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HEABT DISEASE. 
 
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\ 
 
 Alfred W. Sanders, del. 
 
 Acute Aortitis From recent 
 
 specimen, showing raised pink 
 
 "Gelatmiform Plaques." 
 
 Geo Waterston & Sous.LiUi, Edia 
 
HEART DISEASE 
 
 AND 
 
 ANEUEYSM OF THE AOETA 
 
 WITH SPECIAL REFERENCE TO 
 
 PROGNOSIS AND TREATMENT. 
 
 SIR WILLIAM H. BROADBENT, Bart., K.C.V.O., 
 
 M.D. Lond., F.R.S., D.Sc. Leeds, LL.D. Edin. axd St. Andrews, F.R.C.P., 
 
 PHYSICIAN IN OEDINARY TO H.JI. THE KING, AND TO H.R.H. THE PRINCE OF WALES ; 
 
 COMMANDEUR DE LA LEGIO.V d'HONNETTR ; HON'. MEMBER OF VEREIN FUR INNERE MEDICIN, BERLIN 
 
 AND OF GESELLSCHAFT FUR INNERE MEDICIN UND KINDEKHEILKUNDE IN WIEN, 
 
 AND OF SOCIETE IMPERIALE, CONSTANTINOPLE; 
 
 VICE-PRESIDENT IMPERIAL CANCER RESEARCH ; CHAIRMAN OF COUNCIL OF 
 
 NATIONAL ASSOCIATION FOR PREVENTION OF TUBERCULOSIS; 
 
 CONSULTING PHXSICIAN TO ST. MARY'S HOSPITAL AND TO THE LONDON FEVER HOSPITAL; 
 
 AND 
 
 JOHN F. H. BROADBENT, 
 
 M.A., M.D. (Oxon.), F.R.C.P., 
 
 PHYSICIAN TO OUT-PATIENTS, ST. MARY'S HOSPITAL; ASSISTANT PHYSICIAN TO THE 
 
 LONDON FEVER HOSPITAL; 
 
 HON. PHYSICIAN TO THE METROPOLITAN CONVALESCENT INSTITUTION; 
 
 FORMERLY ASSISTANT PATHOLOGIST AND MEDICAL REGISTRAR TO ST. MARY'S HOSPITAL. 
 
 FOURTH EDITION. 
 
 NEW YORK: 
 WILLIAM WOOD & COMPANY. 
 
 MCMVI. 
 

PREFACE TO FOURTH EDITION. 
 
 My father, Sir William Broadbent, has entrusted to rne the 
 preparation of the new edition of this work, and with his 
 approval I have rearranged the subject-matter, and have 
 added chapters on the pulse, disease of the coronary arteries, 
 bradycardia, and atheroma of the aorta. I have also revised 
 and rewritten the chapters on acute and malignant (or per- 
 nicious) endocarditis, and that on affections of the myocar- 
 dium, a subject at which I have been working recently. 
 I am indebted to Messrs. Green for permission to make 
 use of the article I wrote for the Encyclopaedia Medica on 
 affections of the pericardium. My father has made several 
 important additions to the chapters on angina pectoris and 
 functional affections of the heart, and has carefully revised 
 the whole of the proofs. 
 
 JOHN F. H. BKOADBENT. 
 
 April, 1906. 
 
PREFACE TO THIRD EDITION. 
 
 Advantage is taken of the demand for a new edition of 
 the work on the Heart to make the book more complete, 
 and with this view chapters on acute affections of the 
 heart, Endocarditis, Pericarditis, Myocarditis, and on 
 Aneurysm of the Arch of the Aorta, have been added. 
 In these, as in the original work, no attempt is made to 
 give a systematic and complete treatise on each subject, 
 or to enter into a discussion of conflicting views which 
 have been entertained on various points of pathology and 
 etiology. The object has been rather to endeavour to 
 place before the reader a clinical picture of each disease 
 and to emphasize the points which are of chief importance 
 in diagnosis and prognosis. 
 
 The task of revision and of making the considerable 
 additions which have been specified has fallen almost 
 entirely on my son, Dr. John Broadbent, as I myself have 
 not had the requisite leisure. The chapters on the inflam- 
 matory affections of the heart are entirely his work, and 
 the chapter on Aneurysm has been arranged and compiled 
 by him from notes and papers of my own which have been 
 published elsewhere. While making this acknowledg- 
 ment, however, I accept the responsibility, as I have 
 carefully perused all the new matter and made some 
 
viii PREFACE. 
 
 additions. Several illustrations have been added, for which, 
 with the exception of Fig. 23, I am indebted to Dr. A. W. 
 Sanders, whose coloured drawing of acute aortitis from a 
 recent specimen is worthy of special notice. 
 
 W. H. BBOADBENT. 
 
 November, 1899. 
 
PREFACE TO FIRST EDITION, 
 
 This book is, for the most part, a reproduction of lectures 
 on " Prognosis in Valvular Disease of the Heart," delivered 
 before the Harveian Society in 1884, and of the Lumleian 
 Lectures at the Koyal College of Physicians on " Prognosis 
 in Structural Diseases of the Heart," delivered in 1891. 
 
 The prognosis of heart disease already engaged my 
 attention when I was house-physician under Sibson at St. 
 Mary's Hospital, and my first paper on this subject was 
 read before the Harveian Society in 1866. Up to that 
 time there had not, so far as I am aware, been any 
 systematic study and exposition of the indications by which 
 the probable course of disease of the heart in different 
 cases might be foreseen, and ideas which tended to obscure 
 the interpretation of the symptoms and physical signs were 
 held by physicians of great experience and authority. 
 Traces of the controversies of those days will still be found 
 in the present work. They have lost much of their interest, 
 but references to them could not well be entirely omitted. 
 
 The prognosis of heart disease is worthy of special study, 
 not only on account of its inherent importance, but also 
 because the knowledge which enables the medical man to 
 forecast clearly the course of the disease constitutes the best 
 preparation for its treatment. The subject of treatment did 
 
x PREFACE. 
 
 not, however, enter into the scheme of the lectures, but it 
 is engrafted upon them in the present work, and for this, 
 and for the rearrangement rendered necessary by it, I am 
 indebted to my son, Dr. John Broadbent, without whose 
 efficient assistance and co-operation the task of preparing 
 this book could not have been accomplished. 
 
 The lectures on which the book is based having been 
 addressed to the College of Physicians and to the Harveian 
 Society, presupposed a knowledge of heart disease on the 
 part of my audience, and a minute exposition and analysis 
 of the symptoms and physical signs, by means of which the 
 diagnosis of the different valvular and structural affections 
 of the heart is arrived at, were therefore unnecessary. This 
 is still taken for granted, but a brief chapter on the exami- 
 nation of the cardiac region, and on the significance of the 
 various departures from normal conditions, has been added. 
 
 The principal motive for reproducing the lectures has 
 been the frequently expressed wish on the part of old 
 pupils to see my teachings on heart disease in a collected 
 form. They have had to wait long, and to them I now 
 dedicate the book. 
 
 W. H. BKOADBENT. 
 
 Sept. 15th, 1897. 
 
PAGE 
 
 CONTENTS, 
 
 CHAPTER I. 
 
 The relations of the heart to the chest walls — Movements of the heart 
 — On the methods of examination by inspection: palpation, per- 
 cussion, and auscultation ... 
 
 CHAPTER II. 
 
 The Pulse. 
 
 Methods of examining the pulse — The use of the sphygtnograph — 
 Arterial tension— Hypertonus of the vessels — Blood pressure and 
 instruments for estimating it — Causes of high arterial tension ... 17 
 
 CHAPTER III. 
 
 Diseases of the Pericardium. 
 
 Pericarditis — Morbid anatomy — Etiology — -Physical signs — Signs of 
 effusion and cardiac dilatation — Symptoms — -Course of the disease 
 — Differential diagnosis — Prognosis : treatment — Adherent peri- 
 cardium — Suppurative pericarditis — Hydropericardium — Pneumo- 
 pericardium, etc , 29 
 
 CHAPTER IV. 
 
 Simple acute endocarditis . . 56 
 
 CHAPTER V. 
 
 "Malignant" ok "Pernicious" Endocarditis. 
 
 Nomenclature of the affection— Morbid anatomy — Etiology— The role 
 played by various micro-organisms— Physical signs and symptoms 
 — Infarction and embolism — Diagnosis— Prognosis— Treatment. 
 Chronic endocarditis 67 
 
CONTENTS. 
 
 CHAPTEE VI. 
 
 PAGE 
 
 Etiology of valvular lesions 84 
 
 CHAPTEE VII. 
 
 Valvular Lesions. 
 
 Points to be considered in studying a case of valvular disease — The 
 physical signs— Cardiac murmurs, their significance as regards the 
 seat and as regards the extent of the lesion — Modification of 
 heart-sounds — The pulse, its importance in diagnosis 89 
 
 CHAPTEE VIII. 
 
 The importance of hypertrophy and dilatation of the heart as a means 
 of estimating the extent of a valvular lesion — Possible objections 
 to this view discussed — Explanation of the way in which the 
 different valvular lesions give rise to hypertrophy and dilatation : 
 (1) Aortic stenosis ; (2) Aortic incompetence; (3) Mitral regurgi- 
 tation ; (4) Mitral obstruction — Compensation 100 
 
 CHAPTEE IX. 
 
 Aortic Stenosis. 
 
 Morbid anatomy and etiology — The murmur of aortic stenosis — Con- 
 ditions other than aortic stenosis which may give rise to systolic 
 aortic murmurs — Differential diagnosis of murmurs — Estimation of 
 extent of lesion by means of the murmur, the changes in the heart 
 and the pulse — Progress of the disease : Symptoms— Prognosis — 
 Treatment 110 
 
 CHAPTEE X. 
 
 Aortic Incompetence. 
 
 Etiology — Physical signs — The diastolic murmur : directions in which 
 it is conducted — Presystolic murmur, its significance — Modifica- 
 tion of the aortic second sound — Pulsation of arteries — Capillary 
 pulsation — The collapsing pulse — -Pulsus bisfuriens — Irregular 
 pulse — Estimation of the amount of regurgitation from the cha- 
 racter of the murmur, of the aortic second sound, of the pulse, and 
 the changes in the heart— Aortic incompetence due to syphilis and 
 causes other than acute endocarditis — Symptoms— Prognosis — 
 Treatment 123 
 
CONTENTS. xiii 
 
 CHAPTER XI. 
 
 Mitral Incompetence or Regurgitation. 
 
 PAGE 
 
 Etiology and morbid anatomy — Physical signs — The murmur of mitral 
 incompetence — The pulse — Explanation of irregularity of pulse — 
 Mitral incompetence due to endocarditis — Estimation of extent of 
 lesion, from character of murmur and first sound and from com- 
 pensatory changes in the heart — Symptoms — Prognosis — Mitral 
 incompetence without damage to valves — Its causation and ex- 
 planation — Differential diagnosis — Treatment 151 
 
 CHAPTER XII. 
 
 Mitral Stenosis. 
 
 Etiology — Predominance in the female sex— Morbid anatomy — Physio- 
 logy of the changes in the heart — Brown induration of lungs — 
 Nutmeg liver — The physical sigus — The pulse — The changes in 
 the heart — The cardiac murmurs — Three stages in the progress of 
 the disease as defined by auscultatory signs— The characteristics 
 of these three stages — Symptoms — Diagnosis — Prognosis — Treat- 
 ment 174 
 
 CHAPTER XIII. 
 
 Valvular Disease op the Right Side of the Heart. 
 
 Tricuspid incompetence and stenosis — Pulmonic incompetence and 
 
 stenosis — Systolic pulmonic murmurs which do not indicate stenosis 200 
 
 CHAPTER XIV. 
 
 Congenital Malformations. 
 
 Varieties of congenital malformations — Relative frequency of occurrence 
 — Of single and combined defects— Physical signs — Symptoms — 
 Cyanosis— Cause of cyanosis — Diagnosis — Prognosis 206 
 
 CHAPTER XV. 
 
 Prognosis in Valvular Disease (General). 
 
 The nature of the lesion : the relative danger attaching to each par- 
 ticular lesion — Sudden death : the valvular diseases in which it 
 is liable to occur— The extent of the lesion — The stationary or 
 progressive character of the lesion as influencing prognosis ... 214 
 
CONTENTS. 
 
 CHAPTER XVI. 
 
 PAGE 
 
 Prognosis continued — Age, sex, heredity —Effects of high arterial 
 tension — Habits and mode of life of the patient— Anaemia — The 
 circumstances under which prognosis may have to be made : (1) 
 Immediately after acute endocarditis; (2) When the valvular 
 lesion is slight and has given rise to no structural changes in the 
 heart ; (3) When compensatory changes have taken place but no 
 symptoms of embarrassment of the circulation are present; (4) 
 When symptoms of failure of compensation have set in ; (5) In 
 advanced valvular disease when severe symptoms of cardiac failure 
 have supervened 223 
 
 CHAPTER XVII. 
 
 Treatment (General). 
 
 Treatment of valvular disease in general — Prophylactic measures — 
 General rules, in cases where lesion is not of serious extent, as to 
 exercise, (Ertel and £chott treatments, climate, choice of residence, 
 diet, stimulants — Treatment where lesion is of more serious nature 
 and has given rise to marked hypertrophy and dilatation of the 
 heart — Precautions to be taken — Selection of winter resort — Rest 
 in bed — Diet — Stimulants — Employment of drugs — Treatment of 
 venous congestion — Venesection — Treatment in aortic disease . . . 232 
 
 CHAPTER XVIII. 
 
 Treatment by Drugs. 
 
 Use and abuse of digitalis — Substitutes for digitalis — The group of 
 cardiac tonics of the digitalis type— Their physiological action: 
 therapeutic effects — Use of digitalis in aortic stenosis, in mitral 
 incompetence, in mitral stenosis 256 
 
 CHAPTER XIX. 
 
 Structural Change in the Heart. 
 
 Hypertrophy — Causes of hypertrophy of the left ventricle, of the right 
 
 ventricle — Physical signs — Symptoms — Prognosis — Treatment ... 2G8 
 
 CHAPTER XX. 
 
 Dilatation. 
 
 Etiology — Valvular disease, exertion, strain, renal disease, acute bac- 
 terial infections — Physical signs — Symptoms —Prognosis —Treat- 
 ment 281 
 
CONTENTS. 
 
 CHAPTEE XXI. 
 
 Structural Change in the Eight Ventricle. 
 
 TAOP, 
 
 Physiological dilatation — Hypertrophy and dilatation — Degeneration 
 
 of the muscular walls 31 1 
 
 CHAPTEE XXII. 
 
 Disease of the Coronary Arteries. 
 
 Atheroma or Sclerosis — Endarteritis — Thrombosis — Embolism — 
 
 Aneurysm ... ... ... ... ... ... ••• ... 320 
 
 CHAPTEE XXIII. 
 
 Affections of the Myocardium. 
 
 Acute myocarditis — Fibroid change — Etiology and morbid anatomy — 
 — Syphilitic affections of the myocardium — Physical signs and 
 symptoms of fibrosis — Diagnosis — Prognosis — Treatment 32G 
 
 CHAPTEE XXIV. 
 
 Affections of the Myocardium (Continued). 
 
 Distinction between fatty infiltration of obesity and fatty degeneration 
 — Causation of fatty degeneration — Symptoms — Spontaneous 
 rupture of the heart — Physical signs — Diagnosis — Prognosis — 
 Treatment — Aneurysm and new growths of the heart 342 
 
 CHAPTEE XXV. 
 
 Angina Pectoris. 
 
 Characteristics of true angina — -Associated symptoms — Exciting causes 
 of paroxysms — Etiology and morbid anatomy — Discussion of 
 theories advanced to explain the pain — Diagnosis — Prognosis — 
 Treatment 359 
 
 CHAPTEE XXVI. 
 
 Functional Affections (so-called) of the Heart. 
 
 Pain in precordial region— Site of pain — Explanation of referred pain 
 and areas of cutaneous hyperalgesia — Disorders of rhythm of the 
 heart — Mechanism by which the rhythm of the heart is regulated 
 — Intermittent and irregular action of the heart — Palpitation : 
 tachycardia .,. ... 381 
 
CONTENTS. 
 
 CHAPTER XXVII. 
 
 Disorders of Rhythm of the Heart (Continued). 
 
 TAGE 
 
 Varieties of slow pulse and their causation— The condition of brady- 
 cardia known as Stokes-Adams disease — Etiology — Symptoms — 
 Diagnosis— Prognosis— Treatment 398 
 
 CHAPTER XXVIII. 
 
 Acute Aortitis or Acute Degenerative Lesions of the Aorta. 
 
 Experimental evidence — Etiology — Morbid anatomy — Pathogeny — 
 
 Prognosis — Treatment 405 
 
 CHAPTER XXIX. 
 
 I Atheroma or Chronic Degenerative Lesions of the Aorta. 
 
 Etiology of general arterio-sclerosis and atheroma — Morbid anatomy — 
 Pathogeny — Different views — Physical signs and symptoms— Aortic 
 incompetence due to degenerative change — Its distinguishing 
 features — Prognosis — Treatment 411 
 
 CHAPTER XXX. 
 
 Aneurysm of the Arch of the Aorta. 
 
 Morbid anatomy — Etiology — Pathogeny — Relations of the arch of the 
 aorta — Physical signs and symptoms — Aneurysm (1) of the intra- 
 pericardial portion of aorta ; (2) of ascending aorta ; (3) of trans- 
 verse part of arch ; (4) of descending aorta — Diagnosis — Prognosis 
 —Treatment 424 
 
 INDEX 475 
 
HEART DISEASE. 
 
 CHAPTEE I. 
 
 THE EELATIONS OP THE HEAET TO THE CHEST WALLS — 
 MOVEMENTS OF THE HEAET — ON THE METHODS OF EX- 
 AMINATION BY INSPECTION : PALPATION, PEECUSSION, 
 AND AUSCULTATION. 
 
 A systematic description of the anatomy and relations of 
 the heart, and a text-book exposition of the physical signs 
 by means of which departures from the normal condition 
 of the heart are recognized, would be out of place in a work 
 of this character. A brief reminder, however, of the rela- 
 tions of the heart to the chest wall, together with a short 
 description of the method in which a clinical examina- 
 tion of the heart should be conducted, and an indication 
 of the significance of the various points observed, will 
 form a useful preliminary to the study of heart disease. 
 This will therefore form the subject of the introductory 
 chapter. 
 
 The first portion of this chapter, dealing with the position 
 and relations of the heart, is mainly taken from the works 
 of Sibson,* who devoted much time and labour to the study 
 of this subject, and under whom I worked while he was 
 engaged upon it. 
 
 * Sibson's Works, edited by Ord. Vol. iii. 
 
 B 
 
2 heart disease. 
 
 The Position of the Heaet and the Eelation of 
 its Cavities to the Chest Walls. 
 
 The heart and great vessels, with their pericardial 
 covering, occupy the central portion of the thoracic cavity. 
 The right auricle and ventricle compose the whole of the 
 front of the heart, with the exception of a narrow strip to 
 
 FIG. 1. — RELATION OF HEART TO CHEST WALLS (Sibson). 
 
 the left, where the left ventricle comes into view from 
 behind. 
 
 The right auricle lies behind the sternum, its upper 
 border being on a level with the third costal cartilages, and 
 extending from a point about one inch to the right of the 
 sternum nearly to its left border. It is broadest above, and 
 narrows down almost to a point at the lower end of the 
 auriculo-ventricular furrow, which forms its left border and 
 runs obliquely downwards from the sternal end of the 
 third left to the sternal end of the seventh right costal 
 
RELATION OF HEART TO CHEST WALLS. 3 
 
 cartilage. Its right border is convex, and lies behind the 
 right costal cartilages, just beyond the right margin of 
 the sternum. 
 
 The right auricle undergoes more change in form during 
 
 X 
 
 y 
 
 p 
 
 p 
 
 FIG. 2. — THE HEART AND GREAT VESSELS, WITH THE ANTERIOR WALLS OF THE 
 RIGHT AURICLE AND RIGHT VENTRICLE DISSECTED OFF TO SHOW POSITION 
 OF THE VALVES AND SEPTA (QUAIN'S Anatomy). 
 
 a, Innominate and left carotid arteries ; b, Transverse part of arch ; c, Vena cava superior ; 
 d. Ascending part of arch of aorta ; e, Pulmonary artery ; /, Pulmonic valves ; g, Appen- 
 dix of left auricle ; h, Inter-auricular septum ; i, Fossa ovalis, with Eustachian valve 
 below; j, Left segment of tricuspid valve; Jc, iDter-ventricular septum; I, Left ventricle ; 
 m, Coronary vein; n, Right segment of tricuspid valve ; 0, Inferior vena cava ; p, Hepatic 
 veins ; q, Left ventricle ; r, Anterior papillary muscle. 
 
 the action of the heart than any other portion of the organ, 
 becoming nearly twice as wide in systole of the ventricles 
 as in diastole. The auriculo-ventricular furrow also sweeps 
 
4 HEART DISEASE. 
 
 backwards and forwards to so great an extent, to the left 
 during systole and to the right during diastole of the 
 ventricles, that it presents no fixed position during life. 
 
 The right ventricle, when exposed to view, presents a 
 pyramidal shape. The base of the pyramid is formed by the 
 lower boundary of the ventricle, which rests on the central 
 tendon of the diaphragm ; the apex of the pyramid is 
 crowned and completed by the pulmonary artery ; the left 
 side is formed by the furrow which divides the left from the 
 right ventricle ; the right side, by the furrow separating 
 the right auricle and ventricle. 
 
 The furrow separating the two ventricles runs from the 
 third to the fifth left costal cartilages, just behind their 
 junction with the ribs. 
 
 The left ventricle forms the convex left border of the 
 heart as seen from the front, and forms a long, narrow strip 
 extending from the third left intercostal space down to the 
 fifth, where it terminates in the apex of the heart. This 
 occupies the fifth space, being usually situated just internal 
 to a line drawn vertically downwards from the nipple. 
 
 The appendix of the left auricle lies just behind the third 
 left costal cartilage, close to its junction with the third rib, 
 and fills up the space between the upper end of the left and 
 right ventricles at the top of the longitudinal or inter- 
 ventricular furrow. 
 
 The area which would be marked out on the chest 
 wall by percussion, indicating the position of the heart 
 beneath and its relation to the chest wall, is termed "the 
 area of deep cardiac dulness." 
 
 The lungs cover the great vessels and the whole of the 
 heart except a portion of the right ventricle. 
 
 The inner margins of the right and left lungs in front 
 meet behind the sternum for its upper two-thirds. The 
 inner margin of the left lung diverges from that of the right 
 at the level of the fourth left costal cartilage. It passes 
 
RELATION' OF HEART TO CHEST WALLS. 
 
 thence to the left along the lower edge of the fourth 
 cartilage in front of the body of the right ventricle, curving 
 downwards just before it reaches the junction of the 
 cartilage with the rib ; it then crosses the fourth space and 
 fifth cartilage, and curving, so as to form a hollow space 
 
 FIG. 3. — TUE HEART WITH LUNGS IN FIG. 4.— THE HEART WITH OVERLYING 
 
 SITU TO ILLUSTRATE AREA OF SUPER- LUNG DISSECTED OFF TO ILLUSTRATE 
 
 FICIAL CARDIAC DULNESS (SibsOJl). AREA OF DEEP DULNESS (Sibson). 
 
 for the lodgment of the apex, ends behind the sixth 
 cartilage. 
 
 The inner margin of the right lung continues its course 
 nearly straight downwards behind and a little to the left 
 of the centre of the sternum, to the level of the sixth 
 chondrosternal articulation. It thus covers the right 
 auricle, the auriculo-ventricular furrow, and the right border 
 of the right ventricle. 
 
6 HEART DISEASE. 
 
 The area on the chest wall corresponding to the part 
 of the heart uncovered by lung can be accurately marked 
 out by percussion, and is known as " the area of superficial 
 cardiac dulness." 
 
 The area thus indicated would be mapped out as follows : 
 its right margin, by a line running from above downwards 
 slightly to the left of the middle line of the sternum from 
 the level of the fourth costal cartilage down to that of the 
 sixth ; its highest point would be at the level of the fourth 
 costal cartilage ; its left limit would be defined by a line 
 running outwards from the sternum at this level, along the 
 lower edge of the fourth left costal cartilage, nearly as far 
 as its junction with the rib, and then dipping downwards 
 and curving slightly outwards to the point on the chest 
 wall where the apex beat is felt. The base or lower limit 
 corresponds to a line drawn from the sixth right costal 
 cartilage to the apex. 
 
 Movements of the Heaet. 
 
 The heart undergoes a marked change in form and 
 diminution in size during systole. At the end of diastole 
 it is globular in shajDe. The apex is rounded, the ventricles 
 are full, the auricles distended, the appendix of the left 
 auricle coming forward to lie in the groove between the 
 right ventricle and aorta. The ventricles yield on handling, 
 and the auricles are dimpled by slight pressure of the 
 finger. The first systolic act is the sudden swift with- 
 drawal of the auricular appendix, due to the contraction 
 of the auricle. Immediately afterwards the ventricles 
 harden, and the change in form produced by the contraction 
 begins. The septum is the centre on which the movements 
 converge, and the most fixed point is about three-quarters 
 of the distance from the apex to the auriculo- ventricular 
 furrow. The pulmonary artery is drawn sharply down- 
 wards, the apex becomes more pointed, and moves spirally 
 
CLINICAL EXAMINATION OF THE HEART. f 
 
 upwards and to the right. The left border converges 
 slightly, and the right border more upon the axis of the 
 heart. 
 
 The general cardiac impulse is due to the contractile 
 hardening of the muscular walls, the apex beat to this 
 hardening and to the rotatory movement forward and to 
 the right. Both impulse and apex beat require a fulcrum 
 posteriorly in order to be felt through the chest wall. 
 This is furnished by the pericardium and spinal column, 
 against which the shoulder of the left ventricle thrusts. 
 
 In the interior of the heart the end of diastole finds the 
 auriculo-ventricular valves floated up into position by the 
 action of elastic fibres on their auricular aspect, and already 
 in contact along their free margins, so as to close the orifice. 
 The chordee tendinese are slightly on the stretch. The 
 pressure on the valves as the ventricles contract closes 
 them more tightly, and the co-ordinate contraction of the 
 papillary muscles neutralizes the approximation of the 
 origin of the chordse tendinete to the base of the heart 
 which results from its diminution in size during systole. 
 The contraction of the circular muscle fibres round the 
 orifices contributes to the complete closure of the valvular 
 flaps. 
 
 The Clinical Examination of the Heart. 
 This is conducted by inspection, palpation, percussion, 
 and auscultation. Much is learnt by careful inspection. 
 Bulging or other general feature of the precordial region 
 is to be noted. Any deformity of the chest giving rise to 
 displacement of the heart, or fixation of one side of the 
 thorax by pleural adhesions, or by fibroid or other disease 
 of the lung, must be taken into account. The position and 
 character of the apex beat should be determined as far as 
 this is possible ; the surface of the chest should be care- 
 fully scrutinized for pulsation in abnormal situations, and 
 
8 FIE ART DISEASE. 
 
 epigastric pulsation or auy visible heave over the right 
 ventricle should be noted. 
 
 These observations will be corroborated or checked by 
 palpation ; but there are other points which can be ascer- 
 tained by the eye alone, such as retraction of intercostal 
 spaces. This is most commonly seen in the third, fourth, 
 and fifth left intercostal spaces and is usually systolic in 
 time ; it may either arise from a direct tug on the spaces 
 by pericardial adhesions, or be due to atmospheric pressure : 
 the latter condition is more common, and in such cases 
 the heart will usually be dilated and hypertrophied, and 
 therefore subject to great diminution in volume during 
 systole. 
 
 Inspection also embraces the neck, where is seen the 
 carotid throb which betrays aortic regurgitation. To be 
 characteristic, it must be visible, not at the root of the 
 neck only, but as high as the hollow between the ramus of 
 the jaw and the sternomastoid. It may, exceptionally, be 
 present where there is no aortic disease, and it may be 
 simulated by pulsation in the deep jugular vein. This, 
 however, is easily distinguished, being readily arrested by 
 light pressure. 
 
 Important information may frequently be derived from 
 careful observation of the veins of the neck. The jugulars 
 on one or both sides may be full and distended. If the dis- 
 tension is present on one side only, it may be due to pressure 
 on the innominate vein of that side by an aneurysm or 
 some other intra-thoracic tumour. If it exists on both side;-, 
 it may be due either to pressure on the superior vena cava 
 or both innominate veins, or to dilatation and engorgement 
 of the right side of the heart from back pressure through 
 the lungs. In the latter case, the veins will be temporarily 
 more or less emptied by a forcible deep inspiration, and will 
 become more distended during expiration : in the former, 
 variations of the intra-thoracic pressure during inspiration 
 
CLINICAL EXAMINATION OF 7 HE HEART. 9 
 
 and expiration will have no appreciable effect in reducing 
 or augmenting the distension. Pulsation of the jugular 
 veins may be present when the right side of the heart is 
 greatly dilated and tricuspid regurgitation has set in. The 
 pulsation is often double, both auricular and ventricular 
 systoles transmitting backward waves. It has been studied 
 with great care by Mackenzie, of Burnley, who has obtained 
 graphic records of two distinct types of jugular pulsation, 
 and established their significance. 
 
 Finally, mention may be made of enlarged and tortuous 
 veins on the surface of the chest, constituting collateral 
 channels between the superior and inferior vense cavse when 
 one or other is compressed, and of pulsating veins occasion- 
 ally seen dipping into an intercostal space near the sternum. 
 
 Palpation. — The information obtained by palpation is 
 second in importance only to that afforded by auscultation. 
 The situation, force, limits, and extent of the cardiac im- 
 pulse are accurately ascertained, and the relative intensity 
 of the apex beat and right ventricle beat must be compared. 
 The examination, to be complete, must be conducted in 
 various ways. 
 
 Firstly, the flat of the right hand should be placed over 
 the cardiac area, the fingers covering the apex region. The 
 powerful heaving impulse of the apex in hypertrophy, the 
 diffuse shock or slap in dilatation, and the peculiar sudden 
 tap in mitral stenosis are often at once diagnostic : a power- 
 ful heave of the lower left costal cartilages, and sometimes 
 of the lower end of the sternum as well, will indicate stress 
 thrown on the right ventricle by back pressure through the 
 pulmonary circulation. Thrills or vibrations, systolic or pre- 
 systolic, over the area of the apex beat or elsewhere will be 
 recognized at the same time. Sometimes a peculiar diastolic 
 shock or retraction may be felt over the apex or the right 
 ventricle, caused by the presence of pericardial adhesions. 
 Next the fingers must be pressed into the right intercostal 
 
io HEART DISEASE. 
 
 spaces in search of pulsation, and the apex region must be 
 explored with the tips of the fingers, and the exact position, 
 extent, force, and deliberate or sudden character of the apex 
 beat must be noted. This investigation must not be limited 
 to the point at which the apex appeared to present itself, 
 when the hand was applied to the praecordium ; the real 
 apex beat may be sometimes far out in the axilla, or high 
 up in the fourth space, or it may be concealed behind the 
 mamma. 
 
 (Speaking generally, displacement of the apex downwards 
 is indicative of hyjDertrophy of the left ventricle, dilatation 
 giving rise to extension of the impulse outwards and down- 
 wards ; displacement of the apex to the left is caused by 
 enlargement of the right ventricle, which is usually due to 
 combined hypertrophy and dilatation. For the most part, 
 any considerable change in the position of the apex beat 
 is the result of hypertrophy and dilatation of both sides 
 of the heart. Special displacement of the apex not due 
 to intrinsic changes in the heart may be the result of 
 various causes, such as pericardial or pleuro-pericardial 
 adhesions, pleural effusion, pneumo-thorax, fibroid condition 
 or cavitation of the lung, or deformity of the chest. It 
 is always well to ascertain whether the aj)ex changes its 
 position in respiration, and with change of posture of the 
 patient from the erect to the recumbent position, and when 
 lying first on one side, then on the other. 
 
 It is not uncommon to find that neither apex beat nor 
 impulse of any kind is to be felt. This does not necessarily 
 imply feeble action of the heart, but may be due to 
 thickness of the parietes or great depth of thorax, or to 
 overlapping emphysematous lung, or to pericardial adhesions. 
 
 Departures from the normal in the cardiac rhythm should 
 also be noted ; they are of two kinds : Irregularity and 
 Intermission — irregularity, when the beats are of varying 
 force and follow each other at unequal intervals; intermission, 
 
CLINICAL EXAMINATION OF THE HEART. n 
 
 when a beat is dropped from time to time, the intervening 
 beats being of equal force and at equal intervals. 
 
 The irregular action of the heart is usually exaggerated 
 in the pulse, as many of the beats may fail to reach the 
 wrist. When the pulse is intermittent, it will usually be 
 found that there is not an entire absence of the beat of the 
 heart, but an imperfect and hurried beat corresponding to 
 the intermission. 
 
 The examination by palpation, to be complete, must 
 embrace the abdomen, and the size of the liver must be 
 carefully ascertained. As the right ventricle begins to fail, 
 and obstruction to the return of blood to the heart from 
 the liver through the inferior vena cava begins to be felt, 
 the liver becomes engorged and congested, and gradually 
 increases in size, till it may become very much enlarged, 
 extending even below the umbilicus. The size of the liver 
 is therefore an important index as to the degree of venous 
 obstruction. 
 
 In examining to ascertain the size of the liver, the 
 patient should be made to lie on his back with the legs 
 drawn up, so that the belly is perfectly flaccid. The flat 
 of the hand should then be placed on the abdomen, and the 
 edge of the liver carefully felt for ; at the same time the 
 other hand should be placed beneath the back of the patient 
 below the false ribs, and the liver lifted from behind, so 
 that if the liver edge is not at first felt, the jogging from 
 behind will press it up against the hand on the abdomen, 
 and render it more obvious. Palpation with the tips of the 
 fingers will probably provoke some rigidity of the abdominal 
 walls, which obscures the resistance presented by the liver 
 behind. When, however, there is fluid present in the 
 abdominal cavity, this method of palpation will be useful, 
 for then on dipping sharply down with the fingers, the 
 fluid between the liver and abdominal walls will be dis- 
 placed, and the firm, hard substance of the liver be felt below. 
 
12 HEART DISEASE. 
 
 Percussion is, as a rule, a very untrustworthy method 
 of ascertaining the size of the liver, owing to conducted 
 resonance from distended coils of intestine ; it will, however, 
 serve to mark out the upper margin of the liver, unless there 
 he consolidation of lung fluid or old pleural adhesions at 
 the base of the right pleural cavity. 
 
 Pulsation of liver is best detected by combined simul- 
 taneous palpation and inspection. The hand should be 
 placed on a part of the liver at some distance from the 
 epigastrium, and gentle pressure being made, it should be 
 carefully watched. If the liver is actually pulsating, and 
 not merely jogged by a hypertrophied right ventricle, the 
 hand will be seen to rise and fall rhythmically even though 
 no actual pulsation is felt on palpation. 
 
 Percussion. — Percussion will verify and perhaps extend 
 the information obtained by inspection and palpation. It 
 is specially useful when no impulse is present. There is 
 normally, as has already been described, a small area of 
 absolute dulness — " the superficial cardiac dulness " — where 
 the heart is not covered by lung, which is easily defined. 
 It may be encroached upon and obliterated when the lungs 
 are emphysematous, or extended when they are shrunken 
 as a result of fibroid contraction or pleural adhesion. The 
 deep dulness indicating the true dimensions of the heart 
 cannot be mapped out with absolute accuracy in all cases, 
 as the overlying lung tissue varies in thickness and extent 
 in different individuals, and in inspiration and expiration. 
 In percussing for this purpose, the finger must be pressed 
 firmly into the intercostal spaces, and the stroke must be 
 delivered smartly and perpendicularly. The note changes 
 gradually as the dull area is left with the increase in the 
 thickness of the overlapping lung, till full lung resonance 
 is reached. The end of expiration, when the cushion of 
 lung is thinnest, should be chosen as the moment to attempt 
 the definition of the comparative dulness which indicates 
 
CLINICAL EXAMINATION OF THE HEART. 13 
 
 the size and position of the heart. The so-called auscul- 
 tatory percussion is, in my opinion, of no value whatever. 
 
 Auscultation. — The physical examination is completed 
 by auscultation. For the most part, a diagnosis has already 
 been arrived at before the stethoscope is applied, and in 
 all cases the information obtained by auscultation must be 
 checked and interpreted by evidence derived from the pulse, 
 and from inspection, palpation, and percussion. Either a 
 flexible or rigid stethoscope may be employed. The former 
 is more convenient and expeditious, as it can be shifted 
 from point to point without moving the head, and it is 
 always under the eye, so that bulging or retraction of spaces 
 can be timed and co-ordinated with the sounds or murmurs 
 heard. On the other hand, it is sometimes difficult to dis- 
 tinguish between the first and second sound, and the rigid 
 stethoscope, by communicating a faint jar to the ear, at 
 once points out the sound which is produced by the systole. 
 
 The stethoscope should be applied successively to the 
 apex region, the tricuspid, pulmonic, and aortic areas, and 
 the character, and absolute and relative loudness of the 
 sounds should be noted at each point ; observations taken 
 simply at the apex or base afford very imperfect information. 
 
 The Mitral Area. — At the apex both sounds are normally 
 audible — the first, comparatively long and low-pitched ; the 
 second, short and sharp. The first sound may undergo 
 various modifications. It may be prolonged, which is 
 usually indicative of hypertrophy; or, on the other hand, 
 it may be short and sharp. If when short it is also loud, 
 it is among the indications of dilatation ; if weak, it may 
 be due either to degeneration or to simple asthenia of the 
 cardiac muscle. A peculiar sharp and snapping character 
 of the first sound at the apex is produced by mitral 
 stenosis. Reduplication of the first sound is an important 
 modification often met with ; it is most distinct when the 
 stethoscope is placed exactly over the septum between the 
 
14 HEART DISEASE. 
 
 apex and right ventricle, i.e. partly over one ventricle, 
 partly over the other. Left of this spot the sound may be 
 merely blurred; right of it, reduplication may still be 
 distinct. The double sound is due to want of synchronism 
 between the two ventricles, and may be produced when- 
 ever undue stress is put upon the left ventricle by high 
 systemic arterial tension, or on the right by obstruction in 
 the pulmonary circulation. The second sound heard at 
 the apex is, for the most part, that produced at the aortic 
 valves ; occasionally it is more distinct here than at the 
 aortic area proper. Its modifications will be described 
 when the sounds at the base are discussed. 
 
 The interval between the first and second sounds indi- 
 cating the duration of the cardiac systole, and that between 
 the second and first sounds, or the diastolic interval, 
 should be carefully observed, and any deviation from the 
 normal noted. The rhythm may be disturbed in one 
 direction by the shortening of the diastolic interval, till 
 the sounds are equidistant and resemble the ticking of a 
 watch, as in palpitation, or the sounds may become equi- 
 distant from prolongation of the systole, when they resemble 
 the beat of a pendulum. In the other direction the systolic 
 interval may be shortened till the second sound follows 
 the first almost without an appreciable pause : this is a 
 serious condition, indicating incomplete contraction of the 
 ventricle, and also, in many cases, impending cardiac 
 failure. 
 
 The murmurs heard at the apex may be systolic, pre- 
 systolic, or diastolic; of these the most frequent is the 
 systolic. It is most commonly smooth and blowing in 
 character ; sometimes a musical element may be present, or 
 the murmur may be rumbling and indistinct ; it is rarely 
 rough and croaking, as is often the case with aortic systolic 
 murmurs. The systolic murmur heard at the apex always 
 signifies more or less regurgitation through the mitral 
 
CLINICAL EXAMINATION OF THE HEART. 15 
 
 orifice, and it will be necessary to note how far outside the 
 apex the murmur is audible, and to what extent it replaces 
 the first sound, as these will be important points in esti- 
 mating its significance. An apex murmur is sometimes 
 more distinct in the recumbent than in the sitting or erect 
 position, or may be brought out by slight exertion. 
 
 A pulmonic or aortic systolic murmur may be conducted 
 to the apex, but it will be of diminished intensity and will 
 not, as a rule, be conducted towards the axilla. 
 
 The presystolic murmur, so named from the fact that it 
 precedes and runs up to the first sound produced by the 
 cardiac systole, is usually vibratory in character. Speaking 
 generally, it indicates the presence of mitral stenosis, and 
 is produced by the rush of blood from the auricle into the 
 ventricle through the narrowed mitral orifice ; but it may be 
 present as a temporary phenomenon after acute disease. 
 In an early stage it is brief in duration, and rises rapidly 
 in intensity, terminating abruptly in the first sound, when 
 it corresponds with and is produced by the auricular systole. 
 It may, however, be greatly prolonged ; that is, it may begin 
 at a much earlier period so as to correspond with the active 
 dilatation stage of the ventricular diastole, which precedes 
 the auricular systole. 
 
 A diastolic murmur audible at the apex is usually that 
 of aortic insufficiency, conducted from the base to the apex 
 by the walls of the heart. 
 
 The Tricuspid Area. — The sounds heard over the tri- 
 cuspid area are mainly those of the right ventricle; the 
 first sound is rather shorter and louder than that at the 
 apex, and the second sound is intensified when there is 
 obstruction in the pulmonary circulation. 
 
 Systolic, presystolic, and diastolic murmurs may be 
 heard in this region, and the former may indicate tricuspid 
 incompetence, but the two latter varieties are most com- 
 monly murmurs conducted from the apex or base, and 
 cannot be relied upon for diagnostic purposes. 
 
16 HEART DISEASE. 
 
 The Aortic Area. — In the pulmonic and aortic areas 
 accentuation of the second sound is the point specially to 
 be observed, denoting increased pressure in the pulmonic 
 or systemic circulation respectively. Keduplication of the 
 second sound is not uncommon, and is due to a synchronous 
 closure of the aortic and pulmonic semilunar valves. 
 
 The murmurs audible over the aortic area in the second 
 right intercostal space may be systolic or diastolic. A 
 systolic murmur may indicate actual obstruction, but is 
 more frequently due to mere roughening or rigidity of the 
 cusps of the valves, or to dilatation of the aorta beyond the 
 valves, or other conditions not necessarily causing narrow- 
 ing of the orifice. It may be loud and rough, or musical, 
 or soft blowing. A diastolic murmur is usually blowing in 
 character, and almost invariably indicates aortic incom- 
 petence, being produced by the regurgitant stream of blood ; 
 it can sometimes be heard lower down over the sternum, 
 or a little to one side of it, at a point nearer the orifice 
 of the aorta, when it is not audible in the so-called aortic 
 area. 
 
