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 C681 .C83 Diseases of the I 
 

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DISEASES OF THE HEART 
 
DISEASES OF THE 
 HEART 
 
 BY 
 
 JOHN COWAN, D.Sc, M.D., F.R.F.P.S. 
 
 PROFESSOR OF MEDICINE, ANDEKSOn's COLLEGE JTEDICAL SCHOOL ; 
 
 PHYSICIAN. ROYAL INFIRMARY ; LECTURER IN CLINICAL 
 
 MEDICINE IN THE UNIVERSITY, GLASGOW ; 
 
 EXAMINER IN MEDICINE, ROYAL ARMY 
 
 MEDICAL COLLEGE 
 
 WITH CHAPTERS ON 
 
 THE ELECTRO-CARDIOGRAPH 
 
 By W. T. RITCHIE, M.D., F.R.C.P. 
 
 PHYSICIAN, DEACONESS HOSPITAL ; ASSISTANT PHYSICIAN, ROYAL 
 INFIRMARY, EDINBURGH 
 
 AND 
 
 THE OCULAR MANIFESTATIONS IN 
 ARTERIOSCLEROSIS 
 
 By ARTHUR J. BALLANTYNE, M.D., F.R.F.P S. 
 
 SURGEON, EYE INFIRMARY, GLASGOW 
 
 LEA & FEBIGER 
 
 PHILADELPHIA AND NEW YORK 
 1914 
 
VY-a-<r 
 
 >\1 
 
 _ 2-i^J 
 
 
TO THE MEMORY OF 
 
 THE OLD 
 GLASGOW HOYAL INFIRMARY 
 
 1794—1912 
 
 WHICH WAS SBEVED IN THEIR GENERATION 
 
 BY 
 
 EGBERT COWAN 
 
 (1769— ISOS) 
 
 EGBERT COWAN 
 
 (1796—1841) 
 
 SOlIETIilE PROFESSOR OF MEDICAL JURISPRUDENCE 
 IN THE UNIVERSITY OF GLASGOW 
 
 ■JOHN BLACK COWAN 
 
 (1S29— 189C) 
 
 SOMETIME PROFESSOR OF MATERIA MEDIC A 
 IN THE UNIVERSITY 0¥ GLASGOW 
 
 AND 
 
 JOHN COWAN 
 
® 
 
PREFACE 
 
 During the last ten years great advances have been made in 
 our knowledge of the diseases of the heart and arteries. Xew 
 methods of histological technique have revealed lesions which 
 were hitherto unappreciated, and experimental research has 
 deciphered their causes. The sphygmomanometer, the poly- 
 graph, the electro-cardiograph, and the Eontgen rays, have 
 become accessible to the chnician, and the data thus acquired 
 have elucidated some of the many problems which awaited 
 solution; while the pharmacologists have defined the uses of 
 such drugs as digitalis more accurately than had been pre- 
 viously possible. 
 
 The following pages are an attempt to review the whole 
 subject in the Hght of these recent advances, and to present 
 to the practitioner the results which have been attained, and 
 their bearing upon the practical work of diagnosis, 'prognosis, 
 and treatment. They are based in the main upon my personal 
 experience and the records in my own wards, though I have 
 utihzed, where it seemed desirable, the numerous monographs 
 and articles which have recently appeared, and the experience 
 of my medical friends. 
 
 The importance of the cardiac muscle in the maintenance of 
 the circulation renders necessary a short account of the diseases 
 by which it is affected. Arterial disease and its influence upon 
 the heart are discussed in the three succeeding chapters. The 
 myogenic theory and the various disturbances of cardiac 
 function are considered at some length, and are accompanied 
 by an account of the electro-cardiograph. Acute endocar- 
 ditis, chronic valvular disease, myocardial weakness, and peri- 
 carditis then follow in order. 
 
 The chapters so kindly contributed by W. T. Eitchie (" The 
 
viii PREFACE 
 
 Electro-Cardiograph"), and A. J.BaUantyne("The Ocular Mani- 
 festations in Arterio-Sclerosis ") are of special value, as they are 
 written by recognized authorities upon these particular subjects. 
 
 The illustrations are mainly original, and I must express 
 my indebtedness to the kindness of Professors Arthur Keith, 
 Robert Muir, and J. H. Teacher for their permission to utihze 
 the specimens in their museums. The former has also allowed 
 me to reproduce three of his diagrams. The microscopic pic- 
 tures have been made from my own collections and those of 
 A. M. Kennedy and A. W. Harrington. The skiagrams were 
 taken from my patients by J. E. Eiddell. 
 
 The polygraph tracings are, with one exception, from my 
 own collection. This I have done purposely, even in cases 
 where more perfect examples might have been obtained else- 
 where, in order to show the frequency with which disturbances 
 of cardiac function occur in the ward work of a general hospital, 
 and the possibiHty of recording them in a busy clinique. Several 
 of them were obtained — ^unaided — by my residents. 
 
 I have not attempted to supply a full bibliography, and the 
 references which are given refer to statements which may not 
 yet be generally accepted or known, or add point to the text. 
 My own papers will be found to contain numerous references 
 to their particular subject. I have made little reference to 
 standard works, but I must acknowledge my indebtedness to 
 the writings of G. W. Balfour, Sir W. Broadbent, A. E. Cushny, 
 G. A. Gibson, W. H. Gaskell, H. Huchard, James Mackenzie, 
 A. E. Sansom, W. Stokes, and Graham Steell; and to the 
 articles in Sir Clifford AUbutt's and in Sir William Osier's 
 " Systems." 
 
 I have great pleasure in acknowledging the kind assistance 
 in my task of many friends, in particular Robert Muir, and my 
 collaborators and colleagues, W. T. Ritchie, Archibald W. 
 Harrington, A. M. Kennedy, J. R. C. Greenlees, David 
 MacDonald, and G. B. Fleming; my past and present residents, 
 without whose willing aid my records must of necessity have 
 been scanty; and last, but not least, Farquhar Macrae. 
 
 J. C. 
 
CONTENTS 
 
 CHAPTEK I 
 THE DISEASES OF THE MYOCARDIUM 
 
 Pages 
 
 The myocardium. Tlie coronary circulation. Tlie muscle cells. 
 Hypertrophy. Atrophy. Ischsemic atrophy. Granular de- 
 generation. Hyaline degeneration. Dissociation. Fatty infil- 
 tration. Fatty degeneration. Fibrosis. Infarct and para- 
 arterial fibrosis. Peri-arterial fibrosis. Syphilis. Aneurism of 
 the heart. Rupture of the heart ... - 1-29 
 
 CHAPTER II 
 
 THE DISEASES OF THE ARTERIES 
 
 The arteries. Arteriosclerosis. The lesions. Etiology. High 
 blood-pressure. Chronic renal disease. Increased viscosity of 
 the blood. Polycythaemia hypertonica. Plethora. The infec- 
 tions. Focal lesions. Atheroma. Mes-arteritis. Endarteritis 
 obliterans. Medial calcification. Etiology - - 30—: 
 
 CHAPTER III 
 
 THE SYMPTOMS OF ARTERIAL DISEASE 
 
 High blood-pressure. Cardiac hypertrophy. Consecutive mitral 
 disease. UrseiTiic symptoms. Emphysema. Dyspnoea. Cere- 
 bral symptoms ------ 54-71 
 
 CHAPTER IV 
 By A. J. Ballantyne 
 
 THE OCULAR MANIFESTATIONS IN ARTERIO- SCLEROSIS 
 
 72-74 
 
PAOKS 
 
 X CONTENTS 
 
 CHAPTER V 
 
 THE TREATMENT OF ARTERIO-SCLEROSIS 
 
 Vaso-ililators. Elimination. Digitalis. Caffeine. Theobromine. The 
 
 treatment of high blood-pressure. Diet. Exercise - 75-97 
 
 CHAPTER VI 
 
 THE MYOGENIC THEORY 
 
 The myogenic theory. The primitive tissue of the heart. The 
 
 polygraph. The interpretation of cervical curves - - 98-113 
 
 CHAPTER VII 
 
 By W. T. Ritchie 
 
 THE ELECTRO-CARDIOGRAPH 
 
 The interpretation of electro-cardiograms - - - 1 14-122 
 
 CHAPTER VIII 
 
 . STBIULUS PRODUCTION 
 Infantile irregularities ...--. 123-124 
 
 CHAPTER IX 
 
 EXCITABILITY 
 
 Tiie extra-systole. Ventricular, auricular, and nodal extra-systoles. 
 
 The significance of extra-systoles - - - - 125-132 
 
 CHAPTER X 
 
 NODAL RHYTHM 
 
 Nodal rhythm: (1) paroxysmal; (2) continuous. The relationship 
 
 of the cardiac valves and the a-v tissues. Myocarditis - 133-158 
 
 CHAPTER XI 
 
 CONTRACTILITY 
 
 Pulsus altcrnaus. The significance of pulsus alternans - - 159-161 
 
CONTENTS xi 
 
 CHAPTER XI 1 
 CONDUCTIVITY 
 
 PAGES 
 
 Heart-block: full; partial. Irregularities of the pulse duo to de- 
 fective conduction. The Stokes-Adams syndrome. 1'he auricular 
 contractions in heart-block. Nervous causes of heart-block. 
 Prognosis. Treatment .... - 162-173 
 
 CHAPTER XIII 
 
 TONICITY 
 Dilatation of the heart - - - - - - 174 
 
 CHAPTER XIV 
 
 COUPLED RHYTHMS 
 
 Coupled rhythm: in heart-block; in auricular fibrillation; from 
 extra-systoles; in nodal rhythm. The significance of coupled 
 rhythms -...--- 175-18! 
 
 CHAPTER XV 
 
 PAROXYSMAL TACHYCARDIA 
 
 The nodal form. Etiology. Symptoms. Prognosis. Treatment. 
 The relationship of paroxysmal tachycardia and auricular 
 flatter . . - • - - - - 184 -I!)? 
 
 CHAPTER XVI 
 
 AURICULAR FLUTTER 
 
 The cervical curves. The arterial curves. Nervous causes. Symp- 
 toms. Prognosis. Treatment. The action of digitalis - 198-210 
 
 CHAPTER XVII 
 
 AURICULAR FIBRILLATION 
 
 The pulsus irregularis perpetuus. Etiology. The cervical curves. 
 The arterial curves. Valvular murmurs in auricular fibrillation. 
 Prognosis. Treatment . . . - - 211-219 
 
 CHAPTER XVIII 
 
 ACUTE ENDOCARDITIS 
 
 The lesions. Etiology. Acute rheumatism and chorea. Simple 
 
 and malignant cases. Blood cultures - - - 220-233 
 
xii CONTENTS 
 
 CHAPTER XIX 
 ACUTE ENDOCARDITIS 
 
 PAGES 
 
 The symptomg. Latent endocarditis. Valvular murmurp. The 
 pulse. Subcutaneous nodules and cutaneous manifestations. 
 Embolism. Fever. Cardiac, cerebral, pulmonary, and general 
 symptoms - - - . - - - - 234-250 
 
 CHAPTER XX 
 
 ACUTE ENDOCARDITIS— Con^wwed 
 
 Diagnosis. Prognosis. Treatment. Rest. Salicylates. Vaccines. 
 
 Sera. General 251-260 
 
 CHAPTER XXI 
 
 CHRONIC VALVULAR DISEASE 
 The lesions. Etiology. The causes of aortic and mitral disease 201-281 
 
 CHAPTER XXII 
 
 THE SYMPTOMS OF CHRONIC VALVULAR DISEASE 
 
 The symptoms of chronic valvular disease. The causes of symptoms. 
 Dyspnoea. Cheyne- Stokes breathing. Paroxysmal dyspnoea. 
 Cough. Cardiac discomfort and pain. Palpitation. (Edema. 
 Gastro - intestinal symptoms. Cerebral symptoms. The 
 symptoms of mitral and aortic disease - - - 282 -30S 
 
 CHAPTER XXIII 
 
 MYOCARDIAL FAILURE WITHOUT VALVULAR DISEASE 
 
 Myocardial failure fin the infections; in myocardial disease - 309-319 
 
 CHAPTER XXIV 
 
 THE DIAGNOSIS OF CHRONIC VALVULAR DISEASE 
 
 The significance of physical signs. Epigastric pulsation. The causes 
 of murmurs. The physical signs of myocardial weakness in the 
 infections. Mitral valvular disease. Aortic valvular disease. 
 Pulmonary valvular disease. Tricuspid valvular disease. Con- 
 genital heart disease. The Bruit de Roger. Patent ductus 
 arteriosus ------- 320--360 
 
CONTENTS xiii 
 
 CHAPTER XXV 
 THE PROGNOSIS IN CHRONIC CARDIAC FAILURE 
 
 PAGES 
 
 The nature of the lesion. The site of the lesion. The grade of 
 the lesion. The rhythm of the heart. The influence of con- 
 current disease. The degree of compensation. The cause of 
 failure. Age. Sex. Social circumstances - - - 361-369 
 
 CHAPTER XXVI 
 
 THE TREATMENT OF CHRONIC CARDIAC^FAILURE 
 
 Work. Nutrition. The treatment of symptoms. Digitalis. 
 
 Caffeine, etc. General ..... 370-384 
 
 CHAPTER XXVII 
 
 ACUTE PERICARDITIS 
 
 The lesions. Etiology. The infections. Intrathoracic disease. 
 Pyaemia. Terminal pericarditis. The symptoms. The effects 
 of effusion. The physical signs. Latent pericarditis. Prog- 
 nosis -....-.- 385-402 
 
 CHAPTER XXVni 
 
 ADHERENT PERICARDIUM 
 
 Indurative mediastino-pericarditis. Pericarditis interna el externa. 
 Etiology. The symptoms. Pick's disease. The signs of ad- 
 herent pericardium ....-- 403-418 
 
 PNEUMO-PERICARDIUM 
 
 Etiology. The physical signs. Prognosis - - - 418-425 
 
 CHAPTER XXIX 
 
 THE TREATMENT OF PERICARDITIS 
 
 The treatment of dry pericarditis; of pericarditis with effusion; of 
 
 adherent pericardium. Operative procedures - - 426-429 
 
 Index ----_-._ 431 
 
LIST OF ILLUSTRATIO^S 
 
 COLOURED PLATES 
 
 FIG. PAGE 
 
 8. Fibrosis of the Anterior Wall op the Left Ventricle - facing 16 
 11. Marked Narrowing of the Orifices of the Coronary 
 Arteries from Syphilitic Disease of the Aorta: In- 
 farct of Heart - - - - - - ,, 18 
 
 44. Right Fundus Oculi prom a Case op Chronic Nephritis 
 
 (A. J. Ballantyne) ----..,, 74 
 
 IN THE TEXT 
 
 1. Diagram of Arterial Circulation of Normal Heart - - 3 
 
 2. Diagram of Arterial Circulation in a Heart where the Left 
 
 Coronary Artery was obstructed .... 6 
 
 3. Diagram of Arterial Circulation in a Heart where the Right 
 
 Coronary Artery was obstructed - - • - - 7 
 
 4. Ischemic Atrophy op Muscle - - - - - 8 
 
 5. Granular Degeneration of Muscle - - - - - 9 
 G. Fatty Degeneration op Muscle: Patchy Form - - - 12 
 7. Fatty Degeneration of Muscle: Difpuse Form - - - 13 
 9. Dystrophic Fibrosis of Wall op Left Ventricle - - - 17 
 
 10. Para-arterial Fibrosis - - - - - - 18 
 
 12. Peri-artbrlal Fibrosis - - - - - - - 19 
 
 13. Interstitial Myocarditis - - - - - - 20 
 
 14. Perifascicular Fibrosis - - - - - - 21 
 
 15. Interstitial Myocarditis: Focal Form (A. M. Kennedy) - - 22 
 
 16. Interstitial Myocarditis: Difpuse Form (A. M. Kennedy) - 23 
 
 17. Gumma op Heart - - - - - - - 25 
 
 18. Syphilitic Myocarditis - - - - - - 27 
 
 19. Infarct of Papillary Muscle, with Rupture - - - 27 
 
 20. Arterio-Sclerosis: Intimal Thickening - - - - 33 
 
 21. Arterio-Sclerosis: Medial Fibrosis - - - - - 34 
 
 22. Arterio-Sclerosis: Medial Fibrosis - - - - - 35 
 
 XV 
 
xvi LIST OF ILLUSTRATIONS 
 
 Firi. PAGE 
 
 23. Blood-Pressure Chart: Large White Kidney - - - 36 
 
 24. Blood-Pressure Chart: Small White Kidney - - - 37 
 
 25. Early Atheroma - - - - - - - 42 
 
 26. Syphilitic Mesaortitis - - - - - - - 43 
 
 27. Syphilitic Mesaortitis - - - - - - - 44 
 
 28. Syphilitic Mesaortitis - - - - - - - 45 
 
 29. Syphilitic Mesaortitis - - - - - - - 45 
 
 30. Endarteritis Obliterans - - - - - - 46 
 
 31. Endarteritis Obliterans: Syphilitic Form (A. W. Harrington) - 47 
 
 32. Skiagram: Medial Calcification (J. R. Riddell) - - - 48 
 
 33. Blood-Pressure Tracing: Aortic Regurgitation - - - 58 
 
 34. Blood-Pressure Tracing: Chronic Nephritis - - - 59 
 
 35. Sphygmogram: Aortic Regurgitation- - - - - 01 
 
 36. Blood-Pressure Chart: Chronic Nephritis - - - - 62 
 
 37. Blood-Pressure Chart: Aortic Valvular Disease - - - 62 
 
 38. Blood-Pressure Chart: Pneumonia - - - - - 63 
 
 39. Blood-Pressure Chart: Mitral Disease - - - - 63 
 
 40. Blood-Pressure Chart: Chronic Nephritis - - - - 64 
 
 41. Blood-Pressure Chart: Mitral Disease - - - - 66 
 
 42. Blood-Pressure Chaut: Mitral Disease; Cirrhotic Kidney - 67 
 
 43. Blood-Pressure Chart: Chronic Nephritis - - - - 68 
 
 45. Blood -Pressure Chart: Chronic Nephritis - - - - 77 
 
 46. Blood -Pressure Chart: Bronchitis - - - - - 78 
 
 47. Blood-Pressure Chart: Mitral Disease; Cirrhotic Kidney - 80 
 
 48. Blood-Pressure Chart: Cirrhotic Kidney - - - - 80 
 
 49. Blood-Pressure Chart: Bronchitis - - - . - - 83 
 
 50. Blood-Pressure Chart: Bronchitis - - - - - 85 
 
 51. Blood-Pressure Chart: Hemiplegia - - - - - 86 
 
 52. Blood -Pressure Chart: Chronic Nephritis - - - - Sg 
 
 53. Blood-Pressure Chart: Chronic Nephritis - - - - 89 
 
 54. Blood-Pressure Chart: Mitral Disease; Cirrhotic Kidney - 90 
 
 55. Heart of Ox, dissected to show the a. v. Bundle (A. Keith) - 100 
 
 56. Human Heart, dissected to show the a.v. Node and Bundle 
 
 (A. Keith) ........ 101 
 
 57. Heart oe Walrus, dissected to show the a. v. Bundle (A. Keith) - 102 
 
 58. The Sino-Auricular Node (A. M. Kennedy) - - - 103 
 
 59. Curves prom Brachial Artery, Right Neck, and Apex-Impulse - 106 
 
 60. Curves from Brachial Artery, Right Neck, and Apex-Impulse - 107 
 
 61. Curves from Brachial Artery, Second Left Intercostal Space, 
 
 AND Apex-Impulse ------- 108 
 
 62. Diagram showing Surface Relations of Carotid Artery and 
 
 Jugular Vein (A. Keith) ------ 109 
 
 63. Curves from Right Neck and Apex-Impulse - - - 113 
 
 64. Electro-Cardiogram: Normal (W. T. Ritchie) - - - 116 
 
LIST OF ILLUSTRATIONS xvii 
 
 "Q- PAGE 
 
 65. Electko-Cardiogbam and Cervical Curves (W. T. Ritchie) - 117 
 
 66. Electro-Cardiograms from Cases of Mitral Stenosis and Aortic 
 
 Regurgitation (W. T. Ritchie) .... ng 
 
 67. Electro-Cardiogram: Partial Heart-Block (W. T. Ritchie) - 119 
 
 68. Electro-Cardiograjm: Full Heart-Block (W. T. Ritchie) - 120 
 
 69. Electro-Cardiogram: Ventricular Extra-Systoles (W. T. Ritchie) 120 
 
 70. Electro-Cardiogram: Auricular Flutter (W. T. Ritchie) - 121 
 
 71. Electro-Cardiogram: Auricular Fibrillation (W. T. Ritchie) - 121 
 
 72. Curves of Radial Pulse and Respiratory Movements - facing 123 
 
 73. Blood-Pressure Tracing, showing Extra-Systole - ,, 123 
 
 74. Curves showing Interpolated Ventricular Extra-Systole ,, 123 
 
 75. Curves showing Ventricular Extra-Systole - - ,, 123 
 
 76. Curves showing Ventricular Extra-Systole - - - 126 
 
 77. Curves showing Ventricular Extra-Systole, followed by Auric- 
 
 ular Extra-Systole - - - - - - 126 
 
 78. Curves showing Auricular Extra-Systole - - - . 127 
 
 79. Curves showing Nodal Extra-Systole .... ^28 
 
 80. Curves of Brachial Artery and Apex-Impulse; Auricular Fib- 
 
 rillation ........ 129 
 
 81. Curves showing Nodal Extra-Systole .... 130 
 
 82. Curves showing Nodal Rhythm ..... 135 
 
 83. Curves showing Nodal Rhythm . . . . . 133 
 
 84. Curves showing Nodal Rhythm ..... 142 
 
 85. Curves showing Nodal Rhythm ..... 145 
 
 86. Curves showing Nodal Rhythm ..... 148 
 
 87. The a. v. Node and Bundle (A. M. Kennedy) - - - 152 
 
 88. Longitudinal Section of the Heart - - " - - 153 
 
 89. Transverse Section of the Heart - - - - - 154 
 
 90. Transverse Section of the Heart - - - - - 155 
 
 91. The a. v. Node and Bundle: Mitral Disease (A. M. Kennedy) - 156 
 
 92. The a. v. Node and Bundle: Mitral and Aortic Disease (A. M. 
 
 Kennedy) ........ 156 
 
 93. The a. v. Node and Bundle: Mitral and Tricuspid Disease (A. M. 
 
 Kennedy) ........ 157 
 
 94. Curves showing Pulsus Alternans succeeding an Extra-Systole 160 
 
 95. Curves showing Pulsus Alternans - - - - . 160 
 
 96. Curves showing Pulsus Alternans - - - - - 160 
 
 97. Curves showing Pulsus Paradoxus ----- 160 
 
 98. Curves showing Full Heart-Block - - - - - 163 
 
 99. Curve of Apex-Impulse showing Full Heart-Block - facing 164 
 
 100. Curves showing Partial Heart-Block - - - ,, 164 
 
 101. Curves showing Partial Heart-Block - - - ,, 164 
 
 102. Brachial Pulse in Full Heart-Block - - - ,, 169 
 
 103. Curves in Coupled Rhythai due to Extra-Systoles - - 176 
 
xviii LIST OF ILLUSTRATIONS 
 
 FIO. PACK 
 
 104. Curves in Cotjpled Rhythm dtte to Pabtial Heakt-Block - 177 
 
 105. CUKVES SHOWING VENTRICULAR ExTRA-SySTOLES, FOLLOWED BY 
 
 AuRicuLAB Extra-Systoles - - - - - 178 
 
 106. Curves in Partial Heart-Block ..... 178 
 
 107. Curves in Fuxl Heart-Block (W. T. Ritchie) - - - 180 
 
 108. Curves of Brachial Artery and Apex-Impulse: Auricular Fib- 
 
 rillation .-..---- 181 
 
 109. Brachial Curve showing the Effects of Pressure upon the Left 
 
 Vagus Nerve ....... 181 
 
 110. Curves in Coupled Rhythm: Xodal Rhythm . . - 182 
 
 111. Curves from Brachial Artery. Right Neck, and Apex-Impulse; 
 
 Paroxysmal Tachycardia ------ 187 
 
 112. Curves sho\ving Varying Sinus Rhythm - - - facing 192 
 
 113. Curves showing Varying Sinus Rhythm - - - ., 192 
 
 114. Curves from Brachial Artery, Right Neck, and Apex- 
 
 Impulse IN Paroxysmal Tachycardia, showing Change 
 
 OF Rhythm - - - - - - - ,, - 192 
 
 115. Curves in Paroxysmal Tachycardia .... 193 
 
 116. Electro-Cardiograju; Auricular Flutter (W. T. Ritchie) - 199 
 
 117. Curves in Auriculak Flutter (5 to 1 Ratio) - - - 200 
 
 118. Curves in Auricular Flutter (4 to 1 Ratio) ... 20O 
 
 119. Curves in Auricular Flutter (2 to 1 Ratio) - - - 201 
 
 120. Curves in Auricular Flutter (Varying a. v. Ratio) - facing 202 
 
 121. Brachial Curve: Auricular Flutter - - - ,, 202 
 
 122. Curves in Auricular Flutter - - - - ,, 202 
 
 123. Brachial Curve: Auricular Flutter . . . . 202 
 
 124. The Radial Pulse in Auricular Fibrillation - - - 212 
 
 125. Curves in Auricular Fibrillation - - - - - 213 
 
 126. Curves in Auricular Fibrillation ----- 214 
 
 127. Acute Verrucose Endocarditis - - - - - 221 
 
 128. Malignant (Pneumococcic) Endocarditis - . . . 223 
 
 129. Malignant Endocarditis, Infecth^e Aortitis - - - 224 
 
 130. Malignant (Pneumococcic) Endocarditis . - . . 225 
 
 131. Malignant (Streptococcic) Endocarditis .... 226 
 
 132. Chart showing Rise of Pulse-Rate on Cessation of Sodium Sali- 
 
 cylate ........ 235 
 
 133. Curves showing Nodal Rhythm ..... 242 
 
 134. Curves showing Nodal Rhythm . . . . . 248 
 
 135. Chart of a Case of Malignant Endocarditis - - - 252 
 
 136. Chaut showing Subnormal Wave of "Pyrexia" - - - 253 
 
 137. Calcareous Infiltration of Aortic Valve - - - - 262 
 
 138. Chronic Mitral and Tricuspid Stenosis - - - . 263 
 
 139. Chronic Mitral Endocarditis - . . . . 264 
 
 140. Aortic Incompetence ....... 265 
 
LIST OF ILLUSTRATIONS xix 
 
 FIG. PAGE 
 
 141. Cheonic Mitral and Atjeiculae Endocarditis . . . 266 
 
 142. Syphilitic Disease of Aortic and Mitral Valves - - 268 
 
 143. Chronic Renal Disease: Patchy Thickening of Mitral Cusps - 272 
 
 144. Chronic Renal Disease: Diffiise Thickening of Mitral Cusps - 273 
 
 145. Chronic Renal Disease: Diffuse Thickening of Aortic and 
 
 Mitral Cusps ....... 274 
 
 146. Brachial and Respiratory Curves in Cheyne-Stokes Breathing 
 
 facing 287 
 
 147. Blood-Pressure Tracing: Aortic Regurgitation - - - 300 
 
 148. DlAGRAJil SHO\VING SURFACE RELATIONS OF THE LuNGS, HeART, AND 
 
 Cardiac Valves (A. Keith) - - - - - 321 
 
 149. Diagram shoaving Surface Relations of the Pericardium, Heart, 
 
 AND Great Vessels (A. Keith) ..... 322 
 
 150. Curves showing " In-verted " Apex-Impulse - - - 323 
 
 151. Curves of Epigastric Pulsation due to Aoria - - - 323 
 
 152. Curves of Epigastric Pulsation due to Right Ventricle - 323 
 
 153. Curves of Epigastric Pulsation due to Left Ventricle - - 324 
 
 154. Curves from Brachial Artery, Second Left Intercostal Space, 
 
 AND Apex -Impulse ....... 324 
 
 155. Curves from Fourth Right Intercostal Space and Apex-Impulse 324 
 
 156. Diagraji showing Surface Relations of Heart and Lungs - 325 
 
 157. DiAGRAii showing Area of Cardiac Dulness - - - 326 
 
 158. Diagram showing Time Relations of the Cardiac Contractions, 
 
 THE Cardiac Sounds, and the Valvular Murmurs - - 328 
 
 159. Skiagram: Hypertrophy of Left Ventricle (J. R. Riddell) - 334 
 
 160. Diagram showing Area of Cardiac Dulness in Mitral Stenosis - 335 
 
 161. Diagram showing Distribution of Presystolic Murmur - - 337 
 
 162. Skiagram: Hypertrophy of Right Ventricle (J. R. Riddell) - 338 
 
 163. Diagram showing Area of Reduplicated Second Sound - - 340 
 
 164. Diagram showing Area of Early Diastolic Mitral Murmur - 340 
 
 165. Blood-Pressure Chart: Mitral Disease - . . . 341 
 
 166. Blood-Pressure Chart: Mitral Disease; Cirrhotic Kidney - 342 
 
 167. Diagram showing Area of Cardiac Dulness in a Dilated Heart 343 
 
 168. Diagram showing Area of Cardiac Dulness in Mitral Reflux - 343 
 
 169. Diagram showing Distribution op Murmur in Mitral Reflux - 344 
 
 170. Diagram showing Distribution of Murmur in Mitral Reflux - 344 
 
 171. Diagram showing Distribution of Murmur in Aortic Stenosis - 348 
 
 172. Diagram showing Distribution of Murmur in Aortic Stenosis - 348 
 
 173. Diagram showing Area of Cardiac Dulness in Aortic Reflux - 349 
 
 174. Diagram showing Distribution of Murmur in Aortic Reflux - 350 
 
 175. Diagram showing Distribution of Murmur in Aortic Reflux - 350 
 
 176. Sphygmogram: Aortic Reflux ..... 351 
 
 177. Diagram showing Distribution of Murmur in Pulmonary Stenosis 355 
 
 1 78. Diagram showing Distribution of ]\1urmur in Pulmonary Reflux - 355 
 
XX LIST OF ILLUSTRATIONS 
 
 PAGE 
 
 179. Diagram SHOWING Distribution OF Murmur IN Tkicuspid Reflux - 357 
 
 ISO. Diagram showing Distribution of Murmur in Tricuspid Stenosis - 357 
 
 181. Diagram showing Distribution of Murmur in Patent Ductus 
 
 Arteriosus ...----- 358 
 
 182. Stenosis of Left Pulmonary Artery by a Secondary Malignant 
 
 Growth ....---. 359 
 
 183. Diagram showing Distribution of Murmur in Stenosis of Left 
 
 Pulmonary Artery ...... 360 
 
 184. Diagram showing Distribution of Murmur in Stenosis op Left 
 
 Pulmonary Artery ...... 360 
 
 185. Chart of Pulse-Rate and Urinary Output, showing the Influence 
 
 of Rest ........ 371 
 
 186. Chart op Pulse-Rate, showing the Influence of Digitalis - 382 
 
 187. Diagram of Area of Dulness in Pericarditis - - - 399 
 
 188. Diagram of Area of Cardiac Dulness of a Dilated Heart - 400 
 
 189. Skiagram: Pericarditis with Effusion; Left Pneumothorax 
 
 (J. R. RiDDELL) - - - - - - - 401 
 
 190. Curves showing Systolic Retraction of Apex-Impulse - - 407 
 
 191. Curves showing Broadbent's Sign - . - . . 408 
 
 192. Curves showing Systolic Retraction op Fourth Right Inter- 
 
 space --------- 408 
 
 193. Curves showing Pulsus Paradoxus .... - 409 
 
 194. Curves showing Systolic Retraction op Lower End of Sternum 414 
 
 195. Skiagram: Mediastino-Pericarditis (J. R. Riddell) - - 417 
 
 196. Diagram of the Physical Signs in a Case of Pneumo-Pericardium 421 
 
 197. Diagram of the Physical Si3ns in a Case of Pneumo-Pericardium 422 
 
 198. Skiagram: Pneumo-Pericardium (J. R. Riddell) - - - 423 
 
 199. Skiagram: Pneumo-Pericardium (J. R. Riddell) - - - 424 
 
 71ie draivings of microscopic stctions are by Richard Muir. The other draivings 
 are hy A. K. Maxwell. 
 
DISEASES OF THE HEART 
 
 CHAPTER I 
 THE DISEASES OF THE MYOCARDIUM 
 
 The Myocardium. — The cardiac muscle is very specialized, and 
 differs in many respects from voluntary and involuntary muscle 
 elsewhere. The cells are irregular in shape, and more or less 
 rhomboidal on longitudinal section, and divide into branches 
 which unite directly with those of adjacent cells. There is no 
 sarcolemma, and while appropriate staining shows the junctions 
 of the adjacent cells very distinctly, these are invisible in un- 
 stained sections, and many observers are inchned to regard the 
 cardiac muscle as forming a syncytium.* The nucleus is large 
 and oval in shape, with a well-marked chromatin network, and 
 lies in the centre of the cell bounded laterally by the fibril 
 bundles. At each pole Hes an ovoid mass of undifferentiated 
 protoplasm, in which some yellowish-brown granules are usually 
 situated. The fibril bundles run longitudinally and show a 
 transverse striation, which is well marked in contracted muscle, 
 though in extended fibres the longitudinal arrangement is more 
 distinct. 
 
 The arrangement of the muscular layers is extremely com- 
 phcated. In the auricles two main layers are apparent — a 
 superficial circular set of fibres passing from one auricle to 
 the other, and a deeper longitudinal layer which is chiefly 
 confined to one chamber. But both are connected with the 
 septum, and their regular arrangement is disturbed where the 
 great veins join on the posterior walls. 
 
 * The structure of the congenital tumours of the heart (rhabdomyomata) 
 supports this theory, for each cell mass contains several nuclei. 
 
 1 
 
2 DISEASES OF THE HEART 
 
 The arrangement in the ventricles is more complex. The 
 walls are much thicker than those of the am-icles, but the thick- 
 ness varies, being minimal at the extreme apex, where it ma}^ 
 only measure 2 to 3 mm.; and maximal in the upper third 
 of the left ventricle, where it may measure 1 cm. The 
 septum is nearly as thick, but the wall of the right ventricle does 
 not exceed 5 mm., and is often thinner. The muscular 
 layers next the endocardium and the pericardium are in a 
 general way arranged longitudinally. The superficial layers 
 run obhquely towards the apex, and then turn suddenly 
 upwards and inwards in a vortex, and ascend on the inner 
 surface. The central bundles are, as a whole, arranged trans- 
 versely : some interlace in the septum and form a figure-of-eight 
 loop embracing both ventricles, while others run more or less 
 obhquely from one ventricle to the other, their musculature 
 being thus intimatety commingled. In any section of the 
 ventricular wall a few fibres are found to be cut longitudinally 
 and a few transversely, but the vast majority are divided more 
 or less obliquely. The connection of the muscle of the two 
 ventricles is thus very close, and contraction of one side is 
 necessarily accompanied by contraction of the other. It is 
 extremely difficult, how^ever, to appreciate the relations of the 
 muscular bundles to the bloodvessels, and this can only be 
 followed accurately in the musculi papillares, whose cells are 
 all arranged longitudinally. 
 
 The connective tissue in the normal heart is extremely scanty. 
 There are thin, loose layers beneath the endocardium and the 
 pericardium, and the two are connected by a fine meshwork^ 
 which surrounds the muscle cells and supports the vessels and 
 nerves. But even the main septa are small, and in sections the 
 muscle cells seem everywhere in close apposition to each other. 
 The connective tissue is, however, more abundant at the tips 
 of the musculi papiUares where they join the chordae tendinese, 
 at the auriculo-ventricular junction, and in the auricular 
 appendices . 
 
 The Coronary Circulation. — The heart is supphed with blood 
 by the coronary arteries, and as any interference with their 
 lumen is hkely to be accompanied by serious damage to the 
 muscle, their anatomy requires consideration in some detail. 
 
THE DISEASES OF THE MYOCARDIUM 
 
 3 
 
 The right coronary artery is usually the smaller of the two, 
 and arises from the anterior sinus of Valsalva. It passes to 
 the right in the auriculo-ventricular groove, giving off branches 
 to the adjacent muscle, and terminates in a large branch 
 which runs downwards in the posterior interventricular sulcus. 
 It supplies blood to the right auricle and almost the whole 
 of the right ventricle, and to the posterior parts of the left 
 ventricle and the interventricular septum. 
 
 The left coronary artery arises from the left posterior sinus 
 of Valsalva, and passes to 
 the left in the auriculo- 
 ventricular groove ; it divides 
 almost at once into two main 
 branches, the larger of which 
 descends in the anterior in- 
 terventricular sulcus, while 
 the smaller continues its 
 course in the auriculo-ven- 
 tricular groove. These sup- 
 ply the left auricle, the 
 anterior two-thirds of the 
 interventricular septum, the 
 bulk of the left ventricle, 
 and a small portion of the 
 anterior surface of the right 
 ventricle. 
 
 The main horizontal and 
 vertical branches of the two 
 arteries anastomose with 
 
 each other at their extremities, and thus form around the heart 
 two rings of vessels which are almost at right angles to each 
 other. From these rings smaller arteries penetrate the muscle, 
 giving off still smaller vessels, which end in a very free capillary 
 system, so extensive, indeed, as to surround each individual 
 muscle cell on almost every side. 
 
 The coronary arteries send a few smaU branches to the aorta 
 and the pulmonary artery; and an anastomosis with corre- 
 sponding branches of the bronchial arteries has been described. 
 
 Supplementary coronary arteries are frequently met with. 
 
 Fig. 1. — Diagram showing the Arterial 
 Circulation of the Normal Heart. 
 
4 DISEASES OF THE HEART 
 
 sometimes arising witli a main vessel from the bottom of a 
 small pit in the aortic wall, in which case they should be con- 
 sidered to be merely branches with an abnormally high origin ; 
 or having a distinct orifice separate from that of the main 
 artery. More than one may be present, and occasionally an 
 artery arises from each of the three sinuses. The importance 
 of supplementary arteries, however, is small, as they are at 
 once distributed to a part of the muscular wall, and only 
 represent nutritive branches. 
 
 Variations in the origin of the coronary arteries are not 
 very uncommon. Both coronary arteries sometimes arise 
 from the same sinus, either as one trunk, which soon divides, 
 or as separate vessels. A specimen in the Western Infirmary 
 Museum shows this latter anomaly, but only two aortic cusps 
 are present, the right posterior cusp being in its usual situa- 
 tion, while the left posterior and the anterior are fused to- 
 gether. Both coronary arteries arise in the latter sinus, the 
 orifices being about 1'5 cm. apart. 
 
 A few cases have been recorded in which one coronary 
 artery arose from the aorta and one from the pulmonary 
 artery. Brooks has reported two cases. In one the branches 
 from the latter vessel were distributed to the pulmonary 
 artery and to the right ventricle; in the other no branches 
 were supplied to the heart, the vessel at once entering a 
 cirsoid mass of dilated vessels around the pulmonary artery, 
 where it was joined by branches from the right coronary artery, 
 the left subclavian, and the transverse arch of the aorta. In 
 both cases the abnormal vessel arose from the right anterior 
 sinus. Krause has described a case similar to Brooks's first, 
 save that the artery arose from the left anterior sinus. Abbott 
 has described a fourth case in which the right coronary artery 
 arose in its normal site, and directly after its origin expanded 
 into a huge, thick-walled loop, from which its descending and 
 transverse branches arose. The left aortic coronary artery 
 was absent, but a large thin-walled trunk emerged from the 
 dilated posterior sinus of the pulmonary artery. From this 
 vessel branches ran downwards along the front of the inter- 
 ventricular septum, and to the left in the auriculo-ventricular 
 groove. A fifth specimen is present in the museum of the 
 
THE DISEASES OF THE MYOCARDIUM 5 
 
 Western Infirmary. The right coronary artery is normal in 
 its origin and distribution, but the left aortic coronary is 
 absent, while an artery of considerable size arises from the 
 left anterior sinus of the pulmonary artery, and is distributed 
 mainly to the left ventricle. In none of these cases was there 
 any other congenital cardiac defect. 
 
 Two cases have, however, been recorded where the aorta 
 and pulmonary artery were transposed, and both coronary 
 arteries arose from the vessel connected with the right ven- 
 tricle, their abnormal origin being evidently due to an erroneous 
 twist in the development of the septum of the primitive aorta . 
 In both cases death ensued within a short period after birth. 
 Three of the first group, however, lived to adult age, two, 
 indeed, being elderly; and it is difiicult to understand how 
 the nutrition of the heart was maintained. Brooks has 
 suggested that the pulmonary vessel might be afferent in 
 nature, and Abbott considers that this might apply also to her 
 case, the arterial supply being confined to the aortic vessel. 
 
 The majority of cases with gross disease of the coronary 
 arteries show more or less change in the cardiac muscle, for 
 the nutrient arteries are end-arteries in Cohnheim's sense, and 
 their complete obstruction entails the death of the area which 
 they supply. The importance of the anastomosis between 
 the main branches has not, however, been fully recognized. 
 Sudden and complete closure, whether experimental or patho- 
 logical, produces as a rule an infarct, though the lesion is 
 smaller than the area anatomically supplied by the obstructed 
 vessel (Hirsch and Spalteholz); but if the closure is gradual, 
 compensatory dilatation of the other vessel may occur and 
 prevent the occurrence of any lesion. Several cases of this kind 
 have been reported, and I have personally examined five 
 specimens. In one (Fig. 2) the descending branch of the left 
 coronary was completely obliterated about halfway down the 
 interventricular septum. The descending branch of the right 
 coronary artery was large and could be traced round the apex, 
 extending upwards in the anterior interventricular sulcus for 
 an inch or more. In another case (Fig. 3) the orifice of the 
 right coronary artery was invisible, being completely blocked 
 
6 
 
 DISEASES OF THE HEART 
 
 by a patch of aortic atheroma. The artery itself was greatly 
 atrophied. The left coronary vessel, on the other hand, was 
 greatly enlarged, and the posterior interventricular artery 
 arose from the transverse branch. There was no gross lesion 
 of the muscle, though microscopic examination showed a few 
 small patches of fibrosis, and as the patient was able to perform 
 his duties until ten days before his death, the anastomosis 
 must have been fairly sufficient. Huchard and Huchard and 
 
 Chiari have recorded similar 
 cases ; and Pagenstecher has 
 ligatured the right coronary 
 artery during an operation 
 without evil result. 
 
 There are two other ways 
 in which the cardiac muscle 
 may be supplied with blood. 
 The foramina Thebesii are 
 present in all the cavities 
 of the heart, though they 
 are most numerous on the 
 right side. And while they 
 are generally considered to 
 be venous in character and 
 to convey blood to the 
 auricles and ventricles, the 
 evidence is somewhat incon- 
 TiG. 2.— Diagram SHOWING THE CoMPENSA- pi,,„,Vp „.-,.] ^-v,p,, mav r^pr- 
 TORY Developments of the Coronary cmsive, anci tne}' may per 
 Circulation in a Case where the haps be arterial in function. 
 Descending Branch of the Left p xj.5 , • j. , 
 
 Coronary Artery was occluded. Jrratt S experiments are m 
 
 favour of the latter view, 
 for he has shown that the hearts of dogs may continue to 
 contract for several hours after removal from the body, even 
 though the coronary arteries are ligatured, if a suitable fluid is 
 allowed to pass into the cardiac cavities. 
 
 There is also evidence that the endocardial blood may 
 furnish nourishment to the adjacent muscle, for, as Muir has 
 pointed out, in cases of healed infarct and in dystrophic 
 fibrosis a thin layer of muscle always persists along the endo- 
 cardial surface. 
 
THE DISEASES OF THE MYOCARDIUM 
 
 It is weU known that the coronary arteries are pecuKarly 
 liable to pathological processes ; in fact, some change is almost 
 constantly piesent after middle life. The orifice may be 
 obstructed by disease of the aorta, or the main trunks may 
 show patchy atheroma or diffuse fibrosis. Such changes are 
 readily seen on naked- eye examination, but the condition of 
 the larger arteries is no criterion of that of the smaller, whose 
 walls may be seriously damaged without the larger vessels 
 being affected. Most com- 
 monly both sets are in- 
 volved, but the degree of 
 the lesions is by no means 
 always comparable. 
 
 The muscle at the apes, 
 that next the endocardium, 
 and the musculi papillares 
 in particular are supplied 
 by the longest branches of 
 the coronary arteries, and 
 will show most often and 
 in greatest degree any 
 lesions Avhich are due to 
 interference with the blood- 
 supply. Under normal con- 
 ditions the work performed 
 by the left ventricle is much 
 greater than that done by 
 the right, but in many 
 diseases (emphysema, mitral 
 stenosis, etc.) the right 
 
 ventricle is overworked, and it is often, in consequence, hyper- 
 trophied. Given a deterioration of the blood, whether in quantity 
 or quahty, the effect upon the muscle will be more manifest, and 
 wiU appear first where the blood-supply is least ample, and 
 where the greatest functional activity obtains. And these, it 
 will be seen, are the cardinal factors in determining the site of 
 almost all the focal lesions which occur in the myocardium. 
 
 Hypertrophy — Atrophy. — The muscle cells in the normal 
 heart vary considerably in size, those on the left side being 
 
 Fig. 3. — Diagram showing the Compensa- 
 TOKY Developments of the Coronaey 
 Circulation in a Case where the 
 Right Coronary Artery was occluded 
 AT ITS Origin. 
 
8 
 
 DISEASES OF THE HEART 
 
 appreciabl}^ larger than those on the right, and the cells jn the 
 auricles are smaller than those in the ventricles. There is 
 often considerable difference even between adjacent cells, and 
 it may be difficult to estimate the average size in anj' particular 
 case. It is, however, always greater than normal in hyper- 
 trophied hearts, the increase being chiefly in the transverse 
 diameter, and in other respects the cells seem normal. There 
 has been considerable discussion as to whether the celLs are 
 more numerous as well as larger, and the question is still un- 
 settled. Most observers (Gotch, Hirschfelder) are against 
 any numerical increase, but G. A. Gibson accepted Zielonko's 
 work as conclusive evidence on the other side. The connective 
 
 tissue, too, in hypertrophied hearts 
 is always increased in amount. 
 
 In atrophied hearts the cells'may 
 be considerably smaller than usual. 
 In some cases no other abnor- 
 mahty can be detected, but in 
 others the perinuclear pigment is 
 excessive. In the normal heart 
 pigment granules appear about 
 the age of ten, and their number 
 increases with advancing years ; 
 the}^ are usually numerous in 
 senile muscle. They are said to 
 be composed of hsematoidin, and 
 are brownish-yeUow in colour and 
 of varying size. They lie in conical 
 masses at each pole of the nucleus in the perinuclear space. 
 Their significance is obscure. In atrophy they may be numerous 
 or very scanty, 
 
 Ischaemic Atrophy. — In extreme cases of simple atrophy 
 and in cases of local starvation from obstruction of the coronary 
 arteries, other changes may be noticed in the cells. In the 
 latter case the size of the cells varies, those around the arterioles 
 being httle smaller than normal, while those a little distance 
 away are distinctly diminutive. They are, too, empty in 
 appearance, the central fibril bundles having disappeared, 
 leaving only a few at the periphery of the cell (Fig. 4). The 
 
 
 -IscHJEMic Atrophy. 
 ( X 120.) 
 
 The cells nearest to the thickened 
 endocardium are least altered. 
 
 Fig. 4. 
 
THE DISEASES OF THE MYOCARDIUM 9 
 
 perinuclear mass is large and stains faintly, and the lesion 
 is readily appreciated in both longitudinal and transverse 
 sections. The nucleus is always abnormal, and is at first large 
 vdth. a scanty chromatin network, which may be here and there 
 aggregated into httle clumps ; while in the later stages, when 
 the ceU is disappearing, it becomes minute and pyknotic. 
 
 Granular Degeneration. — Granular degeneration (cloudy 
 swelling) is in some ways comparable to ischsemic atrophy. 
 In the early stages the proper detail of the ceU is obscured by 
 somewhat coarse granules, which are scattered widespread 
 over the cell, though they are most numerous in the central 
 parts where the striation is almost lost. But in the later 
 stages (Fig. 5) the cells become smaller and the perinuclear 
 mass enlarged, only a few fibrils with poorly marked striation 
 persisting at the periphery ; while still later all trace of stria- 
 tion has disappeared, and a granular mass of an irregular oval 
 shape alone remains. In ischajmic atrophy the fibril bundles 
 
 
 'mUTiWTM— ~"'V~i'T~ili''iiii Mi"riMiiiii''iir' 
 
 Fig. 5. — Granular Degeneration in an Advanced Stage, (x 1,000.) 
 
 always show transverse striation so long as they are recog- 
 nizable as definite muscle cells. In granular degeneration the 
 striation is obscured at a very early period, even before the 
 cells begin to atrophy. 
 
 Granular degeneration occurs in the acute infections, and is 
 most extreme in cases where the illness has lasted for more 
 than a few days. It is often accompanied by some degree of 
 fatty and hyahne degeneration. 
 
 Hyaline Degeneration. — H3'aline degeneration is compara- 
 tively uncommon. The affected ceUs are homogeneous and 
 glistening in appearance, and displaj^ none of the characteristic 
 features of the cardiac muscle, the nucleus and the striation 
 having disappeared. The staining reactions are altered, and 
 the cells colour yellow instead of red-brown vrith. Ehrhch's 
 triple stain. The distribution of the change varies. Some- 
 times only a part of a cell is affected ; more often a whole ceU 
 
10 DISEASES OF THE HEART 
 
 or a group of contiguous cells. And while as a rule the area 
 involved is small, it is sometimes large and widespread. 
 
 Hyaline degeneration is evidently a coagulation necrosis, 
 and is always present in recent infarcts of the heart ; but it 
 may also be produced by toxic causes, as it can always be 
 seen in the immediate vicinity of inflammatory foci, and may 
 be found in a few cells in the acute infections. 
 
 Dissociation. — The cells of the heart, when examined 
 microscopically, are often seen to be dissociated. Sometimes 
 the cleavage takes place along their line of junction (segmenta- 
 tion), each cell lying separate from its neighbom*s ; and some- 
 times it occurs through the cells themselves (fragmentation). 
 The change may be discrete and limited, or ma}'^ be widespread. 
 
 It has been suggested that dissociation (fragmentation in 
 particular) is merely an artefact occurring during section 
 cutting ; at any rate, appearances evidently due to this cause 
 are often met with locally; but when it is widespread, it is 
 probably vital in origin. It is, however, present in some 
 degree in the majority of hearts which are examined, and it 
 has been found in atrophied and in hypertrophied hearts, in 
 hearts which are degenerate and in hearts which are sound, 
 and in particular in the hearts of individuals whose death has 
 been sudden and abrupt (trauma, hanging, etc.). Its presence 
 seems, then, to be of little importance, and it is probably due, 
 as V. Recklinghausen suggested, to irregular and perhaps 
 excessive contraction of the cardiac muscle during the death 
 agony. It is in no way the cause of death, but rather its 
 result. 
 
 Fatty Infiltration. — There is always some fat in the sub- 
 pericardial connective tissue, the amount var3ang in different 
 cases, being sometimes very scanty and sometimes so con- 
 siderable that it covers and obscures the ventricular muscle. 
 It is normally thickest in the auriculo-ventricular sulcus, and 
 over the right heart. 
 
 Under pathological conditions the fat is sometimes found 
 to be infiltrating the muscle, spreading along the main fibrous 
 septa, in particular around the bloodvessels, and even between 
 individual muscle fibres. As a rule the infiltration is con- 
 
THE DISEASES OF THE MYOCARDIUM 11 
 
 fined to tlie superficial layers, but in some cases it may pene- 
 trate the muscular Avail, and in advanced stages the fat may 
 ■even be visible in httle patches beneath the endocardium. 
 Whenever the external fat is excessive, some infiltration always 
 obtains, but marked infiltration may occur without notable 
 •excess of the superficial fat. Fatty infiltration is always 
 most extreme on the right side of the heart, where it is often 
 considerable when the left side is but little affected. 
 
 In normal hearts one or two laj-ers of muscle cells in the 
 immediate vicinity of the superficial fat always show some 
 fatty degeneration, but the change is strictly limited. In fatty 
 infiltration a similar condition obtains, but to a far greater 
 -extent, and a majority of the muscle cells may be involved. 
 
 Fatty infiltration is usually a part of a general tendency 
 to obesity. In exceptional cases whose nature is not under- 
 stood, it may, however, affect the heart alone. 
 
 Fatty Degeneration. — Fatty infiltration is readily appre- 
 •ciatecl on naked-eye examination, but fatty degeneration 
 frequently can only be recognized microscopically, even in 
 •cases where it is well marked ; for the colour changes by which 
 its presence is known may be obscured in hearts whose blood- 
 vessels are congested, in hypertrophied and atrophied hearts, 
 and in jaundice. Special staining methods, too, are required, 
 for by the usual methods of preparation the fat is dissolved 
 out of the cells, and although the honeycomb appearance in 
 extreme cases is quite distinctive, the lesser degrees are readily 
 missed. Fatty degeneration is extremely common, but the 
 frequency of its occurrence is considerably underestimated 
 on account of the want of the special technique necessary for 
 its detection. 
 
 In a typical case the appearance of the heart is very character- 
 istic, many minute spots of buff or yellow colour being scattered 
 over the endocardial surface in an irregular wa}^ The 
 motthng is sometimes very fine and more or less diffuse, but 
 more commonly the spots are massed together, forming bands 
 which, on the papillary muscles, run transversely. These 
 bands are irregular and often zigzag in contour, and when 
 distinct, are aptly compared to the markings on a thrush's 
 breast. The colour change is usually apparent onty beneath 
 
12 DISEASES OF THE HEART 
 
 the endocardium, and on section is seen to penetrate for but 
 a short distance into the muscle, and to fade gradualh^ away. 
 But occasionally it involves the whole wall, and may even be 
 seen beneath the pericardium. Very rarel}- it is apparent only 
 on the pericardial surface. 
 
 The whole of the heart is never equally affected, and most 
 frequently only a part is involved. It is most common in the 
 left ventricle, less so in the right, and it occurs but rarely in 
 
 Fig. 6. — Fatty Degenekation : Paka-Arterial Distribution, (x 200.) 
 (From a case of ansemia.) 
 
 the auricles. One ventricle may be extensively diseased, and 
 the other but slightl}-. In the left ventricle the papillary 
 muscles, the adjacent muscle on the posterior waU, and the- 
 septum are most often degenerate ; on the right side the papillary 
 muscles and the muscle in their vicinity. The left ventricle 
 suffers alone, or to the greatest extent, in anaemia and aortic 
 valvular disease. In chronic pulmonarj^ disease and in mitral 
 affections the right ventricle is chiefly involved. 
 
 On microscopic examination of sections stained with osmie 
 
THE DISEASES OF THE MYOCARDIIBI 13 
 
 acid, the fatty granules are seen to be distributed irregularly 
 within the ceUs, being largest and most numerous in the 
 central parts around the nucleus ; but even in advanced cases 
 the whole of the muscle fibrils are never destroyed. Eatty 
 degeneration does not affect the size of the cell, and may be 
 present in cells which are larger or smaller than normal. 
 
 Examination Avith a low power distinguishes two forms. 
 In one (thrush breast) the distribution of the fatty ceUs is very 
 irregular, little islets of more or less normal cells being sur- 
 
 FiG. 7. — Fatty Degexeeatiox : Diffuse Foem, of Toxic ORiors'. (x 200.) 
 
 rounded on all sides by masses of degenerate cells (Eig. 6). 
 As a rule the transition is gradual, but sometimes a cell whoUy 
 free from fat may he next one which is extensively disorganized. 
 Sometimes almost every cell is fatty, but a patchy distribution 
 is stiU apparent, islets of ceUs with comparatively little change 
 lying "^-ithin areas whose ceUs are greatly altered. In sections 
 of the walls it is often difficult to determine the relationship 
 of the islets to the bloodvessels, but in sections of the muscuh 
 papillares, where the ceUs are arranged longitudinally, it can 
 be seen that those around the arterioles are less affected than 
 
14 DISEASES OF THE HEART 
 
 those farther awaj' (para-arterial distribution). In the second 
 form the fatty change is generally less extreme than it is in 
 the former, but it is diffuse and almost equally distributed 
 (Fig. 7). 
 
 The patchy degeneration is seen in its most exquisite form 
 in the left ventricle in cases of anaemia, and it is always best 
 marked on the musculi papiUares. It occurs, therefore, in 
 those muscle cells which are most distant from their nutrient 
 arterioles, and in the parts of the ventricle supplied by the 
 longest branches of the coronary arteries ; and it is evidently 
 due to a relatively insufficient supply of blood, arising partly 
 from the blood condition, and partly from the anatomical 
 distribution of the vessels. In cases where the maximal change 
 is situated elsewhere, a special reason for the particular site 
 can usually be found. Thus, in a case of aortic valvular 
 disease, the right ventricle was found to be more fatty than 
 the left, but the orifice of the right coronary artery was partly 
 occluded by aortic atheroma. In another case, that of a child 
 who died somewhat suddenly a few days after a burn, the 
 right ventricle was again more fatty than the left ; but as the 
 patient was at the time of the burn suffering from bronchitis, 
 the right ventricle was overtaxed, and the lesion was, in conse- 
 quence, situated at the point of greatest functional strain. 
 
 The diffuse degeneration is of toxic origin. In local 
 toxaemias, such as occur in abscess and pericarditis, a few fatty 
 cells can always be seen in the vicinity of the lesion, and a 
 diffuse degeneration can be readily produced in animals by 
 the administration of chloroform and phosphorus. In such 
 experiments the animals may die rapidly, in which case the 
 degeneration is slight and periarterial in distribution, or may 
 survive for several days, when it is invariably widespread and 
 uniform. 
 
 CUnically it is particularly associated with severe anaemia, 
 emphj^sema, chronic renal disease, and alcoholism. In the 
 ordinary work of a laboratory it is difficult to secure "pure " 
 cases of chronic alcoholism, as many causes may have co- 
 operated in producing death; but in one case which I have 
 examined the association seemed definite. A man, who had 
 been drinking heavily for a fortnight, was crushed between 
 
THE DISEASES OF THE MYOCARDIUM 15 
 
 a cart and a wall, and died within a few hours from rupture 
 of a kidney and fractured ribs. His heart, which seemed 
 normal on macroscopic examination, proved to be the seat 
 of an extensive and diffuse fatty degeneration. 
 
 A diffuse degeneration is not absolutelj^ uniform in its 
 distribution, and some parts of the heart always show more 
 change than others; but this is not fatal to the general con- 
 tention. The very special arrangements of the muscular 
 fibres and of their vascular supply are adapted to secure the 
 successful performance of work which varies greatty in its 
 amount from time to time, and which may be at a maximum 
 in either ventricle under certain circumstances. It seems 
 probable, too, that in normal conditions the whole of each 
 ventricle is not called upon to perform an equal amount of 
 work, and given a blood poison, it wiU act most rapidly on 
 those parts which are working nearest to their maximum 
 capacity ; for ceUs working well within their power will require 
 less nourishment, and will suffer to a less degree from any 
 vitiation of the blood. The causes of death are often multiple, 
 pneumonia, for example, showing a maximal mortality in 
 alcohohcs and persons with degenerate tissues ; and an acute 
 infection is often the terminal event in a case of chronic renal 
 disease where the coronary arteries are not as supple as normal, 
 and perhaps have a narrow lumen. In such a case it is 
 difficult to predict the precise locality of maximal strain or 
 to estimate the relative value of the different factors — anaemia, 
 toxaemia, high blood-pressure — which maj^ be active in pro- 
 ducing the condition. 
 
 The Fibroses of the Heart. — The connective tissue of the 
 heart is not infrequently increased in amount, but the fibrosis 
 is never uniform in distribution, being scattered in httle islets 
 or bands irregularly throughout the muscle. Sometimes only 
 a single patch is present, but more frequently there are several, 
 and they may be very numerous. They may be of any size 
 or shape; sometimes mere pin-points, and sometimes blocks 
 an inch or more thick ; often rounded, or oval, or star-shaped ; 
 sometimes a long ribbon; their greatest diameter usually 
 corresponding with the general direction of the muscle fibres. 
 
16 DISEASES OF THE HEART 
 
 Their consistence varies with their age, recent nodules being 
 soft and vascular, and the cut surface being flush with the 
 surrounding muscle; while the older patches are firm and 
 depressed, and the surrounding muscle stands out prominently 
 around them. If a large area of the wall is involved, it is 
 often notably thinned, and may only measure a quarter of its 
 normal thickness (Fig. 8). 
 
 Fibroid patches are most commonly found in the left 
 ventricle, though they may occur anywhere. They are rarely 
 met with on the right side. The musculi papillares are most 
 frequently affected and are often shrunken and deformed ; and 
 then, in order, the apical third of the left ventricle, the lower 
 part of the septum, and the posterior wall of the left ventricle 
 about the junction of its upper and middle third. The most 
 usual sites in the right ventricle are the musculi papiUares and 
 the apex. The patches are generally situated deeply in 
 the muscle, the ribbon form often lying about the junction 
 of the inner and middle third of the wall, and do not always 
 extend to the surface; but in extreme cases the overlying 
 endocardium is thick and opaque, and the visceral pericardium 
 may be similarly involved and sometimes adherent to its 
 outer layer. In lesser degrees one or other covering may alone 
 be impHcated. 
 
 Fibrosis is most frequently the result of obstruction of the 
 coronary arteries. These vessels supply practically the whole 
 of the cardiac muscle, and the nutrient vessels are end-arteries, 
 although the main trunks anastomose. Obstruction of the 
 former, therefore, necessarily causes necrosis of the tissues 
 which they supply, though obstruction of the latter may be 
 compensated by anastomotic developments ; but as the anas- 
 tomoses are slight, unless the occlusion is gradual in its onset 
 the muscle is generally more or less damaged. If the occlu- 
 sion is sudden, the lesions are always considerable. 
 
 Infarct — Myomalacia Cordis. — The nutrient arteries may be 
 occluded by emboli or thrombi, the latter being more common. 
 The tissues which are involved necrose, and if the patient 
 survives, are gradually absorbed and replaced by connective 
 tissue. Large infarcts are generally due to sudden occlusion 
 to a main artery, the abruptness of the closure preventing 
 
Fig. 8. Fibrosis of the Anterior Wall of the Left Ventricle 
 W.I. Museum. 
 
THE DISEASES OF THE MYOCARDIIBI 17 
 
 tlie successful development of the anastomotic connections. 
 They occur towards the peripheral distribution of the main 
 vessels, near the apex between the extremities of the descend- 
 ing branches, and on the posterior wall of the left ventricle 
 in the area between the extremities of the transverse branches. 
 The whole of the muscle fibres never disappear in these cases, 
 a few cells always persisting along the margins of the walls 
 (Fig. 9), those along the inner aspect being kept aUve by the 
 
 - ■;■ - . ;***>J'»> ■■ 
 
 ^' 
 
 
 
 Pericardium. Endocardium. 
 
 Fig. 9. — Dysteophic Fibrosis of Wall op Left Venteicle. (x 20.) 
 Some muscle cells still persist along tlie pericardial and the endocardial margins. 
 
 endocardial blood, and those on the outer by the superficial 
 subpericardial anastomosis. 
 
 The appearance of infarcts varies. They may be dull yellow 
 in colour from fatty changes (Fig. 11), or uniformly red or 
 mottled from extravasation of blood. White infarcts are 
 usually fairly firm in consistence, but some are soft and friable 
 from the development of autolytic processes. Haemorrhagic 
 infarcts are soft and may be almost diffluent, in Avhich case 
 rupture of the heart is not unusual. 
 
 Para-Arterial (Dystrophic) Fibrosis. — Partial occlusion of the 
 arteries, or complete obstruction of gradual onset, leads to 
 somewhat similar results, the muscle cells suppHed by the 
 
 2 
 
18 DISEASES OF THE HEART 
 
 particular branch which is affected suffering in nutrition, and 
 in extreme cases gradually atrophying and being replaced by 
 connective tissue. The process is seen best in well-marked 
 examples in the papillary muscles, as their cells are arranged 
 longitudinally. 
 
 ^Microscopic sections (Fig. 10) show that the distribution of 
 the fibrosis is exactty similar to that of the fat in the para- 
 arterial form of fatty degeneration, little islets of more or 
 less normal muscle being embedded in diffuse patches of fibrous 
 tissue. In the centre of the muscular islet around the arteriole 
 
 )^;.-. 
 
 "^^'^ '•" 9 
 
 
 
 
 .^. -,' 
 
 .« 'jft 
 
 ■•# ■ 
 
 •• ■^*.-' -.•' 
 
 .- "r*','^*^ *■*■:- 
 
 -» , ■ ii ■ .■ 
 
 .*.■■•.'■•■' ' ' ■ ' », 
 
 s. " 
 
 -• Si ■ 
 
 FiG. 10. — Paea-Aeterial (Dystrophic) Fibrosis. (x50. ) 
 
 the muscle cells may be normal, but those at the periphery 
 show every grade of ischaemic atrophy, and are widely 
 separated from each other. In the centre of the fibrotic area 
 the connective tissue is sparsely nucleated and often hyaline^ 
 with few bloodvessels, but in the vicinit}^ of "the muscle it 
 may be thickly nucleated and very vascular. Little collections 
 of pigmentary debris may be visible. 
 
 In both infarct and para-arterial fibrosis the process is 
 clearly dystrophic, the muscular degeneration being primary 
 
Fig. 11. Marked Xarrowixg of the Orifices of the Coronary Arteries 
 
 FROM Syphilitic Disease of the Aorta. Infarct, with Fatty 
 
 Degeneration of the Walls of the Left Ventricle. R.I. Museum. 
 
THE DISEASES OF THE MYOCARDIUM 
 
 19 
 
 and the fibrous overgrowth its result; and in both cases the 
 change is patchy and rarely of ribbon shape. The ultimate 
 result, too, is similar, and in old-standing cases the precise 
 mechanism of the process cannot be distinguished. Their 
 usual cause is endarteritis, but they may follow occlusion of 
 the orifice of a coronary artery by a patch of atheroma in the 
 aorta, as in the case reported by Gibson and Muir, and in one 
 which I have personaU}- observed. But coronary disease 
 does not necessarily cause fibrosis. This only ensues when 
 the lumen of the vessel is narrowed or occluded, and the main 
 trunks are often larger than normal when their walls are 
 
 Fig. 12. — Periaeterial Fibrosis, (x 50.) 
 
 diseased, the weakening of the wall inducing dilatation; 
 though when the smaller vessels are affected, the lumen is 
 generally narrowed. 
 
 Periarterial Fibrosis. — In some cases of fibrosis the new- 
 formed connective tissue is situated immediately around the 
 arteries (Fig. 12), and this periarterial fibrosis must be clearly 
 differentiated from that which has just been described, for it 
 is due to entirely cliff' erent causes. 
 
 The adventitia of the normal artery is sharph' demarcated 
 on one side by the muscle cells of the media, but on the other 
 cannot be accurately defined, as it blends with the general 
 connective tissue of the heart. In certain cases of fibrosis 
 
20 
 
 DISEASES OF THE HEART 
 
 the connective tissue around the arteries is notably excessive, 
 and forms an oval or a star-shaped mass of varying size. In 
 the smaller patches the muscle in the vicinity may not be 
 imphcated in the process, but in the larger patches the strands 
 pass in between the muscle cells and separate them from each 
 other (Figs. 13, 14). In early cases (Fig. 13) the connective 
 tissue may be vascular and very cellular, but in older examples 
 (Fig. 14) it is often hyaline and sparsely nucleated. 
 
 Periarterial fibrosis is generally less gross and more diffuse 
 than the para-arterial type, and is sometimes of ribbon 
 iorm. 
 
 Inflammatory lesions are not infrequently present in the 
 walls of the heart. It is unusual to fmd large abscesses, for 
 
 
 ■^ . 
 
 Fig. IS.-r-^EW^-FOEMED eONJfECTIVE TiS&UE IN THE ViCINITY 
 
 OF AN Arteriole. (x500.) 
 (From a cas,^ of malignant endocarditis. ) 
 
 patients suffering from pyaemia with metastatic deposits in 
 this situation generally die early, but microscopic abscesses 
 are not uncommon, and are often present in mahgnant endo- 
 carditis. They are frequently due to direct extension of the 
 infection from the base of the affected valve ; and are occasion- 
 ally found a little distance away beneath a patch of mural 
 endocarditis ; and they may- be disseminated fairly widely in 
 the substance of the muscle from infection of the coronary 
 blood. In the majority of cases of this kind death ensues 
 during the period of infection, but in a small minority recovery 
 ensues, and the scar beneath a thickened patch on the endo- 
 
THE DISEASES OF THE MYOCARDIIDI 21 
 
 cardiiim reveals the nature of the process. It is conceivable 
 that some examples of myocardial fibrosis may result from 
 infective lesions, but the unfavourable result in such cases 
 renders it improbable that this cause is often active. 
 
 In some cases of chronic mitral disease the inflammatory 
 lesion is not strictly limited to the valves, and the cusps, the 
 chordae tenclinse, and the papiUarj^ muscles are aU welded 
 firmly together into a more or less hard fibroid mass (the 
 typical funnel-shaped mitral stenosis, Fig. 139). The fibrosis 
 in these cases is rarely confined to the parts already men- 
 tioned, but also extends from the base of the valves into the 
 
 ^ jS^^ ^^ '^zL *z* ^ is^^^ 
 
 Fig. 14. — Perifascicixlaii Fibeosis. (x200.) 
 
 adjoining muscle in the direction of theoentral fibrous body ; and 
 a patchy fibrosis in the substance of the muscle often coexists. 
 It has been known for long that the rheumatic infection has 
 a special predilection for the cardiac valves, and is, indeed, 
 the most common cause of chronic valvular disease; and it 
 is also recognized to be a frequent cause of the subcutaneous 
 nodules which occur in childhood. The earher writers who 
 first noticed this association failed to appreciate its full 
 significance, but the researches of Barlow and Warner and 
 Cheadle showed that there was a close connection between 
 
22 DISEASES OF THE HEART 
 
 the occurrence of endocarditis and the eruption of nodules, 
 and that the presence of large subcutaneous ncdules was an 
 invariable sign of serious valvular involvement. In 1899 
 Pojaiton demonstrated the existence in the cardiac muscle 
 in cases of acute rheumatism of minute nodules, which were 
 exactly comparable to those found beneath the skin, and 
 subsequent observers have emphasized the frequency and the 
 multiphcity of these lesions. The nodules are invariably 
 small, and are generally invisible on naked-eye examination. 
 
 ^^[i^^, ;^;v:■:-i,•^^:N::^■;;,■ 
 
 
 Fig. 15. — Round-Celled Infiltration of the Myocardium: Focal Form. 
 
 (X 90.) (A. M. K.) 
 
 They occur most frequently in the ventricles, especially on 
 the left side, and are generally situated in the vicinity of, or 
 around, an arteriole. 
 
 jNIicroscopic examination shows that the essential lesion is 
 a round-celled infiltration of the interstitial tissue. It is 
 situated around an arteriole or in its immediate vicinity, and 
 sometimes involves the vessel wall, which may be so swollen 
 that the lumen is narrowed. The cells may be few in number 
 and the adjacent muscle apparently normal; but if they are 
 
THE DISEASES OF THE MYOCARDIUM 
 
 23 
 
 numerous, tliey inj&ltrate between the muscle cells, whicli in 
 this case are degenerate. In most cases the cells are arranged 
 in discrete foci, perhaps widely separated from each other 
 (Fig. 15); but in others the infiltration is diffuse (Fig. 16), 
 and larger areas are involved. The cells are mainl^^ mono- 
 nuclear, the majority being evidently lymphocytes, but a few 
 larger ceUs with, a fair amount of protoplasm, which are 
 probabty of connective-tissue origin, are often present; and 
 occasionally a few multinucleated giant cells. A few poly- 
 
 FiG. 16. — Rouxd-Celled Infiltratiok of the Myocardium: Diffuse 
 Form, (x 90.) (A. M. K.) 
 
 morphonuclear cells, too, may be found. These cellular in- 
 filtrations are commonly present in the tissues at the base of 
 inflamed valves, and are also widely disseminated tliroughout 
 the heart. Bacteria have not hitherto been found in them. 
 As regards their ultimate fate, the smaller nodules may be 
 completely absorbed, but the larger lesions persist. 
 
 Myocardial nodules are not confined to cases of acute 
 rheumatism, and have been found in many varieties of acute, 
 infection (pneumonia, pleurisy, smallpox, blackwater fever 
 
24 : \ DISEASES OF THE HEART 
 
 enteric feveTy sepsis, diphtheria, scarlatina, chorea, leukaemia ). 
 The indiYidual lesion is minute and. of comparatively Httle 
 importance, but their situation, or numbers may produce con- 
 siderable 'interference with the proper working of the heart, 
 both in the acute and in the. chronic stages. The heart, it 
 must be remembered, cannot be immobilized like a broken 
 leg, and its constant movement produces a "callus " quite 
 out of proportion to the original lesion. 
 
 Periarterial fibrosis must be sharply differentiated from 
 the para-arterial form. The latter is dystrophic, and the 
 result of coronary narrowing ; while the former is inflammatory 
 in nature. 
 
 The Mixed Form of Fibrosis. — Para-arterial and peri- 
 arterial fibrosis may occur as individual lesions, but, in perhaps 
 the majority of cases of fibrosis, occur together, though the 
 amount of each kind varies. This is the necessary result of 
 the arterial causes. Endarteritis may, it is true, be the sole 
 lesion in an artery, but in all extreme cases the other coats 
 are also involved ; and in adventitial lesions the vasa yasorum 
 are often affected and intimal changes ensue, so that fre- 
 quently intimal and adventitial lesions coincide, and both 
 forms of fibrosis coexist. 
 
 The special localization of cardiac fibrosis is due to the 
 frequency with which it is dependent upon coronary disease, 
 Huchard has pointed out that the left coronarj^ artery, its 
 descending branch in particular, is much more frequently 
 abnormal than the right. The work which it has to perform 
 is greater, extra strain is more frequently imposed upon it, 
 and it divides rapidly into many branches. The right artery, 
 too, in its bed of fat in the auriculo-ventricular sulcus, is 
 much better protected and much less strained during the 
 cardiac contractions. The arteries of the musculi papillares 
 are the longest branches of the system, and have a course 
 which is particularly tortuous, and are, in consequence, likely 
 to suffer in any disadvantageous circumstance. 
 
 Another factor, a local spread of inflammation from the 
 auriculo-ventricular valve, may also be active in the case of 
 the musculi papiUares, for, in all marked cases of mitral disease 
 the papillae are sclerosed, the fibrosis being most extreme at 
 
THE DISEASES OF THE MYOCARDIUM 
 
 25 
 
 tlie tip, and the chordae are thickened and shortened. So 
 that, although the anatomical peculiarity of their blood- 
 supply is in itself sufficient to explain the special frequency 
 
 Fig. 17. — Gumma of Heart. 
 (From a water-colour drawing by Dr. Ales Macphail, W. I. Mus.) 
 
 with which they are diseased, another factor inflammatory in 
 origin assists to make the pre-eminence still more marked. 
 
 The other possible causes of fibrosis are of comparatively 
 Httle importance. 
 
26 DISEASES OF THE HEART 
 
 Hcemorrhages are not infrequently found post-mortem. 
 They are generally subpericardial, but also occur beneath the 
 endocardium and in the substance of the muscle. They are 
 usually small and cause little damage to the muscle, but are 
 occasionally large, and the muscle in their vicinity is degenerate. 
 In such cases death as a rule occurs early, but if recovery takes 
 place, scar formation may conceivably result. 
 
 Tumours and tubercular masses in the cardiac waU are rare, 
 and are usually secondary ; hydatid cysts have been occasionally 
 
 Fig. 18. — Fibrosis of the Myocardium, ^x 50.) 
 (From a case of syphilis during the secondary stage.) 
 
 found ; and all these lesions occasion fibrosis in their vicinity. 
 Wotmds of the heart and trauma (Pleasants), even without 
 actual penetration, may lead to scar formation. 
 
 Syphilitic lesio7is may be met with. The most important 
 is specific endarteritis of the coronar}?^ arteries, whose lumen 
 may be narrowed or occluded, in which case a dystrophic 
 fibrosis results (Fig. 10). Gummata (Fig. 17) have been 
 found in a not inconsiderable number of cases, and maj^ con- 
 ceivably be responsible for some mj^ccardial scars; and a 
 diffuse periarterial fibrosis (Fig. 18) is recognized as occurring 
 
THE DISEASES OF THE MYOCARDIUM 
 
 27 
 
 during the secondary stages of the acquired disease, and in 
 congenital infections.* 
 
 Fibrosis of the heart may thus be due to several causes. 
 In the great majorit}- of cases, and in all examples of gross 
 disease, it is the result of ischsemic destruction of the muscle 
 
 Fig. 19. — Infakct of a Papillahy Muscle, with Rupture, from Disease of 
 THE Coronary Arteries. (R. I. Mus.) j ^ 
 
 cells, following obstruction of the coronar}^ arteries and second- 
 ary connective-tissue hyperplasia. In other cases the fibrosis 
 Kes around the arterioles, and is a primary connective-tissue 
 reaction. These two forms often coexist. 
 
 Fibroid patches may be due to mural endocarditis, but the 
 lesions are never large ; they are rarely, if ever, due to pericarditis . 
 * Wartliin, Amer. Journ. Med. Sci., 1911, vol. cxli., p, 398. 
 
28 DISEASES OF THE HEART 
 
 S}T3liilis and trauma very occasionally produce scars. 
 
 Chronic valvular disease seems alwaj^s to be accompanied 
 by some degree of fibrosis which is most extreme in the vicinity 
 of the affected valve, though it also occurs throughout the 
 heart in lesser degree. 
 
 Hypertrophied hearts are not necessarily fibroid, though 
 this frequently obtains from associated arterial disease. 
 
 Aneurism of the Heart is comparatively rare. It may be 
 situated anywhere, but is most common in the lower part of 
 the left ventricle. The right ventricle is seldom imphcated, 
 and the auricles still less frequently. The aneurism may be 
 of any size, and is sometimes as large as an orange. 
 
 Aneurism is always secondary to myocardial lesions, which 
 so weaken the wall that the intracardiac pressure causes 
 bulging. The myocardial lesions may be of various kinds. 
 An acute mural endocarditis is occasionally the cause, and 
 usually involves the septum. Myomalacia and dystrophic | 
 fibrosis are more common, and most frequently affect the' 
 lower part of the left ventricle. A traumatic scar, the result 
 of a stab ten years before death, has been followed by the 
 formation of an aneurism. 
 
 In the majority of cases the wall is fibroid and greatly 
 thinned, being sometimes only a fourth of the normal thick- 
 ness. The endocardium is thickened and opaque, and often 
 Hned by laminated clot. The visceral pericardium is thickened 
 and frequently adherent to its parietal layer. The bulk of 
 the muscle has disappeared, though a few cells may persist 
 beneath the endocardium and the pericardium. 
 
 Rupture o£ the Heart is most frequently due to myomalacia 
 the result of coronary occlusion. If an infarct occurs and 
 the patient survives, an inflammatory reaction takes place in 
 the periphery of the necrotic area, with resultant weakening of 
 the tissues. If it extends near the endocardium, the endo- 
 cardial blood soon forces an entrance, and tearing its way 
 along the track of the softening with each successive heart-beat, 
 it ultimately reaches and perforates the pericardium. The 
 path of the blood may thus be devious, and the endocardial 
 
THE DISEASES OF THE MYOCARDIUM 29 
 
 and pericardial lacerations may not correspond unless the 
 communication is large. 
 
 Rupture may also occur from trauma, intramural abscess, 
 and aneurism. 
 
 EEFEEENCES. 
 John Cowan: 
 
 On Obstruction of the Coronary Arteries. Trans. Path, and Clin. Soc, 
 
 Glasgow, 1902, vol. ix., p. 49. 
 
 Fatty Degeneration of the Myocardium. Joum. of Path., London, 1903, 
 
 vol. viii., p. 177. 
 
 The Heart in Acute Disease. Ihid., 1904, vol. ix., p. 87. 
 
 The Fibroses of the Heart. Ihid., 1904, vol. ix., p. 209. 
 
 Cakey Coombs: 
 
 Submiliary Nodules of Acute Rheumatic Carditis. Ihid., 1911, vol. xv., 
 
 p. 489. 
 
 The Histology of Experimental Rheumatism. Lancet, London, 1912, 
 
 vol. ii., p. 1209. 
 
 Louis Gallavardin: La Degenerescence Graisseuse du Myocarde. These 
 
 de Paris, 1900. 
 
 Rene Marie: L'Infarctus du Myocarde. These de Paris, 1896. 
 
CHAPTER II 
 
 THE DISEASES OF THE ARTERIES 
 
 The Arteries. — It has been customary to consider the arterial 
 wall as composed of three layers — the intima, the media, and 
 the adventitia ; but while this is useful from the descriptive 
 point of view, it tends to produce the idea that, physiologi- 
 cally, the layers are distinct and separate, an idea which is 
 essentially inaccurate. The internal elastic lamina, it is true, 
 in the smaller vessels marks abruptly the line of division 
 between intima and media, but it is absent in the aorta and 
 the larger arteries, and the precise limits of the layers are, in 
 consequence, indefinite. Muscular fibres are not confined 
 to the media alone, but are present in both the intima and 
 the adventitia; and though they are in the smaller vessels 
 the main constituent of the middle layer, in the larger trunks 
 they are relatively scanty, and the elastic tissue is the essential 
 element. The two groups of vessels must be sharply separated. 
 One group are the " mains " for the supply of blood to the 
 tissues, with a calibre proportionate to the amount of blood 
 which they have to accommodate, and a structure adapted to 
 resist the varying degrees of blood-pressure to which they are 
 exposed. The other group are the " supply-pipes " with 
 "taps," which can be partially closed and so rearrange the 
 distribution of the blood to the different viscera. The adven- 
 titia is but a part of the general connective tissue, and can 
 seldom be exactly demarcated, and the connective tissue and 
 the elastic framework of the three layers are structurally in 
 contact. The essential constituent of the bloodvessels, as 
 the late Professor Coats maintained, is the intimal pavement 
 endothelium. 
 
 The relations of the three layers may vary even in the same 
 
 30 
 
THE DISEASES OF THE ARTERIES 31 
 
 artery in different portions of its course. Particular parts 
 may be exposed to special stress, and the liability to local 
 damage is to a certain extent compensated. The upper wall 
 of the ascending aortic arch, exposed to the full force of the 
 ventricular systole, is much thicker than the opposite side, 
 where the systolic impact is less direct, and vessels are always 
 thickened at bifurcations and around the origins of branches 
 to meet the extra strain. Arteries such as the facial superior 
 mesenteric and brachial are exposed to injury from the 
 movements of the neighbouring parts, and possess, in conse- 
 quence, an adventitia which is notably thick; while others 
 such as the abdominal aorta and the nutrient arteries of the 
 bones are protected from such influences by their situation, 
 and have an adventitia of little thickness. The relative 
 proportion of the different elements of each layer varies in 
 different vessels of similar size. The media of the renal 
 arteries, for example, contains a much larger proportion of 
 muscle, and a much smaller amount of elastic tissue than such 
 a vessel as the carotid; and one cannot predicate what the 
 exact constitution of an artery will be, since the individual 
 elements may var}^ in amount from its special function or its 
 special site. 
 
 The vascular arrangements of the arterial wall point the 
 same moral. The nutrition of the vessel is maintained by 
 two sources. The vasa of the adventitia penetrate for a 
 certain distance into the media of the larger arteries, but under 
 normal circumstances do not trespass far. The minute 
 vessels have no vasa, and must be largely dependent upon the 
 blood within them, although no definite lymphatic connection 
 is apparent. It is difficult to estimate how much of the wall 
 is supphed from each source, but in endarteritis the cells 
 nearest the blood-stream are always less degenerate than 
 those farther away; and in some cases of medial fibrosis the 
 innermost muscle cells persist, while those in the centre of the 
 layer have disappeared (Fig. 21); so that it seems clear that 
 in abnormal circumstances both media and intima may be 
 nourished by the intra-arterial blood. All the muscle cells 
 of the media, however, may be intact in cases of endarteritis, 
 and the vasa are sometimes seen to penetrate into the intima. 
 
32 DISEASES OF THE HEART 
 
 so that both layers may at times be supphed from without. 
 It seems probable that normally the medial source is mainly 
 vasal, and the intimal source mainly intra-arterial, while 
 under abnormal conditions a defect in one supply can be 
 more or less compensated by the other. New-formed blood- 
 vessels in the media and the intima are, however, always 
 branches of the vasa. 
 
 Lymphatic flow takes place from within outwards, although 
 no definite lymph channels are present in the vessel wall. 
 But in early cases of endarteritis the muscle cells in the vicinity 
 of the degenerate intima are not infrequently fatty, as the 
 result of the local toxsemia. 
 
 The functional and structural arrangements of the arterial 
 wall thus necessarily entail some damage to more than one 
 layer in all but the very slightest lesions. In advanced cases 
 all the layers are ahnormal, though the degree to which each 
 is involved may vary, and this occurs quite irrespective of the 
 site of the initial lesion. 
 
 A clear distinction must be drawn between the two main 
 groups of arterial disease: (l).The di-ffuse form, and (2) the 
 focal or nodidar lesions ; for the causes and the results of the 
 two are notably different. The second group comprises 
 atheroma, patchy mesarteritis, endarteritis obliterans, and 
 medial calcification; the first arterio-sclerosis, using the term 
 in its more restricted sense. 
 
 Arterio-Sclerosis. — Arterio-sclerosis is a diffuse affection, 
 and all the arteries and capillaries, and, according to some 
 writers, the veins as weU, are abnormal. The lesions are best 
 marked in the smaller vessels whose walls are distinctly and 
 uniformly thickened. The medium-sized arteries (renal, etc.) 
 are also thickened, and their consistence may be firmer than 
 normal. The aorta is thickened generally, and, in addition, 
 in old-standing cases shows many atheromatous patches. In 
 th^ early stages the resilience of the vessels may be good, but 
 in advanced cases is distinctly impaired. 
 
 Microscopic examination shows alterations in all the three 
 layers. The intima is usually more or less thickened (Fig. 20), 
 
THE DISEASES OF THE ARTERIES 33 
 
 There is always great hypertrophy of the elastic fibrils, and 
 two or more laminae, sometimes of considerable thickness, 
 may be evident. In older cases degenerative changes are 
 present, the elastic tissue becoming granular and the connective 
 tissue hyahne and sparsely nucleated, but the gross fatty and 
 calcareous deposits, which are met with in atheroma, are 
 rarely, if ever, seen. The media is always abnormal. In early 
 
 Fig. 20. — Arteeio-Sclerosis: Elastic Tissue stained to show the 
 Hyperplasia ik the Intima. (x 75.) 
 
 cases it is thicker than usual, but the relative proportions of 
 muscle, elastic and connective tissue, are preserved, the only 
 alteration being the hypertrophy. In other cases it may be 
 thinned, the muscle ceUs being atrophied and perhaps fatty; 
 while in a third group the connective and elastic elements 
 are in excess and the muscle cells are degenerate and few in 
 number, in advanced cases only persisting along the edges of 
 the coat (Fig. 21). They are most numerous and least altered 
 
 3 
 
34 
 
 DISEASES OE THE HEART 
 
 along the outer margin, but may persist along the inner edge, 
 while those in the centre have disappeared. The connective 
 tissue is usually hj^ahne or granular, and sparsely nucleated; 
 and the elastic fibrils, though excessive in number, are 
 degenerate and granular (Fig. 22). The adventitial changes are 
 less variable. The outer coat is almost invariablv thickened, 
 
 Fig. 21. — Aeteeio-Scleeosis. (xoO.) 
 The media is fibroid, and only a few muscle cells persist along the margins. 
 
 being in the early stages thickly nucleated, and in old-standing 
 cases hyahne and sparsely nucleated. The elastic tissue, 
 here as elsewhere, is always excessive. 
 
 The adventitial thickening is the onl}^ constant change in 
 these cases. If the media is thickened or fibroid, the intima 
 may be but little abnormal; but if the former is atrophied, the 
 latter is generally hj^ertrophied. WiUiam Russell states 
 that the changes in the intrarenal vessels tend to intimal 
 thickening, while the medial hypertrophy is best marked in 
 
THE DISEASES OF THE ARTERIES 
 
 35 
 
 the extrarenal vessels ; but this may be due to the renal lesion 
 being of older date. There has been considerable discussion 
 in the past as to the precise histological details of the arterial 
 lesions. But it is now generally agreed that medial hyper- 
 trophy (hypermyotrophy) is an early and essential phase 
 
 Fig. 22. — Akteeio-Sclerosis. (x 75.) 
 
 The same vessel as Fig. 21, stained to show the degenerate new-formed elastic 
 
 fibres. 
 
 that it occurs throughout the whole arterial system, and that 
 fibroid changes supervene both here and in the adventitia 
 •at a comparatively early period. 
 
 The capillary vessels are also abnormal. A healthy capillary 
 •cut transversely is apt to escape observation, the waU being 
 ■8b mere hair-hne; but in the cases which we are considering, 
 •a double contour is usually visible, the wall being several 
 times its usual thickness; the lumen, too, may be somewhat 
 iiarrow^d. 
 
36 
 
 DISEASES OF THE HEART 
 
 It has been known for long that the blood-pressure in cases 
 of cirrhotic kidney is almost always elevated, sometimes to 
 an extraordinary degree ; and it was at first supposed that this 
 was due to the associated arterial disease. In 1903, how- 
 ever, Sir Clifford AUbutt published a paper,* in which he 
 urged that arterial disease was not the cause of an elevated 
 blood-pressui^e, but rather its result. "The pressure may 
 be, and often is, low throughout the course of arterial degenera- 
 tion; or, again, having been high, it may fall; though, of 
 course, in some elderty persons with arterial decay, occasional 
 transient attacks of high pressure, such as occur at times in all 
 
 of us, maj' be observed." Con- 
 versely, high blood-pressure can- 
 not be maintained for long 
 without arterial strain; and 
 arteriosclerosis results from long 
 persisting high Mood- 'pressure of 
 tvhatsoever origin. 
 
 The process is well seen in cases 
 of nephritis. In acute nephritis 
 the blood-pressure is almost in- 
 variabh^ elevated in the presence 
 of symptoms and falls with their 
 remission, reaching normal read- 
 ings in the majoritj^ of cases long 
 before the albuminuria disappears. 
 In the chronic forms of nephritis 
 the blood-pressure is not invariably elevated, and is, indeed, 
 as a rule low in cases of large white kidney (Fig. 23), but it 
 is always high in contracted kidneys (Fig. 24), whether these 
 are primary or foUow an acute attack. In cirrhotic kidney, 
 as Dickinson has shown, the whole of the arterial tree is 
 affected, and the walls of the aorta and the great vessels, as 
 well as the smaller branches, are notably thickened. 
 
 The elevation of pressure in these cases si due to an increase 
 in the peripheral resistance, which can only result from one 
 of two causes : a diminution in the calibre of the vessels, or an 
 increased viscosity of the blood. Arterial disease does in many 
 
 * Lizncet, 1903, vol. i., pp. 170, 329, 472, 645, 
 
 MAR APR MAy JUN JUL AUG SEP 
 
 mm 
 
 140 
 
 130 
 
 120 
 
 no 
 «oo 
 
 90 
 80 
 
 70 
 
 Fig. 23. — Blo od-Peesstjee 
 Chaet. 
 
 M„ aged 23. Large white kidneys 
 weighing 16 ounces. The heart 
 weighed 6J ounces. 
 
 28 
 
 25 
 
 24 
 
 9 
 
 28 
 
 2Q 
 
 22 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 y 
 
 /N 
 
 V 
 
 
 
 
 >r^ 
 
 >^ 
 
 
 N 
 
 v- 
 
 ^ 
 
 
 
 
 
 
 
 
 
 
 
 A 
 
 ^ 
 
 
 
 
 
 / 
 
 
 
 
 
 
 
 
 
 
 
 
THE DISEASES OF THE ARTERIES 
 
 37 
 
 cases narrow the lumen, but it also 'sometimes widens it; 
 ■and if it lessens it in some places, the local narrowing may 
 be compensated by dilatation elsewhere. In syphilitic disease 
 •of the arteries, the lumen is often greatly narrowed, though 
 the blood-pressure may never be above the normal. 
 
 The second factor, increased viscosity of the blood, may 
 ■conceivably be active in certain cases, but accurate observa- 
 tions on this point are difficult to obtain, for the methods of 
 estimation are not above suspicion even in 
 laboratory experiments, and many diverse 
 factors which may influence it, but cannot 
 be accurately measured, come into opera- 
 tion in the wards. The viscosity of the 
 whole blood rises steadily during the period 
 of growth, and is higher in men than in 
 women. It is affected by menstruation and 
 pregnancy, by sweating exercise, by alti- 
 tude, by variations in the red-ceU and the 
 white-cell counts, and by the percentage of 
 oxygen and of carbonic acid in the blood, 
 as well as by the saline and the colloid con- 
 tent ; while it has no constant relation to 
 the specific gravity of the blood or the 
 height of the blood-pressure.* 
 
 The viscosity is almost always increased 
 in polycythsemia, and Parkes Weberf and 
 others have shown that it may be twice Fig. 24.— Blood-Pbes- 
 or thrice, or even four times, greater than ^"^^^ Chart, 
 
 normal in cases of erythremia, in which \Xeyt wfjhtg"i2| 
 disease the blood-pressure is usually in- 
 creased, apparently in consequence; for 
 although this might be due to renal disease, which is a common 
 accompaniment in these cases, the kidneys may be normal, 
 as in Case 21 of Weber's series, in which the heart was 
 "somewhat hypertrophied." 
 In one group, the polyoythcenla hypzrtonica of Grsisbock and 
 
 * Sir CiiEfjrd Allbitfc, Q ixrl. Joitrn,. of MiL, 1310-11, vol.riv., p. 342. 
 W. H. Welsh: ' He%rt; 1911-12, vol, iii., p. 118. 
 t Qmrt. Journ. of Med., 1908-09, vol. ii.,"p. 85. 
 
 9 
 
 10 
 
 V 
 
 
 
 
 
 
 
 ,, 
 
 
 
 
 Sr^ 
 
 ^ 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 as 
 
 N» 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 NOV 
 
 Hg. 
 mm 
 
 210 
 
 190 
 ISO 
 170 
 160 
 150 
 140 
 130 
 120 
 110 
 100 
 90 
 80 
 70 
 
 ouaces. The heart 
 weighed 18 ouaces. 
 
38 DISEASES OF THE HEART 
 
 Hess, the same relationship apparently obtains. I have seerc 
 one case of this kind. 
 
 The patient, a solicitor aged thirty-nine, had been steadily 
 losing strength and flesh for at least a jesbT, and had been, 
 noticed to be " blue " in colour for the same time. He had 
 had several attacks of "influenza," in which he was fevered, 
 and shivered frequently, and experienced very severe head- 
 ache, while there was but little catarrh; and during these 
 illnesses he became notably c^^anosed, while his urine con- 
 tained much albumin. He was a well-built but badly 
 nourished man, and sweated profusely. The cyanosis was 
 always considerable, and once when I saw him during cold 
 weather extraordinary in its degree, and, although general,. 
 much more intense in the head and neck than elsewhere. The 
 jugular veins were turgid and prominent. The heart was 
 shghtly enlarged, the second aortic sound loud and ringing, 
 and the peripheral arteries thick and tortuous. The retinal 
 arteries were of characteristic silver wire appearance. The 
 brachial systohc pressure measured 175 to 180 mm. Hg. 
 The hver and spleen were shghtly enlarged, and the urine 
 habituafly contained albumm in varying amount, sometimes,, 
 however, only a trace. The red cells numbered 10,000,000, 
 the haemoglobin value was 120 per cent., and the white ceUs- 
 numbered 22,400 per c. mm. The average size of red cell wa& 
 rather above the normal, and a few cells were certainly 
 megalocytes. No erythroblasts were seen. The white cells 
 were chiefly polymorphonuclear. 
 
 The patient himself was definite that his illness had lasted 
 for some twenty years, though it was only recently that he- 
 had been seriously inconvenienced; and he had conducted a 
 considerable business during this period. He was a married 
 man with a healthy family. He had alwaj^s been liable tO' 
 bilious headaches, even as a boy at school, and these had 
 gradually become more severe and of longer duration. They 
 recurred every few weeks, and his tongue became coated and 
 his bowels confined during their persistence. He was, he 
 said, a "fair" hoj, but his complexion darkened in the 
 twenties, and in the early thirties he became "plethoric." 
 His father, too, had been "blue " for the last twenly years 
 
THE DISEASES OF THE ARTERIES 39 
 
 of his Life; but he had carried on business until shortly before 
 his death at the age of seventy, after an iUness of ten days' 
 dui'ation. 
 
 This patient died about two years after I first saw him, 
 and there was no post-mortem examination, so that the con- 
 dition of his kidneys was not ascertained. But it seems 
 probable that the polycythaemia was the primary event and 
 the cause of the increased blood - pressure and the cardio- 
 vascular hypertroph}". 
 
 There has been some difference of opinion as to the site of 
 the increased peripheral resistance. Sir Chfforcl thinks that 
 it is in the capiUary network as in normal individuals, while 
 Sir Douglas PoweU, Russell, and others maintain that it is 
 situated in the finer arterioles. Broadbent and Sansom 
 thought that both factors might be active. The last opinion 
 seems probably correct, for although the first theory seems 
 applicable to the polj^cythaemic group, vasodilator drugs 
 can often in other cases relieve high pressure, at any rate 
 temporarity, and their action can only influence the muscular 
 arterioles . 
 
 The blood-pressure in elderly persons may be elevated 
 without any evidence of renal lesions (hyperpiesis), and Sir 
 Chfford thinks that the most important cause is "repletion, 
 relative or absolute — i.e., tempered or untempered by air and 
 exercise." Although at first the elevation may disappear as 
 the result of suitable treatment, it tends as a rule to recur 
 and to become permanent, and to be ultimately associated 
 with arterial thickening. WilHam Russell has also brought 
 forward evidence in support of the same theory. He differs 
 from Sir Chfford in his contention that the initial error is 
 always an excessive ingestion of food greater than the work 
 done requires or ehmination can overtake; and suggests that 
 in many cases the chief cause is an intoxication due to gastro- 
 intestinal indigestion and the production of hypertonic 
 substances. There seems to be little doubt that both ob- 
 servers have right on their side, but it seems certain that other 
 causes may also be active, for the association of gout and 
 
40 DISEASES OF THE HEART 
 
 chronic lead-poisoning with arterio-sclerosis has been recog- 
 nized for long, though the precise mechanism by which the 
 blood-pressure is elevated is still undetermined. Renal disease, 
 in these cases, though commonly present, may be absent, 
 though the arterial lesions are well marked. 
 
 The isolation of adrencilin and the discover}^ by Josue of 
 its action in producing arterial disease in rabbits have focussed 
 the attention of man}^ observers upon the suprarenal capsules, 
 and it has been demonstrated that these bodies are very often 
 enlarged both in chronic renal disease and in cases of arterial 
 disease. The chief alterations which have been described 
 have, however, been situated in the cortical parts of these 
 organs, while it is known that adrenahn is the product of the 
 medulla ; but Josue has shown that substances obtained from 
 the cortex, though not adrenahn, have also a hypertonic action 
 upon the vessels, and maintains that cortical hj^perplasia, 
 however it may act, whether by some reaction preparatory 
 to the secretion of adrenalin by the meduUa, or by its own 
 effects, is an index to the activity of the gland as a whole. 
 
 Thayer* has pointed out that the blood-pressure is often 
 elevated following an attack of enteric fever, and states that 
 the average systolic pressure in such individuals is appreciably 
 higher than that of healthy individuals of the same age, and 
 that the radial arteries are palpable nearly three times as 
 often as they are in health}^ persons who have never had the 
 disease. It is difficult to understand vihj this should occur, 
 as the blood-pressure during an attack is low, and tends to 
 fall rather than to rise. The small arteries, however, are not 
 infrequently affected in the acute infections [vide p. 48), and 
 the lesions are often associated with microscopic damage to 
 the viscera (submiliary nodules in the heart, focal necrosis 
 in the liver, cellular collections in the kidneys, etc.), and 
 although the separate lesions are individually negligible, 
 their collective result in cases where they are "wddespread may 
 be considerable, and may lead to such an increas^e of the 
 peripheral resistance that an elevation of the blood-pressure 
 is produced. 
 
 * Amer. Journ. Med. Set., 1904, vol. cxxvii., p. 391 ; Johns Hopkins Hosp. 
 Bull, 1904, vol. XV., p. 323. 
 
THE DISEASES OF THE ARTERIES 41 
 
 Hypertrophy of the media, and probably of the adventitia 
 as well, ensues as the natural sequel of the increased work 
 imposed upon the vessels, but there is a very fine distinction 
 Ibetween the degree which induces hypertrophy and that 
 which initiates degenerative changes; and "sooner or later 
 the body meets with circumstances in which either the nutri- 
 tion is not maintained, or the stimuli acting on the media 
 hecome greater than can be sustained " (Klotz), and degenera- 
 tive changes ensue with atrophy of the "noble" muscular 
 •cells, and hypertrophy of the less highly speciahzed connective 
 tissue according to the usual rules. The causes of the in- 
 timal thickening, when it occurs, may be similar, or it may 
 I)e due to continued irritation by toxic materials in the blood- 
 stream. 
 
 2. The Focal Lesions — Atheroma {Endarteritis nodosa vel defor- 
 mans). — Atheromatous patches are almost invariably present in 
 the arteries of elderly persons, though, of course, their number, 
 .«ize, and distribution vary in different cases. The patches are 
 ■elevated above the surface with more or less abrupt edges, and 
 <even in small vessels rarely involve the whole circumference. 
 Sometimes they are mere pin-points, sometimes plaques as 
 large as a shilling, and they may, by coalescence, involve 
 ■comparatively large areas. In the early stages th.ey are soft 
 and gelatinous and translucent; in the later stages opaque 
 And fu-m, or hardened by calcareous deposits. Ulceration 
 is not uncommon, and thrombi may be deposited upon 
 them. 
 
 It is generally agreed that the first portions of the aorta are 
 axLost often involved, but there is a difference of opinion as to 
 the frequency with which the other arteries are affected, 
 ' The coronary arteries of the heart, the cerebral and the 
 peripheral arteries, are, however, affected more often than 
 those of the abdominal viscera, and the pulmonary arteries are 
 but seldom damaged, save in cases of clironic pulmonary or 
 cardiac valvular disease. 
 
 The early lesions are found in the deeper layers of the intima 
 (Fig. 25), but in advanced examples the whole thickness of 
 the wall is found, on microscopic examination, to be involved, 
 though the degree to which each layer is affected varies in 
 
42 DISEASES OF THE HEART 
 
 different cases. The intima is always thickened, often greatly^ 
 and in the early stages is very cellular, the elastic tissue- 
 sharing in the hj^erplasia. In the later stages degeneration 
 occurs, and fatty, granular, mucoid, hyahne, or calcareous 
 changes may be found, always most extreme near, though not 
 necessarih" next, to the outer margin of the coat. The media- 
 
 FiG. 25.— Early Atheroma, (x 40.) 
 The intima alone is thickened; elastic stain. 
 
 is atrophied often to a notable degree, and may be entirely'' 
 destroj^ed, and its elastic tissue may be excessive and de- 
 generate. The adventitia as a rule is less abnormal than the 
 other coats, but it is sometimes grossly affected. In early 
 cases it is thickened and very cellular, with httle foci of mono- 
 nuclear ceUs scattered here and there. In older examples 
 it is distinctly sclerosed, and the new-formed tissue is more 
 or less degenerate. Here, too, as in the intima and the media, 
 elastic hyperplasia and degeneration may be distinct. The 
 
THE DISEASES OF THE ARTERIES 43 
 
 vasa vasorum often show gross disease, the arteries being 
 affected by an endarteritis obhterans, and the veins may show- 
 thickening of their coats. 
 
 Patchy Mesarteritis.* — ^The naked-eye appearance of this 
 form resembles in some degree the atheromatous lesions. The 
 patches in the early stage are elevated and soft, and have a 
 
 Fig. 26. — Syphilitic Mesaoetitis. (x 150.) 
 
 The vasa in the adventitia show endarteritis obliterans, and are surrounded by 
 many mononuclear cells. 
 
 greyish gelatinous appearance, and are generall}^ most 
 numerous in the first (ascending) part of the aorta. In older 
 cases they are tough and fibrous and pearh^ white, and may 
 present a depressed, stellate-shaped scar (Fig. 11). Calcareous 
 deposits are infrequent, and are never massive, and ulceration 
 does not occur. 
 
 * The description of these lesions is based upon the syphilitic form. 
 
