed will often in cases of extreme dilatation suffice to frustrate all attempts at a reduc- tion in the size of the organ. Therefore, dropsical patients should have the necessity of physical repose clearly explained to them, and should be kept at rest until all traces of oedema have disappeared. In mitral disease this precaution will of itself often do much towards removing symptoms. In cases of uncompensated aortic insufficiency al)solute re])Ose is of the utmost importance, since a single injudicious effort may occasion paralysis of the overdistended left ventricle in diastole. Another danger arising from exertion in cases of extreme and long-continued back pressure in the lungs is the establishment of relative pulmonary regurgitation. When this once supervenes, it is in my experience impossible to ever again restore compensa- tion, and the end is not far distant. Exercise. — Only after the cardiac cavities have become un- loaded, and compensatory hypertrophy has begun to be restored, THE TREATMENT OP VALVULAR HEART-DISEASE 503 dare the patient be allowed to indulge in exercise. Even then exertion must be very slight at first, and the medical attendant should observe the effects of effort, and thus form an intelligent opinion of how far cardiac strength has become re-established. I make it a rule to be present the first time walking is attempted, so as to note the effect of exertion on the pulse. Baths. — In this critical stage of cardiac incompetence I believe ISTauheim baths contra-indicated, and even in the matter of bathing for the sake of cleanliness patients must content themselves with the morning sponge-bath given by the nurse. It involves too much exertion for them to bathe themselves, and particularly to get into a tub. Receiving Visitors. — Aj)parently trivial influences may make for or against the restoration of heart-power. Consequently, when there is a damming back of the blood into the lungs and right heart, this latter chamber should not be additionally strained by prolonged conversation. The reason for this lies in the consid- eration that when words are uttered the breath is held, and that with expiratory effort air is driven out through the partially closed glottis. That this throws additional burden on the heart is plain, and is proved, moreover, by the clinical observation that cardiopaths nearly always exhibit breathlessness while talking. Therefore, these invalids should not be allowed to receive visits from friends, unless perhaps from a few who can be relied on to monopolize the conversation, and who know enough to leave so soon as the patients exhibit signs of w^eariness. Diet. — This is a matter of the very greatest importance, and must not be left to the whims of the invalid or the zealous but ignorant notions of friends. The considerations and principles which obtain in cases of failing but not yet wholly lost heart- power apply with added emphasis to these, and hence the reader is referred to what has been already said. Although the management of this stage of valvular lesions is to be conducted along definite lines, still it is and must of a neces- sity be largely symptomatic. There is a certain routine about it, and yet the physician must be ever alert to detect signs of danger and avert it by prompt action, and equally to take advantage of all circumstances that exert an influence for good. He should not exhaust his patient by unnecessary examinations, and yet he 504 DISEASES OF THE HEART should look over the case daily with sufficient care to detect the earliest signs of any of the man}' complications to which the patient is liable. It is especially necessary to make frequent and thorough analyses of the urine, and he should insist on a record being kept of the temperatiire for the detection of some of the terminal infections so frequent in these cases. If he cannot restore cardiac energy, he can at least prolong life and do much to minister to the patient's comfort. If he be so fortunate as to aid Nature in re-establishing some degree of cardiac power, the case then becomes one of the second class, and is to be managed along the lines laid down in the second portion of this chapter. SECTION III DISEASES OF THE MYOCARDIUM CHAPTER XIX ACUTE MYOCARDITIS It is not the design in this chapter to consider acute inflam- mation of the myocardium in association with acute peri- or endo- carditis, but the acute inflammation observed in the course of spe- cific fevers and other acute infectious processes, and which usu- ally exists independently of inflammation of those membranes. This form of myocarditis is described by authors as acute intersti- tial and acute parenchymatous myocarditis, the latter, as re- marked by Osier, being regarded by some as a degenerative process. The history of acute myocarditis is not clear until we come to the works of comparatively recent years. Suppurative myocar- ditis has been recognised since the earliest days of medicine, and by Galen was regarded as the disease of gladiators (Huchard). Beniveni, in the fifteenth century, discovered an abscess in the wall of the left ventricle, and in 1553 Nicolas Massa found an abscess in the right ventricle with a sinuous tract extending into and perforating the auricle. Morgagni was familiar with myocardial inflammation, and Senac devoted a chapter to this affection. Since the beginning of the last century the names of innumer- able workers, including Corvisart, Hope, Andral, Laennec, and Stokes are linked with the history of myocarditis, but their views were more or less obscure. For the most part the changes were spoken of as a softening of the heart-muscle. Bouillaud considered this softening as due to infl^ammation of 34 505 506 DISEASES OF THE HEART both the muscle-fibres and interstitial connective tissue, and dis- tinguished three varieties: The red, which is acute; the white or gray, which is purulent ; and the yellow, which is a chronic phleg- masia. Rokitansky distinguished acute interstitial and acute paren- chymatous myocarditis, and gave an excellent description of them as he observed them in cases of typhus fever. Virchow's studies on parenchymatous myocarditis opened a ncAv era, for in place of the old-time changes in the consistency of the heart-muscle he described definitely recognisable micro- scopic and chemical changes in the structure of the muscle-fibres. lie was followed, in Germany, by Stein, von Zenker, and others, while in France, Hayem did noteworthy work along the same lines. The three divisions, which Hayem made according to the duration of the process, were thought, how^ever, to be too sharply drawn. Among more recent German writers who have made valuable contributions to acute myocarditis as observed particularly in diphtheria, are to be found the names of Birch-IIirschfeld, Ley- den, Rosenbach, and Romberg. Tlie last-named is considered by Fraentzel to have added greatly to our knowledge on this subject, and I desire to acknowledge my indebtedness to his lucid and eminently practical exposition of the clinical features of acute myfx'urditis, as .set forth in Ebstein's Practice. Morbid Anatomy. — The myocardium is the muscle layer of the heart, and corresponds to the media of the arteries. It is tliick in the walls of the ventricles and thinner in those of the auri(*les. The lesions of myocarditis are usually most pronounced in the ventricular walls on account of the greater work thrown on these portions of the heart-muscle. The fibre of the heart-muscle is structurally between that of voluntary and involuntary muscle. The individual cells are short cylindrical bodies, containing one nucleus each. The greater portion of the protoplasm is differen- tiated into contractile fibrilkc which possess the optical character- istics necessary to give the appearance of striation, the fibre being thus striated in both the cross and longitudinal direction. The myocardium possesses a very rich capillary blood-supply which is derived from the coronary arteries, and also from minute ACUTE* MYOCARDITIS 507 arteries opening directly from the left ventricle. Normally there is but little interstitial tissue in the myocardium, which is sepa- rated from the pericardium by a variable layer of fat, while the endocardium lies directly on the muscle layer. Acute myocarditis is either parenchymatous or interstitial. The parenchymatous form includes the various acute degenera- tions of the myocardium, which are usually dependent on the presence of irritants in the circulation, such as the toxines of the infectious fevers. Cloudy swelling and granular degeneration are the most common manifestations of the process. In them the myocardium appears pale and opaque, and is soft, flabby, and easily torn. Microscopically the fibres are swollen, their protoplasm more or less granular, and both the cross and longitudinal striations are obscured. The degeneration induces a more fragile condition of the fibres, so that . they are often found ruptured or separated along the cell boundaries — a condition of fragmentation or seg- mentation. In these cases the rupture probably takes place in articulo mortis. Both these forms of degeneration are usually diffuse and not confined to any special areas. A form of acute myocarditis which may be classed as paren- chymatous, and which sometimes leads to serious results, is that which follows embolism of the coronary arteries. Infarction of the heart is followed by coagulation necrosis of the tissue involved, and is usually attended by some inflammatory infiltration of the area. Ultimately the necrotic area is replaced by scar tissue in the manner to be considered under the heading of the chronic form of the disease. Acute interstitial myocarditis may be purulent or simple. The purulent form is usually characterized by the formation of ab- scesses, which may be many or few in number. On section these appear as whitish or grayish areas of softening, which are de- pressed below the plane of the cut. The larger abscesses may con- tain fluid or semi-fluid pus. Often associated with acute endocarditis, it may be a direct extension from the disease of the endocardium. In this case the foci of suppuration are larger and less numerous than in the case of suppurative myocarditis dependent on a general pysemia when the foci are numerous, widely scattered, and may be so small as to 508 DISEASES OF THE HEART be barely visible to the unaided eye. Microscopically the smaller foci appear as masses of polymorphonuclear leucocytes surrounded by a zone of degenerating muscle. Bacteria can often be demonstrated by appropriate methods. The abscesses rarely attain large size on account of the early su- pervention of death. They may rupture into the heart or into the pericardium, or the wall may become so weakened as to produce rupture through the entire thickness of the heart. The simple form of acute interstitial myocarditis is a rare condition which is found in some of the infectious diseases, nota- bly typhoid fever and diphtheria. In this the chief lesion is the infiltration of the tissue with lymphoid and plasma cells. These foci of infiltration are more numerous in the left than in the right ventricle, and are usually situated close beneath the endocardium. In these foci of infiltration there is usually considerable degener- ation of the muscular tissue, which is characterized by swelling and destruction of the nuclei. Associated with acute myocarditis are the various conditions to which the disease is secondary. Chronic myocarditis may often, though not always, be secondary to the acute form. In abscess of the heart, rupture into the circulation may cause gen- eral ])va'mia and septic embolism. Etiology. — Acute inflammation of the heart-muscle is ob- served in connection with such acute infectious diseases as diph- theria, typhoid and typhus fever, small-pox, scarlatina, gonor- rhoea, and even articular rheumatism. Freund has described a case of acute diffuse myocarditis of the purulent variety in a forty-eight-year-old butcher who fur- nished no evidence either before or after death of any other infec- tion than that of inflammatory rheumatism. He also cites simi- lar instances collected from the literature. Whether in cases of rheumatic arthritis there is some secondary infection that is re- sponsible for the myocarditis, or it is the rheumatic poison itself that creates the mischief, it is impossible to decide. In the spe- cific fevers it is the specific infection probably which gains access to the heart-muscle and there excites inflammation. It may also be that the character of the myocarditis is determined by the viru- lence of the micro-organism. Romberg thinks it is the intensity of the poison and not its continued action which determines the ACUTE? MYOCARDITIS 509 ultimate course of the inflainniatory process, for " in many cases the disease of the heart-muscle reaches its highest point a consid- erable time after the decline of the infection, and it is not to be assumed that all this time the toxic agency continues to increase in activity." The process may possibly be compared, he thinks, to the in- flammatory reaction set up in a part whose function has been destroyed by a burn, or to the tabes dorsalis which develops as an after effect of syphilitic infection. In May, 1900, Poynton reported a comparative study of the changes in the heart-wall in one case each of diphtheria, rheuma- tism, and chorea. In the first-named affection, which occurred in a child of five years, and proved fatal on the seventeenth day, the changes were those of acute parenchymatous degeneration, the muscle-fibres showing profound destruction, in some places even to the disappearance of the muscle-cells with retention of only the reticulum. Associated therewith was a cellular infiltration of the interstitial connective tissue. The endocardium and pericardium were free from disease. In the heart of the rheumatic patient, a young man with clini- cal evidence of mitral disease on admission, and a day or two later of fresh pericarditis, which lesions were found after death, the muscle-fibres showed extensive fatty degeneration, but were not so profoundly disintegrated as in the case of diphtheria. There was also an exudation of cells into the connective tissue here and there around the blood-vessels. In the case of chorea, a child that had manifested great rapidity of cardiac action, the muscle-fibres of the heart also showed more or less fatty degeneration with scattered areas of cell exudation into the interstitial connective tissue. The changes resembled those found in the heart of a rabbit that had been ren- dered pya^mic by the injection into the circulation of streptococci. In commenting on the microscopic findings in the diphtheritic heart, Poynton pointed out their close similarity to those de- scribed by Mollet and Eegaud, and produced by the injection of diphtheria toxines into lower animals. As to the myocardial changes in the rheumatic case Poynton was of the opinion that they were without doubt due to the rheumatic poison, and that they strongly suggested the likelihood of the rheumatic virus 510 DISEASES OF THE HEART being a toxine of microbic origin ; their clinical significance was very obvious and proved that the cardiac failure in rheumatic pa- tients with valve defects is not always to be attributed to mechan- ical causes. Whereas these observations of Poynton are not new, they are of value because contrasting and illustrating the effects on the myocardium of these two important diseases, diphtheria and rheumatic fever. Purulent inflammation of the myocardium is found in connec- tion with pyipmia and ulcerative endocarditis, the bacteria being brought to the heart-muscle in the blood or gaining access directly from the endocarditic affection. Septic emboli may enter a coronary artery and give rise to abscesses. The primary focus of infection may be a suppurating wound, or micrococci may effect an entrance into the system without leaving any trace of their port of entry behind. In rare instances acute myocarditis has appeared to follow trauma, as in a case reported by Rindfleisch of a man who gave no other etiological factor than a fall from a considerable height, and striking on the left side of his chest. Symptoms. — The observations of Romberg and Schmaltz have shown that in diphtheria the symptoms of acute myocarditis occur in from 10 to 20 per cent of all cases, and in the majority of instances appear in the second or third week of the illness, occasionally towards the end of the first, and rarely as late as the sixth or tenth week. These symptoms are the expression of dimin- ished heart-power, and naturally, as regards intensity, depend upon the degree of the myocardial inflammation. Although for the most part they are so apparent that they cannot escape detec- tion by a careful observer, yet there are cases in which death takes place suddenly without previously recognisable symptoms. On the oth(!r hand, according to Romlierg, the symptoms of acute myocarditis, when occurring in typhoid fever, scarlatina, small- pox, gonorrhoea, and acute articular rheumatism, are less conspicu- ous than those of diphtheria; particularly is this true during the stage of fever. Furthermore, it is often impossible without post- mortem inspection of the heart-muscle to determine whether the symptoms are not due merely to functional derangement of the heart's action. ACUTE MYOCARDITIS 511 In all cases of acute myocarditis which is not purulent it is a subject for sjDeculation whether the weakening of cardiac energy is due to destruction of the muscular elements, or to the mechanical effect of cell exudation into the interstitial con- nective tissue, or depends merely upon functional depression (Romberg). Subjective symptoms are not aways present, and if not wholly lacking are not always pronounced, and therefore close observa- tion on the part of the medical attendant should never fail. Pal- lor of the countenance is present, and is often a striking phenome- non. Poynton mentions it in both of his cases of diphtheria and rheumatic fever, especially the former. It is due, according to Romberg, to defective filling of the cutaneous vessels, since the blood is of normal composition. Vomiting is another symptom sometimes of great importance, and has been dwelt on by Villy in connection with the cardiac failure of diphtheria. It may be so persistent as to suggest some abdominal disorder. There is anorexia, and the patient is often strikingly weak and listless, or instead of apathy may display restless anxiety. In a word, the patient conveys the impression of being profoundly ill. The features of the case, however, that most strongly point to myocarditis pertain to the seat of mischief — i. e., the heart. The pulse is more frequent than normal, although as a rule its rate is not greatly accelerated, being 100 or thereabouts. • Arrhythmia may or may not be present; often there is only irregularity in force and volume. Its striking characteristics are feebleness and emptiness, and as the disease progresses loss of stability as well as volume, very slight exertion being sufficient to send up the pulse-rate out of all proportion to the degree of effort. Examination of the heart at this time may disclose some in- crease of dulness, particularly of the relative, to the left and upward, but also to the right. Yet in the beginning, sometimes even throughout the course of the malady, marked dilatation is not detected. Cardiac impulse is absent, and the sounds are nota- bly feeble, especially the first at the apex, which is often so toneless as to be almost inaudible. In a few cases dilatation of the left ven- tricle reaches such a degree as to permit muscular incompetence of the mitral valves, which is declared by a soft, it may be feeble systolic apex-murmur. The disturbance of the circulation may 512 DISEASES OF THE HEART be further shown by hepatic engorgement, and in some cases patients complain of pain in the region of the liver. The presence or absence of other signs of venous stasis, as oedema and scanty, albuminous urine, is determined by the degree of circulatory embarrassment. In some cases there is much pra3- cordial oppression and anxiety that may amount even to pain of a dull and ojipressive or poignant character. Freund lays great stress on substernal pain, and thinks it a highly significant symp- tom and far more pronounced than in endocarditis. In his case the patient often indicated the sternal region as the seat of his dis- comfort, and declared he knew he was going to die. The course of acute myocarditis is very variable. It may set in abruptly and progress rapidly with severe symptoms, leading to death in two or three days or one or two weeks; or it may arise insidiously and be latent throughout, even up to the moment of sudden, unexpected deatli ; or there may be alternation of periods of entire absence of subjective symptoms, with times of alarming weakness and indications of threatening dissolution. The cases which in one sense are the most dangerous are those in which the myocarditis develops weeks after the disa])])oarance of the diphtheria, at a time when convalescence is thought to be progressing satisfactorily, and the patient has perhaps passed out from under the care of the physician. In such the child, uncon- scious or uncomplaining of symptoms, plays about as usual, and one day making some extra exertion falls to the floor and exj)ires without warning. Romberg is of the opinion that the circulatory disturbance is not to be explained on the hypothesis of mechanical obstruction merely, the same as in cases of chronic cardiac disease, inasmuch as cyanosis, dyspnoea, and (edema are not prominent symptoms. The pallor and arterial emptiness af6 rather the eff"ects of the toxines on the vaso-motor centre, of the kind shown by his and Passler's experiments to result froui acute infections. It is pos- sible also that splanchnic neuritis, as suggested by Veronese, may be a factor, producing stasis within the great abdominal vessels, paralysis of the vagus being out of the question. Only in some such way can one account for the absence of pulmonary congestion and dyspna-a. As regards myocarditis from rheumatic fever, it usually ACUTE 'MYOCARDITIS 513 attacks hearts already the seat of acute or chronic endocarditis, or is associated with pericarditis, although, the muscle alone may sometimes be affected. For this reason it is not easy to recog- nise or definitely determine the myocarditic complication. More- over, experience proves the folly of attributing to myocardial in- flammation the cardiac asthenia, or even dilatation, so often wit- nessed in acute rheumatism, for it is often but a manifestation of the poison upon the function of the organ. At all events, it is the part of wisdom in such cases to refrain from a positive opinion. In typhoid and scarlet fever it is not uncommon to observe during the height of the attack symptoms of heart weakness, which in most instances subside with convalescence, and which are perhaps the result of the action of the infection on the vaso- motor centre in the cord, together with exhaustion of the heart- muscle. JSTevertheless, one should guard against an inclination to look on all such manifestations as not due to myocarditis. The onset of acute inflammation of the heart-wall is often so insidious during the febrile stage, and the symptoms are so latent, that the real nature of the heart disorder is readily overlooked. On the contrary, when after subsidence of all active symptoms referable to the primary disease and during convalescence the pulse begins to assume the characters already described — i. e., feebleness, emptiness, irregularity, and conspicuous instability — one should at once suspect the existence of myocarditis. We frequently encounter individuals who have successfully weathered a severe typhoid fever many months, even two or three years before, and still display undue rapidity and even irritabil- ity of the heart's action, I am always inclined to speculate on the possibility of such patients having suffered from unsuspected myocarditis of mild form, and yet sufficient to have left its traces behind. Should the heart-muscle become inflamed during or after the subsidence of acute rheumatic manifestations, the symptoms of circulatory embarrassment will be out of proportion to the clinical evidence of cardiac disease, and yet are very likely to be attributed to such structural alterations as are discovered. There is far more feebleness, emptiness, inequality, perhaps intermit- tence, and particularly instability of the pulse, than there is evi- dence of visceral engorgement and mechanical obstruction in the 514: DISEASES OF THE HEART extremities, at all events until sufficient time has elapsed for the endocardial mischief to become intensified by the myocarditis. The sjinptoms of j)urulent myocarditis depend somewhat upon the nature and extent of the changes induced, but are essen- tially the same as in malignant endocarditis — i. e., rigors, inter- mittent fever, sweatings, and splenic enlargement. If an abscess of the myocardium breaks into the blood-stream, there are in- farcts in the skin, kidneys, brain, or other organs, or in event of rupture of the heart-wall, collapse and death. The clinical picture is usually such as to direct attention to the heart as the seat of the disorder. Yet in cases of diffuse myocarditis like that narrated by Freund, symptoms referable to the heart may be few and obscure, wholly out of proportion to the gravity of the malady. Physical Signs. — Inspection. — Pallor is said to be conspicu- ous, and, associated with either apathy or restlessness, is very suggestive. Falpaiion. — The pulse is weak, empty, and strikingly unsta- ble, and the cardiac impulse is feeble or absent. In some instances the liver and spleen may be palpable. Percussion. — This may or may not disclose an increase in the area of deep-seated cardiac dulness, but if such increase is associated with the characters of the pulse just mentioned, it • greatly strengthens the diagnosis. Auscultation. — As a general tiling tlic ear detects no more than enfeeblement and perhaps muftting of the heart-sounds. IMurmurs are present only when dilatation leads tO' muscular valvuhir incompetence or endocarditis or pericarditis is associated. Diagnosis. — Unfortunately the diagnosis of acute myocar- ditis is usually a matter of conjecture, and reliance must be placed on the history of some infection that may act as an etiological factor, even more than on the symptoms and physical findings. During the height of an acute infection, as diphtheria, acute rheu- marthritis, and typhoid fever, it may be utterly impossible to diagnosticate with certainty the existence of acute myocarditis, whereas the occurrence of the physical signs described during convalescence renders the presence of the disease highly probable. If in a case of stispected myocarditis phenomena of sepsis are observed, they point strongly to a suppurative process. ACUTE ^MYOCARDITIS 515 Prognosis. — It goes without saying that the prognosis is always grave, even in simple myocarditis, and in the purulent form is absolutely unfavourable. Although there is post-mortem evidence that small, scattered abscesses in the heart-wall some- times undergo a process of cure, still a case that is sufficiently outspoken to be clinically recognisable is from its nature incura- ble. In acute interstitial myocarditis of diphtheria Komberg computes the fatal termination as taking place in about one-third of the recognised cases. It is not unlikely that in rheumatism the percentage of recov- ery is larger. This would appear reasonable when we consider that the parenchymatous degeneration is not so intense as in diphtheria. Although all cases do not die, yet the possibility of sudden death should never be forgotten; and, moreover, this pos- sibility is not wanting in any given case simply because the evi- dence of cardiac mischief is slight. It is often precisely in this class of cases that danger is most imminent, since the physician, patient, and friends are likely to be thrown off their guard, and hence permit or commit indiscreet effort. When, on the other hand, symptoms of collapse appear, the danger of death is very imminent. Increasing acceleration of the pulse and marked instability, the heart evincing a degree. of fee- bleness out of all proportion to the demand made upon it, are signs of great danger. So also is abnormal retardation of the pulse-rate, as is exceptionally observed. Delirium renders the prognosis more grave ; and the occurrence of emboli is an exceed- ingly bad omen, since we cannot predict how many are likely to follow or where they will lodge. Favourable indications are to be found in a gradual return of strength, volume, and regularity to the pulse. Treatment. — We possess no means of directly influencing the inflammatory process after it has attacked the myocardium, and therefore our efforts must, in the first place, be directed to the prevention of myocarditis, if possible, and secondly, to pro- tecting the heart-wall from all extraneous influences which can intensify the damage it is sustaining from the inflammation. To the former end is the early employment of such measures as may lessen the activity of the primary disease, which in diphtheria involves the earliest possible use of the antitoxine. The harm 516 DISEASES OF THE HEART tluit may result from delay in the eiiiployiuent of this remedy becomes at once apparent when we rcHect on liomberg's statement that the symjjtoms of acute myocarditis may arise at a time sub- sequent to the administration of diphtheria antitoxine, which goes to prove that the longer the infection is at work in the system the greater the likelihood of the heart-muscle becoming affected. In streptococcus infection the antistreptococcic serum would cer- tainly be indicated ; but in scarlatina, typhoid fever, and rheu- matism we have no specific remedy, unless with the exception of salicylic acid in rheumatic fever ; and hence we must endeavour to promote elimination through the kidneys by administering copious and frequent draughts of water, and subcutaneous and rectal injections of physiological salt solution. So soon as symptoms of myocarditis are detected the indica- tion is to maintain the patient in absolute repose of mind and body. Physical effort is dangerous, and so long as cardiac weak- ness exists the patient must remain in bed. lie should receive as much highly nutritious and simple food as he can assimilate — milk, eggs, broths, etc. The bowels are to be kept active, though depleting purgatives are to be avoided. Strychnine is highly ser- viceable, and should alcoholic stinndants or ammonia be thought indicated, they are to be administered. The character of the pulse would appear to call for digitalis, strophanthus, etc., but if prescribed, it should be cautiously and tentatively, for we are not in position to predicate how much of the myocardium is left uninjured and capable of responding, or whether damage may not accrue to fibres that have imdergone extensive degeneration. Prsecordial pain and restlessness are to be allayed, and for this purpose there is nothing better than mor- phine. In conclusion, it may Ix' rejH'ated that the agencies of greatest service are rest, food, strychnine, and stimulants, in the order mentioned. In diphtheria it is often perilous to allow the patient to even rise up in bed to take a drink or to evacuate bladder or rectum ; he must hv kept as motionless as ])ossil)le. Moreover, it will often be necessary to retain the ])atient in bed for many weeks or months. A rigid enforcement of this rule, even though it seems liard and cruel, is in fact a disjday of greatest kindness. When at length such a measure of improvement has been reached that abao- ACUTE 'MYOCARDITIS 517 lute rest is no longer needful, the patient is to resume exercise by degrees, and at first with the utmost caution. Under no cir- cumstances is an attempt to ascend stairs to be permitted before weeks perhaps of gentle moving about the bed-chamber have proved that the heart is no longer unduly taxed by such efforts. During this period of convalescence cautious attempts may be made to strengthen the heart by resistance exercises and saline baths. At this time benefit may be derived from iron, arsenic, and other ha?matics and nerve tonics. It is needless to add that in the case of young children it is often most difficult, yet no less important, to enforce the quiet and other measures necessary. CHAPTER XX CHRONIC MYOCARDITIS SYN.: FATTY DEGENERATION— FIBROID DEGENERATION— MYOFIBROSIS — WEAKENED HEART— CHRONIC CARDIAC INADEQUACY By far the largest number of persons who at or after middle age begin to manifest signs of cardio-vascnlar disturbance are not victims of valvular disease. Clinically they present evidence of failing circulation with enlargement of the heart (In'pertrophy with dilatation), and with more or less thickening of the arteries. In some instances certain symptoms, as angina pectoris, point unmistakably to coronary sclerosis, with its consequent alteration of myocardial nutrition, but for the most part there is nothing that serves as a criterion of the nature and extent of the change in the heart-muscle. The microscope has revealed not only a con- siderable variety of pathological changes in these cases, but also a want of uniformity or constancy in the relation of these to the symptoms. In other words, various myocardial alterations seem capable of producing the same clinical picture, and conversely, various clinical pictures appear to result from one and the same pathological change. There is consequently much confusion and uncertainty still regarding the patliogenesis and precise relation- ship of the pathological findings, so that in dealing with this phase of cardiac disease one is at a loss whether to attempt to consider it from the standpoint of the pathologist or of the clinician. In either case one is pretty sure to get himself into trouble. German writers, as Romberg and Rosenbach, group the cases under the head of Chronic Cardiac Insufficiency. The latter maintains that as the various changes in the heart-muscle are but different mani- festations of one process, it is impossible to diagnosticate anything more than heart-weakness, while Romberg classifies the cases ac- cording to their etiological factors. Thus he considers in one 518 CHRONIC MYOCARDITIS 519 group those due to coronary disease, those to obesity, those to strain, and those to nephritis, those to excessive consumption of beer, etc. Such a division is in accord with the uncertainty of our knowledge on many points, and also has the merit of sim- plicity, but it is open to the objection that we cannot always be sure of the exact etiology of all cases or of the precise mode of operation of supposed causes. It also, as he himself admits, necessitates much repetition, and therefore I have decided to deal with these cases under the heading given to this chapter. I am well aware of the objections to such a grouping, and know that many times it seems simpler, and non-committal in a sense, to diagnose them according to the gross clinical findings of hyper- trophy or dilatation or idiopathic enlargement of the heart. Still in most cases the microscope shows more or less myocardial de- generation, and therefore I prefer the term Chronic Myocarditis. Morbid Anatomy. — Under chronic myocarditis the ana- tomical conditions usually considered are those of fibrosis and fatty degeneration. Conditions interfering with the nutrition of the heart may produce either or both of these changes, or the fibroid may be dependent on the fatty change. Fibroid degeneration of the heart-muscle, or chronic intersti- tial myocarditis, may represent the final or reparative stage of the various acute forms of the disease. It is then to be regarded as a conservative rather than as a pathologic process. Thus in the case of infarction of the heart, or myomalacia cordis, the necrotic area is invaded by young connective-tissue elements, which finally are metamorphosed into a firm fibroid cicatrix. Such areas of fibrosis, or scleroses, are large or small according to the size of the original lesion. Very large areas are rarely found, as the acute disease would have probably proved fatal. Except by the forma- tion of other infarcts this process does not tend to progress. It is only when the occlusion of many small arteries has produced mul- tiple scleroses that the function of the heart is impaired. Extreme fatty or parenchymatous degeneration, leading to de- struction of the muscle tissue, may be the cause of a progressive fibrosis of the myocardium. Often the destructive process preced- ing the interstitial increase is a coagulation necrosis. As a rule this process is not strictly diffuse, and the appearance on section is of numerous scattered streaks and spots of a grayish or whitish 520 DISEASES OP THE HEART colour, which project slightly above the plane of the section. In- terstitial increase is not always dependent on antecedent degen- eration, but progressive atrophy of the muscle and increase of the fibrous interstitial tissue may occur pari passu in such a way as to render it difficult to determine which is the primary and which the secondary process. In this case the fibrosis is more evenly distributed than in either of the above cases. Scleroses are most frequently observed in the wall of the left ventricle, near the apex, and (m the posterior side in the upper two thirds, near the auricle, in the papillary muscles of the left side, and in the interventricular Sieptum. The fibrous increase nuiy cause a thickening of the wall of the heart — connective-tissue hypertrophy — or the presence of the connective-tissue elements may so reduce the tone of the wall as to cause it to yield to the intracardiac pressure with the formation of bulgings, the so- called partial cardiac aneurysm, or in extreme cases with rupture of the heart. Fatty degeneration is manifested by a general paleness with streaks and patches of a yellowish-brown colour. The markings of such a heart have been compared to those of a faded leaf. The muscle is softer than normal and easily torn. Fatty degeneration is most common in the wall of the left ventricle near the apex, next in the right ventricle, the interventricular Sicptum, and the right and left auricles in the order given. It usually affects the muscle close beneath the endocardium more than that near the pericardium, and the brownish or yellowish mottling is sometimes plainly observable from within the heart. Microscopically the protoplasm of the fibres is seen to be replaced to a greater or less extent by fat droplets. These are arranged in rows, and are said to be situated at the junction of the cross and longitudinal striations. Very advanced fatty degeneration leads to a disinte- gration of the fibres, and their consequent replacement by fibrous tissue. Fatty overgrowth consists in an increase of the normal subepi- cardial layer of adipose tissue. This is normally noticeable only along the course of the large vessels, but in well-marked cases of fatty overgrowth the fat covers the entire organ and no muscle is to be seen. A thick 1)liiiikc( of fat over the heart acts as an effectual impediment to its work, but it is in the nature of an out- CHRONIC MYOCARDITIS 521 side force, and not, as is the case in fatty degeneration, a disease of the muscle itself. Sometimes, however, the adipose tissue invades the subjacent myocardium, first penetrating between the fibres and later causing the complete atrophy and disappearance of the muscle elements. This process may penetrate the entire thickness of a ventricular wall, and of course greatly impairs its functionating power. The senile heart presents a varying picture made up of ele- ments from all of these conditions. As a rule the failing nutri- tion of old age induces a mixture of fibrous and fatty degenera- tion. Fatty overgrowth is common in those elderly persons who incline to obesity. The senile heart may be hypertrophied — this when associated with chronic nephritis and general arteriosclero- sis — or atrophied in consequence of malnutrition and inaction. Very frequently this atrophy is combined with the condition of autochthonous pigmentation already described. This condition of brown atrophy is almost characteristic of the senile heart. The nutritional disturbance which is accountable for these degenerations is frequently the result of the gradual narrowing or occlusion of the coronary arteries or their branches. This may be due to a sclerosis that is part of a general disease of all the arteries, or it may be due to obliterating endarteritis or to a local atheroma of the coronaries either at their orifices or branches. This local process is more apt to take place in the descending branch of the left coronary artery, and this accounts for the spe- cial predisposition of the apical portion of the left ventricular wall to fatty and fibroid degeneration. Thrombosis or embolism of the coronaries induces the condi- tion of myomalacia cordis already considered. The walls of the arteries may become of bony hardness, or atheromatous in patches. The terminal branches may be converted into fibrous cords im- pervious to the circulating fluid. If the obliteration of one artery takes place gradually the circulation may be established through branches of the other. The reduction of the blood-supply to the parts affected, and especially the lack of oxygen, indr.ces fatty degeneration, and often subsequent fibrosis. The heart-muscle, probably on account of its constant activity, feels immediately any lack of oxygen, and hence the myocardium is especially prone to fatty degeneration. 35 522 DISEASES OF THE HEART Changes in the myocardinm are ahnost always found associ- ated with the various valvular lesions, and with hypertrophy and dilatation of the heart from any cause. Etiology. — The changes of the heart-muscle which I have chosen to group under the generic term of chronic myocarditis are of slow development, and presuppose the protracted working of influences injurious to the function of the organ. These influ- ences are for the most part conditions which cause a dispropor- tion between the demands made on the heart and its nutritive supply — in other words, which require the heart to work in ex- cess of its nutrition. The influences which put an abnormal demand on the heart may reside within the organism or may come from without, or there may be a iniion of both. Under the first head are degenerative changes of the vascular coats and chronic kidney diseases, conditions which persistently augment peripheral resistance. Conditions residing outside the body are those which produce long-continued overstrain, as manual toil, the hardships of the soldier's or the sailor's life, the toilsome daily exertions of the mountaineer, excessive consumption of beer, etc. In many instances influences from within and without are conjoined. Something more is required, however, than mere in- crease of work, and this is to be found in disorders of cardiac nu- trition. The blood itself may be of poor quality, or it may be viti- ated by toxines of one kind or another, or the blood remaining healthy, its supply to the heart may be curtailed. It is in the first way that fatty degeneration of the heart is brought about by wast- ing diseases, cancer, chronic suppurations, repeated loss of blood, secondary and pernicious auirmia, exhausting discharges, as chronic diarrhcea, by insuflicient food, etc. The blood may be vitiated by the toxines of acute infectious diseases, by chemical poisons, and prol^ably by toxic substances developed within the gastro-intestinal tract, some of them of bacterial and some of pu- trefactive origin. Typlioid and scarlet fever, diplitheria, acute rheumatism, and iiiflncii/a ai'c all (•a|)able of setting U]i not only acute myocarditis, but chronic niyocanlial changes of an allied if not identical, yet of a more slowly acting nature. Phosphorus, arsenical poisoning, and alcohol are well-recognised causes of fatty degeneration of the heart. The myocardial degeneration of chronic kidney disease may CHRONIC MYOCARDITIS 523 be diiG in part, at least, to chronic toxa-mia acting in conjunc- tion with prolonged high arterial tension. The degenerations de- pending upon coronary sclerosis are instances of the third kind — i. e., of defective blood-su23ply. When the two great factors, work and excessive or deficient nutrition out of proportion to that required for the work, are combined, then we not onl}^ have myocardial degeneration, but in time also inevitable cardiac inadequacy. The hypertrophy which so often develops in association with chronic myocarditis is the expression of an attempt at compensa- tion. It probably evinces an effort on the part of ISTature to repair the damages going on in the heart, but it also results from the necessity on the part of this organ to overcome peripheral re- sistance. Fraentzel's idiopathic enlargement of the heart was thought by him to result from the consumption of an amount of food in excess of the requirements of the organism and of the individual's bodily exercise. Hence it is found in its most typical form in persons who are large eaters, and who, in consequence of their particular line of work, are compelled to be sedentary. Accord- ing to Rosenbach, physical inactivity is an important element in this class of cases. When these individuals reach middle age they are usually found to have developed corpulent abdomens, and they generally continue to increase in weight. In many at this time the previously existing high-pulse tension is still further aug- mented by degeneration of the blood-vessels and kidneys, often also of the liver, which retrograde changes are probably to be referred to the same etiological factors. So long as cardiac hyper- trophy enables the organ to meet its demands its functional in- tegrity is intact. At length, however, either because its nutrition has suffered to such an extent that it cannot meet the ordinary demands made upon it, or because extraordinary work is sud- denly required, as from some undue physical effort, the heart finds itself overpowered, and symptoms of myocardial incompe- tence set in. In the working classes, in soldiers, in sailors, and mountain- eers, in persons addicted to the abuse of beer and other alcoholic beverages, who at the same time perform manual toil, influences of various kinds are active. Food defective in quality or quantity, 524 DISEASES OF THE HEART privations and hardships, and toxic agencies serve to intensify the injurious effects of overstrain. In southern Germany, notably Munich, hypertrophy and degeneration of the heart in its most, typical form are attributed to the excessive consumption of beer. Some have thought this due to the great vascular strain incident to the daily intake of many litres of fluid, but Krehl, Rosenbach, and others recognise in addition the etiological influence of toil and the nutritive elements contained in the beer as well as of the strain put upon the circulatory apparatus by the consumption of excessive amounts of the fluid. In soldiers and mountaineers who carry heavy knapsacks strapped upon their shoulders, and thus loaded perform wearisome marches day after day, Rosenbach thinks cardiac function is impaired through respiratory embar- rassment occasioned by constriction of the chest, and through the necessity of overcoming abnormal peripheral resistance. Athletic sports, as well as coffee, tobacco, and alcohol, he considers injuri- ous only in the abuse, not their use. Myocardial degeneration from coronary sclerosis is an expres- sion of inadequate blood-supply, either circumscribed or general; and that one may understand the diverse appearances encountered I think it well to quote in a general way Leyden's views of the mode of production of the changes in this class of cases. He divides these into four groups in accordance Avith the de- gree of coronary changes and the rapidity with which blood- supply to the heart-muscle is shut off, as follows : (1) The coronary arteries present more or less evidence of sclerosis, but are still able to supply the heart with sufficient blood to maintain its nutrition. Degeneration does not take place, and the organ performs its functions without symptoms referable to coronary disease. Death results from an intercurrent affection, and knowledge of any alteration of the coronary vessels is but the accidental revelation of an autopsy. (2) One of the coronary arteries, usually the anterior de- scending branch of the left, which has become thickened, subse- quently undergoes obstruction by t]irond)osis. When this takes place slowly, or when the circuhition is but imperfectly cut off from the area supplied by the affected vessel, the wall of the heart within this space undergoes fatty or fibroid degeneration. If the thrombosis, on the other hand, suddenly and completely deprives CHRONIC MYOCARDITIS 525 the part of its nutrition, then this area breaks down into the " myomalacia cordis " of Ziegler. Occasionally the extravasation of blood into this softened area gives it an appearance of a hsem- orrhagic infarct. When rupture of the heart occurs, it is gener- ally within such a spot of acute softening. (3) Sclerosis of the coronary arteries is general and has come on gradually, giving rise to correspondingly gradual changes in the heart — i. e., fibroid degeneration either circumscribed or gen- eral. When this chronic or fibrous myocarditis is diffused, the ventricular walls are apt to be thin and dilated, whereas circum- scribed areas of induration are frequently associated with hyper- trophy. In rare instances this development of new connective tissue is attended with atrophy of the muscle-fibres, and the organ shrinks in size after the fashion of a cirrhotic kidney. (4) In this group, the coronary sclerosis, although essentially chronic, has been hastened and intensified from time to time by acute exacerbations of the process, thrombosis, etc. The changes in the heart are therefore twofold; areas of acute softening and fatty degeneration are interspersed among those of chronic myocarditis. This group, which blends the second and third, therefore, is the one most often encountered by the physician. The causes of coronary sclerosis are obscure, but are probably those of arteriosclerosis in general. That age is of influence seems attested by the fact that more or less evidence of the change is found post mortem in persons past middle age, while it is rare under forty and wanting in children. Some families seem to pre- sent a remarkable tendency to sclerosis of the coronaries and con- sequent myocardial disease. This has led to the suggestion of a possible hereditary influence in its production. Some individuals appear to be endowed with " arterial tissue or vital rubber of poor quality, which cannot be explained in any other way," as is so aptly expressed by Osier, " than that in the make-up of the ma- chine bad material was used for the tubing." In my experience individuals who display this tendency to early sclerosis usually manifest distinct gouty diathesis. They may be said to be suffer- ing for the sins of their ancestors. I have long had the conviction that in some families the heart is the locus minoris resistentice, in some displaying particular vulnerability to the rheumatic poi- son, and in others appearing unable to withstand the wear and 526 DISEASES OP THE HEART tear of modern business life. Certainly it is not very nncommon to elicit from a patient, himself suffering with myocardial disease, a history of a parent, usually his father, and one or more of his brothers and sisters having died suddenly of heart-disease. I have in mind now a family in which the father is reported to have died of '' ossification of the heart," while of three of the seven sons one had attacks of angina pectoris, another had heart- disease, developed at middle age, and the third died suddenly with a dilated heart, after having suffered from one or two out- spoken anginal paroxysms. Males suffer from chronic myocarditis more often than do females, but this is probably owing to their greater exposure to those conditions favouring the development of myocardial incom- petence rather than to any inherent tendency residing in the fact of sex alone. Women frecpiently manifest clinical and post-mor- tem evidence of cardiac degeneration, and according to Rosen- bach, it is particularly those who bear children in rapid succes- sion, and are still further depleted by lactation and insufficient nourishment. The immediate causes of cardiac incompetence cannot always be ascertained. It not infrequently develops as a direct result of heart-strain through indiscreet physical efforts ; but it also may appear without any such determining factor, and is then the end- act of all those factors that have led to the degeneration. Worry, grief, excessive business cares, as in times of financial stress, and even emotional excitement of other kinds, may not only occasion loss of power in hearts already the seat of myocardial disease, but are said to be an etiological element in the development of the muscle-disease itself. The cardiac inadequacy of chronic nephritis is generally the result of the organ's inability to longer withstand the excessive tension in the vascular system. It may develop slowly or may be precipitated by some extra exertion or other source of added heart- strain. Symptoms. — The cardiac incompetence of myocardial dis- ease disj[)hiy8 clinical pictures of considerable variety in detail, yet which possess the same fundamental characters. It may be seen as Fraentzel's Idiopathic Enlargement of the Heart, as the Senile Heart so graphically jwrtrayed by Balfour, as a case of angina CHRONIC MYOCARDITIS 527 pectoris from coronary sclerosis in nocturnal attacks of dys- pnoia, known as cardiac astlinia, and in connection with chronic nephritis or diabetes, or both, and occasionally as a mitral or aortic regurgitation due to relative insufficiency from dilatation. Idiopathic cardiac enlargement occurs for the most part in middle-aged men of powerful physique, who are intellectually active, but physically inactive. It is especially frequent, therefore, in men of affairs, as merchants and railroad magnates, and in professional men, as lawyers and clergymen, who, in addition to sitting for long hours at their desks, generally consume large amounts of food. For years there is in such individuals an abnor- mally high and sustained pulse-tension, which resulting, perhaps in part, from abnormal blood-pressure within the abdominal cav- ity, increases as the girth of the waist increases. This state of things is borne without special discomfort until the man gets well along in his forties, or has even passed his fiftieth year. Then he begins little by little to notice he does not breathe quite so easily as formerly on ascending stairs, walking up a slight hill, or hurry- ing to catch a street-car. At times, particularly after breakfast or a more than ordinarily hearty meal, he finds that walking at his accustomed pace is attended by a feeling of uneasiness, ful- ness, or even dull pain in the region of the heart. As the weeks go on he finds these two symptoms become decidedly annoying, and instead of wholly subsiding after he sits down they remain as a vague sense of discomfort in the chest. He also perceives, perhaps, that the old exertion or some excitement incident to his occupation produces consciousness of his heart's action, a verita- ble though not violent palpitation. As a rule this last symptom is not at all pronounced, being subordinate to the breathlessness and pra?cordial fulness. By the time things have reached this pass he concludes to con- sult his j^hysician, who finds a strong, usually regular pulse, no cardiac impulse, an apparently normal heart's dulness, and clear heart-tones without murmur, but the aortic second sound decid- edly accentuated. If the radial arteries are not noticeably stiff, and the urine is negative, the real nature of the case is apt to be overlooked, and the symptoms are attributed to the man's increas- ing weight. He is told to exercise more, eat rather less, and not to worry. Perhaps he is advised to go to some springs, where he 628 DISEASES OF THE HEART can drink laxative waters, or be goes thither on the recommenda- tion of some friend. At first the waters and active exercise seem to make him feel better, but after returning home, and having re- sumed his former mode of life, his symptoms reassert themselves, this time in greater intensity. He again seeks his physician, who now finds the pulse is accelerated, the heart a little enlarged, and the liver palpable. The urine is scantier than before, and it maybe contains a trace of albumin. He is put upon digitalis and strych- nine, or he is sent to Bad Nauheim. This treatment improves his condition to a greater or less degree. His symptoms are less- ened or disappear entirely for a number of months. Then, in consequence of return to his old ways and his neglect of his doc- tor's injunctions, he finds his enemy has again attacked him. The former course of treatments is repeated with less brilliant results. He is now permanently crippled, but is still able to attend to a l)art of his duties. As months go on, however, his shortness of breath and other symptoms of cardiac inadequacy grow more and more pronounced, therapeutic measures are less and less effective, and at length this once powerful and active man of affairs is laid by, a pronounced suiferer from dyspna3a, hepatic stasis, increasing (pdema, scanty, perhaps albuminous urine, insomnia, a dull, con- gestive headache, cough, and frothy, or even blood-tinged sputum, a feeble and often arrhythmic pulse, a dilated and feeble heart — in short, all the signs of advanced cardiac insufficiency. In other cases the course of the disease from initial breathless- ness to complete breakdown of heart-power is much more rapid. Instead of extending over two, three, or more years, it passes through its several phases in a few months, or even five or six weeks, as I have more than once observed. In some instances the clinical history is merely that of ever-increasing cardiac debility, while in others there are some of the special features, as cardiac asthma, brady(;ardia, or even the so-called Stokes-Adams symp- toms, which are described in full in a special article. Whatever the variety of colouring, the general picture is that of more or less rapidly progressing loss of heart-power, and the ultimate out- come is always the same. Cases of chronic myocarditis are conveniently divided into three great groups, according to the predominance of their clin- ical manifestations. These are : CHROOTC MYOCARDITIS 529 (1) The arrhythmic form, in which the pulse is strikingly irregular and intermittent, now slow and strong for a few beats, now perhaps rapid and feeble, or again made up of a perfect jum- ble of large and small, distinct and imperceptible, slow, rapid, in- termittent waves that seem to fairly tumble over each other in their hurry, or to lag back until driven hastily onward again by the impetuously rushing waves behind. In a word, the pulse is so lacking in regularity of rhythm, force, and volume tliat to count it accurately is impossible. (2) This is the form characterized by tachycardia and called the tachycardial form. The pulse is persistently accelerated, or in a few instances become so, in paroxysms which so annoy or even terrify the patient that he comes to stand in mortal dread of his attacks of palpitation. (3) The asthmatic form, distinguished by attacks of acute pulmonary ttdema, which not only occasion distress and terror to the patient, but throw the friends into a state of scarcely less alarm. I have under observation at the present writing a power- fully built, active business man of sixty-three, with moderately stiff arteries and a hypertrophied heart, with feeble tones, and a scratching systolic murmur, who for the past several months has lived in a state of well-nigh intolerable nervousness and apprehen- sion. As he says, he has completely lost his nerve, because last September, after some weeks of neglected shortness of breath, he was one evening seized with an attack of urgent dyspnoea, during which the pulse was scarcely perceptible, and the chest emitted a multitude of fine crackling sounds. He coughed from time to time and expectorated a frothy white sputum. The attack sub- sided after the hypodermic administration of morphine and atro- pine. This gentleman has had one recurrence of the kind, but in the meantime has scarcely passed a week without hours or even days during which his heart has " thumped and bumped," to use his expressive words, in a manner which throws him into a state of great alarm. He never knows when this palpitation is to occur, but it seems in some way connected with temporary aug- mentation of pulse tension. It is also quite certain to folloAV excitement over business affairs. The pulse-rate averages from 88 to 95, but often runs up to 120 or even 140, and such is the throbbing that he can at any 530 DISEASES OF THE HEART time count his heart-beats witlioiit feeling his radial pnlse. There is danger of death during his attacks and he knows it, whic^ of course keeps him in a state of hourly apj)rehension. The fore- going case shows the occasional blending of the tachycardial and asthmatic types. Patients of the arrhythmic form are very common and display the greatest tolerance of the really serious cardiac condition. Thus I knew a man of fifty-five who, notwithstanding an enormously dilated heart and exceedingly arrhythmic pulse, managed to drag on for nine years from the beginning of symptoms. These were not very severe; panting respiration on exercise, a feeling of weakness, so that he could not attend to business, and consider- able fermentative indigestion. That was about all, and at last his end came through ascites rather than distinctively' cardiac inadetpuicy. It must not be supposed that cases of chronic myocarditis can always be clearly separated into the forms just described. Many of them blend the symptoms belonging to each in a way to make a very complex clinical picture. Neither are the disturbances of which these patients complain always strictly cardiac. These lat- ter may be said to be dyspnrea, heart-pain, ])alpitation, visceral congestions, attacks of pulmonary (fdema, cough, and dropsy. They are all present in varying proportion, not perhaps in every case, but in many cases. In addition, however, there are very sure to be numerous other complaints which in all likelihood depend more or less remotely upon the disordered circulation and per- verted visceral function arising from disordered blood-flow. Ver- tigo, insomnia, neuralgias and myalgias, nervousness, irritability of temper, indefinite sensations in the region of the heart, numb- ness, and formication — in short, a score of sensations which the patient connects directly willi his heart, aiid calls on the medical attendant to explain and relieve. They are a large part of the daily plaint of these chronic sufferers when able to be about and in a state of partial compensation. When, however, really serious symptoms of cardiac insufficiency set in, they are so much worse that they drive away more trifling sensations and dominate the scene. All cases do not fall distinctly into the class of Idiopathic Cardiac Enlargement or of the Senile Heart, but occupy a sort of CHRONIC MYOCARDITIS 531 intermediate ground. Nevertheless, it is conducive to clearness to try to classify them, as is essayed to do in this chapter. The senile lieart forms but a part of a general degenerative process. In one case the arteries are markedly stiff and tortuous ; in anutlior tlio urine shows evidence of pronounced interstitial nephritis, but in all the phenomena of cardiac incompetence domi- nate the scene. There are breathlessness on even slight exertion, feebleness, digestive disorders, sensitiveness to cold and changes of weather, a tendency to bronchitis, and insomnia. In some there are attacks of nocturnal dyspnoea of greater or less intensity, flut- terings of the heart, vertigo, or even syncopal attacks. In other cases the breathing assinnes more or less typically the Cheyne-Stokes type (see article on Cheyne-Stokes Respiration), with or without oedema, pulmonary congestions, arrhythmic feeble pulse, and the usual nuinifestations of progressing asystolism. The course is usually slow, the symptoms being sometimes mild, and the patient cut off by some intercurrent affection, as senile pneiunonia. In some instances there is history of attacks of angina. pectoris for five, ten, or even twenty years, and death at last is sudden and unexpected. There are other cases, chiefly men, whose cardiac inadequacy is shown by acceleration and arrhythmia of the heart's action, inclination to cough and wheeze, and various so-called gouty manifestations rather than by pro- nounced dyspnoea or venous stasis ; the so-called arrhythmic form. They get rather breathless on exercise, and yet then can walk at a moderate rate of speed without much difficulty. They have times when from some illness, as acute bronchitis, injudicious strain of one kind or another, they are laid up in their room with a trace of oedema and indications of failing heart-power that look very threatening, and yet under good nursing and proper medical attention they rally, and after weeks or months are again able to be about, a little weaker and thinner, a little more breathless, but on the whole capable of getting considerable enjoyment out of their quiet existence. I recall an old gentleman of eighty with stiff arteries, urine of poor quality, and a greatly hypertrophied heart, the first sound accompanied by a loud systolic basic murmur, the aortic second intensely ringing, who yet attended daily to the cares of a large personal property besides many other duties of a public and pri- 532 DISEASES OP THE HEART vate nature. At length one spring he and his friends noticed that he began to breathe with difficulty upon ascending stairs, and at rest displayed a peculiar sort of breathing which they had never observed before. Notwithstanding this difficulty he came to con- sult nie at my office, and seemed surprised when he was told to return home, give up his business, and remain in the house. His pulse was rather unstable, occasionally intermittent, but not nota- bly accelerated. Ilis respiration was only moderately dyspnoeic as he moved about the room, but after he had been sitting still for some time, and particularly M'hen asleep, it became irregular, with short ])eriods of nearly but not quite complete cessation of breathing, which were then succeeded by gradually deepening in- spirations until they grew full and vigorous. They then died away rapidly into apparent apncea. Close observation detected that at some of these times he yet breathed faintly, while at others he breathed not at all. Some of the dyspnoeic periods were longer and more pronounced than others, and for minutes together others of them presented all the characters of typical Cheyne- Stokes respiration. During these periods he did not seem subjectively conscious of distress. Under appropriate treatment of a stimulating and elimi- nating kind and prolonged confinement to one floor, afterward to the house, his irregular type of breathing gradually left, the heart grew steadier and stronger in action, and he came to look upon himself as pretty well. He required rather close watching to pre- vent indiscretions, chiefly in way of exercise, but as time went on he was able to transact a little business and to enjoy the visits of his friends. In this manner this gentleman was able to live on for two years. When at length the final struggle came, it was in the form of a renewal not of incomplete Cheyne-Stokes respira- tion, but of a most distressing dyspnoea, which gave him no peace even when (piict in bed. It was not attended with notable signs of cardiac failure, and no particular evidence of renal insuffi- ciency. It may have been due to bulbar sclerosis ; but at all events it at length necessitated the hypodermic administration of such heroic and frequent doses of morjihine, that he at last ex- pired in a state of complete narcosis. In tlie case of a man of seventy-one, wlio had been a well- known journalist, the initial symi)t,om so far as could be ascer- CHRONIC MYOCARDITIS 583 tallied was an attack of dyspnoea, which seized him one night after he had retired. He fell asleep, and after a few minutes sprang up in bed, clutching at his throat, exclaiming he was going to stran- gle. This so terrified him that at length he arose, dressed, and compelled his valet to keep him walking up and down in the gar- den for the remainder of the night. When I saw him the follow- ing afternoon he was still greatly agitated and suffering from choking spells. A hypodermic of an -} of morphine, with atropine in the ordinary combination, gave six hours' uninterrupted sleep the next night, although during his repose his breathing was typi- cally Cheyne-Stokes. This patient's pulse was very arrhythmic, his arteries sclerotic, his heart dilated, with a blowing apex-mur- mur and feeble sounds. His urine was that of a moderate renal cirrhosis, and he suffered from prostatic enlargement. His stom- ach was dilated, and he had any amount of flatulent distention of the bowels. Altogether it was an unpromising case, yet persistent and vigorous treatment with cardiac tonics and cathartics, with as strict a control of the dietary as was possible with an irritable, self-willed old gentleman, at length pulled him out of his deplor- able condition. For four years he was an invalid, having times of profound physical and mental depression, and periods of grave cardio-vascular disturbance, during which oedema more than once appeared. These periods of distress were alternated with seasons of comparative immunity from symptoms, and yet they were in- terspersed with numerous attacks of bronchitis, mild ursemic manifestations, and once an acute pleurisy with effusion that even- tually necessitated paracentesis. More than once he rallied from what it seemed must prove his final illness ; and thus actually kept alive by cardiac tonics, he man- aged to drag out four years of chronic cardiac inadequacy. When at length his end came, it was quite sudden, although preceded by days of more than usual feebleness that had confined him to his bed. Although this patient displayed marked general debility, with slowly increasing cardiac asthenia, he never again suffered to any extent from his nocturnal dyspnoea, and never had an attack of angina pectoris. He frequently complained of obstinate chest pains, but these were unmistakably an intercostal neuralgia, as shown by numerous hypersesthetic areas. This case belonged to what may be styled the arrhythmic 534 DISEASES OF THE HEART group, in which the cardiac insufficiency is shown by such an irregularity and intermittence of the heart's action that it consti- tutes a veritable delirium cordis. Radizewsky has shown, conclusively as it seems to me, that when the pulse displays these characters there is extensive fibroid degeneration, chiefly of the auricles, which both clinically and post mortem are found dilated. In his communication upon the subject he quotes Hampeln's researches, which demonstrated that perfect regularity of the pidse is frequently seen in cases in which subsequent necropsy discloses extensive fatty degeneration of the left ventricle. In other words, the state of the ventricle cannot be determined by the state of the pulse. Radizewsky's findings have always seemed to me to explain the protracted course which so often characterizes cases in which the pulse is strikingly arrhythmic. Degeneration and dilatation of the auricles impair the func- tional integrity of the heart-muscle, but can never so seriously threaten life as when the wall of the left ventricle is degenerated. I have seen many of these cases with unmistakable cardiac inade- quacy drag along for months and even years after the heart had become so feeble and arrhythmic that it seemed impossible for it to maintain the circulation. On the other hand, exi)erience has taught me to dread those degenerated and senile hearts, which are apparently not much dilated, yet give rise to dyspna'a of effort, while the pulse remains accelerated, but perfectly regular. Sueli hearts are usually refrac- tory to treatment, and are apt to surprise one disagreeably by stopping suddenly and unexpectedly. They belong to the tachy- cardial form of chronic myocarditis. In my experience the clinical picture of the senile heart is very rarely that of great dropsy and extensive visceral congestion with overdistention of the cardiac chambers, as in the terminal stage of Fraentzel's Tdio])athic Enlargement of the Heart. In the heai't with, coronary sclerosis the consequent interfer- ence with nutrition of the heart-muscle leads to changes of a chronic nature in tlic majority of cases. In others, circulation within the coronarv arteries is more or less suddenly shut oif, and the heart-muscle suffers with corresponding acuteness. Consequently the symptoms due to coronary diseasQ are di- CHRONic MYOCARDITIS 535 verse, and are best divided, as by Leyden, into acute, subacute, and chronic. In the acute form the clinical history is confined to a few days, hours, or even minutes. The symptoms are due to coronary thrombosis with secondary myocardial softening, to sudden rup- ture of the heart in some area of insidious fatty degeneration, or of acute molecular necrosis (myomalacia cordis), or the symptoms consist only of a sudden diastolic arrest of the heart's action. The symptoms of Jieart-rujjhux may be a sudden sharp attack of angina pectoris or of vague pra^cordial distress and oppression with profound prostration. The action of the heart is feeble and disordered, and the organ fails to respond to stimulants. The in- tellect is generally clear, but unconsciousness may be present. In some cases there are symptoms of gastric disturbance, even vomit- ing, and the case is thought to be one of gastric disorder. If life is prolonged for several days, as very rarely happens, the first vio- lence of the attack abates, not to be renewed, or the angina and pra^cordial distress recur from time to time with steadily increas- ing asystolism and death. In other cases of cardiac rupture the symptoms are chiefly those of rapidly failing circulation with insensibility and death from acute pulmonary oedema. With the onset of symptoms the nearest physician is hastily summoned, and on arriving at the patient's side finds him mori- bund. Stimulants prove inert, and the doctor signs the death certificate without having been able to accurately diagnose the condition. If he examines the heart he discovers clear feeble sounds without any appreciable increase in the area of dulness. In other cases cardiac dulness is increased, but unless a slow escape of blood into the pericardium produces the outline charac- teristic of pericardial efi^usion, the augmentation of dulness is attributed to dilatation, and a diagnosis is made of paralysis of the heart (acute asystolism), which seems borne out by the weak- ness of the sounds and strikingly poor quality of the pulse. In such a case recently narrated to me death supervened in half an hour from supposed acute dilatation, and yet the sac was found absolutely distended with blood. In another form of this acute type of coronary sclerosis the patient appears as well as ordinary, having made no complaint that led to a suspicion of his having heart-disease, and yet in the 536 DISEASES OP THE HEART midst of his activities, while at work in his office, on rising from dinner, etc., he suddenly falls dead. lie may turn pale, speak of vertigo, give a groan, or in some way attract the attention of his family, who spring to catch him as he sinks to the floor in fatal syncope. The mahogany flushing of the face and few gasping in- spirations suggest death from apoplexy, but in reality it is from sudden diastolic arrest of the heart. In such instances the degen- erative process has invaded some of the vital centres in the heart, probably in the upper portion of the interventricular sssptum. In cases which, according to Leyden's classification, may be called subacute, there are attacks of angina pectoris extending over a period of weeks or months. They differ much in difi"erent cases, as regards severity and frequency of occurrence. As a rule, however, they grow more intense and more frequent. The suf- ferer speedily becomes incapacitated for business, keeps in the house, or ventures forth only on mild, still days, grows daily weaker and paler, and is very apt to lose flesh. Death comes at last either from slowly increasing asystolism, or suddenly during an anginal paroxysm. The pulse in such cases is usually regular, and but moderately if at all accelerated, while examination of the heart is generally negative. The arteries may display some stiffness, but aside from the patient's age and his attacks of pain there is little to indicate chronic myocarditis. Cases coming under the chronic head run a slow course and extend over years, instead of months, five, ten, or even twenty. The individuals are always conscious of their liability to an attack, and hence deport themselves most circumspectly, eating and drinking moderately, walking and exercising carefully, avoid- ing raw cold winds, and shunning excitement tind provocation to anger, lest at once their cn(>niy he upon them. Their general health does not suffer greatly at first, although as years go by they look and act like invalids. A few experience some shortness of breath, or may exceptionally suffer from veritable cardiac asthma. As a rule, however, their one symptom is their terrible angina. Their pulse is generally regular, always appreciably tense, and their hearts are negative on examination. Deatli comes through intercurrent disease or during an attack. For further particulars the reader is referred to the chapter on Angina Pec- toris. CHRONIC MYOCARDITIS 537 In general arteriosclerosis there are often symptoms of circu- latory failure which are apt to be attributed to cardiac inadequacy alone, when in reality it is the arterial stiffness that is responsible for the stasis and a'dema. The heart may in such be atrophied or of normal size, but as a rule it is hypertrophied. The condi- tion of the myocardium depends upon the degree of its nutrition with relation to its work, and as the aorta and coronaries share to a greater or less extent in the sclerotic process, the heart-muscle is not intact. Xevertheless, its driving power is often adequate for years after the blood-vessels have become rigid and beady. At length it reaches the limit of its compensatory ability, and vas- cular resistance still augmenting, the heart-walls begin gradually to yield to the strain of maintaining arterial circulation, and dila- tation slowly supersedes hypertrophy. In some cases injudicious physical effort, suddenly or too often exerted, causes acute overstrain of the already too greatly taxed heart, and symptoms of cardiac