 The Pulmonic Area. — Systolic and diastolic murmurs 
 may also be heard in the pulmonic area, the third left 
 intercostal space, and may indicate stenosis or incompetence 
 of the pulmonic valves. These affections are, however, 
 rare, and are usually of congenital origin. The murmurs 
 heard in the pulmonic region are for the most part either 
 conducted from the region of the aorta or apex, or are 
 hseinic murmurs dependent on abnormal conditions of the 
 blood, or they may occasionally be due to vibrations caused 
 by the contact of the conus arteriosus with the chest wall. 
 A diastolic aortic murmur is frequently louder in the pul- 
 monic area than at the right second space, and may be 
 audible here when it cannot be heard in the aortic area. 
 
CHAPTER II. 
 THE PULSE. 
 
 METHODS OF EXAMINING THE PULSE —THE USE OP THE 
 SPHYGMOGRAPH — ARTERIAL TENSION — HYPERTONUS OF 
 THE VESSELS — BLOOD PRESSURE AND INSTRUMENTS 
 FOR ESTIMATING IT — CAUSES OF HIGH ARTERIAL 
 TENSION. 
 
 A careful and systematic examination of the pulse is of 
 the first importance, inasmuch as the heart and arteries 
 together constitute one system, and are in close mechanical 
 and functional relation. 
 
 In feeling the pulse, three fingers should be placed on 
 the vessel, and careful palpation be made with varying 
 degrees of pressure. The following points should be care- 
 fully noted : — 
 
 1. The frequency, that is, the number of beats per 
 
 minute ; the regularity or irregularity of the beats, 
 and their equality or inequality in force. 
 
 2. The size of the vessel, whether large or small. 
 
 3. The character of the beat, whether abrupt or 
 
 gradual, long-sustained or short, subsiding gra- 
 dually or falling abruptly. 
 
 4. The force or strength of each beat. 
 
 5. The condition of the vessel between the beats, whether 
 
 full and resistant or readily compressible. 
 
 6. The state of the arterial wall, whether smooth, 
 
 regular, and supple, or irregular, tortuous, and rigid. 
 
 c 
 
1 8 HEART DISEASE, 
 
 The determination of the frequency, the regularity or 
 irregularity of the pulse, the size of the vessel, the character 
 of the beat, presents little difficulty. 
 
 To estimate the force of each beat, three fingers should 
 be placed on the vessel, and pressure made by the finger 
 nearest the heart till the wave is arrested, so that it is not 
 felt by the two lower fingers. By varying the degree of 
 pressure with one and all three fingers, some idea is formed 
 of the force of the pulse wave. 
 
 It must be recollected that the radial artery when 
 compressed by the finger is more or less flattened. When 
 distended by the increased pressure from the volume of 
 blood injected into the arterial system at each beat of the 
 heart it tends to resume the circular shape, and this is felt 
 by the finger as the pulse wave. It yields gradually as 
 the pressure within subsides, and in the normal sphygmo- 
 graphic tracing the cycle is represented graphically by a 
 sudden sharp systolic rise, followed by a gradual fall, 
 which is interrupted by a slight secondary elevation due to 
 the dicrotic wave. 
 
 Condition of the Artery between the Beats. — The artery is 
 more or less distended with blood between the beats after 
 the wave has passed, and the degree of pressure within 
 the vessel during that period may be termed the constant 
 mean blood pressure. It is also known as the " diastolic 
 pressure," but the term is misleading, as the pressure is 
 maintained by the elastic recoil of the aorta and large 
 vessels, and has no reference to the heart. The term 
 " systolic pressure " is more justifiably employed to denote 
 the increased or variable pressure due to the blood in- 
 jected at each beat of the heart. If the arterial walls 
 are relaxed and the blood pressure is low, the vessel can 
 readily be flattened, and can scarcely be felt by the 
 finger between the beats. The filling of the artery at each 
 systole of the heart will then make a greater impression on 
 
THE PULSE. 19 
 
 the finger, and will jerk up the lever of the sphygraograph 
 more rapidly and to a greater height, while the fall will be 
 more abrupt and the dicrotic rebound well marked. 
 
 FIG. 5. — LOW-TENSION PULSE, SHOWING DICROTISM. 
 
 -FIG. 6. — HIGH-TENSION PULSE. 
 
 When the artery is contracted and in a condition of 
 hypertonus (to which reference will be made later), and the 
 blood pressure is high, the vessel is not easily flattened by 
 the finger or lever of the sphygmograph. The wave 
 appears to be small and the excursion of the lever is 
 limited, so that the pulse may appear to be weak, until 
 more pressure is made, when its true character will be 
 brought out, and the greater the pressure made the stronger 
 the pulse will appear to be. The tracing will have a less 
 abrupt upstroke, and will be of no great height, while the 
 summit may be rounded, and the descent gradual, and 
 unbroken by a dicrotic wave. By the fingers the artery 
 will be felt as a firm rounded cord, and will not be easily 
 compressed. 
 
 It is important, therefore, to carefully examine the 
 artery between the beats, rolling it beneath the fingers and 
 
20 HEART DISEASE. 
 
 making varying degrees of pressure, so as to form an esti- 
 mate of the mean or constant blood pressure — in other words, 
 of the " arterial tension." 
 
 The condition of the arterial walls should also be 
 noted, as to whether they are soft and flexible, thickened 
 from hypertrophy, or rigid, tortuous, and deformed from 
 degenerative changes. For this purpose the blood is 
 pressed out of the vessel, which is then rolled under the 
 fingers and carefully palpated by carrying them along it, 
 so that rigidity or inequalities in its course may be detected. 
 
 Most of these points, such as the force and frequency 
 and height of the pulse wave, the size of the vessel, its ful- 
 ness or collapse between the beats, and thickening of its 
 walls, can readily be determined by the fingers of the 
 practised observer. 
 
 A sphygmographic tracing will form a useful supple- 
 mentary graphic record of the character of the pulse wave, 
 and will be the most trustworthy criterion as to its height 
 and duration, a^ to whether its rise and subsidence are 
 gradual or abrupt, and as to the presence or absence of 
 dicrotism, etc. A comparison of a sphygmographic tracing 
 from the radials of both sides will indicate whether the two 
 pulses differ in character, and will often be of great value 
 as an aid to the diagnosis of aneurysm. Marey's sphygmo- 
 graph is the most trustworthy instrument, as the instru- 
 mental oscillations in Dudgeon's sphygmograph often 
 vitiate results, especially when the rise of the wave is 
 sudden and violent and its fall abrupt. 
 
 Arterial Tension. — There is, however, one important point 
 as to which confusion is liable to arise. This is the question 
 as to the meaning of the term " arterial tension." As this 
 has an important bearing on prognosis, and reference will 
 be frequently made to it in this volume, it may be as well 
 to discuss the subject fully now. By " arterial tension " 
 is here meant the strain to which the arterial wall is 
 
ARTERIAL TENSION. 21 
 
 subjected by the contained blood between the beats of the 
 heart — in other words, it is a measure of the constant mean 
 blood pressure, as expressed by the strain it exerts on the 
 arterial walls. 
 
 The factors which enter into its production are, first and 
 foremost, the peripheral resistance in the capillaries and 
 arterioles ; secondly, the volume of blood thrown into the 
 aorta at each systole of the heart ; thirdly, the force of the 
 heart beat. 
 
 To take a simple illustration, if we have a fire-hose with 
 a powerful pump at one end and a narrow nozzle at the 
 other, the hose-pipe will remain full and distended between 
 each stroke of the pump, and the mean tension maintained 
 will be very high. If we remove the nozzle, whatever be 
 the force of each stroke of the pump and the quantity of 
 water injected, the mean constant tension will be practically 
 nil, or very low, and the hose-pipe will be flaccid between 
 each stroke of the pump. By increasing the force of the 
 pump and the volume of water injected, the momentary 
 strain on the walls of the hose at each stroke will be 
 greater, but the constant mean tension will still be very 
 low if there is no nozzle at the distal end. 
 
 The heart corresponds to the pump, the arterial tree 
 to the hose-pipe, and the peripheral resistance afforded by 
 the arterioles and capillaries to that generated by the 
 narrow nozzle at the distal end of the hose-pipe. It is 
 true that the analogy does not hold good in all points, for 
 in the hose-pipe we have an inelastic, more or less rigid, 
 tube, whereas the arterial system is composed of a series of 
 elastic contractile vessels ; moreover, the aorta constitutes 
 an elastic reservoir, which tends to make the flow of blood 
 less jerky and more continuous, the pressure more constant, 
 and the strain less severe, in the arteries of less size. I 
 have thought it worth while to give this simple illustration, 
 as the statement is made by Professor Clifford Allbutt 
 
22 HEART DISEASE. 
 
 " That in aortic regurgitation the mean arterial tension 
 is higher than in any other disease." * And again, " The in- 
 comprehensible statement is commonly repeated that in 
 aortic regurgitation the tension is low." f 
 
 If we apply our illustration to aortic regurgitation (ex- 
 cluding that due to strain or degenerative changes), we shall 
 see that it is impossible for the mean arterial tension to be 
 high. 
 
 For though in aortic regurgitation we have a more 
 powerful pump than normal from the hypertrophy of the 
 heart, and a greater volume of blood injected into the 
 arterial sj^stem at each beat, from the increased capacity of 
 the dilated left ventricle, and the initial momentary strain 
 on the vessel walls during systole is severe, yet immedi- 
 ately after the systole blood leaks back into the heart ; the 
 vessel walls are consequently not kept on the stretch by the 
 contained fluid, but tend to collapse, so that the mean con- 
 stant tension between each heart-beat will necessarily be 
 low, in proportion as the regurgitation is considerable. 
 Clifford Allbutt, in his article, obviously does not use the 
 term " arterial tension " in the same sense as it is employed 
 here, but rather as a synonym for the initial distensile 
 strain at the moment of the cardiac systole. 
 
 The mean constant tension or strain on the arterial 
 walls can be most accurately estimated by determining the 
 blood pressure in each instance, and if in man we could, as 
 in animals, connect the column of blood within an artery 
 with a manometer by means of a rigid tube, this would 
 afford a trustworthy criterion. 
 
 Obviously this method is impracticable in dealing with 
 man, and various instruments have been devised in its 
 place, the essential principle of which is an attempt to 
 balance the pressure of the blood within an artery by 
 
 * "System of Medicine," vol. v. p. 937, line 32; article on "Aortic 
 Regurgitation." 
 t Ibid., p. 93G. 
 
BLOOD PRESSURE. 23 
 
 graduated pressure applied externally to its walls. The 
 degree of pressure required to arrest trie flow of blood 
 through the vessel, or the degree at which the maximum 
 oscillations of pressure are registered by the manometer, is 
 taken as a measure of the blood pressure within. 
 
 The instruments usually employed are of two kinds — 
 
 1. Those in which pressure is applied to the walls of a 
 superficial artery, such as the radial, by a small rubber bag 
 distended with air or fluid, and connected with a mano- 
 meter, e.g. those of Hill and Barnard (small), Oliver, 
 Vierordt, and Von Basch. 
 
 2. Those in which pressure is applied to the whole 
 circumference of a limb, e.g. the arm, by a large rubber bag 
 which completely encircles it, e.g. those of Riva Rocci, Hill 
 and Barnard (large), and Gartner. 
 
 In both groups pressure is made by the rubber bag 
 distended with air or fluid, either till the pulse wave below 
 is obliterated or till maximum oscillations of pressure are 
 attained. The former indicates the systolic pressure, the 
 latter according to Jane way the diastolic, according to Hill * 
 the mean blood pressure. The point at which these pheno- 
 mena occur is read off on a manometer. 
 
 It would be out of place to discuss these instruments 
 so ably described by Janeway,| the merits and demerits of 
 which have been recently reviewed in an article by C. J. 
 Martin ; % but it may be well to point out why the deter- 
 mination of the blood pressure by these methods does not 
 give a trustworthy estimate of the arterial tension. The 
 wall of the vessel varies greatly in elasticity and thick- 
 ness in different individuals at different periods of life, and 
 in health and disease, and the varying pressure required to 
 overcome the resistance of the arterial wall in such diverse 
 
 * " Text-book of Physiology," edited by Scb'afer, vol. ii. p. 80. 
 t " The Clinical Study of Blood Pressure " (Appleton). 
 % British Medical Journal, 1905, vol. i. pp. 865 et seq. 
 
24 HEART DISEASE. 
 
 conditions must prove a source of error. Martin, as a 
 result of a series of experiments on portions of dead arteries, 
 claims that the range of error is small, and that an approxi- 
 mately accurate allowance can be made in the case of 
 vessels the walls of which are rigid from degenerative 
 changes. Granting that this is so, the conditions in the 
 living vessel are essentially different, and are scarcely com- 
 parable. The element of muscular tone in the vessel wall 
 must be taken into consideration. When the arterial ten- 
 sion is low and the vessel wall normal, this is perhaps a 
 negligible quantity, but in states of high arterial tension, 
 such as are associated with chronic Bright's disease, there is 
 a condition of overtone or contraction of the muscular coat 
 almost amounting to spasm, and the resistance to compres- 
 sion by the pneumatic rubber bag offered thereby must be 
 very considerable. Moreover, in these circumstances there 
 is also actual hypertrophy of the muscular coat, which will 
 intensify this resistance, and it is scarcely possible to make 
 accurate allowance for these sources of error, which will 
 render the blood-pressure reading too high. Especially 
 will this be the case in the later stages, when the heart is 
 beginning to fail, and we have a condition of comparatively 
 low blood pressure or arterial tension associated with hyper- 
 trophied rigid vessels, difficult to compress. 
 
 The hypertrophy of the muscular coat of the radial or 
 other vessels can be readily demonstrated post-mortem by 
 microscopical examination of sections of the vessel, and 
 I have never failed to find it in some twenty or thirty 
 cases associated with granular kidney which I have exam- 
 ined. The condition of overtone or hypertonus is not so 
 readily proved, though it can be readily recognized in 
 life by a practised observer by careful palpation of the 
 vessel. Dr. William Russell * has, however, demonstrated 
 clinically rhe existence of this hypertonus by an ingenious 
 
 * Lancet, 1901, vol. i. pp. 1519 et seq. 
 
BLOOD PRESSURE. 25 
 
 experiment. He argues that if this condition of hypertonus 
 exists the diameter of the radial artery ought to vary 
 according to the degree of tone or contraction of the 
 muscular coat. He measured the diameter of an artery in 
 a state of hypertonus by Oliver's arteriometer, taking at the 
 same time a pulse tracing. He then gives erythrol tetra- 
 nitrate or some vaso-dilator, and, allowing time for this to 
 take effect, he again measures the diameter of the vessel by 
 the arteriometer, and takes another pulse tracing. He finds 
 that the diameter of the artery is increased and the cha- 
 racter of the pulse altered correspondingly to the reduction 
 of tension. 
 
 In spite of these sources of error, the determination of 
 the blood pressure by these instruments will afford a useful 
 comparative estimate of the blood pressure and arterial 
 tension, and this may with advantage be supplemented by 
 sphygmographic tracings. The scientific results obtained 
 by Oliver, Mackenzie, and others in this way are of great 
 value and interest. It is, however, not always practicable 
 to employ instruments, nor is it essential for clinical pur- 
 poses, as the finger can by practice be educated so that a 
 trustworthy comparative estimate of the arterial tension can 
 be made. For this purpose three fingers should be placed 
 on the radial artery and varying degrees of pressure made. 
 If the vessel remains full between the beats of the pulse, 
 distended by the contained blood, so that it can be rolled 
 like a cord beneath the fingers, the mean arterial tension is 
 high. Some estimate as to the degree may be inferred from 
 the pressure which has to be made by the finger before the 
 flow of blood is arrested and the pulse wave obliterated. 
 Care must be taken not to mistake a thickening of the 
 arterial wall from degenerative changes for tension due to 
 pressure from the contained blood. In cases of arterio- 
 sclerosis the condition can usually be diagnosed from the 
 tortuous brachial, and the irregularity, rigidity, and loss of 
 
26 HEART DISEASE. 
 
 elasticity of the vessel wall, which is quite different to 
 the firm, cord-like, smooth, elastic artery in a condition of 
 hypertonus. If the vessel remains soft and flaccid between 
 the beats, so that it can scarcely be felt, it is obvious that 
 the tension or blood pressure is low. 
 
 I have laid some stress on the condition of hypertonus 
 as manifested in the medium-sized and larger arteries as 
 exemplified in the radial, but it exists throughout the 
 arterial system, and it is the narrowing of the vast network 
 of arterioles which entails a great increase in the peripheral 
 resistance to the onward flow of the blood, which is of the 
 first importance. The increased resistance necessitates 
 greater driving jDower by the heart, which consequently 
 hypertrophies sometimes to an enormous degree. The blood 
 pressure is of necessity correspondingly raised, and the 
 muscular coat of the large and medium-sized arteries hyper- 
 trophies, or they would give way under the strain. 
 
 It is a debatable question how far the condition of 
 hypertonus in these vessels is due to the condition akin to 
 spasm which affects the smaller arterioles, and how far it is 
 a natural sequence of the increased peripheral resistance. 
 For it is obvious that to overcome the increased resistance, 
 increased contractile force is necessary, not only on the part 
 of the heart, but of the whole arterial system. 
 
 This, however, is a matter of minor importance as long 
 as we recognize that increased peripheral resistance entails 
 increased driving power by the heart and increased con- 
 tractile energy by the larger and medium-sized arteries. 
 This gives rise to considerable increase in the blood pres- 
 sure, and, consequently, to increased strain on the arterial 
 walls, or, in other words, to high arterial tension. When 
 the heart begins to give out under the strain, we have a 
 decreased blood pressure and a condition of low or moderate 
 tension, and in these circumstances we must be careful not 
 to mistake the resistance offered to the fingers by the 
 
HIGH ARTERIAL TENSION. 27 
 
 hypertrophied or thickened vessel walls for one of high 
 tension due to high pressure from within. 
 
 The Causes of Hypertonus and High Arterial Tension. — 
 The most typical instances of hypertonus and high arterial 
 tension are found in association with chronic interstitial 
 nephritis or granular kidney. A reasonable explanation of 
 the mechanism of its production is, that poisonous products 
 are retained in the blood as the result of imperfect elimina- 
 tion by the kidneys, and that these act as an irritant on 
 the walls of the capillaries and arterioles, setting up a 
 reflex spasm or hypertonic condition of their walls, and 
 creating increased peripheral resistance. 
 
 Of predisposing causes heredity is the most important, 
 and we see the tendency to high tension and vascular de- 
 generation transmitted from generation to generation, and 
 sometimes apparent at a very early age. 
 
 Certain constitutional diatheses, gout, diabetes, and 
 rheumatoid arthritis, are frequently associated with high 
 arterial tension. Over- eating, more especially excessive 
 meat eating, in those hereditarily predisposed may be a 
 cause, and it is probable that in this instance and in gout, 
 perverted or defective metabolism, with resulting absorption 
 of toxic products into the blood, and imperfect elimination, 
 are the important etiological factors. 
 
 In the later stages of pregnancy the blood pressure is 
 raised, and in the affection known as eclampsia the arterial 
 tension is always extremely high. The explanation of this 
 condition would seem to be that though the kidneys are not 
 diseased, the extra work of eliminating the waste products 
 of the foetus in addition to those of the mother is too much 
 for them, and toxic products accumulate in the blood, as in 
 the case of granular kidney, and produce similar phenomena. 
 
 Lead poisoning is unquestionably an important and 
 common cause. Alcohol and tobacco have been incrimi- 
 nated, but the part played by them is doubtful. Since the 
 
28 HEART DISEASE. 
 
 discovery of the tonic action of adrenalin on the arterial 
 system, it has been suggested that excessive secretion of 
 the suprarenal glands may be a cause, but there is no evi- 
 dence in support of this. Whatever be the underlying 
 cause of high arterial tension, it seems probable that it acts 
 by generating increased peripheral resistance in the smaller 
 arterioles and capillaries. 
 
 Confusion has arisen by mistaking the condition of 
 hypertonus and hypertrophy of the muscular coat of the 
 artery for arterio-sclerosis or degenerative change, because 
 the artery feels hard and cord-like. But in the majority of 
 cases, in the earlier stages, the radial artery will, on micro- 
 scopic examination, be found to be perfectly normal except 
 for hypertrophy of the media. 
 
 Later on degenerative changes set in in the hyper- 
 trophied vessels, and patches of atheroma or necrosis will 
 be found in the sub-endothelial tissue, possibly as a result 
 of the prolonged strain and impaired nutrition, or due to 
 the action of the toxins which have given rise to the high 
 tension. Of these, lead is especially prone to give rise to 
 early vascular degeneration. The arteries most affected are 
 usually the cerebral, the coronary arteries of the heart, and 
 the aorta, so that the patient, if he escapes the perils of 
 uraemia, is liable to succumb to cerebral hemorrhage, or to 
 cardiac failure from degenerative changes in the heart, or 
 to aneurysm of the aorta. 
 
CHAPTER III. 
 DISEASES OF THE PERICARDIUM. 
 
 PERICARDITIS — MORBID ANATOMY — ETIOLOGY — PHYSICAL 
 SIGNS — SIGNS OF EFFUSION AND CARDIAC DILATATION — 
 SYMPTOMS — COURSE OF THE DISEASE — DIFFERENTIAL 
 DIAGNOSIS — PROGNOSIS : TREATMENT — ADHERENT PERI- 
 CARDIUM — SUPPURATIVE PERICARDITIS — HYDROPERI- 
 CARDIUM — PNEUMOPERICARDIUM, ETC. 
 
 The pericardium is a nbro-serous sac which envelops the 
 heart. The fibrous portion is pyramidal in shape, and at 
 its base is firmly attached to the central tendon of the 
 diaphragm and the adjoining muscular substance ; above 
 it is continued as a tubular prolongation on to the root of 
 the aorta and pulmonary artery, and is gradually lost in 
 the connective tissue of their external coats. The serous 
 membrane lining the sac, termed the parietal layer of 
 pericardium, passes up to the root of the great vessels, 
 which it envelops in a common sheath for an inch to an 
 inch and a half from their origin, and is thence reflected 
 on to the surface of the heart, which it closely invests, 
 constituting the visceral layer of pericardium. Laterally 
 and anteriorly, save for a small triangular area in front 
 termed the anterior mediastinum, the pericardium is in 
 contact with the pleura ; posteriorly it is in relation with 
 the oesophagus, aorta, trachea, and the root of the left 
 lung. The phrenic nerves pass down, one on either side 
 of the sac. 
 
3° HEART DISEASE. 
 
 Morbid Anatomy. — In the early stages the pericardium 
 becomes hyperseinic and congested. Then exudation of 
 serum and leucocytes takes place from the congested 
 vessels, and soon both visceral and parietal layers of peri- 
 cardium become coated in patches or throughout their 
 surface with a thick layer of yellow sticky lymph. From 
 the friction together of the two inflamed surfaces the 
 lymph coating them acquires an irregular, ragged, or 
 honeycomb appearance. The lymph on the surface of the 
 pericardium may be reabsorbed, but frequently becomes 
 vascularized and organized into fibrous tissue, gluing 
 together the two layers of pericardium where they come 
 into contact, and giving rise to partial or universal adhesion 
 between the heart and pericardium. 
 
 Effusion may take place into the pericardial sac to a 
 varying extent. Usually it is small in amount, but excep- 
 tionally it may be very large. In rheumatic cases a large 
 effusion is uncommon. 
 
 The effusion consists of a yellowish serous fluid in 
 which leucocytes, shreds of fibrin, and endothelial cells 
 are present in varying quantity. The fluid is usually clear, 
 but may be turbid if there is much cellular exudation, and 
 may contain flakes of lymph. Sometimes it is blood- 
 stained, and in scurvy may consist almost entirely of 
 blood. 
 
 It may from the outset be purulent, constituting " sup- 
 purative pericarditis," which differs so materially in its 
 clinical features from the simple plastic or fibrinous form 
 that its consideration will be reserved for another section. 
 
 " Milk spots," or white opaque patches sometimes found 
 at autopsies on the surface of the visceral pericardium, are 
 not, as a rule, due to pericarditis, but to a localized growth 
 of connective tissue from irritation, and they occur at some 
 point where the heart in its movements comes into contact 
 with the chest wall. 
 
DISEASES OF THE PERICARDIUM. 31 
 
 The Myocardium. — The heart muscle is almost invariably 
 affected, and there is myocarditis to a varying degree, with 
 resulting granular and fatty degeneration of the muscle 
 fibres. In the more protracted cases areas of round-celled 
 infiltration may sometimes be found in the interstitial 
 tissue between the muscle fibres. 
 
 It is to this accompanying myocarditis that we must 
 attribute the cardiac dilatation which is so marked a feature 
 in pericarditis. One of the chief dangers in rheumatic 
 inflammation of the heart, of which pericarditis is a part, 
 lies in the damage to the cardiac muscle. 
 
 Etiology. 
 
 Rheumatism is by far the most common and important 
 cause of pericarditis. So close is the connection between 
 the two that, as Dr. Frederick Roberts says,* "The peri- 
 cardial inflammation is not to be looked upon as a mere 
 complication of rheumatism, but is an integral part of the 
 disease." Furthermore, pericarditis must not be regarded 
 as a separate entity, but as part of a general inflammation of 
 the heart, aptly termed " carditis " by the late Dr. Sturges,t 
 the myocardium being almost invariably, and the endo- 
 cardium frequently, affected. Pericarditis occurring in asso- 
 ciation with chorea may be regarded as of rheumatic origin. 
 
 Rheumatism. — In childhood and early adolescence rheu- 
 matism is especially liable to attack the heart, while the 
 joints may be so slightly affected that attention is not 
 drawn to them. In later life the joints are more apt to 
 suffer severely while the heart frequently escapes. 
 
 The belief has long been held that acute rheumatism 
 is a disease of microbic origin, and that pericarditis and 
 endocarditis are local manifestations of the activity of a 
 specific micro-organism. From the experimental researches 
 
 * Allbutt's " System of Medicine," vol. v. p. 752. 
 f Lumleiau Lectures, 189L 
 
32 HEART DISEASE. 
 
 of Triboulet, Wasserman, Paine and Poynton, Shaw, Ainley, 
 Walker, Beattie, and others, it would appear that acute 
 rheumatism is due to a minute diplococcus, which may- 
 grow in chains like a streptococcus. This micro-organism 
 they have succeeded in isolating from the pericardial fluid 
 and blood of patients suffering from rheumatic fever, and, 
 after growing it on suitable culture media, have inoculated 
 it into rabbits and reproduced pericarditis, arthritis, and 
 endocarditis, or a disease indistinguishable from acute rheu- 
 matism. Pericarditis, therefore, occurring in association 
 with rheumatism, may be regarded as due to a micro- 
 organism. The question as to whether this is the specific 
 micro-organism of rheumatism, is further discussed in the 
 chapter on acute endocarditis. 
 
 Pneumonia. — Pericarditis may occur as a complication 
 of pneumonia or pleurisy, or even, in the absence of these 
 affections as a primary disease, from infection by the pneumo- 
 coccus, which can, as a rule, be readily isolated from the 
 fluid in the pericardium in cases of pneumococcal origin. 
 
 The Acute Specific Diseases. — Acute pericarditis may 
 ensue as a complication of scarlet fever, variola, erysipelas 
 — rarely of measles and typhus fever. 
 
 Bright's Disease. — Pericarditis is met with in Bright's 
 disease most commonly in association with the later stages 
 of granular kidney or subacute parenchymatous nephritis. 
 
 Traumatism. — Injuries to the pericardium by a gunshot 
 or punctured wound, or by a fractured rib, or by a fish-bone 
 lodged in the cesophagus, may set up pericarditis. 
 
 Tubercular pericarditis may occur as part of a general 
 miliary tuberculosis, or from the extension of the disease 
 from a tubercular lung or bronchial gland. 
 
 Physical Signs. 
 
 Friction rub. — The most trustworthy sign of pericarditis 
 is the characteristic to-and-fro friction sound heard on 
 
DISEASES OF THE PERICARDIUM. 33 
 
 auscultation. For this reason, auscultation will be considered 
 before percussion. The friction sound is caused by the 
 rubbing together of the two inflamed surfaces of the peri- 
 cardium at each beat of the heart. It is a curious scratching 
 rub which appears to be very superficial, and somewhat 
 resembles the noise made by scratching a piece of rough 
 paper with the finger-nail. It is modified by pressure with 
 the stethoscope, and may be rendered more distinct and 
 longer or almost extinguished. It is usually of a to- 
 and-fro character, corresponding more or less, but not 
 accurately, to the movements of the heart in systole and 
 diastole. It may be only systolic in time and not present 
 the to-and-fro character ; this is usually the case when 
 it is heard near the apex, and not over the base. On the 
 other hand, over the base of the heart the friction sound 
 may be triple or cantering instead of merely to and fro, the 
 auricular systole being attended with an audible inde- 
 pendent rub. It is said to be first heard, as a rule, over 
 the base of the heart, but frequently it is first audible at 
 the apex as a single scratch at each systole. As the in- 
 flammation spreads, a to-and-fro friction rub is heard over 
 the whole or a large proportion of the precordial area, and 
 since the heart is usually dilated it may be heard an inch 
 or more to the right of the sternum in children. The rub 
 may be present for a day or two only in mild cases ; in 
 cases of effusion it may be present for a few days, then 
 disappear and reappear when the fluid is absorbed or drawn 
 off by paracentesis. In subacute or chronic cases the rub 
 persists for some days or weeks, only disappearing as the 
 layers of pericardium become adherent. 
 
 Disappearance of the rub may thus indicate (1) sub- 
 sidence of the attack ; (2) effusion into the pericardium ; 
 (3) formation of adhesion between the two layers of the 
 pericardium. 
 
 Friction fremitus may be felt on palpation in well- 
 
 D 
 
34 HEART DISEASE. 
 
 marked cases over the area where the friction sound is best 
 heard. 
 
 The action of the heart is excited and the pulse almost 
 invariably accelerated, as a rule, before the friction rub 
 becomes audible. Sometimes in children it may be irregular 
 in rhythm for a time. After the friction rub has apjDeared, 
 a peculiar triple cantering rhythm of the heart is frequently 
 heard on auscultation at the apex, and is very characteristic. 
 It is apparently due to reduplication of the first sound. 
 
 Increase in the Aeea of Caediac Dulness. 
 
 Increase in the area of cardiac dulness is usually one 
 of the earliest physical signs. This is especially marked 
 in children, in whom it is most easily mapped out on 
 percussion. It is more rapid and extensive in proportion 
 to the severity and acuteness of the attack. The dulness may 
 extend upwards as far as the second left intercostal space, 
 and outwards for an inch outside the vertical nipple line, 
 and in the opposite direction for an inch or more to the 
 right of the sternum, but it is usually not so extensive in 
 adults as in children, and is less easily made out, because 
 of the thickness of the chest wall and errors that may 
 arise from pathological conditions in the lungs. 
 
 The view was held by Sibson * that this increase in the 
 area of cardiac dulness indicates pericardial effusion, and 
 that increase in effusion is indicated by extension of the 
 cardiac dulness. In a certain proportion of cases this is 
 undoubtedly true ; but much evidence has been accumulated 
 which tends to show that this is by no means the rule, 
 and that the increase in dulness indicates in the large 
 majority of cases of rheumatic pericarditis, increase in the 
 size of the heart, or cardiac dilatation. 
 
 In 1895, in a monograph on " Adherent Pericardium," 
 
 * Sibson'e Works, edited by Ord. 
 
DISEASES OF THE PERICARDIUM. 35 
 
 I described a series of cases where marked increase in 
 the area of cardiac dulness was found, post-mortem, to 
 be due, not to effusion, but to cardiac dilatation. In two 
 cases where the physical signs and symptoms seemed to 
 point conclusively to considerable pericardial effusion 
 paracentesis was resorted to, but in neither instance was 
 fluid found, and the increase in dulness was found to be 
 due to increase in the size of the heart. 
 
 Lees and Poynton * drew attention to the acute dilata- 
 tion of the heart that occurs in the rheumatism and chorea 
 of childhood. From an analysis of the post-mortem records 
 of 150 cases of fatal rheumatic heart disease in children, 
 they showed that cardiac dilatation is usually present, and 
 marked excess of pericardial fluid rare ; in only 12 cases 
 out of 150 was there excess of pericardial fluid amounting 
 to more than two ounces. 
 
 Out of 79 cases of paracentesis pericardii, collected by 
 Dr. Samuel West,f only 11 were of rheumatic origin, and 
 in only one of these eleven was the effusion large in 
 amount. 
 
 Clinically, it is not an uncommon experience, even 
 when the area of cardiac dulness is very much enlarged, 
 extending to the right of the sternum, to hear a pericardial 
 rub at several points over the dull area. This seems incom- 
 patible with the presence of fluid, and in many of these cases, 
 at the post-mortem, no excess of pericardial fluid is found, 
 but a dilated heart with the pericardium partially adherent. 
 Effusion. — In effusion the outline of the area of cardiac 
 dulness tends to assume a pyramidal or pyriform shape, 
 with the base or widest portion below. The transition 
 from the dull area to the resonant lung is sudden and 
 well-marked, and the extent and shape of the area of 
 
 * Trans. Med: Chi. Soc, June, 1898. 
 
 t West, S., " Paracentesis Pericardii," Trans. Med. Chi. Soc, vol. 66, 
 p. 235. 
 
36 HEART DISEASE. 
 
 cardiac dulness will vary somewhat with the position of 
 the patient. 
 
 Sibson gave a series of diagrams to illustrate the shape 
 assumed by the pericardial sac in the different stages of 
 effusion, but it is doubtful how far these are of practical 
 value for differential diagnosis, as they were not confirmed 
 by post-mortem examination, and he appears to have 
 taken it for granted that increase in the area of cardiac 
 dulness invariably indicated effusion. It is, however, by 
 no means an easy matter to decide by percussion alone, 
 whether the increased area of dulness indicates effusion, 
 cardiac dilatation, or dilated heart with the pericardium 
 adherent. 
 
 There is much diversity of opinion as to the position 
 assumed by the heart in effusion. Sibson maintained that 
 it was usually pushed upwards and outwards, and the apex 
 beat similarly displaced ; but this is not invariably the case, 
 and pericardial adhesions may fix the apex in various positions, 
 and in effusion of any extent it is not as a rule palpable. 
 
 Bulging of the precordial area as a whole, more 
 especially of the intercostal spaces over this area, which is 
 usually best marked in purulent pericarditis, is a more 
 trustworthy sign of effusion. 
 
 Gradual enfeeblement of the apex beat from day to 
 day, or even its eventual disappearance, together with 
 increasing weakness and distance of the sounds heard 
 at the apex, especially if there is at the same time an 
 increase in the severity of the symptoms, and marked 
 dyspnoea, are strongly suggestive of increasing effusion 
 into the pericardium. 
 
 Symptoms. 
 
 The symptoms are partly local, due to the pericarditis 
 itself, and partly constitutional, or due to a general toxamiia. 
 
DISEASES OF THE PERICARDIUM. 37 
 
 Pain in the precordial region, increase in the pulse- 
 rate, excited action of the heart, dyspnoea varying in degree, 
 rise of temperature, restlessness at night, are symptoms 
 usually well marked in acute pericarditis ; but in the sub- 
 acute variety, common in children, there may be little or 
 no pain or fever, and very slight dyspnoea, though there is 
 usually acceleration of the pulse. The symptoms, as a 
 rule, precede the development of the pericardial rub, and 
 are more marked when it appears. In children there 
 may be premonitory symptoms of nervous origin, such as 
 night terrors, crying out, and wandering in sleep, restless- 
 ness, and even slight delirium on first waking. Vomiting 
 may set in, and is generally of serious prognostic signifi- 
 cance. The face may be pale or flushed, the expression is 
 often anxious or distressed, and the respiration hurried. 
 There may be some pain or difficulty in swallowing from 
 the proximity of the pericardium to the oesophagus, if the 
 posterior aspect is inflamed, or if there is much effusion 
 into the sac. The temperature ranges between 100° and 
 103°, and is usually higher in adults than in children, in 
 whom the attack is commonly less acute and more insidious 
 in its onset. The dyspnoea may become very considerable, 
 not only in cases of effusion, but in cases where there is 
 great cardiac dilatation and the pericardium is becoming 
 adherent ; the patient has to be propped up with pillows, 
 and when there is much effusion or extreme dilatation of 
 the heart, may find most comfort in leaning forward over a 
 bed-board, with his head on his hands. 
 
 In severe cases, nervous symptoms may predominate, 
 and there may be delirium, involuntary passage of motions 
 and urine, great restlessness, or a state resembling collapse. 
 Vomiting is always a serious symptom, and not infrequently 
 ushers in the closing scene. 
 
3§ heart disease. 
 
 Course of the Disease and Terminations. 
 
 The disease as a rule runs a somewhat different 
 course in adults and in children. In adults it is usually 
 acute, and the symptoms are more marked at the onset ; in 
 children it may from the first be sub-acute or chronic 
 in character, and it results frequently in the formation of 
 adhesions between the heart and pericardium. It must 
 not be forgotten that the prognosis to a great extent 
 depends on the degree to which the cardiac muscle is 
 attacked by the inflammatory process. In very severe 
 attacks death may ensue within two or three days from 
 the time at which the disease is first recognizable by the 
 pericardial rub. In such cases there is usually rapid in- 
 crease in the area of cardiac dulness, and in the severity 
 of symptoms, and sometimes attacks of vomiting. Post- 
 mortem there is commonly little or no effusion beyond the 
 lymph on the serous surfaces, but great cardiac dilatation, 
 and it would seem as if the severity of the inflammation 
 had caused paresis of the cardiac muscle, analogous to that 
 which occurs in the muscular coats of the intestines in 
 acute peritonitis. 
 
 In a mild case, though the symptoms at the onset may 
 be severe, the friction rub persists for a few days only, 
 23erhaps not more than one or two ; the area of cardiac 
 dulness does not greatly increase, and rapidly decreases to 
 normal when the friction rub has disappeared : convalescence 
 is soon established. In the more severe type of acute cases, 
 effusion may occur, and require removal by paracentesis. 
 
 In the sub-acute type, common in children, the onset 
 is insidious, and the symptoms are ill marked. The friction 
 rub may persist for some days or weeks, the area of 
 cardiac dulness becomes greatly enlarged, and remains 
 so permanently, and eventually, when the friction rub 
 disappears, the pericardium is left partially or universally 
 
DISEASES OF THE PERICARDIUM. 39 
 
 adherent to the heart. The child, even after convales- 
 cence is established, remains pale and thin, is short of 
 breath, and incapable of exertion, as the heart with its 
 mnscle damaged by myocarditis and hampered by pericardial 
 adhesions, remains permanently crippled. 
 
 In another class of sub-acute cases where the inflam- 
 matory process persists for some months, or repeated attacks 
 in close succession ensue, dropsy may supervene, the liver 
 becoming enlarged and the cardiac dilatation extreme, the 
 patient dying with all the symptoms of cardiac failure from 
 extensive damage to the cardiac muscle by myocarditis. 
 
 As an illustration of the life history of such a case, the 
 following may be quoted : — 
 
 H. D., set. 9, was admitted to the Children's Hospital? 
 Great Orrnond Street, 11th December, 1893, with a history 
 of pains in the joints, fourteen days previous to his admission. 
 When first seen, his heart was considerably dilated, and a 
 mitral systolic murmur was audible at the apex. Five 
 days after admission a pericardial rub was heard, which 
 persisted for about a week, during which time the cardiac 
 dilatation increased. A week later he began to improve, 
 and the area of cardiac dulness gradually decreased. On 
 the 15th February, 1894, two months after the onset of the 
 pericarditis, the area of cardiac dulness was almost normal 
 in extent, and he was sufficiently recovered to go to a con- 
 valescent home. A month later, he had a fresh attack of 
 rheumatism with an eruption of nodules, and was readmitted 
 15th March ; there was slight oedema of the legs, and 
 rheumatic nodules were present on the elbows ; the area of 
 cardiac dulness was again greatly enlarged, and he suffered 
 from severe dyspnoea. From this time he steadily got 
 worse, the oadema of the legs rapidly increased, the liver 
 became greatly enlarged, the veins of the neck distended 
 and pulsating, and he died on the 21st April, with extreme 
 symptoms of venous engorgement and right ventricle 
 
40 HEART DISEASE. 
 
 failure. At the post-mortem all the cavities of the heart 
 were greatly dilated ; the pericardium was universally 
 adherent by recent adhesions, the muscle was soft, and 
 showed evidence microscopically of myocarditis ; there was 
 no serious valvular lesion, though a few vegetations were 
 present on the mitral valve, and its orifice was much 
 dilated. Myocarditis and adherence of the pericardium to 
 the dilated heart were thus responsible for his death. The 
 symptoms were those of venous engorgement and right 
 ventricle failure, as the right ventricle with its comparatively 
 thin walls was more rapidly rendered helpless by the myo- 
 carditis, and more hampered by the adherent pericardium 
 than the left, with its greater thickness of muscular tissue. 
 
 Effusion of any extent is rare in the sub-acute rheumatic 
 cases in children, adhesions, partial or universal, between 
 the heart and pericardium being the most common termina- 
 tion. Effusion is more likely to occur in acute attacks 
 in adults, especially those associated with pneumonia or 
 Bright's disease, and effusion of blood into the pericardium 
 is common in scurvy. 
 
 Diagnosis. 
 
 Till the pericardial friction rub is heard, a certain 
 diagnosis of pericarditis cannot be made. Usually, how- 
 ever, in acute attacks there are premonitory symptoms, such 
 as pain in the precordial region, restlessness, dyspnoea, 
 acceleration of pulse, and rise of temperature which enable 
 us in some measure to anticipate the appearance of the 
 friction rub. These symptoms may in some cases appear 
 to be only exacerbations of those already existing, as the 
 result of rheumatism, pneumonia, or, possibly, scarlet fever, 
 but as the patient is then confined to his bed, we shall be 
 on the look-out for cardiac complications, and are not 
 Hkely to miss the first definite signs of pericarditis. 
 
 The sub-acute attacks so common in children are. on the 
 
DISEASES OF THE PERICARDIUM. 41 
 
 contrary, as a rule, very insidious in their onset, and the 
 child may be going about with pericarditis, especially in 
 the eyent of a second attack, before the symptoms are so 
 severe as to attract attention to the child's condition, and 
 cause the parents to seek medical advice, or the physician 
 to examine the heart. Much damage may thus be done to 
 the heart before the existence of pericarditis is discovered. 
 
 The articular manifestations of rheumatism in children 
 are, moreover, slight, as a rule, while the heart is commonly 
 attacked. It is important, therefore, not to neglect the 
 slightest evidence of rheumatism in children, and if we 
 have reason to suspect its existence, to keep a careful watch 
 over the child, and examine the heart at frequent intervals. 
 
 Differential Diagnosis. 
 
 A friction rub due to pleurisy in the neighbourhood of 
 the heart will be readily distinguished by the fact that 
 its rhythm is synchronous with the respiratory movements, 
 and not with those of the heart. Some difficulty may, 
 however, arise when, from friction between the pericardium 
 and the pleura overlapping or adjoining it, the rhythm is 
 of a to-and-fro character corresponding to the beats of the 
 heart. A friction rub arising from this cause will be 
 intensified by the respiratory movements, and will usually 
 be extinguished when the breath is held in deep inspiration. 
 It will, as a rule, be heard only at the left border of the 
 heart over the ventricles, and not at the base of the heart, 
 or to the right of the sternum. Moreover, as the pleurisy 
 will seldom be confined to the precordial region, a well- 
 marked respiratory friction rub will usually be heard in 
 the adjoining area. 
 