44 DISEASES OF THE HEART 
 
 The microscopic picture is characteristic. In Ihe early 
 stage the vasa in the adventitia are surrounded b}- clumps of 
 mononuclear cells, and their walls are infiltrated and thickened, 
 and their lumen is narrowed (Fig. 26). The media shows areas 
 of necrosis (Fig. 27), into which new-formed branches of the 
 vasa penetrate, surrounded by a Yerj cellular granulation 
 tissue; and the intima is thickened and cellular opposite the 
 
 Fig. 27. — Syphilitic Mesaortitis, showing a Patch of Necrosis ix the 
 
 Media. (x90.) 
 
 patch. In older specimens the adventitia is thickened and 
 sclerosed, and the vasa maj^ be almost completely obstructed; 
 the media may have disappeared complete^ in places and 
 be replaced by new-formed connective tissue (Fig. 29), and 
 the intima, invaded by the vasal branches, though thickened to 
 a greater or a less degree, may show some cicatricial slu-inking. 
 
 Endarteritis Obliterans. — Endarteritis obliterans occurs 
 chiefly in the smallest arteries and the arterioles; it is often 
 
Fig, 28. — Syphilitic Mesaortitis (Elastic Stain), showing the Degenera- 
 tion OP THE Elastic Tissue in a Gkantjlomatous Patch. ( x 90.) 
 
 Fig. 29. — Syphtlitio Mesaortitis (Elastic Stain), (x 8.) 
 The media (the thick black iJne) is completely destroyed in two places. 
 
46 
 
 DISEASES OF THE HEART 
 
 present in the cerebral arteries and in the vasa of the aorta 
 It is always local in its distribution, and never involves more, 
 than a short length of a vessel, but as the whole circumference 
 of the wall is involved, the lumen is always narrowed and 
 sometimes completely blocked, and its clinical importance is, 
 in consequence, considerable. 
 
 The intima is always greatly thickened, the new-formed con- 
 nective tissue being in the early stage loose and very cellular, 
 
 Fig. 30. — Endarteritis OsLiTEEAisrs. ( x 150.) 
 (From a case of acute rheumatism.) 
 
 with much hypertrophy of the elastic elements, (Fig. 30), 
 but in the later stages poorly nucleated and hyahne, with 
 degeneration of the new-formed elastic fibres. The tnedia 
 may be but little altered or definitely atrophied. The adven- 
 titia is always thickened, sometimes to an extraordinary degree 
 (Fig. 31), and, like the intima, shows new formation of elastic 
 tissue. The relative thickness of the intima and the adven- 
 
THE DISEASES OF THE ARTERIES 47 
 
 titia varies considerably in different cases, and sometimes one, 
 sometimes the other, shows the greater change. Gross fatty 
 or calcareous degeneration is rarely met with. 
 
 Medial Calcification. — ^Medial calcification occurs in two 
 forms. In those cases of atheroma in which extensive calci- 
 fication of the thickened intima has occurred, the medial layers 
 in the immediate vicinity may be similarly affected. It also 
 
 Fig. 31. — Syphilitic Endaeteeitis Obliterak-s. (x 90.) (A. W. H.) 
 The adventitia is greatly hypertrophied. 
 
 occurs, however, in a widespread manner, though stiU patchy 
 in distribution, mthout any, or with only minimal, alterations 
 in the intima. In this case it is most often found in the 
 peripheral arteries, and is readily detected during life by the 
 finger, which, as it runs along the vessel, meets now a hard 
 and now a soft patch (Fig. 32). The vessels are frequently 
 dilated. On microscopic examination in well-marked cases 
 the proper structure of the media has wholly disappeared, and 
 
48 
 
 DISEASES OF THE HEART 
 
 is replaced by a mass of calcareous granules, often welded 
 together and encircling the vessel. In the larger vessels the 
 whole of the circumference is rarely affected. 
 
 The Etiology of Focal Lesions. — Local lesions own a local cause, 
 but it must be admitted that our information as to the precise 
 
 etiology of focal ar- 
 terial disease is at pre- 
 sent imperfect. The 
 distinction between 
 atheroma and patchy 
 mesarteritis is impor- 
 tant. In the former 
 the primary lesion is 
 intimal hyperplasia, 
 and the media atro- 
 phies before the pres- 
 sure of the nodule 
 under the influence 
 of the intra-arterial 
 blood - pressure. In 
 the latter the primary 
 lesion is in the middle 
 coat. Patchy mesar- 
 teritis is most fre- 
 quently due to 
 syphihs, and repre- 
 sents the reaction pro- 
 duced by the invasion 
 of spirochsetes (which 
 have been demon- 
 strated in situ by 
 Schmorl, Burda, 
 Wright, and Klotz), or follows obstruction of the vasa in the 
 adventitia and resultant medial necrosis. But while early 
 lesions may be accuratel}' classified, the ultimate scars are 
 essentially similar, and the question must be approached in a 
 general way. 
 
 Evidence is steadily accumulating in favour of the view 
 that the infections as a w^hole are a not uncommon cause cf 
 
 Fig. 32. — Medial Calcification-. (J. E. R.) 
 Skiagram showing the ulnar and radial arteries. 
 
THE DISEASES OF THE ARTERIES 49 
 
 focal lesions. It has been known for long that in cases of 
 pysemia patches similar in their nature to those sometimes 
 found on the valves of the heart may be present on the arterial 
 walls, and that an infective arteritis may occur by extension 
 from a neighbouring infective focus (Fig. 129). As a rule, 
 however, bacteria are not found in early specimens of 
 atheroma, and spirochaetes also are usually absent in cases of 
 syphihtic disease, but tubercle baciUi, pneumococci, anthrax 
 baciUi, streptococci, and staphjdococci have all been found in 
 exceptional cases. Usually the infection takes place from the 
 blood-stream, but an embolic origin is conceivable, and an 
 acute mesarteritis has been observed in acute rheumatism, 
 enteric fever, and diphtheria. Plaques of recent atheroma 
 are often present in the aortas of individuals who have died 
 from acute disease. They have been reported in cases of 
 smallpox, diphtheria, erj'sipelas, pneumonia, acute rheumatism, 
 influenza, scarlatina, measles, and enteric fever, being present 
 in the latter in twenty-one of fifty-two 'post-mortems (Thayer 
 and Brush). Experimental research, too, has shown similar 
 results, and intimal changes have been produced by inocula- 
 tions with streptococci, medial changes with diphtheria toxin 
 and the Micrococcus rheumaticus, and intimal and medial 
 ■changes in conjunction with staphylococci. 
 
 Josue's experiments with adrenalin have opened out a new 
 field of observation. He showed that repeated injections 
 of this drug into rabbits produced local thinning and calcifica- 
 tion of the aortic media with, in some cases, a local thickening 
 •of the overlying intima; and his results have been confirmed 
 by numerous observers. Other drugs, too, of similar h\-per- 
 tonica ction (nicotine, digitahn, hydrastine, barium chloride) 
 have also been shown to produce similar results, and Croftan 
 'has produced various lesions in the vessels with solutions 
 of xanthin and hj-poxanthin. 
 
 The exact mechanism of these procedures is not 3'et under- 
 stood, but Klotz has sho^vn that medial calcification may 
 follow an increase of the blood-pressure produced by suspending 
 rabbits by the hind-legs for short periods over mam- daj^s, 
 the lesions being confined to those vessels (carotids and aorta) 
 in which the blood-pressure was raised, and absent in those 
 
50 DISEASES OF THE HEART 
 
 below the diaphragm ; atheromatous lesions, too, were 
 found in the carotid arteries, which suggests that both medial 
 and intimal lesions maj- result from elevation of the blood- 
 pressure. 
 
 Although it is not difficult to demonstrate the various ways 
 in which focal lesions may be produced, it is not easy to define 
 their actual causes, taking into consideration their frequency 
 in persons over middle age and their special sites of election 
 in the arterial tree. 
 
 The frequency with which the}^ occur makes it evident that 
 some of the possible causes which we have considered have 
 but little to do with their origin. Tuberculosis and syphilis, 
 for example, must be ruled out of court, for these diseases, 
 though prevalent enough, are by no means universal. The 
 infections as a Avhole can hardly be responsible for many cases . 
 It is true that acute arterial lesions are not infrequently met 
 ^^dth in these diseases, but post-mortein records show that gross- 
 changes are, on the whole, uncommon, and that when present 
 they are rarely extensive. The frequency, however, with 
 which infections occur during life, the exanthemata in child- 
 hood, and influenza, pneumonia, enteric fever, etc., in later 
 years make it possible that their influence is greater than has 
 been otherwise supposed, and that the little lesions thus 
 initiated may, perhaps, as places of lessened resistance, allow 
 other causes to produce greater results than would otherwise 
 be possible. 
 
 Nodular lesions are not uncommon in cases of diffuse 
 arterio-sclerosis. The lumen of the smaller vessels is often 
 narrowed, and the fibrous overgrowth of the adventitia some- 
 times spreads into the tissues and produces little islets of 
 fibrosis in the viscera, entanghng and destroying the adjacent 
 cells. Any of the organs may be affected, but the heart and 
 the kidneys are chiefly involved. It seems probable that in 
 arterio-sclerosis nodular lesions vnsuj arise in the larger 
 vessels, such as the aorta, from a similar affection of their 
 vasa . 
 
 On the whole, however, the explanations seem insufficient,, 
 and other causes must come into action. 
 
 The special distribution of the focal lesions has long been 
 
THE DISEASES OF THE ARTERIES 51 
 
 held to indicate that mechanical irritation plays an important 
 part in their etiology. The buttressing of particular parts 
 of the arterial system shows that special stress obtains at these 
 special points even in normal circumstances ; and certain 
 vessels, such as the corona.ry arteries of the heart, the intes- 
 tinal arteries and those of the limbs, must be more hable to 
 injury than those contained within organs which move but 
 little or are deeply situated. (Pophteal aneurisms, for instance, 
 seem almost to have disappeared with the post-boys, and 
 tortuosity of the temporal arteries is of common occurrence, 
 as it is produced by the pressure of the hat against the skull.) 
 It is true that provision seems to have been made for such 
 varying needs, but the continued slight trauma of the systolic 
 pulse-waves must nevertheless exert an influence which in 
 time will produce damage, and this is most likely to occur in 
 cases where physical labour is the chief occupation. Medial 
 calcification is thus common in the femoral and iliac arteries 
 of persons such as poHcemen, who are constantly standing, 
 and in the brachial and radial arteries of individuals whose 
 work entails continued use of their arms, and is even, according 
 to Klotz, more common on the right side in right-handed 
 persons. The arterial blood-pressure is Mable to many altera- 
 tions from phj^siological influences, and these are almost 
 always in the direction of temporary elevation above the 
 normal. Exercise, the ingestion of food, cerebral excitement, 
 etc., all produce an increase, and this may be considerable 
 if the stimulus is great or frequently repeated, and the proba- 
 bihty of injurious irritation will, under these circumstances, 
 be greater than in normal conditions. 
 
 The form and site of the initial lesion depend upon several 
 factors. In some instances overuse of limbs leads to their 
 special involvement; in other cases the aortic strain may be 
 greatest; in others, again, a previous lesion may suggest a 
 particular site. 
 
 The special HabiHty of the aorta and the cerebral arteries 
 to syphilitic disease has not yet obtained a satisfactory ex- 
 planation, but it maj' be pointed out that their structure is 
 very speciahzed, and that the aorta is exposed to the full 
 force of the ventricular systole, while disease of the cerebral 
 arteries is so prejudicial to the proper working of the brain. 
 
52 DISEASES OF THE HEART 
 
 and even to life itself, that it has probably attracted more 
 than its fair share of attention. 
 
 Endarteritis obhterans is not always of pathological sig- 
 nificance. It occurs, for instance, in the umbiHcal vessels after 
 their special function has ceased ; in the ^vessels of a stump 
 after amputation; and in arteries whose lumen has been 
 narrowed or obstructed by any cause, the normal proliferative 
 changes exceeding the degree which is required. 
 
 It is of common occurrence in the infections, and has 
 been found in acute rheumatism, diphtheria, scarlatina, 
 smallpox, and enteric fever. It is particularly frequent in 
 tuberculosis of the cerebral membranes and in syphilis, the 
 adventitial changes in the latter case being usually extreme. 
 
 Medial calcification is most frequently associated with 
 mechanical sources of irritation. 
 
 1. Arterio-Sclerosis. — A diffuse affection involving the whole 
 
 arterial tree. 
 
 Caused by High Blood-Pressure: 
 
 {a) Associated with renal disease. 
 
 (6) From "repletion," relative or absolute. 
 
 (c) From intoxications due to — 
 
 (1) Metabolic errors; gout, digestive disturb- 
 
 ances, etc. 
 
 (2) Poisons introduced from without — lead, 
 
 nicotine, etc. 
 
 (d) Following the infections. 
 
 (e) In polycythsemia. 
 
 2. Focal Lesions. — A patchy affection involving small por- 
 
 tions of the arteries. 
 {a) Infective Lesions: due to staphylococci, strepto- 
 cocci, B. anthrax, B. tuberculosis, Spirochceta 
 pallida. 
 (6) Without Definite Evidence of Infection: 
 (1) Atheroma, caused by — 
 
 (i.) The infections: Enteric fever, tuber- 
 culosis, diphthjeria, smallpox, 
 measles, scarlatina, erysipelas, pneu- 
 monia, acute rheumatism, influenza. 
 
THE DISEASES OF THE ARTERIES 53 
 
 (ii.) Intermittent elevation of the blood- 
 pressure. 
 
 (2) Mesarteritis, caused by — 
 
 Syphilis, acute rheumatism, enteric fever, 
 diphtheria . 
 
 (3) Endarteritis obliterans, caused by — 
 
 (i.) Syphilis, tuberculosis, acute rheu- 
 matism, diphtheria, scarlatina, 
 smallpox, enteric fever. 
 
 (ii.) Occlusion of the lumen from whatever 
 cause. 
 
 (4) Medial Calcification, caused by — 
 
 (i.) Trauma (excessive use of limbs, inter- 
 mittent or continuous elevation of 
 the blood-pressure), 
 (ii.) Adrenalin, nicotine, digitalin, hydras- 
 tine, barium chloride. 
 
 REFERENCES. 
 John Cowan: 
 
 A Review of Recent Work upon Blood-Pressure. Practitioner, 1904, 
 
 vol. Ixxiii., p. 218. 
 The Current Theories regarding the Causation of Arterio-Sclerosls. Ibia., 
 1905, vol. Ixsv., p. 203; ihid., 1906, vol. Ixxvi., p. 317; ihid., 1909, vol. 
 Ixxxiii., p. 614; ihid., 1911, vol. Ixxxvi., p. 750. 
 The Influence of the Acute Infections upon the Arteries. Glasgow Med. 
 Joum., 1906, vol. Ixvi., p. 88. 
 Louis Galiavaed in: La Tension Arterielle en Clinique. Paris, 1910. 
 H. Hitohakd: Arterio-Sclerose. Paris, 1910. 
 
 T. C. Janeway: The Clinical Study of Blood- Pressure. New York, 1904. 
 O. Josue: Traite de I'Arterio-Sclerose. Paris, 1909. 
 O. Klotz: Arterio-Sclerosis. Diseases of the Media. Publications from th e 
 
 University of Pittsburgh Medical School, 1911. 
 W. Russell: Arterial Hypertonus. Edinburgh, 1907. 
 
CHAPTER III 
 THE SYMPTOMS OF ARTERIAL DISEASE 
 
 The symptoms of arterial disease vary greatly in different 
 patients, as they depend both upon the variety of the arterial 
 lesion and upon its special site, and are, in the majority of 
 cases, the results of defective function of the various viscera 
 rather than an indication of the process which has produced 
 them. The symptoms of an aneurism, for example, arise 
 chiefly from pressure upon neighbouring structures, and tumour 
 and pulsation are the only evidence of the arterial dilatation. 
 
 The two main groups of arterial disease contrast in almost 
 every particular. In the focal or nodular group the lesions 
 are always local and never of great size, although they may be 
 numerous, and by coalescence affect considerable tracts of the 
 vessels. The larger arteries are chiefly involved. In atheroma 
 and mesarteritis the wall is weakened, and dilatation of the 
 vessel, or even rupture, may ensue. In medial calcification 
 the artery is often wider than normal. In endarteritis 
 obhterans the arterial lumen is narrowed, and thrombosis 
 often follows, a result which is unusual in the others. 
 
 In arteriosclerosis, on the other hand, the whole of the 
 arterial tree is involved, and the change is most considerable 
 in the smaller vessels. The walls are thickened and on the 
 whole strengthened, so that dilatation or rupture is uncommon 
 fcT.ve in the cerebral arteries, where miliary aneurisms, the 
 common cause of cerebral haemorrhage, are often found. 
 Thrombosis is comparatively rare, but the lumen is generally 
 narrowed, and the visceral blood-supply may be hmited in 
 consequence. 
 
 The focal lesions may be widespread, and even extreme, 
 without causing any abnormal strain uponjthe left ventricle. 
 
 54 
 
THE SYMPTOMS OF ARTERIAL DISEASE 55 
 
 In other cases, however, where the thoracic aorta or the 
 splanchnic arteries are involved, the left ventricle may be 
 considerably hypertrophied. In arterio-sclerosis, on the other 
 hand, the left ventricle is always hypertrophied, sometimes to 
 an extraordinary degree; and, as in valvular disease, the 
 reserve power is necessarily more limited than in health, and 
 the " field of response " is correspondingly diminished. The 
 essential cause of arterio-sclerosis is continued elevation of the 
 arterial pressure, and the arteries as well as the heart are at 
 first thickened by muscular hjrpertrophy. In time, however, 
 fibrosis supervenes, and their elasticity is largely lost. 
 
 One must distinguish between the two types of arteries. 
 One set are the " mains " for the distribution of the blood, 
 affording an elastic assistance to the heart, and insuring a con- 
 tinuous flow, at equable pressures, through the capillaries. 
 The other set are the "supply-pipes," with "taps "which can 
 be shut, at any rate partially, and thus alter the distribution 
 of the blood among the various organs as necessity dictates. 
 If the mains are rigid, the heart has more work to do, and the 
 capillary current is less even in its flow. If the supply-pipes 
 are stiff, the " taps " cannot be altered at discretion, and 
 variations in the functional demands of the tissues can only be 
 inadequately supplied, and that by variations in the general 
 blood-pressure and an increased strain upon an already over- 
 taxed ventricle. 
 
 The symptoms in the two groups arise in different ways. 
 In the focal cases they are the results of hcemoirhage, thrombosis, 
 or arterial dilatation. The results of haemorrhage vary mainly 
 ■with its amount, and also, to some extent, with its site, cere- 
 bral haemorrhage, for instance, causing death with a loss of 
 blood which, if external, would occasion little, if any, discom- 
 fort. The results of thrombosis depend both upon its site 
 and upon the rapidity of the closure; sudden occlusion of a 
 coronary artery may produce myocardial infarct or rupture 
 of the heart, while a gradual narrowing may allow of com- 
 pensatory dilatation of anastomotic vessels, with but little 
 interference with the nutrition of the cells involved. The 
 results of dilatation depend mainly upon its extent and its 
 site, and are most marked when it obtains within a cavit}- of 
 
56 DISEASES OF THE HEART 
 
 fixed dimensions- — e.g., within the cranium or the thorax. 
 The lesions which are thus produced are as a rule isolated and 
 single, though sometimes of considerable size. 
 
 In arteriosclerosis visceral lesions are widespread, multiple, 
 and individually of trifling degree, though their collective in- 
 fluence may be great. Dilatation and haemorrhage are un- 
 usual, save in the case of the cerebral arteries, and thrombosis 
 is also infrequent. But the lumen of the vessels is often 
 narrowed, and the visceral blood-supply is in consequence 
 diminished — an effect which is intensified by the limitation of 
 the response to vasomotor influences entailed by the fibrosis 
 of the vessel walls. This fibrosis, too, not infrequently spreads 
 into the tissues from the adventitia, and produces little islets 
 of fibrosis in the organs, entangling and destroying the ad- 
 jacent cells. Any of the viscera may be involved, but the 
 heart and the kidneys are the common sufferers . Renal changes 
 are the rule in arterio-sclercsis. The initial fault is often 
 renal, a cirrhosis of acute or chronic type; and a somewhat 
 similar condition, the arterio-sclerotic kidney, is generally more 
 or less evident in cases which have arisen from other than renal 
 fault. 
 
 The symptoms of the two groups contrast correspondingly. 
 In the focal group aneurism, infarct, and haemorrhage are 
 the essential conditions. In arteriosclerosis the heart is 
 always overtaxed, renal excretion is generally inadequate, and 
 other viscera are apt to be damaged ; while their function is still 
 further impaired by the limitation of their blood-supply pro- 
 duced by the arterial disease and the relative cardiac insuffi- 
 ciency. At first symptoms only occur on special strain, 
 whether physical, mental, or visceral ; but ultimately even the 
 normal work is imperfectly performed. The onset of symptoms 
 is thus insidious, unless some special cause precipitates their 
 advent. In the focal group symptoms often ensue suddenl}^, 
 and are acute from the outset. 
 
 "^ From yet another standpoint the two groups contrast. The 
 causes of the first group are numerous, syphihs, tuberculosis, 
 trauma, intoxications, and infections of various kinds; and 
 while some of these may be continuous in their action, others 
 have only a hmited period of harmful activity. Focal lesions 
 
THE SYMPTOMS OF ARTERIAL DISEASE 57 
 
 may thus be progressive or merely the healed scars of ancient 
 wounds. Arterio-sclerosis, on the other hand, is due to con- 
 tinued high arterial pressure; and although in some cases the 
 initial elevation is probably of functional origin, and so re- 
 movable on removal of its cause, in others it is secondary to 
 visceral lesions which are incurable. When once permanent 
 changes have occurred in the vessels, the high pressure is per- 
 manent ; the strain upon the heart and vessels continues ; and, 
 as time goes on, the lesions inevitably progress. 
 
 The symptoms in arterial disease may thus be produced in 
 various ways, and as they may be related to almost any organ, 
 and may simulate even closely symptoms due to other patho- 
 logical lesions, their exact significance may be difficult to 
 determine. This is particularly the case with the focal 
 diseases. In arterio-sclerosis the under Ijdng general condi- 
 tion can in most cases be readily recognized. 
 
 The essential and constant feature in arterio-sclerosis, at 
 any rate until cardiac failure is weU marked, is elevation of the 
 aortic blood-pressure. In a large group of cases, renal cir- 
 rhosis occurs, if not antecedent to, at least pari passu with, the 
 cardio-vascular changes which are compensatory and per- 
 manent. Sometimes the cardio-vascular hjrpertrophy is not 
 well marked, and death then seems to ensue more rapidly than 
 is the rule when the hypertrophy is considerable. The cause of 
 the failure may he in anaemia and debihty consequent on the 
 renal disease or other coincident causes, but is sometimes, at 
 any rate, congenital in origin. We cannot all of us become 
 Sanclows, even if we follow a similar hne of training, and the 
 vascular musculature is in many w^ays comparable to the 
 muscles of the hmbs. 
 
 But in another group of cases, as Sir Chfford Allbutt has 
 urged, no renal disease at first coexists. The primary fault is 
 an intoxication of varied origin, w^hich produces an increase 
 of the peripheral resistance, and consequent elevation of the 
 aortic blood-pressure; but an elevation which at first depends 
 upon removable causes, and can thus for a time be dissipated 
 by suitable treatment. "^ 
 
 The recent introduction into clinical methods of the Riva- 
 
58 
 
 DISEASES OF THE HEART 
 
 Rocci sphygmomanometer and its numerous modifications has 
 put within the reach of the practitioner a method by which the 
 arterial pressure may be measured with fair accuracy, and 
 without any special difficulty of technique. But while it is 
 
 12Q, 
 
 7' 
 
 
 ■ -VlAU ^AA^AVMUJ\f^MM/J^'^~VJ 
 
 VlWMAMMWWMMl 
 
 Aortic 
 
 Fig. 33. — Blood-Pkessure Tracing (Gibson Sphygmomanometer) 
 
 Regurgitation. 
 
 The pulse is much larger than in Fig. 34, though the systolic blood-pressure is 
 much lower. The pulse-pressures are equal. 
 
 useful to have figures which can be contrasted, and give a 
 measure in some way of the severity of the disturbance, it 
 must be remembered that the blood-pressure varies to a con- 
 siderable extent in the healthy individual from causes of a 
 temporary and often trivial nature (emotion, exercise, diet, 
 
THE SY^IPTOMS OF ARTERIAL DISEASE 
 
 59 
 
 ■NW^ 
 
 
 Fig. 34.— Blood-Pressuee Tracing (Gibson Sphygmomanometek): 
 Chronic Nephritis, 
 
 Contrast with Fig. 33. 
 
 etc.), the influence of which cannot always be accurately 
 correlated, and that similar results may be noted even in well- 
 marked examples of high blood-pressure. The earlier readings m 
 
60 DISEASES OF THE HEART 
 
 hospital patients confined to bed are often shown by continued 
 observation to be inaccurate, from causes of this temporary 
 kind, and but little importance should be attached to isolated 
 observations, though daily records are of considerable value. 
 
 The information which is desired can, too, be obtained from 
 other data. Digital examination of the pulse is at the present 
 day too much depreciated ; and while I must acknowledge that 
 my impressions of the arterial pressure from, such exam.inations 
 have not infrequently been at variance with instrumental 
 readings, a constant comparison has led to greater accuracy. 
 The error seems to Me in the failure to appreciate that the 
 size of the pulse-wave and the amount of the pulse-pressure* 
 have no constant relation to the height of the aortic pressure; 
 to take a concrete example, the large quick pulse of aortic 
 regurgitation may be of much lower pressure than a small 
 but wir}- pulse (Figs. 33, 34). 
 
 The sphj'gmomanometer, too, gives no information with 
 regard to the condition of the arterial walls, information which 
 is readily afforded by the finger; and if all the accessible 
 arteries (retinal, radial, brachial, temporal, facial, femoral, 
 dorsahs pedis) are explored, a fairlj' accurate idea of the con- 
 dition of the vessels as a whole may be obtained. It is true 
 that the condition of the peripheral and the visceral vessels 
 by no means always corresponds, and changes may be extreme 
 in one set without the other being seriousty involved, but on 
 the whole the comparison is apt . The failure in correspondence 
 is seen chiefly in the focal lesions ; in arterio -sclerosis the asso- 
 ciation is more absolute, so that, while irregularities in the 
 vessel walls convey only a hmited significance, general thicken- 
 ing is always important. The ophthalmoscopic evidence may 
 be unmistakable. 
 
 Examination of the heart is, of course, equally essential. 
 A weU-sustained apex impulse displaced downwards into the 
 sixth or seventh interspace, prolongation and cluUing of the 
 first apical sound, and accentuation of the second aortic sound 
 are, in the absence of valvular flaws, positive evidence of high 
 aortic blood-pressure. The second aortic sound may be in- 
 
 * The pulse-pressure is the difierence in pressure between the systolic and 
 the diastolic pressures. 
 
THE SYMPTOMS OF ARTERIAL DISEASE 
 
 61 
 
 toned and ringing in quality, but this is probably due to aortic 
 dilatation, whether local or diffuse. 
 
 It is easy to recognize such cases when they come under 
 observation from casual reasons, such as insurance examination, 
 etc., at a time when the compensatory mechanism is well 
 estabhshed and sufficient, and symptoms are in abeyance, but 
 an accurate diagnosis may be extremely difficult in the later 
 stages if cardiac failure has supervened. The blood-pressure 
 may be within normal limits, the second aortic sound may not 
 be notably emphatic, and the first apical sound may be short 
 and sharp, or obscured by murmur if the mitral valve has 
 given way before the strain. 
 
 Cardiac hypertrophy is not necessarily associated with high 
 arterial pressure. In well-compensated cases of mitral regur- 
 gitation and aortic stenosis, for example, the degree of ven- 
 tricular hypertrophy is simply that required to insure the 
 
 Fig. 35.— Pulse of Aortic Regurgitation. 
 
 entrance into the aorta, in the proper time, of the proper 
 amount of blood at the proper pressure. In aortic regurgita- 
 tion other factors come into operation. If an average amount 
 of blood is to be left in the arteries at the end of diastole, the 
 amount which is thrown into them during systole must be 
 greater than normal, so as to allow for that which returns into 
 the ventricle as soon as systole has ceased ; and the rapid fall 
 of pressure during diastole requires an excessive systolic 
 pressure. The pulse-pressure is the true index of the degree 
 of the mechanical fault. But such a pulse differs notably from 
 that associated with granular kidneys , In aortic regurgitation, 
 as sphygmographic tracings show so well (Eig. 35), the pressure 
 faUs rapidly, and the mean pressure is low relatively to the 
 maximum. In renal cases the pressure is well maintained, 
 and the mean pressure is high relatively to the maximum. 
 A high blood-pressure is not invariably evidence of cardiac 
 
62 
 
 DISEASES OF THE HEART 
 
 sufficiency, and may, indeed, be accompanied by definite signs 
 of cardiac failure. The most striking example which I have 
 observed occurred in a man, aged fifty-one, who was com- 
 plaining of breathlessness and slight oedema of the feet. The 
 sudden occurrence of a left facial pals}^, accompanied by some 
 difficult}^ in speech, followed a few days later by a partial 
 right hemiplegia, was considered to be the result of cerebral 
 haemorrhage, as the systohc brachial pressure varied from 
 170 to 210 mm. Hg. But 'post-mortem examination revealed 
 
 DEC. 
 
 Hg. 
 mm. 
 
 200 
 190 
 180 
 170 
 160 
 150 
 140 
 130 
 120 
 no 
 100 
 90 
 80 
 70 
 
 12 
 
 14 
 
 W 
 
 18 
 
 21 
 
 23 
 
 25 
 
 27 
 
 30 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 \ 
 
 \ 
 
 
 
 
 
 
 •^ 
 
 --^ 
 
 
 \ 
 
 
 
 
 
 
 
 \ 
 
 N. 
 
 V 
 
 N 
 
 
 
 
 
 
 
 \ 
 
 
 
 ^ 
 
 ^^ 
 
 
 
 
 
 \ 
 
 
 
 
 \ 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 V. 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 Fig. 36. — Blood-Pressure Chart. 
 
 M., aged 47: Chronic nephritis, bronchitis; 
 steady improvement. 
 
 2 
 
 12 
 
 26 
 
 
 
 
 
 
 
 
 
 
 Steady 
 Progress 
 
 / 
 
 
 J 
 
 f 
 
 
 / 
 
 E 
 
 / 
 
 
 
 
 
 .g^ 
 
 
 
 
 ^ 
 
 ^ 
 
 
 
 
 k 
 
 
 
 
 fEB 
 
 Hg. 
 mm. 
 
 170 
 
 IGO 
 
 150 
 
 140 
 
 130 
 
 120 
 
 no 
 
 100 
 
 90 
 
 80 
 
 70 
 
 Fig. 37.— Blood-Pres- 
 sure Chart, 
 
 M., aged 57: Aortic val- 
 vular disease; steady 
 improvement. 
 
 in the cortical vessels multiple emboli which were derived from 
 clots in the dilated left ventricle. And the highest pressure 
 which I have observed — 270 mm. Hg — occurred in a man 
 who became breathless on the least exertion, and developed 
 oedema in the feet and legs whenever he v/as allowed out of 
 bed. 
 
 Such failure is, of course, relative and not absolute. The 
 ventricular waU may be greatly thickened, and the cells may 
 be normal on microscopic examination, but the heart may yet 
 be overtaxed and unable to accomphsh its necessary work. 
 
THE SYMPTOMS OF ARTERIAL DISEASE 
 
 63 
 
 Cardiac strain may arise in two different ways. The heart 
 may be unable to overtake extra work imposed upon it, or 
 may from intrinsic causes (fibroid, fatty degeneration, etc.) 
 be unable to accomplish even a normal amount. The arterial 
 pressure may thus vary either upwards or downwards in the 
 presence of symptoms, and it may be impossible for a time 
 to say whether the actual pressure is too high or too low for 
 the particular individual. If improvement occurs, the 
 pressure may rise or fall; as death approaches, it may also 
 rise or fall. In Fig. 36 the pressure is seen to faU coincidently 
 
 APRIL 1908 MAY JUNE 
 
 23 
 
 24 
 
 25 
 
 26 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 / 
 
 
 r 
 
 ^ 
 
 
 / 
 
 
 
 
 
 
 y 
 
 V 
 
 y 
 
 ^ 
 
 
 
 NOV 
 
 Hg. 
 mm. 
 
 170 
 160 
 150 
 140 
 130 
 120 
 110 
 100 
 
 90 
 
 80 
 
 70 
 
 Fig. 38.— Blood. 
 
 Presstjre Chart. 
 
 M., aged 40 : Alcohol- 
 ism ; pneumonia. 
 Death on Novem- 
 ber 26. 
 
 Hg. 
 mm. 
 
 170 
 160 
 150 
 KO 
 130 
 120 
 110 
 100 
 90 
 80 
 70 
 
 F., 
 
 J7 
 
 25 
 
 29 
 
 7 
 
 29 
 
 8 
 
 13 
 
 17 
 
 28 
 
 3 
 
 8 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 V 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 A 
 
 
 
 
 
 
 
 
 
 
 V 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 \ 
 
 
 
 
 
 
 *v. 
 
 
 
 
 
 V 
 
 "-v^ 
 
 
 ^^ 
 
 ^ 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 
 
 \^ 
 
 ^\ 
 
 < 
 
 _a^ 
 
 ^^ 
 
 — 
 
 
 
 
 
 
 
 
 V 
 
 .'•^ 
 
 
 
 Fig. 39. — Blood-Pressure Chart. 
 aged 35 : Mitral disease. Death on July 23. 
 
 with improvement in the general condition; in Fig. 37 the 
 pressure rose with improvement; in Fig. 38 the pressure rose 
 as death approached; in Fig. 39 it fell. 
 
 The blood-pressure may be elevated for a time independently 
 of arterial or renal disease. Fig. 40 shows the blood-pressure 
 in a man, aged thirty-eight, who was an iron-moulder by trade. 
 He had always been healthy, save for an attack of pneumonia 
 at the age of twenty-three, but had caught cold a fortnight 
 before admission, though this had not kept him away from 
 
64 
 
 DISEASES OF THE HEART 
 
 MARCH WOS 
 
 work. Ten days later he noticed that his eyelids were swollen 
 in the morning, but the swelling disappeared as the day wore 
 on; his back, he said, was sore when he stooped. He had a 
 headache next day, and his feet were swollen at night. On 
 admission, all these symptoms had lessened. There was a 
 trifling albuminuria, and a little oedema in the legs below the 
 knees, but the latter soon disappeared. The urinary output 
 was always ample, and the albuminuria was trifling, and some- 
 times absent. But it was eight days before the pressure fell 
 
 within normal limits, 
 and three weeks more 
 before the minimum 
 reading was recorded. 
 There was no evidence 
 otherwise of organic 
 disease, and the eleva- 
 tion of blood-pressure 
 was presumably toxic 
 in origin. 
 
 High blood - pres- 
 sure per se is thus no 
 certain evidence of 
 arterio-sclerosis, as it 
 may be due to tem- 
 porary causes, and 
 obtains in some forms 
 of valvular disease of 
 the heart. In the 
 absence of aortic re- 
 gurgitation, however, 
 its indefijiite persistence despite treatment, and the presence 
 of hypertrophy of the left ventricle, are extremely suggestive 
 of the disease. Widespread focal lesions in the thoracic aorta 
 or the splanchnic arteries are the only other factors which can 
 produce such a condition. 
 
 The apex impulse is an uncertain guide in some cases of 
 arterio-sclerosis. It may be hidden by pulmonary emphysema, 
 which not infrequently ensues in arterio-sclerotic cases. It 
 may be weak, diffuse, and ill-sustained if cardiac failure has 
 
 Hg. 
 mm. 
 
 210 
 200 
 190 
 160 
 170 
 160 
 150 
 140 
 130 
 120 
 no 
 100 
 90 
 80 
 70 
 
 18 
 
 20 
 
 22 
 
 25 
 
 26 
 
 30 
 
 31 
 
 8 
 
 16 
 
 19 
 
 23 
 
 
 
 
 
 
 
 
 
 
 
 
 — ♦— 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 
 > 
 
 V 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 
 
 L 
 
 A 
 
 
 
 
 
 
 
 
 
 
 V 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 
 K 
 
 Ni 
 
 
 
 
 
 
 
 
 
 
 
 ^S 
 
 N^ 
 
 ?«*s; 
 
 ^^ 
 
 
 
 •v 
 
 5s*-. 
 
 
 
 
 
 
 
 \ 
 
 V 
 
 
 
 A 
 
 V 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 
 
 V 
 
 
 
 
 . 
 
 /^ 
 
 ^x 
 
 ^ 
 
 
 
 
 
 
 
 
 
 
 
 Fig. 40. 
 
 -Blood-Pkessube Chakt. 
 M., aged 38. 
 
THE SYIVIPTOMS OF ARTERIAL DISEASE 65 
 
 supervened; but, on the other hand, may still be punctate, 
 powerful, and well sustained even when oedema is widespread 
 and general. In emphysema the cardiac sounds may often be 
 heard best outside the left border of the cardiac duhiess, even 
 in the axillary line, thus indicating enlargement of the ventricle. 
 
 The cardiac sounds cannot be relied upon. The second 
 aortic sound may be weakened, with failure, to such a degree 
 as to be within normal limits, though it is often distinctly 
 emphatic ; or it may be whoUy obscured by murmur. The 
 special qualities of the first apical sound are often at fault, and 
 it teUs merely of mitral reflux or myocardial weakness. 
 
 In the absence of these data, the condition of the arteries 
 may still be sufficient evidence, and it is here that ophthalmo- 
 scopic examination is so valuable, as the changes are present in 
 the large majority of cases, and persist irrespective of cardiac 
 insufficiency. ^ 
 
 The presence or absence of albuminuria is of little value from 
 the diagnostic point of view. Renal disease is a common 
 accompaniment of arterio-sclerosis, but it may also occur in- 
 dependently. The small red kidney and the arterio-sclerotic 
 kidney are usually associated with an albuminuria which is 
 trifling in degree, and may even be wholly absent, at any rate 
 for a time; and the coincidence of considerable albuminuria 
 indicates the presence of some new factor, such as passive 
 venous congestion or some accidental intoxication or toxaemia. 
 
 The symptoms which are met with in arterio-sclerosis are 
 quite as varied as one would expect from consideration of the 
 pathological lesions. Few of the viscera are absolutely normal, 
 and any one of them may be specially damaged. But the 
 kidneys are almost always more or less involved, and renal 
 excretion is frequently inadequate; and the heart, habitually 
 working close to its maximum power, has a reserve which is 
 but small, and in consequence readily exhausted; so that in 
 practice cardiac and renal symptoms form the bulk of the com- 
 plaints. 
 
 The symptoms which ensue on cardiac failure do not differ 
 appreciably from those that may occur in cardiac insufficiency 
 due to other causes ; shortness of breath, palpitation or other 
 cardiac discomforts, gastro-intestinal disturbances, oedema, 
 
 5 
 
66 
 
 DISEASES OF THE HEART 
 
 etc., are tlie common complaints. In the earlier stages, when 
 the failm-e is slight and relative, the diagnosis is easily made 
 on routine examination; but in the later stages, and in Ihe 
 presence of well-defined valvular flaws, one is apt to miss the 
 
 underlying general condition. 
 Valvular flaws may arise 
 in various ways. Arterio- 
 sclerosis may hit a patient 
 whose heart is already 
 damaged by an acute endo- 
 carditis, or the converse may 
 obtain. Arterio-sclerosis may 
 cause local lesions in the- 
 arteries as well as in the 
 viscera, and the valves may 
 be deformed by a chronic 
 degenerative lesion. The 
 ventricle may give way before 
 the strain, and dilate, with 
 relative mitral insufficiency. 
 French "v\Titers are in the habit 
 of emphasizing this difference 
 in origin of mitral reflux by 
 the statement that in one 
 group the lesion begins at the 
 valves and ends at the 
 myocardium, while in the 
 other it begins in the myocar- 
 dium and ends at the valves. 
 In uncomphcated cases of 
 mitral disease the sequel of 
 rheumatic endocarditis, the 
 blood-pressure is uniformly 
 normal or below normal. It 
 is commonly asserted that 
 the presence of oedema causes variations in the blood-pressure 
 readings from the pressm^e exercised upon the capillary network 
 in the tissues, but my own experience is not consonant with this 
 conclusion. The presence of oedema in the arms, however, inter- 
 
 
 
 
 
 ^ 
 
 
 
 
 
 
 
 CO 
 
 
 
 Co 
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THE SYMPTOMS OF ARTERIAL DISEASE 
 
 67 
 
 JUNE 190R 
 
 fering with the proper apposition of the armlet or the correct 
 appreciation of the radial pulse, of necessity introduces factors 
 which areHkely to prevent accurate records ; but in its absence 
 it is astonishing to find how little variation occurs even in the 
 presence of notable s^-mptoms. In Fig. 41, for example, the 
 systohc pressure only varied from 120 to 95 mm. Hg. diu-ing 
 the course of observations extending over nearly six months. 
 The patient, who was aged thirty, was admitted mth orthop- 
 noea, dropsy invading the trunk, ascites, and much catarrh 
 in the chest. For a time all 
 these symptoms were in abey- 
 ance, and she was out of bed 
 and walking about the ward 
 \^dthout discomfort, but the 
 improvement was only tem- 
 porary. She spat blood for 
 over a month from pulmonary 
 infarcts, and ultimate!}^ left 
 hospital during a reciurence 
 of the symptoms . The highest 
 readings were obtained at a 
 time when compensation was 
 fairly well estabhshed. 
 
 But other mitral cases occur 
 with symptoms of a similar 
 kind in which the blood-pres- 
 sure is elevated, sometimes 
 greatly, above the normal. 
 
 Hg. 
 mm 
 
 180 
 170 
 150 
 150 
 140 
 130 
 120 
 110 
 100 
 90 
 80 
 70 
 
 7 
 
 17 
 
 28 
 
 3 
 
 
 
 1 
 
 6th 
 
 2th 
 
 
 
 
 
 (Edema 
 Ascites 
 
 
 
 
 
 
 
 tap 
 
 oed 
 
 
 
 _*> 
 
 ^ 
 
 
 
 
 
 
 
 / 
 
 
 
 
 
 
 
 J 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 '^' 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 Fig. 42. — Blood-Peesstjee Chart. 
 
 F., aged 50: IVIitral disease; cirrhotic 
 kidney. 
 
 This is shown in Fig. 42, which shows the pressure in a patient, 
 aged fifty, who was admitted to hospital with orthopnoea^ 
 dropsy, and ascites, in whom, with improvement, the pressure 
 rose to even higher levels. 
 
 It is extremely important to distinguish between these two 
 groups of cases. In aortic stenosis, and in both the mitral 
 lesions, the blood-pressure is not elevated to any excessive 
 degree, no matter how large the left ventricle may be. The 
 hj-pertrophy or dilatation is exactly calculated to compensate 
 the valvular flaw, to insure the entrance into the aorta of the 
 normal amount of blood, and to maintain the aortic blood- 
 
68 
 
 DISEASES OF THE HEART 
 
 pre£ sure at normal levels . An intrinsic cardiac lesion (excluding 
 aortic regurgitation, whose effects have already been discussed) 
 is incapable of elevating the aortic pressure, and the presence 
 of a high blood-pressure indicates the presence of some ex- 
 
 
 a 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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 pq 
 
 trinsic influence — an intoxication, renal disease, or arterior 
 sclerosis. 
 
 The converse proposition is not, however, equally true. As 
 one would expect, an elevated blood-pressure may fall to, or 
 even below, normal from mere failure of the vis a tergo. The 
 point is exemphfied by Fig. 43. The patient, who was suffer- 
 
THE SYMPTOMS OF ARTERIAL DISEASE 69 
 
 ing from chronic nephritis, was admitted complaining of head- 
 ache, vomiting, and dimness of vision. The radial arteries were 
 thickened, the left ventricle was enlarged, and the ophthalmo- 
 scopic picture was indicative of widespread vascular disease, 
 and included several examples of mihary aneurism. He was 
 kept on a diet of milk alone from May 14 to June 18, in the 
 hope of allaying the renal mischief, and during this period the 
 pressure steadily fell, ultimately reaching normal or perhaps 
 subnormal levels. But it rose again on the resumption of a 
 more ample dietary, and on his dismissal was distinctly high. 
 His symptoms were in complete abeyance, and he was able to 
 take a fair amount of exercise. It seems clear that, in this 
 case, the blood-pressure required to be above normal on 
 account of the renal and arterial disease, and that the normal 
 pressure on June 18 was due to cardiac weakness from relative 
 starvation. There were no symptoms indicative of cardiac 
 failure at this time, but he was, of course, confined to bed, and 
 they would, I suspect, have appeared if he had been allowed 
 out of bed. He again came under observation in October, 
 ^vith similar symptoms, and a systohc blood-pressure of 225- 
 180 mm. Hg. Treatment was of little avail, and he died of 
 uraemia shortly afterwards. 
 
 In those cases in which arterio-sclerosis and valvular flaws 
 co-exist, a correct diagnosis may only be possible from observa- 
 tion of the arteries, the puLse, and the fundus of the eye. The 
 cardiac evidence may wholly fail. The second aortic sound 
 may be weakened from stiffness of the cusps, or replaced by 
 miu-mur, and the first apical sound and the character of the 
 apex impulse may be useless as guides. It should be remem- 
 bered, however, that in uncomphcated mitral disease the 
 second aortic sound is never accentuated, the pulse is never 
 hard or weU sustained, and that, with failure, the apex impulse 
 becomes weak, diffuse, and of short duration. 
 
 The lesser urcemic manifestations are more hkely to escape 
 recognition than the serious symptoms, for the latter are 
 usually associated with well-marked evidences of both cardiac 
 and renal disease ; but the diagnosis is generally definite on a 
 careful routine examination. The symptoms not infrequently 
 foUow some special additional intoxication, often due to a 
 
70 DISEASES OF THE HEART 
 
 gastro-intestinal upset, and may remain for long in abeyance 
 if circumstances permit a mode of living on physiological lines. 
 
 Shortness of breath is a symptom of which arterio-sclerotic 
 patients frequently complain, and requires some special atten- 
 tion, as it may arise in several ways. 
 
 Emphysema not infrequently occurs in middle-aged people 
 from causes which are apparently trivial in their character. 
 A cough, which is not necessarily of long duration or of great 
 intensity, and may never have seriously inconvenienced the 
 patient, may be the only apparent cause. But it will often 
 be found, in such cases, that the pulse is hard, the arteries 
 thick, and the second aortic sound accentuated. The lesion 
 has resulted from apparently trivial causes on account of the 
 impaired nutrition produced by the arterial disease. And it 
 is often combined with more or less chronic bronchitis, which 
 may produce symptoms quite out of proportion to the in- 
 tensity of the catarrh. 
 
 Both of these points were emphasized recently in my wards. 
 Three men were admitted at the same time, suffering from 
 bronchitis. One, aged forty-six, had been liable to bronchitis 
 for many years, and on this account had been able to do but 
 little work during the three preceding winters. His chest, as 
 one would expect, was notably emphysematous. His heart 
 and blood-pressure were normal. Another, aged fift^-nine, 
 who was almost equally emphysematous, had never, he said, 
 been ofi work previously from ill-health, and had never pre- 
 viously suffered from bronchitis. His left heart was consider- 
 ably enlarged, and his blood-pressure, when the symptoms had 
 abated, measured 175 mm. Hg. The third patient, aged thirty- 
 eight, had no emphysema, and the pulmonary symptoms were 
 not grave ; but general oedema was so extreme that micturition 
 was difficult from the tumefaction of the prepuce and scrotum. 
 Some years before he had suffered from an acute nephritis, 
 and, although the renal symptoms were trivial, possessed a heart 
 whose apex impulse was 4| inches distant from mid-sternum. 
 
 £n another group of cases shortness of breath is related to 
 exertion, and is evidently due to relative cardiac insufficiency, 
 even though the pulse is full and hard, and the left ventricle 
 hypertrophied and powerful. 
 
THE SYMPTOMS OF ARTERIAL DISEASE 71 
 
 But in a third group of cases the dyspnoea is probably toxic 
 in origin. Cheyne-Stokes respiration, for example, occurs 
 almost exclusively in cases of nephritis and the " senile " 
 t3rpe of cardiac disease, and is then present in the class of case 
 in which ehmination is likety to be insufficient; while it is 
 conspicuously absent in the cardiac failure which accompanies 
 acute endocarditis. Cardiac "asthma," too, is less common 
 in the latter group than in the former, and primary asthma, 
 as is well known, is not infrequently dependent on causes of a 
 toxic nature. The slighter manifestations of dyspnoea some- 
 times own a similar origin, and eliminative treatment should 
 always be pursued whenever dyspnoea is nocturnal or paroxys- 
 mal in character, or of a severity" which seems disproportionate 
 to the other evidences of cardiac or pulmonary embarrassment.. 
 
 It is impossible to enumerate all the symptoms which may 
 emerge in arterio-sclerosis. Many of them are cerebral (giddi- 
 ness, faintings, etc.), many are peripheral (cramp, inter- 
 mittent Hmp, etc.), many are visceral (indigestion, etc.), while 
 even such diseases as gastric ulcer, pancreatic diabetes, and 
 enlargement of the prostate, have been considered to be the 
 result of arterial disease. It seems probable, too, that in some 
 instances the proposition is accurate, though of course these 
 symptoms may be produced by very different pathological 
 conditions . 
 
 But it must be recognized that not infrequently in middle- 
 aged and elderly people there is, underlying any local symp- 
 tom which may require attention, a widespread general disease 
 — -arterio-sclerosis — a disease which is essentially progressive, 
 though its progress may be delayed by suitable treatment ; and 
 in which, quite apart from any special lesion, the arteries are 
 everjrwhere more or less damaged, the cardiac reserve is always 
 lessened, and the renal functions are more or less impaired. 
 
 Arterio-sclerosis is no new disease. It is "plethora "; it is 
 often "renal inadequacy "; it is often "senile heart "; it is 
 often "goutof the aberrant type "and the "uric acid diathesis." 
 In many cases it is " old age," which is but rarely the wearing 
 out of undamaged tissues, and too generally the result of 
 physiological misbehaviour in the past — misbehaviour which 
 leaves its first marks upon the arteries. — 
 
CHAPTER IV 
 THE OCULAR MANIFESTATIONS IN ARTERIO-SCLEROSIS 
 
 By Aethue, J. Ballantyne 
 
 The earliest and most common ophthalmoscopic evidences of 
 arterio-sclerosis in the retina are irregularities in the calibre of 
 the arteries due to local thickenings of the intima, and con- 
 striction of the veins where they are crossed by the rigid 
 arteries. The narrowing of the arterial lumen is sometimes 
 more uniform, and may be such that the blood-columns are 
 reduced to mere threads. To the same stage belong two 
 other conditions, namely, undue tortuosity of the arteries, 
 and an excessive brightness of the central light streak, which 
 gives to the arteries the so-called " silver-wire " appearance. 
 Globular or fusiform dilatations of the arteries, the miHary 
 aneurism, may also be found. 
 
 The walls of normal retinal vessels are inv'sible, so that we 
 see only the blood-stream. The more advanced stages of 
 arterio-sclerosis render the vessel walls visible. The first evi- 
 dence of loss of transparency of the wall is that the blood- 
 column looks paler, and the central light-streak less striking 
 than normal. At a later stage the process of thickening and 
 degeneration in the vessel walls proceeds so far as to produce 
 the ophthalmoscopic feature described as "perivasculitis," 
 the blood-stream being bounded on each side by a clear white 
 line, or entirely concealed for a greater or smaller part of ils 
 course by a dense white band, which represents the opaque 
 wall of the artery. Bright, glistening spots in the walls of the 
 vessels may represent deposits of lime or cholesterin. 
 
 The veins may, but do not usually, show as marked changes 
 as the arteries. Constriction of the veins, where crossed by 
 the arteries, has already been mentioned. In the more ad- 
 
 72 
 
THE OCULAR MANIFESTATIONS 73 
 
 vanced stages the veins become dilated and tortuous, and 
 may show irregularities of cahbre, or beading, similar to those 
 seen in the arteries. Excessive prominence and tortuosity of 
 the finer venous radicles is rather a characteristic appearance. 
 
 The optic nerve also alters in appearance. It becomes con- 
 gested, and oedema, either confined to the disc and to its 
 immediate neighbourhood, or affecting the whole of the retina, 
 may be observed. 
 
 Retinal haemorrhages are common, and may be present even 
 when the only visible vessel changes are irregularities of the 
 arterial cahbre and constriction of the veins by the arteries. 
 With or without retinal haemorrhages, we may see white spots 
 and patches, due to retinal degeneration. These occur even 
 in the absence of renal disease, and it is indeed uncertain 
 whether the characteristic changes of albuminuric retinitis are 
 due to the accompanying vascular changes, or whether both 
 are attributable to the one underlying cause. 
 
 Besides the changes described in the retinal vessels, sclerosis 
 of the choToidal vessels may be seen, giving the appearance of a 
 network of white hnes which represent the opaque vessel 
 walls. 
 
 Two conditions which present very striking and characteristic 
 ophthalmoscopic pictures may be referred to as strong evidence 
 of the existence of local vascular disease. These are obstruc- 
 tion of the central artery of the retina and obstruction of the 
 central vein. In the former case the retina at the posterior 
 pole of the fundus presents a milky-white opacity, in the centre 
 of which the fovea stands out as a bright, cherry-red spot. 
 The disc is pale, the arteries are reduced to threads, and the 
 veins are also somewhat narrow. While these appearances 
 used to be considered characteristic of embolism of the central 
 artery of the retina, it has been proved that in many cases they 
 are brought about by obstruction of the artery either from 
 endarteritis or from endarteritis flus thrombosis. Obstruction 
 of the central vein of the retina is usually caused by thrombosis 
 associated with local disease of the vessel wall. On ophthalmo- 
 scopic examination the veins are seen to be dark, distended, 
 and tortuous, the arteries are narrow, the nerve head is con- 
 gested and oedematous, and the retina contains abundant 
 
74 DISEASES OF THE HEART 
 
 haemorrliages and wliite exudative patches. This condition 
 is apt to lead to destruction of sight by the development of 
 glaucoma (hsemorrhagic glaucoma), or of a proliferative retinitis. 
 
 Other ocular evidences of angio- sclerosis which may be men- 
 tioned are — the slowly progressive optic atrophy which some- 
 times results from pressure of a sclerosed ophthalmic artery on 
 the optic nerve within the optic foramen; the pupillary dis- 
 turbances due to sclerosis of the vessels of the iris, and those 
 which sometimes accompam^ disease of the aorta; and the 
 visual defects which result from focal brain disease of vascular 
 origin. 
 
 The somewhat rare retinal condition called "retinitis cir- 
 cinata " is thought by some to be due to disease of the retinal 
 vessels. 
 
 The plate (Fig. 44) illustrates many of the ocular changes 
 referred to in the accompanying note. It represents the right 
 fundus ocuH of a man suffering from chronic renal disease. There 
 was also some indistinctness of the disc margin due to oedema, 
 which is not represented in the drawing. The lower temporal 
 artery is undul}^ tortuous, and presents the "silver wire" 
 appearance referred to. Three months before this drawing 
 was made three or four small aneurisms were present on this 
 artery where the white spots are now seen. A branch which 
 leaves the same artery nearer the disc passes out across the 
 fundus as a white opaque streak. The upper nasal arter}' 
 shows sudden and marked reduction of calibre a short distance 
 from the disc. The veins on the whole are overdistended, 
 and are seen to be constricted where they are crossed by the 
 arteries. The fine terminal twigs are abnormally distended 
 and tortuous. In the lower inner region of the fundus one 
 of these twigs shows something resembhng an aneurismal 
 dilatation. The retinal haemorrhages and white spots were 
 much larger and more numerous at an earlier stage of the 
 disease. 
 

CHAPTER V 
 
 THE TREATMENT OF ARTERIO-SCLEROSIS ^ 
 
 The treatment of arterio-sclerosis is essentially preventive, 
 and thus lies to the hand of the medical attendant. The disease 
 is very chronic, and one in which, as a rule, the early symptoms 
 are trivial, though serious symptoms may develop suddenly; 
 and even when the shghter manifestations are equivocal, the 
 underlying condition is generaUy apparent whm it is looked 
 for. And if, as I beheve, Sir Clifford AUbutt's theory of its 
 origin is appKcable to a large number of cases, its develop- 
 ment may be prevented, or at any rate its progress may be 
 retarded to a degree which as yet seems scarcely to be appre- 
 ciated. But, as Huchard weU said, the treatment is a regiine, 
 and not a drug, and a regime which may be impossible for 
 a busy man to foUow; and in such cases we can but dehver 
 to our patients the ultimatum — a radical change of habits 
 or a short life— and abide by the decision of the person most 
 
 concerned. 
 
 The introduction of the Riva-Rocci sphygmomanometer into 
 cHnical work naturaUy evoked the hope that the blood-pressure 
 chart would supply more definite indications for treatment 
 than had hitherto been available, but a very short experience 
 sufficed to show that this was erroneous, and that it was per se 
 an unrehable guide. Onreflection, too, the fallacy was obvious. 
 In acute nephritis the blood-pressure is elevated in the presence 
 of symptoms, and returns to normal long before the albuminuria 
 has disappeared. But in those forms of chronic nephritis with 
 induration, the smaU white and the small red kidney, the 
 blood-pressure, even in the absence of symptoms, never runs 
 at a normal level. Structural changes have occurred, and the 
 
 75 
 
76 DISEASES OF THE HEART 
 
 ^ arteries are permanently thickened ; the heart is permanently 
 enlarged, and the blood-pressure is permanently elevated. 
 And just as the amount of albumin in the urine is an unreliable 
 guide to the functional activity of the kidneys, so the height 
 of the blood-pressure fails to reveal the degree of damage that 
 has been done to the arteries and to the heart. In arterio- 
 sclerotic patients whose elimination is even relatively insuffi- 
 cient, the blood-pressure varies considerably from apparently 
 trivial causes ; a mere catarrh may suffice to elevate it, cardiac 
 failure may lower it, and every nicety of examination and the 
 most careful survey of the case may for a time prove incapable 
 of solving the important question of the height of blood-pressure 
 which must now be considered " normal " to the particular 
 individual. A reading of 180 mm. Hg may be too low for 
 perfect ehmination, or too high for the heart to cope with 
 successfully. 
 
 Notwithstanding these strictures, routine estimation of the 
 blood-pressure and a daily chart are of great value in guiding 
 the treatment of the case. Isolated observations are of little 
 use, particularly those taken in the consulting-room, where 
 so many factors (emotion, fatigue, etc.) may be in action, pro- 
 ducing a variation from the average reading. And the blood- 
 pressure chart by itself is equally unreHable, and is only helpful 
 when it is taken into consideration along with those other data 
 
 A, jwhich are usually available. 
 ^^ In the early stages of the disease it is often difficult to relate 
 the trifling symptoms to their exciting cause, and as it is more 
 easy to discern the process in cases where the symptoms are 
 well marked, the latter will be considered first. 
 
 The onset of serious symptoms is as a rule more or less 
 abrupt, and the result of the operation of some new factor. A 
 ""^priori, it might be thought that the onset would be gradual 
 in response to the steady increase in the grade of the arterial 
 lesions or the renal inadequacy, or the gradual diminution of 
 the cardiac reserve ; but such a course, though it may occur, 
 is distinctly unusual. The minor symptoms occur insidiousty, 
 but the individual is curiously tolerant of visceral weaknesses 
 of gradual onset, and instinctively learns to protect himself 
 
THE TREATMENT OF ARTERIO-SCLEROSIS 77 
 
 from his increasing disabilities. Business responsibilities are 
 turned on to younger shoulders, the " single " game of golf is 
 replaced by the "foursome," alcohol and tobacco are thrown 
 overboard or their consumption is restricted, and a quiet life 
 with little sudden strain permits the overtaxed organs to per- 
 form their work with but small inconvenience to their owner. 
 There is, however, little or no reserve, and serious symptoms 
 result from conditions which, in a healthy individual, would 
 occasion no anxiety. 
 
 Bronchitis is a common cause of trouble. Chronic bron- 
 chitis is a very frequent accompaniment of arterio-sclerosis, 
 and an exacerbation of the 
 catarrh may produce symp- >fc. 
 toms which are quite out of ng. 
 
 mm. 
 
 proportion to the intensity jqo 
 of the pulmonary lesions. ,90 
 A man of forty-seven years, 
 a stonebreaker by occupa- 
 tion and an alcoholic by 
 choice, contracted a cold, to 
 which he at first paid little 
 attention. A week later he 
 had become very short of 
 breath, and his feet were 
 swollen. When he was ad- 
 mitted to hospital a fort- 
 night after the onset 
 {Fig. 45), oedema was uni- 
 versal and considerable. 
 There were copious albu- 
 minuria and sUght hsema- 
 turia, and a well-marked 
 
 bronchitis. Within the next ten days the cedema disappeared, 
 and he lost 1 stone IQi pounds in weight, the albuminuria 
 became trivial, and the bronchitis subsided. His arteries were 
 tortuous and but shghtly thickened. The blood-pressure, on 
 admission 200 mm. Hg, fell steadily during convalescence, 
 and soon reached subnormal registers. 
 
 The illness in this case seemed wholly attributable to the 
 
 180 
 170 
 160 
 150 
 140 
 130 
 120 
 110 
 100 
 90 
 80 
 70 
 
 12 
 
 14 
 
 16 
 
 18 
 
 21 
 
 23 
 
 25 
 
 27 
 
 30 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 \ 
 
 V 
 
 
 
 
 
 
 •^ 
 
 1 — « 
 
 
 \ 
 
 
 
 
 
 
 
 v 
 
 N, 
 
 V 
 
 N 
 
 
 
 
 
 
 
 \ 
 
 
 
 V. 
 
 ■>.-, 
 
 
 
 
 
 \ 
 
 
 
 
 N 
 
 ^ 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 V. 
 
 
 
 
 
 
 
 
 
 
 ^ 
 
 ^»^ 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 Fig. 45. — Blood-Peessube Chart. 
 
 M., aged 47; Chronic nephritis ; bron- 
 chitis; improvement. 
 
78 
 
 DISEASES OF THE HEART 
 
 bronchitis, which was, however, associated with symptoms 
 which are not its usual accompaniments. The rapid improve- 
 ment in the renal symptoms negatived the diagnosis of an 
 acute nephritis, and suggested the irritation of an already 
 damaged kidney, an inference which was strengthened by the 
 arterial thickening and the presence of a white patch in the 
 retina of the right eye. 
 
 Evidence of cardiac failure may be well marked in these 
 cases. A man, aged sixty-six, who was habitually intemperate 
 and suffered from a chronic cough, contracted a fresh bion- 
 chitis. He became very short of breath, and had to be propped 
 
 up in bed at night, and suffered from 
 severe pain in the epigastrium. 
 Within a week he was forced to cease 
 work and to seek admission to 
 hospital. He was now notably 
 cyanosed and very breathless, re- 
 quiring to sit almost upright in bed. 
 The bronchitis was widespread, and 
 the liver was enlarged and tender; 
 the feet were sKghtly swollen, and the 
 mitral valve was incompetent. The 
 urine contained a trace of albumin. 
 Improvement was rapid, and he was 
 soon lying flat in bed, while the apical 
 murmur and the enlargement of the 
 liver had disappeared. Coincidently 
 the blood - pressure rose from 
 125-170 mm. Hg (Fig. 46). The 
 bronchitis had evidently put a 
 strain upon an already overtaxed 
 heart which it was unable to overtake, and the consequent 
 failure was severe and alarming. 
 
 Excessive indulgence in alcohol may produce serious symp- 
 toms. A tailor, aged fifty-one, who had enjoyed good health 
 prior to the onset of the symptoms for which he sought advice, 
 save for two attacks of renal disease, one at the age of twenty 
 five, following scarlatina, the second of obscure origin at the 
 age of forty-one, from both of which he had made good re- 
 
 APRtL 
 
 Hg 
 mm. 
 
 200 
 
 190 
 180 
 170 
 160 
 150 
 140 
 130 
 120 
 110 
 100 
 90 
 80 
 70 
 
 Fig, 
 
 15 
 
 20 
 
 23 
 
 28 
 
 5 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 ^ 
 
 ^ 
 
 
 
 / 
 
 
 
 
 / 
 
 
 
 
 / 
 
 r 
 
 
 
 
 J 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 46. — Blood-Pressure 
 Chart. 
 
 M., aged 66: Bronchitis. 
 
THE TREATMENT OF ARTERIO-SCLEROSIS 79 
 
 coveries, took one day drink to excess. He went to his work 
 next morning, but about three o'clock in the afternoon was 
 noticed to be somewhat stupid. He walked to the door to 
 get some fresh air, and soon after his return to the workshop 
 became unconscious and had a short general convulsion, from 
 which he rapidly recovered. His blood-pressure was 220-145 
 mm. Hg. Six weeks later he again got drunk, and again 
 had a convulsion; and a fortnight later another fit occurred, 
 this time apart from alcoholic excess. He subsequently be- 
 came fairly temperate, and the convulsions did not recur, 
 but he "aged " rapidly and became less fit for work. Two 
 years later headaches ensued, and he had to leave off his trade, 
 and in a few months succumbed to an apoplectic seizure asso- 
 ciated with hemiplegia. 
 
 Sepsis is another, but less frequent, cause. A man, aged 
 fifty-two, who had probably suffered from syphiHs, and had 
 had an attack of nephritis at the age of forty-six, tore the 
 instep of his foot with a rough boot-eyelet. The wound sup- 
 purated, and was poulticed. A week later the other foot was 
 found to be swollen. In a day or two the eyelids became 
 baggy, and he complained of headache and of frequency of 
 micturition. He was very breathless too, and had to sit up- 
 right in bed. A similar origin was observed in a man, aged 
 seventy-jSve, whose increasing difficulties had been carefully 
 watched for some years. A not very large gumboil formed 
 about a carious tooth, and he was fevered for twenty-four hours 
 until it was evacuated. But general symptoms ensued, and 
 he became drowsy and mildly delirious and extremely weak, 
 and the symptoms only subsided slowly. The minor forms of 
 sepsis, particularly those associated with carious teeth, are 
 probably of more importance in this respect than is generally 
 reahzed. 
 
 Symptoms not infrequently succeed severe haemorrhage, 
 whether gastric or intestinal, or, as in the following case, 
 occurring post-partum. A woman, aged thirty-five, who had 
 always been healthy save for an attack of rheumatic fever at 
 the age of twenty, which kept her in bed for three months, 
 noticed that her feet were swollen in the latter half of her 
 ourth pregnancy. Labour was difficult and prolonged (twins), 
 
80 
 
 DISEASES OF THE HEART 
 
 and she lost much blood. The oedema, however, rapidly dis- 
 appeared, and she felt quite well when she got up out of bed 
 on the ninth day; but it soon recurred and became extreme. 
 She was now (Fig. 47) very short of breath, with a troublesome 
 cough and spit ; the bowels were loose, and she felt sick and 
 vomited on several occasions. The symptoms steadily in- 
 creased in severity, and she died three months later. The 
 strain of pregnancy and the debihty consequent on the haemor- 
 rhage proved too great for a heart which 
 had little reserve power. 
 
 Starvation often produces notable 
 symptoms. A woman, aged sixty years, 
 
 NOV 
 
 Hg. 
 mm. 
 
 210 
 
 APRIL 1908 MAY 
 
 JUNE 
 
 JULY 
 
 200 
 190 
 180 
 170 
 150 
 rSO 
 140 
 130 
 120 
 110 
 100 
 
 90 
 
 80 
 
 70 
 
 Fig. 48. — Blood-Pres- 
 sure Chart. 
 
 F., aged 60: Cirrhotic 
 kidney. 
 
 who was in extremely poor circumstances, and who had 
 been starving for some weeks, noticed that her feet had 
 become swollen. The oedema rapidly involved the trunk 
 and face, and she was forced to stay in bed. She felt sick, 
 vomited repeatedly, and was very short of breath. The 
 striking feature in her condition on admission to hospital was 
 the emaciation. The muscles were tiny and soft, the skin 
 was dry and wrinkled, and the subcutaneous fat was minimal ; 
 in notable contrast with a full, hard pulse and a blood-pressure 
 
 Hg. 
 mm. 
 
 170 
 160 
 
 ISO 
 140 
 130 
 120 
 
 no 
 
 100 
 90 
 80 
 7Q 
 
 17 25 1 
 
 29 
 
 7 
 
 29 
 
 8 
 
 73 
 
 77 
 
 28 
 
 3 
 
 8 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 k 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 A 
 
 
 
 
 
 
 
 
 
 
 V 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 \ 
 
 
 
 
 
 
 •v 
 
 
 
 
 
 V. 
 
 
 
 '^m^ 
 
 ^ 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 
 
 Si^ 
 
 "N 
 
 V, 
 
 j^ 
 
 
 
 
 ~* 
 
 
 
 
 
 
 V 
 
 ^^ 
 
 22 
 
 25 
 
 29 
 
 26 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 ^ 
 
 p.. 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 — 
 
 ^, 
 
 
 
 
 
 \^ 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 DEC 
 
 Fig. 47. — Bloou-Pressure Chart. 
 
 F., aged 35: Mitral disease; cirrhotic kidney. Death 
 on July 23. 
 
THE TREATMENT OF ARTERIO-SCLEROSIS 81 
 
 of 190-135 mm. Hg (Fig. 48). The symptoms subsided as 
 Ker general nutrition improved, but the blood-pressure re- 
 mained high. 
 
 One is apt to forget, when treating a patient with a local 
 disease, that the symptoms may be due to a general condition, 
 and not to the local lesion, although both the prognosis and 
 the treatment depend upon the correot appreciation of the 
 factors which are producing symptoms at the particular 
 moment. When symptoms arise insidiously, the outlook is as 
 a rule more serious than is the case when they occur as the 
 result of some new additional factor, for the lesions are usually 
 already advanced. Speaking generally, the immediate prog- 
 nosis in private practice is worse than among hospital patients, 
 for in the former the conditions of life are more satisfactory 
 and the breaking-strain has been but slight. If immediate 
 recovery occurs, however, the prognosis in private cases is 
 generally the better, for a reasonable life of leisure is usually 
 unattainable among the older hospital patients. Their 
 financial position, for instance, is rarely comfortable, and their 
 alternative lies between continuance of labour and, at any rate, 
 relative starvation and discomfort; so that it is generally 
 impossible for the first and most important indication for 
 treatment — the removal of the cause which induced the occur- 
 rence of symptoms and the prevention of its repetition, if 
 that be possible — to be followed. 
 
 The symptoms of arterio-sclerosis may be referable to the 
 heart, the kidneys, or the vessels. 
 
 Cardiac failure produces symptoms similar to those which 
 occur in chronic valvular disease — shortness of breath, oedema, 
 etc. — and in the main the comparison is exact. In some 
 respects, however, a difference may be observed. A patient 
 who is dying from the cardiac failure of pernicious anaemia 
 as a rule hes flat in bed, and is rarely orthopnoeic even when 
 oedema is considerable and widespread. Cases of serious 
 failure in valvular disease in early life may have notable 
 distress in breathing, and may have to sit almost upright, but 
 there is generally some special adequate reason for the dyspnoea, 
 bronchitis, infarct, or pleural effusion. But in arterio-sclerosis 
 
 6 
 
82 DISEASES OF THE HEART 
 
 dyspnoea may be extreme and orthopncEa absolute without 
 any obvious pulmonary lesion, though of course such a con- 
 dition ma}^ be present, and then intensifies the distress. 
 Paroyxsmal dyspnoea, whether of the asthmatic or Cheyne- 
 Stokes type, rarely, if ever, occurs in uncomplicated cardiac 
 disease ; its presence seems alwaj's to indicate imperfect elimina- 
 tion, as a rule of renal origin. 
 
 The chief difficulty in the treatment of these cardiac cases 
 is the difficult}^ of recognizing the precise mode of the failure, 
 for failure ma 3" occur in two ways. In one type ehmination 
 becomes insufficient, and the blood-pressure is in conse- 
 quence elevated to a height at which the heart is unable 
 to work easily. In the other, the cardiac failure is 
 primary. 
 
 ' In acute nephritis, as is weU known, the blood-pressure is 
 higher than normal. With improvement and the disappearanc e 
 of symptoms it returns to the normal as a rule long before the 
 albumin has disappeared from the urine. In art erio -sclerosis, 
 on the other hand, the blood-pressure is permanently elevated. 
 If elimination is insufficient, in arterio-sclerosis, as in acute 
 nephritis, the blood-pressure rises, in the former case to 
 extraordinary heights, and the heart may give way before the 
 extra strain — a mode of failure which is, indeed, well known 
 to occur occasionally in acute nephritis. But we do not know,, 
 in an elderty person with cardiac failure and high blocd-pressure, 
 hoiv inuch of the latter is due to permanent conditions and how 
 much to tem'porary causes, unless our observations have been 
 continuous and antecedent to the onset of symptoms. In 
 arterio-sclerosis the permanent elevation of pressure gradually 
 becomes higher as time rolls on, and in due course the heart wiU 
 fail before its task, and the blood-pressure will fall, sometimes 
 very considerabh', with the onset of symptoms. To foUow 
 the weU-known simile of the horse and cart of coals that has 
 stopped on a hill, we are in doubt whether to apply the whip 
 or to hghten the load so as to enable the height to be sur- 
 mounted, and we have often to pursue — tentatively and with 
 care— both courses. 
 
 The vagaries of blood-pressure charts are extremely curious,, 
 and their interpretation may be impossible for a time. 
 
THE TREATMENT OF ARTERIO-SCLEROSIS 83 
 
 FEB 
 
 A baker, aged tliirtj'-eiglit, was admitted to hospital, com- 
 plaining of headache, nausea, breathless ness, and swelling of 
 his legs and body, which had ensued about four or five days 
 previously, coincident with the onset of an attack of bronchitis, 
 to which he was subject (Fig. 49). The left heart was dilated, 
 the hver enlarged and tender, and oedema was widespread 
 and considerable. The blood-pressure was elevated. He was 
 given a dietary of milk, evacuant treatment was pursued, and 
 caffein citrate administered, and in a few days the symptoms 
 had abated. Coincidently the 
 blood-pressure fell, the cliastohc 
 fall being relatively greater 
 than the systohc. The bron- 
 chitis seems to have been 
 responsible for an increase in 
 the blood-pressure before which 
 the heart gave way; with the 
 subsidence of the bronchitis and 
 cardiac stimulation, the pres- 
 sure fell within the bounds of 
 the cardiac strength. 
 
 Bronchitis, as is well known, 
 imposes extra work upon the 
 kidneys, and in nephritis even 
 a catarrh may produce serious 
 sjTuptoms. A striking example 
 occurred recently in my wards. 
 A man who was convalescing 
 from nephritis contracted a 
 catarrh which was prevalent in 
 the ward. Coincidently his urine, which had been copious 
 and had contained a mere trace of blood, became scanty and 
 of the colour of porter. The chest seemed normal, but there 
 was a cough and a slight muco-purulent spit, and some redden- 
 ing of the fauces. 
 
 In the baker's case cardiac failure occurred before an acci- 
 dental elevation of the blood-pressure, but it may also fail before 
 the permanent increase of pressure due to arterial disease, as in 
 the case of a man, aged forty, who became breathless on the 
 
 JAN 
 
 Hg. 
 mm. 
 
 210 
 
 200 
 190 
 180 
 170 
 160 
 150 
 140 
 130 
 120 
 110 
 100 
 
 90 
 
 80 
 
 70 
 
 Fig 
 
 21 ^3 
 
 25 
 
 27 
 
 29 
 
 1 
 
 22 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 X 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 ' 
 
 
 
 
 * 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 V. 
 
 "^, 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 49. — Blood-Pbessitee Chart. 
 M., aged 38: Bronchitis. 
 
84 DISEASES OF THE HEART 
 
 least exertion, and developed oedema of his'] legs whenever 
 he was allowed out of bed, though his blood-pressure was 
 270-190 mm. Hg. 
 
 /'It is easy to lower blood-pressure. It falls notably with a 
 sharp attack of diarrhoea, for instance, and drastic purgation 
 and a restricted dietary can almost always reduce it con- 
 siderably. But the fall is not necessarily beneficial to the 
 patient if it results from cardiac failure. In the majority of 
 patients, however, in the presence of symptoms, a high blood- 
 pressure indicates imperfect elimination, and care should be 
 taken to insure that excretion is ample. In a large number of 
 cases relief occurs. 
 
 A high blood-pressure in arterio-sclerosis is not necessarily 
 an index of intoxication, for in this disease the blood-pressure 
 is always elevated, and the " normal " pressure is that at 
 which the heart works easily and elimination is sufficient — 
 i.e., the pressure at which symptoms are in abej-ance — and 
 it can only be gauged by repeated observations over long 
 periods of time. 
 
 Vasodilator drugs have been much lauded and much depre- 
 ciated at different times. There is little use in giving them 
 to a patient whose ehmination is insufficient and peripheral 
 resistance in consequence increased; we are giving with one 
 hand and taking away M'ith the other; and they can have 
 but little action upon fibroid vessels. Their chief value is in 
 temporary emergencies, and their continued use in patients 
 who are, so to speak, convalescent is a confession of failure — 
 our failure to insure that elimination is sufficient in the par- 
 ticular case. 
 
 The action of the digitalis series in cases of arterio-scleiosis 
 when cardiac failure has supervened is in the majority of 
 patients injurious, and the dyspncea is intensified and the 
 venous stasis increased. The special cardiac functions, too, 
 may be disturbed, and an irregular pulse may give evidence of 
 a hitherto latent heart-block or an excessive excitabihty; or 
 the pulsus alternans may occur. Caffeine, diuretin, alcohol, 
 and the ammonium salts are more generally useful, and should 
 be tried first, and should be aided by the milder diuretics, 
 such as the citrate or acetate of potassium, and liquor ammonii 
 
THE TREATMENT OF ARTERIO-SCLEROSIS 85 
 
 JUNE 
 
 acetatis. Strong, freshly infused tea and coffee are often usetul. 
 But it must be acknowledged that in many instances these 
 drugs prove useless, and we are forced to resort to the digitalis 
 group. 
 
 French writers advocate isolated massive doses in cardiac 
 failure, but the repeated administration of small doses seems 
 preferable in the cases which we are now considering, as the 
 minor adverse symptoms can 
 then be quickly checked by 
 thejvithdrawal of the drug. 
 A standardized tinctui'e, the 
 Nativelle granules, Trous- 
 seau's wine, or Guy's pills, 
 may be utihzed ; the granules 
 and the wine scarcely ever 
 upset the stomach. Some 
 patients are very susceptible 
 to mercury, and I have seen 
 well-marked salivation occur 
 after the administration of 
 fourteen Guy's pills in seven 
 days. Oral sepsis was ex- 
 treme in this patient, but the 
 use of mercury should always 
 be carefully watched in these 
 cases, particularly if the renal 
 functions are also notably 
 disturbed. 
 
 The actual height of the 
 blood-pressure is a matter of 
 no practical importance, and 
 I have given even large doses 
 
 MAY 
 
 Hg. 
 mm. 
 
 250 
 250 
 240 
 230 
 220 
 210 
 200 
 190 
 180 
 170 
 160 
 150 
 KO 
 130 
 120 
 110 
 100 
 30 
 80 
 70 
 
 7 
 
 6 
 
 12 
 
 18 
 
 31 
 
 13 
 
 23 
 
 26 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 r 
 
 
 
 
 
 
 
 / 
 
 
 
 
 
 
 
 1 
 
 
 
 
 
 
 
 1 
 
 ' 
 
 
 
 
 
 
 
 J 
 
 
 
 
 
 
 / 
 
 / 
 
 
 
 
 
 
 
 / 
 
 
 
 
 
 
 
 I 
 
 / 
 
 
 
 
 
 
 
 J 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 Fig. 50. — Blood-Peesstjre Chart. 
 F., aged 58: IVIitral disease; cirrhotic kidney. 
 
 of digitalis in high-pressure cases with benefit. A woman, aged 
 fifty-eight, was admitted to hospital orthopnoeic and very 
 short of breath, with extensive oedema and a large effusion 
 into the left pleural sac (Fig. 50). Paroxysmal attacks of 
 dyspnoea occurred at night. The effusion had to be tapped 
 on five occasions, but she left hospital after two months' 
 residence, fairly comfortable and \vithout any oedema, though 
 
86 
 
 DISEASES OF THE HEART 
 
 she was short of breath when she was walking about. Coin- 
 cident with the improvement, the blood-pressure rose from 
 160-250 mm. Hg. The improvement, however, was of 
 short duration, and she returned to hospital in a moribund 
 condition two months later. 
 
 The height of the blood-pressure is no index to cardiac suffi- 
 ciency. A man, aged sixty-eight, was admitted to hospital 
 two days after the occurrence of a right-sided hemiplegia 
 
 (Fig. 51). Three days 
 later he was more stupid 
 than on admission, 
 deglutition was difficult, 
 and incontinence of urine 
 complete, and the 
 breatliing was typically 
 Chej'ne-Stokes in char- 
 acter and associated 
 with pupillary and pulse 
 phenomena. The ex- 
 tremities were cold and 
 blue. Three days later, 
 when improvement was 
 distinct, the blood-pres- 
 sure was practically the 
 same, although all the 
 evidences of venous 
 stasis had passed away. 
 It is difficult to realize 
 
 DEC 
 
 Hg. 
 
 mm. 
 
 210 
 200 
 190 
 180 
 170 
 160 
 150 
 HO 
 130 
 120 
 
 no 
 
 100 
 30 
 80 
 70 
 
 12 
 
 13 
 
 ?4 
 
 15 
 
 16 17 
 
 18 
 
 79 
 
 20 
 
 21 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 "A 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 V 
 
 
 
 
 
 
 
 
 
 ■n 
 
 
 \ 
 
 \/ 
 
 
 \ 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 V 
 
 
 ^ 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 
 
 
 
 v 
 
 
 
 
 
 
 
 
 
 
 
 ^ 
 
 
 -■•^v, 
 
 N.^ 
 
 
 
 ^ 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 Fig. 51. — Blood-Peessxtre Chart. 
 M., aged 68: Hemiplegia. 
 
 that cardiac failure may be present with a blood-pressure of 
 over 150 mm. Hg, but improvement ensued after the adminis- 
 tration of strong tea and whisky and a more ample dietary — 
 treatment which could hardly have any great effect upon a 
 gross cerebral lesion. In another case the demonstration was 
 more complete. The patient, a man aged fifty-one, who was 
 suffering from renal cirrhosis, developed cerebral symptoms 
 which the post-mortem examination showed were the result of 
 cortical emboli derived from clots in the left ventricle. His 
 blood-pressure had ranged from 170 to 210 mm. Hg. 
 '" In many of these cases of cardiac failure the whip is not 
 
THE TREATMENT OF ARTERIO-SCLEROSIS 87 
 
 required, for if some of the coals be removed from the cart, 
 the bm-den can be borne, and with adequate rest the heart 
 regains its strength. 
 
 Cases with symptoms of urcemic type react well to treatment 
 of this kind. Free purgation, packs, cupping, and an ample 
 supply of fluid are the main elements in treatment, and the 
 cardiac dilatation often rapidly subsides, and the pulse becomes 
 less frequent. The administration of water is important. It 
 can often be retained when any food is at once ejected, and, 
 of course, can be given subcutaneously or by the bowel. Con- 
 tinuous rectal injections, as practised by surgeons after ab- 
 dominal operations, are sometimes useful. But here again 
 the behaviour of the blood-pressure varies. 
 
 As a rule, with increased elimination and the disappearance 
 of symptoms, the blood-pressure falls. This is well shown in 
 Fig. 52 — that of a man, aged thirty-six, who was admitted 
 suffering from chronic nephritis, and complaining of headache, 
 vomiting, and dimness of vision. On a diet of milk and 
 ehminant treatment the symptoms rapidly subsided and the 
 blood-pressure fell, though it rose again on the resumption of a 
 more ample dietary. 
 
 But the fall in pressure may be slight even when improve- 
 ment occurs. A woman, aged 45, terminated her eleventh 
 pregnancy prematurely in January. In June she began to 
 suffer from headache, which steadily became more severe and 
 persistent, and at times prevented sleep. Nausea and vomit- 
 ing ensued in December, and in January was very severe, 
 almost all food being rejected at once. On admission, in 
 February, she was extremely ill, with a pale, anxious expression, 
 yawning continually, and complaining bitterly of headache 
 and nausea (Fig. 53). For forty-eight hours after admission 
 she vomited almost constantly, but the symptoms afterwards 
 improved rapidly, and she left hospital in fair health. The 
 blood-pressure in this case fell at first, but rose again before 
 dismissal. Treatment was eliminant, and she was able to 
 retain even large quantities of water in the stomach at a time 
 when all varieties of food were at once rejected. 
 
 The blood-pressure may even rise under similar treatment. 
 A woman, aged forty-six, who had suffered from rheumatic 
 
88 
 
 DISEASES OF THE HEART 
 
 fever in early life, began to be troubled, about the age of thirty- 
 eight, with breathlessness and palpitation, and became subject 
 to attacks of bronchitis. Six years later oedema made its 
 appearance, at first in the face and then in the feet, and nausea 
 and vomiting ensued. When she was admitted to hospital a 
 
 
 Ol 
 
 
 
 
 
 
 
 
 
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 I 1 
 
 
 
 
 
 
 
 
 
 
 
 s. 
 
 
 
 
 
 
 
 
 k^ 
 
 
 en 
 
 
 
 
 
 
 
 
 
 
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 V 
 
 
 
 
 
 
 M 
 
 s> 
 
 en 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
 1 
 
 -3 
 
 
 
 
 
 
 
 
 
 
 
 
 \ 
 
 
 
 
 
 
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 O 
 
 
 
 
 
 
 
 
 
 
 
 
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 ^ 
 
 
 
 
 
 
 
 
 
 
 
 
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 •OB P 
 
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 year afterwards, there was slight general cedema and a small 
 ascitic collection, and she was emaciated and weak (Fig. 54, 
 March, 1908). Rest in bed, a milk diet, and increased elimina- 
 tion rapidly dissipated all the symptoms, and coincidently 
 the blood-pressure rose from 155 to 175 mm. Hg. The only 
 
THE TREATMENT OF ARTERIO-SCLEROSIS 89 
 
 stimulant administered was some Easton's syrup. The further 
 history is instructive. The symptoms recurred, and she was 
 readmitted into hospital with similar but more severe symp- 
 toms. On this occasion Trousseau's wine was given, and she 
 made a slow recovery, and again the blood-pressure rose from 
 150 to 175 mm. Hg. She was again admitted to hospital, 
 sixteen months after dismissal. The blood-pressure was 
 then 140 mm. Hg, and 
 treatment failed to pro- 
 duce any distinct improve- 
 ment, the blood-pres- 
 sure remaining practically 
 constant. Post-mortem 
 examination revealed the 
 widespread nature of the 
 disease, for there was 
 found, besides mitral 
 stenosis and thickened 
 degenerate vessels, well- 
 marked cirrhosis of the 
 kidneys and pulmonary 
 emphysema, and an early 
 cirrhosis of the liver. 
 
 In the milder forms of 
 cardiac failure, then, elimi- 
 nant treatment is the main 
 indication, and not infre- 
 quently is sufficient in 
 itself to relieve the symp- 
 toms, but in more severe 
 failure cardiac stimulants 
 may be required in addi- 
 tion. The essential point in treatment is, however, improved 
 elimination ; without it stimulation is frequently unsuccessful. 
 
 The arterial lesions in arterio-sclerosis are often serious, and 
 the urgency of the local lesion is apt to distract attention from 
 the underlying cause. In aneurism and in cardiac and renal 
 cases the condition of the vessels is investigated as a matter 
 of routine; but in many other diseases, such as epistaxis. 
 
 FEB 
 
 6 
 
 8 
 
 JO 
 
 12 
 
 14 
 
 16 
 
 18 
 
 20 
 
 21 
 
 Hg. 
 
 
 
 
 
 
 
 
 
 
 mm. 
 
 
 A 
 
 
 
 
 
 
 
 
 250 
 
 / 
 
 '\ 
 
 
 
 
 
 
 
 
 240 
 
 J 
 
 \ 
 
 [ 
 
 
 
 
 
 
 
 ?in 
 
 
 
 \ 
 
 
 
 
 
 
 / 
 
 220 
 
 
 
 V 
 
 
 
 
 A 
 
 J 
 
 
 210 
 
 
 
 \ 
 
 ^ 
 
 -^ 
 
 ^/ 
 
 
 
 
 200 
 
 
 
 
 
 
 
 
 
 
 190 
 
 
 
 
 
 
 
 
 
 
 ISO 
 
 
 
 
 
 
 
 
 
 
 i7n 
 
 
 
 
 
 
 
 
 
 
 ISO 
 
 
 A 
 
 
 
 A 
 
 
 
 
 
 isn 
 
 
 
 
 
 A 
 
 
 
 
 
 140 
 
 1 
 
 [ 
 
 \ 
 
 / 
 
 ' 
 
 \ 
 
 
 
 
 130 
 
 1 
 
 
 V 
 
 7 
 
 
 \ 
 
 y 
 
 / 
 
 
 120 
 
 
 
 
 
 
 
 
 
 
 HO 
 
 
 
 
 
 
 
 
 
 
 too 
 
 
 
 
 
 
 
 
 
 
 30 
 
 
 
 
 
 
 
 
 
 
 80 
 
 
 
 
 
 
 
 
 
 
 70 
 
 
 
 
 
 
 
 
 
 
 Fig. 53. — Blood-Peessuee Chaet. 
 F., aged 45: Chronic nephritis. 
 
90 
 
 DISEASES OF THE HEART 
 
 gastric ulcer, etc., in which arterial lesions are only occasionally 
 the cause, their condition is apt to be neglected, though the 
 bearing upon treatment is necessarily considerable. 
 
 There has been much diversity of opinion as to the rela- 
 tionship between aneurism and heightened blood-pressure, a 
 diversity which is, in part at any rate, due to erroneous deduc- 
 tions from the available facts. The blood-pressure is measured 
 in the brachial artery, which is a branch of the subclavian. 
 It is manifest that the blood-pressure in the subclavian artery 
 cannot be high if a distensible aneurismal sac intervenes 
 
 
 
 
 
 
 
 
 JUN 
 
 
 
 
 
 DEC 
 
 MAR 
 
 }2 
 
 25 
 
 MAr 
 
 7 
 
 17 
 
 28 
 
 3 
 
 NOV 
 
 20 
 
 25 
 
 29 
 
 19 
 
 US 
 
 He- 
 
 mm. 
 
 190 
 
 
 
 
 
 
 
 
 09 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 180 
 
 
 
 
 
 
 
 
 
 
 
 
 
 170 
 
 
 / 
 
 
 
 
 ^ 
 
 ^ 
 
 
 
 
 
 
 160 
 
 J 
 
 / 
 
 
 
 
 f 
 
 
 
 
 
 
 
 150 
 
 / 
 
 
 
 
 / 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 130 
 
 
 
 
 
 
 
 
 
 
 
 •v 
 
 ^ 
 
 120 
 
 
 
 
 
 
 
 
 
 
 
 
 
 1 1 
 
 
 
 
 
 
 
 
 
 
 
 
 
 100 
 
 / 
 
 / 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 ^ 
 
 90 
 80 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 7n 
 
 
 
 
 
 
 
 
 
 
 
 
 
 Fig. 54. — Blood-Pbesstjre Chart. 
 F., aged 46: Mitral disease; cirrhotic kidney. 
 
 between it and the heart ; while, on the other hand, an abdom- 
 inal aneurism will not influence the subclavian pressure. In 
 cases of aortic regurgitation, too, the aortic blood-pressure 
 depends largely on the degree of the incompetence, and the 
 aortic valves are often affected in cases of aneurism. But all 
 cases of aneurism are combined, and a general conclusion is 
 stated which has been based upon a collection of facts which 
 are not truly comparable. 
 
 A similar error has been made in regard to organic mitral 
 disease, and the pulse has been stated to be hard or soft, large 
 
THE TREATMENT OF ARTERIO-SCLEROSIS 91 
 
 or small, regular or irregular, by various writers. The frequent 
 association of chronic renal disease and mitral stenosis has 
 been recognized for many years in the post-mortem room, but 
 the chnical appHcation of this fact seems to have escaped 
 notice. There are two kinds of mitral disease, as G. A. Gibson 
 said — those with low arterial pressure and those with high 
 pressure — and the difference lies in extracardiac lesions in the 
 arteries and in the kidneys. In the second group these 
 systems are more or less involved ; in the first they are normal 
 (c/. Figs. 41, 42, and p. 269). 
 
 The treatment of arterio-sclerosis in the early stages, when 
 the symptoms are obscure and slight, is most important, for 
 it is then that its effect is greatest, not only in the relief of 
 symptoms, but in arresting the progress of the disease. 
 
 The general indications have aheady been laid down. The 
 blood-pressure is elevated by the presence of various dele- 
 terious substances in the blood. Continued high pressure 
 produces permanent structural alterations in the heart and 
 bloodvessels — arterio-sclerosis. In every case of arterio- 
 sclerosis renal ehmination is more or less insufficient, the cardiac 
 reserve is lessened, the viscera are poorly nourished, and their 
 functions are imperfectly discharged. 
 
 There is a general consensus of opinion that a generous diet 
 and excessive consumption of alcohol lead in time to " plethora" 
 and increased arterial pressure. Sir Clifford AUbutt has 
 crystallized this in his statement that the most important 
 cause is " repletion, relative or positive — i.e., tempered or un- 
 tempered by air and exercise," hindering the capillary flow, 
 and augmenting the arterial blood-pressure. It seems prob- 
 able that Sir CUfford AUbutt 's theory is appHcable to many 
 cases, the type of which is the big, burly individual, energetic 
 in aU his habits, and overburdened with adipose tissue. But 
 the disease is not uncommon in quite another type, under- 
 average in size and weight, of sedentary habit, and from cir- 
 cumstances or choice exceeding neither in eating or drinking. 
 William Russell has suggested the probable explanation. It is 
 not the quantity of the food that is at fault in these patients, 
 but imperfect digestion. The primary error may be very 
 
92 DISEASES OF THE HEART 
 
 varied, an injudicious choice of food, gastric, intestinal, hepatic, 
 or pancreatic insufficiency ; but the ultimate result is the same — ■ 
 imperfect and disturbed metabolism and persistent intoxica- 
 tion. 
 
 The kidneys are mainly concerned with the removal of the 
 waste products of protein metabolism. If this be excessive, 
 their functions ma 3^ be overtaxed ; if it be abnormal, abnormal 
 substances may be formed and excreted in the urine {e.g., 
 sugar, indican, etc.), and there is evidence that most of these 
 bodies irritate the kidneys during their excretion. Under 
 normal conditions, carbohydrate and fat metaboHsm impose 
 Uttle work upon the kidneys, unless their consumption be 
 excessive {e.g., aHmentary glycosuria), but in disease their 
 metabolism may be imperfect, and the products may be 
 excreted in the urine {e.g., sugar, acetone series, oxalates, etc.). 
 
 In a general way the intake of food must be carefully super- 
 vised and excess avoided, and a minimum of protein food 
 allowed. But the proverb, " One man's meat is another man's 
 poison," is peculiarly apphcable to arterio-sclerotic patients, 
 and a failure of digestion and the consequent irritation of the 
 tissues from the presence of injurious substances in the blood 
 may lead to the occurrence of serious symptoms. 
 
 Appetite, for instance, is probably essential to perfect diges- 
 tion, and may fail before the "simple hfe and food." Vege- 
 tarian diet is weU recognized to be difficult of digestion, and the 
 glass of wine at meals, or savoury dishes, may be necessary 
 stimulants for the individual. If digestion is imperfect, the 
 undigested foodstuffs in the bowel may ferment or putrefy, 
 and a new series of irritant materials may become available 
 for absorption. As a result of "fermentative" processes, 
 acetic, lactic, propionic, butjTic acids, etc., may be formed; 
 while from protein "putrefaction," neurin, chohn, putrescin, 
 cadaverin, mercaptan,^_ HgS, phenol, cresol, skatol, indol, etc, 
 may be produced. 
 
 This point dees not seem to have been sufficiently recog- 
 nized, perhaps because the effects of indigestion vary so greatly 
 even when the digestive disturbances are apparently com- 
 parable. But in one patient a bout of vomiting or an 
 attack of diarrhoea may rapidly remove the irritant, while in 
 
THE TREATMENT OF ARTERIO-SCLEROSIS 93 
 
 another headache, depression, irritabihty, etc., show that 
 absorption has occurred. There is no exact relationship be- 
 tween the amount available for absorption and that actually 
 absorbed ; for, as Herter has shown, indicanuria may be well 
 marked when the faecal indol is inconsiderable, and insig- 
 nificant when the latter is excessive. 
 
 A suitable dietary, then, cannot be rigidly laid down with- 
 out considerable experiment. It is important to make changes 
 slowly, and to regard the general condition of the patient as a 
 whole. One is apt to limit the amount of food too strictly, 
 and the latter error may be as injurious as overfeeding. But 
 no diet is suitable unless the tongue is clean, gastro-intestinal 
 symptoms wholly absent, and the stools normal in colour and 
 odour and consistence. 
 
 The "output " in these cases is quite as important as the 
 "intake," and requires equal attention. A daily evacuation 
 of the bowels may, for instance, be insufficient, and I have 
 more than once been able to feel the colon throughout its 
 course, though the bowels moved regularly every day. In 
 some of these cases regular laxative medicine may be required, 
 in others only occasional doses; but the weekly "wash-out " 
 is probably alwa^-s salutary even when it seems unnecessary. 
 The kind of drug employed is of less importance than the 
 thoroughness of the process. My own preference is for a mer- 
 curial, in particular, blue pill, with a saline as the occa- 
 sional purge, and the milder salines, cascara, or senna, for 
 regular use. 
 
 The kidneys, too, require regular flushing. A simple di- 
 uretic mixture is often helpful, but it should be subservient 
 to the ingestion of water in amount, the daily output of urine 
 being kept over 60 ounces. But here, again, care is necessary, 
 for the " long " drink at meals is not unhkely to disturb 
 digestion. Fluid should be taken when the stomach is empty, 
 the first thing in the morning, a full half-hour before luncheon 
 and dinner, and perhaps at bedtime. 
 
 The skin, too, must be kept active. A Turkish bath once 
 or twice a week is often well borne, but regular toilet ablutions 
 and mild sweating exercises are probably a better substitute; 
 and many amusements may be utilized — golf, riding, tennis, 
 
94 DISEASES OF THE HEART 
 
 shooting, fishing, etc. — if they are available, and of a degree 
 adapted to the physique of the particular individual. 
 
 In the treatment of an individual patient it is generally wise 
 to insist at the outset upon a strict regime. The details are 
 thus better learnt, and as the symptoms remit, relaxations can 
 be readily allowed, while an increase of the restrictions after 
 a period of treatment is naturally disappointing to the patient. 
 
 In any case where the symptoms are severe, confinement to 
 bed is generally advisable at first. The bowels should be kept 
 freely open by salines and blue pill, the fluid intake increased 
 so that 60 to 90 ounces of urine are passed per diem, and 
 ehmination assisted by a simple diuretic mixture. The skin 
 should be kept active by a daily warm bath, and the diet 
 restricted to three or four pints of milk, with or without the 
 addition of some farinacea. Milk is usually weU borne by 
 these patients ; if there is any digestive discomfort, it can be 
 overcome by peptonizing or citrating the milk, or by giving 
 it as curds or "soured." As a rule the symptoms rapidly 
 subside as soon as excretion is ample. But restrictions of this 
 kind cannot be maintained for long with benefit, and in the 
 absence of symptoms some addition should be made to the 
 diet after a few days. The quantity of farinacea is increased, 
 and white fish and eggs are given in addition, but their amount 
 must at first be limited and only gradually augmented. The 
 cooking must be of the plainest kind, but every possible 
 variation should be used, so as to encourage appetite and 
 promote digestion. In the majority of cases improvement 
 continues, and the diet may then be still further varied by 
 the inclusion of chicken and rabbit and a little potato. The 
 key to treatment at this stage is the condition of the digestive 
 functions and the general well-being of the patient rather 
 than the height of the blood-pressure or the amount of albumin 
 in the urine. 
 
 Some digestive help may be required — some rhubarb or soda, 
 or a pepsin mixture — and the tongue must be clean, the stools 
 normal, and gastro-intestinal symptoms in abeyance before any 
 notable addition to the diet is made. Digestive disturbances 
 are not infrequently the result of oral wrongdoing, and every 
 
THE TREATMENT OF ARTERIO-SCLEROSIS 95 
 
 effort should be made at the outset to insure that oral sepsis is 
 absent, and that efficient mastication is possible ; and the 
 patient's attention should be drawn to the necessity that it 
 should be thorough and complete. 
 
 Mild massage may be commenced at this stage as a pre- 
 liminary to a certain amount of exercise, and the latter, when 
 permitted, must be supervised at first by the physician as 
 sedulously as it is done in a sanatorium, for tuberculous patients, 
 for the general feeling of weU-being, often coupled with a loss 
 of superfluous fat, is apt to incline the patient to an amount 
 of physical exertion which is too great for his flabby muscles. 
 
 There is always difficulty in regulating these details when 
 a return to work is finally allowed, for the exigencies of busi- 
 ness necessarily interfere with the placid, orderly routine of 
 life wliich is so essential to an arterio-sclerotic patient. The 
 daily time-table must be laid down by the physician, and par- 
 ticular care taken that the meals are regular and of suitable 
 quality; and that some rest is possible both before and after 
 them . 
 
 The diet in convalescence is often restricted within too narrow 
 limits. The cause of the disease is often dietetic, and the 
 error ma}^ arise in different ways. In one case it is the quantity 
 of food that is at fault, in another the quahty ; while in a third 
 both of these factors may be satisfactory, and the error lies in 
 faulty digestion. It is, of course, manifest that all foods which 
 are notoriously difficult of digestion (crab, goose, etc.) or decom- 
 posing (high game) must be avoided, as well as all salted foods, 
 for it is notorious that the excretion of salt is almost always 
 defective. The red meats are usually interdicted. In a general 
 way they are as easil}' digested as the white, and contain 
 httle more extractives ; but they are essentially the savoury 
 foods, and so Hkely to encourage overeating; and they are 
 often spiced and salted in the cooking to a degree that must 
 entail considerable strain on elimination. The ordinary con- 
 soTrnne, for example, contains a minimum of nourishment and a 
 maximum of substances to be excreted by the kidney, so that 
 aU soups made with meat stock should be prohibited. Vege- 
 table stock, however, may be utihzed. 
 
 A little roasted mutton or a lightty shot, fresh young bird 
 
96 DISEASES OF THE HEART 
 
 is, however, certainly permissible as an occasional variation. 
 The viscera are, of course, objectionable on account of their 
 purin content. The vegetables only require consideration from 
 the digestive point of view, and the majority of the fruits can 
 be allowed in their season. 
 
 The use of drugs in arterio-sclerosis requires some further 
 consideration. There is no specific medicine, and the essential 
 fart of the treatment is the regulation of the life of the patient 
 on the lines that have been suggested. But in arterio-sclerosis, 
 as in other chronic diseases, various symptoms may arise from 
 time to time, and the particular measures that are required 
 for their relief are generally indicated by the special disorder. 
 
 It has been urged that an elevated blood-pressm-e requires 
 reduction, and a host of vasodilators have been recommended 
 for this purpose. But in arterio-sclerosis the high blood- 
 pressure is really a conservative process, an attempt to remedy 
 circulatory difficulties that have arisen, and any interference 
 with it is just as likely to do harm as good. It is true that in 
 the presence of symptoms the pressure may be temporarily 
 high for the particular case, and with improvement often 
 falls, but in other cases it rises ; and in the absence of symptoms 
 it is always above normal. It is not rational to conclude that, 
 because the blood-pressure sometimes falls coincidently with 
 improvement, improvement will occur whenever and however 
 the pressure is lowered. In many cases this can only be done 
 by depressing the cardiac action — ^in short, by inducing cardiac 
 failure. 
 
 It must, however, be admitted that practical experience has 
 shown that in certain cases vasodilator drugs may be of service. 
 In angina pectoris, for example, the inhalation of amyl nitrite 
 is often of great value during the paroxysm, as well as the 
 administration of nitro-glycerin in the intervals between 
 attacks. But the action of all drugs of this kind is very fleet- 
 ing, erythrol tetranitrate, which is said to have the most pro- 
 longed action, losing its effect within five or six hours after its 
 administration; and I have so far failed to find that their 
 continued use has had any appreciable effect upon the blood- 
 pressure curves. 
 
 It is somewhat difficult to understand the high reputation 
 
THE TREATMENT OF ARTERIO-SCLEROSIS 97 
 
 of iodine and the iodides in this disease, for it seems certain 
 that they exercise Httie or no influence upon the blood-pressure, 
 and their action upon fibrous tissue is only likely to be effective 
 when it is of syphilitic origin. The general conclusion as to 
 their good effect is, however, too strong to be hghtly dis- 
 regarded, and moderate doses may be given. Care should be 
 taken, however, that iodism does not occur. 
 
 Mercury is another drug which has a well-established repu- 
 tation in this disease, from its action in increasing renal and 
 intestinal excretion, and in limiting bacterial processes in the 
 intestine. Calomel and blue pill seem to be the most useful 
 preparations. The toilet of the mouth must be carefully 
 supervised, particularly in those cases in which renal symp- 
 toms are prominent. 
 