insufficiency set in rapidly instead of slowly. These are not peculiar, but possess the ordinary char- acters of retarded circulation, breathlessness, slight a^dema of the ankles, scanty, perhaps albuminous urine, pulmonary and hepatic congestion. The superficial veins stand forth still more promi- nently, the rigid, tortuous, uneven arteries show a thready, often flickering pulse, which is accelerated and often irregular both in force and rhythm. The heart is found more or less increased in size, and its sounds are altered in quality and proper relative intensity. There may or may not be murmurs at apex or base indicative of atheromatous changes in the valves, but the aortic second tone is nearly always ringing and metallic. The patient loses strength, and finally takes to the house per- manently. Dyspnoea grows apace and not infrequently assumes the characters of cardiac asthma or of Cheyne-Stokes respiration. Urine grows still scantier, dropsy advances, orthopnoea sets in, troublesome cough, and frothy, blood-tinged expectoration, betoken ever-increasing stasis within the pulmonary vessels, and the pa- tient succumbs after weeks or months to general exhaustion, car- diac asthenia, or an attack of acute pulmonary oedema. Chronicity is the essential feature of this type of cardio-vascu- lar inadequacy. It is not uncommon for cases of arteriosclerosis to drag on for several years under the picture of senility and gen- 35* 538 DISEASES OF THE HEART eral decrepitude, and deatli to come at last as a result of acute bronchitis, pneumonia, or even of renal inadequacy. Exceptionally, although the total number of such eases is not snuill, the termination is through cerebral thrombosis. Rupture of a blood-vessel in the brain is not so frequent in senile arterio- sclerosis as in younger persons whose renal cirrhosis leads to enor- mous left-ventricle hypertrophy. Chronic nephritis leads to very serious changes in the heart- muscle. Clinically, this is shown by hypertrophy of the left ven- tricle either alone or as a part of a general cardiac enlargement. The myocardium may or may not be seriously degenerated, but whether it is or not, it is subjected to an enormous peripheral resistance to successfully cope with which it is compelled to un- dergo hypertrophy. I do not intend to discuss the various theories which have been advanced to explain this increase ; for these the reader is referred to works dealing with kidney diseases. The pulse of chronic nephritis shows prolonged high tension, which is primarily of renal, not cardiac, origin. If the kidney changes are of slow development, as in chronic interstitial nephri- tis, or if the patient is not carried off by the sudden onset of renal inadequacy, there surely comes a time when the heart, struggling with abnormally high endocardial blood-pressure, is able only with difficulty to withstand the enormous resistance in the arterial system. Then gradually or suddenly, according to circumstances, the wall of the left ventricle gives way. If slowly, the volume of urine begins to fall off, and the patient finds his wonted physical efforts are attended by shortness of breath and palpitation, and his pulse-rate is found to be decidedly augmented. Signs of venous congestion and pronounced cardiac dilatation are usually wanting at this stage. Unless the danger is recognised and means are resorted to of restoring the equilibri- um between pulse-tension and heart-power, cardiac insufficiency grows daily more apparent, and the patient is at length compelled to remain inactive. Examined at this time, he is found to evince unmistakable signs of failing circulation. The pulse is rapid and perhaps of poor quality ; the liver is palpable and more or less ten- der; tension, and it may be pitting of the ankles, is detected; the tongue is coated, breath foul, and the urine is apt to be 'decidedly scanty and albuminous. If the heart is examined, the apex is CHRONlC xMYOCARDITIS 539 displaced and lacking in concentration and force, the second sound at the right of the sternum is somewha-t enfeebled, and the pul- monic is nearly or quite as intense. The striking alteration in the heart-findings consists in the peculiar reduplication of the sounds at tlie apex, which is known as gallop rhythm (see introductory chapter). Occurring in the course of chronic Bright's disease this phenomenon is of very evil portent, for it indicates that the left ventricle is yielding to the abnormal strain and tottering on the verge of an irreparable breakdown. In most cases treatment is unavailing, symptoms of stasis progress, and dyspnoea becomes most distressing. It may be of the C'heyne-Stokes type, but is more often of a paroxysmal nature, coming in waves, as it were, with evidences of great agita- tion, even alarm, on the part of the patient, yet without corre- sponding signs of more than usual cardiac failure. This form of dyspncea is probably partly of toxic (urtemic) and partly of cardiac origin. jSTevertheless, the insufficiency of the heart aug- ments, renal excretion fails correspondingly, and after the lapse of weeks or a few months the patient dies with ursemic manifesta- tions or from acute pulmonary oedema. There are other cases of Bright's disease in which cardiac in- competence sets in abruptly. This is usually owing to some indis- creet effort or excess which causes rapid dilatation of the left ven- tricle. The symptoms are much the same as in the more gradu- ally evolved loss of compensation, but are apt to be of far greater intensity. Examination shows feeble apex-beat, displaced far to the left and perhaps downward, enormous increase of cardiac dulness, and a systolic apex-murmur, which often replaces the first sound, and a feeble second tone except in the pulmonary area, where it is intensified. The liver swells rapidly, is often painful and very tender, particularly in the epigastrium. Dropsy sets in, extends rapidly upward, and invades the serous cavities. The pa- tient suffers from orthopnoea with paroxysmal exacerbations, from severe, tensive headache, insomnia, or it may be somnolence, and many other distressing symptoms of combined cardiac and renal inadequacy. Few clinical pictures are more distressing, and 7ione are more hopeless. In many cases in which there are enlarged hearts with stiff- ened arteries and urinarv findin2,'s of renal sclerosis it is difficult 540 DISEASES OF THE HEART to say whether the symptoms of failing circulation are due pri- marily to incompetence on the part of the heart or of the kidneys. Some of these patients manifest symptoms of slowly failing heart- power for many months before being compelled to regard them- selves as hopeless invalids. I recall one gentleman of fifty-eight with this combination of cardio-vascnlar and renal degeneration, who, nearly two years before his death, suft'ered from paroxysms of dyspnoea which becanse of his rapid, unsteady pulse was thought cardiac, but seemed to me in reality ura:^mic. It did not yield until pulse-tension was reduced by frequent doses of nitro- glycerin. Another gentleman of forty-seven with the same asso- ciation of diseases used to complain that he could not breathe " more than an inch deep." This patient's heart manifested clinically the most enormous enlargement I have ever seen. His breakdown was initiated three years before by a " century run " on his bicycle. Diabetes melliius occurring after middle age, and usually con- joined with vascular and renal changes, is often seriously compli- cated by symptoms of cardiac incompetence. The arteries are more or less stiff, the heart is hypertrophied and dilated, and its action is rapid or ])ounding, sometimes intermittent. Glycosuria is the feature which has especially to be combated, and yet one must never lose sight of the cardio-vascular symptoms. At the present writing I have under observation two ladies who have dia- betes mellitus with atheromatous arteries and hypertrophied hearts. In one, whose age is not far from seventy, the main com- plaint (so long as strict diet keeps down the glycosuria) is of great weakness, palpitation, and shortness of breath upon exertion. The other patient, of about sixty, suffers chictiy from dyspnoea, attacks of palpitation, and faintness. On two occasions in the early morning hours she has been awakened by a sense of suffoca- tion, and has nearly died from acute ])ulmonary (rdema. Signs of cardiac inadequacy are present at all times, and yet she shows no traces of dropsy or special venous congestion. In both of these cases hypertrophy still predominates, and is able to endure the high endocardial blood-pressure so long as this is not intensified by the strain of physical effort. The nocturnal seizures in the second lady were probably due to the augmentation of blood-pressure in the arteries occasioned by the reciunbent position in sleep. This CHROMC MYOCARDITIS 541 at length overpowered the left ventricle, which temporarily became weaker than the right, and acute pulmonary a'dema supervened. In some of these cases of chronic myocarditis such attacks form the principal feature, and the cases are particularly grave on this account. Cases of Secondary Valvular Insufficiency. — Lastly, one occa- sionally meets with cases of myocardial degeneration which mas- querade in the guise of a mitral or aortic regurgitation. I do not refer to atheromatous valvular disease, but to cases in which the valvular incompetence is relative or muscular. Arthur R. Ed- wards has reported a case of relative aortic insufficiency from ex- tensive myocardial degeneration, and I have myself observed three cases in which the necropsy revealed the same condition. In all of them the clinical history was that of aortic regurgitation. Mitral incompetence is common and may be relative, but more often is muscular from degeneration of the papillaries or slight ventricular dilatation. I do not now refer to Balfour's Curable Mitral Regurgitation, which is seen in chlorosis and anaemia, or to that form seen in young athletes as an effect of acute strain. These all yield to appropriate treatment. I am now speaking of left-ventricle dilatation and secondary mitral insufficiency seen in cases of chronic myocarditis. I have under observation a man of sixty-five, a veteran of the late civil war, whose mitral valve leaks in consequence of great dilatation of the ventricle. There is no history of inflammatory rheumatism or any other disease to occa- sion endocarditis, but there is history of severe physical effort (climbing a mountain) ten years ago. Previous to that strain he had no cardiac symptoms, but since then his mitral murmur and dilatation of the ventricle have been present. At times the mur- mur wholly replaces the first sound, but as the ventricle retracts under treatment by baths and resistance exercises, the first sound becomes audible and cardiac impulse palpable. I think few would venture to assert that in this case the myocardium is healthy. I have notes of the case of another gentleman of forty who presented the signs of a typical mitral regurgitation, and who for four years struggled to preserve his compensation. He gave a his- tory of mild inflammatory rheumatism, of gonorrhoea, and of a thrombophlebitis of the right femoral vein, and therefore his valvular incompetence was quite naturally supposed to be of endo- 542 DISEASES OF THE HEART carditic origin, a conclusion that was sti-engthened by the occur- rence of two attacks of subacute articular rheumatism during the time he was under observation. He at last died, after having been confined to his bed for only a week, with symptoms of cardiac exhaustion. There was no o?dema, very insignifi.cant venous sta- sis, and at first a profound sense of weakness rather than of short- ness of breath. Towards the close of his illness, however, dyspna^a asserted itself, becoming rather spasmodic. His temperature grew subnormal, the pulse feebler and slightly more rapid, and he died apparently of simple cardiac asthenia. The necropsy made by Dr. W. A. Evans disclosed a perfectly healthy mitral valve, and on the tricuspid, chijnges too insignifi- cant to have aifected their function. The myocardium was in- tensely fatty, particularly of the right ventricle ; the cavities were all more or less dilated. The coronary arteries were healthy, but the aorta was congenitally small throughout. This man had been an athlete in college, and subsequent to his death I learned that before his symptoms of cardiac inadequacy began he had over- strained his heart by a long, hard bicycle ride. Owing to the apparent integrity of the coronary arteries in this case, I believe there can be only two explanation^; of his myocardial decay. It was either an expression of chronic myocarditis in the strict sense of toxic origin, or of a disproportion between the w^ork required of it and its nutrition, this latter being restricted by reason of the congenital smallness of the aorta, which also had served to put undue strain upon the myocardium. Finally, in concluding what I have to say upon the symptoma- tology of myocardial inadequacy, I desire to add a few words concerning two symptoms which are generally thought indicative of fatty degeneration of the heart. These are yawning and sigh- ing. I have never, however, been able to satisfy myself of the import of these two symptoms. Indeed, I not only have seen many cases of myocardial inadeqmicy in which they were absent, but I have, on the other hand, observed them in patients who pre- sented no suspicion of myocardial disease, as in young neurotic or ana?mic w^omen. I should certainly attach no value to yawning and sighing in the absence of other less doubtful symptoms, and in suspected cases of cardiac degeneratioTi I should esteem them of very minor importance. CHRONit MYOCARDITIS 543 Physical Signs. — Inspection. — In most cases inspection is negative. If the eye detects signs of stasis, there is nothing in this fact to indicate the underlying condition. The general ap- pearance of the individual may show to the experienced physi- cian signs of premature or senile decay. When hypertrophy of the left ventricle is present, this may be shown by the displaced apex-beat. But in the class of cases in which it is the most diffi- cult to arrive at a definite conclusion — that is, middle-aged and well-preserved men with capacious chests, the cardiac impulse is not visible becaiise of the chest-capacity and lung-volume. Conse- quently, it may be said that the chief value of inspection lies in the fact of its negativeness, for other disorders of the heart than myocardial degeneration are very apt to furnish some visible indi- cation of their nature. Palpation. — This is of value in the determination of oedema and of hepatic engorgement even more than in the examination of the heart. Yet by careful palpation of the prascordium one is often able to locate an apex-beat which is too feeble to be visible. It may enable one also to perceive that the cardiac impulse has the dif- fused jogging character of dil- atation with hypertrophy^, or the feeble, slapping shock of dilatation. Palpation is of special value in disclosing the state of the arterial coats. If these feel thick and resisting, or tortuous and uneven, like a string of beads, they furnish presumptive evidence that the heart-muscle is not sound. In searching for signs of cardiac incompetence one should always endeavour to palpate the liver. If the lower border of this organ can be felt below the costal arch, and particularly if it is smooth, rounded, firm, and perhaps tender, there is hepatic con- gestion, probably secondary to more or less cardiac inadequacy. Fig. 103. — Showing Shape of Kei.ative Dul- NESs IN Hypekteophy. Quadrilateral with rounded corners. 544 DISEASES OF THE HEART Percussion. — This means of investigation should never be neg- lected, for verv much depends upon the size of the heart. Abso- lute dulness may or may not be increased, but as the organ is enlarged in most cases of myocardial degeneration, careful percus- sion usually elicits an augmentation in the area of cardiac dulness. If this is found increased to the left and upward, it indicates left- ventricle hypertrophy; if to the right and downward, enlarge- ment of the right ventricle. In general cardiac hypertrophy the area of deep-seated dulness is of a quadrilateral outline with rounded corners (see Fig. 103). In estimating the size of the heart it is customary to take the left verticle nipple-line as the normal boundary of deep-seated dulness at the left. But Fraentzel dwells particularly on the lia- bility to error existing in the custom of considering the left nipple as the normal boundary of relative dulness on that side. If the dulness is not found to pass beyond this mark it is taken for granted that the size of the heart is nornuil. It should be remem- Age. Weight. Height. Circumfer- ence of chest. Distance from sternum to left nipple. K. A 29 24 25 30 28 29 42 24 24 33 23 33 28 23 23 31 If 23 21 32 29 30 30 25 25 27 24 22 43 155 135 130 150 145 157 191 149 185 170 160 125 161 195 158 145 155 140 130 165 im 135 162 189 204 150 130 145 189 Feet. iDches. 5 7 5 7 5 7 5 9 5 6 5 9 6 1 5 6 5 7 5 8 5 10 5 4 5 9 5 10 5 7:t 5 9" 5 n 5 10' 5 74 (i 1 5 10^ 5 4 5 H 6 6 5 74 5 6" 5 8i 6 0" Inches. 33 34 34 34 34 354 40t 36 36 36 34 30 35 40 35 34 37 334 33 35 35i 33 38 39 39i 38 33 35 39 Inches. H T. B 3 C. B E.B w.o S. D 3* 3f H 3i H. De V R. E 3f 3i H 3i 21 E. E S. E F. G G.G C. H H..I 3i 4 P. J G. L L ... F. M J. M H. M 3 3 2* 3* H. S 3i 3 J. s J S 3i 3i W. V .F. W .1. \V 4i 3i J. W 3 C 3i C. H 3^ CHRONIC MYOCARDITIS 545 bered, however, that the distance between the midsternal and left maniinary lines is by no means always, the case. I have not in- frequently found the left nipple situated 5 inches from the mid- sternum. Measurements of twenty-nine of my students, taken for the purpose of determining variations in this regard, gave the results shown in the table on the opposite page. These figures indicate plainly that the only accurate means of determining the boundaries of the heart by percussion lies in measuring the distance to which the area of deep-seated dulness extends to the left of the median line. The size of the normal heart, as shown by percussion, has already been stated in the in- troductory chapter. One often obtains valuable information by the sense of in- creased resistance on firm percussion, and hence the value of Ebstein's palpatory percussion. I am in the habit of verifying the results of percussion in the ordinary way, by recourse to aus- cultatory percussion, and am frequently surprised and gratified to see how closely they correspond. Auscultation. — Here, too, much depends upon the thickness or thinness of the chest-wall. If hypertrophy exists the first sound at the apex is prolonged and of low pitch, while the second is usu- ally clear and ringing. In some cases the systolic sound is muf- fled and indistinct. At the base of the heart the aortic second is sharply accentuated, ringing, or it may be so intense as to be actually banging. There is also intensification of the pulmonic second sound when the left ventricle begins to fail, and at the base of the heart one sometimes detects reduplication of the sec- ond sound. If the first in the region of the apex is short and sharp, resembling the normal second, it indicates dilatation rather than hypertrophy. Occasionally the heart-sounds take on the canter-rhythm de- scribed at length in the introductory chapter. This character- istic rhythm is limited to one or the other ventricle, and there- fore to the neighbourhood of the left nipple. It is especially likely to appear in left-ventricle dilatation consequent upon a granular kidney, but, according to Fraentzel, occurs, although rarely, in enlargement of the heart from other causes. This gallop rhythm must be kept distinct from reduplication of the second sound heard at the base, and from that apparent or simu- 36 546 DISEASES OF THE HEART lated doubling of the second sound that is not infrequently dis- covered in the mitral area in cases of stenosis of that orifice. A full, tense, not accelerated pulse, a dull first sound, and an accentuated aortic second, form a combination of signs highly sug- gestive of hyjDertrophy of the heart, even though its area of rela- tive dulness cannot be defined with certainty. There is no pathognomonic sign of degeneration from coro- nary sclerosis, and often the heart-sounds appear normal. It is highly important, however, and sometimes yields valuable infor- mation, to study the relative pitch and intensity of the several sounds. If, as there is good reason to believe, one of the elements entering into the make-up of the first sound is a muscular ele- ment, imparting to the sound its booming quality, and caused by contraction of the ventricular and papillary muscles, then impair- ment of their contractility through disease should theoretically diminish the intensity of the first heart-sound. Experience shows that this is precisely what takes place in some instances. Over the weakened left ventricle this sound at the apex may be weaker than that over the right ventricle, having a distant or muffled character. The pitch of the sound may be raised also and its dura- tion somewhat shortened. The second sound at the apex is often relatively louder than the systolic, and on moving the stethoscope to the base of the heart this intensification of the second sound is found due to accentuation of the aortic second, which may even possess a ringing character from sclerosis of the aorta. In other cases the second sound at the right of the sternum is feebler than that in the pulmonary area. As the aortic second sound should be the louder of the two in persons of the age at which myocardial degeneration usu- ally develops, relative weakening of the second sound in the aortic notch points to diminished vigour in ventricular contrac- tions, and honco furnishes indirect evidence in favour of degen- eration. Murmurs are accidental findings, and are due either to rela- tive incompetence of the valves or to atheromatous roughening of the orifices. In either event they may afford valuable testimony as to the state of the heart-muscle. A murmur may, of course, in some instances be the result of a rheumatic valvular defect, as will be shown by the history. CHRONIC MYOCARDITIS 547 Diagnosis. — From the foregoing, it is evident that in the diagnosis of degeneration of the myocardium, but limited in- formation is derived from a study of the heart. There is no form of cardiac disease, therefore, in the diagnosis of which so much dej)ends on the judgment and experience of the physician. In valvular defects there are murmurs to serve as guide-posts; in hypertrophy or dilatation there is obvious alteration of size. In the affection under consideration the volume of the organ may or may not be changed, and therefore great dependence must be placed on age, state of the vessels, history, and symptoms. Age is so important an etiological factor that the development of cardiac insufficiency in an individual well on in years may be set down to degenerative changes with tolerable certainty. It is quite otherwise when heart-weakness, without obvious signs of disease, develops in a person about the middle period of life. In such persons careful search should be made for traces of prema- ture decay, for indications of renal disease, or a gouty diathesis, etc. There is an old saying that a man is as old as his arteries, and therefore the radials, temporals, and other peripheral vessels should be carefully palpated for evidences of thickening or for nodular deposits of lime-salts. It may be necessary in some cases to make an ophthalmoscopic examination of the retinal artery for the signs of sclerotic change which are said to first manifest themselves in this situation. The physician should note the appearance or not of premature whiten- ing of the hair, and examine the texture of the skin. I have more than once observed that persons with a strong suspicion of fatty degeneration of the heart have a skin that has lost its elasticity and feels peculiarly soft, as is often the case in the aged. The examiner should scrutinize the fingers and ears for chalky deposits, and the nails for those longitudinal ridges said to be indicative of the gouty state. In this way valuable hints may often be obtained. The wine should be analyzed carefully, and repeatedly if nec- essary, for evidence of nephritis, since it is well known that de- generation of the myocardium is a frequent accompaniment of chronic renal disease, particularly the interstitial form. Minute inquiry into the patient's history may elicit facts con- cerning family tendencies, personal habits, previous diseases, etc., 548 DISEASES OF THE HEART that may throw light upon the nature of the present malady. It is particularly important to ascertain whether the patient has suf- fered from attacks of angina pectoris or cardiac asthma. The significance of the former in individuals past middle age is very different from that of anginoid seizures in adults under forty, especially women. Even in spite of the most painstaking investigation and atten- tion to all circumstances, however trivial, a positive diagnosis in this class of cases is not always possible without awaiting the results of therapeutic management. If decay of the heart-muscle is present, it will be ultimately shown by the gradual or more rapid development of symptoms sufficiently characteristic to settle the diagnosis. Aneurysm of the heart is only possible of diagnosis wdien it is of sufficient size to affect the outline of cardiac dulness in a way to suggest localized bulging of the heart-wall. It is stated that cardiac aneurysm may be suspected when there is a striking disproportion between the force of the cardiac impulse at or near the apex and the smallness and feebleness of the pulse. Its exist- ence can probably be determined by fluorescopic examination. In most cases of- cardiac rupture its occurrence can only be suspected but not determined before the death of the patient. It may be surmised in cases running the extremely acute course de- scribed in Symptoms. Physical signs pointing to fluid disten- tion of the pericardium, with a pale, anxious countenance, a small, feeble, irregular, it may be intermittent pulse, and other symp- toms of profound shock, furnish strong evidence that rupture of the heart-wall has taken place. If life is sufficiently prolonged a correct diagnosis is often possible, but when death occurs within a few minutes the physician can rarely do more than conjecture the occurrence of rupture. The diagnosis of chronic myocarditis is largely a matter of probabilities, since there are no pathognomonic signs of the con- dition. Physical examination nuiy disclose certain gross changes, as hypertrophy or dilatation, or a combination of l)ot,li, and pathol- ogy teaches that such hc^arts arc as a rule more or less degenerated, but we possess no means of determining outside the dead-house to what extent the heart-muscle is diseased or the precise nature of its degeneration. The majority of elderly individuals who consult CHRONIC MYOCARDITIS 549 lis because of cardiac symptoms do not suffer from tlio conse- quences of rheumatic endocarditis as do. the young. Tliey pre- sent evidence of cardiac incompetence ; of this we can he certain, but concerning the state of the myocardium we must take much for granted. Prognosis. — This depends upon the cause, the degree of the hypertrophy, and the state of the heart-muscle. If the high pulse- tension is due to luxus consumption, and the individual is young and robust, correction of his habits may lessen peripheral resist- ance, and may retard, if not wholly prevent, development of car- diac inadequacy. In cases of advanced renal or vascular disease there are two dangers : occurrence of apoplexy and the breakdown of the heart under conditions of unwonted strain. If the cause, whatever its nature, is persistent and not amenable to treatment, the ultimate prognosis is unfavourable, because there will at length come a limit to the hypertrophy and the heart-wall will give way. So long as the myocardium is functionally healthy — that is, receives sufficient nourishment — the hypertrophy proves a pre- servative measure ; but when incompetence sets in, the most fa- vourable management can do no more than defer the evil day. Palpitation, and particularly intermittence of the pulse, are unfa- vourable signs ; they may be the first evidence that the heart is yielding to the unequal struggle, or by occasioning incomplete emptying, and hence distention of the cardiac chambers, they may hasten the coming on of dilatation. In forming a prognosis in any given case one must take into consideration also the age and temperament of the patient, and the state of his general nutrition. The younger the patient and the greater his self-control, the better his prospects of maintaining compensatory hypertrophy and the less the likelihood of injury from excesses, emotional or otherwise. The further one gets be- yond middle age the stronger the probability of the cardiac in- sufficiency being due to myocardial degeneration, and of the obstacle to circulation proving too much for the weakened heart- walls. When serious symptoms at length set in there is small pros- pect of medical skill being able to do more than patch up the crip- pled heart. In a word, the prognosis depends upon the relation 550 DISEASES OF THE HEART existing between the demands made npon the heart and its ability to respond. It is therefore abnost entirely a qnestion of cardiac nutrition. The yonnger the individnal the less the likelihood of serious degenerative changes, but after middle age such changes are usually present and compensatory hypertrophy is rarely re-es- tablished after it has once seriously given way. One should make a careful study, therefore, of the condition of the vascular coats, as they furnish presumable indication of the state of the heart- muscle. Nevertheless, experience teaches that the latter may be extensively diseased while the arteries appear healthy. The de- tection of the gallop-rhythm over one or the other ventricle, most often the left, is of evil import, as it indicates a loss of muscu- lar tone and either incipient or fully developed dilatation. In the cardiac inadecpiacy of chronic nephritis this symptom may be regarded as indicating a not very distant termination of the case. In coronary sclerosis the prognosis is most grave. We pos- sess no means of ascertaining the location and extent of degenera- tion, and hence cannot say whether life will persist a single hour. Indeed, a person with fatty degeneration of the heart-muscle can never be sure of his life from one moment to another. He may live for years, and he may die suddenly when apparently in the best of health. The occurrence of angina pectoris makes prognosis doubly bad. In acute and subacute cases death is not likely to be long deferred, and except in the most acute forms, which are usually rapidly fatal, no one can venture to predict the length of life. Chronic forms of coronary sclerosis may persist for many years with ever-recurring attacks of angina. As a rule it may be stated that the more easily and frequently pain is induced the graver is the prognosis. The arrhyllimic form of chronic myocarditis is apt to run a very chronic course, wdiercas those showing attacks of cardiac asthma or of acute pulmonary oedema are in danger of terminat- ing abruptly in such an attack. The development of Cheyne- Slokes r(;spiration is in most instances an indication tliat the end is not far off (see article on this type of breathing). Syncopal attacks are likewise of evil port(int, owing to the danger of sudden death from asystolism at such times. The cardiac insufficiency of Uright's disease and diabetes is of CHRONfC MYOCARDITIS 551 particularly great gravity, since the abnormally high pulse-ten- sion, which is the cause of the cardiac embarrassment, cannot be removed, and prevents the left ventricle from regaining its lost power. A serious breakdown in this class of cases, therefore, may be said to be irreparable. Finally, the prognosis is also determined by the presence or absence of sclerotic changes in the kidneys, lungs, and liver, since the healthier these organs the less the strain upon the diseased heart. Chj'onic gastritis, with its flatulent distention of the hol- low viscera, influences prognosis both through mechanical pres- sure and the generation of injurious toxines. Acute bronchitis or other illnesses, in particular pneumonia and influenza, must always fill the medical attendant with alarm, since it requires but little to throw the balance one way or the other in these cases, and acute infections are very liable to prove the immediate cause of death in cases of chronic myocarditis, which, without such an intercurrent affection, might have persisted for years longer. Conditions of environment also affect prognosis, an individual who is able to spend his winters in a mild climate and avail himself of all other means of warding off injurious in- fluences being, ceteris 'paribus, likely to live longer than he who is compelled to toil on for his daily bread. In conclusion may be quoted Huchard's emphatic statement concerning cases of myocardial disease : " Their evolution is latent, their beginnings insidious, their course paroxysmal, their progress interrupted, their visceral complications various, and their explosions of cardiac insufficiency are sudden." Treatment. — This must be considered first with regard to preservation of cardiac competence, and second with reference to the stage in which heart-power is either showing signs of failure or has actually been lost — pronounced cardiac insufficiency. Medical aid is not sought so long as the myocardium is adequate, and if the discovery of hypertrophy is made, it is only by accident. When, however, such discovery is made, it should be the physi- cian's duty to call the j)atient's attention to the dangers threaten- ing him in the future, and to show him how his habits of life are likely to affect his heart. The management is now along the line of prevention ; patients who habitually eat or drink too much must have the evils of glut- 552 DISEASES OF THE HEART tonj explained to them, and be put upon a diet that will not over- tax kidneys, vessels, and heart. The man who takes little or no exercise, and is too rapidly gaining weight, must be sent to the gymnasium to be put in training, or must be made to walk more and ride less. // vessels are sound and heart still competent there is noth- ing better for such patients than moderate bicycling, tennis, ball- playing, etc. If such sports are thought too vigorous, there is golf, which is an ideal form of exercise, since it trains the eyes and muscles without subjecting weak organs to undue strain. Those with corpulent, flabby abdomen are much benefited by a course of massage and Swedish movements. .The processes of digestion and assimilation are improved, and constipation, if present, is generally corrected. Gouty individuals or persons suffering from defective excre- tion usually derive benefit from a semi-weekly or a weekly Turk- ish bath. This not only increases elimination, but lessens blood- pressure. This seems especially beneficial to persons addicted to the abuse of alcohol and tobacco. If the cause of the hypertrophy is not preventable, or if vascular and renal changes are pro- nounced, then patients should be frankly informed of their con- dition, and warned against undue muscular effort, or whatever may serve as an additional and unnecessary strain to the heart- muscle. Arterial and kidney disease call for still greater strict- ness in the matter of diet. A highly nitrogenous dietary often serves to intensify the already existing high arterial tension, while a vegetarian diet, or one bordering thereon, lowers blood-pressure. Digestive disturbance and constipation must, if possible, be corrected, since they not only increase arterial tension, but may produce palpitation and intermittence, which, if allowed to go on, may ultimately impair the integrity of the heart-muscle, which in this stage it is our aim to preserve. Cardiac tonics, especially digitalis, are not needed at this time, and if administered are likely to do harm. Our attention is to be addressed not to the heart itself, but to its protection from all injurious influences. Unless induced acutely by severe heart-strain, signs of inade- quacy begin to declare •tliomselves slowly and at first very insidi- CHRONIC Myocarditis 553 onsly, so that the maiiagciiicnt may bo said to pass almost im- perceptibly into tlie treatment of symptoms directly due to: Commencing Loss of Heart-power. — Among the earliest signs of this second stage may be tachycardia and palpitation. These do not indicate excessive hypertrophy, for snch does not exist, bnt are tokens that the organ is finding its work too heavy. Therefore an attempt shonld be made to discover and remove possible sources of irritation and increased peripheral resistance before aconite or veratrum, digitalis, or strophanthns are pre- scribed. The former are powerful cardiac depressents and must be used carefully, but in the past three years have been employed by me frequently. The precise indications for their use cannot be stated, but seem to be a dangerously high blood-pressure with con- sequent strain of the heart-walls. A too rapid or violent action of the heart in this stage may be due to digestive disorders, constipation, or faulty elimination which raise blood-pressure and hence subside with removal of the cause. To this end I find very satisfactory a periodic dose of calomel, or blue pill followed by an aperient water. It may be well to restrict the diet by cutting down the red meats and limiting the total amount of water and other fluids which is taken by the patient. The former raise pulse-tension by reason of their extractives, while the latter distend the stom- ach and abdominal vessels, thus increasing the strain on the left ventricle. Should blood-pressure still be too high, it may be reduced by one of the nitrites or by an iodide. Three to five grains of potas- sium iodide may be given in essence of pepsin after meals with- out disturbing the stomach, or nitroglycerin, to -g- of a grain, may be given every three hours. Erythrol is said to be more lasting in its effects on the arterioles, but this advantage has not seemed to me sufficient to compensate for its greatly increased cost. Should such treatment fail to control cardiac action, then it is well to resort to digitalis or allied remedies. They may be given in conjunction with iron, arsenious acid, or strychnine. Gentle exercise is now very beneficial by its action on the heart and vascular system. It causes dilatation of the intermuscular arterioles, promotes venous flow, and thus tends to restore circulatory equilibrium, re- 554 DISEASES OP THE HEART moves waste products from the tissues, and flushes the heart-muscle with freshly oxygenated blood. This explains why patients who feel priecordial ojipression upon starting out for a walk often ex- perience a sense of relief and well-being after their exercise has " warmed them up," as they say. Gentle pedestrian exercise is to be recommended, therefore, in this stage of commencing cardiac incompetence, but under certain restrictions. Patients must be cautioned to begin their walk at a slow pace, and to increase their speed only as they find exercise and breathing grow easier. Walking against a cold or strong wind is very trying, and on such days they should walk with and not in the face of such wind. The carrying of, heavy parcels is to be forbidden, and the restraint of trunk or limbs by tight clothing is inadmissible. The ascent of stairs and hills is fraught with danger to the failing heart, and should be avoided. Oertel's plan of hill-climb- ing is to be advised only for patients whose hearts still retain a fair measure of their integrity and whose judgment can be relied upon. The principle underlying this mode of treatment consists in the ascent of gentle inclines at a rate of speed that does not cause dyspnoea or palpitation. Only when such acclivity can be surmounted with ease is a steeper grade to be allowed. If hill- climbing is done so as not to occasion respiratory or circulatory embarrassment, the heart-walls are gradually strengthened and a tendency to dilatation is overcome. This form of exercise requires excellent judgment on the part of the patient lest he overdo, and on the part of the physician in the selection of suitable cases. Another kind of cardiac exercise not open to the same objec- tion, and suited to a larger number of cases becauses its effects can be more accurately gauged, arc the " resistance exercises," which were described in detail in the chapter devoted to Treat- ment of Valvular Disease. If golf is permitted to patients in this stage of deficient cardiac power it sliould be restricted to put- ting, or at most to the playing of a liiiiited mnnber of holes. Whatever tlie form of outdoor exercise allowed, the following restrictions should be imposed: (1) Patients must not exer- cise immediately after eating, the length of time devoted to rest being determined by the degree of cardiac weakness. In most cases patients should remain ([uiet for at least an hour, and CHRONIC • MYOCARDITIS 555 when the heart is feeble Fracntzel does not allow exercise before three or four hours after a meal. (2) Walking or other exercise should not be indulged in to the point of fatigue. In some cases indeed it should be for only a short period, several times repeated during the day. (3) In cases showing decided indications of a threatened loss of adequacy, rest in a recumbent posture must be insisted on at the close of exercise. As our aim at this time is to prevent the heart from becoming still more taxed in its labours, and blood-pressure is increased by hearty feeding, it is necessary to restrict the diet. It is quantity even more than quality that is harmful, and hence patients should be told to eat lightly. Too much liquid raises blood-pressure in the abdominal vessels, and therefore it is well to restrict it to 8 or at most 10 ounces with each meal. Alcoholic stimulants, if permitted at all, must be in the form of a light, dry wine, or still better of a modicum of whisky, largely diluted with water. To- bacco is to be allowed in great moderation, a small light cigar or a single pipeful of mild tobacco after meals. Huchard, Fraent- zel, Krehl, and others are very strenuous in their opposition to strong Havana cigars on the ground that they augment arterial tension, and state that many middle-aged men with weak hearts find out for themselves that they are obliged to substitute mild domestic cigars for the heavy Havana ones to which they have been accustomed. Excesses of all kinds are injurious, and these patients are to be warned against the harmful effect of frequent sexual indul- gence. Indeed, the principle that must govern the daily life of these individuals is moderation in all things. If patients give due heed to the doctor's admonitions they may succeed in holding their hearts in statu quo for a considerable time. Unfortunately, how- ever, the tendency of myocardial decay is downward, and hence we are called on, soon or late, to institute active treatment for the relief of symptoms which mark the arrival of the third stage. Cardiac Incompetence Pronounced. — Venous and visceral congestion now begins to manifest itself, and calls for the more vigorous and frequent use of cathartic remedies. It is also gen- erally necessary to resort to cardiac tonics, and of these digitalis heads the list, although strophanthus, spartein, convallaria, adonis vernalis, and caffeine are all useful. Whenever digitalis is admin- 556 DISEASES OF THE HEART istered to a patient who exhibits higli pulse-tension, particnhirly if this depends on arterial thickening, it should always be given in conjunction with an iodide salt or nitroglycerin to counteract its effect on the arterioles. So long as cardiac weakness is not ex- treme the dose of digitalis may be small, 10 drops of a fat-free tincture thrice daily, or 15 drops every twelve hours. Given in this way it may be continued for weeks or even months without losing its effect or exhibiting its cumulative action. In more than one instance of myocardial inadequacy with stiff arteries I have seen striking results follow the prolonged use of strophanthus. It is sometimes well to combine these two remedies, a few drops of each being taken at a dose. Spartein sulphate is highly recom- mended by the French when the pulse is irregular, but although I have tried it repeatedly I have never been able to satisfy myself of its beneficial effect or advantage over digitalis. Strychnine is so indispensable a heart-tonic that I believe it should be taken by this class of cardiopaths as regularly as is their food. A fortieth or even a thirtieth of a grain three times a day is not at all too much for the average patient. The one form of treatment from which I have seen patients with myocardial insufficiency derive most benefit are the natural or artificial Nauheim baths (see page 466). They should be com- bined with resistance exercises. In my opinion this form of treat- ment is particularly adapted to this class of cardiopaths, and I have rarely seen a case of dilated hypertrophy which has not been improved by its judicious employment. I recall a typical example of this form of heart-disease in a medical man of forty-four, who began to manifest symptoms of threatening dilatation. His area of absolute cardiac dulness was greatly increased, particularly to the left, and anything more than moderate exercise occasioned a very considerable degree of discomfort. Six weeks of baths com- pletely restored the heart's power, and although five years have now elapsed, the doctor is still able to attend to the duties of a large and exacting practice. His professional calls have required him to daily clind) many flights of stairs, and although unwonted exertion still calls forth some degree of l)rcathlessness, he has, by keeping down his pulse-tension through a somewhat restricted diet and an occasional -purgative, never again displayed the same threatening symptoms. The last time I heard from him he had CHRONIC MYOCARDITIS 557 taken to a bicycle, and by careful riding succeeded in still further strengthening his heart. At the close of hi's course of baths abso- lute dulness had returned to normal, and the relative become manifestly reduced. He weighed over 200 pounds, and of course still has a considerable degree of cardiac hypertrophy. In the summer of 1899 I treated by means of baths and resistance exer- cises two middle-aged gentlemen, each with enormous hyper- trophy. The symptom chiefly complained of by one was great pra3Cordial oppression, amounting almost to what Gairdner would call " angina sine dolore,^^ whenever walking was attempted about an hour after meals. His pulse was slow and tense, and his heart enormously enlarged. At the end of treatment the heart was not much reduced in size, but the sounds were manifestly stronger, and the pulse had become fuller, stronger, and slightly more rapid. He then passed a month at his summer cottage, where he daily indulged in light carpentering, and was able to ascend the sandy hill on which his home stood without experiencing the former discomfort. A very restricted diet and the daily use of small doses of the tincture of strophanthus and iodide of sodium have been rewarded by continued improvement. The second patient also derived much benefit from the baths and exercises, although, as in the preceding case, the area of deep-seated cardiac dulness did not become permanently diminished. I was frequently able to determine a reduction in the size of the heart following a bath, and he always experienced a sense of well-being and lightness in the chest. In this case there was a very obstinate indigestion, and the urine always contained an excess of solids, although it never showed albumin or casts. His pulse was for the most part irregu- lar and intermittent, seeming to be governed in this respect by the intestinal indigestion, for every time his digestive disturbance became aggravated his pulse grew more irregular. He was subse- quently induced to take a course of massage and Swedish gymnas- tics, with the result that not only did his corpulent abdomen be- come greatly reduced in size, but his digestion improved, his pulse became regular for days together, and he said he felt as well as he ever did in his life. The heart, however, still showed great en- largement. In both these cases a change of habit as to food and exer- cise lowered blood-pressure, treatment of the heart restored its 558 DISEASES OF THE REART competence, and threatening dilatation was averted. I should add that all these three patients continued their professional and busi- ness duties while undergoing treatment. In most cases that have reached this stage restoration of heart- power is out of the question. The problem confronting the physi- cian is how to relieve symptoms and postpone the final catas- trophe. In such, exercise is likely to do harm instead of good, and yet my experience has convinced me that harm is also likely to result from a too rigid enforcement of rest. If the breakdown is complete, the sufferer may be forced to remain in bed or his easy chair. If things have not reached this pass, I believe it is better to allow the invalid to move quietly about his room that venous circulation may be aided by muscular contraction and the deepened respiration consequent upon this exercise. In some in- stances venous circulation may be assisted by gentle massage, and carefully conducted resistance exercises may, by dilating the arterioles, and thus flushing the muscles, help to unload the over- distended heart. Romberg and Fraentzef are both emphatic concerning the in- jury of too strictly enforced rest in chronic myocarditis, and expe- rience has convinced me of the soundness of their advice. In the earlier years of my practice I used to consider prolonged rest indi- cated in all cases of cardiac incompetence from whatever cause, but I ultimately found that elderly individuals, who were not suffering from valvular disease, showed an acceleration of their downward course when they were denied all exercise and kept rig- orously in bed. The aggravation of symptoms thus resulting is attributed by Romberg to the enervating effects of inaction, the same as is ob- served in the case of the voluntary muscles from disuse. The same thing is observed in previously healthy persons who are obliged to remain in bed a long time, from one cause or another; when again permitted to get up they not only find their legs weak, but the first attempt at walking produces slight shortness of breath and acceleration of the pulse. This explanation is in accordance with that given by Fraentzel, and is doubtless correct so far as it goes. In the case of a degenerative heart, there is another reason whicli I thiiik holds good. When a patient remains quiet in a recumbent position the venous circulation is deprived of two fac- CHRONIC 'MYOCARDITIS 559 tors of great importance in its maintenance. These are muscular effort and deepened respiration. Muscular contraction aided by the venous valves exerts a pumping action on the venous current, and also the flow within the absorbents. Abolish the use of the muscles and you remove one of the well-known causes of venous circulation. Furthermore, with rest in bed the patient breathes more slowly and superficially, and hence blood is less rapidly aspi- rated out of the great veins into the right heart, and a second important factor in maintaining venous flow is diminished. The work of maintaining the circulation now devolves upon the heart even more than under normal conditions. It must con- tract more powerfully that its driving force may be felt through- out the entire circle propelling the blood onward in the veins. Tn those cases in which breathlessness on effort is a pronounced fea- ture absolute rest for a time may be beneficial, hut it will not do to let these ijcitients remain quiet for too long a iieriod. The heart-muscle is weak, and cannot be left for too long a time to cope unaided with the labour of maintaining adequate blood-flow. Instead, therefore, of complete rest, it is better that the physical repose be interrupted by short periods of gentle exer- cise. This last, however, is to be strictly controlled. The patient must only be allowed to walk about his room, or at the most into the adjoining room. Under no circumstances is he to be allowed to climb stairs nor to walk about soon after a meal. He must be impressed with the danger of jumping up suddenly and of hurry- ing across the room. If very weak, and dyspnoea is considerable, he had better lean upon the arm of an attendant while taking his • exercises. The patient should also not be allowed to dress himself un- aided, and he must be instructed not to strain at micturition or defecation, since, according to Sommerbrodt, straining during such acts raises blood-pressure reflexly, and has more than once caused sudden diastolic arrest of the left ventricle. If massage is employed it must not be applied to the abdomen, unless very cautiously, since it raises blood-pressure. Also, if re- sistance exercises form a part of the management at this time, those are not permissible which constrict the abdomen or necessi- tate the elevation of the arms to a level above the patient's head, as they are likely to occasion dyspnoea and do harm. 560 DISEASES OF THE HEART In the matter of food, it is well to reniomber that these patients require a relatively small amount of nourishment on account of the enforced inactivity of their lives. They should consume a lim- ited quantity of liuids, since it is an easy matter to ingest more than can be excreted by the kidneys because of congestion, and only such an amount is to be allowed as is found by actual trial to promote the renal function. Special care is to be had in order- ing such foods as do not induce flatulent distention of the stomach and bowels, and when this occurs it must be relieved by carmina- tives and medicines that assist feeble digestion. Of equal importance with the prevention of fermentative indi- gestion is the correction of constipation. This is injurious not only because it necessitates straining at stool, but also on account of its raising arterial blood-pressure, and thereby increasing dys- pnoea, and the liability to attacks of angina pectoris and cardiac asthma. The patient should therefore take a laxative pill at bed- time, containing some of the well-known combinations of aloes, cascara, podophyllin, rhubarb, and colocynth, or a morning draught of some aj^erient water. It will not do to purge these patients repeatedly and violently, since there is danger of aug- menting the already existing debility, and yet a considerable degree of hepatic engorgement may render necessary an occasional sharp purge. Having in this way endeavoured to remove or lessen the vari- ous conditions which may embarrass heart-action, the medical adviser should next turn his attention to those therapeutic meas- ures which usually afford a prf)spect of strengthening the heart- muscle. Digitalis is the agent usually employed in this as well as other forms of cardiac debility. It should be prescribed, however, with care and judgment. If the heart-muscle is greatly damaged, it is not likely to respond to the remedy, which will then exert itself chiefly on the arterioles. Through contraction of the latter blood-pressure is raised, so that instead of strengthening the heart digitalis may actually increase its labour. If given in such a case, the remedy should be prescribed in moderate doses, 5 or 10 drojis of the tincture, twice or thrice daily, and its constricting effects on the vessels should be counteracted by nitroglycerin. In coronary sclerosis the nature of the degenerative changes that take place in the heart jirecludes the possibility of doing any- CHRONie MYOCARDITIS 561 tiling more than to relieve symptoms. In the most acute manifes- tations of the disease, the physician, ^vllo. has been hastily sum- moned, is usually able to do no more than attest the fact of death. In the somewhat less acutely fatal cases with manifestations of profound shock stimulation is urgently indicated. Time should not be lost by sending for some favourite stimulant, but use should be made of whatever is at hand. A tablet of nitroglycerin, with which every physician is usually provided, may be placed upon the tongue ; and while an attendant follows this with ^ an ounce of whisky or brandy, the physician should inject under the skin -J of a grain of morphine. Twenty drops of spirits of cam- phor, or ^ a drachm of aromatic spirits of ammonia, j)i"op6rly diluted, is also an efficient stimulant, and may be repeated at inter- vals of twenty minutes. Meanwhile, members of the family should fill bottles with hot water and place them about the body and limbs of the patient, who is then to be wrapped in blankets. A hot bag or bottle should also be j^laced at the pra^cordium. By these and other means every attempt is to be made to restore the failing circulation. In some cases, unfortunately, all efforts are unavailing, but should the patient rally somewhat, stimulation is to be continued in such doses and at such intervals as will main- tain the heart's action. If after the lapse of a few hours it be thought best to administer food to the patient, this should be liquid and hot, as a cupful of soup or hot milk, to which the am- monia, whisky, or brandy may be added. It may now be well to order strychnine hypodermically, in doses of :o^ or ^V of a grain every two or three hours ; but digitalis, strophanthus, and the like are contra-indicated or are to be given cautiously. If the initial symptom is an attack of angina pectoris, nitro- glycerin, 1 minim, and ^ of a grain of morphine under the skin, will probably afford relief, and may be followed by hot whisky, and hot applications to the extremities and pra?cordium, the subse- quent use of stimulants being left to the judgment of the attend- ing physician. In subacute cases, which run their course in a few weeks, or at the most in a few months, the serious changes which the heart- muscle has undergone place the restoration of compensation out of the question. Both the physician and patient must concern themselves with such measures as tend to make the downward 37 562 DISEASES OP THE HEART career as slow as possible. What strength the heart still retains must be carefully preserved, and all unnecessary demands upon it studiously avoided. The management of chronic cases of coronary sclerosis is also largely preventive and symptomatic, but there is often enough re- serve power left in the organ for considerable improvement fol- lowing measures calculated to roinstatc the heart-muscle to a lim- ited degree. Exercise and diet must be governed by the same rules that apply to the more severe cases, although as time progresses and the heart appears to gain strength these restrictions do not need to be so rigorously enforced. The patient should be made to understand, however, that upon his obedience to the physician's in- structions, and his care in avoiding unwise effort as well as ex- cesses in eating or any other kind, depends his hope of prolonging life. In such cases more depends upon habit and daily routine than upon remedies. It is often interesting to observe how true it is that these patients can only learn by personal experience the wisdom which their physician has vainly tried to teach them. They may be repeatedly and emphatically warned against infrac- tion of rules of diet and exercise, lest they thereby bring on a paroxysm of angina pectoris, or aggravate the already existing dyspnoea, and yet so soon as symptoms that serve as a monitor have become lessened, they think they can allow themselves more latitude and commit some indiscretion. A speedy return of angina or cardiac asthma brings them to their senses, and they are again ready to submit to any restriction. The going and coming of these patients must be ordered by their medical adviser, who therefore should keep them under surveil- lance that he may discover early signs of impending trouble, and take prompt action accordingly. Attacks of cardiac asthma are most surely and quickly allevi- ated by hypodermic injections of -J of a grain of morphine combined with ^^o of atropine. A prompt effect is more surely obtained by throwing the medicine into the arm instead of the leg. "JMie relief thus afforded is sometimes almost miraculous within a few minutes, the patient being able to lie down and fall into a refreshing slnndier. In the less severe forms of cardiac asthma tlu; administration of the mor]>hine at 10 or 11 p. m. will often carry the sufferer through the night without one of his CHRONIC MYOCARDITIS 563 dreaded attacks. The remedy is never so efficiently administered in any other way as under the skin, and the dose should be as small as will produce the desired effect. This will rarely be less than ^ of a grain, which dose should be administered nightly with- out increase. Should it be thought best for any reason to with- hold this remedy, then insomnia may be overcome by paralde- hyde, chloralamide, and bromide together, or by sulphonal. The treatment of cardiac asthma is of a necessity that of the paroxysm and the protection of the patient against influences which may precipitate an attack. If Cohnheim's explanation of its mode of production is correct — namely, that it is the result of temporary increase of left-ventricle weakness, in consequence of which its systoles are relatively feebler than those of the right — then efforts must be directed to the protection of the degenerated left heart against conditions which by raising arterial tension tend to overj)Ower the left ventricle. Blood-pressure may be in- juriously raised by the horizontal position of sleep without other factors, and the augmentation of peripheral resistance thus in- duced serves to overstrain this relatively too weak portion of the heart. We cannot abolish the need for sleep, nor can the patient be required to pass his nights in an easy chair, but we can guard him against other harmful influences, as constipation and flatulent distention of the bowels. The former raises blood-pressure in the aortic system ; and the latter exerts injurious pressure upon the weakened heart. Dropsy is to be combated in the usual way, by an infusion of digitalis or diuretin-Knoll, as laid down in the treatment of oedema from valvular disease. The physician is not infrequently called to see a patient suf- fering from excessive distention of the right heart, consequent it may be upon the rapid giving way of hypertrophy. Two lines of treatment are open to him : a resort of free catharsis by some one of the drastic purgatives, as elaterium, or to venesection. There is no doubt of the speedy relief often following the abstraction of 16 to 20 ounces of blood from the arm, and if the urgency of the symptoms or the patient's exhaustion make the medical man hesitate to administer a drastic cathartic, no objection can be urged against the opening of a vein and the letting of blood. The relief thus afforded is justification enough for the procedure. 564 DISEASES OF THE HEART Moreover, this operation can then be followed by the administra- tion of elateriuni, jalap, or any other hydragogue cathartic. In a case of extreme dilatation of the heart, seen for the first time it may be, in this dire condition, the administration of large doses of digitalis, before having depleted the heart and venous system by venesection or hydragogue catharsis, is bad 'practice. Thus overdistended, the heart cannot respond to the drug and only struggles vainly to perform its work, like the poor horse that in response to blows strives in vain to draw the too heavy load up hill. So it is with the overburdened heart. It may be better in some cases to administer diffusible stimulants, as ammonia, cam- phor, ether, and the like, before })rescribing digitalis, and only order the latter after the pulse has been improved in strength and volume by ammonia, etc. Dropsical accumulation in the serous cavities may be with- drawn by aspiration, often to the relief of the sufferer. Such a l)roeedure is of course not calculated to help permanently; it may, however, by lessening pressure for a short time, enable the heart to respond to stimulation. When at length all measures have been tried and found of no permanent benefit, the medical attendant nuiy then resort to opium in some one of its many forms to lessen the patient's sufferings. If we cannot promote restora- tion to health, we are justified in producing euthanasia. It is a physician's duty to prolong life, I presume; but I have seen pa- tients kept alive for days by drugs when it seemed to me it would have been far kinder not to prolong the struggle after it became manifest that the end was not far off. CHAPTER XXI HYPERTROPHY OF THE HEART Morbid Anatomy. — In hypertrophy the heart-muscle is in- creased in thickness and weight. Hypertrophy of the organ as a whole is judged hy its weight, while that of a single chamher is better estimated by a measurement of the thickness of its walls. This increase in size seems, according to the latest investigations, to be dependent on an increase in the size of the individual mus- cle-fibres. According to Gutch, the increase in breadth of the fibres is insufficient to account for the total increase in- weight of the organ. He thinks, therefore, that the discrepancy can be ex- plained by taking into consideration the increase in interstitial fibrous tissue that is almost always present in hypertrophied hearts, and also by the supposition that there is, with the increase in width of the fibre, a corresponding increase in length. These two factors he considers sufficient to account for the increase with- out supposing any numerical increase in the fibres, and indeed evidence of the latter is wanting. The question can, however, hardly be considered settled as yet. The hypertrophied muscle is firm, cuts with increased resist- ance, and is usually of a deep-red colour. Increase of muscular tissue without any corresponding increase in the blood-supply causes retrograde changes to be common in hypertrophied hearts, and in consequence yellowish streaks of fatty degeneration, or gray or whitish areas of local fibrosis, are not uncommon. This is seen especially in the hypertrophy accompanying arteriosclero- sis and renal disease, in which affections the blood-supply to the myocardium may be reduced by reason of narrowing of the coro- nary vessels. The normal heart weighs about 300 grammes (10 ounces) in the male and 250 grammes (8.5 ounces) in the female. These 565 h HYPERTROPHY OP THE HEART 567 figures are for individuals of the average size, but of course the heart weight varies with that of the whole body. In hypertrophy the weight may be doubled or even tripled. Stokes is said to have reported a heart weighing 60 ounces, but one weighing more than 000 grammes (20 ounces) is a very large organ. According to Eichhorst, a generally enlarged heart may attain such dimen- sions as to extend from the right mamillary to the left midaxil- lary line. When the left ventricle is chiefly involved the organ is conical and its apex blunt and broad (Fig. lO-i). When the right chamber is also enlarged it assumes a more quadrangular form, and the apex is formed wholly by the right ventricle (Plate III). The papillary muscles and columnge earner share in the gen- eral hypertrophy, the latter especially in the right chamber (Osier). Hypertrophy may be circumscribed, however, and then the trabecular, papillary muscles, either conus, or one of the au- ricular appendices, may be the seat of the change. Such local hypertrophy is not common and probably is due to trophic changes rather than to any circulatory disturbances. Post-mortem rigidity of the heart-muscle may simulate hyper- trophy by causing the heart-wall to be thicker than normal, and hence increase in weight is the only trustworthy sign. Concentric hypertrophy, or thickening of the wall of a cham- ber without increase in its capacity, is but rarely met with (Fig. 10). It is usually the result of stenosis. Hypertrophy combined with more or less dilatation of the chamber — i. e., eccentric hyper- trophy — is by far the more usual condition. When such a heart comes to autopsy, the dilatation has, as a rule, broken down the hypertrophy and is the predominating feature. For the purposes of comparison, I give the following figures, quoted by Eichhorst, from Thoma's tables : Weight of Heart Until the end of the first year 37 grammes. Second to fifth year 50 to 70 Sixth to tenth year 70 to 115 Eleventh to fifteenth year 130 to 205 Sixteenth to twentieth year 218 to 254 Twenty-first to thirtieth year 260 to 294 Thirty-first to fiftieth year 297 to 308 Fiftieth to sixty-fifth year 308 to 332 Sixty-fifth to eighty-fifth year 832 to 303 568 DISEASES OF THE HEART Eichliorst also furnishes the foHowing table from Bizot In males. Length of tlic heart .... Widtli of tlie heart Thickness of tlie heart Thickness of the left ventricle at the base Thickness of the left ventricle at the middle Thickness of the right ventricle at the base Thickness of the right ventricle at the middle Thickness of the right ventricle at the apex Thickness of the sa^ptum ventriculorum at the middle.. Millimetres. 85 to 90 93 to 105 30 to 35 10.1 11.6 4.5 3.1 2.5 11.0 In females. Millimetres. 