 Endocardial murmurs differ so completely in their 
 character from pericardial friction sounds, that confusion 
 will seldom arise. They will not, of course, be modified 
 by pressure with the stethoscope. 
 
HEART DISEASE. 
 
 Pkognosis. 
 
 Pericarditis is always a disease of considerable gravity 
 owing to the myocarditis which usually accompanies it. 
 In acute attacks, associated with rheumatism or pneumonia, 
 death may take place within the first few days, but this 
 is not a common occurrence. In a large proportion of 
 rheumatic cases the immediate prognosis is favourable, 
 though the liability to repeated attacks, the probable 
 damage to the heart by myocarditis, and the formation of 
 adhesions between the heart and pericardium, render the 
 ultimate chances of long life unfavourable. When associ- 
 ated with Bright's disease, the prognosis is usually bad, and 
 the chance of recovery small. 
 
 In sub- acute and prolonged cases the prognosis seems to 
 depend on the degree to which the myocardium is affected 
 bv the inflammatory process. If the inflammation is of 
 short duration and the changes in the muscle are slight, the 
 heart may rapidly contract down again to its normal size, 
 and be little the worse ; if the inflammation is protracted 
 and severe, involving great destruction of the myocardium, 
 the heart is unable to recover for some time, and in the 
 process of repair fibrous tissue takes the place of the damaged 
 muscle, so the heart is permanently weakened. The peri- 
 cardium may also become adherent to it. 
 
 Children, once attacked, are liable to repeated and pro- 
 longed attacks of cardiac inflammation, both pericardial, 
 myocardial, and endocardial. They seldom grow up to 
 maturity ; or, if they do, it is with hearts so crippled that 
 they do not survive many years. 
 
 Adults attacked by pericarditis usually fare better than 
 children, for though the symptoms are usually more acute 
 at the time of the attack, its duration is short, and the heart 
 often seems to escape without serious damage. 
 
diseases of the pericardium. 43 
 
 Tkeatment. 
 
 In the treatment of pericarditis various local applications, 
 such as ice-bags, leeches, or blisters over the prsecordial 
 area, have been advocated. Of these, ice-bags are the most 
 useful, as they relieve pain in acute pericarditis, and, accord- 
 ing to Lees, modify the inflammation and limit the dila- 
 tation of the heart. Leeches are often of service at the outset 
 of pericarditis, and may be followed by ice-bags ; blisters 
 are better suited for the later and more chronic stages. The 
 administration of salicylates, which in the acute articular 
 rheumatism of adults are given with such marked beneficial 
 results, is of doubtful service. If the pain is severe, opium 
 or morphia may be given with marked benefit ; if stimulants 
 are required, brandy, ammonia, and ether, or strychnine, 
 may be given. Digitalis, and similar cardiac tonics, should 
 not be given during the acute stage. As a general tonic, 
 an effervescing mixture, containing quinine and bicarbonate 
 of potash, is perhaps as useful as any. Nothing, however, 
 in severe cases seems to arrest or exert any controlling 
 influence on the course of cardiac inflammation in children, 
 when once it has gained a firm hold. It is, therefore, of 
 the first importance that any indications of danger threaten- 
 ing the heart should be recognized as early as possible, 
 and due precautions taken. If, then, a suspicion of rheu- 
 matism is aroused by complaints of stiffness in the joints 
 or pains in the limbs, in a child who comes of a rheumatic 
 stock, or who has previously suffered from chorea or some 
 other rheumatic manifestation, more especially if rheumatic 
 nodules are present, the patient should be kept under 
 careful observation, and the heart examined every two 
 or three days for some weeks. Any exposure to chill 
 should be guarded against, and exercise should be limited 
 in amount for some time after all apparent symptoms have 
 subsided. 
 
44 HEART DISEASE. 
 
 Effusion. — If extensive effusion into the pericardial sac 
 takes place, its removal by paracentesis may be necessary, 
 and it is important that this should not be long delayed, as 
 death from syncope is liable to occur from embarrassment 
 of the heart by the pressure of the fluid. It is, however, 
 frequently a difficult matter to determine whether the 
 symptoms of cardiac embarrassment and the increase of 
 cardiac dulness are due to cardiac dilatation or to the 
 presence of effusion, and not infrequently the right ventricle 
 has been punctured by mistake. I have seen two such 
 cases in which blood was withdrawn from the right ventricle 
 but no ill results followed. I have, however, known of 
 two cases in which death from haemorrhage resulted from 
 a similar procedure where cardiac dilatation was mistaken 
 for effusion. The best site for puncture when aspiration is 
 decided on, is in the fifth left intercostal space, about one 
 inch or one and a half inch external to the border of the 
 sternum, outside the course of the internal mammary 
 artery. Some advocate that this puncture should be 
 made in the angle between the xiphoid cartilage and the 
 costal margin, as this would penetrate the lowest part of the 
 sac. A small aspirating needle should be used, and previous 
 to its insertion, an incision should be made down through 
 the skin to the intercostal muscles. Any bulging of the 
 intercostal space can then be seen, and any risk of wounding 
 the intercostal arteries be avoided by keeping close to the 
 upper border of the rib. 
 
 The above description applies to the type of pericar- 
 ditis which is met with in association with rheumatism or 
 pneumonia, and it will be necessary here to briefly allude 
 to the form it may assume in Bright 's disease. 
 
 In Bright 's disease pericarditis occurs most commonly as 
 a complication of subacute parenchymatous nephritis or of 
 the chronic interstitial variety. Statistics vary as to its fre- 
 quency, from 3 to 14 per cent., according to different authors. 
 
ADHERENT PERICARDIUM. 45 
 
 The onset of pericarditis in Bright's disease occurring, 
 as it usually does, m debilitated subjects, may be insidious 
 and unattended by any marked symptoms of local reaction. 
 
 There may be little or no rise of temperature, no pre- 
 cordial pain, and little beyond increase in the pulse-rate 
 and slight exacerbation of pre-existing systems, such as 
 dyspnoea and restlessness due to uraemia, to call attention 
 to its presence. A friction rub is usually present and is 
 well marked. A pleuritic friction rub may accompany it, 
 and in some cases a pleuro-pericardial rub alone is heard, 
 between which and a true pericardial rub it may be diffi- 
 cult to distinguish. The prognosis is always very grave and 
 the treatment must be directed to the primary disease. 
 
 It is important, therefore, that the heart should be 
 examined as a matter of routine, or the onset of peri- 
 carditis may easily escape notice. 
 
 ADHEBENT PEBICABDIUM. 
 
 By the term "adherent pericardium" is implied the exist- 
 ence of adhesions between the visceral and parietal layers 
 of the pericardium, the result of pericarditis. 
 
 Morbid Anatomy. — The adhesions may be limited to fibrous bands 
 stretching across the pericardial cavity, or they may be universal, in 
 which case the pericardium and heart are so intimately connected 
 that the pericardial cavity is entirely obliterated. Adhesions may 
 also exist between the chest-wall or pleura and the pericardium, as 
 a result of so-called mediastino-pericarditis. The adhesions if of old 
 standing are tough and fibrous, so that the pericardium cannot be 
 stripped from the heart without tearing the heart-substance. There 
 is also commonly some fibroid change in the heart- wall due to sub- 
 stitution of fibrous tissue for muscle fibres damaged by previous 
 inflammation. In the case of recent adhesions or lymph undergoing 
 organization into fibrous tissue, the two layers of pericardium on 
 being separated will present a honeycomb or bread-and-butter-like 
 appearance, owing to the layer of thick, sticky lymph which coats 
 the surface. 
 
46 heart disease. 
 
 Physical Signs. 
 
 The physical signs differ according as the adhesions 
 exist only between the two layers of the pericardium, or 
 between the pericardium and chest-wall, or adjoining 
 pleura as well. In the latter case they are more numerous 
 and distinctive. Among them are the following : — 
 
 Fixation of the apex beat, so that it does not alter its 
 position in deep inspiration and expiration or in change 
 of posture of the body. 
 
 Systolic depression of one or more intercostal spaces to 
 the left of the sternum, or of the lower end of the sternum 
 and the adjoining costal cartilages, which may be caused 
 by the heart dragging on them at each systole, through 
 the agency of the pericardial adhesions. The systolic 
 recession of spaces alone is, however, not a trustworthy 
 indication, as it may be due to atmospheric pressure, more 
 especially when the heart is much hypertrophied. When the 
 costal cartilages or lower end of the sternum are dragged 
 in there can be little doubt as to the diagnosis, as this could 
 not be effected by atmospheric pressure. 
 
 Systolic recession of the site of the apex beat is an 
 important sign when a definite apex beat can be felt ; 
 when there is no palpable apex beat, systolic pitting over 
 its site may be due to atmospheric pressure. 
 
 A diastolic shock may sometimes be felt on palpation 
 with the flat of the hand over areas on the chest-wall where 
 systolic recession is present. It is due to the elastic recoil 
 of the chest-wall at the commencement of diastole as soon 
 as the pulling force exerted during the systole ceases. 
 
 Systolic retraction of the lower portions of the posterior 
 or lateral walls of the thorax may indicate the presence 
 of a universally adherent pericardium. Such retraction 
 may, however, be seen though the pericardium is not 
 adherent to the heart, but only to a larger extent than 
 
ADHERENT PERICARDIUM. 47 
 
 normal to the central tendon of the diaphragm and the 
 muscular substance on either side, and to the chest-wall as 
 well. In such cases the heart is usually greatly enlarged and 
 hypertrophied from old valvular disease. The explanation 
 seems to be that the portion of the diaphragm to which 
 the pericardium is adherent is dragged upwards at each 
 systole of the heart, so that the points of attachment of 
 the digitations of the diaphragm to the lower ribs and 
 costal cartilages are dragged inwards and retracted. 
 
 The descent of the diaphragm in inspiration may be inter- 
 fered with by pericardial adhesions between the heart and 
 diaphragm, more especially if the pericardium is adherent 
 to the chest-wall in front as well. This will be shown by 
 impaired movement in respiration of the upper part of the 
 abdominal wall in the epigastrium and left subcostal region. 
 The area of cardiac dulness will be increased, and will 
 remain unchanged in inspiration and expiration, where 
 there are extensive adhesions between the pericardium and 
 chest- wall, as the lung, which normally overlaps part of 
 the heart, will have been pushed aside, or perhaps have 
 become involved in the adhesions, and be collapsed. 
 
 Enlargement of Heart. — It is common with adherent 
 pericardium to find the heart, more especially the right 
 ventricle, considerably enlarged, in the absence of valvular 
 disease or other obvious cause to account for it. 
 
 It seems probable that such enlargement may be 
 indirectly due to pericardial adhesions as follows : The 
 heart becomes dilated during an attack of pericarditis, 
 and, before it recovers its tone or can contract down 
 again to its normal size, the pericardium becomes adherent 
 and fixes it in this condition of dilatation, the right 
 ventricle suffering more than the left, owing to its thinner 
 walls, as well as for other reasons. 
 
 Hypertrophy and dilatation of the heart, more especially 
 of the right ventricle, may therefore, in the absence of 
 
4 8 HEART DISEASE. 
 
 other obvious causes, such as valvular disease, high arterial 
 tension, etc., to explain it, be a physical sign of consider- 
 able importance. 
 
 Diastolic collapse of cervical veins was held by Friedreich 
 to be. of great diagnostic value when accompanied by systolic 
 retraction of spaces; but I have never found it to be of service. 
 
 Systolic emptying of veins on the surface of the thorax 
 may sometimes be observed, due to suction action, in- 
 duced by the walls of the internal mammary veins being 
 dragged apart by pericardial adhesions during systole of 
 the heart. 
 
 When there are no adhesions between the pericardium 
 and chest-wall the physical signs that may be present 
 will be limited in number. There will be no recession of 
 spaces except as the result of atmospheric pressure, no 
 fixation of apex beat, no diastolic shock. As the pericardium 
 is normally attached by fibrous bands to the central tendon 
 of the diaphragm and to the muscular substance on either 
 side of it, there may be some interference with the move- 
 ments of the diaphragm in respiration. There may also 
 be considerable enlargement of the heart, but in these 
 cases a diagnosis will usually have to be made from other 
 indications than physical signs alone. 
 
 Symptoms. — The symptoms in themselves are not in any 
 sense characteristic. They are usually such as arise from 
 cardiac embarrassment, more especially from the giving way 
 of the right ventricle, such as oedeina of the extremities, 
 enlargement of liver, ascites, dyspnoea, etc. 
 
 Diagnosis. 
 
 The physical signs or symptoms of adherent pericardium, 
 few of which may be present, are often in themselves 
 insufficient to allow of a diagnosis being made, or even to 
 arouse suspicion of its presence ; but valuable help may be 
 derived from careful consideration of the physical signs and 
 
ADHERENT PERICARDIUM. 49 
 
 symptoms together, and by balancing the former against 
 the latter, so that the question is raised, "Do the physical 
 signs present afford evidence of sufficient disease to account 
 for the symptoms that have arisen?" When the symp- 
 toms are those of right ventricle failure, and are more 
 severe than the physical signs present would lead one to 
 expect, and have not been induced by undue exertion or 
 imprudence, adherent pericardium must be thought of as 
 being possibly responsible. For it is the right side of 
 the heart more especially that is seriously hampered by 
 pericardial adhesions, so that their presence may account 
 for the unexpected breakdown of the right ventricle when 
 the physical signs indicate that the valvular lesion is 
 slight. It must also be borne in mind that the heart-wall 
 has in all probability been weakened by the substitution 
 of fibrous tissue for muscle fibres destroyed by inflammation 
 at the time of the attack of pericarditis. 
 
 When with symptoms of right ventricle failure there is 
 an absence of cyanosis, or of pulmonary congestion or lung 
 mischief, this is further evidence in favour of adherent 
 pericardium as a possible cause of the breakdown of the 
 right ventricle. If by these means a suspicion of the 
 presence of adherent pericardium has been aroused, con- 
 firmatory physical signs should be carefully sought for. 
 
 The above remarks apply to the question of diagnosis 
 in cases where, with or without valvular disease, there is no 
 history of pericarditis, and the adhesions are of old standing. 
 
 In cases of pericarditis, which can be kept under 
 observation after the attack, there will be less difficulty in 
 arriving at a diagnosis, and the indications which would 
 lead one to suspect that the pericardium was becoming- 
 adherent are as follows : — 
 
 1. Prolongation of the attack of pericarditis evidenced 
 by a harsh friction rub over the precordial area, which may 
 persist for some weeks. When at the margins of the area of 
 
 E 
 
50 HEART DISEASE. 
 
 cardiac dulness a pleuro-pericardial friction is also heard, it 
 will indicate that adhesions are probably taking place between 
 the pericardium and adjoining pleura or chest-wall as well. 
 
 2. Permanent enlargement of the area of cardiac dulness 
 to a marked extent after the subsidence of the pericarditis. 
 
 3. The occurrence of symptoms of right ventricle failure 
 after a period of temporary improvement, there being no 
 apparent exciting cause for the breakdown of the right ven- 
 tricle. Damage to the cardiac muscle by fresh myocarditis 
 may, however, be responsible, and should be first excluded. 
 
 Prognosis. 
 
 When the heart remains normal in size, and there are 
 no adhesions between the pericardium and chest-wall, the 
 universal adherence of the pericardium to the heart may 
 not in an adult tend to materially shorten life. When 
 the heart is enlarged, or when the pericardium is also 
 adherent to the chest-wall, the prognosis is more serious. 
 When adherent pericardium exists as a complication of 
 valvular disease, it is still more likely to prove fatal 
 eventually, by so hampering the right ventricle as to 
 prevent its recovery when once compensation has broken 
 down. The detection of adherent pericardium has also an 
 important bearing on prognosis, inasmuch as it affords pre- 
 sumptive evidence of fibroid change in the heart- wall, and 
 therefore renders the outlook even more unfavourable. 
 
 Treatment. 
 
 The discovery of adherent pericardium, when present, is 
 important from the point of view of treatment, not because 
 anything can be done to remedy or remove the pericardial 
 adhesions, once they are formed, but because, when it is 
 present, it will be necessary to impose additional restrictions 
 on the patient, so that no undue risks may be run of 
 upsetting the compensatory balance, which would only be 
 restored with great difficulty. 
 
SUPPURATIVE PERICARDITIS. 51 
 
 SUPPURATIVE PERICARDITIS. 
 
 Purulent pericarditis may occur as part of a general 
 pyasrnic or septicemic condition, or in association with 
 einpysenia or some pneumococcal infection, abscess of the 
 lung, suppuration of mediastinal or cervical glands, or of 
 other adjacent structures. Sometimes no apparent cause 
 can be found. 
 
 The inflammatory process is almost invariably septic from 
 the onset, and is attended by effusion of pus into the peri- 
 cardium : seldom, if ever, does a serous effusion of rheumatic 
 origin become purulent. 
 
 The outset of the disease is, as a rule, insidious, and the 
 discovery of pus in the pericardium is often not made till 
 the post-mortem examination. 
 
 The micro-organisms which have been found are the 
 staphylococcus pyogenes aureus, albus, and citreus, the 
 streptococcus, and the pneumococcus. 
 
 Physical Signs. — There is seldom any definite friction rub 
 to announce the onset of the attack. 
 
 The physical signs present will be those of pericardial 
 effusion, which have already been discussed. Chief of these 
 is increase in the area of cardiac dulness, and the difficulty 
 of distinguishing whether this be clue to cardiac dilatation 
 or effusion will be intensified when no friction rub has been 
 heard to suggest the possibility of effusion. Furthermore, 
 it not infrequently happens that the area of cardiac dulness 
 is encroached upon by, or runs into, a large dull area due 
 to empysenia. 
 
 Feebleness or loss of the apex beat, and weak or distant 
 heart-sounds may be noted, but will not be of great value, 
 unless the case has been watched from the outset, so that 
 a standard of comparison could be formed. There may, 
 occasionally, be oedema over the precordial region. 
 
5 2 
 
 HEART DISEASE. 
 
 Symptoms. — The temperature is usually that character- 
 istic of some septic infection, but may sometimes be normal 
 throughout. Eigors seldom occur unless as part of a general 
 septicaemia, except in the somewhat rare event of a serous 
 pericardial effusion becoming purulent. Pain is absent, as 
 a rule, but there may be a feeling of oppression in the 
 precordial region. The pulse rate and respiration are 
 accelerated, and there may be marked dyspnoea, especially 
 on movement. 
 
 Diagnosis. — The diagnosis presents many difficulties, and 
 is frequently not made during life. 
 
 In the absence of an antecedent friction rub effusion 
 may not be suspected, and the intermittent pyrexia may be 
 attributed to an empyaema, or suppuration elsewhere than 
 in the pericardium. 
 
 If effusion is suspected, an exploring- needle may be 
 employed. The skin should be incised parallel to the ribs, 
 as described under paracentesis pericardii, and the intercostal 
 muscles divided before the needle is inserted into the peri- 
 cardium, so that any bulging of the space may be noted, and 
 the needle be accurately directed. 
 
 Prognosis. — The prognosis is always very serious, but 
 there are reasonable grounds for hope in cases where the 
 suppuration is not part of a general septic infection, but 
 is a sequela of an empyema or other localized abscess. 
 
 The earlier the diagnosis is made and surgical inter- 
 ference is sought, the better will be the chance of recovery. 
 The percentage of recoveries is, however, very small. 
 
 Treatment. — Abscess in the pericardium must be treated 
 like any other abscess. It should be opened and drained as 
 soon as the diagnosis is made, by an incision in the fifth 
 space, close to the sternum on the right or left side, wherein 
 any bulging of the intercostal space is apparent, 
 
 Hydropericardium. — By hydropericardimn is meant 
 effusion of serous fluid into the pericardial sac, as the 
 
SUPPURATIVE PERICARDITIS. 53 
 
 result, not of inflammation, but of passive dropsical trans- 
 udation. 
 
 Effusion of such degree, as to be clinically recognizable, 
 occurs most commonly as part of a general dropsical trans- 
 udation from whatever cause, and is therefore most frequently 
 associated with Bright's disease or morbus cordis. It is much 
 less common than effusion into other serous cavities, and 
 when present is a late feature in the disease, and is gradual 
 in onset. It is said also to occur as the result of mechanical 
 obstruction, to the return of blood from the pericardial 
 and cardiac veins from some local cause, such as pressure 
 by mediastinal tumours, enlarged glands, or fibrous 
 adhesions, but this must be very exceptional. 
 
 Symptoms and Physical Signs and Diagnosis. — The 
 symptoms are increasing dyspncea and precordial oppres- 
 sion with enfeeblement of the pulse, and the physical signs 
 are those of pericardial effusion, increase of the area of 
 cardiac dulness, with progressive enfeeblement of the apex 
 beat and weakness of the heart-sounds. As there is no 
 antecedent friction rub to call attention to the possibility 
 of effusion, it may readily escape notice in the earlier stages. 
 The diagnosis cannot be made unless the effusion amounts 
 to several ounces, and when there is effusion into one or 
 both pleural cavities as well it is very difficult, and may be 
 impossible. 
 
 Treatment. — Practically the treatment is that of the 
 original disease to which the general dropsy and hydro- 
 pericardium are due. Belief may occasionally be afforded 
 by aspiration of the pericardium when the diagnosis of 
 effusion can be made with certainty ; but it is rarely em- 
 ployed or called for, as the relief can but be temporary, and 
 does not long delay the fatal result. 
 
 Pneumopericardium. — The presence of gas in the peri- 
 cardial sac is rare. It may be due to penetrating wounds 
 of the pericardium by a sharp instrument or a fractured rib, 
 
54 HEART DISEASE. 
 
 but is more commonly the result of ulceration, Ly which a 
 communication is established between the pericardial sac 
 and an air-containing cavity. Thus, an old phthisical cavity, 
 an abscess in the lung, a pneumothorax, a subphrenic abscess 
 that has made its way through the diaphragm, may open 
 into the pericardium, or a communication may be established 
 with the oesophagus by ulceration, giving rise in each in- 
 stance to pneumopericardium. Pus may find its way into 
 the pericardium with the air giving rise to pyo-pneumo- 
 pericardium, or blood in the case of punctured wounds, when 
 the condition is termed hasmo-pneuniopericardiuni. 
 
 Physical Signs. — Uniform bulging of the precordial area 
 may be noted. The apex beat is usually absent or feeble, 
 but can sometimes be felt when the patient bends forwards. 
 
 On percussion the note varies with change of position, 
 being dull over the fluid and tympanitic, or high pitched 
 over the air-containing cavity. The gas always rises to the 
 highest part of the cavity with change of posture of the 
 patient. The relations of the gas and fluid will be remark- 
 ably altered by changes of posture, and can be readily made 
 out by percussion. 
 
 On auscultation the heart-sounds acquire a peculiar 
 metallic character, and are unusually loud and clear, so that 
 they may sometimes be heard at some distance off, and are 
 a source of annoyance to the patient himself. Splashing 
 sounds, and metallic tinkling, and a bell note with coins 
 can usually be heard. 
 
 Treatment. — As pneumopericardium is usually a com- 
 plication of some grave disease, treatment must vary accord- 
 ingly. Aspiration may be required to remove the gas or 
 fluid, or possibly free incision may be necessary to allow 
 of the escape of pus. 
 
 Tuberculosis of the pericardium may occur as part of a 
 general acute miliary tuberculosis, when miliary tubercles 
 will be found scattered over its surface, post-mortem, or 
 
SUPPURATIVE PERICARDITIS. 55 
 
 from direct infection by adjacent tubercular lung or pleura, 
 in which case the onset is insidious and the progress of the 
 disease is usually chronic. The two layers of pericardium 
 become thickened and tend to become adherent, so that 
 the physical signs are those of chronic mediastinitis, or 
 adherent pericardium. 
 
 New growth of the pericardium is very rare, and when 
 found is usually due to invasion of the pericardium by a 
 new growth in adjacent structures. 
 
CHAPTEE IV. 
 
 SIMPLE ACUTE ENDOCARDITIS. 
 
 Acute endocarditis means, strictly speaking, an acute 
 inflammation of the endocardium or lining membrane of 
 the heart. The inflammatory process is, however, as a rule, 
 chiefly manifested on the valves, so that by the term endo- 
 carditis is usually understood inflammation of the valves 
 of the heart. The mitral and aortic valves are most com- 
 monly attacked ; rarely are the valves of the right side 
 of the heart affected except as a result of endocarditis 
 occurring during intra-uterine life. It must be borne in 
 mind that acute endocarditis is commonly accompanied by 
 myocarditis of varying extent, which may seriously and 
 permanently damage the walls of the heart. 
 
 On etiological and pathological grounds it is doubtful 
 whether simple or rheumatic endocarditis should be 
 differentiated from malignant or pernicious endocarditis, 
 and this question is discussed fully in the chapter on 
 the latter affection. Clinically, the two diseases are more 
 or less distinct, and for that reason they are here considered 
 separately. 
 
 Morbid Anatomy and Pathology. — On naked-eye exami- 
 nation of an affected valve it is seen to be studded along 
 the free margin with small greyish-yellow or pinkish opaque 
 bodies, the so-called " vegetations," as shown on the aortic 
 valves in Fig. 7. Microscopically these are seen to consist 
 of a superficial layer of coagulated fibrin and necrotic tissue, 
 in the upper stratum of which are entangled leucocytes 
 
SIMPLE ACUTE ENDOCARDITIS. 
 
 57 
 
 and a few red corpuscles deposited from the blood stream. 
 Deeper down is a layer of simple fibrin free from corpus- 
 cular elements, and below this, again, is a layer of granula- 
 tion tissue, formed by proliferation of the endothelial cells 
 
 as a result of the inflammatory process. The inappropriately 
 named " vegetations " are thus simply necrotic tissue, 
 coagulated fibrin and leucocytes deposited from the blood 
 stream on an inflamed surface. They may become partially 
 absorbed, but, for the most part, the granulation tissue 
 
58 HEART DISEASE. 
 
 undergoes organization, and, later on, cicatricial con- 
 traction, so that the valves become puckered and mis- 
 shapen, sometimes glued together at their margins, and 
 incompetence or obstruction, or both combined, result. 
 When the mitral valve is affected, the chordae tendinese 
 are also, as a rule, more or less involved in the inflam- 
 matory process, so that they become shortened, thickened 
 and deformed, and lose their flexibility. The shortening 
 and fusing together of their fine subdivisions near the valves 
 may be carried to such an extent that the margins of the 
 valves seem to be directly attached to the papillary muscles. 
 
 Etiology. — Acute endocarditis is in the great majority 
 of cases a complication, or rather an essential feature of 
 rheumatism. 
 
 Of late years much evidence has been accumulated 
 tending to prove that rheumatism is a disease of microbic 
 origin, and that the valvulitis associated with it is a local 
 manifestation of the activity of specific micro-organisms. 
 The micro-organism in question is a minute diplococcus 
 which has been isolated from the blood and pericardial fluid 
 of patients suffering from acute rheumatism by various 
 observers, Triboulet,* Wasserman,f Paine % and Poynton, 
 Shaw,§ Ainley Walker, Beattie, and others. This diplo- 
 coccus, grown on suitable media and inoculated into rabbits, 
 has in their hands produced arthritis, endocarditis, and 
 valvulitis, and in early cases of rheumatic endocarditis 
 minute diplococci can sometimes be demonstrated micro- 
 scopically in the vegetations on the affected valves. Acute 
 endocarditis occurring in association with chorea may be 
 regarded as of rheumatic origin. 
 
 It is not uncommon as a sequela to scarlet fever. 
 The type sometimes met with in smallpox, measles, and 
 
 * Bulletin de la Soc. des hopitaux, 1898, p. 93, n. 
 f Berliner Klin. Woch., 1899, No. 29, p. 638. 
 X Lancet, Sept. 1900. 
 § Journal Path, and Bad., Dec. 1903. 
 
SIMPLE ACUTE ENDOCARDITIS. 59 
 
 pneumonia belongs rather to the category discussed in the 
 next chapter. 
 
 Cole * has succeeded in producing valvulitis and 
 arthritis in rabbits by inoculating them with different 
 brands of streptococci obtained from cases of puerperal 
 fever, septic peritonitis, and other sources, in which there 
 was no history of rheumatism, the results being similar 
 to those obtained by Paine and Poynton, Shaw, etc., by 
 inoculation with the diplococcus isolated from cases of 
 rheumatism. He therefore argues that there is no such 
 thing as a specific rheumatic micro-organism, and the 
 question is still to a certain extent sub judice. But, in 
 view of the results obtained by Paine and Poynton and 
 others, it scarcely seems fair to argue that because micro- 
 organisms other than those associated with rheumatism can 
 produce endocarditis in animals, as has long been known in 
 the case of man, therefore there is no specific rheumatic 
 organism. Moreover, rheumatism, whether in the child or 
 adult, is such a definite clinical entity, that one would 
 expect to find a specific organism, and would be confusing to 
 vaguely classify it as a form of " septicaemia " in the ordinary 
 sense of the term. We must hope that further work will 
 be done on this subject, and that future investigators will 
 be able to definitely settle the controversy. 
 
 It is most common in childhood and early adolescence, 
 and is rare after middle age. It may also occur during foetal 
 life, when it is usually confined to the right side of the heart. 
 
 Physical Signs. 
 
 The development of a valvular murmur, or, in the case 
 of a second attack, of some change in the character of an 
 existing murmur, is the only trustworthy indication of the 
 presence of endocarditis. Evidence, however, of its exist- 
 ence is frequently found post-mortem in cases where no 
 
 * Journal Infect. Diseases, vol. i., No. 4, pp. 714-737. 
 
60 HEART DISEASE. 
 
 murmur has been audible during life, so that it is prob- 
 able that in many instances the inflammatory process may 
 be active for some little time before a murmur is developed. 
 It is important, therefore, to be on the look-out for other 
 indications of its presence which may precede the develop- 
 ment of a murmur, however indefinite and uncertain 
 they may be. Of these the most significant is some 
 alteration in the first sound, which may be reduplicated, 
 prolonged and muffled, or rumbling in character, when the 
 mitral valve is affected. The action of the heart may be 
 tumultuous or irregular, and the area of cardiac dulness may 
 become much enlarged, when the inflammatory process 
 involves the muscular substance of the heart as well. 
 
 These indefinite signs are chiefly of value when present in 
 cases in which an attack of endocarditis is to be anticipated, 
 and it is therefore necessary that we should recognize such 
 cases at the earliest possible moment. Of course, in a well- 
 marked attack of rheumatism of the usual type in adults, we 
 shall be on our guard ; but in children, as pointed out by 
 Cheadle,* the articular manifestations are usually slight, 
 and may be confined to fugitive pains in the joints, while 
 the heart is frequently attacked. The symptoms of 
 rheumatism may thus be so ill-defined as to escape notice, 
 and the onset of endocarditis may be very insidious. 
 
 To give an illustration of a case in point. Patrick D., 
 aet. 14, employed at one of the large shops in London, 
 walked up to the out-patient department at St. Mary's 
 Hospital on 2nd January, 1897. He stated that he had 
 vomited the previous day after having some pork for 
 dinner, and complained of being rather short of breath. It 
 was noticed that he was somewhat cyanosed, and was 
 breathing rapidly, and the pulse rate was 132. On 
 examining his chest, well-marked pulsation in the epigas- 
 trium, and in the third, fourth, and fifth left intercostal 
 * Harveian Lectures, 3889. 
 
SIMPLE ACUTE ENDOCARDITIS. 61 
 
 spaces, was noted. The apex beat was diffuse, and was 
 visible in the fifth left space just outside the vertical nipple 
 line. The area of cardiac dulness was enlarged and 
 extended to the right, half an inch beyond the right border 
 of the sternum ; to the left, just beyond the vertical nipple 
 line; and above, to the third space. At the apex a loud 
 blowing systolic murmur was heard, conducted into the 
 axilla, and at the base, over the aortic area, a soft diastolic 
 murmur conducted down the sternum. There was no marked 
 throbbing of the carotids, the pulse was not collapsing in 
 character, and a distinct aortic second sound was audible at 
 the base as well as the diastolic murmur; the pulmonic 
 second sound was accentuated. The liver was somewhat 
 enlarged, but there was no oedema of the extremities. 
 Rheumatic nodules were present on the elbows and knees. 
 
 The history given by the boy was that, two months ago 
 he had felt some stiffness in the knees, and had remained at 
 home two days. He soon felt all right again, and up to 
 the day on which he came up to the hospital he had been 
 at work as usual. He was at once admitted, but got rapidly 
 worse, suffering from great dyspnoea, and repeated attacks 
 of vomiting ; the diastolic murmur became more pronounced, 
 and the pulse collapsing in character ; the cardiac dilatation 
 increased : the liver became more and more enlarged, and 
 oedema of the lower extremities set in, and soon became 
 extreme. He died on 17th February, six and a half weeks 
 from the date of his admission. 
 
 The stiffness in the knees, two months before he came 
 up to the hospital, seems to have been the only warning of 
 the attack of rheumatism which gave rise to such serious 
 cardiac mischief ; and so slight were the symptoms, that 
 the boy was undoubtedly going about his work with active 
 endocarditis and myocarditis for some time before he sought 
 medical advice, and by that time the heart had become 
 dilated to an extreme decree. This case illustrates the 
 
62 HEART DISEASE. 
 
 insidious form that the rheumatism of early adolescence or 
 childhood may assume, and shows how much damage may 
 be done to the heart before any serious symptoms compel 
 the patient to give in. 
 
 A history of pains in the joints or limbs, with slight 
 febrile disturbance in children, should, therefore, put us on 
 our guard, even though there be no appreciable swelling or 
 tenderness of the joints, and the heart should be examined, 
 not only when the patient is first seen, but from time to 
 time for some weeks afterwards. A family history of 
 rheumatism, or of a previous attack of chorea, should make 
 us doubly suspicious of these ill-marked symptoms. 
 
 There are, however, certain unmistakable danger-signals 
 for which we should be on the look-out, in children or 
 young adolescents, when a suspicion of rheumatism is 
 aroused. These are rheumatic nodules — small fibrous 
 growths, commonly about the size of a split pea, some- 
 times much larger. They are found in the neighbourhood 
 of joints over the bony prominences, and are attached by 
 their base to the fascia, sheaths of tendons, or some under- 
 lying fibrous tissue. The skin over them is freely movable, 
 and they are best seen by flexing the joint over which 
 they are situated, so that the skin is rendered tense. 
 They were first described by Barlow * and Warner ; and 
 Cheadle, in his book on the rheumatic state in children, 
 has called attention to their evil prognostic significance. 
 In themselves they are painless, and cause little or no 
 discomfort to the patient, but they indicate that the 
 rheumatism, to which they owe their existence, has got a 
 firm hold on its victim, and where they are present in 
 force, repeated attacks of cardiac inflammation are to be 
 apprehended, though cases do occur in which the heart 
 escapes. They are not present in all, or in the greater pro- 
 portion of cases in which the heart is attacked, but a careful 
 
 * Tram. Internal. Med. Congress. Londou, 1SS1. 
 
SIMPLE ACUTE ENDOCARDITIS. 63 
 
 search for them should never be omitted, as they are of 
 great clinical importance. They are seldom found in adults. 
 
 Exudative erythcmata, of the type of erythema margi- 
 natum, or less commonly papular or urticarial in character, 
 may occur in rheumatic subjects ; they are not so frequently 
 met with as nodules, but they may occur in conjunction 
 with them, or alone. 
 
 In erythema marginatum, small raised patches about 
 the size of a sixpence, with sharply defined margins, and 
 of a dull red colour, make their appearance. The centre of 
 the patch usually undergoes absorption, and becomes of a 
 pinkish or pale colour, while the margins continue to spread 
 as narrow raised red bands with irregular outline. The 
 eruption is usually accompanied by some rise of tempera- 
 ture, and lasts a few days, gradually fading and leaving a 
 slight brownish discoloration. 
 
 Erythema nodosum is sometimes looked upon as evidence 
 of rheumatism, but it is by no means certain that it can be 
 regarded as such. 
 
 Symptoms. 
 The symptoms are not specially characteristic, and are, 
 to a great extent, merged in those of the rheumatic affection 
 of which endocarditis is a part. Dyspncea, a tendency to 
 sigh, a feeling of oppression in the precordial region, rest- 
 lessness, prolonged fever (the temperature not ranging high, 
 as a rule, but from 99° to 101° F.), a fresh rise of tempera- 
 ture after a period of quiescence, increase of the pulse rate, 
 are all symptoms which may give rise to a suspicion of 
 endocarditis, and be present during an attack ; but reliance 
 cannot be placed on these alone for purposes of diagnosis. 
 
 Pkognosis. 
 
 During an attack of endocarditis, it is practically im- 
 possible to determine exactly the extent of the damage 
 
64 HEART DISEASE. 
 
 done to the valves attacked. It is not till some time after 
 the inflammatory process has subsided and compensatory 
 changes have in some degree developed, that we are able 
 to estimate the extent of the lesion. If, in the course of 
 an attack, a diastolic murmur develops over the aortic area, 
 we may be certain that the aortic valves have been damaged, 
 and a certain degree of aortic incompetence will perma- 
 nently result. It does not, however, in the case of the 
 mitral valve, necessarily follow, when a systolic murmur is 
 developed at the apex, that the mitral incompetence which 
 the murmur indicates will be permanent, though this may 
 be the case. For the contractile ring surrounding the 
 mitral orifice, and the musculi papillares may be tempo- 
 rarily thrown out of gear by the inflammatory process, so 
 that the valves, though undamaged, do not come together 
 at their margins, and some regurgitation takes place, or 
 the murmur may be the result of dilatation of the ventricle. 
 As the muscular fibres recover their tone after the 
 inflammation has subsided, the valves may again become 
 competent, and the systolic murmur disappear. If, how- 
 ever, the valves themselves, or the chordae tendinese, are 
 seriously attacked, the former may become rigid and 
 deformed, the latter puckered and shortened, and permanent 
 incompetence results. 
 
 When the valves become thickened and glued together 
 at their margins, stenosis of the orifice will ensue, which 
 gradually increases as cicatricial contraction of the freshly 
 organized fibrous tissue at the bases of the valves and round 
 the mitral orifice takes place. Not infrequently incompe- 
 tence and stenosis co-exist, the valves being thickened and 
 depressed so that they cannot function effectively, while 
 they are also adherent where they meet at their attach- 
 ment to the margin of the orifice. 
 
simple acute endocarditis. 65 
 
 Diagnosis. 
 
 When no cardiac murmur is present, a diagnosis of 
 endocarditis is not possible. It is not always easy on 
 discovering, for the first time, the existence of a cardiac 
 murmur, to decide whether or not it indicates acute endo- 
 carditis. It may be due to a recent or old attack of 
 endocarditis, to cardiac dilatation, or to anseniia. When 
 hypertrophy or other compensatory changes of the heart 
 are present, they will testify to a valvular lesion of old 
 standing, but in such cases we must bear in mind the 
 possibility and probability of a second attack, and watch 
 carefully for any change in the character of the existing 
 murmur, or for the development of a new murmur. The 
 history of the case, the presence of nodules, articular pains, 
 or other rheumatic manifestations, will be of assistance 
 in arousing suspicion of acute endocarditis, and confirma- 
 tory evidence may be found in an irregular slightly raised 
 temperature, or restlessness and dyspnoea, and other 
 symptoms of cardiac disturbance. The murmurs of anaemia 
 have been discussed elsewhere ; the history of the case, 
 the aspect of the patient, and the character of the murmur 
 will usually enable us to distinguish these. Exocardial 
 murmurs, whether due to pericarditis or pleurisy, are, as a 
 rule, readily distinguished by their harsh grating or rubbing 
 character, their position, and their relation to the cardiac 
 rhythm. 
 
 The murmur caused by compression of a thin layer of 
 lung between the heart and chest wall may be excluded by 
 its occurring only during inspiration, and disappearing 
 when the patient is told to make a deep expiration and hold 
 his breath. 
 
 Treatment. 
 
 Neither drugs nor local applications seem to be of avail 
 to arrest the progress of endocarditis, or modify its course 
 
66 HEART DISEASE. 
 
 in an appreciable degree. Salicylates, alkalies, iodides, 
 quinine, internally, and applications over the prsecordial 
 area of blisters, sinapisms, leeches, and ice-bags have been 
 tried, but it is impossible to estimate with any degree of 
 confidence their influence on the inflammatory process. 
 Salicylates and salicin, while exercising an undoubted 
 influence on the rheumatic condition, have no effect 
 on the inflammatory process as such, and they weaken 
 the heart when taken continuously for any considerable 
 time. Alkalies are less open to objection, especially when 
 given with quinine : citrates may lessen the tendency to 
 deposition of fibrin on the valves by diminishing the 
 coagulability of the blood, and thus perhaps prove of 
 service. We shall do the best for the patient by keeping 
 him in bed and treating symptoms as they arise, giving 
 only an effervescing mixture of quinine and citrate of 
 potash. At any rate, no active measures should be taken 
 which could in any way impair his strength or increase 
 his discomfort. The patient should be kept in bed, not 
 only during the attack, but for some weeks or months after 
 it has subsided, till sufficient time has elapsed for the 
 heart to recover, and for compensatory changes to take 
 place. In children who come of a rheumatic stock, a 
 careful look-out must be kept for any of the premonitory 
 symptoms of rheumatism or heart inflammation, and if 
 any suspicion is aroused that the heart is being attacked, 
 the child should be kept in bed till all doubt is over. 
 
CHAPTER V. 
 
 "MALIGNANT" OR "PERNICIOUS" ENDO- 
 CARDITIS. 
 
 NOMENCLATURE OF THE AFFECTION — MORBID ANATOMY — 
 ETIOLOGY— THE ROLE PLAYED BY VARIOUS MICRO- 
 ORGANISMS—PHYSICAL SIGNS AND SYMPTOMS— INFARC- 
 TION AND EMBOLISM — DIAGNOSIS — PROGNOSIS — TREAT- 
 MENT. CHRONIC ENDOCARDITIS. 
 
 To this form of endocarditis various epithets have been 
 applied to distinguish it from " simple or rheumatic " 
 endocarditis : " infective " because of its microbic origin, 
 " malignant " because of its fatal tendency, " ulcerative " 
 because of the severity of the lesions in the valves attacked. 
 In view of recent researches, which tend to prove that 
 rheumatism is a disease due to a specific micro-organism 
 which may be widely distributed in the body, the term 
 " infective " is no longer appropriate, nor is " ulcerative " 
 specially suitable, as ulceration of the valves, though 
 frequent and extensive, is not an essential characteristic. 
 We are left, then, with " malignant," which, though not a 
 highly scientific effort, may be truthfully employed as 
 expressing the grave nature of the malady ; but, inasmuch 
 as recovery undoubtedly occurs in some cases, it is not 
 employed in quite the same sense as when we speak of 
 "malignant" disease as a synonym for carcinoma. We 
 would venture to suggest the term " pernicious as a more 
 
68 HEART DISEASE. 
 
 appropriate epithet, used in the same sense as in " pernicious 
 anaemia," which, while it denotes the serious nature of the 
 disease, does not necessarily connote a fatal issue. 
 