 In patients who are more or less convalescent, these drugs 
 should be given intermittently rather than continuously, and 
 their effects are probably best marked if they are given every 
 alternate week or fortnight, with occasional longer intervals 
 of intermission. 
 
CHAPTER VI 
 THE MYOGENIC THEORY 
 
 The cardiac muscle differs morphologically from voluntary 
 and involuntary muscle elsewhere, and the anatomical differ- 
 ences are associated with differences in physiological action. 
 Stimulation of voluntary muscle, for example, is followed, after 
 the latent period, by contraction of the muscle, and this in 
 turn by relaxation; and the cardiac muscle also responds to 
 similar stimuli, whether mechanical, chemical, thermal, or 
 electric ; but there are fundamental differences in the response. 
 During a contraction the heart is refiactory to stimuli, and a 
 tetanus cannot, in consequence, be produced. With voluntary 
 muscle the degree of contraction in response to stimulation 
 varies in direct accordance with the intensity of the stimulus, 
 a strong stimulus producing a large contraction, and vice versa ; 
 but the cardiac muscle reacts to all stimuli, whether great or 
 small, in exactly the same way. During systole its powder 
 of contraction is lost, and immediately afterwards is at a 
 minimum; during diastole it rapidly recovers, and a contrac- 
 tion excited artificially towards the end of diastole is greater 
 than one produced in the earlier periods ; but this is quite in- 
 dependent of the degree of stimulation, the muscle, if excitable, 
 reacting as strongly to a weak stimulus as to a strong one, 
 the "all or nothing " motto of the heart. And, lastly, the 
 heart beats regularly and rhythmically during hfe, while^ 
 voluntary muscle is inactive for long periods of time. 
 
 The current theory of the cardiac action is in some respects 
 a revival of an old idea. It was at first supposed that the 
 contractions were due to the direct action of the blood as it 
 flowed into the auricle, and followed as soon as the chambers 
 were sufficiently distended; but it was soon shown that this. 
 
 98 
 
THE MYOGENIC THEORY 99 
 
 could not be the case, as the frog's heart, when separated from 
 the body and empty of blood, would beat rhythmically for a 
 considerable time if it was placed under favourable conditions 
 of moisture and warmth, so that its rhythmic action must be 
 due to an inherent property of the myocardium. The dis- 
 covery of nerve cells and fibres in the heart then followed, and, 
 as respiration was at the time considered to be due to the 
 automatic action of nerve cells, the cardiac contractions were 
 ascribed to a similar cause. The earlier theory was, however, 
 reverted to when Gaskell showed that the isolated apex of the 
 heart, which is devoid of nerve cells, may contract rhythmically 
 for long periods, so that the cardiac beat must be due to an 
 inherent power of the muscle to produce rhythmic stimuH. 
 
 The wave of contraction starts at the great veins and travels 
 through auricle to ventricle, and a controversy arose as to 
 whether the stimulus was conducted by nerve or by muscle. 
 But Gaskell showed that in the tortoise, at any rate, the route 
 must be muscular, for the coronary nerve, the sole nervous 
 connection between auricle and ventricle in this animal, lies 
 outside the heart and can be severed without disturbing the 
 normal sequence of events ; while section of the muscle alone 
 leads to asynchronous contractions of the chambers. His 
 deductions were at first alleged to be inconclusive and in- 
 apphcable to mammalian hearts, as no muscular connection 
 between auricle and ventricle was known; but Stanley Kent 
 and His soon afterwards demonstrated the connecting fibres, 
 the auriculo-ventricular, or a.v. bundle. 
 
 The primitive tissue of the heart comprises the sino-auricular 
 node of Keith and Flack, the auriculo-ventricular node of 
 Tawara, and the auriculo-ventricular bundle of Stanley Kent. 
 The cells of which these are composed differ in some respects 
 from the muscle cells elsewhere, being fusiform in shape 
 rather than rhomboidal, and showing striation only at the 
 periphery of the cells. They interlace with each other, and 
 possess a rather lar[;G ovoid nucleus, and are surrounded by 
 connective tissue which is somewhat dense in the sino-auricular 
 node, and more clehcate in the auriculo-ventricular node. 
 They have a well-developed vascular supply, and are accom- 
 panied in the sino-auricular node by many nerve fibres and 
 
100 
 
 DISEASES OF THE HEART 
 
 ganglion cells (Fig. 58), which are directly connected with the 
 vagus and sympathetic nerves. The auriculo-ventricular node 
 contains nerve fibres, but no ganghon cells. 
 
 Fig. 55. — Heart of Ox, dissected to show the a. v. Btjxdle feom the Right 
 Side of the Heakt. (A. Keith.) 
 
 The sino-auricular node is situated at the junction of the 
 superior vena cava and the right auricular appendix immedi- 
 ately beneath the epicardium. It measures about 2 mm. in 
 
THE MYOGENIC THEORY 
 
 101 
 
 thickness, and extends downwards along the sulcus terminalis 
 for about 2 cm. The auriculo-ventricular node is pear-shaped, 
 and measures about 6 mm. longitudinally, and about 3 mm. 
 transverse^. It is situated (Fig. 56) on the right side of the 
 interauricular septum close to the anterior edge of the 
 
 Fig. 56. 
 
 -HiTiiAN Heart, dissected to show the a.v. jSTode ksd Bundle 
 TEOM THE Right Side of the Heart. (A. Keith.) 
 
 coronary sinus, and immediately above the insertion of the 
 median cusp of the tricuspid valve. The fibres, as they leave 
 the node, are collected together into the auriculo-ventricular 
 bundle (Figs. 55, 56, 57), which passes forwards in the inter- 
 auricular septum, and then turns abruptly downwards, pre- 
 forating the central fibrous body of the heart to reach the 
 
102 
 
 DISEASES OF THE HEART 
 
 interventricular septum immediately behind tlie membranous 
 space. As it approaches the lower border of the space, it 
 divides into two main branches, which separate and run 
 downwards beneath the endocardium on each side of the 
 
 Fig. 57. — Heart of Waxbus, dissected to show the a. v. Bundle from the 
 Left Side of the Heart. (A. Keith.) 
 
 septum. The branches, as they descend, spread out fanwise, 
 and apparently end in the muscle cells which clothe the in- 
 terior of the ventricles, the papillary muscles in particular 
 receiving an ample supply. 
 
 The cells of the system vary somewhat in size in the lower 
 
THE MYOGENIC THEORY 
 
 103 
 
 animals, the Purkinje fibres being tbe largest and those in the 
 nodes the smallest. The cells of the auriculo-ventricular node 
 and bundle are in direct connection with each other, but those 
 of the sino-auricular and auriculo-ventricular nodes have not 
 yet been shown to be continuous, as their cells seem to pass 
 gradually into the auricular muscle and to lose their special 
 characters. 
 
 The primitive tissue of the heart is recognized to be the 
 representative of the primitive tubular heart which is formed 
 by the coalescence of the 
 two symmetrical ventral 
 tubes of the hsemoccelum. 
 In the course of the 
 development of the heart 
 saccular chambers are 
 formed, which ultimately 
 become the auricles and 
 ventricles, and these are 
 at first separated from 
 each other by the auri- 
 cular canal. In the lower 
 vertebrates, however, the 
 auricular canal, owing to 
 the telescoping of auricles 
 and ventricles upon each 
 other, is merely repre- 
 sented by the circular 
 fibres at the auriculo- 
 ventricular junction, 
 though the sinus venosus, 
 
 auricles, ventricles, and bulbus cordis are still distinct. In 
 the mammahan heart the distinction is still more confused, 
 for the sinus has become lost in the great veins and the adja- 
 cent auricular tissue, and the bulbus incorporated in the 
 infundibulum of the right ventricle. The s.a. node is a remnant 
 of the sinus venosus, and the a.v. node and bundle are the sole 
 surviving cells of the auricular canal. The ceUs of the bulbus 
 are indistinguishable from the ventricular muscle. 
 
 At the present time it is generally believed that the rhythmic 
 
 Fig. 58. — The SiJfo-AuEicuLAR Node, show- 
 ing Nodal Tissue and Ganglion Cells. 
 
104 DISEASES OF THE HEART 
 
 action of the heart and the proper sequence of contraction of 
 the various chambers are intimately connected with the in- 
 tegrity of the primitive tissue. The histological differences 
 between these fibres and the rest of the cardiac muscle imply 
 functions of a different nature, and the bundle, at any 
 rate, has been definitely proved to be concerned mth the 
 passage of the stimulus from auricle to ventricle, for it has 
 been shown repeatedly that its destruction produces heart- 
 block. 
 
 In the course of development specialization of function has 
 occurred. In the primitive heart rhj'thmicity and contractile 
 power are fairty equally- developed, and a contraction can 
 originate in any part of its length. But in the vertebrate 
 heart the auricles and ventricles have developed their con- 
 tractile power, and lost to some extent their power of originat- 
 ing contractions, and they only respond with an isolated beat 
 to a single (experimental) stimulus. The parts, however, 
 which remain least altered — the sinus, the a.v. tissues, and the 
 bulb — have, however, in the frog a rhythmic power which is 
 greatty in excess of that of auricle and ventricle, and readily 
 initiate contractions spontaneously, and respond in answer to 
 minimal stimuli, not with an isolated contraction, but with a 
 series of beats. The normal contraction of the auricle starts 
 in the vicinity of the s.a. node, and an extra-systole produced 
 experimentally by stimulation of this area gives an electrical 
 response precisely similar to that of the normal beat, so that 
 the normal auricular stimuli presumably arise in this situa- 
 tion. The response, however, is universal, all the cardiac 
 muscle contracting in sequence, a sequence which is regular in 
 cases where the a.v. bundle is intact. If the latter, however, 
 is functionally inactive, the regular sequence is interrupted, 
 and the auricles and ventricles, if they contract at all, do so 
 irrespective of each other, and at a totally different rate, the 
 auricular contractions numbering about seventy and the ven- 
 tricular contractions about thirty per minute. 
 
 The ventricular contractions in this case are not in response 
 to the normal sinus stimuli, but in answer to stimuh which 
 arise in the ventricular substance; and James Mackenzie has 
 suggested that the^^ may arise in that part of the primitive 
 
THE MYOGENIC THEORY 105 
 
 tissue — the terminal branches of the a.v. bundle — which are 
 present in the ventricles. In full heart-block the rhythm of 
 the ventricles may be quite regular, a fact which suggests that 
 the stimuli habitually arise in the same situation; and electro- 
 cardiograms show a normal ventricular complex, so that the 
 contractions originate in the vicinity of the auriculo-ventricular 
 junction in the region where the a.v. bundle is situated. The 
 theory is attractive, but the evidence in its favour, though 
 suggestive, is not yet conclusive. It must, too, be remem- 
 bered that the cardiac contraction starts in the great veins, 
 and not in the auricles. The nodes may be the "clearing- 
 house," rather than the head office of the bank. 
 
 The influence of the nervous system upon the heart is very 
 apparent both in experiment and in the clinique, but it is 
 regulative rather than essential, for the isolated heart can con- 
 tract regularly for considerable periods under favourable con- 
 ditions. All the functions of the heart — stimulus production, 
 excitability, contractility, conductivit}-, and tonicity — may be 
 affected, but our present knowledge is as yet insufficient to 
 enable us to determine, unless in very exceptional instances, 
 whether functional disturbances of the cardiac action are due 
 to intrinsic or to extrinsic causes. Both may be in action at 
 the same time, or one or other alone, and it seems probable 
 that in the former case the actions of the two are sometimes 
 antagonistic, the one endeavouring to minimize or to prevent 
 a detrimental activity of the other. The present position is 
 thus too indefinite for useful discussion, but it may be stated 
 that the available evidence suggests that exactly similar dis- 
 turbances may be produced by either cause, or at any rate 
 may be due to causes originating without the heart as well as 
 within it. 
 
 The investigation of the special functions of the cardiac 
 muscle, its power of producing rhythmic stimuli, its excita- 
 bihty and contractihty, the variations in the rate of conduc- 
 tion of the stimuli from part to part, and the tonicity of the 
 organ as a whole, has been pursued in the laboratory' for many 
 years past; but it has only been possible within the last few 
 years to apply laboratory methods to chnical work, and to 
 
106 DISEASES OF THE HEART 
 
 investigate tlie different functions individually. By graphic 
 methods the relationship of the contractions of the various 
 chambers can be readily demonstrated, and the advance in 
 our knowledge of cardiac disease has been, in consequence, 
 considerable. Much work has been done, and some problems 
 have already been solved, but many more await solution. 
 Some of the current theories may be disproved in course of 
 time, and others may be verified, but the newer methods have 
 added greatly to precision in diagnosis, prognosis, and treat- 
 ment; and a proper conception of the processes which have 
 produced cardiac failure in the individual case can only be 
 attained by appreciation of the character and the site of the 
 special disturbance. 
 
 la I -75 I a I -8 I B I 7^-1 a I ^♦-^-^ 
 
 Fig. 59. — Brachial, Cervxcal, ksb Apex Curves, showing the Relationship 
 OF THE Various Waves. 
 
 1, Commencement of auricular wave on apex tracing; 2, commencement of ven- 
 tricular upstroke on apex tracing; 3, appearance of carotid wave in cervical 
 curve; 4, appearance of brachial wave; 5, termination of ventricular plateau 
 on apex tracing; 6, termination of ventricular wave on apex tracing. 
 
 The Interpretation of Polygraph Curves. — ^The interpretation 
 of the cervical curves requires detailed consideration, for it 
 must be remembered that the causes producing the variations 
 in pressiKe within the cavities of the heart, as shown experi- 
 mentally, are not yet accurately known, while the data avail- 
 able in chnical work are even less numerous and more obscure. 
 The main points, however, can be seen on examination of 
 Figs. 59 and 60. In both figures the upper curve is from the 
 brachial artery at the level of the elbow; the central curve is 
 from the right neck immediately above the clavicle, and just 
 outside the sterno-mastoid muscle; while the lowest curve is 
 
THE MYOGENIC THEORY 
 
 107 
 
 from tlie apex impulse. The curves are thus not strictly com- 
 parable, for while the first two are records of changes in the 
 volume (mainly) and the pressure within the vessels, the third 
 is the record of the varying relationship of the apex impulse 
 to the chest wall, and not of the intraventricular pressure. 
 
 The apex tracings show as a rule one well-sustained wave 
 and several smaller ones, the large wave representing the 
 ventricular systole. Three phases of the latter can be recog- 
 nized : the more or less abrupt but inclined line of ascent, the 
 flat-topped plateau of the summit, which may be broken up 
 into several minor waves, and the gradual fall to the base-line. 
 During the first phase the intraventricular pressure is rising 
 until it becomes greater than the pressure within the great 
 arteries, when the valves open and blood commences to flow 
 out of the heart. The exact time of this occurrence is not 
 
 Fig. 60. — Brachial, Cervical, ajs^d Apex Ctjeves, showing Absence of 
 X Negative Wave. 
 
 precisely indicated on the curve, and, indeed, is variable in 
 different cases (presphygmic interval, 0'02 to 0*085 second 
 Lewis; cf. Fig. 61), from variations in the aortic pressm'e at 
 the end of diastole and in the relative strength of the ven- 
 tricular systole. During the period covered by the plateau 
 the output is maintained, and about its termination diastole 
 commences and the semilunar cusps close. With relaxation 
 of the ventricle the curve rapidly falls, and as soon as the 
 pressure within the auricle exceeds the pressure within the 
 ventricle, the auriculo-ventricular valves open — a time which 
 coincides fairly accuratelj^ with the lowest point upon the 
 tracing. Succeeding the fall there is often a well-marked wave 
 — an instrumental fault due to the momentum of the recording 
 lever, and best marked in cases where the fall is most abrupt. 
 As diastole proceeds, the curve gradually rises as the ventricle 
 
108 DISEASES OF THE HEART 
 
 again becomes distended with blood. Towards the end of 
 ventricular diastole the small wave a is seen, the result of the 
 contraction of the auricle. The a wave is not invariably 
 present in the tracing, and may be absent in cases where other 
 evidence of auricular activity is undoubtedly present. 
 
 The rise in the brachial curve is distinctly later than the 
 commencement of the ventricular wave on the apex tracing, 
 the delay being due to the presphygmic interval, and to the 
 time occupied in the transmission of the pulse wave from the 
 aorta to the brachial artery {cf. Fig. 61) — a period which neces- 
 sarily varies according to the distance between the two points. 
 
 The cervical curve shows a variable number of waves, which 
 are due to various causes. The receiver of the polygraph is 
 
 <3,^>vto J) ^y-«- '*- 
 
 Fig. 61. — Brachial and Apex Curves, and Tracing (Centre) from Second 
 Left Intercostal Space Close to the Sternum. 
 
 The wave P is evidently derived from the pulmonary artery, and succeeds the 
 rise of the ventricular wave on the apex tracing. The interval between 
 these events is the presphygmic interval. 
 
 placed (Fig. 62) immediately over the carotid arter}' and the 
 jugular vein, and the resultant tracing is a complex of the 
 variations in volume and in pressure which are occiirring in 
 these vessels. 
 
 The essential point in the interpretation of the curve is the 
 detection of the carotid wave c (3), which makes its appear- 
 ance shortly after the commencement of the ventricular con- 
 traction (2), as shown on the apex tracing, and shortly before 
 the appearance of the pulse in the brachial artery (4), and c 
 may be identified by reference to either. If there is any doubt, 
 the receiver may be moved slightly higher up the neck above 
 the valves in the jugular vein, and a pure carotid tracing 
 obtained for comparison. There has been some discussion as 
 to the precise significance of the c wave, for a wave has been 
 
THE MYOGENIC THEORY 
 
 109 
 
 recorded at practically the same time in tracings of intra- 
 auricular pressm^e, as well as in animals whose jugular vein 
 has been dissected out free from all Connection with the carotid 
 artery, so that it must be admitted to be possibly due to causes 
 operating in the jugular bulb. The wave in question arises 
 during the period of ventricular systole, and is probably due 
 to ballooning upwards of the auriculo-ventricular valve during 
 
 :Sterno mastoid 
 i 
 
 ^i-O 
 
 Clavicle 
 
 Manubrium sterni 
 
 Fig. 62. — Diagram showing the Situation of the Carotid Artery and the 
 JuGUi/AR Vein. (A. Keith.) 
 
 The circle shows the position of the receiver of the polygraph. 
 
 that event; but it is not invariably present in all tracings of 
 intra-auricular pressure, and it is usually small. Firm pres- 
 sure of the receiver in the neck frequently produces a wave of 
 typical arterial form, and — in the vast majority of cases, at 
 any rate — the c wave is due to the carotid pulse. 
 
 Immediately preceding c is the wave a. It occurs about 
 0*15 to 0"20 second before c, and synchronously with, or im- 
 mediately after, the a wave on the apex tracing, and is the 
 
110 DISEASES OF THE HEART 
 
 result of auricular contraction. There is but little delay in 
 its appearance, for there are no valves between the auricle and 
 the jugular bulb beneath the receiver, and the distance is but 
 short ; so that variations in pressure within the auricle are 
 rapidly transmitted to the jugular vein. There is still some 
 doubt as to its exact significance, and it has been ascribed to 
 regurgitation into the veins during auricular systole, and to 
 stasis in the veins without regurgitation, following the sudden 
 rise of auricular pressure during systole. From a practical 
 point of view the distinction is immaterial, and the wave may 
 be considered as definite evidence of auricular contraction. 
 
 The wave v following c varies considerably in different cases, 
 both in the time of its occurrence and in its form. In many 
 cases it is separated from c b}- the negative depression x, and 
 it may be single or double (wi-Vg). 
 
 The early part at any rate occurs during ventricular systole, 
 and the notch between the two peaks of the double wave is 
 generally synchronous with the termination of the systohc 
 plateau (5) in the apex tracing. With the onset of ventricular 
 systole the auriculo-ventricular valve is closed, and the pres- 
 sure within the auricle is at its minimum. During ventricular 
 systole venous blood gradually enters the auricle, and the 
 pressure within it rises steadily until at the completion of 
 ventricular systole the auriculo-ventricular valves again open, 
 and the auricular pressure falls as the blood flows from the 
 auricle into the ventricle, and the wave in consequence dies 
 away. 
 
 The second wave V2, however, occurs after the systolic 
 plateau has ended, and is therefore ventricular diastohc in 
 time, and its occurrence must be due to other causes. 
 
 During the contraction of the heart the apex is the only 
 part which remains constant in position within the chest- 
 During auricular systole the auriculo-ventricular junction is 
 pulled upwards towards the great veins, and during ventricular 
 systole pulled downwards towards the apex (Keith), and the 
 ventricular movement downwards expanding the auricle is 
 probably the chief cause of the negative depression or wave x. 
 When ventricular systole ceases, the pull on the auriculo- 
 ventricular junction ceases, too, and it resumes its mean 
 
THE MYOGENIC THEORY 111 
 
 position, and the "rebound," when it is active, produces the 
 positive variation, wave v<i, in the jugular curve. 
 
 In certain cases v vnsbj occur earlier in the tracing, and it 
 may even merge into c, as in Fig. 60. This may be due to two 
 causes : v will appear the earlier the more rapid the diastohc 
 filling of the auricle, and this will obtain whenever there is 
 venous engorgement ; and it will also occur early if the auriculo- 
 ventricular valve is incompetent, and blood regurgitates into 
 the auricle at the commencement of ventricular systole. 
 
 The depression x has alreadj^ been ascribed — in part, at any 
 rate — ^to the negative pressure produced in the auricle during 
 ventricular systole by the displacement of the auriculo-ven- 
 tricular junction. Another factor probably coexists. During 
 ventricular systole blood is forced out of the chest into the 
 arteries, and the intrapleural pressure falls as a result, and the 
 intra-auricular pressure will foUow suit. 
 
 The depression y (Fig. 59), which foUows v, is the result of 
 ventricular diastole. As soon as the auriculo-ventricular 
 valves open, blood flows from auricle to ventricle, and the 
 auricular and the jugular pressures fall until, with the lapse of 
 time, both auricle and ventricle are again filled by the inflow 
 of the venous blood, and, in consequence, the lever gradually 
 rises during diastole. 
 
 There has been much difference of opinion as to the precise 
 time of the closure of the semilunar valves and the opening of 
 the auriculo-ventricular valves. 
 
 It seems quite certain that the time of the opening and the 
 closure of the semilunar valves cannot be recognized upon the 
 apex tracing. The valves open synchronously with the ap- 
 pearance of the aortic pulse, and close coincidently with the 
 occurrence of the dicrotic notch, and experimental curves show 
 that these events have no constant relationship with the apex 
 tracing, varying considerably in different cases, the opening 
 occurring during the fine of ascent, and the closure before, 
 at, or after the termination of the plateau. The trans- 
 mission time, too, varies, and corresponding periods in the 
 carotid or brachial pulse cannot be accurately related to the 
 same events in the aorta. 
 
112 DISEASES OF THE HEART 
 
 A similar conclusion must be asserted with regard to the 
 period when the auriculo-ventricular valves open. It seems 
 certain that they close synchronously with the commencement 
 of the upstroke of the sj^stoHc plateau, and that the}^ open 
 after ventricular systole has ceased, as soon as ventricular 
 relaxation has reduced the intraventricular pressure below 
 that in the auricle ; but the pressure within the auricle, at the 
 commencement of ventricular diastole, maj^ var}^ even in the 
 same case from varying degrees of engorgement of the veins, 
 varying length of ventricular systole, etc., and the rapidity of 
 lowering of ventricular pressure is also inconstant, so that the 
 relationship on the apex tracing cannot be fixed. The cervical 
 curve is, however, a more accurate guide, and the apex of v 
 (or the notch between v^ and Vg) seems probabty the period 
 required. 
 
 The a-c interval in the cervical curve has acquired con- 
 siderable importance, since it is used as an index of the time 
 occupied b}^ the transmission of the stimulus from auricle to- 
 ventricle. In a general way the deduction is justified, but it 
 must not be carried too far. During the a-c interval five 
 events occur: (1) The contraction of the auricle; (2) the pas- 
 sage of the stimulus from auricle to ventricle; (3) the latent 
 period after the stimulus has reached the ventricle; (4) the 
 presphygmic interval; and (5) the time occupied by the trans- 
 mission of the pulse wave from aorta to carotid. The a wave 
 is not an accurate index of the duration of auricular systole, 
 for experimental evidence points to the continuance of auricular 
 contraction after ventricular contraction has commenced. We 
 have no knowledge of the duration of the latent period, but 
 we know that the presphygmic interval varies considerably 
 (0"02 to 0'085 second) in experimental curves, and that the 
 transmission time depends upon the distance traversed, the 
 aortic pressure at the end of diastole, and the pressure reached 
 during the presphygmic interval. Chnically, the two items can- 
 not be separated, but together (commencement of V in apex 
 tracing — appearance of c in cervical curve) they may vary from 
 0-03 to 0*11 second. 
 
 The a-c interval measures as a rule 0' 15 to 0-20 second, and 
 it is not likely to be greatly prolonged by variations in factors 
 
THE MYOGENIC THEORY 113 
 
 1, 3, 4, 5. If it exceeds 0-25 second, conduction is probably 
 defective and prolonged, but smaller variations from tlie 
 average may perhaps be produced by other causes. 
 
 H (b) Wave. — In slowly beating hearts a wave {h or h) may 
 be seen in the cervical curves between v and the succeeding 
 a waves (Fig. 63). Its time relationship to the preceding 
 c wave is constant in the particular case (about 0* 50 second), 
 and it has been ascribed by A. G. Gibson and Hirschfelder to 
 
 EiG. 63. — Ceevical a^-d Apex Ctteves, showing the Wave Ti or h. 
 
 the snapping together of the cusps of the aiu'iculo-ventricular 
 valve at the end of ventricular filling in micl-diastole. A 
 similar wave may be present in oesophageal tracings. When 
 the pulse quickens, the wave in question disappears. 
 
 In cases of lengthened a-c interval the possibility of h and a 
 being mingled together must be borne in mind. The fallacy 
 can be detected by reference to the apex tracing, as the com- 
 mencement of a in the cervical curve and a in the apex tracing 
 do not coincide. 
 
 REFERENCES. 
 
 G. A. Gibson: The Nervous AfEections of the Heart, Edinburgh, 1904. 
 W. H. Gaskell: Article in Schafer's Textbook of Physiology, vol. ii. Edin- 
 burgh and London, 1900. 
 JoknIIay: Graphic Methods in Heart Disease. London, 1909. 
 T.Lewis: 
 
 Article in Hill's Further Advances in Physiology. London, 1909. 
 
 Mechanism of the Heart-Beat. London, 1911. 
 James Mackenzie: 
 
 The Study of the Pulse. Edinburgh and London, 1902. 
 
 Diseases of the Heart. London, 1908. 
 P. Mkrklen: Les Troubles Functionnels du Coeur. Paris, 1908. 
 W. T. Ritchie : The Action of the Vagus on the Human Heart. Quart. Journ. 
 
 of Med., 1912, Oxford, vol. vi., p. 47. 
 H. Vaquez: Les Arythmies. Paris, 1911. 
 K. F. Wenckebach: Arhythmia of the Heart. Edinburgh, 1904. 
 
 8 
 
CHAPTER VII 
 THE ELECTRO-CARDIOGRAPH 
 
 By W. T. Ritchie 
 
 When any point of a muscle or other excitable tissue is 
 stimulated, a change of electric potential is induced. The part 
 which is stimulated and in activity becomes electro-negative 
 to the parts at rest, and may be regarded as corresponding to 
 the zinc plate of a galvanic cell; the remainder of the muscle, 
 which is at rest, corresponds to the copper plate. If the active 
 and passive portions of a muscle are connected by means of 
 electrodes to a sensitive galvanometer, the changes in electric 
 potential accompanying muscular activity — the action currents 
 of the muscle — can be recorded by the instrument. Waller, 
 in 1887, was the first to register the action currents of the 
 human heart. He employed a capillary electrometer, and 
 showed that they were transmitted throughout the body, and 
 could be led off from moist skin surfaces. But as action cur- 
 rents are extremely feeble, and as the interpretation of capil- 
 lary electrometer curves is attended with considerable diffi- 
 culty, Einthoven employed the string galvanometer, and it is 
 this instrument, with his modifications, that is now being used 
 extensively in physiological and chnical work. 
 
 The string galvanometer is based on the principle that a 
 moving conductor (a fijie fibre), suspended in a magnetic field 
 at right angles to the lines of force, tends to be deflected to 
 one side or other according to the direction of the current. 
 The extent to which the fibre is deflected varies in direct pro- 
 portion to the intensity of the current passing through it, and 
 to the strength of the magnetic field, and inversely to the 
 weight and tension of the fibre. In Einthoven's string gal- 
 vanometer the currents are led through an extremely fine 
 
 114 
 
THE ELECTHO-CARDIOGRAPH 115 
 
 silvered glass or quartz fibre, which is stretched between the 
 poles of a powerful electro-magnet. Accompanying each con- 
 traction of the heart there are changes of electric potential;, 
 the fibre oscillates to and fro, and its shadow can be projected 
 upon a moving photographic plate. The record thus obtained 
 is termed an " electro-cardiogram." 
 
 The records should be taken while the patient is recumbent 
 or rechning quietly in a chair, so as to avoid as far as possible 
 all tremor of the somatic muscles, which distort the electro- 
 cardiogram. The currents are led off from the two hands, or 
 from one hand and one foot, immersed in porous jars filled with 
 sahne solution. These jars He within earthenware pots con- 
 taining zinc sulphate solution and an amalgamated zinc rod,, 
 which can be connected to the ends of the fibre. The proce- 
 dure is consequently not more irksome to the patient than 
 that entailed in obtaining a graphic record by means of the 
 polygraph. As compared with the polygraph, the string gal- 
 vanometer has the great advantage of ehminating the fallacies 
 dependent upon inertia, and upon the delay in the transmis- 
 sion of mechanical impulses. Its chief value, however, con- 
 sists in the fact that by it alone do we obtain information 
 regarding the essential nature of each heart-beat. 
 
 The form of the electro-cardiogram varies according to the 
 derivation that is employed. Follo\\dng Einthoven's nomen- 
 clature, a lead from the right hand and left hand is termed 
 "Derivation /.," that from the right hand and left foot is 
 ''Derivation //.," and that from the left hand and left foot 
 is "Derivation ///." When recording electro-cardiograms it 
 is customary to adopt Einthoven's standard, and to a-djust the 
 tension of the fibre so that, -with a constant magnification, its 
 shadow is deflected 1 cm. when a difference of potential of 
 1 milhvolt is introduced into the circuit containing the gal- 
 vanometer and the patient. It is, therefore, possible to insti- 
 tute a comparison of the amphtude of the individual deflexions 
 in different records. 
 
 Fig. 64 shows a normal electro-cardiogram by Derivation II, 
 Each upward deflexion P, R, and T, indicates that either the 
 base or right side of the heart was electro-negative, and there- 
 fore in predominant activity, whereas the downward deflexions 
 
116 DISEASES OF THE HEART 
 
 Q and & signify negativity — ^.e., predominant activity — of the 
 apex or left side of the heart. P is the auricular deflexion; 
 Q, R, S, and T are ventricular deflexions. In some instances 
 T is succeeded by another upward deflexion, U. Fig. 65 
 demonstrates the time relation of the waves in the cervical 
 cm've to the electro-cardiographic deflexions. The auricular 
 wave, a, in the jugulo-carotid tracing is later than the electro- 
 cardiographic deflexion P, owing to the material delay in the 
 transmission of impulses recorded by the potygraph. The 
 carotid wave, c, is later than the deflexion R for the same 
 reason, and also because of the presphygmic period and the 
 delay in the transmission of the pulse wave from the aortic 
 valve to the carotid artery. 
 
 The Electro-Cardiographic Deflexions. — In a healthy heart the 
 auricular deflexion, P, is a simple upward deflexion. Although 
 
 Fig. 64. — ^Normal Electeo-Cabdiogkam. 
 Derivation II. 1 mi]livolt=l cm. Time record is 28'o per second. 
 
 the amphtude of the electro-cardiographic deflexions cannot be 
 regarded as a definite measure of the electro-motive force of 
 the heart, we nevertheless find that P is larger than normal in 
 cases of auricular hypertrophy, and more especially in cases 
 of mitral stenosis. When P is of abnormal form — diphasic, 
 inverted, etc. — it is generally supposed that the auricular con- 
 traction has started at some other site than the normal one in 
 the sino-auricular node. For example, diphasic auricular de- 
 flexions may ensue when the heart is retarded by stimulation 
 of the vagus, or when the auricles are in flutter (Fig. 70). 
 According to Rothberger and Winterberg, P becomes inverted 
 when the left accelerator nerve is stimulated, and it is prob- 
 able that under these circumstances the left auricle begins to 
 contract before the right. 
 
THE ELECTRO-CARDIOGRAPH 117 
 
 During the interval between P and Q, while the curve 
 remains horizontal, the ventricles are still at rest ; and although 
 a stimulus is passing along the auriculo-ventricular system to 
 the ventricles, the accompanying change of potential is too 
 weak to cause any deflexion of the fibre. 
 
 Q, B, S, and T are the deflexions resulting from ventricular 
 activity. Their precise interpretation is still a matter of 
 doubt and discussion. The deflexions Q, R, and S probably 
 indicate that the stimulus passing from the auricles along the 
 terminal ramifications of the a.v. bundle reaches different parts 
 of the ventricles ahnost simultaneously. E is the most con- 
 stant of all the deflexions, and is generally regarded as signi- 
 
 Fig. 65. — Simultaneous Records of the CER\acAL Curve axd of the Electro- 
 Cardiogram (Derivation //.). illustrating the Time Relation of the 
 Waves in the Cervical Curve and the Deflexions of the Electro- 
 Cardiogram. 
 
 P precedes a, and R precedes c. 
 
 fying contraction of the basal part of the papillary muscle 
 system. The fijst sound commences 0'02 to 0"03 second after 
 the beginning of the first ventricular deflexion. The period 
 between S and T, during which the line of the curve is again 
 horizontal, coincides with the contraction of the main mass of 
 ventricular muscle. The action currents compensate one 
 another meanwhile, so that there is no predominance of activity 
 either at base or apex or of one ventricle over the other. In 
 the case of a healthy heart, the final deflexion, T, is upwards. 
 Some authorities regard an upward T as signifying that the 
 right ventricle remains in contraction longer than does the 
 left, whereas others conclude that when each contraction wave 
 
118 
 
 DISEASES OF THE HEART 
 
 spreads through the ventricular muscle the last portion to con- 
 tract is that near the aorta and pulmonary artery. Jolly and 
 the writer have concluded that in records by Derivation I. 
 an upward T may be regarded as indicating that the activity 
 of the right ventricle at the end of systole predominates over 
 that of the left, whereas a downward T, as recorded by Deriva- 
 tion /., imphes predominant activity of the left ventricle. 
 
 In some cardiac affections the electro-cardiogram presents 
 ^.bnormal features. 
 
 1. Heart Failure.— In a healthy heart, T, as recorded by 
 Derivation /., is always an upward deflexion. An inverted T 
 
 3 
 
 Fig. 66. 
 
 1 and ^ are electro-cardiograms by Derivations /. and ///. from a case of mitral 
 stenosis; 3 and 4 are electro-cardiograms by Derivations /. and III. from a 
 case of aortic incompetence. 
 
 deflexion (by Derivation /.) is one of the most constant and 
 reUable electro-cardiographic indications of ventricular weak- 
 ness, and is probably evidence of relative failure of the conus 
 arteriosus of the right ventricle. 
 
 2. Mitral Stenosis. — Many cases of mitral stenosis (Fig. 66: 
 1, 2) yield electro-cardiograms in which the ventricular de- 
 flexions present the following characteristic features — namely, 
 M by Derivation /. is smaller than R by Derivation ///., and 
 8 by Derivation I. is larger than 8 by Derivation ///. These 
 
THE ELECTRO-CARDIOGRAPH 119 
 
 changes are due to the predominant hypertrophy of the right 
 ventricle that results from the mitral lesion. 
 
 3. Aortic Incompetence. — In many instances the character- 
 istic electro-cardiographic features (Fig. 66: 3, 4) are the 
 reverse of those observed in mitral stenosis. R by Deriva- 
 tion I. is larger than R by Derivation ///., while 8 by Deriva- 
 tion /. is smaller than 8 by Derivation ///. The changes are 
 the expression of predominant hypertrophy of the left ven- 
 tricle. 
 
 4. Defects o£ Conduction — Heart-Block. — Dm-ing the in- 
 terval P-Q (or P-R), the stimulus is being transmitted along 
 the conducting system from auricles to ventricles, and the 
 duration of this interval indicates the rate at which the stimulus 
 
 IAJ.>vJp^Jl>\JJ 
 
 Fig. 67. — Partial Heart-Block. 
 
 The cervical curve and the electro -cardiogram (Derivation II.) from a case of 
 mitral stenosis without presystolic murmur. 
 
 is being conducted. The P-Q or P-R interval is a better index 
 of the rate of conduction than the a-c interval in a jugular 
 tracing, for the electro-cardiogram obviates the fallacies of an 
 unknown presphygmic period and of the time that has to 
 elapse between the opening of the aortic valve and transmis- 
 sion of the pulse wave to the artery in the neck. 
 
 Minor degrees of impaired conductivity in the bundle can 
 be recognized readily in electro-cardiograms. In Fig. 67, 
 from a case of mitral stenosis, the P-R interval measures from 
 0'28 to 0*31 second, which is approximately twice the duration 
 of the P-R interval in health (0' 14 second). 
 
 When conductivity in the auriculo-ventricular bundle is still 
 further impaired, so that either partial or complete heart- 
 block results, the defect is well seen in electro-cardiograms. 
 
120 
 
 DISEASES OF THE HEART 
 
 Fig. 68, obtained from a man aged seventy-five, is an illustra- 
 tion of complete heart-block. The auricular deflexions, P, 
 occur rhythmicall}^ at a rate of ninety-seven per minute; the 
 ventricular deflexions are rhythmic at a rate of thirty-eight 
 per minute, and there is complete dissociation of the auricular 
 and the ventricular rhythms . 
 
 By means of the electro-cardiograph a complete severance 
 of either the right or left branch of the bundle may be recog- 
 
 
 
 Fig. 68. — Electeo-Caediogram from a Case of Full Heart-Block (Deriva- 
 tion /.). 
 
 The auricular rate is 97, the ventricular rate 38, per minute. 
 
 nized. When, for example, the right branch is severed, each 
 auricular stimulus passes to the two ventricles through the 
 left branch alone, and all the ventricular deflexions have the 
 same characters as those of an extra-systole originating in the 
 left ventricle. 
 
 5. Extra-Systoles can be recognized with great precision 
 in electro-cardiograms. An auricular extra-systole is repre- 
 
 ^^l^ 
 
 Fig. 69. — Coupled Rhythm of Ventricles, due to kegulaely eecuering 
 Ventricular Extra-Systoles. 
 
 The auricular deflexions P are rhythmic throughout (Derivation //.). 
 
 sented by an initial auricular deflexion which is premature, 
 usually of abnormal form, and often inverted, indicating 
 that the beat does not originate in the sino-auricular node, 
 but is of ectopic origin. This auricular deflexion is suc- 
 ceeded by ventricular deflexions which are usually of normal 
 form. 
 
THE ELECTRO-CARDIOGRAPH 
 
 121 
 
 A ventricular extra-systole yields an " atypical " electro- 
 cardiogram because the stimulus exciting the premature beat 
 spreads through the ventricular musculature in an abnormal 
 manner. The deflexions representing a ventricular extra- 
 systole are usually of larger amphtude than those of a physio- 
 logical beat, and are in striking contrast to the feeble puLse- 
 
 iiiiniiiiiiiihiiiiaauiiuiuiiiiUiiiiiiiiuiAiiiiimmiiuiiiuiiiitiiuiiiiiiiiiiiAiiiiiiiiiiiiuiii.uuiiiiuiiiiiiyuiiiiti 
 
 Fig. 70. — AtrRicuLAR Flutter. 
 
 The auricular deflexions are diphasic and rhjiihmic, and number 281 per minute. 
 The ventricular contractions number 70'25 (Derivation //.). 
 
 wave transinitted into the arteries. Two main varieties of 
 ventricular extra-systole are recognized: (1) Left apical extra- 
 systoles, in which the deflexion is first downwards and then 
 upwards ; and (2) right basal extra-systoles, in which the de- 
 flexion is first upwards and then downwards (Fig. 69). It is 
 important to note that the first variety of extra-systole, 
 
 u^..4v.-4. 
 
 nniiiiiiimuiiiuuimiiUiJiUiuJiiiJiiiiiiuiiiiijUiUiimiiiMMiiUiMUiiiiiiAtiiiuuiuimiuiuuiiiiiiMiiniiiiiiiiiiiiiiiiiiiiiit 
 
 Fig. 71. — Aukicitlar Fibkillation. 
 
 The auricular deflexions are small, irregular, and frequent, 
 rhythm is irregular (Derivation //.). 
 
 The ventricular 
 
 when recorded by Derivation /., usually yields the same 
 form of electro-cardiogram as does the second variety 
 by Derivation ///., and that the latter bj^ Derivation I. 
 presents the same form as does the first variety by Deriva- 
 tion III. 
 
 Nodal extra-systoles present ventricular deflexions similar to 
 
122 DISEASES OF THE HEART 
 
 those of a genuine ventricular extra-systole, but tlie auricular 
 deflexion is also premature, and may be inverted. 
 
 6. Auricular Flutter is characterized by rhythmic co-ordinate 
 contractions of the auricular musculature at a greatly acceler- 
 ated rate — usually 250 to 300 per minute. In most instances 
 the ventricles respond to every second or every fourth auricular 
 beat. Electro-cardiograms are extremely helpful in deter- 
 mining the existence of auricular flutter. In Fig. 70 the 
 diphasic auricular deflexions occur rhythmically at a rate of 
 281 per minute ; the ventricles, meanwhile, are beating rhythmi- 
 cally at a rate of 70' 25 per minute. In earher records from 
 this case the auricular and ventricular rates were 283 and 
 141" 5 respectively. After digitahs had been administered for 
 several days the auricular flutter became replaced by fibrilla- 
 tion. 
 
 7. Auricular Fibrillation. — As this subject is discussed fuUy 
 in Chapter XVII., one electro-cardiogram wiU suffice to illus- 
 trate the essential features. Throughout the record in Fig. 71 
 there is a series of small, rapid deflexions, irregular in time and 
 form, characteristic of auricular fibrillation. The record also 
 shows the whoUy irregular rhythm of the ventricles in conse- 
 quence of the auricular fibrillation. The rate of the auricular 
 deflexions in cases of fibrillation is usually from 400 to 600 per 
 minute. 
 
^^Ovjv>jvJv_juCa^^ 
 
 Fig. 72.~RBSPiRATORr and Pcjlse Curves, 
 
 ; Variations in the Cahdiao Rhythm which abe sometimes 
 
 _AAAivJvjVJVMVjviv^.JvAJ^.K 
 
 Rhythm of the Respibations. 
 
 116 S^st. 
 '^7 JJin^C 
 
 TL___MUl)»'»'''~"™"M««n 
 
 ■WVMWWWWMWMWWWW/MWJl 
 
 I'la. 73.— SrilYOMOMMOMKTEIO TEiCINO, SnOWINO Tl 
 LOWEK PllBSSDBE 01 TUE ExTEA-SysTOUO BbaT, 
 
 -^'i L ■■■? 
 
 i Lli I Mt 
 
 f^^fcS=!t 
 
 Fio. 74.— Ihteepolatbd Vektrioolae Extea-Systole. 
 Tho rhythm of the heart is otherwise unchanged. 
 
 Fig. 75. — Venteicdlae Extea-Systolb. 
 
 The ventricular contractiun precedes the regular auricular contraction, 
 which is not succeeded by a ventricular contraction, as the ventricle is 
 still refractory. 
 
CHAPTER VIII 
 STIMULUS PRODUCTION 
 
 In the healthy adult the pulse beats fairly regularly, and 
 about seventy times per minute when the individual is at rest. 
 In infancy and childhood, however, the rate is more frequent, 
 and it may vary very considerably, becoming more rapid on 
 exertion, with emotion, and after the ingestion of food. The 
 rhythm, too, is often irregular, especially during sleep, but 
 polygraph tracings show a normal a, c, v. curve, so that the dis- 
 turbance must be due to a disordered sinus rhythm in response 
 to causes arising outside the heart. 
 
 The maximal irregularities are associated with irregularity 
 in the respiratory phases. The breathing of a child at rest 
 and during sleep is often irregular, and the pulse corresponds 
 ■with this in a general way, and becomes more frequent and 
 more regular when the breathing does the same. In adoles- 
 cents, and less frequently in adults, a similar irregularity is 
 not uncommonl}' observed, and it is important to recognize its 
 nature, for it has no serious significance. A diagnosis can be 
 easily made on examination, for the irregularity is found to 
 correspond "wdth voluntary irregularity in breathing, and to 
 disappear wholly or in part when the patient breathes fre- 
 quently and regularly, or ceases breathing altogether. The 
 association is clearly seen in Fig. 72. At the commencement 
 of the tracing the pulse during quiet breathing is notably 
 irregular, long diastoles occurring before each inspiration. 
 When voluntary apnoea is produced, the long diastoles are 
 more frequent; but diastole is shorter when the respirations 
 become more frequent and the pulse is much more regular. 
 
 As a matter of fact, careful measurement of normal tracings 
 in adults shows that the regularity of the cardiac action is 
 
 123 
 
124 DISEASES OF THE HEART 
 
 apparent, and not real, though the rhythm appears regular to 
 the finger and even on auscultation. In childhood all the 
 functions are unstable. Children laugh and cry on shght 
 provocation ; their temperature rises to inordinate heights from 
 trivial causes ; and an irregular pulse should be looked upon as 
 an indication of the same tendenc}^ 
 
 In disease both the rhythm and the rate of the pulse may 
 vary considerably. The pulse is almost always more frequent 
 in fever, and it is often notably infrequent during convalescence 
 from acute disease, in intoxications such as jaundice, and in 
 cerebral diseases such as meningitis, haemorrhage, and tumour. 
 In Cheyne-Stokes or cyclic breathing the pulse-rate often 
 varies during the different respiratory phases (Fig. 146), but the 
 association is not constant, for it may be unaltered or more or 
 less frequent during, say, apnoea in different individuals. The 
 curves, too, do not correspond, and the maximal changes are 
 not coincident, while polygraph curves are normal. Irregu- 
 larities of this kind have no cardiac significance, and must be 
 regarded as evidence of an intoxication. They disappear with 
 improvement in the other symptoms. 
 
 These variations in the rate and rhythm of the pulse are 
 probably due to variations in the rate and rhythm of stimulus 
 production, though they might, of course, result from dis- 
 turbances of excitabihty, a smaller stimulus sufficing to produce 
 a contraction when this function is exalted, and vice versa. 
 
CHAPTER IX 
 EXCITABILITY 
 
 The regular sinus rhythm of the heart may be at times inter- 
 rupted by the occurrence of a " premature or extra- systole in 
 response to a stimulus arising at some abnormal site in the 
 heart, the fundamental or sinus rhythm being otherwise main- 
 tained " (James Mackenzie), An extra-systole is readil}^ recog- 
 nized when feehng the pulse, the regular sequence of beats 
 being interrupted by the occurrence of an early wave, which 
 is followed by an interval of longer duration than the average. 
 An extra-systohc beat is always of smaller volume, of shorter 
 duration, and of lower pressure (Fig. 73) than the normal 
 beat ; for, as a result of the shorter diastole, the ventricle is not 
 well filled with blood, and its output is, in consequence, les- 
 sened; its contractility is not fully restored, and the maximal 
 contraction possible is of shorter duration and lessened power : 
 while the aortic blood-pressure is still at a higher level than is 
 reached after an interval of normal length. The post-extra- 
 systohc beat, too, is abnormal as a rule, being, on account of the 
 prolonged diastole, a larger, stronger, and better sustained wave. 
 
 Three varieties of extra-systole are now recognized — namely, 
 ventricular, auricular , and nodal. 
 
 Ventricular Extra-Systoles. — A ventricular extra-systole may 
 not interfere with the normal sinus rhythm (interpolated ven- 
 tricular extra-systole). An example is shown in Fig. 74, where 
 the premature wave r' in the brachial tracing (the result of a 
 contraction of the left ventricle) corresponds with c' in the 
 cervical curve, its equivalent carotid expression, and c' is 
 succeeded by the auricular wave a at the usual time. A con- 
 traction of the left ventricle has occurred prematurely, but 
 otherwise the sinus rhythm remains unaltered. 
 
 125 
 
126 
 
 DISEASES OF THE HEART 
 
 Ventricular extra-systoles do not as a rule interfere with the 
 rhythmic beats of the auricle. In Fig. 75 a "sinus " ventricu- 
 lar contraction is lost, for the ventricle being aheady in con- 
 traction as a result of the abnormal stimulus, is, in consequence, 
 refractory, and cannot respond when the " normal " stimulus 
 
 Fig. 76. — Vektricular Extea-Systole. 
 
 The double period 3-4 is exactly equal to twice the normal pulse period. 
 The post-extra-systolic pause is fully compensatory. 
 
 arrives from the auricle. Ventricular extra-systoles may, as 
 in this case, precede an auricular contraction, or they may 
 succeed it or may occur synchronously. In the latter case, 
 since the auriculo-ventricular valves are shut during ven- 
 tricular systole, the " wave in the cervical curve is large, as 
 the contents of the auricle are returned into the jugular vein. 
 
 t^ 
 
 ■bS 
 
 ■ts 
 
 •feS- 1-35 I -7 I -7 1-3 g I -7 I 7 I -65- |av^cPi^ 
 
 (Xc V o-c V a-c V CO. ^^a c vMac v cQu olc \/ a^c w ac \j ac v 
 
 Fig. 77. — Venteictjlar Extra-Systole, followed by an Auriculae Extea- 
 Systole. 
 
 The post-extra-systolic pause is'short. 
 
 The pause which occurs after a ventricular extra-sj-stole is 
 as a rule prolonged, and of such a length that, taken in conjunc- 
 tion with the pulse period preceding the extra-systole, it measures 
 exactly double the normal pulse period, the post-extra-systoHc 
 ventricular contraction being delayed until the next sinus 
 
EXCITABILITY 
 
 127 
 
 stimulus, whose rhythm is undisturbed, passes through the 
 auricle, and reaches the ventricle (Fig. 76). 
 
 In certain cases the post-extra-systolic pause is not fulh^ 
 compensatory, as in Fig. 77, where it is of normal length, an 
 auricular extra-systole succeeding the ventricular extra-systole 
 and disturbing the sinus rhythm. Auricular extra-systoles not 
 infrequently succeed ventricular extra-systoles, for when, as 
 in this case, the auricular and the ventricular contractions 
 coincide, the auricle at the termination of systole is incom- 
 pletely emptied, and being rapidly distended during diastole 
 by the blood flowing quickly into it from the over-distended 
 vena cava, is induced to contract prematurely by the sudden 
 increase of pressure within its cavity. 
 
 Fig. 78. — Auricular Extra-Systoles. 
 The a-c interval is prolonged (0"25 second) with the extra- systolic beats. 
 
 Auricular Extra-Systoles. — In auricular extra-systoles 
 (Fig. 78) the premature contraction commences in the auricle, 
 and is followed by a premature ventricular contraction. As 
 diastole in these cases is short, conductivity is imperfectly 
 restored, and the interval between the auricular and the ven- 
 tricular contractions is unduly prolonged. The presphygmic 
 interval and the transmission time are also necessarily in- 
 creased, and the a-c interval in the cervical curve exceeds the 
 normal 0-15 to 0*20 second. The post-extra-systohc pause is 
 rarely fuUy compensatory, for the sinus rhythm is dis- 
 turbed, its stimulus material being " exploded " prematurely, 
 and the succeeding "sinus " beat is, in consequence, pre- 
 mature. 
 
 Nodal Extra-Systoles. — The third form of extra-systole is 
 styled "nodal " b}' James Mackenzie, on the ground that the 
 stimulus probabl}^ arises in the vicinity of the a.v. node. A 
 
128 
 
 DISEASES OF THE HEART 
 
 nodal extra-systole is shown in Fig. 79, where both the a' and 
 the c' waves are premature. 
 
 The a-c interval in normal cervical curves measures about 
 
 0"15 to 0"20 second, being slightly 
 shorter if the pulse-rate is fre- 
 quent. During the a-c terval 
 five events occur : (1) The auricular 
 systole, which lasts for about 0*10 
 second; (2) the passage of the 
 stimulus from auricle to ventricle ; 
 (3) the latent period of ventricular 
 contraction; (4) the period of 
 ventricular systole prior to the 
 opening of the aortic cusps (pre- 
 sphygmic interval) ; (5) the trans- 
 mission of the aortic wave to the 
 carotid artery. The average period 
 between the commencement of 
 ventricular systole and the ap- 
 pearance of the carotid wave in 
 the 'neck (4 and 5) is 0"06 second 
 (0-03 to 0-11 second), while the 
 commencement of auricular sys- 
 tole practically coincides with the 
 appearance of the a wave in the 
 jugulo-carotid tracing. The pre- 
 sphygmic interval and the trans- 
 mission time are invariably 
 lengthened in premature systoles 
 (Fig. 80), and it thus seems proba- 
 ble that whenever the a-c interval 
 in the cervical cmve measures less 
 than 0"10 second, the auricle and 
 ventricle respond to a common 
 stimulus which arises between 
 them. 
 
 Tracings of a comparable kind have been produced experi- 
 mentally, and Lewis has shown that in the cases which we are 
 considering the auricular electric complex is inverted, resembhng 
 
EXCITABILITY 
 
 129 
 
 an auricular complex produced by stimulation of the auricular 
 muscle near the auriculo-ventricular sulcus ; while the ven- 
 
 tricular complex is normal, and re- 
 sembles a ventricular contraction pro- 
 duced by a stimulus arising near the 
 auricle. 
 
 (The meaning of an inverted P is, 
 however, by no means decided, for 
 Rothberger and Winterberg have shown 
 that it may occur when the left auricle 
 commences to contract before the right.) 
 
 As a rule in these cases a' precedes 
 c', but sometimes c' precedes a' (Fig. 81), 
 and in other cases a' and c' are inex- 
 tricably mingled, and the " wave is 
 large, for the auricular contraction is 
 occurring at a time when the auriculo- 
 ventricular valves are shut, and the 
 auricular contents are, in consequence, 
 thrown back into the veins. But in 
 all three varieties the auricular and the 
 ventricular contractions are prematuie, 
 and separated by an extremely short 
 interval. They differ in this respect 
 from auricular extra-systoles in which 
 the a-c interval is always prolonged. 
 
 \ 
 
 Little information is as yet available 
 regarding the causes of extra-systoles. 
 Experimentally they can be produced 
 in various ways : by direct application 
 of mechanical, thermal, electrical, or 
 chemical stimuH ; by clamping the aorta, 
 the pulmonary artery, or the great veins ; 
 by ligation of a branch of the coronary 
 arteries ; and by the injection of digitahn, 
 adrenahn, aconitine, muscarine, and 
 physostigmine. It is well known that they can be produced 
 in hearts which are isolated or whose nervous connections 
 
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130 
 
 DISEASES OF THE HEART 
 
 m 
 
 kin 
 
 are wholly severed, so that it seems that the cause must be 
 sought for in the heart itself. 
 
 The direct apphcation of stimuli to excitable muscle natur- 
 ally provokes a contraction ; the obstruction of a great artery" 
 
 produces over-distension of the cavities 
 behind the block, and provides a 
 mechanical stimulus ; ligation of a 
 coronary branch interferes with the 
 nutrition of the part concerned bj^ 
 reason of the ischsemia which follows ; 
 and the injection of drugs involves a 
 chemical as well as a mechanical stimu- 
 lus. But it is well known that an 
 extra-systole has per se no serious 
 prognostic significance. Extra-systoles 
 occur at all ages, though they are least 
 common in childhood, and in hearts, 
 which are apparently normal as well 
 as in those which are obviously 
 diseased; and it is difficult, in conse- 
 quence, to understand the mechanism 
 by which they are produced during 
 hf e, though it must be somewhat simi- 
 lar to those which have been utilized 
 in experiment. 
 
 As a general rule, the type of extra- 
 systole in any particular individual,, 
 whether it is auricular, ventricular, or 
 nodal, remains constant; and extra- 
 systoles can often be produced at will 
 in persons in whom they occur spon- 
 taneously by slight physical exertion, 
 or by the cessation of respiration. In 
 a general way, again, extra-systoles 
 are most common in cases with myo- 
 cardial changes, the result of acute 
 rheumatic endocarditis or chronic disease of the coronary^ 
 arteries, and they are frequently present in the later stages 
 of acute endocarditis at a time when submihary nodules 
 
 T 
 
 — Y 
 
 -4 
 
 ^ .2 
 
EXCITABILITY 131 
 
 are being formed. It seems probable that in many cases some 
 local lesion has produced a local hyper-irritability which 
 induces a premature contraction in response to stimuli of 
 minimal degree. 
 
 This inference is supported by some of the phenomena which 
 are associated with heart-block and nodal rhythm. 
 
 In chronic heart-block the ventricular rhythm is infrequent 
 and fairly regular, but in the early stages the pulse may be 
 extremely irregular, a series of beats in rapid succession alter- 
 nating with contractions that occur at widely spaced intervals 
 (Fig. 102). The scar of the lesion which has interrupted the 
 passage of the stimuK is unirritating, and the inherent ven- 
 tricular rhythm comes into action in the chronic cases ; but in 
 the acute stages the connective-tissue hyperplasia is irritant, 
 and now provokes frequent contractions, now inhibits aU con- 
 tractions for a time. A comparable phenomenon has been 
 noticed in nodal rhythm, nodal extra-systoles preceding the 
 onset of the rhythm. The irritation of the node at first 
 produced occasional ectopic beats, but eventually every con- 
 traction, the sinus influence becoming effaced. 
 
 The pressure within the chambers of the heart is constantly 
 varying with the varying phases of systole and diastole, with 
 the respiratory movements, and with physical exertion, and 
 it is known that elevation of the pressure within the heart may 
 evoke ectopic beats. It seems probable that they are often 
 due to such causes, a prior lesion having rendered some part 
 unduly irritable. 
 
 In other cases, however, the irritabihty is probably of 
 functional origin. The cardiac rhythm is unstable in fever, 
 and the pulse-rate alters notably from causes (emotion, exer- 
 tion) which in a healthy individual would produce httle change. 
 Extra-systoles are not uncommon in those diseases, and may 
 be due to a heightened general irritability induced by the 
 fever, toxaemia, etc., rather than to local lesions within the 
 muscle, though these are often present even in the absence of 
 endocarditis. Extra-systoles, too, may occur in persons who 
 are suffering from alcohohc or nicotine poisoning, cr from the 
 metabolic disturbances associated with the presence of uric 
 acid or oxalates in excess in the urine, and they tend to dis- 
 
132 DISEASES OF THE HEART 
 
 appear when the intoxication is remedied. In these diseases 
 the blood-pressure is generally elevated, and as Knoll and 
 Hering have shown that ectopic beats can be produced by 
 reflex disturbance of the vasomotor centres, the association is 
 extremely suggestive. 
 
 The cKnical significance of extra-systoles thus varies in dif- 
 ferent cases. In acute endocarditis they may be regarded as 
 probable evidence of myocarditis, and thus of somewhat serious 
 import. In other diseases they indicate a local or a general 
 hyper-irritability of the heart, and careful search should be 
 made for its cause. In the absence of any sign of cardiac 
 insufficiency, the immediate prognosis is good ; but every effort 
 should be made to discover the source of the irritation, and. if 
 possible, to remove it. There is a general feeling that auricular 
 extra-systoles have a more serious significance than the ven- 
 tricular forms, but the evidence as yet is inconclusive. Nodal 
 extra-systoles should probably be placed with the auricular 
 group as regards their import. 
 
CHAPTER X 
 NODAL RHYTHM 
 
 In certain cases the rhythm of the heart seems to be set by 
 stimuli arising in the vicinity of the a.v. node (James Mac- 
 kenzie), for every beat shows a greatly shortened a-c interval 
 (c/. p. 127, Nodal Extra-Systole). The rhythm is regular, but 
 the pulse-rate varies in different cases, being sometimes very 
 frequent (over 200), and more rarely normal or but shghtly 
 increased. Two groups can be recognized: in one the rhythm 
 is intermittent and paroxysmal, alternating with a rhythm of 
 normal type (paroxysmal tachycardia of the auricular form; 
 c/. Chapter XV.) ; in the other the new rhythm is permanent. 
 
 The onset and the cessation of the paroxysms in the first 
 group are practically instantaneous, and they may recur at 
 varying intervals and last for varying periods, sometimes for 
 but a few seconds, sometimes for hours or even days. In the 
 second group the rhythm continues indefinitely. 
 
 I have observed seven examples of the second group. In 
 six of these patients, who were suffering from acute endo- 
 carditis, we were able to examine the hearts after death, and 
 serial sections of the a.v. node and bundle (A. M. Kennedy) 
 showed that the node was the site of an inflammatory disturb- 
 ance which seemed sufficient to account for its undue excita- 
 bility. 
 
 The first two cases are recorded elsewhere in detail, Case 1 
 on p. 246, and Case 2 on p. 240. 
 
 Case 3. — The patient, a man aged forty-two, was admitted 
 to hospital on January 31, 1911, complaining of breathlessness 
 and of swelling of the feet and legs of some six months' dura- 
 tion. 
 
 He had always enjoyed good health prior to the onset of his 
 
 133 
 
134 DISEASES OF THE HEART 
 
 illness, save for pneumonia at the age of thirty, and attacks of 
 measles in childhood and at the age of thirty- two. He had 
 habitually used tobacco and alcohol to excess. 
 
 In the preceding April he had caught cold, and had never 
 been weU since. The cough and spit persisted, and he lost 
 appetite and felt weak and unable to do his work. In July 
 he noticed that his feet were sometimes swollen at night, and 
 he began to be very breathless on exertion. In August the 
 oedema became permanent, and, steadily increasing in amount, 
 soon compelled him to remain in bed. In December he one 
 day suddenly felt severe pain in his right side, and spat blood 
 in considerable quantities for some weeks. He had to be 
 propped up in bed on account of breathlessness, the spit and 
 the oedema steadily increased in amount, and his general 
 strength rapidly failed. In January he attempted a short 
 walk, but fell down in a faint on the pavement. 
 
 On admission, the patient was extremely ill. He sat bolt 
 upright in bed, coughing continually and spitting up large 
 quantities of watery mucoid material. CEdema was universal, 
 and very marked in the legs and scrotum. Detailed examina- 
 tion was impossible, but evidence was found of a consolidation 
 of the middle lobe of the right lung and of pleurisy on the 
 same side. The heart was enlarged, and double aortic mur- 
 murs were audible over the sternum. Progress was con- 
 tinually in the wrong direction. The hsemoptysis recurred, 
 the dyspnoea and oedema increased, exhaustion became more 
 and more extreme, and he died suddenly on February 5. 
 
 The respiratory difficulty prevented continuous observation 
 of the cardiac irregularities. The pulse on admission was 
 notably irregular in rhj^thm from the frequent occurrence of 
 extra-systoles, but a series of twenty or thirty fairly regular 
 beats of slow rate occasionally obtained. The extra-systoles 
 were sometimes isolated and sometimes in salvos of two, three, 
 or four. On February 1 the same state continued. On the 
 2nd the pulse was very irregular and very mobile, a bout of 
 coughing quickening the rate from about 90 to about 120 to 130, 
 the frequent rate persisting for a minute or two after the 
 cough ceased. On the 3rd the irregularity was more marked, 
 but on the 4th had disappeared, the pulse being quite regular. 
 
NODAL RHYTHM 135 
 
 with a rate of 110 to 120. Alternation was distinct. The 
 rhythm remained regular until death. 
 
 Cervical curves were only obtained on February 2 and 4, 
 and were somewhat deformed by the respiratory movements. 
 Tracings on the 2nd demonstrated that while the a-c interval 
 in the case of the larger beats was of normal length, it was 
 much shorter with the extra-systoles, varying between O'lO 
 and 0"15 second. On the 4th, when the rhythm was regular 
 but more frequent, the a-c interval was always short, and 
 measured 0*10 second (Fig. 82). The tracings thus seem to 
 show that on the 2nd extra-systoles were arising in the vicinity 
 of the node, the sinus rhythm, however, on the whole pre- 
 
 1 ■' I a-c 
 
 C-iJ.H^vO'H . 4.ii'.lO. 
 
 Fig. 82. 
 
 Case 3: The pulse is regular, and the a-c interval measures 0' 10 second- 
 Respiratory movements deform the cervical curve in places. 
 
 dominating ; while on the 4th the pacemaker had changed, the 
 sinus influence had been lost, and every contraction originated 
 in the auriculo-ventricular node. 
 
 On post-tnortem examination the heart was found to be 
 greatly enlarged, weighing 25| ounces. The aortic valve was 
 incompetent, the septal cusp having a fairly large perforation 
 with well-defined margins a little below its free border. All 
 the cusps showed some small recent warty vegetations, but 
 were not thickened. The other valves were not affected, but 
 the auriculo - ventricular valves were incompetent. Two 
 patches of superficial mural fibrosis were present in the left 
 ventricle. One, which was small, was situated near the apex ; 
 the other, which measured about | inch in diameter, was 
 situated on the interventricular septum underneath the an- 
 terior mitral cusp, its anterior border being fully | inch behind 
 the posterior border of the pars membranacea. The coronary 
 arteries and the aorta showed little abnormality. 
 
136 DISEASES OF THE HEART 
 
 A small abscess was found in the middle lobe of the right lung 
 as well as a large infarction; both pleurse were adherent. The 
 Hver was adherent to the diaphragm, and there was a well- 
 marked perisplenitis. The kidneys showed slight evidences of 
 arterio-sclerotic fibrosis, and one or two small infarcts. 
 
 Microscopic examination of the heart showed that the a. v. 
 node was involved in an acute inflammatory process. Many 
 focal cellular collections were present, and some small diffuse 
 infiltrations, the muscular fibres in their vicinity showing 
 granular degeneration. The reaction was best marked in the 
 upper portion of the node, and in the parts which were nearest 
 to the base of the mitral valve. The cells were chiefly mono- 
 nuclear, and mainly lymphocytes, with only an occasional 
 polymorphonuclear leucocyte. The a.v. bundle was not de- 
 finitely affected, but was slightly implicated by a nodule in 
 the cardiac muscle immediately beneath and posterior to it. 
 The fibrous tissue around the bundle appeared excessive in 
 amount, and showed traces of calcification. The s.a. node was 
 normal. 
 
 The cardiac muscle throughout showed evidences of cloudy 
 swelling and a few inflammatory " nodules," which were most 
 numerous at the base of the mitral valve and in the auricular 
 muscle just above the node. 
 
 Case 4. — The patient, a girl aged ten, was admitted to 
 hospital on June 10, 1911, ccmplaining of shortness of breath 
 and of swelling of the feet of a week's duration. 
 
 The girl had enjoyed good health, with the exception of 
 three attacks of "measles," until about two months before 
 admission, when she was noticed to be taking her food badly, 
 to be losing flesh, and to be disinchnecl for her usual pla3^ She 
 continued, however, to go to school until the beginning of 
 June, when she contracted a cough unaccompanied by spit, 
 and became short of breath on exertion. Her face and feet 
 were noticed to be swollen, and she complained of pain in the 
 abdomen and beneath the sternum when she coughed. She 
 had sometimes to sit upright in bed at night on account of 
 dyspnoea, and in the mornings she complained of headache. 
 
 On admission the child looked ill and exhausted, and was 
 inclined to be drowsy. The face was palhd and looked puffy, 
 
NODAL RHYTHM 137 
 
 but there was no oedema. The tongue was thickly coated, 
 and the tonsils were sHghtly hypertrophied. Both hearts were 
 enlarged, and there was pulsation in the second, third, fourth, 
 fifth, and sixth left interspaces, the apical impulse in the fifth 
 space being diffuse. A long, soft, blowing murmur was audible 
 at the apex, partly replacing and partly following the first 
 sound, while the second sound was " doubled." Over the 
 xiphoid the systoHc murmur was loud and harsh, and resembled 
 a friction sound. 
 
 During the next fortnight the patient's general condition 
 improved shghtly, but she still looked ill and exhausted, and 
 complained at times of substernal pain. An urticarial rash 
 appeared upon the 24th, and persisted for a few days. On the 
 29th pericardial friction was well marked, and a small pleural 
 effusion was discovered at the base of the left lung. In the 
 beginning of July the symptoms became more serious, and she 
 grew steadily weaker, and sometimes sweated profusely at 
 night. A crop of minute subcutaneous nodules developed on 
 the backs of the hands, and persisted for a few days. On the 
 14th vomiting set in, and continued severely for the next three 
 days. Exhaustion became more extreme, and she died on 
 July 22. 
 
 The nature of the infection was obscure. There was no 
 history of arthritis, and the joints were never swollen or painful 
 during her residence, and the tonsils, though large, were not 
 acutely inflamed. She was habitually slightly fevered at night, 
 but the temperature only once rose above 101° F., and was 
 more usually under 100°. The leucocyte counts varied be- 
 tween 8,000 and 23,000. No other focus of infection was dis- 
 covered, and the symptoms seemed to point to a rheumatic 
 infection of the heart without arthritis. 
 
 The pulse on admission was regular, small, and extremely 
 soft. At first the rate was 100 to 110, but it steadily increased, 
 and for the last two weeks of her illness never ran below 120, 
 though it only numbered 140 on two occasions. Tracings 
 were frequently obtained, and were regular and normal 
 until July 3, when a ventricular extra-systole was recorded. 
 During the succeeding days the pulse was often shghtly ir- 
 regular from extra-systoles, but no satisf actor}' curves were 
 
138 DISEASES OF THE HEART 
 
 obtained until July 17 (Fig. 83). The respiratory movements 
 were frequent, and deformed ( + ) every alternate pulse-beat, 
 but a, c, v are distinct in the intervening contractions, and the 
 a-c interval regularly measures O'lO second. A tracing on 
 July 22 again showed a regular pulse, with an a-c interval of 
 the same length. 
 
 Post-mortem examination revealed a well-marked subacute 
 pericarditis, the two layers of the pericardium being closely 
 adherent to each other over the front of the heart by fibrinous 
 adhesions, but only slightly over the posterior surface. The 
 parietal pericardium was adherent in several places to the 
 chest wall. The heart generally was enlarged. The mitral 
 and tricuspid valves were both dilated, and showed rows of 
 recent pearly vegetations upon their auricular surfaces. 
 
 Fig. 83. 
 
 Case 4: The pulse is regular, and the a-c interval regularly measures O'lO second. 
 Respiratory movements deform the cervical curve in places. 
 
 One or two caseous glands were found at the root of the 
 right lung. Both pleurae showed evidences of subacute 
 pleurisy. 
 
 Microscopic examination of the heart showed a well-marked 
 interstitial myocarditis. The nodules varied somewhat in 
 their character. The majority were composed of mononuclear 
 cells, with a few polymorphonuclear leucocytes ; others were 
 of the " rheumatic " type, consisting chiefly of multinucleated 
 giant cells, with only an occasional lymphocyte ; and a few were 
 " mixed " with a few giant cells, many lymphocytes, and an 
 occasional polymorphonuclear leucocyte. The muscle cells in 
 the vicinity were evidently degenerate. 
 
 The lesions were most extreme in the neighbourhood of the 
 mitral and tricuspid valves. The a.v. bundle was involved in 
 a large focus which, occurring near the tricuspid valve, infil- 
 
NODAL RHYTHM 139 
 
 trated the bundle for a short distance. The a.v. node was 
 notably affected; none of the infiltrating cells, however, were 
 multinucleated. The capillaries were extremely congested, and 
 the lymphatic vessels could be seen plugged with solid masses 
 of lymphocytes. The principal vein of the node showed an 
 acute phlebitis and periphlebitis. The greater part of the 
 phlebitis was above the node. Just before the vein left the 
 node it was joined by a moderately large branch, and the vein 
 above the junction was thrombosed. The thrombus was 
 attached to the side of the vein, but did not completely occlude 
 it, and could be traced through several sections. The s.a. node 
 was not examined. 
 
 Case 5. — A married woman, aged twenty-seven, was ad- 
 mitted into hospital on March 12, 1910, suffering from acute 
 arthritis of about a fortnight's duration. Her previous health 
 had been good, save for an attack of " rheumatics " at the 
 age of seventeen, which involved the feet and ankles, and per- 
 sisted in varying intensity for nearly a year, though she was 
 never acutely ill. 
 
 Her illness had commenced abruptly with feverish symp- 
 toms on February 23, and next day several joints were swollen 
 and painful. The arthritis continued, and she slept badly at 
 night on account of the pain, and for a week before her admis- 
 sion had been short of breath even when lying quietly in bed. 
 
 She was a poorly nourished woman of medium size, and 
 looked exhausted. Many joints were inflamed and swoUen, 
 and she was fevered and sweated profusely. There was no 
 cyanosis or oedema. The tongue was moist and raw, and 
 digestion was good. There was considerable catarrh in the 
 chest, and a small patch of consolidation at the extreme left 
 base. 
 
 Improvement at first was considerable, and within a week 
 the arthritis had subsided, but the pyrexia continued ; and on 
 March 18 she had three attacks of dyspnoea, during which the 
 pulse became very small and weak. By the end of the month, 
 however, improvement was definite, and the chest was nearly 
 clear. But in the second week of April the arthritis recurred, 
 and many small subcutaneous nodules Avere discovered on the 
 hands and elbows. The arthritis subsided within a few days, 
 
140 DISEASES OF THE HEART 
 
 but on April 28 she suddenly complained of pain in the front 
 of the chest, and pericardial friction was discovered. A large 
 effusion developed, and she became very gravely ill, the cardiac 
 weakness being extreme and accompanied by widespread 
 bronchitis ; but in a week improvement was obvious, and her 
 progress thereafter was good. The arthritis recurred in June, 
 and was accompanied by dry pleurisy on the right side, but 
 the symptoms passed away in a few days. Another recur- 
 rence of arthritis occurred in July, this time of trivial degree 
 and of short duration. She left hospital on account of domestic 
 trouble in September, 1910. 
 
 The heart on her admission was of normal size, but a systolic 
 murmur replacing and succeeding the first sound was audible 
 at the apex. During the recmTence of the arthritis in April 
 the heart became notably dilated, and with the onset of peri- 
 carditis the pulse became very frequent and soft, and the 
 cardiac sounds were very faint and distant. She was, too, 
 extremely breathless when she was moved in bed. In June, 
 however, the dilatation lessened, but the right heart was stiU 
 large when she left hospital. The pulse was of fair quality, 
 but habitually ran between 90 and 100. 
 
 The case at first presented some difficulty in diagnosis, for 
 the fever which was present on admission persisted after the 
 arthritis had subsided, and lasted in greater or less degree 
 until the middle of May. It was associated with a leucocj^- 
 tosis, which varied from 16,000 to 26,000. The only visceral 
 abnormahty at first was the mitral lesion, but the recurrence 
 of the arthritis and the occurrence of pericarditis and sub- 
 cutaneous nodules indicated a persistent rheumatic infection. 
 Blood-cultures were sterile. 
 
 She continued in good health for a year after leaving hos- 
 pital, but then began to suffer from pains in her ankles and 
 shoulders. In October, 1911, she gave birth to a healthy baby. 
 She made a good recovery from the confinement, which was 
 easy and uncomplicated, and nursed the child satisfactorily 
 until February 10, 1912, when the right shoulder became 
 painful, and she had to take to bed. She was evidently fevered 
 at this time, and on February 19 commenced to cough and 
 became very breathless. She was again admitted to hospital 
 
NODAL RHYTHM 141 
 
 on February 22. She was now seriously ill, with a flushed, 
 anxious countenance. The right \vrist was swollen and pain- 
 ful. The lower part of the right lung was consolidated, and 
 there was a profuse muco-purulent spit. The heart was en- 
 larged, and the mitral murmur persisted. The pulse was 
 fairly large and quite regular, but frequent ( 104 to 1 12), and was 
 soft and quick. 
 
 Her progress afterwards was unsatisfactory, though for a 
 few days towards the end of March some improvement oc- 
 curred. She was very breathless, and had to sit up in bed; 
 the fever persisted, she sweated profusely and became very 
 weak. The pneumonia at the right base cleared up, but 
 coincidently spread to the upper and middle lobes. The knees 
 and wrists became swollen and painful for a few days. On 
 April 9 she had an attack of faintness, from which she ralUed 
 with, difficulty, and faints recurred on several occasions, though 
 there seemed little change in the cardiac condition, save that 
 the pulse became steadily less full and more quick, though its 
 rate was but little increased. CEdema made its appearance in 
 the feet and at the bases of the lungs, and she died from cardiac 
 failure on April 15, 1912. The pulmonary affection prevented 
 accurate observations of the cardiac sounds. 
 
 Her temperature throughout was habitually febrile, but was 
 generally remittent. The usual daily maximum was between 
 100° and 102° P., but on one occasion 103' 6° was touched. 
 The pulse was always regular, and ranged between 110 to 120, 
 reaching 140 on those occasions when the temperature was 
 high. The maximum leucocyte count was 20,400. 
 
 The cervical curves which were obtained during her first 
 residence were always normal. During her second residence 
 the curves at first were normal, but on March 16, 1912, the 
 a-c interval was short, and on March 17 (Fig. 84) and subse- 
 quently measured O'lO second or less, save for an isolated 
 curve on April 4, which seemed to show a slightly greater 
 duration. The apex tracings showed a very short A.V. in- 
 terval (0'06 second). 
 
 Post-mortem examination showed a patchy pneumonia of the 
 right lung, which was most extensive in the middle lobe, and 
 much passive venous congestion of lungs, liver, and spleen. 
 
142 DISEASES OF THE HEART 
 
 The cortex of the kidneys was narrowed, the capsules were 
 thickened and adherent, and the surface was markedly granu- 
 lar. The arteries were slightly thickened. 
 
 The pericardium was uniformh^ thickened, and the two 
 layers were everywhere adherent. There was a slight medias- 
 tinitis. The heart was greatly enlarged and hypertrophied. 
 The aortic valve was incompetent, and the mitral valve was 
 sHghtly narrowed, their cusps being sHghtly thickened from 
 chronic endocarditis. The chordse and the tips of the musculi 
 papillares were also thickened and fibroid. Fresh granulations 
 were present on both valves, and also on the tricuspid, the 
 largest being on the aortic cusps. The coronarj' arteries were 
 healthy. 
 
 The tissues in the vicinity of the a.v. system were examined 
 microscopically in esrial section. An extensive fibrosis was 
 
 CC V CC V CC V 
 
 Fig. 84. 
 Case 5. The pulse is regular, and the a-c interral measures less than O'lO second. 
 
 present at the base of the mitral valve, dense fibrous tissue 
 spreading from the valve right up to the a.v. node, which was 
 traversed by several narrow strands between Avhich there were 
 many fibroblasts and round cells. The cellular infiltration 
 extended above and beyond the node into the muscle of the 
 auricle. Around the artery of the node there was well-marked 
 periarterial fibrosis, which in one part was ver}- thick and dense, 
 surrounding the artery like a collar. The a.v. bundle was not 
 involved, though its arteries were affected by periarterial 
 thickening. The s.a. node was normal, though an enlarged 
 gland was adherent to the pericardium immediately over it. 
 The vagus nerves were normal. 
 
 The lesions found were evidently of different date, and it 
 
NODAL RHYTHM 143 
 
 seems probable that those of older date were the result of the 
 illness two years before death. The more recent lesions, too, 
 were evidently of some standing, as fibroblasts were numerous 
 in the cellular infiltrations, a fact which may be correlated to 
 the appearance of nodal rhythm a month before death. The 
 node had evidently been acutely inflamed in 1910, but no 
 evidence of a new rhythm was obtained at that time; and in 
 February, 1912, the cervical curves were normal, so that it 
 appears that the sinus rhythm was then predominant. The 
 attacks of dyspnoea on March 18, 1910, however, suggested a 
 cardiac cause, and may have been due to involvement of the 
 node and the inception of a temporarj^ nodal rhythm. Tracings, 
 however, were not obtained at this time. 
 
 Case 6. — 'A weU-grown girl, aged fifteen, who had had no 
 serious illness of any kind, contracted rheumatic fever in 
 December, 1910, which confined her to bed for two months. 
 In April, 1911, an attack of chorea supervened, for which she 
 was admitted into hospital. The movements ceased com- 
 pletely after five weeks, and she was sent to a convalescent 
 home, but a week after her return to her own home in the end 
 of June the movements recurred. The attack was not severe^ 
 and she was dismissed from hospital in the second week of 
 August, She remained in good health, and worked regularly 
 in a laundry until November 8, when a second attack of acute 
 rheumatism occurred, for which she was at once admitted to 
 hospital. The arthritis lasted for three weeks, and she seemed 
 to be convalescent; but it recurred for a few days in the first 
 week of Januar}', 1912, and again in the first week of March. 
 In the middle of April an attack of pericarditis with consider- 
 able effusion occurred. She was at this time very iU, with 
 distinct evidences of cardiac weakness ; but she eventually 
 improved somewhat rapidly, and she was allowed to go to her 
 own home in the end of August. 
 
 She remained in fair health during the autumn, and was 
 able to do hght housework without distress, but on Novem- 
 ber 24, 1912, she was suddenly seized with acute pain in the 
 left chest, which was aggravated by respiration and accom- 
 panied by cough and a bloody spit. She became extremely 
 short of breath, and vomited repeatedl}' and had to take to 
 
144 DISEASES OF THE HEART 
 
 bed. The pain and sickness disappeared in two or three days, 
 but the dyspnoea continued, and she experienced discomfort 
 over the front of the chest, and had to sit upright in bed. The 
 haemoptysis ceased within a fortnight, but the other symptoms 
 persisted, and a week later oedema made its appearance in the 
 feet, and rapidly spread upwards. She was again admitted to 
 hospital on December 31. She was now extremely ill, in full 
 orthopncea, with small amounts of fluid in the serous sacs and 
 universal oedema, which was very great in the legs. The liver 
 was enlarged and tender. 
 
 The symptoms steadily increased in severity, and more 
 pulmonary infarctions ensued. Towards the end of January, 
 1913, active delirium ensued, and she slept badly and took 
 little nourishment. The leucocyte count rose to 17,500. She 
 died somewhat suddenly on February 3, 1913, some twenty- 
 five months after her initial rheumatic attack. 
 
 On her first admission in April, 1911, the heart was of normal 
 size, but a systohc murmur running out of the first sound for a. 
 considerable distance into the short pause was audible at the 
 apex. During her second residence in June, 1911, the val- 
 vular lesion seemed unaltered, but on her admission i'n Novem- 
 ber, 1911, the heart was dilated, though it regained its former 
 dimensions within a month. In the middle of December a 
 new diastoUc murmur of aortic distribution made its appear- 
 ance, and in March, 1912, double murmurs were apparent over 
 the sternum. The heart was now definitely enlarged, and 
 after the subsidence of the pericarditis the area of dulness was 
 larger than it had been previously, and pulsation was forcible 
 and widespread in the second, third, fourth, and fifth inter- 
 spaces. The oedema on the chest prevented accurate observa- 
 tions during her last residence, but the area of dulness was 
 very large on both sides of the sternum, and pulsation 
 was widespread, the whole prsecordium heaving with each 
 systole. The maximum impulse was in the sixth interspace, 
 well outside the nipple line, and pulsation was felt also 
 in the interspace below. The liver showed an expansile 
 pulsation. 
 
 There was a notable disproportion between the radial pulse 
 and the pulsation in the chest, the former being soft and badly 
 
NODAL RHYTHM 145 
 
 sustained, though of moderate volume, while the latter was 
 violent and widespread. 
 
 During her numerous residences in hospital tracings were 
 taken on many occasions. The cervical curves were always 
 normal until March, 1912. On March 3 she complained of 
 severe pain in the cardiac region. The heart became dilated, 
 and the pulse-rate rose to 148. Tracings on the 4th showed 
 an OrC interval of less than 0*10 second. Xext da^-, however, 
 the dilatation had lessened, the pulse numbered 104 to 120, and 
 the a-c interval exceeded 0* 10 second, and thereafter was never 
 shorter than this, though it never approximated to 0-20 second. 
 Tracings taken on March 10 suggested the occurrence of 
 auricular flutter, but those taken subsequently were of normal 
 
 Fig. 85. 
 Case 6: The pulse is regular, and the a-c interval measures O'lO second, 
 
 character. The pulse, too, was always quite regular, though 
 the rate varied considerably from, time to time, and never fell 
 below 72, usually rumiing between 90 and 100. 
 
 During her last residence in hospital satisfactory tracings 
 were obtained on January 9 and 26, 1913 (Fig. 85). In each 
 the pulse was regular, numbering on the first date 130 and on 
 the second 145 beats per minute. Venous congestion was 
 extreme, and x was absent in the cervical curve, v being 
 mingled with c. In both tracings a was distinct, and preceded 
 c by less than O'lO second. 
 
 Post-mortem examination showed that the visceral and 
 parietal layers of the pericardium were universaUj- adherent, 
 the layers being connected by fine, loose, fibrous tissue. There 
 was a sHght loose fibrosis in the mediastinum. The heart was 
 greatly dilated, and the muscle was hj-pertrophied, the changes 
 being most extreme in the left ventricle. The aortic valve 
 
 10 
 
146 DISEASES OF THE HEART 
 
 was markedly incompetent, all the cusps being shortened and 
 shghtly thickened ; small recent vegetations were also present 
 in the usual site. There was a large patch of atheroma on the 
 aortic wall just above the posterior cusp. The mitral valve 
 admitted three fingers. The curtains were uniformly thick 
 and stiff, and smaU fresh vegetations were present on the 
 cusps and on the chordae tendinese, but the muscuh papillares 
 were not affected. The tricuspid valve admitted four fingers ; 
 the septal cusp showed a small acute ulcer at its free margin. 
 The pulmonary valve was normal. The other viscera showed 
 evidences of gross venous congestion, and there was consider- 
 able effusion into the serous sacs. Cultures from the spleen 
 were sterile. 
 
 Microscopic examination showed an extensive fibrosis spread- 
 ing into the tissues from the base of the aortic and the mitral 
 valves, and several strands passing into the a.v. node. A 
 recent inflammatory reaction was superadded, which also in- 
 volved the node. A similar state was found at the base of the 
 tricuspid valve spreading backwards towards the node, and a 
 few lymphatic vessels in this situation were plugged with 
 leucocytes. The cells were mainly lymphocytes, with some 
 fibroblasts. The reaction was particularly marked around the 
 arterioles, some of which were surrounded by whorls of fibro- 
 cellular tissue, while others were embedded in mononuclear 
 collections. This was especially the case in the node and in 
 the surrounding auricular tissue. The a.v. bundle was normal 
 for the greater part of its course, but a few strands infiltrated 
 the lower part as it passed behind the pars membranacea. 
 The s.a. node was notably oedematous, but otherwise normal. 
 The pericardium overlying it was thickened and adherent. 
 
 It seems clear, on looking back upon the case, that a sub- 
 acute endocarditis arising during the attack of acute rheuma- 
 tism in December, 1910, never really healed, and that the 
 aortic and the tricuspid disease, as weU as the pericarditis, 
 were due to a spread of the infection from the mitral lesion. 
 In March, 1912, a nodule of myocardial inflammation or a 
 vascular occlusion occurred in the vicinity of the a.v. node, 
 occasioning the transient attack of nodal rhythm, and perhaps 
 the auricular flutter as weU ; while the permanent nodal rhythm 
 
NODAL RHYTHM 147 
 
 observed in January, 1913, arose from direct involvement of 
 the a.v. node. At any rate, the transient character of the 
 alterations in rhythm observed in March, 1912, suggests a 
 trivial or an evanescent cause for their occurrence. But it 
 was difficult to reahze during the summer of 1911 that the 
 cardiac valvuhtis was acute. The temperature was normal, 
 and the mitral lesion did not seem to be progressive, and a 
 sHght frequency of the pulse alone suggested the presence of 
 an acute cardiac infection. 
 
 The tonsils in this patient were enlarged, and may perhaps 
 have been the source of the recurring infections. Their 
 removal subsequent to the attacks of chorea seemed desirable, 
 but the operation was postponed in view of the cerebral in- 
 stabihty, and no further opportunity was afforded later on, 
 owing to the state of her general health. 
 
 The last case differs from those which have just been re- 
 ported, in that the patient was suffering from a chronic endo- 
 carditis. He was a painter by trade, aged forty-four, and had 
 complained of cough, dj'spnoea, and dropsy for six months 
 before admission to hospital. The dropsy at this time was 
 extreme, and associated with a large pleural effusion, and his 
 mucous membranes were very cyanotic. The heart was con- 
 siderably enlarged, and double aortic and systolic mitral 
 m.urmurs were present. The urine contained a consider- 
 able quantity of albumin. His condition was extremely 
 critical for a few days, but he ultimately improved, though he 
 was still breathless on trivial exertion, and was never able to 
 lie flat in bed. 
 
 Notwithstanding the serious degree of cardiac failure, the 
 pulse-rate was never frequent, and usually numbered about 
 80. For some time the pulse beat in couples and occasionally 
 in trios, but the rhythm abruptly changed at varying intervals 
 into a regular beat. The cervical curves invariably showed a 
 short a-c interval measuring 0*10 second (Fig. 86). His sub- 
 sequent history is unknown. 
 
 The first six cases present certain resemblances and certain 
 differences. In all an acute endocarditis was present, which 
 affected the aortic valve alone in one case, and the mitral 
 
148 DISEASES OF THE HEART 
 
 valve, and sometimes the aortic and tricuspid valves as well, 
 in the others. Four seemed to be due to a rheumatic infection, 
 though the organism was only isolated in one case, and one to 
 a streptococcic infection. In five of the cases a chronic endo- 
 carditis was also present. 
 
 In all six cases the a.v. node was involved in an inflammatorj'' 
 focus of recent date, and in four evidences of an old myocar- 
 ditis co-existed. In five the a.v. bundle was also slightly in- 
 volved, but the lesions here were always minimal. 
 
 In all six cases gross disturbances of the cardiac functions 
 were observed during life. In Case 1 a coupled rhythm from 
 ventricular extra-systoles was observed preceding the nodal 
 rhj^thm ; in Case 3 nodal extra -systoles ; in Case 4 ventricular 
 extra -systoles. The pulse in Case 3 was at one time extremely 
 
 Fig. 86. 
 Case 7. The pulse is regular, and the a-c interval measures 10 second. 
 
 mobile, a bout of coughing quickening the rate from about 
 90 to about 120 to 130, the frequent rate persisting for a minute 
 or two after the cough ceased. In Case 2 the puLse, which 
 was large and collapsing, became much smaller in volume for 
 two days without obvious cause, and on another occasion was 
 gi'ossly irregular for a couple of hours, during which grave 
 symptoms of cardiac exhaustion were present. In Case 5 
 attacks of extreme d^^spnoea and faintness without obvious 
 cause occurred on several occasions. In Case 6 the pulse-rate 
 at times varied very greatly in its rate, ranging from 110 to 
 148 in a few hom-s on one occasion, and on another from 130 
 to 180. In all evidences of increasing cardiac weakness were 
 very evident, and a regular pulse-rate, which varied from 110 
 to 145, was found to be associated with a shortened a-c interval 
 in the cervical curves. 
 
NODAL RHYTHM 149 
 
 The close conjunction of the auricular and the ventricular 
 contractions suggests that the stimuli arose between auricle 
 and ventricle. The precedence of the auricular contraction 
 suggests that they arose in the vicinity of the a.v. node. The 
 regularity of the rhythm suggests that they habitually arose 
 in one situation. In all six cases the a.v. node was involved in 
 an acute inflammatory reaction, such as might render the part 
 unduly irritable, and so initiate stimuli which dominated the 
 sinus influence, and set the rhj-thm of the heart. 
 
 I have been unable to find any similar records in the litera- 
 ture,* but many comparable tracings from cases of paroxysmal 
 tachycardia have been pubhshed, as well as one electro- 
 cardiogram (Lewis). It seems probable that paroxysmal 
 tachycardia is alwaj's due to stimuH arising in some abnormal 
 situation, as the result of a functional disturbance enhancing 
 the irritabihty of the part. A permanent change in site of the 
 pacemaker suggests that the enhanced irritability is due to a 
 pathological lesion. 
 
 The mechanical interference with the cardiac work in nodal 
 rhythm must be considerable, and rapidly produce cardiac 
 failure ; for the closure of the am-iculo -ventricular valves during 
 auricular sj'stole entails stagnation of the blood in the auricles 
 and great veins, a deficient supply of blood to the ventricles, 
 and relative ischsemia of the arterial system. 
 
 The prognosis in cases of nodal rhythm must alwaj^s be 
 grave, for its presence indicates the existence of an acute 
 myocarditis. In the sixth case, however, its appearance was 
 at first transient, and the patient lived for ten months after- 
 wards. The seventh patient left hospital in fair health. 
 
 REFERENCES. 
 
 CowAX, KE:!fXEDY, Patebson, and Teacher: Quart. Joum. of Med., 1910-11, 
 
 vol. iv., p. 35. 
 Cowan, Fleming, and Kennedy: Lancet, 1912, vol. i., p. 277. 
 Cowan, Fleminci, and Kennedy : Trans, of the Internat. Congress, London, 
 
 1913. 
 
 * W. T. Ritche informs me that he has recently obtained comparable 
 electro-cardiogram?, the P— R interval being habitually short. The P wave 
 is positive. 
 
150 DISEASES OF THE HEART 
 
 It has been known for more than a century that acute 
 rheumatism is peculiarly prone to affect the pericardium and 
 the cardiac valves, and is, indeed, the most common cause of 
 chronic valvular disease ; but it is only recently that its special 
 action upon the cardiac muscle has been recognized. 
 
 Acute rheumatism sometimes produces gross lesions in the 
 connective tissues. The occurrence of subcutaneous nodules 
 was first described hy Hillier in a case of chorea, and Meynet 
 and others subsequently recorded their association with acute 
 rheumatism ; but the full significance of their appearance was 
 only appreciated in 1881, when Sir T, Barlow and Warner 
 pointed out that the eruption of nodules was almost always 
 accompanied by acute endocarditis of a grave type. It had 
 aheady been recognized that in certain fatal cases of rheumatic 
 endocarditis the latter seemed insufficient to account for the 
 fatal issue. In some instances pericarditis co-existed, and 
 doubtless aided in the progress towards death; but in others 
 it was absent, and the chief clinical phenomenon was progres- 
 sive weakness and dilatation of the heart; and Sturges, in his 
 Lumleian Lectures, maintained that the rheumatic affection 
 of the heart was not merely endocarditis or pericarditis, but 
 carditis, as all the tissues of the organ were involved in greater 
 or in less degree. It was known that fatty and granular 
 changes were not infrequently present in the cardiac muscle 
 cells in the acute infections, and in 1899 Poynton demon- 
 strated the essential lesion, the microscopic submiliary nodule, 
 which, though usually smaller, is exactly comparable to the 
 lesions which occur in the subcutaneous tissues. Recent 
 observations have shown that those lesions are not confined 
 to acute rheumatism, but may be found in almost any infec- 
 tion, and may occur in cases where the valves and the peri- 
 cardium are unaffected, though they are most common in 
 cases where endocarditis co-exists. The reaction, too, is not 
 confined to the myocardium, but may obtain in any or in all 
 of the viscera. The microscopic appearance of these lesions 
 has already been described (p. 20). 
 
 Cellular infiltrations are commonly present in the tissues at 
 the bases of inflamed valves, and from the close proximity of 
 the a.v. system to the mitral, aortic, and tricuspid valves, it is 
 
NODAL RHYTHM 151 
 
 often involved, and characteristic disturbances of the cardiac 
 rhythm make their appearance. The results are of two kinds, 
 according to the degree of the disturbance, and the system may 
 become unduly irritable, or may have its functions completely 
 abohshed. In the first case extra-systoles or nodal rhj^thm 
 may occur, in the second heart-block of varying degree. 
 
 The relations of the a.v. node and bundle to the adjacent 
 structures are somewhat perplexing, for they are rarely demon- 
 strated in the dissection of the heart. The node (Fig. 87) is 
 situated on the right side of the interam-icular septum close to 
 the anterior edge of the coronary sinus, and immediately above 
 the insertion of the median cusp of the tricuspid valve. The 
 bundle issuing from the node at first passes forwards in the 
 interauricular septum, and then turns abruptly downwards 
 through the central fibrous body to reach the interventricular 
 septum immediately behind the membranous septum; and 
 running forwards along its lower margin, divides into two 
 branches, which descend to the right and left ventricles. 
 Figs. 88, 89, 90 show clearly the relations of the membranous 
 septum. Fig. 88 is a longitudinal section of the heart, and 
 demonstrates the insertion of the median cusp of the tricuspid 
 valve. The aortic cusps are rather above the membranous 
 septum, and the mitral valve is rather posterior. Fig. 89 is 
 a transverse section of the heart through the septum looked 
 at from below, and shows from another aspect the relation of 
 the septum to the aortic and tricuspid valves. Fig. 90 is also 
 a transverse section, but at a rather higher level, and viewed 
 from above. It is in practically the same plane as the micro- 
 photograph Fig. 87. The orifice of the coronary sinus is 
 seen immediately below the Eustachian valve. To its right is 
 the interauricular septum and the central fibrous body, at the 
 lower margin of which is a cusp of the aortic valve cut trans- 
 versely, exposing the recesses of one of the sinuses of Valsalva. 
 To its right is a fragment of another aortic cusp, and to its 
 left the membranous septum and the tricuspid valve. 
 
 The relations of the valves to the a.v. node and bundle are 
 weU shown in the micro-photograph (Fig. 87). The plane of 
 the section is not quite horizontal, but slopes downwards from 
 behind. In the uppe part of the photograph the muscular 
 
^ 
 
 'A 
 
Aortic Cusp, cut transversely. 
 
 Pulmonary Artery. 
 
 Membranous Septum 
 
 Fro. 89. — Transverse Sectiok of the Heart, viewed from below, showing 
 THE Relation of the Membranous Septum to the Valves. 
 
Tricuspid Valve. 
 
 Orifice of ^^^^^^ ^^^^_ 
 
 Coronary Stnus. ^^^ transversely 
 
 Membranous Septum. 
 
 L. Vent. 
 
 Fig. 90. — Traissveesb Section of the Heakt, viewed from above, showing 
 THE Relation of the Membranous Septum to the Valves. 
 
NODAL RHYTHM 
 
 157 
 
 tissue of the auricle and the insertion of the anterior cusp of 
 the mitral valve (M) are visible, and the section then sweeps 
 forwards along the lower part of the membranous septum, 
 terminating in the muscle of the interventricular septum. 
 The relations of the tricuspid valve (T) to the posterior part, 
 
 X 
 
 Fig. 93. — Micro-Photograph of the a.v. Node, SHOwrNG the iNFLAJViMATORy 
 Reactions at the I^tsertions of the Mitrai and Tricuspid Valves. 
 (x5.) (A.M. K.) 
 
 and of the aortic valve [A] to the anterior part, of the mem- 
 branous septum are also shown, as well as the main bulk of 
 the a.v. node, and almost the whole length of the a.v. bundle. 
 The node is most nearly related to the mitral, and the bundle 
 to the aortic and the tricuspid valves. 
 
 Fig. 91 represents a similar section. The mitral valve in 
 
158 DISEASES OF THE HEART 
 
 this case was the site of an acute endocarditis engrafted upon 
 a chronic lesion, and a dense fibrosis can be seen spreading 
 from the base of the mitral valve into the adjacent auricular 
 muscle and along the membranous septum, which is greatly 
 thickened. There is a well-marked cellular infiltration at the 
 junction of the auricular muscle and the base of the mitra 
 valve spreading into the node itself. In Fig. 92 the fibrosis is 
 more extensive, and involves the membranous septum to a 
 greater extent. The aortic valve in this case was involved as 
 weU as the mitral, and the spread of the fibrosis from the base 
 of the aortic valve into the membranous septum can be clearly 
 seen. In Eig. 93 a similar fibrosis is visible with a cellular 
 infiltration spreading from the tricuspid valve along the septum 
 in the direction of the a.v. node. 
 
 The artery of th.Qa.v. node, a branch of the right coronary 
 artery, is visible in Fig. 87, and many of the lesions which 
 affect the a.v. system are due to interference with its lumen. 
 
CHAPTER XI 
 CONTRACTILITY 
 
 Contractility is the most important individual function of 
 the heart, for the maintenance of the circulation is dependent 
 upon its integrity, and if it fails, death ensues. It may be 
 measured by the size of the pulse-wave, for, as has been aheady 
 stated, the contraction of the heart is always maximal irre- 
 spective of the degree of the stimulus. 
 
 In extra-systoles the size of the pulse-waves varies with 
 successive beats (Fig. 94). In this figure the first six beats 
 are practically of the same size, and are succeeded by a small 
 premature wave c', a nodal extra-systole. The small size of 
 c' is not an indication of defective contractility. During 
 systole all the functions of the heart are in abeyance, contrac- 
 tility among the rest, and are only gradually restored during 
 diastole. If a contraction is premature, contractility is neces- 
 sarily less restored, and as diastole is short, the ventricle is 
 imperfectly filled, and the aortic blood-pressure is relatively 
 high, so that the brachial wave is smaller than before. The 
 eighth (post extra-systohc) beat is larger than normal, for as 
 diastole after an extra-systole is longer than usual, contrac- 
 tility is more active, the ventricular content is larger, and the 
 aortic blood-pressure is relatively low. The small size of the 
 extra-systolic wave and the large size of the wave succeeding 
 it are merely the sequel to the varying duration of diastole. 
 
 The waves succeeding the post-extra-systolic beat vary, 
 however, in their size, though the pulse periods are equal, the 
 ninth and eleventh beats being smaller than the tenth and 
 twelfth, and this alternation in size, when the rhythm is regular, 
 is an indication of defective contractility. Succeeding the 
 extra-systole the diastole is prolonged, and the popt-extra- 
 
 159 
 
160 
 
 DISEASES OF THE HEART 
 
 p^ 
 
 ^ 
 
CONTRACTILITY 161 
 
 systolic contraction is larger and more 'prolonged than usual. 
 In consequence, when the next beat comes after an interval 
 of normal length, the diastole is shortened, and contractility, if 
 it is defective, is imperfectly recovered, and systole is less 
 powerful and shorter. The shortness of systole entails pro- 
 longation of diastole, and the next beat is in consequence 
 larger and longer ; and the process is repeated indefinitely. 
 
 The pulsus alternans often continues for long periods of 
 time. The pulse may be quite regular (Fig. 95), or the small 
 wave may be " delayed " (Fig. 96), but the significance is the 
 same, for the delay results because the weaker contractions 
 require a longer presphygmic interval and transmission time; 
 the apical tracing is almost quite regular. 
 
 Extra-systoles must not be confounded with the pulsus 
 alternans. The distinction is easy, for an extra-systolic beat 
 is always small and premature, and is never "delayed." The 
 pulsus alternans may, however, be closely simulated in Cheyne- 
 Stokes breathing (Fig. 97). In this tracing the size of the 
 brachial beats alternate, but the alternation is of respiratory 
 origin, and only obtains when the respirations increase in 
 frequency to such a degree that they number half the pulse -rate. 
 During inspiration the pulse is smaller than it is during expira- 
 tion, the pulsus paradoxus. 
 
 The pulsus alternans, when continuous, is always of evil 
 import, and its presence, even if only for a few beats after an 
 extra-systole, is also serious, for in hearts of normal strength 
 the beats succeeding an extra-systole do not show the abnor- 
 mahty (Fig. 77). 
 
 11 
 
CHAPTER XII 
 CONDUCTIVITY 
 
 Defective conduction is generalty associated with gross 
 lesions in the a.v. bundle. The earliest experiments were per- 
 formed by Gaskell, who clamped the auriculo-ventricular ring 
 in the hearts of the tortoise and frog, and found that as the 
 clamp was gradual]}^ tightened, the interval between auricular 
 and ventricular contractions gradually lengthened. With 
 variations in the degree of compression the ventricle could be 
 made to respond to every second, third, fourth auricular con- 
 traction, or to remain quiescent. But in the last case, after 
 a time, it recommenced beating, but independently of th& 
 auricle and with a slower rhythm of its own. Stanley Kent 
 verified Gaskell's conclusions in the rat's heart, and His and 
 many others have demonstrated the fact in many mammals 
 beyond any possible doubt. 
 
 Chnical experience has now verified in man the experimental 
 deductions, and numerous cases are on record where some 
 degree of heart-block was present during hfe, and post-mortem 
 the a.v. bundle was affected by various lesions interfering in 
 greater or less degree with its functional activity. 
 
 There is some evidence, however, which suggests that func- 
 tional defect may exist without gross disease of the bundle. 
 Heart-block has been produced experimentally in many 
 ways : by the administration of digitahs, by the induction 
 of asphj^xia, and hj vagus stimulation. Chnically James 
 Mackenzie has found that a pre-existing defect (increased 
 a-c interval) may be intensified by the administration of 
 medicinal doses of digitahs and by the act of swallowing ; and 
 Ritchie and others have noticed a similar result to follow the 
 apphcation of pressure upon the vagus nerve in the neck. In 
 full heart-block, however, as a rule the subcutaneous injection. 
 