80 to 85 85 to 92 30 to 35 9.8 10.8 3.7 2.8 2.1 9.0 Etiology. — Hypertrophy of the heart is rarely met with clinically except as secondary to some other condition. Thus we have seen that it is a part of the process styled chronic myocar- ditis, and is present also in valvular disease and adherent peri- cardium. It is often, though not necessarily, associated with arteriosclerosis. These affections may all he ranked among its etiological factors, but, as it is not of hypertrophy thus occasioned that I intend now to speak, they may be dismissed with this bare mention. liypertroi)liy of the whole heart, but chiefly of the left ventri- cle, is an almost invariable sequel to chronic disease of the kidneys, especially of interstitial nephritis, although also of the chronic parenchymatous variety and, according to Fraentzel, of long- standing pyelonephritis. There is persistently high pulse-tension in these cases, but there is probably some additional influence at work in the production of the hypertrophy — to-xtrmia, it may be, or atheroma. Cardiac hypertroi)hy of this origin becomes a clini- cal entity only as it is incidentally discovered in connection with the nephritis or after indications of myocardial inadequacy have declared themselves. A much less frecpiont but by no ineaus unimportant cause of ]iy])(ifi-(iphy of th(^ left ventricle is congenital smallness of the aorta or of the entire arterial system. There is usually some otlier abnormality, as persistence of Botalli's duct, whenever the narrowing is limited to the isthmus of the aorta or is extreme; but ill minor degrees of narrowing an increase in the thickness of the heart-wall is the only result. This condition is not unimportant, for, according to German authors, it leads to cardiac incompe- HYPERTROPflY OF THE HEART 569 tence and dilatation in young soldiers who arc subjected to the strain of long, toilsome marches. In chronic Bright's disease and congenital smallness of the aorta, hypertrophy develops in consequence of abnormal periph- eral resistance, which forces the heart-muscle to perform extra work. It therefore becomes increased in size (see Morbid Anat- omy), the same as does a skeletal muscle under like conditions. Yet the muscular fibres could not grow in thickness and length if they did not receive sufficient nourishment, and hence aug- mented nutritive supply is indispensable. It is this consideration which leads German writers to regard the consumption of inordi- nate quantities of beer as an undoubted cause of the enormous hearts seen among excessive beer-drinkers of Bavaria. The intake of large amounts of fluid alone would not be capable of producing cardiac hypertrophy, no matter how greatly they increase periph- eral resistance, but containing no inconsiderable proportion of nutritive elements, as it does, the excessive consumption of beer furnishes all the requisites for the causation of hypertrophy. It is believed that contestants for athletic honours, particu- larly oarsmen and professional bicyclists, develop this form of heart-disease, and doubtless some of them do. The hypertrophy is thought to result from the heart having to overcome abnormal pe- ripheral resistance created by severe muscular effort. This is not the correct explanation, since the initial rise of blood-pressure oc- casioned by muscular contraction is later on followed by a fall as the intermuscular arterioles become dilated. Therefore some other factor is responsible for the hypertrophy. This may lie in some unrecognised abnormality of the vascular system, but in the case of professional wheelmen and rowers is probably due to the constrained position they take during their exertions. As seen in the next chapter, the heart-strain of athletic contests is much more likely to result in dilatation. In the case of soldiers, mountaineers, peddlers, labourers, or others who carry heavy packs stra2")ped on their shoulders, the in- jurious effect on the heart is to be attributed to the combined influ- ence of respiratory embarrassment and arduous physical exertion, even granting that there are no such influences at work as abuse of alcohol, atheroma, etc. Rapid and violent action of the heart of a psychical origin is 570 DISEASES OF THE HEART also thought to produce hypertroj^hy, but it is likely that tachy- cardia and palpitation alone are incapable of such a result. The hypertrophy and dilatation of the heart observed in exophthalmic goitre is to be attributed not to tachycardia but to the underlying condition, whatever that may be. Hypertrophy of the right ventricle is a sequel of various tho- racic disorders — i. e., pulmonary emphysema, cirrhosis of the lungs, pleuropericardial adhesions and chest deformity, as kyphoscoliosis. In these conditions there is excessive peripheral resistance in the lesser circulation from compression or even oblit- eration of pulmonary capillaries. In time, as the nutrition of the heart suffers, its undue strain leads to dilatation and even to de- generation. A so-called physiological hypertrophy of the left ventricle is said, especially by the French, to take place during pregnancy. There probably does develop an increased weight of the heart, a true hypertrophy of the muscle-fibres, but it is never so consider- able as to become of clinical importance. To sum up : As remarked by Krehl, the development of hyper- trophy has to do essentially with the propulsion of an increased volume of blood, with the overcoming of abnormal resistance, or with a union of both these factors, and. each one of them may depend upon a variety of causes. Symptoms. — Hypertrophy of the heart is to be regarded as a wise provision on the part of Nature by which the organ is enabled not alone to perform increased work but to accommodate itself to those conditions which render increased work necessary. The normal heart can perform increased labour by putting forth extra exertion, but its ability in this direction is limited. If, therefore, the heart did not respond to demands for extra effort by the development of hypertrophy, its accommodative power to diseased conditions would soon reach its limit. Consequently car- diac hypertrophy may be regarded as a conservative process. These considerations make it a])parent that there are no symp- toms directly referable to hyj)ertr()])liy of the heart as such. If tachycardia, attacks of palpitation, and irregular or intermittent action of the organ disturb the patient, they are not due to the increase in its size but to disturbing conditions without, or are to be regarded as an indication of beginning inadequacy. In other HYPERTROPHY OP THE HEART 571 words, tlu; extra labour required of the lieart is beginning to tell on it, and if the undue strain is continuef 5,280 feet. As this patient was moderately corpulent, weighing 192 pounds, his heart was probably not sound at the time of his exertion, and yet it had been adequate to all demands made on it previously. We sometimes observe dilatation of the heart when we have no reason to assume that the organ is the seat of wide-spread structural disease and there may be no extensive post-mortem al- terations that can be recognised. The heart-walls are soft and flabby, and that is all that can be said of them. In such a case the individual may have been ana-mic, or his heart-muscle as well as his skeletal muscles has been weakened by ycArs of close applica- tion to business or intellectual pursuits. Without any preparation such an individual takes to bicycling and at once indulges in long tours at a scorching pace up hill and down, over I'ough sandy roads and against heavy winds. Under the absurd impression that such exercise is good for his weak muscles, he heeds not his panting respirations and rapid heart-beats. But outraged Nature avenges the insult by permitting the gradual if not sudden development of cardiac dilatation. I once had under treatment for a time a clergyman of mid- dle age who had left-ventricle' dilatation with relative mitral incompetence as the result of a single injudicious effort of this kind. As he expressed it, " he had pumped up " the steepest road on the banks of the Hudson River a thousand feet up the face of the Palisades — a road so steep that very few were ever able to make the ascent on their wheels. Although not aware of injury at the time, ho not long thereafter began to suffer from alarming fainting spells, the first of which seized him while delivering a sermon. Fortunately for him his heart-muscle was sound and ultimately recovered its tone. It is rather singular that I have been called on to treat for car- diac incompetence due to dilatation from strain throe men whose occupations required them to inspect buildings in the process of construction. Failing to discover any sntisfactory cause for their dilatation, I was led to inquire minutely concerning possible heart- strain, and found they were in the habit of climbing ladders or ascending many fliglits of stairs in order to reach tlie different parts of tlieir l)uil(lings. It lias sccnicd to me very reasonable to DILATATION OF THE HEART 579 assume the likelihood of heart-strain by such exertion, and in the case of one of these men intermittence persisted in spite of treat- ment until he exchanged his work as building inspector for a sedentary occupation in an ofSce. In not a few instances the resistance of the myocardium is diminished by the inordinate use of tobacco or by sexual excesses, late hours and social dissipation, dancing, etc. In one case the young man breaks down in his nervous system, a second develops a cough, while still another manifests signs of cardiac dilatation that may have been suddenly or gradually induced. In most of such cases complete restoration of heart-power follows removal of the cause and appropriate treatment. In some the heart remains permanently impaired, and in others every fresh excess is followed by renewed dilatation until at length irreparable cardiac stretch- ing and insufficiency remain. Such examples are not confined to the male sex. Anajmia and chlorosis predispose to this form of heart-disease, and more than one society belle pays for the season's round of dancing and other gaiety by slowly or acutely induced incompe- tence of the dilated heart. Many a jaded matron who declares she is " worn out " by the demands of society is really suffering from serious though perhaps not extensive stretching of the heart-cham- bers. Her heart-muscle has grown flabby and is not always capa- ble of entire restoration. Fortunately the heart-muscle is susceptible of development the same as are the voluntary muscles. Were it not so, the athlete would be incapable of competing for the laurel wreath of victory. If, however, he is overtrained or if his training prove inadequate, the heart may be the part that suffers. Under such circumstances acute dilatation may result from a single contest. It usually affects the right ventricle, and stretching of the right auriculo-ven- tricular ring permits the " safety-valve action of the tricuspid " to come into play. (See the chapter on Tricuspid Regurgitation.) It is possible, however, for the left ventricle also to become acutely overdistended, as was shown by cases reported by Harold Wil- liams. If muscular incompetence of these valves is set up, then the strain is lifted somewhat from the walls of the left ventricle and shared by those of the left auricle and pulmonary veins. This is 580 DISEASES OF THE HEART likewise a compensatory provision on the part of iSTatiirc, for with- out it there would be positive danger of diastolic arrest of the overtaxed left ventricle. In carefully trained athletes, or in the young with a robust myocardium, such a degree of cardiac strain is usually recovered from s])eedily and permanently. If the walls are not perfectly sound, or if there is sustained high blood-pres- sure in the aortic system because of vascular or renal disease, or if the heart is too frequently subjected to overstrain, permanent dilatation may result with all its consequences. Finally I desire here to dwell on the harm in this regard that is likely to accrue to young children from the immoderate use of the bicycle and from games that necessitate long, hard running. There is actual, not fancied, danger of cardiac dilatation. If their hearts are sound no permanent injury may ensue, unless, of course, the strain be too oft repeated. In many cases the children have suffered from undetected rheumatism and latent pericarditis or endocarditis, and in such, unrestrained indulgence will surely result disastrously through the dcvcloinnent of dilatation of the heart with possible coincident inflammation of some of its struc- tures. The heart of a growing boy endures a degree of strain disas- trous in a man of forty, and yet if overstrain be too frequently repeated during one of the " fatigue periods " of childhood, it may, I am convinced, ultimately enfeeble the heart's resistance even in a boy. The overdistention of the heart is due probably to ineffectual systoles, which allow a residue of blood to remain in the distended cavities, while with the continuance of muscular effort and deepened respirations blood is passed on to the heart more rajudly and in larger amounts than can be expelled. Another factor that should not be ignored in considering the question of cardiac strain are those unknown " fatigue products " developed during severe exercise and to which particular attention has boon called by Clifford Allbutt. Symptoms. — The symptoms of cardiac dilatation develop slowly or rapidly according to the development of the dilatation. The stretching and often thinning <»f the heart-walls impair their contractility, and there is a tendency to stasis within the organ which leads to loss of equilibrium between the arterial and venous streams. As the heart-power begins to fail the pulse grows more DILATATION OF THE HEART 581 rapid, often irregular in force and volume, and in many cases in- termittent. Cardiac impulse becomes weaker, its area of dulness increased, and its sounds feeble. The patient begins to notice more or less breatlilessness on exertion and a feeling of unwonted lassitude that may amount to actual weakness. Ilis colour changes from the reddish hue of health to the bluish gray tint of increasing capillary stasis. As cardiac inadequacy advances, symptoms of visceral congestion ap- pear. The urine lessens in amount and becomes of high specific gravity, often containing a trace of albumin. The liver increases in size, which may cause a feeling of fulness in the right hypo- chondrium or of dull pain in the back below the shoulder. Its inferior margin becomes more or less distinctly palpable, being smooth, firm, and rounded, and palpation of the organ may be somewhat painful. Congestion within the gastro-intestinal veins is shown by im- pairment of appetite and more or less flatulent indigestion, so that the patient feels bloated after meals and complains of windy con- stipated bowel movement. Piles may develop, sexual power be- come deficient, and women are apt to suffer from leucorrh(pa and derangement of menstrual function. Congestion within the lower extremities leads at first to puffiness of the ankles, which by night feel tense and uncomfortable. When the shoes are removed the skin is found creased, and a ridge indicates where the upper edge of the shoe pressed. After a night's rest this swelling of the feet and ankles may have subsided, but as cardiac incompetence pro- gresses, oedema remains permanent. Pitting on pressure is now pronounced and found to gradually extend upward. Thus gradually but steadily grow the symptoms of failing cir- culation, and at length, if the condition is not arrested by treat- ment, the patient is compelled to keep his room. Pulmonary con- gestion is no longer shown merely by dyspnoea on effort, but by cough with frothy, perhaps bloody expectoration, and by orthop- noea. . Talking causes breatlilessness and so much fatigue that the patient dreads or even shuns the effort. Examination of the lungs discloses more or less dulness at the bases behind with fine crack- ling rales — in short, the signs of hypostatic congestion. The apex-beat is now imperceptible or is but a feeble tap much outside the left nipple. Absolute and relative cardiac dul- 582 DISEASES OF THE HEART iiess are greatly increased, of a quadrangular outline, and in ex- treme cases may extend from close to the right nipple on the one hand nearly to the anterior axillary line on tlic other. The heart-sounds are almost inaudihle and there is very apt to be a systolic murmur denoting relative mitral or tricuspid in- sufficiency or both. The leak through the tricuspid valves is shown by the positive venous pulse in the external jugulars and liver. The veins of the neck stand out like blue cords, and if pul- sation in them is not apparent at all times, becomes plainly visible so soon as the patient coughs or makes a forcible expiratory effort. The pulse is now rapid, feeble, and often arrhythmic. The state of things has now become pitiable, and if not re- lieved grows steadily worse, with the development of general dropsy, transudation into the serous cavities, somnolence, even low muttering delirium and death. This last may occupy hours, appearing to come from gradual exhaustion, or it may be ushered in by pulmonary oedema. In such a case fine crackling rales de- velop, spread throughout the lungs, and at last become plainly heard at a distance with every laboured ros]>iration. In other in- stances pulmonary infarction occurs, as shown by cough and the expectoration of bright-red blood. In some the heart stops ab- ruptly and unexpectedly, while the patient is at rest or making some slight exertion, although this sudden cessation of the heart's action has been preceded for several days by signs of such increas- ing weakness that its final arrest is scarcely a matter for surprise. In some cases symptoms of cardiac dilatation, even extreme, persist for many months or even two or three years. I recall a man of fifty odd whom I treated in 1893 and who was a striking example of this chronicity. For more than a year he had been incapacitated for attention to business and yet had managed to keep about in spite of very apparent shortness of breath, a rapid, exceedingly arrhythmic pulse, enormously increased cardiac dul- ness, and feeble heart-sounds. The liver could be felt thin-bor- dered and hard, and this patient eventually died apparently from the pressure-eifects of ascites rather than from independent asys- tolism. This man's heart was undoubtedly degenerated and very thin-walled. It might be reckoned as an example of cardiac in- a(l('(|uacy from chronic myocarditis, but it was a typical picture of chrcjiiic dilatation of the heart. DILATATION OF THE HEART 583 I have recently treated with liiglily gratifying results, by means of batlis and resistance exercises, ii powerfully built man of thirty-eight who was suffering from the effects of heart-strain four years before. When in apparently perfect health he endured a day of terrible fatigue from the exertion of journeying in a severe snow-storm at the altitude of 18,000 feet. By night he was completely exhausted, looked blue, felt cold, had a feeling of great prtrcordial oppression, and could not get his breath. After a few days' rest he felt better and returned to the East. He remained at business, but when summer came on, Avent abroad for a rest, and in London consulted a well-known medical authority. By him he was told he had suffered a heart-strain and was advised to give up business. He did not do so, however, with the result that he gradually developed symptoms of chronic heart-disease. For some months before I saw him he suffered from dyspnoea of effort, a feeling by night of profound exhaustion, and the convic- tion that he was liable to die suddenly at any time. He neverthe- less remained at business. When I first saw^ him he presented the signs of mitral regurgi- tation with secondary enlargement of the heart, chiefly of the left ventricle. Lungs were negative, but the liver was palpable. There was no pitting, but the tissues everywhere felt tense and hard, and the patient said he " felt swollen." Preliminary treat- ment by rest in bed, cathartics, and a milk diet for two days re- duced capillary stasis, improved the quality of the pulse, and re- moved the patient's sense of air-hunger. There was 2 per cent of albumin in the urine, but although repeated search was made for casts, they were never found. At the end of less than four months this patient declared he felt perfectly well and desired to return to business. The heart w^as manifestly smaller and its action greatly improved, but the mitral systolic murmur still remained. It was less loud and less harsh, however, and the first sound, originally inaudible, could be heard distinctly. The liver could not be felt, but albuminuria persisted. This man had never had articular rheumatism or any disease to lead to endocarditis, and prior to his arduous mountain climbing had never had even the slightest symptoms of heart weakness. I have no doubt that his heart-muscle has suffered in its integrity, but I look upon this as an instance of chronic left- 584 DISEASES OF THE HEART ventricle dilatation due primarily to strain and leading to relative mitral incompetence. Acute dilatation of tlie heart from strain most commonly affects the right ventricle, but it may also take place in the left. This was shown in the cases of the young men who were examined by Harold Williams immediately before and after a run of twenty- five miles. Cardiac dilatation was shown by exhaustion, cyanosis, a rapid thready pulse, manifest increase in heart's dulness both to right and left, and by a systolic murmur having the characters of a mitral bruit. The safety-valve action of tricuspid regurgita- tion may be rather quickly induced as compared to the time it would take to set up such a left-ventricle dilatation as would pro- duce relative mitral incompetence. In a run of twenty-five miles requiring three or four hours, time would be given for the safety- valve action of mitral insufficiency to occur. Were this not so, the left ventricle would be subjected to a degree of strain that might prove dangerous and even fatal. The symptoms of acute heart-strain are those of deficient arte- rial circulation (relative arterial auu'mia), a rapid, weak, and it may be irregular or intermittent pulse with signs of an overloaded venous and pulmonary system, dyspnoea, exhaustion, pra^cordial discomfort, perhaps pain, and cyanosis, congestion of the liver, and positive venous pulse of tricuspid regurgitation. Within the last year I have seen two instances of acutely in- duced dilatation of the right ventricle in powerfully built young men belonging to college foot-ball teams. One of them walked off the field after the contest was over, but he looked blue in the face, complained of dull pain behind the lower end of the sternum, and the physician having charge of the team detected increase of abso- lute dulness to the right. Symptoms did not disappear for a num- ber of days, and it was months before the heart's action regained its wonted steadiness. When the heart-muscle is healthy, acute dilatation from over- strain may be recovered from, yet if too frequently repeated may without doubt result in permanent cardiac incompetence. I be- lieve this is a very positive danger attending college athletics, par- ticularly in foot-ball and rowing matches. When the heart-muscle is not healthy, and therefore when per- sons have passed their forty-fifth year and have arrived at a time DILATATIOfN OF THE HEART 585 of life in which the state of the myocardiinn is questionable, acute cardiac dilatation from overstrain becomes a very serious matter. The first symptoms of heart-strain may be recovered from, but more or less inadequacy is likely to remain. In time, as a result of renewed but less severe strain, evidence of weakness sets in and the patient ultimately presents a clinical picture of gradually increasing dilatation of the heart. Physical Signs. — Inspection. — The multiplicity of condi- tions which affect the results of inspection renders this means of investigation of comparatively small value. The eye may per- ceive the well-known manifestations of cardiac weakness, but it cannot furnish information as to the actual state of the heart. There is usually an absence of visible cardiac impulse, but this alone is of no value, since it is normal to many individuals to have no visible apex-beat on account of the volume of the lungs or the thickness of the chest-wall. In emphysema, which so com- monly leads to ultimate dilatation of the right heart, visible im- pulse is also likely to be wanting. In all cases in which the apex- beat is not plainly visible the patient should be placed in a strong light and inspection made across the front of the chest from the side or from above downward. If dilatation exists a feeble aj)ex- shock may thus be sometimes perceived outside of and below the nipple or in the epigastric notch. Palpation. — Aside from the knowledge which this affords con- cerning the pulse and hepatic congestion, palpation is of service in the estimation of the feebleness or strength of cardiac contractions. Thin-walled and dilated hearts may give no perceptible shock to the chest-wall, or they may occasionally produce a sudden quick tap whenever the organ gathers itself, as it were, for an extra effort. When the apex-beat persists, it is not like the broad heav- ing impulse of hypertrophy, but is a circumscribed feeble stroke of a slapping character. This is particularly the case in long- standing dilatation with still some degree of efficiency. Percussion. — This is, as a rule, our most valuable means of determining if dilatation of the heart is present, but it may afford very unreliable evidence in cases of pulmonary emphysema. If the state of the lungs and of the thoracic parietes renders percus- sion available and if dilatation exists, the area of deep-seated if not of superficial dulness is found increased in accordance with the 586 DISEASES OF THE HEART degree of dilatation and the chambers affected. In dilatation of the left ventricle relative dulness is increased towards the left and upward, while in stretching of the right heart it is augmented to the right and downward. When general dilatation of the heart exists the area of dulness is found to have assumed a quadrangular outline with broadly rounded corners and sides. Auscultation. — The licf|rt-sounds are feeble, altered in intensity and rhythm, and are frequently accompanied or obscured by nuir- murs of relative or muscular mitral or tricuspid incompetence. The systolic tone becomes shortened and valvular like the second, and with lessening of the long pause the rhythm of the sounds tends to assume that of the ticking of a small clock or watch. In cases of gi'eat weakness and rapidity of heart-action the tones follow each other in quick succession, or but a single sound may be detected. The aortic second tone is usually diminished, while the pulmonic second is accentuated. If murmurs exist, they are, as already stated, those of relative or muscular incompetence of one or both auriculo- ventricular valves depending on the degree of dilatiition. The auscultator should not forget, however, that it is possible for bruits of pre-existing valvular disease to be present, and therefore he must not hastily conclude that the murmur is necessarily due to dilatation alone. In many cases he must await the result of treat- ment before deciding definitely on its real nature. Diagnosis. — The recognition of cardiac dilatation is ordi- narily nut difficult, especially if it has been acutely induced or has progressed to the production of considerable inadequacy. Minor degrees of stretching are not always easy of detection and require minute inquiiy into the history and symptoms, as well as pains- taking physical examination. In slowly induced dilatation there is history of gradual onset and progressive increase of symptoms of cardiac incompetence, while tliere are clinical findings of (1) a more or less rapid and feeble, it may be irregular or intermittent, pulse; (2) feeble, tapping, or even imperceptible cardiac impulse; (3) increase of relative and perhaps superficial dulness in one or nion; directions according to the cliandx'r affected; (4) feeble tick- ing sounds and perhaps systolic munnui's of relative or muscular mitral or tricuspid insufficiency. In acute overstrain the phenomena of cardiac embarrassment follow some unusual exertion and are easily recognised, while the DILATATION OF THE HEART 587 patient is apt to display more or less cyanosis and other evidence of impending stasis. Differential Diagnosis. — Acute dilatation of the heart can scarcely be mistaken or confounded with any other condition pro- vided due attention is paid to history and objective symptoms. Distention of the cardiac cavities that has developed more slowly and has grown extreme may, however, be mistaken for pericar- dial effusion. The differential points are fully dealt with in that chapter, but special emphasis may here be laid on the necessity of determining the relation of the outer and inferior margin of deep-seated dulness to the position of the apex-beat. In car- diac dilatation dulness does not pass beyond the limits of car- diac impulse, whereas in pericardial distention the apex-im- pulse is situated within the outer border of dulness. This, and this alone, is the trustworthy criterion of difference between the two affections. In other respects there is often a striking similarity. Dilatation and hypertrophy can scarcely be confounded if due attention is paid to the characters of the pulse, to the nature of the impulse, and to the greater feebleness and rapidity of the sounds in dilatation. A simply dilated and yet not specially de- generated heart cannot often be distinguished from a degenerated and hence secondarily dilated organ, and it is not always prudent to attempt such distinction. Prognosis. — Dilatation of the heart should never be regarded as a trivial matter, and yet the degree of its gravity depends upon the state of the heart-muscle, the extent of the dilatation, and the length of time it has existed. It is the integrity of the myocar- dium in the young and in trained athletes which in them makes the heart recover so quickly and well from the overdistention caused by strain. On the other hand, it is the likelihood of the heart-walls being not quite sound which renders prognosis serious when dilatation supplants hypertrophy or when elderly individ- uals suffer heart-strain. Stiffened arteries do not necessarily mean that the heart-walls are seriously degenerated, and experi- ence abundantly proves that in some cases proper treatment may restore a dilated heart even when the vascular coats are thickened. ISTevertheless, under such conditions stretching of the cardiac chambers is always a grave affair, and only too often there is but 588 DISEASES OF THE HEART little prospect of the heart-walls again becoming as sound as before the injury. Cardiac dilatation associated with a granular kidney may al- ways be said to furnish a very grave prognosis, for the resistance in the arterial system is so great that in all likelihood the heart has been gradually yielding, and having once given way, cannot re- gain its lost adequacy. In such a case the prognosis depends both upon the state of the heart-muscle and the possibility of lessening the high pulse-tension by treatment. In the face of both arteriosclerosis and interstitial nephritis a seriously dilated heart is likely never again to recover its former compensatory hypertrophy^ It is so evident a fact as to scarcely require statement that the more extensive the dilatation the more serious the prognosis. With care and proper management minor degrees of the condition may endure for a long time — even years — yet in such a case the tenure of life is always uncertain, for the reason that some addi- tional and unexpected strain may at any time convert a not alto- gether unfavourable into a most serious prognosis. Stretching of the auricles or of the right ventricle is not so grave a matter as is left-ventricle dilatation. Owing to the thin- ness of their walls they may not be so amenable to treatment — that is, not so likely to have their hypertrophy restored ; but on the other hand, the right ventricle is more likely to be relieved by stretching of its auriculo-ventricular ring, and therefore is less liable to paralytic overdistention and diastolic arrest. This con- sideration leads me to the belief that in cases of left-ventricle dila- tation the development of a systolic murmur at the apex is a favourable rather than an unfavourable prognostic indication. Such a murmur is usually held to indicate relative mitral insuffi- ciency, and by the giving way of the mitral valve a part of the excessive endocardial blood-pressure becomes transferred to the auricle and pulmonary veins, and thus the wall of tlie left ventri- cle is relieved, in a measure at least. I can recall more than one instance of sudden and unexpected death in men whose hearts were seriously dilated and in whom such a systolic apex-murmur did not exist. On the otlicr IuiihI, T liavc iiioi-c tlian once observed that when the mitral valve gave way tlio progress to asystolism was gradual, and death was usually preceded by the symptoms and DILATATION OF THE HEART 589 signs of venous stasis, extending through a period of weeks or months. « It is also evident that prognosis is largely governed by the length of time the dilatation has existed. If the myocardium is still healthy, as in the young, a chronic dilatation may yet be recovered from. In persons past middle age the condition is likely to resist treatment if it has become chronic, and if in such the pulse is persistently arrhythmic, it is to be looked upon as an in- dication that the heart-muscle is not sound or that the auricles are greatly dilated. According to Radizewsky, habitual irregularity of the pulse points to preponderating degeneration of the walls of one or both auricles. If this be correct, then arrhythmia in con- nection with chronic dilatation of the heart is a better prognostic sign as regards length of life than is tachycardia with perfect regularity of rhythm due to a dilated ventricle. In acute dilatation from overstrain, as in foot-ball or mountain climbing, the progno- sis is as a rule good, for with rest and proper treatment the heart is likely to return to its former healthy condition. Repetitions of its abuse may, however, eventually induce j^ermanent inadequacy. Another element that enters into the question of prognosis is the degree of subjective symptoms produced by the dilatation. If dyspnoea be less than one would be led to expect from the appar- ent gravity of the condition, the case is likely to pursue a chronic course ; if, on the other hand, the shortness of breath be out of proportion to the apparent size of the organ, or to the amount of exertion performed by the patient, or if the dyspnoea assumes the form of cardiac asthma, then the prognosis is bad, unless the urgency of this symptom can be accounted for by an associated emphysema or bronchitis. If skilful treatment succeeds in producing only temporary im- provement, and the heart drops back to its former state so soon as treatment is discontinued, or less vigorous, it is an indication that the heart-muscle is either too weak to be regenerated, or the peripheral resistance is too great to be permanently overcome. A steady though gradual loss of ground, in spite of treatment, proves that very little is to be expected from any management, no matter how skilful. Except ill cardiac strain of effort in the young, one should never venture to prognosticate the length of time it will take for 590 DISEASES OF THE HEART the heart to be restored to health, or in those in which this is mani- festly impossible, to predict how long the disease is likely to last. If the left heart is the one chiefly affected, the end may come sud- denly and unexpectedly, but in those cases in which the right heart is the one chiefly at fault, and particularly when the right auricle is much dilated, pulmonary infarcts are very likely to occur and to be the immediately determining cause of death. Two states of mind on the part of the patient, if they come on after the disease has existed for some time, and serious symptoms of stasis are present, always make me apprehensive of the near approach of the end. These are, great restlessness and an ill- defined nervousness that keep the patient constantly moving about, and on the other hand a sudden lull in the patient's sense of distress. After days or perhaps weeks of severe suffering he suddenly has a day in which he feels remarkably well and free from distress. This is often like the calm that precedes the storm. I have more than once seen death speedily succeed such a day of apparent well-being. Apropos of the former state I recall a large middle-aged num presenting all the symptoms and signs of ex- treme cardiac dilatation whom I examined in consultation with Dr. Harrison late one afternoon and in whom I saw no evidence that the end was imminent; he had been in that condition for a week, and, although very dyspnceic, walked into an adjoining room. He displayed, however, an indescribable restlessness, and less tliaii tlirec hours after we left him he died suddenly. Treatment. — In dilatation of the heart suddenly induced through strain the first indication is to place the patient at rest in the recumbent or semi-recumbent position for the purpose of lessening the heart's work so far as that is possible. Muscular in- action and a more tranquil respiration bring the venous blood to the right heart less rapidly, and if the circulatory apparatus is healthy, as in the youthful athlete, iSTaturc alone, under favourable conditions, will speedily effect a restoration of the blood-stream to its former equilibrium. If, on the contrary, the patient's age or state of general nutri- tion justifies the inference that the heart cannot return to normal without further aid, tlicii a morcui-ial ])ill and digitalis should be prescribed. 15y uiiloadiui: I lie portal system the cathartic tends to restore balance within the abdominal vessels and secondarily DILATATION OP THE HEART 591 in the system at large. Five grains of bine mass followed by ^^ onnce of Epsom salts eight honrs thereafter, or a grain or two of calomel at bedtime and a glassful of the solution of citrate of magnesia next morning, or any one of the numerous aperient waters in the market, will prove highly efficient to that end. The purjiose of the digitalis is to slow down the heart and en- able it to empty its distended cavities effectively. This may be accomplished by the administration of 10 to 15 minims of the tincture every six hours for four or five days. Improvement will be shown by a reduction in the rate and corresponding gain in the force and strength of the pulse, by disappearance of cyanosis and other signs of venous congestion, by increased diuresis, and a gradual return to normal in the size and sounds of the heart. Strychnine and nitroglycerin will probably not be required. It is well, however, to insist on light yet nutritious diet until the normal state of the circulation has been regained. When permanent cardiac insufficiency is threatened from re- peated heart-strain or from the gradual giving way of hypertrophy in the face of relatively too great peripheral resistance, the prin- ciples of treatnient must be the same as in any other form of heart-weakness. The first indication is to relieve the overtaxed heart. Therefore the patient must be put at physical rest for a length of time which is to be determined by results. 'To the pa- tient's query, " How long must I stay in bed ? " do not permit yourself to make a definite answer, but tell him that is to be de- termined by the rapidity and degree of improvement. In other respects the same general plan of action previously detailed for cases of lost compensation is to be followed, but varied to meet the peculiarities of each case. Most cases of cardiac dilatation which the physician is called on to treat are not instances of acute strain, but of chronic cardiac insufficiency. They are to be managed, therefore, in accordance with the principles laid down for the treatment of inadequacy from chronic myocarditis, and the reader is referred to that chap- ter for details. There are three measures, however, of which it may be well to speak with special relation to cardiac dilatation : (1) Bloodletting. — Occasionally a patient is encountered who from one cause or another is suffering from great overdistention of 592 DISEASES OF THE HEART the right heart. The action is extremely feeble and disordered, the face is congested, the veins are turgid, dyspnoea is profound, the lungs are filled with rales of pulmonary redema, there is cough and bloody, frothy expectoration, there is no redema, but the ex- tremities are cold and cyanosed. Percussion shows enormous dilatation of the heart, and, so well as can be determined, the heart-tones are very weak and impure. Dissolution appears immi- nent. Under such circumstances the physician realizes that what- ever is to bring relief must be done quickly. There is not time for digitalis and cathartics to be tried ; they are too slow. In such an extremity there is nothing that usually affords such prompt relief as venesection. Twenty or more ounces of blood taken from the arm are generally followed by diminution of cyanosis, noticeable improvement in the quality of the pulse, and increased clearness and strength of the heart-sounds. Of course such improvement will be only temporary if nothing else is done. This treatment must be followed up, therefore, by the judicious use of digitalis, strychnine, and cathartics, to secure what is gained by the abstraction of blood, since this latter is of course only a temporary measure resorted to foi* the dire emer- gency. Many a patient's life has been saved by such treatment, but, unfortunately, it will not save all. (2) Nmiheim Baths. — By some authors who seem to make a fad of this mode of treatment these saline and effervescing baths are advised even in cases of extreme and long-standing dilatation. Judging from my experience, such treatment is a mistake in cases in which, from the arrhythmic pulse, enormous area of cardiac dulness, and feeble tumultuous heart-sounds, it is clear that the cardiac walls are too thin to ever regain their old-time power. Th(>- oretically these baths should unload the cardiac cavities and tlms assist the heart in its labours. As a matter of fact, I believe in these cases they do not accomplish this result. Such persons can- not be materially benefited by anything, yet if any remedy can help them it should be digitalis, strychnine, and cathartics judi- ciously administered for an indefinite time. (3) Resistance Exercises. — If given by an attendant who thoroughly understands how to apply the proper degree of resist- ance to a feeble heart, these exercises may ])rove of real benefit even to a seriously dilated heart. They ai-e supposed to relieve DILATATION OP THE HEART 593 the cardiac cavities by diverting a part of their contents to the peripheral vessels, and as a matter of fact they are followed by a demonstrable decrease in the area of cardiac dulness. Neverthe- less I do not believe it is possible to create so remarkable a decrease as is claimed by Theodor Schott, who finds in this effect a means of differential diagnosis between a dilated organ and a pericardial effnsion. When employed in the condition now considered they must be given with very great gentleness, and movements are to be omitted which necessitate the elevation of the arms above the head as well as bending of the trunk at the hips, which are capable of augmenting dyspnosa and aggravating the dilatation. Even when permanent improvement in the patient's condition does not result it is generally found that for a time at least there is a less- ening of his distress and an improvement in his colour. I therefore recommend their trial in all cases of chronic cardiac dilatation. Should cases of chronic cardiac incompetence be not improved by the measures just spoken of, then it is reasonable to infer that the case has passed beyond the stage in which anything more is to be hoped from treatment than the amelioration of symp- toms. One may yet do what he can with digitalis, strychnine, nitroglycerin, diffusible stimulants, and cathartics. In the ma- jority of cases morphine will now have to be given^ and if admin- istered hypodermically to secure comfortable nights, the remedy is generally of the greatest service. In many instances mor- phine thus given will jDrolong life and ease the sufferer's path to the grave. Only a few months ago Dr. George F. Roberts, of Minneapo- lis, called me to see a gentleman of nearly sixty who presented a typical picture of a dilated heart. The myocardium was probably degenerated, but his arteries were soft and urine was negative, so that one could not say there was more than cardiac incompetence from dilatation. He was in bed and dyspnoeic, but his suffering arose from vertigo, which came every few minutes and lasted from a few seconds to a minute or more. During the vertigo his radial pulse wholly disappeared and the heart-sounds became exceedingly rapid and feeble but perfectly regular ; the cavities were not being emptied. Suddenly the action of the heart would change, becom- ing slow, strong, but irregular ; the pulse would return and the 39 594 DISEASES OP THE HEART patient would exclaim, " There ! it is gone ! " meaning, of course, his dizziness. The cervical veins were distended, liver was palpable, urine scanty, but no oedema and no turgescence of the superficial veins over the trunk and limbs. Cardiac impulse was absent and the area of dulness enormously increased and of a quadrangular out- line. It seemed as if the large vessels of the abdominal and portal systems were holding the most of the blood. Venesection was indicated and might have afforded temporary relief, but for certain reasons it was not performed. Instead, nitroglycerin, camphor, and valerianate of caffeine were injected subcutaneously at short intervals and the bowels were opened by calomel and a saline. Vertigo was relieved by this means, but circulation was not materially improved. The heart-walls were too greatly stretched and probably degenerated to regain their ade- quacy, and the i)atient died about ten days subsequently. II. RELATIVE AND MUSCULAR MITRAL INSUFFICIENCY Relative. — By this term is meant that variety of incompetence which results from over-distention of the left ventricle and is en- countered in its most typical form in the acute heart-strain just described. When so produced the insufficiency is sometimes spoken of as primary, to distinguish it from the subdivision known as secondary. It is the latter, or secondary, that not infrequently develops in the late stage of aortic stenosis and regurgitation and has so often been referred to in the foregoing pages. Balfour's terui. Curable Mitral Regurgitation, was intended to cover cases of primary relative mitral incompetence, particularly as seen in chlorotic girls, since it is very amenable to treatment. The term was based on the supposition of such a stretching of the mitral ostium as precluded the adequate closure of the valve-flaps. In the light of more recent knowledge, however, it is likely that the insufficiency described by that distinguished author is in reality the form now to be considered. Muscular. — This term, which may be applied to incompetence whether of the mitral or tricuspid valve, denotes a form of in- sufficiency depending not on over-distention of the ventricle with corresponding dilatation of the ring, ])ut on a functional defect of the muscular mechanism by which iioniially the valve is enabled KELATIVE AND MUSCULAR MITRAL INSUFFICIENCY 595 to close. Tor our knowledge of the facts underlying this sub- division of mitral incompetence we are indebted to the Leipzig School, whose views it must be confessed have been very tardily accepted by English and American authors. Pathology.^ — The morbid anatomical condition underlying relative insufficiency of the auriculo-ventricular valves is dilatation of the ventricle. This dilatation must reach such an extreme grade, however, as to carry with it more or less stretching of the mitral ring, as shown by its admitting more than three fingers. The valve itself is structurally intact, or in cases of long standing the cusps may be longer and broader than normal and the papillary muscles be flattened and elongated as a result of the pressure to which they have been subjected. In brief, the organ presents the changes previously described under Dilatation of the Heart, either with or without structural disease at the aortic orifice. In muscular mitral insufficiency the left ventricle may or may not present evidence of dilatation, but if this condition existed dur- ing life it was not of so high a grade as is the case when relative incompetence oocurs. In many instances the pathologist is sur- prised by finding nothing at first sight to explain the murmur heard before death. The mitral ostium is not dilated and the valves are intact. Closer examination, however, discloses changes in the muscula- ture which interfered with the perfect coaptation of the valve-flaps. These are the changes of acute or chronic myocarditis, which favour the occurrence of more or less dilatation and defective action on the part of the ring muscle or papillaries, or both. Three factors are concerned in the closure of the auriculo- ventricular valves, (1) the pressure of the blood within the ventri- cle upon their ventricular surface, (2) the contraction of the ring muscle at the base of the ventricle by which the orifice is nar- rowed to a mere chink, and (3) the contraction of the papillary muscles and consequent tightening of the cordse tendineas. The combined effect of all these elements is the perfect apposition of the valve-flaps throughout practically their entire surface, and not merely at their margins. If now, in consequence of inflammation or degeneration, the wall of the ventricle dilates sufficiently to prevent the mitral ostium from becoming adequately contracted during systole, or to inter- 596 DISEASES OP THE HEART fere with the i^roper pull of the papillaries, then the condition is present which permits more or less regurgitation; the valve is rendered muscularlj incompetent. Consequently, in any case in which the clinical diagnosis of mitral insuthciency has been made and in which the valves are found intact after death, careful examination must be made of the state of the myocardium, since in degeneration of the wall or of the papillaries may be discovered the pathological cause of the regurgitation. Etiology. — Primary relative insufficiency of the mitral valve is the result of acute dilatation of the left ventricle from excessive physical exertion, i. e., acute strain. This was well shown by Har- old Williams's observations. He found that of 1-] healthy young men examined immediately after a run of 25 miles, 11 presented appreciable dilatation of the left ventricle with a mitral systolic murmur and vascular evidence of stasis. When the myocardium is degenerated and the arteries arc stiff, indiscreet physical effort is especially likely to occasion cardiac overstrain, and I have more than once discovered this form of valvular incompetence in elderly men after a business or hunting ti'i]) in the Ivocky Mountains. Secondary relative mitral insufficiency may be said to be the result of chronic heart-strain. It is jwssible, therefore, when the left ventricle has been compelled for a long time to labour against great peri])heral resistance, as in cases of acu'tic stenosis. It is seen not infrequently in chronic interstitial nephritis when the hyjjer- trophied ventricle is no longer able to cope with the excessive blood- pressure in the aortic system, or when the ventricle struggling to preserve its adequacy is overpowered by the addition of some un- Avonted ])liysical or mental strain. Tlie same holds true of the mi- tral incoiujK'tence secondary to hmg-standing aortic r(\gurgitation. The causes of muscular mitral itisuffirirnry are id(Mitical with those of the secondary relative foi-ni. Less dilatation of the left ventricle is required to produce it, however, hence it is a more frecpient occurrence. ]\roreover, degeneration of tlie ])apillaries is a condition wliicli often leads to museular incompetence, whereas it cannot pro(hu'ti()ii of this form of dyspncra. According to his explanation, the deficiency of oxy- gen and excess of carbonic acid in the blood, which result from the period of apnosa, stimulate the vaso-motor centre, and the CHEYNE-STOKES RESPIRATION 619 arterioles of the brain, as well as those throughout the body, become contracted. This constriction of the arterioles diminishes the supply of blood to the respiratory centre, and in consequence this centre is stimulated to discharge, and inspiration begins. So soon, however, as respiration has become energetic and the blood proj)erly aerated, stimulation of the vaso-motor centre ceases, arte- rial spasm is no longer maintained, the respiratory centre receives a proper supply of arterialized blood, and dyspnoea is no longer experienced. The respiratory acts gradually die away and the period of apnoea is again reached. There again occurs stimulation of the vaso-motor centre, and another cycle is repeated. Bram- well is of the opinion that if Filehne's theory is correct, then Cheyne-Stokes breathing should occur much more frequently than it really does. He says : " I am disposed, therefore, to think with Dr. Sansom that something more is necessary, and that there must be some alteration of the respiratory centre itself in addition to the condition which Filehne's theory supplies. A state of irri- table weakness would, in my opinion, account for this condition." BramiDelV s theory in explanation of Cheyne-Stokes breathing is based on the supposition that the respiratory centre consists of two parts : , an inspiratory and an expiratory, and that, as sug- gested by Rosenthal, " the inspiratory centre is the seat~ of two conflicting forces, one tending to generate inspiratory impulses, (the discharging portion of the inspiratory centre as we may call it), and the other offering resistance to the generation of these impulses (the restraining or inhibiting portion of the inspira- tory centre) — the one and the other alternately gaining the vic- tory, and thus leading to rhythmical discharge." Bramwell as- sumes that venous blood excites the discharging portion, restrains the inhibiting portion; while oxygenated blood depresses the for- mer portion, and intensifies the action of the restraining portion. If the discharging portion is in a condition of irritable weakness, and therefore more easily excited to discharge, but also more quickly and easily exhausted, or if both portions are in a condi- tion of irritable weakness, then there is a condition of things, Bramwell thinks, which satisfactorily explains the phenomena of Cheyne-Stokes breathing. At the end of apnoea the blood is highly venous, and therefore gradually excites a paroxysm of dyspnoea, by stimulating the discharging and restraining the inhibitory 620 DISEASES OF THE HEART portion of the centre. In the second place, the carbonic acid in the blood stinmlates to action the vaso-motor centre, the arterioles become contracted, and the supply of oxygen to the respiratory centre is still further diminished. Furthermore, the irritable weakness of the discharging centre causes its impulses to become excessive, and the state of dyspna^a results. Moreover, the weak- ness of the discharging portion of the inspiratory centre causes it to become quickly overexhausted and the dyspnoja subsides. In consequence of the energetic respiratory effort during the stage of dyspna?a the blood becomes arterialized and the discharging portion of the inspiratory centre is no longer stimulated, but the reverse takes place as regards the restraining portion, which gains the ascendency over the weakened and exhausted discharging por- tion, and the state of apno3a is produced. During this period of rest the oxygenated blood, which had stimulated the restraining and depressed the discharging portion of the inspiratory centre be- comes replaced by carbonic dioxide ; the discharging centre is aroused into action again, and the inhibiting is restrained ; inspir- atory efforts are renewed and another cycle is repeated. Of the foregoing theories, conceived to account for this distress- ing rhythmic form of dyspna'a, Bramwell's is the most satisfac- tory, and yet, as he himself suggests, it is difficult to explain how this condition of irritable weakness of the respiratory and vaso- motor centres is produced. Bramwell assumes that in those cases of Cheyne-Stokes breathing displaying a contracted pulse and pallid countenance, there is local anaemia of the centres in conse- quence of arterial spasm, and irritable weakness takes place. In other cases not showing arterial spasm he suggests that this unstable state of the centres may be due to disease within the medulla or to impressions received from nervous centres situated higher up or from the periphery, especially from the heart or lungs, through the agency of the pneumogastric and superior laryn- geal nerves. Such peripheral stinndi are ])iirti('ularly likely to be received by the centres in those cases of heart-disease manifesting right-ventricle dilatation with diminished supply of blood to the lungs. Rosenhach's Theory. — After, as he states, a searching analysis of tlie various theories, Rosenbach has adopted the following ex- planation. Under the influence of certain anomalies of brain- CHEYNE-STOKES RESPIRATION 621 nutrition there develop localized disturbances in the brain or in individual centres, particularly in that of respiration, which dis- turbances lessen the excitability of the affected part and augment the normal exhaustibility of the same. Thereby are produced remissions in the activity of the respective centres with loss of tone in the vaso-motor and vagus centres, or complete intermissions, such as a pause in the respiratory act, with a kind of paralytic state of the cerebrum, manifested by a periodic sleep with contrac- tion of the pupils and movements of the eyeballs. So soon as the fatigue and exhaustion of the centre have disappeared in conse- quence of cessation of respiration and an augmented internal ac- tivity, and its excitability returns, respirations again set in and con- tinue to increase, because the excitability of the nervous apparatus grows out of proportion or waxes more rapidly than the stimulus to activity wanes in consequence of organic work. So soon now as the abnormal exhaustibility of the centre again begins to be felt, it supersedes the stimulus, and therefore the functional activity of the centre lessens, and finally ceases altogether when at last the centre has become completely exhausted. Whether or not res- I^iration takes place is determined by the ability of the centre to respond to stimulus, and the depth of the respiratory act depends not upon the strength of the impulse, but on the functional capa- bility of the nervous apparatus. He thinks that of the various nervous centres the respiratory is the one that suffers most readily and often alone, while the vaso-motor centre is relatively much less frequently affected, and paralysis of this means death. He furthermore thinks that a regularly intermitting pulse, pulsus bigeminus and alternans, may be a manifestation of' peri- odicity in the function of the vagus and vaso-motor centres in certain cases of nutritional disturbance of the brain, and are analo- gous to the Cheyne-Stokes phenomenon. As Rosenbach states, this explanation of this abnormal type of breathing differs from others in the assumption, not of a periodic alteration of the stimulus, but in a rhythmic change in the excitability of the centre which pre- sides over respiration, even to a complete abeyance of its function for the time being. He assumes that this rhythmical periodicity as regards excitability is to be referred to some peculiar charac- teristic inherent in the nervous apparatus by virtue of which it is capable of being exhausted and again aroused to activity. 622 DISEASES OF THE HEART It is needless to add that, however ingeniously the pathology of Cheyne-Stokes respiration may be speculated upon, the subject is still enveloped in great obscurity. Prognosis. — The development of Cheyne-Stokes breathing is generally held to be of unfavourable significance, by indicating that a fatal termination is not far off. Yet weeks or even months may sometimes intervene between the appearance of this symptom and death. Murri reported a case in which the phenomenon per- sisted for forty days, and Sansom one for one hundred and eight days. In the Lancet of April 5, 1890, is the report of a case of a man of ninety-two who manifested the symptom for several years. This type of dyspnoea has also been known to' appear, then cease, and reappear after a lapse of several months. In most of the cases that recover, or in which the symptom is greatly protracted, the disease upon which it dejiends is either some brain-lesion or an acute affection, as influenza. When Cheyne-Stokes breathing is observed in cardiac patients, the underlying malady is itself of a grave nature, and the occurrence of this symptom usually por- tends a not distant termination of the case. To this rule there are exceptions, however. In April, 1895, I was consulted by an old gentleman of eighty who manifested this symptom. He had pro- nounced thickening of the peripheral arteries, a greatly hypertro- j)hied and dilated heart, a harsh bruit along the course of the aorta, and a remarkably intense and metallic aortic second sound. In addition to his arteriosclerosis and myocardial degeneration, his liver was cirrhotic and the urine gave evidence of chronic in- terstitial nephritis. Cheyne-Stokes dyspnoea was typical, and in consequence a well-known Chicago consultant had given a sombre prognosis on the ground that he had never known this symptom to endure for more than three weeks in such cases. Yet pari passu with iuiproveincnt in cardiac tones the dyspncea gradually abated, and after about two weeks was entirely lost, never again to return during the two years that this patient was spared to his family. Another gentlenuin of seventy-one displayed this form of breathing, rather irregularly by day but typically by night, dur- ing the time, in which cardiac asthenia was marked, yet recovered from it with gradual improvement in his condition. It has seemed t(» nic that wlicii ( 'hcync-Stokcs respiration is more ])rononneed, or ])erchance is nuiniiVstcd only during sleep, CHEYNE-STOKES RESPIRATION 623 it is not of so grave a prognosis as when present with equal inten- sity both waking and sleeping. Miirri, and recently Pembrie, have called attention to a physiological Cheyne-Stokes respiration observed in healthy persons during sleep. But the patient of sev- enty-one was not healthy, and therefore the nocturnal manifesta- tion of Cheyne-Stokes dyspnoea during his periods of unconscious- ness in sleep could not be regarded as physiological. Finally, the prognosis must be looked upon as specially grave in those cases which also manifest obscuration of the mental faculties. Treatment. — When Cheyne-Stokes dyspnoea is a symptom of cardiac disease the treatment must be essentially that of the un- derlying condition. Yet we are called on to mitigate the patient's distress so far as this is possible. This is best accomplished by the hypodermic administration of morphine, which, if it does not remove the dyspnoea, blunts the patient's sensibility. The value of morphine in this class of cases has been the subject of some contention in Germany. At the meeting of the Congress for In- ternal Medicine at Wiesbaden in 1892, Unverricht read a paper in which he expressed the decided opinion that morphine and atropine are powerless for the removal of Cheyne-Stokes breath- ing. Other observers have gone so far as to assert that morphine intensifies rather than relieves this symptom. Stadelmann made 25 observations upon the effect of morphine and atropine, alone and combined, upon this type of breathing. The observations were made upon two patients, and the doses were 0.01 to 0.02 (-| to -J) of a grain of morphine, and 0.001 to 0.0015 (-^ to ■£^) of a grain of atropine. The effects were neither uniform nor constant. They sometimes shortened the period of apnoea, sometimes that of dyspnoea, and at other times they lengthened one or the other or both. In 5 experiments morphine lessened or removed the Cheyne-Stokes respiration, and in 4 it aggravated the symptom. Although Stadelmann's observations were so inconstant and unreliable as to the effect of morphine that they seemed to con- firm Unverricht's assertion, he nevertheless concluded that on the whole the effect of this agent was to mitigate the severity of the attack. Morphine certainly seems to exert no injurious effects ; and since it undoubtedly blunts the patient's sensibility and in- duces sleep, there can be no contra-indication to its employment, even if it seems occasionally to change an irregular or unperiodic G24 DISEASES OF THE HEART form of this dyspna?a into the periodic rhythm characteristic of Cheyne-Stokes respiration. A word of caution should be spoken, however, regarding its use in these cases. This symptom is usually observed in elderly individuals with stiffened arteries and degenerated hearts, and as the kidneys very commonly participate in this pathological pro- cess one should bear in mind the possibility of these patients being more profoundly affected by the morphine than is desirable or even safe. For this, as well as other reasons, one should employ the smallest dose that will render the patient comfortable. In my experience this is generally -1 of a grain, an amount which I have rarely found necessary to exceed. In this dose the remedy is also a powerful cardiac stimulant, and as such beneficial to this class of patients. III. BRADYCARDIA Bradycardia and brachycardia are terms applied to an abnor- mally slow pulse-rate — that is, to one of less than GO beats to the minute. Allbutt in his system of medicine objects strenuously to their employment on the ground that, as slowness of the pulse is but a symptom, they are likely to mislead the student by seem- ing to raise the symptom to the importance of an independent dis- ease. Nevertheless the term bradycardia has come to be so gen- erally used that I have thought best to follow the custom of most writers and give it special consideration. I know by experience that practitioners not only regard it with apprehension, but are often at a loss to account for it, and consequently seek for a state- ment of those conditions in which it occurs and for an explanation of its significance. Slo^vness of the pulse may be cither physiological or pathologi- cal. A normal pulse-rate of less than 60 is occasionally observed, but when it is as slow as 30 or 28, of which instances have been reported, it becomes a truly remarkable ])henomenon. Napoleon Bonaparte is often cited as an instance of a physiologically slow pulse, having had only 40 heart-beats to the minute. It has been thought by some that he was a victim of epilepsy, and that his bradycardia was explicable on that ground. Physiological brady- cardia is very exceptional, yet when encountered is not to be re- garded as anywise likely to affect the general health. BRADYCARDIA 625 Osier states that slowness of the pulse sufficient to merit the appellation of bradycardia is sometimes- a family peculiarity. Under physiological bradycardia must also be included those in- stances sometimes yet very rarely observed in connection with hunger and cases of transient slowing of the pulse said by Blot to be seen in about 25 per cent of women during the puerperium. In such cases the rate may sink to 44 or even to 34, Allbutt has noted bradycardia in a healthy man of forty-nine given to excessive sexual indulgence, and has likewise seen it in children as a result, he thinks, of masturbation. In his own case his pulse-rate fell to 48 and to 44 in consequence of exhaustion, for it was restored to its normal rate after a refreshing sleep. Romberg, in writing on diseases of the heart in Ebstein's Prac- tice, displays characteristic German exactitude by limiting his consideration of bradycardia to cases associated with cardiac dis- ease. This appears to me to be too exact, since slowness of the pulse may by the ignorant be thought to indicate heart-disease. I have decided, therefore, to enumerate the diseased conditions of whatever kind which, according to Riegel, may be associated with abnormal retardation of the pulse. As a basis for his classification he made a study of 1,047 cases in which a pulse-rate of less than 60 was observed. (1) Bradycardia may occur during convales- cence from acute infectious diseases, as pneumonia, diphtheria, typhoid fever, erysipelas, and acute rheumatism. Sansom also includes influenza among the acute disorders capable of producing slowness of the pulse, an observation in which Allbutt concurs. It is believed that exhaustion is the cause in such cases. (2) Riegel observed this symptom in 379 cases of disorders of the digestive organs, as chronic dysjoepsia, gastric ulcer, cancer, and icterus. The occurrence of a slow pulse in cholsemia is a matter of frequent observation. Grob is also said to have seen bradycardia in connec- tion with oesophageal cancer and typhlitis. (3) The phenomenon under consideration is sometimes met with in diseases of the respiratory organs, particularly emphysema and (4) in diseases of the heart and blood-vessels, specially degenerations of the myo- cardium depending on coronary sclerosis, atheroma of the aorta (Sansom), but is not frequent in valvular defects unassociated with other alterations of rhythm. In 1 recorded case embolism of a coronary artery was attended with a pulse-rate of 8 to the 41 626 DISEASES OF THE HEART minute. (5) Bradycardia is occasionally seen in acute nephritis, in ura3mia, and was seen in 1 case of hematuria (Sansom). (6) Aside from uraemia, bradycardia may be produced by other poi- sons, as lead, tobacco and coffee, alcohol and digitalis. (7) It is sometimes seen in cases of diabetes, chlorosis, and anaemia. (8) Apoplexy, epilepsy, brain tumours, diseases of the medulla and of the cervical portion of the spinal cord, paresis, melancholia, mania, are all said to sometimes be accompanied by slowness of the pulse. (9) It is sometimes seen in skin disease, affections of the geni- talia, insolation and exhaustion from whatever cause. Finally, with regard to the pathology of bradycardia it may be of interest to give the following summary of Regnard's conclu- sions presented in a doctoral thesis in July, 1890, entitled Etude sur la pathologic du pouls lent permanent. He is of the opinion that every chronic lesion which causes irritation of any portion of the moderator apparatus of the heart may suffice to produce permanent slowness of the pulse and give rise to the aggregate of s^nnptoms. Such nervous irritation may have many causes, as local anaemia through the influence of atheroma on the periph- eral circulation and blood-supply to the nerve-centres, deficient blood-supply to the bulbous portion of the pneumogastric, tumours of the meninges of the bulb, or in the mediastinum acting on the vagus, morbid excitation of the laryngeal and gastric branches of this nerve, but most frequently some affection of the heart itself, as fatty degeneration or coronary sclerosis. The predisposing conditions are stated to be arteriosclerosis, whether syphilitic, alcoholic, gouty, or rheumatic in origin. It is not within the scope of this work to consider the signifi- cance of bradycardia in other conditions than of the circulatory apparatus. In these conditions marked slowing of the pulse is generally regarded as of serious import, because it is most com- monly observed in cases of sclerosis of the aorta or coronary arte- ries, and in such the heart-walls are likely to be degenerated. The lengthening of diastole incident to slow cardiac contractions sub- jects the heart to the possibility of diastolic arrest and the patient to the possibility, therefore, of sudden doatli in syncope. Moreover, the heart-muscle is extremely feeble in such cases, and hence it may require very little additional strain or depression to bring it to a standstill. STOKES-ADAMS DISEASE 627 I have notes of an old man witJi rigid arteries and clironic myocarditis in whom for several years prror to death the pulse- rate was persistently abont 28. In another the heart Avas actually slow, but as only every other systole sent a blood-wave to the wrist, the pulse-rate was in reality only half as fast. It is essential, therefore, in every instance of suspected bradycardia that the heart be auscultated to determine whether there may not be appar- ent instead of actual bradycardia. IV. STOKE^ADAMS DISEASE {Heart-Block) By this term is designated a remarkable symptom-complex con- sisting in bradycardia, vertigo or syncope and epileptiform convul- sions. Adams in 1827 and later Stokes were the first to describe cases, and hence this syndrome is called by their names. For many years it was considered a special disease and was studied chiefly by English and French clinicians, but recently German and American physicians have contributed valuable additions to our knowledge, particularly concerning the so-called bundle of His. Heart-hloch is a more general term, since it includes not only the Stokes-Adams syndrome but all cases in which there is inter- ference with the conduction of stimulus to contraction from auricle to ventricle through the bundle of His. ISTotwithstanding previous work, it may be said, it is the experimental study of Erlanger which has made intelligible the pathology of instances of Stokes- Adams disease that have come to autopsy in the past few years. Etiology and Pathology. — These are no longer obscure and a subject for speculation, as was the case up to 1903 when the first edition of this Avork appeared. The various theories once pro- pounded are now only of historical interest and hence will not be described in this place. Experiments and post mortem exam- inations have explained not alone the pathology of heart-block, but also the morbid anatomical changes underlying the Stokes-Adams syndrome. But before the causation of this symptom-complex can be stated it is advisable to describe briefly the system of conducting fibres which are shown by Aschoff and Tawara to connect the right auricle with the ventricles. This system of fibres begins at the anterior edge of the coronary vein, thence passes along the right side of the interauricular sep- 628 DISEASES OF THE HEART turn below the foramen ovale to the auriciilo-veiitricular septum, where directly above the point of insertion of the median flap of the tricuspid valve and before its entrance into the connective tissue of the septum it forms a knotlike mass of muscle fibres. From this knot a band penetrates the fibrous portion of the septum and running below the nunnbranous part of the interventricular septum to its muscular portion here divides into two main branches which pass obliquely downward beneath the endocardium one on each side. These two branches finally reaching the lower third of the ventricles penetrate the pa])illary muscles, and up to this point remain close underneath the endocardium, through which they usu- ally may be seen by reason of their lighter color. Leaving the papillaries some of the fibres pass along the course of small tra- becular to the parietal wall of the ventricle, where running up and down beneath the endocardial lining they fuse with ordinary cardiac muscle fibres. Aschoff further points out that whereas the right main trunk is fairly narrow, the left spreads out quickly like a fan and increasing in width as it descends divides into two broad but thin branches, of which each passes to a papillary muscle. These conducting fibres, especially in the brownish hearts of the old, but even in the young, may be discerned by the unaided eye because of their light yellow hue. The microscope shows them relatively poorer in sarcoplasm than are ordinary cardiac muscle fibres, and to hav(; a tendency to a reticular arrangement, being in this respect rather like embryonic muscle fibres. This ap- pearance is most marked in the auricular portion of the bundle anTis consist in two or more visible pulsations of the internal jugular veins without corresponding ai)ex-beats or carotid pulses, yet synchronous with distant, feeble heart tones. In other words, for every systole of the ventricle there are two, three or more auricular contractions whicli declare themselves by scarcely audible heart sounds and simultaneous waves or ])ulsations in the jugulars without answering ])ulse-waves in the arteries. Such a state of things can exist only when there is a block to the passage STOKES-ADAMS DISEASE 635 of stimuli from tlic auricle to the ventricles and lionce the detec- tion of these cardio-vascnlar signs esta^blishes the nature of the case beyond peradventure. Stokes-Adams disease must be differentiated from epilepsy and from functional disorders of the heart's action. It is distin- guished from the former by the absence of the epileptic cry, of biting of the tongue and of involuntary evacuation of bladder and rectum and, if the physician be so fortunate as to witness the attack, by the extreme slowness of the pulse and the cardio-vascular signs of heart-block. Functional disturbances of cardiac rhythm may be differenti- ated in favorable cases by inspection of the cervical veins and auscultation of the heart, but the only precise method of identi- fying extra-systoles on the part of auricles or ventricles wbich may simulate partial heart-block is by resort to some form of poly- graph, Mackenzie's or Hirschfelder's modification of the Erlanger sphygiuomanometer. By careful measurement of the venous and arterial tracings thus obtained one can determine the exact time- relation of the pulsations and so ascertain whether or not a block- ing of the contraction-waves exists. Prognosis. — This is exceedingly grave since complete heart- block is liable to cause death at any' moment. A few cases have been reported which appear to have recovered, but since Stokes- Adams disease is generally due to structural lesions within the bundle of His, the probability of recovery is very remote. The cases offering such a possibility are those presenting a specific history in which the symptoms may be due to gumma involving the conducting fibres. Even in such, however, the administration of iodides is not always capable of bringing about a cure. If the patient is old and sclerotic he will succumb to his malady in all likelihood during an attack. Treatment of this disease is highly unsatisfactory because of the fact that with the possible exception of syphilitic disorders of the heart we have no means of removing the cause under- lying the heart-block. We are restricted, therefore, to a symp- tomatic line of therapy, and even this is unprofitable in most instances. Between attacks the general health may receive atten- tion, and digestive disorders, constipation, etc., should be removed. The individual should be warned against acts which may over- 636 DISEASES OF THE HEART strain his heart and should lead as orderly an existence, free from excitement, as possible. Experience has proven that no stimulants of any sort are capable of terminating an attack. Nevertheless, ammonia or camphor may be administered, but digitalis and allied drugs are distinctly dangerous. The fact is, the symptoms will disappear or not as the case itself may determine, and hence stimulants may receive the credit when no credit is due. CHAPTEK XXV ANGINA PECTORIS Definition. — Attacks of intense pain in the region of the heart, with more or less disturbance of cardiac action, usually accompa- nied by a feeling of constriction of the chest and a sense of im- pending death. History. — Although this form of heart-pain was not systematic- ally described until the latter part of the eighteenth century, yet a graphic account of his own sufferings from this complaint was given by Seneca, and in 1707 Morgagni gave a clear description of a paroxysm in a case of aortic aneurysm. In February, 1768, Rougnon addressed a letter to M. Lorry which contained the de- scription of the death of a certain Captain Charles, who, from the account given by Rougnon, appears to have suffered from at- tacks of angina pectoris. It was Heberden, however, who in July, 1768, first systematically described this formidable complaint and who gave it the name by which it is now universally recognised. The names of John Hunter, Edward Jenner, and Parry are also intimately associated with its early history. Hunter having expe- rienced it in his own person, and having ultimately died in an attack. Jenner in 1799 pointed out a definite connection between scle- rosis of the coronary arteries and angina pectoris. He is said to have refrained from publishing his views at an earlier date out of consideration for his famous friend, John Hunter, who during his life had held contrary opinions concerning its etiology. Parry gave it the name of " syncope anginosa," for, although he recog- nised its connection with coronary disease, he considered the at- tacks due to paralysis of the heart. From this time forward the literature of the profession teems with contributions on the subject and with divers theories con- 637 638 DISEASES OF THE HEART cerning its pathogenesis. Most of the earlier writers attributed the complaint to morbid anatomical changes in the heart itself. In 181G Kreysig definitely stated that it was due to ischwmia of the myocardium in consequence of defective blood-supply from sclerosis of the coronary arteries. In 1821 Reeder amplified the theory of cardiac ischa-mia by asserting that this condition might proceed not only from ossification of the coronaries, but also from any other disease — i. e., as atheroma of the aorta— which might be capable of shutting off the blood-supply to the heart-muscle. This same theory was likewise espoused by Tiedemann in 1843, and in 1875 Germain See described the case of an elderly man who had suffered from anginal seizures and in whom after his sudden death the mouths of the coronary arteries were found almost obliterated by atheromatous plaques situated on the intima of the aorta. Throughout the balance of their course the coro- nary vessels were healthy. These few instances are sufficient to show in a general way the trend of opinion on the part of the sup- porters of the so-called anatomical theory. In 1834, says Iluchard, the theory of the purely nervous mech- anism of the attacks was formally announced by Gintrac, although its neuralgic character had been previously asserted by Baumes in 1808, and others. Gintrac attributed the pain to irritation of the fibres of the cardiac plexus, and in 1863 Lancereaux published 3 cases in which the autopsy revealed inflammatory or other changes of this plexus. There has been wide variance of opinion among French au- thors concerning the nerves implicated. Thus Laennec considered it an affection of the sympathetic system and called it neuralgia cordis. Bouilhnul regarded it as an affection of the phrenic nerves, and Peter, while accepting this view as applicable to some cases, also believed there was a neuritis of the cardiac nerves. Trousseau termed it an epileptiform neuralgia. In Germany also the subject was extensively discussed and re- ceived a variety of explanations. Rond)erg considers it as a mere neuralgia of the cardiac plexus, a view not unlike^ that of FricdnM'ch, who tliought it due to hyper- a'sthesia of" thnt plexus. Tlic ujiuics ol" I>aml)erger, Tnnilx', Noth- tiag(!l, Landois, Eulcultcvg, (luttniaiui, Leyden, Kosenbach, and numy others are identified with the literature of this interesting ANGi:5rA PECTORIS G39 subject. Landois, who in 1863 subjected the question to a critical study from a physiological standj)oint, divided angina pectoris into four groups, as follows: (1) Cases caused by disturbance of the excito-motor or accelerator nerves of the heart; (2) those due to irritation of the cardiac branches of the vagus; (3) cases aris- ing from reflex irritation of the abdominal viscera — " angina re- flectoria " ; (4) such as arise from vaso-motor disturbance in vari- ous parts of the body — " angina vaso-motoria." Eulenberg also contributed an elaborate article on this subject in Ziemssen's Cy- clopaedia of Medicine, vol. xiv. Leyden considers the attack due to degenerative and inflam- matory changes in the heart-muscle depending upon disease of the coronary arteries, which changes lead to impairment of the heart's function. According to Rosenbach, some alteration in the contractions of the cardiac muscle takes place, which alteration may, but does not necessarily, lead to functional weakness. In consequence of this change, irritation is imparted to the sensory tract, and this stimulus sets free the various forms of pain and anxiety character- istic of stenocardia, in accordance with irritability of the sensory apparatus and the function of the respective nerves composing it. Painful sensations are more or less pronounced according to whether the sensory centres are or are not accustomed to the irri- tation to which they are subjected. According to Rosenbach's view, this true heart-pain is an indi- cation of the heart-muscle being less able than usual to accommo- date itself to sudden change taking place in the performance of its work ; or, in other words, its ability to respond to demands from without for a display of extra effort is impaired. I^ow and then, also, obstacles residing in the heart itself and capable of in- terfering with its perfect action may interrupt the performance of its regular work and in like manner give rise to the phenomena of angina pectoris. During the century just ended many contributions to this in- teresting subject have appeared in England and America, of which the most noteworthy were by Latham, Gairdner, and Osier. The last mentioned, in his Angina Pectoris and Allied States, deals with the affection in a very complete and entertaining man- ner. The most exhaustive discussion of the subject, however, to 640 DISEASES OF THE HEART vvliich I have had access is that by Huchard. His historical resume of the various theories is complete and shows painstaking research. His own view of the pathogenesis of this formidable complaint is highly suggestive and will be stated in the appropri- ate place. Pathology and Etiology. — It should be clearly understood at the outset that angina pectoris is but a symptom and not an independent affection. It therefore can have no morbid anatom- ical characters peculiar to itself. Its patljology is obscure, and hence there have been, and are still, various theories to explain its nature and mode of production. It may be stated in a general way that .angina pectoris is divisible into two forms: one incurable and likely to terminate in death, the other curable and not likely to end fatally. Some authors, therefore, following Walshe's classification, speak of a true and a false angina. Osier makes this distinction, while Bal- four, Gibson, and others consider such a division irrational and unscientific, on the ground that all pain is real, and that there can be no such thing as true pain and false pain. There can be no great objection to these terms if it is understood that they are employed for the sake of convenience, to distinguish grave cases from those that are not grave. Huchard also classifies cases of angina which are purely neu- rotic and not likely to terminate fatally under the head of pseudo- angina, which he makes include the reflex and toxic forms. In certain cases, however, he believes that nicotine poisoning is capa- ble of producing the fatal form of angina pectoris. The confusion and obscurity wliich so long characterized the consideration of this subject, and which indeed may be said to prevail largely even now, arose from the attempt to make the same pathology responsible for all cases of pain that merit the term of angina pectoris. On the other hand, the recognition of two en- tirely diverse groups renders the subject clear and simple, so that we are able to get a tolerably definite notion of its pathology. The angina which always carries with it the possibility of sud- den death, and which therefore may be called true or grave, is usu- ally associated with, and therefore thought to be dependent upon, structural disease of the heart. Various lesions have been found in fatal cases, but they are all of such a kind as to interfere with ANGINA PECTORIS 641 the blood-supply to the heart-muscle. Coronary sclerosis is the most frequent, but inasmuch as all cases' of this disease are not attended with angina pectoris, it is evident that there must be something more than mere sclerosis of these arteries. According- ly it has been determined that it is not so much the fact of disease of these vessels as it is that this disease must interfere with cardiac circulation if it is to give rise to attacks of angina pectoris. Shutting off of the blood-supply to a limited portion of the myocardium — i. e., by thrombosis of terminal twigs or even of a branch of considerable size — does not apparently always occasion this pain. If, however, one main trunk, or, still more, if both trunks are occluded, or if their lumen is sufficiently narrowed without being actually obstructed, then attacks of angina are very likely to occur. Accordingly, a condition which is specially apt to result in anginal seizures is narrowing of the mouths of the coronary arteries by the sclerotic process, as has been repeatedly proved at the necropsy in cases of this terrible agony. It is upon the evidence furnished by such discoveries that the theory has been reared of ischa?mia of the heart-muscle being the essential pathological factor in the causation of the fatal form known as true or grave angina pectoris. In this variety pain is usually absent so long as the individual is at rest or is not making exertion that requires unwonted labour on the part of the heart. Under such conditions the circulation of blood within the myo- cardium is sufficient for its needs, but when some emotion or extra physical effort calls for unusual heart-work, the narrowed coronary arteries are incapable of supplying the organ with an additional volume of blood and the ischsemia is intensified for the time being. Thereupon an attack of angina pectoris is evoked. According to this hypothesis, the nerve-filaments or ganglia with which the myocardium is so richly supplied become irritated by this depriva- tion of required blood and send an impression through the cardiac plexus up to the centre, which then responds by discharging a sensation of pain along certain nerve-trunks connected with cer- tain segments of the spinal cord. This will again be considered in greater detail. The pain thus induced promptly causes a cessation of exertion and consequent lessening of the heart's work. As the organ re- sumes its accustomed tranquility its blood-supply proves again 42 642 DISEASES OP THE HEART sufficient for its needs, irritation ceases, and with it at last goes the pain. Whether or not this is the actual modus operandi of the attack, the assumption that it depends upon a diminution of the blood-supply seems borne ovit by the nature of other cardiac and vascular lesions sometimes discovered in fatal cases of angina — i. e., aneurysm and atheroma of the ascending aorta, insufficiency of the aortic valves, and very rarely extreme degrees of aortic and mitral stenosis. In cases of angina that appear due to aortic scle- rosis the mouths of the coronary arteries are very commonly found extremely reduced in size by reason of calcareous plaques on the surface of the intima or by calcareous thickening of the aortic wall, while the coats of the nutrient arteries. are also generally invaded by the same sclerotic process. In cases of aneurysm the coronaries are narrowed either by the direct effect of the aneurysm or by associated atheroma. In the diseases just mentioned the changes must be of a kind to obstruct blood-flow into the coronary arteries if they are to occasion the agonizing symptom under con- sideration. In aortic regurgitation adequate blood-pressure in the nutrient vessels is not maintained, and under conditions of extra effort rela- tive ischa'mia of the hypertrophied left ventricle is produced. Mitral and aortic stenosis prevent the discharge of a normal vol- ume of blood into the aorta, and consequently hinder the adequate flushing of the coronary arteries. By some authors the influence of valvular defects in the causation of angina is denied without associated sclerosis of aorta or coronaries, and certainly angina pectoris is exceedingly rare in valvular disease. Nevertheless, I have observed typical angina pectoris in one case of pronounced aortic stenosis that was, from the history and patient's age, presumably of rheumatic origin and in two instances of aortic insufficiency. In the first case no autopsy was obtained, but in one of the patients whose aortic incompetence was associ- ated with angina and whose case was described in the chapter on aortic regurgitation, the pain was foinul to 1)0 clearly due to scle- rotic narrowing of the coronaries. I am inclined to believe, there- fore, that aortic incompetence of itself is not so likely to lead to angina as is stenosis. Post-mortem observation proves undeniably that the nutrition of the heart-muscle may suffer seriously in cases of valve-disease ANGINA PECTORIS 643 without associated coronary sclerosis, and that such myocardial degeneration is particularly likely to be found in long-standing and extreme stenosis of the aortic orifice. This indicates that dur- ing a long period of time the demands on the energy of the heart outstripped its nutrition owing to the small supply of blood sent through the stenosed orifice into the aorta and coronary system. If in such a state of things the supply of blood to the heart- muscle is still further diminished, although but temporarily, then it is possible for a paroxysm of angina pectoris to occur. The in- fluences capable of determining such a temporary increase of car- diac ischasmia may be vaso-motor spasm, affecting the coronaries, as suggested by Powell, or the continuance of undue physical exer- tion after such effort has begun to overtax the heart. In extreme aortic stenosis cardiac overstrain is shown by still greater feeble- ness of the pulse, and when such is the case the coronaries are still more imperfectly flushed. There is temporarily a relative cardiac ischsemia which makes an attack of angina pectoris possible. For- tunately such attacks are rare, yet on the hypothesis of cardiac ischsemia as the cause of angina the conditions favourable to its production are present. Finally, it should be stated that the degenerative changes dis- covered in the myocardium of persons who have died in a parox- ysm of angina pectoris probably bear no direct etiological rela- tionship to the pain. Were it not so, this formidable agony would be far more common than it really is. Such degenerations of the heart-muscle are to be looked upon as the result of the pathological condition in the coronaries or aorta which have led to the angina. It now remains to consider how the morbid anatomical condi- tions just mentioned act in the pathogenesis of this obscure com- plaint. They are to be regarded as predisposing factors merely, which to be operative require some additional influence, since, if such were not the case, all persons in whose heart such changes are found after death ought to have suffered from angina pec- toris. This we know is not the case. It is this consideration which has given rise to the various hypotheses propounded in explanation of the symptom-complex. The best known of the the- ories have been stated already in the history of the complaint and do not call for repetition. I would direct attention particularly to Rosenbach's and to that of cardiac ischsemia. 