 It is indeed difficult, if not impossible, to draw a hard- 
 and-fast line between "simple or rheumatic" and "per- 
 nicious " endocarditis, and, as will be seen later in the 
 section on etiology, there is convincing evidence in favour 
 of the view that " pernicious " endocarditis, in a certain 
 proportion of cases, is a virulent form of rheumatic endo- 
 carditis, and due to the same micro-organism. 
 
 Because simple endocarditis is not a fatal malady, we 
 rarely find at autopsies the small bead-like vegetations on 
 the valves supposed to be characteristic of this affection, 
 unless the patient has succumbed to pericarditis or some 
 intercurrent malady. But in children it is a common ex- 
 perience to meet with repeated and prolonged attacks of 
 endocarditis, in which the temperature ranges from 99 to 101 
 degrees for some weeks, and the cardiac murmur changes 
 in character, the child becoming progressively anseinic, 
 but eventually recovering, with well-marked signs of mitral 
 incompetence. Because there is no evidence of infarc- 
 tion, and the temperature is not high, and the child does 
 not succumb at the time, it is customary to classify these 
 as cases of simple rheumatic endocarditis, though probably 
 they form an intermediate group between the two extremes. 
 Again, when we meet with old cicatrized lesions of the 
 valves, such as the " button-hole " mitral orifice, or great 
 deformity of the aortic valves, in patients who succumb 
 from the effects of these chronic valvular lesions, which 
 from their very appearance must have been due to extensive 
 damage and ulceration of the valves which have healed and 
 cicatrized, we may justly infer that these were cases of 
 ulcerative endocarditis at the outset, and they form another 
 link in the chain between the mild and fatal varieties of 
 acute endocarditis. 
 
"MALIGNANT" OR "PERNICIOUS" ENDOCARDITIS 69 
 
 Gibson, in his treatise on the Heart, does not make any 
 distinction in nomenclature between the various grades, but 
 includes all varieties under the term "acute endocarditis." 
 
 It is, however, convenient for clinical purposes to dif- 
 ferentiate two main groups, as we have done here, as there 
 
 FIG. 8.— DESTRUCTION OF PULMONIC VALVES BY PERNICIOUS ENDOCARDITIS, 
 AND VEGETATIONS ON THE PULMONARY ARTERY. 
 
 are certain clinical and pathological features which mark 
 them off one from the other. 
 
 Morbid Anatomy. — The affected valves are usually 
 masked by large, fungating vegetations readily detachable 
 and extremely friable. On removal of these vegetations, 
 
7o HEART DISEASE. 
 
 the valve is frequently found to be partially or wholly 
 destroyed by ulceration. The disease is often not limited 
 to the valves, and vegetations or erosions may be present on 
 the endocardium lining the cavities of the heart, especially 
 the auricles, on the inner surface of the walls of the great 
 vessels, as in Fig. 8, and along the chordse tendinese, which 
 may be eroded or completely ulcerated through. 
 
 Microscopically, these vegetations are seen to consist of 
 necrotic tissue, fibrin deposited from the blood stream in 
 which may be entangled some red corpuscles and leucocytes, 
 and in the deeper layers leucocytes and proliferating endo- 
 thelial cells, or granulation tissue. Micro-organisms, usually 
 micrococci in large masses, are invariably present in the 
 superficial layers. Vide, Fig. 9. The necrotic and amorphous 
 appearance of the tissues in which the micro-organisms are 
 embedded is very striking. 
 
 In certain of the more chronic cases the vegetations 
 may assume a rounded, opaque, or verrucose form, and be 
 of considerable size, consisting of pale, lobulated excres- 
 cences with smooth, rounded surfaces. Microscopically, it 
 will be seen that the deeper layers consist of actively 
 proliferating endothelial and connective tissue cells in 
 process of organization into fibrous tissue, while the upper 
 layers consist of fibrin and leucocytes more or less necrotic 
 and amorphous, with few nuclei, staining very faintly. 
 Micro-organisms are not present in large masses on the 
 free borders, but may be undiscoverable or very difficult to 
 find, and only revealed after careful search through many 
 sections. If found, they do not take the stain well, and 
 appear to be dead or moribund. Because of this absence 
 or scarcity of micro-organisms, some observers have held 
 that this was a special variety of simple rheumatic 
 endocarditis, and have differentiated it under the name 
 " verrucose endocarditis " (vide Fig. 10). These " verrucose " 
 vegetations are, however, usually found in cases of long 
 
"MALIGNANT" OR "PERNICIOUS" ENDOCARDITIS. 71 
 
 duration, and they are in all probability, from the patho- 
 logical appearances, cases in which the disease has been 
 wholly or partially arrested and repair is taking place, but 
 the patient succumbs from exhaustion or from the effect of 
 the valvular lesion. 
 
 Besides the cardiac lesions, there are commonly secondary 
 lesions in the spleen, kidney, or brain, due to embolism from 
 portions of the vegetations which are detached from the 
 valves and lodge in the smaller arterioles. In the organs 
 
 FIG. 9.— SHOWING MASSES OF MICRO-OEGANISMS IN THE VALVES (X 560). 
 
 above mentioned, the lodgment of an embolus in one of 
 the terminal arterioles causes the death of the tissue sup- 
 plied by that branch, as there is insufficient collateral 
 circulation to nourish the part when its blood supply is 
 suddenly cut off. The portion of tissue therefore under- 
 goes coagulation necrosis, and the resulting condition is 
 known as an " infarct." Infarcts in the kidney and spleen 
 are usually wedge-shaped, but may be of irregular outline, 
 
72 
 
 HEART DISEASE. 
 
 FIG. 10. — MITRAL VALVE, SHOWING " VEBELCOSE : 
 VEGETATIONS. 
 
 and are almost invariably ansemic, i.e. of a pale, dead 
 white colour, with a zone of congestion round the nerotic 
 
 area, though occa- 
 sionally in the 
 spleen they are red 
 or hsernorrhagic. 
 
 Etiology. — Micro- 
 organisms are almost 
 invariably present in 
 abundance in the 
 vegetations on the 
 affected valves, where 
 they can be readily 
 demonstrated by mi- 
 croscopic examina- 
 tion, and they can frequently be isolated in pure culture 
 from the blood of the patient during life. They are usually 
 micrococci. Some difference of opinion exists as to their 
 nature, and as to whether any one specific micro-organism 
 is the etiological factor in this disease. Previous to the 
 isolation and identification of the diplococcus isolated in 
 rheumatism, various observers had experimented with pure 
 cultures obtained from the valves in malignant endocarditis. 
 By injection of these into the jugular veins of animals, 
 some experimenters with, and some without previous injury 
 to the valves, had produced valvulitis, in some instances 
 accompanied by metastatic infarcts. The organism found 
 was not the same in all cases. Among the organisms 
 which have been isolated from cases of malignant endocar- 
 ditis are, the staphylococcus aureus and albus, and citreus, 
 the streptococcus pyogenes, the pneumococcus, and the 
 gonococcus, and the influenza bacillus. 
 
 In 1903,* Poynton and Paine read an important paper, 
 in which they show that malignant endocarditis may be 
 * Med. Chir. Trans., Vol. 85. 
 
"MALIGNANT" OR "PERNICIOUS" ENDOCARDITIS. 73 
 
 set up by a diplococcus, indistinguishable from that which 
 they have isolated in rheumatic fever. They give an 
 account of a series of cases of pernicious endocarditis, 
 with a clinical history and an account of the post-mortem 
 examination, in which they obtained from the affected 
 valves a diplococcus, cultures of which, inoculated into 
 rabbits, reproduced pernicious endocarditis in those 
 animals. This diplococcus they considered to be identical 
 with that which they have previously isolated in cases of 
 pericarditis and endocarditis associated with rheumatic 
 fever. By inoculating rabbits with an attenuated culture 
 of this diplococcus obtained from a case of pernicious en- 
 docarditis, they showed that it might give rise to pericar- 
 ditis without valvulitis, or to a disease indistinguishable 
 from rheumatic fever. Conversely, by inoculating a rabbit 
 with a culture of a diplococcus originally obtained from a 
 case of rheumatic fever, the virulence of which had been 
 raised by passage through several rabbits, they produced 
 in the animal well-marked pernicious endocarditis. 
 
 In all the cases they describe in this paper there was 
 a history of rheumatic fever at some period previous to the 
 attack of pernicious endocarditis. 
 
 In view of these results, it is only fair to admit that 
 pernicious endocarditis may in some cases, if not in a large 
 proportion, be due to infection by the rheumatic diplococcus, 
 and that it occurs either because the virulence of the micro- 
 organism is great, or more probably because the resistance 
 of the individual attacked is very low. Injury to the valve 
 is probably an important etiological factor, for in the 
 majority of cases pernicious endocarditis affects valves which 
 have been damaged in a previous attack of rheumatism. 
 
 We must now consider the role played by other micro- 
 organisms which have been met with in this disease. 
 
 1. The Pyogenic Organisms. — Numerous observers have 
 testified to the presence of the streptococcus pyogenes, the 
 
74 HEART DISEASE. 
 
 staphylococcus aureus and albus in the vegetatioDS on the 
 affected valve and in the blood, and cultures have been 
 made from the blood during life and from the vegetations 
 after death. 
 
 Of these, the streptococcus pyogenes is the most com- 
 monly found, and next in frequency the staphylococcus 
 aureus. Combinations of two of these organisms are also fre- 
 quently met with, e.g. of the streptococcus and staphylococcus 
 aureus, or albus, or of the staphylococcus aureus and albus. 
 If we admit the possibility of a specific rheumatic diplococcus 
 being a cause of pernicious endocarditis, it is probable that 
 it may frequently be one of the organisms in a mixed infec- 
 tion, but not be recognized, because it is a delicate organism 
 and requires special culture media for its growth. 
 
 It is a remarkable fact that while many observers 
 have succeeded in producing endocarditis in rabbits by 
 inoculation of pure cultures obtained from a case of pernicious 
 endocarditis in man, few have succeeded in producing this 
 condition by inoculation of cultures of the streptococcus or 
 staphylococcus pyogenes obtained from other sources, e.g. 
 cases of pyaemia or septicaemia. Cole * has succeeded in 
 doing so with cultures derived from puerperal fever and 
 peritonitis, as already mentioned. Poynton and Paine f 
 made several attempts with different brands of pyogenic 
 organisms, and succeeded in some instances, but the usual 
 result was septicaemia and the early death of the inoculated 
 animal. Again, though ulcerative endocarditis is met with 
 sometimes in cases of septicaemia, pyaemia, puerperal fever, 
 erysipelas, osteomyelitis, etc., it is the exception rather than 
 the rule, and we would expect it to be very common were 
 the pyogenic organisms mainly responsible for the disease 
 known as malignant or pernicious endocarditis. It is also 
 remarkable that infarcts in this affection so rarely suppurate. 
 
 * Journ. Infect. Diseases, vol. i. No. 4, 1004. 
 t Trans, Med. Chir. Soc, Vol. 85. 
 
"MALIGNANT" OR "PERNICIOUS" ENDOCARDITIS. 75 
 
 These considerations tend to support the view of Paine 
 and Poynton that pernicious endocarditis may in some 
 instances be a form of pernicious rheumatism. 
 
 The Pneumococcus. — Pernicious endocarditis is sometimes 
 met with in association with pneumonia and pneumococcal 
 meningitis, and the pneumococcus has been frequently iso- 
 lated from the affected valves. Netter * has written several 
 important papers on this subject, and has produced an 
 ulcerative endocarditis in rabbits after injury to a valve 
 by inoculation of cultures of the pneumococcus. Michaelis f 
 has also produced the affection in dogs by repeated inocula- 
 tion of cultures of the pneumococcus at frequent intervals. 
 Osier, Weichselbaum, Huchard, and many others have 
 published cases of pneumococcal endocarditis. 
 
 We must therefore admit the pneumococcus as one of the 
 causes of pernicious endocarditis, though, when it is found, 
 pneumonia or meningitis is usually the primary disease. 
 
 The Gonococcus. — That ulcerative endocarditis can be 
 caused by the genococcus was first shown by Gluzinski. 
 Schedler, His, % Councilman,^ and others have confirmed 
 his observations. Harris || and Johnson have recently 
 described two cases of gonococcal endocarditis, and in a 
 paper read before the Pathological Society in April, 1905, 
 Horder describes a case of malignant endocarditis, in which 
 he isolated the gonococeus from the blood during life and 
 from the affected valve post mortem. 
 
 Pfeiffer's Influenza Bacillus. — Some cases of ulcerative en- 
 docarditis due to this organism have recently been described. 
 
 Austin 1 has published an account of three cases in 
 which he found Pfeiffer's influenza bacillus in the affected 
 valves. Horder** has also published two cases which he 
 attributes to this bacillus. 
 
 * Soc. Anat., March, 1886 ; Arch, de Phys., 1886, etc. 
 
 t Med. Soc. of Berlin, 1895. t Berlin Klin. Woch., 1892. 
 
 § Amer. Jour. Med. Sc., 1893. || Joum. Amer. Phys., 1902. 
 
 ^ John Hopkins' Reports, 1899. ** Trans. Path. Soc, April, 1905. 
 
76 BE ART DISEASE. 
 
 Other micro-organisms which have occasionally been 
 found in the affected valves in pernicious endocarditis 
 are the bacillus endocarditis griseus of Weichselbaum, the 
 bacillus capsulatus of the same author, and the bacillus coli. 
 
 Pernicious endocarditis may occur as a complication in 
 scarlet fever and smallpox, and in erysipelas, puerperal 
 fever, 'pyaemia, septicaemia, esteomyelitis, and pneumonia, as 
 has already been stated. 
 
 Modes of Infection. — The ways in which the micro- 
 organisms which attack the valves may obtain admittance 
 to the circulation are manifold : by the skin, as in cases of 
 open wounds; by the mucous membranes of the pharynx, 
 especially the tonsils, or of the intestines ; by the genito- 
 urinary, and by the respiratory tracts. All, therefore, may 
 be, at one time or other, exposed to the attacks of the 
 pyogenic microbes, which give rise to this form of endo- 
 carditis, but in only a small proportion of cases are the 
 endocardial tissues specially susceptible. 
 
 Symptoms and Physical Signs. — While it is difficult to draw 
 a hard-and-fast line between simple and pernicious endocar- 
 ditis, there are certain clinical features which may be said to 
 distinguish the latter. These are prolonged irregular pyrexia 
 of a septicemic type, the occurrence of embolism, change in 
 the character of the cardiac murmurs, progressive anaemia 
 aud loss of flesh. Rigors may occur, but are not common. 
 
 The age of the patient is also of importance. Malignant 
 endocarditis appears to be a disease of young adult, or 
 middle life, and is rare in young children. From an 
 analysis of seventeen cases on which I made post-mortem 
 examinations during the years 1900 to 1904 at St. Mary's 
 Hospital, I find the average age works out at 84. Curiously 
 enough, this almost exactly coincides with the average age 
 arrived at by Dreschfield from an analysis of cases during a 
 period of four years at the Manchester Infirmary, namely 34^. 
 
 The youngest of the patients in the St. Mary's cases was 
 
"MALIGNANT" OR "PERNICIOUS" ENDOCARDITIS. 77 
 
 16, the oldest 54, and no less than thirteen out of seventeen 
 were between the ages of 22 and 45. 
 
 The Temperature. — This may vary considerably. Some- 
 times the onset is insidious and the temperature is little 
 raised above normal, ranging from 99 to 100, with intervals of 
 apyrexia for some clays. Later on, as the symptoms become 
 more pronounced, the temperature ranges high, and assumes 
 a septicemic type, running up to 102, 103, or 104 in some 
 period of the twenty-four hours, and dropping to 99 or 100 at 
 another. In the final stages, when the patient is exhausted 
 by the disease, it is frequently subnormal in the morning and 
 
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 TEMPERATURE CHART PROM CASE OP PERNICIOUS ENDOCARDITIS 
 
 only slightly above normal in the evening. Exacerbations 
 of temperature usually mark the occurrence of infarcts. 
 
 The above temperature chart, from the later stages of 
 a severe case, shows the extreme irregularity of tempera- 
 ture that may occur. 
 
 There was evidence of infarction of the kidney and spleen 
 respectively when the temperature rose to 103° and 104° F. 
 at the points marked A and B on the chart. 
 
 Infarction. — Infarction of the spleen will commonly be 
 attended with pain in the left hypochondriac region, with 
 tenderness of and possibly some enlargement of the spleen. 
 Infarct of the kidney is usually marked by pain in the 
 loin, followed by hematuria and albuminuria, but these may 
 
78 HEART DISEASE. 
 
 sometimes be absent, and hseroaturia may occur as a result 
 of nephritis without infarction. 
 
 Of the cerebral vessels, the middle cerebral artery is the 
 most common seat of embolism, an embolus being especially 
 liable to lodge where it divides into its four main branches 
 opposite the island of Eeil. 
 
 Hemiplegia may result with aphasia if on the left side ; 
 sometimes this may pass off in four to six days from shrink- 
 age of the embolus or establishment of some collateral 
 circulation. In a case of which the specimen is in the 
 St. Mary's Hospital Museum, a man of 23, suffering from 
 malignant endocarditis, suddenly became aphasic and lost 
 all power in his right side. In five days he had completely 
 recovered his speech and almost entirely the power in his 
 limbs. Post mortem the embolus was found to have lodged 
 in the left middle cerebral artery where it divides into its 
 main branches. The embolus had apparently shrunk, and 
 did not occlude two of the branches. 
 
 Embolism of the superior mesenteric artery may occur, 
 o-iving rise to gangrene of the small intestine, with symptoms 
 of collapse and shock followed by profuse melsena. 
 
 Embolism of the arteries of the extremities may cause 
 pain and temporary numbness with pallor and coldness of 
 the limb if a large vessel is blocked, but usually collateral 
 circulation is established and the symptoms pass off. 
 
 Aneurysms are occasionally met with as a result of 
 lodgment of emboli containing micro-organisms in an artery 
 and the destructive action of the toxins of the organisms in 
 the vessel wall. They may be multiple or single. In the 
 St. Mary's Hospital Museum is a specimen with thirteen 
 aneurysms of the coronary artery of the heart. I have seen 
 two instances of aneurysm of the gluteal artery, and one 
 of the femoral, and aneurysms of the cerebral and various 
 other arteries have been described, so that it would appear 
 that almost any artery may be affected. 
 
"MALIGNANT" OR "PERNICIOUS" ENDOCARDITIS. 79 
 
 Infarcts in the lung are exceptional, not merely because 
 the disease is commonly confined to the left side of the 
 heart, but because lodgment of an embolus in a small 
 branch of the pulmonary artery, if the valves of the right 
 side of the heart are affected, would probably not cause an 
 infarct, unless there is in addition extreme pulmonary con- 
 gestion from back working. 
 
 Sometimes numerous capillary embolisms occur, giving 
 rise to petechia? on the skin. 
 
 The Cardiac Murmurs. — The development of a murmur 
 in association with a previously healthy valve will, of course, 
 give a clue to the condition, but not infrequently the valve 
 attacked is already the seat of a previous lesion, and a 
 murmur may already be present. Change in the character 
 of the murmur should be carefully watched for and noted ; 
 it may become softer and weaker, or louder and musical. 
 The development of a fresh murmur at another orifice should 
 also be looked out for. 
 
 Anaemia is usually pronounced and progressive, and the 
 complexion assumes a waxy and sallow hue. 
 
 The Appetite may remain good and the tongue clean till 
 a very late stage in the disease, and gastro-intestinal 
 troubles are not usually marked, though diarrhoea is often 
 present in the septicemic types. 
 
 Diagnosis. — When a cardiac murmur of recent develop- 
 ment is present, associated with pyrexia, a high range of 
 temperature of an irregular or septicemic type and the 
 occurrence of embolism will usually enable a diagnosis to be 
 made early in the course of the disease. The persistence of 
 the irregular pyrexia, the progressive anaemia, the sallow 
 complexion, loss of flesh, and occurrence of embolism, will 
 afford confirmatory evidence of the malignant character of 
 the endocarditis. In young children we frequently meet 
 with prolonged subacute attacks of cardiac rheumatism, 
 in which a valvular murmur may be present, associated with 
 
8o HEART DISEASE. 
 
 pyrexia, lasting many weeks ; but in these cases recurrent 
 attacks of pericarditis are the rule, and this, with the 
 accompanying myocarditis leading to cardiac dilatation, is 
 the more serious malady, and is readily recognized. It 
 would, indeed, seem that in young children we have a type 
 of pernicious pericarditis corresponding to the pernicious 
 endocarditis of adults. 
 
 When no murmur exists, or when a valvular murmur of 
 old standing is present, in association with pyrexia of unex- 
 plained cause, a differential diagnosis may have to be made 
 from typhoid fever, septicaemia, and acute miliary tubercu- 
 losis. Typhoid can, after a week or ten days, be identified 
 by the eruption of spots, abdominal symptoms, condition of 
 the tongue, and Widal's reaction. Septicaemia, in the 
 ordinary sense of the term, may be usually traced to some 
 source of septic infection, but inasmuch as pernicious endo- 
 carditis is a septicaemia complicated by a valvular lesion, 
 it is out of place to use the term " differential diagnosis " in 
 this connection. In acute miliary tuberculosis, if we cannot 
 discover any old tubercular lesion, we may have to wait till 
 definite signs in the lungs or the onset of tubercular 
 meningitis disclose its nature. 
 
 Change in the character of a pre-existing murmur, or 
 the development of a valvular murmur, and the occurrence 
 of embolism will usually, sooner or later, make clear the 
 nature of the malady in pernicious endocarditis. 
 
 In the acute cases cultures of micrococii can frequently 
 be made from 10 c.c. of blood withdrawn under aseptic 
 precautions by a sterile syringe from the median basilic vein, 
 and inoculated into suitable culture media. 
 
 It must be borne in mind that possibly the rheumatic 
 diplococcus is responsible for a certain number of cases, and 
 the culture media must be selected accordingly. These 
 micro-organisms do not flourish in broth or on agar, though 
 they may grow feebly, but, according to Poynton and 
 
"MALIGNANT" OR "PERNICIOUS" ENDOCARDITIS. Si 
 
 Paine, grow best in milk, so this, or blood agar, on which 
 Shaw * finds they grow freely, should be included. 
 
 Prognosis. — The prognosis is, as the name implies, very 
 grave. In the acute cases, when the temperature ranges 
 high, and embolism takes place early, recovery is rare, and 
 the disease may prove fatal in a few weeks. In the more 
 chronic cases of insidious onset, unexpected recovery some- 
 times takes place after the lapse of two months or more, 
 when the patient seems almost reduced to the last extremity. 
 That a certain proportion of cases recover in which severe 
 ulceration of the valves has taken place, attended with 
 infarction of the kidney or spleen, is demonstrated from 
 time to time by post-mortem examinations, in which greatly 
 deformed cicatrized valves or cicatrices on the endocardium 
 and old cicatrized infarcts are found some years later. In 
 a large group of cases, in which there is no evidence of 
 infarction, the lesions found in the valves indicate that 
 extensive ulceration and destruction must have taken place 
 during the attack of acute endocarditis. The two last- 
 mentioned groups could scarcely be classified as "malig- 
 nant," inasmuch as the acute disease did not prove fatal, 
 though they were undoubtedly instances of " ulcerative 
 endocarditis." The question of prognosis will therefore vary 
 with the degree of virulence of the causative micro-organ- 
 ism and the resistance of the individual, as evidenced by the 
 formation of protective substances in the blood, or the reverse. 
 
 Treatment. — Various drugs have been tried without any 
 appreciable result. Salicylates are useless : salol, sulpho- 
 carbolate of soda, and benzoate of soda have been freely 
 given, but have not proved to be of service. Perchloride of 
 mercury, administered freely, has seemed to be efficacious 
 in some cases. General tonics, such as iron quinine and 
 strychnine, are of most value, as they help to maintain the 
 
 * Etiology of Acute Rheumatic Fever, Journal of Path, and Bad. 
 December, 1903. 
 
82 HEART DISEASE. 
 
 strength, of the patient, though they are not in any sense 
 a specific remedy. Citric acid may be given with advantage, 
 as it reduces the coagulability of the blood by combining 
 with the calcium salts, and thereby lessens the tendency to 
 formation of clot on the diseased valve and the chances 
 of embolism. Possibly thymus gland may be of service by 
 stimulating the production of leucocytes. 
 
 Good results have been claimed from time to time by 
 various authors from the injection of antistreptococcic 
 serum. As the disease may be set up possibly by the 
 rheumatic organism, possibly by streptococci, or pneumo- 
 cocci, or gonococci, it is obvious that the indiscriminate 
 use of a so-called antistreptococcic serum is not rational 
 or scientific, even if one were sure that the serum really 
 possessed any antitoxic substances, and this we have as 
 yet no accurate means of determining. 
 
 CHBONIC ENDOCARDITIS. 
 
 Under this heading are comprised certain chronic de- 
 generative changes in the valves which set in insidiously 
 in later life, and are usually associated with degenerative 
 changes in the aorta. They are to be distinguished from 
 chronic valvular lesions, which are the result of cicatrization 
 after an attack of acute endocarditis. 
 
 Morbid Anatomy. 
 The valves become thickened and opaque and lose their 
 elasticity. The aorta is usually dilated and atheromatous. 
 The aortic valves are chiefly affected, and though there is 
 no actual loss of substance, the rigidity of the cusps, together 
 with the dilatation of the aorta, occasions a certain degree of 
 incompetence. Sometimes calcareous plates may be present 
 in the aorta at the root of the valves, and project into the 
 cusps themselves. A certain degree of obstruction may result, 
 giving rise to a systolic aortic murmur, but this may be due to 
 
CHRONIC ENDOCARDITIS. S3 
 
 roughening- of the valves without actual stenosis. The mitral 
 valve is affected to a less degree than the aortic, but becomes 
 thickened and opaque, and slight incompetence may result. 
 
 Etiology. — Among the recognized causes of chronic 
 degenerative valvular lesions are lead poisoning, gout, 
 kidney disease, and what Murchison termed lithfemia, from 
 excessive eating and drinking with defective elimination. 
 These are conditions associated with high arterial tension, 
 involving constant undue strain on the aorta and its valves. 
 
 Valvular change of like character is common in men 
 following certain arduous occupations, such as those of the 
 miner, collier, blacksmith, hammerman, and soldier. Here we 
 have undue intermittent pressure within the aorta. As was 
 pointed out by Clifford Allbutt, Fothergill, and others, in the 
 occupations mentioned the undue pressure is created by effort 
 in a constrained and cramped position, or by work of such 
 a character as to require prolonged closure of the glottis 
 and fixation of the chest by holding the breath, or by violent 
 muscular exertion constantly repeated throughout the day. 
 
 Heredity is an important factor in connection with high 
 arterial tension, due to gout or lithseinia, as the tendency 
 may be transmitted through many generations. 
 
 Age. — Degenerative changes in the valves usually set in 
 after middle life, from the age of 40 to 45 onwards, and are 
 frequently associated with degenerative changes in the 
 aorta or cerebral vessels. 
 
 In later life, apart from actual disease, there is a ten- 
 dency to thickening, opacity, and loss of elasticity in the 
 valves, which in some instances may give rise to a murmur. 
 
 Syphilis may be incriminated in a certain proportion of 
 cases, especially where degenerative changes occur early in 
 life. 
 
 The symptoms and physical signs vary according to the 
 valve affected, and are discussed later in the chapters on 
 the different valvular lesions. 
 
CHAPTER VI. 
 
 ETIOLOGY OF VALVDLAIi LESIONS. 
 
 Acute Endocarditis. — This is by far the most common cause 
 of valvular lesions. This has already been fully discussed 
 in a previous chapter. The acute inflammatory process 
 may rapidly impair the efficiency of the valve and render 
 it incompetent. Subsequent cicatricial contraction of the 
 fibrous tissue formed in the process of repair may still 
 farther impair its efficiency, or give rise to progressive 
 stenosis, which may result, in extreme cases, in a narrow 
 funnel-shaped rigid orifice less than half an inch in diameter. 
 
 Chronic Endocarditis, — Chronic endocarditis is an in- 
 sidious affection occurring in middle or later life, usually 
 due to high arterial tension, whether from gout, kidney 
 disease, or other causes, and intimately associated with 
 the degenerative change known as atheroma of the aorta. 
 The valves become thickened, and lose their elasticity, and 
 incompetence usually results from this in conjunction with 
 dilatation of the aorta. Syphilis may be a cause, especially 
 when atheroma of the aorta occurs early in life, associated 
 with degenerative change in the valves. 
 
 Rupture of a Valve. — Rupture of a valve is of rare 
 occurrence. It is usually the aortic valve which suffers, 
 and, except as a result of direct violence, the rupture will 
 nearly always have been preceded by disease in its 
 structure, and by the cause of such disease, high arterial 
 tension. The rupture usually takes place during some 
 severe muscular exertion, and is attended by great pain 
 
ETIOLOGY OF VALVULAR LESIONS. 85 
 
 in the region of the heart. It may be a complete or partial 
 rupture of one of the cusps of the aortic valve, or may be a 
 mere slit in it. 
 
 One or more tendinous cords of the mitral valve may be 
 found ruptured when this valve has been the seat of disease ; 
 but this occurrence can rarely be dated by any recognized 
 accession of symptoms, though it must give rise to a con- 
 siderable increase in the derangement of the circulation. 
 
 Dilatation of the Orifice of a Valve. — Dilatation of the 
 orifice may upset the functional efficiency of a valve while 
 the valve itself has not undergone any material change. 
 The aortic orifice is less liable to be stretched and enlarged 
 than the mitral, as would be expected from the difference 
 in the structures surrounding the two. It is only com- 
 paratively late in life that the strong fibrous ring at the 
 root of the aorta ever yields, and it will then only take 
 place as part of a general dilatation of the first part of 
 this vessel, the result of atheroma or chronic degenerative 
 changes. The usual result is more or less insufficiency 
 or regurgitation; but, paradoxical as it may appear, there 
 may actually be obstruction as well, the valves being rigid 
 and projecting, even during systole, across the dilated 
 mouth of the aorta. 
 
 Mitral insufficiency from failure of fairly healthy valves 
 to close the orifice is not uncommon. Sometimes the 
 orifice is very much enlarged, admitting four or five fingers 
 instead of three. Frequently, however, there is no stretch- 
 ing of the opening, and the valves themselves are un- 
 affected, although during life there has certainly been 
 regurgitation. Various explanations of this fact have been 
 offered. It has been supposed that irregular action of the 
 papillary muscles interferes with the accurate adjustment 
 of the valvular curtains ; and, again, that the papillary 
 muscles, being carried by dilatation of the ventricle so far 
 from the valvular ring that the tendinous cords are dragged 
 
86 HEART DISEASE. 
 
 down too far, do not allow the margins of the valves to meet 
 during the systole. 
 
 The real cause of the imperfect closure of the valves 
 is that originally suggested by Donald McAlister.* He 
 pointed out that an important factor in the valvular 
 mechanism is the active contraction of the mitral orifice 
 with the systole of the ventricle. We are accustomed to 
 imagine that this opening, like the aortic, is surrounded by 
 a strong fibrous ring, maintaining its form and patency 
 under all circumstances ; but this is not the case, as was 
 shown by Sibson in dissections and specimens, which I had 
 the pleasure of assisting him to prepare ; for it was demon- 
 strated that the mitral ring of fibrous tissue, taking its 
 origin from the central fibro-cartilage of the heart, gradually 
 thins out till at the opposite side of the orifice it is practically 
 non-existent. There is nothing, therefore, to keejD the mitral 
 orifice rigid, or prevent it from altering its shape ; hence we 
 find that, during systole, the transversely circular fibres of 
 the cardiac muscle, by their contraction, cause a narrowing 
 of the mitral orifice, and partially close it independently of 
 the valves. Such a closure is in effect a part of the 
 general obliteration of the ventricular cavity during systole. 
 When, therefore, there is dilatation of the ventricle, this 
 active constriction of the auriculo-ventricular opening is 
 imperfectly performed, and the valve fails to cover the 
 whole area of the orifice. 
 
 Mitral regurgitation caused in this way, may occur at 
 any period of life, and under very different conditions. The 
 cardiac dilatation may be the result of imperfect nutrition 
 in advancing years, or of debilitating influences, or it may 
 be induced by acute disease, such as enteric fever or acute 
 rheumatism. Perhaps the most common and important 
 cause is aneeinia ; it is most important because of its fre- 
 quency in young adults, and because, though curable, it 
 
 * British Medical Journal, August, 18S2. 
 
ETIOLOGY OF VALVULAR LESIONS. 87 
 
 is yet liable to be rendered permanent by imprudence 
 and neglect. George Balfour has rendered good service by 
 calling attention to this condition under the head of 
 " Curable Mitral Regurgitation." Now, although weakness 
 of the cardiac muscular fibres, or want of energy in their 
 contraction, is perhaps an essential condition in the pro- 
 duction of dilatation, another factor plays an important 
 part, namely, high arterial tension. We should not expect 
 anaemia to be attended with any such state of the circulation, 
 but this is very frequently the case in the ordinary type. 
 
 Pernicious anaemia, however, is less commonly attended 
 with high arterial tension, perhaps because of the frequent 
 intercurrent attacks of pyrexia ; for pyrexia, as is well 
 known, relaxes arteries and lowers the arterial tension. 
 
 It may be remarked in passing, that the low arterial 
 tension which accompanies pyrexia probably renders the 
 occurrence of dilatation of the ventricle much less frequent 
 in acute disease than we should expect as a result of the 
 debilitating effect of the accompanying myocarditis or 
 " cloudy swelling " of the muscular walls of the heart. 
 
 Mitral incompetence may, further, be a secondary con- 
 sequence of aortic incompetence, through the dilatation of 
 the left ventricle. But, unless cardiac debility have a share 
 in the production of this dilatation, a comparison between 
 it and the dilatation just spoken of is illusory. The one is 
 the result of asthenia, the other of over-distension of the 
 ventricular cavity ; in the one, the contraction of the 
 ventricle is never completed ; in the other, it is carried 
 through energetically. 
 
 Congenital Valvular Affections. — Lesions of one or more 
 of the valves of the heart are sometimes found at birth. 
 They may be the result of a congenital malformation, or 
 of endocarditis occurring while the foetus was in utero. In 
 the former case the pulmonic valve is most commonly at 
 fault, the lesion being usually constriction of the orifice, 
 
HEART DISEASE. 
 
 and frequently the valvular defect is associated with a 
 malformation of some other portion of the heart. In the 
 latter case the valves of the right side of the heart usually 
 suffer, but those of the left side may also be affected, the 
 aortic more commonly than the mitral. 
 
CHAPTER VII. 
 YALYULAE LESIONS. 
 
 POINTS TO BE CONSIDEEED IN STUDYING A CASE OF 
 VALVULAE DISEASE — THE PHYSICAL SIGNS— CAEDI AC 
 MUEMUES, THEIE SIGNIFICANCE AS EEGAEDS THE SEAT 
 AND AS EEGAEDS THE EXTENT OF THE LESION — 
 MODIFICATION OF HEAET-SOUNDS — THE PULSE, ITS 
 IMPOETANCE IN DIAGNOSIS. 
 
 Diseases of the heart are classified as structural and 
 valvular, according as the morbid change affects the 
 muscular walls or the valves. There are, again, functional 
 derangements which must be included among the affec- 
 tions of the heart. 
 
 The valvular lesions will be first discussed: they 
 are what is usually understood by heart disease, and are 
 most important because most numerous. We know more 
 about them, and can be more certain of their diagnosis, 
 thanks to the murmurs to which alterations in the valves 
 give rise. We are also in a better position to estimate 
 the extent of the lesion, and to give an accurate prognosis 
 in valvular disease than in structural. The estimation of 
 the obstruction produced by a certain degree of narrowing 
 of one or other orifice, or of the amount of reflux resulting 
 from incompetence of a given valve, is a problem of hydro- 
 statics capable of solution, but no such definite conclusion 
 can be arrived at, when in structural disease we have to 
 form an opinion as to the contractile power and durability 
 of muscular fibres in a certain stage of degeneration. 
 
9 o HEART DISEASE. 
 
 The Clinical Study of Yalvulae Disease. 
 
 In studying a case of valvular disease of the heart, 
 the following are the points which must be taken into 
 consideration : — 
 
 1. The valve affected, and the relative danger attaching 
 
 to the particular lesion. 
 
 2. The actual condition of the orifice and valve — the 
 
 degree of obstruction or amount of regurgitation to 
 which the lesion has given rise. 
 
 3. The origin of the lesion, whether due to acute 
 
 rheumatism, degenerative changes, or other causes. 
 
 4. The degree of soundness and vigour, functional and 
 
 nutritional ; firstly, of the muscular substance of 
 the heart itself; secondly, of the tissues generally. 
 How far, in fact, and for how long compensatory 
 changes can be counted upon. In considering this 
 question, family history will have an important 
 place. 
 
 Localization of the Valvular Disease. — Significance 
 of the Cardiac Murmurs. 
 
 The chief guide in localizing disease in the valves of 
 the heart is a murmur, produced, either by obstruction to 
 the current of blood when one or other orifice is narrowed 
 or roughened, or by regurgitation of the blood when a 
 valve no longer closes perfectly. The term stenosis or 
 constriction is employed to denote the condition of an 
 orifice which is narrowed, the result of the narrowing being 
 obstruction : the term insufficiency or incompetence is 
 employed to characterize the state of a valve which fails to 
 close the opening it ought to protect, while regurgitation 
 or reflux expresses the functional effect. It is well, as far 
 as possible, to observe the distinction between the names 
 
THE CARDIAC MURMURS. 91 
 
 indicative of structural change and those expressive of 
 functional derangement resulting therefrom, but the terms 
 " obstruction " and " regurgitation " are in such familiar use 
 that they are frequently employed when "stenosis" and 
 " insufficiency " would be more exact. 
 
 By means of the murmurs we learn definitely which 
 valve is affected and what is the nature of the affection — 
 whether such as to produce obstruction or regurgitation — 
 but they fail altogether by themselves to indicate the 
 amount of damage which a valve has sustained. A loud 
 murmur may be produced by a very slight change, and 
 a murmur which is scarcely audible may be indicative of 
 extensive destruction of valves. Some information, however, 
 may be gathered from a careful study of murmurs. 
 
 Different Characters of Murmurs : their Value as 
 regards Estimation of the Extent of the 
 Valvular Lesion. 
 
 Murmurs may be compared or contrasted in several 
 respects : in intensity, they may be loud or soft ; in duration, 
 they may be long or short ; they may be blowing, or musical, 
 or mixed, rough and vibratory, or smooth. Again, they may 
 begin with an accent, or rise gradually to a maximum 
 intensity. 
 
 A loud murmur is, on the whole, of less serious import 
 than one which is weak and soft. It is, at any rate, 
 indicative of force in the heart's action, and of vigour in the 
 movement of the blood ; and weakness of the heart con- 
 stitutes the greatest of all dangers. Then, again, although 
 a rough edge to a large opening in aortic or mitral 
 incompetence may generate vibrations which will produce 
 a loud murmur, a mere slit in a membranous valve, or a 
 shred of fibrin hanging by one end, is more likely to have 
 such an effect. 
 
92 HEART DISEASE. 
 
 In a case seen with. Dr. Parrott of Hayes, a systolic 
 mitral niurinur, of such intensity as to be heard distinctly 
 across a billiard-table, had been present for fifteen or twenty 
 years without giving rise to symptoms, until dilatation of 
 the heart was induced by extreme over-exertion. Another 
 very loud murmur which came under my notice was attended 
 with no important symptoms for the several months during 
 which the patient was under observation. It was systolic 
 aortic, and could be heard half a yard or more from the 
 chest, through the man's clothes. In another case, a 
 murmur almost as loud was found, after death, to be due 
 to a delicate fibrinous thread at the free margin of one of 
 the aortic valves. 
 
 On the other hand, cases are met with in which the 
 pulse may indicate serious aortic regurgitation while no 
 diastolic murmur can be heard, and a murmur gradually 
 develops itself as the patient gains strength and recovers 
 from a state of extreme prostration; and it is common in 
 mitral stenosis for murmurs to disappear with the super- 
 vention of serious symptoms, and to reappear as these are 
 abated by treatment. It must not be concluded that a soft 
 or weak murmur is necessarily indicative of either a failing 
 heart or greatly damaged valve ; but a diminution in the 
 intensity of a murmur, gradual or sudden, may confirm 
 unfavourable indications given by symptoms. 
 
 The character of a murmur — its roughness or vibratory 
 character or smoothness — may have diagnostic significance, 
 as will be pointed out later, but it does not give any infor- 
 mation with regard to the extent of structural change or 
 functional derangement. A musical murmur would seem 
 to require for its production either a very fine chink with 
 thin margins, or a thin membrane capable of vibrating like 
 a string, and would therefore seem to be inconsistent with 
 serious disease ; but this cannot be laid down as an absolute 
 rule. A musical note is often heard in the midst of a blowing 
 
MODIFICATIONS OF THE SOUNDS OF THE HEART. 93 
 
 murmur or at the beginning or end of such a murmur. A 
 long murmur, except in the case of mitral or aortic stenosis, 
 is usually indicative of early and comparatively slight dis- 
 ease and of efficient action of the heart. A short murmur 
 may be innocent of prognostic import, but it is very 
 frequently an indication of ruined valves and of a failing 
 heart : it may, for instance, indicate that the orifice is so 
 patent, say, in aortic insufficiency, that the refluent blood 
 passes through it rapidly and with little hindrance ; or in 
 mitral disease, that the systole is brief and imperfect, the 
 heart being on the point of breaking down. 
 
 The accent at the beginning of a murmur is chiefly 
 observed in the regurgitant diastolic murmur of aortic 
 insufficiency where it represents the second sound, and it 
 is important as showing that the valves still act as a check 
 on the reflux of blood from the aorta. It has the same 
 significance in a minor degree as persistence of the aortic 
 second sound — a very important fact, which will be fully 
 explained later, in the chapter on aortic regurgitation. 
 
 It will thus be seen that the murmurs, while pointing 
 out distinctly and certainly what valve is affected, afford also 
 some information as to the extent of change which has 
 taken place, though only of a vague character. 
 
 Modification of Heaet-Sounds. 
 
 The heart-sounds may be modified by murmurs in 
 various ways. A mitral systolic or an aortic diastolic 
 murmur may accompany, replace, or follow the sound with 
 which it is associated in the cardiac cycle. Generally 
 speaking, when the heart-sound is distinctly heard as well 
 as the accompanying murmur, the lesion is slight : when, 
 on the contrary, it is entirely replaced by the murmur, the 
 lesion is probably severe. 
 