 162 
 
CONDUCTIVITY 163 
 
 of atropine in doses sufficient to abolish all vagus influence 
 fails to influence the block, though in the partial defects 
 the degree has been at all events lessened (Gibson and 
 Ritchie, Rihl, Volhard). There is only one case on record 
 (Hoist and Monrad-Krohn) in which the a.v. bundle was found 
 to be normal post-mortem, though heart-block had been 
 demonstrated during life. In this instance both vagi nerves 
 showed well-marked degenerative changes.* 
 
 Three grades of defective conductivity are recognized : 
 1. Full Heart-Block. — In full heart-block the auricular and 
 the ventricular contractions occur independently of each other. 
 In many cases the auricular contractions are normal in rate 
 
 Fig. 98. — Fitll Heart-Block. 
 
 There is complete dissociation of the auricular and the ventricular contractions. 
 When these coincide, the cervical wave is large as the auriculo-ventricular 
 valve is shut, and the auricular blood is thrown backwards into the jugular 
 vein. 
 
 and rhythm, and occur evidently in response to sinus stimuli, 
 as the rate alters on exertion, etc., as in normal hearts; while 
 the ventricular contractions are infrequent, numbering about 
 thirty per minute, and, though fairly legular, are the result of 
 impulses arising in the ventricle itself. But both the auricular 
 and the ventricular contractions may vary greatly in rate and 
 rhythm from time to time, and a diagnosis can only be made 
 by instrumental methods. The dissociation is usually distinct 
 in cervical curves, and often in apex tracings. 
 
 The cervical curve (Fig. 98) shows no regular relationship 
 between the a and c waves, a now preceding, now following, 
 and now coinciding with the carotid beat. In the last case 
 (Beat 3), the auricular wave is large, for as the auricle is 
 contracting at the same time as the ventricle, the auriculo- 
 ventricular valves are shut, and the auricular blood is, in 
 consequence, thrown backwards into the veins. In the apex 
 
 * W. T. Ritcliie informs me that the a.v. tissues were normal in a case 
 recently examined by him, though the electro-cardiogram showed full 
 heart-block. 
 
164 DISEASES OF THE HEART 
 
 tracings (Fig. 99) the a wave is generally lost when aiu'icular 
 and ventricular systole coincide, but it is distinct during 
 ventricular diastole. 
 
 2. Partial- Heart- Block. — In the lesser degrees of defective con- 
 duction (Fig. 100), the ventricular rhythm may be fairly regular, 
 and occur in response to sinus stimuli, but the interval between 
 the auricular and the ventricular contractions is increased. 
 
 The a-c interval in cervical curves measures in the normal 
 individual 0-15 to 0-20 second, being slightly shorter when the 
 pulse-rate is frequent . During the a-c interval five events 
 occur: (1) The contraction of the auricle; (2) the passage of the 
 stimulus from auricle to ventricle ; (3) the latent period before 
 the ventricle contracts; (4) the presphygmic interval; (5) the 
 transmission of the aortic wave to the carotid artery. The 
 average peiiod between the commencement of ventricular 
 sj'stole and the appearance of the carotid wave is 0-066 second, 
 while the commencement of auricular contraction is practically 
 S5mchronous with the appearance of the a wave in the cervical 
 '^urve. The presphygmic interval and the transmission {time 
 (4 and 5) vary inversety with the frequency of the"' ventric- 
 ular contractions, and are relative^ short when diastole is 
 prolonged (Fig. 80); auricular systole, even in cases of mitral 
 stenosis, seems rarely to last for more than 0-10 second; and 
 it seems certain that whenever the a-c interval measures more 
 than 0-25 second, the conduction of the stimulus from auricle 
 to ventricle is unduly delayed. A possible fallacy must be 
 borne in mind. When the heart is beating 'frequently, the 
 period of ventricular contraction may overlap the period of the 
 succeeding auricular contraction, and a may be merged in the 
 preceding v. |A similar overlapping of h and a may also occur. 
 But these occurrences may be distinguished by an apical 
 tracing, which will show that the a wave succeeds the appear- 
 ance of the composite ^, or ^ wave. 
 
 3. In the third form a ventricular contraction occasionally 
 fails as a result of the defect (Fig. 101). With each contraction 
 of the heart all its inherent functions 'are in abeyance for the 
 time, 'the stimulus material being exploded, the excitabihty 
 ost, 'Contractility abolished, and conductivity minimal if 'it. 
 exists, though all these functions are rapidly restored during 
 
/AWl*kv IT . 27 TT 9 
 
 Fig. 100. — Defectr^b CoNDUCTIO^*j)l. — Pabtial Heart-Block. 
 The a-c interval measures 0-35 second-d ventricular contraction fails. 
 
 [To face page 161. 
 
Fig. 99. — ^Apex Tracing in Full Heaet-Block. 
 The auricular and the ventricular contractions are fairly regular. 
 
 ■'V..:'i:.'r.:V-.:'i':: 
 
 ^ 
 
 B5 I 1-65 I 95 I 15 I 95 
 
 ¥ 
 
 Fig. 100. — Defecth'e Conduotiox. 
 The a-c interval measures 0'35 second. 
 
 ^^<>^^\^J\]\r^W^ 
 
 Fig. lOl.— Paktial Hbaet-Blook. 
 Every third rentricular contraction fails. 
 
 ITo face page 164. 
 
CONDUCTIVITY 165 
 
 diastole. When conductivity is defective, frequent exercise of 
 the function entails further defect. In Fig. 101 conductivity 
 is;S0 defective that even after a ventricular rest of 1-35 seconds 
 the a-c interval measures 0-30 second. The succeeding 
 auricular contraction occurs 0-55 second later, and the shorter 
 rest necessitates a longer period (0-40 second) for the trans- 
 mission of the stimulus ; and when another auricular contraction 
 occurs 0-35 second later, the stimulus fails to pass, and a 
 ventricular contraction is missed. But the longer rest which 
 thus ensues improves conductivity, and ventricular con- 
 traction succeeds the ensuing auricular contraction by a shorter 
 interval, [and the process is repeated indefinitely. The radial 
 pulse may be almost regular in these cases if every second 
 auricular contraction fails ; or every third or fourth, ven- 
 tricular beat alone maj^ be missed. 
 
 The chronic 'forms of full heart-block are not necessarily 
 associated with any definite signs of cardiac distress, and Sir 
 WiUiam Gairdner,* for example, who died at the age of eighty- 
 two, enjoyed fair health for the last four years of his life, 
 though there was complete dissociation for all this period. In 
 the majority of cases, however, some degree of cardiac in- 
 sufficiency is present — weakness, shortness of breath upon 
 exertion, etc. — though these are to be related rather to the 
 causes which produced the block than to the block itself. 
 The heart itself is rarely normal, valvular flaws are common, 
 and the musculature is apt to be affected diffusely by lesions 
 similar to those which have involved the a. v. bundle. 
 
 The pulse in these circumstances is uniformly infrequent, 
 numbering [about 30 per minute, and is generally regular 
 in rhythm. The rate may vary slightly from time to time, 
 but it is little influenced by emotion, exercise, fever, etc., which 
 produce [notable effects upon a normal heart. A pulse-rate 
 of under 40 per minute of itself suggests heart-block, as the 
 other conditions which may produce so slow a rate are much 
 more rare, and I have only observed it twice, once in jaundice 
 and once in cerebral tumour, in both of which the rate was 39, 
 
 * G. A. Gibson and W. T. Ritchie: Edin. Med. Joum. N.S., vol. ii.. 
 pp., 315, 507; Lancet, 1909, vol. i., p. 533. 
 
166 DISEASES OF THE HEART 
 
 with normal cervical curves. In the first case the pulse rose to 
 normal rates when the jaundice passed away, and a similar 
 event occurred in the latter after a decompression operation. 
 In a patient w^ho was suffering from tobacco intoxication the 
 pulse numbered 40, and I have pulse-rates of 46 after pneu- 
 monia and 48 after influenza, with normal curves. 
 
 The evidences of auricular action in the jugular veins may 
 be visible, as was described by Stokes : "A new symptom 
 appeared, namely, a remarkable pulsation in the right jugular 
 vein. This was most evident when the patient lay down. 
 The number of the reflex pulsations was difficult to be 
 estabhshed, but the}^ were more than double the number of 
 the manifest ventricular contractions. About every third 
 pulsation was strong and sudden, and could be seen at a 
 distance; the remaining waves Were much less distinct, and 
 some very minor ones could be perceived."* 
 
 Auscultation furnishes another sign. If the pulse is regular 
 and a mitral systohc murmur co-exists, regurgitation into the 
 auricle wiU cease when ventricular and auricular contraction 
 coincide, and the murmur will, in consequence, disappear or 
 weaken {cf. Fig. 98). The murmur of mitral reflux, of course, 
 varies in its intensity and duration in cases of auricular 
 fibrillation, according to the duration of diastole and the degree 
 of filling of the ventricle ; but it does not alter in cases with 
 regular ventricular contractions unless auricular contractions 
 coincide with the ventricular. 
 
 In some cases the auricular contractions may produce 
 audible (single) sounds, but this is hx no means constant, even 
 in cases where the auricles have been sho^\Ti to contract 
 rhythmically, and not to be in flutter or in fibrillation. Person- 
 ally I have never heard them. 
 
 A diagnosis can be readily made with instrumental aid, the 
 dissociation being shown in the cervical or the apex curves. 
 
 In full heart-block a very striking series of symptoms, the 
 Stokes-Adams syndrome, is not infrequently observed. It may 
 occur at any period, but is most common in the early stages 
 
 * " Diseases of the Heart," 1854, p. 315. Dublin Quart. Journ. of Med. Sci., 
 1846, vol. ii., p. 73. 
 
CONDUCTIVITY 167 
 
 during the development of the fuU block, and it often dis- 
 appears with its estabhshment, though in exceptional cases 
 it has recurred later on. A typical example is recorded below. 
 
 The patient, an engineer, aged fifty-seven, had been employed 
 in tropical chmates for some thirty years . His health had been 
 good while abroad, save for occasional attacks of ague. He had 
 suffered from gonorrhoea twenty years before, accompanied by 
 a sore which was not considered to be syphilitic, and was not 
 followed by any secondary symptoms. Four years before his 
 illness, however, he began to " feel the tropics," and two years 
 later he came home on a year's furlough. He did not return to 
 his work, as he felt that he was not fit for it, though he had no 
 definite symptoms save on one occasion slight swelling of the 
 feet, which disappeared in a few days . 
 
 The symptoms for which he came under observation com- 
 menced quite suddenly three months before, when he was 
 living in Stirhng. He was going to the Perth race-meeting and 
 was late in rising, so that his breakfast was hurried. When he 
 was walking smartly to the railway-station, he suddenly felt 
 faint and had to clutch hold of some raihngs to prevent himself 
 from falling ; but the f aintness passed away in a few moments . 
 When walking to the luncheon-stand at Perth in the afternoon 
 he again felt faint, and on this occasion lost consciousness, and 
 feU to the ground, but he rapidly recovered. He attributed the 
 seizures to starvation, and after lunch he felt better and stayed 
 on at the races . He slept well at night, but next morning, while 
 sitting quieth" in his rooms, he had some thirty seizures of a 
 similar kind. 
 
 These attacks have continued at irregular intervals ever 
 since. He was sometimes free from them for as long as a 
 week, but sometimes they recurred several days in succession. 
 On one occasion he fell down and cut his face. Two weeks 
 before admission the attacks became more numerous and 
 more severe. For hours at a time, the}^ recurred frequently, 
 and lasted for longer periods, and were associated with 
 twitchings of the muscles, and in consequence he felt weak 
 and exhausted. The}- were generally preceded by a dull 
 pain in the upper part of the right chest. 
 
 For three days after his admission to hospital the attacks 
 
168 DISEASES OF THE HEART 
 
 did not recur, but they recommenced next day at 7 a.m., and 
 continued all daj^ at short intervals ; some 200 occurred in 
 the twenty-four hours. Next day he had seven attacks, and 
 on the succeeding day thirteen, but there were only_^ eleven m 
 the next eight days, and about twenty on the last day of his 
 residence. They subsequently continued to be infrequent and 
 of short duration. 
 
 Manyjattacks were observed. They were all similar in type. 
 The apex impulse was large and prominent, and the first thing 
 that was noticed was the cessation of the apex impulse and 
 the radial pulse. Simultaneously he said that he felt giddy 
 and that a fit was impending, his countenance became white 
 and anxious, and he moved his arms restlessly and tried to 
 catch hold of the bedstead. In two or three seconds he 
 became unconscious, and a slight tonic spasm, which some- 
 times seemed purposeful, ensued ; and this was followed, if the 
 ventricular asystole continued, by clonic spasms, which com- 
 menced in the face and spread to the arms and sometimes also 
 to the legs. In a few seconds the face suddenly fiushed, and 
 the apex impulse and radial pulse reappeared ; he straightened 
 his head, and consciousness returned. 
 
 Convulsions did not occur in every attack. Many were of 
 very short duration, and only lasted for five or six seconds 
 (Fig. 102), in which case no convulsion ensued, but others 
 lasted for ten to fifteen seconds, and were then accompanied 
 by muscular movements. These, however, even when general, 
 were never gross, and incontinence never occurred. Recovery 
 after jthe attacks was rapid and complete, but he said that he 
 felt tired and exhausted. 
 
 He was a tall, well-developed man, but his muscles were 
 small and soft,' and the subcutaneous tissue scanty. His hair 
 was white, and he looked older than his years, and somewhat 
 weakly. There was no oedema, but the liver seemed to be 
 enlarged. There was a sHght bronchial catarrh, and a trace 
 of albumin in the urine. 
 
 The apex impulse was situated in the fifth interspace, 
 4| inches from mid-sternum, and was punctate and prominent 
 and well-sustained. The area of cardiac dulness measured 
 4| inches transversely. The cardiac sounds were faint; the 
 
Fig, 102. — Brachial Curve from a Case oe Full Heart-Blook. 
 The auricular contractions are distinctly visible. 
 
CONDUCTIVITY 169 
 
 second aortic sound was intoned and ringing ; the first sound 
 at the apex was prolonged and impure, and on some days suc- 
 ceeded by a rather harsh murmur. The auricular contractions 
 were never audible. The arteries generally were thickened, 
 hard, and tortuous. The pulse was fuU, and the blood- 
 pressure^measured 145 — llOmm.Hg. 
 
 The pulse as a rule was fairly regular and infrequent, 
 usually running] about 28 to 32 per minute (Fig. 99), and 
 at these times attacks did not occur. On other occasions 
 it was extremely irregular (Fig. 102), and a pause of several 
 seconds might appear between successive beats, or the pulse- 
 rate [might increase, and number even 56 per minute, a rate 
 which was observed on two or three occasions. 
 
 ^Cervical curves were not obtainable as the clavicles were 
 deformed and covered the jugular bulb, but the apex and 
 brachial tracings showed plainly the dissociation of the 
 auricular and the ventricular contractions, the auricular beats 
 being fairly regular and numbering about 66 per minute, quite 
 irrespective of the rate or the rhythm of the ventricles. 
 
 The attacks may be of varying nature and duration. In the 
 shorter seiziKes they are simple syncopes, while in ,those of 
 longer duration convulsions often supervene both of the tonic 
 and the clonic kind. Recurring attacks at short intervals 
 may persist for hours on end, or even for a day or two, and 
 while in some cases they are isolated events, they may return 
 after intervals of weeks or months for two years (Sir W. 
 Gairdner), or, for fourteen years, as in one of Mackenzie's cases. 
 
 It must be clearly understood that heart-block and the 
 Stokes-Adams syndrome, though frequently associated, are 
 not synonymous. Many cases of full heart-block without the 
 syndrome have been recorded, and the Jsyndrome may occur 
 without block. In heart-block the pulse is quite regular, and 
 numbers about 30 per minute. In the syndrome the pulse 
 is irregular and ver^' infrequent, numbering 5 to 20 per 
 minute, and long intervals of [many seconds' length may 
 occur between beats. jThis latter featm-e is the essential point. 
 Kussmaul and Tenner showed that cerebral anaemia, induced 
 by hgature or compression of the carotid arteries, produced 
 
170 DISEASES OF THE HEART 
 
 loss of consciousness, and, if continued, convulsion; and 
 observations of many attacks by numerous observers have 
 made it clear that the ventricular contractions cease prior 
 to the onset of the cerebral symptoms ; and that this is the 
 cause of the attacks. 
 
 Sir William Osier has reported two cases of the syndrome 
 in which heart-block seems definitely excluded. In one the 
 patient suffered from tubercular disease of the first and 
 second cervical vertebrae, and had on several occasions attacks 
 of syncope and slow pulse. Another patient suffered from a 
 sarcoma of the medulla, and experienced similar seizures.* 
 
 The cause of the cessation of the ventricular contractions 
 is in all probability the lesion which produces the block. 
 Gaskell pointed out that if a cut was made close against the 
 ventricle in the auriculo-ventricular groove, the ventricle beats 
 rapidly for a time, and then gradually slows until at last it 
 stands still ; and after a variable period it begins to beat again, 
 at first very slowly, but ultimately more frequently and 
 regularly. If, on the other hand, the junction is clamped very 
 slowly, the ventricle ceases to beat without any initial increase 
 in its rate of contraction. A sudden stimulus produces an 
 initial rhythm of excitation ; a slowly applied stimulus merely 
 abohshes the function ; while in time, after either, the inherent 
 rhythmicity of the ventricle comes into play, and the ventricular 
 contractions develop with their own special rate. 
 
 The lesions which have been found in heart- olock in the 
 a.v. tissues are of various kinds. In some cases they are of 
 acute character, abscess, arterial occlusion, etc. ; in others, they 
 are chronic, a dystrophic fibrosis, tumour, etc., and acute or 
 chronic inflammatory reactions may occur in their vicinity. 
 
 In some cases, then, the lesion may irritate and provoke a 
 frequent ventricular rate, and in other cases inhibit the 
 ventricular contractions for a time. And fresh lesions or an 
 exacerbation of the secondary inflammatory reaction may 
 repeat for an indefinite period the symptoms which ensued 
 at the onset. An old scar is unirritating, 'and the chronic 
 form of heart-block with a regular infrequent pulse is its 
 accompaniment . 
 
 * Article in AUbutt's System, 1909, vol. vi., p. 130. 
 
CONDUCTIVITY 171 
 
 The dangerous period of heart-block is thus the initial stage, 
 the period when lesions are forming in the a.v. tissues. When 
 once the block is full and the scar contracted, the danger of 
 ventricular asystole from this cause is past. 
 
 In full heart-block the ventricles seem to be outwith the 
 influence of external stimuli, such as vagus pressure or the 
 injection of atropine, though these may a£Pect the rate of the 
 auricular contractions, a fact which harmonizes with the 
 current conception that the a.v. bundle is the onlj channel 
 through which impulses of any kind travel from auricle to 
 ventricle. In partial block, however, the administration of 
 atropine may lessen the degree of block, and vagus pressure 
 may increase it, though as a rule such procedures have httle 
 effect. 
 
 The Auricular Contractions in Heart-Block. — The auricular 
 action in heart-block is not always normal, for the auricles may 
 be fibrillating (Mackenzie, Lewis), or in flutter (Ritchie); but 
 these seem to occur only in exceptional cases. The actual 
 condition of the auricles is apparently immaterial with regard 
 to the prognosis ; the important factor is the rate of the ven- 
 tricular contractions. Ritchie's patient, with flutter and block, 
 is stiU ahve and in fair health, though the condition was recog- 
 nized more than seven years ago ; and one of Mackenzie's cases 
 of fibrillation and block was working regularly four years after 
 the condition was recognized. 
 
 Cases with partial heart-block, too, have no necessary incon- 
 venience from their disability. In some instances the block 
 may become complete for a time, the pulse may run at a very 
 slow rate, and the Stokes-Adams syndrome may ensue, but 
 in the majority they are recognized on critical examination of 
 an irregular pulse or on routine examination of a faihng 
 heart. Symptoms of cardiac insufficiency may or may not be 
 apparent, but if present are only in small degree the result of 
 the block. Palpitation is frequently experienced by these 
 patients . 
 
 The lesions which are found in Ithe a.v. tissues on post- 
 mortem examination are varied. The following hst is derived 
 from those of Hirschfelder and Lewis : Gumma, 7 ; calcification, 
 7; fibrosis, 11; tumour, 2; anaemic infarction, 2; round-celled 
 
172 DISEASES OF THE HEART 
 
 infiltration, 4; mural ulceration, 1; fatty degeneration, 1; 
 arterio-sclerosis of a.v. arterj', 1. 
 
 Tlie majority of these cases are thus chronic in their nature, 
 but heart-block may occur in acute disease. In 1905 James 
 Mackenzie repoited the transient occurrence of the milder 
 grades of block in patients who were suffering from acute 
 rheumatism and influenza, and since then several cases of full 
 heart-block, -vvith post-mortem examinations, have been recorded 
 (gonococcic endocarditis, ulcerative endocarditis, diphtheria, 
 acute rheumatism, quickly followed b}- enteric fever). Clinic- 
 ally it has been observed, either complete or partial, in pneu- 
 monia, scarlatina, and enteric fever. 
 
 Transient defects are not uncommon in acute rheumatic 
 endocarditis, and I have observed five examples. In one case 
 the defect persisted for nearty four weeks ; in another it dis- 
 appeared after six days, recurred three days later, and again 
 lasted for six days . In none of these cases was there complete 
 block, but in one the ventricles only responded to every second 
 auricular contraction. All the cases made good recoveries, 
 and in one alone was the ultimate valvular lesion severe. 
 
 In exceptional cases the Stokes-Adams syndrome may occur. 
 My colleague, W. D. Macfarlane, observed this in a case of 
 acutCj rheumatic endocarditis, in which the pulse-rate fell 
 as low as 15 per minute, with occasional long intervals 
 between the beats. On these occasions the patient lost con- 
 sciousness, and the muscles of the face and arms twitched. 
 The convulsions recurred for two or tlu'ee weeks, but recovery 
 ensued after a tedious convalescence. He lived for more than 
 ten years, and eventually died from chi'onic valvular disease. 
 
 The prognosis in heart-block is based upon two factors, the 
 degree of the block and its cause. In a general way the prog- 
 nosis is grave, for |its presence, whether partial or complete, is 
 an indication of serious mj'^ocardial disease. The presence of 
 valvular lesions is probably of little moment. The a.v. tissues 
 are most frequently affected in valvular disease, but this is 
 owing to their close proximit}^ to the valves, and the myo- 
 carditis is not necessarily mdespread. If the lesion is due to 
 an acute process, it may subside (acute rheumatism) or progress 
 (mahgnant endocarditis); if due to a chronic arterial change, it 
 
CONDUCTIVITY 173 
 
 wiU tend steadily to increase. A syphilitic lesion may resolve 
 under treatment (Osier). The presence or absence of signs of 
 myocardial insufficiency is necessarily important. 
 
 Chronic full heart-block is not incompatible with many 
 years of fair health. A partial block may become complete 
 or may pass away. And as the danger of the cessation of 
 ventricular contraction occurs in cases of partial block, and 
 in full block about the period of its development, the lower 
 grades are probably more important than the complete form. 
 Here again, as usual, the experience of the individual patient 
 is important, and a low rate of the pulse or the occurrence of 
 even trivial syncope or convulsion renders the immediate 
 prognosis extremely grave. 
 
 Chronic full heart-block demands no special treatment beyond 
 that indicated by the general symptoms. 
 
 In partial block 'complete rest is certainly indicated, for 
 exertion is bound to increase the work of the heart, and so to 
 increase in some measure the inflammatory reaction and the 
 ultimate scar. The administration of digitalis is contra- 
 indicated, for it tends to exaggerate defective conductivity, 
 and vagus pressure has a similar effect. 'In certain cases the 
 administration of atropine {-xlrn ^^ tV grain) has lessened or 
 abohshed the block and so increased the number of the iven- 
 tricular contractions, and it should certainly be given if the 
 ventricular rate becomes infrequent. In most cases it has no 
 action of this kind. The diffusible stimulants — strychnine, 
 hot fomentations to the prsecordia, etc. — are most likely to be 
 useful. 
 
 'In full block, digitahs, atropine, and vagus pressure have no 
 influence upon the rate of the ventricular contractions . 
 
CHAPTER XIII 
 TONICITY 
 
 The recurring contractions of the heart interfere with the 
 recognition of the tone of the cardiac muscle at any particular 
 moment, for it is evident that the degree of diastoHc relaxation 
 is dependent upon the duration of diastole as well as upon the 
 tone of the muscle. But it has been clearly shown that the 
 heart possesses this quahty, for the application of drugs, such 
 as sodium hydrate, to the beating heart, is followed by less 
 and less complete relaxation, until finally the heart remains 
 in a condition of systolic standstill. The apphcation of other 
 drugs, such as lactic acid, moreover, produces atony, and the 
 contractions become more and more feeble until the heart 
 stands still in complete relaxation. 
 
 When tone is defective, the heart becomes dilated, the 
 apical pulsation is displaced and diffuse, the area of cardiac 
 dulness is increased transversely, and evidences of general 
 venous engorgement make their appearance. The mitral or 
 the tricuspid valve may become incompetent. 
 
 174 
 
CHAPTER XIV 
 COUPLED RHYTHMS 
 
 In pulsus alternans a large and a small pulse-beat alternate, 
 and a somewhat similar allorrhythmia obtains in coupled 
 rhythm. There is, however, an essential difference, for in 
 pulsus alternans the interval between the smaller beat and 
 that preceding it is longer than, if not equal to, the interval 
 between the smaller beat and that which succeeds it (Figs. 95 
 and 96) ; while in coupled rhythm the period between the small 
 beat and the succeeding larger wave is always the longer 
 (Fig. 103). 
 
 Coupled rhythm may be due to various causes. The most 
 common form is the result of a regularly recurring ventricular 
 extra-systole, or, less frequently, a nodal extra-systole. It may 
 obtain in nodal rhj^thm, in auricular fibrillation, and in the 
 various degrees of heart-block. In some instances both auricle 
 and ventricle share in the coupling ; in others the ventricles 
 alone are involved. 
 
 A coupled rhythm may occur in partial heart-block. This is 
 shown in Fig. 104, which was obtained from a patient suffering 
 with acute rheumatism, in whom defective conduction obtained 
 for a month. In the tracing the a-c interval is always pro- 
 longed, the first auricular contraction being followed by the 
 carotid wave after an interval of 0-30 second. The second a-c 
 interval measures 0-35 second, and with the third auricular 
 contraction the stimulus fails to pass. During the lengthened 
 rest which ensues in consequence, conductivity is restored, so 
 that the fourth auricular contraction is followed by a ven- 
 tricular contraction after an interval of again 0-30 second; 
 but with the next beat, as the period of rest is shortened, the 
 a-c interval is longer (0-40 second), and the sixth auricular beat 
 again fails to produce a ventricular response. 
 
 175 
 
176 
 
 DISEASES OF THE HEART 
 
 The coupled rhythm wliich occurs in auricular fibrillation 
 
 resembles somewhat closely those forms in which it is due to 
 
 a regularly recurring extra-systole. As will be seen (p. 213), 
 
 the ventricular beats in auricular fibrilla- 
 
 3 tion are in response to impulses which 
 
 o descend from the fibrillating auricle, and 
 
 % are therefore comparable to phj^siological 
 
 g contractions of the ventricle, and electro- 
 
 g cardiographic investigations have shown 
 
 1^ that the smaller beat of the couple in these 
 
 fc, cases is due to an intrinsic ventricular 
 
 o 
 
 jH contraction, or, in other words, to a 
 
 % ventricular extra-sj^stole. 
 
 -i 
 
 -i 
 
 -C 
 
 -r 
 
 H 
 
 
 Henschen* pointed out that coupled 
 rhythm occurs most frequently in cases of 
 mitral disease with a feeble heart, and a 
 pulse-rate which is infrequent from full 
 doses of digitalis ; and, arguing from radial 
 tracings alone, suggested that in these 
 cases, on account of the prolonged diastole 
 produced bj^ the drug, the auricles were 
 incompletely emptied at their regular sys- 
 tole. With the succeeding ventricular 
 contraction the reflux from the ventricle 
 still further distended the left auricle, and 
 the excessive pressure which resulted in- 
 cited the auricle to contract prematurely. 
 As diastole was short, the ventricle was 
 imperfectly filled, and the aortic wave was in 
 consequence small. Following the extra- 
 systole, the auricular excitability was so far 
 reduced that a complete distension of its 
 cavity was required to provoke a new con- 
 traction, and the succeeding diastole was in 
 consequence prolonged, and more or less compensatory. But 
 while this theory is extremely plausible, it is only applicable 
 to cases in which the second beat of each couple is a regularly 
 * Mitteil. a. d. me:l. Klinih zu Upsala, 1898, i. 
 
COUPLED RHYTHMS 
 
 177 
 
 recurring auricular extra-systole, an undoubted example of 
 which has not yet been recorded, the large majority of cases 
 being due to ventricular extra-systoles. 
 
 The question is discussed at length in the Quarterly Journal 
 of Medicine by Ritchie and myself,* and we have suggested 
 that " whenever an enfeebled heart is unduly irritable in an 
 abnormal site, any excessive rise of intracardiac pressure may 
 produce a regularly recurring premature systole which origi- 
 nates at the irritable area." 
 
 Extra-systoles may arise in any part of the heart, and are 
 probably the result of a local hyper-excitability produced in 
 some cases by local myocardial lesions, and in others by 
 functional disturbances . Experimental researches have demon 
 
 /Au/i*+ij^ jr . 27"n- 9 
 
 Fig. 104. — Coupled Pv,hythm:, due to Partial Heart- Block, every Third 
 Ventricular Contraction failing. 
 
 strated that extra-systoles may be induced by constriction of 
 the aorta or the pulmonary artery, or by reflex stimulation of 
 the vasomotor centres, which produces a rise in the intra- 
 cardiac pressure ; and a rise will also certainly accompany the 
 synchronous contraction of auricle and ventricle, or any undue 
 prolongation of diastole. 
 
 Synchronous contraction of auricle and ventricle is often 
 followed by a premature auricular or ventricular contrac- 
 tion. In Fig. 105 the fourth ventricular contraction occurs 
 sjaichronously with a regular auricular contraction. As a result 
 the auricle is unable to empty its contents into the ventricle 
 and at the end of its diastole is notably engorged. The intra- 
 auricular pressure is rapidly increased by the influx of blood 
 
 * 1910-11, vol. iv., p. 55. 
 
 12 
 
178 
 
 DISEASES OF THE HEART 
 
 from the congested veins, and the fifth auricular contraction is 
 in consequence premature, 
 
 A similar coincidence is sometimes observed in heart-block. 
 In Fig. 106 a partial heart-block is present, and occasional 
 ventricular contractions drop out. Reference to the accom- 
 
 
 6S- I 'n-^Fi. 
 
 '(>S I -^ I bS I '65- I -45 r~^«S- I 'fcs I ••> I -65 \^^-:'^^~ 
 
 acvac vac vcg ^a c vMac v ca^o-c v a^c \r gc \y ac v 
 
 Fig. 105. 
 The ventricular extra-systoles are followed by premature auricular contractions. 
 
 panying diagram shows that the auricular rhythm is also 
 irregular, the a-a periods varying between 0-50 to 0-70 second. 
 The sphygmic periods are plotted out in the diagram, and it is 
 evident that the shorter a-a periods succeed synchronous con- 
 traction of auricle and ventricle, the periods being shorter, 
 
 E 
 
 3^ 
 
 •S5 
 
 •65 
 
 
 •6S 
 
 ^ 
 
 ::^ 
 
 nK 
 
 E 
 
 xs 
 
 e: 
 
 s 
 
 a. e 4 
 
 aeok ca a, c a. 
 
 a. c oi 
 
 a c 
 
 <x. tf a. C a 
 
 Ok. ce 
 
 K 
 
 Fig. lOG. — Partial Heaet-Blook. 
 
 The auricular contractions succeeding synchronous contractions of auricle and 
 ventricle are premature. 
 
 the more nearly do the commencements of auricular and ven- 
 tricular systole coincide. To a4, occurring immediately after 
 a ventricular contraction, succeeds an a-a period of 0'70 second ; 
 while to a 5, which occurs in the middle of ventricular con- 
 traction, succeeds a period of 0-55 second. aQ occurs during 
 
COUPLED RHYTHMS 179 
 
 ventricular diastole, and is followed by an auricular contraction 
 after an interval of 0-70 second. 
 
 The block in this case was suspected on auscultation. A 
 regular rhythm of 96 beats per minute alternated at times 
 with a much less frequent and irregular rhythm, long pauses 
 occurring after one, two, three, or more beats. During the 
 frequent rate the first sound at the apex was followed by a 
 short, soft whiff ; with the infrequent beats the murmur was 
 longer and louder, replaced a considerable portion of the first 
 sound, and ran for some distance into the short pause. As the 
 tracing shows, during the frequent ventricular rate the delay 
 in the conduction of the stimulus from auricle to ventricle was 
 so great that ventricular contraction occurred immediately 
 before the succeeding auricular contraction, and at a time 
 when the auricle was so full that regurgitation from ventricle 
 to auricle could only be minimal, however great the incompe- 
 tence of the valve. With infrequent ventricular beats, how- 
 ever, the prolonged rest restored conductivity to such a degree 
 that ventricular contraction occurred relatively early in relation 
 to the succeeding auricular systole, and at a time when, the 
 auricle being as yet not nearly full, a maximal regurgitation 
 was possible, and a longer murmur was, in consequence, 
 audible. 
 
 In some instances the synchronous contraction of auricle and 
 ventricle is followed by a ventricular extra-systole. This is 
 shown in Fig. 107, which was obtained from a case of full 
 heart-block. 
 
 An undue prolongation of diastole may also be followed by a 
 premature beat. This is shown in Fig. 108, obtained from a 
 patient whose auricles were in fibrillation. Another example 
 is shown in Fig. 109, obtained from a patient whose pulse 
 often beat in couples for hours at a time. The sinus rhythm 
 was extremely mobile, but it can be seen that the first ven- 
 tricular extra-systole succeeded a lengthened diastole, though 
 at the end of the tracing an even longer diastohc period was 
 not accompanied by an extra-systole. His pulse was easily 
 influenced by pressure upon the left vagus nerve, and the 
 diastohc lengthening, which was readily produced in this way, 
 was generally followed by an extra-systole, which might recur 
 
ISO 
 
 DISEASES OF THE HEART 
 
 for a few beats or for hours. The post-extra-systoHc pause in 
 this patient, when the coupled rhythm was continuous, was 
 also generally increased by pressure upon the nerve. 
 
 The coupled rhythm shown in Fig. 110 differs from these 
 cases which we have just been considering in that both heats 
 are in response to similar stimuli, which, however, arise in 
 an abnormal situation (nodal rhythm). It is this type of 
 coupled rhythm that Wenckebach calls " true " bigeminy, 
 inasmuch as beats of different origin cannot be considered 
 as " true " twins. 
 
 Brae/it'al 
 
 Fig. 107.— Full Heart-Block. (W. T. R.) 
 
 The third ventricular contraction coincides with an auricular contraction, and is 
 quickly followed by a premature ventricular beat. 
 
 Coupled rhythm is apparently invariably associated with 
 evidence of cardiac weakness, and very often with mitral 
 reflux. Cases in which coupled rhythm is long maintained 
 are usually cases of chronic heart failure; but in other cases 
 presenting a coupled rhythm for shorter periods, the degree of 
 cardiac failure may be equally severe. The ventricular rate is 
 usually of moderate frequency. 
 
 The origin of a coupled rhythm may be stated as follows : 
 1. The ventricle is assumed to be unduly irritable, and 
 mitral reflux to co-exist. If on any one occasion, from 
 
COUPLED RHYTHMS 
 
 181 
 
 lengthening of diastole or synchronous contraction of auricle 
 and ventrrcle, the ventricle at the end of ventncular con. 
 
 'o 
 
 to . 
 
 3 I 
 
 go 
 
 s o 
 
 > r? 
 
 
 
 to tJ 
 
 <S o 
 
 
 -fit 
 
 H 
 
 .action is imperfectly e^ptiea J^— Jf ^ ^n.!^ 
 auricle wiU rapidly produce so great a cieg 
 
182 
 
 DISEASES OF THE HEART 
 
 tkat the irritable area in the ventricular wall initiates a 
 premature contraction. 
 
 The prematurity of the contraction insures complete empty- 
 ing of the ventricle, for the auricle is as yet relatively empty, 
 and the systoUc reflux is, in consequence, full; and no over- 
 distension of the ventricle will occur before the succeeding 
 sinus stimulus arrives. The lengthened diastole which thus 
 ensues entails again over-distension of the ventricle, even 
 though its contractility has improved during the longer period 
 of rest, and so an imperfect emptying of its contents ; and the 
 process may be continued indefijiitely. 
 
 2. In cases of regularly recurring auricular or nodal extra- 
 systoles the process is comparable, the irritable focus being 
 
 hi I 05 [55 [ 95 1-6 [^ 1-0 I 
 
 55 -95 -55 
 
 ■95 
 
 as 
 
 Fig. 110. — Nodal Rhythih. 
 Case 7, p. 147. True bigeminy. 
 
 situated in the auricle. If the auricle, from prolongation of 
 diastole or synchronous contraction of auricle and ventricle, 
 becomes over-distended, it will be unable to empty itself com- 
 pletely. With the succeeding ventricular systole it will be 
 rapidly over- distended by the reflux of blood from the left 
 ventricle, and the excessive intra-auricular pressure will excite 
 a premature contraction in auricle or node, followed in due time 
 by a ventricular systole. As this ventricular contraction is pre- 
 mature, the ventricle is incompletely filled, and the regurgitant 
 blood is smaU in amount, and insufficient to distend the auricle 
 to such a degree as to excite a new contraction, which will 
 only obtain when the next sinus stimulus reaches it. The 
 long diastole, however, entails again auricular over-distension, 
 and the coupled rhythm will continue indefinitely until from 
 
COUPLED RHYTHMS 183 
 
 some external influence (respiration, exertion, etc.) the flow of 
 blood into the auricle is lessened, and with an auricular con- 
 traction of sinus origin no over-distension of its cavity 
 coincides . 
 
 In " true " bigeminy the mechanism is similar, the only 
 difference being that beats of sinus origin are replaced by beats 
 which arise in the a.v. node. 
 
 There is probably no essential difference in the origin of 
 regularly recurring ventricular, nodal, or auricular extra- 
 systoles. The difference is merely a difference in site of the 
 irritable area, which in one case initiates a contraction in the 
 ventricle, in the second in the node, in the third in the auricle. 
 
 The significance of coupled rhythms is that of its cause — 
 extra-systole, heart-block, etc. In cases where it is produced 
 by the administration of digitaHs, it is an indication to cease 
 or to lessen the dose. 
 
CHAPTER XV 
 PAROXYSMAL TACHYCARDIA 
 
 The Nodal Form. 
 
 The occurrence of paroxysms of rapid cardiac action was 
 first described by Cotton in 1867, and since then numerous 
 eases have been reported, and many theories as to the nature 
 of the disturbance have been suggested. Considerable light 
 has been thrown upon the subject recently by means of the 
 polygraph and the electro-cardiograph, and it appears probable 
 that the essential feature is a disturbance of the intrinsic cardiac 
 mechanism, which is not, however, always of the same nature, 
 even in cases which otherwise seem comparable. The clinical 
 symptoms are extremely striking, and were well exemphfied in 
 the following case : 
 
 An iron-dresser, aged forty, was admitted into my wards 
 on April 16, 1908, complaining of attacks of breathlessness and 
 palpitation. He had been hable to these for seven or eight 
 years, 'but until Christmas, 1907, they were of short duration 
 and of infrequent occurrence, and rarely ensued save upon 
 exertion. Since then, however, they had been more frequent, 
 and occurred when he was at rest as well as when he was 
 at work, both during the day and at night, and had even 
 wakened him from sleep. At first they only lasted for at most 
 a few minutes, but recently they had continued for several 
 hours at 'a [time; one attack persisted for two days. He had 
 found, too, that he was more easily tired, and_^ he^[had felt 
 weak and unfit for exertion, though he had continued at his 
 work. There had been no oedema, giddiness, headache, or 
 other discomfort. i 
 
 He had always been a healthy man, save for ]a pleurisy jten 
 years before. His work was arduous, and exposed him to 
 
 184 
 
PAROXYSMAL TACHYCARDIA 185 
 
 extremes of temperature. He smoked heavily, and frequently 
 took too much liquor. 
 
 On admission he was found to be a well-built, muscular man. 
 He lay quietly in bed without any discomfort. The skin per- 
 spired fairly freely. There was no oedema. The apex impulse 
 was heaving in character and a little displaced to the left, and 
 the area of dulness was increased in the same direction. The 
 cardiac sounds were pure ; the first sound at the apex was dull 
 and long, and the second aortic sound was intoned. The 
 pulse was regular, infrequent (60 to 64), full, and slow; the 
 arterial walls were shghtly thickened. The blood-pressure was 
 140-115 mm. Hg. The urine contained a haze of albumin. 
 The other viscera were normal. 
 
 For the first few days after admission he remained in bed 
 and experienced no discomfort, and felt better in every way; 
 and on May 21 it was noted that the apex impulse and the left 
 border of cardiac dulness had receded to their normal sites. 
 The urinary output was free, and the albumin had disappeared 
 from the urine. 
 
 On the evening of May 24, however, an attack of palpitation 
 ensued at 7.45 p.m. He went to sleep notwithstanding, and 
 when he awoke at 2 a.m. (May 25) the pulse-rate was normal. 
 At 6 a.m. the tachycardia recurred, and lasted until 9.45 p.m. 
 Both attacks commenced and ended suddenly, and his general 
 condition remained unaltered. He sweated fairly freely, but 
 there was no dyspnoea or discomfort beyond the feeling of 
 palpitation, and he took the ordinary ward diet without dis- 
 turbance. The liver was slightly tender during the afternoon 
 of the 25th. 
 
 For the four succeeding days he remained well, but on 
 May 30 another attack supervened at 9.40 a.m., and continued 
 until 3.45 a.m. on June 1, when it ceased as suddenly as it had 
 commenced. There was again Uttle subjective discomfort 
 beyond the palpitation, but he complained of slight headache. 
 The left heart dilated a httle on May 31, and the Hver became 
 shghtly tender and swollen ; but on the day after the palpitation 
 had ceased they were again of normal size. 
 
 The cardiac action during the [attacks was always quite 
 regukir, the rate varying between '134 and 180. The pulse 
 
186 DISEASES OF THE HEART 
 
 during the paroxysms was fairly full, but very quick and 
 soft, the systohc blood-pressure falling to 85 mm. during 
 the four attacks in which it was recorded, as contrasted 
 with 125 to 115 mm. in the intervals. Sphygmographic 
 tracings at the higher rates were often monocrotic and the 
 vessel seemed empty between the beats. The pulsation on 
 the front of the chest was widespread and well-marked, and 
 the cardiac over-action contrasted strongly with the softness 
 of the pulse. In the intervals between attacks the pulse 
 numbered 56 to 68, and was usually quite regular; on a few 
 occasions an extra-systole (ventricular) was observed. 
 
 He remained in hospital under observation until August 21. 
 On dismissal he had gained a stone in weight, and felt in good 
 health and stronger than he had been, but he had never made 
 any complaint save of breathlessness and palpitation during 
 the attacks. 
 
 During the fourteen weeks twenty-one attacks of tachycardia 
 were observed— May 24, 30; June 4, 10 (three), 12, 13 (two), 
 15, 18, 19 (two), 20 (two); July 2, 5; August 8, 13, 18 (two)— 
 and on many other occasions he was conscious of an attack, but 
 of such short duration that it had subsided before the nurse's 
 attention was attracted. 
 
 The attacks commenced suddenly and without apparent 
 cause, and occurred at any period of the twenty-four hours, 
 during sleep as well as at other times. Their termination, 
 which was as abrupt as their commencement, was observed on 
 several occasions, and was absolutely sudden, the normal rate 
 instantly succeeding the rapid action. He was but slightly 
 incommoded during the attacks, and though he usually appre- 
 ciated their commencement and end, and the palpitation during 
 their continuance, he was not always conscious of the tachy- 
 cardia, and was accustomed to feel his pulse to ascertain what 
 the rate was. He had no dyspnoea, orthopnoea, cyanosis, or 
 oedema during the attacks ; his skin, however, was congested, 
 and he sweated fairly freely, but he took his food and went 
 to sleep as usual during a paroxysm, and would probably have 
 walked about save that he was confined to bed by order. The 
 attacks varied in their duration. The shortest lasted for but 
 a few minutes, the longest for forty-two hours. 
 
PAROXYSMAL TACHYCARDIA 187 
 
 He was again admitted to hospital on June 11, 1910. He 
 had maintained fair health in the interval, and had continued 
 his work as an iron-dresser, though attacks of palpitation of 
 short duration recurred about every fortnight. In March, 
 1910, however, an attack lasted for two days, and he was off 
 work for a week. On June 7 an attack commenced and con- 
 tinued without interruption until June 11, the longest attack 
 that he had had. This paroxysm was preceded by abdominal 
 pain, and was accompanied by nausea and retching, and sub- 
 sided after a bout of vomiting, after which the pain disappeared. 
 He remained in hospital until July 5, and had only a few 
 paroxysms, the longest of which lasted for twelve hours. The 
 highest pulse-rate recorded was 180. His general condition 
 was good, and no change was found in the viscera. 
 
 a, V a V 
 
 't^-^'^,^.2^.v!!c^>^^^v!::" ' '''V'-vr>j 
 
 Fig. 111. — Paroxysmal Tachycardia. 
 The a-c interval is less than O'lO second; P.R., 180. 
 
 Tracings (Fig. Ill) were obtained on many occasions during 
 the paroxysms, and always presented the same features, a 
 small c wave followed by a large and early v, indicative of 
 venous engorgement, and succeeded, ere the base-line was 
 reached, by a distinct a, which was almost synchronous with the 
 a wave in the apex curve. The transmission time is short, for c 
 in the cervical curve rapidly succeeds the rise of the ventricular 
 impulse. The a-c interval is regularly less than 0-10 second. 
 
 There is a marked similarity between attacks even in different 
 patients. The onset of the tachycardia is sudden and appar- 
 ently instantaneous, and the termination is equally abrupt. 
 Attacks may commence without obvious cause, but are fre- 
 quently, especially in the earlier phases, the sequel to physical 
 exertion. As time goes on, the degree of exertion required 
 often diminishes, so that attacks ensue on apparently trivial 
 
188 DISEASES OF THE HEART 
 
 physical strain. Sometimes they follow straining at stool. 
 In a patient under my care they at first succeeded severe fits 
 of coughing, during which the patient became extremely livid, 
 her face swelling rapidly to nearly double its usual size, and 
 the jugular veins becoming distended to three or four times 
 their usual diameter. The pulse became extremely frequent 
 and uncountable, and lost markedly in volume and strength, 
 and continued in this way for several minutes, when the 
 infrequent rate was rapidty resumed. 
 
 jSometimes they seem to succeed mental excitement, and, in 
 consequence, they not infrequently occur 'in the consulting- 
 room, or at demonstration in the wards . In one of my patients, 
 who required operation on account of acute appendicitis, the 
 frequency of the pulse-rate excited apprehension of widespread 
 peritoneal involvement, which proved, however, to be un- 
 founded, and the pulse rapidly resumed its normal rate after 
 operation. Flatulent distension of the stomach, too, may be 
 an exciting cause. 
 
 The cardiac phenomena are characteristic. The pulse-rate 
 is greatly increased, and numbers 150 and upwards; 160 to 
 180 seem to be common figures, but I have records of 214 and 
 234 beats per minute, and even higher figures have been re- 
 ported, the maximum being about 300. Coincidently the pulse 
 loses both in force and in volume, and becomes small and soft 
 and quick, irrespective of its previous character. The cardiac 
 pulsations, too. become exaggerated, pulsation] being notice- 
 able in several interspaces on both sides of the sternum, though 
 diffuse and badly sustained. The whole chest may shake, and 
 the vehemence of the heart's contractions contrasts in a striking 
 way with the smallness and softness of the pulse. 
 
 The symptoms of the patient seem to depend upon the 
 amount of the cardiac reserve. In uncomplicated cases the^^ 
 are often surprisingly slight, and the consciousness of the heart- 
 beats may be the sole subjective sensation. In long-continued 
 paroxysms, however, evidence of venous stasis [may be 
 observed — breathlessness, congestion of the liver, albuminuria, 
 a scanty concentrated urine, and oedema of the extremities. 
 In patients who are already seriously ill the occurrence of 
 tachycardia rapidly augments the distress. 
 
PAROXYSMAL TACHYCARDIA 189 
 
 A labourer, aged thirty-eight, was admitted into my wards 
 complaining of headache, palpitation, and general weakness 
 of six months' duration. The earliest symptom was the 
 occurrence of attacks of palpitation, which were generally 
 nocturnal, and rarely came on during the day. At first they 
 occurred about once a week, and lasted from thirty minutes 
 to three hours, but they had gradually become more frequent 
 and of longer duration. He noticed that he was easily made 
 short of breath upon exertion, and his weakness increased so 
 that he was forced to take to bed a fortnight before admission 
 into hospital. Since then the palpitation had not recurred, 
 but he had had several attacks of breathlessness . 
 
 On admission he M^as extremely ill, in full orthopnoea, the 
 respirations being laboured and cychc. The heart was greatly 
 enlarged, and double aortic murmurs were audible on auscul- 
 tation. The hver was enlarged, and the urine contained much 
 albumin. The pulse was regular and shotty, and numbered 88, 
 In ten days improvement was marked, and he was breathing 
 easily and lying low in bed. The liver was smaller, and the 
 albuminuria was trifling. Four days later, however, an attack 
 of tachycardia ensued, and lasted from 9 a.m. until 5 p.m., the 
 pulse-rate varying between 152 and 180; and all the old 
 symptoms at once recurred. Next day he was much better, 
 but the breathing was still difficult and cyclic, and he required 
 three pillows. The symptoms continued, and a few days 
 later he had an attack of vomiting, during which he nearly 
 died, his face becoming livid, and the jugular veins greatly 
 distended. Five days later Janother attack of tachycardia 
 supervened, and though it only lasted for an hour, notably 
 intensified his distress. The pulse-rate, too, only fell to 110 
 after the attack had passed off. In the evening another 
 paroxysm ensued, the pulse numbering about 200. The 
 cyanosis became extreme and the dyspnoea urgent, and after 
 three hours the heart suddenly ceased to beat. 
 
 On examination the heart was very large, weighing 
 25| ounces. The aortic valve was notably incompetent from 
 chronic sclerotic changes, the aorta was very atheromatous, 
 and the orifices of the coronary arteries were considerably 
 narrowed. The kidneys showed widespread fibroid change. 
 
190 DISEASES OF THE HEART 
 
 In this case the tachycardia seemed directly responsible for 
 the fatal termination, as improvement had been considerable 
 after his admission to hospital. The post-mortem examination, 
 however, showed widespread valvular and myocardial disease, 
 so that the cardiac reserve must have been small. 
 
 A similar sequence was observed in a case of chronic bron- 
 chitis and emphysema. The paroxysms were sharply related 
 to bouts of coughing, and at first ceased shortly after the 
 cough, but later on continued indefinitel3^ and rapidly pro- 
 duced fatal cardiac failure. 
 
 A married woman, aged fifty-three, was admitted to hospital, 
 complaining of a cough and spit and severe sickness. She had 
 had an attack of pleurisy twenty years before, and had been 
 subject to a winter cough ever since. A fortnight before her 
 admission she caught cold, and the cough became more trouble- 
 some. Three days later vomiting ensued and continued. It 
 was, in part at any rate, induced by the cough, and prevented 
 her from retaining any food at all, and she had become very 
 exhausted. 
 
 She was a big, stout woman, but flabby and soft, and on 
 admission was verj^ ill, the mucous membranes being extremely 
 livid, and the feet oedematous. The finger-tips were slightly 
 clubbed. She retched continuously, but only brought up a 
 Httle mucus. The pulse was small, and so frequent as to be 
 uncountable. The heart was greatly enlarged, and a systolic 
 murmur was audible at the apex. There was widespread 
 bronchitis, and a chronic consohdation at the right apex. 
 The urine contained albumin in abundance. 
 
 For a few days after admission she improved considerably, 
 the vomiting ceasing, and enabhng her to retain a fair quantity 
 of fluid food; but she had at times severe bouts of cough, 
 during which she became extremely hvid, the face swelhng 
 enormously, and the jugular veins becoming distended to many 
 times their usual size. The pulse became tiny and very 
 frequent and uncountable, and she appeared at the point of 
 death. The symptoms, however, rapidly subsided when the 
 coughing ceased. On October 20, after a restless night, she 
 had a severe fit of coughing, and was collapsed and weak for 
 some hours. At 11 a.m. on the 21st the pulse was found to 
 
PAROXYSMAL TACHYCARDIA 191 
 
 be extremely rapid (200), and small and soft, but she did not 
 seem to be notably distressed. In the evening the vomiting 
 recurred, and she was extremely weak and feeble, but next 
 morning she had improved, and the pulse w^as fuller and 
 stronger, and numbered 80. A few extra-systoles were observed 
 at this time. The tachycardia, however, returned at noon on 
 October 23, and continued until her death on the 25th from 
 cardiac failure. 
 
 Ko cervical tracings were obtained in this patient, but epi- 
 gastric curves showed a rate of 222 beats per minute on 
 October 21, and 234 per minute on October 23. 
 
 All the available evidence goes to show that paroxysms of 
 tachycardia are due to the inception of a new cardiac rhytlim, 
 the contractions originating in some abnormal situation in the 
 heart. The pulse-rate, it is true, varies considerably in indi- 
 viduals, and rates approximating to the lower figures reached 
 in paroxysmal tachycardia have been recorded in patients 
 whose cervical curves were of normal type ; but the onset and 
 the cessation of the frequent action are almost invariably 
 gradual, and a sudden change is rarely seen. In only one case 
 have I observed a comparable change in rate. 
 
 The patient, a labourer aged fiity-four, was admitted to 
 hospital complaining of breathlessness and praecordial pain of 
 three weeks' duration. He had suffered from acute rheu- 
 matism five years previously, and had since then been subject 
 to breathlessness and palpitation upon exertion, but these 
 had not interfered with his work. Three weeks before 
 admission, however, after a severe strain at his work, he 
 suddenly became extremely short of breath, and felt his heart 
 fluttering, and experienced severe pain in the prsecordial 
 region. These symptoms steadily progressed; his feet and 
 legs began to swell, and he was forced to seek admission to 
 hospital. 
 
 He was a well-built man and weU nourished. On admission 
 he was extremely breathless, and had to sit upright in his bed. 
 The cedema extended as high as the sacrum, but was not 
 excessive. His heart was large, and double aortic murmurs 
 were audible over the sternum. The pulse was very shotty 
 but quite regular, and numbered 92. His progress was con- 
 
192 DISEASES OF THE HEART 
 
 tinuousl}' in the right direction, and he made a good conva- 
 lescence. 
 
 The point of interest lay in pulse disturbances which appeared 
 four clays after admission at a time when improvement was 
 already manifest. The oedema had gone, and he was lying 
 low in bed, and feeling quite comfortable. The breathing was 
 less difficult, but was now for the first time Cheyne-Stokes in 
 character, the periods of apnoea being of considerable length. 
 The pulse was infrequent and irregular, little runs of two, three, 
 or more beats at a quicker rate occurring at frequent intervals 
 and irrespective of the respirator}^ phases. The tracings were 
 always of the same character whatever the duration of the 
 "tachycardia." In Fig. 112 the first three pulse periods are 
 practically equal ; period 4 is shorter, period 5 is shorter still, 
 period 6 is longer, but not so long as the first three, and the 
 initial rhythm then recurs. In Fig. 113 the first two periods 
 are long and equal, 3 is shorter, and then comes a series of 25 
 beats in rapid succession before the slower rhythm is resumed. 
 The pulse periods of the frequent rate are practically equal, 
 save in the case of beats 8 and 9, period 8 being shorter and 
 period 9 longer than the others. The jugular curve shows 
 that all the beats are apparently of sinus rhythm, the a-c 
 interval being of normal duration, save in the case of beat 9, 
 where it is short. The ventricular contraction is premature, 
 but the auricular rhythm is unaltered, so that beat 9 is a 
 ventricular extra-systole. 
 
 The case is, of course, not one of paroxj^smal " tachycardia," 
 though it shows an abrupt change from a pulse-rate of about 
 63 beats per minute to one of 117, the normal sinus rhythm 
 continuing unchanged. There was no constant relationship 
 between the cardiac and the respiratory irregularities, and 
 both the pulse and the respirations became regular mthin 
 three or four days. 
 
 The cervical curves in paroxj^smal tachycardia are often 
 difficult to interpret on account of the frequency of the cardiac 
 contractions, for with a pulse-rate of 180 or more diastole is 
 so short that auricular systole occurs before the preceding 
 ventricular contraction has ceased, and v and a are inex- 
 tricably mingled. In some cases, however, they are more 
 
WA/U^'WU'AJ'^ 
 
 Fig. 113.— a Paroxysm of Fi 
 Beat! 
 
 The rhythm of the he 
 
 ^^ vac vq c V d c u AC V a c « ^'^yf 
 
 Fig. 
 res showing the sudden transition fro 
 
 [To face page 192. 
 
JvJV^JMUJiAAJiJiWJi 
 
 Fig. 112. 
 The rhythm of fcho heart varies, bub the o-c interval is always normal. 
 
 JiAji/i_i.iJUyijjijij/j4WJiAjA/uUwU'iU'j^/j-AJ^iiu^i/ii'/u%i |i,J.jJV^/«JiJjiMJj'JJ'^ 
 
 Fig. 113.— a P 
 
 oir Frequent Caediac Beats with a Normal a-c Interval. 
 Beat 9 is a ventricular estra-syatole. 
 
 Fio. 114. — Paroxysmal Tachycardia. 
 Curves showing the sudden transition from boats with a short a-c interval to those with a normal a-c interval. 
 
PAROXYSMAL TACHYCARDIA 193 
 
 intelligible, and v and a are distinct, perhaps as the result of 
 insufficiency of the tricuspid valve, so that v occurs early in 
 the cycle and precedes a. 
 
 Fig. Ill was obtained when the pulse numbered 180 per 
 minute. The cervical curve is regular and shows three waves, 
 the smallest being c. This is rapidly succeeded by an early 
 and prominent v, on the downstroke of which a is distinct, and 
 precedes c by less than 0-10 second. The apical curve is also 
 clear, and a is rapidly succeeded by v before the base-line has 
 been reached. In Fig. 114 the transition between the normal 
 and abnormal rhythm is distinctly shown. The pulse-rate is 
 gradually slowing before the central ordinates (one beat), but 
 the essential change occurs between the second and third beats 
 following them. In the cervical curve a is unfortunately 
 
 Fig. 115. — Paroxysmal Tachycaedia. 
 The a-c interval is less than O'lO second; P.R., 214. 
 
 mingled with v and somewhat indefinite, but the apical curve 
 is clear. The a-c interval in the former changes suddenly 
 from less than 0-10 to 0*20 second; and the A.V. interval in the 
 latter from 0-05 second to nearly 0-10 second. As has been 
 already shown (p. 127), so short an a-c interval indicates that 
 the contractions originate between the auricle and the ventricle, 
 and are not in response to normal stimuh. 
 
 The majority of the curves which have been published are 
 similar to those which have just been described, and another 
 example is shown in Fig, 115 with a pulse-rate of 214. Lewis, 
 too, has published comparable electro-cardiograms (Fig. 218, 
 Plate II.), with a short P.R, interval and an inverted P, so 
 that the evidence seems complete that attacks of tachycardia 
 may be due to the inception of a nodal rhythm as the curves 
 are similar, save in the frequency of the contractions, to those 
 which I have already designated by this term, 
 
 13 
 
194 DISEASES OF THE HEART 
 
 Experimental evidence (Lewis, Hirschfelder), however, 
 strongly suggests that similar paroxysms may occur from 
 stimuli arising lower down in the ventricle which precedes the 
 auricle in its contraction. A " retrograde " contraction of the 
 auricle rarely succeeds an isolated ventricular premature 
 systole, but if the latter recurs for several beats, the auricular 
 contractions change their rhythm, apparently in response to 
 stimuli passing backwards from the ventricle. 
 
 Variations in the exact site of origin of the stimuli may 
 conceivably produce slight variations in polygraphic and 
 electric curves. If they arise in the node, the auricular con- 
 tractions precede the ventricular; but if lower down, the- 
 auricular and ventricular responses may be simultaneous,* and 
 if lower still, the ventricles may contract first. In each case^ 
 however, the a-c or the c-a interval is excessively short. 
 
 It seems probable, too, that paroxysmal tachycardia may 
 be due to auricular flutter, and that many of the cases hithertO' 
 pubhshed as examples of the former are really cases of the 
 latter. The patient from whom Fig. 115 was obtained, for 
 example, had certainly auricular flutter a few days after the 
 tracing was obtained, and varying degrees of conductivity 
 might conceivably account for the varying number of the 
 ventricular contractions. Sudden doubUng or halving of the 
 ventricular rate — at one time supposed to be characteristic of 
 paroxysmal tachycardia — is probably always indicative of 
 auricular flutter. Hertz and Goodhart's case probably comes 
 under this category. 
 
 The essential feature of paroxysmal tachycardia appears tO' 
 be the inception of a new site of stimulus production. The 
 cause of this is obscure, but is probably to be sought for apart 
 from organic lesions of the a.v. tissues, for in those cases which 
 I have described as "nodal rhj'thm," where definite lesions 
 were found post-mortem, the pulse-rate was never extremely 
 frequent, and no sudden changes in rate ever ensued. The 
 causes which produce premature systoles are probably those 
 
 * A case recorded by Falconer and Dean (" Heart," 1912-13, vol. iv., p. 137) 
 showed short paroxysms of tachycardia during which the a and c waves in the 
 cervical curve were synchronous ; and on post-mortem examination an acute? 
 inflammatory lesion in the middle third of the a.v. bundle. 
 
PAROXYSMAL TACHYCARDIA 195 
 
 wliicli may produce paroxysms of frequent contractions, but the 
 nature of the underlying excitability of the parts concerned 
 still awaits elucidation. A. M. Kennedy has examined the a.v, 
 tissues in one case, and found that they were apparently 
 normal, though the s.a. node was involved in a chronic and an 
 acute injBlammatory reaction. 
 
 The coincidence of the auricular and the ventricular con- 
 tractions explains several of the characteristic features of the 
 paroxysms. During ventricular systole the auriculo-ventric- 
 ular valves are shut, and the auricle contracting simultaneously 
 is, in consequence, unable to supply the ventricle with its 
 normal quantity of blood. The ventricular output is thus les- 
 sened, and the pulse loses both in volume and in force. 
 
 The auricular contraction drives the blood backward into 
 the veins, and thus initiates venous stasis ; which, if the 
 paroxysm is prolonged, rapidly becomes serious in its degree, 
 the lungs and the liver becoming engorged, and oedema making 
 its appearance in the dependent parts. The pulsations in the 
 neck, too, become larger and more distinct. 
 
 The obstacle to the output from the auricle stimulates it 
 to increased effort, and the pulsations on the front of the chest 
 become more forcible and more widespread, and the apparent 
 strength of the cardiac contractions contrasts markedly with 
 the smallness and softness of the arterial pulse. 
 
 At the present time accurate data of the incidence of 
 paroxysmal tachycardia are necessarily awanting, for the 
 nodal rhj'thms, auricular fibrillation, and auricular flutter have 
 only recently been differentiated from each other, and our 
 present knowledge of the relationship between them is ex- 
 tremely scanty. Electrical stimulation of the auricle may 
 produce extra-systoles, and, if continued, auricular flutter, and 
 in time auricular fibrillation ; and James Mackenzie has observed 
 flutter pass into fibrillation in patients under the influence of 
 digitalis. (I have once seen this occur.) Some of the cases of 
 paroxysmal tachj^cardia show at one time tracings of "nodal 
 rhythm," and later on of flutter; and in the constant nodal 
 rhythms extra-systoles have been observed to precede the 
 onset of the rhythm. It seems probable that extra-systoles, 
 the nodal rhythms and auricular flutter, are closely allied and 
 
196 DISEASES OF THE HEART 
 
 that the last two are merely series of extra-systoles originating 
 in different situations. Lewis thinks that auricular fibrillation 
 is of similar nature, the stimuli arising in many places in the 
 auricular muscle instead of in one constant situation; but 
 Gaskell's theory that fibrillation is due to defects in conduction 
 between the auricular muscle cells seems a more probable 
 explanation. 
 
 It is, however, apparent that paroxysmal tachycardia, 
 auricular flutter, and auricular fibrillation may occur in both 
 sexes and at every age, though they are all less frequent in 
 early childhood ; in every form of organic cardiac disease, and 
 in hearts that are apparently normal; in hypertrophied hearts, 
 and in hearts of normal size. They may arise suddenly and 
 cease suddenly, both in experiment and in the clinique, and 
 may thus be the result of functional disturbances. Fibrillation 
 and nodal rhythm may also be permanent, and are then, in all 
 probability, the sequel to organic disease. 
 
 The prognosis in paroxysmal tachycardia must be based 
 upon several factors. Paroxysms of short duration and infre- 
 quent occurrence, which have never produced any signs of 
 cardiac insufficiency, occurring in patients with no obvious 
 diminution in the field of response, are of little practical 
 importance, save that they indicate a tendency to functional 
 disturbance which may in time prove serious. Herringham* 
 states that the condition seems always to tend to get worse 
 and in the end to kill, and that after thirty the patient is never 
 safe, though the progress may be slow, since people who have 
 been affected in childhood have been known to pass fifty years. 
 On the other hand, paroxysms of considerable duration and 
 frequent occurrence, which produce signs of obvious cardiac 
 distress and obtain in patients whose hearts in the intervals 
 exhibit little cardiac reserve, are in a condition of extreme 
 danger. A paroxysm which la its for two or three days seems 
 always to produce symptoms, and the duration of the 
 paroxysms is probably of most importance in this respect. 
 
 The treatment of the paroxysms is still unsatisfactory. The 
 vast majority of attacks end spontaneously, and the patient is 
 restored to his usual health, but there is little that can be done 
 
 * Edin. Med. Journ., 1897, N.S., vol. i., p. '^m. 
 
PAROXYSMAL TACHYCARDIA 197 
 
 to induce the cessation of the frequent action. I have seen 
 attacks cease after deep breathing, holding the breath, exertion, 
 the act of vomiting, the appHcation of fomentations to the 
 praecordia, and they have been described as terminating after 
 pressure had been exercised upon the chest or upon the vagus 
 nerve in the neck. But everyone is agreed that those measures 
 usually fail, and that their effects are rarely uniform even in 
 the same patient. Digitalis, too, has proved equally useless 
 in my hands, although good results have been recorded after 
 its administration. 
 
 Much, however, can be done in the intervals to lessen the 
 frequency of the attacks. A careful detailed survey of the 
 case usually shows some manifest error in the mode of life, or 
 some functional disturbance in one or other of the viscera. 
 As Herringham points out, the over-use of tea, coffee, alcohol, 
 or tobacco, or some digestive disturbance, are sometimes 
 responsible. The cardiac reserve m.a.ry be limited, even in the 
 absence of organic valvular or myocardial disease, and the 
 usual modes of treatment are necessarily indicated. Or the 
 cares of business or domestic worries may press unduly upon 
 the patient. 
 
 It may appear unnecessary to limit the phj^sical exercise of 
 these patients if, when seen between attacks, their general 
 health and nutrition seem unimpaired, but my personal ex- 
 perience has taught me caution in this respect. A paroxysm 
 in esse is always a period of danger, for it is impossible tc 
 predict its duration, and if it continues for more than a day 
 or two, definite signs of cardiac failure are sure to appear. 
 The heart, too, is unduly irritable, whatever the source of this 
 may be, and an irritable organ is hypersensitive to strain and 
 stress, so that it is generally advisable to exercise precautions 
 in this direction ; and if the attacks are frequent, however short 
 their duration, or if any evidence of cardiac insufficiency is 
 present, the patient should be confined for a time to bed. In 
 the milder cases less restriction is indicated. The obvious 
 errors should at the same time be corrected, special attention 
 being paid to the alimentary tract, and a general tonic may be 
 added. Small doses of digitalis seem in many cases to help. 
 
CHAPTER XVI 
 
 AURICULAR FLUTTER 
 
 In 1905 the late G. A. Gibson and W. T. Ritchie reported a 
 case in which polygraphic tracings showed that the auricular 
 contractions were extremely frequent (about 270 per minute) 
 and perfectly rhj^thmic, though the ventricular contractions were 
 infrequent (about 35 per minute) and fairly regular, the result, 
 apparently, of full heart-block; and in 1906 they recorded a 
 second case in which the auricular contractions numbered 
 about 350, while the ventricular contractions numbered about 
 40. In 1909 Morrison reported a case of very rapid auricular 
 contractions, in which the ventricles usually beat at haK the 
 auricular rate; and in the same year Hertz and Goodhart 
 described a fourth case in which the ventricles contracted 
 about 80 times per minute, while the auricles beat four times 
 as frequently. In 1910 Jolly and Ritchie* published the 
 results of electro-cardiographic investigations of the case 
 which had been reported in 1905, and showed that there were 
 distinct differences between the curves of the auricular con- 
 tractions in this case and in patients in whom the auricles were 
 in fibrillation. The rate was less frequent, the rhythm was 
 quite regular, and tracings showed with Derivations II. and 
 III. a diphasic deflexion. MacWilliam had already found that 
 the application of a faradic current to the auricles might — in 
 experiment — produce a rapid co-ordinate " flutter " of the 
 auricles, the contractions originating in the stimulated area; 
 and Jolly and Ritchie, recognizing the similarity of the clinical 
 and experimental tracings, designated the condition "auric- 
 ular flutter." Recent papers by Ritchief and Lewis, J with 
 
 * Heart, 1910-11, vol. ii., p. 177. 
 t Edin. Med. Journ., 1912, N.S., vol. ix., p. 485. 
 % Heart, 1912-13, vol. iv., p. 171. 
 198 
 
AURICULAR FLUTTER 199 
 
 tracings from other cases, seem to have estabhshed the 
 identit}^ of a new rhythm, and one, too, that is of frequent 
 occurrence. 
 
 Auricular flutter is most readily recognized in electro- 
 cardiograms, and is well shown in Fig. 116, which is 
 reproduced by kind permission of W. T. Ritchie. The ven- 
 tricular contractions show well-marked R and 8 deflexions, 
 and the successive beats are separated from each other by 
 regularly recurring diphasic waves of considerable size, which 
 in this figure overlap and obliterate the Q and T deflections of 
 the normal ventricular complex. The auricular waves are 
 regular in rhythm, and number 281 per minute, and differ in 
 their regularity, their less frequent rate, and their diphasic 
 character from the waves which are present in auricular 
 fibrillation. The ventricular rate is almost constant (72-25 per 
 minute). 
 
 R 
 
 ' ' ' ' ff 
 
 iiiiiiiiiiiiiiiiiiiiituuuuiiiiiiiuiiiiuiiiUJiiiimuiiikiiiiiiiiiiiUiiuuiniiiiiiiAiiiiiiiniimiiimuiiiuuiiiiHUiiiiiiii 
 
 Fig. 116. — ELECTEO-CARMOGEAjii OF Atjeicular Flitttee. (W. T. R.) 
 
 The rate of the ventricular contractions varies considerably 
 in auricular flutter, and if it is infrequent the auricular waves 
 may be readily seen in polygraphic tracings (Figs. 117, 118). 
 Their size varies. The waves synchronous with the carotid 
 impulse and those immediatelj^ succeeding it are ample, as 
 auricular contraction coincides with ventricular contraction 
 (c and v), and the auricle is thus unable to force its contents 
 through the closed auriculo-ventricular valve ; the blood 
 is, in consequence, thrown back into the jugular vein. As 
 ventricular diastole ensues, the waves at first are smaller, 
 but they again increase in size as systole approaches, owing to 
 the increasing fulness of the ventricle and the increasing diffi- 
 culty in still further augmenting its blood-content. The 
 rhythm of the auricular waves is fairly constant, but in poly- 
 graph curves is somewhat disturbed by carotid waves occurring 
 
200 
 
 DISEASES OF THE HEART 
 
 approximate^ at the same moment, or by respiratory move- 
 ments of the sterno-mastoid muscle. If measurements are 
 taken, however, at corresponding respiratory phases and from 
 points which are not coincident with carotid beats, the number 
 of a waves in stretches of equal length is exactly the same. 
 In Figs. 117, 118, 119 the waves number about 270 and 240 
 per minute. 
 
 Fig. 117. — Cervical Curve rs Auricular Flutter, (a. v. 
 
 5 to 1.) 
 
 The rate of the auricular contractions is generally in the 
 neighbourhood of 300, and the highest record is 350. Ritchie's 
 Case 5 suggests that thej^ may reach 454. 
 
 Tlie rate and rhythm of the ventricular contractions, on 
 the other hand, vary within very large limits. In Fig. 116 
 the}' number 72, the A.V. ratio being regularly 4 to 1. In 
 Figs. 117, 118, 119 they number 54-5, 60, and 120 per minute, 
 the A.V. ratios being 5 to 1, 4 to 1, 2 to 1. The cervical 
 curves are most easilj' deciphered in Fig. 117. In this figure 
 
 a-: 7.tfO. v : 6o 
 
 Fig. 118. — Cervical Curve in Auricular Flutter. {a.v. = 4 to 1.) 
 
 each cardiac cycle is represented by fi^ve waves, the largest of 
 which is evidently synchronous with the carotid pulse. The 
 succeeding wave, however, is almost as great, and can only be 
 partly due to v ; and an evident auricular wave a precedes 
 each carotid elevation. The intermediate waves occur, as is 
 evident on reference to the radial pulse, during the diastole 
 of the ventricle, and are of equal duration and of the same 
 
AURICULAR FLUTTER 
 
 201 
 
 length as a, and the period c-c is five times the length of a. 
 Each wave, then, is in part or in whole the result of a regularh' 
 recurring auricular contraction, and the auricles are contract- 
 ing five times as often as the ventricles . In Fig .118 the cardiac 
 cycle shows four waves which, b}' the same argument, are also, 
 in whole or in part, of auricular origin, but the A.V. ratio is 
 4 to 1. In Fig. 119 only two waves are present in the cervical 
 curve, but as the largest wave coincides mth v and not -^nth c, 
 it is eviclentlv only in part the result of ventricular contraction ; 
 and as the radial pulse-rate is exactly double that of the 
 preceding figure, it is clear that each represents in part an 
 auricular contraction, the A.V. ratio being 2 to 1. 
 
 The ventricular contractions, however, are not necessarily 
 always regular. In Fig. 120 the first two and the last ^our 
 pulse periods are of 
 equal length, but the 
 intervening periods are 
 all shorter and varj^ in 
 duration, though four 
 in series are in one place 
 equal. On examination 
 of the cervical curve 
 the number of the waves 
 
 between successive carotid beats is found to varj-, the series 
 being 4, 4, 2, 2, 3, 2, 2, 2, 2, 1, 2, 4, 4, 4, 4; but as each 
 carotid wave evidently overlaps an auricular wave, the 
 series of auricular contractions is evidently 5, 5, 3, 3, 4, 3, 3, 3, 
 3, 2, 3, 5, 5, 5, 5, and the ventricles are either responding to 
 every second, third, fourth, or fifth auricular contraction, 
 or contracting independenth- of the auricles. The ventricular 
 electric complex in Fig. 116 is of normal character so far as 
 can be seen, which indicates that the contraction is originating 
 near the auriculo -ventricular junction. In Ritchie's first case 
 full heart-block was present, and the ventricular contractions 
 were quite regular, with a pulse-rate of 30 to 40 per minute, 
 the usual idiopathic ventricular rate. But in Fig. 120 the 
 ventricular contractions are never less than 50, a figure 
 greater than those which occur in cases of full heart-block, so 
 that the latter condition mav be excluded. A partial heart 
 
 Fig. 
 
 119. — Cervical Cukve in Auricular 
 Flutter, (a. v. = 2 to 1.) 
 
202 DISEASES OF THE HEART 
 
 block may occur in cases of sinus rhythm, and a partial block 
 seems the probable explanation of the varying pulse-rate in 
 auricular flutter. The most common A.V. ratios seem to be 
 2-1 and 4-1, and an abrupt change from one to the other may 
 double or halve the pulse-rate instantaneously. 
 
 The arterial curves show as a rule a characteristic appearance, 
 and can generally be distinguished from those of auricular 
 fibrillation. The pulse periods in the latter are totally 
 irregular, and occur without any recognizable sequence, or 
 definite relationship between individual beats. In auricular 
 flutter, on the other hand, series of rhythmic ventricular beats 
 occur at times (Fig. 121), and the periods of an irregular rhj^thm 
 tend to recur and to bear a deflnite relationship to each other. 
 The two longer pulse periods in Fig. 122 are thus^ equal, and 
 
 Fig. 123. — Brachial Curve in Auricular Flutter. 
 The underlined groups of beats are of equal duration. 
 
 bear to the intervening beats the ratio 7 to 6. In Fig. 120 
 the correspondence is less close. A premature ventricular 
 systole is accompanied by a prolongation of both the presphyg- 
 mic interval and the transmission time, and the arteiial wave 
 is, in consequence, separated from its precursor by a longer 
 interval than obtains between the ventricular contractions, as 
 shown on the apex tracing (c/. Fig. 80). If the ventricular 
 contraction is delayed, the presphygmic and transmission 
 periods are shortened, and the pulse period is then shortened 
 as weU. 
 
 Comparable stretches may, however, be found if care be 
 taken to contrast stretches which are preceded and ended by 
 equal pulse periods (Fig. 123), so that the transmission time 
 and presphygmic period are equal in the two cases. In 
 Fig. 121 five beats of the frequent rate exactly equal three of 
 the infrequent rate. 
 
Five 
 
 slow rhvthm. 
 
 iTo face paffe 2.02. 
 
3 3 3 3-3 
 
 Fig. 120. — Cervical Cfrve in Auricular Flutter. 
 The A.V. ratio is incoiatant. 
 
 Fig. 121. — Brachial Curve in Auricular Flutter, 
 Five pulse periods of the frequent rhythm equal three pulse periods of the slow rhythn: 
 
 AJUU 
 
 Fig. 122.— Cervical Curve in Auricular Flutter. 
 The two longer pulse periods are equal. 
 
AURICULAR FLUTTER 203 
 
 Auricular flutter has been recognized for too short a time 
 to enable any definite conclusion to be stated with regard to 
 its significance, but it is already evident that it may occur 
 under various conditions, and it has been found in acute and 
 chronic valvular disease, in hearts that are enlarged and evi- 
 dently degenerate, and in hearts that are of normal size and 
 probably healthy. It may arise and continue for varying 
 intervals, hours, days, and certainly weeks, and may cease and 
 recur from time to time. In some cases it has been succeeded 
 by auricular fibrillation; in others by a normal rhythm, and 
 the transition may be extremely abrupt. 
 
 The symptoms that are met with in auricular flutter are 
 often subjective rather than objective. This seems to be due 
 to the fact that it occurs in patients whose cardiac reserve is 
 ample as well as in those who are already suffering from cardiac 
 insufficiency; and while in the former its appearance is of 
 ■comparatively Mttle significance if the paroxysms are of short 
 duration, in the latter its onset rapidly induces extreme failure. 
 
 There is little doubt that auricular flutter is not uncommon, 
 though the number of cases that have been reported is still 
 small, but many patients whose auricles are probably fluttering 
 a.re too ill to allow a detailed examination, and the recorded 
 cases are thus the less serious, and the prognosis on the avail- 
 able data is, in consequence, erroneous. 
 
 The cases which are narrated below illustrate this point. 
 In the first the objective signs of cardiac failure were slight, in 
 the second severe, and in the third completely absent. 
 
 Case 1. — A shipyard labourer, aged fifty-one, was admitted 
 into my wards complaining of palpitation, shortness of breath, 
 and pain in the epigastrium. i 
 
 The symptoms made their appearance about a year before 
 his admission, when he first became conscious of his heart's 
 contractions. At the outset the attacks only occurred on 
 severe exertion, and ceased shortly after he stopped work, and 
 they were, he thought, more frequent after alcoholic excess. 
 He was short of breath during the paroxysms, and often giddy 
 as well, but he never fell down. During the last few months 
 the attacks had been more easily induced by exertion, and the 
 breathlessness had been exaggerated, and for three weeks he 
 
204 DISEx4SES OF THE HEART 
 
 had had a constant gnawing pain in the epigastrium. The 
 palpitation, he says, is a frequent action of the heart, " Hke a 
 bird fluttering, with occasional irregular thumps." Ten days 
 before admission, after a bout of drinking, it became constant, 
 and did not remit during rest. The pain in the epigastrium 
 was constant, not related to the ingestion of food, and steadily 
 became more severe, and he was forced to cease work five 
 days after the onset of the attack. He felt very weak and. 
 ill, and was only able to reach the hospital with the greatest 
 difficulty, though he quickly rallied after being put to bed. 
 
 He was a big, muscular man, and lay easily in bed with two 
 pillows. The respirations were somewhat frequent (36 to 42)' 
 and irregular, and at times sighing in character. There was 
 no oedema, but the liver was large and somewhat tender. The 
 other viscera, save the heart, appeared normal, but the urine 
 contained a fair quantity of albumin. 
 
 The apex impulse was indistinct and badly sustained, and 
 was situated in the fifth interspace in the nipple Une. The- 
 area of cardiac cluhiess measured 5| inches transversely, both 
 sides of the heart being slightly dilated. The sounds were- 
 muffled and indistinct, but pure. The second sounds at the- 
 base were emphatic, the emphasis being on the pulmonic 
 element. The cardiac action was frequent, numbering 136 tO' 
 150, and extremelj^ irregular, little runs of five to twenty beats 
 of even rhj^thm and force being separated from each other by 
 pauses of slightly longer duration, or by runs of beats at a less 
 frequent rate. The pulse w^as of good volume, but soft. 
 
 His condition remained unchanged for forty-eight hours 
 after admission, during which he took his food fairly well and 
 slept for reasonable periods, being apparently comfortable- 
 when at rest, but very breathless and weak on even trivial 
 exertion (stool, etc.). Between midnight and 2 a.m., however, 
 the cardiac action suddenly altered, the pulse-rate falling ta 
 80, and the rhythm becoming perfectly regular. The patient 
 was conscious of his improvement and of the cessation of the 
 flutter. His progress afterwards was good. The pulse re- 
 mained infrequent and regular, save for a few ventricular 
 extra-systoles which were noticed in the succeeding twenty- 
 four hours ; the area of cardiac clulness rapidly diminished to 
 
AURICULAR FLUTTER 205 
 
 4J inches, and the hepatic engorgement and pain passed 
 away. 
 
 The habits of this patient were unsatisfactory in every way- 
 He drank and smoked heavity, and was engaged in arduous 
 manual labour, circumstances which seemed to be the chief 
 cause of his cardiac disabilities. 
 
 Case 2. — ^A wire-drawer, aged sixty-one, was admitted to 
 my wards on April 5, complaining of shortness of breath and 
 swelling of the feet a nd legs . 
 
 He had been a healthy man until the preceding December, 
 save for an attack of dropsy, which only lasted for a few days, 
 three years before. His early symptoms consisted of a feeling 
 of sickness after taking food, accompanied by giddiness, but 
 he continued at his work until he caught cold early in January. 
 At this time he had a harassing cough and spit, accompanied 
 by pain in the chest, and he was forced to take to bed. He 
 was very breathless and had paroxysms of dyspnoea at night, 
 which lasted for about haK an hour. A few days after he went 
 to bed his feet began to swell. After nine days the symptoms 
 subsided, and he was able to resume work; but he felt weak 
 and ill, and became breathless on slight exertion. The oedema 
 was always greater at night after his work, and the paroxysms 
 of dyspnoea still continued. He was giddy at times, particu- 
 larly when at work, and as all the symptoms increased, he 
 sought admission to hospital. 
 
 He was a badly nourished man of poor physique, and re- 
 quired to be propped up in bed on account of shortness of 
 breath. Qi]clema was well marked and extended on to the 
 trunk. The chest was barrel-shaped, and there was wide- 
 spread catarrh of the lungs, with rales at the bases. The hver 
 was enlarged, but was not tender. The left heart was enlarged, 
 the apex impulse being felt in the nipple line in the fifth space. 
 Double aortic murmurs were audible over the sternum; the 
 second aortic sound was inaudible. The arteries were very 
 hard and tortuous, and the pulse numbered 90, and was 
 regular and notably shotty. The urine contained a trace of 
 albumin. The knee-jerks were slight, but equal; the pupil- 
 lary reactions were trivial; and the Wassermann test was 
 frankly positive. His symptoms rapidly subsided, and he 
 
206 DISEASES OF THE HEART 
 
 left hospital a week later of his own accord, though the oedema 
 was still present. A week later he resumed work, but he was 
 never able to do a full day's darg, as the slightest exertion made 
 him very breathless. A few weeks afterwards the cough 
 returned, and all his symptoms became exaggerated. The 
 nocturnal dj'spnoea reappeared, and he had again to be propped 
 up in bed, and he slept badly and the oedema steadily increased. 
 He was readmitted to hospital on May 23. He now looked ill 
 and collapsed, and was in full orthopnoea. The oedema again 
 invaded the trunk; the bases of the lungs were congested, and 
 the liver was enlarged and tender. The respirations were 
 shallow and frequent, and slightly irregular. The heart was 
 a little larger than on his previous residence, pulsation being 
 apparent in the sixth interspace. The rate was very frequent 
 (about 150), but the rhythm was quite regular. The systohc 
 aortic murmur was still distinct, but the second sound was 
 closed, the diastolic murmur having disappeared. The pulse 
 was fairly full and still shotty. 
 
 After his admission his symptoms steadily impioved. The 
 urinary output became ample, and the oedema diminished 
 and the orthopnoea became less marked. A pulmonary infarct 
 occurred on May 27, but this did not interfere with his progress. 
 
 The frequent cardiac action, however, continued until June 3, 
 the rate varying between 140 and 178; but on that morning, 
 between 6 a.m. and 8 a.m., it suddenly fell to 92, and after- 
 wards to 76. It was now notably irregular from auricular fibrilla- 
 tion. At 2 p.m. on June 4 the rhythm again altered, and the 
 pulse became quite regular, but very frequent (140 to 174). 
 This continued until 8 a.m. on June 5, when the rate again fell 
 suddenly to 88. The rhj'thm was now quite regular, save for 
 the presence of an occasional extra-systole, which was appar- 
 ently always ventricular in origin. 
 
 There are several points of interest in the case. The patient 
 was never conscious of the cardiac action, and was unable to 
 state whether the tachycardia had occurred prior to his second 
 admission, or the time of its onset. He was given 60 minims of 
 tinct. cligitaHs daily at first, a week later 75 minims, and two 
 days later (June 1), 90 minims, and with apparent benefit, 
 though there was no change in the pulse-rate. 
 
AURICULAR FLUTTER 207 
 
 Cervical tracings were frequently obtained during the period 
 of tachycardia. The a wave was always distinct, and preceded 
 the c by O'lO second, while v occurred early, and filled up the 
 rest of the curve. Two interpretations are possible: a 
 "nodal " tachycardia or a 2-1 auricular flutter, every other 
 auricular contraction being hidden beneath the c-v waves; 
 and as the paroxysm passed into undoubted auricular fibrilla- 
 tion, the second explanation seems the more probable. No 
 tracings were obtained during the second paroxysm, which was 
 succeeded by a normal rhythm. 
 
 The disappearance of the diastolic aortic murmur during the 
 tachycardia was presumably due to the shortness of diastole, 
 which did not permit sufficient regurgitation to produce audible 
 vibrations, and the murmur reappeared as soon as the rate 
 became sufficiently slow and diastole lengthened. The pulse 
 altered considerably in volume with the change in rate, 
 and became larger with the less frequent beats ; but it varied 
 httle in force, the systolic pressure only varying between 145 
 and 152 mm. during the periods of tachycardia and fibrillation, 
 though it fell to 130 mm. when the regular rhythm reappeared. 
 This fall, however, accompanied the disappearance of the 
 oedema, and the higher levels may have been due to its presence. 
 
 The beneficial action of digitalis was clearly shown by the 
 lessening of the dyspnoea and the oedema, and the increase of 
 the urinary output; but the improvement occurred without 
 any reduction of the pulse-rate — a most unusual occurrence. 
 James Mackenzie has described the occurrence of fibrillation 
 following flutter on the administration of full doses of digitahs, 
 but this is the only example of the sequel which has come under 
 my own observation. 
 
 Case 3. — Another patient, a lad of seventeen, who com- 
 plained of palpitation, dated his attacks from a fright which 
 he had received at the age of twelve on being chased by a 
 drunken man. Two months before his admission to hospital 
 he slid for 12 feet down a ladder, and, though merely bruised, 
 was greatly frightened. The attacks of palpitation became 
 more frequent, and he became very breathless on exertion, 
 and easily tired. He was a very nervous boy, and was anxious 
 about his condition, as his previous health had not been good 
 
208 DISEASES OF THE HEART 
 
 He had suffered from growing-pains when at school, and had 
 had his right arm broken by an accident ; and enlarged glands 
 had been removed from the left side of his neck at the age of 
 nine. The scars were sound, but the wounds had evidently 
 been deep ; they ran downwards from the angle of the jaw to 
 the thyroid cartilage, and the vagus nerve might well have 
 been nipped in the cicatrix. 
 
 The pulse was extremely unstable, varying between 60 and 
 214, and the beats were sometimes in twins or triplets even on 
 the same day. The tachycardia commenced and ended 
 abruptly, and the paroxysms lasted for varying periods — a 
 minute or two, or twenty-four hours — but they generally ceased 
 more or less completely during sleep, and were intensified during 
 examination. He complained of discomfort in the cardiac 
 region during their continuance, and sweated profusely, and 
 breathed heavily, but he lay comfortably flat in bed. When 
 the pulse-rate was frequent, the right heart and the liver be- 
 came enlarged, but they rapidly regained their normal size 
 when the paroxysms ceased. A mitral sj^stohc murmur was 
 present on his first admission, but a year later the cardiac 
 sounds were pure and the heart was of normal size, so that 
 the incompetence was probably functional. The attacks at 
 this time were much less frequent, and none occurred during 
 a week's residence in hospital . 
 
 Tracings were obtained on many occasions. In one, when 
 the pulse numbered 214 per minute, the a-c interval measured 
 less than O'lO second (Fig. 115). At other times, however, 
 the auricles passed into flutter, and the pulse became extra- 
 ordinarily mobile (Fig. 120). On these occasions a bigeminal 
 or a trigeminal rhythm might be maintained for several seconds 
 or minutes. 
 
 When the auricles were fluttering, the pulse-rate was curi- 
 ously mobile, the records taken at about hourly intervals one 
 day numbering 156, 214, 168, 128, 108, 100, 128 (120, 128, 116, 
 80, 84, 80, 76, 90, while he was sleeping), 104, 112, 64, 196, 
 224, 168. The condition persisted for nearly three months. 
 
 The case is interesting on account of the neurotic character 
 of the patient. The symptoms succeeded a fright ; the pulse- 
 rate was always increased by examination and lessened when 
 
AURICULAR FLUTTER 209 
 
 he was asleep, and the patient was extremely excitable. 
 Digitalis, opium, tinct. belladonnse, vagal pressure, etc., seemed 
 to have little influence, and a watchful neglect appeared to 
 be the most useful therapeutic measure. The subsequent 
 course of events confirmed the impression that the cause of 
 the attacks was probably situated outside the heart. 
 
 The depth of the cervical scars suggested the possibility of 
 irritation of the vagus nerve, but pressure upon the other vagus 
 and the administration of belladonna seemed to have no effect 
 upon the cardiac action. Ritchie's Case 4 also suffered from 
 enlarged glands and sinuses in the neck. 
 
 The papers of Ritchie and Lewis contain reports of 23 cases, 
 to which I have added 7 of my own, in which the polj^graphic 
 records seem clear. Of these patients 24 were males and 
 6 were females ;* 21 were over forty years of age, the youngest 
 patient being aged fourteen and the oldest seventy-four; 
 3 suffered from disease of the aortic (in 2 cases of acute char- 
 acter), and 9 from disease of the mitral valve, and 1 from 
 adherent pericardium; 5 patients had a high blood-pressure; 
 9 complained chiefly of paroxysms of tachycardia; in 3 at 
 least the heart was probably normal; in 1 case the flutter 
 developed and ceased during an operation for osteomyelitis. 
 
 In Ritchie's Case 1, flutter has lasted almost continuously for 
 seven years. Thirteen cases passed at one time or another 
 into auricular fibrillation. 
 
 Only 2 cases are reported as having died under observa- 
 tion, while 1 was moribund when last seen. The records, 
 Jiowever, on this point are insufficient, and the true mortality 
 is probably, as akeady mentioned, greater than would appear. 
 The prognosis in an individual case depends upon several 
 factors, the most important being, as akeady mentioned, the 
 ■degree of the cardiac reserve. The frequency and the (Juration 
 
 Age. 
 
 Cases. 
 
 * 10 to 19 years 
 
 .. 4 
 
 20 „ 29 „ 
 
 .. 2 
 
 30 „ 39 „ 
 
 .. 3 
 
 40 „ 49 „ 
 
 .. 6 
 
 50 „ 59 „ 
 
 .. 6 
 
 60 „ 69 „ 
 
 .. 6 
 
 70 „ 79 „ 
 
 .. 3 
 
 14 
 
210 DISEASES OF THE HEART 
 
 of the paroxysms, their relation to removable causes (alcohol, 
 tobacco, etc.), are also important. In Ritchie's Case 1 full 
 heart-block was present, and the ventricular action was in- 
 frequent and regular. The block was in all probabihty useful, 
 as it prevented undue frequency of the ventricular contractions, 
 and my observations point to the conclusion that rapid ven- 
 tricular contractions lead much more quickly to cardiac failure 
 than rapidity of the auricular contractions accompanied by a 
 moderate ventricular rate. The same conclusion probably 
 apphes to auricular fibrillation. The occurrence of auricular 
 flutter in acute endocarditis is not necessarily followed by per- 
 manent irregularity- of the cardiac action, for in one case in 
 which it arose and persisted for at least ten days under my 
 observation, the cardiac rhythm was quite normal two years, 
 later. The flutter had not recurred in the interval. 
 
 Treatment. — James Mackenzie states that auricular fibrilla- 
 tion may be induced in flutter by full doses of digitalis, and that 
 if the drug be then intermitted a normal rhythm may ensue. 
 A similar sequence has been observed by Lewis and by myself, 
 and this treatment by digitalis should be pursued whenever 
 the disturbance is recognized ; but it is not invariably success- 
 ful, and has failed in some cases. In one of my cases, too, the 
 auricular fibrillation continued until the patient's dismissal, 
 though her general condition improved very greatly. 
 
 The administration of digitalis is, moreover, only a part of 
 a rational treatment, and aU the other measures indicated in 
 cardiac failure should be carried out — in particular, absolute 
 mental and physical rest. 
 
CHAPTER XVII 
 AURICULAR FIBRILLATION 
 
 In many forms of cardiac disease, and particularly in mitral 
 stenosis, the pulse is notably irregular in rhythm for long 
 periods of time. The condition has been known for many 
 years, and has been called the "mitral pulse," " dehrium 
 cordis," "pulsus irregularis perpetuus," etc., by various 
 writers ; but its cause, until recently, remained obscure. In 
 1906, however, Cushny and Edmunds pointed out the close 
 resemblance of this irregular pulse to that which occurs in 
 animals whose auricles are fibrillating, and suggested that it 
 might be due to the same cause. In 1907 James Mackenzie 
 formulated the same theory as a result of his investigations of 
 the venous pulse, though later on he attributed this irregularity 
 to other causes. In 1909 Rothberger and Winterberg,* using 
 the electro-cardiograph, brought forward strong evidence in 
 favour of Cushny and Edmunds' conclusions, and the indepen- 
 dent work of Lewis, t and Jolly and Ritchie, J using similar 
 methods, has placed the association beyond doubt, the cervical 
 and electrical curves in dehrium cordis being exactly similar 
 to those obtained from animals whose auricles are fibrillating. 
 
 Auricular fibrillation is easily produced in animals. It 
 occurs frequently in the dying heart, and follows faradic 
 stimulation of the auricles, ligature of a coronary artery, 
 and the administration of various drugs (potassium bromide, 
 adrenalin, etc.). When fibrillation ensues, the normal co- 
 ordinate contraction of the auricle as a whole ceases, and 
 the chamber dilates; the muscular fibres contract in little 
 bundles here and there, so that the surface is in a state of per- 
 
 * Wien. Iclin. Wochenschr., 1909, vol. xxii., p. 839. 
 ■\ Heart, 1909-10, vol. i., p. 306. 
 t Ibid., 1910-11, vol. ii., p. 177. 
 211 
 
212 
 
 DISEASES OF THE HEART 
 
 petual quivering or flickering, very similar to that wliicli may 
 be seen in the tongue and systemic muscles (fibrillation) in 
 cases of progressive muscular atrophy. The ventricular con- 
 tractions remain co-ordinate, but their rhythm is disturbed, 
 and the beats are notably irregular. Auricular fibrillation is 
 often permanent when once it has ensued, and continues until 
 the heart ceases to beat; but it may stop and the normal 
 sequence of contractions may reappear if the stimulus is 
 removed and the vagus nerve strongly stimulated, or if the 
 heart is perfused with a suitable fluid. 
 
 The yulse in auricular fibrillation is very characteristic, the 
 beats being wholly irregular in their sequence and their size. 
 
 Fig. 124. — The Radial Pulse in Auricular Fib rill ateon'. 
 
 The varying size of the waves is extremely striking, and is 
 not dependent upon the duration of the preceding diastole as 
 in a normal heart-beat, but may be now large and now small, 
 though the pulse periods are nearly equal (Fig. 124). 
 
 The cervical curve is equally distinctive. If the pulse-rate 
 is frequent, it usually shows a single large wave, perhaps 
 broken up into two or more summits, commencing synchron- 
 ously with the carotid beat (Fig. 125). The a wave has dis- 
 appeared from its usual situation immediately before c, and the 
 X depression is also ab-^ent. The v wave may " anticipate " 
 and succeed c without any interval, or may be separated from 
 it by an interval of short duration. If the pulse-rate is infre- 
 quent, a new series of waves may be recognized during the 
 
AURICULAR FIBRILLATION 
 
 213 
 
 fe 
 
 diastole (Figs. 125, 126). These are generally smaU and of 
 varying size and duration, numbering from 300 to 600 per 
 minute; but accurate enumeration is impossible, as some of 
 the wavelets are lost when c and v l ^ i 
 
 supervene. The wavelets may be quite 
 distinct in the apex tracing, and the a 
 wave is always absent both here and 
 in the liver tracing. 
 
 Electro-cardiographic curves show a 
 comparable curve (Fig. 71). The normal 
 P wave has disappeared, and ventricu- 
 lar diastole is occupied by a series of 
 tiny deflexions exactly similar to those 
 that are found in the cervical curves. 
 The ventricular complex is normal. 
 
 The rate of the pulse varies within 
 large limits. It is often about normal, 
 and in this case symptoms of cardiac 
 weakness are usually trivial or in abey- 
 ance; it may be greatly increased, 
 running about 120 or even as high as 
 160, and then symptoms of cardiac 
 weakness are generally apparent ; vevy 
 rarely it is infrequent, numbering about 
 30, or even less. 
 
 There has been considerable dis- 
 cussion as to the site of origin of the 
 stimuli which produce the ventricular 
 systoles, for it is conceivable that the 
 ventricles may follow their own intrinsic 
 rhythm, or may respond to some of the 
 stimuli which are continually^ being 
 showered upon them by the auricles ; 
 but it seems certain that the 'latter 
 conception applies to most cases. An intrinsic ventricular 
 rhythm is infrequent and regular, the pulse numbering about 
 30 beats per minute, the antithesis of that in most cases of 
 auricular fibrillation ; the ventricular electric complex is normal, 
 so that the ventricles are responding to stimuli passing to it 
 
 o 
 
214 
 
 DISEASES OF THE HEART 
 
 •^ 
 
 i 
 
 i 
 
 along their usual route ; and the a.v.]node and bundle may be 
 normal on histological examination (Monckeberg, Koch, A. M. 
 Kennedy), so that the usual pathway 
 of the stimuli is intact and available. 
 
 In a few cases, however, the ventri- 
 cles have been shown to follow their 
 own intrinsic rhythm, presumably from 
 accompanying heart-block. Lewis and 
 James Mackenzie have recorded cases 
 in which the ventricular rate was 
 generally infrequent and regular, though 
 auricular fibrillation was demonstrated 
 by the electro-cardiograph, and in which 
 premature ventricular contractions were 
 foUowed by a pulse period of normal 
 length, a characteristic feature of a 
 ventricular rhythm, Fredericq too has 
 severed the a.v. bundle experimentally 
 in animals whose auricles were fibrilla- 
 ting, and has recorded the occurrence 
 of a regular infrequent ventricular 
 beat. It seems probable that minor 
 degrees of defective conduction may 
 also occur, and impress their own special 
 characters upon the pulse. 
 
 The onset of auricular fibrillation in 
 
 experiment seems always to be abrupt ; 
 
 and a similar onset has been observed 
 
 clinically (James Mackenzie), cardiac 
 
 symptoms ensuing abruptly, and being 
 
 accompanied by notable irregularity of 
 
 the heart. In some cases, however, the 
 
 mode of onset cannot be ascertained, 
 
 as the patients are unconscious of the 
 
 irregularity, and their symptoms are 
 
 insidious in onset. 
 
 The duration of auricular fibrillation varies. In some cases 
 
 it is continuous, and it may be present for years in persons 
 
 who are enjoying average health. In others, however, its 
 
 s ^ 
 
AURICULAR FIBRILLATION 215 
 
 occurrence is the signal of serious symptoms, and life may be 
 rapidly endangered. In the majority of cases, when once 
 established, it is permanently present, but in a few cases it 
 ceases as abruptly as it begins, after a period of varying 
 duration, the paroxysms lasting for minutes, hours, or days. 
 
 A man aged forty-seven, who was suffering from acute 
 pneumonia, had two attacks of auricular fibrillation under my 
 observation. The pulse, though frequent, was quite regular 
 until the morning of the eighth day, when quite suddenly, 
 about 3 a.m., it presented the characteristic irregularity, the 
 beats numbering about 120 per minute. This continued until 
 11 p.m., when it again became quite regular. About 1 a.m. 
 on the ninth day the auricles again passed into fibrillation for 
 a short time, but subsequently the pulse remained regular, and 
 convalescence, though slow, was good. SHght oedema of the 
 feet ensued for a few days after he got up out of bed, but this 
 was the only evidence of cardiac weakness throughout the ill- 
 ness. 
 
 In exceptional cases its occurrence has been at first inter- 
 mittent, but ultimately continuous. 
 
 The causes of auricular fibrillation are at present unknown, 
 but several considerations may be borne in mind. In experi- 
 ment auricular fibrillation may be produced by functional dis- 
 turbances {e.g., faradic stimulation), and may cease when the 
 disturbing factor is withdrawn. From the clinical standpoint 
 the cases may be divided into two groups : one in which it 
 occurs occasionally and in paroxysms ; and another in which 
 it is constantly present, perhaps for years ; and in the latter 
 case the patient may enjoy fair health. It seems probable 
 that the cause is not always the same. One can hardly con- 
 ceive that a functional disturbance can produce an effect which 
 continues for years, or that a functional disturbance can be 
 present for years without producing very obvious symptoms . 
 
 Auricular fibrillation occurs in many forms of cardiac dis- 
 ease, but is particularly common in mitral stenosis and in 
 hypertrophied and degenerate hearts. In mitral stenosis the 
 maximal strain is laid upon the left auricle, and is continuous, 
 and functional disturbance of auricular action is extremely 
 likely to foUow. In mitral disease and in degenerate hyper- 
 
216 DISEASES OF THE HEART 
 
 trophied hearts myocardial fibrosis is often present, and may 
 involve the auricles in particular. Pathological observations 
 are stiU scanty, but the a.v. node and bundle have been found 
 healthy in cases of auricular fibrillation, while the s.a. node 
 has been found to be involved in an inflammatory focus in a 
 case where auricular contractions took place regularly during 
 life (Krumbhaar), so that it seems improbable that the irregu- 
 larity is produced by lesions in the primitive tissue.* 
 
 Gaskell has suggested that fibrillar contractions may be 
 brought about by a blocking in the connections between the 
 branching muscle cells, and that, in consequence, the contrac- 
 tions travel at different rates and are blocked at varying dis- 
 tances in the muscular mass, thus giving the appearance of 
 inco-ordinate contractions. As the stimuli are weak and of 
 var^ang intensity, ventricular contractions only occur occa- 
 sionally whenever maximal stimuh happen to reach them. 
 