64:4 DISEASES OF THE HEART AVith reference to the latter, I tliink one should also hear in mind the suggestion of Sir Douglas Powell that oftentimes we are obliged to assume the possibility of relative cardiac ischmmia if we are to understand how some cases originate — i. e., the condi- tions under which they originate, and the beneficial influence of certain lines of medication. According to this hypothesis, vaso- motor spasm may affect the coronary arteries and temporarily seriously diminish the flushing of the heart-muscle with arterial- ized blood. The irritation thus evoked is declared by pain and often by disordered cardiac action. AVhen, upon administration of vaso-dilators or on cessation of arterial spasm from other influ- ences, the coronaries become relaxed, and hence better flushed, irritation ceases. Whatever is the exact condition, however, the generally ac- cepted view is that there is abnornuil and excessive cardiac irrita- tion which initiates the paroxysm. This is Huchard's view at all events, and herein he appears to coincide with Rosenbach. According to Iluchard, the course of vents in cases of grave angina is as follows: The heart itself is the starting-point of the attack. From here the stimulus ascends by way of the sensory centres and finally reaches the medulla. Thence it is reflected along the intercostal nerves and brachial plexus as a manifestation of pain. The stimulus next reaches the vagus centre, and from here an inhibitory impulse is sent down to the heart, the original start- ing-place, and declares itself by slowed, and it may be intermittent action of the heart. Such an inhibitory action explains the sense of constriction and of impending death, as well as tlie dilatation of the cardiac cavities sometimes noted. In pseudo-angina, on the contrary, the point of departure of the irritation is an intercostal nerve or some other peripheral or visceral nerve, whence, as in true angina, it also passes to the medulla. From there an impulse is sent out not along intercostal nerves and brachial plexus, but is passed down along the vagus or accelerator nerves of the heart to this organ. According to the route thus selected, the action of the heart becomes either rapid or slow and otherwise disordered. In these two forms, therefore, the original source of irritation is entirely different and the circuit is traversed in a contrary di- ANGK^A l^ECTORIS 645 rection. To my mind this is a highly satisfactory explanation of the differences in their clinical phenomena. It likewise proves seryiceable in making up diagnosis and prognosis and in deciding on the mode of management. Leaving now the pathology of angina pectoris, which, however much we may speculate upon it, is undeniably obscure, we come to the consideration of the remaining predisposing causes as well as the influences which directly excite an attack. Aside from the anatomical conditions already considered, we are at once impressed by the important part played by age. An- gina pectoris of coronary origin is emphatically a complaint of individuals who have passed middle age and have entered their sixth or seventh decade. This is an age in which the effects of arteriosclerosis usually declare themselves, and yet angina of this origin is sometimes observed before the fiftieth or even the fortieth year. One or two instances are on record of its occurrence in chil- dren. ISTevertheless such facts do not invalidate the correctness of the statements made concerning the importance of age. Males are much more frequently affected than are females, and of men who are befallen it is a noteworthy fact that it is espe- cially the well-to-do and well-fed. Regarding the influence of sex, Osier states that out of his 40 cases but 3 occurred in women. I have notes of 32 cases, and of these, 7 were in the female sex. Of '2 that came to autopsy, 1 was a woman of sixty-six with aortic and mitral stenosis, with sclerosis of the aorta and coronaries ; while in the other, as already stated, there was coronary obstruc- tion and aortic regurgitation, both of sclerotic origin. Of the re- maining 5 cases, 1 was in an aged woman presenting well-marked signs of arteriosclerosis, a hypertrophied left ventricle, and a harsh systolic basic bruit. Another was a comparatively young female with aortic regurgitation of uncertain origin, but whose questionable habits always made me suspicious of the likelihood of syphilitic infection. The third was in the lady of forty-four with signs of pure aortic stenosis whose case has been already de- scribed in the chapter on Aortic Stenosis, and will be again alluded to in this. The fourth was in a woman of fifty with aortic regurgitation, due probably to arteriosclerosis, to judge from her history and the arterial thickening. The fifth case was that of a woman of fifty-six who was corpulent and had thickened arteries G46 DISEASES OF THE HEART with a greatly hypertropliied and dilated heart. As regards this striking discrepancy between the two sexes, it may be stated that the greater prevalence of angina pectoris among elderly men is to be referred not so much to sex per se as to those conditions which are responsible for the greater frequency of arteriosclerosis in the male sex. Heredity is also a predisposing factor, what was said under this head concerning coronary sclerosis and myocardial degenera- tion being also applicable to the symptom now considered. In- stances are on record of this formidable complaint having been passed down through three generations. It is not at all uncom- mon for both father and son to suffer or eveii die from angina pectoris. The most notable instances of the kind occurred in the persons of Thomas Arnold, of Kugby, and his equally well-known son, Matthew Arnold. Gout predisposes to arteriosclerosis, and therefore to angina pectoris. Syphilis, alcohol, and, according to Huchard, tobacco, are also predisposing causes. The last named may, however, be an exciting cause. The exciting causes of true, or coronary angina, as Huchard calls it, are conditions that suddenly raise blood-pressure in the aortic system, or, according to the theory of cardiac ischamiia, re- quire more work of the heart than it can perform in consequence of its diminished blood-supply. Foremost among these is muscu- lar effort. The patient may have had no premonition of the mal- ady, when, one day, perchance immediately after breakfast, he starts out for a walk and is arrested by an indescribable attack of praecordial pain. In other instances the first paroxysm is expe- rienced upon the patient attempting to hurry to reach a car, or the like, and thereafter is repeated whenever he quickens his foot- steps beyond his usual pace. Atmospheric conditions undoubtedly intensify the influence of exertion, for on a day when the wind is easterly and raw these patients find themselves imable to walk at even their accustomed gait ; while in warm weather and on still days, or here in Chicago, even in the depth of winter when the air is dry and cold and the sun bright, these patients frequently find themselves able to get about with comparative comfort. I have known patients who could walk with ease when the ANGINA PECTORIS 647 stomach was empty, yet who invariably experienced pain, of greater or less severity, whenever attempting to walk soon after breakfast. This is undoubtedly to be explained by the augmenta- tion of arterial tension, produced by the presence of food in the stomach. Nevertheless the rise of blood-pressure thus occasioned is of itself not sufficient to evoke an attack, since it requires in addition physical exertion. Emotional states, as anger, worry, or excitement from what- ever cause, which accelerate and intensify cardiac action, are also capable of evoking an attack of angina pectoris. This was illus- trated in the historic case of John Hunter, who was wont to say that " his life was in the hands of any rascal who chose to annoy or tease him." As a matter of fact. Hunter died during a parox- ysm brought on by a fit of silent rage in consequence of having been flatly contradicted at a meeting of the Board of Governors of St. George's Hospital, October 16, 1793. His coronary arteries were found ossified and the aorta dilated. I knew a gentleman of this city, a great sufferer from ferocious attacks of angina for many years, who frequently declared that nothing was so bad for him as a fit of temper. It is very remarkable how diverse are the effects of exertion in different persons, or in the same individual at different times. I recall the instance of a gentleman of fifty-two, who, by the way, had been an inveterate smoker of strong Havana cigars, and who could not walk out of an evening without suffering from his an- gina. Yet on one occasion he assisted in carrying a loaded book- case up a flight of stairs without experiencing the slightest pain. This patient ul'timately died suddenly. I have another gentleman under occasional observation who invariably experiences more or less pain of a true anginal character the first thing in the morning when he goes into the bath-room to dress. The taking of a cool bath is almost sure to evoke one of his seizures. Excitement and exertion combined are particularly apt to call forth an attack. For this reason coitus is especially injiirious to some of these pa- tients. The influence of cold in determining a paroxysm has been referred to, and is shoAvn by the inability of patients to face a cold wind, particularly when damp as well as cold, and by the effect of a cold bath. Distention of the abdominal viscera by flatus and the taking 648 DISEASES OF THE HEART of a full meal are enumerated among the exciting causes by some authors, but in my experience these have been operative only in connection with other determining factors, as exertion. Tobacco is counted by Huchard as both an exciting and a predisposing cause, and he narrates instances of individuals who had abandoned smoking because of the attacks of angina it induced, and who upon returning to their former habit again found it promptly followed by the same unpleasant effect, Gibson likewise speaks of tea and coffee in this connection, say- ing they also claim their victims. Regarding the angina due to tobacco, Huchard recognises three forms: (1) Functional or rela- tively benign form, resulting from spasm of the coronary arteries, without disease of the myocardium, and which is the " Angina spasmo-tabagique," and which is recovered from by giving up the use of tobacco. (2) An organic angina of a grave character, re- sulting from coronary sclerosis and which is not recovered from by the abandonment of the tobacco habit. This is the " Angina sclero-tabagique." (3) The form most benign of all results from digestive troubles produced by the tobacco habit (gastralgia, dila- tation of the stomach, and insensibility of the mucous membrane). This is the " Angina gastro-tabagique." Strictly speaking, these all, with the possible exceptions of the second form, belong to the pseudo-angina. In the group of cases known as false angina, and which, ac- cording to Huchard, belong to the peripheral or visceral neuralgias, and which will be considered in connection with cardiac neuroses, the exciting causes are not always easy of recognition, yet, as stated emphatically by Huchard, are never due to effort. Herein, therefore, lies the great distinction between true and false an- gina. Occasionally in true angina, the paroxysms occur at night, arousing the patient from sleep, but, according to Huchard, this does not invalidate the statement that coronary angina is evoked by effort, nor arc these cases to be classed as pseudo, because com- ing on at night. Their advent during sloo]) is referable to some condition which augments blood-pressure and acts in the same manner as does effort made by these individuals. Some of these conditions may be flatulent distention of the bowels, coldness of the air in the sleeping apartment, an uncomfortable position during sleep, or ANGIl^A PECTORIS 649 the recumbent posture itself, which is known to augment blood- pressure (llucliard). Clinical History and Features of an Attack. — The sufferer from angina of coronary disease is most often an elderly man of about sixty years of age who has been engaged in mercantile, profes- sional, or literary pursuits rather than in manual labour, and who often presents the appearance of well-preserved health. He not infrequently states that prior to his first attack of angina he never had any symptoms that made him think his heart was affected, and that were it not for this symptom he would still think his heart as sound as ever. Questioned concerning the symptoms for which he consults the physician, he says he has a pain in the front of the chest, which he locates at the upper and middle portion, frequently putting his hand over the manubrium sterni. He describes this pain as coming on suddenly, usually during a walk, and becoming so intense as to compel him to stand still until it goes away, which it usually does in a few moments. Further inquiry brings out the fact that associated with the pain is a feeling of oppression or weight on the chest, and in some cases a sense of impending death. The essential features of an attack, therefore, or the char- acteristic triad of symptoms, as it may be called, are (1) a subster- nal pain, that is usually so severe as to be an indescribable agony, (2) a sense of great constriction of the chest, a feeling as if this were being crushed or squeezed together, and (3) a sense of speedy or impending dissolution. The duration of a paroxysm is not long, generally not more than a few minutes, probably because the violence of the agony necessitates a cessation of the effort occasioning it, and with the removal of its exciting cause the attack subsides. Occasionally it persists for twenty minutes or more, and when it occurs in the middle of the night it is apt to last longer than do day attacks. Thus it is seen that the pain may come on either by day or by night, but as a rule and particularly in mild cases it is more likely to manifest itself during the waking hours and when the patient is exposed to some obviously exciting cause. I^octurnal seizures are apt to be more severe as well as of greater duration, because, according to-Huchard, the rise of blood-pressure incident to the recumbent posture does not subside quickly even after the 650 DISEASES OP THE HEART patient leaves his bed, whereas that due to effort or emotion yields promptly to the removal of the cause. The first seizure has been known to prove fatal, and on the other hand attacks have recurred at varying intervals for five, ten, fifteen, and even twenty-five years. A single sharp paroxysm has been followed by years of immimity, and in other instances, after having been absent for a long period, the malady has then assumed a frequently recurring type. Huchard speaks of the paroxj^sms as sometimes occurring with such frequency as to over- lap each other, and thus become practically continuous with only remissions in severity, a condition which he terms I'etat de mal angineux. Some patients are aware so soon as they arise in the morning that they are going to have a " bad day," as they say, or that they will have to be more than usually cautious lest they pre- cipitate an attack. As a rule, however, anginal seizures come on abruptly without warning and with such agonizing intensity that the sufferer is compelled to stop in his tracks and remain standing, scarcely daring to stir or breathe lest he intensify his pain beyond all possibility of endurance. At other times he leans against a tree or wall for support, or he stands in some peculiar attitude which experience has taught him will somewhat mitigate the severity of the pain. He may lean forward or bend backward, let his arms hang motionless at his side or stretch them above his head in an effort to fix the pectoral muscles so as to thereby increase the expansion of his chest, which seems to him to be compressed and too small for its contents. But whatever his attitude, it is, according to Huchard, always an upright rather than a recumbent position, which latter, by augmenting arterial tension, increases the severity of the attack. Most happily for the patient the angina usually departs as quickly as it comes, and unless the attack has been one of un- usual length or severity tlie victim feels as well immediately after as he did before the seizure. He is generally able to resume his walk, although perhaps rather more cautiously than before. Such is the history of a comparatively mild angina pectoris, but in some sad cases thg attacks grow more fro(picnt and more agonizing until at length the patient is not al)le to move in bed or engage in con- versation witliout frightful suffering, iiud life becomes a miserable existence. ANGINA PECTORIS 651 It now becomes necessary to consider the features of anginal attacks in detail. It has been stated that the pain is subster- nal; that is, that its seat of maximum intensity or its point of departure is beneath the upper or middle third of the breast- bone. It is for this reason that Baumes applied to the complaint the name of sternalgia. The pain may remain centred beneath the sternum, but in most instances it radiates into the side of the thorax and along the course of the brachial plexus into the left shoulder or down the corresponding arm to the elbow or still farther, as far as the wrist, or even into the two fingers supplied by the ulnar nerve. In some cases the pain takes origin in the region of the apex-beat or epigastrium, or, as in the case of one of my patients, just above the ensiform appen- dix, whence it shoots into the left shoulder and down the left arm. In rare instances the attack starts in the arm, at the wrist or elbow, and thence passes into the chest to the region of the heart. In one of Trousseau's patients the paroxysm began in the back of the neck, and then darted forward into the tongue and front of the thorax. Very exceptionally the pain may take origin in the left interscapular region or at the adjacent dorsal spines. But whatever is its point of departure the anguish radiates more or less widely throughout the chest, flashing from the cardiac area into the left, sometimes the right arm, and in some cases into both arms, or upward into the side of the neck or the occiput, or, instead, downward into the left half of the abdomen, and now and then even to the thigh. These latter lines of radiation are, how- ever, very uncommon as compared with its course into the left shoulder and arm. Very diverse terms are employed by patients in attempts to describe their agony. It is spoken of as crushing, grinding, tear- ing, cutting, burning, scalding, or, in want of appropriate adjec- tives, as indescribable, frightful, and the like. One of my pa- tients, a lady with extreme aortic stenosis, depicted her anguish as " a feeling as if my chest were being crushed beneath the wheels of a passing train." The sensation of pain is sometimes lost in the terrible distress occasioned by the sensation of the chest being squeezed in a vise, or of the walls being forced together from before backward. 652 DISEASES OP THE HEART Balfour describes it as if the heart were being " grasped by a mailed hand." Then, as if this were not enough, the sensation of impending death is added, to complete this awful suffering. The lady just mentioned, said in reply to a query upon this point : '' Oh, yes ! of course I feel as though I were going to die, but I have learned by experience that I do not die, and therefore I no longer speak about it. I always used to declare that I knew I was going to die." Nearly all sufferers from severe angina pectoris agree in the assertion that no other pain can compare with the awfulness of its agony, and if it were not happily of short duration, life could not endure. The physician is not often a witness of the terrible agony, the attack being over before he arrives, or his attention is so occupied in efforts for the patient's relief that he cannot note the several features. Nevertheless, from such observations as have been re- corded, we possess certain facts concerning objective symptoms. The face is expressive of unspeakable agony ; it is anxious and usually pale, and bedewed with perspiration, but it may be con- gested. The patient is usually motionless during the height of the Ijaroxysm, yet it may be ushered in and terminated by restlessness. The extremities are usually cold, and the pulse is variable. It is sometimes stated to be unchanged, but is for the most part small and tense. It may be regular or irregular and, if accelerated in the be- ginning, is likely to become slower than normal before the cessa- tion of the pain. The size and rate of the pulse have given rise to much discussion, but the consensus of opinion seems to be that it is small, sharing in the condition of spasm, and that its rate is slow, indicating vagus stimulation. The heart sounds are usually clear, but feeble, although in some instances a systolic apex-mur- mur has been audible. As already stated, the seizure usually subsides suddenly, leav- ing TKithiiig more than a feeling of weakness behind. The pain in th(! uj)p('r extremities may be accom]>anied but is more often fcjllowed by a feeling of numbness, even by transient paresis. The lady to whom reference has been repeatedly made, said her left arm was always helpless after cessation of the suffering. In the case of my aged female patient, already mentioned as ANGINA PECTORIS 653 having arteriosclerosis, the face was flushed during the attack, and the cessation of pain was followed by vomiting. I have stated that i)atients remain motionless during the paroxysms, yet I have known two instances, both men, who thought they obtained some relief by walking gently about the room while the pain was on. One of them was a well-known attorney, in whom the necropsy verified the diagnosis of coronary sclerosis and fatty degen- eration of the left ventricle. In the other case the age of the patient, the thickened peripheral arteries, and the history of the attacks, left no doubt as to the nature of his angina. Douglas Powell states that when relief is produced by quiet walking it has seemed to him to indicate a fairly sound state of the heart-muscle. This may be so in some but not all cases. Mr. H., the attorney, was found to have extensive myocardial degeneration, and hence some other exjDlanation is needed in his case. In my other pa- tient, the gentleman was not only able to endure without pain certain gymnastic and breathing exercises which produced great perspiration, but he declared that he felt better for them. That they did not call forth his suffering the same as did walking against a wind, may have been due to the lowering of arterial ten- sion which they induced. The extremely variable course of the malady and its not in- frequent termination in death during an attack are also note- worthy features. An historic instance is that of the Rev. Dr. Chalmers, who is thought to have died during a paroxysm of angina, since he was found dead in his bed with a bowl beside him into which he had emptied the contents of his stomach. I knew a similar instance of an old gentleman who, after having suffered attacks of angina pectoris for twenty years, was found lifeless in his bed in a hotel with a wash-bowl resting on the bed in front of him and containing vomited matter. I knew of another elderly gentleman who, while in attendance upon a lawn fete, was seized with a paroxysm of prsecordial pain, vomited, and imme- diately died before assistance could reach him. So far as could be ascertained, it was his first and only attack. Before leaving this subject, it should be mentioned that Gaird- ner has described what he calls angina sine dolore. What he means by the term is best described in his own words : " Apart from what has been variously termed cardiac asthma, dyspnoea, 654 DISEASES OF THE HEART or orthopnoea, which in many cases receives its clear explanation from the associated states, either of the pulmonary circulation or of the lungs, bronchi, and pleura^, as disclosed by physical signs, there is often an element of subjective abnormal sensation present in cardiac diseases, which, when it is not localized through the coincidence of pain, is a specially indefinable and indescrib- able sensation, almost always felt to be such by the patient him- self. I make this remark deliberately, as the result of experience, and well knowing it is liable to be brought into question in par- ticular instances — that, in fact, a large part of what has been de- scribed under the titles given at the commencement of this para- graph has been inextricably confounded by systematic writers with the sensation, or group of sensations, to which I refer. To this group of sensations, when not distinctly accompanied by local pain, I have, in various instances, given the name of angina sine dolore, recognising thereby what I believe to be its true diagnostic and pathological significance, and its alliance with the painful angina of Heberden ; the pain in which, however, as we have already seen, is an exceedingly variable element, both in degree and in kind." Diagnosis. — Two questions present themselves for answer in the diagnosis of this formidable complaint: First, is the attack of pain angina pectoris ? and second, what is the pathological con- dition underlying the attack ? In other words, is the paroxysm to be classed as coronary angina ? or is it a disorder of the nervous system independent of any cardiac or vascular disease ? In at- tempting to answer the first query, one should keep clearly in mind the fact that all pra'cordial or so-called heart-pains are not attacks of angina pectoris. Many of these pains are simple inter- costal neuralgias, and although variously described as cutting, stabbing, tearing, shooting, darting, l)urning, smarting, or only as dull, sore, heavy, and the like, they lack two features essential to angina pectoris — namely, the feeling of the chest being crushed, and the sense of the near presence of deatli. The fact that pain is felt in the region of the left nipple or that it radiates from that point into the left shoulder and arm does not warrant the conclusion that it is angina. Indeed, a pain that takes its jK)iiil df departure at llic stcnud end of the fourth left interspace or iji tlie fifth left intersj)ace below the breast, whatever ANGINA PECTORIS G55 be its direction of radiation, is more likely to be an intercostal neuralgia, since the agonizing suffering meriting the name .angina pectoris is most frequently substernal. MoreoV'Cr, in cases of in- tercostal neuralgia there are usually well-defined tender spots cor- resi)onding to the points of origin of the pain. Another character- istic of these intercostal neuralgias is their coming like a sudden stab or thrust, and then leaving as quickly, the points where they aj)peared being sore to the touch. When, as in some instances, the pain is permanent or is continuous, with exacerbations and remis- sions, the very length of the attack stamps it as intercostal neural- gia and not angina pectoris. Moreover, these jjains are most frequently met with in anae- mic, neurasthenic, or otherwise neurotic individuals, or such as present symptoms of gastric disorder, and although by no means limited to the female sex, they are more frequent in women than in men, and generally in such as have not yet reached the age at which vascular degenerations are to be expected. In most cases attention to the points just mentioned enables one to readily differ- entiate intercostal neuralgias from the true heart-pain of angina. It is far otherwise, however, with those attacks of prsecordial pain which display the features of true angina pectoris, yet which in reality do not belong to that class. In other words, is it Heberden's angina with its possibility of sudden death ? or is the pain a pseudo-angina, and hence not of the same serious import ? The answer to these queries is to be found in the consideration of the following points: (1) the age and sex of the individual, (2) the state of the arteries and heart, (3) the influence of effort in evoking a paroxysm. Attacks of prsecordial pain that occur in young persons, no matter how closely they resemble coronary angina, are presumably symptomatic of irritation in some other organ than the heart, and if such attacks are in women the presumption is the stronger that they are false angina. If, on the contrary, they occur at an age when vascular degeneration is common, they are much more likely to be of the grave kind, even though they occur in females. The detection of stiff arteries or of signs of heart-disease is in favour of true angina, and jet pain of visceral disturbance may occur in women past forty with hypertrophied hearts, particularly at the menopause or in such as have suffered all their life from 656 DISEASES OP THE HEART constipation and defective elimination. The same thing may be said of young persons of either sex who long before they reach forty are victims of aortic valvular disease. Consequently in all such cases particular attention is to be paid to the influence of pli^'sical exertion over the attacks of pain. If the initial paroxysm took place during exercise, if the pain is aroused by a hurried walk or by walking after a meal or against a cold damp wind, if it compels the patient to stop in his tracks and remain standing until it passes away, it is in all probability a true angina. If, on the other hand, the person is able to con- tinue his walk, if he sits or lies down, instead of standing, during the acme of the pain, and if he is restless, moaning, and throwing himself about, the attack is probably one of pseudo-angina pec- toris. In cases of a mixed nature described by Huchard, in which cardiac or vascular disease is complicated with- attacks of pain of an hysterical nature, there is often great difficulty of diagnosis. Their precise nature can only be determined by noting carefully the influence of effort in provoking the seizures and by the discov- ery of the stigmata of hysteria. Furthermore, in attempting to distinguish the false from the true angina, one should never forget that the occurrence of pain alone is not sufficient for a trustworthy diagnosis, but that the symptom-complex of pain, constriction of the chest and a sense of impending death, is essential. Pain is the paramount sensation, but in typical coronary angina there is more or less blending of the other two. There are doubtless horder-line cases, as they may be called, in which it is impossible to assert positively the real nature of the pain, especially in elderly well-to-do males with stiff arteries, yet in whom constriction and the feeling of overhanging death are wanting or not pronounced. If, on the other hand, the patient is young and a female and the two symptoms just men- tioned are absent, tlie pain may quite safely be set down as a false angina pectoris. Finally, the pathological condition underlying the angina is to be determined so far as possible. Thickened arteries in a person past forty and signs of sclerosis of the aorta should be carefully sought for. Curschmann has pointed out that tlic elongation and widening of the arch incident to sclerotic changes may be recog- ■^ ANGINA PECTORIS 657 nised by careful study of the cervical arteries. In the fossa jugu- laris, particularly during the act of swallowing, may be seen, or, still better, felt the pulsation of the transverse portion of the aorta, while the pulsation of the subclavians is situated abnor- mally high and the carotids arch unnaturally forward and feel stiff and perhaps slightly irregular. There may be slight dulness at right of the sternum, appreciable only upon deep percussion, and the second aortic tone is sharp and ringing. The detection of such signs would strongly support the conclusion that the angina was due to coronary degeneration, and was therefore most grave. Musser has reported a series of cases in which there was typi- cal anginal seizures so long as the left ventricle was hypertrophied, yet in which with supervention of dilatation the attacks of pain disappeared. These observations have led Musser to conclude that in some cases angina pectoris is due to increased intracardiac blood-pressure. In all such instances the exact nature of the underlying condition cannot be made with certainty, and one must content himself with the diagnosis of the angina and of the car- diac condition without attempting to do more than speculate on the connection between the two. Prognosis. — As has been repeatedly stated, there is always a possibility, and, according to Huchard, a strong probability of sudden death in a paroxysm of angina pectoris. Even if the patient does not succumb during an attack, the complaint is in- curable. He should be advised, therefore, concerning the gravity of his affection, and his immediate family should be warned of the likelihood of a fatal termination. How long a patient is likely to live, subject to these attacks, is a matter of too great uncertainty for an expression of opinion by a prudent physician. It is always well to reassure the sufferer, however, by the state- ment that patients have been known to experience the symptom for a long term of years, and that its severity and the frequency of its occurrence are likely to be modified by appropriate medical treatment and by the care exercised by the patient. Other things being equal, it may be said that the more severe the attacks the greater the danger of death. Also, the more easily the paroxysms are evoked, the more extensive is the coronary ob- struction, and the graver the complaint. Increasing frequency of 48 658 DISEASES OF THE HEART recurrence is likewise of evil import. On the contrary, the prog- nosis may be said to improve in proi)ortion as the attacks become less severe and the intervals between them longer. According to Powell's assumption, previously mentioned, the prognosis should be better when relief is afforded by slow walking, but the case I have cited of the attorney proves the contrary. Moreover, in the case of my other patient his condition grew stead- ily worse in spite of his ability to endure the exercises to which he resorted in the vain hope of improving his general health, since his attacks of pain became more frequent if not more intense. Treatment. — This includes, first, measures addressed to the relief of the paroxysms, and second, the management of the pa- tient's daily life during the intervals between the seizures, with a view if possible to lessening their frequency and severity. The treatment of the attacks has already been considered in the chap- ter dealing with myocardial diseases secondary to coronary scle- rosis, but may be again discussed at this time at somewhat greater length. Very many and divers remedies have been used either solely to relieve the pain, or to strengthen and regulate the heart's action, and are therefore either anodynes or stimulants. Inhalations of chloroform and ether, Hoffman's anodyne, aromatic spirits of ammonia, opiates, carminative draughts, such were the measures relied upon prior to the discovery and introduction by Richardson and Lauder Brunton of nitrite of amyl. Two medicaments which in the experience of the profession the world over have proved of tlie liighest value in controlling the attacks of angina pectoris, and now universally employed, are the nitrites and opium. The action of the nitrite of sodium is too slow, and therefore Ave have recourse either to the inhalation of a few drops of nitrite of amyl, or to a minim of a 1-per-cent solution of nitroglycerin dropped on the tongue. If amyl nitrite is preferred, it should be carried about by the patient in the form of nitrite-of-amyl pearls, containing 3 to 5 minims each of the remedy. Kept in this way the drug does not lose strength. So soon as the patient perceives his pain a pearl is to be crushed in the handkerchief, or a few drops from a vial may be poured thereon and the fumes inhaled, or the suf- ferer may breathe them directly from the vial. The action of the remedy is usually very prompt, rarely failing to afford relief. ANGINA PECTORIS 659 There is usually no danger attending its use; at the most, only a dull headache is produced. If nitroglycerin be preferred, it is most conveniently and usually administered in the form of a tablet triturate containing 1 minim of a 1-per-cent solution. If the tablet is dissolved on the tongue instead of being swallowed, its effect is more promptly induced. This is especially the case if the occasion for its use is soon after the taking of food. The remedy can also be dropped on the tongue or taken in a swallow of water when the solution is preferred, but this method is not only less convenient, but it necessitates the loss of valuable time, when seconds of agony seem like hours to the sufferer. Abatement or cessation of the attack generally takes place in a few seconds ; but should this not be the case a second or even a third tablet may be employed at intervals of two or three minutes. Special indications for one or another of these remedies are found in pallor of the countenance and a small and tense pulse, whether slow or accelerated, regular or irregular, and intermittent or not, and in other signs of arterial spasm. The nitrites are essentially vaso-dilators, and stimulate the heart only indirectly through their dilating influence on the arterioles. Through their action, the wiry, and it may be slow, pulse grows softer, fuller, and more rapid, while at the same time there may be felt some constriction of the throat and tense or throbbing headache, spnptoms which to the patient are of small moment in comparison with the relief from his frightful agony. It has generally been my observation that in elderly individ- uals with sclerosis of the temporal, and presumably therefore of the cerebral arteries, the head symptoms occasioned by the nitrites are far less pronounced than in younger persons whose vessels are less stiff, and hence more responsive to the action of the drug. When phenomena of vascular spasm are absent or when relief does not promptly follow the use of the nitrites, recourse would better be had to opium in some form. A method of administration that yields speedy results is indicated, and therefore it is best to give morphine hypodermically and in a dose that will suffice without repetition — e. g., ^ or even -| of a grain. X The lady to whom reference has been repeatedly made was compelled to resort to both nitroglycerin and morphine, and in addition frequently took a teaspoonful of sulphuric ether in sweet- H60 DISEASES OP THE HEART eiied iec-watcr. Ivclief was not obtained initil under their com- bined effect the pnlse became fnll and bonnding, and the skin, pre- viously cold and perspiring, grew flushed and warm. In her case there was extreme aortic stenosis with, it may be, coronary scle- rosis, and a more decided stimulation of the heart was required than was indirectly occasioned by nitroglycerin. Under the influ- ence of the ether, cardiac contractions are both invigorated and quickened, so that the coronaries previously dilated by nitroglyc- erin receive a more adequate supply of blood. In comparatively mild cases relief may sometimes be obtained by the administration of diff'usible stimulants, as aromatic spirits of ammonia, Hoffman's anodyne, camphor, whisky, or brandy, and their effect is hastened by being taken in hot water. Elixir of valerianate of anmionia in tcaspoonful doses is a particularly eligible ])reparation, and admirably meets the indications when rapid stimulation is required. Any one of these remedies may be administered directly following the nitroglycerin and Mill sometimes obviate the necessity for morphine, a consideration of some importance in elderly individuals who, as well known, arc sometimes peculiarly sensitive to this drug. In nocturnal attacks, which are apt to be severe and prolonged, it is often well to supplement the action of medicinal agents by the application of hot bottles to the extremities or by heat to the pnpcordium, the epigastrium, or between the shoulders. There is no indication during an attack for the use of digitalis and strych- nine, for not only is their action too slow, but when arterial S])asm is responsible for the paroxysm the former will do harm. Aco- nite and veratrum viride should never be employed at such a time. During the intervals between attacks the daily life of the pa- tient should be so regulated as to minimize if possible both the fre- quency and severity of his seizures. If the complaint has existed for some time the sufferer is likely to have learned by experience that moderation in tlu; matter of exercise is absolutely indispensa- ble to iiiiiinuiity from his attacks. Nevertheless it may be well to caution him against undue exposure during cold and inclement weather, or going about insufticiently clad, against carrying heavy hand l)aggage or parcels, against attem])ting to walk soon aft^r a meal, hurrying to catch a train or street car, etc. He should l)o explicitly instructed to make use of surface transportation in pref- ANGINA PECTORIS OGl oreiK'o to elevated roads, which have to be reached by long flights of stairs, since the inclination to hasten Tip the last few steps as the train is heard approaching is almost irresistible, and such a spurt may precipitate an attack. Patients should also be in- structed concerning the harmfulness of immoderate coitus, fits of passion, overeating, the too free indulgence in tobacco and alco- holic stimulants, of becoming excessively fatigued, etc. The hands and feet should be kept warmly covered, and it is often well for these patients to wear a chest-protector both front and back. Those who can afford to pass the inclement seasons in a warm, equable climate should be advised to. do so, since they can there take outdoor exercise without fear of encountering cold winds and of contracting attacks of bronchitis. Sufferers from coronary angina have habitually high and sus- tained arterial tension, and as it is sudden and unexpected aug- mentation of this tension which often precipitates a paroxysm, it is essential that their blood-pressure be lowered. This can usually be accomplished, in a measure at least, by revision of the dietary — that is, by the restriction, or in some instances by the exclusion, of meats and the substitution of a largely vegetable dietary. E,umpf, of Hamburg, interdicts the use of foods rich in lime- salts, as eggs, milk, cheese, spinach, etc. Theoretically, such a restriction is called for when there is arteriosclerosis, but practi- cally, it will be found difficult to adequately nourish the patient if all foods rich in phosphates as well as meats are excluded. Turthermore, a too restricted dietary grows monotonous and leads to anorexia and feeble digestion. The principles laid down for the dietary of cases of myocar- dial degeneration are equally applicable to these patients, and therefore the reader is referred to that chapter for details. Should arterial tension be not sufficiently reduced by regulation of the diet, then attempts must be made to accomplish this in other ways. To this end appropriate doses of nitroglycerin may be given every two or three hours during the day, or moderate doses of an iodide salt, three times daily, may accomplish the result. That such is the effect of iodine internally is generally held, and yet Komberg asserts that both clinical observation and experiment show this not to be the case. In some cases it may not be necessary to give nitroglycerin daily, but only on those days when the patient finds 662 DISEASES OF THE HEART walking particularly difficult, or there is a raw easterly wind. I have known striking amelioration of the patient's condition follow regulation of the diet, together with the prolonged use of nitro- glycerin and iodide of soda. Men addicted to the use of tobacco should be informed of its baneful effects and advised to abandon the habit altogether. If this is not acceded to, then the matter may be compromised by the patient's being allowed to smoke only mild domestic cigars. This will sometimes affect a cure of the tobacco habit in those who have been accustomed to choice Ilavanas. In cases that have begun to manifest cardiac insufficiency or in which abnormally high blood-pressure threatens to soon over- power the heart, attempts must be made to restore cardiac strength or at least to stay its further decline. To this end recourse may be had to the usual heart-tonics. Strophanthus appears to me prefer- able to digitalis by reason of its inferior constricting effect on the arterioles, a virtue of the drug to which Frazer originally directed attention. If digitalis is selected, then its vaso-constrictor effect must be offset by the iodides or nitroglycerin. Strychnine and arsenious acid are also of benefit, and the former may be continued in moderate doses for many months. Strychnine is generally be- lieved to raise pulse-tension, but this action is slight and not to be weighed in the balance as against its value as a heart-tonic. The one method of treatment that is particularly adapted to this class of patients at this time are the so-called resistance exer- cises, and very favourable results have been reported from their employment in angina pectoris. Theoretical considerations, and indeed actual experience, indicate that benefit is also likely to fol- low the careful use of the saline baths with artificial as well as natural waters. iN^evertheless, the lady whose case has been so often cited in these pages experienced her first severe paroxysm of angina pectoris shortly after her first bath at Bad Nauheim upon having been wheeled to her hotel, and then attempting to walk slowly from her wheel-chair to the elevator on her way to her apartments. Subsequent baths, however, were not followed by a similar distressful effect. Details concerning this mode of treat- ment are found elsewhere. (See chapter on Treatment of Valvu- lar Disease in General.) CHAPTER XXVI SYPHILIS OF THE MYOCARDIUM — NEW GROWTHS IN THE MYOCARDIUM— ATROPHY OF THE HEART —SEGMENTATION AND FRAGMENTATION OF THE MYOCARDIUM I. SYPHILIS OF THE MYOCARDIUM Morbid Ana-tomy. — The most common myocardial mani- festation of syphilitic infection consists in fatty degeneration of the cardiac muscle. This is not different in any way from fatty degeneration from other causes, and so is not recognisable except in the presence of other evidences of the disease. Associated with the arteriosclerosis of syphilis is a diffuse interstitial myocarditis, which is also usually classed as a luetic lesion. It seems probable, however, that in many cases the induration is due to the presence of the arterial disease, rather than to the direct action of the syphilitic poison. Gumma of the heart is very rare, and especially so in the con- genital form of the affection. The part of the heart most com- monly affected is the wall of the left ventricle. The gummata appear as soft grayish masses surrounded by hyperplastic fibrous tissue, or if older, as dry caseous areas of a yellowish white colour. Very rarely a softening gumma may rupture into one of the cavi- ties of the heart. Etiology. — Syphilis attacks the myocardium only in the ter- tiary period of the disease, and after a lapse of five or ten years or longer following the initial sore. It is not confined to either sex, but appears to have been rather more frequently discovered in males. As regards age, it may be said to be more frequent at or after middle life, rarely in childhood for the reason that the dis- ease is generally acquired, not congenital. 663 664 DISEASES OF THE HEART Symptoms. — Xot only is heart-syphilis a comparatively rare affection, having been for the first time detected by Ricord, but its clinical recognition is still less frequent than is its post-mortem discovery. This is due to the fact of its possessing no pathogno- monic features as yet recognised. Not only have patients, in whom this myocardial disease has been discovered after death, been known to exhibit no clinical evidence of heart-affection during life, but when symptoms were present they were found on analysis to differ in nowise from those displayed by persons suffering from other non-syphilitic forms of myocardial degeneration. Most ob- servers agree in this statement that the cardiac action is likely to be disordered. This is generally though not invariably acceler- ated, and some authors, as Semmola, lay great stress on arrhyth- mia and acceleration of the pulse. Another symptom that has been noted is an indescribable prircordial distress which may or may not amount to actual pain. Philips has called attention to angina-like pain as having been present in one or two cases ob- served by him. This symptom was remarkably distressing on one occasion in a professional man, who subsequently died suddenly and in whom Philips found syphilis of the myocardium at the autopsy. Cardiac dyspnoea has also been complained of by some patients, but there was nothing about the difficulty of breathing that was in anywise peculiar. Upon examination of the patient there may or may not be evidence of specific infection, such as old scars on the skin or mucous membranes, glandular induration, gummata, etc., and the arterial system may or may not furnish evidence of sclerosis. Physical examination of the heart is not infrequently negative, while in some cases there are signs of cardiac disease. When these are present, they are apt to be those of dilatation with feebleness or altered quality of the sounds, ^rurniurs are not ])rcsent as a rule unless as an accidental complication or due to the dilatation — i. e., to relative insufficiency of the mitral valves, for example. Diagnosis. — Unless there is a clear history of previous sypliililic infection the diagnosis of myocardial syphilis is not pos- sible with certainty. On the other hand, even with such a history, one is not always justified in making the diagnosis merely because an individual of middle age disjilays cardiac symptoms. They may be due to changes in the heart-muscle incident to his age and SYPHILIS 0^ THE MYOCARDIUM 665 not at all to sypliilis. If one cannot discover sypbilides of one sort or another, he should give the patient the benefit of the doubt until the futility of all other modes of treatment has been proved. The association of symptoms and signs of myocardial disease with a history and with clearly demonstrable lesions of the specific in- fection renders the existence of syphilis of the heart-wall very probable. If the cardiac manifestations occur in an individual not yet fifty years of age the supposition is greatly strengthened. Very often the diagnosis will have to be deferred until the results of specific treatment have been ascertained. Except by men of wide exj)erience in this particular line of diseases the diagnosis of this cardiac affection must necessarily be a matter of guesswork in most instances. The clinical obscurity enveloping this affection is shown by the relative frequency with which it is found at the autopsy as compared with its intra vitani recognitioji. Prognosis. — This may be said to be good provided the disease is recognised in time to institute proper treatment. In undiag- nosed cases the prognosis is bad, since they are likely to terminate fatally. Death is apt to be sudden and unexpected. I know of no statistics going to show how long may be the duration of the dis- ease, but it is probably a very chronic affection, having existed years, it may be, before the coming on of cardiac symptoms. The rapidity with which death is likely to follow the development of symptoms is likewise a matter of individual difference depending on the extent of the myocardial change, which is itself a matter we cannot obtain definite knowledge of during life. If the heart be extensively dilated, its action greatly disturbed, and the pa- tient's symptoms pronounced, the prognosis is grave, and even specific treatment is not likely to do more than effect a partial recovery. Treatment. — This, it needs hardly be stated, is the employ- ment of iodides, with or without mercurials, as the physician de- termines. Being a tertiary manifestation, reliance is to be placed chiefly on the iodides. Ordinarily other remedies of the class of cardiac tonics are not necessary. But here again the medical ad- viser must decide. Their employment is symptomatic, and digi- talis in conjunction with the specific medication may be of service in cases in which the action of the heart is much deranged and the patient's distress from dyspnoea is considerable. What has 666 DISEASES OF THE HEART been said in other chapters on the hygienic management of heart patients applies equally to these, so long as cardiac power is de- ficient. II. NEW GROWTHS IN THE MYOCARDIUM Under this head are included various tumours and parasites. They are rare, some of them as parasites being excessively so, and aside from gummata just considered possess interest for the pathologist rather than the clinician. They will therefore receive only brief mention in this work. Tubercles of the myocardium may be encountered as miliary nodules scattered through the heart-muscle, or still more rarely as caseous masses. The affection may also be declared as an inter- stitial myocarditis, which, however, possesses no distinctive fea- tures. Parasites and cysts in this situation are still more infrequent and usually fail to declare their presence by either subjective or objective symptoms. Thus Knaggs, in the Lancet of 1896, vol. i, p. 29, narates the instance of a man who died suddenly, and had not previously manifested evidence of cardiac disease, yet in the wall of whose left ventricle a hydatid cyst was found at the necropsy. Of other growths in the myocardium cancer is the most fre- quent, and yet this is absolutely very uncommon. Lipoma and fibroma have also been met with, but are still more rare. Ma- lignant tumours occur in either the primary or secondary form, but of the two the latter is much the more frequent. The rarity of the primary form may be judged of by Gibson's statement that in 21,954 autopsies mentioned by Koehler, Tanchon, and Willigk there were only 21 instances of heart-cancer, while Petit found but 7 in the literature. From Bodenheimer's analysis of 45 cases of secondary can- cer, also cited by Gibson, it appears that the growth occurs most often as multiple nodules scattered throughout the myocardium, since it was limited to the wall of the left ventricle but seven times, to that of the right ventricle three times, and to the right auricle twice. It may occur at any age, even in infancy, but most often after forty-five, and is more frequent in males. The clinical manifestations of myocardial cancer are too in- ATROPHY OF THE HEART 667 definite and uncertain to permit an intra-vitam diagnosis. The heart may be irregular and feeble in action, may furnish percus- sion evidence of dilatation, but in such findings there is nothing to distinguish these from ordinary cases of myocardial degen- eration. The prognosis is unfavourable, and yet for the most part life is destroyed in secondary cases by the original disease. In pri- mary heart-cancer the tenure of life will depend largely upon the seat and nature of the tumour. Treatment is of course purely symptomatic, since if the ac- tion of the heart is disordered and the real cause of the disorder is unsuspected or not, physicians find themselves limited to the administration of heart-tonics. III. ATROPHY OF THE HEART By atrophy of the heart is meant a diminution of the organ in weight and size. The condition may be partial or general. The former is exemplified in the smallness of the left ventricle seen in extreme mitral stenosis. General atrophy may be the result of age, when it is spoken of as physiological, or the effect of disease — i. e., pathological. Congenital smallness of the heart is sometimes designated as atrophy, but, as preferred by Virchow, should be properly termed hypoplasia of the heart. It is usually associated with con- genital smallness of the genitalia. Morbid Anatomy. — The atrophied heart is of a brownish red or yellowish colour, often firmer than normal, sometimes pre- senting a wrinkled appearance, owing to puckering of the epicar- dium (like a withered pear, Eichhorst); and beneath the micro- scope the individual muscle-fibres are seen to be diminished in size, their transverse striation obscured and stained by a deposit of brown or yellow pigment near their nuclei. Adipose tissue is everywhere absent. Etiology. — Various causes of general cardiac atrophy are enumerated, but those most often and powerfully operative are conditions which induce marasmus — i. e., pulmonary phthisis, cancer, diabetes, and chronic suppuration, as from disease of a bone. Thus W. Church is said to have obtained from the body of a woman who died of slow starvation in consequence of pylorus 668 DISEASES OF THE HEART obstruction by eareinoivia a heart tliat woii>,lio(l only P)-^^ oinices. Of ]71 cases of phthisis analyzed by (^iiain the heart was atro- phied in 54.4 per cent, ^\diile Engel is reported to have found cardiac atrophy in about 25 per cent of males who died of the same wasting disease between the ages of twenty-eight and thirty. It may here be stated that, according to Wunderlich, a heart is to be regarded as atrophied if it weighs less than 200 grammes. Symptoms. — The clinical manifestations of atrophy of the myocardium are obscured by those of the general complaint, but may be said to be such as always characterize cardiac inadequacy — i. e., rapidity and weakness of the pulse, feebleness of cardiac impulse and sounds, without, however, signs of .venous stasis other than slight oedema. As a matter of fact this oedema is due to mal- nutrition rather than to stasis. Diagnosis. — The diagnosis is likewise obscured by the signs of the primary disease. It rests on the determination by percus- sion, or better by the fluoroscoijc, of marked decrease in the size of the heart, together with evidence of prolonged and extreme emaciation. Prognosis. — The prognosis is that of the general cachexia, and yet a wasted lieart may become so feeble as to cause death. Treatment. — The treatment is that of the primary disorder, since it can do but little good to administer heart-tonics. IV. SEGMENTATION AND FRAGMENTATION OF THE MYOCARDIUM The precise nature of this condition has been, and still is, a matter of dispute. Opinion is still unsettled as regards its causa- tion, the time of its occurrence, whether prior to or during the death agony, and consequently on the question whether or not it possesses any practical clinical importance. Renaut first de- scribed it as a segmentation of the heart-muscle due to chemical and nutritional changes and assigned to it definite clinical fea- tures. His original view was that the muscle-fibres became broken up, segmented, in consequence of softening of the cement sub- stance liolding the cells together. Various French and German writers, notably Przewoski and Klein and l)rowicz, confirmed Renaut's observations and indorsed his views. Others, chiefly von Recklinghausen and Tedeschi, discovered disintegration of SEGMENTATION AND FRAGMENTATION OF THE MYOCARDIUM 669 the cardiac muscle-libres, but declared it was due to rupture, i. e., fragmentation of the cells, which occurred during the death agony in consequence of overstimulation and irregular contractions. Although they found fragmentation in otherwise normal hearts of individuals who had died suddenly by violence or other- wise, still in the majority of instances it was in hearts that showed chronic fibrous and fatty change, or the fragmentation was discov- ered in persons who had suffered from acute infections or lesions of the central nervous system. Indeed, Tedeschi found the condi- tion in 48 per cent of 236 cases of death from all sorts of causes. The statements of von Recklinghausen caused Eenaut to modify his views somewhat, and in 1804, at the first French Congress for Internal Medicine, he described the process as due to swelling, " gigantism " of the muscle-cells and alteration of the intercon- tractile plasma which render the cells brittle and disposed to fracture, while at the same time there is softening of the cement that leads to segmentation. Eenaut still held, therefore, to his assertion that the process constitutes a distinct and recognisable clinical entity. Since that time the subject has been discussed by numerous observers, chiefly in France and Germany, English and Ameri- can writers have had little or nothing to say on the subject, be- cause, it may be, of its being still sub judice, and as yet not be- lieved to possess practical value to the clinician. The only impor- tant contributions that have, so far as I know, appeared in this country at this present writing, are by Ludwig Hektoen and John Bruce MacCallum. The former made a careful study of a large number of hearts from lower animals, both small and large, and from over 100 human beings that had died suddenly as a result of violence, or slowly or suddenly in consequence of a great variety of acute and chronic affections, some of them cases of either in- dependent or secondary heart-disease. Hektoen's observations agreed with those of writers on the Continent as respects the fre- quency with which dissociation of the heart-muscle occurs in both sexes, at all ages, in all sorts of acute infectious and chronic dis- eases without associated cardiac lesions and in hearts manifest- ing the ordinary myocardial degenerations, hypertrophy and atroj^hy. Thus, of 190 cases of deaths from a great variety of causes 670 DISEASES OF THE HEART and in both sexes, lie found segmentation in G5.78 per cent, while in 10 instances of traumatic and usually instantaneous death the condition was present in all. Hektoen states that whenever seg- mentation was present to any extent there was also more or less fragmentation. It is his opinion that segmentation is due to a disproportion between tlie violence of fibrillar contractions and the cohesive strength of the cement substance, and thinks that in- travital alterati(m of the muscle-cells may predispose to cement- softening and consequent segmentation ; it is not impossible, there- fore, for excessive cardiac contractions during excitement, coitus, etc., to lead to sudden death through segmentation of the myocar- dium. The symptoms attributed by Renaut to disintegration of the muscle-fibres are disordered action and feeble apex-impulse of the heart, some increase in the area of cardiac dulness, an uncertain systolic murmur, and it may be slight a'dema. These are, how- ever, not at all peculiar to segmented hearts, but are observed in hearts that have undergone other forms of degeneration. It is strange, therefore, that Renaut and his pupils should consider the process susceptible of clinical recognition. I shall not devote more space to its consideration, but allow the following sentences, taken from Plektoen's paper, to sum up the whole matter. " All the other authors regard general and focal segmentation as an acci- dental or secondary phenomenon occurring in the course of infections and intoxications in connection with tlie primary and secondary lesions of asystolic hearts, and with fatal traumatism. It constitutes an episode in the course of the principal affection. While it possesses an anatomical individuality, it is so common that it would be difficult to say in what disease it would surely be absent after, say, the twentieth year, and it would take a very long time to enumerate all the diseases in Avhicli it has been found present." CHAPTER XXYII PEDUNCULATED AND BALL-THROMBI OF THE HEART Among the tumours of the heart may be included those rare formations which are found in the cardiac cavities and are in reality thrombi. They differ from cardiac thrombosis (marantic) in the chronicity of their development, the changes they undergo, and in their clinical history, since they do not give rise to emboli. Like vascular thrombi, some of them undergo organization, and when attached to the inner surface of the heart-wall by a pedicle are known as pedunculated thrombi or true polypi of the heart. Others, called hall-thrombi, have either become detached from their pedicle, or having been formed by the deposition of suc- cessive layers of fibrin upon a primary nucleus, and unattached, roll about free in the chamber where they are formed. Both varieties are exceedingly rare, but of the two, ball-thrombi have been much less frequently encountered. At the Reunion of Russian Physicians at St. Petersburg in 1893, in honour of Pirogoff, Pawlowski reported a case of true heart polypus that had come under his observation. In this paper he stated that diligent research in the literature up to that date had enabled him to collect only 25 cases, including his own. Wil- liam Welch, however, in his admirable article on cardiac throm- bosis in Allbutt's System of Medicine, states that he has found 8 others in the literature, making 33 in all. Small as is this num- ber, that of ball-thrombi is still less. Von Ziemssen, in the report of a case at the Vienna meeting of the German Congress for In- ternal Medicine in 1890, stated that he had been able to collect only 4 cases besides his own. His research for published cases had been superficial, however, for Welch mentions 4 cases, with a reference to a fifth, that had been reported in England prior even to von Recklinghausen's, which by German authors was consid- 671 672 DISEASES OF THE HEART ered the earliest recorded. Since von Ziemssen's there have been others reported, so that uj) to date there have been 20 published instances of ball-throHd)i. Sonic oi these I had myself discovered in the literatniic before I had the good fortune to peruse Welch's article. The others have been taken from Welch's list. The en- tire number will be found at the close of this chapter. Pedunculated thrombi may be found in any of the cardiac cavities excepting the right ventricle, although by far most fre- quently in the left auricle. Twenty-five were in this cavity, 4 in the right auricle, and a like number in the left ventricle. The point of attachment is various, although the interauricular sa^p- tum seems to be the most frequent seat of the polypi, near the foramen ovale. Of Pawlowski's list of cases, 12 arose from the sseptum, 5 being from the fossa ovalis. Two, including Paw- lowski's, were attached to the posterior wall of the left auricle, 2 within the appendix, and 1 to the mitral valve. In the other cases the precise point of attachment is not stated. In size and form the polypi diifer, being likened to a pear, a small heart, a cone, a bullet, a walnut, and a hen's egg, the average comparison being to a walnijt. The pedicle is generally compact and strong, and in most cases the polyp is covered by a thin membrane thought to be an extension of the endocardium (Pawlowski). He also states that, according to Wilkinson King, some polypi could be injected through the coronary vessels, while in others this did not succeed. In some of the r(>corded cases the tumours contained calcareous deposits, others were cystic. In all instances of these heart- thrombi there is disease, usually narrowing, at the auriculo-ven- tricular orifice or some other condition, as dilatation, that has led to stagnation of the blood in the cardiac cavity containing the tumour. In Pawlowski's case there was mitral stenosis of an extreme degree. Von Ziemssen states that ImlJ-thromhi are for the most part of the size of a walnut, spherical, smooth, with no rounded cor- ners, and showing no trace of a pedicle. In liis case the mass was beautifully round and smooth, as if turned by machinery, and ex- hibited numerous indentations upon its surface. The thrombus was firm, and ii))oii being sliced into sections sliowcd successive layers of fibrin-f 'S '^_: 5p. a^ g^ a 3 o § o g g "« g'sgs go's ■2 2 d J- s ,- 3 S ^ ^ J- " ^ p ^ ^^ s s ^ ^ -4^ Cl '^^ "a. ^ ti ^"q., OJ ^ OJ "Oh^ pSri ^, -;;; r-. T- ^, O.' .> •35 ^'S Si gj g -i^ g OJ a^ g cti^?i-r ftiii (7} g /)ccir/j(Z}032?^ C/JCO (5 cAj ^ CO 5 ^/i 2 £ 2° o o o<3 o ^ -^ ^ ^ fq 1) C- 05 "* T)* lo o iffl 00 -co lO • O Ci -* C5 lO CO TtH l-H CD CO ICCO '^ ^ -CO CO • CO CO t- to CO I- Sf3 s p;p:SS^E::; :£:; S :^»"^'t^^* r ^• T-H T)5 T)H s ^ £,£> J§g -^ ■'I com •Ti 03 ^ ., CQ PQ ^ M k;cio.;^-GO ^ ci ;^, ^ C:,M CO ^- «5 . cS "3 q ^ 03 d 't3 'd r-f a d _: ■^ ;zi pa pq oi , ., ^ ;-) ■^ .-h' ^ O o-j <^'> S 00 -« „ • . ^<^^ r-l CO GO =1 .o o to '^ ;:i .22 « 3 ji s a '"^00 ^C5 OJ C? c3 '-' J> l-H 03 ^co 03 03 '^ _; ^ ^T-l 1-1 • |g||^oco| H g-Si^". . s g g^ H 03 ■713 ■^ CO 4^ g^ r . G«D 05 O -rH oi CO '^ id T-H l-H 1-1 tH T-H 1-1 1-1 1-1 1-1 C 56.2 3i Ol • • CO ^ O CO • • CO CO '^ ^.y-s 00 00 • • 00 00 o-i r-i T-H - - ^~' 1— 1 • 4J S ai coco CO CO lO lO iO lO O CO 00 O^ t- lO to CO O-JOT CO 000 tH 1-H 1— Ii-Hi-Hi-HtHi-Hi-Hi— ( 1 680 DISEASES OF THE HEART ticated. The associated valve-lesion will cause death eventually, and we can do no more than ameliorate the patient's distress. Indeed, we may deem ourselves fortunate if we can accomplish this. Bibliography of Cases of Ball-Thrombi Arnold. Bcitriige zur pathologisclien Anatoniie und zur iillgemcincn Patho- logie, Jena, 1890. BosTROEM. Deutsches Archiv fur klin. Med., 1895, Iv, p. 219. EwART. Trans. Clin. Soc, London, 1896-97, xxx, p. 190. IlARTiLL. Brit. Med. Jour., May 22, 1886, p. 973. Hertz. Deutsches Archiv flir klin. Med., Bd. xxxvii, S. 74. OsLER. Johns Hopkins Hospital Reports, 1890, ii, p. 56. Montreal Med. Jour., 1897, XXV, p. 729. Pawlowski. Zeitschrift fur klin. Med., 1894, xxvi, p. 482.