 When a mitral murmur follows the first sound at a brief 
 
94 HEART DISEASE. 
 
 but appreciable interval, constituting a " retarded systolic " 
 murmur, it seems to show that the valves come together 
 accurately at first, but fail to remain in apposition through- 
 out the whole period of the ventricular contraction. It 
 indicates, therefore, that the changes in the valves, and 
 consequently the amount of leakage, can only be slight. 
 A " retarded diastolic " aortic murmur is sometimes met 
 with, but it has not the same favourable significance. 
 
 The first sound in association with the presystolic 
 murmur of mitral stenosis may be greatly modified. It is 
 not replaced by the murmur, but is usually altered in 
 character, becoming short, sharp, and high-pitched. 
 
 The Pulmonic Second Sound. 
 
 i 
 
 This is usually accentuated to a varying degree in 
 mitral affections, owing to increase of pressure in the 
 pulmonary circulation. There are two factors instrumental 
 in causing this increase of pressure — obstruction to the 
 outflow of blood from the pulmonary veins into the left 
 auricle, due to the mitral lesion; and increased driving 
 power of the right ventricle, the result of compensatory 
 hypertrophy. The degree of accentuation of the pulmonic 
 second sound depends on the degree of pressure in the 
 pulmonary circulation : it will thus afford important 
 evidence as to the amount of reflux or obstruction caused 
 by the mitral lesion, and also as to the state of efficiency 
 of the right ventricle. For instance, if in a case of 
 mitral disease the pulmonic second sound is greatly 
 accentuated, it will tend to show that the mitral lesion is 
 one of some severity, and, as confirmatory evidence, we 
 should expect to find hypertrophy of the right ventricle. 
 Bronchitis, or any intercurrent lung trouble, increasing the 
 obstruction to the flow of blood through the lungs, will 
 tend to cause still greater accentuation of the pulmonic 
 
ALTERATIONS IN THE CARDIAC RHYTHM. 95 
 
 second sound, provided that the right ventricle does not 
 break down under the strain. If in a severe case of mitral 
 disease the pulmonic second sound, from being greatly 
 accentuated, becomes feeble or much diminished in in- 
 tensity, it will indicate, not, of course, that the valvular 
 lesion is less, but that the right ventricle is beginning to 
 fail. 
 
 The aortic second sound will be accentuated when the 
 tension in the systemic circulation is high from any cause ; 
 it will be altered in intensity and pitch in aneurysm, or in 
 dilatation of the aorta. 
 
 Reduplication of Heart-Sounds. 
 
 Reduplication of the second sound heard at the apex of 
 the heart indicates that the pulmonic and aortic valves 
 do not close synchronously. It is of common occurrence 
 in mitral disease, especially in mitral stenosis, when it 
 indicates that the pressure in the pulmonary circulation 
 has become so considerable as to cause the pulmonic valves 
 to close before the aortic. 
 
 Reduplication of the first sound heard at the apex in- 
 dicates that the two ventricles do not accomplish their 
 systole simultaneously, owing to the fact that one is 
 beginning to give way under extra strain imposed on it. 
 It is not infrequently met with in advanced aortic stenosis, 
 or in cases of high arterial tension, such as results from 
 kidney disease; it will then show that the left ventricle 
 is beginning to fail. 
 
 Alterations in the Cardiac Rhythm. 
 
 Intermission is less frequent than irregularity as a result 
 of valvular disease. The particular affections in which 
 this deviation from the normal rhythm is most liable to 
 occur are aortic incompetence, when it indicates a faltering 
 
96 HEART DISEASE. 
 
 of the heart's action, and certain functional disturbances 
 due to a reflex from gastric troubles. Irregularity is 
 very common as a result of mitral incompetence, when it 
 is not of serious import. It may also occur in association 
 with fibroid degeneration of the heart walls in conjunction 
 with general arterio-sclerosis, when the prognosis is grave, 
 as death may occur from a syncopal attack, or hemiplegia 
 result from rupture of a cerebral vessel. 
 
 THE PULSE. 
 
 Information to be gathered from the Pulse as to 
 the Nature and Extent of Valvular Lesion. 
 
 In aortic stenosis the artery will be somewhat small, and 
 full between the beats ; the initial percussion-wave will be 
 slight and gradual, and the pulse-wave prolonged. This 
 modification of the pulse is due to the fact that the blood 
 has to pass through a narrowed orifice on its way from the 
 left ventricle into the aorta. Hence the impact of the 
 systole upon the column of blood in the aorta will be 
 diminished, and more time will be required for the passage 
 of the contents of the ventricle into the arterial system. 
 
 In aortic incompetence we have the well-known collapsing 
 or water-hammer pulse ; the artery is large, and empty 
 between the beats ; the pulse-wave is sudden, forcible, short, 
 and ill-sustained, and its cessation is very abrupt. 
 
 In mitral stenosis the artery is small, full between the 
 beats, with higher tension than would be expected, and the 
 pulse-wave is long. 
 
 In all these three forms of valve-lesion the pulse is 
 regular till the heart begins to break down. 
 
 In mitral regurgitation, on the other hand, the pulse is 
 usually irregular, both in force and frecpuency, if the lesion 
 
THE PULSE IN VALVULAR LESIONS. 97 
 
 is at all severe. The pulse-wave is also short, and passes 
 the finger rapidly. 
 
 The characteristics of the different types of pulse, as 
 brought out by the sphygmograph, are shown in the accom- 
 panying tracings. 
 
 FIG. 11. — AOKTIC STENOSIS. 
 
 FIG. 12. AOKTIC INCOMPETENCE. 
 
 FIG. 13. — MITRAL STENOSIS. 
 
 FIG 14. — MITRAL INCOMPETENCE. 
 
 In Fig. 11, the pulse of aortic stenosis, it will be seen 
 that the wave is of little altitude, and has a sloping 
 upstroke, with a rounded top and a gradual descent ; that 
 is to say, the wave is small, and attains its maximum 
 gradually, is persistent or long, and subsides slowly. There 
 
 H 
 
98 HEART DISEASE. 
 
 is no dicrotic wave, as the conditions necessary for its pro- 
 duction, great fluctuation of the blood-pressure and rapid 
 contraction of the ventricle, are absent. 
 
 In Fig. 12, the pulse of aortic incompetence, the upstroke 
 is high, perpendicular, has a sharp top, and falls rapidly ; 
 that is, the wave is large, owing to the size of the artery, 
 is sudden and rapidly attains its maximum, is very short 
 and rapidly falls. Dicrotism is not altogether absent, but, 
 owing to want of the fulcrum formed by the aortic valves, 
 it is much less marked than might be exj)ected from the 
 violence of the fluctuations and the rapidity of the systole. 
 
 In Fig. 13, the pulse of mitral stenosis, the upstroke or 
 percussion-wave is short, and soon attains its maximum ; 
 the wave is long, and is slowly extinguished. Dicrotism 
 is absent. 
 
 In Fig. 14, the pulse of severe mitral incompetence, the 
 tracing shows that the pulse is very irregular both in force 
 and frequency ; the wave is short and small, and ill-sustained. 
 When, however, the amount of regurgitation is slight and 
 compensation is good, the pulse will usually be regular. 
 
 The character of the pulse, therefore, affords important 
 information as to the nature of the lesion ; while the degree 
 in which the special peculiarities are developed, in each 
 instance gives some clue to the extent of the valvular 
 mischief. The pulse, however, may be modified in various 
 ways; for instance, where aortic stenosis co-exists with 
 regurgitation, the collapsing and sudden character of the 
 regurgitant pulse will, to a great extent, be lost. Such 
 modification, when present, is in itself a valuable help to 
 diagnosis, as it enables us to say with certainty that there 
 is real aortic stenosis, and not merely roughening of the 
 aortic valves, either of which might be indicated by the 
 presence of a systolic basic murmur. 
 
 Much information may thus be gained from the pulse ; 
 but the character of the pulse, even when taken in 
 
THE PULSE IN VALVULAR LESIONS. 99 
 
 connection with the murmurs, is not sufficient to enable 
 us to estimate the degree of obstruction or the amount of 
 regurgitation in a given case. Further indications are to 
 be obtained, firstly, from the effects on the cavities and 
 walls of the heart produced by the mechanical difficulties 
 resulting from the valvular imperfections ; secondly, from 
 the evidences of obstructed circulation in the lungs or 
 system. 
 
CHAPTEK VIII. 
 
 THE IMPOETANCE OP HYPEETEOPHY AND DILATATION OF 
 THE HEAKT AS A MEANS OF ESTIMATING THE EXTENT 
 OF A VALVULAE LESION — POSSIBLE OBJECTIONS TO THIS 
 VIEW DISCUSSED— EXPLANATION OF THE WAY IN WHICH 
 THE DIFFEEENT VALVULAE LESIONS GIVE EISE TO 
 HYPEETEOPHY AND DILATATION : (1) AOETIC STENOSIS ; 
 (2) AOETIC INCOMPETENCE ; (3) MITEAL EEGUEGITA- 
 TION; (4) MITEAL OBSTEUCTION — COMPENSATION. 
 
 The most important indications as to the extent of a 
 valvular lesion are to be gathered from its effects on the 
 walls and cavities of the heart, resulting in hypertrophy of 
 the former and dilatation of the latter. These changes are 
 due to the efforts of the heart to overcome the mechanical 
 difficulties in the circulation occasioned by the regurgitation 
 or obstruction to which the valvular lesion has given rise. 
 
 Hypertrophy and dilatation must be looked upon as 
 caused by the valvular lesion, and as affording a measure 
 of its extent. The degree of these structural changes is 
 ascertained by the increased area of deep cardiac dulness, 
 by the displacement and modification of the apex beat, by 
 the situation and character of the impulse, and by associated 
 changes in the character and rhythm of the heart-sounds ; 
 the more pronounced these changes, the greater is the 
 mechanical difficulty in the propulsion of the blood, and the 
 more grave is the prognosis. 
 
 Not that a given degree of hypertrophy or dilatation, 
 
IlYPERTROriTY AND DILATATION OF THE HEART. 101 
 
 or of the two combined, is indicative in all cases of the 
 same extent of valvular change. Each kind of valvular 
 disease has its own special form and degree of structural 
 change, and comparisons, to be valid, must be made between 
 like cases ; a degree of hypertrophy and dilatation, which 
 would have little significance in aortic insufficiency, might 
 indicate a serious amount of mitral regurgitation ; and 
 again, mitral stenosis, which has reached a dangerous 
 degree, may be attended with less conspicuous structural 
 change than a degree of mitral insufficiency which gives 
 rise neither to danger nor to inconvenience. It will be 
 well, indeed, to exclude mitral stenosis while the general 
 question under consideration is argued out. Numerous 
 other modifying influences are also in operation, so that, 
 while it is generally true that the greater the dilatation and 
 hypertrophy, the greater the functional imperfection of the 
 valves, the converse statement, that the less the hypertrophy 
 or dilatation, the smaller the valvular damage, must not be 
 taken without important qualifications. This statement is 
 indeed usually true in the absence of serious symptoms, but 
 sometimes the very failure of the heart to undergo the 
 changes required for the compensation of valvular in- 
 efficiency causes severe embarrassment of the circulation, 
 and gives rise to an early fatal termination. 
 
 It is stated by Walshe, and is undoubtedly true, that no 
 direct ratio constantly holds good between the amount of 
 hypertrophy and valvular change, as ascertained by post- 
 mortem examinations. This, however, is capable of explana- 
 tion, if we take into account the various circumstances that 
 may modify the development of the hypertrophy. 
 
 Firstly. The age of the patient at the time when the 
 lesions of the valves take place is an important factor. The 
 enormous hypertrophy and dilatation sometimes met with 
 are produced almost exclusively in early life, when the 
 heart is still developing and its muscular substance is 
 
io2 HEART DISEASE. 
 
 capable of active growth ; later, trie heart loses its adaptive 
 capability in great measure, and thus a valvular lesion 
 which, at the age of fifteen or twenty, would be survived 
 with enormous hypertrophy, would at forty or fifty prove 
 fatal with very little change. 
 
 Secondly. Time is an important element in the develop- 
 ment of hypertrophy, which may take years to reach its 
 maximum growth ; and it is often very difficult to assign 
 a date to the origin of a given morbid condition. For 
 instance, of two cases in which the extent of the valvular 
 mischief, as seen by post-mortem, is apparently the same, 
 in one the heart may be found to be considerably hyper- 
 trophied, because the patient did not at once succumb to 
 the injury ; in the other there is perhaps little hypertrophy 
 but great dilatation, because the difficulty of carrying on 
 the circulation increased more rapidly than the power of the 
 heart to cope with it, so that death occurred quickly. 
 
 Thirdly. We must take into account the fact that 
 different affections of the valves have inherently and 
 mechanically different degrees of tendency to the pro- 
 duction of structural alterations. For instance, aortic in- 
 competence gives rise to enormous hypertrophy of the left 
 ventricle, whereas mitral incompetence gives rise to very 
 moderate hypertrophy, and uncomplicated mitral stenosis 
 to atrophy rather than hypertrophy. 
 
 Fourthly. The mode of life, whether active and accom- 
 panied by considerable muscular exertion, or sedentary and 
 unattended by anxiety and excitement, will be an important 
 consideration. The amount of work the heart is called upon 
 to do will vary in each instance, and the hypertrophy will 
 vary in direct proportion. 
 
 Again, the presence of high tension in the vascular 
 system will tend to increase the degree of hypertrophy to 
 a considerable extent. 
 
 Fifthly. The period after the occurrence of the valvular 
 
HYPERTROPHY AND DILATATION OF THE HEART. 103 
 
 change at which active exertion is undertaken, allowing or 
 not allowing the heart to adapt itself gradually to this 
 change, will have great influence on the condition of its 
 walls and cavities. For example, after endocarditis, which 
 has given rise to damage of the aortic or mitral valve, one 
 patient has prolonged rest, care, comforts, and change of air, 
 so that dilating influences are postponed by the rest while 
 the heart is weak and liable to yield, and the muscular 
 walls are enabled, by a good state of nutrition, to resist 
 dilatation ; another must return to work, or is allowed to 
 exert himself before the heart has recovered from the effects 
 of the illness, and its badly nourished fibres give way and 
 permit of dilatation, which will be followed later, if the 
 patient lives, by hypertrophy. 
 
 We have in the above conditions the quota of causation, 
 beyond the mechanical difficulty at the valves, which 
 explains the variation observed ; and it will be evident, 
 from these considerations, that an unvarying direct ratio 
 between the valvular and structural changes is not to 
 be looked for, and that its absence furnishes no valid 
 objection to their standing in the relation of cause and 
 effect. 
 
 Mechanism of Causation op Hypeeteophy in the 
 dlffebent valvulae diseases : its beneficial 
 
 Effects. 
 
 Aortic Stenosis. — Taking first the most simple case. If 
 the constriction of the aortic orifice is sufficient in amount 
 to give rise to mechanical obstruction to the flow of blood 
 through it, there must either be increase in the propulsive 
 power of the heart, or a slowing of the circulation ; for it 
 is obvious that the same force will not propel the same 
 amount of blood in the same time through a narrowed 
 orifice as through one of normal size. We find, however. 
 
io4 HEART DISEASE. 
 
 that the rate of circulation is maintained, the increased 
 power necessary to drive the blood through the narrowed 
 orifice at a more rapid rate being gained by hypertrophy 
 of the heart, which takes place to a degree necessary to 
 overcome the obstruction. This is a simple illustration of the 
 physiological law, that increased functional activity gives 
 rise to increase of structure. If the hypertrophy did not 
 take place, there would be a slowing and finally a standstill 
 of the circulation. 
 
 Aortic Insufficiency. — In this lesion a certain proportion 
 of the blood driven into the aorta at each systole returns 
 into the ventricle through the leaking valves ; conse- 
 quently, in order that the same rate of circulation may be 
 maintained, there must be either an increase in the number 
 of heart-beats per minute, or an increase in the quantity of 
 blood expelled by the ventricle at each contraction. Mere 
 augmentation of the force of the systole would not answer 
 the requirement : for instance, if five ounces of blood are 
 driven into the aorta at each systole, and one ounce re- 
 turns, the normal, supply of blood would obviously not be 
 maintained by propelling the five ounces more forcibly ; 
 what is needed is that six ounces of blood should be driven 
 into the aorta, so that when one ounce has regurgitated 
 into the ventricle, five ounces would still remain in the 
 arterial system. This requirement is met by an increased 
 capacity of the left ventricle, which is the primary com- 
 pensatory change taking place in aortic insufficiency. 
 Increased capacity is, in other words, dilatation. In this 
 instance, therefore, dilatation of the left ventricle, which 
 under other conditions is injurious, is actually a beneficial 
 and conservative change when reinforced by hypertrophy, 
 and this we shall see is a natural sequence. 
 
 It is true there is no direct provocation to hypertrophy in 
 the shape of increased resistance to the blood-flow ; but there 
 is a call for increased exercise of force in the additional 
 
HYPERTROPHY AND DILATATION OF THE HEART. 105 
 
 quantity of blood to be projected from the ventricle into 
 the aorta at each systole. Further, the total internal area 
 of the walls of the ventricle is greatly increased owing 
 to the increase in its capacity, while the same pressure is 
 exerted on each square inch during systole, hence the 
 amount of force to be exercised by the muscular walls of 
 the heart must be proportionately augmented. These two 
 causes give rise to the hypertrophy present in so remark- 
 able a degree in aortic regurgitation. 
 
 It must not be supposed that, because the dilatation which 
 takes place in aortic regurgitation is compensatory and 
 necessary, this is a sufficient explanation of its occurrence. 
 It is produced in the following way : During diastole, the 
 most defenceless period of the heart in the cardiac cycle, 
 when the muscular fibres are in a state of relaxation, the 
 ventricle is exposed to a double distending force. Firstly, 
 the entry of blood from the left auricle and pulmonary 
 veins ; secondly, the backward rush of the blood from the 
 aorta: the greater the amount of the regurgitation, the 
 greater will be the distending force, and consequently 
 the greater the dilatation of the left ventricle. This dila- 
 tation, however, is a totally different thing from the dilata- 
 tion which is sometimes met with as the result of structural 
 change and degeneracy of the muscular walls of the heart : 
 in the latter case, the walls yield because they are in- 
 herently weak, and the effect on the circulation is dis- 
 astrous, a gradually increasing stagnation from deficient 
 vis a tergo ; in the former case the walls yield, not because 
 they are weak, but because they are subjected to an 
 abnormal distending force while in a condition of relaxation 
 and least able to resist it ; ultimately, when this dilatation 
 is backed by hypertrophy, the effect on the circulation ig 
 beneficial, since it neutralizes, more or less completely, the 
 tendency to stagnation produced by the regurgitation. 
 
 When, however, aortic regurgitant disease is set up late 
 
ro6 HEART DISEASE. 
 
 in life from degenerative changes in the valves, there is 
 frequently also degeneration and consequent weakening of 
 the muscular substance of the heart ; then, owing to the 
 inherent weakness of the walls of the heart, the dilatation 
 due to the aortic regurgitation will be excessive, unless 
 the case is cut short by sudden death, and, as there is 
 little chance of sufficient compensatory hypertrophy taking 
 place, the condition will be one of distress and danger, if 
 the regurgitation is extensive. 
 
 MlTKAL BeGURGITATION AND MlTRAL OBSTRUCTION. 
 
 In affections of the mitral valve the effects of the 
 derangement of the circulation due to the lesion no longer 
 fall mainly on the left ventricle, but primarily on the left 
 auricle and lungs, and eventually on the right ventricle. 
 The left auricle in mitral lesions corresponds in its relation 
 to the current of blood to the left ventricle in aortic lesions ; 
 hence, by analogy, in mitral regurgitation, we should expect 
 to find hypertrophy and dilatation, and in mitral obstruction 
 marked hypertrophy of the left auricle. This is what occurs 
 to a certain extent, but as the auricle is thin walled and 
 poor in muscular substance, it is impossible for it to take 
 on hypertrophy and compensate for the mitral lesions in 
 the same way that the ventricle does for aortic lesions; 
 it may, indeed, be distended so as to form a thin walled 
 sac of considerable size. The result is that the burden of 
 the work of compensation is thrown on the right ventricle 
 by back pressure through the pulmonary circulation, which 
 thus becomes the channel through which the effects of the 
 mitral regurgitation or obstruction are transmitted from the 
 left auricle to the right ventricle. We find, therefore, 
 that the right ventricle undergoes hypertrophy and dila- 
 tation as a result of mitral lesions, while the pressure 
 
HYPERTROPHY AND DILATATION OF THE HEART 107 
 
 in the pulmonary circulation, the connecting channel, is 
 enormously increased. 
 
 It thus comes to pass that the right ventricle, by the 
 additional force it gains from hypertrophy and the ad- 
 ditional capacity it gains from dilatation, aids in supplying 
 the left ventricle with blood, and in neutralizing the dis- 
 turbing effects of mitral lesions on the circulation ; for the 
 increased pressure in the pulmonary system and left auricle 
 will send the blood more rapidly through a constricted 
 orifice in case of mitral stenosis, and will resist the regur- 
 itation in mitral incompetence. 
 
 Dilatation of the Left Venteicle in Miteal 
 Incompetence. 
 
 A certain limited amount of dilatation and hypertrophy 
 of the left ventricle, as well as of the right, takes place 
 in mitral incompetence, the explanation of which is as 
 follows : — 
 
 During diastole, in consequence of the increased pressure 
 in the pulmonary circulation and left auricle, the blood 
 will rush through the mitral orifice with greater force and 
 rapidity than normal ; hence the pressure on the walls of 
 the left ventricle will be greater than normal, and the 
 muscular fibres, being relaxed and defenceless, readily yield 
 to the extra distending force : in this way some degree of 
 dilatation results. Then as the dilatation increases the 
 area of ventricular wall exposed to pressure, it increases 
 also the amount of work to be done in systole, and thus 
 creates a demand for hypertrophy, which also takes place 
 to a moderate extent. 
 
 In mitral stenosis, though there is increased pressure 
 in the pulmonary circulation which would tend to cause 
 dilatation of the left ventricle during diastole in the same 
 way as in mitral incompetence, the mitral orifice, being 
 
ioS HEART DISEASE. 
 
 narrowed, does not allow a volume of blood, sufficient to 
 exert a distending force, to pass through ; indeed, in severe 
 cases, the constriction may be so great that the ventricle 
 has never time to fill during diastole, so that it tends rather 
 to decrease in size than dilate, and there will be no demand 
 for hypertrophy. 
 
 In incompetence of the mitral valve, therefore, the amount 
 of hypertrophy and dilatation of the right ventricle and 
 the degree of pressure in the pulmonary circulation are 
 among the most important indications of the extent of the 
 lesion. 
 
 In mitral stenosis this holds good up to a certain point, 
 but the changes in the right ventricle are not so safe a 
 guide, since the dilatation and hypertrophy sometimes 
 appear to be restricted in extent by the absence of accom- 
 panying changes of a similar character in the left ventricle, 
 which remains very small. 
 
 Compensation. 
 
 It has thus been seen that dilatation and hypertrophy 
 of the left or right ventricle or of both are a necessary 
 consequence of valvular disease of any severity, if the 
 patient lives, and the mechanism of their production has 
 also been discussed. These changes in the cardiac walls 
 are spoken of as compensatory, that is, they are changes 
 which must take place to enable the heart to cope with 
 the extra work thrown upon it as a result of the valvular 
 lesions ; in the case of aortic disease it is the left ventricles 
 in the case of mitral lesions the right ventricle, more 
 especially, which undergoes compensatory changes. Com- 
 pensation is said to be established when the hypertrophy 
 and dilatation, the former especially, have so far developed 
 that they neutralize the disturbing effects on the circulation 
 which the valvular lesions would otherwise produce, and 
 
COMPENSATION. 109 
 
 enable the patient to live his ordinary life without dis- 
 comfort, and without any marked symptoms. 
 
 When compensation is imperfect, the symptoms incident 
 to the valvular disease from which the patient is suffering 
 will present themselves more or less readily under moderate 
 exercise or exertion, their severity varying inversely with 
 the degree of compensation established. 
 
 For instance, a boy who is allowed to go about imme- 
 diately after he has contracted a valvular lesion of some 
 severity, and is suffering, say, from aortic incompetence, 
 will be extremely short of breath, and incapable of walking 
 any distance, will have attacks of severe pain in the pra3- 
 cordium, and perhaps fainting fits, one of which may prove 
 fatal ; whereas the same patient, if he is kept at rest till the 
 compensatory changes have had time to develop, will be 
 able to take moderate exercise comfortably and go about 
 his work free from pain or respiratory distress, though he 
 may be incapable of any prolonged or violent exertion. 
 
 In mitral disease dyspnoea, cyanosis, and oedema of the 
 lower extremities are among the earlier symptoms of failing 
 compensation. In the later stages one of the most impor- 
 tant guides as to the state of compensation is the size of the 
 liver. When this organ becomes engorged and enlarged, 
 owing to obstruction to the flow of blood from the inferior 
 vena cava to the right auricle, it will indicate that the 
 right ventricle is unable to cope efficiently with the in- 
 creased pressure in the pulmonary circulation caused by 
 the mitral lesion, and consequently that compensation is 
 imperfect. A further indication will be pulsation and 
 fulness of the veins of the neck, which may sometimes be 
 seen to fill from below. The liver may attain a consider- 
 able size, extending below the umbilicus, and may even- 
 tually pulsate when tricuspid regurgitation has become 
 established. 
 
CHAPTER IX. 
 AORTIC STENOSIS. 
 
 MORBID ANATOMY AND ETIOLOGY — THE MURMUR OF AORTIC 
 STENOSIS— CONDITIONS OTHER THAN AORTIC STENOSIS 
 WHICH MAY GIVE RISE TO SYSTOLIC AORTIC MURMURS 
 — DIFFERENTIAL DIAGNOSIS OF MURMURS — ESTIMATION 
 OF EXTENT OF LESION BY MEANS OF THE MURMUR, 
 THE CHANGES IN THE HEART AND THE PULSE — 
 PROGRESS OF THE DISEASE : SYMPTOMS— PROGNOSIS — 
 TREATMENT. 
 
 The first valvular change to be considered will be aortic 
 stenosis. This is the least common of the valvular affections 
 of the left side of the heart, as shown both by post-mortem 
 statistics and clinical experience. 
 
 Morbid Anatomy and Etiology. 
 
 Actual narrowing of the mouth of the aorta is almost 
 always due to changes in the valves, the cusps of which 
 may be stiff and rigid from cicatricial contraction of fibrous 
 tissue after endocarditis, with rounded and thickened 
 margins, a condition which does not permit them to fall 
 back into the sinuses of Valsalva before the current of 
 blood. Instead, therefore, of a circular orifice of the same 
 size as the vessel beyond, there is a roughly triangular 
 opening of reduced area, formed by the edges of the 
 cusps : subsequent calcification may render the valves 
 
AORTIC STENOSIS. in 
 
 still more rigid and deformed. Sometimes adhesions take 
 place between damaged valves at the angle in which they 
 meet, so that a narrow funnel-shaped orifice results. This 
 condition may be left by endocarditis, whether rheumatic 
 or occurring in the course of scarlet fever or other bacterial, 
 infection of the valves. Or the valves may be deformed 
 by atheroma or chronic degenerative changes, which destroy 
 their flexibility, cause puckering and contraction of their 
 margins, and lead to calcareous deposits in their substance. 
 
 It is also possible that by dilatation of the ring at the 
 root of the aorta, a slight and unimportant obstruction may 
 be produced ; valves, not themselves greatly diseased, being 
 so put on the stretch that they cannot fall back, but remain 
 as an obstacle to the stream of blood. 
 
 Physical Signs. 
 
 The characteristic physical sign to which aortic stenosis 
 gives rise is a murmur systolic in time which usually has 
 its maximum intensity in the second right intercostal space 
 close to the sternum, in the so-called aortic area. All 
 systolic murmurs heard over this area do not, however, 
 necessarily imply actual obstruction of the aortic orifice, 
 but may have other significance. 
 
 The Murmur. — The systolic aortic murmur, as is indicated 
 by its name, is heard during the systole of the left ventricle, 
 and is produced by the rush of blood through the obstructed 
 aortic orifice from the ventricle into the aorta. Its 
 commencement coincides in time with the first sound 
 of the heart, and may either accompany or replace it, 
 and it may begin with a burst or accent, or gradually. 
 The duration of the murmur varies ; it is usually long, 
 sometimes occupying the entire interval between the first 
 and second sounds, which interval may be prolonged, but it 
 may be short. It is audible over the sternum at the level 
 of the third intercostal space, but is most distinct just 
 
U2 HEART DISEASE. 
 
 outside the right edge of the sternum in the second space, 
 or sometimes over the third costal cartilage, at which point 
 on the surface the aorta comes from under the pulmonary 
 artery, and nearly touches the anterior wall of the chest. 
 It is conducted upwards, as the phrase is, along the right 
 side of the sternum to the right sterno-clavicular articu- 
 lation, where it is distinctly audible, and it is also heard 
 over the carotids in the neck and occasionally over the 
 thoracic aorta along the spine. It is frequently heard along 
 the right margin of the sternum lower down, sometimes 
 to the fourth or fifth space right or left of the sternum, 
 more especially when the aorta is dilated and elon- 
 gated, and it may have its maximum intensity over the 
 sternum near its left edge at the level of the third rib or 
 space, i.e. immediately over the aortic valves. This, however, 
 is not common, as the root of the aorta is deeply seated in 
 the chest, and has, between it and the surface, the conus 
 arteriosus of the pulmonary artery. The murmur is lost 
 over the right ventricle, but is again audible, as a rule, at 
 the apex, being conducted to this point by the wall of the 
 left ventricle. This murmur may be loud — sometimes 
 extremely loud — and when this is the case, it may be heard 
 all over the chest behind, as well as in front, or it may be 
 comparatively soft ; it is often rough and vibratory, more 
 rarely, croaking in character, but it may be smooth and 
 blowing, or musical. Occasionally it is accompanied by a 
 systolic thrill felt in the second or third right space, or in 
 both close to the edge of the sternum. 
 
 Causes other than Aortic Stenosis which may give rise to 
 a Basic Systolic Murmur. — Such a murmur in one or other 
 of its varieties may be due to several causes, which will 
 now be enumerated. 
 
 1. Anaemia may be mentioned first. It is not well 
 understood how it is that this condition gives rise to 
 murmurs, but the fact is exemplified by the venous hum 
 
AORTIC STENOSIS. 113 
 
 heard in the neck, by pulmonic and mitral murmurs, and 
 also, though less commonly, by a systolic aortic murmur. 
 This murmur is rarely rough or loud, but it is often distinct 
 and audible along the edge of the sternum upwards to the 
 sterno-clavicular articulation, and in the neck. It accom- 
 panies the first sound, and does not substitute itself for it. 
 Haemic murmurs are commonly multiple, which renders 
 their diagnosis more easy. 
 
 With the uremic aortic murmur may be grouped the 
 murmur of similar character, sometimes accompanying or 
 following acute febrile disease of long duration, such as 
 rheumatic fever and typhoid fever, although it is not certain 
 that the causation is exactly the same. A systolic mitral 
 murmur is more common, and is usually present as well as 
 the aortic murmur. Such murmurs may perhaps be attri- 
 buted to a temporary loss of tone of the heart and vessels. 
 They usually disappear as the patient regains health and 
 strength. 
 
 2. Mere roughening of the orifice or valves, or impaired 
 flexibility of the latter, slight congenital malformation, 
 fenestration of one or more of the cusps, a shred of fibrin 
 hanging from the edge of a valve, may give rise to a loud 
 systolic murmur without offering any appreciable obstruc- 
 tion to the course of the blood. 
 
 3. An aortic murmur may be produced by acute or sub- 
 acute aortitis, a rare and obscure disease which may be 
 suspected when, with a murmur not previously known to be 
 present, there are irregular pyrexia, dull sub-sternal pain, 
 and rapid and apparently unaccountable failure of the heart. 
 
 4. Dilatation of the aorta just above the valves, the 
 orifice and valves remaining unchanged, produces a murmur. 
 The fibrous ring at the root of the aorta, which gives attach- 
 ment to the muscular fibres of the ventricle, and supports 
 the semilunar valves, is extremely strong, so that it does 
 not readily give way and allow the orifice to be enlarged, 
 
 1 
 
H4 HEART DISEASE. 
 
 but the aorta just above the ring is prone to dilatation, and 
 the blood passing- through an opening of normal size into a 
 larger cavity beyond is thrown into eddies, the vibrations 
 attending which produce the sound heard as a murmur. 
 
 In none of these conditions is there stenosis of the 
 orifice, or obstruction to the stream as it issues from the 
 heart ; the condition last mentioned has dangers of its own, 
 but they do not arise from aortic obstruction. 
 
 Differential Diagnosis of Basic Systolic Murmurs. — It 
 is clear that the first point to be ascertained when a 
 systolic murmur is present is, whether it indicates the 
 existence of obstruction or not. In this we shall be greatly 
 assisted by the history, aspect, and age of the patient. 
 We should, for example, suspect that the murmur was 
 hsemiCj and not produced by obstruction if the patient 
 were a young and ansemic girl, or if it were first heard 
 during convalescence from an acute illness, more especially if 
 similar blowing murmurs were heard at other valves as well. 
 
 The history of an attack of rheumatic fever would, on 
 the other hand, favour the conclusion that the orifice was 
 actually narrowed. 
 
 A systolic murmur over the aorta, appearing after middle 
 age, or in advanced life, or discovered for the first time at 
 this period, will seldom be due to actual narrowing of the 
 orifice, but will be caused by roughness or rigidity of the 
 valves, or by dilatation of the aorta above the valves with 
 perhaps atheromatous irregularities in its walls. Fortu- 
 nately the aortic second sound is of very great assistance 
 in determining the point. Under the condition just 
 mentioned it will almost certainly be unduly loud and 
 accentuated from co-existing high arterial tension, while 
 stenosis diminishes the intensity of the second sound in two 
 ways : by the changes present in the valves impairing their 
 flexibility, and by the less sudden recoil which follows 
 the slower distension of the arterial system. Prolonged 
 
AORTIC STENOSIS. 115 
 
 observation of cases of high arterial tension from gout, lead 
 poisoning, renal disease, or other causes in advanced life, 
 will not unfrequently afford the medical attendant the 
 opportunity of noting the first appearance and gradual 
 development of a murmur over the aorta in addition to the 
 accentuated second sound. 
 
 The loudness or character of the murmur, or the extent 
 to which it is conducted along the aorta, does not give us 
 much help. Hamiic aortic murmurs are usually soft and 
 smooth, but so also may murmurs be which are due to 
 extreme narrowing. It has been stated by some that when 
 the margins of the thickened valves are smooth and rounded 
 there may be no murmur in spite of considerable narrow- 
 ing ; but if the fact be true, the explanation can scarcely 
 be accepted, since it is not the friction of the blood against 
 the valves as it passes over them which generates sonorous 
 vibrations, but the eddies produced by the passage of the 
 blood through a small orifice into a large channel. A 
 more probable explanation is weakness of the ventricle and 
 languid propulsion of the blood which may render the 
 murmur weak or inaudible ; thus the gradual enfeeblement 
 and ultimate disappearance of a systolic aortic murmur may 
 be a serious prognostic indication. The loudest murmurs, 
 such as have already been mentioned, are most frequently 
 produced by rigidity or deformity of one or more of the 
 cusps or by a calcareous deposit in the valve, or some- 
 times by a delicate band stretched across a part of the 
 orifice, but it would not be safe to conclude that all loud 
 murmurs are harmless. All we can safely infer is that a 
 long, loud murmur indicates a vigorous ventricular systole 
 which is a good prognostic element. 
 
 It is thus evident that from the murmurs alone it may 
 be impossible to make a certain diagnosis of aortic stenosis, 
 and still less to estimate the amount of the constriction. 
 
 The Heart : Estimation of Degree of Stenosis by Degree of 
 
n6 HEART DISEASE. 
 
 Cardiac Hypertrophy. — We turn, then, to the condition of 
 the heart. If there is actual obstruction its existence will 
 be betrayed either by the changes in the walls and cavities 
 which are required in order to overcome it, or by some 
 evidences of derangement in the circulation. 
 
 The change by which aortic obstruction will be over- 
 come will be more or less pure hypertrophy of the left 
 ventricle. This does not bring the heart to the gigantic 
 size which it reaches as a consequence of aortic regurgi- 
 tation. The apex beat will be lower than the normal 
 position by an intercostal space, or perhaps more, but it 
 will not be greatly displaced outwards ; it will be a well- 
 defined and deliberate push of no great violence. The 
 first sound here will be dull and prolonged, and not very 
 loud ; perhaps accompanied by a murmur which may be 
 mitral, but most commonly is, in the early period of the 
 disease, the aortic murmur conducted to the apex by the 
 walls of the left ventricle. The other sounds will present 
 nothing remarkable, except that the aortic second sound 
 will be weak. If we get such evidence of hypertrophy of 
 the left ventricle as this, i.e. the downward displacement 
 and definite push of the apex with a prolonged first sound, 
 in a young person without kidney disease, together with 
 a systolic aortic murmur, there can be no hesitation in 
 inferring: stenosis of the aortic orifice. At and after middle 
 age it would be necessary to consider whether the hyper- 
 trophy might not have been produced by long-continued, 
 antecedent resistance in the peripheral circulation and high 
 arterial tension ; but in this case the apex would usually be 
 less defined, the first sound louder and less deliberate, and 
 the aortic second sound much accentuated. When aortic 
 incompetence has preceded the stenosis, as is often the case 
 when it is due to acute endocarditis, the left ventricle will 
 attain a greater size by reason of the previous dilatation to 
 which hypertrophy has succeeded. 
 
AORTIC STENOSIS. 1*7 
 
 The Pulse. — Almost more important than the hyper- 
 trophy of the left ventricle will be the character of the 
 pulse. The orifice being narrowed, the blood discharged 
 from the ventricle will require more time to pass through 
 it, and the pressure in the arterial system will not at once 
 rise to its maximum ; in other words, the so-called percus- 
 sion element of the sphygmographic trace will be weakened 
 and the pulse wave will be long and slow, not striking the 
 finger or lever abruptly and vigorously, but raising it gradu- 
 ally. The artery will, for the most part, be small and full 
 between the beats of the pulse. A large sudden pulse is 
 incompatible with aortic stenosis unaccompanied by regur- 
 gitation, and Avhen it is a question whether or not an aortic 
 systolic murmur is due to obstruction at the orifice, the 
 pulse becomes the most certain criterion to which we can 
 appeal ; if there is an apparent contradiction between the 
 indications of the heart and those of the pulse, the latter 
 must dominate. 
 
 For instance, if with a systolic and diastolic aortic 
 murmur and a hypertrophied heart, the pulse is large, 
 sudden and collapsing, we shall infer that there is no real 
 stenosis of the aortic orifice ; if, on the other hand, the 
 pulse lacks these features characteristic of aortic incom- 
 petence, we shall conclude that there is aortic stenosis 
 which has interfered with their development ; and we shall 
 estimate the degree of stenosis from the extent to which it 
 has modified the pulse. 
 
 A systolic murmur heard over the aortic valves and 
 along the aorta will not, in the absence of cardiac hyper- 
 trophy and the long, small pulse described above, indicate 
 stenosis of the aortic orifice, and even when there is hyper- 
 trophy, if the pulse is large, short and abrupt, there can be 
 no real narrowing. 
 
n8 HEART DISEASE. 
 
 Effects of the Disease : Symptoms. 
 
 When the constriction is moderate in amount and is a 
 result of endocarditis, in a young subject the heart will 
 usually undergo hypertrophy sufficiently to overcome the ob- 
 struction, and no serious or troublesome symptoms will arise. 
 In severe cases there may be dyspnoea and anginoicl pains. 
 There is a tendency for the constriction to increase, and 
 when this is so considerable as to have given rise to great 
 hypertrophy of the left ventricle, the latter is sure to give 
 out sooner or later. As a consequence of the deficient pro- 
 pulsive power resulting therefrom, there will be a tendency 
 to systemic stagnation, and as a result of the incomplete 
 emptying of the ventricular cavity in systole, there will be 
 insufficient room for the whole contents of the left auricle 
 in diastole, and consequent back pressure through the left 
 auricle and pulmonary circulation. Mitral incompetence 
 may ensue as a result of the giving out of the left 
 ventricle, but there will also be other injurious influences 
 at work which may give rise to regurgitation in the 
 following way : The pressure in the ventricular cavity 
 will be greatly increased owing to the powerful contraction 
 of the muscular walls, which is necessary to overcome the 
 obstruction at the orifice ; as a consequence of this, there is 
 a constant and severe strain upon the flaps of the mitral 
 valve and the chordse tendinete, so that eventually they 
 become stretched or give way, and mitral incompetence 
 results, or chronic degenerative changes may take place, 
 leading to thickening and contraction of the valves and 
 cords. It will thus be seen that in aortic stenosis of any 
 severity there is little chance of the mitral valve escaping 
 damage in the long run, and if it has at the outset been 
 injured by the same attack of endocarditis which gave rise 
 to the aortic mischief, the outlook is far more serious. The 
 barrier formed by the mitral valve being thus broken 
 
AORTIC STENOSIS. "9 
 
 down, the door is open to backward pressure through the 
 auricle, which will take effect upon the pulmonary circula- 
 tion and right ventricle. It has been said by some that 
 timely yielding of the mitral valve acts as a safety valve, 
 as tricuspid regurgitation is supposed to do for the right 
 ventricle, preventing sudden death through over-distension 
 and consequent paralysis of the left ventricle. This view 
 does not commend itself to my judgment, and must, in the 
 nature of things, be purely hypothetical. There can be no 
 doubt that the establishment of mitral regurgitation marks 
 a downward step and renders the prognosis grave. The 
 obstacle to the outflow of blood from the ventricle, which 
 has given rise to the whole train of consequences, remains 
 irremovable, and the setting in of mitral symptoms marks 
 the failure of compensation. 
 
 Prognosis. 
 
 Nearly all authors concur in making aortic stenosis the 
 least dangerous of the valvular affections, and on a priori 
 considerations such would seem to be probable ; but this 
 conclusion will scarcely seem quite secure if the cases of 
 systolic aortic murmur without actual narrowing of the 
 orifice are eliminated. Just as the inclusion of all cases in 
 which a systolic aortic murmur is heard makes aortic stenosis 
 apparently the most frequent valvular disease, while on 
 post-mortem evidence it is seen to be the least common, so 
 the dilution of the death-rate by the cases in which no 
 real narrowing exists makes it appear to be the least fatal. 
 The relative danger of real stenosis cannot be estimated 
 with confidence, but it is certainly greater than has been 
 supposed, and though, perhaps, it is not so serious as aortic 
 incompetence or mitral stenosis, it is more so than mitral 
 incompetence. The average age of the cases of this disease 
 in the post-mortem statistics referred to in the chapter on 
 prognosis was about forty, and would have been higher had 
 
120 HEART DISEASE. 
 
 deaths by intercurrent independent disease been excluded. 
 The age of the oldest patient among these, however, was 
 fifty-three; this would bear out the above statement that 
 aortic stenosis must be looked upon as more dangerous 
 than mitral incompetence, of which numerous examples are 
 known to have reached the age of seventy. 
 