 Disturbances of conduction between the auricle and ven- 
 tricle may be produced by functional disturbance, as well as 
 by organic disease of the a.v. bundle, and functional disturbance 
 of conduction in the auricular muscle would explain paroxysmal 
 fibrillation, while organic disease of the auricle would produce 
 a permanent defect. Further chnical and pathological observa- 
 tions are still required for the elucidation of the problem, but it 
 is already known that the auricle is frequently affected by a 
 diffuse (Fig. 14) as well as by a patchy fibrosis. 
 
 It has been suggested (Lewis) that auricular fibrillation is 
 the result of an increased excitability of the auricular muscle, 
 whereby ectopic stimuli are constantly arising at every part 
 of the wall. It can be reaclih' produced by strong faradization 
 of the auricle; its occurrence clinically may be preceded by the 
 appearance of auricular extra-systoles ; paroxysms of tachy- 
 cardia of auricular origin and of fibrillation may occur in the 
 same individual; and, as already mentioned, inflammatory 
 foci are often present in the auricular wall. But the failure 
 of vagus stimulation to influence auricular fibrillation, though 
 it undoubtedly depresses the excitability of the auricular 
 
 * In 14 cases of auricular fibrillation the s.a. node was normal in 3, the a.v, 
 node in 9, and the a.v. bundle in 8. In 3 cases all three were normal. (Cowan. 
 Fleming, and Kennedy: Trans. Interna*. Congiess, 1913.) 
 
AURICULAR FIBRILLATION 217 
 
 muccle in animal experiments, makes GaskeU's theory the 
 more probable, as under it the auricular conductivity would be 
 still further depressed by vagal stimulation, and the inco- 
 ordinate action of the auricle would be intensified. 
 
 In the majority of cases auricular fibrillation is first recog- 
 nized during a period of cardiac insufficiency, and the date of 
 its onset is, in consequence, unknoTvoi. As a rule, its occur- 
 rence is associated mth the onset of defmite sj^mptoms, or, at 
 any rate, with some limitation of the field of response ; but the 
 severity of the sjmiptoms varies considerably in different cases, 
 very largely in correspondence with the rate of the ventricular 
 contractions, a pulse-rate of 140 being accompanied by well- 
 marked evidences of failure, while a pulse of normal rate may 
 be associated with but few. The radial pulse-rate is often 
 misleading, since mam^ of the beats may be missed, and the 
 rate should be ascertained hj auscultation 'or by palpation of 
 the apex impulse. The importance of this factor is often seen 
 in the clinique, a patient admitted with oedema, orthopnoea, etc., 
 and a pulse of 120 or over, losing all his symptoms coincidently 
 with a reduction of the pulse to 70 or its neighbourhood, 
 though the irregularity persists unchanged. 
 
 It is in mitral stenosis in particular that auricular fibrillation 
 is most common. In this lesion the strain upon the left auricle 
 is constant, as the obstruction at the mitral valve is permanent, 
 in contrast with the intermittent strain in mitral insufficiency 
 where the auricular congestion is rapidly reheved during 
 ventricular diastole. The cessation of co-ordinate auricular 
 contractions, however, makes the characteristic crescendo 
 murmur disappear, so that the recognition of the stenosis is 
 difficult, unless its existence is already known. It should, 
 however, be suspected if a systohc murmur is present, or if 
 the second sound at the base is doubled, or the second 
 pulmonic element unduly emphatic, and its existence may be 
 confidently affirmed if the apical diastolic murmur is recog- 
 nized. 
 
 In auricular fibrillation, as alreadj^ mentioned, the auricle 
 dilates, and the area of cardiac clulness is altered in correspond- 
 ing degree, extending outwards to the right as far as, or 
 beyond, the right sternal border. 
 
218 DISEASES OF THE HEART 
 
 The murmurs at the apex in auricular fibrillation are ex- 
 tremely variable, and are often impossible to define in cases 
 where the cardiac contractions are frequent; for in this case 
 the shortness of diastole prevents adequate fiUing of the 
 ventricle, and so minimizes systolic reflux, and the murmur 
 may only be audible after the longer pauses ; while, for a similar 
 reason, the diastolic murmur may also fail. Aortic murmurs 
 are also variable, the systolic murmur being shorter and softer 
 with shortened pulse periods, and longer and harsher after 
 longer intervals. The diastolic murmur may be unrecognizable 
 if the pulse is very frequent. 
 
 The prognosis in cases where auricular fibrillation has ensued 
 is always more grave than in comparable cases with a sinus 
 rhythm, and I have never seen a patient with this condition 
 whose cardiac power was not at any rate subjectively lessened. 
 James Mackenzie states that he has known patients lead 
 arduous lives for as long as ten years, but such cases are cer- 
 tainly exceptional. One of my patients, who died at the age 
 of thirty-six, had persistent auricular fibrillation for at least 
 three years before his death, and enjoyed fair health for 
 months at a time. He suffered from double mitral disease, 
 and the first symptoms were associated with a pulmonary 
 infarct. 
 
 The cases which are associated with mitral stenosis seem to 
 have a better prognosis than those which are due to other 
 cardiac lesions. In mitral stenosis the left auricle is over- 
 strained, and its action is perhaps more easily disturbed. In 
 other lesions the auricles merely share in the general stress, 
 and fibrillation indicates a widespread disorganization of the 
 heart. 
 
 In a general way the inception of permanent auricular 
 fibrillation is the beginning of the end, though many patients 
 are able to lead quiet fives for a year or two after the onset. 
 
 The dilatation of the auricles, which always ensues, is of 
 particular importance, for it seems to be a main factor in 
 producing clotting in the appendices, and the strain of a 
 pulmonary infarct is badly borne. Infarcts are much more 
 common than is perhaps reahzed. They are generally accom- 
 panied by frank haemoptysis or pleural friction, and by the 
 
AURICULAR FIBRILLATION 219 
 
 ■evidences of consolidation; but I have often found more in- 
 farcts on post-mortem examination than were suspected from 
 clinical observation, and their occurrence need not be accom- 
 panied by any obvious physical sign. A central infarct, out- 
 with the sphere of clinical examination, is a not infrequent 
 cause of the onset of acute cardiac sj-mptoms. 
 
 The immediate prognosis seems to depend chiefly, if not 
 entirely, upon the rate of the ventricular contractions, and upon 
 the response to the administration of digitalis. Patients differ 
 considerably in these respects, and the prognosis is better if the 
 pulse, with or without drugging, can be kept within normal 
 limits. One of Mackenzie's cases ^vith heart-block and a 
 regular infrequent pulse was working regularly two years later, 
 ^nd a degree of defective conductivity is, in all probabihty, 
 beneficial rather than the reverse. The case which I have 
 just mentioned seems to belong to this category. 
 
 In many patients the administration of digitahs leads to a 
 reduction in the pulse-rate and to the disappearance of symp- 
 toms, and the pulse subsequently remains within normal rates. 
 But in other cases the drug requires to be administered con- 
 stantly, for on its cessation the pulse becomes frequent and 
 the symptoms recur. This was the case with a woman at one 
 time under my care, who stated that she had taken digitalis 
 constantly for seven years. Her symptoms rapidly subsided 
 upon its administration, but they recurred on more than one 
 ■occasion within a fortnight of its being stopped. 
 
 The treatment of auricular fibrillation is mainly a matter 
 ■of treatment by digitalis, and is discussed in detail in 
 Chapter XXVI. The drug should be stopped when the pulse 
 numbers 60, or if a coupled rhythm supervenes. 
 
CHAPTER XVIII 
 ACUTE ENDOCARDITIS 
 
 The clinical distinction between simple and malignant forms 
 of acute endocarditis is apt to convey an erroneous idea of 
 their true nature. Both are due to bacterial invasion, and 
 the pathological difference is merely a matter of degree, the 
 infection in the one case being readily overcome, and in the 
 other progressing indefinitely ; and an intermediate group con- 
 nects the links at each end of the chain. The difference may 
 be due to several causes : to the particular variety of bacterium, 
 to its virulence or its dose, or to the resistance of the tissues tO' 
 the infection. 
 
 The distinction, too, is inaccurate from the chnical stand- 
 point. As Sir William Osier says, there is no benign endo- 
 carditis, for even the most trivial acute infection may in- 
 augurate changes of a chronic character, which sooner or later 
 lead to death ; and an* infection which is at first trivial in its 
 grade may suddenly assume a virulent character and rapidly 
 produce a fatal issue. The malignant cases, too, may change 
 their character, and the fire which blazed brightly at first may 
 ultimately burn itself out. 
 
 The Lesions. — In the majority of cases acute endocarditis 
 involves the valves of the heart alone, and does not affect the 
 endothelial lining of the auricles and ventricles. In an early 
 case the characteristic festoons of little translucent white or 
 yellow beads are visible running round the cusps, a little dis- 
 tance from the free margins, at the points where the contact is 
 most intimate when the valves are shut (Fig. 127). The surface 
 which is exposed to the blood-stream, the ventricular aspect 
 of the arterial valves, and the auricular aspect of the auriculo- 
 ventricular valves is alone implicated. Microscopic examina- 
 
 220 
 
ACUTE ENDOCARDITIS 
 
 221 
 
 tion shows that the vegetations are mainly composed of 
 fibrin, with a few cells scattered throughout the mass, and a 
 larger number along the free margins. At the base the connec- 
 tive tissue of the valve is hypergemic and proliferating, and a 
 
 Fig. 127. — Actjte Veektjcose Endocarditis, following a Rheumatic (or 
 GoNOCoccic) Arthritis (W. I. Museum). 
 
 cellular infiltration may be found. Micro-organisms may be 
 detected with suitable staining, and are as a rule most numerous 
 in the superficial layers, though they are sometimes seen in 
 the deeper layers and in the valve itself. 
 
 The infection of the valve is presumably derived from the 
 
222 DISEASES OF THE HEART 
 
 blood-stream in, at any rate, aortic endocarditis ; for there are 
 no bloodvessels in the normal aortic valve, and the bacteria 
 gain access to the tissues through some abrasion of the protec- 
 tive endothelium produced by the toxaemia and the mechanical 
 stress imposed upon the parts. In mitral endocarditis, how- 
 ever, as vessels are present in the valve, the deeper structures 
 may be first affected by a bacterial embolus, and the fibrinous 
 exudate forms when the inflammation reaches the surface, and 
 the protective endothelium is, in consequence, shed. In a case 
 of septicaemia which was shown to me by Kennedy, the infection 
 arose in an unusual way. An abscess had formed in the inter- 
 ventricular septum, and reached the interior of the right 
 ventricle immediately beneath the septal cusp of the tricuspid 
 valve. The latter became involved by direct infection, and 
 a perforation measuring nearly 1 cm. in diameter ensued 
 in the centre of the cusp. The free margin was not affected. 
 Acute endocarditis is most common on the aortic and mitral 
 valves, which are exposed to the highest blood-pressure, and 
 bathed in the most thoroughly oxygenated blood. 
 
 In some cases no bacteria are found on microscopic examina- 
 tion, and the reaction in the valve is minimal. This is the 
 general rule in the endocarditis of acute rheumatism, but 
 although the lesion might follow a toxic and traumatic 
 damage to the valve, the general evidence in favour of an 
 infective origin of acute rheumatism is so strong that one is 
 forced to the conclusion that the cardiac condition is due to a 
 similar but minimal infection of the valve. In the majority of 
 cases of this type the inflammation in time subsides. The 
 vegetations are penetrated by new-formed connective tissue, 
 and the surrounding endothelium grows over the denuded 
 surface, leaving a thickened scar of greater or of less extent. 
 
 In the malignant type of case the ultimate result is very 
 different, the bacterial infection is not overcome, and the infec- 
 tion spreads. In some cases the vegetations are large and 
 luxuriant, measuring many millimetres in length (Fig. 128), 
 and interfering by their mere bulk with the proper action of 
 the valves. In others the process is destructive, gross necrotic 
 and ulcerative processes ensue, and the cusps may be per- 
 forated (Fig. 129), or their attachments may be severed, and 
 
ACUTE ENDOCARDITIS 
 
 223 
 
 their function may be almost wholly abolished. The inflam- 
 mation, too, in some cases, spreads from the valves to the 
 adjacent parts. The spread is often direct, and takes place in 
 any direction. If the aortic valve is involved, the aorta may 
 be affected, and an acute infective aortitis results, with some- 
 times aneurismal dilatation (Figs. 129, 130); or the inter- 
 
 -Pneitmococcic Endocarditis of Aoetic Valve spreadikg on to 
 
 THE illTPvAL CirSPS (W. I. MuSETUl). 
 
 Fig. 128.- 
 Embolic gangrene of the foot ensued ten days after the onset of the pneumonia 
 
 ventricular septum may be infected (mural endocarditis), and 
 the ulceration may spread deeply into the tissues, and even 
 open up communication with the right side of the heart. When 
 the mitral valve is implicated, either auricle or ventricle may 
 be invaded. The most common spread is upwards on to the 
 auricular wall opposite to the foramen ovale (contra-fossal 
 
224 
 
 DISEASES OF THE HEART 
 
 wall) (Fig. 131), and downwards on to the chordae tendinese 
 (which may be ruptured in the process), sometimes invading 
 even the tips of the musculi papillares. 
 
 In other cases the infected area is situated a little distance 
 
 Fig. 129. — Malignant Endocarditis of Aortic V.-vlves, with Aneurisms and 
 Perforations of the Cusps; Infective Aortitis; and Aneurism of 
 Aorta rupturing into Pericardial Sac (R. I. Museum). 
 
 from the valve, by an infected " tag " waving to and fro in 
 the blood-stream, and hitting and infecting the ventricular, 
 auricular, or aortic walls. Or a fragment of a vegetation 
 
ACUTE ENDOCARDITIS 225 
 
 may be broken off, enter the coronary artery, and produce an 
 embolic abscess anywhere in the heart. 
 
 The infective character of mahgnant cases is always well 
 marked, and large collections of bacteria may be seen on the sur- 
 face of the vegetations, or more deeply situated in the valve itself. 
 
 Fig. 130. — Pnetjmococcic Endocaeditis of the Aortic Valve 
 (W. I. Museum). 
 
 One cusp is partly severed from its attachments. An aneurism, the size of a 
 walnut, sprang from the aorta immediately above the valve, and projected 
 into the right auricle. 
 
 In the intermediate cases the lesions are less extreme and 
 more chronic in their character. The general evidences of 
 septicsemia are absent or trifling, but a progressive valvular 
 lesion can be detected on physical examination. In the valves 
 themselves progressive and reparative changes may be seen 
 
 15 
 
226 
 
 DISEASES OF THE HEART 
 
 side by side, but the valvular defect is always severe, and the 
 patient often dies from the mechanical fault even when healing 
 has taken place. 
 
 It seems probable that in the mildest cases a complete re- 
 covery may occur, but pathological data are necessarily absent ; 
 
 Tig. 131. — Stkeptococcic Endocarditis of Mitral Valve speeadestg on to 
 THE Left Auricular Wall (W. I. Museum). 
 
 The chordae tendinese are also involved. 
 
 and in the majority of cases, though the infection is overcome, 
 a scar is left behind. The cardiac valves have, however, no 
 rest, either by day or by night, and chronic fibrous changes 
 ensue, the cusps becoming thickened and shrunken and often 
 adherent to each other, and the valvular defect gradually but 
 steadily increases in degree. In time, after perhaps many 
 
ACUTE ENDOCARDITIS 227 
 
 years, it becomes extreme, and the cardiac "pump " fails to 
 accomplish its necessary work. 
 
 In acute endocarditis the cardiac muscle is invariably 
 damaged to a greater or a less degree. The gross infective 
 and ulcerative lesions which occasionally occur in mahgnant 
 cases have, of course, for long attracted notice, but the 
 microscopic lesions have failed to receive their due share of 
 attention, though myocarditis is an almost constant accom- 
 paniment of acute endocarditis (c/. p. 150). The lesions are 
 usually most extreme in the vicinity of the base of the affected 
 valves, but they are often disseminated widely through the 
 muscle. Their degree does not necessarily correspond with 
 that of the valvular inflammation, and they may be well 
 marked in cases where the valvulitis is but trivial. In some 
 cases clinical evidence of an acute myocarditis is available, 
 for the a.v. node and bundle are in close proximity to the 
 mitral, aortic, and tricuspid valves, and may be involved in 
 the inflammation; and heart-block, extra-systoles, or nodal 
 rhythm may, in consequence, occur. 
 
 Pericarditis is a frequent comphcation. The flow of blood 
 and lymph takes place towards the pericardium, and its in- 
 fection is of common occurrence, and necessarily adds greatly 
 to the gravity of the case. 
 
 The Causes of "Acute Endocarditis. — Acute Simple Endo- 
 carditis occurs most frequently in childhood and in adoles- 
 cence, though it may be found at any period of life ; but accu- 
 rate statistics are not available, for it rarely causes death 
 during the acute stage, and post-mortem data are, in conse- 
 quence, awanting. This predominance is chiefly due to its 
 close connection with acute rheumatism — a connection which 
 has been amply proved by clinical observation. In a series of 
 1,750 cases collected from the literature, 933 patients suffered 
 from endocarditis ; and its incidence is twice as great in persons 
 under twenty years of age as it is in older persons. In children 
 under ten endocarditis and acute rheumatism are almost 
 always conjoined, and Norman Moore aptly named the disease 
 cardiac fever. Endocarditis is said to occur most frequently 
 in the first attack of rheumatism, and within the first fortnight 
 
228 DISEASES OF THE HEART 
 
 of the fever; and its incidence is not directly related to the 
 severity of the arthritis, as it is of common occurrence in cases 
 where the arthritis is trifling or subacute, but may be absent 
 though the arthritis is severe and prolonged. A recent 
 " claim " in my insurance office illustrates the point. The 
 man died at the age of fifty-eight from mitral stenosis. He 
 had had muscular rheumatism in 1874, and rheumatic pains 
 in his joints — " not rheumatic fever " — for two or three months 
 in 1884. 
 
 The mitral valve is most frequently affected, and the valves 
 of the right heart are but seldom involved. 
 
 Endocarditis is frequently associated with chorea, and was 
 present in 154 cases of a series of 171 examined post-mortem. 
 Valvular lesions are extremely common in choreic patients, and 
 were present in 262 out of 829 patients who were examined during 
 or after the illness. The endocarditis is usually of the simple 
 type, and though so often present in fatal cases, is rarely the 
 immediate cause of death. 
 
 Among the exanthemata endocarditis is comparatively rare, 
 but here again post-mortem data are misleading, as in some 
 diseases endocarditis is apt to be of the malignant type, 
 and an active factor in producing death; and its relative im- 
 portance is, in consequence, over-estimated. In pneumonia, 
 for example, it was found post-mortem in 16 out of 100 cases 
 (Osier), but its clinical incidence is shght (0-44 per cent., Musser 
 and Norris). In scarlatina it only occurred in 0-65 per cent. 
 (McCollum). Macrae reported its occurrence in 6 of 1,500 
 cases of enteric fever, and Horton-Smith in 4 of 290 cases ex- 
 amined post-mortem ; and Councilman in 1 out of 54 (post- 
 mortem) cases of smallpox. Horder has recorded its occurrence 
 in influenza. 
 
 The causes of acute endocarditis, with the exception of acute 
 rheumatism and chorea, are thus unknown, and it has been 
 suggested that the other " rheumatic " manifestations, acute 
 tonsillitis, erythema nodosum, etc., may be responsible. The 
 suggestion is extremely plausible, for the tonsils are recognized 
 to be the harbourers of many micro-organisms, and they not 
 infrequently show on section macroscopic evidence of gross 
 infection of the crypts which was not evident on examination 
 
ACUTE ENDOCARDITIS 229 
 
 of the surface; and the probabihty of a blood-infection is 
 increased if the middle ears and the naso-pharynx are, as is so 
 frequently the case, also inflamed. 
 
 It must be remembered, however, that the portal of entry in 
 malignant cases is not always evident, even on post-mortem 
 examination, and in these cases must have been trivial and of 
 short duration ; and a similar trivial sepsis may be responsible 
 for some of the simple cases. 
 
 In the malignant cases the valves which are involved have 
 been as a rule already damaged, and are, in consequence, 
 places of lessened resistance, so that the disease affects older 
 people than in the case of the simple form. In Kanthack and 
 Tickell's series of 84 cases, only 25 were under twenty years 
 of age, and in Border's series of 150, only 45. In my series 
 the proportion is larger — 14 out of 30 cases. The valves 
 had been previously damaged in 64 per cent, of Kanthack's 
 and 80 per cent, of Kelynack's series; in 108 cases out of 
 118 of Border's series; and in 24 of my series of 30. Malig- 
 nant cases are, however, not uncommon in the second decade, 
 perhaps in consequence of the special incidence of acute rheu- 
 matism at this period. 
 
 The association with acute rheumatism is again extremely 
 close, but the nature of the connection is not clear. Rheuma- 
 tism may act merely as a predisposing cause by damaging the 
 valves and so allowing a subsequent bacterial infection from 
 a minimal dose ; or by producing a mahgnant form of endo- 
 carditis. Poynton has emphasized the latter view, and has 
 isolated the micrococcus in blood-culture on several occasions. 
 In one of my cases Kennedy isolated a similar organism both 
 during life and after death. But Horder considers that mahg- 
 nant rheumatic cases are due to a superadded infection. In 
 the typical endocarditis of acute rheumatism, at any rate, blood- 
 cultures are ahnost always sterile. 
 
 The association with other infections is by no means close. 
 The majority of these patients have, of course, suffered from 
 some of the exanthemata in early life, or from some infection, 
 but in a few cases no antecedent illness has been known. In 
 others, however, many infections have been present, and one 
 of my patients, a man of twenty-four year?, had suffered from 
 
230 DISEASES OF THE HEART 
 
 growing-pains, enteric fever, diplitlieria, pneumonia, and gonor- 
 rhoea ; lie was, too, liable to boils, and his mouth was extremely- 
 septic, the gums being swollen and bleeding on shght provoca- 
 tion. A similar state of extreme oral sepsis was present in 
 another patient, while a third had an offensive rhinitis, and a 
 fourth a chronic otorrhoea. In two of my cases the symptoms 
 developed during lactation, though there was no obvious source 
 of sepsis about the uterus or breasts. 
 
 In another case the symptoms succeeded the birth of the 
 patient's second child. She had frequent rigors, with profuse 
 perspiration, which recurred every two or three days. The 
 lochia persisted for six weeks, and only finally cleared after 
 " a copious discharge " had continued for a few days. 
 
 In another the sj^mptoms succeeded a " cross-birth " twelve 
 weeks before admission to hospital. Rigors occurred on the 
 third or fourth day afterwards, and were frequently repeated, 
 and she felt pain in her left side when she coughed. Post- 
 mortem examination revealed the association. The uterus was 
 small and involuted, but the endometrium showed evidence of 
 recent ulceration, and many thrombosed veins were present 
 in the muscular wall. The right ovarian vein contained a long 
 thrombus, and there were clots in the iliac veins and the lower 
 3 inches of the inferior vena cava ; these did not, however, com- 
 pletely block the lumen. There. was a large, dense, mobile 
 thrombus, the size of a marble, in the right auricle, and a 
 smaller one attached to the wall. The mitral valve was covered 
 with fairly large, soft, fibrinous vegetations, and the tricuspid 
 valve was also affected, but in lesser degree. Septic abscesses 
 were present in the spleen and in the lungs, and a large necrosis 
 of the visceral pleura had produced a pneumothorax, which was 
 the immediate cause of death. Blood-cultures during life were 
 sterile. 
 
 Hearts with congenital defects are not infrequently affected. 
 
 The valves on the left side of the heart are those which are 
 most frequently involved, but the great predominance of mitral 
 disease in simple endocarditis is not approached, though this 
 valve is more often infected than the others. Two or more 
 valves are involved in nearly hah the cases, and a mural 
 infection occurs in about a quarter. 
 
ACUTE ENDOCARDITIS 
 
 231 
 
 Recent improvements in blood-culture have led to the isola- 
 tion, during life, of the causal micro-organism in a large number 
 of cases, but Horder's positive results (29 out of 32) are more 
 numerous than are usually obtained. The micro-organism is 
 generally isolated in acute cases, and less frequentty in the 
 chronic types — at any rate, until shorth^ before death. In my 
 series positive results were obtained in 3 out of 11 cases; in Sir 
 William Osier's, in 3 out of 6. The most common organism is 
 a streptococcus of low virulence, which is closely "allied to 
 the saprophytic streptococci of the ahmentary tract " (Horder). 
 
 The characters of the vegetations are not specific, but in a 
 general way the pneumococcic and gonococcic vegetations are 
 numerous and small, while staphylococci produce a spreading 
 ulceration. 
 
 Acute Soiple Exdocakditis. 
 
 
 Cases of Acute 
 Rheumatism. 
 
 Cases of 
 Endocarditis. 
 
 Sibson 
 
 Macrae 
 
 Churcli 
 
 Moore 
 
 Latham 
 
 325 
 300 
 
 889 
 100 
 136 
 
 161 
 105 
 
 494 
 99 
 
 74 
 
 1,750 
 
 933 
 
 First Attacks (Church) — 
 
 16 cases under 10 years: endocarditis in 12 — 75 per cent, 
 
 109 ,, between 10 and 20: „ 60—55 „ 
 
 75 „ between 20 and 30: ,, 38—50 „ 
 
 36 ,, between 30 and 40: „ 13—36 „ 
 
 8 „ over 40: „ 1—12 „ 
 
 Endocarditis was present in 149 out of 150 fatal cases of acute 
 rheumatism under the age of twelve (Poynton). In Macrae's 
 series it was present in 45 per cent, of cases under twenty years, 
 but only in 20 per cent, of cases over twenty years. 
 
 In Sibson's series murmurs made their appearance in 25 per 
 cent, of cases within the first week, and in 66 per cent, within 
 the first two weeks of the disease. 
 
 In Macrae's series the mitral valve alone was affected in 
 77 per cent., the aortic valve alone in 5 per cent., and both in 
 
232 
 
 DISEASES OF THE HEART 
 
 18 per cent. At St. Thomas's Hospital the corresponding 
 figures were: Mitral valve alone, 85 per cent.; aortic valve 
 alone, 3 per cent. ; and both in 12 per cent. 
 
 Malignant Acute Endocarditis. 
 
 
 Horder, 
 
 Personal, 
 
 Age. 
 
 150. 
 
 30. 
 
 1 to 10 
 
 7 
 
 1 
 
 10 „ 20 
 
 38 
 
 13 
 
 20 „ 30 
 
 39 
 
 8 
 
 30 „ 40 
 
 31 
 
 2 
 
 40 „ 50 
 
 23 
 
 3 
 
 50 „ 60 
 
 8 
 
 3 
 
 60 and over 
 
 4 
 
 — 
 
 Sex: 
 
 
 
 Male 
 
 79 
 
 17 
 
 Female 
 
 71 
 
 13 
 
 
 Osier, 
 
 Horder, 
 
 Personal, 
 
 Total, 
 
 
 209 Cases. 
 
 lis Cases. 
 
 •29 Cases. 
 
 356. 
 
 Mitral 
 
 77 
 
 38 
 
 8 
 
 123 
 
 Aortic 
 
 53 
 
 22 
 
 2 
 
 77 
 
 Mitral and aortic . . 
 
 41 
 
 63 
 
 13 
 
 117 
 
 Tricuspid and others 
 
 19 
 
 14 
 
 5 
 
 38 
 
 Pulmonary and others 
 
 15 
 
 7 
 
 1 
 
 23 
 
 Mural infection 
 
 33 
 
 51 
 
 4 
 
 88 
 
 Valves of right heart alone 
 
 9 
 
 — 
 
 — 
 
 9 
 
 Congenital defects in heart 
 
 — 
 
 8 
 
 1 
 
 9 
 
 Previous Infections. 
 
 Personal, 
 28 Cases. 
 
 Horder, 
 loO Cases. 
 
 Acute rheumatism 
 
 13 
 
 } 72 
 
 Chorea 
 
 
 
 4 
 
 Tonsillitis . . 
 
 
 
 3 
 
 
 
 Pneumonia 
 
 
 
 6 
 
 1 
 
 Enteric fever 
 
 
 
 1 
 
 4 
 
 Diphtheria . . 
 
 
 
 1 
 
 — 
 
 Scarlet fever 
 
 
 
 — 
 
 10 
 
 Influenza . . 
 
 
 
 — 
 
 2 
 
 Dysentery . . 
 
 
 
 — 
 
 1 
 
 Gonorrhoea 
 
 
 
 — 
 
 7 
 
 Extreme oral sepsis 
 
 
 
 2 
 
 
 
 Atrophic rhinitis . . 
 
 
 
 1 
 
 — 
 
 Otorrhcea . . 
 
 
 
 1 
 
 — 
 
 Lactation , . 
 
 
 
 2 
 
 
 
 Fistula 
 
 
 I 
 
 
ACUTE ENDOCARDITIS 
 
 233 
 
 The records being derived from hospital patients are almost 
 certainly defective in many respects. 
 
 Organisms isolated during Life. 
 
 Horder. 
 
 Personal. 
 
 Streptococcus 
 
 Bacillus infliienzcE 
 
 Pneumococcus 
 
 Gonococcus 
 
 Staphylococcus alhus 
 
 Doubtful 
 
 26 
 5 
 5 
 2 
 1 
 1 
 
 1 
 1 
 1 
 
 E. Libman has recently described a group of cases of sub- 
 acute endocarditis and has isolated a streptococcus in 71 out 
 of 75 cases. He names the organism Streptococcus mitis. It 
 is probably the same as the >S', viridans and the S. salivarius 
 of other writers. 
 
 In surgical cases the most common organisms are the 
 Staphylococcus aureus and the Streptococcus pyogenes. 
 
 EEFERENCES. 
 
 T. J. Hoeder: Quart. Joum. of Med., 1908-09, vol. ii. 
 SmW. Oslek: 
 
 Ibid., p. 133. 
 
 Osier's System, 1908, vol. iv., p. 219. 
 E. Libman: 
 
 Amer. Journ. Med. Sci., 1912, vol. cxliv., p. 313. 
 
 Ibid., 1913, vol. cxlvi., p. 625. 
 
 Trans. Intemat. Med. Congress, London, 1913. 
 
 p. 289. 
 
CHAPTER XIX 
 ACUTE ENDOCARDITIS— Co7^iwM 
 
 The Symptoms. 
 
 In the majority of cases of simple acute endocarcTitis occur- 
 ring in the course of rheumatic fever, the patient makes no 
 complaint of any cardiac symptoms, and a valvular lesion 
 is discovered on routine examination of the heart. Occasion- 
 ally palpitation or discomfort or even slight pain in the cardiac 
 region may be experienced, but these are rare in the absence 
 of pericarditis. There is seldom any dyspnoea, and the chief 
 discomforts are the pain of the arthritis or the profuse sweating. 
 
 The onset of endocarditis is, however, as a rule associated 
 "\\ith definite evidence of cardiac embarrassment. The most 
 constant signs are found in the pulse, which may be more fre- 
 quent than the degree of fever would suggest, or infrequent, or 
 irregular; and the abnormahty may persist, even unchanged, 
 though the fever and the arthritis subside, and convalescence 
 is apparently attained. As an isolated symptom, an abnormal 
 rate or rhythm is extremely suggestive, and may be present at 
 a time when valvular murmurs are absent. 
 
 A girl of fifteen was admitted to my wards suffering from 
 subacute rheumatism which had lasted for some six weeks. 
 Within a week the arthritis had subsided, and the joints were 
 mobile and painless. The heart seemed normal on examina- 
 tion, but the pulse-rate continued to be high (90 to 100) after 
 the fever had disappeared. A month later a very soft blowing 
 murmur made its appearance for the first time at the apex, 
 and the second pulmonic sound became accentuated. Four 
 months afterwards the recognition of a typical presystohc 
 murmur placed the diagnosis of organic valvular disease beyond 
 doubt. 
 
 234 
 
ACUTE ENDOCARDITIS 
 
 235 
 
 In manv of these cases the recurrence of rheumatic symp- 
 -toms (arthritis, tonsilhtis, chorea, nodules) emphasizes the fact 
 that the infection is 
 not completely 
 •eradicated, but re- 
 currence is extremely 
 rare if the pulse-rate 
 has returned to nor- 
 mal figures . One 
 iaUacy, however, 
 must be remembered . 
 The pulse-rate during 
 the administration of 
 -saUcylates is often 
 within normal hmits, 
 but rises on its with- 
 •drawal, so that the 
 pulse should be ob- 
 served for at least a 
 week after the ad- 
 ministration of sali- 
 cylates has been 
 ■ceased before any 
 conclusion is reached 
 <Fig. 132). 
 
 The pulse in endo- 
 carditis is not infre- 
 •q u e n 1 1 y itregular . 
 This may be due to 
 partial heart-block, 
 which I have now 
 observed in six cases. 
 In one the defect per- 
 sisted for nearly four 
 weeks ; in another it 
 disappeared after six 
 days, but recurred three days later, again lasting for six days ; 
 in a third it was present for several weeks before death; in 
 the others it was transient, and only present for a few days. 
 
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 ^ 
 
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 ^ 
 
 II 
 
 
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 1 
 
 ^ 
 
 105- 
 104- 
 
 102- 
 
 lor 
 :co- 
 sr 
 
 33- 
 S7- 
 160 
 150 
 140 
 
 :3o 
 
 1 
 
 i 
 
 ^ 
 
 i 
 
 zE 
 
 ^ 
 
 ^ 
 
 Ez 
 
 = 
 
 = 
 
 = 
 
 
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 ^ 
 
 :^^ 
 
 
 EE 
 
 = 
 
 1 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 dp 
 1 
 
 = 
 
 ^ 
 
 1 
 
 ^ 
 
 ^ 
 
 1 
 
 1 
 
 1 
 
 1 
 
 
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 ¥ 
 
 1 
 
 1 
 
 i 
 
 
 1 
 
 1 
 
 no 
 ;:o 
 so 
 
 £0 
 70 
 
 eo 
 
 60 
 40 
 30 
 CO 
 
 :o 
 
 1 
 
 90 
 
 M 
 
 ^ 
 
 1 
 
 ^ 
 
 M 
 
 I— 
 1 
 
 1 
 
 e^ 
 
 g 
 ♦* 
 
 1 
 
 1 
 
 
 o^a 
 
 
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 1 
 
 
 m 
 
 ^ 
 
 M 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 1 la.e 
 
 11 
 
 12 
 
 !3 
 
 14 
 
 15 
 
 ?e 
 
 ;/ 
 
 18 
 
 19 
 
 ijo 
 
 ji 
 
 22 . 
 
 3 2-i 
 
 il 
 
 26 . 
 
 7 28 
 
 \m 
 
 w 
 
 ^ 
 
 Fig. 132.— Chakt of J. McK., Aged 7. Acute 
 Rheumatism; JIiteal Endocaeditis. 
 
 Note rise of pulse-rate on cessation of salicylate ( X ). 
 The temperature had been normal for thirteen 
 days. 
 
236 DISEASES OF THE HEART 
 
 Heart-block in varying degree has been reported in gonococcic 
 and streptococcic infections, and though it may occur in the 
 infections apart from endocarditis (diphtheria — Fleming), the 
 two are so commonly associated that their co-existence is 
 extremely probable. An infrequent pulse is generally due to 
 full heart-block. 
 
 Extra-systoles may also occur. I have seen them in seven 
 patients, in three of whom nodal rhythm ultimately ensued. 
 Extra-systoles are, of course, of common occurrence in various 
 forms of cardiac disease, as well as in patients whose hearts 
 are apparently normal, and their appearance can only b& 
 taken as suggestive of an acute cardiac lesion when they recur 
 frequently without other signs of cardiac distress. 
 
 Auricular fibrillation occurs occasionally, but I have only 
 seen it as a terminal event, and it obtains in so many dying 
 hearts that its significance is slight. 
 
 The persistent form of nodal rhythm seems usually to be 
 associated with acute endocarditis, which was found to be 
 present in six of my cases on post-mortem examination. In a 
 seventh case the clinical course of the illness suggested a similar 
 diagnosis, but no post-mortem examination was obtained. In 
 another case the lesions were perhaps chronic. 
 
 " Cardiac overaciion " is often present, the vehemence of the 
 cardiac pulsations widely diffused over many interspaces being 
 associated with a pulse which is small and soft to a degree 
 which is quite out of proportion to the apparent strength of the- 
 heart. Cardiac overaction, however, owns several causes. 
 
 It is often present in hypertrophied hearts — in particular, 
 those associated with aortic regurgitation. It is almost always 
 present in paroxj^smal tachycardia, and is frequently seen in 
 cases of exophthalmic goitre when the pulse-rate is frequent. 
 
 In paroxysmal tachycardia its origin is obvious. Auricle 
 and ventricle are contracting simultaneously, and the auriculo- 
 ventricular valves are consequently shut, so that the ventricular 
 output must be limited; while the obstacle opposed to the 
 auricles, and to the right ventricle in consequence, leads to 
 vigorous though ineffective attempts to overcome the diffi- 
 culty. A similar state of matters may also obtain in cases 
 where the pulse-rate is frequent, though the beats are of 
 
ACUTE ENDOCARDITIS 237 
 
 sinus origin ; for if the rate of stimulus production is sufficient^ 
 rapid, auricular systole will occur before the preceding ven- 
 tricular systole has ended, and a similar interference with the 
 onward flow of blood will, in consequence, ensue. 
 
 The auscultatory evidence of endocarditis may be definite 
 quite early in the illness, even before the arthritis has subsided 
 or the associated fever gone. But a systolic murmur, it must 
 be remembered, may be of functional (myocardial) origin, and 
 is extremely likely to accompany the anaemia which is so 
 rapidly produced by acute rheumatism. In some cases, too, 
 the cardiac sounds are pure at first, and a murmur only develops 
 during convalescence. 
 
 The early auscultatory signs may be very trivial, and a slight 
 blurring or roughening of the first sound, or a short distant 
 and muffled sound, or a short sharp often loud sound, approxi- 
 mating in character to that of the normal second sound, may 
 be the precursors of the permanent murmur of organic valvular 
 disease. Murmurs are apt to be intermittent in the early 
 stages, and may be distinct one day, and faint or gone upon 
 the next, to recur in course of time. I have noticed this on 
 many occasions, and in some which were examined 'post- 
 mortem the valves were covered with very large vegetations, 
 which by their bulk were quite capable of closing the aperture. 
 In one case where an infective endocarditis involved a pulmonic 
 valve which was congenitally defective, one of the longest 
 and loudest diastolic murmurs which I have ever heard dis- 
 appeared altogether for several days, though it returned before 
 death. 
 
 The occurrence of pericarditis or the appearance of sub- 
 cutaneous nodules are additional evidence in favour of an endo- 
 carditis being acute. Pericarditis is almost invariably accom- 
 panied by endocarditis, though the degree of the two is by no 
 means proportionate, and either may be severe when the other 
 is slight. Subcutaneous nodules are generally considered to 
 be indicative of gross cardiac inflammation — endocardial, peri- 
 cardial, or myocardial — an opinion with which my own 
 experience agrees, but the endocarditis is not necessarily 
 severe. 
 
 Subcutaneous nodules are usually small (pin-head to a large 
 
238 DISEASES OF THE HEART 
 
 pea), fairh- firm in consistence, painless and not tender, and 
 freely movable beneath the skin and upon the subjacent 
 tissues. Tenderness may be present if they are mechanically 
 irritated. They are most common about the back of the hand, 
 the elbow, the knee, the scapula, and the occiput, occurring in 
 relation to the fibrous planes, the hgaments, and the tendon 
 sheaths ; but I have seen them on almost every part of the 
 body save the face. Comparable lesions, too, occur in the 
 muscles. In one case the patient frequently complained of 
 pain in different muscles, which were tender to the touch. 
 As a rule, nothing abnormal could be felt, but sometimes an 
 indefinite induration was apparent, which disappeared in a 
 day or two. In another patient the lesions were ver\' large, 
 and one reached the size of a hen's egg, the surrounding tissues 
 becoming brawny and infiltrated. The left sterno-mastoid 
 was affected at one time, and the swelling which commenced 
 at its uppey extremity gradually spread downwards to the 
 sternal insertion. Suppuration did not result, but the muscle 
 remained indurated and hard for a week after the swelling had 
 subsided. 
 
 In the majority of cases the nodules are discovered acci- 
 dentally, and a routine examination reveals several. In some 
 patients fifty or more may be present at one time. Thej^ last 
 for a variable period — a da}^ or two or several weeks — irrespec- 
 tive of their size, and resolution is complete. A migrator}- 
 circinate erythema is a common accompaniment. 
 
 The continuance of fever after the arthritis has subsided, or 
 a want of correspondence between its degree and that of the 
 joint affection, have as their most common cause an endocar- 
 ditis. Endocarditis is generall}- present in cases where the 
 arthritis relapses, even if the recrudescence is shght and tem- 
 porary; and in cases where the other manifestations of the 
 rheumatic poison, chorea, tonsiUitis, erythema, etc., occur 
 subsequently, perhaps, in quick succession. 
 
 The symptoms of the graver forms of the disease are very 
 varied, as they may be referable to almost any organ. Endo- 
 carditis may be merely a part of a general pyaemia, a meta- 
 stasis from the original septic focus, and may occasion httle in 
 the w-ay of symptoms, and have little direct comiection with 
 
ACUTE ENDOCARDITIS 239 
 
 the fatal issue of the case. A girl of nine, for instance, who 
 had suffered from otitis media, noticed that her ears had again 
 begun to discharge. A few days later a broncho-pneumonia 
 developed, from which she seemed to be convalescing, when 
 meningeal symptoms made their appearance and rapidly caused 
 death. At the post-mortem examination vegetations were 
 found on the aortic, mitral, and pulmonary valves, and seemed 
 the probable source of the meningeal infection. 
 
 In another group of cases endocarditis is merely a terminal 
 event, occurring in a patient who is dying slowly from a 
 chronic disease. In one of my patients who suffered from a 
 pneumococcic endocarditis of the aortic and mitral valves and 
 the left auricle, there was found 'post-mortem a quiescent tuber- 
 cular lesion at an apex, a cancerous ulcer in the stomach, 
 granular kidneys, and several strictures of the urethra ! In 
 another group embohc phenomena may be the first indication 
 of the presence of serious cardiac mischief. A woman aged 
 thirt^'-four, who had suffered from several attacks of acute 
 rheumatism during adolescence, complained of epistaxis and 
 of throbbing in the head during the later months of her fourth 
 pregnancy. The confinement (triplets) in August was unevent- 
 ful, and she made a good convalescence, though the throbbing 
 continued. In the second week of October hemiplegia sud- 
 denly ensued, from which she died three days later. Post- 
 mortem examination revealed an acute endocarditis of the 
 mitral valve and the left auricle, and a cerebral haemorrhage 
 which had ruptured into the ventricles. 
 
 The symptoms are perhaps best illustrated by consideration 
 of a number of cases in detail. 
 
 In some instances endocarditis is subacute but persistent, 
 and serious symptoms only ensue after many months. The 
 bacteria concerned may be of various kinds, and the cardiac 
 infection may seem trivial at first, even when it is the source of 
 the recurring symptoms elsewhere. This is often the case in 
 the "rheumatic " group. 
 
 Case 1. — A well-grown girl of fifteen, who had had no serious 
 illness, contracted an attack of acute rheumatism in December, 
 1910, which kept her in bed for two months. In April, 1911, 
 chorea supervened and persisted for six weeks, and it recurred in 
 
240 DISEASES OF THE HEART 
 
 June for nearly a month. In November she again suffered from 
 arthritis, this time for three weeks, and it returned in January 
 and in April, 1912, for a few days. 
 
 The associated cardiac phenomena were instructive. On 
 her first admission in April, 1911, the heart was of normal size, 
 but a systolic murmur was audible at the apex, running out 
 of the first sound for a considerable distance into the short 
 pause. The second pulmonic sound was accentuated. No 
 change was apparent during her second residence in June, save 
 that the murmur was longer and louder. On admission in 
 November the left heart was distinctly larger than before, but 
 it resumed its former size within a month, coincidently with 
 the subsidence of the arthritis. The murmur was unchanged, 
 but a new diastolic murmur of aortic distribution made its 
 appearance in the middle of December. Towards the end of 
 that month she complained of pain in the upper part of the 
 chest for a few days, and this recurred in the middle of Febru- 
 ary, 1912, and in the first week of March. A double murmur 
 was now audible over the sternum, and she complained con- 
 tinually of pain in the chest, though no pericardial friction 
 could be detected. But in the middle of April the tempera- 
 ture again rose, and friction sounds became audible all over 
 the heart, and an effusion of moderate size rapidly developed . 
 By the end of May the effusion had to a large extent dis- 
 appeared, but both hearts were large, and the aortic and mitral 
 murmurs persisted. She made a fair convalescence, and in 
 the autumn was able to do her share of the housework. In 
 December a pulmonary infarct occurred, and she died in 
 February, 1913, from cardiac failure (c/. p. 143). 
 
 In rheumatic endocarditis the arthritic symptoms may 
 be trifling, even when the cardiac affection is severe, and 
 this is more hkely to be the case in childhood than in adult 
 life. The cardiac inflammation, too, may run an acute course. 
 
 Case 2. — An Italian, aged eighteen, was admitted into my 
 wards complaining of pains in the joints and in the chest and 
 of palpitation and general weakness. He had suffered from 
 acute rheumatism three years before, but had made a good 
 recovery, and his present symptoms only began five weeks 
 before admission. He rapidly became pale and felt weak and 
 
ACUTE ENDOCARDITIS 241 
 
 giddy when at work, so that he was forced to take to bed ten 
 days after the onset of symptoms . 
 
 On admission, he was found to be well developed and well 
 nourished. He looked extremely pale and complained of pain 
 in his joints on movement, though the left ankle alone was 
 tender and swollen. There was slight oedema in both feet. 
 He lay fiat in bed, and breathed easity and quietty ; the lungs 
 were normal. The mouth contained many carious teeth, and 
 the tongue was slightly furred. The liver was enlarged and 
 shghtly tender; the stools were normal. The thj^roid gland 
 was shghtly enlarged and was tender on palpation. The 
 urine contained a trace of albumin. Eor two days after ad- 
 mission he seemed to improve, his discomforts abating and 
 his puhe and temperature rumiing at normal rates, but on the 
 evening of December 5 his temperature rose to 99' 6"^ F. and to 
 higher hmits in the days succeeding, touching a maximum of 
 104*4° F. on December 21, though the morning remission 
 touched or approached the normal. Fresh symptoms, too, 
 began to appear, and he complained at this time, for a couple 
 of days, of pain in his right forearm, which was found to be 
 tender and shghtly swollen. A few days later his left shoulder- 
 joint Avas painful on movement, though nothing objective 
 could be discovered. The fever persisted, and he became 
 steadily weaker. Rales appeared at the bases of the lungs in the 
 second week of January, and the oedema of the feet reappeared. 
 Blood was found in the urine on January 22, and became 
 considerable in amount, incontinence of urine ensued, and he 
 became delirious at night. He died from increasing cardiac 
 weakness on January 31. 
 
 The special interest of the case is concerned with the heart, 
 Avhich, on admission, was enlarged on both sides. 
 
 Double murmurs were audible all over the sternum as well 
 as a systohc murmur at the apex, which was thought to indi- 
 cate mitral reflux. The pulse was large and notably shotty. 
 For the first few days of his residence its rate varied from 
 80 to 89, but it then increased to 90-110, and touched 128 
 on the evening of December 31, when the fever was high. It 
 was habitually regular and large, but from December 25 to 27 
 
 was noticed to be much less in volume than before, though no 
 
 16 
 
242 DISEASES OF THE HEART 
 
 other abnormality was detected. After January 14 it became 
 more frequent and averaged about 110, and after January 21, 
 1912, numbered about 120 beats per minute, touching a maxi- 
 mum of 140 on January 28. It was habitually regular save 
 on January 24, when it was noticed to be grossly irregular 
 for a couple of hours, and this was accompanied by grave 
 symptoms of cardiac exhaustion, from which, however, he 
 rallied next morning; and after January 29, until death on 
 January 31. 
 
 The highest leucocyte count, on January 24, numbered 
 13,000. A blood-culture on January 17 showed the presence 
 of diplococci (? Micrococcus rheumaticus) . 
 
 Polygraph records were taken regularl}^ and were easily 
 secured until January 16, but thereafter were difficult to 
 
 Fig. 133. — Nodal Rhythm (Case 2.). 
 
 obtain on account of the respiratory distress and overaction 
 of the sterno-mastoid muscle. In the early tracings the a-c 
 interval averaged, or even exceeded, 0*20 second, and a partial 
 block was carefully watched for; but the interval tended to 
 decrease rather than to increase, and on January 8 was dis- 
 tinctly less than 0*20 second, and it barely exceeded 0*10 second 
 on January 16. On January 19 the A-V interval in the apex 
 tracing only ohghtly exceeded 0"05 second, and on January 25, 
 following the period of irregularity on the preceding evening, 
 the a-c interval in the jugular curve was definitely shown to 
 be habitually less than O'lO second. Tracings thereafter were 
 undecipherable (c/. Nodal Rhythm, Chapter X.). 
 
 On post-mortem examination, the heart was found to be 
 greatly enlarged. The pericardial sac contained a small 
 amount of fibrinous exudation, and the parietal pericardium 
 presented several patches of fibrosis over both auricles and 
 ventricles. The aortic cusps were covered with luxuriant 
 
ACUTE ENDOCARDITIS 243 
 
 vegetations, which spread downwards for a short distance on 
 to the adjacent ventricular wall. The mitral valve was simi- 
 larly affected, and the vegetations involved some of the chords 
 tendineae and the left auricular wall. Both valves showed 
 evidence of old-standing fibrosis. The spleen showed many 
 infarctions, and an acute parenchymatous nephritis was super- 
 added to a chronic interstitial inflammation. 
 
 The cardiac muscle was seriously damaged. Extensive 
 cellular infiltrations were found in both ventricle and auricle, 
 in greatest degree around the bases of the valves, and diffuse 
 and focal collections were present farther away, involving to 
 a notable degree the a.v. node, but barely touching the a.v. 
 bundle. The s.a. node showed no evidence of recent in- 
 flammation, but around its artery there was considerable 
 fibrosis, which spread into the adjacent nodal tissue. The 
 epicardium was somewhat thickened, and strands of fibrinous 
 tissue spread from it into the node, and infiltrated between 
 the nerve fibres and the ganglion cells . 
 
 The diagnosis in this case was not difficult, the continuance 
 of the fever being associated with a visceral lesion in the heart 
 alone. The progressive cardiac weakness and the occurrence 
 of nodal rhythm pointed in the same direction. 
 
 In other cases, however, the cardiac symptoms may be shght 
 and the duration of a valvular flaw unknown, so that its rela- 
 tion to septicsemic symptoms is difficult to establish. The 
 occurrence of embolic phenomena is, however, extremely sug- 
 gestive of acute endocarditis, and in the following case led to a 
 correct diagnosis. 
 
 Case 3. — 'The patient, a man aged twenty-six years, was 
 admitted into hospital on June 5, 1909, complaining of weak- 
 ness and of breathlessness on exertion of some months' 
 duration. 
 
 The patient's health had been good, save for occasional 
 "growing-pains," an attack of tonsillitis in boyhood, and 
 gonorrhoea in the early part of 1903, until an attack of enteric 
 fever later in the same year, for which he was in hospital in 
 Japan for about three months. He never regained his former 
 health, and his feet were often swollen at night, but he was 
 able to work until July, 1908, when he was thrown out of em- 
 
2.44 DISEASES OF THE HEART 
 
 ployment by the failure of his firm. He stayed at home in 
 fairly comfortable circumstances until he procured a new 
 situation on February 19, 1909. In the early part of February 
 he had caught cold, and he was feeling " run down " when he 
 commenced his new work. This entailed a daily walk of four 
 miles, and he felt exhausted at night and also during the day 
 when walking uphill; but though he steadily became weaker, 
 he continued at his post until six weeks before admission. 
 when he was compelled to go to bed. His cough, accompanied 
 by a sMght mucoid spit, persisted from February until May. 
 He had frequent attacks of shivering at night after getting 
 home ; they were fairty severe, and lasted for fifteen to twenty 
 minutes, and he felt hot after he got into bed, and often 
 sweated profusely in the early morning. About a fortnight 
 before admission his right forearm and elbow became sore to 
 the touch and on movement, and this continued for a few days. 
 Four days before admission, the left hip and ankle became 
 painful, and this persisted. 
 
 On admission, the patient was found to be a thin, pale, 
 badly nourished man, with flabby muscles and little sub- 
 cutaneous fat. The left hip and ankle were painful and tender, 
 and there was a small tejider area of induration on the back of 
 the left forearm. The right caK was, he said, painful; but 
 nothing abnormal could be detected. There were several 
 minute ecchymoses on the conjunctival surface of the right 
 lower eyehd, and a fairly large one on the conjunctiva of the 
 left bulb, while ophthalmoscopic examination revealed a 
 medium-sized flame shaped haemorrhage in the course of the 
 left superior temporal vein. The lungs were normal, the 
 tongue was clean, the digestion good; the Hver and spleen 
 were shghtly enlarged ; the urine contained a small amount of 
 albumin. The heart was but little enlarged, though there 
 was a weU-marked mitral systohc murmur. The pulse was 
 frequent, regular, small, and soft; and he was shghtly 
 fevered at n^'ght. The leucocj-te count never rose above 
 15,000. 
 
 Progress after admission was slowly but continuously in the 
 wrong direction. Many embohsms occurred, chiefly in the 
 Hmbs, but once, at any rate, in the spleen, and twice in the 
 
ACUTE ENDOCARDITIS 245 
 
 kidneys. He had several "faint turns " of a feAv minutes' 
 duration without obvious cause. The weakness increased, 
 and after the middle of Juh' oedema was more or less continu- 
 ally present in the legs. There were occasional rigors and 
 generally profuse sweats at night. On August 25 a left hemi- 
 plegia occurred, and he died on August 29. 
 
 The pulse during the patient's residence in hospital was 
 always regular until immediately before death ; and the venous 
 curves were normal, save that the a-c interval was invariably 
 prolonged, measuring about 0'25 second, and never touching 
 0-2 second or O'S second. 
 
 Post-7nortem examination revealed an acute endocarditis 
 of the mitral valve. Two emboli were present in the 
 right middle cerebral arteries, and septic infarctions were 
 present in the left kidney and the spleen. Erom the latter the 
 pneumococcus and Bacillus coli communis were ^isolated in 
 culture. Blood-cultures during life had proved sterile. 
 
 The mitral valve was dilated. Numerous vegetations were 
 present on the cusps, some small and wart-like, others long and 
 luxuriant. The endocardium of the left auricle was thick and 
 opaque, and a few minute granulations were present on the 
 contra-fossal wall immediately above the valve; the endo- 
 cardium at this point was notably thickened. There was no 
 evidence of mural impHcation elsewhere. 
 
 Microscopic examiiuLtion of the a.v. node and bundle re- 
 vealed well-marked congestion. The node was otherwise 
 normal, though two small foci of round-cells were found in 
 the auricular muscle in its immediate vicinity. The bundle 
 was involved in three separate places by foci of the "-ame kind. 
 The first was of small size and was situated immediately below 
 the node ; the second, which was considerably larger, was found 
 a httle lower down, between the auricular muscle and the 
 bundle, and imphcated both; the third, of fair size, occupied 
 the central part of the bundle, and occurred inmiediately above 
 the point where it passed through the central fibrous body. 
 The cehs were all mononuclear and chiefl}' l^-mphocytes . The 
 fibres of the a.v. bundle seemed normal, save in the immediate 
 vicinity of the two larger foci, where they were evidently de- 
 generate. The fibrous tissue of the bundle was not excessive 
 
246 DISEASES OF THE HEART 
 
 in amount. The s.a. node was normal. The cardiac muscle 
 generally showed evidence of interstitial myocarditis in an 
 early stage, and the muscle fibres in some of the patches were 
 degenerate. 
 
 In some cases the symptoms point to the existence of gross 
 lesions in the central nervous system, and the diagnosis may 
 be extremely difficult or impossible. An old man was admitted 
 to hospital on account of cerebral symptoms which had ensued 
 •somewhat rapidly, and as an aural discharge was found to 
 exist, the mastoid cells were exposed and drained, but without 
 effect. Post-mortem examination showed that the symptoms 
 were due to embohc occlusion of the cerebral vessels associated 
 with a mahgnant endocarditis of the mitral valve. The otitis 
 media was quiescent. In the following case the correct diag- 
 nosis was considered to be probable on account of the sudden 
 occurrence of the cerebral symptoms and their association 
 Avith a cardiac lesion, fever, and rigors. The significance of 
 the occurrence of extra-systoles and nodal rhythm was not fully 
 reaHzed until the post-mortem examination. 
 
 Case 4. — The patient, a man aged twenty -four, was ad- 
 mitted into hospital on July 15, 1909. His previous health 
 had been good, save for attacks of measles and enteric fever 
 in childhood; but he was often troubled with gumboils, and 
 was frequently wetted at his work. 
 
 The patient's present illness dated from July 1, when he 
 had had one of his molars extracted on account of a gumboil 
 from which he had suffered for a day or two. In the evening 
 he felt sick and shivery, and probably was fevered. Thes 
 symptoms continued, and on the afternoon of July 4 he had 
 a definite rigor. On the 7th he felt better, and on the 8th he 
 went to Ardrossan, walking from the station to the house at 
 which he stayed (a distance of two miles). After this he im- 
 proved until the 12th, though he had a shght cough after the 
 6th, with discomfort in the left chest; but on the 12th he had 
 to go to bed as the pain in the side became worse and was 
 much intensified on coughing. The left arm, too, was stiff, 
 and he was very breathless and had to sit up in bed at night. 
 On the evening of the 13th he was better, and able to sleep 
 quietly lying down. 
 
ACUTE ENDOCARDITIS 247 
 
 On July 14 the man felt so well that he dressed and went 
 downstairs, which he did without any difficulty and without 
 assistance. After breakfast he sat down on a chair, and on 
 attempting to rise an hour later found that his legs were power- 
 less and " had no feeling " in them. He had to be carried 
 back to bed. 
 
 On admission, the patient was found to be notabh' emaciated, 
 with small muscles and scanty subcutaneous fat. His com- 
 plexion was somewhat sallow and his expression anxious, 
 while he had to be propped up in bed on account of breathless - 
 ness. The skin was hot and dry and there was a little oedema 
 of the feet and slight pitting with the stethoscope on ausculta- 
 tion over the cardiac area. He was shghtly fevered at night. 
 The patient, though weak, was quite clear mentally, spoke 
 correctly, and answered questions accurately and sharply. 
 He had little power in his legs, but was able to pull up both 
 knees, though he was unable to move the toes of the right foot. 
 The movements were more free on the left side. There was 
 considerable anaesthesia in both legs. Power was perhaps de- 
 ficient to some slight extent in the left arm, but in the right 
 was good, and sensation seemed normal. The right pupil was 
 shghtly smaller than the left; both reacted to light and on 
 accommodation. 
 
 The tongue was dry and coated, many of the teeth were 
 absent, most of the remainder were carious, and the mouth 
 generally was very foul. The pulse was soft, regular, and in- 
 frequent. Palpation of the apex-beat, which was full and 
 widespread, showed that ever}^ other beat was missed at the 
 radial, the cardiac action being regularly coupled. A systoHc 
 murmur was audible all over the cardiac area. It was heard 
 best at the apex, where it was long and soft, replacing and 
 running out of the first sound ; the second sound was not audible 
 here. The respirations were difficult and cycHc, but without 
 any full apnoea. A consohdation was found in the upper part 
 of the right chest, and in the left lower axilla friction sounds 
 were audible. The urine contained a trace of albumin. 
 
 For a few days the patient's general condition improved 
 slightly. The coupled rhythm ceased on the 16th, and he 
 rested fairly well at night. On the 17th movement was more 
 
248 DISEASES OF THE HEART 
 
 free in the left leg, but the palsy below the right knee persisted. 
 About midnight on the 18th he was noticed to be restless, and 
 was found to be semi-conscious and unable to say more than 
 "Yes," and there was a well-marked full right hemiplegia. 
 He gradually became weaker and more comatose, and he died 
 from cardiac failure on Juh' 27. 
 
 The pulse remained "single " until the day of death, when 
 it was noticed to be " coupled " again for a short time. The 
 tracings, which were obtained in this case during the coupled 
 rhythm, showed that there was a shght increase of the a-c 
 interval (0"25 second) with the first or larger beat of the couple, 
 and that the second or smaller beat was a ventricular extra- 
 systole which did not interfere with the auricular rhythm. 
 Tracings of the " single " pulse obtained on July 23 showed 
 . „ a regular pulse and a 
 
 °-- ac as. Q(z ac ftc ac ac a.c ac , 
 
 very short a-c interval, 
 measuring httle more 
 ?3^.<x? " " than 0'05 second. 
 
 ,S^ Post-mortem ex- 
 amination revealed an 
 acute ulcerative endo- 
 carditis of the mitral valve, engrafted on a lesion of older 
 standing. The upper and middle lobes of the right lung were 
 sohd from a somewhat chronic pneumonia, and there were 
 numerous infarcts in the spleen and kichiej's. The left middle 
 cerebral artery was occluded by a large pale embolus, which 
 resembled the vegetations on the mitral valve, and was associ- 
 ated mth a ver}- extensive softening. Streptococci were 
 isolated on culture from the spleen. No blood-cultures were 
 made during life. 
 
 The mitral valve was stenosed, the cusps being notably 
 shortened, the chordae tendineae short and thick, and the tips 
 of the papillar}^ muscles fibrous. There was well-marked 
 evidence of fibrosis spreading upwards from the bases of the 
 cusps in the direction of the central fibrous body of the heart. 
 Enormous soft recent vegetations almost occluded the valve, 
 and there was, in addition, extensive ulceration and perforation 
 of the anterior mitral cusp . There was no evidence of any acute 
 mural endocarditis ; but the endocardium of the left auricle 
 
 viU^^KKUAiv^^^'' 
 
 Fig. 134. — Nodal Rhythm (Case 1.). 
 
ACUTE ENDOCARDITIS 249 
 
 was thick and opaque, with, a special area of thickening about as 
 large as a shilling on the contra -fossal wall just above the valve. 
 
 Microscopic examination of the a.v. tissues revealed con- 
 siderable congestion of the tissues generally. The node was 
 the site of a profound inflammatory disturbance, many focal 
 collections of round-cells being present, as well as, in places, a 
 diffuse infiltration. The fibres of the a.v. bundle were probably 
 normal, and there was no evidence of old-standing fibrosis. 
 The walls of a microscopic artery were infiltrated with round- 
 cells, though the lumen was patent; the other vessels seemed 
 normal. The intensity" of the lesions varied at different levels, 
 but the whole of the node was more or less affected. The 
 bundle, on the other hand, was not implicated, save at one place 
 immediately below the node, where one or two small foci in the 
 auricular muscle immediately adjoining it passed in for a short 
 distance between a few of its fibres. The s.a. node was normal. 
 
 There was a weU-marked myocarditis, involving both ven- 
 tricle and auricle, but it was onh' extreme at the base of the 
 mitral valve, and in the auricular sections immediately above 
 the node itself. 
 
 The following case is instructive on account of the duration 
 of the fever, which lasted from May 15 until 'July 28, and the 
 ultimate good result. The fever was not high, and only once 
 exceeded 103° F. The mitral and the aortic valves became 
 affected under observation. 
 
 Case 5. — D. L., aged twenty, fireman, was admitted on 
 May 21, 1909, complaining of pains in his joints of six days' 
 duration. His previous health had, on the whole, been good, 
 save for an attack of measles when a child, and pneumonia at 
 the age of sixteen. He was, however, hable to tonsillitis until 
 he was thirteen years of age, but subsequently it had ceased 
 to trouble him. Three weeks before admission, however, his 
 tonsils again became acutely inflamed, and he was in bed for 
 a week. As he had then quite recovered, he resumed his work, 
 which exposed him to the weather, as he was on a night shift. 
 On the evening of May 16 he began to feel pains in the " small 
 of his back " ; on the evening of May 18 his shoulders began to 
 be painful, and on May 19 the hips were affected, and he was 
 compelled to go to bed. Xext day manj' more joints were 
 
250 DISEASES OF THE HEART 
 
 implicated, and he sweated profusely. On admission to 
 hospital he M'as found to be a well-nourished man of good 
 physique. His face was flushed and he was sweating profusety, 
 and evidently suffering considerable pain. The tongue was 
 furred, the mouth foul, and both tonsils were enlarged and 
 shghtlj' inflamed. The knees and ankles, the wrists, and man}' 
 of the phalangeal, metacarpo-phalangeal, and metatarso- 
 phalangeal joints were swollen and tender. There was a con- 
 siderable amount of fluid in the right knee-joint. The other 
 viscera seemed normal, save for a httle catarrh in the lungs 
 The arthritis rapidly became less acute, but persisted in one 
 or other joint until the end of June. The tonsillitis persisted 
 for some time after admission, but had subsided by the first 
 week of June. In July, however, it returned and persisted 
 for a week, and again in the last week of November. His 
 general condition slowly but steadily improved after acbnission, 
 and he was always able to take an adequate supply of nourish- 
 ment. Bacteriological examinations of the blood on May 7 
 and July 11 were negative. The leucocyte count reached a 
 maximum of lu,800 on May 24. The cardiac condition never 
 gave rise to any anxiety from the sj^mptomatic point of view, 
 though the auscultatorj' phenomena indicated grave myo- 
 cardial weakness. The apex impulse was faint and was not 
 displaced. On auscultation the sounds were pure, but the 
 first sound was extremely short and indistinct, and somewhat 
 distant. The pulse was regular and fairly full, but soft and 
 frequent. The first sound remained short and distant, but 
 pure for about a fortnight, after which it began to lengthen 
 from the addition of a sj^stohc murmur of mitral distribution. 
 Towards the end of July a short, soft diastohc murmur became 
 audible in the third left space about an inch from the sternal 
 margin, succeeding an emphatic second sound. The pulse- 
 rate only reached normal hmits at the end of July. He was 
 allowed out of bed in the commencement of October, and 
 when dismissed home on Januar}^ 24, 1910, was able to take a 
 fair amoimt of exercise and to walk upstairs without any 
 evident discomfort. The heart was shghtly enlarged, and the 
 aortic and mitral murmurs persisted. 
 
 Three years later he was in good health, and playing cricket 
 on occasion. 
 
CHAPTER XX 
 ACUTE ENBOCARDITIS— Continued 
 
 The Diagnosis o! Acute Endocarditis.^ — The diagnosis of acute 
 endocarditis, though often self-evident, may be at times ex- 
 tremely difficult or even impossible, for in some cases the 
 symptoms are general, and in some point to the involvement 
 of other organs than the heart. In my hospital cases the symp- 
 toms in 19 were cardiac, in 6 cerebral, in 2 pulmonary, and in 
 2 of a general kind ; one patient died during an attack of chorea. 
 
 In the majority of cases fever co-exists (Fig. 135), but it is of 
 no special type, and may be high or low, and continuous 
 remittent or intermittent; in the latter case rigors often occur. 
 It may, too, be absent. This obtained in two cases, in one of 
 which it was perhaps merely a measure of the debility of the 
 patient; but in the other the temperature was normal during 
 the last five weeks of the illness. Fever is not infrequently 
 absent during the acute stages of rheumatic endocarditis, and 
 the temperature may even be subnormal ; sometimes the 
 evening temperature rises occasionally to 99° or 100° F. without 
 any obvious cause; or a subnormal wave of " pyrexia," lasting 
 for a week or more, may be apparent on the chart (Fig. 136.) 
 Both of these signs are significant. 
 
 The essential feature is the recognition of a valvular murmur, 
 but the cardiac sounds may be unaccompanied for some weeks 
 (c./. p. 234). As a rule the valvular disease is well marked, 
 but previous observation may be wanting, or the presence of 
 a pre-existing flaw may be known, and the separation of an 
 acute from a chronic endocarditis is required. Horder has 
 suggested that the occurrence of embolism and the isolation of 
 organisms from the blood are almost conclusive evidence of an 
 infective endocarditis ; but while this is probably accurate, it 
 
 251 
 
252 
 
 DISEASES OF THE HEART 
 
ACUTE ENDOCARDITIS 
 
 253 
 
 excludes practically all the cases of rheumatic origin, as well 
 as manj' others in which blood-cultures are sterile, and thus 
 restricts the recogni- 
 tion of the disease. 
 It is on the cardiac 
 evidence that most 
 reliance must be 
 placed. 
 
 I would again em- 
 phasize the impor- 
 tance of the pulse- 
 rate in the diagnosis . 
 The pulse-rate may 
 be unduly frequent in 
 fever, from emotion, 
 from cardiac weak- 
 ness, and in a few 
 diseases, such as 
 phthisis, exophthal- 
 mic goitre, rheuma- 
 toid arthritis, and 
 diphtheria , apart 
 from cardiac com- 
 phcations. But the 
 absence of these 
 factors can be readity 
 determined by a few 
 observations, and in 
 their absence a fre- 
 quent pulse -rate is 
 generall}^ due to an 
 acute cardiac lesion. 
 The sudden appear- 
 ance of irregularity 
 has a similar signifi- 
 cance. Heart-block is so generally due to a myocardial fault 
 that its appearance, even in trivial and transient degree, suggests 
 that an associated endocarditis is acute and not chronic ; and the 
 sudden appearance and continuance of extra-systoles, without 
 
 Fig. 
 
 133.— Chart of H. O'K., Aged 12: Acute 
 Rheujiatisji; Acute EN^DDOAnorTis. 
 
 Xote siibnormnl wave of " p'/revi'i ' 
 frequent pulse-rate. 
 
 and uaiuly 
 
254 DISEASES OF THE HEART 
 
 obvious pulmonary complications or increase of cardiac weak- 
 ness, point the same moral. Nodal rliytlmi seems to be most 
 frequently associated with an acute endocarditis. Paroxys- 
 mal tachycardia and auricular fibrillation have no particular 
 significance. 
 
 The appearance of new murmurs is as a rule decisive, and 
 the temporary disappearance of murmurs is equally suggestive, 
 but one exception must be remembered. The characteristic 
 crescendo murmur of mitral stenosis always disappears if 
 auricular fibrillation or nodal rhythm occurs ; and may disappear 
 in partial heart-block.* If a sinus rhythm, continues, the con- 
 clusion that there is an acute lesion is probabl}^ always correct. 
 
 Embolism is of frequent occurrence. It may of course 
 occur in chronic endocarditis from the separation of clots in 
 the auricles, but it is often multiple and recurrent in acute 
 cases. In chronic valvular disease puhnonary embohsm is 
 more common ; in acute endocarditis embolism of the systemic 
 arteries. The spleen is often involved (Horder, 47 cases) and 
 becomes enlarged. Occasionally the enlargement is great, and 
 in one of my cases the lower border reached down to the 
 umbihcus. The occurrence of an infarct may be acutely 
 painful, and friction may be audible from associated peri- 
 tonitis. Renal infarct is also common. Gross haematuria was 
 present in 46 of Horder's cases and in 8 of my own; but, as 
 Horder points out, the incidence is probably greater, for the 
 lesser degrees are not always accompanied by macroscopic 
 evidence of the presence of blood. The brain is less frequently 
 affected, but the cerebral vessels were occluded in 22 of Horder's 
 cases and in 3 of my own. The result is most frequently 
 softening, but haemorrhage is not very rare. Meningitis 
 occurred in 4 of my cases. 
 
 Infective aneurisms may form. Horder reports 2 cases; in 
 one the aneurisms were multiple, the right ulnar, the superior 
 mesenteric, and the hepatic arteries being involved. In one 
 of my cases, a boy of fourteen years, there was a small aneurism 
 of the aorta just above the valves, and a fusiform aneurism, 
 the size of a plum, at the lower end of the left iliac artery. 
 Both the artery and vein were occluded, but the leg, though 
 * W. T. Ritchie, Edin. Med, Journ., 1913, vol. x., N.S., p. 410. 
 
ACUTE ENDOCARDITIS 255 
 
 oedematous, showed no signs of gangrene. Cutaneous mani- 
 festations are not uncommon. Petechial eruptions are the 
 most frequent, and were present in 43 of Horcler's series and 
 in 6 of my own. Subcutaneous nodules occurred in 3 cases in 
 my series, and persistent erythema and urticaria in 3 instances. 
 Fugitive tender indurations in the deeper structures have a 
 similar significance. 
 
 Gross visceral lesions are by no means uncommon, and the 
 co-existence of pneumonia, pleurisy, pericarditis, etc., with a 
 valvular murmur, should always suggest the possibility of an 
 endocarditis being acute. 
 
 The occurrence of a leucocytosis has no particular diagnostic 
 significance. It is always present in mahgnant cases save in 
 the terminal stages, when it is sometimes absent; but it is 
 merely evidence of a septicaemia, whose presence is clearly 
 shown in other ways, and not of a cardiac infection. A count 
 of over 25,000 is uncommon in the rheumatic forms. 
 
 The Prognosis in Acute Endocarditis. — The prognosis in acute 
 endocarditis is clifiicult to assess. The majority of rheumatic 
 cases recover, but with damaged valves; while patients from 
 whom positive blood-cultures have been obtained usually die. 
 
 In the individual case the risk must be assessed from con- 
 sideration of the usual factors, the general condition of the 
 patient, the height of the fever, and the rapidity of the pulse- 
 rate ; and the prognosis should be guarded until the fever has 
 gone and the pulse-rate is wdthin normal limits. The occur- 
 rence of rigors, emboL'sm, and petechial eruptions ; the appear- 
 ance of oedema, and progressive dilatation of the heart; and 
 alterations in the rhj^thm of the heart, are of serious signifi- 
 cance. Comphcations, such as pericarditis, pleurisy, and 
 pneumonia add greatly to the danger. Dehrium is generally- 
 the immediate precursor of death. But I have seen patients 
 recover in whom each of these symptoms was present, and I 
 am inchned to lay most stress upon the general nutrition of 
 the patient. If this can be maintained, the prognosis is never 
 hopeless ; but if it fails, the cardiac infection always progresses. 
 
 The Treatment of Acute Endocarditis. — ^There is no specific^ 
 treatment of acute endocarditis, for, as has been shown, its 
 
256 DISEASES OF THE HEART 
 
 causes are diverse. But the general indications are clear, and 
 the essential part of the treatment is rest. 
 
 It is of course impossible to secure physiological rest to the 
 heart, for life ceases when the heart stops beating ; but absolute 
 confinement to bed in the recumbent posture diminishes the 
 frequency of the cardiac contractions and insures a minimal 
 blood-pressure ; for both the pulse-rate and the blood-pressure 
 are appreciably raised even by sitting up in bed. Absolute 
 rest necessitates full nursing, the patient doing nothing that 
 can be done for him by a nurse, and being fed and washed 
 and dressed with as little voluntary movement as is possible. 
 The use of a bed-pan and a slipper is essential. The rest, too, 
 must be long continued, for even after the symptoms have 
 disappeared and the curves are normal, the valves are infil- 
 trated and soft, and resolution is incomplete ; and the size of 
 the ultimate scar depends upon the degree of movement of 
 the cusps. 
 
 In too many instances the duration of the rest allowed is in- 
 sufficient. It is impossible to assess accurately the extent of 
 the inflammation, but analogy from lesions elsewhere, such as 
 pneumonia and fractures, shows that the rate of resolution 
 varies considerably in individual cases ; and the only wise plan 
 is to play for safety, and rather to prolong the rest unnecessarity 
 than allow exercise at a time when it will, or may, cause harm. 
 The effects of exertion on the incidence of endocarditis in acute 
 rheumatism are well known, and the lesions are less common 
 and less severe in cases where the severity of the arthritis has 
 driven the patient at once to bed, as contrasted with the milder 
 cases where the patient has been able to go about for days or 
 even weeks. 
 
 Absolute rest, then, is indicated until aU symptoms have 
 disappeared, and the rate and rhythm of the pulse are normal . 
 When this has occurred, the patient may be allowed to sit up 
 in bed for short periods, the size of the area of cardiac duhiess 
 and the pulse-rate being carefully watched ; and the periods 
 may be gradually increased if no untoward result follows. He 
 should, however, be confined to bed for at least two months 
 longer, and for another month merely moved on to a couch; 
 before he is allowed to stand up and walk. Restrictions as to 
 
ACUTE ENDOCARDITIS 257 
 
 exercise must be continued for at least three to six months 
 longer, and violent exercise, such as games, interdicted for a 
 year or so afterwards. 
 
 Massage is useful during the period of rest, and may be 
 commenced as soon as the patient is allowed to sit up, the 
 massage being at first slight and of short duration, and only 
 increased very gradually. Every effort, too, should be made 
 to improve the general health, and plenty of fresh air and a 
 variety of food utilized with this in view. In suitable weather 
 much time may be spent out of doors. 
 
 The results obtained by these means are surprising. One 
 patient, aged forty when I saw him, had a heart so full of mur- 
 murs that no valve could be pronounced sound, but its size was 
 normal. He was a lawyer in busy practice who took much exer- 
 cise, and he had never had any cardiac symptoms since his 
 attack of acute rheumatism twenty years before. But at that 
 time he was for six months in bed and for six months on a 
 couch, and he was not allowed to walk quickly for another 
 year. . -'^' 
 
 From the clinical standpoint cases of endocarditis may be 
 divided into three groups: (1) Those which are of rheumatic 
 origin ; (2) those in which blood-cultures reveal the presence of 
 bacteria; and (3) those in which blood-cultures are sterile, 
 though they seem to have no connection with acute rheu- 
 matism. 
 
 1. The incidence of endocarditis in acute rheumatism, as 
 gauged by statistics in the literature, does not seem to be 
 appreciably lessening, so that it appears that sahcylate treat- 
 ment has little effect in preventing this complication. Every- 
 one knows how difficult it is in some cases to overcome the 
 tendency of the arthritis to relapse in this disease ; and most 
 of us have watched cases of rheumatic endocarditis progress 
 steadily, notwithstanding sahcylate treatment. It has, in 
 consequence, been suggested that the failure of the salicylates 
 indicates a non-rheumatic infection. The inference, however, 
 does not seem justifiable, for cases of malaria or syphilis may 
 run a mahgnant course in spite of treatment by quinine or 
 mercury ; and the obvious conclusion is that acute rheumatism 
 may run a malignant course. A progressive lesion merely 
 
 17 
 
258 DISEASES OF THE HEART 
 
 indicates a severe infection, not necessarily different in 
 nature. 
 
 The action of large doses of salicylates upon the heart, 
 slowing its rate and weakening its action and lowering the 
 blood-pressure, has been held to contra-indicate their adminis- 
 tration in cases where the heart is involved. If there is any 
 evidence of cardiac weakness, the contention is obviously 
 sound, but in its absence the drug should be exhibited, as 
 apart from the question of a specific action upon the infection, 
 the lessening in rate and the lowering of blood-pressure are 
 beneficial to the local lesion. Large doses are, however, 
 unwise, but 60 to 90 grains may be given daily to an adult in 
 combination with equal dose^, of sodium bicarbonate.* 
 
 Sahcylate poisoning is comparatively^ infrequent. The 
 lesser degrees are most frequently observed in patients who are 
 suffering from high blood-pressure and defective elimination. 
 In any case attention should be paid to the smallest mani- 
 festations of intolerance, and the drug should be intermitted 
 if they appear. 
 
 2. The isolation of bacteria from the blood necessarily raises 
 the question of specific treatment, and it seems reasonable to 
 administer the corresponding antiserum in these cases, even 
 though one must as a rule employ a polyvalent serum, and not 
 one specially prepared from the particular organism. The 
 results which have been obtained, however, are extremely 
 disappointing, and only one or two cases have been recorded 
 in which recovery ensued. My own experience has been uni- 
 formly unsatisfactory. 
 
 Vaccine treatment, too, has had equally poor results, and it 
 seems extremely doubtful if good results will ever be obtained 
 in this way. The production of antibodies, which is the aim 
 of this treatment, takes place in disease in response to the 
 presence of bacteria or of their products, and may fail to be 
 sufficient if the infection is local and absorption minimal; or 
 if the infection is intense and the defensive processes are over- 
 powered. Of all the conceivable sites of infection, the endo- 
 
 * The administration of alkali in an amount sufficient to render the urine 
 alkaline, and the prevention of constipation, obviates the risk of salicylate 
 poisoning (Lees), which is perhaps due to an acid intoxication. 
 
ACUTE ENDOCARDITIS 259 
 
 cardium is surely that most certain to produce a general 
 intoxication, and I fail to comprehend how in these general 
 " arterial " septicsemias an additional dose of the poison can be 
 of benefit to the patient. 
 
 In four cases, however, recovery has ensued after treatment 
 of this kind, and although the satisfactory result may not have 
 been due to the specific treatment, the uniformly fatal ter- 
 mination in cases in which such treatment has not been tried 
 should perhaps encourage further experiments.* 
 
 3. In the third group the indications for treatment of a 
 specific kind are lacking. The salicylates have generally been 
 already tried and have failed, and serum or vaccine treatment 
 are negatived by the failure to isolate a bacterium. General 
 treatment of the kind that has been already laid down — com- 
 plete rest, fresh air, an abundant dietary (solid food can often be 
 well digested by fevered patients) — is of course already in action. 
 
 It seems probable that in many of these cases continual 
 reinfections of the blood-stream (and of the valves) are occur- 
 ring from local septic foci which may exist in different situa- 
 tions . The tonsils are often large and deeply pitted ; the nose 
 or middle ears are septic; or the teeth are carious and the 
 mouth is foul. The urethra, the bladder, the uterus, etc.. may 
 be infected. The influence of such septic foci in the production 
 of a visceral infection is difficult to estimate, but an impression 
 is gradually arising that they are, at any rate, of greater im- 
 portance than has hitherto been recognized; and that little 
 good result is likely to occur unless the reinfections of the 
 valves are stopped by eradication of the source of the re- 
 infection. The general condition of the patient, or the nature 
 of the primary focus, may make it difficult to secure asepsis, but 
 I have on two occasions seen permanent improvement ensue 
 in cases which seemed to be progressing downhill, after removal 
 of enlarged tonsils ; and on one occasion a great, though un- 
 fortunately only temporary, relief after removal of some dozen 
 carious teeth. 
 
 * Sir James Barr, W. Blair Bell, and Captain S. R. Douglas, Lancet^ 
 London, 1907, vcl. i., p. 499. A. Latham and E. L. Hunt, Proc. Royal Soc. 
 Med., London, 1910, vol. iv. (Clinical Section), p. 14. G. Jochmann, Berlin 
 Klin. Woch., 1912, p. 436. H. Hemstead and T. J. Horder, Lancet, London,. 
 1913, vol. i., p. 10. 
 
260 DISEASES OF THE HEART 
 
 From the preventive point of view, in any case, such measures 
 are urgently required, and no " rheumatic " patient should be 
 allowed to harbour septic foci, even in the absence of cardiac 
 disease. 
 
 Many drugs have been advocated in these cases — horse 
 serum (to supply complement), arsenic, mercury, quinine, 
 silver in the colloidal form, etc. I have once or twice thought 
 that coUargol injected intravenously, and applied as Crede's 
 ointment to the skin of the trunk, was responsible for improve- 
 ment, but in most cases it has no effect. The most important 
 factor is probably the digestion; and so long as the nutrition 
 of the patient can be maintained or improved, recovery may 
 be hoped for; with anorexia or digestive disturbance the pro- 
 gress is invariably in the wrong direction. Cardiac weakness 
 must be combated by the usual means, but its appearance in 
 acute endocarditis is always of grave significance. 
 
CHAPTER XXI 
 CHRONIC VALVULAR DISEASE 
 
 The Lesions. — Chronic valvular disease of the heart interferes 
 in greater or less degree with the proper working of the valves, 
 and thus imposes an extra strain upon the heart ; but as the 
 lesions differ in their grade and are not necessarily confined 
 to the cusps but may involve the " cyhnder " as well, the 
 ultimate result varies in different cases, and the interference 
 with the valvular action may be considerable or of little 
 moment. 
 
 The conditions which are found post-mortem are of various 
 kinds. The normal soft, pliable, translucent appearance is 
 lost, and the cusps are hardened, stiffened, and opaque, the 
 change being in some cases uniformly distributed throughout, 
 and in others confined to, or most extreme at, the free margins 
 or the lines of attachment. Calcareous and atheromatous 
 deposits are not uncommon, and although usually merely an 
 addition to a general change, are sometimes an isolated lesion 
 in a fairly normal cusp. The calcareous deposits are occa- 
 sionally so large that by their mere bulk they interfere with the 
 proper action of the valve, and may prevent its closure or 
 obstruct its orifice (Fig. 137). 
 
 The cusps may be shortened or adherent to each other ; and 
 while shortening produces incompetence, adhesion causes nar- 
 rowing of the orifice ; the two results frequently co-exist. The 
 ultimate result varies. Sometimes the cusps are more or less 
 uniformly joined together, and a funnel or dome-shaped ap- 
 pearance is produced ; and sometimes the longitudinal shrinkage 
 is extreme, and a diaphragm results (Fig. 138). The chordae 
 tendineae, and even the musculi papillares, may be imphcated 
 in the fibrosis of the mitral valve, and the whole apparatus 
 
 261 
 
262 
 
 DISEASES OF THE HEART 
 
 may be welded together into a single mass (Fig. 139). The 
 orifice is often greatly narrowed, and may be rounded or linear 
 or stellate. 
 
 In many cases warty outgrowths of varying size and con- 
 sistence are visible at the margins of the cusps ; in others erosion 
 and loss of substance are the main feature, and the edges are 
 puckered and uneven. The line of attachment may be eroded 
 and part of a cusp may be freely mobile in the blood-stream ; 
 or, if it is calcified, project stiffly into the lumen. These results 
 are most common in the aortic valve, for destruction of the 
 chordae tendineae of the mitral valve usually produces so great 
 
 an interference with the cardiac 
 action that death ensues during 
 the acute stage. 
 
 The cusps may be perforated 
 through their substance. This is 
 most commonly the result of acute 
 endocarditis, but sometimes follows 
 severe muscular effort or an external 
 trauma. Those pathological per- 
 forations must not be confounded 
 with fenestration of the cusps, a 
 congenital defect of no importance, 
 which does not interfere with the 
 action of the valves. The dis- 
 tinction is easy, as the fenestras are situated close to the 
 margins of the cusps, and on surfaces which are opposed during 
 closure; while the edges are unaltered, and neither thick nor 
 hard. In the former the cusps are abnormal, and the per- 
 forations are at the centre of the cusps or near their attach- 
 ments. 
 
 In the majority of chronic aortic defects the edges of the 
 cusps are more or less inverted ; in rare instances the edges are 
 everted.* In the latter case (Fig. 140) the curtains are usually 
 voluminous rather than shortened, but, though thickened, are 
 so soft that they fall downwards towards the ventricle and 
 impose no obstacle to the regurgitation of blood ; there is rarely 
 necrosis or ulceration, and vegetations, if present, are generally 
 
 Fig. 137. — Calcaeeotjs Infil- 
 tration ? OF Aortic Valve 
 (R. I. Museum). 
 
 Cowan, Glasgow Med. Journ., 1902, vol. Iviii., p. 198. 
 
CHRONIC VALVULAR DISEASE 
 
 263 
 
 scanty and small. Microscopic sections show that the con- 
 nective tissue of the cusps is loose and degenerate, with patches 
 of leucocytic infiltration which are most numerous at the base 
 of the valve and in the aortic wall; the vessels here show in- 
 flammatory changes and a narrowed lumen interfering with the 
 
 Fig. 138. — Teaxsverse Section of Heart, viewed from above 
 (W. I. Museum). 
 
 The mitral valve is greatly, and the tricuspid valve slightly, stenosed. Both 
 auricles are greatly dilated. 
 
 nutrition of the valve and producing degeneration of the new- 
 formed connective tissue. 
 
 The lesions frequently extend beyond the valve. The waU 
 of the aorta is often affected, showing either a diffuse thicken- 
 ing or a patchy change ; the orifice may be so greatly dilated 
 that even cusps of normal size would be insufficient to occlude 
 it. The mitral orifice, on the other hand is more often 
 
264 
 
 DISEASES OF THE HEART 
 
 CHORD/E TENDlNE/€ 
 
 ANTERIOR. CUSP 
 
 MUSCULI PAPILLARES 
 
 Fig. 139.— Ftjnnel-Shaped Miteal Endocarditis (W. I. Museum). 
 
 The mitral cusps, the chordse tendinese, and the musculi papillares are all welded 
 
 together. 
 
CHRONIC VALVULAR DISEASE 265 
 
 narrowed than dilated, for the inflammatory spread into the 
 muscle in the course of cicatrization leads to narrowing. The 
 auricular wall may be affected. 
 
 Valvular defects are rarely pure. Stenosis is almost always 
 associated with some degree of incompetence ; and conversely 
 incompetence is generally accompanied by some degree of 
 narrowing. In aortic cases incompetence is the rule, and 
 stenosis is minimal and rarely extreme. In mitral cases 
 stenosis is the rule, and incompetence co-exists ; for the ana- 
 tomical division of the mitral valve into an anterior and a 
 posterior cusp is inaccurate, as it is reallj^ a circidar curtain 
 
 Fig. 140. — Flabby "Wash-Leather" THiCKExrs:G or Aortic Valve, which 
 
 WAS NOTABLY InCOMPETEXT (W. I. MuSEUM). 
 
 with special developments of certain parts; and if it is uni- 
 formly involved, the lumen is necessarily narrowed by the con- 
 traction of the scar tissue. 
 
 The close proximity of the valves to particular structures is 
 an important factor in the ultimate progress of the case. The 
 orifices of the coronary arteries are frequently involved in 
 aortic disease, and the a.v. node and bundle are often damaged 
 in mitral and in aortic lesions. The interference mth the 
 nutrition of the heart produced by the former, and the dis- 
 turbance of the cardiac rhythm entailed by the latter, imprint 
 special characters upon the sj^mptoms of these diseases. 
 
 The Etiology of Chronic Valvular Disease. — There is con- 
 siderable difficulty in determining the precise causes of chronic 
 valvular lesions. More than one cause is frequently active; 
 the effects of different causes are very similar ; the chronicity 
 
266 
 
 DISEASES OF THE HEART 
 
 of the disease prevents accurate observation of its progress ; and 
 the ultimate result depends on the site of the affection rather 
 than on the nature of the cause. 
 
 Chronic valvular disease may follow (1) acute endocarditis; 
 (2) syphihs; or (3) mechanical strain; or may be (4) merely a 
 part of a general cardio-vascular degeneration, or (5) a defect 
 of development. 
 
 Fig. 141. — IMiteal Endocarditis, showing a Large Healed Scar on the Wall 
 OF THE Left Auricle (c/. Fig. 131) (R. I. Museum). 
 
 1. Acute Endocarditis. — A priori it seems probable that a 
 slight acute endocarditis may resolve completely, but patho- 
 logical data are necessarily lacking, and the cHnical evidence is 
 insufficient to prove the point. In the majority of cases the 
 wound heals in course of time, but resolution is imperfect and 
 a scar is left behind, which from the constant movements of 
 the parts, is larger than it would have been if it had been 
 situated on a less mobile site. Necrotic lesions of course 
 cannot be replaced, so that in practically every case of acute 
 endocarditis a valvular defect is left. If the lesion is small, 
 
CHRONIC VALVULAR DISEASE 267 
 
 the mechanical defect may be minimal, but the damage makes 
 the valve more vulnerable, and more liable to be seriously 
 injured by causes which would produce little effect upon a 
 healthy valve. The free margins of the cusps are most 
 -affected, and the lesions may be confined to these parts, or 
 may involve the whole of the cusp. 
 
 2. Syphilis. — The effects of syphihs are only gradually 
 l»eing appreciated at their true value. The specific arterial 
 lesions have but recently been distinguished ; a syphiUtic scar 
 upon a valve closely resembles those produced by other causes ; 
 ^nd the chronic disease can only be recognized by the presence 
 ■of other syphihtic stigmata, though the acute lesions are distinc- 
 tive. These are well shown in Fig. 142. The patches on the 
 ■aorta are characteristic, and the thick yellow nodules upon 
 the aortic and mitral cusps are exactly similar. The damage is 
 more widespread than would appear from mere inspection of 
 the surface ; and the cut surface of the cusp to the left of the 
 •drawing shows a widespread thickening. Syphihtic nodules 
 tend to break down in their centre, and the resultant scar 
 leads to shortening and puckering of the cusps . The valvular 
 ■disease may occur at any stage of the disease, and though most 
 •common as a late sequel, may also obtain comparatively early 
 if treatment is defective. Accurate data are difficult to pro- 
 cure, but in one case where the patient died mth aortic and 
 mitral disease, the symptoms of cardiac distress appeared two 
 years after the chancre, and two years before death. No 
 specific treatment had been undergone. The patient was 
 incKned to athletic exercises, and the symptoms may have 
 I)een accelerated by physical exertion. 
 
 3. Mechanical Strain. — The relations of mechanical injury to 
 chronic valvular disease are equally difficult to assess, though 
 isolated cases have proved beyond doubt that acute lesions 
 may be produced in this way. Sir Cfifford Allbutt* quotes 
 many examples. A healthy man, aged thirty-six, was crushed 
 between a cart-wheel and a post, and died a few days after- 
 wards ; the healthy aortic valves had been torn away from the 
 healthy aorta. A man, aged nineteen, had an aortic cusp 
 ruptured from the free margin to the base by a blow upon the 
 
 * Allbutt's " System," 1909, vol. vi., p. 425. 
 
268 
 
 DISEASES OF THE HEART 
 
 chest. A man, aged twenty, fell from a scaffold and developed 
 well-marked aortic regurgitation. And in a certain number 
 
 Fig. 142. — Syphilitic Aortitis, with Involvement of Aortic and IMitrai* 
 Valves (R. I. Museum). 
 
 of cases the severe strain of some physical exertion has been 
 so rapidty followed b}^ serious cardiac symptoms that the 
 
CHRONIC VALVULAR DISEASE 269 
 
 association seems clear. A porter, for example, who was Kfting 
 a heavy trunk on to a barrow, suddenly became exceedingly 
 breathless, and when I saw him a few days later, was the 
 subject of well-marked aortic regurgitation. No other cause 
 than the strain could be discovered. But such cases are rare, 
 and in most the evidence points to valvular disease being 
 antecedent to the trauma, which produced gross results in con- 
 sequence of some local weakness. 
 
 Two other groups of cases of mechanical strain require con- 
 sideration. In some occupations (moulders, draymen, riveters, 
 et alii) severe physical exertion is constantly undertaken, 
 with, in consequence, high blood-pressure during the period of 
 stress; and in some diseases (arterio-sclerosis, chronic renal 
 disease) the blood-pressure is constantly above normal. The 
 question of the influence of an intermittent or a constant high 
 blood-pressure upon the valves naturally arises. 
 
 There is no doubt that men in arduous employments grow 
 old before their time ; the Clyde shipbuilders are rarely in active 
 work after the age of fifty-five ; and the main damage falls upon 
 the heart and the arteries. But the habits of these men are 
 often loose. Sweating labour is often associated with the con- 
 sumption of large quantities of alcohol; and syphihs and other 
 infections and intoxications not infrequently co-exist ; so that 
 it is difficult to ascertain the exact value of the mechanical 
 factor. 
 
 The influence of intermittent strain can hardh/ be determined 
 by pathological examination, though microscopic haemorrhages 
 and local scars have been found in such cases. A correct 
 appreciation of the frequency of its action can only be 
 gauged by clinical data on the large scale. But there is 
 already much information available with regard to the occur- 
 rence of chronic valvular disease in cases of high blood-pressure, 
 and it has been found that the valves are very frequently 
 damaged. 
 
 The connection between mitral and renal disease was first 
 noticed by Barclay in 1848, and several writers have in the 
 interval investigated the question from post-mortem data. 
 Goodhart found that, of 97 cases of renal cirrhosis, 47 had mitral 
 lesions ; while of 215 cases of (clinically) primary mitral disease, 
 
270 DISEASES OF THE HEART 
 
 31 had. cirrhotic kidneys. Newton Pitt found that, of 542 
 cases of renal cirrhosis, 33 had mitral stenosis, and that 33 per 
 cent, of 115 cases of mitral stenosis had renal cirrhosis. In a 
 series of 335 cases of renal fibrosis (capsules adherent ; surface 
 more or less granular) reported by Fleming and myself,* 60 
 had organic disease of the mitral valve (17"9 per cent.), and of 
 93 cases of mitral disease 60 had fibroid kidneys. It seems 
 certain, too, that the association is not accidental, for in a 
 corresponding series of 807 cases, in which the kidneys 
 were not fibroid, only 33 (4 per cent.) had organic mitral 
 disease. 
 
 The relationship between mitral and renal disease is not 
 always the same. 
 
 1. In some cases it seems clear that the cardiac lesion is 
 primary. A man who died at the age of twenty-one had 
 suffered from chorea at the age of three ; the mitral valve was 
 notably hard and deformed, while the kidneys were only slightly 
 affected. A woman who died at the age of forty-eight had 
 suffered from acute rheumatism at twenty-two; the mitral 
 lesion was extensive and the interstitial nephritis "early"; 
 while a woman who died at the age of thirty-five had had 
 several attacks of acute rheumatism before twenty-eight ; and 
 her kidneys, though granular, were still large. In all three 
 cases the symptoms were cardiac. 
 
 ' It seems improbable that the renal lesion is due to chronic 
 venous congestion as has been suggested, for if that were the 
 case, the liver should suffer as frequently as the kidneys ; but 
 in our series of 93 cases of organic mitral disease, the kidneys 
 were affected in 60 and the liver in but 9. The causes of renal 
 cirrhosis are still unknown, but there is considerable evidence 
 in favour of the view that it may be due to faulty metabolism 
 and the consequent irritation of the kidneys by abnormal 
 substances which are excreted in the urine ; and chronic venous 
 congestion of the digestive organs is extremely likely to derange 
 their proper action, and is not infrequently accompanied by 
 gastro-intestinal catarrh, which will exert its own special 
 action. 
 ^ 2. But in another group of chronic mitral cases the usual 
 
 * Quart. Journ. of Med., 1912, vol. v., p, 309. 
 
CHRONIC VALVULAR DISEASE 
 
 271 
 
 causes of acute endocarditis are conspicuously absent. A 
 woman who died at the age of forty-five would not admit 
 having had any illness whatever before the onset of that which 
 ultimately proved fatal. A woman, aged forty-three, had had 
 measles and scarlatina in childhood, but had always been 
 healthy until a few winters before her death, when she became 
 hable to bronchitis and short of breath on exertion. A man, 
 aged forty-seven, had had no previous iUness, with the ex- 
 ception of an attack of " gastric " fever at the age of fourteen. 
 And there are a small number of cases on record in which 
 mitral stenosis has been observed to develop in the absence of 
 all acute disease (Sansom). It is generally agreed that the 
 most frequent causes of those chronic cases are arterio- 
 sclerosis and chronic nephritis, and in these three cases the 
 kidneys were more or less granular and their capsules were 
 adherent. 
 
 Huchard has outhned the process by which the lesion is 
 produced. The vessels of the valve are frequently degenerate, 
 their lumen is diminished, and minute haemorrhages are not 
 uncommon. As a result the overlying endothelium is lost 
 and fibrin is deposited upon the uncovered surface; and the 
 constant movements of the part produce a " callus " which is 
 large and out of proportion to the original lesion. Kennedy, 
 too, has investigated the point and finds that the basal portions 
 of the mitral cusps are almost always thickened and fibroid in 
 chronic renal disease (Figs. 143, 144, 145). 
 
 It thus seems evident that in some cases the renal lesion is 
 the cause of the mitral one, but it is improbable that this is 
 the common sequence. It is true that the incidence of mitral 
 disease in cases of renal fibrosis is much greater than in cases 
 where the kidneys are normal, but the incidence is much 
 greater in women than in men,* a fact which suggests that the 
 connection often arises in other ways. 
 
 3. Mitral and renal disease may conceivably be due to the 
 same cause, and though actual proof of this association is 
 
 
 Renal Fibrosis. 
 
 Mitral Disease. 
 
 Per Cent. 
 
 Men 
 Women 
 
 201 
 134 
 
 27 
 33 
 
 13-4 
 24-6 
 
272 
 
 DISEASES OF THE HEART 
 
 lacking, the evidence in its favour is suggestive. Newton Pitt 
 and Sansom maintained that acute endocarditis and nephritis 
 might both originate during the puerperium, and so initiate the 
 chronic disease, and Rolleston has suggested that they might 
 result from syphilis. Acute syphihs at the present day rarely 
 causes death, and its real importance as a cause of chronic 
 mischief is apt to be obscured by its chronicity. I have ob- 
 served one case in which both the kidneys and the cardiac 
 
 Fig. 143. — Chronic Renal Disease: Patchy Thickening towards the Base 
 OF the Mitral Valve (R. I. Museitm). 
 
 valves were affected. The patient had contracted a chancre 
 four years before, for which he had not received specific treat- 
 ment. The arteries were extensively diseased, the aortic valve 
 was notably deformed and grossly incompetent, the mitral 
 valve was dilated and the cusps shortened and thickened, and 
 the cortex of the kidneys was slightly atrophied and their 
 surface somewhat granular. Scarlatina, too, is a not infre- 
 quent cause of acute endocarditis and acute nephritis, and 
 might affect the heart and the kidneys simultaneously. 
 
CHRONIC VALVULAR DISEASE 
 
 273 
 
 Some recent papers have thrown a new hght upon the matter. 
 The subacute forms of acute endocarditis from which Horder 
 and Libman have so frequently isolated streptococci are very 
 often accompanied by glomerular changes in the kidneys of 
 embohc origin. An interstitial leucocytic infiltration occurs 
 in the vicinity of the affected tufts, while the tubules are only 
 slightly affected. Most of the patients in whom blood-cultures 
 
 / 
 
 / 
 
 Fig. 144. — Chronic Renal Disease: Diffuse Thickening of the Base, of the 
 MiTKAL Valve (R. I. Museum). 
 
 have been positive have died, and only a few have recovered ; 
 but it seems probable that a mild infection of the same kind 
 is not uncommon, though blood-cultures are negative, and that 
 healing takes place, leaving, however, a chronic valvular 
 defect and a chronic renal lesion.* 
 
 * P. Baehr, Amer. Journ. Med. Sci., 1912, vol. cxliv., p. 317. J. F. Gaskell, 
 Journ of Pathol., 1911-12, vol. xvi., p. 287. E. Libman, Zoc. cit. 
 
 18 
 
274 
 
 DISEASES OF THE HEART 
 
 The association between aortic and renal disease is also 
 striking, and h,as been recognized for many years . MacDonald * 
 has examined post-mortem data upon this point and found that 
 of 200 cases of renal fibrosis, 34 (17 per cent.) had organic lesions 
 of the aortic valve, while in 25 more the valves showed " com- 
 pensatory thickening." Of 32 cases of aortic disease, 25 (78 
 per cent.) had renal fibrosis, which was present in 18 (81 per 
 
 Fig, 145. — Chronic Eenal Disease: Diffuse Thickening in Mitral and Aortic 
 Valves and the Adjacent Endocardium (R. I. Museum). 
 
 cent.) of 22 cases in which both aortic and mitral valves were 
 diseased. 
 
 The varying relationships which exist between mitral and 
 renal disease may also occur between the latter and aortic 
 disease, but it seems probable that the renal lesion is less fre- 
 quently secondary to the cardiac disease. 
 
 4. General Car dio- Vascular Degeneration. — The influence of 
 a generalized cardio-vascular degeneration in the production 
 of chronic valvular disease has been in part considered in the 
 * Glasgoiv Med. Journ., 1914. 
 
CHRONIC VALVULAR DISEASE 275 
 
 preceding paragraphs. No clear distinction can be drawn 
 between the heart and the arteries. The intimal Hning is 
 exactly similar, and the valves are merely a double layer of 
 endothelium enclosing a delicate connective tissue; and in 
 cases of chronic arterial disease comparable lesions are often 
 found on the cusps. The aortic valve suffers most frequently, 
 but atheromatous and calcareous plaques are not uncommonly 
 found on the anterior mitral flap, and presumably own the 
 same causes as the arterial disease. The mitral cusps, at any 
 rate, possess arteries of their own, and any interference with 
 their lumen will necessarily entail defective nutrition of the 
 valves and produce lesions comparable to those which occur in 
 the great vessels from such causes. 
 
 5. Congenital Defects. — Congenital defects of the heart are not 
 common, and though they generally involve the great vessels 
 or the muscular septa, in many instances the valves also are 
 affected. The aortic and pulmonary cusps may thus be more 
 or less numerous than usual, or represented by a diaphragm 
 or a cone-shaped funnel. The orifice may be involved; one 
 vessel may be narrowed and the other widened; or one alone 
 may persist. The defects arise during the division of the 
 truncus arteriosus into the pulmonary artery and the aorta 
 vera. Many such cases have been recorded, but in Abbott's 
 valuable article in Osier's "System" only four examples of de- 
 velopmental malformation of the mitral valve are recorded. 
 It seems almost incredible that the auriculo-ventricular septum 
 is so rarely abnormal, and much more probable that the nature 
 of the defect has not been recognized. It is well known that 
 valves which are congenitally defective are not infrequently 
 attacked by acute endocarditis, and this may so disguise the 
 abnormahty that its real nature is not appreciated. A con- 
 genital defect may be the cause of some of these valvular 
 lesions, which seem to own none of the more usual causes. 
 