- Proust. Conipte rendu d. .sc. med. et do l)iologie, 1864, i, p. 41. Recklinghausen, von. Handbuch dcr allg. Path, des Kreislaufs u. d. Ernah- rung, 1883, p. 131. Redtenbacher. Wien. klin. Wocli., 1892, v, p. 689. RoLLESTON. Lancet, 1897, vi, p. 1546. Stance. Arb. a. d. path. Inst, in Gtittingen, Berlin, 1893, S. 232-234. Welch. Allbutt's System of Medicine. Wood. Edinburgh Med. and Surg. Jour., 1814, x, p. 50. Ziemssen, von. Vortrag gehaltcn auf dem IX. Congresse fiir inneren Med. in Wien, 1890, S. 281. CHAPTER XXVIII DEXTROCARDIA This term signifies a transposition of the heart into the right side of the thorax. This condition may be congenital or acquired. Most congenital displacements of the heart occasionally met with possess interest chiefly for the pathologist. The organ may be situated in the cervical region, within the abdominal cavity or upon the exterior of the chest (ectopia cordis). CONGENITAL DEXTROCARDIA This form is the most frequent of all displacements and is of clinical as well as pathological interest, inasmuch as the physi- cian may be called on to determine whether the displacement is pathological or normal to the individual concerned, and therefore devoid of danger. In most instances this abnormal situation of the heart is associated with transposition of the other viscera, a condition which has received the name situs viscerum inversus. That this is not invariable has been noticed by Breschet. The displaced heart occupies the same relative position on the right side as it does normally at the left, while the stomach and spleen are in the right and the liver in the left hypochondrium. The position of the intestines is also reversed, so that the rectum lies in the right instead of in the left iliac fossa. Symptoms. — Congenital dextrocardia occasions no symp- toms unless it be associated with other cardiac anomalies, as some- times is the case. It is stated, however, that patients with this displacement of the heart are apt to develop pulmonary tubercu- losis. Apropos of this possibility I recall the case of a Miss A., who applied to me for an examination because she had had her attention directed to the fact that her heart pulsated upon her right side, and she desired to learn if it possessed any special im- 681 682 DISEASES OF THE HEART portance. Examination showed the apex-shock was in the fifth right interspace, about 1 inch inside the vertical nipple-line. Car- diac dnlness was of normal extent, and beginning a finger's breadth to the left of the sternnm, reached nearly to the right mamillary line. The heart-sounds were of normal strength and clearness, and were situated at the right of the sternum. Per- cussion of the abdomen showed gastric tympany beneath the right costal arcli and hepatic dnlness in the left hypochondrium. At that time the patient was in perfect health and gave no history of tuberculosis in the family. Yet before two years had elapsed she developed pulmonary tuberculosis, to which she succumbed about a year later. Diagnosis. — The detection of the dextrocardia depends upon the recognition of the cardiac impidse, dnlness, and sounds to the right of the median line and their absence at the left. Its congeni- tal nature is shown by the transposition of the abdominal viscera, which can scarcely be a matter of difficulty of determination. ACQUIRED DEXTROCARDIA Morbid Anatomy. — This form of dextrocardia may be complete, the heart lying entirely within the right half of the thorax, or it may be partial, in which case the organ is situated mainly but not wholly to the right of the median line. As this transposition of the heart is a pathological condition, the other viscera remain in their customary position. The morbid anatom- ical appearances in these cases are found chiefly in the lungs and their investing membranes, since the heart is not necessarily the seat of any other disease than that incident to the torsion of its supports. The organ is fixed at its base by the great vessels, and cannot become displaced in either direction without undergoing more or less rotation upon its long axis. In dextrocardia there must be twisting of the arteries and veins at its l)ase, aud hence authors have speculated on the direction in which the heart must turn to admit of displacement to the right. Sibson maintained that the heart rotates in such manner as to bring the left ventricle to the front and flic riglit chambers to the rcai-, wliilc von Schroetter argued tbat the right ventricle turns towards llie left so that the left ventricle recedes still further into the background. DEXTROCARDIA 683 A inomeut's reflection will ('onvinco one, however, tliat the direction in which the heart rotates is determined hy the displace- ment and twisting of its sn})ports or by the point of attachment of adhesions and the angle in which they pull. In a paper on dex- trocardia, contributed by me in 1888, this question was fully dis- cussed, and I there reported 2 cases which proved conclusively that the heart may rotate in either direction, so that both Sibson and von Schroetter were right. (For details see Medical jSTews, 1884-1888.) The twisting and strain to which the aorta and pulmonary artery are subjected may exert a detrimental effect on the heart. Thus in the case of a child which I reported the aorta was found constricted by the superior vena cava, which was stretched tightly across it, and the narrowing of the aorta thus occasioned had led to dilatation of the left ventricle. It is possible, therefore, for this abnormal and constrained position of the heart to lead to its hypertrophy and dilatation and to constriction as well as stretch- ing of the large vessels at its base. Etiology. — This is found in pathological processes that exert either pressure or traction upon the heart. The former is brought about through the accumulation in the left pleural cavity of air (pneumothorax) or of liquids (pleuritis with effusion and empy- ema). With the absorption or artificial removal of the exuda- tion the heart usually returns to its normal situation, but the formation of pleuritic adhesions and obliteration of the left pleural sac may serve to maintain the organ in its acquired loca- tion. The pressure exerted may be sufficient to push the heart entirely beyond the median line, so that its apex strikes the chest- wall outside the right mamillary line, and Walshe says this may take place wdthin thirty-six hours. Ordinarily the organ is not greatly displaced, and the apex may come to lie at any point between the midsternal line and the right nipple. When the heart is drawn over into the right side, it is through the traction exerted by pleuro-pericardial adhesions acting in con- junction with more or less cirrhosis of the right lung. This was the cause in all three of my cases. The primary cause may be a trauma, or tuberculosis of the lung may be the initial etiological factor. Whatever be the predisposing cause, the pleuritic adhe- sions undergo contraction slowlv, and a considerable length of 684 DISEASES OP THE HEART time must elapse before the dextrocardia is completed. In this class of cases, moreover, are seen the most extreme examples of cardiac transposition, the heart assuming a nearly horizontal posi- tion in its new situation. It lies, of course, under these condi- tions, immediately beneath the anterior chest-wall and is uncov- ered by hmir. Symptoms. — These may consist of those phenomena ordi- narily associated with venous stasis — i. e., cyanosis, dyspnoea, fee- bleness and rapidity of the pulse, palpitation, and after a time oedema, scantiness of the urine^ and other evidences of visceral congestion, or the clinical picture may be rather that of the pul- monary aifection with or without symptoms . of cardiac insuffi- ciency. The symptoms may be of a severe type throughout, but more frequently the course of the disease is protracted, and the symptoms are mild, depending upon the nature of the associated pulmonary aifection. In a word, there is nothing distinctive of the clinical history of these cases unless it be their chronicity. Diagnosis. — The detection of the fact of the dextrocardia can hardly be a matter of difficulty, particularly in cases in which it is associated with or dependent upon chronic disease of the right lung. When due to accumulaticm of air or liquid in the left pleu- ral cavity with compensatory emphysema of the right lung, the condition may escape the detection of the careless observer. It is conceivable also that an aneurysm pulsating low down and to the right of the sternum, or a pulsating empyema between the ster- num and right nipple, might mislead the inexperienced or super- ficial examiner. The history of the case and careful exploration of the chest ought, however, to protect against so gross an error. Inspection and Palpation. — These disclose pulsation in the region of the right nipple and its absence in its usual situation. Percussion. — This reveals an area of absolute and relative dulness to the right of the sternum having the characteristic out- line of the heart, while a similar area of dulness is absent on the left. Unlike congenital cases, percussion discloses gastric tym- pany and hepatic dulness in their normal position. Auscultation. — This enables one to perceive that, instead of the heart-sounds being audible in their normal situation, they are heard at the right of the median line. The physical signs, by wliicli are recognised the i)ulmonary DEXTROCARDIA 685 diseases that bring about an acquired dextrocardia, do not need to be here stated. If occasionally cardiac murmurs are heard in this class of cases, it is not always easy to determine whether they are organic from valvular disease, or are accidental and due in some way to the alterations in the cardiac walls and large vessels incident to the rotation of the organ. The history of cases of acquired dextro- cardia shows that accidental bruits are not uncommon. For the differentiation of the murmurs one must rely on the rules that have been stated already in the introductory chapter. Prognosis. — In most instances this may be said to be that of the lung condition, and yet in a case of complete acquired dex- trocardia with presumably considerable torsion of the vessels, the condition is likely to shorten the prospect of the patient's life. Nevertheless, one of my patients was alive and in ordinary health fourteen years after my first examination. The prognosis in each case depends upon the evidence or not of cardiac feeble- ness and disordered circulation, all of which signs have been suffi- ciently set forth in previous chapters. Treatment. — This must be based on the indications of each case and the principles that apply to other forms of cardiac in- adequacy. It is needless to remark that nothing can be done for the relief of the dextrocardia in those instances in which it is owing to traction from permanent disease within the right half of the thorax. CHAPTEK XXIX CONGENITAL DISEASES OF THE HEART Some of these possess a pathological rather than a clinical in- terest, since they render extra-iiterinc existence impossible. For a detailed description of snch the reader is referred to works on pathology, (^jngenital cardiac aifections were the object of much interest and even of superstition in the early days of anatomic investigation. It is to Meckel, Bonilland, Rokitansky, Dorsch, Peacock, Knssniaul, and Lcbcrt that the profession is chiefly in- debted for a scientific elucidation of their various modes of de- velopment. Morbid Anatomy. — Of the congenital defects of the heart that are the result of developmental errors, the most frequently found and at the same time the least important clinicall}^, is an increase in the number of cusps in the semilunar valves of the aorta or })ulmonary artery. This condition is more frequent at the pulmonary than at the aortic opening. Four and even five segments have been found. The supernumerary cusps are usu- ally smaller than the others, but the ring may be equally divided between the increased nimiber of segments. The presence of a diminished number is of less frequent occurrence. Two cusps have then become united, leaving no trace of the line of union, or at best a very slight one. According to Osier, this condition is more common at the aortic orifice, but two of his twenty-one instances having occurred at the pulmonary. Osier further states that this defect is an important one, as the conjoined cusjis are very a))t to nndergo sclerotic changes. Stenosis of the puhnonary or aortic orifices may result from the more or less complete fusion of all three cusps (Fig. 78), and this may even ])roceed to complete atresia. The fusion may be the result of fcr-tal endocarditis or developmontMl error. In the former case the valve ])resents mnch the same ai)poarancc as after 686 CONGENITAL DISEASES OF THE HEART 687 postnatal endocarditis. Vegetations may cover the cusps, project into tlie ventricle, or fill the sinuses of Valsalva. At other times, however, the nnited valves may present no signs of endocarditis, being combined to form a funnel, which may show signs of very slight sclerosis. Stenosis or atresia of the auriculo-ventricular orifices is of much less frequent occurrence than of the arterial openings. In either case the congenital disease is more frequent on the right side on account of the more frequent location of foetal endocarditis on that side. Pott says that for one congenital aortic defect there are twenty-five pulmonary and tricuspid. Fig. 105. — Perforate Interventricular Septum. Pulmonary stenosis, already considered in a special chapter, is a by no means infrequent congenital anomaly. Aortic obstruction is far less frequently congenital. In either case if the obstruction 688 DISEASES OF THE HEART arises earlier than the eighth week of foetal life, it leads to an imperfect formation of the interventricular sa^i:)tum. This is due to the inequality of blood-pressure in the two ventricles occa- sioned by the stenosis, and the consequent passage of a stream of blood from one to the other through the still imperfect septum, with each systole of the ventricles. This stream prevents the union of the two fundaments of the sa>ptum, and in consequence, the imperfection is almost always situated at the pars memhrana- cea, or point where the two embryonic fundaments fuse (Fig. 105). This is high up on the sa^ptum in the portion separating the two coni arteriosi. If the obstruction be established later in embryonic life, the interventricular sa^ptum is usually found entire, but the inter- auricular sa^ptum is usually imperfect, and the ductus arteriosus open. The stenosis need not necessarily be located at the valve to produce these effects, since narrowing of the conus on either side, the so-called stenosis of the heart, acts in the same way. It is not always possible to say whether the imperfect closure of the sa?ptum preceded the obstruction of the pulmonary ostium or of the conus, or whether it followed the other lesion. In the light of Kiissmaul's conclusions, that defects of development predisposes to endocarditis, the former hypothesis is not unlikely. Patency of the foramen ovale results from any condition causing a considerable inequality in the blood-pressure in the two auricles at the time when it is normally closed. This may be due to stenosis of one or the other of the auriculo-ventricular orifices, or obstruction at either of the arterial openings may secondarily influence the blood-pressure in the auricles, and so cause persist- ence of the foramen. The condition is often combined with a de- fective interventricular sa'ptuiii, or j)atent ductus arteriosus, for the reason that all these imperfections are due to the same cause. Patency of the foramen ovale, or rather an incomplete union of the valve with the ring, is by no means always to be considered a pathological condition. According to Romberg, such a condi- tion exists in at least half of all cases. This may not produce symptoms, however, as when the valvular flap is of suflicient size the pressure of the blood in the left iiuriclc keeps it closed and prevents any interchange of blood. The ductus arteriosus j)crsists as a patulous vessel, when, at CONGENITAL DISEASES OF THE HEART 689 the time it should normally be obliterated, the blood-pressure in the aorta and pulmonary artery is so unequal that a current flows through the ductus from one to the other. Thus in a case of pul- monary stenosis developing early in f(jotal life, the contents of the right ventricle, experiencing difficulty in passing through the pul- monary orifice, enter the left chamber through the imperfect in- terventricular sfcptum, and only a diminished quantity of blood passes into the pulmonary artery. On the other hand, the aorta receives an increased amount of blood on account of the extra supply to the left ventricle from the right chamber through the imperfect sffiptum. Thus the ten- sion in the aorta is rendered higher than that in the pulmo- nary artery, and a portion of blood passes into the latter vessel through the ductus Botalli. The stream in the ductus, it is to be noted, is in this case flowing in a direction opposite to that normal in foetal life, which is from the pulmonary artery into the aorta. Persistence of the ductus may depend on aortic as well as pulmonary defect, and may be due to a congenital reduction of the calibre of the vessel, as in Fig. lOY. The extreme case of atresia of either artery necessitates the patency of the ductus for the carrying on of the circulation. Etiology. — There has been much speculation upon the de- termining factors in the development of congenital affections of the heart. Foetal endocarditis is quite generally attributed to the agency of infectious diseases operating through the maternal circu- lation. It has not been at all clear what influences lead to the pro- duction of developmental anomalies. Some have sought to ac- count for these in tendency or inclination to perversion of growth impressed upon the germ by the parent, and hence regard such abnormalities as stigmata of degeneracy.* This hypothesis is based largely on the fact that developmental defects of other parts of the body are not infrequently associated with congenital car- diac anomalies. Others, again, hold that these abnormalities, de- * F. Simpson, in 4,253 autopsies of the insane, found fenestration of the aortic valve 75 times; of the right semilunar, 18; of the mitral, 6; and of the tricuspid, 2. It was especially frequent in men. Supernumerary and rudimentary valves were found very often. It would be interesting to ]mo- giobin, until a l)alancc is struck between tlic production and de- struction (d' the bl(jod-corpuscles." CONGENITAL DISEASES OF THE HEART 695 In contrast to the usual results of blood examinations in these cases Mouille is cited by Vierordt as having found a reduction, the red cells ranging between 3,500,000 and 4,500,000, yet this in no way invalidates the general proposition that the corpuscu- lar elements are increased in cyanosis. Finally, it should be stated that a similar though less striking increase is observable in cyanosis in acquired heart disorders. Laennec and Rokitansky attributed to cyanosis a protective influence against the development of pulmonary tuberculosis. Their views are erroneous, however, since it is a well-known fact, as has been stated in the chapter on Pulmonary Stenosis, that patients with this affection, in which cyanosis is particularly apt to occur, are especially prone to tuberculous disease of the lungs. Another symptom in cases of cyanosis is coldness of the skin, particularly of the extremities, and hence these patients are re- markably sensitive to cool atmospheres. They are also very sub- ject to dyspnoea and often manifest pronounced shortness of breath on comparatively trifling exertion, as was present in my case ; but this, as we have seen, is a symptom common to all forms of cardiac disease in the stage of defective compensation. In these cases, when dyspnoea is a marked feature, there is usually evidence of considerable visceral stasis. In congenital cases, on the contrary, breathlessness is not infrequently pronounced out of all proportion to the signs of engorgement in the various organs, aside from the capillary dilatation emphasized by Vierordt. This lack of such venous stasis as would ordinarily be ex- pected in cardiac disorders of such evident gravity, is attributed by Romberg to the slowness with which the veins have been re- quired to accommodate themselves to their abnormal burden (uebetiastung) . Nevertheless, the deficient arterial blood-supply and the sluggish return of venous blood and the defective metab- olism lead to disturbances of function on the part of the various viscera rriore or less severe and commensurate with heart-power. The variations in the pulse will be spoken of in connection with the physical signs now to be considered. Physical Signs. — Ins'pection. — This is of special value only in the cases in which there are cyanosis, a dwarfish appear- ance, clubbing of the fingers, praecordial bulging, and other signs 696 DISEASES OF THE HEART of a long-standing circulatory embarrassment. In such a case, moreover, there is nsnally the history that the patient " was a bine baby." Scrutiny of the cardiac area may detect displacement of the apex indicative of hypertrophy, but in all this there is noth- ing to attest the exact nature of the lesion. In not severe cases of congenital disease, as persistence of the ductus or patency of the foramen ovale, there may be nothing whatever in the j)atient's aspect to suggest the existence of cardiac mischief. Palpation. — Of the serious congenital defects which come to a clinical recognition stenosis of the pulmonary orifice or conus is by far the most frequent, and it is in this affection that palpation is of special value. This usually detects a systolic thrill in the second and third left intercostal spaces close to the sternum. This may be so soft and weak as to be scarcely percejitible, or so coarse and strong as to tickle the hand. In patency of the foramen, of the duct, or even of the interventricular saeptum, there may be no thrill unless associated with some obstructive lesion, as just men- tioned. For the most part authors pay but little attention to the pulse, since it is thought to possess no distinctive characters. It should, however, be given particular study in cases of pulmonary steno- sis, since, according to Starck and Renvers, its volume assists in determining the question whether or not there is closure of the interventricular sa'ptum. If the Sieptum is perfect the supply of blood to the left heart is diminished, and hence the pulses of the upper extremities are small. When, on the contrary, communica- tion exists between the ventricles, a side channel is provided by which the left ventricle receives a large supply of blood, and hence the pulses are of greater volume. Consequently, if in a given case of pulmonary constriction the pulse shows a degree of strength and volume out of proportion to what would be naturally expected, it suggests the likelihood of incomplete closure of one or both of the septa. Kolisko is reported to have stated that when persistence of Botalli's duct exists secondary to atresia or great narrowing of the isthmus of the aorta or to congenital stenosis of its ostium, the pulses in the lower extremities are larger tliau tliose in the upper. This is due to the fact that the arteries given off from the aortic arch receive an abnormally small volume of blood, whereas a por- CONGENITAL DISEASES OF THE HEART 697 tion of the blood pent up in the puhnonary artery and intended for the ascending- aorta through the left ventricle is switched off through the patent duct and enters the descending aorta, thus supplying the lower extremities with a disproportionate share of blood. Percussion. — As in acquired heart-disease this means of in- vestigation should not be neglected, since it is of extreme impor- tance to discover possible modifications of cardiac dulness. In pulmonary obstruction the absolute and relative dulness are both increased to the right and downward in consequence of the right- ventricle hypertrophy. In patent foramen ovale and a defective ventricular sseptum the cardiac outline may or may not be in- creased transversely, according to the severity of the lesion. When the ventricular sii'ptum is incomplete the greater blood- jDressure in the left ventricle forces a portion of the contents through into the cavity of the right ventricle. This chamber be- comes surcharged, and tends therefore to hypertrophy and dilata- tion, which condition is shown by increase of cardiac dulness in that direction. Nevertheless, in both patency of the S£eptum and foramen unassociated with other lesions prsecordial dulness may in some cases remain normal. Auscultation. — This usually furnishes the most valuable in- formation concerning the presence and nature of these congenital affections by the detection of a murmur. Yet in cases of sseptum defects, including of course the foramen, there may be no mur- mur of any kind. When such a bruit exists, it is usually a loud systolic murmur heard throughout the cardiac area, particularly over the base. It does not appear to be limited to any area, as are the murmurs of acquired valvular disease ; and this fact, when noted, possesses a certain amount of value. Robert Maguire thinks that the systolic bruit of a defective ventricular saeptum is most distinct over the situation of the inter- ventricular groove, and decreases in intensity as the stethoscope recedes from this line in either direction. As, however, the only case he has reported, so far as I have been able to learn, has not yet come to a necropsy, the proof of his contention is wanting, and although the statement may appear plausible, it cannot yet be accepted unreservedly. Worcester has reported a case of patency of the foramen ovale, 698 DISEASES OF THE HEART toe-ether witli a small defect in the interventricular Sicptimi just below the right semilunar vahes, which was discovered post mor- tem in a negro of fifty-seven who died of general paralysis. Sev- eral years before there was detected a long loud systolic murmur audible over the entire chest. The absence of symptoms during life is to be inferred from the fact that he served as a soldier during the civil Avar. The heart was found only moderately hypertrophied. There is nothing, therefore, distinctive of the mur- mur of foramen or ventricular sa'ptum patency. Cabot speaks of the quality of the bruit as harsh and vibrant; but there is in this statement nothing at all distinctive. In the case of a boy recently seen by me there was a loud systolic murmur not trace- able to any particular ostium. For a description of the murmur of pulmonary stenosis, as well as the other signs, the reader is referred to the chapter on that subject. The auscultatory phenomena due to persistence of Botalli's duct are best described in the narration of a case I had under observation for several years, and which finally came to necropsy. The patient was an undersized woman of twenty-one who suffered from breathlessness upon rapid walking and an uncomfortable pounding of the heart. Her mother reported her as having been a small delicate baby, but as not having shown cyanosis even dur- ing fits of crying. Her only illness had been scarlatina at the age of nine. The radial pulses were small, regular, equal, and in rate between 90 and 100. There was no cyanosis or venous turgescence. The pra?cordium was prominent, particularly at the left of the sternum, but was not pigeon-breasted. The apex-beat was in the sixth left interspace, 2 inches from the sternum, strong and diffused. There was a soft, not very distinct thrill in the second and third left interspaces close to the sternum, which was not syn- chronous with either systole or diastole, but was most pronounced at the end of expiration and beginning of inspiration. It seemed to follow the apex-shock by a very brief instant, and to run into the long pause. Absolute cardiac diihicss was but slightly in- creased, whereas the relative appeared rather too broad. The heart-sounds were feeble and obscured l)y ;i loud harsh murmur that seemed to be systolic and audible throughout the entire prae- CONGENITAL DISEASES OF THE HEART 699 cordia, but most plainly at the base, and , was transmitted to the lower angle of the left scapula. Upon closer observation it was perceived that at the site of the thrill the murmur became a continuous remitting roar, having Fig. 107. — IIkakt from Case on p. «y8, shovvinu Cuncentkic IIvpertuophv uf Left \'kntricle and Sound passed through Patent Ductus Arteriosus. its maximum intensity just after the first sound and its minimum towards the end of the long silence, but never entirely ceasing. 700 DISEASES OF THE HEART Everywhere the quality of the bruit seemed to be the same. The lungs, abdomen, and urine were negative, but the blood examina- tion showed a pronounced reduction in the percentage of hsemo- globin. The precise nature of this lesion was not clear, but was evi- dently congenital. In time, however, the affection was decided to be either patency of the foramen or of the ductus arteriosus. As compensation appeared threatened, appropriate treatment was in- stituted, and soon a satisfactory degree of hypertrophy became re- established. To make a long story short, this patient ultimately married and was delivered of a child, passing through both pregnancy and labour without special difficulty. Unfortunately she became infected through the carelessness of her nurse, and died of sep- ticoemia in the second week of her puerperium. The necropsy was made by Dr. W. A. Evans, who found foci of suppuration in the right kidney and liver, but no evidence of inflannnation in the cardiac structures. The specimen is pre- sented in Fig. 107. The left ventricle was concentrically hyper- trophied, its wall measuring 22 millimetres. The wall of the right ventricle measured 11 millimetres, and was therefore also thicker than normal. Both septa were complete and the foramen was not patent. All four sets of valves were healthy, but the aortic orifice was so small as to barely admit the index finger. This was found, however, to correspond in size to the lumen of the artery, whieli was abnormally narrow throughout. The circmuference of the aortic ring was 43 millimetres ; of the aorta, just central to branches, 45 millimetres ; at opening of ductus, 43 millimetres ; and 6 centimetres beyond, 40 millimetres. Of pulmonary ring, 55 millimetres; and of pulmonary artery, 55 millimetres. The ductus was patulous, and u])on searching for the cause of this persistence it was found that, instead of the isthmus being constricted, or the aortic arch smaller than the portion of the artery below the origin of the duct, it was as a matter of fact half a centimetre wider. In this case the narrowing of the aorta below the origin of the duct, slight as it was, was yet sufficient to cause a portion of the blood-wave to be diverted into the duct and through it into the ])ulmonary artery, thus giving rise to the ninnnnr and thrill. The CONGENITAL DISEASES OF THE HEART TOl left-ventricle hypertrophy was secondary to the aortic narrowing. This was an instance of chlorosis aortica, and accounted for the fact that treatment had never been able to restore the haemo- globin to its normal percentage. I have under observation at the present time two other pa- tients, one a woman, the other a young man, who present almost identical physical signs and who, I believe, are also instances of this same congenital anomaly. Diagnosis. — As there are several affections embraced by the term Congenital Cardiac Affections, it would be wearisome and unnecessary to recapitulate the physical signs by which each may be diagnosticated, and hence the reader is referred to what is stated above under the caption of physical signs. It only needs to be here stated that the congenital nature of the affection must be determined by the history and in some cases by a blood exami- nation. If there is a history of the individual having been " a blue baby " or of his having been feeble from birth with evi- dence of circulatory embarrassment directly after birth, and if the child's appearance corresponds more or less to that described under inspection, there is strong likelihood of the cardiac dis- ease being congenital. In many instances the parents are able to state that the family doctor discovered signs of heart-disease as soon as the infant was born or in its earliest weeks of life. If the person presents well-marked cyanosis, and if exami- nation of the blood discloses the changes previously described — i. e., an increase of haemoglobin and red corpuscles over the nor- mal — the diagnosis of a congenital defect can be positively made. In some cases, as of pulmonary stenosis, there may be nothing to prove conclusively during life whether the disease is congenital or acquired. In such a case, however, probabilities are always in favour of its prenatal origin, owing to the great rarity of the acquired form. Finally, in doubtful cases of persistence of Botalli's duct, it is stated that by means of the fluoroscope a positive diagnosis may be made. Prognosis. — As stated in the symptomatology of persistence of the foramen, this abnormality may occasion no signs of its pres- ence, and patients may reach an advanced age, and die of some intercurrent affection. Unassociated with an affection of the pul- 702 DISEASES OP THE HEART moiiic or other orifice, a defective sreptnin ventriciilonun or a patu- lous ductus arteriosus may also in no wise aiiect the prospect of longevity. It is far otherwise, however, as regards pulmonary stenosis. Even when the patient does not succumb to the heart- lesion directly, he is most likely to develop tuberculosis of the lungs. In comparing the gravity of this with other forms of con- genital cardiac disease, excepting, of course, the uncomplicated SiTpptum anomalies just mentioned, Komberg states that up to the twelfth year of life affections of the pulmonary ostium and conus constitute three-fifths of all cases, whereas after the twelfth year, owing to the mortality of other lesions, these comprise four-fifths of the cases. Taking all forms of congenital cardiac defects to- gether, he cites Stoelker's figures, which, condensed, are as fol- lows: Out of 79 cases of all kinds, 24 died in the first six months of life, 42 had died before the end of the first year, 56 before the tenth year, and 71 had died before the twentieth year of life was reached. It should be remendjered, moreover, that, according to Kuss- maid, C(mgcnital disorders of the heart predispose to endocarditis. In other respects the prognosis is influenced favourably or not by all those conditions of environment that have been fully consid- ered in previous chapters. Lastl}^, when compensation has once begun to fail in these cases there is small prospect of much being accomplished by treatment. Treatment. — As may be inferred from the preceding sen- tence, this must be largely or wholly symptomatic — that is, in accordance with the indications of each case. The reader is re- ferred, therefore, to the discussion of the management of valvular diseases in general for the principles of treatment. SECTION IV OAEDIAC ISTEUEOSES SYN. : FUNCTIONAL DISORDERS OF THE HEART CHAPTER XXX PALPITATION, TACHYCARDIA, CARDIAC PAIN, PSEUDO-ANGINA PECTORIS * Pathology. — There is a class of disorders which manifest themselves clinically by a perverted action of the heart, or by pain and other sensations in the cardiac region, or by a combina- tion of the two, yet in which no structural alteration of the organ can be detected. They are often spoken of, therefore, as func- tional disorders of the heart. Objection is made to this term on the ground that in organic cardiac disease there is a disturbance of function, and, strictly speaking, such affections may also be des- ignated functional derangements. Furthermore, it cannot be affirmed absolutely that some as yet undiscoverable alteration of the structure of the heart does not underlie or attend its perver- sion of function. However logical such reasoning may be, the term functional has been sanctioned by usage, and is generally understood by the profession and the laity to mean an affection which is not associated with demonstrable structural lesion. Tor this very reason it is often advisable in speaking to the patient or his friends to designate the disturbance as functional. A fear or an exaggerated notion of the gravity of the complaint may thus be allayed. Although from force of habit I frequently speak of these affections as functional, I yet prefer the designation cardiac neuroses, since one cannot observe these cases without coming to the conclusion that the manifestations on the side of the heart are the expression of a disorder of the nervous system. . 703 704: DISEASES OF THE HEART One may be unable to detect any definite pathological lesion underlying this disturbance of the nervous nieehanisni, and yet it cannot be doubted that some neurosis is responsible for^the cardiac symptoms. In some instances the disorder of the heart's ac- tion points to vagus influence, while in others the accelerator nerves of the heart are responsible for the manifestations. The exciting cause may or may not be discoverable, but an attentive study of the history and close analysis of the symptoms during and between attacks render no other conclusion tenable than that the cardiac and circulatory phenomena are secondary and sub- ordinate to some disturbance of the nervous system, and hence outside the cardio-vascular apparatus. It would no doubt be more in accord with the pathology of these cases to relegate these so-called cardiac neuroses to the do- main of neurology, wdiere they properly belong ; but the symptoms calling attention to the heart are so often the dominant ones that they mislead the patient into the belief he has heart-disease. In- deed, the correct interpretation of the sensations is often puzzling to the physician, and hence it is customary to consider these cases in works of this kind. Romberg classifies them as neurasthenic, hj-sterical, and reflex, in accordance with the nervous disorder underlying them. This would be well if all cases belonged strictly to these categories, or if the pathology of these neuroses was clearly understood. Such is not the case, and therefore I prefer to describe the various manifestations without attempting to divide them according to their apparent etiology into special groups. Symptoms Palpitation.- — Tliis is a transient derangement of cardiac ac- tion characterized by an increase in both the frequency and force of its contractions. Without warning, the heart suddenly begins to beat in a more or less disordered manner, and to give to the individual the sensation of a pounding or knocking against the ribs. Whatever may be the variations in rate and rhythm in in- dividual cases, it is this subjective consciousness of the lieart's action that constitutes tlie special cliaracteristic of an attack of palpitation, and it appears to ])e lliis feature wliich alarms the patient. The heart may be rapid, 120, 130, or more, or it may FUNCTIONAL DISORDERS 705 remain below 100, but whatever its rate its action is violent. In the matter of rhythm also there are differences. Ordinarily the pulse is regular, but it may be irregular in frequency and force, and may be even intermittent. When this is the case the indi- vidual is likely to be thrown into a state of great alarm. Each time the heart intermits, it is announced by a sensa- tion of the organ suddenly falling or sinking in the chest; it is often described as a " sinking feeling." This is succeeded the next instant by a powerful throb, a sensation as if the heart gave a flop or jumped up into the throat, and with this very uncom- fortable feeling the patient is apt to make a sudden exclamation or outcry, and perhaps quickly press the hand against the pra^cor- dia, as if trying to grasp the refractory organ. The heart may then quiet down, or it may race off as madly as before. It appears to me that in strictly neurotic persons without any discoverable organic mischief it is more common for the heart's action at these times to be rapid and regular (tachycardia). During the attack of palpitation there is often a violent throb- bing or pulsation in the arteries of the neck or in the abdominal aorta, or in both situations. The hand placed against the prse- cordium readily appreciates the energetic beating of the organ, and not infrequently the eye perceives a rapid rising and falling of the cardiac region. As it is so often expressed by the friends, " you can see the heart beat through the clothes." If the radial pulse is examined during such an attack or " spell with the heart," to quote the popular phrase, it may be found full and quick, or if the rate be extremely rapid, small and feeble. Vaso-motor changes are also very apt to accompany the seizure. The face flushes or pales, as the case may be, and the hands and feet are usually cold. One of the most typical examples of palpitation was presented in a young man who consulted me only a few days ago. He was twenty-two and an athlete of superb physique, standing 6 feet 2^ inches, weighing 200 pounds, and with muscles of steel. He is an expert boxer, and can endure an arduous sparring-match with- out palpitation or shortness of breath. Two years ago he passed through an unusually severe typhoid fever, from which he made a good recovery with the single exception of sudden attacks of rapid, violent beating of the heart, that almost invariably came on 46 706 DISEASES OF THE HEART shortly after a meal. They were accompanied and followed by a feeling of exliaustion, and were, naturally enough, very alarming to both the patient and his family. The attacks were of frequent occurrence, sometimes daily, I examined the young man at that time and was unable to discover any indication whatever of car- diac disease. The history of a recent severe typhoid fever made me con- sider the possibility either of an acute myocarditis during his ill- ness or of the myocardium having been seriously enfeebled in con- sequence of fatty degeneration, such as has been so well described by Quain. But the heart's dulneso and the heart-sounds were nor- mal, and inquiry elicited the statement that he was able to exer- cise, indeed had but just returned from a shooting trip in the mountains of North Carolina, without experiencing any shortness of breath, vertigo, or palpitation. The pulse was rapid during my examination, but its volume and force were excellent. I there- fore assured him that his attacks were of a functional nature and did not indicate heart-disease. His flesh at that time was rather too flabby, and he said he had been gaining weight rapidly since his recovery from his fever. IMinute inquiry into his habits, diet, etc., brought out the fact that he was eating enormously and altogether too much carbohydrates, and was in the habit of drinking a large amount of water with his meals. He acknowledged some feeling of being bloated after eating. It was concluded, in the absence of other etiological fac- tors, that gastronomic errors were at the bottom of his complaint, and he was advised to cut out his sweets and starches, to limit his consumption of fluids at meals, to drink lithia water between meals, and to begin his former systematic exercise both in the gymnasium and out of doors. This regime was faithfully carried out, with the result that his palpitations almost entirely disappeared. During the follow- ing two years he came to see me twice, once a few weeks after his initial visit, merely to report progress, and the second time to re- ceive an examination for life insurance, which on my recommen- dation was granted him. This past week, however, he came again with liis father, who said he wanted to know how it could be that so robust a young man could still have his attacks of palpitation without there being FUNCTIpNAL DISORDERS 707 something wrong with his heart. He then explained that the Sun- day previous his son was about to start for church with his mother, when all at once he was discovered by his father lying on the floor and his heart beating so fast and hard that it could be seen through the clothes. The attack lasted about twenty minutes. The young man then spoke up and said he did not see any use of being concerned about the affair, as he knew perfectly well what had brought the attack on. He had eaten too hearty a breakfast, consisting of coffee and three pieces of German coffee cake, besides fried chicken and fruit. An examination was then made, and a more normal heart I have never listened to. The pulse was steady, regular, and 80, standing. The apex-beat was in the nor- mal situation, absolute dulness was not increased, and the rela- tive measured 3 inches to the left and 1 inch to the right of the sternum. The sounds were clear, of normal relative intensity, and entirely free from murmurs of any kind. It was without hesitation, therefore, that the opinion expressed two years previously was reiterated. It was not quite clear why the attacks should take place in so powerful and an apparently perfectly well young man, but there was certainly an etiological connection between the attacks and indiscretions in the way of a too liberal allowance of carbohydrates. There was either a tem- porary abeyance of vagus control or a stimulation of the acceler- ator nerves of the heart. Whether this was an instance of reflex irritation or of some toxic influence resulting from indigestion, was not at all clear. But it would be ordinarily classified as a reflex cardiac neorosis. In the foregoing case precordial pain or other sensations of an allied nature were never complained of. It is quite common for an attack of palpitation to be accompanied by a painful sen- sation in the region of the heart or for the exaggerated cardiac action to follow the pain. At other times the patient may com- plain of the heart's pulsations as painful. In still other cases the chief complaint is of an indescribable feeling of distress or dis- comfort " at the heart," which is usually but not invariably at- tended or succeeded by palpitation. Such symptoms are frequent in individuals who are hysterical. This class of cases is well illustrated by the following example : A physician, aged twenty-four, height 6 feet 1 inch, weight 708 DISEASES OF THE HEART 150 ijoiinds, gave a history of " heart-weakness " for a year. His parents, brothers, and sisters were all living and in good health and free from neurotic tendency, so far as the patient knew. With exception of measles in childhood he had never been ill, and he denied venereal disease or sexual excess, and did not use tobacco, alcohol, or narcotics. During the siunmer of 1899 he had been particularly hard worked in his profession, and compelled to lose much sleep. In iN^ovember he suddenly developed attacks of pain in the region of the heart that were speedily followed by accelerated forcible beat- ing of the organ. It seemed to him that every throb of the heart produced pain just below the left nipple. These attacks were pre- cipitated by exertion, such as walking, or even a long drive into the country. After they had endured for about ten days he be- came so bad that he used to faint away during his attacks, and he remained unconscious for an hour or more in spite of efforts to revive him. This statement made me suspicious that the so-called syncope was not in reality a true fainting fit, and he was asked if he be- came absolutely insensible to his surroundings, or whether or not he knew in a dim w^ay what was being done to him. He then replied that he believed he was vaguely conscious of his surround- ings at those times. These attacks recurred for about four months, and were finally cured by the taking of | of a grain of codeine 4 times daily dur- ing three weeks. The drug then had to be discontinued because of the obstinate constipation it occasioned. During those four months he was much troubled by insomnia. Since April, 1900, his condition had improved somewhat, but at the date of his ex- amination by me, October, 1900, he was still unable to endure exertion because of the palpitation it evoked. The young man was a blond, evidently highly nervous and not strong, since he lolled on the lounge in my office, as though too weak to sit up. His hands were cold and moist, and his arm trem- bled while the pulse was being examined. This was full, tense, regular, and varied from 10.5 to 110. The apex-beat was in the fifth left interspace well inside the nipple, and the strong, rather broad shock was accompanied In- a coarse thiill. Absolute and relative cardiac dulness were normal, the latter measuring 3 FUNCTIONAL DISORDERS 709 inches to the left of the sternal margin and 1 inch outside the right sternal border. The first sound at the apex was partially obscured by a rough vibrant murmur of whizzing quality, which was loudest in the erect position, disappeared in the fight lateral decubitus, and was scarcely audible when the patient lay on his left side. It was increased in intensity at the end of deep inspiration and grew almost inaudible at the close of expiration. The second pulmonic sound was not accentuated. The liver was not palpable and its dulness did not pass below the inferior costal margin, right nipple-line. The abdomen was negative. The patient reported his urine as negative, containing neither albumin nor sugar. He was not conscious of indigestion, and the bowels were not constipated. The diagnosis was made of a cardiac neurosis with an acci- dental murmur and palpitation. The patient was advised to spend the winter in the South, where he could be in the open air, to take moderate, regular exer- cise, and endeavour to build up his nervous system, and to school himself to regard his malady as not organic. In the way of medication he was advised to take strychnine, give up the use of digitalis and allied heart tonics. Up to the present writing I have had no further report from this case. This patient illustrated another feature of hysterical patients with disordered heart action. He declared he was always con- scious of its pulsations, and could tell how it was beating without having to feel his pulse. To test him in this matter I took hold of the wrist and counted the pulse, and then told him to count aloud his heart-beats. In this he utterly failed, and I became con- vinced that his sensations were imaginary. This is not always the case, however, for in some instances the cardiac action is suffi- ciently exaggerated to be perceived by the patient. Sometimes, too, when the pulse-tension is high the individual can perceive pulsations in the extremities. The powerful influence of the imagination and the readiness with which an attack of palpitation can be elicited by trivial causes are illustrated by the following case : A law student, aged twenty-four, sought advice because of palpitations since the age of fourteen. Family history was nega- 710 DISEASES OF THE HEART tive, and the patient had not suffered from any acute disease that might have led to endocarditis or pericarditis. lie thought his trouble with his heart dated from his study of physiology in school, when he observed that his pulse was too rapid. At all events, from that time on he has been subject to fre- quent attacks of violent, rapid beating of the heart, and has been told repeatedly that he had heart-disease. He is greatly fright- ened by his attacks, which often come on without apparent cause or when fatigued by study, during unwonted exercise and excite- ment, or even too close application to his books. He is greatly troubled with flatulence, and this often sets the heart to palpi- tating. During an attack he is exhausted, alarnied, and notices particularly a violent beating in the stomach. Pollutions occur every two or three weeks, and are folloM'ed next day by extreme weariness, nervousness, and liability to his palpitations. Examination showed him to be a tall, slender man with thin chest and broad intercostal spaces. The abdomen was thin, rather scaphoid when in the dorsal decubitus, and the abdominal aorta pulsated visibly. There was gurgling in the course of the trans- verse colon, but no dilatation of the stomach, and no demonstrable enteroptosis. The pulse was full, soft, rapid, and regular. The action of the heart was excited and abnormally forcible, and the cervical arteries pulsated strongly. The apex-beat was in the normal position, cardiac dulness was not increased, and the sounds were clear, but too ringing. No murmurs could be detected. During the examination the patient became very nervous and exhibited a fine tremor, the hands being warm and moist. There could be no doubt of the nature of his fancied heart- disease, and he was emphatically assured that his trouble was a neurosis and that he need apprehend no danger from his attacks. It was concluded also that in this case there was a reflex element, and that the cause of his palpitations lay in such an excitability of tlie cardiac accelerator nerves that they were sensitive to con- ditions which would be wholly inadequate to arouse them in a normal individ'iuil. Tlie chronicity of the affection made prog- nosis rather unfavourable. So much suffering was caused by the pollutions that the ure- thra was explored, resulting in the detection of nothing more than FUNCTIONAL DISORDERS Til hypera3sthesia of its posterior portion. Local treatment was in- stituted by the specialist to whom the patient was referred, but with no appreciable effect on his attacks of palpitation. The following extremely instructive case exemplifies the as- sociation of a veritable phobia with a distinct hysterical element and a reflex irritation, or at all events an imaginary reflex irrita- tion: The patient was a German-American, married, aged twenty- six, of medium height and weight. She sought medical aid be- cause of " weakness, palpitation, and sinking spells." Her fam- ily history was negative, excepting that her mother and sisters were nervous. The patient was doubtful concerning her having had the ordinary diseases of childhood, but denied rheumatism or other illness of an acute or infectious nature. Said she had had stomach trouble and been nervous all her life, and at ten years of age had heart-trouble that came from her stomach and persisted about a year. From that attack she recovered without treatment, and she remained well with exception of nervousness until two or three years before marriage, at which time she had some nervous trouble that lasted a year and a half. During her pregnancy she suffered much with her heart and stomach. The confinement was difficult, necessitating the admin- istration of chloroform and delivery with forceps. She thought the chloroform weakened her heart very much, and she was not strong enough to nurse her baby. That was two and a half years ago, and ever since she has been a nervous wreck. She has " heart attacks " from exercise, excitement, and after eating. These have been much worse the last four months in spite of treatment, and last week came as often as twice a day. Excitement, as from anger or domestic wrangles, which unfortu- nately are too frequent, at once give her a sinking spell, and she lies exhausted for hours, her heart beating very rapidly at such times, occasionally as much as 160 a minute, in this respect re- sembling paroxysmal tachycardia. At times the taking of some article of food or a remedy which disagrees with her stomach will instantly produce palpitation with extreme exhaustion. At these times she is alarmed, but is speedily quieted and her pulse slows down upon the arrival of a physician. She thinks she has been relieved a little by strophanthus, and has very strong notions re- 712 DISEASES OF THE HEART garding the effect on her of certain medicaments — e. g., dilute hydrochloric acid, which twice gave her a violent and prolonged attack of palpitation. Her symptoms are always more likely to occur about ten days before menstruation, but when the menses have become estab- lished, her heart is more quiet and she feels better. Attacks are also very apt to follow looseness of the bowels, and conversely are not so easily called forth when she is constipated. Ever since the birth of her child she has been subject to the appearance on her extremities of " spots that look just like bruises, are dark red, gradually grow yellowish and fade away." Of late she has eaten only beef and wine, because anything else produced gas on the stomach and the attacks of palpitation and sinking spells. She notices some shortness of breath on fast walking and as- cending stairs; has appetite, and could eat if her stomach would let her, and after eating her stomach feels heavy. The bowel movements are irregular, but menses are regular, lasting two days. Her sleep is disturbed by palpitation, and she nearly always feels dizzy. During the rapid heart's action she notices pulsation in the carotids and in the stomach, and she has a feeling as if her lungs filled up with blood, her face, feet, and hands are cold, and she feels also as if she could not breathe. The attacks persist from half an hour to several hours, and are not followed by a flow of copious pale urine. In a word, there is, excepting severe pain, scarcely a sensation connected with the heart of which this highly neurotic and imaginative woman does not complain. It is apparent that she is only too glad and ready to talk and dilate upon her symptoms. She is sure she is going to die in one of her attacks. Physical examination showed pulse 106, small, regular, but not of noticeably low tension, and carotids throbbed slightly. Apex-beat was in fifth left interspace, 3^ inches from midsternal line, and accompanied by a slight thrill, which disappeared in the recumbent posture, although the apex-shock became more defined. Relative cardiac dulness reached from 1 inch to right of sternum to 3| inches to the left of that l)one. The first sound was accom- pained by a faint, short, high-pitched systolic whiff, which was of limited transmission upward and to right and was slightly louder at end of inspiration — and both jiuliiionic and aortic second FUNCTIONAL DISORDERS Y13 sounds seemed accentuated. In the standing position the abdomen bulged relatively too much below and was too flat above the um- bilicus. The right kidney descended to a little below the costal arch, but could not be grasj)ed. The liver could not be made out as having dropped downward. Gastric tympany reached 3 inches below and 1 inch too far to right of the umbilicus, and there was splashing. The abdominal aorta pulsated with abnormal force, but could not be distinctly palpated. The abdominal viscera evidently dragged somewhat upon their supports, and gas- troptosis was undoubtedly present. The pelvic organs were nega- tive. The lungs were negative, and there was no oedema about the ankles. A week subsequently, after having been limited to two meals a day, and having enjoyed a week of immunity from her attacks, her heart's action was found slow but somewhat irregular in fre- quency. The apex-thrill previously noted was discovered to be a short but very distinct presystolic one, and the first sound was unmistakably thumping. Upon the patient assuming the recum- bent posture the second sound, exactly at the seat of apex, was doubled and a low-pitched short murmur accompanied the first sound. I was therefore forced to conclude that this patient had mitral stenosis, l^evertheless, her symptoms were those of a car- diac neurosis rather than of an organic lesion. She was sent to a well-known neurologist, who reported that, although distinct hysterical stigmata were not discoverable, he yet believed there was an hysterical element in the case. In addi- tion, I could not rid myself of the belief that the condition of the stomach and bowels had much to do with the production of her attacks. At one time they w^ould follow an indigestible meal or a relaxation of the bowels sufficient to merit the term of diarrhoea, at another some emotional disturbance, as a quarrel with her hus- band or an ungratified sexual desire — in short, a considerable variety of disturbing causes. This case gave me endless trouble and perplexity, until at last, acting on a hint furnished by her statements concerning the etiological influence of diarrhoea, I prescribed a combination of astringents which kept her bowel somewhat constipated. She then became more and more free from her fearful attacks, and with in- creasing freedom from them regained a measure of confidence, so 714 DISEASES OF THE HEART that at the present writing, 1901, I have not seen her for nearly two months. Augtist, 1902, heart's action heing quiet, there was entire absence of cardiac murmurs, and the organ was to all apjpearances free from disease. The presystolic murmur and doubling of second sound above noted must therefore have been of acci- dental origin a/nd in some way due to the disturbed cardiac rhythm. A clergyman's widow, German, consulted me because she was sure s(miething was wrong with her heart, and she feared she was suffering from the disease her husband died of. This was Grave.s's disease, the man having been frequently seen by me during his life and final illness. For two years after his death she remained in her usual health, but about a year ago she began to suffer from " si)ells with her heart," which were brought on by excitement, and sometimes, she thought, by the taking of food that did not agree with her stomach, for with the eructation of gas the palpi- tation began. At still other times the attacks came on without any apparent cause. The action of the heart was likened to " rope jumping." She feels a " clutch at the heart," then her heart begins, and the next moment she is " entirely gone," the face being " deathly pale and the hands cold as ice." Nothing relieves her so quickly as a little brandy. Last week she had two attacks. She said she often noticed a gurgling in the left side of her abdomen, and this gave her much uneasiness. Her appetite was poor, and she was in the habit of drinking coffee four or five times a day. She was con- stipated, but her menses were regular. Her account of her com- plaint was not that of a neurasthenic, and there was nothing in her symptoms or appearance to suggest that she belonged to that class of sufferers. Neither was there any history of neurotic dis- turbances in her family. She was thirty years of age, rather spare, and of medium height. There was no throbbing of the carotids, no tremor, no perspirations, no enlargement of the thyroid — in short, no indica- tion of Graves's disease. Tlie ])ulse was 90, equal, regular, and of fair tension. The apex-beat was in the normal situation, cardiac dulness was normal, and the heart-sounds were normal excepting, perhaps, that the first was rather too ringing. There were no murmurs. The lungs were negative also. Within the abdomen was the interesting finding that acconnled for licr gurgling. The FUNCTIONAL DISORDERS Tl5 abdominal walls were relaxed, depending baglike and bulging in the hypogastrinm, while the epigastric region was too flat. An indistinct splashing was elicited, and gastric tympany extended well down into the pelvis, but not more than an inch to the right of the median line. It began at the level of the ninth instead of the seventh costal cartilage, and was too long vertically in propor- tion to its lateral dimensions. The kidneys and other viscera could not be made ont as prolapsed. She looked ansemic. Here, then, was an individual whose organs were apparently normal with exception of the stomach, which was prolapsed but not dilated. !No other condition could be discovered to account for her palpitations, and accordingly she was told that the attacks were probably due to the gastric disorder, perhaps intensified by the undue use of cofi:"ee. She was emphatically assured that her attacks were not dangerous and was ordered to secure an abdom- inal supporter, and so adjust her clothing as to avoid the dragging of her skirts upon the abdominal parietes and pressure upon her stomach. She was given tincture of nux vomica before and dilute hydro- chloric acid in essence of pepsin after meals. For the attack of palpitation with pallor of face and coldness of the extremities she was given tablets of nitroglycerin. Coifee was forbidden, and in- structions were given regarding a simple and nourishing diet. At present Avriting the symptoms still persist, but are less severe. Tachycardia. — The physician is frequently called on to treat cases of habitually rapid heart's action, which are so annoying to the patient by reason of his subjective consciousness of the same that they may be said to be a persistent palpitation. In many in- stances this is the exaggerated cardiac action of Graves's disease, yet it is so prominent a symptom that it brings the patient to the doctor in the belief that the heart is the real seat of the trouble. As exophthalmic goitre is a disorder of the nervous system instead of the heart, it will not receive special consideration in this work. There is another class of cases, however, which likewise present tachycardia and attacks of palpitation as their main symptoms, and which because sometimes associated with thyroid enlargement would seem to be incomplete forms of Graves's disease. The indi- viduals are highly nervous, easily agitated, manifest more or less tremor, and in some instances have a warm unduly perspiring 716 DISEASES OP THE HEART skin. They do not show cxoplithahiios, and if goitre is not pres- ent, it is often exceedingly difficult to say whether they belong to the category of exophthalmic goitre or not. Most, if not all, the cases I have seen have been in women, who, as a rule, are below the age of forty. T have frequently discovered enteroptosis in these persons, and I am not able to escape the conviction that there is some intimate etiological connection between this condition and that of the nerv- ous system. In some there has been evidence of moderate cardiac hypertrophy and in others, not. This form of cardiac neurosis, as it may not inaptly be termed, was well illustrated by the case of a married woman of twenty- seven who came for treatment on account of symptoms that made her fear heart-disease. One sister had died of pulmonary tuber- culosis at the age of twenty-four, and I may say, in passing, that in my cases I have been struck by the frequency with which a history of consumption in some near relative has been obtained. The patient had not been in her previously good health since her last confinement, two and a half years before. Her home was in a remote suburb in a lonely situation, and as night approached and her husband did not return she regularly grew nervous and appre- hensive. She had lost weight, and for a considerable time had noticed that her heart beat too fast. Recently it had taken to giving a " flop," and every time this occurred it threw her into a state of alarm and agitation. Her neck had grown full, but she had given this no attention in comparison with the action of her heart. She was a hearty feeder, and all her functions appeared to be normal. Physical examination showed pronounced enlarge- ment of the thyroid, which was firm and without thrill. There was no prominence of the eyeballs, but there w^as a fine tremor and the pulse was so rapid, in consequence of extreme nervous agi- tation, that no attempt was made to count it. Cardiac impulse was exaggerated, but the area of dulness was not demonstrably increased, and the sounds were clear, ringing, and free from mur- murs. The lungs were negative and there was no enteroptosis. The case was regarded as one of incomplete exophthalmic goitre, and a guarded prognosis was expressed. The patient was assured that she had no heart-disease, and T observed that this assurance at once favourably influenced the heart's action and nervousness. FUNCTIONAL DISORDERS 717 In conclusion, it may be stated that under the prolonged use of iodine to the neck and internal medication addressed to relief of symptoms and improvement of digestion and general health, this patient ultimately made a complete recovery, the thyroid becoming of normal size and the tachycardia disappearing en- tirely. There was evidently a neurosis in this case, as shown by the powerful domination of her emotions over the action of her heart. Whether there was any direct connection between the thy- roid enlargement and the tachycardia and palpitations I am not able to say, but her nervousness certainly disappeared pari passu with the decrease in the size of the gland. ISTevertheless, her pulse-rate was invariably influenced by the state of her digestion and elimination. I recall another case of rapid and pounding cardiac action in a female who presented fine tremor of the extremities, but no other signs of Graves's disease, and who was ultimately found to be pregnant at the time. As she was positive that her symptoms had first attracted her notice after the cessation of her menses, and the heart's action quieted down somewhat as the pregnancy advanced, I have not been able to determine what the connec- tion, if any, was between the two conditions. This patient was unmistakably neurotic, as shown by both her family and personal history. Whether such cases are instances of incipient or incom- plete Graves's disease or not, they are instances of cardiac neuro- sis so far as the action of the heart is concerned. The foregoing cases present some of the symptomatology of heart-neuroses so graphically that it was thought best to intro- duce them before considering the etiology, although in so doing the general plan of this work is departed from. It is believed they will throw some light on the causation of some of the most common manifestations of functional cardiac disorders. As there is no demonstrable alteration in the structure of the refractory organ in typical cases, there is no morbid anatomy to be described. If a valvular lesion or dilatation of the heart is found in a person displaying the symptoms of neurotic disturbance of cardiac ac- tion, a combination which is not at all infrequent, the anatomico- pathological changes on the part of the heart are not to be re- garded as dependent upon the neurosis. There may be an etiologi- cal connection in so far as the organic heart-lesion may, through 718 DISEASES OF THE HEART its influence over metabolism, aid in the development or the main- tenance of the neurosis and may help to explain the ease with which the heart's action is perturbed. It may also be claimed that the palpitation and tachycardia induce the dilatation; but in my experience these cases do not display permanent cardiac enlarge- ment to an extent that calls for treatment. As previously stated, the pathology of palpitation is ohsciire. It is argued that it may be due to loss of vagus control, which allows the accelerator to gain the ascendency, or that there may be stimu- lation of this latter independent of an abeyance of the inhibitory apparatus. Again, it is not at all certain that there may not exist some histological change in the heart structures or nerve-centres which may account for the readiness with Avhich the action of the heart becomes disturbed under conditions that are inoperable in the healthy individual. As Romberg saj^s, arteriosclerosis some- times develops in neurasthenics at an unusually early period of life; and who can say that there may not be some connection be- tween this fact and the cardiac manifestations ? These are mat- ters of speculation purely, and in the present state of our knowl- edge we must content ourselves with speculation and theory. Cardiac Pain. — This is another exceedingly frequent symptom in neurotic patients who suffer from fancied disease of the heart. It possesses no uniformity in intensity or character, being in one case sharp and darting, in another dull and continuous. Its one feature, common to all, is its location in the heart-region, usually in close proximity to the left nipple. It is sometimes intensified or even evoked by exercise — e. g., sweeping, which calls into use the muscles of that portion of the chest. In some instances it seems to be influenced, in part at least, by atmosplieric conditions. Very frequently this pain is associated with a feeling of anxiety or oppression in the prtecordia, which, because it occasions a vague feeling of apprehension, is by the Germans called herz angst, or anxiety of the heart. This sensation may be wholly independent of any demon- strable change in the heart action, but is apt to be attended by palpitation, coldness of the hands and feet, and other indications of vaso-motor disturbance. As stated, it may accompany, but as a rule it seems to replace, actual pain. Whatever the exact char- acters of this j)ru'Cordial feeling, it is very unlike, and is not to FUNCTIONAL DISORDERS 719 be confounded with tlio painful seizures wliicli are designated angina pectoris, whether true or false. The differences are so marked that no mistake ought to be made, and yet it is possible for the feeling of cardiac anxiety to be mistaken for the constric- tion of the chest present in grave angina and the feeling of appre- hension for the sense of impending death. Pseudo-angina Pectoris. — From the standpoint of scientific ac- curacy this term may be and doubtless is objectionable, since there can be no such thing as a false chest pain. jSTevertheless, this term is sanctioned by the usage of the best writers in this country and Europe. It includes those precordial pains which closely re- semble attacks of coronar^^ angina, and are therefore spoken of by Osier as " allied states." The essential difference between them lies in the fact that pseudo-angina is independent of structural disease of the heart or its nutrient vessels, and that it is not likely to cause sudden death. In true angina there is some condition within the heart which initiates the stimulus sent to the nerve-centres. In the pseudo form the starting-point of the painful attack is, according to Huchard, not the heart, but some peripheral or visceral nerve, most commonly one of the intercostals. The impulse thence passes to the medulla, and there, reaching the sensory centres, evokes a sensation of pain that radiates into the chest or down the arm with phenomena that point to a coincident stimulation of the vaso- motor and vagus centres. Often it is some painful point on the chest, generally one in the region of the left nipple, which acts as the starting-place for an attack. Whether such is the pathology of these cases or not, it certainly seems to me to afford a fairly satis- factory explanation of the essential difference betw^een these two forms of angina. Writers recognise three great varieties of this neurotic form: the reflex, the vaso-motor, and the toxic. Of these, angina re- flectoria is the most common, although no one can observe these cases without coming to the conclusion that they are all very apt to blend indistinguishably with each other. Irritation within the abdominal organs is thought to be the most common starting-point of an attack of the reflex variety, and yet the vaso-motor form may likewise find its origin in some disturbance within the abdo- men as well as in any part of the body. Huchard dwells much on 720 DISEASES OF THE HEART the toxic angina and finds its cansation in toxic agencies intro- dnced into the system from without, snch as tobacco. An attack of pseudo-angina pectoris is agonizing, and because it usually begins in the cardiac area it excites a feeling of fear or apprehension that is closely allied to a sense of impending death. Ordinarily, however, the patient admits that this feeling is subor- dinate to that of pain. This latter radiates throughout the chest and into the left arm, which is apt to feel numb and cold. There is often a " clutching feeling at the heart," and the patient is apt to have a sensation as if she were " sinking away." At such times the pulse is said to become " very low," by which seems to be meant slow and weak. In cases of the vaso-motor type the face is pale and anxious, the extremities cold and clammy, and the pulse is small, usually slow, and often irregular or intermittent. The sufferer from pseudo-angina is not compelled to assume an erect, motionless attitude, as in true angina, but lying on the bed or couch moves about restlessly and moans or cries aloud with pain. It is this feature of the attack on which reliance is chiefly placed in the determination of its real nature. Exceptionally, patients pass into a cataleptic state, apparently though not actu- ally unconscious, rigid, and it may be cold, presenting in this state an appearance which is very alarming to the friends, who think it presages speedy death. The attacks usually come on sud- denly and without warning, frequently at night, but in some in- stances there are prodromata, such as chilliness, restlessness, or vague nervous sensations. Some authors state that this neurotic form of angina displays a tendency to periodicity by recurring at the same hour on successive days. The duration of the seizures is longer than that of true angina, lasting for one or more hours ; their departure is apt to leave the patient weak and exhausted. They may abate gradually or suddenly or they may terminate in an attack of violent palpita- tion. Numbness and helplessness of the arm into which the pain radiates are not infrequent sequels of a paroxysm. Patients are naturally terrified, not only by the seizure, but also by the pros- pect of its return. Its frequency of occurrence is variable, but usually the intervals of freedom from pain are not long. Hu- chard observed cases in Avhicli as many as 200 or 300 attacks were experienced In tlie course of a single year. FUNCTIONAL DISORDERS 721 In pure angina reflectoria without vaso-motor phenomena irritation originates in some distant part and the pain radiates thence into the cardiac area^, from which it spreads along the in- tercostal nerves and even into the left arm. There is usually an associated feeling of anxiety and constriction, but the neuralgic element is the more pronounced, Iluchard cites a case, not ob- served by himself, however, in which the paroxysms of pain origi- nated in the cicatrix of a wound received many years before. This was situated at the bend of the elbow, and the attack of pain was precipitated by movements of the joint, by friction of the clothing, and even by gentle stroking of the scar. Squeezing of the middle finger was also capable of arousing a paroxysm, and this fact together with their cure by acupuncture led him to con- clude there must have been an hysterical element in the case. He also quotes the instance of an officer who experienced an attack of pseudo-angina in consequence of painful irritation of his foot by one of his decorations, which had fallen into his boot, and there remained during the day. In such an individual there must be a highly neurotic tendency. Osier narrates a single case in which this form of angina followed attacks of vomiting, and there- fore appeared due to gastro-intestinal irritation. Such attacks have also been known to result from exposure to cold. In the vaso-motor foi^m the exciting cause may likewise be exposure to cold or even the washing of the hands in very cold water. In this group there are phenomena of widespread vaso- motor spasm as well as pain, as might be expected. • The strictly toxic form is exceedingly uncommon and presents considerable diversity as regards the severity of the attacks and the prominence of certain features. Pain is often subordinate to a feeling of anxiety or prsecordial oppression and there is dis- turbed cardiac rhythm in the way of retardation or acceleration, irregularity, and intermittence of the pulse. In tobacco angina there may be vertigo, pallor, a contracted pulse, tendency to syn- cope, prsecordial anxiety, coldness of the hands and feet, and cold perspirations. According to Iluchard, there may be other asso- ciated symptoms which are referable to nicotine intoxication, as dizziness, tinnitus aurium, dysphagia, and cephalalgia, a sense of suffocation or dyspnoea, general weakness, cerebral confusion, spinal tenderness, and disorders of vision. Although anginal 47 722 DISEASES OF THE PIEART attacks from tobacco may be incomplete in all their manifesta- tions, they are none the less severe, and may be of great intensity. Etiology. — Althongh the automatic action of the heart prob- ably depends upon some quality inherent in the cardiac muscle- cells, and not upon the nerve filaments or ganglia situated in the heart-walls, still there can be no doubt of the powerful influence of mental and nervous states ui)on cardiac action. The class of disorders now considered is generally thought independent of structural disease of the heart, although persons with organic car- diac lesions may undoubtedly present some symptoms closely akin to those of the so-called cardiac neuroses. The predisposing