 There is no risk of sudden death as in aortic incompe- 
 tence, and there is little danger as long as the patient is free 
 from symptoms ; but when once dropsy has set in from back 
 pressure due to dilatation of the left ventricle, there is 
 a smaller possibility of recovery than in other valvular 
 affections. For when the left ventricle has given way 
 under the resistance it encounters, it has little chance of 
 regaining its normal condition, since the resistance persists 
 undiminished, and there is no other compensatory influence 
 which can be called upon. Further, if the break-down 
 occurs after middle life, it is probable that degenerative 
 change is taking place in the hypertrophied left ventricle, 
 which will render the prognosis still more unfavourable. 
 
 In regard to this it must be borne in mind that at and 
 after middle age, a systolic aortic murmur appearing for the 
 first time may be indicative of degenerative change, and 
 obstruction is the smallest of the dangers to which degenera- 
 tive change in or about the root of the aorta may give 
 rise. The loss of flexibility in the valve Avhich gives 
 rise to obstruction may permit of regurgitation. Again, 
 the degeneration may affect one of the sinuses of Valsalva 
 and produce aneurysm here, or may implicate the orifice 
 of the coronary arteries, and by cutting off the supply of 
 blood lead to fatty change in the walls of the heart. Any 
 murmur at the aortic orifice, then, in an elderly person, 
 must be looked upon as a possible forerunner of serious 
 disease, though I. have known of cases in which a rough 
 systolic murmur has been present for upwards of ten years 
 without any serious symptoms arising. 
 
aortic stenosis. 121 
 
 Treatment. 
 
 In regard to the treatment of aortic stenosis, there is 
 little to add to what has been said on the treatment of 
 valvular disease in general. We cannot hope to rectify the 
 constriction which has already taken place, and can do 
 little to modify the process of narrowing, which may be 
 going on as a result of cicatricial contraction, or adhesion 
 of the valvular curtains, after acute endocarditis has 
 subsided. When, however, the valves are being damaged 
 by a chronic inflammatory process due to syphilis, benefit 
 may be sometimes obtained by the administration of large 
 doses of iodide of potassium. 
 
 Supposing the contraction of the aortic orifice to have 
 reached a certain point and become stationary ; the dangers 
 likely to arise out of this condition will be, at an early 
 period, an imperfect degree of compensatory hypertrophy 
 and later degeneration of the hypertrophied muscular wall, 
 with, in both cases, secondary dilatation of the left ventricle. 
 From this, mitral incompetence may result, and subsequently 
 right ventricle failure with its train of symptoms of venous 
 obstruction. 
 
 The hypertrophy is usually sufficient in the first instance, 
 as the contraction of the orifice takes place slowly, so that 
 the structural increase can keep pace with it, provided that 
 the patient is a young subject. A moderate degree of 
 constriction may therefore exist for years without apparently 
 affecting the health or well-being, or interfering with 
 ordinary occupations, giving rise to no symptoms except 
 perhaps shortness of breath and precordial pain on too 
 great exertion. Even considerable stenosis is not incom- 
 patible with moderate exercise and work and apparent 
 health. 
 
 Exceptions occur when the patient is weak and anaemic, 
 either as a result of protracted illness, or from other causes, 
 
122 HEART DISEASE. 
 
 and nutrition being poor, the hypertrophy is inadequate 
 and accompanied by dilatation. In such cases prolonged 
 rest may be of great service. 
 
 Secondary dilatation and break-down of the left ventricle 
 is to be averted by carefully avoiding over-exertion, fatigue, 
 and anxiety, and by attention to general health. Modera- 
 tion in food and drink is necessary, as the amount of 
 exercise which can be taken is limited, and anything that 
 may lead to high arterial tension and increased peripheral 
 resistance is especially to be guarded against. Tonics may 
 be given when required, and ansernia is to be combated by 
 all means in our power. The protracted administration of 
 digitalis is of very questionable utility. When the left 
 ventricle has begun to give way, and symptoms of back- 
 ward pressure through the lungs and embarrassment of 
 the right ventricle supervene, then digitalis and similar 
 remedies will be of service. If, however, these symptoms 
 have come on insidiously, and are not traceable to over- 
 exertion, chill, or any definite cause, drugs will rarely be 
 able to improve materially the condition of the patient or 
 postpone for long the fatal termination. 
 
 When the hypertrophied walls of the heart have begun 
 to undergo degeneration, and there is precordial pain and 
 oppression, the administration of nitro-glycerine and nitrites, 
 or the nitrates of erythrol and mannitol, by diminishing the 
 arterio-capillary resistance, and thus relieving the stress 
 on the left ventricle, will often afford the heart distinct 
 relief, and produce a general amelioration of symptoms. 
 These drugs may be given at the same time with digitalis. 
 
 On the other hand, I have more than once known aconite, 
 given with a similar object, completely overthrow the 
 compensation established by hypertrophy, and cause rapid 
 cardiac dilatation, with frequent Aveak and small pulse 
 accompanied by pallor and cold sweats. 
 
CHAPTER X. 
 AORTIC INCOMPETENCE. 
 
 etiology — physical signs — the diastolic murmur : 
 directions in which it is conducted— presystolic 
 murmur, its significance — modification of the 
 aortic second sound — pulsation of arteries — 
 capillary pulsation — the collapsing pulse — 
 pulsus bisferiens — irregular pulse— estimation 
 of the amount of regurgitation from the 
 character of the murmuk, of the aortic second 
 sound, of the pulse, and the changes in the 
 heart — aortic incompetence due to syphilis and 
 causes other than acute endocarditis— symptoms 
 — prognosis — treatment. 
 
 Etiology. 
 
 The commonest cause of this affection in childhood and 
 early adult life is acute endocarditis. As the clinical 
 features of aortic incompetence which develops in later life 
 from other causes, differ materially, discussion of these 
 will be deferred till later on in this chapter. 
 
 Physical Signs. 
 The Diastolic Murmur. — The diagnostic sign of this con- 
 dition is a murmur produced by the backward rush of the 
 blood from the aorta into the left ventricle during its 
 
124 HEART DISEASE. 
 
 diastole. Two forces will be at work in its production — the 
 suction action of the ventricle, and the pressure in the 
 arterial system generally and in the aorta in particular, due 
 to the elastic recoil of the walls of the great vessels. The 
 cause of the murmur is not necessarily roughness or irregu- 
 larity of the valves or orifice ; it may be due partially or 
 entirely to the vibrations generated by the passage of liquid 
 through a constricted point in a channel, into a large cavity 
 beyond. 
 
 The seat of production of the murmur being the valves 
 which encircle the root of the aorta, the point on the 
 surface of the chest immediately over and nearest to the 
 origin of the sound will be close to the left margin of 
 the sternum at the level of the third cartilage ; but it is not 
 always here that the murmur is best heard, as the con as 
 arteriosus of the pulmonary artery is interposed between the 
 aorta and the chest wall. 
 
 The murmur is conducted in various directions, and the 
 seat of its maximum intensity differs in different cases. It 
 is, with rare excejotions, audible in the so-called aortic area 
 just outside the right edge of the sternum in the second 
 intercostal space, or over the second costal cartilage, and 
 is usually conducted upwards from this point along the 
 sternal margin as far as the sterno-clavicular articulation, 
 though losing rapidly in intensity the while. It can 
 frequently be followed downwards along the side of the 
 sternum to the fourth space, or even lower, sometimes with 
 increasing intensity over one or two ribs ; it is also fre- 
 quently heard along the sternum itself, or to the left of it, 
 the seat of maximum intensity being frequently in the 
 fourth or fifth spaces near the left edge of the sternum, 
 where it may be audible when not heard over the aortic 
 area. It may again be audible at the apex after having 
 been lost over the right ventricle, but it is usually weakened 
 here, and is not at its loudest. Another point at which it 
 
AORTIC INCOMPETENCE. 125 
 
 may be heard is the third left space exactly over the 
 pulmonic valves or artery. 
 
 Cause of the Conduction of the Murmur. — In a certain 
 degree we may say that the distribution of the murmur 
 described is explained by its conduction downwards by 
 the current of the regurgitant blood, and this must be 
 held to account for the difference between obstructive and 
 regurgitant aortic murmurs, in regard to the points on the 
 chest wall where they are best heard. But the direction which 
 the blood takes will be towards the apex, and if the current 
 carried the murmur, it would be at the apex that we should 
 hear it most distinctly, which is not the case. The truth is 
 that we are apt to lose sight of the fact that much more blood 
 enters the ventricle from the auricle than from the aorta — 
 any other state of things would be incompatible with onward 
 movement of the blood in the systemic arteries, and therefore 
 with life — and also that the regurgitant stream through the 
 valves is comparatively small if rapid. We are also perhaps 
 given to figure in our imagination, this stream as falling 
 into an empty vessel, whence has arisen such an explanation 
 as the collision of the blood with the ventricular wall, to 
 account for some abnormal sound or other. The ventricle is 
 never an empty cavity into which blood can fall with 
 violence as into a bottle or jar ; there is no large and 
 powerful stream rushing straight from the aorta down to the 
 apex ; during diastole, in a case of aortic insufficiency, there 
 must be complicated cross currents in the ventricle, rendering 
 conduction of sound in any definite direction impossible. 
 The vibrations, then, must be conveyed by the walls of the 
 ventricles, and not by the contained blood, or at any rate the 
 blood thrown into sonorous eddies will communicate the vibra- 
 tions to all parts of the ventricular wall indifferently, and not 
 impinge upon any special point carrying thither the sound. 
 Presystolic Murmur. — Sometimes, more usually when 
 there is stenosis as well as incompetence of the aortic 
 
126 HEART DISEASE. 
 
 orifice, a presystolic murmur is heard in the region of the 
 apex, resembling very closely that of mitral stenosis, which 
 does not, however, denote constriction of the mitral orifice. 
 This is sometimes termed the Flint murmur, as it was first 
 described by him. It is, of course, possible that mitral 
 stenosis may co-exist with double aortic disease ; but in 
 some Cases in which a presystolic murmur has been audible 
 at the apex, together with a systolic and diastolic murmur 
 in the aortic area, the mitral orifice has been found to be 
 normal at the autopsy, and the only lesion has been 
 constriction and incompetence of the aortic orifice. The 
 following explanation of the origin of this murmur has 
 been suggested. The mitral and aortic orifices are in 
 close apposition, and it is probable that the regurgitant 
 stream from the aorta impinges to a certain extent on 
 the anterior or aortic flap of the mitral valve. It is con- 
 ceivable that the murmur may be due to this flap of the 
 mitral valve being thrown into vibration by the regurgi- 
 tant stream from the aorta, the vibration being conducted to 
 the apex by the chordse tendinepe and papillary muscles, 
 or, on the other hand, that the backward rush of blood 
 from the aorta prevents the complete falling back of this 
 flap of the mitral valve, so that some actual obstruction of 
 the mitral orifice results, giving rise to a presystolic murmur. 
 Violent Arterial Pulsation. — One of the most striking 
 features in aortic regurgitation is the sudden, abrupt, and 
 violent pulsation of the arteries throughout the body, most 
 conspicuous in the carotids. So marked is this that one can 
 often make a diagnosis at sight. The pulse is visible at the 
 wrist, the brachials at the bend of the elbow throw them- 
 selves into violent curves, the femoral and anterior tibial 
 arteries are scarcely less visible ; the temporals, facials, and 
 labials may be seen beating ; even the digital arteries may 
 be seen as well as felt to an unpleasant degree. As was 
 first pointed out by Sibson, the radial pulse is audible when 
 
AORTIC INCOMPETENCE. 127 
 
 the hand is raised, a sign more interesting perhaps than 
 valuable. 
 
 The arteries, as may be easily seen in the radial at the 
 wrist, are large, because the entire contents of the left 
 ventricle, expanded to two or three times its normal capacity, 
 are launched into the arterial system, distending it 
 momentarily to a corresponding degree. 
 
 Capillary and Venous Pulsation. — Another interesting- 
 effect is capillary pulsation, a pulsatile reddening of the 
 skin, which is sometimes observed in the palms of the 
 hand when warm, especially when pyrexia is present, and 
 a similar phenomenon may at any time be provoked at 
 various parts of the surface, most conveniently perhaps 
 on the forehead, by bringing out a red patch or line by 
 friction, the margins of which will be seen alternately to 
 extend and fade, synchronously with the pulse. This is 
 due to the extension of the arterial relaxation into the 
 capillaries, and when it is general the pulsatile movement 
 of the blood may even reach the veins. To render this 
 visible the hand should be so held as to drop at the wrist 
 when the veins on the dorsum will fill, and sometimes will 
 be seen to pulsate, not with the sudden beat of the artery, 
 or like the rapid flush of the capillaries, but with a gentle 
 and deliberate movement followed with difficulty, but which 
 a filament of sealing-wax across the vein will render visible. 
 
 Capillary pulsation, however, is not a phenomenon 
 peculiar to aortic incompetence, as it may be produced 
 sometimes in pneumonia, or phthisis, or enteric fever, or 
 other conditions associated with a pulse of low tension. 
 
 The Pulse. — This is the well-known collapsing or water- 
 hammer pulse, sometimes named after Corrigan, who is 
 believed to have first called attention to it. The artery at 
 the wrist is large. In the intervals between the pulsations 
 it is empty and allows itself to be completely flattened 
 against the bone; then the wave comes with a sudden 
 
128 HEART DISEASE. 
 
 violent rush, filling the vessel and lifting the fingers 
 forcibly. It is as short as it is sudden, and the artery at 
 once collapses again under the pressure of the fingers. In 
 order that all these features may be fully realized, the hand 
 must be above the level of the heart and above the shoulder 
 or elbow. When the patient is lying in bed, the act of 
 giving the hand for the pulse to be felt brings about this 
 condition, but when he is sitting, as during an interview in 
 the consulting-room, or standing with the arm hanging 
 down, although the artery may be large and the beat 
 sudden, the collapse will not take place. 
 
 The cause of the collapse is, that in consequence of the 
 loss of the support of the aortic valves, the column of blood 
 is not sustained, and therefore drops out of any vessel 
 which is above the level of the heart in obedience to 
 gravity. If, then, the hand is hanging down, the radial 
 artery remains full, having above it a column of blood up 
 to the arch of the sub-clavian. 
 
 The collapsing character of the pulse is indispensable as 
 an evidence of aortic regurgitation, though certain compli- 
 cations, which will be enumerated later, may interfere with 
 the degree of collapse. 
 
 In cases of pulmonic regurgitation, which are rarely 
 met with, the absence of the collapsing pulse and of undue 
 carotid pulsation will be the most important distinguishing 
 features. Similarly their presence, in cases where the 
 diastolic murmur is heard loudest or exclusively over the 
 pulmonic area, will clear up all doubts as to diagnosis. 
 
 The evidence afforded by the collapsing pulse is corro- 
 borated by conspicuous pulsation in the carotid arteries. 
 This is visible not only at the root of the neck, where 
 pulsation is often seen, but can be followed upwards along 
 the entire course of the artery in front of the sterno-mastoid 
 and between this muscle and the ramus of the jaw, also 
 in front of the ear. 
 
AORTIC INCOMPETENCE. 129 
 
 The Delay of Pulse. — The pulse in aortic regurgitation is 
 always retarded or delayed — that is, there is an appreciably 
 longer interval than normal between the beat of the heart 
 and the pulsation in the radial artery, which varies 
 according to the extent of the incompetence. This delay 
 is due partly to the collapsed and empty state of the 
 arteries between the beats, and partly to their large size 
 and loss of tone. The tension in the arterial system has 
 to be considerably augmented by the launching of a 
 large volume of blood into the aorta, before the vessels 
 are rendered sufficiently tense for a pulse-wave to be 
 transmitted. Clifford Allbutt,* in his article on Aortic 
 Kegurgitation, states that delay of the pulse seems to him 
 to be "contrary to observation both physiological and 
 pathological." He qualifies this statement later on in 
 a postscript,! and admits that there is delay, as shown 
 by tracings taken by Dr. Chapman of Hereford, the delay 
 being attributed to prolongation of the cardiac systole. 
 Mackenzie % published a series of tracings which he claims 
 prove the opposite of this, namely, that there is no delay. 
 The explanation of this conflict of evidence may be that 
 the cases investigated were of different types. Mackenzie 
 states that some of his were taken from cases of incompetence 
 due to degenerative changes, and in these conditions one 
 would not expect much delay, as the aorta is converted into 
 a rigid inelastic tube, and the loss of elasticity would tend 
 to lessen the amount of regurgitation and to do away with 
 the delay which the expansion of the walls of the great 
 vessels entails. Moreover, in seeking the clinical evidence 
 of delay in the pulse, the hand is raised so as to bring out 
 the significant effects in the circulation, whereas in instru- 
 mental estimation of the retardation of the pulse wave, the 
 forearm rests on a table below the level of the shoulder, 
 
 * " System of Medicine," vol. v. p. 939. f Ibid., p. 965, 
 
 % Edinburgh Medical Journal, 189S. 
 
 K 
 
*30 HEART DISEASE. 
 
 so that the column of blood in the arm does not fall back 
 towards the heart, tending to empty the vessel, but is ready 
 to transmit the systolic pressure. 
 
 The pulsus bisferiens is sometimes met with in aortic 
 incompetence, more commonly when there is concomitant 
 stenosis. It is a peculiar double beat, best felt when the 
 fingers exert a moderate pressure on the artery, less than is 
 necessary to bring out fully the collapsing character of the 
 pulse, but more than is employed to appreciate dichrotism. 
 It can be readily demonstrated by the sphygmograph. It is 
 produced by a double systolic effort, which can sometimes 
 be felt or heard in the heart itself, and which frequently 
 gives rise to a double rush of blood audible in the carotids. 
 
 FIG. 15. — PULSUS BISFERIENS. 
 
 According to D'Espine, of Geneva, the normal systole of the 
 heart is a deux temps, or a double contraction, of which this is 
 an exaggeration. The pulsus bisferiens can not uncommonly 
 be induced by an effort, which throws additional work on 
 the heart ; for instance, in one case it was not present while 
 the patient lay quietly in bed, but was brought out when 
 he held up both his hands. 
 
 Irregularity of Pulse. — Though the pulse of aortic in- 
 competence is for the most part regular in force and 
 frequency, in advanced cases, especially when the heart is 
 beginning to fail, irregularity of pulse is not uncommon. 
 The irregularity, which may be described as faltering, is 
 first manifested by the occurrence of a short and rapid 
 pulsation of less force and amplitude than the ordinary 
 
AORTIC INCOMPETENCE. 
 
 131 
 
 wave, and occurring at irregular intervals. It succeeds 
 the previous beat very quickly, and is followed by a longer 
 interval than usual. It would seem to indicate an effort 
 of the heart to supplement an inadequate and inefficient 
 preceding contraction, or to be an abortive systole. Later 
 on, the irregularity, both in force and frequency, becomes 
 more general and more marked, though the pulse is still 
 recognizable as that of aortic regurgitation. 
 
 Estimation of the Extent of the Lesion. 
 
 The amount of blood which returns into the ventricle 
 is a matter of the first importance in estimating the 
 prospects of life and comfort before the patient, and we 
 have now to consider the different sources of information 
 on this point. 
 
 The diastolic murmur itself affords but vague indications. 
 As has been already mentioned, it may be loud or feeble, 
 rough or smooth, long or short. It usually begins with an 
 accent. Speaking generally, a long loud murmur shows 
 that a considerable degree of pressure is kept up in the 
 aorta, which is a desirable thing in itself, and a proof that 
 the heart is acting with vigour, and also that the leakage 
 of the valves is not excessive ; it is usually, therefore, among 
 the favourable auguries. On the other hand, a weak short 
 murmur indicating an opposite state of things may be a 
 note of impending danger or death. But there are so many 
 exceptions to the rule hinted at that it is not to be relied 
 upon. 
 
 Aortic Second Sound. — A very important auscultatory 
 sign, however, is the presence or absence of the aortic 
 second sound. We must listen for this, not at the apex or 
 in the aortic area, but in the neck. A second sound of 
 some kind, probably the pulmonic conducted, is often heard 
 c at the apex or base, but it has not the same favourable 
 
132 HEART DISEASE. 
 
 significance. The point of the sign is this : the aortic 
 second sound is produced by the sudden tension of the 
 aorta and its semilunar valves at the moment of closure of 
 the valves ; it is not their clicking as they meet, or the 
 tension of the valves alone under the column of blood, 
 but the vibration or sudden strain on the entire ascending 
 aorta. If, then, the incompetence is considerable, there 
 cannot be the sudden check to the column of blood which 
 sets the aorta vibrating, and the diastolic murmur takes 
 the place of the second sound ; if, on the contrary, the 
 leakage is only small, the required check or shock is given 
 by the closing valves, and the second sound is distinct, 
 although there may be a murmur. It is not the murmur, 
 which may be loud or feeble, that drowns the second sound 
 and prevents it being heard. In listening in the neck over 
 the carotid artery, we have the advantage of being out of 
 reach both of the diastolic murmur and of the pulmonic 
 second sound, and the tension in the aorta must be real in 
 order that the second sound may be heard here. A second 
 sound, therefore, heard in the neck indicates that the 
 regurgitation is small in amount and is consequently a 
 favourable prognostic element. The second sound is usually 
 loud and ringing when the incompetence is the result of 
 dilatation of the aorta involving the orifice, but this is not 
 of favourable prognostic significance, as the lesion is due to 
 degeneritive change and is likely to be progressive. 
 
 The Pulse. — The degree of collapse in the pulse is an 
 important factor in the estimation of the amount of the 
 regurgitation. The greater the regurgitation, the more 
 pronounced will be the collapsing character of the pulse. 
 In the absence of any marked collapse in the pulse, a 
 diastolic murmur, whatever its character, would not indicate 
 any serious degree of incompetence. While this may be 
 taken as a general rule, three important exceptions must 
 be mentioned : 
 
AORTIC INCOMPETENCE. 
 
 133 
 
 1. Concomitant aortic stenosis may interfere with the 
 suddenness and completeness of the collapse, when the 
 amount of regurgitation would have to be estimated by 
 other means than by the pulse. 
 
 2. In the last stages of aortic regurgitation, when the 
 heart is failing, there may not be sufficient force in the 
 cardiac systole to produce the collapsing pulse. 
 
 3. In aortic disease, acquired in later life from dilatation 
 of the aorta or degenerative changes in the valves, the 
 
 FIG. 1G. — COLLAPSING PULSE OF AORTIC FvEGURGITATION DUE TO ACUTE ENDOCARDITIS. 
 
 FIG. 17. 
 
 FIGS. 18. — LOSS OF COLLAPSE IN PULSE OF AORTIC REGURGITATION 
 DUE TO DEGENERATIVE CHANGES. 
 
 pulse has not the typical sudden and collapsing character. 
 (Figs. 17 and 18.) This absence of collapse in the pulse is 
 partly due to the rigidity and loss of elasticity in the 
 vessels, partly to the fact that the incompetence is not great, 
 as in such cases life is rarely prolonged if the regurgitation 
 becomes considerable. 
 
 The difference between the pulse of aortic incompetence, 
 due to degenerative changes in the valves, and the ordinary 
 collapsing pulse is well brought out by a sphygmographic 
 tracing. 
 
134 HEART DISEASE. 
 
 The Heart. — Other evidence as to the amount of regurgi- 
 tation is obtained from the changes which it has induced in 
 the heart. It has already been pointed out that if the 
 normal amount of blood is to be propelled through the 
 systemic arteries, while a certain proportion of that sent 
 by each systole into the aorta is returned into the ventricle, 
 an increase in the capacity of the ventricle is necessary. 
 In other words, it must be dilated. We are not arguing 
 that, because the necessity exists, therefore the provision 
 is made, but showing that the dilatation always found is 
 not injurious but useful, inasmuch as increased force in the 
 ventricular contraction would not alone meet the difficulty. 
 
 The process by which the dilatation is effected is the 
 distending influence of the backward pressure from the aorta, 
 during the diastole of the ventricle, when the muscular 
 fibres are relaxed and unresisting. Finally, hypertrophy 
 results from the excessive functional activity imposed upon 
 the walls of the ventricle by the mechanical conditions 
 present. It is in aortic incompetence that the extremes 
 of dilatation and hypertrophy of the left ventricle are met 
 with, and we have the apex beat displaced downwards to 
 the sixth, seventh, or eighth space, and carried beyond the 
 nipple or, in exceptional cases, up to or beyond the anterior 
 axillary line. The apex beat may be well defined, or 
 spread over a large area, and will be powerful. Sometimes 
 the wall of the chest between the apex and the sternum 
 is visibly lifted by the forcible contraction of the left 
 ventricle. Very frequently two or three spaces, between 
 the nipple line and the sternum, will be depressed with 
 the systole, and this systolic recession of intercostal spaces 
 has been supposed to prove the existence of adhesion 
 between the pericardium and heart. It is, however, 
 frequently only the result of atmospheric pressure con- 
 tributing to fill up the space left by the great diminution 
 of volume of the heart during systole. 
 
AORTIC INCOMPETENCE. i?>i 
 
 Estimation of the Extent of the Lesion by Degree 
 of Dilatation and Hypertkophy of the Heart. 
 
 The dilatation and hypertrophy being the effects, are 
 also, with certain qualifications, the measure of the 
 regurgitation, in the absence of symptoms such as con- 
 spicuous breathlessness on very slight exertion, or faltering 
 action of the heart and tendency to fainting or giddiness. 
 The most important qualification is that arising out of 
 the inability of the heart to take on these compensatory 
 changes late in life ; so that when aortic insufficiency 
 develops for the first time after the age of thirty, an 
 opinion as to its degree, and as to the danger attending it, 
 can only be arrived at after prolonged observation and 
 repeated examination. It is an interesting and important 
 question up to what age effectual compensation for serious 
 aortic regurgitation is possible. In my own experience all 
 really satisfactory examples have been among those in 
 whom the valvular lesion has been established under the 
 age of twenty. Cases have come under my observation in 
 hospital practice in which the valves have been extensively 
 damaged between the age of twenty and thirty, and the 
 patients have remained under observation for some time 
 afterwards, without developing symptoms of cardiac failure ; 
 but such cases are too soon lost sight of for trustworthy 
 conclusions to be based upon them. 
 
 The amount of dilatation attending a given degree of 
 incompetence will also vary according to the amount and 
 duration of the care bestowed upon the patient during the 
 first few months of its existence. If he has been allowed to 
 leave his bed too early and engage in exercise, or has 
 undertaken work before the heart has fully recovered from 
 the effects of acute disease, the dilatation will have gone 
 further than would have been the case if due precautions 
 had been observed till the strength was fully restored. 
 
136 HEART DISEASE. 
 
 Dilatation, moreover, may be increased during subsequent 
 illness attended with pyrexia or ansemia. In all such cases, 
 however, if the extent of the changes in the cavities and 
 walls of the heart does not accurately correspond with the 
 degree of change in the valves, it indicates the extent to 
 which the functional efficiency of the heart is endangered. 
 
 Aoetic Incompetence due to other Causes than 
 Acute Endocarditis. 
 
 In the account just given of the physical signs of aortic 
 incompetence, reference has been made from time to time 
 to differences observed when the valvular disease is 
 established during or after middle life, and from causes 
 other than rheumatism. Such causes are syphilitic affection 
 of the valves and the wall of the aorta, degenerative 
 changes included under the general term atheroma, and 
 rupture of a cusp of the valve. 
 
 Syphilis may be suspected as the cause of aortic 
 incompetence, which comes on in early adult life or middle 
 age, and is not traceable to rheumatic endocarditis or to 
 gout or high arterial tension. It is usually associated with 
 degenerative changes and dilatation of the aorta. Aneurysm 
 is indeed more common than aortic incompetence as a 
 result of syphilis. The regurgitation may rapidly become 
 considerable, and as regards the murmur and the character 
 of the pulse, there will be no important deviations from 
 the description given. The principal difference will arise 
 from the fact that the heart-walls and cavities do not so 
 readily take on compensatory changes; consequently the 
 relation between the degree of dilatation and hypertrophy 
 which makes the latter approximately a criterion by which 
 to estimate the former, no longer holds good. There may, 
 therefore, be considerable regurgitation with comparatively 
 little enlargement of the heart. 
 
AORTIC INCOMPETENCE. 137 
 
 Atheroma of the Aorta. — Atheroma may involve the 
 aortic valves or give rise to dilatation of the aorta, in- 
 cluding the aortic orifice, and thus produce insufficiency. 
 When the incompetence is the result of such degenerative 
 changes, there will be hypertrophy and dilatation of the 
 heart, not, however, induced by and compensatory of 
 the valvular defect, but developed antecedently to it by 
 the high arterial tension which has given rise to the 
 aortic disease. The pulse will exhibit only partially and 
 imperfectly the collapsing character ; the artery will be 
 large, and the wave sudden and brief; but when the hand 
 is held up the vessel does not collapse, but can be rolled 
 under the finger throughout the diastolic interval. It will 
 be visible, not however from the sudden filling of the 
 previously collapsed artery, but from the artery being 
 thrown into curves. Further, there will not be the marked 
 loss of time between the apex beat and the pulse at the 
 wrist. The second sound is usually heard in the neck, 
 and has the low pitch and ringing character indicative of 
 dilatation of the aorta and high arterial tension. Very 
 frequently the diastolic murmur is audible across the 
 manubrium, along the course of the aorta. 
 
 The insufficiency in such cases is produced, not simply 
 by changes in the valve, but by concurrent dilatation of the 
 aorta implicating its orifice, which is sometimes, indeed, so 
 stretched that the valves, even when retaining their normal 
 size, fail to close it, and the actual amount of regurgitation can 
 never become considerable without producing fatal syncope. 
 
 Rupture of Valve. — Rupture of a valve is always a 
 very serious lesion. It may occur as the result of severe 
 exertion when the valve has been weakened by degenerative 
 changes. The valve affected is usually the aortic, and the 
 sudden and severe strain on the heart, which has no time 
 to accommodate itself to the altered conditions of the circu- 
 lation, leads to dilatation of the left ventricle and the 
 
138 HEART DISEASE. 
 
 consequent onset of severe symptoms wnen the rupture of a 
 cusp is complete. The patient may be seized by a syncopal 
 attack, which will at once prove fatal. He may, however, 
 appear to progress favourably for some time, but will rarely 
 recover sufficiently to be able to go about again as usual, 
 for the accident usually takes place at a time in life when 
 degenerative changes are already beginning to take place 
 in the walls of the heart, and it is incapable of under- 
 going sufficient hypertrophy to compensate for the valvular 
 lesion. Hence the ultimate cause of death, if the patient 
 survives, is a gradual stasis of the circulation, the pre- 
 monitory indications being a rapid increase in the size of 
 the liver, with dilatation of the right ventricle following on 
 that of the left, and later the onset of cedema of the ex- 
 tremities. It may be some weeks or months after the 
 accident before the fatal termination ensues. 
 
 The early symptoms, however, are not necessarily so 
 severe. 
 
 In a case that was under my care at St. Mary's Hospital 
 in 1893, the patient, a man aged fifty-two, walked up to the 
 casualty room, complaining that he could not use his right 
 arm, and saying that he thought he had sprained it while 
 lifting a heavy weight. The history of the accident was 
 that he was carrying a heavy bag on his shoulder ; and 
 when throwing it off his shoulder he tried to prevent 
 it falling with too much violence on to the ground by 
 catching hold of it with his right hand. He then felt a 
 sudden pain in his arm and chest, and was violently sick. 
 He walked up to the hospital, apparently without much 
 discomfort. He was somewhat pale, but was not suffering 
 from dyspnoea, and complained chiefly of his right arm. 
 On examination, the right radial pulse was found to be 
 absent owing to thrombosis of the brachial and axillary 
 arteries. The pulse in the left radial was 98, regular in 
 force and frequency, slightly collapsing ; respirations, 18. 
 
AORTIC INCOMPETENCE. 139 
 
 On examining the heart, the apex beat was found to be 
 in the fifth space, just inside the nipple line ; a faint systolic 
 and diastolic murmur were audible at the apex, and a 
 diastolic murmur was also heard at the aortic cartilage and 
 down the sternum. The liver was not enlarged. 
 
 He remained in hospital from April 22 till May 13, 
 when he left at his own request. During this time no 
 serious symptoms had developed, and he had been up and 
 walking about the ward without any discomfort beyond a 
 little shortness of breath. 
 
 Bather more than a fortnight later, on May 30, he 
 came back to the hospital complaining of extreme short- 
 ness of breath and swelling of the legs. The pulse was 
 then 116, the respirations 34. The legs were cedematous, 
 and the face was very pale and ansemic. On examining the 
 heart, it was found to be much dilated, the area of cardiac 
 dulness extending up to the third rib above and inwards to 
 the middle of the sternum, outwards for half an inch 
 outside the nipple line. 
 
 The apex beat was not visible or palpable, but the 
 sounds were best heard in the seventh space, half an inch 
 outside the nipple line. A systolic and long soft diastolic 
 murmur were audible at that point, and the diastolic murmur 
 was heard down the sternum. The aortic second sound was 
 almost entirely replaced by the murmur, and the first sound 
 was very feeble. The liver was much enlarged, extending 
 down to within two inches of the umbilicus, and was 
 pulsating. 
 
 Kest and treatment failed to improve his condition, 
 which got steadily worse, the symptoms increasing in 
 severity till he died on August 9, some ten weeks later. 
 At the autopsy it was found that the anterior flap of the 
 aortic valve was ruptured, and that there was extensive 
 incompetence. There was considerable dilatation of the 
 cardiac cavities, and little or no compensatory hypertrophy. 
 
HO HEART DISEASE. 
 
 Symptoms. 
 
 The symptoms in well-marked aortic regurgitation are 
 those of deficient and unsustained blood supply in the 
 systemic circulation. The patient is pale, anaemic, short of 
 breath on slight exertion, and liable to fainting or syncopal 
 attacks, one of which may prove fatal. Pain, or a sense of 
 oppression in the cardiac region, may be present, amounting 
 in severe cases to angina pectoris. There may be sleepless- 
 ness or paroxysms of severe dyspnoea, and vomiting is 
 sometimes persistent in severe cases where compensation 
 has not been established or suddenly breaks down. 
 
 The above may be termed " aortic " symptoms, as dis- 
 tinguished from the train of symptoms which set in when 
 the mitral valve has given way under the strain and mitral 
 incompetence is established. The burden of compensation 
 then, as in mitral disease, falls on the right ventricle, and 
 we get a train of " mitral " symptoms in addition to the 
 already existing " aortic " symptoms. 
 
 There will be back pressure in the pulmonary veins 
 with congestion of the lungs, increased dyspnoea, and 
 perhaps cyanosis. Dilatation of the right ventricle eventu- 
 ally occurs, and enlargement of the liver and dropsy 
 supervene. 
 
 Secondary mitral symptoms are less common in aortic 
 regurgitation than stenosis, as if the lesion is severe the 
 patient is liable to sudden death from syncopal attack. 
 When stenosis supervenes in a severe case of regurgitation, 
 it appears to have a beneficial effect, and limits the amount 
 of reflux, so that the patient has a better chance of sur- 
 viving for a time ; and it is in cases of double aortic lesions 
 that we usually meet with the train of secondary mitral 
 symptoms, when the patient eventually succumbs from 
 right ventricle failure. 
 
aortic incompetence. 141 
 
 Pkognosis. 
 
 When, with a diastolic murmur, the aortic second 
 sound is distinctly audible in the neck, the pulse exhibits 
 the collapsing character only in a moderate degree, and 
 the dilatation and hypertrophy of the heart are inconsider- 
 able; that is, when the physical signs indicate that the 
 lesion is slight in extent, the patient may enjoy life and 
 do hard work untroubled by symptoms for many years, 
 provided that the lesion is due to acute endocarditis and 
 not to degenerative changes. 
 
 This may be illustrated by an example. A medical 
 man, aged forty, called on me in October, 1883, whom 
 I had known and examined sixteen or eighteen years 
 previously, when he was under Dr. Sibson's care as a 
 student at the hospital. He had had aortic incompetence 
 ever since an attack of acute rheumatism at the age of 
 fourteen, so that its duration was twer>ty-six years. The 
 following is an account of the physical signs, they were 
 identical with those present when he was at the hospital : 
 " Apex beat in sixth space not much below and very little to 
 the left of the normal situation, being a good push, but not 
 violent or extensive ; the first sound good, the second 
 sound also distinct. A systolic murmur, probably con- 
 ducted from the aorta, is audible at the apex. At the right 
 second intercostal space a weak systolic murmur is audible, 
 and along the right edge of the sternum, from the third 
 cartilage downwards, over the lower part of the sternum and 
 over the left costal cartilages, a very distinct, long, smooth 
 diastolic murmur is heard. There is a good second sound, 
 audible at the right second space and sterno-clavicular 
 articulation and in the neck. The pulse is short and is 
 felt in the fingers as well as at the wrist, but is scarcely 
 collapsing ; the carotid pulsation is marked, but the pulse 
 at the wrist and in the temporals is not visible." He had 
 
142 HEART DISEASE. 
 
 gone through his medical studies with distinction, and 
 had ever since carried on a hard-working country practice, 
 with all its incidents of night-work and exposure and 
 excessive fatigue. He could walk uphill or run upstairs 
 without experiencing any inconvenience, and it was not for 
 any cardiac symptoms that he consulted me in 1883. 
 
 Aortic incompetence sufficient to abolish the second 
 sound in the neck, and to give rise to considerable dilatation 
 and hypertrophy and to well-marked collapsing pulse is 
 serious, though it may for many years be compatible with 
 apparent health and strength. The patient will be capable 
 of ordinary work and exercise, but will be sooner out of 
 breath on going uphill or from any unusual exertion than 
 a man in health, or may feel suddenly faint and giddy 
 instead of losing his breath ; emotion again will more 
 readily induce palpitation. The future in such circum- 
 stances must be estimated on the principles laid down in 
 the chapter on general prognosis. After calculation of 
 the degree of valvular inefficiency, we must consider the 
 tenacity of the family constitution and the vigour of the 
 individual, as well as his age, habits, occupation, and 
 circumstances, bearing in mind always that even in the 
 most favourable cases the nutrition of the enlarged heart 
 will not be well maintained after middle age, and that as 
 years go on there is a tendency to increased resistance in 
 the peripheral circulation. We must look, therefore, for 
 failure of the heart and accession of symptoms sooner or 
 later, at best long before the natural term of life. There is 
 also the possibility that the compensatory equilibrium may 
 at any time be dangerously disturbed or finally overthrown 
 by imprudent exertion or anxiety or acute illness of any 
 kind. 
 
 The Age of the patient at the time when the lesion is 
 acquired is a most important consideration in prognosis, 
 and a case may be quoted to show how long a severe lesion 
 
AORTIC INCOMPETENCE. 143 
 
 may be survived even under unfavourable circumstances, 
 when the patient is young, and the heart can take on 
 compensatory changes. The patient, a boy of fifteen, came 
 under my observation in 1868, when he was admitted to 
 St. Mary's Hospital, complaining of shortness of breath. 
 His condition on admission was as follows : " Heart impulse 
 extensive and violent, apex beat in the fifth and sixth 
 spaces just outside the nipple line. Loud systolic and 
 diastolic murmurs, audible over all the cardiac area, 
 especially at the lower end and down the right border of 
 the sternum. Pulse large, sudden, and collapsing ; no 
 second sound audible in the neck." The patient was a 
 greengrocer, and continued to do his work, but frequently 
 attended the hospital as an out-patient. Five years later, 
 a mitral systolic murmur first developed, and by that time 
 the heart was of great size ; the apex beat was in the 
 seventh space in the axillary line, and was a forcible thrust, 
 which could be seen through his clothes. Dilatation and 
 elongation of the aorta had carried the outer side of the 
 ascending arch beyond the right edge of the sternum, so 
 that, pressed into the second, third, and fourth spaces, the 
 fingers came upon marked pulsation and thrill. He was 
 still able to do his work, and a year later, at the age of 
 twenty-one, he married and set up in business for himself. 
 He had now to go to the early market regularly instead of 
 occasionally, and had more work. This he did pretty well 
 for a time, but he soon had to spare himself, and his 
 business fell off. In 1875, seven years from the time he 
 was first seen, he was ill at home with rheumatism, and then 
 lived in a basement. In 1880, when again attacked by 
 rheumatism, he consented to enter the hospital as in-patient, 
 which he had refused to do previously. He was again in 
 the hospital for sub-acute rheumatism from March 5 to 
 May 8, 1882. The rheumatism quickly subsided, and there 
 was no pain after March 18 ; he had, however, a severe 
 
144 HEART DISEASE. 
 
 cough. During his convalescence, the kind of irregularity 
 of pulse and heart beat characteristic of cardiac failure in 
 aortic regurgitation was manifest ; after three or four 
 regular and fairly equal beats, a weak supplementary beat 
 would follow too quickly, or while perceptible at the 
 heart would be missing at the wrist, or the irregularity 
 might go further than this ; sometimes also the pulse would 
 reveal two distinct efforts of the ventricle in its systole, and 
 have the " bis feriens " character. Occasionally he had a 
 severe attack of dyspnoea. He improved, however, and after 
 being up and about the wards for some time, was sent to a 
 convalescent hospital, where after doing well and gaining 
 strength, he died suddenly, fourteen years after he was 
 first seen. A post-mortem examination revealed old-stand- 
 ing extensive disease of the valves, which had in effect 
 ceased to exist as valves, great general dilatation of the 
 aorta, some thickening of the mitral flaps and shortening 
 of the tendinous cords, extreme dilatation and hypertrophy 
 of the left ventricle, some dilatation and hypertrophy of 
 the right ventricle without any affection of the valves 
 of this side of the heart. The weight of the heart was 
 forty-two and a half ounces. 
 
 But even in young subjects, as soon as marked symptoms 
 begin to present themselves, danger is at hand ; when they 
 are not habitually present, the readiness with which they 
 are induced by exertion serves as a dynamic test of great 
 prognostic value. Some years since, I examined, within a 
 short time of each other, two boys with very extensive 
 aortic incompetence, attended with almost the maximum 
 degree of dilatation and hypertrophy. The physical signs 
 could only tell us that there was great incompetence, and 
 great compensatory change in both, but in the one the 
 heart was readily put off its balance, and serious symptoms 
 were induced by slight exertion ; in the other, this was not 
 so. The prognosis was, therefore, widely different in the two 
 
AORTIC INCOMPETENCE. 145 
 
 cases. The former died suddenly three years after I first 
 saw him, while the latter did not die till ten years later. 
 