 The Causes o£ Aortic and Mitral Disease. — The tables pub- 
 lished by Lockhart Gillespie and by Grant Andrew, showing 
 the age and sex incidence of chronic valvular disease, contain 
 important indications as to its etiology, though the conclu- 
 sions arrived at are only approximately correct, as the figures are 
 
276 
 
 DISEASES OF THE HEART 
 
 merely those obtained at the time of admission to hospital, and 
 show neither the age at which the disease originated nor the 
 age at death, but merely that at which serious symptoms were 
 present. 
 
 Age. 
 
 Aortic. j 
 
 JIlTRAL. 1 
 
 Gillespie. 
 
 Andrew. 
 
 M:wDonald. 
 
 Gille 
 
 -pie. 
 
 Aud 
 
 •ew. 
 
 MacDonald. 
 
 
 M. K. 
 
 M. F. 
 
 M. F. 
 
 M. 
 
 F. 
 
 M. 
 
 F. 
 
 M. F. 
 
 1 to 9 
 
 — 
 
 2 — 
 
 — 
 
 17 
 
 10 
 
 8 
 
 10 
 
 1 1 
 
 10 .. 19 
 
 13 2 
 
 22 5 
 
 6 — 
 
 78 
 
 114 
 
 76 
 
 118 
 
 8 10 
 
 20 ,. 29 
 
 43 15 
 
 44 18 
 
 2 4 
 
 92 
 
 150 
 
 84 
 
 118 
 
 5 12 
 
 30 „ 39 
 
 66 14 
 
 65 17 
 
 11 2 
 
 106 
 
 96 
 
 93 
 
 96 
 
 7 12 1 
 
 40 „ 49 
 
 95 13 
 
 76 14 
 
 12 3 
 
 81 
 
 63 
 
 85 
 
 76 
 
 6 29 , 
 
 50 ,. 59 
 60 .. 69 
 
 70 
 
 |l26 13/ 
 11 
 
 354 57 
 
 48 8 
 
 13 — 
 5 — 
 
 |210 
 13 
 
 86 1 
 4 
 
 75 
 
 37 
 
 1 9 
 
 i 
 
 273 63 
 
 49 9 
 
 597 
 
 523 
 
 465 
 
 468 
 
 29 73 
 
 LocKHAKT Gillespie: Edin. Hospital Reports, 1898, vol. v., p. 293. 
 Grant Andrew: Age Incidence, Sex, and Comparative Frequency in Disease 
 1909. 
 
 The causes of aortic and mitral lesions are evidently different, 
 for while the majority of aortic cases occur after the age of 
 forty, the majority of mitral cases occur before that age; and 
 while aortic disease is much more prevalent in men than in 
 women, mitral disease affects the sexes in approximately equal 
 proportions . The chief incidence of aortic disease in men is after 
 forty ; in women between twenty and fifty. Mitral disease is most 
 c ommon in men in the fourth decade, and in women in the third. 
 
 The causes which we have considered are Hkely to be active 
 at particular periods of hfe. Developmental defects of course 
 occur during intra-uterine life; acute endocarditis is most 
 common in adolescence and in early adult life; syphihs and 
 physical strain in early manhood ; and high blood-pressure and 
 cardio-va^cular degeneration after middle life. Aortic disease 
 in men thus seems likely to be mainly due to the influence of 
 syphilis and physical strain ; while in women acute endocarditis 
 should be an important factor. Mitral disease in men seems 
 likely to be mainly due to acute endocarditis and high blood- 
 ]">ressure and general degenerative changes ; in women to acute 
 endocarditis. 
 
CHRONIC VALVULAR DISEASE 277 
 
 David MacDonald has examined my hospital records from this 
 point of view. The numbers are small (aortic cases, 58 ; mitral 
 cases, 102) and the numerical fallacy must be borne in mind; 
 but no other observations are available, and the conclusions 
 on the whole agree with those deduced from the more general 
 considerations . 
 
 Congenital Defects. — Obvious congenital defects are not in- 
 cluded in his series. 
 
 1. Acute Endocarditis — Aortic Cases. — A history of "rheu- 
 matism " was given in 20 cases (34 per cent.); in 13 it seemed 
 to be clearly acute rheumatism ; in 2 it was described as " grow- 
 ing-pains," in one of which it was associated with chorea; in 
 the other cases its nature was indefinite. In 16 cases other 
 infections were recorded: scarlatina, 6; measles, 3; smallpox, 
 pneumonia, 2 ; typhus fever, influenza, pleurisy, 1 ; but the hst 
 is obviously incomplete. Smallpox, measles, and typhus 
 fever are rarely accompanied by endocarditis, so that the 
 incidence of endocarditis in this series is not Ukely to be 
 greater than 30 (51 per cent.), and in all probability is 
 less . 
 
 Mitral Cases. — A history of " rheumatism " was given in 68 
 cases (66 per cent.) ; in 47 it seemed to be clearly acute rheu- 
 matism; in 9 it was subacute; in 4 it was described as "grow- 
 ing-pains " ; in 1 it was gonorrhceal. Three patients had had 
 chorea, 2 recurring tonsilhtis, and 2 had suffered from muscular 
 rheumatism. In 25 cases other infections are recorded: 
 Measles, 8; scarlet fever, 5; scarlet fever and measles, 5; in- 
 fluenza, 5; typhoid fever and measles, diphtheria, 1. The list, 
 again is obviously incomplete. ^Excluding measles, typhoid 
 fever, and diphtheria, the incidence of acute endocarditis in 
 this series is not hkely to be greater than 83 (81 per cent.), and 
 in all probabihty is less . 
 
 2. Syphilis — Aortic Cases. — In 10 cases (17 per cent.) the 
 patients had suffered from syphilis, but the figures certainly 
 minimize the incidence, as the evidence of the Wassermann 
 reaction shows that the proportion should be larger. Routine 
 examinations have only recently been instituted in my wards, 
 but the test was positive in 9 out of 13 cases ; and in 18 out of 
 
278 DISEASES OF THE HEART 
 
 22 cases collected from the literature.* Aneurism, too, which 
 is so frequently syphilitic in origin, co-existed in 9 of my aortic 
 cases. 
 
 Mitral C'ases. — Syphilis was known to have existed in only 
 1 case. Aneurism co-existed in 1 case. 
 
 3. Mechanical Strain. — No examples of gross trauma occurred 
 in the series. The influence of a continuously high blood- 
 pressure, too, cannot be estimated in aortic disease, for in aortic 
 regurgitation it occurs as a necessary result of the valvular 
 disease, and independently of any associated defect else- 
 where. In mitral disease a high blood-pressure is often present 
 (36 out of 59 cases), but in many cases the evidence points to 
 the elevation occurring subsequently to the onset of the cardiac 
 lesion. In some cases, however, it seems probable that the 
 connection is reversed, and that the valvular flaw is secondary 
 to changes arising elsewhere. The association has already 
 been considered at length on p. 271. 
 
 4. General Cardio- Vascular Degeneration. — The evidence of 
 vascular disease is not infrequently well marked in cases of 
 chronic valvular affections. The brachial arteries are often 
 notably tortuous, and the radials distinctly thickened, and one 
 may be doubtful whether to catalogue a patient as a cardiac or 
 an arterial case. In some the lesions may be very extensive, 
 A man, aged flfty- seven, was admitted into my wards com- 
 plaining of a cough, accompanied by spit, and of great breath- 
 lessness, which had ensued flve weeks previously after a chill. 
 The heart was considerably enlarged, and double aortic murmurs 
 were audible, as well as that of mitral incompetence ; the pulse 
 was notably shotty. The whole of the arterial tree and most of 
 
 
 Cases of Aortic 
 lusuflBcieney. 
 
 W 
 
 assermann Test, 
 Pofcitive. 
 
 *Clough 1 
 Collins and Sachs 2 . , 
 
 .. 9 .. 
 .. 13 .. 
 
 Aortic and Mitral 
 Disease. 
 
 
 .. 6 
 .. 12 
 
 
 5 .. 
 
 
 .. 2 
 
 
 Mitral Disease. 
 
 
 
 
 11 .. 
 
 
 2 
 
 1 Johns Hopkins Hasp. Bull., 1910, vol. xxi., p. 70. 
 
 a Trans. Assoc. Amer. Phys., 1909, vol. xxiv., p. 351. Cf. Longcope, Journ. 
 Amir. Med. Assoc, 1910, vol. liv., p. 118. 
 
CHRONIC VALVULAR DISEASE 279 
 
 the accessible veins were diseased. Skiagrams disclosed a 
 general dilatation of the aortic arch without any localized 
 aneurism; and the temporal, facial, brachial, radial, ulnar, 
 superficial volar, femoral, posterior tibial, and dorsaHs pedis 
 arteries were thickened, tortuous, and hard, though no 
 calcification was apparent on X-ray examination. Ophthalmo- 
 scopic examination showed that the retinal arteries were 
 normal. 
 
 The superficial veins of the legs were large and varicose, and 
 the capillaries were dilated and visible halfway up the legs, the 
 dilatation being maximal in the feet. The veins of the arms 
 were large and tortuous ; and an anastomotic vein as large as a 
 lead pencil crossed the hypogastrium from groin to groin, the 
 flow of blood being from left to right. 
 
 The patient was a moulder by trade, and had been intem- 
 perate in early life, though for a number of years he had been 
 an abstainer ; the Wassermann reaction was frankly positive. 
 His symptoms were only cardiac in part. The right dorsahs 
 pedis, though easily felt, did not pulsate, and several scars on 
 the toes remained as evidence of gangrene which had occurred 
 two years before admission. The oedema which was present 
 on admission w^as trivial in degree and rapidly disappeared, and 
 might quite well have resulted from the varicosity of the veins. 
 Cheyne-Stokes breathing and a copious albuminuria showed 
 that the kidneys were grossly diseased. 
 
 His early symptoms, however, were cardiac. Eive years 
 previously he had strained himseK when at work, and had had 
 to lie up for several weeks on account of breathlessness on 
 exertion, oedema and prsecordial pain; and he had fainted re- 
 peatedly during the intervening years. During his convales- 
 cence in the ward he overexerted himself on one occasion and 
 the oedema recurred, and the liver and the heart became 
 definitely enlarged, so that the cardiac reserve was evidently 
 small. From the general point of view, however, the arterial 
 mischief seemed the essential lesion, the aortic cusps being 
 probably affected as a secondary result. 
 
 One must bear in mind that the presence of arterial disease 
 does not necessarily indicate that the cardiac lesion is its 
 result, for, as already mentioned, renal fibrosis and general 
 
280 
 
 DISEASES OF THE HEART 
 
 arterio-sclerosis are not infrequently secondary effects of 
 chronic valvular disease. The whole history of the case must 
 be investigated and the evidence carefully weighed before a 
 decision is made and a prognosis given, for the primary arterial 
 group are not far distant fromi their end when the cardiac 
 valves have become incompetent, and have, in consequence, 
 a worse outlook than cases in whom the valvular disease is 
 primary. But in both definite arterial damage is always 
 serious, for it may kill rapidly and with but little warning. 
 
 Exact figures as to the incidence of vascular disease were 
 unfortunately not available in this series. 
 
 The special incidence of mitral disease in the female sex 
 between the ages of ten and thirty requires further considera- 
 tion. It occurs at a period of life when acute endocarditis is 
 most frequent, and is thus most likely to be due to rheumatic 
 conditions. Grant Andrew's figures, however, show that acute 
 rheumatism is more common in males than in females at those 
 ages, and there is no evidence that endocarditis occurs more 
 frequently in one sex rather than in the other during acute 
 rheumatism. The explanation is probably to be found in its 
 association with chorea, which is three times as common in 
 girls as in boys.* 
 
 MacDonald's conclusions thus seem to support those which 
 were deduced from more general considerations. Acute endo- 
 carditis is the most common cause of chronic mitral disease. 
 Syphilis and physical stress are probably of almost equal im- 
 
 Age. 
 
 Acute Rheumatism. 
 
 Chorea. 
 
 
 
 
 
 
 Grant Andrew. 
 
 MaoDouald. 
 
 [ Grant Andrew. 
 
 1 
 
 JIacDonald. 
 
 
 M. F. 
 
 M. F. 
 
 i\r. F. 
 
 M. F. 
 
 1 to 9 
 
 7 5 
 
 2 2 
 
 11 45 
 
 2 5 
 
 10 „ 19 
 
 
 
 77 82 
 
 23 23 
 
 46 134 
 
 11 27 
 
 20 „ 29 
 
 
 
 132 95 
 
 31 18 
 
 1 17 
 
 — 2 
 
 30 „ 39 
 
 
 
 69 32 
 
 19 12 
 
 ! 4 - 
 
 
 
 40 „ 49 
 
 
 
 24 19 
 
 6 4 
 
 — 
 
 
 
 50 ., 59 
 
 
 
 13 3 
 
 1 1 
 
 — 
 
 — 
 
 60 
 
 
 
 2 
 
 — 
 
 — 
 
 — 
 
 
 
 
 324 236 
 
 82 60 
 
 62 196 
 
 13 34 
 
CHRONIC VALVULAR DISEASE 281 
 
 portance to acute endocarditis in causing aortic disease. And 
 both aortic and mitral disease may occur in later life associated 
 with chronic renal and arterial disease. The last group may 
 arise in several ways ; from high blood-pressure, from arterial 
 lesions, or from the chronic intoxication which accompanies 
 all chronic renal disease ; all three factors may be active at the 
 same time. 
 
 A special group may be mentioned here. Chronic valvular 
 disease is not uncommon in women who have borne many 
 children, and is often accompanied by renal mischief. It 
 seems probable that in some instances the orgin is to be 
 ascribed to parturition producing coincident lesions in both 
 heart and kidneys. 
 
 In individual cases the cause of the valvular mischief is 
 sometimes obscure, and all the usual factors may seem to be 
 absent. An example was recently brought to my notice by a 
 medical friend whose sister had been found, on a routine ex- 
 amination for insurance, to have well-marked mitral stenosis. 
 Her age was twenty-four, and the most careful investigations 
 failed to ehcit any evidence of antecedent illness beyond a mild 
 attack of measles. She had never suffered from rheumatism, 
 tonsillitis, chorea, or scarlet fever, was httlehable to "colds," 
 and had always enjoyed excellent health. Her general develop- 
 ment and nutrition were, if anything, above the average, and a 
 developmental defect seemed the most probable explanation. 
 In another case, in whom mitral stenosis was discovered at 
 the age of sixteen, the girl had never suffered from any illness. 
 
CHAPTER XXII 
 
 THE SYMPTOMS OF CHRONIC VALVULAR DISEASE 
 
 The symptoms of the various forms of chronic valvular 
 disease differ in their incidence and their degree rather than in 
 their nature, and may conveniently be considered together 
 irrespective of the lesions with which they are most commonly 
 associated. The special significance of particular symptoms 
 will be considered subsequently. 
 
 The Causes o! Symptoms. — Chronic valvular disease is not 
 necessarily accompanied by symptoms of cardiac discomfort, 
 and many individuals with valvular flaws are able to lead lives 
 of average activity without distress. A valvular flaw, of 
 course, imposes an extra strain upon the heart, but compen- 
 satory arrangements are made which overcome the particular 
 difficulty. In aortic stenosis, for example, the lumen of the 
 valve is narrowed, and the flow of blood into the aorta is, in 
 consequence, impeded. But if the ventricle contracts more for- 
 cibly, and the rate of flow through the valve is sufficiently 
 increased, the normal quantity of blood will enter the aorta in 
 the normal period, and the disability will be overcome. Under 
 ordinary circumstances, the heart works at less than half its 
 full power, the reserve being retained to meet the extra strain 
 of physical exertion, and so any small degree of valvular incom- 
 petence is readily compensated. 
 
 The additional work thrown upon the heart causes hyper- 
 trophy of the muscular fibres which are concerned, in exactly 
 the same way that regular exercise causes hypertrophy of the 
 systemic muscles ; so that the additional work is carried on 
 easily and well. But there is a limit to hypertrophy, and even 
 when it is considerable, the power that can be developed is 
 never so largely in excess of that ordinarily required as in a normal 
 
 282 
 
SYMPTOMS OF CHRONIC VALVULAR DISEASE 283 
 
 heart. The reserve is only 30 or 20, or 10 per cent, instead of 
 the normal 50, and what James Mackenzie calls "the field of 
 response " is, in consequence, limited. A man may become 
 breathless, for example, during a hard game of tennis, though 
 able to walk about without discomfort. He may only be able to 
 walk up a flight of stairs which formerly he could run up ; he 
 may only be able to walk quietly on the level; or he may be 
 incapable of any exertion, though perfectly comfortable when 
 seated on a chair. The difference is merely a matter of degree, 
 but the response of the heart to demands for increased activity 
 is more or less insufficient. 
 
 With a stationary lesion of trivial degree and good general 
 nutrition, the field of response may be large and ample, and the 
 patient's disabihties trivial or imperceptible, and many indi- 
 viduals live for years without discomfort. Sir William Broad- 
 bent has recorded the case of a doctor, aged forty, in busy 
 country practice, who had had aortic regurgitation for twenty - 
 six years. Sir William Osier reported the case of a lady, aged 
 sixty-three, who had mitral regurgitation from the age of 
 fifteen, but nevertheless possessed a healthy family of eleven 
 children ! Balfour knew a hale old gentleman of eighty-eight 
 who had had a mitral leak for sixty-six years ! ! And, per- 
 sonally, I know two men, aged forty -four and thirty-four, with 
 well-marked congenital defects, who have never suffered from 
 any cardiac symptoms. 
 
 With a stationary lesion and ample compensation, symptoms 
 then are absent, and continue absent indefinitely; but in the 
 majority of cases they make their appearance in course of time. 
 Their appearance is generally due to the activity of some new 
 factor, originating in the heart itself and affecting the valves 
 or the muscle ; or in some other viscus and producing a disturb- 
 ance of its action which indirectly affects the heart. ^^ 
 
 The valvular lesion may be 'progressive, and the mechanical 
 difficulty may steadily increase. Congenital disease is as a 
 rule associated with so great a disturbance of the circulation 
 that it is incompatible with normal growth. Many of these 
 children die shortly after birth; some survive for a few years, 
 but with stunted growth and imperfect nutrition, and readily 
 succumb to accidental infections. But a congenital defect 
 
284 DISEASES OF THE HEART 
 
 which has not interfered with normal growth or nutrition, 
 and has not produced smy symptoms before adult Hfe is 
 attained, is, in one respect, the valvular lesion which has the 
 best prognosis, for it is one which is not progressive, and in 
 which no recurrence of the causal factor can arise. The de- 
 generative va Ivular lesions associated with widespread arterial 
 disease are, on the other hand, essentially progressive in their 
 nature, and as years pass the defect necessarily becomes 
 greater, and the cardiac reserve becomes smaller and smaller. 
 The lesions which are due to acute endocarditis are interme- 
 diate in their tendency. A rheumatic scar of course contracts 
 for a period of months or 3'ears, but not indefinitely, and an old- 
 standing chronic lesion is, in consequence, a stationary one. 
 But acute rheumatism tends to recur and is pecuharly apt to 
 reinfect damaged valves, so that the cause may again come 
 into action and the lesion may again become progressive. 
 Muscular hypertrophy jnay attain to enormous size (a heart 
 weighing 53 ounces has been recorded), but there is a limit to 
 its development, and a progressive lesion in course of time 
 produces mechanical difficulties which no possible hypertrophy 
 can compensate. With a progressive lesion cardiac failure 
 sooner or later ensues. 
 
 ^^h.e symptoms may be due to failure of the cardiac muscle. 
 An individual's adaptability to his environment is always 
 relative rather than absolute; we cannot add a cubit to our 
 stature; and the most carefully regulated course of physical 
 exercises may fail to produce an athlete if he comes of poor 
 stock. This vital factor is almost incalculable. A long-lived 
 stock means a good family vitaUty, and the heart of a member 
 of such a family is more likely to develop satisfactory hyper 
 trophy, if it is required, than that of one belonging to a family 
 whose members usually die in early life. Muscular failure 
 arises in various ways, and may arise, too, in hearts which 
 have no valvular defect. 
 
 The general nutrition of the patient is always a matter of 
 importance, for the cardiac muscle shares in any general 
 weakness. In mild cardiac failure a vicious circle is often 
 estabhshed. Shght venous stasis occurs, the gastro-intestinal 
 tract becomes congested, digestion and absorption become de- 
 
SY^IPTOMS OF CHROmC VALVULAR DISEASE 285 
 
 fective, the general nutrition and the cardiac nutrition are 
 impaired, and the cardiac insufficiency is augmented. 
 
 The cardiac nutrition alone may be defective. This, too, 
 is of common occurrence, for it is dependent almost wholly 
 upon the integrity of the coronary arteries. And if, as is often 
 the case, the blood-supply is lessened by narrowing of these 
 arteries, at their origin or in their course, the cardiac power may 
 be notably decreased. 
 
 The cardiac rhythm may be disturbed, and all the abnormal 
 rhythms of themselves impose an extra strain. Heart-block, 
 auricular flutter and auricular fibrillation, nodal rhythm, and 
 even extra-systoles, are all injurious. The effects are well 
 seen in parox3^smal tachycardia, in which the heart dilates 
 and the hver swells and oedema makes its appearance in 
 the extremities, if the paroxysm lasts longer than a few^^ 
 hours. 
 
 Extrinsic factors may come into action. They are innumer- 
 able and may act in various ways. The records of athletics 
 contain many examples of a heart strained by severe physical 
 exertion, and even death may result, as in the recent Marathon 
 race at Stockholm. Failure is more likely to occur in a heart 
 whose reserve is lessened b}^ chronic valvular disease, and the 
 exertion need not be great or long-continued. In cases of high 
 blood-pressure, the pressure usualh^ rises as years pass, and 
 the extra strain one day becomes too great for the muscle to 
 overtake. 
 
 The strain may fall upon the right ventricle instead of the 
 left, from some affection of the lungs, bronchitis, pneumonia^ 
 or the Hke; and the strain may be progressive, if progressive 
 emphysema ensues. The right heart, it must be remembered, 
 is already overworked in mitral disease and in affections of the 
 pulmonary and tricuspid valves. . 
 
 Symptoms may succeed a gastro-intestinal upset ^dth its 
 accompanying disturbance of nutrition and its varied intoxi- 
 cations ; an operation ; a mental shock ; or starvation in any 
 form. An acute exacerbation of chronic renal mischief is fre^^ 
 quently the last straw. 
 
 In another group symptoms ensue as a result of the cardiac 
 disease, but yet indirectly. An embolus may be set free from a 
 
286 DISEASES OF THE HEART 
 
 clot in the auricles or on a valve, and a coronary artery may be 
 blocked, or an infarct of the lungs or a cerebral softening may 
 take place, and cardiac failure follow. 
 
 The most frequent symptom in chronic valvular disease is 
 shortness of breath, of which the majority of patients make more 
 or less complaint. It may be frequency of respiration (poly- 
 pncea) or difficulty in breathing (dyspnoea), or associated with 
 distress when lying dowTi, so that the patient is forced to main- 
 tain the upright position (orthopnoea). Cheyne-Stokes or 
 cyclic breathing maj' occur. The distress may only be felt on 
 exertion, or may obtain during rest as well; and not infre- 
 quently is most marked during the night. 
 
 ' Shortness of breath occurs in many diseases. It may be due 
 to anaemia or to disease of the lungs ; it may be associated with 
 abdominal conditions, such as the enlarged uterus of late preg- 
 nancy, which mechanically interfere with the free movements 
 of the diaphragm; or may be the result of toxaemia. Com- 
 parable causes may be active in cardiac disease. Some patients 
 are notably anaemic. The weakness of the left heart may be 
 so great that systemic ischaemia ensues even on trivial exertion. 
 The lungs are often more or less engorged and pulmonary 
 oedema is the rule, if the failure is well marked ; bronchitis and 
 emphysema often co-exist ; and an infarct or pleural effusion 
 may add to the respiratory difficulties. An enlarged liver 
 or ascites may hinder the movements of the diaphragm. Asso- 
 ciated renal or hepatic disease may produce toxaemia. 
 \^ It is important to recognize in each individual case the par- 
 ^ ticular factor that is in action, and this is usually easy if a 
 routine examination is made, for the signs of bronchitis, pul- 
 monary oedema, ascites, etc., are distinctive. Toxic causes 
 may occasion difficulty, for chronic renal disease of the cirrhotic 
 type is not invariably accompanied by albuminuria; which, 
 conversel}", may be merely the result of chronic venous conges- 
 tion. The blood-pressure is here a useful guide, for it is not 
 elevated in simple valvular disease, save in cases of aortic 
 regurgitation, so that a high blood-pressure indicates the 
 existence of some extra-cardiac comphcation, such as arterial 
 or renal disease, and so, most frequently, defective ehmination. 
 
FlU. 140. — BuiCIItAL AND KE31'L 
 
 'URVES IN GhEVNE-StOKES IJRBiTniNa, SdOWING VARIATIONS IN THl:; PeILSE-RATE. 
 
 The two uurvus, however, do uot cuiacido. 
 
SYMPTOMS OF CHRONIC VALVULAR DISEASE 287 
 
 The character of the respiratory distress, too, is important, for 
 paroxysmal dyspnoea is always toxic in origin ; while orthopncea, 
 in the absence of gross pulmonary or abdominal mischief, owns 
 a similar cause. 
 
 In the typical form of Cheyne-8tokes breathing periods of 
 apnoea and dyspnoea alternate. The respirations, at first weak 
 and infrequent, gradually become deeper and more numerous, 
 and then gradually wane until respiration wholly ceases. The 
 alternation is sometimes incomplete, and no real apnoea occurs, 
 though periods of weak infrequent breathing alternate with 
 periods during which it is full and frequent. Similar variations 
 may occur in the pulse-rate, which is generally more rapid 
 during apnoea, but the respiratory and pulse variations do not 
 coincide exactly, though they exhibit similar curves (Fig. 146); 
 and the relationship may be reversed, so that the pulse-rate is 
 more frequent during dyspnoea; it is often unchanged. A 
 " pulsus alternans " may occur during dyspnoea, if the respira- 
 tions number half the pulse-rate (Fig. 97); the smaller beat 
 occurs at the maximum of inspiration. 
 
 The periods of apnoea vary in duration and may last for a 
 second or two, or for nearly half a minute or even longer. If 
 the period is long, the patient often becomes unconscious 
 and may close his eyes and cease talking, individual muscles 
 may twitch, and, rarelj^, general convulsions occur. In the 
 lesser degrees the intelligence may be unimpaired. If the eye- 
 lids remain open, the size of the pupils may be seen to vary ; they 
 usually contract during apnoea, and dilate during dyspnoea ; 
 but the phenomenon is inconstant and variable. 
 
 Cheyne-Stokes breathing is most frequently noticed at night, 
 though it may be continuous ; and in many cases the patient is 
 greatly distressed, for as soon as he goes to sleep the period- 
 icity is exaggerated and apnoea prolonged, and at the end of 
 each period he wakens up in distress, covered with profuse 
 perspiration, and may have to sit up in bed to recover his 
 breath. In the lesser grades symptoms maj^ be absent. In 
 some cases the breathing is periodic or cycHc, the waxing and 
 waning of the typical Cheyne-Stokes paroxysm being absent, 
 the patient merely ceasing to breathe for a few seconds at more 
 or less irregular intervals. 
 
288 DISEASES OF THE HEART 
 
 Paroxysmal attacks of breathlessness occasionally occur. 
 They are most common at night, the patient as a rule suddenly 
 awakening from sleep in an access of intense dyspnoea, which 
 necessitates his sitting bolt upright in bed. Expiration is 
 prolonged, and the chest is full of rhonchi. After an interval 
 of some duration (minutes to hours), relief is obtained, but 
 some orthopnoea generally persists. The attacks tend to recur, 
 and the distress may be so great that the patients are afraid to 
 go to sleep, 
 
 A cough and spit are not uncommon. The cough is usually 
 accompanied by spit, and due to a slight catarrh, or oedema of 
 the lungs ; but it is sometimes an isolated symptom and may be 
 extremely troublesome. The sputum may be of varied kind; 
 mucoid or muco-purulent from catarrh; watery and perhaps 
 copious in oedema of the lungs, when a spittoonful or more may 
 be expectorated in twenty -four hours ; or haemorrhagic . Haemop- 
 tysis in chronic mitral disease is verj^ seldom due to pulmonary 
 phthisis. In mitral stenosis it occasionally occurs from capil- 
 lary rupture when the congestion of the vessels is extreme; 
 aud several ounces may be voided. As a rule it ceases quickly, 
 though it may recur, and the patient is conscious of improve- 
 ment in his general condition. In one of my patients, a girl 
 who had been sent to a sanatorium from an error in diagnosis, 
 the relief was so distinct that she welcomed the recurrence of the 
 haemorrhage. In the other valvular lesions simple rupture is 
 unusual, and the most common cause of blood in the sputum 
 is a pulmonary infarct. The bleeding in this case is not accom- 
 panied by relief, but rather by an exaggeration of the symp- 
 toms, and the breathlessness may be suddenly intensified and 
 accompanied by pain in the side from associated pleurisy. The 
 physical signs of a consolidation are usually apparent on ex- 
 amination. The prognosis is always serious, for a pulmonary 
 infarct is evidence as a rule of gross stasis in the right auricle, 
 and is thus the accompaniment of a considerable failure of 
 compensation, and is hkely to occur towards the end of the 
 iUness ; but in exceptional cases a fair recovery may ensue and 
 persist. 
 
 Cough without spit is by no means common. Sir William 
 Osier has reported some cases of mitral stenosis with laryngeal 
 
SYMPTOMS OF CHRONIC VALVULAR DISEASE 289 
 
 palsy, in which the recurrent laryngeal nerve was pressed upon 
 by the dilated right auricle ; in some cough was persistent. 
 
 Cardiac discomfort or pain is frequently experienced. The 
 most common complaint is of palpitation, the patient becoming 
 conscious of the cardiac contractions as a fluttering or throbbing 
 sensation within the chest. 
 
 Palpitation, of course, obtains in healthy individuals under 
 the stress of severe physical exertion or deep emotion; and is 
 not unusual in other persons whose cardiac work is carried on 
 easily and well; its most common cause is gastric flatulence. 
 But its occurrence without obvious cause is always a matter of 
 importance, and calls for a detailed examination of the heart. 
 In cardiac disease it may be due to several causes. It occurs 
 on slight exertion in cases where the cardiac work is being 
 carried on with difficulty. The disability is generally apparent 
 in other ways as well, and a mild degree of cyanosis or oedema, 
 an enlarged and tender liver, or a frequent pulse-rate, are 
 obvious on examination. Palpitation of this kind is most 
 common in patients with large hearts, in particular those asso- 
 ciated with renal disease, arterio-sclerosis, and aortic regurgita- 
 tion. In the latter case the arterial pulsations may be very 
 forcible and the patient's head may shake visibly with each 
 pulsation ; and I have even felt the bedstead on which a pn tient 
 was lying shake with each beat of the heart. 
 
 In other cases palpitation occurs even when the patient is at 
 rest, and is then most often due to a disturbance of the normal 
 rhythm of the heart. The occurrence of an extra-systole may 
 thus be apparent, the individual being conscious either of the 
 long pause — the intermission — or of the strong post-extra- 
 systolic contraction. More rarely the extra-systole itseK is 
 felt. But in many cases, particularly if extra-systoles are 
 frequent, or if the post-extra-systolic pause is short, the patient 
 may be unaware of the irregularity. Palpitation is usual in 
 auricular flutter, auricular fibrillation, nodal rhythm, and 
 heart-block, the irregularity in the force of the ventricular 
 contractions in the second, and the shock of the auricular con- 
 traction when the auriculo- ventricular values are shut in the 
 others, being perceptible. The palpitation of the tachycardia 
 
 19 
 
290 DISEASES OF THE HEART 
 
 of exophthalmic goitre maj" be due to a similar cause ; for when 
 the pulse is very frequent, ventricular diastole is of short dura- 
 tion, and auricular contraction may ensue before the preceding 
 ventricular systole is ended. 
 
 Palpitation is most common when the cardiac action is fre- 
 quent, and is comparatively rare when the pulse-rate is below 
 normal. In full heart-block, however, occasional beats may 
 be felt, presumably when auricle and ventricle happen to con- 
 tract simultaneously. 
 
 / Pain may be occasioned in several ways and may be referred 
 to various situations. Epigastric pain of a dull, aching char- 
 acter, intensified by pressure and often by the ingestion of 
 food, is usually associated with a large congested liver, which 
 can easily be felt upon palpation ; and somewhat rarely may be 
 due to cholecystitis, which occurred in a patient who was 
 recently under my care for severe cardiac failure. Embolism 
 often occasions abdominal pain, which may be very severe. 
 The most common cause is embolism of the spleen, in which 
 case the pain is generally referred to the left side, and friction 
 may be audible on auscultation; but the pain may be general. 
 A woman, aged forty-six, who had suffered from symptoms of 
 mild cardiac failure for a couple of years, was one day seized, 
 without obvious cause, with griping abdominal pain, which 
 was so severe that she fell down upon the floor and was unable 
 to move until her husband came home from work five hours later 
 and lifted her into bed. The only obvious cause on 'post-mortem 
 examination was a splenic infarct. In another patient who 
 was already in hospital, abdominal pain of severe character 
 suddenly ensued when he was lying quietly in bed, and re- 
 quired the administration of morphia ; the stools on the next 
 day contained blood in large amount. Post-mortem examina- 
 tion revealed a blocked mesenteric artery with necrosis of 
 several feet of the small bowel, and general peritonitis. 
 
 Thoracic pain also owns several causes. It may be due to 
 pulmonary infarct and pleurisy, and is then usually referred to 
 the side of the chest.^ It may be due to pericarditis, and is then- 
 prsecordial in site. It may be paroxysmal and of anginous 
 type, preecordial in site, but often spreading to the head and 
 arms. A clear distinction should be drawn between con- 
 
SYMPTOMS OF CHRONIC VALVULAR DISEASE 291 
 
 tinuous and paroxysmal pain, for the former is almost always 
 associated with a gross visceral lesion, while the latter may be 
 due to functional disturbance. 
 
 The degree of thoracic discomfort varies considerably in 
 different patients. In some the complaint is frequent, but the 
 distress is probably trivial, and no objective evidence of cardiac 
 weakness may be apparent. A choking sensation, a short bout 
 of palpitation, or a sense of constriction round the chest, may 
 thus be called pain by some individuals, while in others Httle 
 reference is made to discomfort, and complaint is made of pain 
 alone. 
 
 Cardiac cedema contrasts with that of renal disease in being 
 most marked in the lower extremities, and first noticed in the 
 evening, if the patient has been walking about during the day ; 
 and minimal in the morning, after he has been lying flat in bed. 
 (Edema may be considerable without attracting the attention 
 of the patient. The rapid variations in the weight of cardiac 
 patients from time to time is generally due to fluctuations in 
 the amount of fluid in the subcutaneous tissue, and a stone's 
 weight may be present without any very obvious signs. In 
 patients who are confined to bed, the sacrum and the back of 
 the thighs may be oedematous, if they are the most dependent 
 parts, though the shins scarcely pit. 
 
 The oedema spreads upwards and may involve the scrotum 
 and the serous sacs. Q^]dema of the prepuce may interfere 
 with micturition, but the difficulty can always be temporarily 
 overcome by firm pressure on the foreskin with the fingers. 
 Pleural effusions, on the right side more frequently than on the 
 left, are perhaps more common than ascites, but ascites may be 
 missed if the patient is orthopnoeic, for the pelvis can contain 
 a considerable quantity of fluid without any obvious signs of 
 its presence. Pleural effusion may occasion considerable 
 respiratory distress even when the amount is small. 
 
 In a general way the oedema and effusions steadily increase 
 from below upwards, and any deviation from the rule indicates 
 the activity of some new factor. Pleural adhesion, for instance, 
 may prevent pleural transudation, and should be suspected, 
 if one pleural cavity is full and the other empty; and thepres- 
 
294 DISEASES OF THE HEART 
 
 lution, may all occur. Many patients complain of constant 
 throbbing in the head ; this is most frequently associated with 
 aortic regurgitation. Headache and insomnia are often accom- 
 panied by paroxysmal dyspnoea or by orthopnoea, and are 
 usually due to toxaemia and associated with a high blood- 
 pressure. Mental symptoms may obtain; cases with nocturnal 
 dyspnoea often suffer from disturbing dreams, which may 
 appear as real occurrences during their waking hours ; or may 
 be mildly dehrious or stupid. Acute mania is rare; dementia 
 is not uncommon, but is most usually associated with evidence 
 of organic cerebral disease. 
 
 The Symptoms of Mitral Disease. — It is impossible to draw 
 a sharp chnical distinction between mitral stenosis and mitral 
 regurgitation. Their causes are similar — acute endocarditis 
 in early life and chronic endocarditis in later years — and both 
 are frequently associated with chronic arterial and renal 
 disease. Regurgitation, however, owns one cause which is 
 pecuhar to itself. The orifice of the mitral valve is large, 
 while the cusps are relatively smaU and quite incapable of 
 closing the aperture unless it is narrowed by the contraction 
 of the sphincter muscle. In anaemia and in debility from any 
 cause, this sphincter action may fail, and a temporary "func- 
 tional " mitral reflux ensue. A comparable reflux may also occur 
 in cases of aortic valvular disease or high blood-pressure, where 
 a special strain is thrown upon the left ventricle. The presys- 
 toUc murmur is always a sign of organic valvular disease, but the 
 systoHc murmur may be due to a temporary and curable cause. 
 
 In the majority of cases of organic valvular disease stenosis 
 and incompetence co-exist, though the degree of each varies in 
 individual cases, the stenosis being sometimes considerable 
 and sometimes trivial; and vice versa. In many cases a double 
 murmur is present, but in others one alone persists, and an 
 accurate diagnosis may be impossible during life. Thus, in 
 auricular fibrillation, the characteristic crescendo murmur dis- 
 appears mth the cessation of co-ordinate auricular contrac- 
 tion ; and it also fails when, as in nodal rhythm and heart-block, 
 the auricular contractions do not regularly precede the ven- 
 tricular contractions. The presystohc murmur, too, may 
 alone obtain in cases where post-mortem the mitral orifice is 
 
SYMPTOMS OF CHRONIC VALVULAR DISEASE 295 
 
 found to be patent, and the cusps so stiff and hard that it 
 seems impossible that it could ever have been closed. Re- 
 gurgitation in these cases is prevented by the high blood- 
 pressure within the auricle, which is raised by the contraction 
 of the right ventricle to such a height that blood can only flow 
 slowly, if at all, from left ventricle to left auricle during ven- 
 tricular systole, and too slowly to produce an audible murmur. 
 The presystolic murmur is the one that most often disappears, 
 and my own experience agrees with that of Graham Steell,* 
 who states that " the murmur most frequently present in 
 cases of mitral stenosis is unquestionably the murmur of 
 coincident incompetence." 
 
 In both lesions the pulmonary blood-pressure is high. In 
 stenosis the elevation is continuous, for the obstruction at the 
 mitral valve necessarily remains constant. In regurgitation, 
 on the other hand, the elevation is intermittent, for though, 
 when the ventricles are in systole, the left auricle is distended 
 by blood flowing into it from the left ventricle and the pul- 
 monary veins, the congestion is rapidly relieved when diastole 
 succeeds, as no obstacle is now presented to the free flow of 
 blood into the left ventricle ; and the auricular blood-pressure 
 in consequence rapidly falLs. Dilatation of the left auricle is 
 for this reason as a rule more extreme in cases of stenosis, and 
 clots in the auricular appendages are more common, and em- 
 bolic phenomena more frequent. 
 
 In mitral incompetence the left ventricle is dilated and hyper- 
 trophied. During ventricular systole the left auricle is dis- 
 tended by blood flowing into it from the left ventricle and the 
 pulmonary veins, and the left ventricle, in consequence, receives 
 during diastole a larger amount of blood than normal. The 
 larger complement, too, is necessary if compensation is to be 
 sufficient, for a normal amount of blood in the left ventricle 
 would be insufficient to supply the aorta with its proper amount, 
 if some of the blood regurgitated at the same time into the 
 left auricle. Mitral stenosis, on the other hand, has no effect 
 upon the left ventricle, but only on the left auricle and the 
 right ventricle ; and left ventricular hypertrophy, when it obtains, 
 is due to other causes, aortic valvular, arterial, or renal disease. 
 * " Diseases of the Heart," Manchester, 1906. 
 
296 DISEASES OF THE HEART 
 
 The onset of symptoms may be gradual or abrupt. The 
 slighter s^^mptoms are often insidious, but those which bring 
 the patient under observation as a rule ensue more or less 
 suddenly. Thus in MacDonald's series the onset was gradual 
 in 36 cases, and more or less sudden in 66. 
 
 In the exceptional case the symptoms may arise with 
 dramatic abruptness, A woman, aged forty-three, had ex- 
 perienced shght breathlessness and palpitation on exertion for 
 some years, but of so trivial a degree that she paid no attention 
 to the discomfort and sought no advice. One morning her 
 husband, on awakening, discovered that she was unable to 
 speak and could not move the right arm or leg. On post- 
 mortem examination a large cortical softening was found in 
 the left cerebral hemisphere, and weU-marked mitral stenosis. 
 The embolus was evidently derived from clots in the left 
 auricle. Such a course of events is, however, uncommon, but 
 serious symptoms may arise within a few days. A man, aged 
 forty-six, a foreman with a firm of horse-dealers, took a ship- 
 load of horses to Canada for sale. On September 21 he ran 
 the horses in the show-yard without discomfort. He imme- 
 diately sailed for home, but on the voyage bad weather was 
 encountered, and on the 27th his cabin was flooded. Bron- 
 chitis ensued, and two days later his legs were cedematous. 
 On admission to hospital the cardiac failure was extreme, but 
 he made a good recovery. The bronchitis had overtaxed a 
 right heart already strained by a double mitral lesion. A 
 woman, aged thirty-five, who had always been healthy save 
 for an attack of acute rheumatism at the age of twenty, 
 noticed that her feet were swollen after the sixth month of her 
 fourth pregnancy. Labour was difficult and prolonged, and 
 chloroform was administered; she lost a considerable quantity 
 of blood. The oedema rapidly disappeared, and she felt quite 
 well when she rose from bed on the ninth day after dehvery, 
 but it returned within a week, and steadily increased in 
 amount, and she became Yevy short of breath, even while at 
 rest. The failure continued, and she died some months after- 
 wards. The strain of pregnancy and a post-haemorrhagic 
 anaemia had occasioned the failure of compensation. 
 
 The onset may be gradual. A httle wizened old woman 
 
SYMPTOMS OF CHRONIC VALVULAR DISEASE 297 
 
 enters my wards every few montiis suffering from extreme 
 general weakness and considerable oedema. She has a well- 
 marked presystolic murmur. Improvement is always rapid, 
 and in a month or six weeks she has gained a stone in weight 
 and feels in excellent health. But she drinks heavily, and after 
 a few weeks invariably loses her employment and is half 
 starved ; and the symptoms slowly recur. 
 
 The onset of symptoms may be determined by various 
 causes. Twenty-two of MacDonald's cases were admitted to 
 hospital on account of other diseases (acute rheumatism, 
 II; influenza (?), 6; scarlatina, gonococcic arthritis, pleurisy, 
 gastritis, ruptured pyloric ulcer, 1). In 13 cases symptoms 
 foUowed exposure to cold and chill, and in 10 cases child- 
 birth, and in 2 more arose during pregnancy ; in 5 they suc- 
 ceeded exertion (a " flitting," a game of football, a dance). 
 Starvation, angina pectoris, the shock of a husband's iUness 
 and death, the extraction of several teeth, etc., are included 
 in his list. 
 
 The Symptoms o! Aortic Disease. — In aortic, as in mitral 
 disease, it is impossible to draw a sharp distinction between 
 stenosis and incompetence, for the two lesions frequently co- 
 exist, though the degree of each varies in individual cases. 
 In a general way incompetence is much more common than 
 stenosis, and the more serious fault; but, whenever the cusps 
 are stiffened, their mobihty is lessened and the orifice is shghtly 
 narrowed, and double murmurs are, in consequence, audible; 
 even trivial vegetations, too, may produce a systohc murmur. 
 
 The diastohc murmur is almost always a sign of organic 
 disease of the valves, or at am' rate of permanent incom- 
 petence, for though it may occur without any lesions of the cusps 
 from dilatation of the aortic orifice, the connective and elastic 
 tissues of the wall, when once stretched, never regain their 
 former condition. 
 
 These cases are uncommon, but my colleague. Dr. George S. 
 Middleton, recently showed me a specimen from a patient 
 who had died in his wards . The valve was grossly incompetent 
 to the water-test, but the cusps were only shghtly thickened 
 and were not retracted, though they were quite incapable of 
 closing the greatly dilated orifice. The ascending aorta, too, 
 
298 DISEASES OF THE HEART 
 
 was dilated, the walls being affected by an advanced syphilitic 
 aortitis . 
 
 In a few rare cases, however, the murmur may be incon- 
 stant, and this may occur both in acute endocarditis and in 
 chronic degenerative lesions . In the former case large vegeta- 
 tions may temporarily stop the leak; in the latter the leak 
 may be minimal for a time. The loudness of a murmur 
 depends upon two factors — the rapidity of the blood-current 
 and the nature of the valvular fault; and may vary from 
 variations in the first factor, though the second remains con- 
 stant. An old man who was attending my out-patient clinique 
 had at one time a diastolic murmur which was only audible 
 immediately after exertion; it disappeared after ten minutes' 
 rest. In the course of some months the murmur was con- 
 stantly present, and as the other symptoms increased he was 
 admitted into hospital and put to bed. Two days later the 
 murmur was absent so long as he was in the recumbent position, 
 though it reappeared whenever he stood erect. 
 
 With physical exercise the blood-pressure rises, and the 
 difference between the blood-pressures within the aorta and the 
 left ventricle during ventricular diastole is, in consequence, 
 increased. The backward flow may now be sufficiently rapid to 
 produce an audible murmur, though during rest the pressures 
 approximate, the rate of flow lessens, and the murmur dis- 
 appears. In this patient, as the incompetence progressed, 
 the murmur became audible whenever gravity was in action 
 and the difference in pressure was augmented, though it was 
 absent when the patient was recumbent. 
 
 An inconstant murmur as a rule in time becomes constant, 
 but a few cases have been recorded in which the murmur has 
 never returned. The explanation is difficult to understand. 
 In a still more rare group the diastolic murmur may be absent, 
 though post-mortem the valve is stenosed, and the cusps so 
 stiff and hard that it seems certain that the orifice was always 
 open, while to the water-test it is markedly incompetent. 
 
 The normal blood-pressure within the aorta is considerable 
 (100 to 130 mm. Hg), while the aortic cusps are thin and 
 fragile, and it has been suggested that they are of themselves 
 insufficient to prevent leakage, unless supported on the ven- 
 
SYMPTOMS OF CHRONIC VALVULAR DISEASE 299 
 
 tricular side by the apposition of the subjacent muscle. If 
 the aortic bulb is dilated, the support fails, and regurgitation 
 ensues. With recovery the muscular pads resume their 
 function, and the leak is stayed ; while, conversely, in valvular 
 disease the muscular mechanism may be sufficient to prevent - 
 regurgitation. Keith considers that though the subaortic 
 musculature does contract and narrow the lumen during the 
 systole of the ventricles, its contraction ceases during diastole, 
 and that it can have little if any effect in preventing regurgita- 
 tion at this period of the cardiac cycle. Stewart, however, 
 maintains that the musculature of the aortic conus enters into 
 contraction later than the rest of the ventricular muscle, and 
 remains contracted during the early part of diastole, thus 
 affording the aortic cusps efficient support until the intra- 
 ventricular pressure rises, with the influx of blood from the left 
 auricle, to such a height that regurgitation can only be minimal. 
 The systoMc aortic murmur, on the other hand, is by no means 
 definite evidence of aortic stenosis. It is often present when 
 the cusps are merely hard and stiff or coated with small vegeta- 
 tions in such trivial degree that little obstruction can obtain, 
 and frequently occurs in anaemia or debihty, and disappears as 
 soon as the general condition is improved. In fact, as an 
 isolated sign, it is more frequently associated with a normal 
 than with an abnormal valve. 
 
 The effects of aortic valvular disease are at first confined to 
 the systemic circulation and to [the left ventricle. In stenosis 
 the lesion hinders the entrance of blood into the aorta and 
 tends to produce systemic anaemia ; in incompetence the blood 
 enters the aorta readily during systole, but re-enters the ven- 
 tricle as soon as diastole succeeds ; the systemic anaemia is 
 intermittent. In stenosis the lesion tends to lower the blood- 
 pressure, though, as a matter of fact, it is generally high from 
 associated arterial and renal disease. In incompetence the 
 blood-pressure is necessarily elevated as a result of the in- 
 competence ; for if the mean blood-pressure within the aorta 
 is to be maintained, the initial pressure must be above the 
 normal to compensate the rapid fall which occurs during the 
 early part of diastole. The variations in pressure may be 
 
300 
 
 DISEASES OF THE HEART 
 
 large if the leak is great, and the pulse-pressure (the difference 
 between the systolic and diastolic pressures) is an accurate 
 index of the degree of the mechanical fault (Fig. 147). Some of 
 the symptoms — the throbbing in the head, palpitation, etc.- — are 
 the result of this sudden variation of the arterial blood-pressure. 
 
 '******, 
 
 ' O <9 rvx >v, . 
 
 Fig. 147. — Blood-Pressuke Chart: Aortic Regurgitation. 
 
 The pulse pressure (55 mm.) exceeds the diastolic pressure. Note the large shotty 
 
 pulse. 
 
 Aortic stenosis is compensated by ventricular hypertrophy, 
 but in incompetence the ventricle must be larger than normal 
 as well as hypertrophied ; for if the normal amount of blood is 
 to be left in the arteries at the end of diastole, the amount 
 thrown into them during systole must be greater than normal 
 to compensate the loss which occurs during diastole. In aortic 
 reflux the left ventricle may be very large. 
 
SYMPTOMS OP CHRONIC VALVULAR DISEASE 301 
 
 The strain of aortic lesions is thus thrown primarily upon 
 the left ventricle, and as long as it is able to do its work, symp- 
 toms are in abeyance. But if the work required is more than 
 it can undertake, it dilates under the strain, the sphincter 
 muscle of the mitral valve fails to close the orifice, mitral 
 reflux occurs, and the symptoms of an engorged pulmonary 
 circulation are superadded to those of the original lesion. In 
 the majority of aortic cases the onset of serious symptoms is 
 synchronous with the onset of mitral reflux, and in great 
 measure its result, and aortic and mitral disease thus produce 
 symptoms of the same type, though they vary in their incidence 
 and in their degree. In mitral disease symptoms ensue when 
 the right heart fails ; in aortic disease when the left heart fails. 
 
 Aortic disease is associated with arterial and renal lesions 
 with even greater frequency than is the case in mitral disease, 
 and the symptoms which obtain are often only partly due to 
 the cardiac element. Their onset may be gradual or sudden, 
 but is most often the former, being sudden in only 15 of 
 MacDonald's series of 58 cases. In some cases they suc- 
 ceed some physical exertion, as was the case with a man, 
 aged fifty-three, in active business, whose aortic valves were 
 known to have been incompetent for two years, though no 
 evidence of cardiac weakness had been shown, and who had a 
 serious faint as the initial symptom after a hard day's work in 
 hot weather. In another case, an engineer aged twenty-five, 
 whose valvular disease had been recognized for several years 
 but had not interfered with his occupation, hemiplegia suddenly 
 ensued when he was running to overtake an uncle whom he 
 saw walking in front of him. Sometimes the symptoms follow 
 a pulmonary catarrh, as was the case with a man, aged forty- 
 seven, who became notably breathless during an influenzal 
 attack, though the evidence of pulmonary disturbance was 
 trivial. And sometimes they arise without evident cause. A 
 man, aged sixty, who had not been looking well for some 
 months according to his medical attendant, whom, however, 
 he had not consulted, took a hot bath one night at 10 p.m. 
 At midnight, when lying quietly in bed reading, he suddenly 
 became extremely breathless and had to sit up in bed. The 
 dyspnoea passed off in ten minutes, but from that time he was 
 
302 DISEASES OF THE HEART 
 
 always conscious of his heart's action as a constant throbbing 
 within the chest. 
 
 The early symptoms, when the onset is insidious, are also 
 often associated with physical exertion. A man, aged forty- 
 six, for instance, who was accustomed to hard physical exercise, 
 admitted that he had been getting more short-winded than he 
 used to be for a year before the symptoms really troubled him. 
 
 Symptoms may, of course, occur without obvious cause. A 
 farmer's wife, aged sixty, who had always been healthy and 
 active, save for an attack of scarlatina at the age of twenty, 
 and blood-poisoning from a prick of the finger at forty-four, 
 noticed in the spring of 1909 that her feet were often swollen 
 at night, and that she became short of breath on trivial exer- 
 tion; but she was able to continue her work notwithstanding 
 her discomforts. In the spring of 1910 the symptoms became 
 exaggerated, and she was forced to take to bed and to seek 
 medical advice. The aortic lesion was progressive, and the 
 symptoms, in consequence, became more serious. 
 
 The onset of symptoms may be due to various causes, 
 but is most frequentty insidious (43 out of 58 cases). In 
 MacDonald's series 5 patients ascribed their illness to ex- 
 posure and chill; 5 were admitted suffering from acute 
 rheumatism; 2 were suffering from notable distress in 
 breathing, which had ensued suddenly when they were at 
 work; 3 were admitted unconscious, 1 after an epileptic fit, 
 and 1 hemiplegic. The modes of onset thus contrast with 
 those of mitral disease, a fact which is to be related to the 
 difference in the incidence of their various causes. In aortic 
 cases these causes are as a rule progressive in their nature, 
 while from the proximity of the coronary arteries to the valve 
 these vessels are extremely apt to be abnormal, and the 
 nutrition of the cardiac muscle suffers in consequence. A 
 rheumatic scar on a mitral valve may cease to contract, and 
 rarely affects the coronary arteries. 
 
 The Symptoms o5 Mitral and Aortic Disease. — The symptoms 
 of mitral disease are most often respiratory, and ninety-one of 
 MacDonald's series complained more or less of breathlessness. 
 In mitral disease the pulmonary circulation is always con- 
 gested, and the normal respiratory activity is impeded ; mitral 
 
SYMPTOMS OF CHRONIC VALVULAR DISEASE 303 
 
 patients are often cyanosed. Bronchitis is a frequent com- 
 plication, and occurred in 39 cases. It may, as already men- 
 tioned, originate sj-mptoms, and in their presence always 
 intensijQes the distress. One of my chronic hospital patients 
 with mitral disease and auricular fibrillation was quite com- 
 fortable and able to do light work so long as his chest was clear, 
 but had serious cardiac failure whenever he contracted a cold 
 in the chest. 
 
 Pulmonary infarct and haemoptysis are common in mitral 
 disease, and occurred in 18 cases. Twenty patients were 
 orthopnceic; in 10 the breathing was difficult; in 3 the 
 dyspnoea was spasmodic and paroxysmal. Orthopnoea is 
 generally accompanied by abdominal distension (due to flatu- 
 lence or ascites) or by an enlarged Hver. The upright position 
 relieves the pressure upon the diaphragm and permits a greater 
 excursion. Dyspnoea is frequently associated with auricular 
 fibrillation, which was present in 19 cases. It may of course 
 be due to other causes, but the sterno-mastoid muscles 
 are almost always habitually in action whenever the pulse is 
 permanently irregular. 
 
 In aortic disease shortness of breath is also the most common 
 symptom, and was present in 54 cases of MacDonald's 
 series. It is not, however, related so closely to passive venous 
 congestion of the lungs as in mitral disease, for this is minimal 
 or absent unless the ventricle dilates and the mitral valve 
 becomes incompetent. Puhnonary embohsm is unusual, and 
 did not occur in this series, so that death seems to occur before 
 any considerable strain is thrown upon the right heart. Short- 
 ness of breath is frequently due to bronchitis, which was 
 present in greater or less degree in 37 cases ; and may also 
 result from systemic ischsemia, being then experienced on 
 exertion. This result is more hkely to foUow if, as is often 
 the case, the patient is anaemic. The degree of anaemia 
 is rarely considerable, but in one case the red ceUs only 
 numbered 2,000,000, with a haemoglobin value of 35 per cent. 
 Auricular fibrillation is uncommon, and was only present in 
 two cases. 
 
 In aortic cases shortness of breath is not unusual when the 
 patient is at rest (20 cases), and is often worse at night. 
 
304 DISEASES OF THE HEART 
 
 Nine patients were orthopnoeic, and 11 had difficulty in 
 breathing ; in 6 of these the dyspnoea was spasmodic and 
 paroxj^smal. The majority of the patients were over forty 
 years of age (over forty, 33; under forty, 25), and the prob- 
 abihty of a toxic origin is, in consequence, considerable. The 
 question is difficult to answer, but 10 of the 13 cases examined 
 post-mortem showed some form of nephritis ; and of the 6 
 patients in whom the dyspnoea was paroxysmal 2 had granular 
 kidnej^s, while all the others had persistent, though shght, 
 albuminuria. 
 
 Forty-nine of the mitral patients complained of palpitation, 
 and 30 suffered from thoracic pain. In one case typical 
 attacks of angina occurred. The distinction between dis- 
 comfort and actual pain is sometimes difficult to establish, 
 for the descriptions of the patients vary according to their 
 sensitiveness, and are often evidently inaccurate. A woman, 
 aged twentj'-seven, who was suffering from a double mitral 
 lesion, became one morning quite suddenly very short of breath. 
 The respirations were more frequent than they had been, and 
 the pulse had doubled in rate and was running about 160. 
 At intervals paroxysms of intense dyspnoea ensued, during which 
 her distress became intensified; the attacks lasted for about 
 fifteen minutes. She said that she had no actual pain, but 
 that her discomfort was unbearable, though she had described 
 her previous attacks as "painful." Paroxysmal tachycardia, 
 then, occasions discomfort, and so may auricular fibrillation 
 and extra-systoles. Pericarditis is probabty a more common 
 cause than is realized, for a local pericarditis is not uncommonly 
 found on fost-7nortem examination, which had given rise to no 
 evident signs during Mfe. A girl who was suffering from an 
 acute endocarditis complained of pain in the upper part of her 
 chest for a few hours on December 29. On February 11 the 
 pain recurred during the night, again lasting for a short time. 
 On March 3 she had severe pain over the heart for twenty -four 
 hours, and on March 5 pericardial friction was audible. It 
 seemed probable that pericarditis was the cause of the recurring 
 attacks, but that the inflammation was local, and subsided on 
 the two first occasions. In another patient thoracic pain was 
 due to arthritis of the sterno-clavicular joints, apparently of 
 
SYIIPTOMS OF CHRONIC VALVULAR DISEASE 305 
 
 rheumatic origin and associated with large crops of subcu- 
 taneous nodules. 
 
 Epigastric pain was present in 15 cases. In many more the 
 liver was tender on palpation. 
 
 Nineteen of the aortic cases complained of palpitation, and 
 22 of thoracic pain, which in 17 cases was preecordial in site. 
 One patient suffered from typical anginous attacks, and 4 ex- 
 perienced a sense of constriction around the chest. Thoracic 
 discomfort is thus almost equally common in mitral and aortic 
 disease, but palpitation is less, and pain is more, frequent in 
 the aortic group. The frequency with which auricular j&brilla- 
 tion occurs in mitral disease (19 of 102 mitral cases; 2 of 58 
 aortic cases) explains the more common complaint of palpita- 
 tion in this group, while the predominance of pain in the aortic 
 cases must be ascribed to the frequency of associated arterial 
 disease involving the aorta and the coronary arteries . Aneurism 
 occurred in 9 of the aortic and in 2 of the mitral cases. 
 Epigastric pain, on the other hand, is unusual, and was only 
 present in 2 instances. _-^ 
 
 (Edema was present in 51 of MacDonald's mitral cases, and 
 was considerable, and invaded the trunk in 22. In some it 
 was trivial and subsided rapidty as soon as the patient Avas 
 -confined to bed, but in others it was extreme, and in 1 case 
 the skin of the legs gave way and the fluid drained through 
 the apertures. The four causes of oedema — cardiac failure, 
 renal disease, anaemia, and obstruction of veins — may all be 
 active in a cardiac case. ,The first three are often present; 
 the last is unusual. Oile of vd.y patients, however, complained 
 of pain in her right calf, which was tender to palpation ; the 
 overlying skin became red and glazed. The discomfort sub- 
 sided in a couple of days, but a fortnight later the left leg 
 became oedematous, and the femoral vein was tender and 
 cord-hke. A pulmonary infarct occurred, but she made a good 
 recovery. Renal oedema is universal, while cardiac oedema 
 is distributed in accordance with the law of gravity. The 
 scalp frequently pits on pressure in renal disease, but I have 
 never found this to occur in cases of cardiac failure where the 
 Sidneys seem to be normal. Local oedema owns a local cause.- 
 
 In aortic disease oedema is slightlj- less frequent, and is rarely 
 
 20 
 
306 DISEASES OF THE HEART 
 
 considerable. It was present in 24 patients, but was only 
 considerable in 5. 
 
 In exceptional cases, however, it may be both persistent 
 and extreme, and in one old lady, aged sixty, who was admitted 
 into my wards it was present for twenty-one months, for ten 
 of which she was, in consequence, confined to bed. On her 
 admission the oedema was extreme, and practically universal, 
 and involved the serous sacs to such a degree that paracentesis 
 was required. The mitral valve, however, was incompetent 
 as well as the aortic, and the right heart was notably dilated. 
 
 Gastric symptoms are frequently present in mitral disease. 
 Twenty-two patients complained of anorexia, 34 of vomiting, 
 12 of varjdng gastric discomfort. One patient suffered from 
 acute gastritis. 
 
 In aortic disease, on the other hand, gastric symptoms are 
 uncommon. Six patients complained of anorexia, and 4 of 
 gastro-intestinal discomfort. 
 
 -/ Embolic phenomena are not uncommon in mitral disease. 
 A married woman, aged forty-six, had suffered for some year& 
 from shortness of breath and palpitation on exertion, but was 
 able to do her household duties without distress . Two months 
 before admission she ran a short distance to catch a tramcar, 
 and, on arriving beside it, was so weak that she was unable to 
 get into it. She felt very breathless and faint, but after 
 leaning against a wall for ten minutes was sufficiently recovered 
 to walk, with her son's assistance, the few hundred yards to 
 her house. She had great difficulty in ascending the stairs, 
 and had to take a rest on several occasions. Next day she felt 
 much better, and got up for a few hours, and within a week 
 was doing her usual work. Two weeks later, when alone in 
 her house, she suddenly, without obvious reason, experienced 
 a griping pain in the abdomen, which was so severe that she 
 fell to the floor, where she lay for five hours, until her husband 
 returned and assisted her to bed. The pain persisted for a 
 day or two, but gradually lessened, though slight attacks 
 recurred from time to time. The palpitation became more 
 troublesome, and continued even when she was at rest. On 
 the day before admission, when she was sitting in a chair, she 
 suddenly felt extremely weak, and vomited, but the discomfort 
 
SYMPTOMS OF CHRONIC VALVULAR DISEASE 307 
 
 ceased within ten minutes. On admission to hospital, on 
 February 15, she was seen to be fairly well developed but 
 poorly nourished, and white hair made her look older than her 
 years. She lay easily in bed, and there was no csdema, but 
 the liver was enlarged and tender, rhonchi were audible all 
 over the chest, and the pulse was frequent and extremely 
 irregular (auricular fibrillation). Both sides of the heart were 
 enlarged. No murmurs were audible, but the first sound at 
 the apex was short and sharp, with an abrupt commencement, 
 and the second pulmonic sound was emphatic. The urine 
 contained blood and albumin in amount, and numerous tube- 
 casts. Some improvement occurred within the next few days, 
 but on the evening of February 28 she experienced pain in her 
 right leg, which prevented her from sleeping ; it had disappeared 
 next day, and nothing abnormal could be seen. On March 19 
 she complained bitterly of numbness in the left leg and foot, 
 but again examination was negative. On the evening of 
 April 6 she suddenly fell back unconscious, her breathing 
 becoming stertorous, and a left facial palsy was apparent. 
 In a few hours consciousness returned. She had a restless 
 night, but next morning spoke clearly and intelligibly ; a shght 
 paresis was evident on the left side, but she could move 
 her limbs. On April 15 she suddenly lost consciousness for 
 ten minutes, but rapidly recovered. On April 20 she com- 
 plained of pain in the right side of the abdomen, and felt sick 
 and vomited. Cyanosis became extreme, but the symptoms 
 subsided in a couple of days . The pain and vomiting recurred 
 on May 14, and lasted again for two days ; but on May 18 she 
 suddenly lost consciousness and passed into coma, dying a few 
 hours later. 
 
 On 'post-inortem examination many infarcts were found, a 
 small one in the lower lobe of the right lung, four in the spleen, 
 and five in the kidneys. In the brain there was a white cica- 
 tricial area above and behind the posterior end of the right 
 internal capsule, and a haemorrhagic infarct of more recent 
 origin in the pons ; the right middle cerebral artery was oc- 
 cluded by an embolus near its origin ; the cerebral vessels were 
 not diseased. The mitral valve was the site of an extreme 
 button-hole stenosis ; the left auricle was greatly enlarged and 
 
308 DISEASES OF THE HEART 
 
 its walls hypertrophied. The auricular appendix was particu- 
 larly large, and completely fiUed by an enormous tough throm- 
 bus, which measured some 3 inches in length, and projected as a 
 polypoid mass into the cavity of the auricle. The free surface 
 was in parts coated with soft recent clot. 
 
 The cause of the various symptoms was thus apparent. The 
 abdominal pain was due to splenic infarcts, the pain on the 
 right side to the pulmonary infarct, and the hsematuria, in 
 part at any rate, to the renal ones. The cerebral symptoms 
 owned a similar cause. 
 
 Embohc phenomena are unusual in aortic disease. None 
 occurred in this series. 
 
 Cerebral sj^mptoms are more common in aortic than in mitral 
 disease. Of the mitral patients, 4 suffered from hemiplegia, 
 18 complained of headache, 9 of giddiness, 8 of faintness, and 
 1 of noises in the head. In the aortic group 2 suffered from 
 hemiplegia, 7 complained of headache, 9 of giddiness. 3 of 
 faintness, 6 of insomnia, and 2 of a sensation of impending 
 death. 
 
 The exact cause of these symptoms may be diificult to 
 determine during hfe. Two of the mitral hemiplegias were 
 due to embohsm, and one to haemorrhage. One of the aortic 
 hemiplegias had a cerebral haemorrhage. No post-mortem 
 examination w^as made in the other cases. The headache 
 sometimes suggests a definite cerebral lesion, but is most 
 often associated wdth high blood-pressure and evidence of 
 renal disease; sometimes it seems to be due to anaemia. Gid- 
 diness is most frequent in patients with degenerate arteries, 
 while faintness is not necessarity associated wdth anaemia or 
 extreme cardiac weakness . In one of my patients who fainted 
 frequently, as a rule after exertion, the only other sign of 
 cardiac disabihty w'as very slight oedema of the shins. In 
 some patients " faints " are probably petit mal. 
 
 Of general sjrmptoms the most frequent is weakness, which 
 was present in 33 mitral cases and in 13 aortic patients. Three 
 mitral patients complained of coldness of the extremities and 
 1 of epistaxis. One aortic patient made complaint of failing 
 eyesight. 
 
CHAPTER XXIII 
 MYOCARDIAL FAILURE WITHOUT VALVULAR DISEASE 
 
 In chronic valvular disease th.e cardiac work maj^ be carried 
 on for many years without any signs of cardiac distress, symp- 
 toms only making their appearance when the muscle becomes 
 unable to accompKsh its necessary task. The failure may be 
 due to many causes ; the occurrence of a new factor, such as 
 bronchitis, throwing an extra strain upon the heart ; an in- 
 crease in the grade of the valvular disturbance to such a point 
 that the reserve is overwhelmed ; or the appearance of patho- 
 logical changes in the muscle itself. 
 
 Myocardial disease may, however, occur in the absence of 
 valvular lesions, and may produce very evident symptoms of 
 cardiac distress ; but though the chnical picture may be purely 
 cardiac, pathological investigation shows that the lesions are 
 rarely, if ever, confined to the heart. The granular degenera- 
 tion of the acute infections is accompanied by cloudy swelling 
 in other viscera ; fatty degeneration of the heart is associated 
 with fatty degeneration elsewhere; fatty infiltration usually 
 affects the whole body, and not the heart alone; while the 
 arterial lesions of fibrosis are rarely hmited to the coronary 
 arteries . 
 
 The symptoms of myocardial weakness are similar to those 
 which occur in valvular disease when compensation has broken 
 down. 
 
 In the infections the symptoms of cardiac failure are obscured 
 by those of the toxaemia and those produced by any local lesions 
 which may be present ; but the increasing weakness, breathless- 
 ness, and cyanosis, which are so commonly present in serious 
 
 309 
 
310 DISEASES OF THE HEART 
 
 cases, are due, ir part at any rate, to cardiac weakness. Cold- 
 ness, pallor, or congestion of the extremities, are by no means 
 infrequent, and faintness or intense prostration may occur 
 even on trivial exertion, such as sitting up in bed. (Edema 
 during the progress of an acute infection is of somewhat rare 
 occurrence, and is most often the result of venous thrombosis ; 
 but it may be purely cardiac, and though usually trivial, is 
 occasionally widespread and extreme. 
 
 A married woman, aged thirty, who had nursed her fourth 
 baby for nine months, gradually began to find that her house- 
 work was becoming exhausting, and that she became short of 
 breath, and felt her heart beating on very slight exertion. 
 Vomiting set in, and continued for several weeks . She lost flesh 
 rapidly, and became pale and sallow in appearance. On admis- 
 sion to hospital, she was very weak and exhausted, and notably 
 emaciated and pale, the red cells only numbering 1,060,000, 
 with a haemoglobin value of 20 per cent. Films showed a well- 
 marked megalocytic reaction. A few days afterwards she 
 became fevered, and a consolidation gradually involved the 
 left lung. With the onset of the pneumonia exhaustion be- 
 came extreme and incontinence ensued, and coincident ly 
 oedema, which on admission had been trivial in amount, became 
 universal and considerable. The pulse was now very small 
 and soft and frequent, and the cardiac sounds were short and 
 weak. Three weeks later the consolidation was resolving, the 
 oedema had disappeared, and the pulse, though still small and 
 soft, approximated to the normal rate. She eventual^ made 
 a good recovery, and four years later was strong and well. 
 
 During convalescence from the infections, on the other hand, 
 the usual symptoms of cardiac weakness, shortness of breath 
 on exertion, and oedema, are extremely common, and are some- 
 times very persistent, though in the vast majority of cases they 
 disappear rapidly with improvement of the general liealth. 
 Cardiac discomfort, palpitation, tachycardia, and pain may 
 also occur, and may suggest from their continuance the possi- 
 bihty of serious mischief, though complete recovery is the rule, 
 unless organic disease is abeady present. The palpitation and 
 tachycardia are extremely trying to the patient, and may con- 
 tinue for months. In the case of a medical friend, after an 
 
MYOCARDIAL FAILURE 311 
 
 influenza] attack, even such trivial exertion as walking slowly 
 upstairs induced profuse perspiration, with throbbing of the 
 Avhole chest and head, while the pulse-rate ran up to the 
 neighbourhood of 200 per minute. A sensation of faintness is 
 common, but actual syncope is rare. 
 
 Fatty Changes. — 'The fatty changes which occur in the heart 
 are as a rule associated with disease elsewhere, and give but 
 little clinical evidence of a specific kind. Fatty degeneration 
 is most common in severe anaemia, in chronic alcohohsm, in 
 emphysema, and in chronic disease of the kidneys, and the 
 cardiac symptoms are only a part of a general disturbance. It 
 co-exists with granular changes in the infections, but its particu- 
 lar degree cannot be appreciated during life; and in disease of 
 the coronar}" 'arteries it is only a phase of an ischsemic atrophy. 
 So that, as an isolated lesion affecting the heart and the heart 
 alone, it is of rare occurrence, although cardiac weakness from 
 fatty changes frequentl}^ occurs. 
 
 Fatty infiltration is as a rule merely a part of a general ten- 
 dency to obesity, whose presence naturally suggests the nature 
 of any existing myocardial weakness. But with obesitj', again, 
 renal and arterial disease are frequently combined, and the 
 cardiac picture is, in consequence, obscured. 
 
 It seems probable that there is no real distinction between 
 fatty infiltration and fatty degeneration, which differ in site 
 rather than in nature. The quality of the fat has been shown 
 to be the same in the two situations in animals in which the lesion 
 has been produced experimentally, and fats which are abnormal 
 to the species may be deposited, if a particular fatty dietary is 
 adopted. Fatty infiltration, too, is invariably accompanied 
 by a certain amount of fatty degeneration, though the converse 
 proposition is by no means universally true. 
 
 In the exceptional case fatty infiltration of the muscle occiu-s 
 without the epicarclial or the general fat being excessive. The 
 causes of this are not yet recognized; but the fact is of im- 
 portance, as the nature of the cardiac weakness is apt to be mis- 
 interpreted. A striking example of this once came under my 
 observation. An old man who was convalescing apparently 
 satisfactorih' from a mild attack of smallpox, somewhat sud- 
 denly became weak and stupid, and passed rapidly into semi- 
 
312 DISEASES OF THE HEART 
 
 coma and into coma, dying within forty-eight hours of the 
 onset of serious symptoms. There had been no symptoms 
 previously which suggested anj' special cardiac weakness, and 
 his general nutrition seemed good, and there was no special 
 obesity-. The heart, however, shoAved extreme fatty infiltra- 
 tion, particularly upon the right side, where fatty deposits were 
 visible even on the endocardial surface; and the muscle cells 
 were also grossly affected. His arteries generally were athero- 
 matous and hard, and the minute arterioles on the right side of 
 the heart were affected to a greater degree than on the left. 
 
 The symptoms of fatt}^ change in the heart do not differ from 
 those of cardiac weakness owning other causes, and the evi- 
 dences of cardiac insufficiency are similar. The heart, too,, 
 from associated lesions may be large or small; the pulse may 
 be hard and full, or small and soft ; and the murmurs indicative 
 of valvular disease, or alterations of the sounds from high 
 blood-pressure or a hardened aorta may be absent or present 
 in particular instances. The thickness of the parietal fat in 
 general obesity may interfere with the examination of the 
 heart, and the character of the pulse may be the sole trust- 
 worthj' guide. One is not infrequently scarcely able to hear 
 the cardiac sounds, though the pulse is full and hard, with a 
 pressure decidedly above the normal. 
 
 Disease of the Coronary Arteries. — The relative frequency 
 with which individual arteries are diseased has been investi- 
 gated b}^ several writers. Everyone is agreed that the aorta 
 is most frequently affected, but while Lobstein states that the 
 splenic and the femoral arteries are more often diseased than 
 the coronary arteries, and Rokitansky gives precedence as well 
 to the iliac vessels, Huchard considers that the arteries of the 
 heart are those which are most frequently abnormal. For this 
 predominance several reasons, he states, are apparent. Their 
 high origin in the aorta, where the blood-pressure is at a maxi- 
 mum, their mainly muscular texture, their numerous and 
 acute curves, their constant activity in supplying blood to 
 tissues constantly in action, etc., all tend to render them unduly 
 liable to disease; while their relationship, however well pro- 
 tected they may be in their bed of fat in the sulci, to the regu- 
 
MYOCARDIAL FAILURE 313 
 
 larly contracting heart, exposes them constantly to jars and 
 contusions. The exact reason for their affection, however, is 
 of less moment than its frequency, and the importance of their 
 integrity cannot be over-estimated, for upon their integrity the 
 nutrition of the heart depends. 
 
 Myocardial disease is rarely, if ever, universal, and the local 
 distribution is dependent upon local and most commonly vas- 
 cular causes ; and, as we have seen, atrophy, fatty, and hyaline 
 degeneration, necrosis and fibrosis, may aU be due to arterial 
 disease. In arterio-sclerosis the arterial change is widespread, 
 and the coronary lesions can be appreciated by recognition 
 of the existence of the change in the peripheral vessels ; but in 
 focal disease the distribution is often erratic and apparently 
 whimsical, and the visceral vessels may be seriously affected 
 Avithout any evident change in the arteries which are accessible 
 to examination. It is this factor which makes prognosis in 
 cardiac disease so imperfect, for our ignorance of the condition 
 of the coronary arteries renders it impossible to assess the most 
 important factor at its true value, and the " happy guess " 
 sometimes turns out to be wrong. An embolus occludes the 
 lumen, a narrowed vessel becomes completely blocked, and the 
 cardiac contractions suddenly and for ever cease. 
 
 Occlusion of the coronary arteries may be of gradual or of 
 sudden onset, and may affect the superficial "rings " or the 
 perforating branches. The anastomotic connections of the 
 rings may prevent any serious damage to the muscle if the 
 occlusion is sufficiently gradual, and several cases in which this 
 occurred have been already considered. But rapid closure 
 prevents adequate compensatory arrangements, and the 
 muscle which is concerned in consequence dies. Even in 
 gradual closure adequate anastomotic developments are excep- 
 tional, and the muscle suffers in greater or less degree. Closure 
 of a nutrient end-artery always produces necrosis. 
 
 The changes which are found post-mortem may thus vary 
 from variations in the rapidity of the closure and in the site 
 of the affected vessel. And while at one end of the chain, 
 where the anastomotic developments are sufficient, the cardiac 
 muscle may be perfectly normal, and at the other, where a large 
 vessel has been suddenly closed, it may show no microscopic 
 
314 DISEASES OF THE HEART 
 
 lesions, because sudden death has prevented structural changes, 
 the intervening hnks exhibit every intervening grade in extent 
 and severity, and the clinical symptoms follow suit. Death 
 may ensue in a moment, or after an illness of many months, 
 and serious failure may pass away if satisfactory anastomotic 
 developments eventually follow. 
 
 Experimental ligation of a coronary artery or of one of the 
 main branches is often rapidly followed by death, but this is 
 by no means invariable, and the animals may live for hours, 
 days, or even weeks without the appearance of any notable 
 symptoms beyond a transient irregularity of the cardiac action ; 
 and a case has been recorded (Pagenstecker, quoted by Hirsch- 
 f elder) in which the right coronary artery of a man was liga- 
 tured without harm. Clinical and pathological observations 
 show similar results, and the changes which are found even in 
 cases of sudden death often show that coronary occlusion must 
 have occurred some time previously. 
 
 If the occlusion is sudden and complete, immediate death 
 may ensue. A woman, aged thirty-two, underwent a some- 
 what tedious operation for gall-stones, and on the next morning 
 was very cheery and well, but about noon died suddenly, and 
 without any warning. On examination, a large mobile embolus 
 was found to block completely the descending branch of the 
 left coronary artery, which was otherwise normal. The embolus 
 had arisen from a clot at the apex of the left ventricle, which 
 was evidently of some age, and must have existed prior to the 
 operation. But in other cases — e.g., in rupture of the heart — 
 necrosis has occurred previously, and the fatal issue, though 
 abrupt, takes place subsequent to the occlusion. An insane 
 woman, aged seventy-eight, who went to bed in her usual health, 
 was found to be dead in the morning, rupture of the left ventricle 
 having occurred on its posterior and upper aspect. The tissues 
 at the site of rupture were soft and friable and necrotic, and 
 the transverse branch of the right coronary artery was found 
 to be thrombosed for nearly an inch. The inflammatory re- 
 action in the periphery of the infarct had so weakened the 
 tissues that the endocardial blood had gained entrance to the 
 muscle, and, forcing its way along the track of the infarct with 
 successive contractions of the heart, ultimately reached and 
 
MYOCARDIAL FAILURE 315 
 
 perforated the pericardial covering. Infarcts, too, are not 
 necessarily fatal, and may produce little sign of cardiac failure. 
 A woman, aged fifty-seven, died after an illness of five days' 
 duration, during which the symptoms were wholly cerebral, 
 the result of streptococcic abscesses in the cerebellum, and 
 meningitis. There were no signs of special cardiac embarrass- 
 ment, even during the last twenty-four hours of life, though 
 the mitral valve was extensively disorganized by recent ulcera- 
 tion superimposed upon a valvular defect of old standing, and 
 a large infarct was present at the apical end of the left ventricle. 
 
 Myocardial Fibrosis. — In cases where the coronary obstruc- 
 tion is gradual, the onset of symptoms is necessarily insidious, 
 and the course of the disease is essentially chronic — a course 
 which is the rule in aneurism of the heart ; for sudden occlusion, 
 if of any extent, causes sudden death or infarct, and in the 
 latter case is more usually associated with rupture than with 
 reparative fibrosis. 
 
 A pohceman, aged forty-nine, caught cold one January, 
 which did not, however, necessitate his ceasing work; but 
 when the cough had gone he noticed that he was somewhat 
 breathless on exertion, and experienced a sensation of tightness 
 in the epigastric region. In April the cough recurred, and was 
 now accompanied by a scanty spit, and he felt so unweU that 
 he went on holiday to the Highlands. Here he improved to 
 some extent, but was still troubled with breathlessness, espe- 
 cially when walking uphill. On his return home he still felt 
 unwell, but he continued at work until September, when his 
 feet for the first time became swollen. At night, too, he was 
 very short of breath, and had to sit up in bed, and slept badly. 
 His weight had decreased, and he was 2 stones lighter than 
 usual. On admission to hospital, the oedema, which was 
 general, was not great, but the right chest was half full of fluid, 
 and he was very breathless and orthopnceic. After the fluid 
 had been removed, his symptoms rapidly abated. The heart 
 was large, especially to the right side, and the sounds were 
 short and distant, but pure. The pulse was regular, but small 
 and weak, and numbered about 100, and even when his other 
 symptoms had disappeared still ran between 90 and 100. 
 After a month's residence in hospital he was sent to a con- 
 
318 DISEASES OF THE HEART 
 
 more or less abruptly without obvious cause, and ultimately 
 passes off. In the following case such a state of matters 
 seemed extremely probable, but the crucial examination is 
 wanting : 
 
 A carter, aged thirty-two, who presented many of the signs 
 of incipient locomotor atax}^, noticed that his feet had become 
 swollen without any obvious cause. The oedema rapidly in- 
 creased, and a week later a slight cough, accompanied by a 
 muco-purulent spit, supervened, and the abdomen became 
 swollen and tender. When admitted into hospital, a fortnight 
 after the onset of the iUness, the oedema was universal and 
 considerable, the penis and scrotum being so much swollen 
 that micturition was difficult. The liver was enlarged and 
 tender, and the heart was large, but the sounds were pure, 
 the first sound at the apex being short and sharp, while the 
 second aortic sound was emphatic. The arteries were thick- 
 ened and tortuous. Three weeks later the oedema had dis- 
 appeared, and the patient's discomforts had ceased, and his 
 convalescence was uninterrupted. The failure seemed to be 
 purely myocardial, and the absence of aU the usual causes of 
 failure and the presence of widespread arterial disease sug- 
 gested that it resulted from disease of the coronary arteries. 
 The area involved, however, was sufficiently sma U for complete 
 recovery to be possible. 
 
 The character of the sounds in valvular disease is neces- 
 sarily obscured by the presence of murmurs, and the physical 
 signs generally may be grossly altered in other directions. 
 The apex impulse may thus be displaced b}^ associated renal 
 cirrhosis, or obscured by emphysema; the relative intensity 
 of the second sounds may be altered by arterial or by pul- 
 monary lesions ; and displacements of the heart may occasion 
 pulsation in abnormal sites, or the conduction of the sounds 
 in abnormal directions. 
 
 It is often helpful in these cases to contrast the character of 
 the apex impulse, the character of the pulse, and the quality of 
 the cardiac sounds ; and if one of these seems disproportionate 
 to the others the prognosis should be based on the more serious 
 sign. In renal cirrhosis, for example, the apex impulse may be 
 stronger than normal, and the pulse of high pressure, while the 
 
MYOCARDIAL FAILURE 319 
 
 cardiac sounds alone suggest myocardial weakness. The first 
 sound in these cases is rarely sharp or loud, and is generally 
 dull and distant and faint ; its termination may be indistinct, 
 though no definite murmur is present . I shall always remember 
 the case of an old man dying slowly from cardiac failure who, 
 a couple of days before his death, when oedema was well 
 marked and widespread, stiU presented a slow, dehberate, 
 strong apex impulse, though the first cardiac sound was almost 
 inaudible. The relative intensity' of the first sound over the 
 right and the left ventricles should also be contrasted, for 
 cardiac strain may be experienced by either one or the other. 
 In pneumonia the difference may be extremely striking, and 
 in valvular disease the sounds in one or other situation may be 
 pure. 
 
CHAPTER XXIV 
 
 THE DIAGNOSIS OF CHRONIC VALVULAR DISEASE 
 
 The diagnosis of the various valvular affections is made on 
 examination of the patient. It is impossible in this place to 
 consider all the details of physical examination, but some 
 points require a Kttle special consideration. 
 
 The Significance of Physical Signs. — Onty a portion of the 
 heart is directly related to the front of the chest, as the lungs 
 overlap all but a smaU part of the right ventricle (Fig. 148). 
 The apex impulse is thus felt through a considerable thickness 
 of pulmonary tissue, and its character may be modified by 
 variations in the condition of the lungs or pleurae, quite apart 
 from any alterations in the heart itself. It is, for example, 
 temporarily weakened on full inspiration and strengthened 
 on full expiration, and it may be permanently abohshecl by 
 emphysema, or its area may be increased by retraction of the 
 lungs. In health}^ individuals it is freely movable, and may 
 be felt even a couple of inches outside its usual site if the 
 individual hes on his left side. The absence of these physio- 
 logical variations is important, as it shows that the anterior 
 margin of the left lung is fixed, or that the apex of the heart 
 is adherent to the anterior chest wall. 
 
 In most healthy persons the apex impulse is the only appre- 
 ciable pulsation on the front of the chest. It is a definite 
 forward thrust or protru 'ion, which lasts for about a third of 
 a second, and precedes the appearance of the carotid pulse. 
 It is produced by the cardiac systole, which alters the shape of 
 the heart as well as its relation to the chest wall, the apex 
 being tilted forward and to the right, and the long axis of the 
 heart being slightly lengthened; coincidenth' the transverse 
 diameter of the heart is diminished. If the interspaces are 
 
 320 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 321 
 
 wide and the chest waU is thin, a recession may be observed 
 above the right ventricle between the apex and the sternum. 
 
 It is often difficult to distinguish, either by the eye or by the 
 hand, between a protrusion and a recession, for in both a for- 
 ward 'movement occurs, though at different periods of the 
 cardiac cycle. (The carotid pulse may be felt and the apex 
 impulse watched.) With graphic methods the distinction is 
 easy, as the arterial pulse can be taken as a guide. Normally 
 
 Aortic 
 
 Tricuspid 
 
 Puhrtonary' 
 
 Mitral 
 
 Fig. 148. — Diagka^i shotting the StrEFACE E.ELATIO^-s of Ltj:sgs, Heaet, and 
 Cahdiac Valves (A. Keith), 
 
 the impulse makes its appearance about O'lO second before 
 the carotid, and 0"20 second before the radial pulse. 
 
 If the left ventricle is hypertrophied, the impulse is wide- 
 spread and well sustained, and its relationship to the arterial 
 pulse is unchanged. If the right ventricle, however, is hyper-, 
 trophied, the apex proper may be displaced backwards from 
 the chest wall, the impulse which is felt being due to the con- 
 traction of the underlying right ventricle. The rhythm of the 
 
 21 
 
322 
 
 DISEASES OF THE HEART 
 
 impulse is thus altered, for during systole the transverse 
 diameter of the heart is lessened and a recession occurs, the 
 cardiogram being "inverted " (Fig. 150). 
 
 In pathological conditions pulsations may be present in 
 various parts of the chest, and their nature can only be recog- 
 nized by appreciation of their character and rhythm. Epigas- 
 
 Aorta 
 
 Pulmonary 
 artery 
 
 .... ^^/^ 
 
 auricular 
 
 appendix 
 
 'Left 
 ventricle 
 
 Ri^ht ventricle 
 
 Fig. 149. — Diagram showing the Surface RELATioisrs of the Peeicakdium, 
 Heart, and Great Vessels (A. Keith). 
 
 trie pulsation, for example, may be due to the pulsation of the 
 abdominal aorta (Fig. 151), to true hepatic pulsation from 
 tricuspid regurgitation, or to communicated pulsation from 
 the heart itself (Fig. 153). The first succeeds the apex im- 
 pulse, and is practical^ synchronous with the brachial pulse, 
 and the others are synchronous with the apex impulse and 
 precede the brachial pulse ; but if the pulsation is due to the 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 323 
 
 contraction of the right ventricle (Fig. 152) the tracing is 
 inverted. The pulsation so often seen in the second left 
 interspace close to the sternum is generally due to the pulsation 
 
 •BTo.eK 
 
 S'i. Lift SpcLCJL. 
 
 Fig. 150. — "Inverted" Apex Imptjlse (c/. Fig. 152). 
 
 of the pulmonary artery, as the main wave succeeds the apex 
 impulse and precedes the brachial pulse (Fig. 154). But it 
 may be synchronous with the apex, and either a protrusion or 
 
 Fig. 151. — Epigastkic Pulsation succeeding the Apex Impulse: ABDOMiNAii 
 
 Aorta. 
 
 a recession, the first if it is due to the conus arteriosus, the 
 second if it is due to contraction of the right ventricle. The 
 contraction of the auricle may be represented upon the tracing, 
 
 Fig 152. — Epigastric Pulsation synchronous with Apex Impulse, put 
 inverted: Right Ventricle. 
 
 usually as a positive wave, more rarely inverted. Pulsation 
 to the right of the sternum generally shows an inverted wave, 
 as it is most frequently due to the contraction of a dilated right 
 heart (Fig. 155). But the wave may be positive if it results 
 
324 
 
 DISEASES OF THE HEART 
 
 from the reflux of blood, tlirough an incompetent tricuspid 
 valve. 
 
 Pulsation on the front of the chest may be produced in many 
 ways, for the heart is often displaced in pulmonary and 
 
 
 Fia. 153. — Epigastkeo Pxtlsation synchronous with Apex Impulse and 
 Positive: Left Ventricle. 
 
 abdominal disease, the viscera may be transposed or an 
 aneurism may be present, and the nature of the pulsation can 
 only be recognized by careful examination. 
 
 Fia. 154. — Curves of Brachial Pulse, Pulsation in Second Left Intercostal 
 Space and Apes Impulse. 
 
 The area of cardiac dulness is often altered by pulmonary 
 disease. Under normal circumstances it is an inaccurate guide 
 to the size of the heart, for, though the left and the upper 
 
 A7M,,S?t 
 
 Fig. 155. — Pulsations prom Fourth Right Intercostal Space and Apex 
 
 Impulse. 
 
 The pulsation on the right side is inverted. 
 
 margins can be deUmited fairly accurately, the right margin 
 is always within the right border of the heart, as the sternal 
 note is representative of the structures underlying it as a 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 325 
 
 whole, and the lower margin runs into the area of hepatic 
 dulness. The so-called areas of superficial and deep dulness 
 are notoriously inaccurate. A medium strength of stroke 
 yields the best result, and the physician must be careful to use 
 the same technique habitually and to form his own estimate of 
 the normal dimensions of the area (Figs. 156, 157). 
 
 The cardiac dulness in healthy individuals varies appreciably 
 with variations in respiration, being diminished during full 
 inspiration and vice-versa. 
 It may be notably less- 
 ened in emphysema and 
 apparently increased in 
 pulmonary consolidation 
 and retraction. Absence 
 of the physiological varia- 
 tions is an important sign, 
 for it indicates fixation of 
 the anterior margins of 
 the lungs. 
 
 The character and the 
 area of audibility of the 
 cardiac sounds and valvu- 
 lar murmurs requires care- 
 ful examination . The fir s t 
 sound is due to the con- 
 traction of the ventricular 
 muscle and to the closure 
 of the auriculo-ventricular 
 valves. If the ventricle 
 is powerful, the sound is 
 long and dull, as the 
 muscular element is well-marked ; but if the muscle is weak, the 
 valvular element becomes predominant, and the sound becomes 
 shorter and sharper, and approximates in character to that of 
 the normal second sound. The second sounds are due to the 
 closure of the arterial valves. They are loud if the arterial 
 pressure is high, and weak if the pressure is low, or the valves 
 stiff and immobile ; absence of a second sound always indicates 
 a gross valvular defect. But the character of the sounds may 
 be greatly altered by the thickness of the overlying structures. 
 
 Fig. 
 
 156. — Diagram showing Surface Ee- 
 LATiONs OF Heart and Lungs. 
 
326 
 
 DISEASES OE THE HEART 
 
 and they are often weakened in fat and in very muscular 
 individuals, and in emphysematous patients ; and they may be 
 loud in thin people or in those Avhose lungs are retracted from 
 the front of the chest, quite apart from an}^ real alteration in 
 the heart itself. The loudness of valvular murmurs may of 
 
 course be affected in the 
 same way. 
 
 The conduction of 
 sounds and murmurs is 
 due to several factors : 
 
 (1) The site of production 
 of the sound. The second 
 sounds are loudest at the 
 base and the first sounds 
 over the ventricles. 
 
 (2) The direction of the 
 flow of blood at the time 
 when the murmur is being 
 produced. The sj'stohc 
 aortic murmur is well con- 
 ducted into the carotid 
 arter}^, and the diastohc 
 murmur doi^aiwards to- 
 wards the ventricles . 
 
 (3) The relationship of the 
 chambers with which they 
 are concerned to the sur- 
 face of the chest. The 
 left auricle, for example, 
 
 is deeply situated, while the left ventricle is relative^ superficial. 
 In mitral stenosis the presystoHc murmur is heard best at the 
 apex, because this is the nearest accessible spot to the mitral 
 valve, and the current of blood which produces the abnormal 
 sound is flowing from auricle to ventricle. 
 
 In mitral regurgitation, too, the murmur is heard best at 
 the apex of the ventricle, though it must be louder in the left 
 auricle, as the current of blood is flowing from ventricle to 
 auricle; but the distance of the left auricle from the front of 
 the chest prevents it being heard best over the auricle. The 
 
 Fig. 157." — Diagram showtng Area of Dtjl- 
 NBss OP Heart astd Liter. 
 
 Author's normal. 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 327 
 
 murmur of stenosis is rarely heard weU at the back of the 
 €hest, as the current is flowing from behind forwards ; and 
 the murmur of insufficiency is often heard weU at the back, 
 as the current which produces it is flowing towards the back 
 of the chest. 
 
 An abnormal conduction of sounds or murmurs indicates 
 some abnormality which occasions it. In consohdations of the 
 middle lobe of the right lung the cardiac sounds are well con- 
 ducted towards the right nipple. In aneurism they are well 
 conducted to any region where the aneurism comes near the 
 surface of the chest. The conduction of the cardiac sounds 
 is thus, like the area of cardiac dulness, dependent upon the 
 condition of the structures surrounding the heart almost as 
 much as upon alterations in heart itself. 
 
 The Causes of Murmurs. — ^The localization of a murmur 
 indicates the site of the valvular lesion, but the character of 
 the murmur conveys little information as to the grade of the 
 defect. Its loudness depends upon two factors — the nature of 
 the lesion and the rate of flow of the current of blood — and a 
 murmur may weaken or even disappear in cardiac failure 
 from variations in the second factor, without any change 
 occurring in the valve itself. Other things being equal, a 
 loud murmur is more satisfactory than a weak murmur, for it 
 is indicative of a powerful cardiac muscle. 
 
 The duration of a murmur, on the other hand, conveys 
 definite information of value . A mi tral murmur which obscures 
 the first sound and occupies the whole of the short pause 
 indicates regurgitation during the whole of ventricular systole, 
 while a mere whiff succeeding a distinct first sound shows that 
 regurgitation is only occurring during a part of systole. 
 
 The character of a murmur may alter from several causes. 
 In acute endocarditis, and less frequently in the chronic disease, 
 the valve itself may undergo notable changes. A cusp may be 
 perforated and becom.e notably incompetent, or vegetations 
 may become so luxuriant that a previously existing incom- 
 petence ceases. The muscle may become too weak to produce 
 audible vibrations, or with increasing strength may generate 
 a longer and a louder sound. The cardiac rhythm may change. 
 This latter factor has already been considered in some detail. 
 
328 DISEASES OF THE HEART 
 
 In auricular fibrillation the co-ordinate contraction of the 
 auricular muscle ceases, and any murmur produced by auricular 
 contraction ceases too, so that in mitral stenosis, with the 
 
 I ^ 
 
 I 
 
 m 
 
 Aurioulap Systole 
 
 wm/////M///M 
 
 W///////////////M 
 
 Ventricular Systole 
 
 \ SHUT 1 
 
 OPEN 
 
 1 SHUT 1 
 
 Aurioulo-Ventricular 
 
 Valves 
 
 1 OPEN 1 
 
 SHUT 
 
 1 OPEN 1 
 
 Arterial Valves 
 
 1 f n 
 
 1 1 n 
 
 Cardiac Sounds 
 
 iiiiinm n I liiiiiiM,. n 
 
 nillln,.,, D lllilllllllllliu.,,, D 
 
 I 1 □ I I niiinin 
 
 I I lllliri I I llliinn. 
 
 Systolic Murmurs 
 
 Diastolic Murmurs 
 
 .-.irllilO 
 
 D 
 
 ,1,11111(0 
 
 D 
 
 • 
 
 „MlllllO 
 
 Dliiiii 
 
 ..11111111110 
 
 Dill, 
 
 iiiO 
 
 Dlllin, 
 
 / 
 
 iMIIIillO 
 
 Dliiii,, 
 
 n 
 
 Oiii. 
 
 Q 
 
 Diiiiii 
 
 Presystolic Murmur 
 
 Full Diastolic Murmur 
 
 Early Diastolic and 
 Presystolic Murmurs 
 
 Early Diastolic Murmur 
 
 Pig. 158. — Diagram showing the Time Relations of the Cabdiac Contrao. 
 TioNS, THE Cardiac Sotxnds and Valvular Murmurs, and the Corre- 
 sponding Condition of the Cardiac Valves. 
 
 onset of fibrillation, the presystolic murmur disappears. Re- 
 gurgitation in mitral incompetence can be only minimal if the 
 auricle and ventricle contract simultaneously, so that in 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 329 
 
 heart-block, partial or complete, and in extra-systoles, the 
 duration and loudness of a murmur may vary with successive 
 beats ; while in nodal rhythm and in paroxysmal tachycardia 
 a systohc mitral murmur may be constantly weakened or may 
 disappear altogether. 
 
 The presence of a murmur does not necessarily indicate 
 structural disease of the valve. The arterial valves are simple 
 mechanical contrivances which probably act independently of 
 muscular action (cf. p. 299), but the auriculo-ventricular valves 
 are in large measure closed by contraction of their muscular 
 sphincter, and may become incompetent from muscular weak- 
 ness without any abnormality of the cusps. Mitral and tri- 
 cuspid reflux may thus be temporarj^ if the muscular weakness 
 is due to removable causes. "Curable " mitral reflux can be 
 recognized by the absence of any of the^f actors which produce 
 valvular disease, and by the presence of conditions which 
 produce weakness of, or throw strain upon, the ventricular 
 muscle. Debilit}^, anaemia, etc., represent the former; physical 
 strain and aortic valvular disease the latter. 
 
 Murmurs are not infrequently present in patients whose 
 cardiac valves are normal. They are always systohc in rhythm, 
 but may be of various characters — soft or harsh, loud or weak, 
 long or short ; and thej may be present over any part of the 
 cardiac area. According to the late Dr. Sansom, the most 
 frequent site is over the pulmonary artery- and the conus 
 arteriosus in the second and third left interspaces close to the 
 sternum (59 per cent.). They may be heard in the aortic area 
 (11 per cent.), and at the apex (7 per cent.) ; and may be present 
 over the conus arteriosus and right ventricle (11 per cent.); 
 and at both the apex and the pulmonary area (9 per cent.). 
 The most frequent causes are anaemia and post-febrile debility ; 
 and they may also occur in excited hearts (as in Graves's 
 disease), in women following child-birth, and in any case 
 where the heart is displaced from its usual site by pleural 
 effusions, abdominal distension, etc. ; they are generallj' present 
 in extreme lateral curvature of the spine. The apical murmur 
 is probably always a sign of mitral reflux. The basal murmurs 
 are probably produced in the aorta or the pulmonary artery, as 
 the case may be, and may well result from kinking of the vessel 
 
f^30 DISEASES OF THE HEART 
 
 in cases where the heart is displaced; but their origin in other 
 cases is unknown, though numerous theories have been suggested. 
 Their recognition is usually easy. Organic disease of the 
 pulmonary valve is very rare save in congenital heart disease, 
 in which the disturbance of the circulation is usually con- 
 siderable, and clubbing of the finger-tips, cyanosis, or other 
 congenital defects, often co-exist; the right heart, too, is 
 generally enlarged in consequence of the excessive strain 
 thrown upon it. Aortic stenosis without regurgitation is 
 unusual, though a systolic murmur is not uncommon in later 
 life, as the result of some stiffening or roughness of the cusps 
 unaccompanied by definite narrowing of the orifice ; in this case 
 the second sound is generally abnormal, and emphatic or 
 intoned or weakened, and the left ventricle is more or less 
 hypertrophied. So that in the presence of a systolic basal 
 murmur as an isolated sign the presumption is against the 
 presence of organic disease. Obvious causes of functional 
 murmurs, too, are usually apparent, and the bruit de diable is 
 frequently heard on auscultation over the jugular vein. The 
 size of the heart is rarely increased, and the second sounds are 
 of normal character. The murmur is usually not loud, and is 
 badly conducted, and is variable or perhaps inconstant, accord- 
 ing to the attitude of the patient and the phase of respiration. 
 It is almost always best marked when the patient is recumbent, 
 and less distinct or absent when he assumes the upright 
 position ; and it can often be altered by the cessation of respira- 
 tion, either on full inspiration or full expiration ; while it may 
 only be present when the patient is at rest, disappearing on 
 even shght exertion. A similar variability ma}^ also occur 
 with the apical systolic murmur. As a rule this murmur 
 observes all the distinctions which connote the presence of 
 mitral regurgitation, though it disappears when the patient's 
 health and the tone of the muscular sphincter are restored. 
 In other instances, however, the murmur itself is suggestive 
 of a functional cause, being most distinct outwith or inside 
 the apex impulse and not over it, and varying with the respira- 
 tory phases, waxing during inspiration and waning during ex- 
 piration. Cessation of respiration on full expiration generally 
 causes this murmur to disappear (carclio-pulmonary murmur). 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 331 
 
 Too much reliance, however, must not be laid upon the 
 -auscultatory signs, and the case must be considered on general 
 lines. The presence at the time, or previously, of any disease, 
 :such as acute rheumatism, which is commonly accompanied 
 by endocarditis, always turns the bias in favour of organic 
 •disease of the valve. 
 
 The Physical Signs oJ Myocardial Weakness in the Infections. 
 
 — The physical signs of chronic myocardial failure are some- 
 times slight and equivocal, for they are often disturbed by 
 pre-existing changes in the heart. The apex impulse in renal 
 cirrhosis, for example, may be more forcible than normal, 
 though it is really weak for the individual case. The borders 
 of the area of cardiac dulness may be displaced on account of 
 compensator}^ enlargement, and not from the dilatation of 
 progressive weakness. And the cardiac sounds may be weak 
 or distant from emphysema or subcutaneous fat. The pulse, 
 too, may convey erroneous ideas, for its rate is not necessarily 
 increased in failure, and it may be less frequent than the 
 •average, and the blood-pressure may be above the normal, 
 though too low for the individual's comfort. The history of 
 the case and the nature of the symptoms are the most useful 
 /guide in both diagnosis and prognosis. 
 
 The physical signs of increasing cardiac weakness are well 
 seen in the injections, in particular those without local cardiac 
 lesions and of severe character, such as typhus fever, for 
 appreciable changes may occur in the course of a few hours, 
 and so at a time when the memory of their former character 
 is acute and accurate. 
 