causes of the so-called functional or neurotic disturbances of cardiac action and of the various sensations refer- able to the heart are those disorders, neurasthenia, hysteria, etc., which for want of definite knowledge of their pathology are called neuroses. Psychoses, such as hypochondria, may also be attended by disturbance of cardiac action and other symptoms referable to the heart. Consequently in every case of cardiac neurosis the physician should endeavour to ascertain and expect to deal with some such underlying neurotic or psychical element. Heredity, age, and sex have an undoubted etiologic influence over functional disorders now considered. Most of these patients present a clear family history of neuroses, and some of them have manifested unstable cardiac action from childhood. It is particu- larly in the female sex that the symptoms which have been de- scribed are encountered, and yet some of the most pronounced cases are seen in young men. Women appea especially prone to these symptoms during the child-bearing period and at the meno- pause. Their attacks of palpitation, heart-pain, or what not, are very apt to be evoked during the days immediately preceding menstruation. This is not because of any direct etiologic connec- tion between the two, but simply because at this time, as at the climacteric, the nervous system is more than usually unstable. Whatever serves to lower nerve tone, or otherwise deteriorate the general health, predisposes to cardiac neuroses, and therefore mas- turbation, excessive venery, loss of sleep, sorrow, worry, too close confinement to mental pursuits, are all predisposing factors. The influences which act as exciting causes are too numerous and various and often too obscure to warrant the attempt to enu- FUNCTIONAL DISORDERS 723 mcrate them in detail. Patients are very apt to speak of having a " nervous shock," by which may be meant some sudden start or fright, an unexpected piece of bad news, and the like. In many instances the mere suggestion, whether subjective or made by an- other, that they have heart-disease suffices to excite an attack of palpitation. This is particularly the case with hysterical sub- jects, and I have known a word casually dropped, by being wrong- ly understood to apply to himself, to throw such a person into a violent fit of palpitation with coldness of the hands and a feeling of intense anxiety. On the other hand, a reassuring word will sometimes as promptly quiet the action of the heart. There is often a close connection between the taking of food or a remedy and the onset of symptoms. This is sometunes doubtless the result of suggestion, at others of the formation of products of indigestion, and when this latter is the case it is dif- ficult to say whether it is through a reflex or mechanical action or is the eifect of the absorption of toxins. The symptoms not infrequently come on so quickly that there would hardly seem to be time for the formation and action of toxins. In neurasthenic individuals fatigue is undoubtedly an exciting factor. I have known a woman to take a short walk and immediately upon her return to be seized by a sinking spell with either rapid or slow and feeble pulse and coldness of the extremities, symptoms easily thought to indicate heart-failure, yet in reality due not at all to cardiac weakness. Ordinarily in cardiac neuroses an attack of palpitation is not produced by a reasonable amount of exercise. In fact, moderate exercise, as walking, is more likely to quiet down the heart. N^evertheless exceptions may occur, as was the case with one of my patients, a highly neurotic young man with- out demonstrable signs of organic disease. Cases of pseudo-angina reflisctoria have been shown in the de- scription of symptoms to result from irritation of the abdominal viscera, from irritation of a peripheral nerve, and undoubtedly also from disturbances within the pelvic organs. It is my opinion that the same sort of influences may excite an attack of palpita- tion instead of pain. The same thing is true, I believe, as regards the impressions which are said to arouse an attack of pseudo- angina through the vaso-motor centres. Palpitation of this origin is not common, however, any more than is pure vaso-motor pseudo- 724: DISEASES OF THE HEART angina. Instances in which an attack of pain is called forth by washing the hands in too cold water or by the impression made by a cold wind n])on the intercostal nerves are certainly excep- tional. Of the toxic agencies accredited with the production of pseudo-angina pectoris, disordered action of the heart, prsecordial anxiety, oppression, etc., tobacco is by far the most frequent. This influence of the weed is not very common, and yet I have under observation at the present time a gentleman wdio assures me that he cannot smoke a single pipeful of mild tobacco without feeling his heart beat more rapidly and strongly than ordinary. Diagnosis. — In deciding the question whether or not a pa- tient's symptoms warrant their being classified as a cardiac neu- rosis, one should bear in mind that they are independent of struc- tural alteration of the heart, and are in reality one of the mani- festations of a disordered nervous system. Consequently one must first seek in the personal and family history and by a care- ful analysis of the symptoms for evidence of hysteria, neuras- thenia, or of a highly neurotic temperament, conditions which have been shown to possess an etiologic influence over the phenom- ena that form a clinical picture of cardiac neurosis. This being so far as possible settled, it is next necessary to determine the presence or absence of organic heart-disease. If such can be excluded, and the patient belongs to the age and sex in which neuroses are most prevalent, a correct diagnosis cannot for the most part be difficult. If, on the contrary, structural altera- tion of the heart is detected, or if the patient has arrived at the time of life wdien myocardial degeneration is likely, then one should be most cautious about expressing a positive opinion. It is very possible that he has to do with a case in which there is a blending of neurosis with structural cardiac disease. In all in- stances, even in the young, one must carefully study the nature of the symptoms, carefully discriminating those pointing to insta- bility of the nervous system from such as indicate cardiac as- thenia. One should therefore inquire minutely concerning the effect of exercise, for although one cannot assert positively that physical effort is without influence upon symptoms in cardiac neuroses, still such is ordinarily the case. This applies as well to anomalies of cardiac action as to the differential diagnosis of pseudo-angina. FUNCTIONAL DISORDERS T25 Furthermore, without wishing to set it down as an infallible guide, 1 desire to give it as the result of years of observation that, if the patient is not subjectively aware of disorders of his cardiac rhythm, there is probably myocardial disease even if objective proof of the same cannot be had. The reverse does not obtain. The matter of dyspnea requires close study. Patients with car- diac inadequacy from whatever cause experience shortness of breath upon exertion and not during repose except in an advanced stage. Neurotic individuals, on the contrary, unless markedly neurasthenic, are able to walk without breathlessness, whereas they are very apt to complain that they are unable to draw a long breath, or that they feel a " catch in their breath." They breathe superficially, and every now and then take an unusually deep in- spiration, which is followed by a feeling of great relief. If one is summoned hastily to administer relief to a patient in an attack of palpitation, a sinking spell, etc., a correct diagnosis is not always easy at first. Valuable information may be obtained, however, from inquiry into the history as regards previous at- tacks, mode of onset, etc., and from attention to the absence of signs of organic heart-disease and of secondary stasis. Further- more, the patient generally displays nervous agitation, fright, etc. In those cases of palpitation which manifest throbbing of the aorta either in the episternal notch or in the epigastrium, the dif- ferential diagnosis from aneurysm may be made by attention to the following points: (1) The history of attacks of palpitation and their association with symptoms of neurasthenia or hysteria ; (2) the age and sex of the patient, who is generally young and more often a female; (3) the absence of pain, of signs and symp- toms of pressure, of a localized tumour having an expansile pulsa- tion and thrill; (4) the absence of an area of dulness upon the manubrium sterni or at either side, or at some point along the course of the abdominal aorta; (5) the failure to detect the aus- cultatory phenomena, of bruit and accentuation of the vascular sounds usually present in aneurysm; (6) the evidence derived from the sphygmograph and the X-ray. In determining the significance and nature of pain in the car- diac region one should meet with but little difficulty if he remem- bers the following points: (1) The absence in neurotic cases of signs of structural cardiac disease ; (2) the spontaneous origin of 726 DISEASES OP THE HEART the pain, independent of exercise or of any other evidently excit- ing cansc; (3) the presence of painful areas in the course of the fourth and tifth intercostal nerves, sliOAvn by Head to be symp- tomatic of both functional and organic disorders of the stomach. These hypersesthetic zones are generally found on the left side as follows: (A) near the left nipple, upon the fifth rib, or in the in- terspace immediately above or below; (B) another upon the fourth costal cartilage or in the fourth interspace near the ster- num ; (C) at the lower end of the sternum or upon its appendix. There are frequently other painful points upon the back near the inferior angle of the scapula. The tender areas symptomatic of disorders of the thoracic organs are, according to the same author, located higher up, being in front on the sternum near the level of the third costal cartilage, and on the third rib, or near by, just within the vertical mamillary line. When the tender points first mentioned are discovered close inquiry will usiially elicit symp- toms of indigestion or the so-called auto-infection. For the most part the correct diagnosis of the pseudo-anginas is difficult only in patients at or after middle age, and in them the question is likely to be rendered still more difficult by the dis- covery of cardiac hypertrophy or arterial thickening. In such an event a positive diagnosis must often be deferred until time throws further light on the case. In most cases, however, a cor- rect diagnosis is possible by the discovery: (1) That the attacks, as previously mentioned, arise independent of, and are as a rule iminfluenced by, physical effort; (2) the suiferer is not compelled to seek the erect posture, but frequently prefers to lie down; (3) he does not present a picture of silent motionless agony, but moans or cries aloud and moves about restlessly; (4) the attack is of much longer duration, often lasting several hours; (5) it is often [)ossible to discover signs of peripheral disease that may exert a reflex influence or to get a history of influences that are operable through the vaso-motor system or act as a toxin. As regards tobac- co, however, it should be needless to suggest that in middle-aged men who are smokers coronary sclerosis is much more likely to be the cause than is their tobacco. Prognosis. — I'his is practically that of the underlying neu- rosis. These cases are often of very long standing, and therefore present a correspondingly unfavourable prospect of cure. In the FUNCTIONAL DISORDERS 727 young, when the case is unmistakably one of neurosis, the assur- ance can unhesitatingly be given that death will not result from the attack of palpitation or pseudo-angina. When the diagnosis is doubtful, the patient may, for the moral effect, be told that his cardiac symptoms are functional, yet the friends should be warned of the possibly grave nature of the case. In strictly neu- rotic subjects the prognosis depends, moreover, upon the possi- bility of the removal of all those influences of environment which unfavourably affect the patient. In Graves's disease, or those allied states associated with enteroptosis, the prospect of obtaining immunity from their tachycardia and palpitations is very un- promising. . Treatment. — This must be directed not alone to the relief of the j)aroxysms of palpitation or pain, but also to the removal if possible of the underlying neurosis. It is not the province of this work to discuss the management of neurasthenia and hysteria, and therefore the reader is referred to works dealing with the sub- ject. It need only be remarked here that the physician who would successfully treat cardiac neuroses must command the entire con- fidence and respect of his patient, and he must use the influence thus gained for their proper moral management. He must dis- play no hesitation or vacillation in his suggestions and no irreso- lution in their enforcement. Treatment of the Attack. — In most instances the medical at- tendant first sees the patient in one of his seizures, and is there- fore called on to act energetically and promptly. Yet he should never be in such haste that he cannot first gain a tolerably correct notion of the nature of the disorder. He should never display alarm, and even if he thinks so, he should never tell the patient he is in danger of dying. On the contrary, he should endeavour to reassure the patient both by word and the calmness of his manner. Whether the attack is one of palpitation merely, or one of intense pain, the treatment is essentially the same, for there are usually associated symptoms of vaso-motor disturbance. Palpitation. — I have never been able to see the wisdom of re- sorting to digitalis or remedies of similar action for the arrest of an attack of palpitation. These remedies are slow of action, the attack is in most instances short-lived, and before the digitalis takes effect the tumultuous heart-action subsides spontaneously, or 728 DISEASES OF THE HEART because some other measure has met tlic indication. If there are pallor of the countenance, coldness of the extremities, and a small contracted pulse, a rapidly diffusible stimulant is indicated. The arterioles should be dilated so as to cause warmth and flush- ing of the surface, even though the pulse be rapid as well as small. To this end nitroglycerin is efficient and usually affords prompt relief. It is better to dissolve a tablet or to drop a minim of a 1-per-cent solution on the tongue, for its action is more prompt than when swallowed. Whisky, ammonia, camphor, or even hot ginger tea or hot peppermint water may be given, while heat should also be applied to the extremities and prsecordium. If in- stead of being cold the surface of the body is warm and the face flushed, pulse full and bounding^ then diffusible stimulants are contra-indicated. It is now better to apply ice to the pra^cordium and to give a full dose of one of the bromides, with possibly 2 or 3 drops of tincture of aconite root. This may be followed by a dose of digitalis or strophanthus. In most cases fear plays an impor- tant part in maintaining the attack, and consequently the very presence of the doctor, provided his manner is calm and reassur- ing, will do much to aid the action of remedies. If the seizure is unusually refractory and the patient's agitation does not subside after a sufficiently long trial of the line of treatment indicated above, then it may be well to inject ^ of a grain of morphine for its calmative effect. The Attach of Pain. — If the pra:'Cordial distress is not suffi- cient to merit the term of pseudo-angina, l)eing plainly a pleuro- dynia with cardiac anxiety, it may yield to the application of a sinapism or of simple heat to the chest. If there are signs of vaso-motor spasm, or if the pulse is weak and perhaps slow and irregular or intermittent, a rapidly acting stimulant of the kind mentioned above should be given. If the paroxysm is a pseudo-angina either one of two remedies is indicated : nitroglycerin where there is arterial spasm, and m(irj)hine subcutaneously where there is or is not such spasm. This latter not only allays pain and acts as an efficient cardiac stimulant, but it calms the patient and promotes subsequent sleep. Nevertheless it is well to bear in mind that there is always danger of these neurotic patients, wlio suffer from fi-ccpient attacks of l)ain, learning to depend ujion the drug, and thus in time becom- FUNCTfONAL DISORDERS 729 ing victims of the morphine habit. The same objection applies to the use of alcoholic stimulants for the treatment of an attack of palpitation, sinking spells, etc., and therefore it is better to rely on other harmless but equally effective stimulants. In conclusion, the physician should search for and endeavour to remove all those sources of visceral or perij^heral irritation which serve to disturb the nervous system between attacks or may seem to act as exciting causes. Enteroptosis, dilatation of the stomach, digestive indiscre- tions, or any other condition that may account for the cardiac symptoms are to be treated in accordance with the principles ap- plicable to such cases and the special indications of each case. Great amelioration and sometimes entire relief of the distressing attacks of palpitation follow so simple a measure as the wearing of a properly fitted abdominal supporter in cases of ptosis of the stomach or other viscera. In addition, attention must be paid to the clothing, that too tight skirt-bands or corsets may not in- crease the dragging of the abdominal contents upon their sup- ports. Properly given, massage is often of much benefit in these cases. Finally, in all cases the exciting causes should be carefully sought out and the patient impressed with the necessity of avoid- ing all those influences which may precipitate an attack. He should be told that if he is to get better he is to aid in his cure by obeying instructions to the letter, since medicines alone are in- capable of eradicating his disorder. CHAPTER XXXI ESSENTIAL PAROXYSMAL TACHYCARDIA This is a highly interesting and very puzzling derangement of the heart's action which has received much attention from the medical profession since 1867, the date, according to Herringham, of the publication by Payne Cotton of the first recorded case. This disorder of cardiac rhythm consists in exceeding rapidity of action, and occurs in attacks of variable duratioxi and frequency, during which the heart-beats number 160 or more to the minute. ]\Iedical men in the British Isles have always been keen observers, and here again, as in angina pectoris and bradycardia, have sig- nalized their powers of observation. Cotton, Edmunds, Watson, and Bowles led the way, and in the next few years other observa- tions were recorded by Nunnely, Cavafy, and Farquharson. On the Continent we find the names of Tuchzek, Gerhardt, Bouveret, Oettinger, Probsting, and many others. Gerhardt suggested the term Tachycardia in the year 1881, and in 1888 Bouveret sug- gested the appellation Essential Paroxysmal Tachycardia, to dis- tinguish cases in which the paroxysms of excessively rapid action furnished the only clinical evidence of cardiac disease. Acceleration of the heart's action to 140, 150, and even to 170 in the minute is sometimes observed in cases of valvular lesion, and may be assumed to depend in some way upon structural alter- ation of the walls due to the valve defect. But in those cases which Bouveret characterizes as essential tachycardia there is no clinical evidence of cardiac disease, and therefore tlio ])arnxysms cannot be considered symptomatic. This distinction is objected to, however, by Herringham, Gibson, and others, who prefer to call the condition simply paroxysmal tachycardia, since this ap- plies broadly to all cases in which typical attacks of excessively rapid action occur. 730 ESSENTIAL PAROXYSMAL TACHYCARDIA Y31 Clifford Allbiitt objects to the term paroxysmal, saying, " The interpretation is that tachycardia is a fairly uniform symptom groii}) ; and, as one of its eminent characters is its paroxysmal occurrence, the addition of this qualification to the name is super- fluous." Pathology. — There are no anatomical changes that can be definitely associated with essential paroxysmal tachycardia, and likewise there is no established pathological basis upon which an explanation of the phenomenon may rest. Prior to 1897 six post- mortem observations had been made in this class of cases, but they failed to disclose any constant or uniform lesion. In one, the wall of the left ventricle was in a state of pronounced fibrous degeneration, and in two the hearts were extensively fatty, while in three others no special changes were noted aside from dilata- tion. As these alterations have been found over and over again, indeed, are very common in hearts that have never manifested this peculiar disorder of action, it is plain that there is nothing in these post-mortem findings to explain the occurrence of parox- ysmal tachycardia. Consequently various theories have been offered to account for the attacks. Tuchzek suggested paralysis of the vagus, and IS^othnagel, irri- tation of the sympathetic, sufficient to overcome the controlling influence of the pneumogastric. It has also been suggested that there may be a combined action of the two, vagus paresis and ac- celerator stimulation. Objections are urged against all of these theories. Tuchzek's theory has been widely accepted, and yet ex- periments on animals have failed to produce so extreme a rapidity of heart-action as is seen in these attacks, and Allbutt believes that in man abeyance of the inhibitory control of the vagus would not send the pulse up beyond 120. Likewise, stimulation of the cardiac accelerator nerve is said not to increase the pulse-rate beyond 150. Ascribing the rapid action to a combination of both necessitates the assumption of some cause which acts simultane- ously on both nerves, and this, in Allbutt's emphatic words, " sins against the economy of causes." Bouveret's suggestion that it is a bulbo-spinal neurosis, and Talamon's that it is of an epilpetic nature, are both not acceptable. Samuel West has urged that the attacks are due to alterations in the myocardium, to which Herringham would add changes in the 732 DISEASES OP THE HEART nerve endings situated in the heart, a view that seems to appeal strongly to Gibson. Other suggestions, as a neuritis, are of still less importance. They are all mere surmises ; and in the present state of our knowledge, without numerous and careful necropsies to throw light on the anatomical changes underlying this interest- ing symptom or disease, whichever it may be, we can only say witli posit iveness that we know nothing concerning its true nature. Etiology. — This is likewise obscure. Most of the recorded cases have been in adults. Of the 53 cases collected by Herring- ham, the age was stated in 40, and of these there were 7 instances in children, 12 between the ages of twenty and thirty, and 13 in the following decade of life, the remainder being in persons past forty. Age, therefore, cannot be said to exert special predispos- ing influence. Both sexes are subject to attacks, and although 30 of Herring-ham's collected instances were in males, the prepon- derance of this sex is so slight that it scarcely warrants the con- clusion that in sex alone resides any predisposing influence. That in some cases there may be an hereditary element ap- pears to be established by Oettinger's case, since there was history of the same sort of attacks in three preceding generations. In some of the reported cases there has been a history of previous disease — rheumatism, influenza, diphtheria, malaria, amemia — that may possibly have been a predisposing factor, but a definite relationship of this kind has not been established. In the way of possible exciting causes have been a blow on the chest, fright or other strong emotion, and a sudden physi- cal effort. Attacks have also followed disturbances in the digest- ive tract. Komberg states that paroxysmal tachycardia rests on a nerv- ous basis, and may arise reflexly from disorder in any of the vis- cera or may result from some cause acting directly througli the central nervous system, and is independent of any demonstrable cardiac disease. Thus it is plain that after all has been written on the subject of its pathogenesis we are no wiser than we were before. Features of the Paroxysm. — Two conditions are essential if rapid action of the heart is to be considered an instance of essen- tial paroxysmal tachycardia: (1) Tlie apparently healthy heart must beat at least 100 times a minute. (2) The onset and ter- ESSENTIAL PAROXYSMAL TACHYCARDIA 733 minatiou of the attack must be so sudden and abrupt as to give it the character of a paroxysm. Although a pulse-rate of less than 160 is frequently observed in persons with some structural disease of the heart, still in essential tachycardia the number of cardiac contractions is often vastly in excess of this number, running as high as 200, and in a few instances even to 300 a minute. The pulse is small, thready, and often uncountable, because the ex- treme frequency of the waves and the emptiness of the vessel cause the pulse-waves to run together in an indistinguishable manner. To determine the heart-rate, therefore, one must count the heart-beats by auscultation instead of by palpating a periph- eral artery. The rhythm of the contractions is usually regular, but irregu- larity and inequality in their force are sometimes observed. The extreme rapidity of the cardiac systoles is at the expense of their Fig. 108. — Sphtgmogram from Case of Paeoxysmal Tachtcaedia. Strength and efficiency, blood-waves of normal volume are not dis- charged into the aorta, the arterial system becomes relatively empty, and the pulse is one of strikingly low pressure. This is illustrated by the appended tracing (Fig. 108) kindly furnished me by Dr. E. F. Wells from one of his cases. The paroxysms begin abruptly and generally without premoni- tion. Indeed, upon the occurrence of the first attack the patient does not always know what is the matter with him, and is only able to say he feels bad. If the tachycardia is short lived, the patient may experience nothing more than a vague feeling of dis- comfort and his outward appearance may not disclose anything unusual to the ordinary observer. There may be, however, pallor or flushing of the countenance. In some instances there are pra3- cordial oppression and even pain, numbness or tingling of the arm (Gibson). Palpitation or fluttering of the heart may be com- plained of, and vertigo is sometimes experienced. Most sufferers from this complaint, notwithstanding repeated attacks and the 734 DISEASES OF THE HEART fact that experience has shown the termination to be in sudden recovery, become greatly alarmed, and if the attack is prolonged to several days fall into a state of great mental and physical dis- tress. If the case is seen early there is usually so little evidence of the actual state of things in the patient's outward appearance that the medical attendant on feeling the radial pulse is usually struck with astonishment and even dismay at its rapidity. If the attack lasts long enough it leads to cardiac inadequacy and the blood tends to accumulate in the heart-cavities. The heart becomes overdistended and the venous side of the circulation en- gorged, as shown by increased cardiac dulness, cyanosis, and it may be by pulsation of the jugulars (Gibson). There is pulmo- nary congestion, possibly also a small amount of oedema, and even albuminuria. The heart-sounds are feeble and the first at the apex may become almost inaudible. In most cases the duration of the paroxysm is not sufficient to lead to such marked signs of stasis. The attack subsides sud- denly after a few hours and the patient is left very much as he was before, feeling perhaps tired and dreading a recurrence, but able to return to his ordinary duties. A striking peculiarity of such a paroxysm, whether long or short, is the persistence of the tachycardia even during sleep. Such attacks are usually repeated through a series of years, and yet cases have been observed in which but a single paroxysm was noted. Although recurrences are the rule, there is no regularity in their repetition. Their duration is likewise variable, since the paroxysms may last from a few minutes to one or more days. In one or two in- stances the tachycardia persisted for two or even three weeks. If the tachycardia is a symptom of some visceral disturbance, or, in other words, is a functional derangement of reflex origin, then it is easy to conceive of but a single attack and to understand how this may be of short duration. But, if it is due to some deli- cate and as yet unrecognisable alteration in the myocardium or bulb, then recurrences should be the rule, as indeed they are, and the nttar-ks slionld be of considerable duration. Diagnosis. — The determination of the fact of tachycardia is not difficult. The point to be decided is whether the rapid ac- ESSENTIAL PAROXYSMAL TACHYCARDIA 735 tion is an instance of essential paroxysmal tachycardia or is of the kind called symptomatic. If it belongs to the former class, it should fulfil the following requirements: (1) A heart-rate for the time being of at least 160 a minute, (2) abruptness of onset and equal suddenness of termination, (3) failure to detect evidence of heart-disease either during or between attacks. If, on the other hand, there is evidence of myocardial or endo- cardial disease, the tachycardia is symptomatic and not essential, no matter how rapid may be the pulse. In this class, however, it is not usual for the heart's action to exceed 150 a minute. Most instances of " heart hurry " belong to this class, and yet it is prob- able that the essential form occurs more often than is reported, either because the attacks come to the notice of the family doctor rather than of the consultant, or because the attacks are so tran- sient that no physician is called in. Although I have repeatedly observed symptomatic tachycardia and have known several indi- viduals who gave a history of the essential form, among them a medical man, I have not actually v^itnessed a paroxysm. Prognosis. — In the essential form the prognosis may be said to be favourable so far as life is concerned. There is always an element of uncertainty in any case of extreme and protracted " heart hurry," but if a paroxysm terminates speedily no damage to the heart may be sustained. The real difficulty lies in the uncertainty of the length of time during which an attack may endure. In the aged, the feeble, and persons having a definite cardiac lesion such paroxysms are. not devoid of danger. In most cases of paroxysmal tachycardia the seizure may be expected to terminate abruptly and spontaneously, but how long the patient is to remain immune from a repetition is a matter of too much uncertainty for the prudent physician to express an opinion. The history of cases shows that in most instances other attacks are to be expected. Treatment. — The plain indication is if possible to arrest the paroxysm. This is called for, notwithstanding the fact that in the majority of cases the tachycardia has not caused death. Al- though a patient may have had repeated attacks that have ceased spontaneously, yet tachycardia is such an uncertain quantity that one can never be quite sure how^ another paroxysm may affect the heart. Unfortunately it is the same with this as with other mala- 736 DISEASES OF THE HEART dies; our therapeutic resources do not always enable us to meet indications satisfactorily. Theoretically, digitalis ought to enable us to slow down a run- aw^ay heart, but experience has shown its inefficiency in most cases. This remedy should not be administered recklessly in paroxysmal tachycardia, for if the attacks were to terminate spontaneously soon after the administration of a single very large dose or of several massive ones in quick succession, there might be positive danger of poisonous effects. If, as stated by Allbutt, digitalis produces diuresis even when it does not control the heart's action, it is likely to be eliminated and evil consequences will not result. Nevertheless, it is well not to administer more than 10 minims of the tincture hourly for six hours, and if at the end of this time no appreciable slowing of the pulse is produced, to have recourse to other means. Ice may be applied to the praecordia, or one may try the effect of prolonged but not too vigorous friction of the skin over the upper portion of the spinal column, which has been said to slow the heart. The vagus may be compressed in the neck, or it may be stimulated by an electric current. It has also been recommended that the patient take a deep inspiration, and then with his arms folded across the front of the chest and his feet pressed firmly against the foot-board of the bed to make a powerful expiratory effort while the glottis is kept closed. One of my patients who is a sufferer from essential paroxysmal tachycardia assures me that she has sometimes been able to check her heart by drawing a full breath, then w^hile her body is flexed so as to compress her abdomen, making a powerful expiratory pressure. In her case also a paroxysm has been known to be arrested by the pouring of cold water over her wrists. Whatever remedy is administered or wdiatev^r method of im- pressing the nervous system is tried, it is often found useless. It then becomes the physician's duty to support the heart until the tachycardia subsides spontaneously, and when cardiac dilatation sets in, this is imperative. To this end reliance must be placed on strychnine, caffeine, digitalis, etc., while the patient is kept at rest. The diet is to be simple and nourishing, and tea, coffee, or other stimulants are to be forbidden. In prolonged attacks it may be well also to administer a "ontle cathartic. ESSENTIAL PAROXYSMAL TACHYCARDIA 737 It may not bo possible to prevent recurrences, and attempts in that direction may seem to be somethiilg like firing in the dark, yet the patient should receive medical attention between attacks. In cases exhibiting subsequent signs of cardiac strain or in which there is an unstable nervous system, such regular treatment is spe- cially advisable. Gibson recommends tonics, a course of the ITau- heim baths with resistance gymnastics and such other measures as the experience of the medical attendant and the exigencies of each case suggests. In some instances it may be well to give digitalis or other heart-tonics for a long time. Every effort should be made to discover and remove any source of reflex irritation, and the daily life should be as healthful and free from excitement as possible. 48 SECTION V DISEASES OF THE ARTERIAL SYSTEM CHAPTER XXXII ARTERIOSCLEROSIS Degenerative changes in the coats of the blood-vessels were observed as long ago as the days of Senac and Morgagni, and by these investigators were described as an inflammatory process. It is to Rokitansky and Virchow, however, that we are indebted for thorough and systematic investigations concerning the origin and nature of the process to which Lobstein had previously given the name of arteriosclerosis. Virchow regarded it as a chronic arteritis and pointed out its similarity to the slow inflammatory process so often seen in the viscera, which is attended by the devel- opment of fibrous tissue. The inflammatory nature of arterio- sclerosis was accepted by other pathologists also, but by certain of them was regarded as an evidence of some infectious process. On the other hand, the cause of the sclerotic change was by Traube and others found in mechanical factors — i. e., in an in- crease of the arterial blood-pressure following persistent contrac- tion of the arterioles. Indeed, some went so far as to attribute to high blood-pressure every case in which they recognised sclero- sis and secondary cardiac hypertrophy. The latest view of the pathology of this vascular change and the one that is coming into general acceptance is that of Thoma. Concisely stated, his conception of the process is that in conse- quence of lessened resistance of the media the vessel becomes widened with resulting slowing of the blood-stream. Connective tissue then develops in the subendothelial layers of the intima as a compensatory process by which to restore the normal relation be- 738 ARTERIOSCLEROSIS 739 tween the artery and its contents. Although in most instances the vascular change is an attempt to make good a loss of elasticity and widening of the artery, still it may develop when the normal relation between the vessel and its contents is lost by reason of decrease in the volume of the blood. Romberg, to whom I am in- debted for the historical data just given, finds Thoma's view highly satisfactory, since it seems to explain the development of arteriosclerosis in cases which were previously unaccountable by Traube's theory. Moreover, it has been founded on an immense amount of carefully studied material. Morbid Anatomy. — Arteriosclerosis consists essentially in a degeneration of the media with secondary compensatory thicken- ing of the intima. It may be localized, constituting the nodular form of Councilman, or it may be diffuse. In the nodular or cir- cumscribed form whitish or yellowish patches are scattered along the inner surface of the vessel, which stand up from the surround- ing level and are of a rounded contour. In the diffuse variety the arterial wall is stiff, and more or less dilated, while on the surface of the intima may be zones of nodular thickening and calcareous or atheromatous patches. In old persons the arteries are stiff, more or less tortuous and dilated. The inner surface presents numerous calcareous plates and atheromatous ulcers. Examined microscopically, the thickening of the intima is found due to development of connective tissue between the endo- thelium and underlying elastic tissue. After a time, degenerative changes take place in this newly formed connective tissue which consist in hyaline transformation of the outer portion with areas nearer the endothelium of fine detritus in which fat droplets are seen. These areas of necrosis constitute the so-called atheroma- tous abscess. When these areas break into the lumen of the vessel depressions are left, known as atheromatous ulcers. The borders and bottoms of such ulcers are rough, and hence may become the seat of white thrombi. By the deposit of lime salts in these ath- eromatous patches calcareous plaques are formed which project above the surface of the intima, while by formation of chalky particles in the wall the artery may become transformed into a tube of almost bony hardness. In the middle coat changes of a degenerative nature take place which lead to weakening and dilatation of the artery and conse- 740 DISEASES OF THE HEART qiient thickening of the intima. The middle tunic becomes thinned in consequence of atrophy and degeneration of its muscle- fibres and of more or less extensive destruction of its elastic ele- ments. In some cases these elements disappear entirely and are replaced by connective tissue. The adventitia in its turn does not escape, but becomes infiltrated with round cells, especially in the neighbourhood of the vasa vasorum. The investing membrane be- comes tough and fibrous and may also be of increased thickness. The changes of arteriosclerosis which have been thus briefly described are not distributed uniformly in the afl'ected vessel or in all parts of the arterial system. The lumen of small arteries is apt to be greatly narrowed and even obliterated by the hyper- plasia of their coats, or it is blocked by thrombosis. The aorta and large arteries, on the contrary, are apt to become more or less dilated while their walls are rigid and the intima rough from the i)resence of calcareous plates and atheromatous patches, as pre- viously described. As already stated, the various parts of the arterial system are not equally involved in the sclerotic process. Thus Bregmann found as a result of analysis of the cases investigated under Thoma's direction, that the ulnar was involved in 94 per cent, anterior tibial in 93, subclavian in 88, cerebral arteries in 87, in- ternal carotid in 87, radial in 86, splenic in 82, popliteal in 79, external carotid in 78, axillary in 71, femoral in 69, common ca- rotid in 68, ascending aorta in 67, abdominal aorta in 64, external iliac in 58, and brachial in 55 per cent. This list shows some very remarkable differences which it is difficult to explain, and so far as I know have not been satisfactorily explained. Why, for instance, should there be so marked a discrepancy in the fre- quency with which the ulnar and radial are affected ? This matter will again be referred to in considering the eti- ology. It should also be mentioned that arteriosclerosis of the nodular variety is encountered in some arteries with greater frequency than in others. These are such as do not run in straight or nearly straight directions, but make numerous turns in their course or give off branches at a shar|) angle. The sclerotic ])rocess is here found at the points wliciice the branches dejjart or where the vessel undergoes a bend or curve. A glance at Bregmann's ARTERIOSCLEROSIS 741 tables, quoted by Romberg, and compiled with special reference to the nodular form, shows that the abdominal aorta heads the list, while the common carotid, internal carotid, ascending aorta, and cerebral arteries follow close after in this order. On the other hand, the radial is generally affected with the diffuse form, owing probably to its nearly direct course and the arrangement of its not numerous branches, conditions which per- mit uniformly high blood-pressure, and hence development of sclerosis throughout its length. Associated with sclerotic changes in the vascular system are alterations of a similar nature in the various organs, particularly heart, kidneys, and liver. In the senile form the heart may be decreased in size, whereas in the diffuse variety, that encountered in comparatively young and robust men, the heart sometimes reaches enormous dimensions. Councilman found instances in which the heart weighed two and nearly three times the normal. The myocardium is apt to show fibrous degeneration, the coro- naries to be sclerotic, and the aortic valve to be opaque, sclerotic, and in some cases incompetent. The kidneys are especially likely to show the sclerotic change on microscopic examination, although to the naked eye the changes may be so slight as to be easily overlooked. The capsule is adher- ent and somewhat roughened on its surface, which may present dark red depressed areas due to atrophy. The capillaries of the glomeruli are thickened and may be obliterated and exhibit ex- tensive hyaline degeneration. Atrophic changes may be present in the liver, particularly in connection with senile arteriosclerosis. Etiology. — The great frequency of sclerotic changes in the arteries of old people very naturally attracted attention and sug- gested a close etiological connection between age and this disease. It has been thought directly due to senility, and hence a necessary part of advanced years. That arteriosclerosis is not an invariable accompaniment of age, however, is well known, and Gibson states that when Thomas Parr died at the age of one hundred and fifty- two his arteries were found by Harvey to be free from any evi- dence of degeneration. Such facts indicate that to the mere influ- ence of age per se cannot be attributed the development of arterial degeneration. The explanation given by Romberg of the connec- tion between the two conditions seems to me to be the best I have 742 DISEASES OF THE HEART yet seen, and is, that when arteriosclerosis is found in an old man, it is because the conditions of blood-pressure which lead to the change have been operative during his many years, and therefore have come to manifest themselves more extensively than in a younger individual. Males are without doubt more often and extensively affected with this change than are females. This is owing not to any special influence inherent in sex, but to the greater exposure of men to occupations, habits, and conditions of life in general which affect blood-pressure injuriously. The influence of occupations which necessitate arduous physical exertion, and thereby subject the arterial system to strain, has long been recognised and empha- sized, particularly by the English, Thus day labourers, smiths, miners, etc., are very apt to develop arteriosclerosis, sometimes at a comparatively early age, and Romberg points out that in them it is the vessels of the extremities that are specially prone to dis- ease. It is probable, also, that among the labouring classes other factors are at work beside physical toil, such as abuse of alcohol and syphilis, l^evertheless, strain of the vascular coats by severe and oft-repeated muscular effort cannot be ignored in the produc- tion of sclerosis. Of diseases which lead to this degenerative process syphilis is perhaps the most important. Its relation to the form of endar- teritis known as obliterans was described by Heubner, and is quite generally recognised. Chronic lead poisoning and chronic alco- holism are also recognised etiological factors, as is likewise gout. How these act is not quite clear, whether as suggested by Traube by causing persistent augmentation of blood-pressure or through the action of their poisons directly on the vascular coats. The excessive use of tobacco is also believed by some w^riters (Iluchard, Romberg) to cause arteriosclerosis, particularly of the coronary arteries. Romberg likewise states that neurasthenic subjects are prone to arterial degeneration, as he believes, in consequence of the frequent alternations in blood-pressure occasioned by their unstable and excitable nervous state. The manner in which these, and other predisposing conditions to be mentioned presently, act in the production of arterial degen- erations has long been thought to be through the persistent in- crease of blood-pressure occasioned by them. Nevertheless expla- ARTERIOSCLEROSIS 743 nation based on such hypothesis was not altogether satisfactory and did not clearly account for the pathology or etiology of the changes observed. In the light of Thoma's investigations and views, however, we are now able to understand much in the etiol- ogy which was before obscure. It will be remembered that, according to his view, the thicken- ing of the intima is an attempt at the preservation of the normal relation existing between the calibre of the vessel and the pressure of its contained blood. The loss of such proper relation or equi- librium, as it may be termed, is brought about either by dilata- tion of the artery in consequence of lessened elasticity or by dimi- nution in the volume of the contents. Loss of elastic resistance on the part of the vessel is due to degeneration and atrophy of the elastic fibres of the media, and this destructive change in the mid- dle coat may be due to the long continuance of excessive blood- pressure or to sudden, frequent alternations of blood-pressure. Diminution of the volume of blood is seen very much less fre- quently, but is met with in the arteries of amputated extremities (Komberg), and, according to the same author, in the renal artery in interstitial nephritis. Of course the former requirement — i. e., increased pressure — is far more often and widely operative than is lessened blood-pressure. Accordingly, when we have to do clinically with arteriosclerosis we have to seek out some under- lying condition, disease, occupation, or habit, that has caused long-continued and greater internal or endarterial strain than the vessel was able to bear. Slowly the middle coat has been forced to give way before the intravascular blood-pressure, pari passu the intima has taken on compensatory thickening and by degrees the sclerotic process has declared itself. In some individuals blood-pressure has been abnormally high quite uniformly throughout the body and arteriosclerosis is gen- eral. More commonly, perhaps, the conditions influencing the change are local and the degeneration is confined to or at least far more pronounced in certain parts, as extremities, brain, coro- naries, etc. For example, the frequency with which the anterior tibial is involved is explained by the fact that this artery is com- pelled to bear the distending weight of a column of blood which is heavy by reason of hydrostatic pressure (Romberg). It has been frequently and forcibly pointed out (Fraenkel, 744 DISEASES OP THE HEART Hasenfeld) that corpulent persons of a sedentary mode of life are especially prone to the development of sclerosis in the splenic, hepatic, and superior mesenteric arteries, and, according to Hasen- feld, earlier in these than elsewhere. The explanation is, that owing to their sedentary pursuits and their habitual consumption of more food than the requirements of their inactive lives demand (luxus consumption) the vessels of their digestive organs are persistently overtaxed. In other words, blood-pressure within them is habitually too high. In time abnor- mally high and sustained pulse-tension is everywhere established, more or less wide-spread arteriosclerosis develops, and in conse- quence secondary cardiac hypertrophy (Fraentzel.'s idiopathic en- largement of the heart) results. Another interesting phase of this question of blood-pressure relates to the development of sclerosis in vessels which are ex- posed to varying degrees of pressure, oscillations from low to high pressure, " schwanlvungen " (Romberg). Such alternations subject the artery to undue strain and probably account for the sclerotic change so frequently present in the arteries of the arms of workingmen. According to Romberg, they also explain the fact that sufferers from migraine sometimes manifest sclerosis of the arteries of the side of the head affected by the pain. It is on this hypothesis likewise that we may explain the pre- ponderance of arteriosclerosis in the cerebral vessels of persons who are engaged in literary pursuits or whose occupations call for spe- cial activity on the part of the brain during a certain number of hours each day. May it not be for this reason that many an ambitious business man succumbs to the stress of modern com- mercial life ? Romberg explains the greater frequency of coro- nary sclerosis in hypertrophied hearts as compared with those that are not hypertrophied, on the ground that coronary blood-pres- sure is higher in the former on account of their more forcible contractions. If his view is correct, then one is tempted to query if the car- diac excitement experienced by stock-brokers and men of affairs under the influence of rapid fluctuations of the stock or grain market may not have much to do with the relatively great fre- quency of coronary angina in modern business men. In illustra- tion of the important etiological influence exerted by variations ARfERIOSCLEROSIS 745 of blood-pressure in circumscribed areas, Romberg cites the re- markable case reported by Erb of an ardent angler who developed a high degree of arteriosclerosis in the lower extremities, in con- sequence, it is thought, of his standing and walking for hours together in the cold water of the streams where he fished. Additional instances of the injurious effect of long-continued high blood-pressure are seen in the degenerative changes found in the pulmonary artery of mitral patients and in chronic phthisis as well as the general arteriosclerosis of diabetic patients (Rom- berg). In short, upon the basis of Thoma's conclusions we are now able to understand many a case of arteriosclerosis the development of which was previously almost unintelligible. Symptoms. — Arteriosclerosis is latent so long as it is of minor degree and not very wide-spread. When at length symptoms are produced, they depend upon the degree and distribution of the process and the organs affected. In some cases the clinical picture is that of renal inadequacy, in others of cardio-vascular disorder, in others again of disturbed cerebral circulation, and in still others of interference with the blood-supply to the extremities, digestive organs, or heart-muscle, as the case may be. Sclerosis of the renal arteries may be secondary to already ex- isting interstitial nephritis in consequence of diminished supply of blood to the renal capillaries, but in most cases it precedes or accompanies the development of the nephritis. The augmented blood-pressure occasioned, first declares itself clinically by in- creased secretion of urine, particularly at night. Examination of the urine in this early stage generally shows nothing more than a lowered specific gravity. When at length the sclerosis has be- come so extreme as to materially interfere with flow of blood in the renal capillaries, the urine grows scanty, and is apt to present characters like those of genuine contracting kidney. In these cases there is apt to be more or less sclerosis of the arteries of other parts, particularly the heart, or general pulse ten- sion becomes too high to be successfully combated by the hyper- trophied left ventricle, and symptoms of cardiac incompetence are added to those of renal disease. Thus I recall the case of a middle- aged physician who, aside from cardiac breathlessness, developed symptoms of serious renal inadequacy. Urine grew persistently scanty, contained an occasional trace of albumin, but rarely casts. 746 DISEASES OF THE HEART He ultimately died with symptoms that were urromic rather than cardiac, and the autopsy disclosed almost complete obliteration of the renal arteries. In other cases the picture is that of slowly increasing, or per- haps suddenly induced, failure of heart-power, with renal symp- toms of very inferior importance. Only to-day I examined a man of seventy-one who for two years past has noticed breathlessness, which of late has become serious cardiac dyspnoea. For more than twenty years he has had increased nocturnal micturition, but no other evidence of renal disease. He has been closely confined to his desk daily, and has been " a pretty heavy eater, particularly at breakfast." His chest is capacious and abdorainal corpulence is quite marked. The radials, temporals, and carotids are stiff, and the heart is enormously enlarged, its impulse feeble, and its sounds distant and muffled. This case is a fair illustration of the etiology and symptomatology of the cases in which the clinical pic- ture is what may be termed cardio-vascular, the chief, it may be the only, complaint being dyspna?a of effort. Many such cases, like the foregoing, very well represent the clinical picture of chronic myocarditis. In others, sj'mptoms of failing heart-power and of chronic interstitial nephritis are so in- timately blended as to make it difficult to determine definitely which organ is the more seriously involved. In others again, gly- cosuria and renal cirrhosis precede the symptoms of vascular and cardiac disease, yet when the latter become marked they may domi- nate the scene. In all these eases, when cardiac incompetence su- pervenes, it is apt to prove most serious and to progress under the every-day appearance of increasing and unconquerable stasis, since the extreme degree of peripheral resistance incident to arte- rial rigidity renders restoration of heart-power impossible. They have been sufficiently portrayed in preceding pages and do not re- quire repetition. In comparatively few cases the symptoms are mainly, almost exclusively, referable to the arteriosclerosis as such. The arteries everywhere feel wiry and nodular, like a string of beads, or thick- ened and tortuous, and the pulse is small and weak. The super- ficial veins stand out prominently; the heart manifests slight if any change, being in some moderately and in others not at all enlarged ; the urine is scanty and of poor quality, and if any albu- ARTERIOSCLEROSIS 747 mill is present, it is a mere trace, while casts are scanty, being hya- line or granular; the patient complains of increasing inability to work or exercise; appetite and digestion fail; slight oedema appears at the ankles ; the individual emaciates, grows sallow, pale, steadily more feeble, and at length takes to bed and dies from what appears to be general asthenia. I have notes of such a typical case in an Englishman who was a farmer of about sixty-eight years of age. Up to a year or so prior to my seeing him he was hale and hearty, and able to perform active work of a not too severe kind. Examination disclosed no distinct evidence of heart or renal disease, but the radials, ulnars, temporals, femorals, and tibials all felt hard and empty and most of them contained deposits of lime that gave them a pronounced beady character. Venous stasis was evident in the turgescent veins, palpable liver, and slight pit- ting of the ankles and shins. He did not complain especially of dyspnoea, but was much concerned over his growing weakness and loss of weight. Treatment benefited him for a time, but he ultimately grew too feeble to report at my office, and as he resided in the country was lost sight of. It was ultimately learned, however, that he died after a few months of what appeared to be general feebleness with failing circulation. In his case, as in many, the heart seemed to be comparatively unaifected and the difficulty of circulation to be due to the impermeability, so to speak^ of the arteries. The rigidity of the arterial system interferes with proper dis- charge into the capillaries — neither are the arteries able to receive the full supply of blood sent from the veins, and stasis occurs. In a considerable proportion of cases the clinical manifesta- tions are not those of disturbed circulation in general, but of dimin- ished or abolished blood-supply to a part, as the brain, extremities, heart, etc. The result is perverted function and structural altera- tion of a more or less serious kind. In some instances such disturb- ances are plainly apparent, while in others the manifestations of arterial degeneration are obscure and often misinterpreted or over- looked altogether. Thus sclerosis of the cerebral arteries may be shown by impair- ment of memory and intellection, headache, transient vertigo, espe- cially upon quickly assuming the erect position, change in disposi- 748 DISEASES OP THE HEART tion, increasing weakness, in a word, by tlie manifold symptoms due to cerebral ana?mia or areas of softening (enceplialomalacia) which result from the shutting off of blood-supply to definite areas. One should not forget also that when epilepsy develops at or after middle age, it may be due to arteriosclerosis within the brain (Hochhaus). Disease of these vessels is also a very frequent, ac- cording to Romberg the most frequent, cause of apoplexy. There may be either luinnorrhage into the brain from rupture of a miliary aneurysm, a condition of the arteries shown by Charcot to be very common, or the apoplectic seizure may result from thrombosis of a narrowed cerebral artery. Sclerosis of the arteries in the medulla is a recognised cause of slowness of the pulse and of recurrent bradycardia known as Stokes-Adams disease, and which has been previously considered. (See page 627.) Sclerosis of the arteries of the feet and legs is not uncommon, but apart from the change it creates in the elasticity of the vessel — i. e., stiffness and tortuosity, as perceived by the palpating finger — ■ it does not often lead to serious disturbance of circulation in the region supplied by the sclerotic artery. The sclerosis may, how- ever, according to Erb, be responsible for disorders of sensation and motion, vaso-motor and even trophic 'disorders. The first may be shown by paraesthesia, formication, pain, and a feeling of heat or coldness; disorders of motility, by intermittent lameness and extreme degrees of arterial narrowing by cramps, rigidity, etc. ; vaso-motor disturbances, by coldness, pallor, cyanosis; and nutri- tional disorders, by circumscribed sloughing of the skin. In cases of obliteration from sclerosis, as is well known, there may be local- ized gangrene (senile gangrene). According to Romberg, sensory and motor disturbances make their appearance at first only when the muscles are put in use — i. e., when tlicre is a call for more blood to the part than can be fur- nished by the thickened arteries. In more advanced degenerations these disturbances are produced by insignificant movements, and at length the limb becomes stiff and useless. Not only are vaso-motor neuroses, such as pain, redness, swell- ing, stiffness, etc., phenomena of arteriosclerosis, but, according to Romberg, there may appear symptoms of Reynaud's disease, cyano- sis, pallor, and even gangrene of portions of the skin, such phenom' ARTERIOSCLEROSIS 749 ena being particularly liable to affect the fingers. Fortunately, however, such serious disturbances are rare, and for the most part only minor degrees of sensory and vaso-motor perversions are present. The heart may be affected by arteriosclerosis in either or both of two ways : It may be degenerated and feeble in consequence of thickening, narrowing or thrombosis of the coronaries, with angina pectoris and the symptom-complex of myocardial incompetence, or the heart may be secondarily hypertrophied in consequence of diffuse sclerosis of the arteries supplying the abdominal viscera. Hasenfeld has dwelt on the intimate connection between sclerosis of the mesenteric vessels and general cardiac hypertrophy, and Romberg also states that it is degeneration of these arteries which calls forth secondary hypertrophy of the left ventricle. Extensive vascular change of the brain and extremities may exist, he states, without appreciable enlargement of the heart. This coincides with my clinical experience, for the largest and most inadequate hearts I have ever seen have been in men whose abdominal cor- pulence and sedentary lives have furnished the conditions neces- sary for the development of vascular disease in the splanchnic area. Moreover, their stiffened radials and high-tension pulse have borne out the correctness of that assumption. On the other hand, I have seen old men with emaciated abdomens, peripheral arteries that were like wires strung with tiny beads, and feeble, even flickering pulses, and yet whose hearts could not be made out as hyper- trophied. In some of these cases, to be sure, pulmonary emphy- sema renders the results of percussion uncertain, but the clinical picture is that of adynamia or of a cachexia, but not of myocardial failure, as in men of the other type. Lastly, there is still another group of cases which present them- selves in guise of chronic bronchitis and emphysema. They are usually at or past middle age, not confined to either sex, yet in my experience more often males of the labouring class. The vascular system is everywhere stiff, urine is of poor quality or may contain a small amount of albumin, and there is manifest hypertrophy of the right ventricle. This may be due in part to the emphysema, but a contributing factor of importance is the sclerosis of the pul- monary arteries. It is not always easy to determine whether this disease of the pulmonary vessels is primary or secondary, but as it 750 DISEASES OP THE HEART is associated with retrograde change of tlie aortic system it is fair to assume that it plajs a role in the causation of the emphysema and bronchial catarrh. For the most part the course of this vascular disease is slow and iijdefinite. Years are usually consumed in its development, and even after symptoms appear the course is protracted or more or less rapid, according to the portion of the arterial system chiefly affected and to the degree of the sclerotic change. Physical Signs. — Inspection. — There are two main types of individuals with arteriosclerosis. In one class they are large and imposing, more or less corpulent and with rather too flabby abdom- inal walls. In such, there may or may not be evidence of vascular disease in the peripheral arteries. The other type is quite the re- verse. The individual is thin, looks ill-nourished, and the tem- poral, perhaps also the carotid, arteries are seen distinctly, the former looking like stiff tortuous cords and pulsating visibly. Superficial veins are also prominent, but cyanosis is not present. The only other information obtained by inspection relates to changes in the strength and location of the apex-beat, and to epi- gastric pulsation, signs which may be directly connected with arteriosclerosis, yet may be independent of the same. Palpation. — This is the best and usually most reliable means of detecting arterial degeneration. If an artery which rests on a firm foundation, as the radial or tibial, is carefully palpated, it is perceived to be thicker and stiffer than nornuil. It can be rolled beneath the finger like a cord, and the vessel is difficult to compress. In many cases this is all, but in others the vessel is tortuous, and when the finger is passed along its course, presents small elevations that feel hard like beads, and hence lead us to speak of the vessel as beady. In some instances the artery shows minute elevations, which when carefully studied are found to be dilatations of the vascular wall — in other words, miliary aneurysms. Particular attention should be paid to the cervical arteries, noting their position, size, regularity or smoothness, rigidity, etc., since changes in tlicin may furnish valuable hints concerning the state of the aorta and inferentially of the coronaries. When the arch of the aorta is tliin-walled and dilated it may sometimes be felt pulsating abnormally high up in the sui)rasternal fossa. Litten is authority for the statement that when the abdominal aorta is scle- ARTERIOSCLEROSIS 751 rotic and accessible to palpaticjii, thrill is elicited by very much less pressure than is required if the vessel is healthy. Percussion is of value only in the detection of changes in the size of the heart secondary to vascular disease. It may, therefore, by demonstrating hypertrophy of the left ventricle, afford a certain amount of corroborative information. Careful and deep percus- sion of the areas overlying the ascending portion of the aortic arch may detect a slight degree of dulness due to dilatation of the vessel. In such a case resonance is apt to be impaired in the first and sec- ond right interspaces close to the sternum. Dilatation and elonga- tion of the arch may displace the heart downward, the same as does true aneurysm ; and hence in cases in which the aorta is suspected of being sclerotic, it is well to percuss the heart carefully, with view, if possible, to ascertaining its exact location. Auscultation. — Almost the only value of this means of investi- gation lies in the study of the second sound in the aortic area. This tone is normally more intense than is the pulmonic second in per- sons after thirty years of age, and hence it is the quality of this sound more than its mere intensification that is significant. Gen- eral arteriosclerosis causes accentuation of the aortic second tone, but so also do other conditions, especially chronic interstitial neph- ritis. Taken in connection with left-ventricle hypertrophy, un- due intensification of this sound is significant of arterial or renal disease or botb. If the sound is not only intensified but is also sharply ringing, even of a metallic quality and is associated with stiff arteries in persons of middle age, it is generally consid- ered to indicate sclerosis of the aorta. Should the sound be not quite pure, as well as accented, it is likely that the valve is also involved in the degenerative process, l^ot infrequently in persons whose vessels are resisting, there is a systolic murmur heard along the course of the ascending arch, and when present is, in the absence of signs and symptoms of aneurysm, to be regarded as due to roughening or dilatation or both of the aorta, not of steno- sis of the ostium. Any other modifications of the cardiac sounds are indicative of secondary or associated changes in the heart- muscle and valves. Diagnosis. — The recognition of sclerotic changes in periph- eral vessels that can be reached by the palpating finger, as radial, ulnar, tibial, etc., is a very simple matter, and has been sufficiently 752 DISEASES OF THE HEART described under palpation. It is far otherwise, however, with the diagnosis of sclerosis of the arteries within the cranial and other cavities. In such, diagnosis is usually a matter of inference in- stead of absolute demonstration, and must be arrived at by study of the patient's history, age, symptoms, etc. It is manifestly beyond the scope of this work to discuss the diagnosis of disease of the cerebral vessels. It may be stated, however, that tortuosity and rigidity of the temporals may, in connection with the head symptoms previously noted, be taken to point strongly to sclerosis of the cerebral arteries. If doubt still remains, or the external vessels are negative, the ophthalmoscope may be appealed to and is said to furnish early and reliable information concerning the state of the cerebral arteries (Thoma, Eehlmann, Koenig). The changes said to indicate sclerosis are pulsation and tortuosity of the retinal artery (when not due to chlorosis or anaemia), opacity of its coats, narrowing, and it may be thrombosis of the artery of the papilla, and miliary aneurysms and punctate haemorrhages into the retina, the choroid, and the enveloping capsule of the optic nerve (Koenig). The diagnosis of sclerosis of the aorta cannot always be defi- nitely made. Romberg states that the condition of peripheral vessels, as radials, affords no criterion of that of the aorta, and hence stiffness of the arm or leg arteries does not warrant a con- clusion that the aorta is also sclerotic. The state of the latter must be inferred, therefore, from careful study of the cervical ves- sels and of changes in the size of the heart or of its sounds. If the carotids appear healthy, if the heart is not appreciably en- larged nor displaced, and the aortic second tone is not unduly ac- centuated, then the aorta is probably healthy. If, on the contrary, the carotids are unyielding, the subclavians are situated abnor- mally high and feel stiff, if the left ventricle is hypertrophied, and lastly, but not least, if the aortic second sound is ringing and metal- lic, there is probably sclerosis of the ascending portion of the arch. The question of the existence or not of arteriosclerosis within the domain of the splanchnic nerves may present great difficulties. The recognition of stiffened radials in a corpulent individual who complains of dyspnoea of effort out of proportion to recognisable changes in the heart, renders extremely probable a similar state of the vessels deeply situated in the abdominal cavity. If, on the eon- ARTERIOSCLEROSIS T53 trary, accessible arteries are not stiff;, one must depend for diagno- sis on the history, symptoms, degree of blood-pressure, and adequacy as well as size of the heart. A history of sedentary pursuits and of luxus consumption; gradually developed and increasing shortness of breath ; abdominal corpulence ; high tension but slow pulse; cardiac hypertrophy without dilatation; these point strongly to arteriosclerosis as the cause of the symptoms. In suspected cases one should test the efficiency of the heart- muscle as well as search carefully for indications of overstrain of the right ventricle. If the pulse is unduly rapid and feeble during repose, if cardiac dulness is increased transversely and downward with pulsation in the epigastrium, if superficial veins are engorged, there is reason to conclude that the heart is no longer quite ade- quate and that the dyspnoea is cardiac. Then if on the patient's making extra exertion, as by hopping about the room, the action of the heart grows unduly accelerated, perhaps irregular or inter- mittent, and the sounds become feeble, perhaps accompanied by an apex-murmur, but little doubt is to be entertained of myocardial insufficiency. Even then the state of the internal vascular system may be a matter of doubt. Prolonged high tension of the pulse, as shown by Gaertner's tonometer, and a ringing metallic quality of the aortic second sound strengthen the assumption that the heart weakness is secondary to arteriosclerosis. It is, of course, presupposed that all other etiological data are wanting. The differential diagnosis of such cases from the cardiac insuf- ficiency of the obese (the so-called fatty heart), is often impossible, and, as a matter of fact, the two conditions are not infrequently combined. In the obese, however, there is a general distribution of adipose tissue far in excess of what exists where there is only excessive abdominal corpulence with arteriosclerosis. Quite recently I examined a gentleman of fifty-three com- plaining of breathlessness on more than moderate exertion. His abdomen was very bulging and flabby, while his extremities and chest were rather thin, his radials were distinctly stiff, but the heart was not appreciably enlarged except on the left, and did not grow too rapid or irregular from the effort of hopping up and down my office. In this case I felt no hesitation in attributing his symptoms to arteriosclerosis, and not to myocardial inadequacy, 49 754 DISEASES OP THE HEART particularly as his habits were such as tended inevitably to its de- velopment. Unfortunately all cases are not so clear, and hence necessitate great reserve. With regard to the diagnosis of vascular disease in other inac- cessible regions, it may be stated that coronary sclerosis is not often possible of positive recognition. It may be assumed when angina pectoris develops in a man past middle age, when there is reason- able evidence of sclerosis of the aorta and its great branches with subjective and objective symptoms of myocardial incompetence. Sclerosis of the pulmonary artery cannot be diagnosed with any degree of certainty, but may be assumed if a patient with stiff arteries is a sufferer from chronic bronchitis and emphysema, and in addition there is unusual hypertrophy of the right ventricle. Kenal arteriosclerosis may be inferred if in conjunction with stiffened peripheral vessels there is nocturnal micturition, the urine being of poor quality. When in an advanced stage there is evidence of positive renal change, as shown by albumin and casts, it is practically impossible to say definitely how much is due to nephritis and how much to arteriosclerosis. Prognosis. — This depends upon the degree of the vascular change discovered and upon the extent and nature of the visceral disturbance resulting therefrom. The process is inherently pro- gressive, and I believe incurable. Symptoms may, however, some- times be held in check by proper treatment. Cardio-vascular symptoms are for the most part subject to the conditions which influence prognosis in cases of myocarditis, and need not here be dwelt upon. For the prognosis of cerebral and renal arteriosclerosis readers are referred to works devoted to dis- eases of the respective organs. The prognosis of sclerosis of the pulmonary vessels is essentially that of the cardiac or pulmonary affections to which it is secondary, while when vascular decay of the arteries of the extremities has once led to definite disturbance of circulation the prognosis is highly unfavourable. Progressive emaciation and loss of strength in general arteriosclerosis indicate so serious an interference with nutrition that it may be regarded as the coiiimencement of the end. Treatment. — This is to be divided into (1) prophylactic, (2) curative, and (3) symptomatic. The institution of preventive measures necessitate (A) the earliest possible recognition of vas- ARTERIOSCLEROSIS 755 cular change and (B) the proper regulation of habits, diet, exercise, and excretion with a view to lessening undue vascular strain and correcting injurious fluctuations of blood-pressure. The disas- trous effect of sedentary pursuits must be counteracted by appro- priate gymnastic and abdominal exercises, including massage in cases of excessive abdominal corpulence. Heavy feeding must be restricted and its effects offset by outdoor exercise and sports, as golf, hunting, and fishing. Furthermore, the character of the dietary should be revised so as to exclude or reduce the eating of meats which are tissue-forming foods and are also harmful on account of the extractives they contain. Theoretically, also, the diet should not consist of foods rich in lime-salts, and as a matter of fact Rumpf, of Hamburg, cuts out such articles from the dietary of his patients. He includes among such forbidden articles milk, eggs, cheese, rice, and spinach. For my part, I am of the opinion that quantity cuts a far greater figure than does quality, since it is a matter of every-day observa- tion that the individuals who live the longest and are the most active with advancing years are those who eat sparingly and of a dietary relatively rich in vegetables, cereals, milk, and fruits. I regard it as a good indication when a person past middle age tends to lose weight gradually rather than to gain. Best of all, he should strive to hold his weight about at a standstill until well on in years. Exercise in the open is a very important matter, especially for the man who having been accustomed to plenty of exercise in col- lege suddenly finds himself tied down to his office desk many hours each day. He should endeavour in every way possible to get out for some sort of active physical exertion. If his profession or busi- ness duties tax his mental powers severely and keep him keyed up to the highest pitch day after day and month after month, then he should make whatever sacrifice is necessary to secure a yearly vacation, during which he can obtain perfect relaxation and recrea- tion. Otherwise sclerosis of cerebral or other arteries will be his fate after middle age. If, as is believed, the splanchnic nerves regulate blood-pressure and irritation of these nerves increases blood-pressure, particularly within the abdominal cavity, then, from a prophylactic standpoint, digestive derangements, including of course chronic constipation, 756 DISEASES OF THE HEART should be corrected. This is desirable from another point of view — namely, that by improving excretion the system may be rid of toxines which may be of influence in augmenting arterial tension, and eventually leading to arteriosclerosis. In a word, the prevention of degenerative changes in the blood- vessels calls for the removal, or at least the minimizing, of all in- jurious influences which are believed to derange blood-pressure, and thereby subject the vascular system locally and generally to strain. The curative treatment of arteriosclerosis is, I believe, unprom- ising. The French, and of late some German clinicians, as Vie- rordt, express faith in the ability of iodine to arrest and even cure vascular degeneration. The remedy is administered in the form of iodide of sodium rather than of potassium because