 In aortic regurgitation, acquired late in life, the prognosis 
 is rarely favourable. Even if the lesion be the result of 
 acute endocarditis, and therefore stationary, the heart is 
 unable to undergo adequate hypertrophy, and efficient 
 compensation will not be established. But after middle 
 age acute endocarditis is of rare occurrence, and the 
 incompetence will usually be due to degenerative changes 
 in the valves ; the lesion will therefore be progressive, 
 especially if the arterial tension, the primary cause in all 
 probability of the trouble, is not carefully kept down by 
 suitable treatment. The prognosis is still more un- 
 favourable if the affection is due to syphilitic disease of 
 the aorta invading the valves. 
 
 Prognosis in Aoetic Kegukgitation with Stenosis. 
 
 When aortic stenosis gradually becomes established in 
 a case where aortic incompetence already exists of such 
 severity that symptoms are readily and easily induced, it 
 may act to a certain degree as a palliative agent, by limiting 
 the amount of regurgitation and making the circulation 
 more equable and regular. As the stenosis makes its 
 effects felt, the pulse will lose to a great extent its collapsing 
 character, and the artery will not empty so completely 
 between the beats. The heart will undergo further hyper- 
 trophy, and the risk of undue dilatation will be diminished. 
 Dyspnoea will be less readily induced, and the patient will 
 be less liable to syncopal attacks. 
 
 I have seen several cases in which a patient, after being 
 in imminent danger from aortic regurgitation, has, on the 
 supervention of aortic stenosis, been enabled to enjoy a life 
 of comparative comfort for many years. It does not follow 
 that the onset of aortic stenosis is of favourable prognostic 
 
 L 
 
146 HEAR! DISEASE. 
 
 import in all cases of incompetence ; it is only when the 
 aortic valves are severely damaged and are incapable of 
 checking the regurgitant stream in any effectual degree 
 that this holds good, and when the patient is still young 
 enough for further cardiac hypertrophy to take place. 
 
 Treatment. 
 
 Perhaps more can be done to prolong life and postpone 
 suffering in aortic regurgitation than in any other form of 
 valvular disease ; at any rate, it is in this disease that the 
 greatest difference can be made by care on the one hand 
 and imprudence on the other. A patient may die suddenly 
 from a single rash act who might have lived twenty years, 
 or condemn himself by a single imprudence to a short and 
 suffering existence when fair health and many years of life 
 were possible for him. It is more especially shortly after 
 the occurrence of the lesion, before full compensatory 
 hypertrophy has had time to take place, that such accidents 
 are likely to happen. Hence it is especially important 
 when aortic regurgitation has been recently established in 
 acute rheumatism that prolonged rest should be insisted 
 upon. 
 
 Six or eight weeks in bed, and after this rest in the 
 recumbent posture for another month or six weeks, is 
 advisable, and the boy should not go to school, or the young 
 man to business for another six, eight, or twelve months, 
 according to circumstances. It is even possible that a 
 diastolic murmur may completely disappear, and with it all 
 symptoms of aortic incompetence, when due care of this 
 kind has been taken. 
 
 Not uncommonly incompetence of the aortic valves is 
 discovered unexpectedly at an interval after an attack of 
 rheumatism during which endocarditis had not been 
 suspected, or had not been revealed by murmurs. It is a 
 
AORTIC INCOMPETENCE. 147 
 
 most important and useful precaution, therefore, to examine 
 the heart at intervals for some time after rheumatic fever, 
 and it is an imperative duty to do so when there has been 
 cardiac complication of any kind or degree. 
 
 In children, as the articular manifestations of rheu- 
 matism are usually so slight, and the heart is so frequently 
 attacked, an examination of this organ should never be 
 omitted : there may be nothing to suggest the presence of 
 endocarditis : but a history of transient pains in the joints 
 with febrile disturbance should at once arouse suspicion, 
 and the presence of rheumatic nodules is almost pathogno- 
 monic of cardiac mischief present or to come. Irreparable 
 damage to the heart not infrequently results from a child 
 being allowed to go about with unsuspected endocarditis. 
 
 Caution and rest are necessary, not only after an attack 
 in which there has been endocarditis setting up aortic 
 regurgitation, but also after a febrile attack of any kind 
 complicating cases of aortic incompetence. Dilatation is 
 easily induced in a heart weakened by fever under the 
 continual strain to which the left ventricle is exposed, and 
 there is special liability to sudden death during the period 
 of convalescence from acute illness. 
 
 On the other hand, provided care and complete rest are 
 insisted on, the heart may actually regain lost ground from 
 the diminution of resistance in peripheral circulation due 
 to the arterio-capillary relaxation attending pyrexia. In 
 a severe case of aortic regurgitation, I have known an old- 
 standing mitral regurgitation from secondary dilatation of 
 the left ventricle, disappear for some time under these 
 circumstances. 
 
 The risk of sudden death makes it imperative that the 
 patient suffering from aortic disease should be specially 
 warned against over-exertion and hurry, such as running 
 to catch a train or running upstairs, or excessive mental 
 excitement of any kind. The fatal event does not always 
 
148 HEART DISEASE. 
 
 take place during the exertion or excitement, but may be 
 postponed till the next day. Periods of rest from time to 
 time may be of striking service. Whenever exaggeration 
 of the short and sudden character of the pulse is observed, 
 especially if there is a faltering in the beat now and then, 
 and still more when the apex of the heart is found to be re- 
 ceding outwards, and the beat is becoming' diffuse, the recum- 
 bent posture should be enforced for some two to six weeks. 
 
 As compensation fails and symptoms become more con- 
 tinuous and severe, they will arise from and take their cha- 
 racteristics from one of two causes : either (1) failure on the 
 part of ;the left ventricle to maintain a sufficient movement 
 of blood in the capillaries, or (2) backward pressure in 
 the veins, the result of right ventricle failure secondary 
 to that of the. left. In the former case, sudden death from 
 syncope with little warning or apparent cause is liable to 
 occur ; failing that, there may be sleeplessness of a 
 peculiarly harassing kind, or painful dyspncea, unexplained 
 by any interference with the entry of air into the lungs, or 
 by want of aeration of the blood. The face will be pale and 
 have an anxious and suffering expression ; the patient will 
 be very restless and weary. Dropsy, if present, will be 
 slight, though there may be some fluid in the pleural 
 cavities with oedema of the bases of the lungs. 
 
 Under these circumstances the object of treatment is to 
 sustain the failing heart by nourishment, stimulants, and 
 such remedies as may contribute to this end — nux vomica 
 or strychnia, with ammonia and ether, to which belladonna or 
 atropin often makes a valuable addition ; sometimes digitalis 
 may be of service, but it must be used with caution ; or 
 strophanthus, which theoretically ought to be safer as 
 having less contractile influence on the arterioles. Morphia 
 hypodermically is often of the greatest possible benefit, 
 giving quiet sleep, which is not only an inexpressible 
 comfort to the sufferer, but frequently recruits the strength, 
 
AORTIC INCOMPETENCE. 149 
 
 and, by rendering the recumbent posture possible, so far 
 relieves the heart that it proves the starting-point for a 
 temporary recovery. Occasionally, however, a patient, after 
 a good night's rest procured in this way, will say he feels 
 better, sit up in bed, and suddenly fall back dead. This 
 danger of syncopal attacks should be explained to patients 
 and friends, so that watchfulness and care on their part may 
 guard against any imprudent effort or sudden movement 
 which might be attended with such fatal consequences. 
 Morphia or opium administered by the mouth is much 
 less effectual, bromides are mostly useless, chloral is 
 positively dangerous. 
 
 Angina pectoris may complicate this form of heart 
 failure. It is usually relieved by nitrite of amyl or nitro- 
 glycerine, and patients suffering from anginoid pain com- 
 plicating aortic regurgitation may come to take the latter 
 remedy in extraordinary doses. When relief cannot be 
 obtained in any other way, morphia may be given hypo- 
 dermically. Whatever tends to strengthen the heart or 
 relieve it from work will tend to prevent the onset of 
 anginoid symptoms, and when such threaten, treatment 
 must be directed to these two points. 
 
 Arsenic, and more esjDecially phosphorus, have had in 
 my hands a very beneficial influence as cardiac tonics in such 
 cases. 
 
 When the preponderating character of the symptoms 
 is that of venous obstruction, the jugular veins being dis- 
 tended and pulsating, the liver enlarged, and dropsy present ; 
 when, in fact, we have with aortic physical signs mitral 
 symptoms, the line of treatment is quite different to that 
 just described. 
 
 Purgatives should be given in full doses, but judgment 
 and caution must be exercised in their administration, as 
 unfavourable effects may develop abruptly. Digitalis may 
 then be given, usually with great benefit, and when there 
 
ISO HEART DISEASE. 
 
 is much dropsy, diuretics in addition to the digitalis will 
 often have a marked effect. It is under such conditions 
 that digitalis finds its opportunity in aortic regurgitation, 
 and justifies the statements of those who find this remedy of 
 the same service in aortic as in mitral disease. 
 
 If the administration of digitalis is persisted in after the 
 recovery from dropsy and the more severe symptoms of 
 venous stasis, it is not uncommon for patients to die 
 suddenly, sometimes before leaving bed, more frequently 
 when they have begun to get up and move about. There 
 are grounds for suspicion that digitalis contributes to this, 
 but sudden death may occur whether it has been left off or 
 not. In the absence of mitral symptoms, it is rarely that 
 digitalis is called for in aortic incompetence or is of service, 
 and it may undoubtedly do harm. It may set up sickness, 
 which is an ominous symptom in this form of disease, and 
 induces a condition of asthenia difficult to remedy. 
 
 Venesection, even when the venous stasis is severe, is 
 rarely to be contemplated. It is true that the relief to the 
 right ventricle so afforded might enable it to regain control 
 over its contents and increase the supply of blood to the 
 left ventricle and the amount available for distribution to 
 the arterial system, but before this occurs there may be a 
 momentary faintness, leading to a fatal attack of syncope. 
 
CHAPTER XL 
 
 MITRAL INCOMPETENCE OR REGURGITATION. 
 
 etiology and morbid anatomy — physical signs — the 
 murmur of mitral incompetence — the pulse — 
 explanation op irregularity of pulse — mitral 
 incompetence due to endocarditis— estimation 
 of extent of lesion, from character of murmur 
 and first sound and from compensatory changes 
 in the heart — symptoms — prognosis — mitral in- 
 competence without damage to valves — its 
 causation and explanation— differential diag- 
 nosis — treatment. 
 
 Etiology and Morbid Anatomy. 
 
 The causation of mitral incompetence is most varied. 
 It may be due to actual damage to the mitral valve by acute 
 or chronic endocarditis, or to imperfect apposition of the 
 valves or stretching of the orifice from dilatation of the 
 left ventricle. The former group, where the valves have 
 been injured by an inflammatory process, will be first con- 
 sidered. 
 
 The kind and degree of deformity produced by endo- 
 carditis may vary greatly. The edges may be thickened 
 and shrunken, presenting, instead of the translucent, thin, 
 flexible curtain, an opaque, inelastic, rounded border, in 
 which the delicate marginal ramifications of the tendinous 
 cords are swallowed up and lost. A considerable area of valve 
 
152 HEART DISEASE. 
 
 may still be available for closing the orifice, although the 
 apposition may not be accurate. In a more advanced state 
 of change, the body of the cusps may be opaque, thickened, 
 and contracted so that a considerable gap must remain, 
 allowing of great reflux even when their approximation is 
 greatest ; and sometimes this is carried so far that, as valves, 
 they are practically non-existent, especially when the 
 chordae tendinese are greatly shortened, which they may be 
 to an extent which brings the margins of the flaps close to 
 the apices of the papillary muscles. 
 
 Chronic endocarditis or degenerative change may 
 produce some opacity, thickening, and deformity, giving 
 rise to insufficiency, and calcification is not uncommon. 
 
 Physical Signs. 
 
 The Murmur. — The evidence of regurgitation through 
 the mitral orifice is a systolic murmur heard in the 
 region of the apex, and very frequently beyond the apex 
 in the fifth or sixth space towards the axilla. It is 
 often audible also at the back of the chest, between the 
 scapula and the spine, at about the middle of the posterior 
 border of the scapula. The murmur reaches the surface at 
 this point, not by extension round the thorax from the 
 axilla, but by an independent route, being conducted by 
 the vertebrae from the base of the ventricle, the shoulder 
 of which rests upon the spinal column. Occasionally 
 the murmur of mitral regurgitation is heard more loudly 
 in the fourth or even in the third space in the vertical nipple 
 line or just outside it, than at the apex. When this is 
 the case, an impulse is usually to be felt at or near the 
 same point. 
 
 Murmurs which may be mistaken for Mitral Regurgitant 
 Murmur.— The only murmurs likely to be mistaken for this 
 are, a systolic aortic murmur conducted to the apex, a 
 
MITRAL INCOMPETENCE. 153 
 
 systolic and therefore regurgitant tricuspid murmur, and 
 the spurious murmur produced by compression of the edge 
 of the lung by the ventricular systole. A pulmonic systolic 
 murmur is also occasionally heard almost at the apex. A 
 question which frequently arises when a systolic murmur 
 is heard both at the base and at the apex, is, whether 
 it is one and the same, in which case it will be aortic, 
 or whether it arises from two independent sources. It is 
 only when the murmur is loudest over the aorta that there 
 can be any uncertainty, and as a rule it is not difficult to 
 decide. Any marked difference in the tone or character of 
 the apex murmur, as compared with that heard at the base, 
 or a superadded musical element in it, would be sufficient 
 to show that it was not the conducted aortic murmur, and 
 where such evidence as this is lacking, if the apex murmur 
 is longer than the aortic, and especially if it is conducted 
 outwards for any distance, or is heard in the left inter- 
 scapular space, there can be no doubt. It must be 
 remembered, however, that a loud, rough, aortic murmur 
 may be heard as a smooth murmur of a different tone at the 
 apex, the thick muscular wall of the ventricle not lending 
 itself to the propagation of coarse vibrations, which are, 
 in fact, vibrations of the aorta itself. A loud aortic 
 murmur, again, may be audible all down the thoracic spine. 
 With regard to the tricuspid murmur a special warning 
 may be of service, as it is not unfrequently set down as 
 mitral. The tricuspid area, so called, is over the lower 
 costal cartilages, near the ensiform appendage, but a 
 systolic tricuspid murmur is often heard as far out as the 
 apex, and occasionally has its maximum intensity just to 
 the inner side of the apex. When a murmur heard at the 
 apex is lost immediately to the left of the beat, while it is 
 audible between the apex and the lower end of the sternum, 
 its seat of production is at the tricuspid, and not at the 
 mitral orifice. 
 
154 HEART DISEASE. 
 
 An imitation of a systolic apex murmur is not un- 
 frequently produced by movement of air in the lungs 
 overlapping the heart as it is compressed by the systole of 
 the heart, and it is sometimes loud enough to be heard by 
 the subject. The imposture is easily detected, by the fact 
 that it is only audible, as a rule, during inspiration, or is, at 
 any rate, much more distinct then, and that its distribution 
 does not coincide with the conduction of the true mitral 
 murmur, but follows the line of the thin edge of the lung 
 across the pericardium from the neighbourhood of the apex 
 towards the sternum. 
 
 The sources of error just mentioned being eliminated, a 
 systolic murmur audible at and to the left of the apex, is 
 mitral in origin, and indicates incompetence in the valve 
 and reflux of blood into the left auricle. There is not the 
 same doubt as to its significance as there is with regard 
 to the constant association of obstruction with an aortic 
 systolic murmur ; a mitral systolic murmur means regurgi- 
 tation. It does not, however, necessarily imply that there 
 is actual disease of the mitral valve, as there are other 
 causes, enumerated later, which may give rise to mitral 
 regurgitation from dilatation of the left ventricle or 
 stretching of the mitral orifice. 
 
 The Pulse. — The distinguishing characteristic is irregu- 
 larity, both in rhythm and in force. In advanced cases no 
 two beats are alike; a few fairly strong, full pulsations, 
 at something like proper intervals, will be followed by a 
 number of feeble, hurried beat's, these again perhaps by 
 a single good stroke, after which there is a pause and then 
 renewed hurried action. Little difference of opinion exists 
 as to the association of mitral incompetence with irregu- 
 larity of pulse. It would not be true to assert that there 
 can be no considerable regurgitation without irregular 
 action of the heart, but it is a safe working hypothesis that 
 a mitral murmur is not attended with serious reflux while 
 
MITRAL INCOMPETENCE. 155 
 
 the pulse remains regular. What, then, is the cause of the 
 irregularity? We find similar irregularity occasionally 
 attending dilatation of the heart, and it might be suggested 
 that, as mitral insufficiency is not unfrequently the result 
 of dilatation of the ventricle, the irregularity of the pulse 
 is symptomatic of the dilatation, and not of the regurgi- 
 tation ; but the irregularity accompanies incompetence 
 caused by rheumatic damage of the valves, quite as 
 constantly as it does the insufficiency due to dilatation. 
 
 Irregular heart action and pulse, again, may be among 
 the final symptoms in any form of valvular disease, though 
 they are rarely quite of the same character as in mitral 
 regurgitation ; but in this latter disease the irregularity 
 supervenes early, and is not inconsistent with fair compensa- 
 tion and apparent health for many years. 
 
 It is probable that the varying pressure to which the 
 heart is subjected in inspiration and expiration may account 
 for it. The variations of intrathoracic pressure in ordinary 
 respiration have no obvious effect on the action of the 
 heart ; but we can at any time slightly disturb the rhythm 
 of the heart and pulse by taking and holding a very 
 deep breath. When again there is incipient irregularity 
 careful observation will almost always show that the break 
 in the rhythm occurs at the moment when there is a 
 change in the intrathoracic pressure at the beginning and 
 end of inspiration or expiration. This is best seen, 
 perhaps, in cases of bronchitis and emphysema with dilated 
 right heart. The thin-walled auricles will be all the more 
 susceptible of this change of pressure when distended and 
 dilated, while it will scarcely affect the ventricles. 
 
 The heart works habitually under a negative pressure due 
 to the elastic traction of the lungs, and is only subjected 
 to positive pressure, strictly speaking, when the chest is 
 filled and the glottis closed in effort. The aspiration re- 
 sulting from the negative pressure is greatest in inspiration, 
 
156 HEART DISEASE. 
 
 and aids the circulation by drawing the blood into the 
 auricles, which then carry it on into the ventricles. In 
 expiration the auricles are more or less compressed as the 
 chest walls collapse. 
 
 When the left auriculo-ventricular valves are incom- 
 petent, the pressure on the auricle during expiration will 
 aid in resisting the systolic reflux from the ventricle, and 
 in driving the blood into the ventricle during diastole ; at 
 the moment when the positive pressure of expiration is 
 exchanged for the negative pressure of inspiration, the 
 resistance to the reflux of blood into the auricle is suddenly 
 diminished, so that more will be allowed to regurgitate, and 
 less will be carried into the aorta, and there will be no 
 compression of the auricle to aid in filling the ventricle. 
 Corresponding differences of an opposite kind will attend 
 the end of inspiration. The varying supply of blood to the 
 ventricle thus induced, cannot fail to produce a tendency to 
 irregularity. 
 
 Estimation of the Extent of the Lesion. — Our first inquiry 
 will be as to the physical signs and symptoms by means 
 of which we may approximately infer the degree of impair- 
 ment of the valves, and the amount of regurgitation which 
 takes place. 
 
 The murmur affords, in some cases, important informa- 
 tion. When it is not conducted much beyond the situation 
 of the apex beat, the apex itself not being greatly displaced, 
 and is not audible in the back, the regurgitation is usually 
 slight. But an exception to this statement may be found 
 at the opposite extreme, when the orifice is gaping and the 
 ventricle weak. Under such circumstances the murmur may 
 be short and scarcely audible ; symptoms, however, will at 
 once distinguish between the two conditions. 
 
 The persistence of the left ventricle first sound is 
 evidence that there is no advanced change in the valves, 
 more especially when the murmur is retarded. This is 
 
MITRAL INCOMPETENCE. 157 
 
 an important point to note. If the regurgitation is con- 
 siderable, the murmur takes the place of the first sound, 
 and is said to hide it ; but it is not a mere question of 
 loudness, there is a true substitution of the murmur for the 
 sound. When, therefore, the first sound is distinctly heard 
 heading the murmur, some difference exists. It would be 
 going too far to say, as in the case of the aortic valves, that 
 the sound indicates sufficient check to the refluent blood to 
 produce tension of the valves and cords, and of the ventri- 
 cular wall, but the inference tends in that direction. With 
 regard to the retarded-systolic mitral murmur, when the 
 murmur follows the first sound at a distinct though very brief 
 interval, it would seem that there is, in the first instance, 
 complete closure of the valves, but that during the contrac- 
 tion of the ventricle, the apposition is deranged so that 
 leakage occurs. Such leakage can scarcely be other than 
 slight. These inferences are confirmed by the fact that the 
 persistent first sound and the retarded systolic murmur are 
 most common in the curable or temporary regurgitation of 
 ansemia, and the conclusions based on this observation may 
 be extended to other cases than those of early life. One 
 caution is necessary, that is, to beware of taking the 
 modified short, sharp, first sound of mitral stenosis, when 
 there is both obstruction and regurgitation, for the normal 
 second sound. 
 
 The general statement made in the first chapter that a 
 loud and long murmur is usually significant of a lesser 
 degree of structural damage and functional imperfection 
 than a short and weak murmur, is another point to be borne 
 in mind. Loudness implies strength of contraction, and 
 length shows that the ventricle goes through with its 
 systole, and also that it is not quickly emptied, as it would 
 be were there a large escape into the auricle. The murmur 
 of worst significance is a short, weak whiff, varying in 
 intensity and duration in successive beats. 
 
158 HEART DISEASE. 
 
 It is the mitral systolic murmur which is most frequently 
 musical ; very commonly, but not perhaps always, the 
 musical murmur indicates a narrow chink, and therefore 
 little reflux. The musical note may be high-pitched or low, 
 nearly always it is accompanied by a blowing murmur, and, 
 according to my experience, has never the pure tone some- 
 times produced at the aortic orifice. It does not always 
 begin at the same time with the blowing murmur, but may 
 be interpolated into it, beginning later and ending sooner. 
 
 As the action of the heart is frequently irregular, the 
 intensity, character, pitch, and length of the murmur may 
 vary from one beat to another. 
 
 For further evidence we must trace the effects of regur- 
 gitation through the mitral orifice. The immediate effect of 
 reflux of blood into the left auricle will be to distend this 
 cavity, but, lying deeply as it does, the physical signs of 
 an early stage of dilatation are not such as can be relied 
 upon for definite information ; but another result which 
 follows early is obstruction to the free outflow of blood 
 from the pulmonary veins into the auricle, and this soon 
 makes itself felt backwards through the capillaries of the 
 lungs, and gives rise to high pressure in the pulmonary 
 artery. Here we come upon audible evidence ; the in- 
 creased tension brings down the semilunar valves with 
 greater force, and gives rise to accentuation of the pul- 
 monic second sound. It is not easy to say what degree of 
 intensification of this second sound is required as proof of 
 obstruction to the flow of blood through the lungs. The 
 aortic second sound has to be taken as a basis for com- 
 parison, and while most observers say that the aortic is the 
 louder of the two, my own conclusion is that the pulmonic 
 is usually louder than the aortic. Again, the pulmonic 
 second sound may be accentuated by resistance arising in 
 the lungs themselves, as in bronchitis and emphysema. 
 Marked and persistent intensification of the pulmonic 
 
MITRAL INCOMPETENCE. 159 
 
 second sound, when a mitral systolic niurmur is present, 
 must, however, be taken as evidence of sufficient reflux to 
 increase the pressure in the pulmonary artery by the 
 obstruction to which it gives rise. 
 
 Changes in the Heart.— From this follow hypertrophy 
 and dilatation of the right ventricle. The call upon the 
 right ventricle for increased force in propelling the blood 
 through the lungs results in a combination of dilatation 
 and hypertrophy, of which the physical signs are displace- 
 ment of the apex outwards or to the left and undue right 
 ventricle impulse, felt when the hand is placed over the 
 lower costal cartilages to the left of the sternum, and seen, 
 and perhaps felt, in the epigastrium and below the left 
 costal margin. The right ventricle in effect comes to the 
 aid of the left ; the heightened pressure maintained by its 
 means in the left auricle resists the reflux of blood from 
 the ventricle, and since life is often sustained when the 
 valves are practically non-existent, the intra-auricular 
 pressure must in such cases almost, if not quite, equal the 
 pressure in the systemic arteries. Further, the same force 
 which resists the reflux must, on the relaxation of the left 
 ventricle, drive the blood violently into it, taking it, so to 
 speak, at a disadvantage, and distending it in the same 
 way, though not to the same degree, as aortic regurgitation, 
 giving rise thus to dilatation, which is accompanied or 
 followed by more or less hypertrophy. In proportion as 
 the left ventricle is enlarged, the apex will be carried 
 downwards and its beat become conspicuous, and the hyper- 
 trophy of the right ventricle pushing it outwards and some- 
 times upwards, the ultimate displacement of the apex will 
 be the resultant of the changes in the two ventricles. 
 There will also be dilatation of the auricles. The volume 
 of the heart as a whole will thus be increased, giving 
 rise to a corresponding extension of the area of deep 
 dulness. 
 
160 HEART DISEASE. 
 
 These changes, the necessary result of the incompetence 
 of the mitral valve, traceable directly to the mechanical 
 difficulty produced by it, become the measure of the diffi- 
 culty and of the incompetence. A systolic mitral murmur 
 without increase in the area of cardiac dulness, without 
 much displacement of the apex, and without marked 
 accentuation of the pulmonic second sound, without, again, 
 symptoms indicative of disturbance of the circulation such 
 as might be due to failure in the compensatory changes, is 
 not attended with any considerable regurgitation, and is not 
 a source of present danger. Unless there is reason to look 
 upon it as the beginning of progressive damage, it may 
 practically be disregarded. As the signs of pressure in the 
 pulmonary circulation and of changes in the walls and 
 cavities of the heart increase, we infer increase in the 
 amount of reflux, for they indicate greater difficulty in 
 neutralizing its injurious effects. We, therefore, calculate 
 on diminished stability of the compensatory balance and 
 on less power of regaining a working equilibrium of the 
 circulatory forces if it is once overthrown. 
 
 To sum up the indications by which the extent of the 
 lesion may be surmised : 
 
 While it may safely be said that if the pulse remains 
 regular the reflux is slight, the degree of irregularity of 
 the pulse will not be any criterion as to the extent of the 
 reflux. More is to be learnt from the degree of vigour of 
 the beat, and the length of the pulse wave. 
 
 Further information will be derived from the character 
 of the murmur, and the extent to which it replaces the 
 first sound, and again from accentuation of the pulmonic 
 second sound ; but the amount of dilatation and hyper- 
 trophy of the heart, more especially of the right ventricle, 
 will afford a more accurate basis for the estimation of the 
 degree of incompetence. The symptoms must also be con- 
 currently taken into consideration. 
 
mitral incompetence. 161 
 
 Symptoms. 
 
 No symptoms will be present in cases of slight regur- 
 gitation even on moderate exertion. In more severe cases, 
 or when compensation is beginning to fail, shortness of 
 breath, a tendency to cyanosis, and slight pitting of the 
 legs at night will be among the earliest symptoms. The 
 dyspnoea and cyanosis will become more marked and per- 
 sistent as time goes on, and are due to congestion and 
 passive hyperemia in the lungs from back pressure in the 
 pulmonary circulation, which gives rise to the secondary 
 changes in the lungs described in the chapter on mitral 
 stenosis. The pressure in the pulmonary circulation, how- 
 ever, is not so high as in mitral stenosis, and hsemioptysis 
 does not occur in pure mitral incompetence, nor is the con- 
 dition of brown induration so definitely established. The 
 tendency is rather to congestion and oedema of the bases 
 of the lungs than to fibrosis, and cough is often a trouble- 
 some symptom, the more so as the patient is especially 
 liable to attacks of bronchitis. (Edema of the legs is a 
 comparatively early symptom, but is at first readily 
 amenable to treatment by rest in bed and suitable 
 medicaments. The liver enlarges as the right ventricle is 
 unable to cope efficiently with the effects of the mitral lesion, 
 and its varying size is therefore an important indication as 
 to the efficiency of compensation. It will pulsate when 
 tricuspid incompetence is established, but, as a rule, it 
 feels less firm and hard than in mitral stenosis, and ascites 
 is less common. 
 
 The morbid anatomy of the secondary changes in the 
 lungs and liver in mitral disease are described in the 
 chapter on mitral stenosis. 
 
 Prognosis. 
 The range of possibilities as regards duration of life in 
 mitral regurgitation, due to actual damage of the valve by 
 
 M 
 
162 HEART DISEASE. 
 
 acute endocarditis, is more extensive than in any other form 
 of valvular disease. It is the least serious and the most 
 amenable to treatment of all the valvular affections. 
 
 When the lesion is slight the patient may live to old 
 age without experiencing inconvenience from the results of 
 the leakage, and may be capable of much hard work and pass 
 through serious illnesses. In moderately severe cases, with 
 reasonable precautions, he may live many years without 
 serious symptoms declaring themselves. Women with 
 mitral regurgitation may bear children with impunity. 
 
 In endeavouring to forecast the further course of a case 
 of mitral incompetence when the regurgitation is incon- 
 siderable, or when compensation has been established, one 
 of the most important considerations will be the degree 
 of arterial tension. Everything, so to speak, will depend 
 upon the amount of resistance in the peripheral systemic 
 circulation, and this may vary extremely. If with a given 
 degree of mitral incompetence, we have undue arterial 
 tension, the force of the regurgitant stream will be great, 
 the back pressure in the auricle and pulmonary circulation 
 high, the demand upon the right ventricle severe, all of 
 which are circumstances tending to the production of 
 structural changes ; if, on the other hand, the arterial 
 tension is low, the conditions are reversed. 
 
 The case of a patient, whom I have known to have 
 mitral regurgitation for at least thirty-five years, may 
 illustrate this. When first seen there were disquieting 
 symptoms, a sense of constriction and oppression at the 
 chest on moderate exercise, and liability to slight fainting 
 attacks. Finding with such symptoms the pulse ex- 
 tremely short, soft, and compressible, it was at first feared 
 that there were degenerative changes in the heart, but the 
 family pulse, as exhibited by several children and grand- 
 children, Avas one of extremely low tension, and this was 
 found to be the explanation of the patient's weak pulse. 
 
MITRAL INCOMPETENCE. 163 
 
 There can be no doubt that the absence of resistance in the 
 systemic arterioles and capillaries had an important share in 
 the prolonged immunity from structural changes which he 
 has enjoyed in spite of work of the most trying and 
 arduous kind. 
 
 One or two other examples of prolonged survival may 
 be mentioned. Two gentlemen, in whom I found mitral 
 regurgitation more than twenty years since, were, when I 
 last saw them, more than forty years of age and in active 
 work. The murmur was loud and long in both, and in 
 one there was considerable hypertrophy of the right ventri- 
 cle and marked irregularity of the pulse. Another gentle- 
 man, whom I have repeatedly examined, and found to have 
 a mitral systolic murmur, was, thirty-five years before I 
 saw him, condemned to life-long inactivity, and I learnt 
 from the family medical man that there had been a con- 
 tinuous history of valvular disease for that length of time ; 
 he rebelled against the sentence, and was still at the 
 age of sixty-four doing strenuous work. Nothing is more 
 common than to find a mitral systolic murmur after the age 
 of seventy, but we cannot say how long it has been present, 
 as it is not often that we can date it. Mitral regurgitation 
 is the disease which sends patients into hospital time after 
 time, often with advanced dropsy or severe pulmonary 
 complication, from which they recover so completely as to 
 resume work for a while. It is again the affection most 
 commonly met with in out-patient hospital practice, while 
 among in-patients and in the post-mortem room it is less 
 frequently represented than mitral stenosis. All these facts 
 point to one conclusion, viz. that mitral incompetence is 
 not a deadly form of heart disease ; I consider it to be less 
 serious than aortic stenosis. It is not merely that in a 
 large number of cases the actual damage to the valve and 
 the consequent functional imperfection is only slight, but 
 there is ample provision for compensatory adjustments, and 
 
1 64 HEART DISEASE. 
 
 very extensive change, if it is stationary, may be survived 
 twenty or thirty years, and not prevent the patient reaching 
 old age in comfort. 
 
 Mitral Incompetence without Damage to Yalves. 
 
 In the large group of cases of mitral regurgitation now 
 to be considered, the cause of the reflux is not actual 
 damage to the mitral valves, but stretching of the orifice 
 or imperfect closure of the valves, due to dilatation of the 
 left ventricle. 
 
 Such dilatation may be secondary to aortic disease, or 
 the result of prolonged high arterial tension ; but mitral 
 regurgitation due to these causes need not be considered 
 here, as its prognosis and treatment are those of the primary 
 affection, and have been discussed elsewhere. 
 
 The chief causes of mitral incompetence in the group 
 to be considered, are : anaemia, acute febrile disorders, and 
 conditions associated with advancing age. 
 
 The so-called hseinic mitral murmurs which have some- 
 times been supposed to have some other significance than 
 actual reflux, as they disappear with improving health, 
 are not unfrequently met with in anseinia, especially in 
 young women, or at times after acute febrile diseases, such 
 as acute rheumatism, typhoid fever, or measles ; the systolic 
 mitral murmurs so commonly present in chorea sometimes 
 belong to the same class, and mitral regurgitation, coming 
 on late in life, not unfrequently has a similar causation, 
 although it may not be removed by treatment. 
 
 It is to all this class of cases that McAlister's* explana- 
 tion of mitral reflux without disease of the valves or en- 
 largement of the orifice, already referred to, applies. It 
 had been forgotten or overlooked, notwithstanding ocular 
 demonstration on the living heart, and preparations 
 
 * British Medical Journal, August, 18S2. 
 
MITRAL INCOMPETENCE. 165 
 
 showing the heart in systole and diastole by Sibson, 
 notwithstanding also measurement of the circumference 
 of the heart in the contracted and relaxed condition and 
 the fact that the opening was only the upper end of 
 the ventricular cavity, that contraction of the orifice con- 
 tributed in an important degree to its perfect closure by the 
 valves. When regurgitation occurred, which was not ex- 
 plained by changes in the valves, it was accounted for by 
 irregular action of the papillary muscles, or by the sup- 
 position that the papillary muscles, and with them the 
 tendinous cords, were carried by dilatation of the ventricle 
 to such a distance from the base of the valves that the 
 margins, being dragged down by the chordae tendineae, 
 could not meet. It was demonstrated in McAlister's 
 paper, that all that is required in order that the reflux in 
 question may occur, is that from languid contraction of the 
 cardiac muscular fibres, or from resistance in the peripheral 
 circulation, the due constriction of the orifice should not 
 take place ; the valvular mechanism will then be deranged 
 and the apposition of the flaps be incomplete. It must be 
 added, however, that if the contraction of the orifice is 
 imperfect, so will be the ventricular systole as a whole, so 
 that the position of the papillary muscles may contribute 
 to the derangement. 
 
 The mitral murmur of anaemia, though only a particular 
 case of regurgitation from dilatation, is worthy of separate 
 consideration. It is met with in only a small proportion 
 of cases of anaemia, and may be absent when the blood- 
 lessness is extreme. It does not, therefore, mark a certain 
 degree of impoverishment of the blood, and may indeed be 
 found when this is by no means advanced. The remarks 
 apply equally to chlorotic anaemia, to anaemia from loss of 
 blood, and to pernicious anaemia. The fact that a mitral 
 murmur is so often absent in fatal pernicious anaemia is 
 perhaps the most remarkable. It seems probable that while 
 
166 HEART DISEASE. 
 
 the poverty of the blood and the consequent innutrition 
 of the heart are the predisposing influences, the proximate 
 cause is some overstrain, Avhich may be sufficient even in 
 the absence of anaemia. 
 
 As an instance of this, may be quoted the case of a young 
 lady whom I saw from time to time during a period of four 
 years. She was well nourished, with well-developed muscles, 
 as well as a fair amount of adipose tissue, and the lips and 
 face were a good colour. When first seen she had a pro- 
 nounced mitral murmur, and the apex beat was displaced to 
 the left of the nipple line. There were no murmurs in the 
 neck or over the pulmonic area or aorta ; the catamenia 
 were excessive. 
 
 This was her condition in July ; in October the murmur 
 had disappeared and the apex had receded. In the following 
 January, after the death of a relation by drowning, which 
 she witnessed, the murmur and dilatation had returned. 
 A month later the murmur could not be heard, but the 
 apex was still outside its normal situation. On examina- 
 tion in July, September, and December of that year, the 
 apex beat was normal and the murmur absent, although 
 the menses were suspended for long periods, and she had 
 lost flesh. No further relapse had occurred when I last 
 saw her. The influences which appeared to determine the 
 occurrence of the regurgitation were the relaxing climate 
 in which her home was placed ; the frequent necessity, from 
 the situation of the house, of walking uphill when tired ; 
 and, probably more than all, domestic worry. 
 
 There is, however, in anaemia, a cause of dilatation of 
 the weakened left ventricle independent of external and 
 accidental circumstances ; this is high arterial tension, 
 which, as has been elsewhere pointed out, nearly always 
 attends this state of the blood. Undue arterial tension 
 implies increased resistance to the emptying of the ventricle, 
 and this gradually distends it. When regurgitation is not 
 
MITRAL INCOMPETENCE. 167 
 
 produced, there are still very frequently the signs of 
 dilatation in displacement outwards and downwards of the 
 apex, and a diffuse character of its beat. The operation of 
 this cause perhaps throws light on the production of 
 permanent valvular disease by anaBinia, which G-oodhart has 
 shown to be probable. The peripheral resistance throws 
 extra stress upon the mitral valves, the action of the heart 
 is liable to be excited and violent in anaemic subjects, which 
 will intensify the effects of the strain, and so valvulitis may 
 be set up. 
 
 Differential Diagnosis. 
 
 It may sometimes be difficult to decide whether a mitral 
 murmur is due to conditions such as have just been described, 
 or to actual changes in the valves. Where there are 
 obvious compensatory changes in the left or right ventricle, 
 there can be no doubt, and in many cases the state of health 
 of the patient with the history will be a sufficient guide ; 
 but difficulties may arise, for example, when there is marked 
 anpeinia in a woman who has had acute rheumatism, or when 
 a murmur is present, without anaamia adequate to account 
 for it, in a patient who is not known to have suffered from 
 rheumatism. In such doubtful cases, the character of the 
 murmur may afford useful information. If the murmur is 
 soft and blowing, and a murmur is heard not only at the 
 apex, but at the pulmonic and aortic areas, the probability 
 is that it is due to anasmia, and not to actual valvular change. 
 
 Hsemic murmurs are usually soft and blowing in 
 character, not harsh or musical, and they do not replace or 
 extinguish the first sound. Generally speaking, they are 
 not conducted to the axilla or heard over the back, and are 
 not accompanied by much displacement of the apex beat. 
 While this is the rule, I have known several cases in which 
 it was departed from, the apex being displaced, and the 
 murmur heard towards the axilla or over the back. 
 
1 68 HEART DISEASE. 
 
 Furthermore, it is the hsemic murmur which is most 
 frequently late-systolic in time, that is, it follows the first 
 sound at an appreciable interval instead of commencing 
 synchronously with it. 
 
 These indications, together with the history of the case 
 and the physical signs present, will as a rule be sufficient to 
 clear up the diagnosis in doubtful cases. 
 
 Regurgitation in Acute Febrile Diseases. — Eegurgitation 
 of similar character resulting from acute disease lasts for 
 a short time only, and is chiefly interesting from the fact 
 that it is not uncommon after acute rheumatism, the great 
 cause of true valvular lesions. It is often impossible 
 to say whether a soft mitral murmur heard towards the 
 close of an attack of rheumatic fever, indicates the begin- 
 ning of actual disease, or is the result of temporary 
 functional imperfection. If it occurs after the commence- 
 ment of systole, and especially if a pulmonic systolic 
 murmur is also present, it may be that the regurgitation 
 is due to dilatation from anasmia or loss of tone of the 
 muscular fibres, the result of myocarditis ; but time alone 
 will decide with certainty. 
 
 Chorea. — The mitral murmur associated with chorea 
 frequently persists after the chorea is cured, and may be 
 the result of endocarditis which has damaged the valves 
 during acute or sub-acute rheumatism, which is so frequently 
 an antecedent or accompaniment of chorea. It may, how- 
 ever, be due to temporary dilatation of the heart, and dis- 
 appear as the chorea subsides and the patient improves in 
 general health. 
 
 The cases considered constitute the mitral incompetence 
 of early life. But the mitral incompetence may be estab- 
 lished during the decline of life, from other causes, and this 
 class of cases must now be considered. 
 
 The Mitral Regurgitation of Middle and Old Age. — 
 It is astonishing how frequently this is met with, and 
 
MITRAL INCOMPETENCE. 169 
 
 how imperceptibly it is established. In some cases there 
 is no obvious organic valvular, or structural alteration ; 
 commonly, however, there is considerable dilatation of the 
 auriculo-ventricular opening, and no definite diagnosis can 
 be made between this condition and degenerative changes, 
 such as thickening and calcification, slowly taking place 
 in the valves. 
 
 Mitral Incompetence and High Arterial Tension— The 
 mitral orifice may be greatly stretched so as to admit 
 three or four fingers. Sometimes, from the condition 
 of rigor mortis in the muscle, the valves seem to be 
 apparently capable of closing it more or less perfectly 
 when tested by water after death, though during life re- 
 gurgitation was permitted as a result of imperfect co- 
 aptation. Dilatation of the ventricle and stretching of the 
 auriculo-ventricular opening usually take place together, 
 but by no means to a corresponding extent ; either orifice 
 or ventricle may be disproportionately enlarged. The 
 regurgitation may be said to be only an incident of 
 dilatation. Undue arterial tension will have a most im- 
 portant place among its causes, and I have watched in many 
 cases the gradual supervention of a murmur upon sounds 
 which have had the loud and sharp character produced 
 by excessive peripheral resistance ; but I have also found 
 a mitral murmur when there has been no arterial tension, 
 the pulse being large, soft, short, and compressible. In 
 chronic disease of the kidneys, which can scarcely escape 
 mention when the effects upon the heart of protracted high 
 tension in the arteries are under consideration, mitral 
 regurgitation is less frequent than might perhaps have 
 been expected, and when it occurs, there is usually actual 
 lesion of the valves. This is probably due to the fact that 
 the hypertrophy, which is associated with the dilatational 
 and is usually the predominant change, renders the ventri- 
 cular systole efficient in constricting the orifice. 
 
170 heart disease. 
 
 Teeatment. 
 
 Mitral incompetence is met with in such varied degree 
 and has such varied causation, that it is necessary in 
 discussing the treatment to differentiate between the most 
 important varieties. 
 