 The apex impulse, as the weakness increases, loses its punc- 
 tate character and becomes more diffuse, while its force and 
 •duration diminish, until it wholly disappears . It can, however, 
 often be recovered if the patient lies on his left side, but may 
 «ven then be lost if the weakness is extreme. The area of 
 dulness is rarely appreciably altered, but shght variations in 
 the position of the various borders may sometimes be deter- 
 mined. The auscultatory signs are more distinct. The first 
 apical sound loses its special emphasis and becomes less 
 loud and more distant, its quality is altered, and it becomes, 
 
332 DISEASES OF THE HEART 
 
 shorter and sharper and. approximates to that of the second 
 sound; so that, if the heart is beating freqluently and diastole 
 is shortened, the sounds closely resemble the tic-tac of the 
 watch or the foetal heart. The change is best appreciated 
 at the apex, where the first sound is normally loudest and most 
 emphatic ; with its weakening the second sound becomes 
 relatively loud, and so apparently accentuated. The sounds 
 at the base are similarly affected, but as the second sound here 
 is in health the loudest, the alteration is less readily recog- 
 nized. The first sound may finally disappear at the base^ 
 though it is still audible at the apex; and eventually may be 
 inaudible anywhere. The pulse-rate as a rule becomes more 
 frequent with increasing weakness, and though the amphtude 
 of the wave is not at first affected, its force and duration are 
 lessened, and it becomes softer and quicker, and perhaps 
 dicrotic ; eventually it becomes smaller as well. The rhythm 
 of the pulse is occasionally changed. An inJrequent pulse in a 
 febrile illness is generally due to a coupled rhythm, the extra- 
 systolic beat being imperceptible to the finger, though it can 
 be recognized on auscultation. The irregularities due to extra- 
 systoles, heart-block, auricular fibrillation, and auricular 
 flutter, may all occur, though they are uncommon even in cases 
 where an acute endocarditis has ensued, but I have observed 
 them all in pneumonia and acute rheumatism. Greoffrey 
 Fleming has been kind enough to give me some statistics 
 (unpublished) upon this point, the result of his investigations 
 in RuchiU Fever Hospital. Of 29 cases (diphtheria, 10; 
 scarlatina, 9 ; enteric fever, 7 ; typhus fever, 3), where routine 
 tracings were taken from the second or third day of the illness,. 
 2 alone showed extra-systoles, and they occurred in only 5 out 
 of 61 patients suffering from various fevers, in whom tracings 
 were taken on account of some cardiac abnormahty. Heart- 
 block was detected in 1 case of diphtheria, in which the a.v, 
 bundle was afterwards found to be involved in an inflammatory 
 lesion; and in another case of diphtheria, a case of enteric 
 fever, and a case of scarlatina, a transient partial] block was 
 recognized. 
 
 The Physical Signs o£ Mitral Disaase. — The general appear- 
 ance of mitral patients is often suggestive, but is, of course, 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 333 
 
 ■only apparent in patients with advanced disease. The face is 
 puffy and congested, and the complexion is dusky, and the 
 lips and ears are more or less blue. A malar flush is common, 
 and the malar capillaries may be permanently dilated. The 
 hands and feet are often cold and clammy, and in chronic 
 cases a mild degree of clubbing of the finger-tips may be found. 
 Difficulty in respiration, too, may be evident even when the 
 patient is at rest. 
 
 Mitral Stenosis. — The apex impulse is punctate and not 
 well defined, and little, if at all, displaced ; it may be impalpable. 
 Pulsation is often present in the second left intercostal space 
 ■close to the sternum, and in the epigastrium. There has been 
 much discussion as to the cause of the former pulsation. George 
 BaKour maintained that it was due to the dilated left auricle en- 
 larging forwards in front of the pulmonary artery and reaching 
 the front of the chest. This undoubtedly does occur, but it is 
 rare (I have only seen one example post-mortem), while the 
 pulsation in question is of common occurrence. It is generally 
 due, as William Russell has shown, to enlargement of the 
 pulmonary artery or of the conus arteriosus, the left auricle 
 seldom presenting more than the tip of the appendix on the 
 front of the heart, and it is outside the pulmonary artery 
 and well away from the sternum. In polygraph tracings 
 [cf. Fig. 154) the chief wave usuaUy succeeds the apex impulse, 
 and is undoubtedly derived from the pulmonary artery, though 
 a smaller wave of auricular rhythm often co-exists. Occasion- 
 ally the chief wave is synchronous with the apex impulse, and 
 presumably due to the contraction of the conus. The epigas- 
 tric pulsation is generally inverted, and therefore due to the 
 contraction of the right ventricle. 
 
 In certain cases of mitral stenosis the apex impulse is large 
 and well marked, and may be considerably displaced both 
 outwards and downwards. This may result from the co- 
 existence of mitral reflux or disease of the aortic valve, which 
 necessarily entail enlargement of the left ventricle. When it 
 obtains without mitral reflux or aortic disease, it is invariably 
 associated with a high blood-pressure and arterio sclerosis or 
 fibroid kidneys. In some of these cases the epigastric pulsa- 
 tion is due to the left ventricle; careful examination of the 
 
334 
 
 DISEASES OF THE HEART 
 
 rhythm of the pulsation -will decide the point. The sternum^ 
 too, may definitely pulsate. 
 
 The thrill is very characteristic, and is frequently present. 
 It commences during diastole as a soft, purring tremor, and 
 
 Fig. 
 
 159. — Skiagram: Reis^al Cirrhosis, Hypertrophy of Left Ventricle 
 (c/. Fig. 162) (J. R. R.). 
 
 rapidly increasing in intensity, ends abruptly as the apex 
 impulse reaches the hand. It is usually limited to the imme- 
 diate vicinity of the apex, but it is sometimes widespread, and 
 I have felt it distinctly beneath the xiphoid cartilage, though 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 335 
 
 post-mortem the tricuspid valve was not narrowed. In another 
 case in which the same distribution was present, tracings showed 
 that the epigastric pulsation was due to the left ventricle, the 
 chest being long and narrow, and the left ventricle hyper- 
 trophied and powerful. 
 
 The area of dulness is as a rule but little altered. In some 
 cases it is enlarged to the right from dilatation of the right 
 heart, or upwards along 
 the left side of the ster- 
 num, even as high as the 
 second costal cartilage, 
 from dilatation of the 
 conus or the pulmonary 
 artery (Fig. 160). 
 
 The murmur is diastolic 
 (presystolic) in rhythm, 
 and at first soft and 
 distant ; but it rapidty 
 becomes loud and rough 
 (crescendo), terminating 
 abruptly with a loud 
 "snap," the shortened 
 representative of the first 
 sound. It is well imitated 
 b}^ vocalizing the symbols 
 rrrh or voot. The exact 
 cause of the murmur has 
 been much disputed. It 
 commences during ven- 
 tricular diastole and ends 
 synchronously with the 
 apex impulse, and thus 
 occurs during the period of auricular systole. It is one of the 
 loudest and roughest of cardiac murmurs, and it seems im- 
 possible that it can be produced by the relatively weak auricular 
 systole; but its chief cause is undoubtedly auricular, for it 
 disappears when auricular fibrillation occurs. Other factors, 
 however, aid in its production. 
 
 In its typical form the murmur begins early in diastole, 
 
 Fig. 160. — Diagraivi showing Area of Dtjl- 
 btess and pulsation ( + ) in mlteal 
 Stenosis. 
 
 This and the following diagrams are actual 
 ease records from my ward journals. 
 
336 DISEASES OF THE HEART 
 
 and so softly tliat the exact commencement is difficult to deter- 
 mine; the "snap " with which it ends is synchronous with the 
 apex impulse. The apex impulse, however, is not exactly 
 synchronous with the commencement of ventricular systole, 
 for a certain period elapses before the muscular contraction 
 so alters the shape and position of the ventricles that the 
 impulse is perceptible outside the chest wall. The early parts 
 of the murmur, therefore, are diastohc in time, while the ter- 
 minal crescendo portion is synchronous, first of all with 
 auricular systole, and, at the very end, with the commence- 
 ment of ventricular systole.* 
 
 The mechanical disturbance in mitral stenosis is peculiar 
 to this lesion. The obstruction at the valve leads to engorge- 
 ment within the left auricle, and its muscle in consequence 
 hypertrophies, but as this is rarely sufficient, the left auricle 
 dilates, the pulmonary circulation becomes engorged, and the 
 right ventricle in consequence hypertrophies. At the con- 
 clusion of ventricular systole the left ventricle is relatively 
 empty and the intraventricular pressure is at a minimum, while 
 the auricular (left) pressure is relatively high, as the chamber 
 has just been refilled from the right heart. If, from the rela- 
 tive difference in pressure within the two cavities, the fiow of 
 blood is rapid, a soft murmur may be produced. In mid- 
 diastole the difference in pressure is less, for the ventricle is now 
 partly filled and the auricle partly emptied, and the flow is less 
 rapid and the murmur becomes more faint or disappears. 
 When auricular systole ensues, the difference in pressure is 
 rapidly augmented, the flow becomes more rapid, and the 
 murmur becomes louder. At the commencement of ventricular 
 systole the intraventricular pressure, on account of the mitral 
 obstruction, is stiU relatively low, and the auricular pressure is 
 
 * The time relations of the commencement of ventricular systole and the 
 first sound of the heart have been investigated by means of the phono-electro- 
 cardiograph, and it is stated by Fahr,i that the former precedes the latter by 
 0-02 to 0-04 second. Weiss and Joachim,^ using similar methods, have found 
 that the terminal portion of the crescendo murmur occurs during ventricular 
 systole. Lewis's conclusions^ are similar. 
 
 1 Heart, 1912, vol. iv., p. 147. 
 
 2 Zeitschr.f. Bin. lied., 1910, vol. siii. 
 
 3 Heart, 1913, vol. iv., p. 241. 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 337 
 
 still relatively high, and until the ventricular pressure rises 
 above the auricular pressure as the result of ventricular con- 
 traction, the valve will not be closed, and blood will continue 
 to flow from auricle into ventricle. This, of course, only 
 occurs for a very short period, as the intraventricular pressure 
 rises very rapidly, but, synchronously with the commencement 
 of ventricular systole, 
 the sphincter muscle of 
 the mitral valve and the 
 muscuH papillares con- 
 tract, so that the shape 
 of the valve and the ten- 
 sion of its cusps are 
 altering while blood is 
 still flowing from auricle 
 into ventricle; and it is just 
 at this moment that the 
 characteristic crescendo 
 part of the murmur oc- 
 curs. As the current 
 ceases to flow, the "snap " 
 is heard. The crescendo 
 character then is due to 
 blood flowing through the 
 mitral valve at a time 
 when changes are taking 
 place in the lumen of the 
 orifice and in the tension 
 of the cusps,* 
 
 The influence of the 
 ventricular contractions 
 is shown as weU by another phenomenon. In slight degrees 
 of mitral stenosis the murmur may be absent when the patient 
 is lying down, but becomes distinct on any physical exertion. 
 such as sitting up, an action which has a definite effect on the 
 strength of the ventricular contraction, and but little effect 
 upon the contraction of the auricle. 
 
 The crescendo murmur is usually heard best a little internal 
 * Cowan, Glasgow Med. Journ., 1898, vol. xlix., p. 166. 
 
 Fig. 161. — Diagbat^i showing Distribution 
 OF Pkesystolic Mtjrmtjk (0) IN Mitral 
 Stenosis. 
 
 fl = accentuation of second pulmonic 
 sound. 
 
338 
 
 DISEASES OF THE HEART 
 
 to and above the apex impulse, and is limited in its distribu- 
 tion, being generally audible over an area which is little larger 
 than a crown piece (Fig. 161). The limited area of audibility 
 is proportionate to the area of left ventricle related to the 
 
 Fig. 
 
 162. — Skiagram: Mitral Stenosis. Dilatation and Hypertrophy of 
 Right Heart (J. R. R.) (c/. Fig. 159). 
 
 front of the chest, which, in uncomphcated cases, is small, as 
 the enlarged right ventricle displaces the left backwards and 
 away from the front of the chest ; but the area is larger when 
 the left ventricle is enlarged from other causes, and the murmur 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 339 
 
 may then be audible right up to the sternum. The murmur is 
 rapidly lost towards the axilla, though the softer systolic 
 murmur is weU conducted in this direction. The reason 
 is obvious. In mitral reflux the ventricle is in systole, and 
 the apex is in intimate contact with the ribs, and the vibra- 
 tions are well conducted along them. In mitral stenosis the 
 murmur is diastolic in rhythm, the apex is not firmly applied 
 to the chest, and the vibrations are, in consequence, rapidly 
 lost. 
 
 If auricular fibrillation ensues, the early diastohc murmur 
 may persist, though the characteristic presystohc murmur 
 disappears ; for when the co-ordinated auricular contraction 
 ceases, the flow of blood at the end of diastole is not sufficiently 
 rapid to produce audible vibrations.* 
 
 If the ventricle is relatively weak, the early diastohc murmur 
 rapidly succeeds the second sound and quickly dies away 
 (lubb-te-te), simulating a doubled second sound, but differing 
 from true doubhng in its distribution, the latter being heard 
 best at the base, the former only at the apex (Figs. 163, 164). 
 If the ventricle is powerful, the diastolic aspiration may be 
 powerful, and the murmur may be of considerable duration. 
 The murmur is necessarily separated from the second sound, 
 for, as Lewis pointed out, the auriculo-ventricular valve only 
 opens after the aortic valve has closed. 
 
 The third murmur of mitral stenosis is of different origin. 
 It is a soft murmur of varying length, running out of the 
 second sound, and heard best to the left of the sternum in the 
 second or third interspace. It is almost certainly due to 
 relative incompetence of the pulmonary valves, the pulmonary 
 
 * James Mackenzie has pointed out that the presystolic murmur may also 
 disappear if conductivity is defective and the auricular and ventricular con- 
 tractions are separated from their usual close connect! on. Ritchie! has demon- 
 strated this in electro- cardiograms (Fig. 67). I have observed it in one case 
 where the murmur was absent when the a-c interval measured 0-25 second, and 
 present when the interval measured 0-20 second. A mid- diastolic murmur 
 synchronous with auricular systole, and separate from both first and second 
 sounds, may appear in these cases, and has been demonstrated by Lewis^ with 
 the phono-electro-cardiograph. 
 
 1 Edin. Med. Journ., 1913, vol. x., N.S., p. 410. 
 
 2 Heart, 1913, vol. iv., p. 241. 
 
340 
 
 DISEASES OF THE HEART 
 
 artery having dilated under the stress of the increased pressure 
 within it to such a degree that the cusps are unable to close the 
 aperture. 
 
 The second pulmonic sound in well-compensated cases is 
 alwaj^s notably emphatic, and may be palpable. As compen- 
 sation fails with dilatation of the right heart, it loses emphasis. 
 Very often the two second sounds are not synchronous, and 
 
 Fig. 163.— Diagram showing Area 
 OF Reduplicated Second Sound. 
 
 Fig. lei. — Diagram showing Area of 
 Early Diastolic Mitral Murjiur. 
 
 a '* reduplication " is audible over the sternum, which may be 
 heard in lessened intensity at the apex. 
 
 The 'pulse in mitral stenosis is in no waj- characteristic. In 
 simple uncomplicated cases it is quite normal so long as com- 
 pensation is good ; but in manj^ cases it is small and hard and 
 well sustained from associated renal disease — a complication 
 which is present in a large proportion of cases, particularly 
 those of some duration (Figs. 165, 166; c/. p. 269). When 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 341 
 
 auricular fibrillation ensues, the characteristic irregular pulse 
 makes its appearance, and generally persists until the end. The 
 blood-pressure as a rule falls to some extent when this occurs. 
 .■' In mitral stenosis com- 
 pensation is at first effected 
 by hypertroph.}^ of the left 
 auricle. In the lesser grades 
 this may be sufficient, but 
 in even average cases it soon 
 fails, and the cavity in con- 
 sequence dilates, with re- 
 sultant stasis and congestion 
 of the pulmonary circuit; to 
 overcome this the right 
 ventricle hypertrophies. It 
 is difficult to appreciate the 
 precise degree of the lesion, 
 for the size of the left auricle 
 and of the right ventricle can 
 rarely be measured. Any 
 notable increase in the area 
 of dulness to the right indi- 
 cates an enlarged right heart 
 (Fig. 167), and the stenosis 
 in these cases is usually con- 
 siderable; but an enlarged 
 right heart is only present 
 when the right ventricle has 
 dilated under the strain, and 
 compensation is, in conse- 
 quence, more or less broken. 
 Notable epigastric pulsation 
 and an indistinct apex im- 
 pulse result from right ven- 
 tricular hypertrophy ; but 
 other causes 
 
 
 
 
 
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 as the}' may also occur from 
 an accurate conclusion is difficult to obtain. 
 If the right ventricle is powerful, the lower end of the sternum 
 may be felt to pulsate ; but this depends in great measure on 
 the softness of the ribs, and is seldom w^ell marked save in 
 
342 
 
 DISEASES OF THE HEART 
 
 childhood and in adolescence. It must be remembered that 
 mitral stenosis 'per se exerts no influence upon the left heart, 
 which, if hypertrophied, is hypertrophied from other causes. 
 
 Mitral Reflux. — The apex impulse is diffuse and heaving, 
 and is displaced to the left and downwards ; it may be felt in 
 several interspaces, and pulsation is usually also evident in 
 the epigastrium. A thrill is sometimes felt at the apex ; it is 
 diminuendo in character, and accompanies and succeeds the 
 apex impulse; it is more often absent than present. The area 
 
 DEC 
 
 MAR 
 08 
 
 He- 
 
 mm. 
 
 190 
 
 180 
 170 
 160 
 150 
 140 
 130 
 120 
 no 
 100 
 90 
 80 
 70 
 
 12 
 
 25 
 
 MAY 
 
 7 
 
 17 
 
 28 
 
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 20 
 
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 29 
 
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 — ^ 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 ^ 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 Fig. 166. — Blood-Peessuee Chart. 
 F., aged 46: Mitral disease; cirrhotic kidneys. 
 
 of dulness is increased to the left and downwards in correspond- 
 ing proportion to the displacement of the apex (Fig. 168). The 
 murmur is systoHc in rhythm, and replaces or follows the first 
 sound. It is usually soft and blowing, and is less harsh than 
 the aortic systoHc murmur. It is heard best at the apex, and 
 is well conducted into the axilla along those ribs with which 
 the apex is in contact (Fig. 169). When the murmur is loud, 
 it may be audible all over the left chest ; and it is often distinct 
 at the back, with maximal intensity at the angle of the left 
 scapula, and in a lessened degree along the spine (Fig. 170). The 
 second pulmonic sound is emphatic. The second sound at the 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 343 
 
 base may be doubled, but this is more frequent in stenosis 
 than in regurgitation. 
 
 The j)ulse is normal in character in simple, well-compensated 
 cases, but is well sustained if, as frequently happens, renal 
 fibrosis co-exists. When auricular fibrillation ensues, the 
 characteristic irregular pulse makes its appearance. The 
 blood-pressure in simple, well-compensated cases is about, or 
 
 Fig. 167.— Diagram showing Area of 
 DuLNESs IN A Dilated Heart. 
 
 Pig. 168. — Diagram showing Area op 
 dulness and pulsation in mitral 
 Reeltjx. 
 
 sHghtly below, the normal reading. In cases where renal 
 fibrosis or arterio-sclerosis co-exist, the pressure is elevated, 
 sometimes to very high readings ; it is generally, but not in- 
 variably, high in the presence of oedema. 
 
 The murmur sometimes shows notable variations in its 
 character with successive beats. This is particularly the case 
 in heart-block {q.v.) when the auricular and the ventricular 
 contractions coincide, as regurgitation is prevented or is 
 
344 
 
 DISEASES or THE HEART 
 
 minimal; and the murmur is, in consequence, absent, or 
 weakened and shortened. A similar phenomenon may occur 
 in auricular fibrillation, for as the degree of distension of the 
 auricle when its co-ordinated contractions cease depends 
 upon the duration of diastole and the aspiratory action of the 
 left ventricle, it may, if the ventricular contractions are fre- 
 
 FlG. 169. — DiAGBAM SHOWING DISTRIBU- 
 TION OP Systolic Murmur in Mitral 
 
 E.EFLUX. 
 
 fi= accentuation of second pulmonic sound. 
 
 Fig. 170. — Diagram showing Distribu- 
 tion OF Systolic Murmur of Mitral 
 Reflux. 
 
 quent, become so distended that free regurgitation is impos- 
 sible. A similar explanation, too, accounts for the frequent 
 absence of a regurgitant murmur in well-marked cases of mitral 
 stenosis, where post-mortem the valve is seen to be so hard 
 and shrunken that the orifice can hardly be closed, even if 
 considerable force is exerted. The obstruction in these cases 
 is often extreme, and the congestion in the auricle too great 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 345 
 
 to allow any appreciable reflux from the ventricle during 
 ventricular systole. 
 
 Mitral regurgitation is compensated by alterations in the left 
 auricle and ventricle, and in the right ventricle. The capacity 
 of the left ventricle is necessarily increased, for, if blood flows 
 back through the mitral valve during ventricular systole, the 
 ventricle must enlarge to accommodate the amount returned 
 into the auricle as well as the normal amount for the aorta ; and 
 the Avail is hypertrophied on account of the extra work which 
 is entailed. During ventricular systole the left auricle is over- 
 distended, for it receives blood from the left ventricle as weU as 
 from the right, and the auricular wall, in consequence, hypertro- 
 phies. The right ventricle, too, hypertrophies, as its work is in- 
 creased by the heightened pressure within the pulmonary circuit , 
 
 The degree of the lesion maj- be gauged by the degree of 
 enlargement of the left ventricle. The length of the murmur, 
 too, is of value in this respect, as a short murmur occurring 
 after the first sound indicates a short duration of the regurgita- 
 tion, and, in consequence, a minimal leak. If the murmur is 
 well heard at the scapular angle, the lesion is probably always 
 organic and gross, for it is only conducted in this direction in 
 cases where the left auricle is dilated and reaches close to the 
 back; and this will not occur in slight or in functional in- 
 sufficiency. In well-marked regurgitation the second pulmonic 
 sound is notably emphatic. If the right ventricle is greatly 
 hypertrophied, the lower end of the sternum may pulsate, and 
 epigastric pulsation is well-marked. The relationship between 
 the size and strength of the pulse and the apex impulse should 
 also be compared, for in well marked regurgitation the pulse 
 is small and soft, though the apex impulse is diffuse and powerful. 
 
 In cases of mitral disease where compensation has failed, the 
 physical signs may alter. The pulsation in the apex region 
 becomes more diffuse and less powerful, and is often better 
 seen than felt, and is not well sustained. Epigastric pulsation is 
 more marked, and pulsation may be felt in the fourth and fifth 
 right intercostal spaces. The area of dulness is increased both 
 to the left and to the right. The murmurs become shorter and 
 less loud, and the second pulmonic soundless emphatic ; reduphca- 
 
346 DISEASES OF THE HEART 
 
 lion generally persists. If auricular fibrillation has ensued, the 
 crescendo thrill and murmur of stenosis disappear, though the 
 early diastohc murmur may persist. The pulse becomes more 
 frequent and the wave loses in strength, volume, and duration. 
 
 The Physical Signs of Aortic Disease. — The general appear- 
 ance of aortic patients may be characteristic. They are often 
 notably pale, and may appear careworn or anxious, frightened 
 or in pain; the carotid or the temporal arteries may visibly 
 pulsate, and the head may shake with each beat of the heart. 
 These symptoms, however, must be referred more frequenth^ 
 to associated disease than to the valvular lesion itself; for 
 while anaemia occurs in aortic valvular disease, it only obtains 
 when the compensatory arrangements have broken down and 
 the general nutrition is, in consequence, defective. Anaemia 
 occurs in syphihs, in arterio-sclerosis, and in chronic renal 
 disease, and its presence in aortic valvular disease is most often 
 due to those causes, and not to the cardiac lesion. Anaemia is 
 by no means constant; some aortic patients are plethoric 
 rather than anaemic ; others are cyanosed ; in some the blood- 
 counts are normal ; though, in a general way, a contrast should 
 be drawn between the cyanosis of mitral and the pallor of 
 aortic disease, A similar distinction holds good with regard 
 to the expression. The cause of angina pectoris is sometimes 
 cardiac and sometimes aortic, and the frequency with which 
 disease of the aorta co-exists in aortic valvular disease makes 
 the symptom of common occurrence. Even the throbbing of 
 the vessels is not pathognomonic, for they throb whenever a 
 large quantity of blood is suddenly thrown into relatively empty 
 vessels ; and it may be notable in exophthalmic goitre and in 
 excited chlorotic girls, quite apart from any valvular disease. 
 
 Aortic Stenosis. — Pure aortic stenosis is comparatively un- 
 common, and I have only seen two or three specimens. In 
 one case in which the valve presented an appearance very 
 similar to that shown in Fig. 137 a systolic murmur alone was 
 present, so that regurgitation must have been minimal. The 
 patient, who was aged sixty- two, was admitted with oedema, 
 Cheyne-Stokes breathing, etc., and died from progressive 
 cardiac failure. A loud, harsh murmur was audible all over 
 the cardiac area, replacing the first sound and occupying a 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 347 
 
 considerable portion of the short pause. It was loudest at the 
 aortic cartilage, and the second sound was inaudible here; a very 
 faint second sound could be heard at the apex. The heart on 
 post-7nortem examination was found to weigh 24|^ ounces. The 
 aortic cusps were adherent to each other for the greater part of 
 their extent, and were thickly infiltrated with large calcareous 
 masses. The lumen was greatly narrowed, and the cusps were 
 practically immobile, and to the water-test notoriously incom- 
 petent, though no diastohc murmur was audible during life. 
 
 The a'pex impulse is large and heaving and well sustained, 
 and is displaced downwards and in lesser degree to the left. 
 A thrill, which is systoHc in rhythm and usually rougher than 
 the thrill of mitral reflux, may be felt at the base. The area 
 of cardiac dulness is increased downwards and to the left in 
 corresponding proportion to the displacement of the apex. 
 The mui'mur is diminuendo and systohc in rhythm, following 
 or replacing the first sound. It is generally harsh and is often 
 loud, and contrasts with the soft murmur of mitral reflux. It 
 is heard best at the aortic cartilage, and is weU conducted 
 upwards into the neck along the carotid and subclavian 
 arteries (Fig. 171). It is sometimes very loud, and may be 
 audible on auscultation over the vertex of the head, the 
 sacrum, and the condyles of the humerus ; or even without 
 direct contact with the patient. When heard at the back, it is 
 loudest close to the left border of the vertebral column, about 
 the level of the fourth dorsal vertebra, where the aorta first 
 comes into contact with the spine (Fig. 172). The second 
 aortic sound ma}' be weakened or inaudible if the stenosis is 
 considerable and the cusps stiff. A second sound is, however, 
 generally audible at the aortic cartilage even in well-marked 
 cases, but is due to the closure of the pulmonic valves. The 
 aortic sound alone is heard on auscultation over the carotid 
 artery, and the character of the sound should be gauged only 
 b}' auscultation above the clavicle, so as to avoid this fallacy. 
 
 The pulse is small, infrequent, and slow, the wave rising 
 gradually beneath the finger. It is weU sustained, and the 
 artery is well fiUed between the beats. These characters, 
 however, are probably due to coincident arterial disease rather 
 than to the valvular defect, but the two frequently co-exist ; 
 
348 
 
 DISEASES OF THE HEART 
 
 an anacrotic pulse is generally the result of arterial hardening, 
 just as intonation of the second sound is an indication of an 
 enlarged and stiff aorta, rather than an index of the height of 
 the blood-pressure. Tracings show the gradual rise of the 
 pulse-Avave, the rounded apex, and the gradual fall ; the normal 
 Avaves on the downstroke are usually poorly marked, and the 
 dicrotic wave may be wholly absent. 
 
 Fig. 171. — Diagram showing Disteibtj. 
 TiON or Murmur of Aortic Stenosis. 
 
 y = weakening of second aortic sound. 
 
 Fig. 172. — Diagram showing DiSTEiBtr- 
 TioN of Murmur of Aortic Stenosis. 
 
 Aortic stenosis is compensated by hypertrophy of the left 
 ventricular muscle, and the degree of the stenosis jnsbj be 
 estimated by the degree of enlargement, but here again the 
 condition of the arteries and kidneys must be taken into 
 account, for the hypertrophy may in large measure be due to 
 arterial or renal disease. Basal systolic murmurs not infre- 
 quently obtain from mere roughening or hardening of the 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 349 
 
 cusps with little or no stenosis ; the condition can be recognized 
 by the absence of ventricular hypertrophy which accompanies 
 any definite narrowing. The character of the second sound is 
 important, for its absence indicates gross valvular disease. 
 
 The relationship between the size and strength of the pulse 
 and apex impulse should also be compared, for in gross stenosis 
 the pulse-wave is small 
 and weak, while the apex 
 impulse is diffuse and well 
 sustained. 
 
 A ortic Regurgitation . — 
 The a'pex impulse is power- 
 ful, well sustained, and 
 diffuse, and is displaced 
 downwards and to the left. 
 Pulsation may be present 
 in several interspaces. 
 Pulsation, too, is often 
 evident elsewhere ; towards 
 the base and in the second 
 and third right inter- 
 spaces, even in the absence 
 of dilatation, and in the 
 carotids and above the 
 sternum; the whole chest 
 may heave. The head is 
 sometimes seen to shake 
 
 with each systole; and the Fig. 173. — Diagbaji showing Area of Dul- 
 
 , p XT 1 J ^Ess AND Pulsation in Aortic Reflux. 
 
 vehemence of the beats 
 
 may be so great that they can be felt by the observer seated 
 on the bed without direct contact with the patient. A th-ill 
 can sometimes be felt over the base, diastoHc in rhythm, and 
 succeeding the second sound. It is more often absent than 
 present. The area of cardiac dulness is increased to the left 
 and downwards, in corresponding proportion to the enlarge- 
 ment of the left ventricle (Fig. 173). 
 
 The murmur is diminuendo and diastolic in rhythm, succeed- 
 ing or replacing the second sound, and running for a variable 
 period into the long pause. It is usually soft and blowing, 
 
350 
 
 DISEASES OF THE HEART 
 
 and may be distant and difficult to detect ; but it is often loud 
 and superficial; it is sometimes musical in character. It is 
 heard best over the sternum, as a rule with maximal intensity 
 about the middle, opposite to the third or fourth interspaces ; 
 and is well conducted down the sternum to the xiphoid carti- 
 lage, and in lessening degree to the apex (Fig. 174). When it 
 is well heard at the apex, it is said (Foster) to indicate a special 
 
 Fig. 174. — Diagram showing Distkibu- 
 TioN OF Diastolic Mtjemue in Aortic 
 Reflux. 
 
 ^ = weakening of second aortic sound. 
 
 Fig. 175. — Diagram showing Area of 
 Diastolic Mtjrmtjr of Aortic Re- 
 flux. 
 
 failure of the left posterior cusp. Sometimes the murmur is 
 heard best at the aortic cartilage (Fig. 175), and it may be 
 conducted into the carotids, but much less frequently than the 
 systolic aortic murmur. OccasionaUy it is heard best towards 
 the xiphoid end of the sternum. In well-marked cases, with a 
 loud murmur, it may be audible all over the chest, and even 
 on auscultation over a large artery hke the femoral in Hunter's 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 351 
 
 canal. As a rule this murmur of Duroziez is absent, but it 
 never occurs in the absence of aortic reflux. 
 
 A presystoKc murmur (Austin Flint's murmur) is sometimes 
 present at the apex in these cases without there being any 
 mitral disease. In the majority of cases, however, in which 
 a presystohc murmur is present mitral stenosis co-exists. 
 
 In the majority of cases the second aortic sound persists and 
 precedes the murmur; but in gross defects, where the cusps are 
 so shrunken or stiffened that they cannot meet, the sound 
 may disappear and be whoUy replaced by the murmur. 
 
 The pulse is large and quick (shotty, collapsing, water- 
 hammer, Corrigan's pulse), rapidly reaching a maximum and 
 rapidly collapsing. This character is exaggerated if the hand 
 is raised above the head, and may be better felt if the forearm 
 is grasped by the whole hand than when the artery alone is 
 felt by the finger. Capillary pulsation is always well marked. 
 
 Fig. 176. — Sphygmogeam in Aoktic REGUBGiTATioir. 
 
 Tracings show an almost vertical abrupt upstroke, a pointed 
 apex, and a sudden fall, the aortic notch being low down and 
 the dicrotic wave poorly developed (Fig. 176). 
 
 Aortic regurgitation is compensated by enlargement and 
 hypertrophy of the left ventricle, and the degree of the reflux 
 may be estimated by the degree of the enlargement. Mere 
 hypertrophy of the ventricular waU is insufficient, the ven- 
 tricular content must be larger; for if the aortic content during 
 diastole is to remain of normal amount, the systohc influx 
 must be abnormally large to compensate the amount lost hy 
 regurgitation. In the same way the pulse-pressure is an index 
 of the degree of the fault, for the systohc pressure must be 
 abnormally high, if, notwithstanding the rapid fall of pressure 
 during diastole, the mean aortic pressure is to remain normal. 
 The pulse-pressure is often a valuable guide in these cases, for 
 it is related to aortic reflux alone. Not infrequently mitral 
 
352 DISEASES OF THE HEART 
 
 and aortic reflux co-exist, and the enlargement of the left 
 ventricle is due to the two causes combined; and it is difficult 
 in other wa^'s to assess the proper value of each individual 
 defect. The point may be determined by the finger, for the 
 pulse is more collapsing and " quicker," the greater the reflux. 
 
 The pulse-pressure, however, is only useful as a gauge of 
 the degree of the leak when compensation is eftective. Two of 
 my patients had blood-pressures which were similar (115-92 
 mm. Hg), but the lesions were in no way comparable. In 
 one there was no evidence of cardiac weakness, the patient 
 being under observation on account of an attack of acute 
 rheumatism, and the lesion was minimal. The other patient 
 was moribund at the time, fainting habitually when at stool, 
 and sometimes when he merely sat up in bed. Muscular 
 weakness was so extreme that the pulse-pressure could not be 
 raised to a satisfactory- level, the lesion being gross . Coincident 
 stenosis may whollj^ alter the characteristic pulse of regurgita- 
 tion if the obstruction is considerable and the outflow of blood 
 gradual and prolonged. 
 
 Weakening or disappearance of the second aortic sound is 
 also an important guide to the grade of the lesion, for the 
 presence of a norma] sound indicates that the valves are 
 fulfilHng their purpose fairly well, notwithstanding the leak. 
 This may be seen in tracings ; a well-marked dicrotic wave has 
 a similar significance. The length of the murmur is an indi- 
 cation of the duration of the regurgitation. In shght cases 
 it mereh' follows the second sound for a short distance, but 
 in severe leaks may occupy the whole of diastole. 
 
 The Physical Signs o! Valvular Disease of the Right Heart. 
 
 — Valvular disease on the right side of the heart is uncommon. 
 Both the pulmonary and the tricuspid valves maj- be affected 
 bj' acute endocarditis, but this is generaU}' malignant in 
 tj-pe and secondary to septic foci elsewhere, the organisms 
 being conveyed directly to the heart through the veins; and is 
 rarely of the simple form, so that chronic lesions are unusual. 
 When chronic lesions occur, they are almost alwaj's accom- 
 panied by disease of the mitral or aortic valves, of older date 
 and more extreme grade. The tricuspid valve is affected 
 much more frequently than the pulmonary. 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 353 
 
 Congenital defects are fairly common, and affect the pul- 
 monary artery in particular, tricuspid lesions, like those of 
 the mitral valve, being extremely rare. As pulmonary defects 
 arise during the development of the septum of the truncus 
 arteriosus, the aortic valve is also frequently involved. 
 
 Functional (secondary) incompetence of the tricuspid valve, 
 on the other hand, is of common occurrence. The tricuspid 
 is similar in its structure to the mitral valve, and becomes 
 incompetent if the right ventricle dilates, the muscular 
 sphincter becoming unable to narrow the orifice sufficiently 
 for the cusps to occlude it. The right ventricle is always over- 
 worked in mitral disease and in chronic pulmonary diseases, 
 such as emphysema and fibroid phthisis, and although com- 
 pensatory hypertrophy ensues and so allows the work to be 
 carried on for a time, it ultimately becomes insufficient, and 
 the ventricle gives way beneath the strain. In acute pul- 
 monary disease a temporary incompetence is not unusual. 
 
 Tricuspid incompetence, even when due to muscular weak- 
 ness, is always extremely serious, for the strain is thrown 
 upon the right auricle, which is incapable of satisfactory 
 compensatory hypertrophy, so that venous stasis follows. 
 The appearance of oedema in the feet and passive venous 
 congestion of the hver are the result. 
 
 Pulmonary incompetence may own a similar cause. In 
 cases of extreme mitral stenosis the blood-pressure in the 
 pulmonary circuit is extremely high, and the artery may 
 dilate and incompetence ensue without any lesion of the cusps. 
 With improvement the characteristic murmur may disappear. 
 The comparable incompetence in cases of high aortic blood- 
 pressure is rare, for the aorta is thicker than the pulmonary 
 artery, and its valves remain competent (in experiment) 
 under a pressure which produces notable regurgitation at 
 the pulmonary valve (G. A. Gibson). 
 
 Tricuspid incompetence is probably the most frequent as 
 well as the most serious valvular lesion, for it occurs in many 
 diseases as a sequel of cardiac failure, and so is the immediate 
 precursor of death. 
 
 Pulmonary Stenosis. — The murmur is usually loud and harsh 
 and superficial, and replaces or follows the first sound. It 
 
 23 
 
354 DISEASES OF THE HEART 
 
 is heard best in the second left interspace close to the sternum, 
 and is well conducted to the left clavicle (Fig. 177). It is 
 not conducted into the carotid artery. The maximum in- 
 tensity at the back is some distance away from the spine, 
 about the centre of the left scapula. The second pulmonic 
 sound is weakened or absent. A thrill which is systolic in 
 rhythm is generally present, with maximum intensity in the 
 second left interspace. The right heart is hypertrophied, 
 and pulsation may be evident in the epigastrium, at the xiphoid 
 end of the sternum, and in the fourth and fifth right inter- 
 spaces. 
 
 Compensation is effected hj hypertrophy of the right 
 ventricle, but its degree is difficult to gauge; but the Iwper- 
 trophy is considerable, and the stenosis is great if the lower 
 end of the sternum pulsates. The duration of the murmur 
 is an important guide to the grade of the defect. Absence of 
 the second sound indicates a gross lesion of the valve. 
 
 Pulmonary Regurgitation. — The murmur is usually soft and 
 blowing in character, and is diastolic in rhythm, replacing or 
 following the second sound. It is heard best in the second 
 or third left interspaces close beside the sternum, and is con- 
 ducted downwards, and in the direction of the xiphoid car- 
 tilage (Fig. 178). The second 'pulmonic sound may be weakened 
 or absent. A soft diastolic thrill may be felt to the left of 
 the sternum. The right heart is hypertrophied, and pulsation 
 may be present in the epigastrium, at the xiphoid end of the 
 sternum and in the fourth and fifth right interspaces . 
 
 The distribution of the murmur, if it is loud, thus closely 
 resembles that of the murmur of aortic regurgitation. The 
 important differences are the enlargement of the right heart, 
 the interference with the pulmonic second sound, and the 
 absence of the characteristic pulse of aortic disease. 
 
 Compensation is effected by hypertrophy of the right ven- 
 tricle, but its degree is difficult to gauge. If the lower end 
 of the sternum pulsates, the hypertrophy is considerable and 
 the reflux is great. Absence of the second sound indicates 
 a gross lesion of the valve. 
 
 Tricuspid Regurgitation. — Pulsation is generally evident at 
 the lower end of the sternum and in the epigastrium, and often 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 355 
 
 in the fourth and fifth right interspaces. The apex impulse 
 IS not displaced, but it may be impalpable. A thrill is rarely 
 present. The area of dulness is increased to the right, but 
 does not trespass upwards above the third costal cartilage 
 (Fig. 167). The murmur is systohc in rhythm, and replaces 
 or succeeds the first sound; it is usually soft and blowing in 
 character, is heard best at the xiphoid end of the sternum 
 
 Fig. 177. — Diagram showing the Dis- 
 tribution OF THE Systolic Murmur 
 OF Pulmonary Stenosis. 
 
 Fig. 178. — Diagram showing Distri- 
 bution OF Diastolic Murmur of 
 Pulmonary Reflux. 
 
 and is well conducted towards the right nipple 
 At the back its maximum intensity is at the an 
 right scapula. The second pulmonic sound is 
 The jugular veins are usually greatly distended, 
 pulsate forcibly. The hver, too, may show an 
 pulsation, and is generally notably enlarged and 
 palpation. 
 
 Tricuspid regurgitation is compensated to some 
 
 (Fig. 179). 
 
 gle of the 
 
 weakened, 
 and may 
 expansile 
 
 tender on 
 
 extent by 
 
356 DISEASES OF THE HEART 
 
 dilatation of the right ventricle and hypertrophy of its wall, 
 and by dilatation and hypertrophy of the right auricle. The 
 results are, however, less satisfactory than in mitral regurgi- 
 tation, for failure of the right auricle entails general venous 
 stasis, as it has no assistance, when in difficulty, that can be 
 compared to the action of the right ventricle in failure of the 
 left auricle. The degree of auricular distension may be 
 measured by the increase in the size of the cardiac dulness 
 to the right, or by the size of the distended veins and the con- 
 gested liver and the amount of oedema. If the liver is cir- 
 rhotic, however, the enlargement is rarely great. The char- 
 acter of the cervical pulse is of help, for in free tricuspid 
 regurgitation the auricle is rapidly distended by the reflux 
 from the ventricle, and the v wave occurs prematurely, and 
 is merged into the carotid wave, the x depression being lost 
 (c/. Fig. 60, p. 107). 
 
 Tricuspid Stenosis. — The murmur is diastolic (presystohc) 
 in rhythm and crescendo and rough in character, but 
 is rarely as loud as the corresponding murmur of mitral 
 stenosis. It is heard best at the xiphoid end of the sternum, 
 and is of limited distribution (Fig. 180). A rough presystolic 
 thrill has been observed in the same situation. 
 
 Tricuspid stenosis is usually associated with other valvular 
 defects, and often with mitral stenosis. In some of these cases 
 two maxima of the murmur have been observed — in the 
 apical region and at the xiphoid end of the sternum — but 
 the two murmurs are often indistinguishable. It must be 
 remembered that, in cases where the left heart is hyper- 
 trophied, the presystolic murmur of mitral stenosis may be 
 well heard even over the sternum, and its thrill may be felt 
 in the epigastrium. 
 
 Tricuspid stenosis is compensated by hypertrophy of the 
 right auricle, which is rarely sufficient . 
 
 The Physical Signs in Congenital Valvular Disease. — The 
 
 murmurs which occur in congenital heart disease are very 
 perplexing, for the defects are frequently multiple, and an 
 accurate diagnosis is usually only possible on post-mortem 
 examination. In cases, however, where there is a defect in 
 the interventricular septum, and in those with a persistent 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 357 
 
 ductus arteriosus, the lesions may manifest characteristic 
 murmurs . 
 
 The murmur which is present in defect of the interventricular 
 septum (bruit de Roger) is usually loud and harsh; it com- 
 mences early in systole, and is prolonged into diastole, so that 
 it hides or covers the second sound, which may, however, 
 be distinctly heard at the base. The murmur has its site of 
 
 Fig. 179. — Diagkam showing Distribu- 
 tion OP Systolic Mukmue of Tri- 
 cuspid Eeflux. 
 
 Fig. 180. — Diagrasi showing Distri- 
 BTJTioN OF Presystolic Murmur of 
 Tricuspid Stenosis.? 
 
 maximum intensity at the left side of the sternum close to 
 the xiphoid, and is not well conducted into the carotid artery 
 or into the axilla.* 
 
 The murmur in patent ductus arteriosus is also long, and 
 occupies both systole and diastole. It is usually loud and 
 harsh, replacing or running out of the first sound, and per- 
 sisting for a variable period into the long pause, sometimes 
 
 * Cowan and L. Storey, Glasgoiv Med. Journ., 1909, vol. Ixxii., p. 425. 
 
358 
 
 DISEASES OF THE HEART 
 
 even up to the commencement of the succeeding first sound. 
 It is usually loudest at its commencement and diminuendo, 
 but it may wax about its middle and then wane. The second 
 sound may be distinctly audible. The murmur is usually 
 heard best in the second left intercostal space, about 2 inches 
 from the sternum, where a thrill can generally be felt with the 
 hand. The murmur is well conducted to the left clavicle 
 (Fig. 181); but it may be heard best at the back over the left 
 
 scapula. This variation in 
 distribution is due to varia- 
 tions in the other defects. 
 The ductus persists when 
 the pulmonary artery is 
 stenosed at its orifice, so 
 that the pulmonary 
 branches may be supplied 
 from the aorta ; but it may 
 also persist if the aortic 
 orifice is narrowed, so that 
 the descending aorta may 
 be filled from the pul- 
 monary artery. In some 
 cases, then, the flow of 
 blood is from aorta to 
 pulmonary artery; in 
 others, from pulmonar}^ 
 artery to aorta. In many 
 cases aortic or pulmonary 
 
 Fig. 181. — Diagkam showing Disteibution stenosis gives a special 
 OF Mtjemur of Patent Ductus Arteki- , . . , • i 
 
 osus, emphasis at a particular 
 
 The distribution of the murmur in this case site to the first portion of 
 IS unusual. themurmur. The murmur 
 
 which is best heard at the back of the chest is probably that 
 which is produced by blood flowing from pulmonary artery 
 into aorta, the vibrations being loudest where the junction 
 of the blood currents is nearest to the surface. 
 
 The murmurs in these two defects resemble each other in 
 one respect — namely, that they occupy both systole and 
 diastole without any interval between the systolic and the 
 
DIAGNOSIS OF CHRONIC VALVULAR DISEASE 359 
 
 diastolic portions. Such murmurs cannot originate at any of 
 the valves, and only obtain when a communication exists 
 between separate cavities or vessels. These murmurs are not 
 confined to congenital defects, and may be met with in 
 
 Fig. 182. — Stenosis of Left Pulmonary Arteey from Pkessuee of a 
 Malignant Growth {a). 
 
 aneurismal varix as weU as in cases of ulcerative endocarditis 
 or aneurism, if rupture takes place into adjacent cavities or 
 vessels. 
 
 The distribution of murmurs produced at the valves is a 
 
360 
 
 DISEASES OF THE HEART 
 
 natural sequel to their anatomical position within the chest. 
 Any abnormality in distribution indicates that some abnormal 
 factor has come into action. In a case of multiple cutaneous 
 cancer, for instance, a secondary growth occurred in the 
 mediastinum, and nipped the left pulmonary artery just after 
 the bifurcation (Fig. 182), and a loud systohc murmur made 
 
 Fig. 183. — Diagram showing Distbi- 
 BXJTION OF Systolic Mubmur. 
 
 Fig. 
 
 its appearance. It was well heard 
 but it was louder beneath the left 
 the left scapula (Figs. 183, 184), 
 stenosis was situated some distance 
 valve and the front of the chest, 
 an intrathoracic tumour, or a 
 may also lead to the conduction 
 directions. 
 
 184. — DiAGRAJVI SHOWING DISTRIBU- 
 TION OF ISystolic Murmur. 
 
 at the second left space, 
 clavicle, and loudest over 
 clearly showing that the 
 away from the pulmonary 
 An aneurismal dilatation, 
 pulmonary consohdation, 
 of murmurs in abnormal 
 
CHAPTER XXV 
 THE PROGNOSIS OF CHRONIC VALVULAR DISEASE 
 
 The difficulty of forming an accurate prognosis in disease of 
 the heart has recently been emphasized by Sir Chfford Allbutt, 
 in a lecture to the Chelsea Chnical Society; but though no one 
 denies the frequency of error, his opinion is probably too 
 gloomy, and a fairly accurate forecast can generally be made 
 if all the facts of the case are carefully scrutinized. A wide 
 outlook, however, is necessary, as the cardiac symptoms and 
 signs are by no means the most important elements. An 
 accurate prognosis, too, requires repeated and continuous ob- 
 servation, and can rarely be made on an isolated examination. 
 
 In the presence of active symptoms their progress from day 
 to day forms, of necessity, the main basis on which an opinion 
 can be formed. The size, the strength and rate of the pulse, 
 the degree of oedema and hepatic enlargement, the frequency 
 of the respirations, and the grade of the dyspnoea or orthopnoea, 
 the pallor or the cyanosis, the amount of urine excreted, the 
 discomfort, the restlessness and the amount of sleep obtained, 
 have all to be accurately recorded and compared from day to 
 day. And it must ever be remembered that the " accidents " of 
 valvular disease, produced by embolism, occur most frequently 
 in the presence of general symptoms of cardiac distress, and 
 may, in a moment, alter the whole aspect of affairs. But em- 
 bohsm is by no means invariably fatal, and I have seen patients 
 hve in comfort for several years after the occurrence of a 
 ■cerebral embohsm or a pulmonary infarct, though this is 
 certainly unusual. 
 
 In exceptional cases, too, recovery may ensue after serious 
 embohc phenomena. A woman, aged forty, was recently in 
 my wards suffering from cardiac failure consequent on mitral 
 disease and auricular fibrillation. Four and a half years pre- 
 
 361 
 
362 DISEASES OF THE HEART 
 
 viously the right hand had suddenly become painful and cold and 
 powerless, and gangrene followed, which necessitated amputa- 
 tion through the forearm . The radial and brachial pulses could 
 not be felt before operation, though the subclavian artery was 
 pulsating, and the condition was apparently the result of an 
 embohc block associated with organic mitral disease of rheu- 
 matic origin. She was able to perform her household duties until 
 a few months before her second admission into hospital. 
 
 Of isolated sj-mptoms, two are particularly important and 
 of evil omen. Few patients recover who display distinct jaun- 
 dice with an enlarged, congested liver, or who lie in the trough 
 of the bed, with lack-lustre ej^es, completely indifferent tO' 
 their surroundings. 
 
 Sir William Brcaclbent laid down a useful scheme of inquiry 
 on which the prognosis should be based in those cases in whom 
 the urgencj" of the symptoms is not immediate. To this I 
 have made some additions. The nature, the site, and the- 
 grade of the lesion ; the rhythm of the heart ; the presence or 
 absence of associated disease in other viscera ; the degree to 
 which compensation has been eft'ected ; the cause of the failure 
 which has brought the patient under observation — have all to 
 be taken into account, as weU as the age and sex of the patient 
 and his social circumstances and habits. 
 
 1. The Nature of the Lesion. — The most favourable cases are 
 those in which the mitral valve has become incompetent as 
 the result of anaemia or debility, if the cause can be removed 
 and its recurrence prevented. The corresponding incompe- 
 tence of the tricuspid valve is more serious, for it rarely pro- 
 duces symptoms in the absence of organic disease of the lungs 
 or left heart, and the cause of its occurrence consequently 
 persists. A congenital defect is not progressive, but the 
 majority of patients die in early life in consequence of the 
 disturbance of the circulation, or, if they survive, are essentially 
 weakhngs; and valves which are so deformed are pecuharly 
 prone to be affected by acute inflammatory processes. In 
 patients, however, who have reached maturity with good 
 physique and nutrition, and absence of any evidence of cardiac 
 distress, the outlook is favourable, but though many cases 
 have been recorded who lived to thirty and forty years of age^ 
 
PROGNOSIS OF CHRONIC VALVULAR DISEASE 363 
 
 the records are less numerous in the fifties, and I can find but 
 few over sixty. Of my own cases, onlj two have as yet 
 reached forty. 
 
 A chronic valvular lesion due to a long antecedent rheumatic 
 infection is unhkely to be progressive unless the exciting cause 
 recurs, and has, in consequence, a good prognosis ; but the age 
 of the patient must be taken into account, for rheumatism 
 often recurs in the teens and twenties, though less frequently 
 after thirty. A syphilitic lesion may become stationary if it 
 is recognized and treated. The progressive lesions are un- 
 favourable. Acute endocarditis can only be gauged by the 
 progress of the case and the degree of the compensatory 
 changes in the size of the chambers. The occurrence of symp- 
 toms of cardiac failure is always a serious sign, particularly if 
 they obtain during the febrile stage. The degenerative chronic 
 lesions are necessarily progressive, though the rate of progress 
 varies in different cases. Patients rarely live for five years 
 after symptoms have once made their appearance. 
 
 2. The Site of the Lesion. — The possibility of sudden death 
 in patients who are the subject of valvular disease has rarely 
 to be considered, so long as the patient is not confined to bed, 
 though it is by no means uncommon in cases where serious 
 sj^mptoms are already present. Sudden death, according to 
 Kisch, is uncommon before the age of thirty, and is most frequent 
 between fifty and sixty. It is apt to occur in fat people with 
 general arterio-sclerosis, and in patients with f att}^ dilated hearts 
 and mitral or aortic insufficiency. It is not uncommon in aortic 
 aneurism, in cases with irregular or infrequent pulses, in fat 
 persons who suffer from angina, and in emphysematous patients 
 who have manifested symptoms of cardiac weakness.* 
 
 The causes of sudden death are thus related to myocardial 
 rather than to valvular lesions, and are often the result of 
 coronarj^ disease. I have notes of 6 cases in which death 
 ensued without warning, and in 4 the heart was ruptured. In 
 the other 2 the coronary arteries were blocked by emboh, which 
 were derived in 1 case from the apex of a dilated left ventricle, 
 and in the other from f ungating vegetations upon the valves. 
 
 * It has been suggested that the occurrence of ventricular fibrillation may- 
 be the cause of sudden death in cases where the auricles are fibrillating. In 
 experiment such a sequel is not uncommon. 
 
364 DISEASES OF THE HEART 
 
 Of the valvular lesions, aortic regurgitation is that which 
 most often ends suddenly. The strain upon the left ventricle 
 is great if the regurgitation is extreme and occurs during 
 diastole, when the ventricle is "defenceless," as it is not in 
 contraction, and a fatal syncope may, in consequence, occur. 
 In aortic disease, too, the coronary arteries are more fre- 
 quently damaged than in mitral disease, and the muscle is 
 thus more likely to be abnormal. In mitral stenosis embohsm 
 is relatively frequent, and may occasion sudden death. The 
 experience at St. Mary's Hospital may be quoted: 4 out of 
 38 cases of aortic regurgitation died suddenly, but only 1 of 
 53 cases of mitral stenosis, and 2 of 44 cases of mitral reflux, 
 and in the latter serious sj^mptoms were already present. In 
 aortic stenosis (11 cases) there were no sudden deaths. 
 
 The most serious valvular lesion is disease of the tricuspid 
 valve. It is uncommon unless in the form of "functional" 
 insufficiency, secondary to left-sided disease, or affections of 
 the lung, but as compensation has to be effected by the right 
 auricle, its degree is usually insufficient, and it is rarely 
 maintained for any length of time. Tricuspid regurgitation, 
 aortic regurgitation, mitral stenosis, aortic stenosis, mitral 
 regurgitation, in order, probably represents fairly accurately 
 the relative danger of the lesions . 
 
 It is impossible to give figures, for the lesions are rarely 
 comparable; for example, the age at death in mitral disease 
 following acute rheumatism in early life cannot be contrasted 
 with the age at death in mitral disease the result of chronic 
 endocarditis which ensued after fiftj-. Balfour's case, where 
 the patient had mitral reflux for sixty-six years, had the 
 longest duration which I can find recorded. 
 
 3. The estimation of the degree of the lesion has already 
 been considered. 
 
 4. The Rhythm of the Heart. — I had hoped to have been able 
 to give definite figures as to the frequency with which irregu- 
 larities occur in mitral and aortic disease in the presence of 
 symptoms, but my records are stiU scanty. In the mitral series 
 (102 cases), auricular fibrillation occurred in 19 cases, paroxys- 
 mal tachycardia in 5, extra-systoles in 2, and heart-block, nodal 
 rhj^thm, and an undecipherable irregularity in 1. In the aortic 
 series (58 cases), extra-systoles occurred in 9, auricular fibril- 
 
PROGNOSIS OF CHRONIC VALVULAR DISEASE 365 
 
 lation in 2, paroxj^smal tachycardia in 1, and nodal rhythm 
 in 3. But the records are imperfect, and irregularities 
 were more frequent than the figures suggest, though the large 
 majority of patients had a regular pulse. Death may occur, 
 in mitral stenosis, without any alteration in the rhythm, 
 even in cases where the valvular lesion is considerable and of 
 old standing. A woman who was under my charge when 
 house physician in 1895 in Dr. Tennent's wards was admitted 
 into my wards in 1912 for a few weeks before her death, at the 
 age of forty-four. The mitral lesion had existed for seventeen 
 3^ears at least, and probably for longer, and the right heart was 
 permanently enlarged ; but not\^'ithstanding the repeated occur- 
 rence of pulmonary infarcts, the cardiac rhythm remainedregular, 
 and the auricular wave persisted in the cervical curve. 
 
 The prognosis in cases with a regular cardiac rhythm is 
 apparently less serious than in those with an irregular rhythm. 
 But the other factors must be comparable if the comparison is 
 to be exact, and as a permanently irregular rhythm is generally 
 due to myocardial changes, the difference may be merely due 
 to the greater incidence of the latter. From the practical 
 point of view, however, the distinction is important.* 
 
 i 
 
 All Cases. 1 "l^ytbm Rhythm 
 
 Regiiiar. IiTegular. j 
 
 1 
 jVIitral disease 
 
 Death in . . 
 
 Per cent. . . 
 Aortic disease 
 
 Death in . . 
 
 Per cent. . . 
 
 102 73 
 32 15 
 31-4 20-5 
 58 43 
 17 11 
 29-3 25-6 
 
 29 
 17 
 58-6 
 15 
 6 
 40 
 
 1 
 
 Mitral Disease. Aortic Disease. 
 
 Auricular fibrillation 
 
 Death in . . 
 Extra-systoles 
 
 Death in . . 
 Paroxysmal tachycardia . . 
 
 Death in . . 
 Heart-block . . 
 
 Death in . . 
 Xodal rhythm 
 
 Death in . . 
 
 
 19 2 
 11 — 
 
 2 9 
 
 2 2 
 
 5 i 1 i 
 2 1 
 1 — 
 
 ■ ■ i 
 
 D. MacDonald. 
 
366 DISEASES OF THE HEART 
 
 5. The PreseThce of Disease in Other Viscera. — I have already 
 indicated the frequency with which cardiac valvular disease 
 is associated with lesions in other viscera, the lungs, the 
 arteries, and the kidneys being most often involved. The 
 presence of other lesions always intensifies the gravity of the 
 prognosis. In young people the}^ occur as a result of the 
 cardiac lesion or irrespective of it, but in elderly persons 
 they are frequently the cause of the valvular disease, and the 
 recognition of the cardiac element alone leads to an erroneous 
 idea of the case; for in many patients the cardiac flaw is 
 immaterial, and the progress is dependent upon, and the 
 symptoms are due to, the other lesions. In comparable cases, 
 of course, the prognosis is better in the purely cardiac group. 
 Patients with cardiac disease and hepatic cirrhosis rarely live 
 long after the latter has been recognized. Notable emacia- 
 tion is always of serious import. 
 
 6. The Degree of Compensation. — James Mackenzie has 
 recently emphasized the well-known, but oft-forgotten, 
 aphorism that the integrity of the cardiac muscle is the most 
 important factor in valvular disease, and that, so long as the 
 cardiac work is carried on easily, the exact degree or nature 
 of the valvular flaw is immaterial — in short, that "the proof 
 of the pudding is in the eating." With this everyone will 
 agree, and so long as the ordinary business of life is conducted, 
 without discomfort, the immediate outlook is satisfactory. 
 
 It is difiicult to estimate the reserve power of the heart, 
 and it can only be gauged by repeated experiment as to the 
 amount of physical exertion which can be undergone without 
 discomfort. Even here a fallacy is at once apparent, for 
 air~of~us who -have entered or passed the forties — the forties 
 which are so often as stormy in life as thej^ are at sea — are 
 well aware of the necessitj^ of taking things quietly at the com- 
 mencement of our annual holiday, and that an amount of 
 exertion which can be indulged in with impunity, or even with 
 benefit, towards its conclusion may be badly borne at its 
 commencement . 
 
 "^In a general way a conclusion may be reached. If a day's 
 goK or shooting is not accompanied by undue weariness or 
 breathlessness, if business activities entail no special dis- 
 
PROGNOSIS OF CHRONIC VALVULAR DISEASE 367 
 
 ability, and if a hill can be surmounted mtH ease, the cardiac 
 reserve is ample, and little apprehension need be felt. Con- 
 Tersely, if a slow walk on the flat is the only comfortable 
 mode of progression, if CBdema appears in the ankles at night, 
 and if breathlessness ensues on walking upstairs, the reserve 
 is shght, and immediate trouble may be anticipated. In 
 the consulting-room similar experiments may be tried, and 
 the results of hopping round the room or walking upstairs 
 may be investigated. The behaviour of the pulse on exertion 
 is often a useful guide. Its rate, when the patient is re- 
 cumbent, is normally some seven to fifteen beats less than 
 when he is standing up. In the milder forms of insufficiency 
 the difference is greater, or no fall in rate ensues when he hes 
 down. On exertion, in healthy individuals, the pulse-rate at 
 first increases, but rapidly regains its former rate when the 
 patient is again seated. The majority of normal persons 
 regain their usual pulse-rate A^dthin a couple of minutes after 
 walking upstairs, but in myocardial insufficiency the period 
 may be delayed for four or ten, or even thirtj", minutes. In 
 exceptional cases the pulse-rate may be slowed by exercise. 
 This is generall}^ due to some of the beats becoming imper- 
 ceptible to the finger, though it is said to result in exceptional 
 instances from true slowing of the ventricular contractions. 
 The occurrence is, in any case, a sign of evil significance. 
 
 7. The Cause of Failure. — In patients who come under 
 observation on account of symptoms of cardiac weakness, 
 the precise cause of the failure is an important element in 
 the prognosis. The symptoms may be due to the activity of 
 some new factor out with the heart itseh, to a progressive 
 lesion of the valve, or to the development of some patho 
 logical condition of the cardiac muscle. 
 
 Extrinsic factors are numerous. Physical exertion, whether 
 short and severe, or moderate and prolonged; bronchitis, 
 pneumonia, etc., throwing extra strain upon the right heart; 
 a gastro-intestinal upset or an alcoholic debauch; an attack 
 of influenza; anaemia or debilitj- pregnancy and parturition; 
 a mental shock or business worries ; so often precede the onset 
 of cardiac symptoms that their relationship to it can hardly 
 be in doubt. Progressive lesions occur both in acute endo- 
 
368 DISEASES OF THE HEART 
 
 carditis and in the degenerative chronic forms, and though 
 usually gradual in their onset, may be sudden, if, for example, 
 a cusp ruptures suddenly. Eatty overgrowth and degenera- 
 tion and fibrosis of the myocardium, are usually of insidious 
 origin, but a sudden blocking of a coronary branch may produce 
 symptoms with great rapidity. 
 
 ^ The prognosis in the individual case varies accordingly. 
 The possibility of a future pregnancy can be prevented; the 
 patient may become teetotal; the occupation majr be changed, 
 or excessive work and strain may be avoided; and climatic 
 change may retard the recurrence of pulmonary disease. 
 The fatty overgrowth may be reduced by the cessation of 
 "indulgence, indolence, and intemperance "; an anaemia may 
 be overcome; while but little can be effected in checking the 
 rapid progress of an acute endocarditis, or the insidious pro- 
 gression of the more chronic lesions which are affecting the 
 valves or the coronary arteries. 
 
 In other cases failure is due to the inception of a new cardiac 
 rhythm, auricular fibrillation, heart-block, paroxysmal tachy- 
 cardia, etc. The prognosis in this event is always serious 
 unless the progress of the case reveals the individual tendency 
 towards convalescence. It may, however, be borne in mind 
 that none of the abnormal rhythms are necessarily incompatible 
 with life, which may be prolonged over a period of years. 
 *^ 8. Ttie, Age, of the Patient. — The age of the patient musFlje 
 taken into account. There is a maxim in my insurance office 
 that in youth the family history, in adult life the habits, and 
 in later years the circumstances, of proposers should be closely 
 scrutinized; and the maxim, on the whole, holds good with 
 regard to the prognosis in cardiac disease. A family tendency 
 to rheumatism; habits of excess, whether at work or at play, 
 in food or in drink; the anxieties of straitened circumstances ; 
 are all necessarily untoward elements in the case. 
 
 Muscular hypertrophy in early life is easily produced, and 
 is generally ample; but the probability of recurrence of a rheu- 
 matic infection is considerable in the teens and in the twenties, 
 when it is most often accompanied by a fresh endocarditis. If 
 growth is incomplete, its extra strain is badly borne, and a 
 considerable lesion is generally followed by a stunted develop- 
 ment and a poor physique. In elderly persons muscular^ 
 
PROGNOSIS OF CHRONIC VALVULAR DISEASE 369 
 
 hypertrophy is often limited in the case of the heart, as it is 
 in the systemic muscles, and compensation may be effected 
 with difficulty. Other viscera, too, are apt to be damaged, 
 and the lungs, the kidneys, or the arteries, are frequently 
 abnormal. The nutritional demand, on the other hand, is 
 lessened. The condition of the ribs is probably important. In" 
 childhood, when they are soft and yielding, the contour of an 
 enlarged heart may be mapped out on the front of the chest ; 
 but in elderly people, protrusion is unusual, and the heart can 
 only enlarge at the expense of the other organs within the 
 thorax. On the whole, early adult life is the least unsatis- 
 factory age, for the strain of growth is past, and the prob- 
 abihty of a fresh infection is less, while muscular hj^pertrophy 
 is likely to be ample, and the other viscera are probably sound. 
 The unsatisfactory feature is the activity of manhood, and a 
 physiological mean must be carefully enjoined. 
 
 9. The Sex of the Patient. — The influence of sex is not very 
 considerable; for while women as a rule escape extremes of 
 heat and cold, and the strenuous physical exertions to which 
 men are so often exposed by reason of their special occupation, 
 the gain is counterbalanced by their maternal functions. 
 Pregnancy, in my experience, is always a dangerous experi- 
 ment in women who are the subjects of chronic valvular 
 disease. Failure often occurs in the later months or following 
 child-birth during lactation, though, curiously enough, it does 
 not seem to be particularly related to the accouchement. 
 It may be due to general debihty or to a fresh endocarditis, 
 or to a renal complication. The latter two are the most fre- 
 quent causes. The cases already recorded instance the 
 connection. _ 
 
 10. The Social Circumstances and Habits of the Patient. — 
 The habits and social circumstances of the patient are im- 
 portant. Arduous employments are, of course, always in- 
 jurious to patients whose cardiac reserve is hmited by valvular 
 disease; but they may be the only means of obtaining a liveh- 
 hood ; and those in receipt of a weekly wage are rarely able 
 to secure the just medium of mental and physical work that 
 is so desirable. The prognosis in hospital cases is in con- 
 sequence less favourable than in private patients. 
 
 24 
 
CHAPTER XXVI 
 THE TREATMENT OF CHRONIC CARDIAC FAILURE 
 
 The general indications for treatment in cases where com- 
 pensation has broken down are comparatively clear. The heart 
 must he relieved of all unnecessary work, and its nutrition must 
 be improved. Symptoms ivhich by their presence throw a strain 
 upon the heart must be relieved. Cardiac stimulation may be 
 required. 
 
 1. Considerable rehef is almost always experienced after the 
 cardiac work has been reduced to a minimum by confining the 
 patient wholly to bed, under the charge of an efficient nurse 
 (Fig. 185). In no other way can the unnecessary work be so 
 thoroughly removed, for the rate of the pulse is always in- 
 creased when the patient is even sitting up, and if 5 beats per 
 minute are saved, it means 7,200 beats in the twenty-four 
 hours. The patient's comfort, however, must be consulted, 
 for discomfort means restlessness, and restlessness entails work, 
 and support by means of pillows or a bedchair is required in 
 cases where orthopnoea exists. In the lesser degrees of failure, 
 of course, such restrictions are unnecessary, and the patient 
 may be able to sit quietly at home or to take a hmited amount 
 of exercise, but the desired result is attained most quickly by 
 absolute confinement to bed ; and it is always easy to diminish 
 restrictions, while it is often difficult to increase them. The 
 rationale is simple: the expenditure must be curtailed until 
 the overdraft is paid off, and when this is accomphshed, must 
 be rearranged on such a scale that the income is not exceeded. 
 
 The rest, too, must be mental as well as physical, for mental 
 worry and strain entail extra work to the heart, as the blood- 
 pressure is thereby raised and the pulse-rate is often increased. 
 
 The return to ordinary habits, when convalescence is estab- 
 
 370 
 
TREATMENT OF CHRONIC CARDIAC FAILURE 371 
 
 lished, must always be gradual and should be closely super- 
 vised, so that any injurious results may be at once recognized. 
 It is often helpful to have patients massaged mildly when they 
 are still confined to bed and its effects can be readily estimated; 
 and the general improvement in nutrition which it produces 
 as a rule shortens the subsequent con- 
 valescence. 
 
 It is impossible to lay down absolute 
 rules as to the period for which patients 
 should be confined to bed, but it is 
 never wise to allow them out of bed 
 until all the symptoms are in abeyance, 
 and the pulse-rate is again normal, and 
 the confinement should even then be 
 continued for one or two or even three 
 weeks longer. In elderly people, how- 
 ever, severe restrictions are sometimes 
 badly borne, confinement to bed pro- 
 ducing loss of appetite, sleeplessness, 
 mental depression, etc., and it is some- 
 times wise in these cases to allow the 
 amount of exertion to be determined 
 by the patient himself rather than by 
 his medical attendant. 
 ji 2. A priori a weak heart requires 
 more nourishment than a healthy one, 
 so that in cardiac failure every effort 
 should be made to insure an adequate 
 supply ; but the digestive disturbances 
 which so often co- exist may render the 
 
 task difficult. In serious failure the symptoms are frequently 
 intensified by abdominal distension, vomiting, and flatulence; 
 diarrhoea is uncommon. The dietary, in consequence, must be 
 of a kind that throws little work upon the digestive organs . The 
 carbohydrates and the vegetables are generally contra-indicated 
 on this account, for both are liable to produce flatulence, and 
 while the latter notoriously entail extra work, the absence of 
 oral digestion in serious cases is Ukely to disturb the proper 
 digestion of the former. Milk is usually well borne in these 
 
 Fig. 185. — Arterio-Sclebo- 
 sis; Auricular Fibrilla- 
 tion; Cardiac Faxlube. 
 
 Dec. 4: (Edema universal 
 
 and considerable. 
 Dec. 10: Qiidema minimal. 
 
 - - - urinary output in 
 
 ounces; — == pulse-rate. 
 Treatment: Rest in bed and 
 
 a simple alkaline mixture. 
 
372 DISEASES OF THE HEART 
 
 cases, and should be given in small quantities and frequently 
 (every two to three or four hours during the day, and every 
 four or five hours at night). It may be predigested or diluted, 
 or flavoured with weak tea, coffee, rum, etc.; 3 or 4 pints may 
 be given in the twenty-four hours. Benger's or Mellin's food 
 can sometimes be added with benefit. 
 
 If the tongue is clean and the stools normal, solid food may 
 be given, small, lean, fine-fibred fishes, such as whiting, had- 
 dock, and sole, the breast of young birds, and eggs lightly 
 boiled or poached, being the most suitable. Carbohydrates 
 should be given in minimal amount and in dry form — toast, 
 rusks, biscuits, etc. — so as to insure thorough mastication. 
 The amount of solid food at first should be small, so as to avoid 
 undue distension of the stomach. As the quantity of sohd 
 food is increased, the intake of milk may be correspondingly 
 diminished. 
 
 The cooking of the food must be of the simplest kind, but 
 as much variety as is possible should be secured, so as to in- 
 crease the psychic appetite; and it may be remembered that 
 a fried fish, free of its batter and oil, is just as digestible as, and 
 infinitely more appetizing than, one which has been plainly 
 boiled. The clear and the thick soups are generally inad- 
 visable, but stewed fruit (apples, pears) may be useful as a 
 medium for the consumption of cream. 
 
 The intake of fluids requires regulation. In many cases 
 dropsy is present, and it seems desirable to limit the intake of 
 water; but in many patients renal complications co-exist, and 
 the blood-pressure is high, and the intoxication is best remedied 
 by the administration of fluid in sufficient amount. The 
 estimation of the blood-pressure is all-important from the 
 point of view of treatment ; for if it is high, free elimination 
 must be secured before any good result will be obtained. In 
 young people, however, the kidneys are generally normal, and 
 the intake of fluid may be restricted with benefit. The 
 amount taken at meals should always be small (less than 
 10 ounces), so as not to interfere with digestion. 
 
 A similar distinction must be made with regard to the con- 
 sumption of table salt. In acute nephritis and in many cases 
 of chronic nephritis the excretion of salt is deficient, and it 
 
TREATMENT OF CHRONIC CARDIAC FAILURE 373 
 
 accumulates in the tissues, and to keep the fluids of the body 
 isotonic attracts fluid to the parts. The resultant dropsy can 
 be, in part at any rate, relieved by the withdrawal of salt 
 from the diet. In cardiac cases with high blood-pressure salt 
 retention frequently occurs, and its intake should, in conse- 
 quence, be restricted. Less than a gramme of salt daily is 
 required by a healthy individual, who, however, habitually 
 exceeds this amount, sometimes to a very notable degree. 
 Salt is present in bread and in almost all cooked dishes, if 
 one excludes sweets from the hst. Its use in bread and in 
 cooking should be interdicted, and the amount used at table 
 carefully restricted to less than the normal requirement of a 
 gramme. 
 
 In elderly persons a sudden and complete change of diet is 
 often badly borne, being apt to produce anorexia or indigestion 
 of varying type and degree. The patient's habits in this 
 respect should be considered, and a detailed list of the articles 
 of food which are habitually consumed will generally be found 
 to contain some elements which are relatively innocuous. The 
 use of tea and alcohol, for example, should often be continued, 
 though the amount or the quahty may require to be altered. 
 
 Balfour recommended the following " dry " dietary in cases 
 of senile heart when there is anasarca : 
 
 Breakfast. — A single slice of dry toast with no butter, and 
 4 ounces of tea infused for not more than four minutes, with 
 cream and sugar. 
 
 Dinner. — Not more than the lean of two chops or their 
 equivalent in fish or chicken; no vegetables ; as much dry toast 
 as may be desired, and \ ounce of spirits in 3 ounces of water. 
 
 Supper. — As much dry toast as is desired, and ^ ounce of 
 spirits in 3 ounces of water. 
 
 He did not consider that it was advisable that a patient in 
 this condition should drink much, even between meals, and 
 only allowed 3 to 4 ounces of hot water, sipped slowly, about 
 an hour before each meal. A dietary so restricted is, however, 
 rarely well borne for any length of time in chronic heart 
 disease, the restriction of fluids in particular leading to much 
 discomfort; but the consumption of 2 pints of fluid in the 
 twenty-four hours is generally tolerated. 
 
374 DISEASES OF THE HEART 
 
 The following diets are in use in my wards, and are generally 
 useful. In private practice they have usually to be modified, 
 but the general idea can be maintained. The chief meal 
 should be taken in the middle of the day. The patient should 
 rest quietly for at least half an hour after the larger meals, and 
 for the same period before them, and efficient mastication must 
 be insisted upon. Every effort should be made to insure a 
 sufficient variety in the foodstuffs, so as to encourage appetite, 
 
 " Cardiac " Diet. 
 
 5 a.m. : Milk, 8 ounces; bread-and-butter, 2 ounces. 
 
 8 a.m.: Tea, 8 ounces; bread-and-butter, 6 ounces; fish, 4 ounces, or a 
 lightly boiled or poached egg. 
 
 11 a.m. : Milk, 8 ounces, or milk and Benger's food, or a switched egg. 
 
 I p.m.: Chicken, boiled or roast mutton, 4 ounces; bread, 4 ounces; 
 milk pudding, 6 ounces. 
 
 5 p.m. : Milk pudding or tea, 8 ounces; bread-and-butter, 6 ounces. 
 
 7 p.m. : Milk, 8 ounces; bread-and-butter, 4 ounces. 
 
 The bread is stale and toasted. The diet is free from salt, 
 which is added at the table if ordered. The total fluid may be 
 restricted to 30 ounces. Milk pudding includes cornflour, 
 ground rice, semofina, tapioca, sago, arrowroot, custard. Milk 
 may be made more digestible by being citrated, "soured," or 
 peptonized, and more palatable by the addition of weak, 
 freshly infused China tea or coffee as flavouring agents, or may 
 be given in the form of curds or junket. 
 
 " Light" Diet. 
 5 a.m. : Milk, 10 ounces. 
 
 8 a.m.: Milk, or milk and weak tea, 10 ounces; bread-and-butter, 2 to 8 
 ounces; white fish, 4 ounces, or an egg lightly boiled or poached. 
 
 II a.m.: Milk or Benger's food, 10 ounces. 
 
 1 p.m. : Chicken or white soup, 10 ounces; chicken or white fish, 4 ounces; 
 potatoes, 2 ounces ; vegetables, 1 ounce (cauliflower, cabbage, sprouts); bread, 
 1 ounce ; milk pudding, 10 ounces. 
 
 5 p.m.: Milk, or weak tea and milk, 10 ounces; bread-and-butter, 2 to 8 
 ounces ; white fish, 4 ounces, or an egg. 
 
 8 p.m. : Milk, 8 ounces. Cream, 10 ounces per diem. 
 
 This diet is salted. 
 
 3. The Treatment of Symptoms. — The relief of particular 
 symptoms is often a necessary antecedent to any real improve- 
 ment, for dropsy, pain or sleeplessness may of themselves 
 
TREATMENT OF CHRONIC CARDIAC FAILURE 375 
 
 prevent that rest which is so essential. In the shghter degrees 
 of dropsy it may be sufficient to keep the bowels loose, but in 
 the graver forms the fluid should be removed without delay, 
 accumulations in the serous sacs being removed by a trocar 
 and canula, and subcutaneous oedema by multiple puncture, 
 which is generally preferable to the use of Southey's tubes^ 
 The punctures should be numerous, but separated from each 
 other by an inch; two or three rows may be made on each 
 side of the legs below the knees. The punctures should not 
 be deep, merely through the skin, the needle being " guarded " 
 by the finger and thumb finch from the point. With a sharp, 
 broad surgical needle the stabs may be made with great 
 rapidity and occasion little pain. Asepsis must, of course, be 
 
 maintained. , 
 
 The dyspnoea, which so frequently aggravates a patient's 
 sufferings, is often extremely difficult to treat. It may be 
 due to bronchitis, to even small amounts of fluid in the 
 pleural sacs, to oedema of the lungs, or to toxic causes; but, 
 however caused, may interfere gravely with sleep and rest. 
 Much can be done by suitable bed-rests, etc., to make the 
 patient comfortable sitting up in bed, but in some cases a 
 chair affords more ease, though in the latter case any oedema 
 in the legs is generally increased. Oxygen is sometimes help- 
 ful. If there is fluid in the chest, it should be removed, even 
 though but half a pint can be taken away ; while bronchitis may 
 be helped by the usual means. (Edema of the lungs can only 
 be remedied b}' improvement of the cardiac condition; but in 
 the toxic cases much relief may be obtained by the use of 
 mercury and morphia, the former being given as blue pill or 
 calomel in sufficient amount to secure two or three loose stools 
 in the day, and the latter hypodermically and combined with 
 atropine.- The dose of morphia at first should be small (gr. |to Jr), 
 but it may be increased if well borne. It rarely occasions trouble, 
 though care must be exercised if there is much secretion in 
 the bronchi, or if the urine is scanty and highly albuminous. 
 A similar hne of treatment is often useful in sleepless patients. 
 Insomnia is frequently accompanied by dyspnoea and by great 
 restlessness, and is but rarely benefited by the usual h3-pnotics. 
 A dose of bromide in hot whisky may be sufficient in the milder 
 
376 DISEASES OF THE HEART 
 
 cases, and may be backed up by chloral. Paraldehyde also is 
 useful at times. In chronic cases, however, morphia is in- 
 valuable, and improvement is often rapid after two or three 
 good nights' sleep have been obtained. In high-pressure cases , 
 W. RusseU finds vaso-dilator drugs useful. Similar treatment 
 may be required for cough, but the cough of irritation must 
 be distinguished from that associated with profuse secretion; 
 and while morphia is indicated in the first case, it is, of course, 
 prejudicial in the second. Haemoptj^sis rarely occasions 
 anxiety, and generally ceases without treatment, though in 
 infarct the spit may continue to be blood-stained for a week 
 or more. 
 
 The milder degrees of cardiac discomfort are generally re- 
 Heved by local appHcations — hot fomentations, blisters, anti- 
 phlogistin, an ice poultice, etc. — but if severe, require opium 
 in some form. The pain of hepatic congestion is best treated 
 by dry-cupping followed by hot poultices, or by leeching, the 
 bowels being kept active by mercurials. 
 
 Gastro - intestinal symptoms sometimes entail anxiety, 
 especially if vomiting is repeated and severe, and interferes 
 with nutrition. Here, again, mercurials are most hkely to be 
 of use,' and it often lessens as soon as the bowels have been 
 freely moved; a mustard poultice over the epigastrium some- 
 times helps. Whey, albumin water, and weak tea are most 
 likely to be retained. The usual gastric sedatives are of httle 
 value. In severe repeated vomiting water is often weU borne 
 and may be retained, at any rate in part, even when all food 
 is rejected. Even if it is returned, it flushes out the stomach 
 and frequently makes the patient less uncomfortable. 
 
 4. The action of digitalis, as shown in animals, is somewhat 
 comphcated, as, besides its local irritant action, it affects the 
 central nervous system, the heart, and the arteries. It stimu- 
 lates the medullary centres, slowing the rate of the heart and 
 lessening its tone and constricting the arteries. It strengthens 
 and prolongs ventricular systole by its direct action upon 
 the heart, and increases its muscular tone, so that relaxation 
 is less complete; and it exalts its irritabihty. It produces 
 constriction of the arteries directly as weU as through the 
 nervous system. The ultimate result, however, varies, as the 
 
TREATMENT OF CHRONIC CARDIAC FAILURE 377 
 
 nervous and cardiac mechanisms are in some ways opposed. 
 With small doses the cardiac contractions become less frequent 
 but more complete, so that the ventricular output is increased, 
 and the arterial pressure is raised. With larger doses the 
 inhibitory action is augmented, the contractions become less 
 frequent and perhaps irregular, and, though diastohc relaxa- 
 tion becomes more ample, the ventricular output lessens. 
 With increasing doses the excitabihty is so exalted that the 
 pulse-rate becomes very frequent, and the auricles may pass 
 into fibrillation, while the ventricular action becomes irregular 
 and the output is still further diminished. The irregularity 
 may be due to several causes. The whole heart may be con- 
 cerned if it is produced by medullary inhibition, or the ven- 
 tricles alone if heart-block or auricular fibrillation ensue. 
 
 The crisp results obtained in experiment on normal hearts 
 do not, however, convey as precise indications for the use of 
 digitahs in actual practice as might be anticipated, as the 
 hearts concerned are never normal, and in cardiac failure the 
 whole metabohsm of the patient is often out of gear. The 
 uses of digitahs have to be determined by actual experience 
 in sick people. 
 
 Withering 's remarks on the " constitution of patients " in 
 his "Account of the Foxglove" are extremely interesting. 
 " Digitalis," he says, " seldom succeeds in men of great natural 
 strength, of tense fibre, of warm skin, of florid complexion, or 
 in those with a tight and cordy pulse. If the belly in ascites 
 be tense, hard, and circumscribed, or the limbs in anasarca 
 sohd and resisting, we have but little to hope. On the contrary, 
 if the pulse be feeble and intermitting, the countenance pale, 
 the lips livid, the skin cold, the swollen belly soft and fluctuat- 
 ing, or the anasarcous limbs readily pitting under the pressure 
 of the finger, we may expect the diuretic effects to follow in 
 a kindly manner." Translated into current phraseology, 
 Withering's remarks mean that digitahs is not hkely to prove 
 helpful in cases of dropsy with high arterial pressure, and that 
 it is hkely to be of value if auricular fibrillation has ensued. ^.^^-^ 
 
 The first point which should be determined in every case-of 
 cardiac failure is the height of the blood-pressure. A sphyg- 
 momanometer is not required — the finger alone can decide 
 
378 DISEASES OF THE HEART 
 
 the point — for if the blood-pressure is high, ehminative treat- 
 ment is required, and digitals will fail unless it is accompanied 
 or preceded by treatment of this kind. A hundred j-ears after 
 Withering wrote, Wilham Murray discussed the point as 
 follows : " The administration of (mercury) in cardiac dropsy 
 ... is as old as the hills, and we old-fashioned physicians know 
 well enough that thirty or forty years ago no one thought of 
 treating those conditions except by a mercurial pill, followed 
 by a saline or jalap purgative, and a diuretic mixture con- 
 taining digitalis." The actual height of the blood-pressure 
 is immaterial. Digitahs frequently acts well in cases where 
 it is greatly above normal, if it is combined with treatment of 
 the kind suggested by Dr. Murray; and, if it is permissible, 
 the administration of digitalis may be delayed with advantage 
 for two or three days. 
 
 There is, of course, the risk that digitahs in these cases may 
 produce such an elevation of the blood-pressure that a cerebral 
 vessel ruptures . I am not aware of such an accident in my own 
 experience, and I am at one with James Mackenzie in his 
 statement that medicinal doses comparatively rarely affect 
 the blood-pressure to any appreciable degree. It is always 
 wise to administer digitahs in a simple diuretic mixture — for 
 example, in combination with citrate of potassium and Hquor 
 ammoniae acetatis, or with iodide of potassium; or the weU- 
 known Guy's piU may be utihzed. 
 
 The question has aheadj" been discussed in detail (p. 84) 
 in connection with arterio-sclerosis, which, I would again 
 remind the reader, is very often associated with valvular 
 disease of the heart. Of other drugs in these cases caffeine 
 citrate and diuretin are probablj^ the most useful. G. A. 
 Gibson recommended the combination of potassium citrate, 
 caffeine citrate, and infusion of digitahs, which I have used 
 with success. 
 
 The majority' of writers state that digitahs is often useless 
 in senile heart disease, and consider that this is due to fibroid 
 or other disease of the cardiac muscle. The fact is, of course, 
 weU known; but the failure of digitalis is more often due to 
 associated arterio-sclerosis and imperfect elimination than to 
 actual disease of the m^^ocardium. 
 
TREATMENT OF CHRONIC CARDIAC FAILURE 379 
 
 The occurrence of a weak, irregular puLse in dropsy was stated 
 by Withering to be an indication for the use of digitahs. Sir 
 WiUiam Broaclbent gave a more detailed description, stating 
 that a frequent weak, irregular pulse, accompanied by oedema 
 and a scanty, concentrated, turbid urine, were the special 
 indications; and James Mackenzie, anatyzing his results from 
 the standpoint of the varying rhj'thms that may be met with 
 in cardiac failure, states that it is most useful in auricular 
 fibrillation the pulse-rate slowdng concurrently with improve- 
 ment, though the irregularity persists, ~^ 
 
 The slowing of the pulse-rate in these cases seems to be due 
 to direct action of the drug upon the heart, and not to stimu- 
 lation of the inhibitory mechanism, as the rate is not affected 
 by atropine (Cushny), and it is most probably due to depres- 
 sion of conductivity, though it might result from a lessening 
 of excitability. In cases with a normal rhj^thm, where the 
 pulse-rate is slowed, the atropine results are variable, so that 
 in some cases the slowing is due to direct action upon the heart, 
 in others to inhibition. In cases with a normal rhythm, the 
 beneficial results of digitalis are rarely accompanied by such 
 striking effects upon the pulse-rate as are seen in auricular 
 fibrillation. The improvement in the tone of the heart which 
 the drug produces is probabl}- the chief factor in the bene- 
 ficial results, and a dilated heart often shrinks rapidly under 
 its administration. The frequency of the pulse of fever, 
 exophthalmic goitre, acute endocarditis, etc., is seldom in- 
 fluenced to any notable degree, though the other good results 
 may be well marked. Even as I write, its value in fever has 
 been well exemphfied. A man aged thirty-nine was admitted 
 into my wards on the fifth day of a pneumonia. He was 
 shghtly jaundiced, and very prostrate, the puLse being soft 
 and quick, and the second sound at the puhnonar}' area less 
 emphatic than the first. Forty-eight hours later, coincidently 
 with the administration of digitalis, the pulse was stronger 
 and less quick, though the rate had not decreased, and it was 
 still running about 120; the second sound had become em- 
 phatic. During the crisis on the eighth day the heart for a 
 few hours showed signs of failure, but it quickly recovered, 
 and convalescence was good. 
 
380 DISEASES OF THE HEART 
 
 It is necessary to administer considerable doses, and to 
 push the drug until either the desired result is obtained or 
 symptoms of intolerance appear. The old rule that nausea or 
 vomiting increased frequency of the pulse, and diminution in 
 the output of urine, indicate cessation of the drug, is a useful 
 guide, and dangerous symptoms will never appear if it is 
 observed. The administration should also be stopped if the 
 pulse-rate falls to 50. 
 
 The dangers of digitalis are in all probability exaggerated. 
 In myocardial disease sudden death is not uncommon, but 
 its occurrence when the patient is taking digitalis is not 
 necessarily the result of the drugging. Balfour quoted a case 
 in which death ensued after 211 grains of the powdered leaves 
 had been taken within five weeks; but marked symptoms of 
 intolerance had been present for four weeks previous to death I 
 I have only seen one case in which sudden death ensued during 
 its administration, and in which the drug might perhaps be 
 blamed for the result. The patient, who was not under my 
 care, was suffering from symptoms of cardiac weakness, 
 which had followed the excessive use of beer. There was 
 no valvular disease, but the heart was very large. Under 
 full doses of digitalis the symptoms were relieved, and the 
 pulse-rate fell to about 50. There were no symptoms of 
 intolerance otherwise; but he died suddenly one morning after 
 getting up out of bed. 
 
 James Mackenzie recommends a daily dose of 1 drachm of 
 the tincture divided into three or four equal doses. Smaller 
 amounts, in my experience, are generally sufl&cient— 20 or 
 30 minims in the day — and I rarely find it necessary to ad- 
 minister the larger dose. The effects are not noticeable for 
 three or four days. In the majority of patients a good result 
 is obtained when the pulse-rate reaches normal, but some 
 pa^iients experience most benefit when it is still lower; and 
 BaKour stated that he had successfully kept the pulse running 
 for days at 40. Such cases are, however, exceptional. The 
 appearance of a coupled rhythm is an indication of approaching 
 intolerance. 
 
 When the symptoms have disappeared and the pulse-rate 
 is within normal limits, the dose may generally be discon- 
 
TREATMENT OF CHRONIC CARDTAC FAILURE 381 
 
 tinued, and general tonics substituted. But in some patients 
 digitalis seems to be necessary to their comfort. A woman 
 who was recently in my wards suffering from mitral disease 
 and auricular fibrillation stated that she had taken digitalis 
 regularly for seven years. Improvement was rapid after her 
 admission to hospital, and the drug was stopped. But as 
 soon as she went to a convalescent home the symptoms 
 recurred, though they were readily kept in abeyance by 
 regular minimal doses. Fig. 186 shows the relation of the 
 pulse-rate to the dose in another mitral fibrillation case. 
 There were few symptoms present after the first week of her 
 residence, but cessation of the drug or diminution of the dose 
 was rapidly followed by an increase in the pulse-rate and the 
 discomforts of the patient, who spontaneously requested the 
 continuance of the drug. 
 
 James Mackenzie has shown that heart-block may be pro- 
 duced by digitalis in the clinic as in the laboratory. He has 
 utilized the reaction to prove the existence of those partial 
 forms of block which are not associated with an intermittent 
 pulse, and finds that the pulse can often be made to intermit 
 in those cases, as the block is exaggerated, and occasional 
 impulses fail to pass through to the ventricle. In exceptional 
 instances, with a normal cervical tracing, heart-block may 
 also ensue, apparently from the existence of a latent weak- 
 ness in conduction. The presence of partial heart-block is 
 thus a contra-indication to the use of digitalis, as the block 
 wiU be intensified by its administration. In the chronic 
 forms of full heart-block, however, this contra-indication dis- 
 appears . 
 
 In cases of paroxysmal tachycardia the pulse-rate is usually 
 unaffected by digitahs (always, in my experience); but Mac- 
 kenzie has found that in auricular fiutter the auricles passed 
 into fibrillation during its use, and that on its cessation the 
 heart resumed its normal rhythm. 
 
 Extra-systoles as a rule are not a contra-indication to its 
 use, for although they are by no means uncommon when the 
 rate of the contractions lessens, their appearance is probably 
 more often due to the prolongation of diastole than to in- 
 creased irritability of the heart. When stimuli occur at 
 
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TREATMENT OF CHRONIC CARDIAC FAILURE 383 
 
 frequent intervals, diastole is too short to allow ectopic stimuli 
 to arise, and a coupled rhythm rarely, if ever, occurs with a 
 pulse-rate of over 100, whether the auricles are in fibrillation 
 or contracting in response to sinus stimuli. 
 
 The use of digitalis in cases of aortic reguj?gitation has been 
 much discussed. Theoretically, prolongation of diastole in 
 these cases seems inadvisable, as it will increase the amount 
 of blood which regurgitates into the ventricle ; but, as has been 
 already mentioned, failure of compensation in aortic cases is 
 due to dilatation of the heart, and is often accompanied by 
 mitral insufficiency. The loss of tone which is present is an 
 indication for the drug, and practical experience has shown 
 that much benefit is often derived from its administration. 
 
 Many preparations of digitalis have been advocated, but 
 the standardized tincture, the fresh infusion, the NativeUe 
 granules, and Guy's (Baillie's) pill, are generally found to be 
 efficacious. It is said that the infusion is particularly valu- 
 able in cardiac dropsy, and the tincture in fibrillation, while the 
 pill is indicated in cases with defective elimination. Trous- 
 seau's wine is a preparation which is often well borne by 
 irritable stomachs. Digitalin may be injected subcutaneously, 
 a procedure which is sometimes useful if sickness prevents 
 oral administration. 
 
 Gtjy's OB Baillie's Pill, 
 
 '^ Pulv. digital, fol. | 
 
 Pulv, scillse J- . . . . . . . . aa gr. i. 
 
 Pil. hydrarg. J 
 
 M. et ft. pil. 
 
 ViN Teotjsseaxt. 
 
 White wine , . . . . . . . 750 grammes. 
 
 Squill bulbs . . . . . . . . 5 ,, 
 
 Juniper berries . , . . , . 50 ,, 
 
 Foxglove leaves . . . . . . 10 ,, 
 
 Macerate for four days; then add potass, acet., 15 grammes, and filter. 
 Dose: One teaspoonful. 
 
 Of the other cardiac tonics, strophanthus and squill have the 
 best reputation, but they rarely succeed when digitahs has 
 failed. Strophanthus is said to have little action upon the 
 arterioles, and thus to be indicated in high blood-pressure 
 cases ; but it is alleged to be an irritant to the kidneys, and so 
 
384 DISEASES OF THE HEART 
 
 contra-indicated when they are abnormal. Caffeine, theo- 
 bromine (diuretin, theobromose), convallaria, are also useful 
 in the milder forms of failure, when a temporary change 
 of drug seems advisable. 
 
 The " diffusible stimulants " — ammonia and alcohol — ^are fre- 
 quently of use. Sal volatile is one of the best immediate 
 stimulants in cases of faintness, though its continued use is 
 rarely of much value. The general opinion of the value of 
 alcohol has been corroborated by my own experience, notwith- 
 standing the variable opinions which have been expressed 
 upon the subject. It may be of more use on account of its 
 vaso-dilator than from its stimulant action. Hot fomenta- 
 tions applied over the heart have an instantaneous action. 
 "^ The general nutrition of the ^patient must never be for- 
 gotten, as symptoms of cardiac failure sometimes ensue on 
 account of a general failure in strength, and often accompany 
 anaemia, however produced. Arsenic, strychnine, iron, and 
 quinine, are frequently of value, in particular after the acute 
 symptoms of failure have abated and convalescence has 
 commenced. 
 
 ^ REFERENCES. 
 
 A. R. CusHNY AND OTHERS: The Action of Digitalis in Therapeutics, Heart, 
 
 1912-13, vol. iv., p. 33. 
 James Mackenzie: Digitalis. Heart, 1910-11, vol. ii., p. 273. 
 William Mukray : Rough Notes on Remedies, London, 1896. 
 W. Withering : An Account of the Foxglove, Birmingham, 1785. 
 
CHAPTER XXVII 
 ACUTE PERICARDITIS 
 
 Pericarditis is less common than endocarditis, and only- 
 occurred in 158 of 3,842 cases who were admitted to hospital 
 on account of heart disease;* but its high mortality (63 of 
 the 158 patients died during their residence) makes it an im- 
 portant cause of death in cardiac diseases. 
 
 The Lesions. — ^Pericarditis may be local or diffuse, and may 
 be acute or chronic. It may be due to many micro-organisms, 
 the pyogenic cocci, the pneumococcus, and the organism of 
 acute rheumatism, being those which are most frequently 
 causal; while a tubercular infection is by no means uncommon, 
 both as a major and as a terminal event. In the acute stage 
 the exudate may be sero- fibrinous, purulent, or haemorrhagic. 
 If recovery ensues, resolution may be complete; but it is 
 usually imperfect, and organization of the exudate occurs, with 
 adhesion, partial or universal, of the visceral and parietal 
 layers. 
 
 In the earliest stage the serous surface is hypersemic, dull, 
 and opaque, and minute haemorrhages may be apparent in the 
 vicinity of the vessels, with here and there a few flakes of 
 fibrin. In the majority of cases, however, a fibrinous or fluid 
 exudation is found on examination. The fibrinous exudate 
 varies in character in different cases. It may be scanty and 
 slight, and situated mainly around the great vessels ; or thin 
 and more diffuse, covering the greater part of the heart wq,ll ; 
 or abundant and universal, involving both the parietal and 
 the visceral layers. The deposit is usually thickest in the 
 vicinity of the coronary vessels. From the constant move- 
 ment of the heart its surface is rarely smooth, generally pre- 
 
 * Lockhart Gillespie ; Grant Andrew. 
 
 385 25 
 
386 DISEASES OF THE HEART 
 
 senting a "rippled," honeycomb, or shaggy appearance, 
 with bands of varying thickness here and there uniting the 
 two layers. In exceptional cases little fluid is effused, but as 
 a rule the sac contains a few ounces, even in those cases in 
 which the fibrinous deposit is most extensive and thick. In 
 other cases the fluid effusion is considerable, and may amount 
 to several pints, and the fibrinous exudate is relatively scanty. 
 The fluid is yellowish-green in colour, and generally fairly 
 clear, but it may be turbid. The specific gravity is about 
 1-018, much albumin is present, and clotting takes place 
 if the fluid is allowed to stand. In severe infections the fluid 
 may be frankly purulent, and it is occasionally hsemorrhagic 
 in character, particularly in tubercular cases. In the slighter 
 infections the exudation may be completely absorbed, but in 
 the majority of cases adhesions form between the two surfaces, 
 and are ultimately organized. In some cases calcareous 
 material is deposited between the two layers. 
 
 In most cases the chief deposit occurs on the visceral peri- 
 cardium, and the pericardial sac is but slightly involved ; but 
 in others the parietal layer is primarily or chiefly involved, 
 and in this case the inflammation may extend outwards into 
 the mediastinum, and not infrequently involves the pleural 
 sacs as well. In a few cases the primary focus is without the 
 sac, and a comparable lesion occurs, but with a different 
 sequence. Tubercular pericarditis sometimes arises in this 
 way by extension from infected mediastinal glands. 
 
 In acute pericarditis the superficial muscle cells may be 
 seriously damaged, showing distinct fatty or other changes ; 
 but the connective tissue of the heart is Httle altered. The 
 fibrous tissue around the main vascular trunks or the super- 
 ficial layers of muscle cells may be more bulky than normal, 
 and more thickly nucleated; but even this is rare, and in any 
 case the lesion is always superficial. In adherent pericardium 
 a similar state of matters is the rule, and I have only twice 
 seen any considerable degree of fibrosis in the heart muscle. 
 In both cases it was patchy in distribution, and in one case 
 there was, in addition, widespread valvular disease. Myo- 
 cardial lesions, however, are probably always related to causes 
 other than the pericarditis. Acute endocarditis is usually 
 
ACUTE PERICARDITIS 387 
 
 accompanied by a varjdng amount of myocarditis, and not 
 infrequently by pericarditis as well; and a myocardial infarct 
 or abscess, if it approaches the surface, is necessarily associated 
 with pericardial changes ; but these are the result, and not the 
 cause, of the myocardial lesion. In tubercular pericarditis, 
 too, the superficial muscular layers alone are usually involved. 
 
 In mural endocarditis, on the other hand, the muscle is 
 always deeply involved, as the infection spreads outwards 
 along the lymphatic channels. In pericarditis the inflamma- 
 tion does not travel far against the lymphatic stream. 
 
 The milk spots which are so often seen are always superficial, 
 and never invade the muscle. It seems probable that they 
 are rarely the result of acute local pericarditis. They are 
 most common in elderly persons, and are rare in childhood. 
 They are generally situated on the front of the heart on the 
 parts which are directly related to the sternum and ribs, and 
 are unusual on the parts which are covered by the lungs ; 
 they are probably due to mechanical irritation produced by 
 the movements of the heart against the unyielding bony 
 thorax. 
 
 The functions of the pericardia] sac are frequently gravely 
 injured. In the acute stages it is infiltrated and thickened 
 by inflammatory exudate, and its strength and resilience are 
 seriously affected if it is at this stage distended by effusion; 
 and they are still more disturbed if the inflammation spreads 
 outwards into the mediastinal structures, and adhesions form 
 between it and the thorax or the neighbouring viscera. 
 
 The adhesions which follow acute pericarditis vary consider- 
 ably in distribution and in site. They may be delicate, tenuous, 
 and long, or dense and thick, and then usually short ; and while 
 they are as a rule, even when considerable, more or less localized, 
 they may, in exceptional cases, be universal, and obHterate 
 the pericardial cavity. Complete obliteration of the sac is 
 unusual, but it is often divided into several compartments. 
 
 Adhesions may be present anywhere, and may interfere 
 with the proper action of the heart, as they may embrace and 
 strangle the vense cavse and the right auricle, or the pulmonary 
 veins and the left auricle ; or involve the aorta, the puhnonary 
 iirtery, or the ventricles. 
 
388 
 
 DISEASES OF THE HEART 
 
 If the inflammation spreads outside the sac, the pericardium 
 may become fixed to neighbouring structures — the sternum 
 and adjacent ribs in front, the diaphragm below, the lungs 
 on either side, or the vertebral column behind. 
 
 The Etiology of Acute Pericarditis. — Pericarditis may be 
 associated with man}- diseases, and is rare as a primary event. It 
 occurs in ( 1 ) the infections generally, in particular acute rheuma- 
 tism; (2) intrathoracic disease of various kinds; (3) general 
 and local sepsis ; and (4) chronic disease, as a terminal 
 event. 
 
 1. Of all the infections acute rheumatism is that with which 
 pericarditis is most frequently associated, and its incidence 
 in this disease is considerable (16 per cent.), though decidedly 
 less than that of endocarditis, by which, however, it is com- 
 monly accompanied. It is almost equally frequent in the two 
 sexes, and, like endocarditis, is much more common in early 
 life, and was present in 94 out of 100 cases of fatal heart 
 disease observed by Sturges* at Ormond Street. It is generally 
 considered to be most usual in first attacks of rheumatism, but 
 in Church's series, 56 per cent, occurred in second or subsequent 
 attacks. Its incidence is greater the more severe the arthritis, 
 and it rarely obtains in those trivial rheumatic illnesses 
 with which endocarditis, on the other hand, is so often 
 associated. I 
 
 * Lancet, 1894, vol. i., pp. 583, 653, 723. 
 
 t The Incidence of Pericarditis in Acute Rheumatism (Garrod). 
 
 
 Acute 
 Rheumatism. 
 
 Pericarditis. 
 
 
 Case 
 
 Cases. 
 
 Latham^ 
 
 136 
 
 18 
 
 Peacock^ 
 
 233 
 
 36 
 
 Sibson^ 
 
 326 
 
 63 
 
 Pye Smith* 
 
 400 
 
 96 
 
 Whipham^ . . 
 
 655 
 
 111 
 
 OslerS 
 
 Totals 
 
 330 
 
 2,080 
 
 20 
 
 344 
 
 Church: Of 155 cases of pericarditis occurrmg in acute rheumatism, 67 
 accompanied the first attack. 
 
 {For continuation of note, see next 'page.) 
 
ACUTE PERICARDITIS 389 
 
 Roberts stated that it is not uncommon between the third 
 and the sixth day of the arthritis. Balfour thought that the 
 majority of cases occurred within the first week; and in 
 Sibson's series* the signs were recognized within eleven days 
 in nearly haK the cases (30 out of 63 cases). But in exceptional 
 instances the onset may be delayed indefinitely, as late as the 
 sixtj^-first day (Sibson), or may supervene during a relapse. 
 A married woman, aged twenty-seven, was admitted to hospital 
 suffering from acute rheumatism on February 23. The 
 arthritis soon subsided, but on March 20 a consolidation 
 appeared at the base of the left lung. In the early part of 
 April crops of subcutaneous nodules appeared, and on the 
 29th — two months after the subsidence of the arthritis — 
 pericarditis was recognized. A girl, aged fifteen, suffered 
 from acute rheumatism in December, 1910, chorea in April and 
 June, 1911, acute rheumatism in November, 1911, and slight 
 arthritis for a few days in January and April, 1912. With 
 the last attack a pericardial effusion developed. In both of 
 these patients acute endocarditis co-existed, and in the latter 
 case the cardiac infection seemed to be persistent and re- 
 sponsible both for the recurring attacks of arthritis and the 
 pericardial infection. 
 