of its being better tolerated. It is begun in small doses, 2 or 3 grains twice or thrice a day at first, and as the system learns to tolerate the remedy it is gradually increased until 15 grains three times a day are reached. In this dose the iodide is continued over a long time — i.e., from eighteen months to three years — but with occasional intervals during which the drug is not taken. Yierordt is said to omit the remedy one week out of five and one month out of every five months. Given in this manner, and from the start increased so cautiously as not to cause undue irritation, he has seen very gratifying results. I have made repeated attempts to get my private patients to perse- vere in the use of iodide of sodium after the manner recommended by Vierordt, but always without success. It has invariably disor- dered appetite and digestion, and at length has had to be discon- tinued. This therapeutic agent may favourably affect the patient's gen- eral condition, and even the vascular disease in cases of syphi- litic origin (although I believe the claim is made that favourable results arc obtained even when there is no specific taint), but it is very difficult to see how any drug can promote resolution of the sclerotic process, or why it should be well to do so. If the develop- ment of connective tissue in the intima is, as Thoma believes, a compensatory process by which is attempted to make good atrophic changes in the media, then how can any line of therapy be bene- ficial that does not restore the media to its former normal state? The iodide may in some way prevent or remove deposits of lime ARTERIOSCLEROSIS 757 and the hyaline degeneration that ultimately occur in the newly formed connective tissue, but can it do more or would it be well to have it do more ? It seems to me, therefore, that when arteriosclerosis has once become pronounced, our efforts must be limited to the prevention or lessening of symptoms — in short, must be symptomatic. To do this we must endeavour to promote better circulation in the arterial system, since it is in this respect that evils arise. Cardio-vascular derangements are to be combated in the same manner as disorders due primarily to cardiac insufficiency, and these do not need to be repeated. I should like to urge the neces- sity, however, of freely using vaso-dilators, as the nitrites, that if possible the arterial paths may be somewhat opened up and the labour of the left ventricle thereby lessened. In this class of cases nitroglycerin, etc., should always be given whenever it is necessary to resort to digitalis. It is because of the constricting action of digitalis on the arterioles that strophanthus ought to be tried instead, and only replaced by digitalis when it has proved in- efficient. Nothing is of greater service in cases of diffuse arteriosclerosis with secondary venous engorgement than a periodic purge by means of calomel. The catharsis should be brisk to be of benefit, for relief does not follow until several watery stools have been secured. I have seen truly surprising results from such simple treatment. One instance in particular comes to mind as I write, that of an old German with very stiff vessels who exhausted both my patience and my resources in a vain endeavour to procure relief from formication and coldness of the thighs. At last, in despair, I prescribed 5 grains each of calomel and jalap for the purpose of preventing his return to my clinic. He did not reappear for two or three months, when one day he returned, and on entering the clinic room exclaimed that he had come back for another powder, as he had never had anything do him so much good. I recall also an Irishman with stiff arteries and an obstinate chronic bronchitis that had defied the efforts of several well-known practitioners, and who obtained greater relief from his dyspnoea and cough by a single dose of 5 grains of calomel than from all the cough anixtures he had previously taken. Traenkel reports the highly interesting and instructive case 758 DISEASES OF THE HEART of a man with general arteriosclerosis who was relieved of his nocturnal asthma for a period of three months by a single sharp attack of epistaxis. This suggests that in cases of cardiac asthma, which so often form a distressing feature in the clinical history of arteriosclerosis of the cardio-vascular type, it might be well to resort to venesection when catharsis has failed of ameliorating the symptom. In cerebral arteriosclerosis I am of the opinion that stimulants and vaso-dilators are indicated. Judgment and caution should be exercised in their administration, however, lest the heart be too vigorously stimulated and rupture of a miliary aneurysm result. The safety of such medication may be estimated by the state of the cardiac muscle. They are certainly indicated when the systoles are feeble and the brain is not sufficiently flushed. The treatment of coronary sclerosis and its resulting angina pectoris has already been considered in the chapters on Chronic Myocarditis and Angina Pectoris. The management of renal sclerosis is essentially that of chronic nephritis, since the two conditions are so frequently com- bined. When vascular disease in the extremities has led to gan- grene, the treatment is of necessity surgical. Sclerosis of the pul- monary artery is practically that of arteriosclerosis in general plus that of bronchitis and emphysema. Only general principles can here be laid down. In every case special symptoms must be left to the judgment of the practitioner. CHAPTER XXXIII ACUTE AORTITIS- ACUTE ARTERITIS - SYPHILITIC ARTERITIS-ENDARTERITIS OBLITERANS-PERI AR- TERITIS NODOSA-STENOSIS OF THE AORTA AND PULMONARY ARTERY-CONGENITAL SMALLNESS OF THE ARTERIES I. ACUTE AORTITIS When acute inflammation of the aorta is discovered it is in most cases associated with the changes of sclerosis in the same situ- tion or with an acute endocarditis. French authors, however, have described a form of acute aortitis which they claim is independent of antecedent sclerotic change and occurs in the course of acute infectious diseases. Such statements are received with consider- able reserve by the Germans, and von Schroetter in jSTothnagel's System seems quite sceptical on the subject, particularly as regards its clinical recognition. Morbid Anatomy. — The aorta is found more or less dilated, and the surface of the intima looks rough from the presence of reddish or grayish translucent more or less thickly scattered patches of a gelatinous consistency. These are minute thrombi, and it is through the detachment of these that cutaneous and other infarcts occur, the same as in acute valvulitis. Indeed, acute aor- titis is so similar to acute endocarditis that the description of the latter may answer for the former. The process may be of a benign type and proceed to the forma- tion of so-called vegetations, or it may behave like ulcerative endo- carditis and lead to serious destruction of the vessel and rupture. In this manner communication may be established between the aorta and one of the auricles, a contiguous vessel or the pericar- dium with fatal haemorrhage (Romberg). The media and even the adventitia becomes infiltrated with round cells, and if the pro- 759 760 DISEASES OF THE HEART cess is sufficiently prolonged newly formed vessels may penetrate into the intima. As already stated, degenerative changes are usually found as- sociated with the evidences of acute inflannnation. There may also be an associated valvulitis affecting previously healthy valves or more often as an acute process ingrafted on an old-standing aortic-valve lesion. In other distant parts of the body there may be discovered local changes due to benign or septic emboli cast off from the aortic intima. Etiology. — The aorta may become acutely inflamed in conse- quence of direct extension of an identical process of the endocar- dium. French clinicians (Huchard, Leger, Siredi, etc.) maintain that acute aortitis may arise in the course of scarlatina, measles, variola, independently of involvement of the endocardium, and Fiessinger is said to have seen it in a case of influenza (Gibson). The latter says also that acute aortitis may be associated with acute pneumonia, pleurisy, and pericarditis. The disease has also been attributed to trauma, and has been observed in the course of chronic nephritis. Symptoms. — Acute aortitis in most instances is latent or is overlooked by reason of its occurrence in the course of some other distinctive affection. The case discovered by Thoma, and which occurred during measles, had produced no symptoms whatever. Von Schroetter appears to think that the clinical features de- scribed by Huchard in such a brilliant and interesting fashion are not to be attributed to acute aortitis per se, but are such as are so often observed in cases of arteriosclerosis affecting the aortic arch. In Chapter IV, page 158, I have depicted a case which I took to be acute endocarditis because of the subjective symptoms and clinical findings, and in which post-mortem examination dis- closed an aortitis together with endocarditis, the acute process hav- ing developed on top of old sclerotic changes that had masqueraded under the guise of aortic insufficiency. I will briefly portray the features that are claimed by the Frencli t(» liave been observed in acute aortitis unconnected with other aortic or endocardial lesions. Fever is usually absent, but if present it is due to the primary infection, not to tlic aortitis as such. The countenance is apt to be pale and anxious. The pulse is small and weak, regular or not, as circumstances in each case may die- ACUTE AORTITIS 761 tate. The patient is likely to complain of pain in the upper ster- nal region, and sometimes extoiidiiig through the mediastinum and down the back along the spinal column. The pain is described as burning, sticking, smarting, etc., and in some instances is said to radiate into the left shoulder and down the arm, very like that of angina pectoris. The resemblance to this latter is enhanced by a feeling of oppression and anxiety in some cases. Peter has observed tenderness on pressure in the intercostal spaces to the left of the manubrium, and undue throbbing of the right subclavian has been noted by French writers (Laboulbene, Faure), and by them is attributed to the greater liability to in- flammation of the left subclavian than of the innominate artery. Von Schroetter, however, believes that if such difference in the pulsation of the two subclavia exists, it is due to sclerotic changes, an opinion in which Gibson concurs. Dysphagia, cough with expectoration, and disturbance of the digestive tract shown by vomiting and flatulent distention of the bowels, have been observed in some cases. In short, the symptoms of this affection are often wholly want- ing, and when present are not at all distinctive. There is noth- ing in them which may not be observed in other affections involv- ing the heart, and hence Romberg states that even when the malig- nant form of acute aortitis occurs, there is nothing in its clinical picture to distinguish it from ulcerative endocarditis. The course of acute aortitis is often protracted and the termi- nation is usually in death. Physical Signs are usually indefinite, or are such as are found in other acute inflammations involving the cardiac struc- tures, or are those of the infection in the course of which acute aortitis occurs. Inspection. — The countenance may be pallid and anxious, the carotids throb strongly, and the right subclavian may pulsate more powerfully than does the left. Palpation is negative unless pressure elicits sensitiveness in the intercostal spaces to left of the sternum and along the course of the aorta. Percussion is likely to be negative unless dulness be revealed at right of the manubrium in cases in which the inflammation leads to dilatation of the aortic arch. 762 DISEASES OF THE HEART Auscultation. — This is not likely to furnish information of a positive kind. A systolic murmur over the situation of the ascend- ing arch may be evoked by dilatation of the vessel, and in cases in which the valve is also affected there may be impurity of the aortic second tone. Diagnosis. — This can rarely if ever be more than conjectural. If the character of the pain and oppression simulate that of angina pectoris, it may possibly be differentiated from it by the fact that in acute aortitis this symptom is likely to persist, or at the most show only remissions, not intermissions. The differentiation from acute endocarditis is not possible in all, perhaps not in most cases. Aid may be obtained, however, if one notes that in the course of a disease resembling endocarditis no changes in the area of cardiac dulness or in the heart-sounds are developed, or if on repeated examinations one should be able to detect increasing dulness over the ascending aorta indicative of dilatation. In my case this was noticed, but was not correctly in- terpreted, owing perhaps to the coincident dilatation of the right auricle. Prognosis. — This may be said to be very unfavourable. The occurrence of embolic phenomena renders the outlook most un- promising. Rupture of the aorta is a possibility that should always he borne in mind in suspected cases of the disease. Treatment cannot be expected to do more than relieve symp- toms. Rest in bed is imperatively indicated, and the strength of the patient must be sustained by highly nourishing, easily digested food. Pain, when severe, should be allayed by morphine, counter- irritation, hot applications, etc. Nitroglycerin may be of service by diminishing intra-aortic blood-pressure, and strychnine is a val- uable general and cardiac tonic. Digitalis is only useful in case of threatening cardiac inadequacy. II. ACUTE ARTERITIS Morbid Anatomy. — Circumscribed inflammation of the larger arteries is sometimes observed in connection with an in- flammatory process of surrounding tissues or in consequence of embolic plugging. Infiltration with small round cells takes place in the outer and middle coats, later on also in the intima. The endothelial lining becomes swollen and of increased thickness, ACUTE ARTERITIS 763 while the underlying layers of the intima show the development of newly formed connective tissue. In cases in which the inflammation is the result of plugging, thrombosis also occurs, and in time the thrombus undergoes organ- ization. If the embolus is infective, the inflammation may spread to the parts outside of the vessel and set up abscess. When the arteritis results from surrounding inflammation, thrombosis and subsequent organization may likewise take place. The etiology has already been stated in the opening sen- tence. Acute arteritis results either from adjacent inflammation or from embolic occlusion. Symptoms are likely to be recognised only when the arteritis is situated in an extremity or a part accessible to palpation, and when thereby one can detect either embolism or thrombosis, or when there is phlegmonous inflammation of the tissues surround- ing an artery of considerable size. When local inflammation invades the artery, involvement of the latter is likely to be masked by the symptoms of associated phlebitis. In the latter event there are circulatory disturbances due to interference with return flow, swelling, and more or less oedema, together with pain and great tenderness. In the case of embolism there are pain and phenomena of obstructed circulation, coldness (local syncope), cyanosis, and numbness. Physical Signs consist of such phenomena of local inflam- mation or of the accompanying phlebitis. Inspection perceives swelling and redness of the affected ex- tremity. Palpation is of greater service. The limb is hot, painful to touch, usually pits on pressure, and at some point careful palpa- tion is generally able to detect resistance due to the embolus or to thrombosis extending for a variable distance above the seat of the plug. Diagnosis. — This is to be made by the history, local symp- toms, and the result of palpation. The differentiation of acute arteritis from phlebitis is not always easy or possible. Prognosis depends upon the nature of the cause and the completeness of collateral circulation. Acute meningitis is a pos- sibility in certain cases, and of course affords a very grave outlook. 764 DISEASES OP THE HEART The prognosis is always unfavourable in cases in which the arte- ritis is secondarv to acute uuilignant endocarditis. The treatment of acute arteritis is partly medical and partly surgical. The affected limb should be elevated, kept at absolute rest, and enveloped in moist heat, as poultices to which anodyne remedies may have been added. Pain is to be allayed by local sedatives or by the use of opimn in some form. Should an abscess occur, it is to receive appropriate surgical management. III. SYPHILITIC ARTERITIS Vascular changes observed in syphilitic subjects have been the object of careful study by numerous investigators, among whom should be mentioned Lanccreaux, ITeubner, Weigert, Doelile, Baumgarten, Vendeler. Some of the changes are unquestionably of luetic origin, while others are by some authors, as von Schroet- ter, accepted with considerable doubt. Morbid Anatomy. — The inflammatory changes in the arter- ies are of a chronic nature and invade circumscribed portions of a vessel or are limited to the arteries of certain regions, as of the brain. The process may show itself as circumscribed patches of a grayish white translucent appearance, or the entire vessel may be changed into a whitish or grayish cord in consequence of the trans- formation of its coats into fibrous tissue. In this form the adven- titia, and ultimately the media and intima, become infiltrated with round or fusiform cells. The process may remain in this stage of inflammatory infiltration (von Schroetter), but as a rule it goes on to formation of fibrous tissue in the several coats. This hyperplasia of the walls is often extreme and leads to very considerable narrowing and even occlusion of the lumen of the artery. In this respect syphilitic arteritis difl'ers from arteriosclerosis, which is more apt to lead to dilatation than to obliteration of a ves- sel, although it may do this latter in the smallest arteries. It has been shown, furthermore, particularly by Baumgarten, that minute gummata are scattered in the middle coat in imme- diate proximity to the vasa vasorum. Atrophy and rupture of the media result, and in time the rents are repaired by the formation of cicatricial tissue. The subsequent contraction of these areas leads to pouchings of the intima, which, when they are found in SYPHILITIC ARTERITIS T65 the ascending aorta, are almost pathognostic of syphilis (Rom- berg). These pouchings of the aortic intima may prove the start- ing-place of future aneurysms. In another form of arterial disease due to syphilis the vessel becomes invaded by a syphilitic process in its neighbourhood. The vessel is surrounded by a gummatous mass or by dense cicatricial tissue, and the coats of the artery are more or less thickened and altered (Ziegler). In the early or inflammatory stage the outer and inner coats are rich in cells, but as the process advances fibrous tissue replaces the cells wholly or in part. The media is not so much invaded by fibrous tissue as are the adventitia and intima. The cerebral arteries appear to be the ones most frequently affected. The aorta and coronary arteries may, however, be the seat of syj^hilitic disease, and in a few cases the vessels of the extremities have been affected. C. O. Weber is said by von Schroet- ter to have found the right branch of the pulmonary artery in a syphilitic girl greatly narrowed by reason of a gumma in its wall. Zeissl is also stated by the same author to have found the left brachial artery invaded by a gummatous infiltration, wdiile Lang- enbeck saw the same sort of process in the right brachial of another case. Etiology. — Syphilitic arteritis is a late manifestation of lues. The symptoms are determined by the seat of the arteritis. In the case of the brain they are those of disturbed or obstructed circulation," loss of memory, dizziness, headache, mental confu- sion, epilepsy, etc. — in short, such as arise from areas of acute softening. When the disease affects the aorta it may lead to aneurysm or to the symptom-complex of sclerosis of the arch. Arteritis of this origin may be a cause of angina pectoris by leading to sclerosis and occlusion of the coronaries, particularly the left anterior descending branch. In very rare instances a coronary artery has been said to be invaded and obliterated by a gumma of the myocardium. In the extremities syphilitic arteritis occasions clinical mani- festations of obstructed circulation the same as may other forms of arterial disease, pallor or cyanosis, coldness, and eventually gangrene. 766 DISEASES OF THE HEART Tlic diagnosis must depend upon the history of hietic infec- tion and on the discovery of unmistakable lesions indicating a late staiic of the disease. Even in such a case one cannot always say positively that the vascular changes observed are of specific origin. They may be due to arteriosclerosis and be independent of syphilis per se. In some cases one may be obliged to await the result of treatment before being able to arrive at a definite diagnosis. The prognosis is not always favourable as regards recovery, although appropriate therapy may in some cases affect a restora- tion of health. If the arteritis has led to pronounced fibrous thick- ening and considerable obstruction, to pouching, or even to aneu- rysm, there is small prospect of favourably influencing the process by antisyphilitic medication no matter how vigorous. The treatment should consist of the administration of ap- proved specific remedies — i. e., mercury and iodides. In addition, one may have to treat certain symptoms, as angina pectoris, cardiac inadequacy, gangrene, cerebral disorders, etc. The management of aortic aneurysm will be found in a succeeding chapter. IV. ENDARTERITIS OBLITERANS The following account is a condensed statement taken from von Schroetter's excellent description of the disease in Notli- nagel's Specielle Pathologic und Therapie. No apology for such a transcript is necessary, since the disease in question is rare, and comparatively few contributions to the subject have been made. The designaticm obliterans was suggested by Winiwarter, whose case is considered so typical by von Schroetter that he makes use of Winiwarter's description. Billroth gave it the name Ilyper- plastica, while Orth called it Productiva. Other observers to whose views or cases von Schroetter refers are Weiss, Brochard, Schlesinger, Sternberg, Wiedermann, Ortmann, Hadden, Gold- flam, Welter, (\>ll('t, Thatin, Roque, Braun. Morbid Anatomy. — The disease occurs most often in the smaller arteries of the foot or leg, occasionally also in the upper extremity, and exceptionally in other parts. Upon macroscopic inspection the vessels are seen to be enveloped by a tough fibrous sheatli wliich binds them firmly together. The individual artery — e. g., posterior tibial — is converted into a firm whitish cord, and on section is seen to be filled with a whitish gray or grayish brown ENDARTERITIS OBLITERANS 7G7 mass, so that a probe can be passed into the vessel only with diffi- culty or not at all. The artery is nevertheless not uniformly so filled, yet on the whole is transformed into a rigid cord in consequence of its inte- rior being filled with a somewhat yielding wide-meshed tissue. The process begins at the jDcriphery and extends upward, reaching from the plantar peroneal and posterior tibial arteries, even in some instances to the femoral, or in the case of the arm, to the brachial. Histological examination reveals in different places a somewhat variable condition, yet which is in reality a hyperplasia of the intima which may augment its thickness to even eight times the normal. In the larger vessels the newly formed connective tissue is composed of round, spindle-shaped, or stellate cells, between which can be recognised an intercellular substance made up of delicate threads. According to Winiwarter and others, several strata of elastic fibres may be seen in the outer portion of the in- tima next to the media. Finally, minute blood-vessels are seen to exist within the connective tissue of the interior, which Winiwarter regards as an extension or formation of new channels by which an attempt is made to provide a collateral circulation, and not as an organization of a thrombus. The capillaries thus formed permit a partial injection of the mass filling up the lumen of the artery. In spite of this attempt at a collateral circulation the stump after an amputation does not bleed freely when the Esmarch bandage is removed. Etiology. — This is practically unknown. It has been ob- served in men far more frequently than in w^omen, and what is especially strange about it is that it attacks comparatively young and previously healthy individuals. The process does not neces- sarily invade all the arteries of a limb, for it has been found in the posterior tibial, while the anterior tibial was free. It has been attributed to occupation, but in von Schroetter's opinion without sufficient warrant. The only theory that seems to appeal to von Schroetter is that the affection is, in some manner as yet unknown, dependent on some nervous influence. Symptoms are made up of prodromata extending through a period of years, as many as twelve, and of such phenomena as depend upon interference with local circulation. Individuals thus 768 DISEASES OP THE HEART afflicted complain, for years of pains in the leg or arm Avhicli are generally thought to be either rheumatoid or neuralgic, and are likely to be treated as such, yet without benefit. After a time perversions of sensation occur (parsesthesiae), as formication, numbness, etc. At first the pains are lessened or disappear when the extremity is at rest, but at length grow extreme, and on use of the affected member become intoler- able. As the obstruction to circulation increases movement be- comes difficult and the extremity feels heavy, so that the patient favours the limb so far as possible and may actually walk lame. When at last the artery is wholly occluded areas of gangrene make their appearance. These may be superficial or may invade a toe or the whole foot, and show a tendency to sj)read rajDidly upward. The extremity now looks either pale or livid and feels cold and lifeless. Unless the gangrenous area is removed by the surgeon septic phenomena may develop and lead to a fatal termi- nation of the case. The course of the disease is progressive, and the termination is usually or invariably fatal in the course of years. The diagnosis is surrounded by considerable difficulty, par- ticularly in tlio prodromal stage. The pains are likely to be con- sidered rheumatic or simply neuralgic, and cannot very well be correctly interpreted before there is evidence of rigidity of and want of pulsation in the arteries. Obliterating endarteritis is to be distinguished from arterio- sclerosis mainly by the age of the patient, since it has been observed most frequently between twenty and thirty, next between forty and fifty, and arteriosclerosis occurs most often past fifty. The disease is likely to be localized, while evidence of vascular degen- eration is usually more wide-spread. Moreover, arteriosclerosis, althougli it may cause gangrene, does so far less constantly than does the endarteritis, and then usually in persons who present well-marked evidence of the arterial change in both legs. Reynaud's disease, for which the endarteritis may be mistaken, occurs most frequently in children and young adults, especially in females, sets in al)ru})tly, and the dead feeling of the fingers of both hands is attended with slight annesthesia. Moreover, the condition is due to a cramplike constriction of the vessels, and is not attended with rigidity and pulselessness of the vessels. PERIARTERITIS NODOSA 769 The prognosis is imf avourablc, since the affection is pro- gressive. Treatment is of a necessity symptomatic and restricted to such measures as may alleviate suffering. The occurrence of gan- grene calls for surgical interference. V. PERIARTERITIS NODOSA. SYN.: CONGENITAL ANEURYSM The very remarkable and rare affection which bears the above titles was first adequately described by Kussmaul and Maier in 1866, although it appears that Rokitansky in 1852, and possibly Pelletan in 1810, observed each a single case (von Schroetter). The designation Periarteritis Nodosa w^as bestowed upon it by Kussmaul because of his conception of the process as an inflam- mation originating in the adventitia. The term Congenital Aneu- rysm is applied to it because it has been thought to be due to con- genital weakness of the arterial coats (Eppinger), leading event- ually to the development of multiple aneurysms. According to von Schroetter, only thirteen authentic cases have been reported. Morbid Anatomy. — The affected artery is studded with nodular thickenings of a whitish colour and of variable size, from that of a pin's head to a pea, which are due to circumscribed fibrous thickening of the intima with cellular infiltration of the adven- titia and media. The lumen of the vessel may be narrowed or the weakening of its coats may lead to circumscribed dilatations — i. e., multiple aneurysms. These may reach such numbers as to be uncountable. The disease affects arteries of medium calibre, and is found with special frequency in the arteries of the muscles and viscera, as the heart, intestines, spleen, liver, and kidneys, and also of the skin. Its etiology is entirely unknown, but inasmuch as the clin- ical picture is very like that of sepsis or an infection it may have some such origin (Romberg). The disease appears to attack both sexes about equally and to occur between the ages of twenty and fifty-two (Osier). Symptoms. — The most striking features of the affection are weakness, rapidly progressing ana?mia, and rapidity of the pulse out of all proportion to the temperature. Fever may be present in the beginning, but is of moderate height, and tends to ultimately disappear. There is pain in the muscles which may eventually 50 770 DISEASES OF THE HEART show atrophic changes and paralysis. Digestive disturbances are present, as anorexia, thirst, and vomiting, and there may be con- stipation or diarrh(pa. There may be albuminuria and casts, and when the arteries of the abdominal organs are affected there is severe epigastric distress. Iljemorrhages from the bowel may also be observed (Romberg) in cases in which the arteries of the intes- tines are the seat of the disease. The course of the malady is progressive as a rule, and a fatal termination occurs in from six weeks to three months. Very ex- ceptionally, however, recovery may ensue. Diagnosis is impossible unless the nodular thickenings can be felt along the course of peripheral arteries or such as situated within the abdomen are yet accessible to palpation. In suspected cases a nodule may be excised and subjected to microscopic exami- nation. Prognosis is unfavourable, although recovery does not appear to be impossible. Treatment is purely symjitomatic and is limited to attempts to alleviate suffering, build up strength, and check or overcome the destruction of the blood. VI. STENOSIS OF THE AORTA AND PULMONARY ARTERY Stenosis of the Aorta may be Congenital or Acquired. — In the former variety the narrowing is situated at the isthmus and may be caused by a too early closure of Botalli's duct and conse- quent failure of the descending aorta to receive the amount of blood necessary for its proper development or expansion, or a membrane may be stretched across the vessel at the isthmus, having at its centre an opening through which the stream of blood must pass. Acquired stenosis may be caused l)y a fibrous band that con- stricts the aorta at some point within the mediastinum, or it may be compressed by a tumour. Such conditions are, however, rare as regards the arch, since this portion of the aorta is capable of successfully withstanding en(;roachment upon it by new growths (Romberg). In the chapter on Dextrocardia is lucntioncd the case of a child in whom the rotation and displacement of the heart had caused the superior vena cava to be stretched tightly across the aorta and STENOSIS OF THE AORTA AND PULMONARY ARTERY 771 constrict its lumen. I have also in the chapter on Aortic Regurgi- tation mentioned the case of a man whose ascending aorta was greatly narrowed by a ring of fibrous tissue that completely encircled the vessel and had induced relative insufficiency of the valve. Symptoms depend upon the degree and seat of the stenosis. In the congenital form collateral circulation may become estab- lished through the intercostal arteries, the internal mammary, or arteries in the integument and muscles of the back. If such side channels are sufficient there may be no obvious hindrance to the blood-supply of the lower parts of the body, and no untoward effects are experienced. Romberg mentions a case observed by him in which the arter- ies of the back provided a means of maintaining the circulation below the point of stenosis, and in which he detected a loud vascu- lar bruit on the posterior aspect of the trunk between the vertebral column and right scapula. The murmur was attributed by him to dilatation of the arteries at that point. In the acquired form narrowing of the aorta is likely to occa- sion compensatory hypertrophy of the left ventricle and possibly also incompetence of the aortic valve, as in my case. The ulti- mate effects are those of cardiac inadequacy. In cases in which relative insufficiency does not occur, but the stenosis leads to left- ventricle hypertrophy, the clinical history is likely to be that of narrowing of the ostium or of the disease which causes the con- striction of the aorta. The diagnosis is very difficult as a rule, and may be impos- sible. One may recognise the signs of obstruction to outflow from the ventricle, but may not be able to determine its real nature. The detection of a mediastinal tumour or of chronic fibrous medi- astinitis, together with the signs of obstruction — i. e., a systolic bruit over the course of the aortic arch with accentuation of the aortic second tone and left-ventricle hypertrophy — might lead to a correct diagnosis. This would be strengthened if as time went on evidence of regurgitation should appear. Congenital narrowing of the isthmus might be diagnosed if one were to discover compensatory dilatation of the arteries by which collateral flow is established together with hypertrophy of the left ventricle. • 772 DISEASES OF THE HEART Prognosis depends upon the cause and degree of the stenosis, the effects on the heart, and in congenital cases the completeness of collateral circulation. The general health may not be seriously influenced, or the heart may suifer in its integrity, and death be ultimately brought about through cardiac inadequacy. In a few cases the prognosis may be that of the etiological condition. Treatment is to be addressed to obviating so far as possible the injurious consequences of the acquired stenosis. We can do nothing towards removing the cause. Stenosis of the Pulmonary Artery is acquired, and is a relatively infrequent condition. It may be due to constriction by a fibrous band, to compression by an aortic aneurysm and a few other con- ditions, of wliich isolated examples have been reported. Thus Romberg states that Litten found stenosis of the pulmonary artery from an " echinococcus embolus," while Gerhardt discovered a case of slight compression of the vessel by the left auricle in conse- quence of this having become distended by a clot. C. O. Weber, cited by von Schroetter, observed pronounced narrowing of this artery by a bean-shaped gumma in its wall. One of the branches of the artery may be constricted through retraction of the lung in interstitial pneumonia. Symptoms are confined in the main to the secondary effects on the right ventricle or to congestion of the lung back of the seat of stenosis when this is situated within the lung at a distance from the bifurcation. If the obstruction is in the nuiin trunk or in a branch suffi- ciently close to the main stem, the right ventricle undergoes hyper- trophy and perhaps dilatation witli consequent turgescence of the veins of the aortic system and corresimnding feel)leness of the pulse. It may even lead to relative incompetence of the pulmonary valve with its evil consequences. Diagnosis is attended with great difficulty, and is likely to be inij)(»ssiblt'. It must depend upon the recognition of right-ventri- cle hypertrophy for which no other cause can be determined, or on this with a systolic murninr in tlic ])uliiionic area together with intensification, instead (if (liiniimtion of tlie second tone, as is the case in stenosis of the puhiiouic ostium. Systolic pulsa- tion in the situation of the trunk of tlie artery — i. e., in the second left intercostal space close to the sternum — together with CONGENITAL SMALLNESS OF THE ARTERIES 773 dulness in tliis area, would greatly strengthen the other signs just mentioned (Romberg). The prognosis is determined by the nature and degree of secondary disturbance. It is of necessity more or less unfavour- able. Treatment is entirely symptomatic, and, as in stenosis of the aorta, must aim at maintaining cardiac adequacy, since the cause cannot be removed. VII. CONGENITAL SMALLNESS OF THE ARTERIES This state of the aorta and arterial system was studied by Virchow, who pointed put its association with chlorosis. Not only are the vessels of small calibre, but their coats are thin and deli- cate, rendering them particularly liable to rupture, and they are abnormally elastic. In extreme cases the lumen of the arteries ma}" be reduced to a third of the normal (Romberg). The heart is also abnormally small, the genitalia are likely to remain undeveloped, and the individuals are small and delicate in appearance. This is especially true of those who present the chlo- rosis spoken of. In other not pronounced cases of arterial hypo- plasia there may be nothing in the appearance and no lack of body development to suggest its existence. Symptoms of this condition as such cannot be said to exist. The heart, by reason of its smallness, is weakened in its re- sistance, and is more than usually liable to infection (Romberg), and indeed general vigour and resistance may be said to be below par. This is readily comprehensible in cases character- ized by chlorosis. The hypoplasia is found more often among females than males. Fraentzel was of the opinion that congenital narrowness of the arteries predisposed to hypertrophy and dilatation of the left ven- tricle, and in support of his view cited instances of the kind in young recruits. Romberg, however, thinks the clinical picture drawn by Fraentzel is to be interpreted as the result of prema- turely developed arteriosclerosis. This is favoured possibly by the smallness of the arterial system ; and yet, as a matter of fact, such arterial degeneration does not occur with special frequency in the subjects of arterial hypoplasia. It is worthy of note that rupture of the aorta and dissecting 774 DISEASES OF THE HEART aneurysm are said to occur with relatively greater frequency when it is congenitally narrow. The patients are also said to bleed more easily than normal persons owing to the thinness of the vascular coats. Diagnosis of arterial hypoplasia is difficult to make with cer- tainty. It may be considered as possibly present when palpation of the large cervical arteries and percussion of the heart show what seems to be abnormal smallness of the same, and when, in addition, the individual is poorly developed, chlorotic, and possesses deform- ity or an infantile state of the genital organs. It is possible that an expert in the use of the fluoroscope might be able to recognise that in a given case the heart and large vessels were abnormally undersized. Prognosis. Congenital narrowness of the arteries affects life prospect only when the hypoplasia is considerable and is at- tended with chlorosis. In such cases there is danger of some of the consequences that have already been considered. Treatment cannot affect the underlying condition, and is therefore limited to attempts at relieving or modifying such effects as may result. CHAPTER XXXIV ANEURYSM OF THE THORACIC AORTA Aneurysms have been the object of interested study for several centuries both to anatomists and clinicians. The names of many celebrated men are connected with the history of this arterial dis- ease, and, as might be expected, they were at first the names of anatomists who studied the subject mainly on the dead body. Methods of diagnosis were crude and, very naturally, not equal to the discovery of such obscure affections as intrathoracic aneurysm. I^evertheless it is worthy of record that Vesalius made a diagnosis of aortic aneurysm in 1567. Malpighi and Morgagni wrote on the subject and added to the facts concerning it. There has been scarcely an author of note since who has not attempted to add to our knowledge on the subject, and to some of them the profession is greatly indebted. Lancisi, Scarpa, Corvisart, Hodgson, Stokes, and in our own time Eppinger and Thoma, are names that are inti- mately linked with the history of aneurysm. In this chapter it is proposed to deal exclusively with the dis- ease as it affects the aorta within the thorax, a condition that pos- sesses peculiar interest for the physician. Aneurysms of periph- eral arteries belong to the province of the surgeon and hence are left to surgical works for consideration. Morbid Anatomy. — An aneurysm is a circumscribed dilata- tion of an artery ; and as such must be distinguished from the uni- form widening of an artery, which results from sclerosis. The three main divisions that are made of aneurysms are, (A) true, (B) dissecting, (C) false. By false aneurysm is meant a circum- scribed collection of blood that has escaped from an artery into the surrounding tissues, hence a ha?matoma. The walls of the tumour are not composed of the arterial coats, and therefore, ac- cording to von Schroetter, it should not have the term aneurysm 775 776 DISEASES OF THE HEART applied to it at all. A dissecting aneurysm is one in which the stream of blood penetrates through a rent in the intima into the parts beneath, and burrowing its way either between the inner and middle coats or in the layers of the media, thus dissects up the intima for a variable distance. In some instances the blood-current again breaks through the intima and becomes reunited with the main stream. This condition may be of long standing and is scarcely open to recognition. True aneurysm is therefore the condition in which are ful- filled the requirements stated in the definition. The two sub- divisions of this form of tumour which best meet the facts as observed by the clinician are (1) fusiform and (2) sacculated aneurysm. By the former is meant a localized dilatation of an artery involving its entire circumference; while by sacculated is meant a dilatation limited to one side, and hence involving but a portion of its circumference. Aneurysm of the aorta may be either fusiform or saccular, but the latter is the more common. All three coats are involved in the bulging but are not all retained in the wall of the aneurysm. The intima extends into the sac to a greater or less distance, but is then lost. The portion that persists usually presents the changes of arteriosclerosis, as does also the inner coat of the aorta, in the neighbourhood of the tumour. The media is also involved in the destructive process which has favoured the fornuition of the aneurysm. Its muscular fibres are degenerated or wholly lost and its elastic elements show signs of granular change. In places, the middle coat may be entirely destroyed; and when such is the case, together with loss of the intima, the wall of the sac is composed solely of the adventitia. This latter is also thickened and infiltrated with inflammatory products. The pouch which has thus been formed communicates with the lumen of the aorta by an opening of variable size, but almost al- ways smaller than is the calibre of the sac. The interior of the aneurysm is apt to be lined by coagula in the form of layers of a whitish colour. The most internal of tliese lamina is likely to be reddish and soft, while the more deeply situated layers are firm as well as white. The degree of thrombus formation within the aneurysm is variable, but does not usually fill up its lumen. ANEURYSM OF THE THORACIC AORTA 777 Exceptionally, however, when the sac is not very large and its opening into the channel of the aorta is small, its cavity may be entirely filled with coagrila so as to obliterate the sac. The inner- most layer of fibrine then forms a firm wall nearly on a level with the intima. Its surface is apt to be rough and calcified. Although an aneurysm may in this manner undergo spontaneous arrest, still the degeneration of the arterial coats which led originally to the formation of that aneurysm is likely to favour the development of others, so that multiple aneurysms are not at all uncommon. Aortic aneurysms differ much in shape and size. Thus a sac- culated aneurysm may have other sacs springing from its walls so that the tumour presents an irregular outline. In size the sac may vary from that of a small nut all the way to that of a man's head. Aneurysms may be situated at any point along the course of the aorta from just above the ring to the termination of the abdominal portion. The disastrous effects of aortic aneurysm are not confined to the vessel, but consist of all the changes in structure and position of neighbouring organs produced by pressure of the sac. The na- ture and extent of these secondary pressure effects are determined by the situation as well as the size of the aneurysm. Aneurysms involving the sinuses of Valsalva are not apt to attain much size, yet their influence on the heart is very disastrous and they are especially liable to rupture into the pericardium, causing sudden death. Aneurysms of the arch displace the heart downward (Fig. 109) and it may be forward or to the left, but they rarely occasion hypertrophy of the left ventricle unless the aortic valves have been rendered incompetent. The latter condition is likely to result when the sac springs from the ascending or transverse arch and has attained great size. I recall a man whom I treated for months for aortic regurgitation without suspecting the existence of an aneurysm until quite suddenly signs of pressure on the left lung arose. Even then other signs of the aneurysm were not at all dis- tinct, yet were of such a kind as to render its presence certain. Other effects of aortic aneurysm than those already mentioned will be left for consideration under S;)Tnptoms. Etiology. — Arteriosclerosis has long been recognised as pre- disposing to the development of aneurysm. It is objected by Ep- 778 DISEASES OF THE HEART pinger that the changes of sclerosis tend to render the vessel more rather than less resisting, an objection that is also recognised by Thoma. Consequently the latter points out that aneurysm is likely to develop during the time of primary degeneration and weakness of the media, before compensatory thickening of the inner coat has taken place. This will be referred to again. Fio. 109. — Skiagraph showing Aneurysm of Aokta with Disi'i.acemext of the Heart Downward and to tiik Lkkt. Syphilis is an uii(l()ul)t('(l factor in tlic causation of aortic aneurysm, and yet wide differences exist in the opinions of writers concerning the frequency of its relation to this form of vascular disease. The extremes are represented by M. Schmidt, who finds syphilis present in 29 per cent of cases, and Drummond, who be- lieves that lues is responsible for aortic aneurysm in every in- stance — i. e., 100 per cent. My exjierience leads me to look upon ANEURYSM OP, THE THORACIC AORTA 7T9 Drummond's opinion as too extreme, and to accept Gerhard t's 53 per cent as much nearer the truth. Age is a predisposing factor of great importance, since aneu- rysm of the thoracic aorta is undoubtedly more frequent after than before the fortieth year. The decade of life in which it is most common is still unsettled, and figures differ all the way from the fourth decade (Crisp) to the seventh (Juda, Barsdorff). Thoma's notion is that persons are especially liable to the development of aortic aneurysm at or about the age of forty, in consequence of diminished resistance of the vascular coats at this time. There is, he thinks, a period of about a year at this age when the weakness of the media has not yet become offset by growth of connective tissue in the intima, and during which time the coats of the vessel are therefore liable to yield to excessive blood-pressure at one or more points resulting in future aneurysm. I have under observation at the present writing a muscular man of forty-four who gives no history or signs of previous syphilis, but who has been a more than usually active, energetic business manager in a line of work that necessitated much physical exer- tion. This patient suffers from symptoms which, together with stiff arteries and suggestive but not conclusive physical signs, are yet suspicious of fusiform aneurysm of the arch. The age of this person, his occupation, and the state of his arteries, are all, from an etiological standpoint, highly suggestive and strengthen the conclusion to be drawn from the clinical findings. Sex is likewise a predisposing element in the class of cases now under consideration. Men are without doubt far more liable to aneurysm than are members of the gentler sex. Thus of a total of 425 cases of aortic aneurysm analyzed by Hodgson, Bizot, and Browne, and cited by Gibson, 380 occurred in males and only 45 in females. This striking preponderance of men is not to be at- tributed to any quality inherent in sex per se as inferior vascular resistance on the part of men^ but to the greater liability of males to all those factors which favour the development of arteriosclero- sis as well as their greater exposure to syphilis and conditions of vascular strain which, acting in conjunction with vascular degeneration, are known to predispose to the occurrence of aneurysm. Sex is therefore only incidentally of etiological in- fluence. Y80 DISEASES OP THE HEART Two other factors that are mentioned as predisposing to aortic aneurysm are the abuse of alcohol and occupations which necessi- tate vascular overstrain. Both are recognised causes of arterio- sclerosis, and as such operate in the production of aneurysm ; but, in addition, overwork subjects the aorta to strain at a period of life when, according to Thoma's view, the vessel-wall is least able to endure high intravascular pressure. Such influences are inde- pendent of sex, and yet are some of the things which render men more liable to aneurysm than are women. Race, which is said to exert a certain degree, of influence, can scarcely be separated from conditions of M'ork, habits, etc., to which peoples of some countries are especially subjected. Thus aoVtic aneurysm is particularly frequent in England. The English appear to be more than commonly subject to arterial degeneration, and this fact, acting in conjunction with heavy toil in the manifold workshops of their country, probably accounts for the relatively great frequency of thoracic aneurysm among them. Traumatism cannot be ignored in the production of aneurysm of peripheral arteries, and probably also of the abdominal aorta, but it is diffi- cult to see how injury can have direct etiological relation to aneu- rysm of that portion of the vessel which is situated deeply within the thorax and is ])rotccted by its bony walls. It certainly could only act in connection with already existing degeneration of the media. If under such conditions trauma — e. g., a fall from a height — were to suddenly raise blood-pressure, it might possibly induce laceration of the middle coat and thus be an indirect cause of aneurysm. The iiilhu'iK'o r»f malignant endocarditis in the causation of so-called mycotic aneurysms has been emphasized by Epi)inger and is generally recognised. Aneurysms of this origin are usually lo- cated in peripheral vessels, and yet it is possible for such aneu- rysm to be aortic, as shown by the case mentioned by Osier as hav- ing occurred in the Montreal General TTos]utal. In this case there were, in addition to ulcerative endocarditis, four saccular dilata- tions of the aorta, one large and three small ones. Embolism may also be a cause of aneurysm of the arch as well as of other arteries, as shown by reported instances in which the lodgment of an em- bolus on the intima of the ascending aorta has been discovered and was associated with circumscribed inflammatory change. Osier ANEURYSM OP THE THORACIC AORTA T81 thinks it possible for such an embolus, if consisting of a calcareous plate, to lacerate the intima and thus initiate aneurysm. Lastly, Osl^ believes there may be an inherent weakness of the vascular coats which predisposes individuals to aneurysm, and cites the instance of Dr. Thomas King Chambers, who, after hav- ing had one of the left popliteal artery, and eleven years after- ward another in the right leg, finally developed " aneurysms of the carotid arteries." Symptoms. — Cases of aortic aneurysm may be divided into three groups : (1) Those in which the tumour fails to declare its presence by either subjective or objective symptoms. Such aneurysms are usu- ally small and are only discovered at the necropsy, when they may be found associated with some other clinically recognisable disease or as the cause of unexpected death through rupture. When the sac is situated just above the aortic ring, it is very apt to rupture into the pericardium. This was found to be the case in 75 out of 289 cases of rupture from a total of 953 instances of aortic aneurysm analyzed by Hare and Holder. (2) Aneurysms which occasion subjective symptoms as the leading feature of the case. In the majority of cases objective signs are also present, but often of so indefinite a character as to furnish no clear information concerning the nature of the tumour occasion- ing pressure. Such cases belong to Bramwell's second category. They may be said to correspond also to Broadbent's subdivision of cases which occasion symptoms but not signs of aneurysm. (3) Aneurysms which produce distinctive physical signs. These are generally united with symptoms of greater or less severity, but the objective manifestations of the disease are sufficiently pro- nounced to warrant their classification in a separate group. Aortic aneurysms may also be classified according to their situation — e. g., of the ascending, of the transverse, and of the descending portion of the arch, etc. Indeed, one cannot deal with this subject adequately and clearly without describing the features distinctive of aneurysm in the several locations. There are, however, certain general features shared to a greater or less extent by all aneurysms, whatever their position along the course of the thoracic aorta, and hence these will be considered first. Such symptoms are the result of pressure, and hence it is plain 782 DISEASES OF THE HEART that variations in pressure phenomena are determined by several factors, as the size of the sac and the direction in which it grows, as well as the portion of the aorta from wliich it springs. More- over, aneurysms are liable to change their direction of growth, so that symptoms sometimes differ in character and intensity from time to time. Indeed it may be said that such lack of constancy is generally regarded as one of the points of distinction in favour of vascular as against solid tumours. Pain is one of the earliest and most constant symptoms of tho- racic aneurysm. Its nature and severity depend upon the direction in which the sac develops. If this is towards the surface of the chest, or, as Walshe termed it, " centrifugal," pain appears earlier, is more constant, and more like what is called neuralgic, is sharp and lancinating or dull and aching, and is not infrequently described as boring, grinding, cutting, burning, etc. As it is due to pressure upon the intercostal nerves or branches of the brachial plexus, it is apt to radiate along the lines of these nerves, hence around the chest, up into the side of the neck, dowm the arm, etc. As a rule, the pain is confined to nerves connected with the first, second, third, and fourth spinal segments (Head), and is associated with tender areas in the upper part of the thorax at either side, but especially at left of the sternum. Such areas of tenderness are not characteristic of aortic aneurysm, however, for they may be sjanptomatic of various diseases of the intrathoracic viscera. The pain of aneurysm is apt to be very constant, and in this regard indicative or suggestive of tumour rather than of any other disease not occasioning pressure. If the sac grows inward towards the more yielding and less sensitive structures, it is not so apt to give rise to such severe pain, and hence this symptom is likely to be overshadowed by some other more distressing symptom, as dyspnoea or cough. The character of the pain, too, when this is experienced, is apt to be more dull and oppressive, and does not radiate so widely in tlie wall of the chest or the upi)er extremity. Although the pain of aneurysm is apt to be constant, it is liable to paroxysmal exacerbations which greatly increase the suffering. Pain is also apt to be influenced somewhat by the position of the patient's body. For example, it is apt to be intensified when the patient lies in such a manner as to permit the sac to gravitate or press more strongly upon the irritated and ANEURYSM OP THE THORACIC AORTA T83 painful nerve. Per contra, suffering is lessened by attitudes which allow the sac to fall away from the part previously pressed upon. Such postural variations in the pain arc not often marked, but are seen sufficiently often to merit attention. It is stated also that in some cases the pain is what is known as intrinsic, by which is meant pain experienced in the sac itself or in the aorta either from acute aortitis or from internal pressure. Pain of this origin is evoked or aggravated by increase of blood- pressure, and is dull or aching in character and substernal in loca- tion. It is likely to be lessened whenever vascular tension is low- ered. Extrinsic pain or that due to pressure may disappear after the structure subjected to pressure has been destroyed — e. g., after the bony wall has been eroded and the tumour is permitted to grow without the restraint of rigid structures. I recall the instance of an enormous aneurysm which had thus penetrated the chest-wall and was covered only by a thin layer of skin, and in which case the man made no complaint of pain whatever. Dyspnoea is another very common symptom of aortic aneurysm, but varies much in severity. It is of course most pronounced when the growth of the tumour is inward and pressure is exerted on the trachea, large bronchi, or lungs. Very distressing paroxysms of dyspnoea are occasioned by irritation, not paralysis, of one of the recurrent laryngeal nerves, more often the left, and are due to laryngeal spasm. There is apt to be an associated feeling of con- striction and perhaps pain in the side of the throat. In a case of the kind coming under my observation, the man felt the painful sense of constriction in the side of the neck corresponding with the recurrent nerve affected, and described the sensation as beginning in the left side of the larynx and running thence along the side to the back of the neck. I have quite recently seen, in consultation with Dr. Grorgas, a man of fifty with aneurysm of the ascending and transverse arch whose dyspnoea was extreme, and compelled him to maintain the right lateral decubitus. Change of position induced a paroxysm of air-hunger accompanied by uncontrollable coughing. It was impossible for him to rest on the left side, or indeed to lie back against the pillows. In this respect his dyspnoea corresponded with what appears to be a quite common experience — i. e., the influence of posture over the intensity of the dyspnoea and of 784 DISEASES OF THE HEART change of position in evoking a paroxysm of respiratory difficulty that is very like an asthmatic attack. The subsequent history of this case is interesting and instructive. Having received a hope- less prognosis from his medical advisers, he resorted to a Christian Science healer. Owing to a coincident change in direction of pressure, his sufferings abated and he again got about, the im- provement being attributed by himself and family to this treat- ment. After a respite from suffering of several weeks, his former symptoms recurred with aggravated intensity and shortly there- after the man died. Dr. Gorgas made an autopsy and discovered an enormous sac that had not only produced pressure on the right lung and sur- rounding structures, but had caused the erosion of several dorsal vertebra?. Difficulty of breathing is very apt to be accompanied by stridor, which may be so intense as to be audible at a distance and occasion pronounced fremitus. This stridulous respiration is due to con- striction of the trachea or of a bronchus and consequent interference with the expulsion of mucus accumulated behind the point of com- pression. Cough is a very common symptom in cases of thoracic aneu- rysm, but is variable in both frequency and severity. In some cases it is so distressing as to rob the patient of needful rest, and when once excited is so prolonged and intractable as to necessitate abso- lute repose in a given position pud even require the free use of morphine. When due to pressure upon the trachea, as occurs most fr('(|uently in cases of aneurysm of the transverse arch, the cough is a])t to possess a harsh strident character; that by Wyllie was likened to the note of a gander, and hence is known as the " goose cough." In some instances it may be of a toneless, muffled charac- ter, probably in consequence of paralysis of a vocal chord. The causes of cough are various, as (A) reflex irritation from pressure on the vagus or recurrent laryngeal nerve, (B) compression of trachea or bronchus, (C) direct impingement on the lung with re- sulting retention of secretions or with an actively destructive process, Expecioraiion is apt to be associated with cough, and may con- sist of mucus and serum, muco-pus, and in cases of ])ulmonary gan- grene, of offensive material characteristic of this affection. AI^EURYSM OF THE THORACIC AORTA 785 Hcemoptysis is by no means uncommon in cases of aortic aneu- rysm, in Avhich event the blood may come from granulations situ- ated on the tracheal mucosa (Osier), from bronchial congestion, or from destruction of a lung, or from the sac itself, what is then known as weeping of the aneurysm. Such hsemoptyses may occur from time to time over a protracted period, even for months. I vividly recall the instance of a man with unmistakable aneu- rysm of the upper portion of the descending aorta, whose clinical picture was that of phthisis. The tumour occasioned destructive pressure on the left lung, with pronounced dulness, bronchial res- piration, and a multitude of coarse and fine bubbling rales, fre- quent harassing cough, and copious purulent sputum which was occasionally streaked with blood. In another case of aneurysm similarly situated, pressure was chiefly exerted upon the left bron- chus with consequent dyspnoea, cough, and copious rales due to retention, since there w^as very little expectoration. Dysphagia is another very frequent subjective symptom, which is occasioned by aneurysms of the transverse and descending por- tions of the arch, or when a sac situated on the descending aorta exerts pressure upon the oesophagus. The patient not infrequently speaks of the ingesta seeming to stick at a certain point in their passage downward. If the aneurysm is situated low down near the diaphragm it may cause regurgitation of the food. Digestive disorders, properly speaking, do not form a part of the clinical history of thoracic aneurysms. They may be present nevertheless, and are then the result, in part at least, of the stasis within the portal system and its tributaries occasioned by pressure on the great veins in the thorax. All aneurysms of the arch do not occasion appreciable inter- ference with the flow of blood out of the venous system. When, however, an aneurysm attains considerable size it can scarcely fail to affect circulation by mechanical pressure. One or both of the vense cavee may be compressed, and to such a degree that the circulation can only be carried on by means of collateral vessels. Such a condition is admirably shown in Fig. 110, which is taken from a photograph kindly furnished me by Dr. Emil Beck. This man, aged thirty-seven, was first seen by Dr. Beck in October of 1901, at which time his complaint was of cough, dyspnoea and in- ability to lie down. He gave a history of syphilis sixteen years 50* 786 DISEASES OF THE HEART FlO. no. — DiLATATInx OF SUPERFICIAL VeINS SeCONHAHY Ti) PuESSUUE BY ANEURYSM ON Ven^ Cav^. before, for which he received very inadequate treatment. His occu- pation was that of a metal-polisher, which necessitates the putting forth of considerable, strength in pressing the metal against a ANEURYSM OF THE THORACIC AORTA 78Y polishing wheel. Here, then, were two factors both operative in the etiology of aneurysm. His one initial symptom of breathlessness on exertion devel- oped slowly, and did not necessitate abandonment of work and the sport of playing baseball until nearly a year after it was first noticed. When Dr. Beck examined the patient there was a per- ceptible fulness of the neck and bulging in the aortic area. This tumour pulsated and gave a systolic bruit. The pulses of the right half of the neck and of the corresponding arm were distinctly smaller than their fellows on the left side. The diagnosis was accordingly made of aneurysm of the ascending and transverse aorta. Cyanosis and turgescent veins were marked. He was then ad- vised to enter St. Joseph's Hospital, in the service of Dr. Carl Beck, for the purpose of treatment. Rest and iodide of potash did not seem to ameliorate his condition, and he left the hospital. An aggravation of symptoms and evident increase in the size of the sac led the patient to re-enter, in January, 1902, when he was given hypodermic injections of gelatin (2 per cent in 30 cubic centimetres of normal salt solution) which were administered once a w^eek, subsequently increased to 45 cubic centimetres, until he had received ten such injections in all. Under this treatment pressure symptoms nearly disappeared, and the patient felt so well that he again left the hospital. Through the courtesy of Dr. E. Beck, I had the opportunity of examining him a number of weeks later. The distention of the superficial veins was then as shown in Fig. 110, while, viewed from the side, there w^as the evident bulging of the chest shown in Fig. 111. The arteries of the right arm and corresponding half of the neck were manifestly less filled than those on the opposite side. There was a feeble pulsation in the prominent area, and tracheal tugging could be plainly felt. Percussion elicited an area of flatness having a semicircular outline below and extending from beneath the middle of one clavi- cle across the upper sternal region to about the same distance on the other side. This area is shown by a shaded area in Fig. 112. Over this area could be heard a dull first tone accompanied by a systolic bruit and succeeded by a loud, ringing second sound. The area of relative cardie dulness is also shown in Fig. 112, 788 DISEASES OF THE HEART Fi iircli and consequent irritation of tlie left recurrent laryngeal nerve. Laryngoscoi)ic examination was next made, and aside from slight congestion of the left arytenoid cartilage was negative. The patient was then submitted to an X-ray examination with the re- sult that the fluoroscopic screen revealed a pulsating tumour be- hind the left edge of the sternum, while a skiagraph showed a distinct though small shadow in the same situation. The diagnosis was thus confirmed and the case was shown to be one of the type just described. It is interesting, furthermore, in two resjoects: first, on account of the early age (thirty-two years) at which thoracic aneurysm has developed, and second, because it was tlie i)eeuliar character of the dyspnoeic attacks which sug- gested the possibility of the disease. The attacks, which in this case were considered asthmatic by the patient, were in reality due to laryngeal spasm ; and could the larnyx have becii inspected during an attack, the arytenoid carti- lages M'ould probably have been found approximated and the left vocal cord occupying the median line. As a matter of fact, an at- tempt to inspect the larynx during a spasm was made, but the attack was passing off and the laryngoscopic examination was negative. It is further worthy of note, that paroxysmal dysphagia was not experienced and that pain was never complained of by this man. This accords with the fact that dyspnoea and dysphagia arc not necessarily associated in all cases. Pressure on the left bronchus is another effect of aneurysms of the transverse arch of the type now considered. If the t\d)e is but slightly constricted, the lung becomes retracted only sufficiently to occasion immobility of the side, tympanitic resonance and di- minished respiratory sounds. When the bronchus is greatly nar- rowed the side becomes perceptibly snuiller than its fellow, the percussion note is dull, and respiratory sounds are abolished. There may be retention of the secretions with rales, bronchorrhoca, :ind bronchiectasis — symptoms which, in the Montreal General lIos])ital, are characterized as "aneurysmal phthisis" (Osier). Aneurysms of this portion of the arch sometimes occasion pres- sure on the thoracic duct. If they develop in such a direction as to involve the innominate or carotid artery, the condition is apt ANEURYSM OP THE THORACIC AORTA 797 to be shown by a symmetry or delay of the pulses on that side. Pressure on the sympathetic is another manifestation of tumours in this situation, and is shown by dilatation and immobility of the Fig. 116. — Trachea from Case of Euptuked Aneurysm, showing Point of Rupture. pupil when the nerve is irritated, and by contraction when the sympathetic is paralyzed. Tracheal tugging is another result of aneurysm of the transverse arch, as was first shown by Oliver. Tt 798 DISEASES OF THE HEART is due to the downward traction of the sac on the trachea at its bifurcation. This si^n will be spoken of ai;ain at greater length under Palpation. Aneurysms in this situation nia}' rupture into the trachea (Figs. 11(>, 117). (3) Aneurysms of the descending portion of fhe arch grow laterally and posteriorly in the majority of instances, and yet it is Fi(i. 117. — Oi'i>o9iTE Side of Specimen shown in Fig. 11)!. Snows Interior of Sac. Pkoke in Opening into Trachea. stated that a tumour of this portion of the vessel may present at the left of the sternum (Sansom, Walshe). Phthisical symptoms are the result of pressui'c on tlic left lung or bronchus, dysphagia of (compression of th(\ii'nll('t, jiaiii fiiuii ei'osion of the dorsal vertebra3 ANEURYSM OF THE THORACIC AORTA T99 (third to sixth), and a tumour in this situation may be the result of backward pressure. Compression of the spinal cord may oc- casion characteristic effects — e. g., paraplegia. (4) Aneurysms of the descending thoracic aorta are usually located low down near the diaphragm and produce oftentimes very obscure symptoms. In an instance of the kind which I saw with Dr. Bayard Holmes, and which was not recognised as aneurysm, the only complaint was dull pain vaguely felt in the lower zone of the thorax and upper abdominal region. The only thing that could be discovered on examination was an area of impaired resonance and feeble broncho-vesicular breath-sounds in the left infrascapu- lar region, close to tlie spinal column. From the history of previous illness, that seemed to have been pleuritic, and from the physical findings, this area was erroneously thought to indicate old adhe- sions. The autopsy, months subsequently, revealed a sac filled with dense coagula pressing on the base of the left lung just above the diajDhragm. Aneurysms in this situation may, as previously stated, cause dysphagia and regurgitation of solid ingesta, but they rarely occa- sion respiratory embarrassment. Aside from deep-seated pain they are not likely to produce subjective symptoms, and unless, by reason of their size, thev ffive rise to lateral dulness and other signs of pressure on the lung, they are likely to escape recognition. It should be borne in mind that an aneurysm which in the beginning is confined to one portion of the arch may as time pro- gresses so increase in dimensions as to eventually invade other divisions of the vessel. Thus, a sac at first limited to the transverse arch may in time spread to the ascending portion, or one in this latter situation may at length involve the entire arch ; so that both subjective and objective symptoms are very liable to exhibit changes corresponding to the extension of the aneurysm. I recall the case of a locomotive engineer w^ho was for many months an inmate of the Cook County Hospital in whom such a change took place. His aneurysm at first presented in such a situ- ation that it was believed to implicate the descending portion of the arch. As months went on, however, the tumour grew enormously towards the front, and at the necropsy was found to have involved the entire arch, which had consequently lost all semblance to an arch, being, in fact, but a huge sac from heart to descending aorta. 800 DISEASES OF THE HEART Physical Signs. — Inspection. — In some cases this is wholly negative, minute scrutiny failing to detect signs of pressure, and the general appearance being that of robust health. In other in- stances, on the contrary, patients look cachectic, and their chests being uncovered present unmistakable evidence of aneurysm. It is not to be supposed that all the signs are present in any one case. Consequently the following are the points to be carefully looked for : (1) Circumscribed bulging of the chest-wall in the folloAving areas: (A) At the right of the sternum, especially in the second and third intercostal spaces, but also the first, and including the stern o-clavicular articulation ; (B) at the upper end of the sternum, including the regions at either side and tlio fossa jugularis; (C) in the intercostal spaces at left of the breastbone, from clavicle to fourth rib ; (D) in the left interscapular region below the level of the fourth dorsal vertebra. These are the areas in which tho- racic aneurysm most commonly makes its appearance. The integument at these points may appear smooth and shin- ing, the prominence being slight, or a tumour of such size may pro- ject and have so eroded the overlying structures that the skin is of a dark red or bluish hue, or may have disappeared in spots, leaving the wall of the aneurysm visible. (2) Signs of interference with the circulation: (A) visible cutaneous capillaries on some portion of the chest, as over the area of bulging; (13) distended, tortuous veins denoting the establish- ment of collateral circulation in consequence of pressure on some of the great internal veins, as superior vena cava, one of the in- nominates or subclavians; (C) localized (edema, as of one arm and corresponding half of the neck, or when bilateral, of the ujipcr part of the body, but not of the lower extremities. Walshe speaks of the neck being in some instances so distended and spongy from capillary turgescence as to look " like a collar of flesh." (3) Pulsation in some abnormal situation — e. g., one of the areas in wliicli l)nlging may appeal-; or an exaggeration of a i)ulsa- tion in a normal situation — e. g., of the cervical arteries, particu- larly on one and not the other side or in the episternal notch. (4) Dislocation of the cardiac impulse, in most instances downward and to the left. The organ may, however, be pushed strongly forward against the anterior chest-wall. ANEURYSM OF THE THORACIC AORTA 801 (5) Diminution or absence of respiratory movement of one half of the thorax, more often the left, with, in some cases of marked bronchial compression, also retraction of the side. This sign in conjunction with pressare-symptoms is highly suggestive. (G) Immobility of one pupil, which may be larger than its fellow, but is more often contracted. (Y) Sweating of the head, sometimes unilateral, and by Walshe said to be very profuse in some instances. This is another sign of pressure on the sympathetic, and taken in conjunction with other pressure-symptoms may be of value, but found alone pos- sesses no significance as respects aortic aneurysm. Palpation is of value chiefly as a means of detecting abnormal pulsation, its extent and character. It is especially likely to give information when employed as bimanual palpation, one hand being pressed firmly against the chest in front and the other behind. In this way, deeply situated pulsation may softietimes be apj)re- ciated that otherwise would escape recognition. If a bulging area is perceived to pulsate, one should endeavour to feel the extent, force, and direction of the pulsation. If the tumour is due to aneurysm, it is likely that the pulsation includes the whole area. If this is forcible, so forcible in fact as to equal in this regard the beat of the heart, it is highly suggestive of aneurysm (Balfour). Finally, the pulsation of aneurysm may be slowly heaving and is exj)ansile, and when by palpation this character can be determined, there is no doubt of the nature of the tumour. Pulsation imparted to a solid tumour by a vessel beneath is a simple forward thrust or shock. In some cases the hand laid iipon a tumour due to aneurysm perceives a distinct diastolic shock which succeeds the systolic im- pulse. This is very characteristic, being due to elastic recoil in the wall of the sac. In some instances a thrill is detected in the bulg- ing area, but in my experience is not at all common, and is of diag- nostic aid only in connection with other signs. Palpation is of value also in the study of the pulse with a view to ascertaining whether or not it is equal and synchronous in cor- responding arteries, since when the innominate or the left common carotid and subclavian arteries are implicated, smallness and per- haps retardation or obliteration of the pulse in the arteries of the corresponding half of the neck or arm are likely to be occasioned. 802 DISEASES OF THE HEART Palpation is of value also in ascertaining displacement of the heart, as well as hepatic congestion due to pressure. The finger pressed gently into the episternal notch may sometimes detect pulsation of the transverse arch of an abnor- mal character, or a thrill, as well as the jogging impulse of aneurysm. The tracheal tug is another iihenomenon sometimes elicited by palpation. It is a distinct downward pull of the trachea caused by the impact of the sac against the windpipe at its bifurcation or against a main bronchus, and although feebly present in some other conditions — e. g., free aortic regurgitation — is never so marked as in aneurysm of the transverse arch. To elicit tracheal tugging the examiner instructs the patient to raise his chin so as to strongly extend the neck, whereupon he inserts the tips of his forefingers into the notch between the thyroid and cricoid cartilages and pulls gently upward. If the sign sought for is present, the trachea is felt to be jerked distinctly downward with each cardiac systole. When well marked, this tug cannot be mistaken, but when not pro- nounced considerable care is required for its detection. Percussion is a valuable means of diagnosis in cases of aneu- rysm, especially when there is no visible tumour. Before the sac leads to protrusion of the chest-wall it may occasion retraction of a lung-border or more or less collapse of a lobe, so that dulness in one of the areas in which aneurysm is usually situated may be de- tected by firm percussion and form an early sign of such tumour. It is especially important to percuss carefully in the right infracla- vicular region close to the sternum, since loss of resonance in this location is, together with symptoms and signs of pressure, strongly suggestive of aneurysm. Dulness over the manubrium is not so suggestive as at either side. Percussion is necessary also for the recognition of pressure eifects on the lungs and of displacement of the heart. Auscultation. — Aneurysms do not always produce acoustic phe- nomena, a statement which applies to some large as well as small ones that are deeply situated. A sac may be filled with coagula, and be thus to all intents and purposes the same as a solid growth, in wbic'li event no adventitious sounds are generated and the aneu- rysm remains silent. In most instances, however, aneurysms occasion abnormal ANEURYSM OF THE THORACIC AORTA 803 sounds or bruits which ar(; UTuIible over the sac or in some neigh- bouring vessel or part to whicli they are propagated. There is no auscultatory phenomenon pathognomonic of aneu- rysm, but certain sounds are more suggestive than are others. The two tones normally heard over one of the great vessels at the base of the neck and in the aortic area are usually altered by the devel- opment of aneurysm. Either the systolic or the diastolic may be modified — i. e., intensified, diminished, or impure. Perhaps the most frequent and striking change is a loud pecul- iarly ringing quality of the second tone heard over the growth or in one of the cervical arteries but not the others. In some instances such a sound is impure or split, in others it is clear and clanging, while the first is not pure or has been replaced by a murmur of harsh quality. In other cases again the systolic tone is pure and accentuated and the diastolic is accompanied or obscured by a dis- tinct bruit, while in still others there is a double to-and-fro murmur of wide propagation. Intensification or modification of the normal vascular sounds occurring in immediate proximity to the heart — e. g., in the aortic area, are not so suggestive as are such changes in regions in which they do not normally exist — e. g., the left interscapular region or one side of the neck. Another very valuable auscultatory sign is the propagation of the heart-tones to a much greater distance than normal — e. g., to the outer limit of an infraclavicular region or into an axilla, the lung tissue not being indurated. This condition is essential, for solidification of lung from tuberculosis may lead to wide transmission of the cardiac sounds without aneurysm. We do not yet understand the conditions wdiich determine changes of one kind and another in the tones heard over an aneu- rysm. These sounds are probably not generated de novo in the wall of the sac, but are merely conducted thither from the heart and are there intensified, reduplicated, or otherwise modified by vibra- tions set up in the sac-wall or by some other condition that escapes our ken. It may well be that bruits are generated in some cases in the sac itself in consequence of the blood-stream swirling into or out of the sac, but probably the murmur is due in other instances to atheromatous roughening of the aorta between the heart and sac or to insufficiency of the aortic leaflets. This is believed to be the explanation of the double aortic bruit not infrequently heard in 804 DISEASES OP THE HEART aneurysm of the ascending portion of the arch. Indeed, Gibson states that lie can recall only three cases in the literature in which such a double bruit was found without associated incompetence of the semilunar valves. It is not strange, therefore, that all possible combinations of tones and murmurs may be heard in cases of intra- thoracic aortic aneurysm. Drummond has called attention to the fact that the pulsation of an aneurysm may be communicated to the trachea and manifested by rhythmical interruption of the expiratory murmur. This is perceived by placing the stethoscope upon the manubrium and aus- cultating while the patient exi)ires slowly through only one nos- tril, the other being closed by his finger. This phenomenon is not peculiar to aneurysm, being perceived in health, but is more pro- nounced. In some cases an aneurysmal bruit may be ])laiuly heard when the bell of the stethoscope is placed between the patient's teeth, his lips being closed about the instrument, Sansom speaks of having thus been able to detect a systolic murmur, and Dr. E. J. Abbott, of St. Paul, has narrated to me an instance in which the detection of such a tracheal bruit was the only evidence of aneurysm he could discover. In Cook County Hospital at present writing is a man with aneurysm in whom both a systolic and diastolic bruit can thus be loudly heard. The phenomenon is due to the conduction of the murmur to the column of air within the trachea. This sign may be of diagnostic value in cases of small sacs of the transverse arch which are too deeply situated to declare their presence by outward pressure-effects. Diagnosis. — Under some circumstances the diagnosis of aneu- rysm of the thoracic aorta may be made almost at a glance, by the discovery of an external tumour displaying the expansile pulsa- tion and other characters of an aneurysm. There are other cases, on the contrary, in which the most painstaking examination fails to positively establish the nature of the malady. Between these two extremes are to be found cases which, although obscure, are yet susceptible of elucidation by minute investigation and by ex- clusion. In a suspected case the following points may be considered of diagnostic importance: (1) A history of syphilis years before or of strain, as by occupation, to which some would add chronic alco- ANEURYSM OF THE TIlORArrC AORTA 805 holic excess. (2) Age, the patient being at or after the middle period of life. (3) The male sex, since men are vastly more liable to aneurysm. (4) Symptoms indicative of intrathoracic pressure ; as, (A) intractable ])ain of the characters previously described; (B) dyspnoea, especially if influenced by posture; (C) cough of a brazen clang, also evoked or intensified by posture; (D) dys- phagia or regurgitation of food. These four symptoms, if all pres- ent, form a very strong chain of evidence in favour of an existing aneurysm. If to the foregoing history and symptoms the following physi- cal signs are added, reasonable doubt can scarcely be entertained: (5) Bulging, even if slight, in some one of the areas in which aneurysm is likely to be present. (6) Dulness in one of these areas even without perceptible bulging. (7) Displacement of the heart, most often downward and to the left. (8) Some of the auscultatory phenomena already described, especially a harsh, aortic systolic bruit with a clanging second sound. If such second tone is split or doubled and is heard most plainly or solely over a dull area or in the cervical arteries, especially if on one side and not on the other, and is accompanied by a diastolic shock, the evidence, taken in connection with pressure-symptoms, may be considered almost conclusive. Aside from an external tumour having a distinctly expansile pulsation or a diastolic shock, there may be said to be no signs so distinctive as to be pathognomonic. Diagnosis is to be found in the association of several important signs rather than in any one alone. ISTevertheless attention may be especially directed to what Balfour considers very trustworthy evidence — namely, a pulsation in an aneurysmal area equal in intensity to the apex-beat, so that there may be said to be two areas of maximum impulse. Even this is not absolute, however ; for a kyphoscoliosis has been known to push the convex portion of the aortic arch so strongly against the anterior chest-wall at right of the sternum as to simulate, with respect to the force of its pulsation, a thoracic aneurysm. Tracheal tugging is a very strong sign of aneurysm of the trans- verse arch, especially in conjunction with other signs ; but as it may be produced by other conditions, it is not infallible. Differential Diagnosis. — This concerns especially the three fol- lowing diseases, which taken in order of frequency and importance 806 DISEASES OF THE HEART are: (1) A solid intrathoracic growth — e.g., carcinoma and the varieties of sarcoma; (2) mediastinal abscess; (3) pulsating em- pyema in close contiguity to the base of the heart. (1) Malignant Tumour. — This disease when situated wdthin the thorax occasions symptoms of pressure so identical in some re- spects with those of aneurysm that they cannot be distinguished. The chief differential points are to be found, therefore, in the his- tory and physical signs. As a rule, the history is of more rapid growth than in aneurysm, accompanied by more pronounced ema- ciation and loss of strength. In the physical signs the main dif- ferences are found in the character of pulsation, when such exists, and in the auscultatory phenomena. A solid tumour occasions pulsation which is not expansile, but is a forward impulse, owing to the circumstance that the growth itself does not pulsate, but receives an impulse imparted to it by the aorta or some other artery or by the heart against which the tumour lies. More commonly, however, such a mass possesses no impulse. It must not be forgotten, on the other hand, that when a sac is filled with dense coagula, it is practically also a solid tumour, and hence under such conditions may be also incapable of producing any perceptible pulsation. I recall such an instance in Cook County Hospital. A large, dense, intensely resisting, non- pulsating tumour protruded close to the sternum in the right infra- clavicular region. It was, moreover, perfectly silent, and very naturally was for a long time mistaken for a malignant growth. Only after the lapse of time had somewhat altered the size of the sac and permitted vascular sounds to be generated was a correct diagnosis possible. As regards the sounds audible over a solid tumour, it may be stated that when such are present they are usually clear and un- changed. It is possible, however, for the cardiac or vascular sounds to be modified in consequence of pressure by the growth. Under such circumstances bruits may be generated or the second sound may take on a ringing intensification. It is not likely to be so clanging as is sometimes the case in aneurysm. Moreover, a tu- mour of the mediastinum which, from its situation and resulting area of dulness, simulates aneurysm of tlie transverse arch, does not occasion a tracheal tug. Neither is such a solid growth when situated in the area at right of sternum, and hence simulating ANEURYSM OP THE THORACIC AORTA 807 aneurysm of the ascending aorta, likely to lead to signs of insuf- ficiency of the semilunar valves. It does not change its direction of growth and cause sudden modification.^ of symptoms, nor is it apt to create asymmetry of the pulses. Finally, in cases of malig- nant growths there may be history or symptoms of an ante- cedent tumour elsewhere, or there may be induration of some of the lymph-nodes in axilla or neck which may aid in the correct inter- pretation of the case. (2) Mediastinal Abscess. — In this infrequent affection there is history of more sudden invasion, and pain is an early symptom, even before pressure has become sufficient to occasion dyspnoea. Fever is likely to be present, and is an early symptom, whereas when it exists in aneurysm it is apt to be late, after the sac has begun to exert pressure on the bronchus or lung with phthisical symptoms. In abscess, moreover, there is not likely to be the change in the vascular sounds or the production of new ones as occurs in aneurysm. The disease may arise at any age and in either sex, showing no predilection for the male sex. (3) Pulsating empyema may simulate an aneurysm when an empyema necessitatis forms in close proximity to the base of the heart. It is, however, exceedingly rare, and may occur in children as well as in adults. The history and examination of the lungs ought to clear uj^ the nature of the case. Should a circumscribed empyema in immediate contiguity to the heart display bulging and pulsation as well as dulness, it may occasion considerable difficulty of correct diagnosis, but ought at length to be diagnosed by exclusion, if not by history and physical signs indicative of its real nature. Other diseases producing signs in the aortic area — i. e., dila- tation of the ascending arch associated with aortic regurgitation, stenosis of the aortic ostium, and sclerosis of the ascending arch — may and have been mistaken for aneurysm. In the case of the first mentioned a positive differential diagnosis is sometimes ex- tremely difficult, when the regurgitation occurs in the male past middle age, but as a rule pressure-effects are absent. Thrill and systolic murmur may in cases of stenosis give rise to suspicion of aneurysm, but error may ordinarily be avoided by study of the history, age, the second sound, the position and size of the heart, and the characters of the pulse. Sclerosis of the aorta may occa- 808 DISEASES OF THE HEART sion a systolic bruit and ringing second sound very suggestive of aneurysm, but does not occasion pressure-effects noted in aneurysm. In all these three affections the subsequent progress will probably clear up the case. Pulmonary tuberculosis, fibrosis and retraction of the lung and throbbing of the aorta sometimes observed in neurotic subjects ought not to occasion material difficulty if due attention is paid to the history, symptoms, and clinical findings. Formerly the sphygmograph used to be depended on to aid in the detection of thoracic aneurysm, and may in favourable cases afford reliable information, by furnishing a tracing of one or both radials in which the usual characters are wholly wanting, but in many instances it fails to record positive evidence. N^owadays we are accustomed to resort to the X-ray in all doubtful or suspected cases. The reader is referred for details to the appropriate article in the Appendix. Prognosis may be said to be extremely unfavourable, for although spontaneous cure through obliteration of a small sac or one with a narrow pedicle sometimes takes place, it is unlikely for such to happen. Furthorniore, the results of medical or surgical treatment are not encouraging. The progress of the disease is not of a necessity steadily downward, although such is apt to be the rule. Remissions may occur both in the gravity of subjective symptoms and growth of the sac. Thoracic aneurysm may run a comparatively rapid course, par- ticularly if the sac develops externally and ruptures, but the dis- ease may persist for years, depending of course upon the size, direc- tion of growth, and physical conditions of the sac. Ten years may be said to be a long period of time for the continuance of thoracic aneurysm, and yet this limit has been reached and even surpassed. Finally, the outlook is influenced largely by the habits, general status, and environment of the individual, the same as in any other form of cardiac or vascular disease. Modes and Causes of Death. — The fatal termination may be said to occur either from rupture or tlio dirc'ct or indirect effects of pressure. Death from rupture is not the most frequent mode of termination, as shown by Hare's and Holder's figures, previously quoted, according to which it was the cause of death in 289 out of 953 cases. Rupture may take place externally or into any one of ANEURYSM OP THE THORACIC AORTA 809 the contiguous structures, pericardium, heart, pleural cavity, bronchus, trachea, a'soplmgus, 'vena cava, pulmonary artery. In such an event death nuiy be immediate or protracted over a period of hours. More commonly, life is terminated in consequence of mechani- cal interference with respiration or circulation and cardiac inade- quacy, or the patient succumbs to " aneurysmal phthisis " or gen- eral exhaustion and cachexia. Under such circumstances the end may come slowly or suddenly after weeks of slowly progressing loss of strength. The last hours are in many cases fraught with ex- treme suffering and death is hailed as a blessed deliverer. Treatment. — The not infrequent post-mortem discovery of the spontaneous cure of thoracic aneurysm by coagulation of the blood within the sac has furnished the hint upon which all thera- peutic measures are based that aim at anything more than pallia- tion of symptoms. The accomplishment of this object presupposes certain favouring conditions in the sac itself. In the first place the aneurysm must be of the saccular variety, and in the second it must communicate with the aorta by a narrow opening. Given these essentials, it is possible for clotting within the sac to take place. If these conditions are not present, there is little or no prospect of cure, and medical skill is powerless to do more than mitigate suffering or furnish advice, which if carried out may retard prog- ress. In the majority of cases, unfortunately, we are compelled to content ourselves with palliative measures and watching the course of the disease. Our aim should be, however, to effect a cure in every case in which there seems to be such a possibility. Consequently, the first measure to be advised is rest in the recumbent 'position. The object of this plan of management is the reduction in the number and force of cardiac contractions that thereby the flow of blood within the aneurysm may be less swift. Ever since its introduction by Val- salva the value and importance of this measure has been recognised. To be effective the rest must be absolute and must include rest of mind as well as of body. Whatever excites the heart to more rapid and powerful systoles must be avoided, and to attain as complete rest as is necessary, the patient should be clearly instructed con- cerning its advantages and necessity. 810 DISEASES OF THE HEART It is also advisable that arterial tension be reduced and the vol- ume of the blood diminished. To this end the diet must be re- stricted, as was recommended by Tufnell, of Dublin. His dietary was extremely rigid, consisting as it did of 2 ounces of bread and butter with 2 ounces of milk for breakfast and supper alike, while for the midday meal 2 to 3 ounces of meat and 3 to 4 ounces of milk were allowed. Such a rigid restriction in the amount of food requires for its successful carrying out courage and determination on the part of the patient, and few persons will submit to such an almost starva- tion diet. It is probable that the daily allowance may be somewhat greater than Tufnell's dietary permitted without destroying the aim of treatment, provided one remembers that if blood-pressure is to be lowered the quantit}^ of fluid allowed must be small. Fur- thermore, if such management is to accomplish results it must be persevered in for several months or until the aneurysm gives evidence of having diminished in size. While carrying out this or any other mode of treatment the bowels are to be kept freely open that there may be no straining at stool or increase of blood-pressure incident to constipation. The next plan of management that promises beneficial results is the administration of iodide of potassium. This mode of treatment was at very nearly the same time recommended by Bouillaud and Chuckerbutty, but has been especially advocated by Balfour. It is not advised because of the syphilitic history obtained in most cases of thoracic aneurysm, but for the purpose of influencing the sac in some as yet unknown manner. Balfour is of the opinion that this salt leads to thickening and contraction of the aneurysmal wall, while others believe its beneficial action lies in decrease of blood-pressure and slowing of the heart's action. \. Whatever be its modus operandi, it is not necessary and it is not advised to prescribe enormous doses, as used to be done, but to administer it in doses of 5, 10, or 15 grains thrice daily, since these moderate doses accomjolish exactly as much as do larger ones. The dose of the salt must not be large enough to produce acceleration of the pulse, the rate of which during repose should have been pre- viously determined. The remedy should be continued for many months, and is advantageously combined with rest and a restricted diet. ANEURYSM OF THE THORACIC AORTA 811 Testimony is universal tha,t the first and ^jronounced effect is relief or very considerable amelioration of pain due to the aneu- rysm. Why this is cannot be said, but there can be no doubt of the empirical fact. This plan of management should be instituted in all cases, yet to promote a cure of the disease favourable condi- tions of the sort explained above must be present in the tumour. The foregoing are the simplest measures, and in most instances are likely to accomplish as much as any other of the various plans of management that have been recommended and will now be mentioned. The surgical procedures sometimes employed in the treatment of this formidable complaint are five in number, as follows: (1) The introduction into the interior of the sac of many feet of fine iron or steel wire, horsehair, catgut, or silk thread. The object of such treatment is the coagulation of the blood in the meshes of this foreign material, wire being preferable to the others. This operation, known as the Moore or Loreta method, has been done a number of times, but not with sufficiently brilliant results to make it a popular mode of treatment. Of the 16 cases collected by White and Gould (Gibson), only 2 were successful, while of the 8 cases of thoracic aneurysm so treated and collected by Hunner prior to 1900 (Osier), all died. The great objection to this method of management is the resulting inflammation and aggravation of the condition. (2) Electrolysis, which consists in passing a galvanic current through the contents of the aneurysm by means of two insulated needles introduced through the wall of the sac. The points of the needles are to be left uncovered by the insulating material. They must not be in contact when inside the tumour. The electrical current thus applied causes coagulation of the sac contents, and in Gibson's opinion promises well, although the results as yet have not been very satisfactory. It is worthy of trial in suitable instances. (3) The Moore-Corradi method, which consists in the combi- nation of the two procedures just mentioned. A fine gold, silver, or steel wire is passed into the sac, and then a galvanic current is sent through the wire. This method is said to have yielded sat- isfactory results in a few instances. It has been performed by Burresi and Hershey. Of 17 cases of thoracic aneurysm thus treated prior to 1900 only 3 were successful. According to Hun- 812 DISEASES OF THE HEART ner, this method is not devoid of the following dangers: (1) embolism; (2) the formation of a secondary bulging of the wall of the sac; and (3) obliteration of an artery springing from the wall of the aneurysm. (4) The scratching of the inner surface of the sac-wall with the point of a thoroughly sterilized needle, a method said to have been introduced by Macewen (Gibson). After the integument has been carefully sterilized an aseptic needle is passed through into the aneurysm until its point comes in contact with the internal surface at the opposite side. The needle may then be left m situ to be moved about and made to scratch the lining of the sac by the pijlsations of the aneurysm, or the surgeon may irritate the wall by moving the point of the needle about first in one place and then in another, but without removing the instrument. If the needle is left in situ, it should not be allowed to remain for longer than twenty-four to thirty-six hours. This method is simple, said to be safe, and to promise well. (5) The subcutaneous injection of a 1-per-cent solution of pure white gelatin in normal salt solution. This method was introduced by Lancereaux in 1896, and by him was highly praised. At first a 2-per-cent solution Avas employed, but at ^lio suggestion of Hu- chard was reduced to half this strength as being safer. The gelatin solution should be carefully filtered and sterilized under pressure at the temperature of 120° C. Two hundred or 250 cubic centimetres of this 1-per-cent solution at a temperature of about 100° F. are to be very slowly injected into the loose subcutaneous tissue of the thigh or abdomen, after which the patient is to be kept perfectly quiet. Injections should be repeated every six to eight days until 20 in all have been given. The objections to this plan of treatment are the intense pain and sometimes local and general reaction that follow. In the case of the patient treated in this manner by Dr. Carl Beck, and previously mentioned in these pages, the tempera- ture rose to 101° F. or thereabouts after the injections. Cures have been reported in France, but in this country, so far as I know, the results have been unsatisfactory. It may be tried in desperate cases; but so many difiiculties and dangers attend its use, that it is not likely to become widely employed. Among the dangers is the risk of sepsis or tetanus, since 10 per cent of ANEURYSM OF THE THORACIC AORTA 813 comiTiercial gelatin is .said to contain germs, especially the tetanus bacillus. Moreover, not many patients will be found willing to bear the pain from the injections and the subsequent febrile re- action. Finally, of the cases in which this treatment has been tried, but a small percentage has shown really encouraging results. The use of gelatin in this manner does not ap})ear to increase the coagulability of the blood, and since the action is as yet not under- stood, it has been suggested that the remedy be given by the mouth as food, 15 grammes being consumed daily. When one considers the pathology of thoracic aneurysm, the great internal pressure to which the wall of the sac may be sub- jected in cases in which the mouth of the aneurysm is a wide one, and usually the advanced stage of the process when the individual applies to the surgeon for relief, it is not strange that failure, or at best only amelioration, of symptoms follows any attempt at a cure. The most that can be done in the great majority of cases is to mitigate the patient's distress. If the iodide of potash does not relieve the pain, recourse must be had to opium in some form. Subcutaneous injections of morphine are the best^ since they, not only rid the sufferer of his pain for a time, but they also lessen his sense of dyspnoea and promote sleep. I have not yet prescribed heroin in a case of aneurysm, but think it ought in the dose of one-twelfth grain not only to prove efficient against the cough, but should diminish the sense of dyspna3a. Venesection is highly recommended for relief of venous con- gestion and to decrease blood-pressure for a time, and thereby the dull pain arising from pressure within the sac. Only a few ounces, 3 to 5, should be taken at a time, since it may have to be frequently repeated, and the abstraction of too much would only serve to w^eaken the patient without doing more' good than do the few recommended. When the sac is external and large, it is said to minister to the patient's comfort to have him wear an elastic bandage over the tumour (Osier). It certainly' ought to lessen the tension to which the integument and thoracic parietes may be subjected, and thereby mitigate pain. In some cases it may be necessary to protect the tumour against violence from external blows by having the patient wear a shield of thin metal or woven wire strapped to his chest. 814 DISEASES OF THE HEART The diet of these sufferers should be light, eveu though they are not placed at complete rest, and they should never be allowed to become constipated, since straining at stool is sure to prove harm- ful. They should take a daily laxative, and now and then, when blood-pressure becomes too high, they should receive a sharp purge from calomel. They should be informed of the dangerous nature of their malady and be warned of the risk attending severe physical efforts, excitement, excesses, etc. There are times when from cardiac inadequacy digitalis or one of its congeners may appear indicated, but one should remem- ber that such agents are likely to injure rather than benefit the aneurysm. Consequently if such a remedy is called for, it should be administered with caution and its effects should be carefully watched. When at length it is plain that the end is near, and, as it approaches, suffering is intense, I am of the opinion that the phy- sician is warranted in the free administration of morphine injec- tions to promote euthanasia. I certainly should not hesitate under such circumstances to inject a dose that would hasten the patient's death. I know of an instance in which this was done to prevent the terrible shock to the friends that was sure to follow the impend- ing rupture of a large external sac. APPENDIX MECHANICAL DEVICES AS AIDS TO DETERMINING CARDIAC DISEASE THE X-RAY Peecussiotst and auscultation are not entirely satisfactory methods of examining the heart, for the reason that thick, rigid parietes, pulmonary emphysema, or other conditions may prove sources of error. Much depends also on the skill of the examiner or on his delicacy of hearing, so that it is quite common for two or more examiners to obtain results that do not wholly agree. When, therefore, the Roentgen-ray came into use it was quite naturally hoped it would furnish a reliable means of detecting diseased con- ditions in the heart. Accordingly, considerable work along this line has been done both in Europe and this country. As a result of such investiga- tions we now know that the X-ray is in many cases a valuable aid to the diagnosis of internal diseases, but cannot altogether replace other and older means of investigation. This is pre-eminently true of cardiac disease. Francis P. Williams, of Boston, is a particularly diligent in- vestigator with the X-ray, and it is to his elaborate paper in the Philadelphia Medical Journal of January 6, 1900, that I am in- debted for much of what is here stated. Percussion of the cardiac area was made by Williams and his friends in a large series of cases both healthy and diseased, and after the limits of deep-seated dul- ness had been carefully marked out on the bare skin the results thus obtained were compared with those of the X-ray by means of the fluorescent screen. The conclusion Williams arrived at was that the fluoroscope is a much more trustworthy means of judging of the size of the heart. He found that in normal hearts the dis- 815 816 DISEASES OF THE HEART crepancies between percussion and the fliioroscope were not so marked as when the heart was either undersized or oversized, and that the greater the enlargement of the organ over the normal, the less frequent is the error by percussion, although the more pro- nounced is such error when made. He furthermore discovered the X-ray to be a more precise method of determining the shape and position of the heart. Thus Williams found that in one case, in which the situation of the apex-beat and the results of percussion led him to conclude that the heart was hypertrophied, the X-ray showed the organ to be merely displaced downward so as to lie transversely. Trans- positions are also discovered by means of the fluorescent screen more certainly than by percussion. This was brought out very clearly in cases of left-side pleuritic effusions. Congenital malformations are stated to be capable of diagnosis by the X-ray, and by this means patency of the ductus arteriosus has been determined. It also enables one to diagnosticate a peri- cardial effusion, as is well illustrated by the figure opposite kindly furnished me by W. C. Fuchs, who took the skiagraph from which the cut has been made (Fig. 118). Cardiac contractions can be observed and differences in size between systole and diastole noted, particularly in cases of valvular incompetence. The value of the X-ray in the diagnosis of aortic aneurysms has been repeatedly proved. Williams finds that certain aneurysms can be more surely detected by this means than by any other mode of examination. It enables one to determine their location and extent and whether or not the tumour is increasing in size. Final- ly, if the aneurysm is situated at the left, it is best seen from behind, while those at the right of the heart show best from the front. Although it is possible for even skilled observers to commit error by incorrectly interpreting normal pulsations seen by aid of the fluoroscope, still there can be no doubt of the. positive value of the X-ray in this class of cases. To sum up, it may be stated that aside from the detection and study of aneurysms the real practical value of the X-ray in cardiac disease lies in its greater accuracy in determining the size of the heart in general, enlargement of any of the chambers, displace- ments and transpositions and certain obscure congenital malforma- tions. Even if it could replace percussion and auscultation, which 818 DISEASES OF THE HEART it cannot, its lack of portability would preclude the possibility of its supplanting older methods. THE SPHYGMOGRAPH The sphygmograph is at tlie same time one of the most useful and most useless of the instruments used in clinical medicine. If used as a routine in his practice by the observing physician it will exceed in value the feeling of the pulse by the fingers, which it should supplement and not supplant. The educated tactile sense, which is always quickly and easily available, can appreciate nearly everything which the sphygmograph can show, and some features which this instrument is unable to delineate, but the impressions cannot be intelligently described and are evanescent. On the con- trary, the sphygmograph, which is not always at hand nor readily applicable, can graphically show nearly everything that the finger can detect and some characteristics which this member cannot appreciate, and the results may be preserved for deliberate study, comparison, future reference, and exhibition to others. The clinician will be able to do good work with any one of the standard sphygmographs, but he can use with the greatest facility, and can interpret most readily and accurately the tracings made by the instrument with which he is most familiar. My own pref- erence is for Dudgeon's sphygmograph, which, because of its por- tability and adaptability, readily lends itself to the exigencies of all kinds of practice. In the practical application of the sphygmograph certain ele- mentary rules must be followed, but the whole secret of success in manipulating the instrument lies in placing and maintaining the metal pad upon the artery in such manner as to give the greatest possible amplitude to the excursions of the lever. The wrist band should be elastic ; the pad properly placed ; the tension correctly adjusted ; the pressure gauged to give the greatest amplitude to the writing lever. In adjusting and maintaining the instrument in proper position it is essential that the operator should rely, mainly, upon his fingers and not upon mechanical appliances. Facility in the use of the sphygmograph can only be attained by practice. It may be noted that the most convenient strips of paper which can be used are made from ordinary heavy writing paper, cut thirty-one thirty-seconds THE SPHYGMOGRAPH 819 of an inch wide, and blackened with smoke from burning camphor. The best varnish for preserving the tracirfgs is the ordinary sandarac varnish used by dentists, suitably thinned by the addition of absolute alcohol. Fig. 119. — From a IIealtiiy Man, Forty-five Years of Age. Tracings of the normal pnlse in health vary infinitely in their characteristics, and no two are ever exactly alike. The above sphygmogram (Fig. 119) may be considerecl fairly typical of the pulse in the healthy middle-aged adult. Fig. 120. — -From a Womaw, Aged Forty-four, During an Attack of Paroxysmal Tachycardia. Pulse, 196 per Minute. Between the extreme frequency of the pulse in paroxysmal tachycardia and the remarkable slowness of bradycardia lies a wide gap which is filled by the rapid pulses of infectious fevers, the varying pulses of health and the slow pulses of age, some of the intoxications, etc. (Figs. 120 and 121). Fig. 121. — From a Man, Aged Twenty-eight, -with Eecuerent Bradycardia. Pulse, 25 per Minute. The sustained arterial tension as shown in the pulse varies within wide limits. The lowest tension is found in some of the acute infections — e. g., general gonorrhoeal or pneumococcal, in which there occurs, very early, profound capillary paresis. In many of these cases the powerful left ventricle throws the blood 820 DISEASES OP THE HEART forcibly into the arteries and tlirouiili the capillaries with prac- tically no resistance, as shown in the following tracing (Fig. 122). Fig. 12i!. — Fkum a Man, AbEu Tweniy-five, with Acute Genekal Gonouuhceal Infection. In some of these cases the capillary and arteriole vaso-motor reflexes respond energetically to an nnnatnral stinmlns, and the dicrotic pnlse of every grade is the result, an example of which is Fig. l2o. — FuoM a Man, Aukd Foinv, with Declining Tvimiuid Fever. given in Fig. 123. The hyperdicrotic pnlse, as shown in Fig. 124, is so often seen in ha?morrhages accompanied by nervous excite- ment — e. g., in ha?moptysis — that it may be considered somewhat distinctive. In aortic regurgitation the po^verful left ventricle vigorously propels a large volume of blood into nearly collapsed arteries, Fig. 124. — liyrEKDiuKoxic Fllue fkom a Woman, Aoeu Tiiiuty-kive, aktek Twelve Hours Kecurkino ILemoptvsis. Pulse, 135. quickly and Avidely distending tlieni, but the flow of blood through the capillaries, during and immediately following the systole, and the reflux of blood through the open valve, the instant ventricu- THE SPHYGMOGRAPH 821 lar action ceases, as quicklj- reduce the arterial tension, and the typical pulse of this condition is the result, as shown in Fig. 125. Fig. 125. — Fkom a Woman, Aged Twenty-five, with Mouekate Aoktic Insufficiency, Well Compensated. In this connection it should be remembered that, other conditions being equal, the pulse will be less frequent and approximate the normal in character, or more frequent and with exaggeration of the distinctive characteristics, according to the degree of valvular incompetency. With failing compensation, the secondary curves in the line of descent may disappear. At the other end of the scale we have the initial and sustained high-tension pulses, which are so often the accompaniment of early Fig. 126. — Initial High-Tension Pulse, from a Man, Aged Forty-eight, with Ar- teriosclerosis and a Small Aneurysm of the Arch of the Aorta. arteriosclerosis, aneurysms of the aorta, and chronic interstitial nephritis, typical tracings of which are given (Figs. 126 and 12Y). Fig. 127. — Sustained High-Tension Pulse from a Woman, Aged Sixty-three, with Chronic Interstitial Nephritis. The following sphygmogram (Fig. 128) may be considered as fairly representing the average in chronic interstitial nephritis, and is typical of those oftenest encountered in this affection. In this connection it is fair for me to state that, highly as I value the sphygmograph, it is my opinion that its tracings in chronic interstitial nephritis have been accorded, in some quarters, a diagnostic value altogether beyond their merits. This is not to the discredit of the instrument, for it afiords the 822 DISEASES OF THE HEART best practicable means for quickly and conveniently estirnating and permanently recording the state of the circulation, cardiac energy, peripheral resistance, arterial resilience, and arterial tension. On the contrary, this fictitious value usually depends upon a faulty appreciation of the infinite variations of the pulse in health and disease, and in the same person at different times. Fio. 128. — Fkom a Man, Aued Fuktv-five, with Ciiitoxic Intekstitial Nephritis. The rhythm of the pulse is very clearly and only satisfactorily shown by the sphygmograph. In health, the rhythm, in every par- ticular, is fairly but not absolutely regular. A moment's reflec- tion upon the ])liysiology of the cardiac cycle and the vaso-motor mechanism should lead us to expect this, and an inspection of any Fifi. 129. — FuoM a Woman, Aged Foirrv-Foin, with Milu Myxcepema. large collection of sphygmograms will confirm the inference. Nevertheless, in ordinary health, the points of difference between the individual pulsations are minute and well within the limits of physiological identity. However, in certain conditions, some of which are understood while others are not, the pulse becomes Fio. 13IJ.— I'Jiu.M Man, Aoed Twkniv-i'ih i:, with VVell-Cumpen8ateu Mitual In- SUFKKJIENCY. decidedly and morbidly irregular — arrhythmic. These irregu- larities may be of almost every conceivable degree and character, some of which are strikingly peculiar. Tims Ibcre may be a marked iucciiiiility in the interval be- tween some of the pulsations, as shown in Fig. 129, or beats may THE SPHYGMOaRAPH 823 be entirely lost, as seen in Fig. 130. It will be found that nnder these circumstances the line of descent reaches a lower level than it does in the regular pulsations, because the artery has had a longer time in which to empty itself through its distributing chan- nels. In some cases the pulsation is not entirely lost, one or more abortive beats showing in the line of descent, as illustrated in Figs. 131 and 132. Such pulses are denominated bigeminal, trigemi- nal, etc. It is to be noted that the elevation that marks the abor- FiG. 131. — Fhum a Woman, Aged Sixty-seven, with Akteriosclerosis and fairly Well-Compensated Mitral Incompetence. tive pulsation in the bigeminal pulse is located nearer the pre- ceding than the following full beat, and that the second abortive pulsation in the trigeminal pulse lies nearer the first abortive beat than does the latter to the preceding full stroke. The arrhythmias thus far mentioned may be irregular in their occurrence, or the prolonged, missed, or abortive pulsations may be repeated at regular intervals. The irregularities of this group may be found rarely in apparent health, and frequently in patients Fig. 132. — From a Woman, Aged Seventy-three, with Arterioscleeosis, and Mitral Insufficiency, Failing Compensation. suffering from digestive disturbances, various intoxications — as, 6. g., tobacco, renal insufficiency, organic disease of the central nervous system, the vagus and the cardiac ganglia, arteriosclerosis of the coronary arteries, myocardial changes, etc. They occur, therefore, in conditions of no, or varying degrees of danger. They often lead to the discovery of conditions which without such warn- ing might be overlooked. They may, by the strain thrown upon the ventricular walls, lead to dilatation, and relative valvular in- 824 DISEASES OF THE HEART competence and thns become an element of danger. As a matter of fact, however, many persons pass throngh the greater portion Fig. 133. — Fitosi a Man, Aged Seventy-three, with Artekiosclerosis, Chronic In- terstitial Nephritis, and Mitral Insufficiency, with Failing Compensation. Cheyne-Stokes Kesvikation. of a long life with such irregularities and without any inconveni- ence whatever. In addition to the above arrhythmias we have another group Fig. 134. — From a Woman, Aged Sixty-two, with Mitral Obstruction and Eeguroi- TATioN, WITH Failing Compensation. Irregularly Recurring Delirium Cordis. in which the irregularities of the pulse, as shown by tracings, abso- lutely defy either analysis or description. Such pulses are simply Fig. 135. — From a Man, Aged Fifty, with Mitral Keguroitation, Lost Compensa- tion, Relative Tricuspid Insufficiency, Ascites, and (Edema of Legs. Later Comparative Recovery with Good Compensation. irregularly arrhythmic, and are endless in their variety, as may be seen in the few examples shown (Figs. 133, 134, 135, and 136). Fio. 136. — From a "Woman, Aged Tiiirty-ekiHT, with Mitral Obstruction and In- sufficiency, Lost Compensatujn, and Uklative Incompetence of the Tricuspid. Delirium Cordis. THE SPHYGMOGRAPH 825 This form of arrhythmia is met with, particularly, in mitral stenosis and incompetence, arid in myocardial insufficiency. It is often a late plienonienon in mitral disease. It is of grave, but not necessarily of fatal import, as the lost compensation may be restored, or the weakened myocardium may regain its tone. Fig. 137. — From a Boy, Aged Twelve, with a Pkeviously Normal Pulse, Ten Days III with Acute Kheumatism, and on the Second Day of Endocakditis. No Murmur. In endocarditis the sphygmograph usually furnishes us Avith diagnostic evidence of valvular involvement several hours or days before murmurs can be heard with the stethoscope. This evidence Fig. 138. — From the Same Patient, Two Years Later, with Developed Aortic Stenosis. (Convalescent from Mumps.) is shown in a more or less radical change in the character of the pulse, as shown in the above sphygmograms (Figs. 137 and 138). In introducing the above tracings it is proper for me to say that, during the past five years, I have had under observation for one, three, and five years respectively, three cases of aortic stenosis in young persons, from each of whom tracings of a similar character were obtained. In the slighter cases of aortic stenosis the character of the pulse approximates the normal. In this connection a word of caution is due. In using the sphygmograph in cases of considerable or great aortic obstruction the most delicate adjustment of the instrument is required to obtain satisfactory results. It may be said, however, that the greater the care bestowed upon this point the more difficult it will be to pro- duce tracings corresponding to some which have been made classic by more than a generation's text-book currency. In early pulmonary tuberculosis the pulse is often of a pecul- iar character, approaching, more or less closely, the infantile type, and the tracings, at this time, possess a distinct diagnostic value. 53 826 DISEASES OF THE HEART One of the curiosities of clinical spliygmography is the mani- fest family resemblance, inherited from the father or mother by their children, often shown in the pulse tracings. Fig. 139. — CAunioGiiAM from a Gikl, Ageu Nine, with Mitral Insifficiency. The sphygmograph may be used to obtain tracings from the heart (an example of which is given in Fig. 139), aneurysms, pul- sating veins, pulsating tumours, etc., but the information to be derived from such tracings is not very great. GAERTNER'S TONOMETER The examination of the circulation includes the observation of the pulse for what is termed the arterial or blood pressure. This is determined by heart contraction, the peripheral resistance in the arteries and tissues, and the quantity of blood contained in the vessels. Among skilled physicians there is often a difference of opinion in regard to the degree of the arterial pressure, even in general terms, such as hard and soft, while subtile differences are entirely beyond registration, and, to most physicians, beyond perception. Numerous attempts have been made to overcome this difficulty in pulse examinations by means of instruments; if suc- cessful, we would then have a more accurate method of comparison of the blood-pressure of individuals, and also of the blood-pressure of the same individual under different conditions. The invention of the sphygmograph was expected to bring accuracy into the subject, but this hope was not realized. Mosso, von Basch, Iluer- thle, Frey, Oliver, Riva-Rocci, and Hill and Barnard may be mentioned as inventors of such instruments. Of these, the von Basch instrument was the most used up to 1899, since when the Gaertner instnmient, on account of greater simplicity of its mech- anism, has supplanted it in the hands of many, and has also intro- duced the practice of taking the arterial pressure to a greater extent than had heretofore been customary. Opinions still vary as to the preferable instrument. James MacKenzie (1902) com- GAERTNER'S TONOMETER 827 pares the action of the Hill and Barnard instrument to that of the sphygmograph and regards it unreliable for blood-pressure registration. So also with the Oliver instrument. Jarotzny be- lieves the Hill and Barnard device superior to those of von Basch, Gaertner, etc. Ilirsch considers the Gaertner less reliable than the von Basch instrument. As the latter is at present the chief rival of the Gaertner in- strument it may be well to state the principle on which it works. There is a small compressible rubber pelote connected by a rubber tube to a metallic manometer. By pressure with the rubber cyl- inder (pelote) a suitable artery may be compressed and the amount of necessary pressure at the point of disappearance or reappearance of the pulse on the peripheral side of the instrument is registered on the manometer. The radial artery may be used, but the temporals are usually selected. The sense of touch is re- quired for this instrument, while in the Gaertner method, soon to be described, sight is employed for observing the re-establish- ment of the circulation; and because in most peoj^le the sense of sight is more acute than the sense of touch, the Gaertner instru- ment requires less practice for its use, and also is believed by many to be more accurate. Von Basch calls his instrument a sphygmomanometer. Gaert- ner' s tonometer consists of a mercury manometer, a rubber bulb, a " Y " rubber tubing, and a small ring consisting of a metal frame- work and encased in a rubber envelope, which on inflation stretches inwardly only, and thus compresses the finger that is introduced into the ring. These rings are of different sizes to fit large and small fingers snugly. One end of the " Y " tube is attached to the manometer, another end to the rubber bulb, and the third end to the rubber finger ring; thus pressure made on the bulb transfers itself to the manometer and the rubber ring, and the elastic rubber on the inside of the ring unfolds itself and makes inward pressure in proportion to the pressure put on the bulb. The manometer, being on the same closed tubing, registers the increase or decrease of the pressure. A small clamp is serviceable for compressing the bulb firmly and steadily. The rubber ring is pressed over the first or second phalanx of any finger or the thumb. It is to fit loosely, and is not to rest on a joint. An ordinary small rubber elastic is now rolled from the tip of finger to the rubber ring. This produces 82S DISEASES OF THE HEART an aiui'inia of the finger. Pressure is now put on the rubber bnlb to a degree that is regarded sufficient to nuiintain the anfcmia. This is usually 180 to 200 millimetres of the mercury manometer. The rubber elastic is now pulled off the finger, after which the anaemic appearance continues on account of the constriction of the ring. The pressure on the rubber bulb is now gradually lessened, 5 millimetres at a time. After each diminution, the finger is ob- served for a few seconds. Wheii the pressure is sufficiently lowered for the arterial pressure to force the blood through thx? arterioles compressed by the rubber ring, the anaemic finger first shows a few spots of purple congestion, and after a little more reduction of the pressure on the bulb, the finger becomes entirely suffused with the purple colour of congestion, showing that the circulation is re- established. At this point the height of the mercury column is observed on the scale of the manometer. This is the arterial pres- sure expressed in millimetres of mercury. One of the principal objections is the small size of the arteries utilized, but Gaertncr and others state that the pressure in the digital arteries is the lateral pressure in the volar arch, and that this is probably only 8 or 10 millimetres lower than the pressure in the radial arteries. Another objection is that such small peripheral arteries are more under the influence of the vaso-motor variations than large vessels, and especially subject to local influences. Cold anaemic fingers sometimes must be immersed in warm water before the test can be made. It is well to follow his instructions for the use of the instrument very closely. The individual may be in the horizontal or upright posture. In the former the pressure is a few millimetres lower than when the person is erect. The manometer must be on a level with the heart. A difference of 10 centimetres in the levels of the heart and manometer ])roduces a change of 7 millimetres in the mercury accordingly. The individual is to breathe regularly. A cough renders the result unreliable on account of the sudden in- crease of the blood-pressure. The test is not to be repeated on the same finger immediately on account of a possible persistence of an arterial s])asm. Thirty seconds will suffice for a test. There is no pain, but at the time of the re-estal)lishm(Mit of the circulation the person feels a throbbing and tingling in the finger. For portability a metallic manometer may be used; but it 18 iiot GAERTNER'S TONOMETER 829 as reliable; it should be frequently compared with the mercury manometer. The advocates of the von Basch method admit the requirement of much more experience and careful manipulation in its use than in that of the Gaertner. The values obtained by both instruments agree fairly, those of the von Basch instrument are probably 8 to 10 millimetres higher ; the range of normal blood-pressure under ordinary conditions is from 100 to 160 milli- metres of mercury. These limits may be narrowed down to 110 to 135 for the greater number of persons. Constant pressure of 150 to 160 should be regarded suspiciously high. It is probable that each organism has a mean arterial pressure towards ivhose maintenance the regulatory mecJianism tenaciously strives as soon as a disturbance occurs. Active influences are numerous. For instance : Posture, food, sleep, physical and mental work, psychical conditions. Several readings should be obtained and the average taken ; according to some authorities the lowest reading is the correct blood-pressure, as more causes are active in increasing than lowering the blood-pressure. According to Jellinek the ar- terial pressure in the fingers of the right side is usually slightly higher than on the left, but Eckart and Hirsch, using von Basch's sphygmomanometer, found the pressure usually higher in the left temporal arteries, and ascribed this to the direct origin of the left carotid artery from the aorta. Hirsch, who prefers von Basch's sphygmomanometer, maintains that the Gaertner instrument reg- isters the blood-pressure 10 to 20 millimetres higher than the von Basch instrument, but admits that in general the values obtained by both instruments agree as to being high, medium, or low. The high pressures are of special interest on account of being associated with diseases in which many of the threatening symp- toms are thought to be due to the high pressure ; thus in uriemia and arteriosclerosis pressures of 170 to 240 or more millimetres are the rule. All observers state that high pressures are frecjuently found in spite of an apparently soft pulse by palpation; here, then, as the general accuracy of these instruments cannot be doubted, their value is undeniable. In many illy defined conditions of mid- dle age an unusually high pressure is found, which returns within the normal limits in the course of treatment. Such cases are often described as due to arteriosclerosis or to some intoxication produc- ing increased arterial pressure. In the treatment of nej)hritis a 830 DISEASES OF THE HEART lowering of the arttn-ial pressure is associate3: in endocarditis, acute, simple, 175; in endocarditis, ulcerative, 190; injection of, in aneurysm, 814; in myocarditis, chronic, 533, 501 ; in pericarditis, dry, 09, 88, 91; in pneumo])ericardium, 135; in regurgitation, aortic, 288, 290, 310; in stenosis, aortic, 333; in stenosis, mitral, 272; in Stokes- Adams disease, 635; in valvular disease, 440, 481, 499. Murmurs, accidental, 20, 32; differential diagnosis of, 34; not accompanied by secondary changes, 35; detection of, 13; endocardial, 21 ; exocardial, 36; musical, 29; pericardial, effect of pressure on, 59; transmission of, 25. (See also Sounds.) Muscle, papillary, degeneration of, a cause of mitral insudicicncy, 596. Mycotic endocarditis. (See Endocar- ditis.) Myocarditis, acute, 505; antitoxin in, 515; associated with endocarditis, 157; diagnosis of, 514; digitalis in, 510; diphtheria in, 508, 511; etiology of, .508; infarction in, 158; iron in, 517; micro-organisms in, .508; morbid anatomy of, 506; palpation in, 514; percussion in, 514; in physical signs in, 514. ^Myocarditis, prognosis in, 515; l)ulse in, 511, 513; rheumatism in, 508, 513, 515; scarlatina in, 508, 516; small-pox in, 508; strophanthus in, 516; symptoms of, 510; treatment of, 515; in typhoid fever, 508, 516. Myocarditis, chronic, 518; atropine in, 502; baths in, Turkish, 552; brandy in, 501 ; Bright's disease, associated with, 539; bromides in, 563; bronchitis, acute, in, 551; camphor in, 561 ; cases of, .520, 531, 540, 541; chloralamide in, 563; diagnosis in, 122, 547; digitalis in, ,522, 564; dropsy in, 530, 563; etiology of, 522; gastritis, chronic, in, 551 ; influenza in, 522, .551; inspection in, 543; massage in, 559; morbid anatomy of, 519; morphine in, 533, 561 ; nitroglycerin in, 553, 560; palpation in, 543; percussion in, 544; physical signs in, 543; pneumonia in, 551; ])rognosis in, 549; ])ulse in, 529; rheumatism in, 522, .541 ; strophanthus in, .553, 561; strychnine in, 553; symptoms of, 526; treatment of, 551 ; typhoid fever in, 522. Myocardium, cancer of, 666; degeneration of, in chronic pericar- ditis, 101; diseases of, .505; fibroma of, 600: fragmentation of, 008; lipoma of, 600; segmentation of, 668. Myocardium, syphilis of, 663; diagnosis of, (»04; digitalis in, 665; etiology of, 003; iodides in, 005. INDEX 845 Myocardium, syphilis of, mercury in, I ()();") ; morbid anatomy of, 003; prognosis in, 005; symptoms of, 004; treatment of, 005. Nephritis, in acute pericarditis, 44. Neuroses, 703, 717, 731; diagnosis of, 724; etiology of, 722; pain in, 728; pathology of, 703; prognosis in, 720; symptoms of, 704; treatment of, 727. Nitroglycerin, in angina pectoris, 058; in aortitis, acute, 702; in arteriosclerosis, 757; in dilatation, 591, 593; in endocarditis, chronic, 202; in fatty heart, Oil; in mitral insufficiency, 594; in myocarditis, chronic, 553, 500; in pseudo-angina pectoris, 728; in regurgitation, aortic, 288, 314,310; in stenosis, aortic, 332, 333; in stenosis, mitral, 272; in Stokes-Adams disease, 635; in tachycardia, 715; in valvular diseases, 442, 444, 440, 488, 498. Occupation, effect of, in valvular dis- eases, 409, 419, 470. CEdema, in mitral stenosis, 250; in valvular diseases, 495; digitalis in, 495. Orthopnoea, in fatty heart, 003; in pericarditis with effusion, 67. Oxygen, in acute endocarditis, 191 ; in Stokes-Adams disease, 035. Pain, in aneurysm of thoracic aorta, 782; attack of, in neuroses, 728; cardiac, 718; in pericarditis, dry, 49. Palpitation, in cardiac neuroses, 727. Paroxysmal tachycardia, 730; features of, 732. Pathogenesis, of thrombi, 074. Pathology of angina pectoris, 640; of fatty heart, 599; of mitral insufficiency, 594; of neuroses, 703. Pathology of Stokes-Adams disease, 027; of tachycardia, 731. Pectoris, angina (see Angina Pec- toris) ; pseudo-angina, 719. Percussion, "abgcdilmpfte" metliod, 7 ; auscultatory, or stcthoscopic, 8; palpatory, 10. Perez's sign in chronic mediastino- pericarditis, 121. Pericarditis, acute, 37; abscess in, 47; alcoholism in, 47; Bright's disease in, 45; bronchitis in, 47; cancer in, 47; caries of rib in, 47; cholera in, 40; diphtheria in, 46; erysipelas in, 40; etiology of, 41; measles in, 46; micro-organisms in, 40, 42; morbid anatomy of, 37; nephritis in, 44; peritonaeum, diseases of, in, 47; pleuritis in, 47; pneumonia in, 40; purulent form, 40; purpura heemoiThagica in, 47; rheumatism in, 42, 40; scarlatina in, 46; scurvy in, 47; serofibrinous form, 40, 42; simplest form, 37; small-pox in, 46; strychnine in, 516; suppurative form, 42; tonsillitis in, 44, 47; typhoid fever in, 4b; ulcer in, 47; valvular defects resulting from, 49. Pericarditis, chronic, 99; baths in, 110, 115; calomel in, 125; cases of, 105, 114, 123; compensation prevented in, 105; course and termination of, 117; diagnosis of, 122 ; diagnosis, differential, from cirrho- sis of liver, 122; digitalis in, 126; diuretin in, 126; etiology of, 103 ; morbid anatomy of, 100. S^Q DISEASES OF THE HEART Pericarditis, chronic, palpation in, 120; percussion in, 121 ; pliysical signs in, 118; prognosis in, 123; rheumatism in, 117; stasis in, 117; strophanthus in, 114; strychnine in, 114, 125; symptoms of, 104; treatment of, 124. Pericarditis, dry, 48; cases of, oO, 52, 61 ; course and termination of, 56; deglutition in, painful, 49; tliagnosis of, 60; dili'erential, 60; digitalis in, 54; inspection in, 56; morplune in, 69, 88, 91; pain in, 49; palpation in, 57; percussion in, 57 ; ])hysical signs in, 56; pneumonia in, 60; prognosis in, 61 ; pyrexia in, 51 ; rheumatism in, 50, 54, 61; strydinine in, 53; symptoms of, 48; hiiMuorrliagic, 40, 47. Pericarditis, with effusion, 64; anodynes in, 88; atrojjine in, 92; belladonna in, 88; blister in, 86, 87; calomel in, 89; cases of, 68, 70, 92; chloroform in, 88; codeine in, 88, 91; course and termination of, 73; diagnosis of, 81 ; dilFerential, 82; digitalis in, 83; fever in, 89; "first rib" sign in, 75; fomentations in, 88; lieroin in, 88; ice-bag in, 87, 89; inspection in, 75; opium in, 8S, 91 ; orthopnci-a in, 67; percussion in, 76; pliysical signs in, 74; I)rf)gnosis in, 84 ; puncture in, site of, 94, 96. Pericarditis, resulting from pneumo- nia, 73; with effusion, resulting from scar- let fever, 72; rheumatism in, 68, 70, 73, 84; sepsis in, 72; signs in, "first rib," 75; Ewart's, 80, 81; Pins', 80; Kotch's, 78; strychnine in, 91 ; symptoms of, 64; treatment of, 86, 90; tuberculosis in, 84. Periarteritis nodosa, 769; etiology of, 7(i9 ; morbid anatomy of, 769; prognosis in, 770; sepsis in, 769; symptoms of, 769; treatment of, 770. Pericardium, adherent, 99; bacteria in, 45; signs in, l^roadbent's, 119; Friedreich "s, 120; Kussmaul's, 120. Pericardium, carcinoma of, 141 ; diseases of, 37 ; perforated by gastric ulcer, 133; sarcoma of, 141; syphilis of, 139; tubercidosis of, 136. Pick's pcricarditic pseudo-cirrhosis of the liver, 123. Pins' sign, in pericarditis with ellu- sion, 80. Pleurisy, mistaken for pericarditis, 83. Pneumonia, in aortitis, acute, 760; in bradycardia, 625; in Cheyne-Stokes respiration, 617; in endocarditis, acute, 185; croupous, 154, 156, 181; recovery from, 155; in myocarditis, chronic, 551 ; in pericarditis, acute, 46; in pericarditis, chronic, 103; in pericarditis, dry. 60; in pericarditis, with efTusion, 73, 97; in regurgitation, mitral, 224; in stenosis, aortic, 341 ; in valvular disease, 440. Pneumopericardium, 132 ; bacilli in, gas forming, 133; brandy in. 135; cases of, 133; diagnosis of, 135. INDEX 847 Pneumopericardium, digitalis in, 13G; etiology of, 132; inspection in, 134; morbid anatomy of, 132; morphine in, 135; prognosis in, 135; resulting from trauma, 133; resulting from ulcer, 133; strychnine in, 130; symptoms of, 133; treatment of, 135. Pregnancy, in valvular defects, 409, 422. Pressure, effect of, on pericardial mur- mur, 59. Pseudo-angina pectoris, 719; -ciri'hosis of liver, Pick's pericar- ditis, 123. Pulmonary artery, stenosis of (see Stenosis). Pulmonary regurgitation (see Re- gurgitation) ; stenosis (see Stenosis). Pulse, capillary, in aortic regurgita- tion, 301; inequality of, in aortic aneurysm, 801; inequality of, in mitral stenosis, 257, 259, 260; instability of, in acute myocarditis, 511, 513; tension of, in chronic myocarditis, 529; venous, in aortic regurgitation, 301 ; " water hammer," in aortic regurgi- tation, 298. Puncture, site of, in pericarditis with effusion, 94, 96. Pyrexia, in endocarditis, acute, 171; in hydropericardium, 129; in pericarditis, dry, 51; in regurgitation, tricuspid, 346. Quincke's sign, in aortic regurgita- tion, 298. Regurgitation, aortic, 278; alcoholism in, 280; cases of, 282, 288, 293, 308, 313; cusp, ruptured in, 278; diagnosis of, 305; digitalis in, 288, 290; Duroziez's sign in, 305; etiology of, 280; gout in, 280, 296; inspection in, 288, 290, 316. llegurgitation, aortic, nitroglycerin in, 288, 314, 316; palpation in, 298; percussion in, 301 ; physical signs in, 297; prognosis in, 300; pulse in, 298, 301; (Quincke's sign in, 298; rheumatism in, 289; scarlatina in, 309 ; strophanthus in, 288, 291; strychnine in, 290, 316; symptoms of, 282; syphilis in, 284. Regurgitation, aortic and mitral, com- bined, 397; diagnosis of, 391, 397; prognosis in, 398; symptoms of, 397. Regurgitation, aortic, and aortic ste- nosis combined, 396. Regurgitation, aortic, and mitral ste- nosis combined, 393; inspection in, 395; palpation in, 395; pei'cussion in, 395; prognosis in, 394, 396; symptoms of, 393. Regurgitation, mitral, 216; Brighfs disease in, 237; cases of, 224, 229, 232, 247; congestion in, 237; diagnosis of, 245; digitalis in, 225; dropsy in, 219, 236, 245; dyspnoea in, 238, 257; etiology of, 252; inspection in, 239; insomnia in, 237; morbid anatomy of, 216; palpation in, 239; percussion in, 240; physical signs in, 239; pneumonia in, 224; prognosis in, 246; resulting in gangrene, 238; rheumatism in, 222, 247; scarlatina in, 222, 224, 229; stasis in, 236; strychnine in, 225; symptoms of, 223; tuberculosis in, 232. Regurgitation, mitral, and aortic ste- nosis combined, 396. Regurgitation, mitral, and mitral ste- nosis combined, 392. 848 DISEASES OF THE HEART Regurgitation, symptoms of, 391. Regurgitation, of pulmonary artery, 772; diagnosis of, 772. Regurgitation, pulmonary, 305; case of, 3G8; diagnosis of, 387 ; etiology of, 380. morbid anatomy of, 3G5; l)a]pation in, 371 ; percussion in, 371; physical signs in, 370; prognosis in, 374; stasis in, 367; symptoms of, 367. Regurgitation, tricuspid, 343; case of, 354; cyant)sis in, 347; diagnosis of, 363; dropsy in, 351 ; etiology of, 350; inspection in, 349; morbid anatomy of, 344; palpation in, 350; percussion in, 350; physical signs in, 349; prognosis in, 354; pyrexia in, 340; resulting from cirrhosis of lung, 340; from fibroid phthisis, 346; from renal cirrhosis, 345; secondary to chronic bronchitis, 34G; stasis in, 347; symptoms of, 347. Rheunuitism, acute, in bradycardia, 625 ; in endocarditis, acute, 146, 181, 186; in endocarditis, chronic, 522; in myocarditis, acute, 513, 515; in pericarditis, acute, 42; in pericarditis, chronic, 117; in pericarditis, dry, 50, 54; in regurgitation, aortic, 289; in regurgitation, mitral, 222; in stenosis, pulmonary, 377; in tachycardia. 732; in valvular disease, 401, 429. Kheiimatism, articidar, 32, 34; in dilalafi(m. 583; in endocarditis, acute, 152, 157, 187: in liydro])ericardium, 129; in mitral insudiciency, 595; in myocarditis, acute, 508. Rheumatism, articular, in pericarditis, acute, 42 ; in pericarditis, dry, 61; in pericarditis, with effusion, 70; in regurgitation, mitral, 247 ; in stenosis, pulmonary, 376; in stenosis, tricuspid, 356; in valvular disease, 441, 479, 485. Rheumatism, inflammatory, in endo- carditis, acute, 153; in myocarditis, chronic, 541 ; in pericarditis, with efTusion, 68, 73, 84; in stenosis, mitral, 274; in valvular disease, 436, 441. Rhythm, gallop or canter, 18; a sign of the end, 20. Rotch's sign, in pericarditis with efTu- sion, 78. Scarlatina, in aortitis, acute, 760; in congenital disease, 698; in endocarditis, acute, 154; in myocarditis, acute, 508, 516; in pericarditis, acute, 46; in regurgitation, aortic, 309 ; in regurgitation, mitral, 222, 224, 229; in si'cnosis, mitral, 274; in stenosis, tricuspid, 358. Scarlet fever. (See Fever.) Sclerosis, 246, 286, 573. Scurvy, in pericarditis, acute, 47. Second sound, simulated doubling of, 17. Segmentation of the myocardium, 668. Sepsis, in acute endocarditis, 170, 193; in periarteritis nodosa, 769 ; in pericarditis with effusion, 72. Septica'mia, in acute endocarditis, 155, 156. Serum, anti-streptococcus, in acute en- docarditis, 193. Signs, Rroadbent's, in adherent peri- cardium, 119; Duroziez's, in aortic regurgitation, 305; Ewart's, in pericarditis with efTu- sion, SO, 81: " first rib," in pericarditis with efTu- sion, 75 ; Friedreich's, in adherent pericar- dium, 120; Kussmaul's, in adherent pericar- dium, 120. INDEX 849 Signs, Perez's, in chronic mediastino- pericarditis, 121; Pins', in pericarditis with effusion, 80; Quincke's, in aortic regurgitation, 298; Rotch's, in pericarditis with effu- sion, 78. Simple endocarditis. (See Endocardi- tis.) Sraallness of arteries, congenital, 773. Small-pox, in acute endocarditis, 154; in acute myocarditis, 508; in acute pericarditis, 4G. Sound-friction, intensity of, 59; location of the pericardial, 58; quality of, 59; rhythm of, 58. Sounds, heart, normal, 13; reduplication of, IC, 18; second, simulated doubling of, 17. Spleen, abscess of, in acute endocardi- tis, 150, 185. Stasis in pericarditis, chronic, 117; in regurgitation, aortic, 297 ; in regurgitation, mitral, 23G; in regurgitation, pulmonary, 367; in regurgitation, tricuspid, 347; in stenosis, mitral, 257 ; in stenosis, tricuspid, 358. Stenosis, of aorta, 770; symptoms of, 771; treatment of, 772. Stenosis, aortic, 319; cases of, 323, 330, 339; cyanosis in, 335; diagnosis of, 338; digitalis in, 326; inspection in, 335; morbid anatomy of, 319; nitroglycerin in, 332, 333; palpation in, 335; percussion in, 336; physical signs in, 335; pneumonia in, 338; prognosis in, 339; strychnine in, 332 ; symptoms of, 323. Stenosis, aortic and mitral combined, 392; diagnosis of, 392; prognosis in, 393 ; symptoms of, 392. Stenosis, mitral, 249; bronchitis in, 256; cases of, 253, 263, 270, 273. Stenosis, mitral, delirium in, 270; diagnosis of, 208; digitalis in, 272; epilepsy in, 212; " fremissement cataire " in, 259; gout in, 254; insomnia in, 256; inspection in, 258; morbid anatomy of, 249; morphine in, 272; nitroglycerin in, 272; oedema in, 256; palpation in, 259; percussion in, 260; physical signs in, 258; prognosis in, 269; pulse in, 257, 259, 260; rheumatism in, 264; scarlatina in, 274; stasis in, 257; strophanthus in, 272; strychnine in, 272; symptoms of, 255; syphilis in, 254. Stenosis, mitral, and pulmonary ste- nosis combined, 387. Stenosis, pulmonary, 376; eases of, 377, 380; diagnosis of, 373; inspection in, 385; morbid anatomy of, 376; percussion in, 386; physical signs in, 385; prognosis in, 374; rheumatism in, 376, 377; symptoms of, 380; tuberculosis in, 380. Stenosis, of pulmonary artery, 772. Stenosis, tricuspid, 355; cases of, 379, 380; diagnosis of, 353; digitalis in, 359; inspection in, 361 ; morbid anatomy of, 355; percussion in, 362; physical signs in, 361 ; prognosis in, 364; rheumatism in, 356; scarlatina in, 358; stasis in, 358; symptoms of, 357. Stokes- Adams disease, 627; cases of, 628. 630, 632; digitalis in, 636; etiology of, 627; morphine in, 635. 850 DISEASES OF THE HEART Stokes-Adams disease, uitroglycerin in, 635; oxygen in, 035 ; pathology of, (i27; prognosis in, 635; symptoms of, 629; syphilis in, 628; treatment of, 635. Strophanthns. in angina pectoris, 662; in arterioselerosis, 757 ; in endocarditis, acute, 169; in fatty heart, 611 ; in functional disorders, 711; in myocarditis, acute, 516; in myocarditis, chronic, 553, 561; in pericarditis, chronic, 114; in regurgitation, aortic, 288, 291; in stenosis, mitral, 272; in vahndar disease, 432. Strychnine, in aortitis, acute, 762; in dilatation, 591 ; in endocarditis, acute, 169, 191; in endocarditis, chronic, 202; in fatty heart, 611; in functional disorders, 709 ; in myocarditis, chronic, 553; in pericarditis, acute, 516; in pericarditis, chronic, 114, 125; in pericarditis, dry, 53; in pericarditis, with effusion, 91; in pneuniopericardiuni, 136; in regurgitation, aortic, 290, 316; in regurgitation, mitral, 225; in stenosis, aortic, 332; in stenosis, mitral, 272; in tachycardia, 736 ; in valvular disease, 439, 443, 445. Syncope, in aortic regurgitation, 287. Syphilis, in aneurysm, 778, 795; in arterioscleiosis, 742 ; in angina pectoris, 646; in endocanlitis, chronic, 204;' in regurgitati(m, aortic, 284; in stenosis, mitral, 254; in stenosis, tricuspid, 356; in Stokes-Adams disease, 628; Syphilis of the myocardium, 663; of the ])ericar(liunK 139. Syphilis vs. rheumatism, in aortic ste- nosis, 388. Syphilitic arteritis, 764, Tachycardia, 730; calleine in, 736; diagnosis of, 734; digitalis in, 736; diphtheria in, 732. Tachycardia, etiology of, 732; ice in, 736; inlluenza in, 732; malaria in, 732 ; nitroglycerin in, 715; pathology of, 731; prognosis in, 735; rheumatism in, 732; strychnine in, 736; treatment of, 735. Temperaments, of cardiopaths, 408. Tendencies, individual, 2U6. Terrain cure, in valvidar disease, 454. Thoracic aorta, aneurysm of, 775. Thoracic cavity, 1. Thrombi, ball, 674; bibliography of, 680; cases of, 676, 680; diagnosis in, 677;' etiology of, 674; pathogenesis of, 674. Thrombi, pedunculated, 674; prognosis in, 678; symptoms of, 675; ti-eatment of, 678. Thrombosis, arterial, causing gan- grene, 676; venous, in valvular disease, 208. Tissue, adipose, in syphilis of pericar- dium, 139. Tonics, accessory, 499; cardiac, 441 ; nerve, 517. Tonsillitis, in endocarditis, acute, 156; in pericarditis, acute, 44, 47. Tonometer, Gaertner's, 826. Tricuspid regurgitation (see Regurgi- tation) ; stenosis (see Stenosis). Tuberculosis, of pericardium, 136; of lungs, 103. Tuberculosis, p\ilmonary. in aneu- rysm, 808; in dextrocardia, 681 ; in functional disorders, 716; in pericarditis, with cfTusion, 84; in regurgitation, mitral, 232; in stenosis, pidmonary, 380; in valvular disease, 406. Typhoid fever, in pericarditis, 46. Typhus, in acute myocarditis, 508. Ulcerative endocarditis. (See Endo- carditis.) Valvular lesions combined, 390; atropine in, 500. INDEX 851 Valvular lesions, baths in, Naulieim, 427, 404, 503; batlis iu, saline, 4GG; cail'cine in, 432; calomel in, 432, 44S, 491, 493; cases of, 393, 436, 440, 469, 479, 482, 485; cathartics in, 492; chloral hydrate in, 501 ; chloralo.se in, 501 ; change of climate in, 432; clotliing in, 425, 470 ; compensation imperfect in, 435; compensation lost in, 478; compensation perfect in, 413; complicated with catarrh, bronchial, 407; with dropsy, 470; with pneumonia, 440; with rheumatism, 406; convallaria in, 432, 497; diet in, 428, 470; digitalis in, 394, 430, 480; drugs in, 430; exercise in, 414, 454, 502; exercise, resistance, in, 455; glonoin in, 432, 446; habits- in, 410, 420, 476; haematics in, 448; home surroundings in, 410; hypnotics in, 500; illnesses in, 429. Valvular lesions, jalap in, 493; marriage in, 422; medicinal agents in, 444; mercury in, 432; morphine in, 440, 4S1, 499; nitroglycerin in, 442, 444, 446, 488, 498; occupation in, 409, 419, 476; oedema in, 495; pregnancy in, 409; prognosis in, 401 ; rest in, 448, 502; rheumatism in, 401, 429, 436, 441, 479, 485; strophanthus in, 432; strychnine in, 439, 443, 445; Terrain cure in, 454; treatment of, 413, 435, 478; tuberculosis in, 406. Vegetative endocarditis. (See Endo- carditis.) Verrucose endocarditis. (See Endo- carditis.) Vessels and valves of heart, position of, 3. Whisky, in acute endocarditis, 192; in angina pectoris, 660; in pseudo-angina, 728; in myocarditis, chronic, 561; in valvular disease, 493. (4) THE EIS"D ADDENDUM Recent Important Discoveries Concerning the Mechanical Effects of Aortic Regurgitation upon the Cardio-vascular System. Under the caption of Experimental and Clinical Investigation of the Pulse and Blood Pressure Changes in Aortic Insufficiency, there appeared in The Archives of Internal Medicine, Vol. I, JSTo. 1, January 15, 1908, a contribution to the knowledge of this valvular lesion of such wide-reaching significance that, if confirmed by other physiologists, it is destined to cause a rewriting of the chapters devoted to this subject in medical text-books. On this account I cannot permit this third edition to be given to the pub- lic without a brief statement of the facts discovered by Dr. Hugh A. Stewart in the physiological laboratory of Johns Hopkins Hos- pital. Inasmuch as this present edition has already come from the press and only awaits binding, it has been decided to incor- porate these novel facts in an addendum rather than to leave them unnoticed. There is the additional advantage that by so doing I shall leave for the reader the original and, as it were, historical conception of the disease which has dominated medical thought since the time of Corrigan, that he may contrast the dif- ferences between Corrigan's and Stewart's explanation of the phe- nomena observed. By a reference to Chapter VIII it will be seen that the pathology of aortic regurgitation is, briefly, as follows : Insuffi- ciency of the aortic semilunar valves causes a portion of the blood discharged into the artery during systole to leak back into the ventricle with the next ensuing diastole. The quantity of blood thus regurgitating depends upon the degree of damage sus- tained by the valve, but whether small or great produces collapse of the pulse and a proportionate dilatation of the ventricle, since the regurgitating stream enters the cavity of the ventricle during its period of diastole. This primary dilatation is soon counter- 853 854 DISEASES OF THE HEAKT balanced bv hypertropby of the wall, in consequence of wliicli the powerful and capacious ventricle is enabled to discharge with abnormal suddenness the increased volume of blood it has received from both auricle and aorta. This large blood wave rapidly dis- tends the arteries during cardiac systole and then ra])i(lly recedes during diastole because of the regurgitation, thus giving rise to the collapsing jjulsc and other vascular phenomena characteristic of aortic incompetence. lentil Stewart's careful studies proved the inaccuracy of Cor- rigan's explanation of the colla])se of the pidse this had seemed to account for the clinical changes fully and satisfactorily. Now, however, the manner in which the mechanical effects on the heart and pulse are produced is found to be quite different and to pos- sess therapeutic and prognostic importance. For a description of the mechanical devices by which were v(^^''*i''"'