 C^Aorea is responsible for many cases of pericarditis. In Sibson's 
 series it occurred in 15 out of 21 cases of acute rheumatism 
 which were associated with chorea. Osier found that it was 
 present in 19 of 73 cases of chorea examined post-mortem ; and 
 Cheadlef has drawn attention to its association with the other 
 
 {Continuation of notz ("f") on previous page.) 
 
 
 Male. Female. 
 
 Church^ 
 
 Lockhart Gillespie . . 
 Sibson . . 
 
 12-22% 10-53'/ -2.2 90 Cttsv.3 
 68 51 
 35 ' 28 
 
 ! 
 
 ^ Quoted by A. E. Garrod. A Treatise on Rheumatism, 1890. 
 
 2 Hem. 3 Log. cit. * Quoted by Garrod. ^ idem. 
 
 ^ " The Principles and Practice of Medicine," 1912. 
 
 '' AUbutt's " System," 1 906, vol. ii., part i., p. 594. 
 
 * Reynolds's "System," 1877, vol. iv., p. 186. 
 
 f " Occasional Lectures on the Practice of Medicine," 1900. 
 
390 DISEASES OF THE HEART 
 
 rheumatic manifestations — erythema, subcutaneous nodules, 
 and tonsillitis. 
 
 Pericarditis is of rare occurrence in the other infections. 
 It is most common in pneumonia (1-2 per cent.), scarlatina 
 (0-65 per cent.), and enteric fever (0-2 per cent.), and may 
 occasionally obtain in smallpox, measles, influenza, diphtheria, 
 and gonorrhoea. In smallpox it is probabty due as a rule to 
 a secondary infection.* 
 
 2. The incidence of pericarditis in thoracic disease is chiefiy 
 due to its association with pneumonia, pleuris}^, and phthisis. 
 Its occurrence in pneumonia is of serious significance, as its 
 post-mortem incidence (12-6 per cent.) is much greater than 
 that reported from the wards (1-2 per cent.). It is uncommon 
 in pleurisy, save in empyema. In phthisis it was found post- 
 mortem in 4' 6 per cent. Some cases were not tuberculous? 
 but were due to a secondary pyogenic infection. 
 
 It may follow inflammatory lesions in the sternum, ribs, 
 or mediastinal glands, whether tubercular or pyogenic; frac- 
 tures of the ribs and perforating wounds of the thorax; and 
 rarely inflammatory lesions below the diaphragm, such as a 
 perforated gastric ulcer with subphrenic abscess. 
 
 3. Pericarditis is sometimes a terminal event in pycemic 
 cases. It may then be secondary to a myocardial abscess, or 
 occur apart from cardiac disease, as the result of a direct 
 blood infection. 
 
 4. Pericarditis is not uncommon as a terminal event in 
 chronic diseases of various kinds, the inflammation occurring 
 on account of the lessened resistance to infection. It has been 
 met with in anaemia, cancer, gout, and renal disease, and is 
 
 Pneumonia 
 
 Post-mortem series (Musser and Norris)^ 
 
 Scarlatina (McCollum)- 
 
 Enteric fever (McCrae)^ . . 
 
 Phthisis {posl-mortem series) (Norris)* . , 
 
 Cases. 
 
 Pericarditis. 
 
 Percent. 
 
 40,773 
 
 499 
 
 1-2 
 
 2,128 
 
 267 
 
 12-6 
 
 2,000 
 
 13 
 
 0-65 
 
 1,500 
 
 3 
 
 0-2 
 
 1,780 
 
 81 
 
 4-6 
 
 1 Osier's " System," 1907, vol. ii., p. 537. 
 
 2 Ihid., p. 334. 3 lud., p. 70. 
 
 * Quoted by Lawrason Brown, ibid., 1908, vol. iii., p. 321. 
 
ACUTE PERICARDITIS 
 
 391 
 
 most common in the latter, in particular in renal cirrhosis, 
 while it is comparatively rare in acute nephritis.* The micro.- 
 organisms concerned are chiefly the pyogenic cocci, but a 
 tubercular infection is by no means rare. 
 
 The actual incidence of these factors varies in different 
 series, mainly on account of variations in the class of case 
 under observation; but the most common accompaniment is 
 endocarditis, which is usually of rheumatic origin. In my 
 series of 30 cases of acute endocarditis, pericarditis occurred 
 in 4. In pneumonia, pericarditis is usually trivial, and merely 
 terminal — an indication of a general septicaemia; but it may 
 occur early, and be severe. In only one of my cases was it 
 considerable, the exudation being mainly fibrinous, and due to 
 the pneumococcus, fthough gonococci were present in an 
 urethral discharge, and the bacillus of diphtheria in the 
 throat ! Of the cases associated with renal disease, one was 
 due to a tubercular infection, and one of those accompanying 
 tuberculosis was caused by a streptococcus. f 
 
 The Symptoms o£ Pericarditis. — ^The symptoms of acute 
 pericarditis vary considerably in different cases, as they may 
 arise in various ways . In the early stages and in small effusions 
 the interference with the cardiac action is shght, but in large 
 
 * PosT-MoETEM Statistics. 
 
 
 Nephritis. 
 
 Amyloid Kidney. 
 
 Cirrhotic Kidney. 
 
 [Cases. 
 
 Pericarditis. 
 
 Cases. 
 
 Peri- 
 carditis. 
 
 Cases. 
 
 Peri- ' 
 carditis. 
 
 Dickinson^ .. 
 Grainger- 
 
 Stewart^ 
 
 Sibson^ 
 
 39 
 
 28 
 
 2-5% 
 7-0% 
 
 48 
 50 
 
 22 
 
 6-2% 
 8-0% 
 
 9-0% 
 
 68 
 13 
 
 162 
 
 23-5% 
 
 7-5% 
 
 14-1% 
 
 1 
 
 Acute 
 Nephritis. 
 
 Chronic 
 Nephritis. 
 
 Cases. 
 
 Peri- 
 carditis. 
 
 ^^^®- carditis. 
 
 21 
 
 19-0% 
 
 62 9-6% 
 
 ^ "Diseases of the Kidney." London, vol. ii., 1877. 
 2 "Diseases of the Kidneys." Edinburgh, 1871. 
 
 f See footnote (a) on page 392 
 
 3 Loc. cit. 
 
392 
 
 DISEASES OF THE HEART 
 
 efihisions the mechanical interference is considerable. The 
 amount of fluid may be large (as much as a gallon, Gibson), 
 and much greater than a normal pericardium can hold (less 
 than 1| pints) ; and although an inflamed pericardium stretches 
 under the strain, the pressure within the sac always rises. 
 Starling* has observed the results in experiment. On intro- 
 ducing oil into a dog's pericardium, the venous pressure 
 steadity rose, though the aortic pressure at first remained 
 constant ; but a critical point was soon reached when the intra- 
 pericardial pressure rose to such a height that it prevented 
 the diastohc filling of the heart, and the supply of blood to 
 the ventricles failed. The pulse then became small, and the 
 blood-pressure rapidly fell. 
 
 The increasing difficulties can be readily observed during 
 the stage of an increasing effusion, the pulse-rate becoming 
 more frequent, and the volume and pressure lessening, 
 while the surface becomes cyanosed and the respirations diffi- 
 cult. Hepatic engorgement is usual, but oedema is uncommon 
 and is rarely extensive. 
 
 Pericardial inflammation has little direct effect upon the 
 
 (a) For reference to this footnote see f in text on page 391. 
 
 Hirschfelderi | 
 (Johns Hopkins ' Personal. 
 Hospital). 
 
 Endocarditis 
 
 
 
 
 53 
 
 Mvocarditis 
 
 
 
 8 
 
 Pneumonia 
 
 
 
 
 39 
 
 Acute rheumatism 
 
 
 
 
 31 
 
 Xephritis 
 
 
 
 
 33 
 
 Tuberculosis 
 
 
 
 
 25 
 
 Pleurisy . . 
 
 
 
 
 17 
 
 Gonorrhoea 
 
 
 
 
 3 
 
 Aneurism 
 
 
 
 
 2 
 
 Leukaemia 
 
 
 
 
 2 
 
 ' Syphilis . . 
 
 
 
 
 1 
 
 Sepsis 
 
 Totals 
 
 
 
 
 — 
 
 214 
 
 28 
 
 142 
 53 
 1 
 
 59* 
 
 " Diseases of the Heart and Aorta." " Philadelphia, 1910. 
 
 One -was tubercular. ^ Q^e -was pyogenic. 
 
 In 17 of these cases the patients had suffered from acute rheumatism. 
 
 Lancet, 1897, vol. i., pp. 569, 652, 723. 
 
ACUTE PERICARDITIS 393 
 
 cardiac muscle, and lesions which are found post-mortem in 
 uncompKcated cases are always trivial and confined to the 
 superficial muscular layers. But pericarditis is rarely, if ever, 
 uncomplicated. Endocardial lesions are often present, and a 
 m^yocarditis not infrequently co-exists. Pleural or pulmonary 
 d'sease may originate or accompany the pericardial inflam- 
 mation. 
 
 The pericardium, too, is situated within the thorax, whose 
 walls are capable of only limited displacement, and an increase 
 in its size can only be accommodated by pressure upon the 
 neighbouring viscera. The lungs are compressed and emptied 
 of their air, the oesophagus is driven against the vertebrae, the 
 superior vena cava is obstructed, and the vagus, phrenic or 
 recurrent laryngeal nerves may be implicated, and the symp- 
 toms in different cases vary accordingly. 
 
 The onset of pericarditis is more frequently attended by the 
 occurrence of definite symptoms than is the case in endocar- 
 ditis, and they general^ suggest a cardiac origin; but peri- 
 carditis may be latent and only recognized on routine examina- 
 tion or post-mortem. This is most likely to happen when the 
 patient is already seriously ill and insensitive to trivial dis- 
 comforts, or in cases where a pulmonary affection interferes 
 with auscultation; but even in subacute rheumatism it may 
 be latent. A boy, aged eighteen, who was resident in my 
 wards on account of an attack of acute rheumatism, suffered 
 from a relapse of the arthritis of short duration and sKght 
 severity, and typical friction sounds and enlargement of the 
 area of cardiac dulness were discovered on routine examina- 
 tion of the chest, though the pulse-rate remained unaltered, 
 and no thoracic discomfort was experienced. 
 
 In about half the cases (15)* the patient complains of 
 discomfort or pain over the front of the chest. The pain is 
 rarely severe, and may be general or referred to the base or 
 to the xiphoid cartilage, and varies in intensity at different 
 times without any obvious cause. It is less frequent and less 
 severe in dry pericarditis than in cases with^effusion ; and if 
 
 * The figures in brackets show the incidence of symptoms in a series of 
 30 cases. 
 
394 DISEASES OF THE HEART 
 
 present in the early stages, may become more marked or may 
 remit with the occurrence of effusion. If the effusion is con- 
 siderable, some complaint is almost invariable, and occasion- 
 ally the anguish is extreme. The pain is generally increased 
 by pressure with the stethoscope, but this probably depends 
 upon the mobihty of the chest wall, and is more constant in 
 children than in elderly persons with calcified costal cartilages. 
 In some cases the pain on pressure is due to tenderness of the 
 skin, and even the slightest pressure with the stethoscope is 
 resented, and poultices and fomentations cannot be borne ; but 
 this is exceptional. Palpitation is not uncommon. 
 
 The pulse is ahnost always affected. In the early stages it 
 is more frequent than normal, and out of proportion to the 
 degree of fever. With the onset of effusion the rate increases 
 and the volume and pressure diminish in corresponding degree 
 to the pressure exercised upon the heart. The pulsus para- 
 doxus may be present, but seldom in characteristic degree. 
 The rhythm of the heart has never, in my experience, altered, 
 though irregularities have often been described. Pericarditis 
 is generally met with in cases where other lesions co-exist, and 
 frequently occurs in persons whose pulse is already irregular, 
 so that extra-systoles, auricular fibrillation, etc., are not rare; 
 but these are seldom, if ever, the result of the pericardial 
 inflammation. 
 
 Shortness of breath is quite as frequently present (18) as 
 prsecordial pain. It may of course be due to associated 
 pulmonary or pleural disease, but it occurs also in uncomph- 
 cated cases. It is never extreme in cases without effusion, and 
 is usually severe in corresponding degree to the amount of 
 fluid, and, if this is considerable, ma3^ be accompanied by 
 orthopnoea (11). Sometimes the breathlessness is paroxysmal 
 and occurs mainly at night, or is of the Cheyne-Stokes type; 
 but this is probably always due to accompanying renal disease, 
 which was present in the 3 cases of this series in which it was 
 observed. 
 
 The other symptoms which may be present are all less con- 
 stant. The facial aspect may be changed, the countenance 
 becoming anxious and unduly pale (2), or distinctly cyanosed 
 (9). This is most usual in effusion, and the degree of cyanosis 
 
ACUTE PERICARDITIS 395 
 
 in particular may be taken as an index of the degree with which 
 the effusion is interfering with the cardiac work. 
 
 Difficulty in swallowing (1) or choking attacks (1) may be 
 present in cases where the effusion is large and presses upon 
 the oesophagus. The difficulty is usually increased if the 
 patient is recumbent, and is reheved by the erect position. 
 The voice may become weak and lost if the laryngeal nerves 
 are specially impHcated. The veins of the neck may be turgid 
 and distended, and the face and head may be swollen and 
 puffy. The systemic veins, too, may be congested; but 
 oedema (1) is rarely extensive. Hepatic enlargement may be 
 distinct, and accompanied by tenderness on pressure in the 
 epigastrium. 
 
 In serious cases the patients are drowsy, or restless and 
 sleepless, and are often mildly dehrious at night. Acute cere- 
 bral symptoms occasionally ensue. Fever is inconstant. In 
 acute rheumatism the temperature rises on the onset of peri- 
 carditis, but the rise may be inconsiderable and hyperpyrexia 
 is rare. In renal cases and in terminal pericarditis fever is 
 generally shght or absent. 
 
 The course of events in an attack of pericarditis varies greatly 
 in individual cases, for the causal factors differ widely, and it 
 may be a minor accompaniment of a serious ailment in which 
 other viscera are gravely involved, or the chief episode of a 
 purely cardiac iUness. In pneumonia, for example, peri- 
 carditis is generally merely an indication of a widespread 
 septicaemia and an additional cause of cardiac strain; in 
 pyaemia it is but an item in a widespread sepsis ; and in renal 
 disease an indication of the way in which death is approaching, 
 rather than its cause. In all three cardiac weakness is often 
 present, and the advent of the serous inflammation merely 
 accentuates the pre-existing symptoms, and it is apt to be 
 missed unless routine examinations are frequently made. Even 
 in the cardiac group associated with acute rheumatism its 
 effects are often indistinct, for endocarditis and myocarditis 
 may co-exist, and the exact influence of each factor can rarely 
 be measured. The amount of the effusion cannot be accurately 
 gauged by the size of the area of cardiac dulness, for this may 
 be enlarged from hypertrophy consequent upon a valvular 
 
396 
 
 DISEASES OF THE HEART 
 
 flaw, from dilatation on account of loss of tone, or from the 
 presence of effusion, or maj- be tlie sum total of all three factors. 
 In the majorit}' of cases the sj-mptoms are only in part due to 
 the pericarditis, their character is necessarity inconstant, and 
 their progress varies within wide limits. 
 
 The anatomical distinctions between dry pericarditis, effu- 
 sion, and adhesion are also onty accurate in a general way, 
 and everj' case does not run the full course. Friction may be 
 audible for days without the occurrence of slitv appreciable 
 effusion, and in a man, aged seventy-two, who died in my 
 wards from bronchitis and renal cirrhosis, it was constantly 
 present from February 22 until April 9, while the pericardial 
 sac on ■post-mortem examination only contained 4 ounces of 
 fluid. Fluid may be poured out rapidly, and within three or 
 four days exert an obvious mechanical influence upon the 
 cardiac action, or maj^ appear and disappear insidiously and 
 gradually — results which must be due to variations in the 
 virulence of the bacterium and in the resistance of the indi- 
 vidual. The effusion in rheumatic cases is usually sero- 
 fibrinous and rarely purulent; in tubercular cases, in cancer, 
 and in scurv\% it is often hsemorrhagic ; and pus is likely to 
 occur in streptococcic infections. And while a purulent effu- 
 sion generally terminates fatally, as in the comparable empy- 
 ema, unless operative interference is successfulh' undertaken, 
 the recoveries which occasionally ensue in the latter disease 
 suggest that a similar result maj^ obtain in purulent pericar- 
 ditis, a suggestion which is borne out by the discovery in a 
 few cases of cretaceous material within the sac. 
 
 The relative frequency of the various forms of pericarditis 
 is indicated by the following table, which shows their incidence 
 in the post-mortem room : 
 
 Sero-fibrinous 
 
 . . 108* 
 
 Hsemorrhagic 
 
 .. 30 
 
 Purulent 
 
 .. 24 
 
 Tubercular (secondary) 
 
 ..24 
 
 Tubercular (primary) 
 
 2 
 
 Partially adherent . . 
 
 '. !! Ill 
 
 Totally adherent 
 
 .. 23 
 
 Ossified 
 
 2 
 
 
 324 
 
 * Breitung, quoted by G. A. Gibson. 
 
 1 
 
ACUTE PERICARDITIS 397 
 
 In acute rheumatism the onset of pericarditis is most usually 
 rapidly followed by effusion, which, within a few days (as a 
 rule three or four, rarely a week) attains a maximum, and 
 then gradually disappears. The process can be followed more 
 or less accurately from day to day by percussion, the area of 
 dulness steadily increasing and then lessening. Considerable 
 differences, however, occur in the duration of the effusion. In" 
 a few cases the area of cardiac dulness regains its normal hmits 
 within a fortnight, but in others not for many weeks. An 
 exudate, which is mainly serous, is rapidly removed, but a 
 thick fibrinous deposit necessitates the formation of granula- 
 tion tissue, and months may elapse before any appreciable 
 alteration in the area of cardiac dulness can be detected. In 
 a large majority of cases recoverj- ensues spontaneously, unless 
 the endocardial lesions are widespread and actively pro- 
 gressive. 
 
 Sir Wilham Osier states that dry pericarditis does not kill, 
 though it frequently occurs in dying patients, and the dictum 
 is probably accurate. In effusion, too, the actual mortality 
 is probably small, and the gravity of the individual prognosis 
 depends chiefly upon the amount of the effusion and the degree 
 of pressure exercised upon the heart; but I have only seen 
 three or four cases in which death seemed to result in this way. 
 The mortality of pericarditis, however, is great (39-8 per cent., 
 G. A. Gibson), so that its advent is always a herald of evil 
 omen, even though it only acts indirectly. 
 
 In exceptional cases pericarditis is chronic, or, at any rate, 
 subacute. The duration of the illness is prolonged, and on 
 2?05^-mor^em examination, a soft, succulent exudation is found 
 loosely uniting the two layers. In tubercular cases, too, the 
 progress may be subacute, and much caseous matter may be 
 found, the parietal and visceral layers being separated at times 
 by half an inch of caseous material. 
 
 The Physical Signs oS Pericarditis. — ^In fibrinous pericarditis 
 the characteristic friction may be felt hj the hand, but 
 it is usually only apparent on auscultation. The sounds 
 are superficial, and seem to originate close to the ear. 
 They are usually double (to and fro) and of cardiac 
 rhythm, but they do not correspond closely to the cardiac 
 
398 DISEASES OF THE HEART 
 
 movements or sounds, occurring a little after systole has 
 commenced, and continuing till a short period before the 
 cessation of diastole, with an interval between the systohc and 
 the diastohc portion, and covering rather than replacing the 
 cardiac sounds. The sounds may be of varying quality — very 
 soft, or harsh and grating, or scratching, or creaking Hke the 
 creaking of new leather. The systohc element is usuallj^ 
 louder and longer than the diastolic. Sometimes the sound is 
 single and systolic in rhythm, and it may be triple if the 
 auricular contractions impart a special emphasis at the end 
 of ventricular diastole. The friction is usually loudest be- 
 tween the apex and the xiphoid cartilage, and may be audible 
 all over the cardiac area and even a little beyond it, or may 
 be hmited to a small area. It is occasionally only audible 
 towards the base, or more rarely at the apex. It is variable 
 in its distribution and character, which may change from day 
 to day. It is often intensified by pressure with the stethoscope 
 over an interspace and by alterations in the respiratory phases, 
 but it may be loudest during either inspiration or expiration; 
 it may be unaffected. The sounds may vary in character 
 and site with changes in position. There are no lines of con- 
 duction outwith the cardiac area, as in aortic valvular disease, 
 and the sound is rapidly lost when the cardiac borders are 
 transgressed. 
 
 There is as a rule little diflficulty in recognizing the nature 
 of the sounds. They may resemble the murmurs of double 
 aortic disease, but these are constant in character and site, and 
 are conducted in definite directions. Pleuro-pericardial fric- 
 tion rarely occasions difficulty. It occurs when the pleural 
 spaces overlving the heart are involved, when the friction may 
 be cardiac in rhythm; but full inspiration or full expiration 
 almost always abolishes the sounds, while in pericarditis the 
 friction never disappears, even though the respiratory move- 
 ments alter its quality. It is only audibly at the periphery of 
 the cardiac area, especially about the upper and left borders, and 
 it is generally accompanied by evident pleural friction elsewhere. 
 
 Difficulty may be experienced when the sound is single, but 
 its quality may be characteristic, and its variations from day 
 to day separate it clearly from an endocardial murmur. 
 
ACUTE PERICARDITIS 
 
 399 
 
 In large effusions in thin persons the physical signs are 
 distinct. The prgecordia may be prominent if the chest wall 
 is soft, and the interspaces may be flush, or even bulging 
 above the ribs, and the overlying skin may be cedematous. 
 The apex impulse becomes weaker, and may disappear, 
 though pulsation may be apparent in the fourth interspace ; 
 and the expansion of the left chest on inspiration is less free 
 than that of the right. 
 The movement of the dia- 
 phragm, too, is less am- 
 ple, in particular upon 
 the left side, and the 
 liver and spleen may be 
 evidently displaced 
 downwards . The area of 
 cardiac dulness is in- 
 creased in all directions. 
 The upper border rises 
 above the third rib, and 
 may extend as high as 
 the fi.rst, the maximum 
 elevation being over the 
 sternum. The left border 
 extends outwards, and 
 may be an inch or more 
 beyond the apex im- 
 pulse, if that still per- 
 sists, and the right border 
 extends towards or as 
 far out as the right nip- 
 ple. The shape, too, is 
 altered, and it is conical instead of rectangular, the maximum 
 diameter being at the xiphoid level (Figs. 187, 188). 
 
 The fifth right interspace is encroached upon early, and the 
 cardio-hepatic angle is obtuse instead of right-angled, as in 
 enlargement of the right auricle. The friction sounds usually 
 persist, but their area of distribution becomes circumscribed. 
 They are generally audible over the base of the heart, or 
 rarely at the extreme apex; but they are sometimes httle 
 
 Pig. 187. — Diageajvi showing the Shape of 
 THE Area of Dulness in Pericardial 
 Effusion. 
 
400 
 
 DISEASES OF THE HEART 
 
 altered if the heart retains its relationship with the front of 
 the chest. The cardiac sounds become weak, muffled, and 
 indistinct, and in large effusions may be short and very- 
 distant. 
 
 Some other signs have been described, but their occurrence 
 is occasional. The shoulder girdle may be raised, so that the 
 finger can be introduced between the left clavicle and the first 
 
 rib close to the sternum. 
 An area of dulness, with 
 diminished respiratory 
 murmur, may be found at 
 the extreme left base close 
 to the vertebral column, 
 and tubular breathing, 
 with segophon}^, may be 
 recognized at the angle of 
 the left scapula. 
 
 In thin subjects the 
 
 diagnosis of pericardial 
 
 effusion is usually made 
 
 without difficulty, but it 
 
 may be difficult in very 
 
 fat people, especially if 
 
 the case only comes under 
 
 observation at a late 
 
 stage. In dilated hearts 
 
 pulsation tends to become 
 
 more widespread, though 
 
 EiG. 188.— Diagram showing the Shape of less ample and of shorter 
 
 THE Area of Dulness in Dilatation of duration, rather than tO 
 
 THE Heart. 
 
 disappear. The area of 
 
 dulness is increased laterally rather than upwards, and in mitral 
 stenosis alone reaches as high as the second rib, unless the heart 
 is displaced upwards by abdominal distension ; and the cardio- 
 hepatic angle is a right angle. The sounds are generally 
 short and sharp and superficial, and are often loud rather than 
 distant and indistinct. The liver and spleen, though fre- 
 quently enlarged, are not grossly displaced. 
 
 The physical signs may, however, mislead. As a rule, with 
 
ACUTE PERICARDITIS 401 
 
 the occurrence of effusion, the fluid collects between the heart 
 and the front of the chest, so that the apex impulse disappears, 
 the friction area diminishes, and the sounds become distant. 
 But the heart may retain its position in front, while the fluid 
 accumulates elsewhere. In one case under my observation a 
 well-marked apex impulse persisted unchanged during the 
 progress of an effusion, and the friction area remained constant, 
 
 Fig. 189. — Skiagram: Pericarditis, with Effusion- and Left Pneumothorax 
 
 (J. R. K). 
 
 as the apex was firmly anchored to the adjacent pericardium 
 by a thick, short band, the residue of an antecedent pericar- 
 ditis. In another case the right border of the area of dulness 
 remained immobile as the right pleural sac was obhterated 
 and adherent to the chest wall. And in a third the area of 
 dulness diminished in size and moved steadily to the right 
 side from the gradual development of a left pneumothorax, 
 
 26 
 
402 DISEASES OF THE HEART 
 
 The pulse, too, may be a fallible guide to the degree of the 
 effusion. As a rule it steadily becomes more frequent, quick, 
 and soft ; but its character may be disguised by arterial thicken- 
 ing, aortic regurgitation, or antecedent high blood-pressure. 
 The shape of the distended pericardium, as shown in a skia- 
 gram (Fig. 189), is characteristic; but examination of this kind 
 is rarety possible. 
 
 The onset of pericarditis may be latent, and the diagnosis 
 may be made on routine examination. In the majority of 
 cases, however, complaint of pain in the cardiac region, or 
 an exacerbation of the fever, attract attention, and are associ- 
 ated with an increase in the rate of the pulse. The latter is 
 rarely absent, and, as in acute endocarditis, the pulse-rate is 
 increased out of proportion to the fever and the number of 
 respirations, the pulse-respiration ratio becoming 5, or even 6, 
 to 1. With the occurrence of effusion, the pulse-rate still 
 further increases, the respirations become more frequent, and 
 the extraordinary muscles of respiration are brought into play, 
 while the mucous membranes become cyanosed, and the 
 patient is forced to sit up in bed. With an increasing effusion, 
 the distress is rapidty augmented, the countenance becomes 
 anxious and distressed, the cyanosis deeper, and the pulse 
 and respirations stiU more frequent. In the later stages 
 the cardiac exhaustion steadily increases, the pulse is smaller 
 and more quick and of lessened pressure, the cyanosis 
 is combined with an ashen pallor, and the patient tends to 
 sink downwards in the bed, his skin often bedewed with a cold 
 sweat, and death ensues from cardiac failure. 
 
 In the individual case attention should be paid to the fea- 
 tures which have just been mentioned. The occurrence of 
 orthopnoea, unassociated with an}" pulmonary lesion, a definite 
 diminution in the volume and strength of the pulse, and the 
 combination of pallor and cyanosis, are all of evil omen. The 
 degree of pyrexia is of little importance, but the rate of the 
 pulse and of the respirations convey their special lesson of 
 cardiac or respiratory embarrassment. Failure to maintain 
 the erect posture, if unaccompanied by definite evidence of 
 improvement, is a most serious symptom. 
 
CHAPTER XXVIII 
 ADHERENT PERICARDIUM 
 
 The term "'adherent pericardium " is generalty used some- 
 what loosely, and comprises all cases in Avhich local or universal 
 adhesions exist between the visceral and parietal layers of the 
 sac. Mediastino-jDericarditis includes two groups : one in which 
 with pericardial adhesions there is a marked increase of the 
 fibrous tissue in the mediastinum, with adhesion of the exterior 
 of the pericardium to surrounding parts [indurative mediastino- 
 pericarditis) ; and a second in which with pericardial adhesions 
 the parietal pericardium is adherent to surrounding parts, with 
 little or no general mediastinitis [pericarditis interna et externa). 
 Chronic mediastinitis implies that there are no internal peri- 
 cardial adhesions. 
 
 Pericardial adhesions necessarily entail additional work for 
 the heart, but this may be insufficient to produce appreciable 
 hj^pertrophy if they are tenuous and lengthy and limited in 
 their distribution, and Sibson* collected 50 cases in which the 
 size of the heart was normal. If, on the other hand, the adhe- 
 sions are thick and extensive, and if, in addition, they extend 
 outside the sac and fix the heart to adjacent parts and limit 
 its free movement, hypertrophy is always considerable and of 
 appreciable degree. When pericardial adhesions and valvular 
 disease co-exist, the heart is alwa^-s hypertrophied, and Sibson 
 found that hearts with valvular defects and adhesions were de- 
 finitely heavier than hearts in which comparable valvular defects 
 were present without adhesions ; so that the latter must be hedl 
 responsible for some part, at any rate, of the hypertrophy. 
 
 Local adhesions are most frequently found at those parts of 
 the heart which alter their relations to the parietal pericardium 
 in least degree during the cardiac movements. The}" are thus 
 most common near the apex and about the left border of the 
 
 * Loc. cit. 
 403 
 
404 DISEASES OF THE HEART 
 
 left ventricle, over the left auricle, and at the basal regions 
 of the great vessels ; and are less common over the right 
 ventricle, the right auricle, and the origins of the great vessels. 
 
 The extra-pericardial adhesions also vary in their site and 
 extent, and the heart may be adherent to the lungs, the 
 diaphragm, the sternum and adjacent ribs, or even to the 
 vertebral column. The inflammatory spread is sometimes 
 minimal and sometimes local, and the symptoms and signs 
 correspond accordingl^^ Pericardial adhesions, too, may vary 
 in their effects upon the different chambers of the heart. They 
 uiaiy surround and entangle the auricles and great veins and 
 hinder the influx of the blood ; or embrace the ventricles and 
 the arteries and impede its exit from the heart. If the pleural 
 cavities are obliterated, or the heart is adherent to the parietes, 
 the respiratory movements will affect the cardiac action. 
 
 The etiology of adherent pericardium is presumably similar 
 to that of acute pericarditis, but the chronicity of the affection 
 makes it difficult to appreciate the various factors at their 
 proper value. In Sibson's series 49 out of 80 cases had valvular 
 lesions, with as a rule some form of chronic renal disease. In 
 3 cases aneurism of the aorta was present, and in 1 cancer of the 
 heart. In 19 cases the valves and aorta were health}-, and in 
 7 of the 19 no other viscus was diseased. In 22 cases which I 
 have observed 13 had valvular disease, of whom 4 had renal 
 disease in addition; and in 9 the valves were normal, of 
 whom 4 had renal lesions ; 4 cases suffered from tuberculosis ; 
 1 from a chronic pulmonary fibrosis, which probably originated 
 in an acute pleuro-pneumonia accompanied by empyema; in 
 1 the origin was unknown, as it was discovered in a patient who 
 died from acute pneumonia ; and in 1 it arose during acute 
 rheumatism, though no valvular lesion was found 'post-7nortem. 
 
 In Harris's series of cases of mediastino-pericarclitis examined 
 post-morte7n, 11 seemed to be due to tuberculosis, 2 to acute 
 rheumatism and enteric fever, and 1 to chronic bronchitis, 
 syphilis, scarlatina, and trauma. In 6 the origin was not ap- 
 parent, and the symptoms commenced insidiously without am- 
 obvious acute thoracic disease. 
 
 The symptoms in adherent pericardium depend upon the 
 amount of interference with the cardiac action which the adhe- 
 
ADHERENT PERICARDIUM 405 
 
 sions produce, and are in many cases absent altogether, as 
 from their extent or from their character they do not incom- 
 mode the heart. In other cases the interference is consider- 
 able, but the co-existence of valvular disease in sufficient 
 degree to account for the symptoms which are present makes 
 the recognition of the pericardial element difficult if not im- 
 possible. So that in the majority of cases the condition is first 
 recognized post-mortem, unless the previous existence of an 
 acute pericarditis is already known. 
 
 In cases, however, where adhesions exist outside the peri- 
 cardial sac, as well as within it (mediastino-pericarditis) 
 symptoms of cardiac insufficiency are generally manifest, as 
 they entail a very considerable amount of extra work on the 
 heart, and so curtail the reserve to an appreciable degree. 
 Sequeira has suggested that the difficulties may originate in 
 another way from that which has been already discussed. The 
 pericardium is strong and indistensible, and under normal con- 
 ditions prevents undue distension of the cardiac cavities under 
 the stress of physical exertion. In acute pericarditis its 
 resistance may be seriously impaired by inflammation, and its 
 cavity may be grossly distended by effusion, and its functions 
 may thus be seriously compromised: a result which is more 
 likely to follow if physical exertion has been undertaken before 
 the inflammation has completely resolved. Dilatation of the 
 heart may thus arise and persist; and if the sac, when dis- 
 tended, contracts adhesions to the neighbouring viscera, and is 
 unable to return to its former dimensions when the inflamma- 
 tion has subsided, the results will be still more serious. 
 
 In this latter group of cases with inflammatory adhesions 
 outside and within the pericardial sac, a characteristic syndrome 
 {Pick^s or Concato^s disease, polyorrhomenitis, polyserositis) is 
 not uncommon. The majority of these patients suffer from 
 ascites and enlargement of the liver with, in addition, evidences 
 of cardiac failure and sometimes effusions into the pleural 
 cavities as well ; jaundice may occur, but is rare. The abdominal 
 symptoms are probably due to chronic peritonitis, which is 
 most marked upon the diaphragmatic surface of the liver, 
 accompanied by a varying degree of hepatic cirrhosis ; but the 
 latter may be, as in one of Harris's cases, wholly absent even 
 
406 DISEASES OF THE HEART 
 
 when ascites is a prominent symptom. In some cases the 
 earliest symptoms are cardiac (as in Case 1), and the in- 
 flammation originates within the pericardium; but in others 
 the primary lesion may be pleural, or both the pleural and 
 pericardial lesions may occur simultaneously. The combina- 
 tion is by no means unusual, and occurred in 3 of my cases of 
 acute pericarditis ; while in 6 more pleurisy developed either 
 before or after the pericarditis. 
 
 In my series of 22 cases, a diagnosis of pericardial adhesion 
 was made in 6, 3 of which are reported below. In 2 the diag- 
 nosis was based upon the previous observation of the acute 
 stage. In the sixth, a patient who died from cardiac failure, 
 the evidences of congestion in the area of the superior vena cava 
 were persistent and in excess of those in the area of the inferior 
 cava. The pericardial and the right pleural sacs were obliterated 
 b}' adhesions, which in some parts were ver}- thick, the medias- 
 tinum showed evidences of chronic inflammation, and the 
 superior cava was narrowed to nearly half its diameter imme- 
 diately above the right auricle. 
 
 The Physical Signs of Adherent Pericardium. — In many 
 cases no evidence of pericardial adhesions is apparent, and the 
 diagnosis is made on yost-ynortem examination. This is most 
 frequently the case when valvular disease co-exists, as the 
 symptoms are naturally ascribed to the valvular defect. A 
 knowledge of the previous occurrence of acute pericarditis 
 maj' suggest the existence of adhesions, but it must be remem- 
 bered that the signs of "adherent pericardium" are really 
 those of chronic mediastino-pericarditis, and do not follow 
 mere adhesion of the visceral and parietal layers. 
 
 In a general way the apex impulse is diffuse and forcible and 
 displaced; pulsation is also evident in the epigastrium, and 
 to the left and often to the right of the sternum ; the latter as 
 well as the ribs may pulsate visibty. In children the prsecordia 
 maj^ be prominent. The apex impulse may be flxed to the 
 chest wall and show little or no alteration in site, when the 
 patient turns on to his left side ; or in force, during full inspira- 
 tion, if the pleural cavity is also obliterated ; but these signs are 
 really evidence of pleural, and not of cardiac, adhesion, and 
 nave been found to be present in cases where the pericardium 
 
ADHERENT PERICARDIUM 407 
 
 was quite normal. Immobility of the lateral borders of cardiac 
 dulness, especially on the left side, during the respiratory move- 
 ments, owns a similar origin, and though generally associated 
 with pericardial adhesions, may also be a fallacious guide. 
 
 The normal systolic protrusion of the apex impulse may be 
 replaced by systohc recession (Fig. 190). The explanation is 
 somewhat difficult to understand, for the true apex impulse 
 must protrude during systole, as the longitudinal axis of the 
 heart is always lengthened. It seems probable that systolic 
 retraction of an interspace in the region of the apex is due to 
 right-sided hypertrophy with displacement of the apex back- 
 wards, and to the retraction of the right ventricle becoming 
 perceptible, owing to its adhesion to the chest wall. A similar 
 recession of the interspaces close to the sternum is often seen 
 
 ■BrokeK 
 
 5 - Ltf t Sf>a.c-e. 
 
 Griil.es ■ "■ 
 
 Fig. 190. — Curves tkom the Brachial Artery and Apex Impulse, showing 
 Systolic Retractioist op the Impuxse. 
 
 in persons with hypertrophied hearts, as the transverse diameter 
 towards the base of the ventricle is always shortened during 
 systole, and the atmospheric pressure upon the surface of the 
 chest causes a recession. The sternum, too, may be retracted 
 during systole (Fig. 194); this is probably always a sign of 
 adhesion. 
 
 A similar systolic recession may be found to the right of the 
 sternum in the fourth and fifth interspaces from similar causes, 
 and even the cartilages may be retracted if they are soft ; but 
 here, too, a fallacy obtains, and Fig. 192 was taken from a 
 patient with mitral stenosis, in whom i)ost-7nortem examination 
 showed neither pericarditis nor meliastinitis, so that the sign 
 is obviously inaccurate. Broadbent has described " visible 
 pulsation, synchronous with the cardiac systole, of the left 
 back in the region of the eleventh and twelfth ribs, and in less 
 degree of the same region on the right side," as strongly sug- 
 
408 DISEASES OF THE HEART 
 
 gestive of the adhesion of the heart to the diaphragm, the 
 cardiac contractions pulHng the diaphragm upwards and so 
 drawing the false ribs inwards with each systole; a similar 
 pulsation may be apparent on the front of the chest at the 
 anterior ends of the sixth and seventh ribs. But he has sub- 
 sequently found the sign to be present in cases of hypertrophied 
 
 Fig. 191. — Curves from the Left Back Immediately Below the Costal 
 Maegin, and Just Outside the Line of the Scapular Angle, and the 
 Radial Artery, showing that the Retraction in the Former Situation 
 IS Systolic in Rhythm (Broadbent's Sign). 
 
 heart without adhesion, and the pericardium was normal in 
 the onty case in which I have observed it (Fig. 192). 
 
 Adhesion of the heart to the diaphragm or to the sternum 
 may prevent or limit their movements during respiration. 
 The defect in abdominal movement is read^'ly appreciated by 
 the eye or by the hand. Deficiency in the respiratory move- 
 ment of the sternum is best shown with the cahpers, for the 
 increase in the antero-posterior diameter of the chest is slight, 
 
 Fig. 192. — Curves from the Fourth Right Interspace and Apex Impulse, 
 SHOWING Systolic Retraction of the Former. 
 
 rarely exceeding 1 inch in normal individuals, and is always 
 limited in emphysema and in pigeon-breast. 
 
 The pulse is generally rather small and somewhat frequent 
 in cases which come under observation on account of cardiac 
 insufficiency. It frequently varies both in volume and force 
 with the respirator}' movements, becoming larger and stronger 
 during expiration {pulsus paradoxus, Fig. 193), the exact oppo- 
 site of the normal, but this has been observed in pericardial 
 
ADHERENT PERICARDIUM 
 
 409 
 
 effusion, and even in cases where the heart was normal. Faihire 
 of the pulse during full inspiration, however, does not seem to 
 occur unless mediastino-pericarditis is present. Pulsus para- 
 doxus is probably due in these cases to adhesions about the 
 root of the heart, embracing the aorta and the great veins ; and 
 to traction exerted upon the fibrous bands during inspiration 
 narrowing their lumen and so limiting both the output and the 
 intake of the heart. Inspiratory filhng of the cervical veins 
 (Kiissmaul's sign) owns a like cause, and may also be present. 
 
 The pulse may of course present the characteristic features 
 of that of aortic regurgitation or renal cirrhosis, should either 
 of these conditions co-exist. 
 
 The other signs which have been described are less frequently 
 present, and may be due to many causes. Sir W. Broadbent 
 
 Fig. 193. 
 
 -Ctteves of Respieatoey Movements and Radial Pulse: Pulsus 
 Paeadoxus. 
 
 The pulse is largest during expiration. 
 
 drew attention to the fact that the diastolic shock of the arterial 
 valvular closure was often well marked and felt over a large 
 area ; but this may also obtain in dilatation of the aorta and in 
 high blood-pressure. Riess has described cases in which the 
 cardiac sounds were of metallic quality and well conducted 
 to the skin surface overlying the stomach. Sewill has reported 
 reduplication of the first sound ; and Thayer thinks that the 
 third cardiac sound is usually very distinct. All these signs, 
 however, are infrequent in adherent pericardium, and may 
 be present in other cardiac abnormahties . 
 
 None of the signs ascribed to pericardial adhesions are thus 
 pathognomonic, and they may all be absent in individual 
 cases. 
 
 A patient died recently in my wards from valvular disease 
 of the heart who had previously suffered from an attack of acute 
 pericarditis of rheumatic origin under my observation. A week 
 
410 DISEASES OF THE HEART 
 
 before her death I carefully examined her for all the signs of 
 adherent pericardium which have been described above, with 
 the exception of Reiss's sign and immobility of the apex impulse 
 on change of position. All were absent, but post-mortem ex- 
 amination showed that the pericardial sac was entirely obliter- 
 ated by fairly firm adhesions. The heart, however, was not 
 adherent to the chest wall, mediastinitis was minimal and in no 
 way indurative, and the pleural cavities were normal. 
 
 The previous existence of pericarditis ; the presence of several 
 signs in conjunction, in particular a well-marked systolic re- 
 traction of a powerful apex impulse or of the sternum ; immo- 
 bihty of the impulse and the borders of cardiac dulness during 
 respiration ; and the occurrence of cardiac insufficiencj^ without 
 any other obvious cause, are strongly in favour of the presence 
 of mediastino-pericarditis. Examination with the Rontgen 
 raj-s is often valuable. The mediastinal induration may be 
 apparent in skiagrams (Fig. 195), and limitation of the move- 
 ment of the diaphragm from the presence of adhesions may be 
 visible with the screen. 
 
 The following cases illustrate the usual symptoms of Pick's 
 disease : 
 
 Case 1. — A boy, aged sixteen, was admitted into hospital 
 on May 11, 1908, complaining of breathlessness and of pain in 
 the left side of the chest, and of swelling of the abdomen and 
 of the face and feet. 
 
 He had always been healthy, save for an attack of scarlatina 
 in childhood, until he contracted rheumatic fever four months 
 before admission. Many joints were affected, and he sweated 
 profusely, and was confined to bed for three weeks. Even 
 when he was lying in bed he was very breathless, and this 
 continued for a month after he got up, being intensified on 
 exertion, and he spent the greater part of this time in bed. 
 The dyspnoea then lessened, but he was still unfit to return to 
 his work at the pit. Three weeks before admission, the lower 
 eyelids and the feet became swollen, and the abdomen was 
 noticed to be enlarging, and he was again forced to return to 
 bed. He had a slight cough without any spit, and his left 
 side became painful at times, but otherwise he had no special 
 discomfort J and his appetite was good. 
 
ADHERENT PERICARDIUM 411 
 
 On admission, he was found to be a well -grown lad of fair 
 nutrition. He lay flat in bed, by preference on his right side. 
 
 There was slight oedema in the legs and over the sacrum, 
 but none in the face, and his complexion was somewhat pale. 
 The tongue was coated and rather dry, and the pharynx was 
 congested. The abdomen was considerably distended and 
 contained a large quantitj^ of free fluid. The spleen could 
 not be felt, but the hver was definitely enlarged. Rhonchi 
 were audible aU over the chest and rales at the posterior 
 bases . 
 
 His progress thereafter was satisfactory. The <Dedema and 
 ascites rapidly disappeared, and he left hospital on September 
 12, 1908, in fair health, and resumed his work as a colher. He 
 continued at work until March, 1909, when the abdomen again 
 began to swell, and as he became unable to stoop he had to 
 cease work. There was no recurrence of the general oedema, 
 and no other symptoms beyond shght breathless ness on exer- 
 tion ; but the ascites increased, and he was again forced to go 
 to bed in July. 
 
 On admission in August, he seemed to have lost flesh, and 
 he was pale and thin. He lay easily in bed and made no 
 complaint, though the ascites was now much greater than on 
 his first admission, but there was no oedema. His progress, 
 however, was not satisfactory. The ascitic accumulation had 
 to be removed frequently, as it rapidly recurred after tapping. 
 The fiuid presented the characters of a transudate, the cellular 
 elements being mainty lymphocytes, with some large endo- 
 thelial cells, which were often en jilaque, and a few polymorpho- 
 nucleated cells. In December he was transferred to a surgical 
 ward for operation. Death ensued suddenty, when he was 
 under the anaesthetic, before any operative interference had 
 been undertaken. 
 
 The physical signs which were observed during life were not 
 very distinctive evidence of adherent pericarditis. There was 
 no pulsation on the front of the chest, though the apex impulse 
 could be felt indistinct^ in the fifth left space when he lay on 
 his left side. The area of cardiac duhiess was of normal site 
 and size, but was not altered by changes in position or in re- 
 spiration. The cardiac sounds were pure but short. On his 
 
412 DISEASES OF THE HEART 
 
 first admission, murmurs were present from time to time, both 
 at the apex and at the base, but they never persisted for any 
 length of time; on his second admission the sounds were pure. 
 The pulse was always quite regular, but a Httle frequent (90 to 
 100). The chest expansion measured 2 inches, and the dia- 
 phragm moved fairly well with respiration. There was no 
 inspiratory distension of the cervical veins, though there was 
 a shght pulsus paradoxus, and there was no systolic drag upon 
 the false ribs ; but the liver was large, and steadily increased 
 in size (the vertical measurement being 7| inches on his second 
 admission), and the ascitic transudation with minimal oedema 
 pointed to a hepatic origin. The antecedent rheumatism 
 accompanied by breathlessness while at rest suggested, in the 
 absence of gross pulmonary lesions, a cardiac origin, and a 
 diagnosis of adherent pericardium and perihepatitis was 
 accordingly made. 
 
 On post-mortem examination, the pleural cavities were found 
 to be completely abolished by firm adhesions everywhere, save 
 at the base of the right lung, where 2 pints of fluid were present 
 between the diaphragm and the base of the lung. The peri- 
 cardial surfaces were united by firm adhesions, which were 
 fully half an inch thick in places, and the diaphragm was 
 firmly adherent to both liver and spleen, the hepatic peritoneum 
 elsewhere being only slightly thickened. The liver was con- 
 siderably enlarged and showed an early fine, monolobular 
 cirrhosis. The cardiac valves were normal. 
 
 Case 2. — ^A pithead w^orker, aged seventeen, was achnitted 
 to hospital on June 10, 1911, complaining of swelling of the 
 feet and legs of five months' duration. 
 
 His previous health had not been good. He had had 
 whooping-cough and measles in childhood, and had fallen and 
 broken two of the right ribs at the age of thirteen, and shortly 
 afterwards was admitted into hospital on account of ascites 
 with occasional attacks of pain in the right iliac fossa. In 
 July, 1907, the abdomen w^as opened, and the intestines were 
 found to be covered with miliary tubercles. He made a good 
 recovery, and worked for eight months at the pithead, but 
 the ascites recurred, and in July, 1908, as the scar of the 
 former wound was thin and distended, the abdomen was again 
 
ADHERENT PERICARDIUM 413 
 
 opened. The liver was now enlarged and rough, so an attempt 
 was made to procure adhesions between it and the parietal 
 peritoneum. On dismissal in September, his general condition 
 had improved, but he was distinctly cyanosed and had a 
 troublesome cough. He was unable to return to work as the 
 cough continued, accompanied by a yellow spit, and he 
 was breathless, and felt his heart beating on any exertion, 
 and oedema appeared at times in the feet and legs. In 
 January, 1911, the oedema became permanent and gradually 
 increased in extent, and the breathlessness became more 
 marked. 
 
 On admission, the patient lay comfortably flat in bed. He 
 was only moderately developed, and was poorh^ nourished, 
 and there was widespread oedema, though it was not extreme. 
 The mucous membranes were very blue, and the face was puffy, 
 and the hands and feet were congested and purple. The malar 
 capillaries were distended and prominent. The tongue was 
 moist and coated. The abdomen was large but not tender. 
 The parietes were oedematous. and there was shght ascites. 
 The hver was enlarged, but not tender, the vertical measure- 
 ment being 6|- inches, the edge and surface being smooth and 
 firm; it moved Yevj slightly with respiration, the movement 
 on the left side being more ample, though distinctty less than 
 normal. The spleen was slighth' enlarged. The respiratory 
 murmur over the right lower back and axilla was deficient and 
 accompanied by much fine, bubbling rale. 
 
 The patient remained in hospital until November, but re- 
 ceived shght benefit from his treatment. He made httle com- 
 plaint, and had few discomforts when he was confined to bed, 
 but the oedema increased whenever he was out of bed for 
 any length of time. 
 
 There was well - marked pulsation over the front of the 
 chest, the whole prsecordia heaving, though it was not unduly 
 prominent. The apex impulse was fixed and was unaltered 
 by changes in position or by the respiratory movements, and 
 was negative, a sj^stolic retraction ; and the third, fourth, 
 fifth, sixth, and seventh cartilages on both sides, but less 
 strongly on the right, and the lower sternum (Fig. 194) showed 
 similar movements, the interspaces moving more freely than 
 
414 DISEASES OF THE HEART 
 
 the cartilages. The sternal pulsation was exaggerated on deep 
 inspiration. The area of dulness was enlarged on both sides, 
 and was not influenced by the respiratory movements. The 
 cardiac sounds were pure, the first sound being everywhere 
 short and sharp and loud. The pulse was always regular, but 
 a little frequent (90 to 100). The blood-pressure was normal. 
 There was distinct pulsus paradoxus, and the sternal move- 
 ment forwards on inspiration was nil. Broadbent's sign was 
 absent, and there was no visible distension of the cervical 
 veins at any time. 
 
 A skiagram showed considerable mottling on each side of 
 the heart, especially to the right. The right heart was en- 
 larged, and the cardio-hepatic angle was obtuse, and the upper 
 margin of the diaphragm was indistinct. 
 
 X nSjbt/1. 
 
 ■*** 
 
 = TolA.£ reA^K 
 
 <-*^^ ^ S h.«^VVK . 
 
 Fig. 194. — Curves of Respiratory Movements and Retraction of Lower 
 
 End of Sternum. 
 
 The history of this case presents an absence of the usual 
 causes of mediastino-pericarclitis, and the injury to the ribs 
 which preceded the onset of the ascites was the only illness 
 known which niight affect the thoracic viscera. The presence 
 of diffuse tuberculosis in the abdomen at the time of the first 
 operation, however, suggests another cause, chronic tuber- 
 culosis in the mediastinum ; and the localization of rale to the 
 right lower lobe alone and the diminution of the respiratory 
 murmur pointed to a local pulmonary lesion, although no de- 
 finite signs of a massive consolidation were present. No tubercle 
 bacilli could be found in the sputum. There is in the Museum 
 of the Western Infirmary a specimen of a heart with an enorm- 
 ously thickened (tubercular) pericarditis, which arose from 
 the direct infection of the pericardium by a tubercular gland 
 in the mediastinum. The whole of the mediastinum was 
 matted together around caseous glands, and a tuberculous 
 pleurisy co-existed, so that the factors required for further 
 
ADHERENT PERICARDIUM 415 
 
 spread were already present. In Harris's series of 25 cases 11 
 seemed to be due to tuberculosis. 
 
 Case 3. — A cabinet-maker, aged twenty-seven, was ad- 
 mitted to hospital on July 1, 1909, on account of a right 
 hemiplegia which had occurred suddenly two days previously. 
 
 His health had been good until two years before admission, 
 when he became subject to " indigestion," which was occasion- 
 ally accompanied by vomiting. His face was at times swollen, 
 and he was short of breath, and for the last six months had 
 been troubled with headache and swelling of the abdomen. 
 Two months' before admission he had to cease work for a 
 fortnight on account of abdominal pain and swelling accom- 
 panied by headache and vomiting. 
 
 He was an unhealthy-looking man, of poor physique. The 
 face was puffy and covered with acne, and the venules on the 
 nose were dilated. The eyeballs were rather prominent, and 
 there were slight nystagmoid movements when the eyes were 
 turned to the side. The veins on the forehead were dilated 
 and prominent, and the left jugular veins were large and full. 
 The muscles were small and soft, and enlarged glands were 
 present in the axillae and groins. The tongue was coated, 
 many of the teeth were carious, and the tonsils were enlarged 
 and inflamed. The abdomen was large, mainly on account of 
 enlargement of the liver, which occupied the greater part of 
 the right hypochondrium ; the area of dulness measured 
 7^ inches vertically. The edge was thickened and hard, 
 and not tender, and moved but little with respiration. A 
 small amount of free fluid was present in the abdomen. Im- 
 provement was rapid, and power steadily returned to the 
 paralyzed limbs, while his speech regained clearness and 
 accuracy. 
 
 In the middle of July he suddenly experienced acute pain 
 in the right hypochondrium, and the pulse became more fre- 
 quent. The liver was distinctly larger than it had been, and 
 was now tender to palpation, and friction was audible over 
 the lower part of the right chest. The symptoms subsided 
 within ten days, and the hepatic tenderness disappeared and 
 the liver returned to its usual dimensions. Improvement 
 continued, and he was able to go home on September 13. 
 
416 DISEASES OF THE HEART 
 
 walking fairly well. His colour, however, had deepened, and 
 he was more cyanotic than on admission. 
 
 He was readmitted to hospital on March 31, 1910, on ac- 
 count of pain and swelling in the abdomen and oedema in the 
 legs. The pain had recurred on five occasions in the interval. 
 It was never very severe, but, commencing gradually, steadily 
 increased for a week or so, and then gradually disappeared 
 after ten days or a fortnight. The bowels were costive during 
 the attacks, but there was no vomiting. The symptoms had been 
 more severe since January, and the legs had become swollen. 
 
 On admission, he was more cyanotic than before, and he 
 required three pillows on his bed. There was severe ascites, 
 and oedema in the limb which had been paralyzed though there 
 was none in the other, and he was short of breath and incap- 
 able of any exertion. 
 
 The prsecordium generally was prominent, and there was well- 
 marked pulsation in the second, third, fourth, fifth, and sixth 
 left interspaces, the maximum being in the fifth and negative, 
 a retraction during systole (Fig. 190) ; and with diastole a well- 
 marked shock was felt on palpation all over the right chest. 
 The impulse moved for nearly an inch when he turned on to 
 his left side, and decreased in force during inspiration. The 
 area of dulness was of normal site and size, but the right border 
 was unaffected by respiration. There was pulsation in the 
 epigastrium, which was S3'stolic in rhythm. All the veins of 
 the body were prominent and full, and the valves stood out dis- 
 tinctly, the veins on the sides of the chest and the left external 
 jugular being most distinct ; one on the left flank was varicose. 
 On auscultation, the sounds were everywhere pure, but every- 
 where triple. The first sound was somewhat loud, but short 
 and sharp, and the emphasis was on the middle sound. The 
 pulse was small and poorly sustained, and about the normal 
 rate. During his first residence it was quite regular, save for 
 occasional extra-systoles, but during his second stay it waS' 
 always irregular (auricular fibrillation). A skiagram showed 
 considerable fibrosis of the right lung, which was most marked 
 at the base, where it was intimately mingled with the shadow 
 of the diaphragm and the right border of the heart (Fig. 195), 
 The lower interspaces of the chest were retracted on inspiration. 
 
ADHERENT PERICARDIUM 417 
 
 The false ribs showed no cardiac movement, SHght pulsus 
 paradoxus was present. 
 
 The diagnosis in this case seemed clear, but the cause was 
 not very apparent at first. On examination, however, a scar 
 
 Fio. 195. — Skiagram from a Case of Mediastixo-Pericarditis, associated 
 WITH Chronic Pleueo-Pneumonia of Right Lung (J. R. R.). 
 
 was found at the lower part of the right chest behind where 
 an " abscess " had been opened in childhood, and there was 
 dulness and deficient respiratory murmur in this situation, so 
 that it seemed probable that an empyema had been present. 
 
 27 
 
418 DISEASES OF THE HEART 
 
 The recurring attacks of perihepatitis, however, suggested the 
 existence of an active focus of infection, but none could be 
 discovered beyond the tonsillar inflammation and a slight 
 catarrh in the lungs. 
 
 REFERENCES. 
 Sm John Broadbent: Adlierent Pericardium, London. 1895. 
 Thomas Harris : Indurative Mediastino -Pericarditis. London. 1895. 
 Pick: Zeitschr. f. klin. Med., 1895, vol. xxix., p. 385. 
 A. O, J. Kelly: Amer. Journ. Med. Sci., 1903, vol. cxxv., p. 116. 
 
 Pneumo - Pericardium. — The presence of gas within the 
 pericardial sac is extremely rare, James, when recording his 
 own case in 1904, being only able to find 37 undoubted 
 cases in the literature. To these I can but add the case 
 recorded by Ljungdahl in 1913, and that which is reported 
 below, 
 
 Pneumo-pericardium may conceivably arise in several ways. 
 In a few cases it has apparently developed post-mortem from 
 infection of the sac by a gas-producing organism ; but no case 
 has yet been recorded in which such an occurrence has been 
 observed during life, and in only 5 of James's cases was the 
 pericardium closed, though in Ljungdahl's and in my own case 
 no evidence of a breach of continuity was discovered. 
 
 In a second group the gas is due to the entrance of air 
 through a wound. This has occurred in compound fractures of 
 the thorax, stabs, gunshot wounds, and operative procedures 
 such as paracentesis of the pleural cavity, and has been pro- 
 duced as a therapeutic measure by Wenckebach in chronic 
 pericardial effusion, apparently with benefit. 
 
 In a third group pneumo-pericardium is due to ulcerative 
 processes connecting the sac with an air-containing viscus. 
 The primary lesions have been varied — ulcerating cavities in 
 the lung, both tubercular and gangrenous ; pyo-pneumo- 
 thorax ; oesophageal ulceration, both cancerous and traumatic ; 
 and subdiaphragmatic abscess due to gastric ulcer, hepatic 
 abscess, and even appendicitis. 
 
 In the majority of cases the lesion which permits the pneumo- 
 pericardium produces in addition an infection of the sac, and 
 effusion sooner or later develops, and very often becomes 
 purulent. The symptoms and the physical signs are, in conse- 
 
ADHERENT PERICARDIUM 419 
 
 quence, as a rule due in part to pericarditis, and in part to the 
 aerial distension of the sac. 
 
 The onset of the symptoms may be gradual or sudden. In 
 the former case the symptoms are those of acute pericarditis ; 
 in the latter the sudden occurrence of cyanosis, collapse, syn- 
 cope, prsecordial oppression, or pain, denotes the advent of the 
 new lesion. 
 
 The physical signs are usually striking. The apex impulse 
 disappears, though it has been noticed to return if the patient 
 assumed the prone position, and the area of cardiac dulness is 
 replaced by an area with a tympanitic or skodaic note. In 
 Stokes's case a b7'uit de pot fele was present for a time. As 
 effusion develops, the area of tympanitic percussion sound 
 becomes diminished and varies in site according to the position 
 of the patient. The auscultatory phenomena at this stage are 
 characteristic, and the cardiac contractions produce the 
 rhythmic churning, splashing, " miU- wheel " sounds, which 
 are distinctive of the presence of air and fluid within the peri- 
 cardium. In Stokes's case they had a peculiar metallic 
 character; metallic tinkhng has frequently been noticed. 
 Friction sounds of the usual kind often co-exist. 
 
 In the majority of cases the diagnosis has been eas}", as only 
 6 of James's cases were not recognized before autopsy. In 
 my case, however, the condition was only diagnosed on 
 examination with the X raj'S, but in this instance the charac- 
 teristic auscultatory and percussion phenomena were absent, 
 as effusion did not develop, and the heart maintained through- 
 out its normal relation to the front of the chest. The disten- 
 sion of the sac, too, at the first X-ray examination was slight. 
 The diagnosis in Ljungdahl's case was also made with the 
 X rays, but no photograph was taken. 
 
 The prognosis in pneumo-pericardium is better than might 
 be anticipated, for 11 of James's cases recovered, so that 13 
 out of 40 cases did not die. In many of the fatal cases, too, 
 the primary lesion was evidently likely to prove fatal. 
 
 The treatynent of this disease must be conducted on orclinar}^ 
 lines. Pyo-pneumo-pericardium suggests the advisabihty of 
 surgical interference if the general condition of the patient 
 permits. 
 
420 DISEASES OF THE HEART 
 
 I have onl}' seen one case of pneumo-pericardium, and the 
 physical signs were somewhat different to those which have 
 been reported. The skiagrams, however, made the diagnosis 
 clear. 
 
 A boy, aged eight, was admitted into hospital on October 2, 
 1912, on account of sickness and vomiting of four days' 
 duration. 
 
 He had always been healthy until his present illness, save 
 for an attack of measles in infanc}', and had seemed in good 
 health on September 28. Next morning he felt sick and 
 vomited, and his mother kept him in bed. The vomiting re- 
 curred, and he became fevered, and was restless and rambled 
 in his talk. The symptoms persisted, and on October 1 he 
 complained of headache, and frequently put his hands up to 
 his occiput. 
 
 On admission, he was mildly delirious and very restless, and 
 constantly moved his limbs in an erratic wa}'. He often placed 
 his hands at the back of his head. The skin was pale, dry, and 
 harsh. The face was flushed and the conjunctivae were in- 
 flamed. He took his drinks well, but passed both urine and 
 faeces in bed. There were few objective signs. There was a 
 slight catarrh in the chest, and the tongue was dry and brown. 
 The left membrana tympani showed some old cicatrices, and 
 the right a large chronic perforation, from which issued a very 
 small quantity of slightly odorous muco-pus ; but there was 
 no mastoid tenderness, and no palsy or spasm or inequality of 
 reflex could be discovered, save that the right pupil was slightly 
 larger than the left. Kernig's sign was negative. During the 
 succeeding week slight improvement ensued, the delirium be- 
 coming less and the pulse-rate diminishing in frequency. On 
 October 5, however, the stools contained a considerable amount 
 of muco-pus, which persisted for twelve days. The pupillary 
 inequality was inconstant. Rales were now audible at the 
 bases of the lungs. On October 14, however, he suddenly 
 became extremely livid and very ill, and appeared to suffer 
 abdominal pain. On October 17 the abdomen was for the 
 first time somewhat distended, and a small consolidation was 
 discovered at the base of the right lung. On the 20th new- 
 physical signs were recognized on the front of the chest. The 
 
ADHERENT PERICARDIUM 
 
 421 
 
 percussion note at the left apex Avas skodaic in character, and 
 an area of dulness ran outwards from the heart to the left 
 shoulder; the respiratory murmur was ver}^ deficient (Fig. 196). 
 The area of cardiac dulness was increased in every direction. 
 The signs at the right base were unaltered. Little change was 
 noticed during the next few days, but the duU area on the 
 front of the chest had disappeared on the 26th, t hough the 
 respiratory murmur at the 
 left apex was stiU very 
 deficient. 
 
 His general condition 
 slowly improved, though 
 the cerebral symptoms 
 still persisted. On No- 
 vember 12 the chest was 
 carefully examined, and 
 the area of tympanitic 
 percussion, shown in Fig. 
 197, was now recognized. 
 It may have been present 
 for a few days previously, 
 as the chest was not ex- 
 amined on every day . The 
 apex impulse persisted in 
 the fifth interspace just 
 within the nipple line. 
 The consolidation at the 
 right base was larger than 
 it had been. Progress 
 thereafter was continuous, 
 though slow . The physical 
 signs gradually cleared up 
 the chest seemed normal. 
 
 20.X.12 
 
 Fig. 196. — Pneumo-Peeicardium. 
 Physical signs on October 20, 
 
 and on December 6 the front of 
 The liver was stiU enlarged and 
 the basal consolidation was resolving. On dismissal, on 
 January 19, 1913, he was fat and well, though the pulse-rate 
 was still rather frequent. In June, 1913, he was very well 
 and attending school regularly. There was still some dulness 
 and deficiency of the respiratory murmur at the right base. 
 During his residence in hospital the fever was slight and 
 
4:22 
 
 DISEASES OF THE HEART 
 
 only exceeded 100° F. on October 19, 20, and 22, reaching a 
 maximum of 100-8° on the latter date. It never rose above 
 99° after December 1 6. The pulse-rate rose to 1 56 on October 3 
 and afterwards ran about 125 until the second week of De- 
 cember, when it tended to run at lower levels, but it was still 
 in the neighbourhood of 100 on dismissal. The respirations 
 numbered 44 on October 5, and thereafter ran about 30, 
 
 falling to normal limits in 
 the middle of December. 
 
 The case presented man}?- 
 interesting features, and 
 an accurate diagnosis of 
 the sequence of events is 
 impossible. On admission 
 it seemed probable that 
 he was suffering from 
 meningitis, but no source 
 of infection was apparent ; 
 the aural sepsis seemed 
 quiescent, and the course 
 of events soon showed that 
 the disturbance was 
 general. The Widal test, 
 etc., were all negative, no 
 sputum could be obtained, 
 and a septicaemia of un- 
 known nature was the only 
 diagnosis. The cause of 
 the exacerbation of the 
 symptoms on October 14 
 was not recognized, and 
 the pneumonia was not apparent until three days later. 
 The interpretation of the new physical signs on October 20 
 was also difficult, and it was only on October 28 that his 
 general condition permitted examination by the X rays, and 
 the pneumo-pericardium was recognized. The skiagrams are 
 instructive. On October 28 the distension of the pericardium 
 was probably uniform, the heart was but little displaced, and 
 the pneumonia was small (Fig. 198). On November 11 the 
 
 12.XI.12. 
 
 Fig. 197. — Pnetjmo -Pericardium. 
 Physical signs on November 12. 
 
ADHERENT PERICARDIUM 
 
 423 
 
 distension of the sac was considerably larger, but only towards 
 the left side and immediately below the apex, and the heart 
 was displaced towards the right. On November 22 the heart 
 still seemed displaced, but the gas was in less amount and almost 
 
 <J c 
 o 
 
 S S 
 
 Ph 
 
 «» CE 
 
 f=H 
 
 wholly on the left side (Fig. 199). On December 6 the disten- 
 sion was less and the heart had returned to its normal site. 
 On December 16 the distension was still less, and subsequent 
 skiagrams failed to reveal any gas in the pericardial sac. The 
 
424 
 
 DISEASES OF THE HEART 
 
 distension of tlie pericardial sac, however, was never quite 
 uniform, for the apex impulse persisted throughout, and the 
 area of cardiac dulness also remained, so that the heart can 
 never have left the front of the chest. There was at no time 
 any evidence of pericarditis, and there was no history of any 
 illness in the past likely to have produced pericardial adhesion, 
 so that the cause of the localization of the gas is unknown. 
 
 M^GLONE 
 
 Fig. 199. — Pneumo-Pekicardium (J. R. R.). 
 Skiagram taken on November 22. 
 
 It seems possible that the original septicaemia provoked (or 
 originated in) a local lesion of the mediastinal glands, which on 
 October 14 became disseminated more widely, involving first of 
 all the right lung and subsequently the pericardium, and per- 
 mitting the entrance of air into the pericardium from the lung. 
 
 Thepossibihty of a gas-producing infection of the pericardium 
 seems slight, for at no time was pericardial friction observed, 
 and the skiagrams exclude the presence of effusion. 
 
ADHERENT PERICARDIUM 425 
 
 Tile only skiagram which I can discover in the hterature is 
 that which was taken in Wenckebach's case. It differs in 
 some respects from Figs. 198 and 199. The heart appears to 
 be in its usual situation, and is not displaced. The pericardial 
 sac is uniformly distended and projects well to the right of the 
 right auricle. The upper margin (as in Fig. 199) extends higher 
 upon the left side of the chest than upon the right. The lower 
 border and the apex impulse are not defined, as the heart in 
 this situation dipped into the fluid effusion in the lower recesses 
 of the sac. 
 
 REFERENCES. 
 
 James: American Medicine, 1904, vol. viii., p. 23. 
 
 LjtnsTGDAHL: Deutsch. Arch. f. klin. Med. Leipzig, 1913, vol.cxi., p. 19. 
 
 Wenckebach: Zeitschr. f. klin. Med. Berlin, 1910, vol. Isxi., p. 402. 
 
CHAPTER XXIX 
 THE TREATMENT OF PERICARDITIS 
 
 The treatment of acute pericarditis must be conducted on 
 lines similar to those which have been considered with reference 
 to acute endocarditis (Chapter XX.). 
 
 The essential feature is absolute rest, both bodily and mental, 
 so as to insure the minimal amount of cardiac strain, and 
 a comfortable bed-rest is often required for patients who are 
 unable to lie flat in bed. The restriction of active movements 
 should be maintained until all the symptoms have disappeared, 
 the pulse-rate has returned to normal, and the area of cardiac 
 dulness has reverted to its usual limits . The patient may then 
 be allowed to move about in bed, but he should not be allowed 
 out of it for at least two months longer ; and for another month 
 should be confined to a couch. Restrictions as to exercise 
 must be continued for three to six months afterwards, and 
 violent exercise prohibited for a j^ear longer. 
 
 It has been suggested that physical exertion should be 
 instituted early in cases of pericarditis, in order to augment 
 the movements of the heart, and so limit the area of adhesion ; 
 but if, as I believe is the case, one of the main functions of the 
 pericardium is to prevent undue distension of the heart during 
 physical exertion, early activity is likely to distend the inflamed 
 sac and so prevent it from exercising this particular function. 
 It is not uncommon, too, to see the right heart dilate tem- 
 porarily^ from even trivial exertion early in convalescence, and 
 the patients in whom the period of rest has been prolonged 
 have always seemed to me to have smaller hearts than those 
 in whom physical exertion has been rapidly resumed. Adhe- 
 sion of the visceral and parietal layers seems to interfere little 
 with the cardiac action, unless mediastinitis co-exists and the 
 
 426 
 
THE TREATMENT OF PERICARDITIS 427 
 
 heart is fixed to the chest wall, or the pericardial sac is unduly 
 large. 
 
 Pain when present must be relieved, in particular in those 
 cases in which it interferes with sleep. Local applications, 
 either hot or cold (an ice poultice is generally comforting) or 
 sedative applications, such as glycerine of belladonna, may be 
 sufficient; leeches or blisters are sometimes successful; but 
 opium is often needed. Pulv. ipecac, co. or a hypodermic 
 injection of morphia is generally useful. 
 
 In many cases no particular line of treatment is indicated 
 beyond that instituted on account of the causal condition. In 
 acute rheumatism salicylate treatment should be continued, 
 but large doses (above 120 grains per diem) should be avoided. 
 In cases where cardiac failure is impending stimulants may 
 be required. Ammonia, nux vomica, and alcohol have seemed 
 to me to be of special value in addition to drugs of the digitalis 
 group. 
 
 In cases with effusion the question of performing para- 
 centesis pericardii naturall}" arises, but the general impression 
 that it is rareh^ required is probably correct, as death is seldom 
 solely due to the pressure exercised upon the heart. The 
 results of operation, too, are by no means favourable. In West's 
 series 33 out of 67 cases died, including 4 out of 11 rheumatic 
 cases; and in Delorme and Mignon's series 65 per cent, of 82 
 cases proved fatal. The results of incision and drainage are 
 also unfavourable, though in a few cases recovery has ensued 
 in apparently moribund patients. In my series no operation 
 was performed, though in one case it seemed desirable. The 
 patient was the boy from whom the skiagram (Fig. 189) was 
 obtained, and the pericarditis, which was sero-fibrinous, was 
 secondary to a septic broncho-pneumonia, accompanied by 
 left pneumothorax. Paracentesis seemed impossible, and the 
 boy's general condition from the pulmonary aspect negatived 
 operative interference of a more extensive kind. In another 
 case post-mortem examination indicated the desirability of the 
 operation. The apex of the heart was, however, firmly ad- 
 herent to the parietal pericardium and to the chest wall, and 
 had remained immobile and well marked during the whole 
 progress of the attack, so that the degree of the effusion was not 
 
428 DISEASES OF THE HEART 
 
 estimated correctly, tlie main factor in the increase of the area 
 of cardiac duhiess being ascribed to dilatation. Six of the 30 
 cases recovered; but in none of the remaining 22 did the peri- 
 carditis appear chiefl}^ responsible for the fatal issue. 
 
 In purulent pericarditis incision and drainage seem indicated. 
 I have never seen a case either during life or on the post-mortem 
 table. 
 
 Many sites have been suggested for the operation, but the 
 most suitable seems that suggested by Baizeau and Delorme 
 and Mignon — namely, puncture as near as is possible to the 
 sternal margin in the fifth or sixth left intercostal space. The 
 internal mammarj^ vessels and the left pleural cavity are thus 
 avoided. The presence of friction at this point, or loud cardiac 
 sounds showing that the heart is immediately underneath, 
 contra-indicate this site, and puncture may then be performed 
 from below upwards through the left costo-sternal angle, or 
 just inside the left border of dulness and outside the cardiac 
 impulse. The pleural cavity is necessarily opened in the 
 latter case. 
 
 The treatment of cases of adherent pericardium in which 
 symptoms of cardiac insufficiency are present must be con- 
 ducted upon lines similar to those which are of value in chronic 
 valvular disease. Fibrolysin has been recommended in those 
 cases with a view to the dissolution of the adhesions, but there 
 are no records of siiry very notable success. In one of my 
 cases the patient seemed slightly better after its use. 
 
 Operative treatment has been advocated in those cases of 
 adherent pericardium where the heart is firmly fixed to the 
 thoracic wall, resection of those portions of the ribs, costal 
 cartilages, or sternum which are involved relieving the heart, 
 from much unnecessary work. A widespread and forcible 
 movement of the bony and cartilaginous chest wall is the 
 special indication for the operation. In many cases of ad- 
 herent pericardium, however, the cardiac difficulties arise in 
 other ways from adhesion to the diaphragm, lungs, or medias- 
 tinum, or from cicatricial bands around the heart or the great 
 vessels ; and suitable cases for operation are by no means fre- 
 quently seen. The dangers of the operation are considerable, 
 sudden death on the operating-table (which occurred in the only 
 
THE TREATMEXT OF PERICARDITIS 429 
 
 case witli which I have been personally concerned) being nat 
 infrequent, and pleurisy often succeeds, as the pleural cavity is 
 almost necessarily opened during the operation. I believe, 
 however, that a more careful selection of cases and an earlier 
 operation than has hitherto been carried out, will in the future 
 lead to better results. 
 
 A similar operation has been suggested in cases of cardiac 
 disease accompanied bj* much enlargement of the heart in adrdt 
 patients. The contour of the chest wall is rarely deformed 
 in adults by cardiac hj-pertroplw, as the rib arches are un- 
 yielding, and the increased space within the thorax demanded 
 hj the heart can only be supplied by depression of the dia- 
 phragm and lessening of the pulmonary- area. The removal of 
 portions of the ribs permits enlargement of the heart forwards 
 and so increases the pulmonary area. The results which have 
 been obtained are at anj^ rate encouraging, 
 
 REFERENCES TO C'ARDIOLYSIS. 
 
 H. T. Bewley: Brit. Med. Jom-n., 1910, vol. i., p. 914. 
 A. Morison: Lancet, 1908, vol. ii., p. 7. (Literature.) 
 W. Thoeburx; Brit. Med. Journ.. 1910, vol. i., p. 10. 
 
INDEX 
 
 Adherent pericardium, 403 
 Adrenalin and arterio-sclerosis, 40 
 Alcohol in chronic cardiac failure, 384 
 
 in arterio-sclerosis, 92 
 Alcoholism and arterio-sclerosis, 78 
 Ammonium salts in arterio-sclerosis, 84 
 Aneurism and arterio-sclerosis, 56, 90 
 blood-pressure and, 90 
 infective, in acute endocarditis, 254 
 of heart, 28, 317 
 sjrphilis and, 277 
 Anginal pain, 289 
 Ante-mortem clots, 306 
 Aorta, rupture of, 267 
 syphilis of, 43, 267 
 Aortic valvular disease, acute endo- 
 carditis and, 276 
 arterial disease and, 274, 
 
 278 
 blood-pressure in, 90, 298 
 cardiac rhythm in, 285, 
 
 364 
 causes of symptoms in, 
 
 282 
 Cheyne-Stokes breathing 
 
 m, 287 
 chorea and, 276 
 comparison with mitral 
 
 disease, 302 
 coronary arteries ua, 265 
 cough in, 288 
 diagnosis of, 346, 349 
 dyspnoea in, 303 
 etiology, 275 
 Flint's murmur in, 351 
 general cardio - vascular 
 degeneration and, 278 
 incidence of, 275 
 left ventricle in, 299 
 mechanical strain and, 
 
 277 
 mitral incompetence and, 
 
 301 
 morbid anatomy of, 261 
 murmurs in, 297 
 myocardial failure m, 284 
 onset of symptoms in, 301 
 oedema in, 291 
 
 Aortic valvular disease, pain in, 289 
 palpitation in, 289 
 prognosis in, 348, 351 
 pulse in, 348, 351 
 renal disease and, 272, 
 
 277, 301 
 symptoms of, 282, 297 
 syphilis and, 277 
 treatment of, 370 
 Aortic valves, mechanism of the, 297 
 Apex tracings, 106, 323 
 
 the a wave in, 108 
 inverted, 323 
 Arterial diseases, 30 
 
 arterio-sclerosis (q.v.) 
 atheroma, 41 
 
 Bright's disease and, 57, 65 
 calcareous degeneration, 47 
 diffuse lesions, 32 
 endarteritis obliterans, 44 
 focal lesions, 41 
 mesarteritis, 43 
 symptoms of, 54 
 syphilitic, 43 
 Arteries, retinal, 72 
 structure of, 30 
 vascular arrangements of, 31 
 Arterio-sclerosis, 32 
 adrenalin and, 40 
 albuminuria in, 65 
 alcoholism and, 78 
 and aneurism, 56, 90 
 and cardiac hypertrophy, 61 
 apex impulse in, 64 
 blood-pressure in, 36, 57, 68, 82 
 bronchitis in, 77 
 cardiac failure in, 65, 78, 81 
 constipation in, 93 
 diagnosis of, 60, 63 
 diet and, 92, 95 
 diuretics and, 93 
 drugs in, 96 
 elastic fibres in, 33 
 emphysema in, 70 
 enteric fever and, 40 
 etiology of, 36 
 exercise and, 93 
 haemorrhage in, 79 
 
 431 
 
432 
 
 DISEASES OF THE HEART 
 
 Arterio-sclerosis. heart-sounds in, 65 
 iodine in, 97 
 lead-poisoning and, 40 
 massage in, 95 
 
 miliary aneurisms and. 54. 74 
 morbid anatomy, 32 
 ocular manifestations in. 72 
 oral sepsis in, 94 
 polycythsemia and, 37 
 purgatives in, 87, 93 
 renal changes in, 36, 56, 57, 65 
 repletion and. 39 
 sepsis and, 79 
 shortness of loreath in, 70 
 symptoms of. 54 
 treatment, 75 
 uraemia in, 69, 87 
 valvular flaws in, 66 
 vaso-dilator drugs in, 84, 96 
 visceral lesions in, 56 
 viscosity of the blood in, 36 
 Ascites in adherent pericardium, 405 
 Atheroma, 41 
 Atrophy of the heart-muscle, 7 
 
 ischsemic, S 
 Auricles, arrangement of musculature 
 
 of, 1 
 Auricular fibrillation, 211 
 
 arterial pulse in, 212 
 
 auricular muscle in, 216 
 
 cervical curve in, 212 
 
 digitalis in, 219 
 
 duration of, 214 
 
 electro -cardiogram in, 122, 213 
 
 etiology of, 215 
 
 experimental production of, 
 211 
 
 infarcts in, 218 
 
 mitral stenosis and, 215 
 
 murmurs in, 218 
 
 presystolic murmui in, 217 
 
 prognosis in, 218 
 
 stimulus production in. 213 
 
 symptoms of, 214 
 
 treatment of, 219 
 Auricular flutter, 198 
 
 arterial curve in, 202 
 
 aortic disease and, 209 
 
 auricular contractions and, 200 
 
 cervical curve in, 199 
 
 digitalis in, 210 
 
 electro-cardiogram of, 199 
 
 etiology of, 195 
 
 incidence of, 209 
 
 mitral disease and, 209 
 
 paroxysmal tachycardia and, 
 209 
 
 prognosis in, 209 
 
 symptoms of, 203 
 
 treatment of, 210 
 
 ventricular contractions in. 
 200 
 
 Auriculo-ventricular bundle. 101 
 
 the relations of, 151 
 
 branches of, 102 
 Auriculo-ventricular node, the. 101 
 
 the relations of, 151 
 Aiu"iculo-ventricular valves, mechanism 
 of the, 294 
 
 Baillie's pill, 383 
 
 Blood-cultures m acute endocarditis. 
 233, 251, 258 
 
 Blood-pressure in aneurism. 90 
 in aortic reflux, 90, 299 
 in aortic stenosis, 67, 299 
 in arterio-sclerosis, 68, 82 
 in mitral disease, 66, 90, 295 
 in paroxysmal tachycardia, 188 
 
 Broadbent's sign, 407 
 
 Bronchitis in mitral disease, 303 
 
 Bruit de Boger, 357 
 
 Caffeine in arterio-sclerosis, 84 
 
 in chronic valvular disease, 384 
 Cardiac failure, causes of, 282 
 
 treatment of, 370 
 Cardiolysis, 428 
 Carditis, rheiunatic, 20 
 
 and endocarditis, 150 
 Cervical curve, 106 
 
 the a wave in, 109 
 the a-c interval in, 112 
 the c wave in, 108 
 the /i wave in, 113 
 the V wave in, 110 
 the .T depression in. 111 
 the y depression in. Ill 
 Cheyne-Stokes respiration, in arterial 
 disease, 71 
 in valvular disease, 287 
 Chordae tendinese, in acute endocar- 
 ditis, 222 
 in mitral disease, 264 
 Chorea and acute endocarditis, 228 
 
 and chronic valvular disease. 20G. 
 
 276 
 and pericarditis, 389 
 Cloudy swelling of myocardium, 9 
 Coagulation necrosis, hyaline degenera- 
 tion and, 9 
 Conductivity, 162. Cf. also Heart - 
 block 
 asphyxia and, 162 
 atropine and, 163 
 digitalis and, 162 
 murmurs in defective, 166 
 swallowuig and, 162 
 vagus stimulation and, 162 
 Congenital heart disease and chronic 
 valvular disease, 274 
 and malignant endocai - 
 
 ditis, 230 
 diagnosis of, 356 
 
INDEX 
 
 433 
 
 Connective tissue of the heart, 2 
 
 in cardiac hypertrophy, 8 
 Contractility, 159 
 
 prognosis in defective, 161 
 pulsus alternans and, 161 
 Convallaria, 384 
 Coronary arteries, the, 2 
 
 anastomosis of. 3 
 
 circulation of, 2 
 
 closure of, 5 
 
 in aortic incompetence. 265 
 
 ligature of, 6 
 
 supplementary, 3 
 
 variations in origin of, 4 
 Coupled rhythms, 175 
 
 auricular fibrillation and, 176 
 
 digitalis and, 380 
 
 etiology of, 176 
 
 extra-systoles and, 175 
 
 partial heart-block and, 175 
 
 Death, sudden, 363 
 
 Derivation L, 115 
 
 Derivation II., 115 
 
 Derivation III., 115 
 
 Diastole, cardiac, 110 
 
 Digitalis, 376 
 
 in aortic incompetence, 383 
 
 in arterio-sclerosis, 84, 378 
 
 iu auricular fibrillation, 219, 381 
 
 in auricular flutter, 210, 381 
 
 in chronic cardiac failure, 380 
 
 dangers of, 380 
 
 in heart-block, 381 
 
 ia paroxysmal tachycardia, 381 
 
 Dissociation, 10 
 
 Diuretin, iu arterio-sclerosis, 84 
 LQ chronic cardiac failure, 384 
 
 Ductus arteriosus, patent, 357 
 
 Duroziez's sign in aortic incompetence, 
 351 
 
 Dysphagia in acute pericarditis, 393 
 
 Dyspnoea, in chronic cardiac failure, 
 286 
 in pericarditis, 394 
 
 Effusion, pericardial, characters of, 386 
 diagnosis of, 399 
 symptoms of, 392 
 treatment of, 426 
 Electro -cardiogram of auricular fibrilla- 
 tion, 122 
 in extra -systoles, 120 
 in aortic incompetence, 119 
 in heart-block, 119 
 in heart-failure, 118 
 in mitral stenosis, 118 
 normal, 116 
 of auricular flutter, 122 
 Electro-cardiograph, the, 114 
 Embolism. 290, 306. 308, 314 
 cardiac, 16 
 
 Embolism, cerebral, 293, 308 
 
 in acute endocarditis, 246, 254 
 in mitral stenosis, 295, 306 
 pulmonary, 303 
 renal, 254, 306 
 
 Emphysema and arterio-sclerosis, 70 
 
 Endarteritis deformans. 41 
 etiology of, 50 
 
 Endarteritis obliterans. 44 
 etiology of, 50 
 
 Endocarditis, acute, 220 
 aortitis in, 223 
 aneurism, infective, in, 224, 
 
 254 
 auscultatorv evidence of, 237 
 blood-cultures in, 230, 258 
 cardiac muscle in, 226 
 cardiac overaction in, 236 
 chorea and, 228 
 cutaneous manifestations ot, 
 
 255 
 diagnosis of, 251 
 embolism in, 254 
 enteric fever, 228 
 etiology of, 227 
 extra-svstoles in, 236 
 fever in, 238, 251 
 heart-block in, 236, 245 
 hemiplegia in, 246 
 incidence of, 227 
 influenza and, 228, 233 
 leucocytosis in, 255 
 local infectious and, 229 
 massage in, 257 
 micro-organisms in, 221, 230 
 morbid anatomy of, 220 
 mural, 223 
 murmurs in, 237, 254 
 nodal rhji}hm in, 236, 242 
 pericarditis and, 227, 237 
 pneumonia and, 228 
 Xjrognosis of, 255 
 puLse in, 235, 253 
 rest in, 256 
 
 rheumatism and, 227, 231, 257 
 scarlatina and, 228 
 septic foci in, 259 
 symptoms of, 234 
 subcutaneous nodules in, 237 
 tonsillitis and, 228 
 treatment of, 255 
 valves affected in, 232 
 
 Endocarditis, chronic. C/. Valvular 
 disease, chronic 
 
 Endocarditis, malignant, 229 
 blood-cultures in, 233 
 I childbirth and, 230 
 
 diagnosis of, 251 
 exanthemata and, 229 
 incidence of, 229, 232 
 micro-organisms in, 230 
 morbid anatomy of, 222 
 28 
 
434 
 
 DISEASES OF THE HEART 
 
 Endocarditis, malignant, predisposing 
 causes of, 232 
 rheumatism and, 229 
 site of lesions in. 232 
 symptoms of, 234 
 treatment of, 257 
 Enteric fever and arterio-sclerosis, 40 
 and acute endocarditis, 228 
 Epigastric pulsation, 323 
 Epileptic convulsions and bradycardia, 
 
 166 
 Excitability, 125 
 Extra systoles, 125 
 auricular, 127 
 causes of, 129 
 in acute endocarditis, 236 
 in alcoholic poisonuig, 131 
 in aortic disease. 363 
 m fevers, 131, 332 
 in mitral disease, 363 
 in nicotme poisonuig, 131 
 interpolated, 125 
 nodal, 127 
 prognosis, 132 
 symptoms, 132 
 treatment, 132 
 ventricular, 125 
 
 Fatty degeneration of the heart, 1 1 
 causes of, 14 
 diffuse, 14 
 distribution of, 12 
 frequency of, 11 
 patchy, 14 
 Fattj' infiltration of the heart, 10 
 
 obesity and, 11 
 Fibrosis, arterio-capillary, 32 
 Fibrosis of heart, 15 
 
 and coronary disease, 24, 26 
 distribution of, 16 
 gummata in, 26 
 haemorrhages in, 26 
 hydatid cj^sts in, 26 
 mixed form, 24 
 para-arterial, 17 
 causes of, 19 
 peri-arterial, 19 
 
 causes of, 20 
 syphilis in, 26 
 trauma in, 26 
 tumours in, 26 
 Fhst-rib sign, the, in pericardial effu- 
 sion, 400 
 Flint's murmur, 351 
 Focal lesions of arteries. 41 
 etiology of, 48 
 Foramina Thebesii, 6 
 Fragmentation of cardiac muscle, 10 
 Friction-sounds in acute pericarditis, 
 
 397 
 Fimdus oculi, the, in arterio-sclerosis, 
 72 
 
 Granular degeneration of the myo- 
 
 cardirun. 9 
 Gumma of the heart, 26 
 
 and heart-block, 170 
 Guy's pill, 383 
 
 H wave, 113 
 
 H asmopericardium , 396 
 
 Haemoptysis ui mitral stenosis, 288 
 
 in pulmonary embolism, 288 
 Heart, congenital diseases of the, 356 
 patent ductus arteriosus, 
 
 357 
 septal defects, 357 
 Heart, aneurism of, 28, 317 
 
 contraction of, 98 
 
 fatty degeneration of, 11 
 
 fatty infiltration of, 10 
 
 fibroid disease of, 15 
 
 in adherent pericardium, 406 
 
 in aortic disease, 297 
 
 in arterio-sclerosis, 60 
 
 in mitral disease, 294 
 
 mobility of, 320 
 
 reserve power of, 283 
 
 wounds of, 26 
 Beart-block, acute, 170, 172 
 
 and Stokes-Adams syndrome, 166 
 
 auricular contractions in, 171 
 
 chronic, 165 
 
 full, 163 
 
 in acute endocarditis, 236, 245 
 
 m the acute infections, 172 
 
 morbid anatomy of, 170 
 
 partial, 164 
 
 prognosis in, 172 
 
 sjTnptoms of, 165 
 
 treatment of, 173 
 Heart-failure, 282 
 
 and high blood-pressure, 62 
 Heart, rupture of, 28 
 Hemiplegia, in acute endocarditis, 247 
 
 in aortic disease, 308 
 
 in mitral disease, 308 
 Hyaline degeneration, 9 
 Hypermyotrophy, 35 
 Hyperpiesis, 39 
 Hypertrophy of heart, 7 
 Hypnotics in chronic cardiac failure, 375 
 
 Infections, acute, and acute endocar- 
 ditis, 228 
 and pericarditis, 390 
 Influenza and acute endocarditis, 228 
 Intermittent claudication and arterio- 
 sclerosis, 71 
 Intestine, infarction of the, 290 
 Iodine in arterio-sclerosis, 97 
 
 Jaundice and bradycardia, 124 
 
 in mitral stenosis, 362 
 Jugular veins, 109 
 
INDEX 
 
 435 
 
 Leucocytosis in acute endocarditis, 255 
 Liver, the, in mitral disease, 290 
 
 in tricuspid reflux, 356 
 Lungs, the, hsemorrhagic infarcts of, 
 288, 303 
 
 in aortic disease, 302 
 
 in mitral disease, 303 
 
 Massage iu acute endocarditis, 257 
 in chronic cardiac failure, 371 
 Medial calcification, 47 
 Mediastinitis, chronic, 403 
 Mediastino-pericarditis, 403 
 Medulla, disease of the, and Stokes- 
 Adams disease, 170 
 Mesarteritis, patchy, 43 
 Miliary aneurisms in arterio-sclerosis, 
 
 54, 74 
 Milk diet in arterio-sclerosis, 92 
 
 in chronic cardiac failure, 374 
 ililk-spots, pericardial, 387 
 Mitral incompetence, 332 
 diagnosis. 342 
 etiology, 362 
 murmurs of, 342 
 prognosis, 363 
 Mitral stenosis, 332 
 
 diagnosis, 333 
 murmurs of, 335 
 prognosis, 363 
 Mitra] valvular disease, acute endocar- 
 ditis and, 277 
 blood-pressure in, 295, 
 
 341 
 cardiac rhythm in, 285 
 causes of, 275 
 causes of symptoms, 282 
 cerebral symptoms in, 293 
 Cheyne-Stokes breathing 
 
 in, 287 
 chorea and, 277 
 comparison with aortic 
 
 disease, 302 
 cough in, 288 
 dyspnoea in, 286 
 embolism in, 293 
 gastro - intestinal symp- 
 toms in, 292 
 general cardio - vascular 
 degeneration and, 278 
 haemoptysis in, 288 
 incidence of, 279, 280 
 in women, 280 
 mechanical strain and, 
 
 277 
 morbid anatomy of, 261 
 murmurs in, 295 
 oedema in, 291 
 onset of symptoms in, 296 
 pain in, 289 
 palpitation in, 289 
 renal disease and, 269 
 
 Mitral valvular disease, rheumatism 
 and, 277 
 symptoms of, 294 
 syphilis and, 277 
 
 Murmurs, 328 
 
 cardio-pulmonary, 330 
 
 conduction of, 326 
 
 in acute endocarditis, 237, 254 
 
 in aortic incompetence, 349, 350 
 
 in aortic stenosis, 348 
 
 in mitral incompetence, 295, 344 
 
 in mitral stenosis, 337, 340 
 
 in patent ductus arteriosus, 358 
 
 in pulmonary incompetence, 355 
 
 in pulmonary stenosis, 355 
 
 in tricuspid incompetence, 357 
 
 in tricuspid stenosis, 357 
 
 presystolic, 337 
 
 Myocarditis, 19 
 
 Myocardium, disease of the, 1 
 
 and acute infections, 309 
 
 Myocardium, the, atrophy of. 7 
 cloudy swelling of, 9 
 coronary arteries and, 312 
 failure of, 309 
 
 fatty degeneration of, 11, 311 
 fatty infiltration of, 10. 311 
 fibrosis of, 315 
 granular degeneration of, 9 
 hyaline degeneration of, 9 
 hypertrophy of, 7 
 infarction of, 16 
 ischsemic atrophy of, 8 
 para-arterial fibrosis of, 17 
 peri-arterial fibrosis of , 19 
 rheumatic nodules in, 21 
 rheumatism and, 150 
 
 Myogenic theory, the, 98 
 
 Myomalacia cordis, 16 
 
 Nativelle's digitalin, 383 
 
 Nerve, recurrent laryngeal, the, in 
 
 mitral obstruction, 288 
 Nervous system and functions of the 
 
 heart, 105 
 Nodal rhythm, 133 
 
 cardiac weakness in, 148 
 in acute endocarditis, 236, 242 
 the a.-v. node in, 148 
 the a.-v. bundle in, 148 
 the pulse in, 148 
 Node, auriculo-ventricular, 101 
 
 sino-auricular, 100 
 Nodules, subcutaneous, 21 
 
 Qildema in aortic disease. 291. 305 ■ 
 in mitral disease, 291, 305 
 in tricuspid incompetence, 356 
 
 CEsophagus, the, obstruction of, ia 
 pericarditis, 395 
 trauma of, and pericarditis, 418 
 
436 
 
 DISEASES OF THE HEART 
 
 P deflection. 116 
 Palpitation, 289 
 Paracentesis pericardii, 428 
 Paroxj-smal tachycardia, 184 
 
 auricular flutter and, 194 
 
 cardiac reserve in, 188 
 
 cervical curve in, 192 
 
 dilatation of heart in, 197 
 
 electro -cardiogram in, 193 
 
 etiology of, 195 
 
 incidence of, 196 
 
 nodal form, 184 
 
 prognosis in, 196 
 
 pulse-rate in, 188 
 
 stimulus production in, 194 
 
 symptoms of, 184 
 
 treatment of, 196 
 Pericarditis, acute, 385 
 
 acute rheumatism and, 388 
 
 chorea and, 389 
 
 diagnosis of, 397 
 
 effusion in, 399 
 
 etiology of, 388 
 
 incidence of, 385 
 
 milk-spots and, 387 
 
 morbid anatomy, 385 
 
 onset of, 393 
 
 paracentesis in, 428 
 
 prognosis in, 402 
 
 pulse in, 394 
 
 pyaemia and, 390 
 
 renal disease and, 390 
 
 symptoms of, 391 
 
 terminal, 390 
 
 the infections and, 390 
 
 thoracic disease and, 390 
 
 treatment, 426 
 X-ray examination in, 401 
 Pericardium, adherent, 403 
 
 Broadbent's sign in, 407 
 
 cardiolysis in, 428 
 
 chronic mediastinitis, 403 
 
 diagnosis of, 406 
 
 etiology of, 404 
 
 indurative mediastino-pericar- 
 
 ditis, 403 
 mediastino-pericarditis, 403 
 morbid anatomy, 403 
 pericarditis interna et externa, 
 
 403 
 Pick's disease, 405 
 pulsus paradoxus in, 409 
 symptoms of, 404 
 treatment of, 428 
 Petit mal and Stokes-Adams disease, 
 
 166 
 Physical signs, in aortic incompetence, 
 349 
 in aortic stenosis, 346 
 in mitral incompetence, 342 
 in mitral stenosis, 333 
 in myocardial failure, 331 
 
 Physical signs, in pulmonary incom- 
 petence, 354 
 in pulmonary stenosis, 353 
 in tricuspid incompetence, 354 
 in tricuspid stenosis, 356 
 of adberent pericardium, 406 
 of fibrinous pericarditis, 397 
 of pericardial effusion, 399 
 of pneumo -pericardium, 419 
 significance of, 320 
 Pick's disease, 405 
 Pneumonia and acute endocarditis, 228 
 
 and pericarditis, 390 
 Pneumo -pericardium, 418 
 diagnosis of, 419 
 etiology, 418 
 prognosis, 419 
 symptoms, 419 
 treatment of, 419 
 Polycythsemia, 37 
 
 Polygraph curves, interpretation of, 106 
 Polyorrhomenitis, or polyserositis, 405 
 Presphygmic interval, 128 
 Primitive cardiac tissue, the, 99 
 Prognosis, 361 
 age and, 368 
 cause of failure and, 367 
 degree of compensation and, 366 
 disease of other viscera and, 366 
 embolism and, 361 
 grade of the lesion and, 364 
 jaundice and, 362 
 nature of lesion and, 362 
 rhythm of the heart and, 364 
 sex and, 369 
 site of lesion and, 363 
 social conditions and, 369 
 Prognosis in acute endocarditis, 255 
 in aiu^icular fibrillation, 218 
 in auricular flutter, 209 
 in coupled rhythms, 183 
 in chronic cardiac failure, 361 
 in dilatation of the heart, 345, 353 
 in extra-systoles, 132 
 in heart-block, 172 
 in infantile irregularity, 124 
 in paroxysmal tachycardia, 196 
 in pericarditis, 402 
 in pneumo-pericardium, 419 
 in pulsus alternans, 161 
 Pulmonary incompetence, 354 
 due to dilatation, 353 
 mitral stenosis and, 339 
 Pulmonary stenosis, 353 
 Pulsation, prsecordial, 323 
 Pulse, the, alternation of, 153 
 
 in acute endocarditis, 235, 253 
 
 in aortic incompetence, 351 
 
 in aortic stenosis, 347 
 
 in Cheyne-Stokes breathing, 124 
 
 in heart-block, 1G5 
 
 in mitral disease, 66, 340 
 
INDEX 
 
 437 
 
 Pulse, the, in paroxysmal tachycardia, 
 188 
 in the Stokes-Adams syndrome, 169 
 palpation of, 60 
 pressure of, 60 
 
 respiratory irregularity of, 123 
 Pulsus alternans, 161 
 bigeminus, 180, 183 
 paradoxus, 409 
 
 in adherent pericardium, 409 
 Purgatives in chronic cardiac failure, 
 
 378 
 Purkinje fibres, 103 
 Pyopericardium. 396 
 
 Q deflection, 117 
 
 R deflection, 117 
 
 Renal disease and aortic disease, 272, 
 277, 301 
 and arterio-sclerosis, 36, 56, 65 
 and high blood-pressure, 36 
 and mitral disease, 66, 271, 301 
 and pericarditis, 390 
 Retinal vessels, 72 
 Rheumatic nodules in myocardium, 21, 
 
 150 
 Rheumatism and acute endocarditis, 
 227, 231, 257 
 and aortic disease, 276 
 and disease of the right side of the 
 
 heart, 353 
 and mitral disease, 277 
 and pericarditis, 388 
 and Stokes-Adams syndrome, 172 
 Rhythm, nodal, of the heart, 133 
 
 coupled, 175 
 Rupture of heart, 28 
 
 S deflection, 116 
 
 Salicylates, the, in acute endocarditis, 
 258 
 in acute pericarditis, 427 
 Scarlet fever and acute endocarditis, 
 228 
 and pericarditis, 390 
 Segmentation of cardiac muscle, 10 
 Semilunar valves, the mechanism of, 
 
 297 
 Septum, congenital defects of the car- 
 diac, 357 
 Sign, Broadbent's, 407 
 
 Duroziez's, 351 
 Sino -auricular node, the, 100 
 Sounds of the heart, the reduplication 
 
 of, 339 
 Stenosis, aortic, 346 
 mitral, 333 
 pulmonary, 353 
 tricuspid, 356 
 Stimulus production, 123 
 Stokes-Adams syndrome, 166 
 
 String galvanometer, 114 
 
 Strophanthus in chronic valvular dis- 
 ease, 383 
 
 Strychnine in chronic valvular disease, 
 384 
 
 Subcutaneous nodules in acute endo- 
 carditis, 149, 237 
 
 Syphilis and aortic disease, 277 
 and arterial degeneration, 43 
 and chronic valvular disease, 267 
 and mitral disease, 277 
 
 Symptoms of acute endocarditis, 234 
 of adherent pericardium, 404 
 of aortic disease, 282, 297 
 of arterial disease, 54 
 of auricular fibrillation, 214 
 of auricular flutter, 203 
 of chronic cardiac failure, 282 
 of mitral disease, 294 
 of myocardial failure in myocardial 
 
 disease, 311 
 of myocardial failure in the infec- 
 tions, 309 
 of paroxysmal tachycardia, 184 
 of pericarditis, 391 
 of pneumo-pericardium, 410 
 
 T deflection, 116 
 Tachycardia, paroxysmal, 184 
 Theobromine, 84, 384 
 Thoracostomy in chronic valvular 
 disease, 429 
 in pericardial adhesions, 428 
 Thrombosis in auricles, 306 
 
 in focal lesions of the arteries, 55 
 Tonicity, 174 
 
 Tonsillitis and acute endocarditis, 228 
 Treatment of acute endocarditis, 255 
 of adherent pericardium, 428 
 of arterio-sclerosis, 75 
 of auricular fibrillation, 219 
 of auricular flutter, 210 
 of extra-systoles, 132 
 of heart-block, 173 
 of paroxysmal tachycardia, 196 
 of pericarditis, 426 
 Treatment of chronic cardiac failure, 
 370 
 alkalies in, 378 
 caffeine in, 384 
 diet in, 371 
 digitalis in, 376 
 mercury in, 378 
 of symptoms, 374 
 rest in, 370 
 squills, 383 
 strophanthus, 383 
 theobromine, 384 
 Tricuspid incompetence, 354 
 stenosis, 356 
 
 valves, endocarditis and, 352 
 Tuberculosis and pericarditis, 396 
 
438 
 
 DISEASES OF THE HEART 
 
 Undefended space, the, 151 
 Uraemia and arterial disease, 69, 87 
 and chronic valvular disease, 286 
 
 Vaccines in acute endocarditis, 258 
 Valvular disease, chronic, 261 
 
 acute endocarditis and 
 
 266 
 and congenital defects, 274 
 and general cardio-vascu- 
 
 lar degeneration, 273 
 cardiac rhythm in, 285 
 Cheyne-Stokes breathing 
 
 •in, 287 
 cough in, 288 
 diagnosis, 320 
 dyspnoea in, 286 
 etiology of, 266 
 gastro-intestinal disturb- 
 ances in, 292 
 
 Valvular disease, chronic, mechanical 
 strain and, 267 
 morbid anatomy of, 261 
 myocardial failure in, 284 
 oedema in, 291 
 pain in, 289 
 . palpitation in, 289 
 prognosis of, 361 
 renal disease and, 269 
 symptoms of, 282 
 syphilis and, 267 
 treatment of, 370 
 Vaso-dilator drugs in arterio-sclcrosis, 
 
 84, 96 
 Ventricles, arrangement of musculature 
 
 of, 2 
 Viscosity of the blood, the, 36 
 
 X-ray examination, 48. 334, 338, 401, 
 417. 423, 424 
 
 BILLING AND SONS, LTD., PKINTKKS, GUILDFORD 
 
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