 1. When there is no valvular lesion, and the regurgita- 
 tion is due to imperfect systolic narrowing of the orifice as 
 in anaemia, and occasionally after acute disease, the principal 
 treatment will be that of the condition which has given rise 
 to the atony of the cardiac muscle. When the heart is dilated 
 after acute disease, a period of absolute rest may occasionally 
 be necessary. Violent or sustained exertion in such cases 
 and in anaemia, must be avoided, as acute dilatation may be 
 produced, or a pre-existing dilatation may be increased by a 
 comparatively slight cause. Gentle regular exercise will be 
 of great importance, and may be gradually increased in 
 duration and vigour, as the heart regains its tone. 
 
 A daily period of repose in the recumbent position 
 should be enjoined, and a complete rest for a certain time 
 before and after meals should be insisted on. 
 
 Climate has an extraordinary influence in this condition 
 of heart, and the GErtel system of graduated exercise at a 
 moderate elevation is often of great service. 
 
 Iron, quinine and strychnine may be given for the 
 anaemia and general weakness, and small doses of digitalis 
 will often make a great difference in the results obtained. 
 
 The systolic apex murmur may be confidently expected 
 to disappear in time, as a result of suitable treatment. 
 
 2. In the case of a systolic apex murmur with extremely 
 little regurgitation, common after middle age, when not 
 due to dilatation of the left ventricle, little treatment is 
 required. 
 
 In most cases, instead of restriction in exercise being 
 necessary, regular exercise will have to be ordered, and a 
 
MITRAL INCOMPETENCE. 171 
 
 sedentary, self-indulgent mode of life modified, as these 
 patients often plead a weak heart as an excuse for avoiding 
 fresh air and exercise, which they dislike. 
 
 When the incompetence is real, and has required 
 compensatory changes to neutralize its effects, it is still 
 desirable that the patient should take regular exercise, the 
 duration and vigour of which must be determined by his 
 strength and breath. So long as respiratory distress is not 
 induced, outdoor exercise will do good and not harm. 
 Standing about indoors is much more likely to be 
 injurious. 
 
 The one contingency to be specially guarded against 
 is bronchitis, or any acute affection of the lungs. The pul- 
 monary circulation is already carried on under difficulties, 
 and superadded obstruction may intercept the compensatory 
 high pressure maintained in the left auricle by the right 
 ventricle ; the result being that there is less opposition to 
 the mitral regurgitant stream, the left ventricle is imper- 
 fectly filled, and the systemic blood supply is impaired : 
 further, the right ventricle, unable to contend with the 
 double obstacle to the transmission of blood through the 
 lungs, becomes over-distended and crippled, so that tricuspid 
 regurgitation and venous stasis result. The dreaded ulterior 
 effects of mitral regurgitation are thus anticipated, and, 
 besides this, recovery from the bronchitis is retarded by 
 the congestion in the pulmonary capillaries. 
 
 High Arterial Tension. — Precautions must also be taken 
 against high arterial tension, which may be due to renal 
 disease or gout, or may be produced by too nitrogenized 
 a system of diet, or by habitual consumption of beer or 
 strong wines, or by constipation. With high arterial 
 tension there will be increase in peripheral resistance, and 
 thus increase in the amount and force of the mitral reflux, 
 causing an additional continuous strain on the compensatory 
 mechanism. Suitable dieting and the habitual use of a 
 
172 HEART DISEASE. 
 
 mild mercurial purge once or twice a week, will tend to 
 keep down high arterial tension when it is present. 
 
 3. When serious symptoms set in, and especially if any 
 exciting cause can be traced, there is more chance of making 
 head against them, and of improvement under treatment, 
 than in other forms of valvular disease. The result of mitral 
 regurgitation is always backward pressure, taking effect 
 first on the lungs, then on the right ventricle, and finally 
 giving rise to obstruction to the systemic venous return, 
 when the right ventricle breaks down. Tricuspid regurgi- 
 tation does not appear to add appreciably to the obstruction 
 in the great veins, and, indeed, is thought by some to 
 prevent paralysis of the right ventricle from over-dis- 
 tension. The two problems in the treatment are the 
 relief of the venous stagnation and the strengthening and 
 restoration of tone and vigour to the right ventricle, so 
 that it can again perform its work efficiently. There is 
 no constricting barrier opposing a fixed mechanical obstruc- 
 tion to the blood current as in mitral stenosis ; the task 
 is therefore easier. 
 
 Fur the Relief of the Venous Obstruction, purgatives, of 
 which mercury in some form is a constituent, will usually 
 be sufficient, repeated according to their effect, and accord- 
 ing to the condition and strength of the patient every 
 second or third day. The application of leeches over the 
 liver, if it is enlarged and tender, will often be of great 
 service, and almost invariably affords relief. Dry cupping 
 may be useful. Yenesection is not often absolutely required, 
 though probably it might more frequently be resorted to 
 with advantage than is the case. 
 
 Concurrently digitalis should be given, and it is in the 
 treatment of dropsy and advanced conditions of mitral 
 incompetence, that it may be administered with the greatest 
 confidence and least apprehension of its so-called cumulative 
 effects. It increases, it is true, the peripheral resistance, 
 
MITRAL INCOMPETENCE. i 73 
 
 but as long as the structures of the heart are sound, it 
 appears to increase the vigour of its contraction in greater 
 proportion; this is especially the case with the right 
 ventricle, and the improvement in the transit of blood 
 through the lungs is perhaps the most important element 
 in its beneficial results. It may be given with satisfactory 
 results for any length of time, as there is no barrier in the 
 shape of a stenosed orifice, against which the increased 
 energy expended by the heart will be exhausted : the only 
 reason for discontinuing it will be nausea or loss of appetite, 
 to which it sometimes gives rise, or marked diminution in 
 the amount of urine excreted. 
 
CHAPTER XII. 
 MITEAL STENOSIS. 
 
 ETIOLOGY — PREDOMINANCE IN THE FEMALE SEX — MOEBID 
 ANATOMY — PHYSIOLOGY OP THE CHANGES IN THE 
 HEART — BROWN INDURATION OP LUNGS — NUTMEG 
 LIVER — THE PHYSICAL SIGNS — THE PULSE — THE 
 CHANGES IN THE HEART — THE CARDIAC MURMURS — 
 THREE STAGES IN THE PROGRESS OP THE DISEASE AS 
 DEFINED BY AUSCULTATORY SIGNS — THE CHARACTER- 
 ISTICS OF THESE THREE STAGES— SYMPTOMS— DIAGNOSIS 
 — PROGNOSIS —TREATMENT. 
 
 Constriction of the mitral orifice is on many grounds the 
 most interesting of the valvular affections of the heart. 
 It is a common, and at the same time a serious form of 
 valvular disease, and its clinical history presents peculi- 
 arities, some of which have long been recognized, while 
 others have not received adequate notice. It was the last 
 of the valvular diseases to be associated with distinctive 
 physical signs, and to Gairdner the credit of this discovery 
 is due. It also presents greater difficulties in diagnosis 
 than any other of the valvular affections. 
 
 Etiology. 
 
 Acute endocarditis is the commonest cause of mitral 
 stenosis, but a certain interval must elapse before con- 
 striction of the mitral orifice results, as this is mainlv due 
 
MITRAL STENOSIS. 175 
 
 to cicatricial contraction of the fibrous tissue formed in the 
 process of repair of the damaged valves after inflammation. 
 A remarkable fact is the relative frequency of its occur- 
 rence in women, whether the basis of the estimate is 
 post-mortem or clinical. Of fifty-three patients dying in 
 St. Mary's Hospital and examined after death, thirty-eight 
 were females and only fifteen males — seventy-two and 
 twenty-eight per cent, respectively. Of eighty-one cases 
 collected by Hayden fifty-four were females and twenty- 
 seven males — 66-6 and 33*3 per cent. Dyce Duckworth, in 
 eighty cases, found no fewer than sixty-three women — 
 78*75 per cent. It cannot be said that any satisfactory 
 explanation of this great disproportion of women affected 
 by mitral stenosis has been given. It is true that rheumatism 
 is more common in girls than in boys, but were this the 
 only reason, there ought only to be a general predominance 
 of valvular disease in women, and not of this particular con- 
 dition. Possibly the greater liability of girls to ansemia at 
 the period of puberty may have some bearing on the greater 
 incidence of mitral stenosis in the female sex, especially 
 when it is borne in mind that ansemia is frequently attended 
 with augmented arterial tension which, by increasing the 
 stress on the mitral valves, is a cause of insidious damage. 
 These two factors may tend to keep going the chronic 
 inflammatory process, which results in adhesion of the cusps 
 of the mitral valve, and in further constriction of its orifice 
 by cicatricial contraction of the fibrous tissue thrown out 
 around it. 
 
 Morbid Anatomy. 
 
 The Heart. — As a rule the heart is not very large. Weights 
 of ten and twelve ounces are common, and fourteen or fifteen 
 will represent about the average. The left ventricle is 
 usually not increased in size, the left auricle is dilated 
 and hypertrophied, and the right ventricle much enlarged 
 
176 HEART DISEASE. 
 
 and its walls greatly thickened. The left ventricle, how- 
 ever, may be enlarged and its walls thickened if mitral 
 incompetence preceded the mitral stenosis, and there may 
 therefore be great differences in the weight of the heart 
 and dimensions of its cavities in different cases. 
 
 The Mitral Orifice. — The condition of the mitral orifice 
 may vary greatly, and an extreme degree of stenosis does 
 not seem to be incompatible with life. The orifice may be 
 so constricted that it will scarcely admit a penholder, and 
 very commonly it will only admit the tip of the little finger. 
 To such conditions the term " button-hole " has been applied, 
 but it is scarcely applicable, as the margins of the orifice 
 are usually rigid and unyielding. In other cases the aperture 
 may be funnel-shaped. Frequently there is no trace of the 
 mitral valves remaining as such, as they are adherent at the 
 margins, contracted down to form a rough irregular lining 
 to what is left of the original mitral orifice. 
 
 The characteristic physiological effect of the lesion upon 
 the heart is dilatation of the left auricle with more or 
 less thickening of its wall, and great hypertrophy with 
 some dilatation of the right ventricle. The left ventricle 
 is not correspondingly enlarged, and may retain its normal 
 size, while the right ventricle, by its growth, may displace 
 it backwards, so that no part of it appears on the anterior 
 aspect of the heart, and its apex is no longer in contact 
 with the chest wall. 
 
 When the mitral orifice is narrowed, it is the left auricle 
 and right ventricle only which are called upon to exert 
 increased force, since there is no obvious cause of increased 
 resistance in the systemic circulation. The same may be 
 said when the valvular lesion is mitral incompetence with 
 regurgitation; but here another element of change comes 
 in, which makes a difference between obstruction and 
 incompetence. The high pressure in the pulmonary veins 
 and left auricle, which is a result of the damming back of 
 
MITRAL STENOSIS. 177 
 
 the blood and of the increased force of the right ventricle, 
 causes a forcible inrush into the left ventricle during 
 diastole ; and this, so long as the orifice remains of the 
 natural size, must distend, and in the long run dilate its 
 cavity, taking effect, as it does, during the unresisting 
 period of the ventricular rhythm. But an increase in the 
 capacity of the cavity multiplies by so much the force 
 required to expel its contents, and this constitutes a 
 demand for hypertrophy. We have, then, as a result of 
 mitral incompetence, dilatation, and more or less hyper- 
 trophy of the left ventricle ; but the hypertrophy here is 
 required as compensation for the dilatation, and not to 
 overcome any direct effect of the impairment of the 
 valvular apparatus. In stenosis of the mitral orifice, the 
 pressure which thus affects the left ventricle is intercepted 
 by the narrowed orifice. There is scarcely time for it to be 
 adequately filled during diastole, still less for any distending 
 effect to be produced. We see, then, how it is that the left 
 ventricle usually remains of normal size and does not in- 
 crease 'pari passu with the right. Frequently, however, 
 the left ventricle is dilated and more or less thickened, 
 and here our reasoning appears to be at fault. But the 
 difficulty disappears on reflection. Not uncommonly the 
 change in the valves, which eventually glues them together 
 and narrows the orifice, only interferes at first with their 
 apposition and permits of regurgitation, which may, indeed, 
 be for a long time the predominant result ; and, in point 
 of fact, incompetence often precedes the establishment of 
 obstruction. We have here abundant cause for differences 
 in the condition of the walls and cavities of the heart found 
 after death, and, it must be added, for variations in the 
 clinical history, and especially for diversity of physical 
 signs. 
 
 The Lungs. Passive Hyperemia. Brown Induration. 
 (Edema. — As a result of prolonged obstruction to the 
 
 N 
 
178 HEART DISEASE. 
 
 flow of blood from the lungs to the left auricle in mitral 
 incompetence and stenosis, there is passive hypereemia of 
 the lungs. To a certain extent this is overcome by the 
 increased driving power of the hypertrophied right ventricle. 
 But the high pressure thus induced in the pulmonary circu- 
 lation gives rise to certain pathological changes in the 
 lungs. 
 
 The capillaries in the walls of the alveoli are over- 
 distended, and become tortuous, projecting into the alveoli. 
 Exudation of white and red blood cells into the alveoli 
 takes place and occasionally capillaries rupture, giving rise 
 to slight haemoptysis, which is frequently met with in 
 mitral stenosis even in the early stages. Some of the 
 extravasated blood may be thus expectorated, some is taken 
 up by the alveolar cells and lymphatics, and the walls and 
 lymphatics of the alveoli are often loaded with granules of 
 pigment derived from the disentegrated haemoglobin. 
 
 As a result of the irritation, proliferative changes take 
 place in the alveolar walls, which become thickened, lose 
 their elasticity, and tend to shrink and collapse, so that 
 the surface available for aeration of the blood is seriously 
 impaired and diminished. It may be still further diminished 
 by patches of catarrhal inflammation. 
 
 This condition of lung, from its tough, inelastic feel, 
 resulting from the diffuse fibrosis, and the brownish colour 
 due to the deposit of blood pigment, is known as " Brown 
 Induration." 
 
 As will be readily understood, this condition is most 
 likely to arise in cases of mitral stenosis, where the hyper- 
 trophied right ventricle has to keep up sufficient pressure 
 in the pulmonary circulation to force the blood through the 
 narrowed mitral orifice which constitutes, in severe cases, 
 an almost impenetrable barrier to the on-flow of the blood. 
 In mitral incompetence the back pressure is more variable 
 and is usually not so severe, and we are more likely to 
 
MITRAL STENOSIS. 179 
 
 meet with, a condition of congestion varying in degree 
 from time to time. When the stagnation of the circulation 
 in the lungs becomes more intense, oedema of the bases 
 of the lungs may supervene, the alveoli becoming filled 
 with serum exuded from the congested vessels. 
 
 Infarction. — In the later and final stages of mitral 
 stenosis, or of mitral stenosis and incompetence combined, 
 infarction of the lungs is very liable to occur. 
 
 As the lung is freely supplied with blood vessels, 
 infarction does not occur from embolism of a small artery 
 in a normal lung, as is the case in the spleen or kidney, 
 since collateral circulation is readily established. This has 
 been proved experimentally by Welch in dogs, and has also 
 been verified at post-mortems by the finding of occluded 
 vessels without any resulting infarct. When, however, 
 there is extreme congestion of the lungs and the circulation 
 is obstructed and stagnant, embolism will give rise to an 
 infarct, as collateral circulation cannot be established. It 
 has been supposed that, in mitral stenosis, embolism 
 occurs from clots forming in the right auricle during life 
 and portions becoming detached and carried to the lungs. 
 I have never seen any foundation in fact for this theory, 
 and it is scarcely conceivable that clotting should take 
 place in the heart during life if its walls are healthy. 
 
 It is probable that the infarction which is common in 
 the later stages of mitral stenosis is the result of thrombosis. 
 There is intense congestion and stagnation in the capillaries 
 and small arteries, and the limit at which the circulation 
 can be maintained is reached at last. Stasis and gradual 
 thrombosis occur in one or more of the smaller arteries, and 
 the result is the same as in embolism. The blood-supply to 
 the area supplied by the artery is cut off, and temporarily it 
 becomes anaemic. But blood soon flows from the adjoining 
 capillaries into the empty vessels, the walls of which, deprived 
 of their nutrition, give way or allow the blood to 
 
I So HEART DISEASE. 
 
 through them into the alveoli, by actual rhexis, or 
 diapedesis, so that we get a large hsemorrhagic infarct. 
 The name " pulmonary apoplexy " has been applied by 
 some authors to this condition, but it scarcely seems a 
 suitable term, as it is not the rupture of a vessel which 
 is primarily responsible for the lesion. 
 
 The infarcted areas are usually of considerable size, and 
 more or less wedge-shaped with their base at the pleura, and 
 may measure from half-inch to three or four inches across 
 at their widest part. They are often multiple, and are 
 usually among the incidents of the closing scenes in the 
 disease. 
 
 The Liver. — As the pressure in the pulmonary circulation 
 is greatly increased, it stands to reason that the pressure in 
 the right ventricle in systole must be raised in proportion. If 
 the ventricle is unequal to the task of maintaining the high- 
 pressure circulation it may dilate, giving rise to incom- 
 petence of the tricuspid valve, or may inconipletety empty 
 itself during systole, which tends, in either case, to dam back 
 the blood in the right auricle. This will cause obstruction 
 to the return of blood to the auricle from the great veins. 
 The blood in the inferior vena cava, and consequently that in 
 the hepatic veins being dammed back, will give rise to conges- 
 tion of the liver. The intra-lobular veins and the capillaries 
 entering them in the centre of the liver lobules, become 
 distended and engorged with blood. The pressure on the 
 adjoining cells in the centre of the lobule, and impairment 
 of their nutrition results in atrophy of these cells, while 
 fatty degeneration is prone to occur in the cells in the 
 periphery of the lobule. The liver is engorged with blood, 
 and greatly increased in size ; and on making a section of 
 the liver post-mortem, we see, naked eye, the congested 
 capillaries and vein in the centre of the lobules as small 
 red areas surrounded by yellowish, opaque rings of cells in 
 a state of fatty degeneration, a condition which is known as 
 
MITRAL STENOSIS. 1S1 
 
 a "Nutmeg Liver " from its appearance. A certain amount 
 of secondary fibrosis may occur in chronic cases of long 
 duration, especially in mitral stenosis. 
 
 The Kidneys.— As a result of chronic congestion pre- 
 valent throughout the venous system, the kidneys become 
 congested. The stellate veins are especially prominent, 
 and the capillaries of the malpighian tufts are swollen and 
 distended with blood. The organ is often of a bluish colour, 
 when seen at the post-mortem, and is hard, rounded, and very 
 firm on section from secondary diffuse fibrosis chiefly marked 
 round the congested vessels. This condition is known as 
 
 " Cyanotic Induration." 
 
 * 
 
 Physical Signs. 
 
 The Pulse. — The pulse of mitral stenosis is interesting. 
 It is almost always regular until the heart is obviously 
 failing, unless the obstruction be complicated by regurgi- 
 tation or by valvular affection of the right side of the 
 heart. 
 
 The artery at the wrist is small, and is full between the 
 beats, presenting the characters of moderately high tension 
 — that is, it can be rolled under the finger and is not very 
 easily compressed. In my experience this modified high 
 tension pulse is almost constant, and it points to resistance 
 in the capillaries ; but the cause of such resistance is not 
 readily perceived. It may be due to contraction of the 
 arterioles, either reflex or by direct stimulation, consequent 
 on the blood being charged with impurities from im- 
 perfect elimination, or possibly be caused by backward 
 pressure in the veins, which makes itself felt through the 
 capillary network. More probably, however, it is simply 
 an effect of the contracting down of the entire arterial 
 system owing to the diminished supply of blood from the 
 imperfectly filled left ventricle. 
 
iS2 HEART DISEASE. 
 
 When irregularity comes on, it is usually at first in- 
 equality in the force of the beats, without marked disturb- 
 ance of the rhythm. Then some of the beats of the heart 
 fail to reach the wrist — no doubt from inadequate filling 
 of the ventricle ; the action of the heart may thus continue 
 to be regular when the pulse is irregular. In some rare 
 instances, there is only one beat of the pulse for every two 
 beats of the heart, the contraction of the left ventricle at 
 every alternate systole being inadequate to raise the aortic 
 valves ; and, on listening to the heart, there will be no 
 aortic second sound with the alternate systoles, the rhythm 
 as expressed by the sounds being one — two — one, one — two 
 - — one, with an accent on the third sound heard. The 
 heart-beats follow each other in couples, and the accentuated 
 first sound, unaccompanied by an aortic second sound, is 
 mainly produced by the abrupt contraction of the right 
 ventricle. 
 
 The Heart. — The cardiac sounds and murmurs are varied, 
 and sometimes perplexing ; but it has appeared to me that 
 they afford a means of estimating approximately the degree 
 of constriction which the mitral orifice has undergone. The 
 contraction does not take place all at once, but increases by 
 slow degrees through many months or years, and it is to be 
 expected that corresponding change in the physical signs 
 will accompany this change of mechanical conditions. The 
 physical signs are not the same in a given case from 
 beginning to end, and by following the modifications of 
 the sounds and murmurs which gradually supervene, 1 have 
 been led to recognize three stages of the disease. 
 
 The heart is not usually greatly enlarged ; the apex is 
 displaced to the left and sometimes also downwards, but 
 it is found, as a rule, not far from the normal situation. 
 
 The dilatation of the left auricle gives rise to an 
 extension of dulness outwards, along the fourth and third 
 left intercostal spaces, and the dilatation of the right 
 
MITRAL STENOSIS. 183 
 
 auricle causes dulness beyond the right border of the 
 sternum. 
 
 The apex beat is not well defined, and in advanced cases 
 a sharp and distinct shock is felt on palpation, which has 
 not the deliberate thrusting character of hypertrophy, but 
 is more like a tap. A thrill, presystolic in time, may 
 usually be felt at the apex or just internal to it. The 
 impulse of the right ventricle is powerful, lifting the lower 
 end of the sternum and adjacent costal cartilages, and 
 making itself seen and felt in the epigastrium. 
 
 Changes in the dimensions of the heart, however, have 
 not the same direct relation to the degree of valvular 
 mischief in mitral stenosis as in other valvular diseases, 
 and it is by means of auscultatory signs that the division 
 into stages is effected. 
 
 The pathognomonic sign of mitral stenosis is usually 
 given as a presystolic murmur heard over a limited area at 
 and to the inner side of the apex beat, between it and the 
 left border of the sternum. It is not a smooth, blowing 
 murmur, but has a rough, vibratory character, and is often 
 accompanied by a thrill perceptible to the hand at the same 
 spot. A further distinctive feature is the way in which 
 it runs up to and suddenly ends in the first sound, which 
 tends to become short and sharp, and is itself highly 
 characteristic. 
 
 Sometimes in children after an attack of pericarditis, 
 possibly as a result of pericardial adhesions, or in association 
 with a mitral systolic murmur, a kind of rumbling pre- 
 systolic murmur is audible, when no constriction of the 
 mitral orifice exists. This murmur has not, however, the 
 vibratory character of the true murmur of mitral stenosis ; 
 nor does it terminate abruptly in the first sound ; nor 
 is the first sound modified in the manner described above. 
 Reduplication of the first sound should not be mistaken 
 for a presystolic murmur. 
 
1 84 HEART DISEASE. 
 
 The pulmonic second sound is accentuated, as a result of 
 the backward pressure in the pulmonary circulation, and 
 very frequently there is reduplication of the second sound, 
 from want of synchronism in the closure of the pulmonic 
 and aortic valves. 
 
 Characteristics of the Three Stages in the Progress 
 of the Disease, as defined by Auscultatory Signs. 
 
 In the first stage a second sound, as well as a presystolic 
 murmur and first sound, will be audible at and to the 
 left of the apex. It is the persistence of the second sound 
 at the apex which is the chief distinctive feature of this 
 stage. The second sound may be reduplicated. 
 
 Under these conditions I have never known serious 
 symptoms to arise from the condition of the heart, and I 
 have seen illnesses of different kinds, even serious attacks 
 of bronchitis, passed through without the intervention of 
 embarrassment of the circulation. It is very rarely that 
 patients are admitted into hospital presenting simply the 
 signs above enumerated, but they are frequently met with 
 in out-patient practice and in consulting-rooms. 
 
 The Second Stage. — This is marked by the disappearance 
 of the second sound at the apex, and by the short, sharp 
 character of the first sound, which also usually becomes 
 very loud ; the first sound, in effect, comes to resemble 
 a second sound. Mistakes in diagnosis may now be easily 
 made. In mitral stenosis, at this stage, and in mitral 
 incompetence there is alike heard at the apex a murmur 
 followed by a short, sharp sound ; but in the former the 
 murmur is presystolic in time, and the sound is the modified 
 first sound, while in the latter the murmur is systolic and 
 the sound is the second sound. Very slight attention would, 
 in most cases, suffice to prevent any confusion between the 
 two, but an apex murmur is liable to be set down as the 
 
MITRAL STENOSIS. 1S5 
 
 familiar systolic murmur of regurgitation without further 
 investigation, and thus mitral stenosis, the most serious of 
 the diseases of the valves, at a period, too, when symptoms 
 may be impending, is taken for incompetence, which is 
 attended with less danger than any other of the valvular 
 affections. To bear this source of error in mind is to avoid 
 it ; but cases are sometimes met with in which, from 
 absence of cardiac impulse and from the similarity between 
 the sounds, it is not easy to follow the rhythm of the heart 
 and time the murmurs and sounds. Flexible stethoscopes are 
 here at a disadvantage as compared with the rigid wooden 
 instrument, which communicates to the ear and head, not 
 only sound, but a sense of shock which at once indicates 
 the moment of the systole, and this when there is no 
 impulse perceptible to the hand. To attempt to time the 
 first sound by the radial pulse is, of course, fallacious. The 
 carotid pulse is a safer guide, but it is not always easy to 
 co-ordinate tactile and auditory impressions. 
 
 The most trustworthy method of determining the 
 relation of sounds to the cardiac rhythm is to find a spot in 
 the region of the base where the first and second sounds are 
 unmistakably recognized, and then from this point to 
 follow the sounds, step by step, toward the apex, when it 
 will be found which of them it is that disappears, or which 
 maintains some distinguishing peculiarity. 
 
 The presystolic murmur itself usually undergoes a 
 modification in this stage. As commonly heard, it occupies 
 the end of the diastolic interval, running up to the first 
 sound, and corresponding therefore with the auricular 
 systole. But it may be a long or a short murmur, and may 
 indeed occupy the entire diastolic interval, when it will 
 correspond, not only with the auricular systole, but also 
 with the active diastolic rebound of the ventricle from 
 contraction ; that is, the murmur is produced by the 
 current of blood sucked into the ventricle as it dilates, as 
 
1 86 
 
 HEART DISEASE. 
 
 well as by that driven into it by the systole of the auricle. 
 This murmur, occupying the whole of the diastolic interval, 
 is most frequent in bad cases. But it may further be cut 
 in two, and, instead of being a continuous rumble from the 
 second sound up to the first, may subside as the active 
 dilatation of the ventricle ends, and before the auricular 
 systole begins ; or the proper presystolic part of the 
 murmur may be lost while the diastolic part remains 
 audible, so that the only murmur heard is diastolic, i.e. 
 a diastolic mitral murmur, strictly speaking. These varieties 
 
 FIG. 19. — 1. PRESYSTOLIC MURMUR CORRESPONDING WITH AURICULAR SYSTOLE. 
 2. MURMUR OCCUPYING WHOLE DIASTOLIC INTERVAL. 3 MURMUR DIVIDED 
 INTO DIASTOLIC AND PRESYSTOLIC PORTIONS. 
 
 of murmur may be represented diagrammatically as shown 
 in Fig. 19. 
 
 The disappearance of the second sound at the left of the 
 apex, which, with the short, sharp character of the first 
 sound, marks the second stage of mitral stenosis, is probably 
 explained by the following considerations. In the normal 
 heart, a second sound is always audible at and to the left 
 of the apex; and repeated careful examinations have con- 
 vinced me that it is the aortic second sound which is here 
 heard, and not the pulmonic, even when this is accentuated 
 and unduly loud. In mitral stenosis, there are two influences 
 tending to prevent the aortic second sound from reaching 
 the surface of the chest. First, the left ventricle, not 
 
MITRAL STENOSIS. 187 
 
 undergoing dilatation and hypertrophy, while the right 
 enlarges greatly, is overlapped by the latter, which usurps 
 the position of the apex, and thus the left ventricle cannot 
 conduct the aortic sound to the chest wall. Again, the 
 aortic second sound will be weak, because the diminished 
 amount of blood entering the ventricle, in consequence 
 of the narrowed mitral orifice, will not distend the aorta, 
 and will, therefore, fail to produce a powerful recoil 
 such as is necessary for the production of a loud second 
 sound. 
 
 The modification of the first sound in mitral stenosis is 
 remarkable, and in searching for an explanation of this, one 
 is struck by the analogy of the sharp, sudden, and tapping 
 character of the apex beat to the shortness and sharpness of 
 the first sound, which would seem to imply that some 
 common cause has been instrumental in the production of 
 these peculiarities in both instances. If this be the case, 
 it is clear that the ventricular wall must be one of the 
 factors, and the following explanation may be suggested. 
 Owing to the narrowing of the mitral orifice there is not 
 time in the diastolic interval for a sufficient amount of 
 blood to flow into the left ventricle to completely fill it. 
 At the commencement of systole, therefore, the ventricular 
 cavity is not fully distended with blood, so that the muscular 
 walls at the first moment of their contraction meet with no 
 resistance ; then, closing down rapidly, they are suddenly 
 brought up and made tense as they encounter the contained 
 blood. It seems plausible that this sudden tension of the 
 muscular walls and the abbreviated systole of the left 
 ventricle, would account both for the sharp and tapping 
 apex beat and for the short first sound. 
 
 In severe palpitation and tachycardia the first sound is 
 also extremely short and sharp, and probably a similar 
 explanation holds good here, namely, that the brief diastolic 
 interval which is the rule in such cases does not afford 
 
188 HEART DISEASE. 
 
 sufficient time for the complete filling and distending of 
 the ventricle with blood. 
 
 The third stage is characterized by the disappearance 
 of the presystolic murmur, so that, the second sound being 
 already lost, the only sound at and outside the apex is 
 the short sharp first sound described. This is not unlike 
 the first sound heard in dilatation with thinning of the 
 left ventricle ; but the absence of the second sound to the 
 left of the apex constitutes a diagnostic difference, since 
 this is distinct in dilatation. 
 
 No careful observer who has devoted much attention to 
 the study of mitral stenosis has failed to notice that the 
 presystolic murmur is sometimes absent in cases in which 
 an advanced stage of this condition is met with after 
 death. The principal justification, however, for taking the 
 disappearance of the presystolic murmur as a distinct 
 stage in the clinical history of mitral stenosis is that, 
 very commonly when pulmonary complications set in, or 
 other serious symptoms arise, the presystolic murmur is 
 lost, and that it again becomes audible when these subside 
 and the patient improves. 
 
 It is a matter of repeated and familiar experience for 
 cases to be admitted into hospital on account of serious 
 symptoms with only the short sharp first sound audible 
 at the apex, and to leave after recovery with a presystolic 
 murmur. The third stage, however, is not necessarily 
 attended with serious symptoms, though this is the rule. 
 
 The probable cause of the disappearance of the murmur 
 is the establishment of tricuspid incompetence. The giving 
 way of the tricuspid valve and the occurrence of con- 
 siderable reflux into the right auricle, make it impossible 
 for the right ventricle to sustain the same high pressure 
 in the pulmonary circulation and left auricle as was 
 present previously. There is not, therefore, sufficient 
 pressure to force the blood through the mitral orifice 
 rapidly enough to generate a murmur. 
 
MITRAL STENOSIS. 
 
 Symptoms. 
 
 The patient, up to a somewhat advanced stage, has not 
 the look of heart disease, is neither pallid, nor dusky, 
 nor anxious-looking, but often has a bright colour and 
 cheerful expression. There is some breathlessness on 
 exertion, but not infrequently, up to the moment when, 
 from some cause or other, serious symptoms set in, he or 
 she is unconscious of serious embarrassment of the circula- 
 tion, and capable of ordinary work. The capillaries over the 
 cheek bones are frequently congested, giving a ruddy colour 
 which might be taken for a sign of good health, were it not 
 contradicted by the dusky cyanotic tinge of the lips. The 
 cyanosis tends to become more marked and permanent and 
 the dyspnoea more severe in the later stages, from the 
 diminution in the aerating capacity of the lungs, which 
 supervenes as their condition approximates that known as 
 " Brown Induration." Such patients are liable to cough 
 and haemoptysis from the constant high pressure in the 
 pulmonic circulation. In the early stages the haemoptysis 
 is slight, being due to rupture of capillaries, and consists of 
 mucus streaked with blood. In the advanced and terminal 
 stages it is often very profuse and repeated, being due 
 to infarction. Cough is often a troublesome symptom, 
 from the bronchial catarrh to which the patient is especially 
 liable. Attacks of tachycardia or palpitation are common 
 and may cause great distress. Another condition more 
 frequently met with as a consequence of mitral stenosis, 
 than in other valvular affections, is great enlargement of 
 the liver, with true pulsation of this organ, which often 
 feels hard and firm on examination ; it is not uncommon 
 to find fluid in the peritoneal cavity before there is 
 cedertia of the feet and legs, or the oedema will dis- 
 appear with rest in bed, while ascites persists, whereas 
 dropsy, in cardiac failure, due to mitral incompetence, as 
 
igo HEART DISEASE. 
 
 a rule, begins in the connective tissue of the most de- 
 pendent parts, and ascites is not common. A reference to 
 the section on morbid anatomy will make clear the causa- 
 tion of most of the symptoms. 
 
 Diagnosis. 
 
 In the first stage, where the vibratory presystolic 
 murmur ending in the short sharp first sound, and the 
 second sound are present, there will be little difficulty in 
 arriving at a diagnosis. The short, rumbling, presystolic 
 murmur often met with during or shortly after an attack 
 of peri- or endo-carditis, more especially in children, may, 
 however, lead to some confusion. This murmur, however, 
 is not of the loud vibratory character of the typical pre- 
 systolic murmur, but is usually short and rumbling ; it does 
 not indicate the presence of mitral stenosis, at any rate, 
 in the sense of an established organic lesion. A further 
 distinctive feature in diagnosis will be the absence of the 
 typical modification of the first sound, which, instead of 
 being short and sharp, will be dull, low-pitched, and 
 possibly reduplicated. 
 
 In the second stage, when the second sound is lost 
 at the apex and only the presystolic murmur and first 
 sound are present, these may possibly be taken for a 
 systolic murmur and second sound which the first sound 
 has come to resemble in character ; the case would then be 
 mistaken for one of mitral incompetence in which the 
 prognosis is much less serious. Due care and accurate 
 timing of the sounds will prevent this. Confusion is, 
 however, liable to occur when mitral regurgitation is 
 present as a complication, which is of very common 
 occurrence. It is then possible to mistake the presystolic 
 and systolic murmurs together for a prolonged systolic 
 murmur, the short sharp first sound being taken for an 
 
MITRAL STENOSIS. 
 
 191 
 
 accentuated second sound. But attention to the character 
 and time of the murmurs will obviate such a mistake. 
 The systolic murmur of mitral regurgitation is blowing 
 or musical, and begins with an accent, whereas the pre- 
 systolic murmur is vibratory and ends with an accent. 
 Accurate observation of the time at which the short sharp 
 sound is heard will also prevent the mistake, but this 
 will not perhaps be so easily distinguished as the character 
 of the murmurs. 
 
 They may be represented diagrammatically as follows : — 
 
 ilBu. 
 
 fig. 20 (Dark shading = presystolic murmur ; light shading = systolic 
 murmur). 
 
 1. ORDINARY PRESYSTOLIC WITH SYSTOLIC MURMUR. 2. PRESYSTOLIC 
 MURMUR OCCUPYING THE WHOLE OF DIASTOLE, WITH SYSTOLIC MURMUR. 
 3. DIASTOLIC PORTION ONLY OP PRESYSTOLIC MURMUR WITH SYSTOLIC 
 MURMUR. 
 
 In the third stage, complicated by mitral regurgitation, 
 recognition of mitral stenosis will often present great 
 difficulties. There will be no presystolic murmur, and 
 only a first sound with a systolic murmur will be audible 
 at the apex. The absence of the second sound will be of 
 great value in identifying the stenosis. If, however, the 
 mitral regurgitation has preceded the onset of stenosis, it 
 may have given rise to a degree of hypertrophy and dilata- 
 tion of the left ventricle, such that the apex-beat, which 
 comes into contact with the chest wall, is still that of 
 the left ventricle and not of the right, so that the aortic 
 second sound is still conducted to the chest wall. In such 
 
192 HEART DISEASE. 
 
 cases the modification of the first sound is an important 
 aid to diagnosis; regurgitation tends to destroy the first 
 sound, stenosis to shorten and intensify it, so that the 
 presence of a short sharp first sound with a systolic murmur, 
 in a case where there is obviously serious cardiac mischief, 
 should at once suggest the probability of the presence of 
 mitral stenosis. 
 
 When, however, compensation has broken down in a 
 case of combined stenosis and regurgitation, extraordinary 
 fluctuations in the physical signs may be present ; at one 
 time a systolic, at another a presystolic murmur, at another 
 time both may be heard, or perhaps only a short sharp 
 sound alternating with murmurs, which it is impossible 
 to time. At the same time the action of the heart will 
 be rapid and markedly irregular. In such cases the ex- 
 traordinary fluctuations must themselves give the chief 
 clue to the diagnosis, though it will be impossible to 
 estimate the extent of either lesion. 
 
 It would appear that when the high pressure in the 
 left auricle is well sustained it generates a presystolic 
 murmur, and prevents regurgitation, so that no systolic 
 murmur is generated, and there is no reflux, even though 
 the typical " buttonhole " mitral orifice is present, in which 
 closure of the orifice is absolutely impossible, as no valves 
 in fact remain as such. When, on the other hand, the 
 pressure in the left auricle and pulmonary circulation falls 
 below a certain point, either from break-down of the right 
 ventricle or from the onset of tricuspid regurgitation, 
 mitral reflux takes place during systole, and there is not 
 sufficient pressure in the left auricle during diastole to 
 generate a presystolic murmur. We may thus explain 
 these extreme and confusing varieties in the physical 
 signs of the third stage of mitral obstruction complicated 
 by regurgitation, and account for the absence of a systolic 
 murmur in many cases where, from the condition of the 
 
MITRAL STENOSIS. 193 
 
 mitral orifice post-mortem, we should have expected mitral 
 regurgitation to have been present during life. 
 
 In aortic incompetence a presystolic murmur is some- 
 times present in addition to the diastolic murmur, which 
 does not necessarily imply the existence of mitral stenosis. 
 The probable significance of this murmur and the explana- 
 tion of its presence have already been discussed in the 
 chapter on Aortic Incompetence. 
 
 Peognosis. 
 
 Mitral stenosis stands next to aortic regurgitation 
 among valvular affections in the order of gravity. The 
 average age at death, as deduced from 53 cases abstracted 
 from the post-mortem records at St. Mary's Hospital, was 
 found to be 33 for males and 37 or 38 for females, which 
 is higher than one would expect. 
 
 A suggestive inquiry is, why mitral stenosis should be 
 so serious, and especially why it should be attended with 
 greater danger to life than mitral incompetence. One 
 reason is, that the effects of obstruction here are not so 
 easily neutralized as are the effects of regurgitation. The 
 high pressure maintained in the pulmonary circulation and 
 in the left auricle, by hypertrophy of the right ventricle, 
 will antagonize incompetence of the valve in two ways — 
 by resisting the reflux during systole, and by more rapid 
 filling of the ventricle during diastole. In stenosis this 
 high pressure can only be of service by increasing the 
 rapidity of the passage of blood through the narrowed 
 orifice during diastole ; and, as diastole only lasts for a 
 certain time, if the contraction be extreme, the ventricle 
 cannot be properly filled before the systole is again due. 
 When such is the case, the compensation is inadequate. 
 On the other hand, since the constriction may reach a 
 degree which, in the absence of experience, would seem 
 quite incompatible with life, and since the subjects of such 
 
 o 
 
i 9 4 HEART DISEASE. 
 
 extensive change must have lived through all the inter- 
 mediate degrees, it can scarcely be simply that obstruction, 
 as such, is specially dangerous. Probably the explanation 
 of the greater danger of obstruction, as compared with 
 regurgitation, lies in the fact that, when once adhesion 
 between the flaps of the valves has set in, it tends to go 
 on, the friction and strain keeping up chronic inflamma- 
 tion, which gives rise to further adhesion of the valves and 
 contraction of the orifice. 
 
 When mitral stenosis is established in childhood or 
 early adolescence, the prognosis is more serious than 
 when it occurs in later life. This is partly owing to the 
 progressive tendency of the constriction of the orifice, 
 which is more marked in early life, and partly to the fact 
 that the stenosed orifice does not increase in size while 
 the growth of the heart continues, so that even though no 
 further actual narrowing takes place, the relative dispropor- 
 tions between the mitral orifice and the cavities of the heart 
 will increase as the heart attains its full development. 
 
 The important point in prognosis, however, is the 
 comparative prospect of life in individual cases, and it is 
 in the estimation of this that the recognition of the 
 different stages is of service. The extent of the hyper- 
 trophy and dilatation of the walls and cavities of the heart 
 does not afford very great assistance, as we have seen that 
 mitral stenosis does not give rise to any marked change 
 in the left ventricle ; a certain amount of information, 
 however, as to the amount of obstruction may be gathered 
 from the degree of hypertrophy and dilatation of the right 
 ventricle, on which has fallen the work of overcoming the 
 obstruction. A careful study of the sounds and murmurs 
 will give more precise information, so that the three stages 
 in the disease, as described above, must be borne in mind 
 in attempting to form a prognosis. So long as the second 
 sound is heard at and beyond the apex, there is little or 
 
MITRAL STENOSIS. 195 
 
 no liability to the occurrence of symptoms, and there is 
 no immediate danger. It must, however, be borne in mind 
 that, owing to the tendency of the stenosis to increase, the 
 prognosis as to prolonged life in the future is not favour- 
 able in the majority of cases. 
 
 When the second sound is lost at the apex, that is, 
 when the second stage is reached, there may still be 
 immunity from symptoms under ordinary conditions of 
 life; but there is no capacity for the adjustment of the 
 circulation to deviations from these, so that any imprudence 
 or slight over-exertion, or even mental worry, on the part 
 of the patient is liable to bring about a break-down of 
 compensation. One must not, therefore, be thrown off 
 one's guard by absence of complaints, or by the apparent 
 good health of the patient. With suitable precautions 
 and care, however, the condition of the patient may remain 
 the same for years, though any tendency to increasing 
 shortness of breath or any fresh attack of rheumatism will 
 be reasons for apprehension, as indicating that the con- 
 striction is increasing. 
 
 When the third stage is reached and serious syrnr)tonis, 
 such as dyspncea, dropsy, pulmonary infarction, and other 
 effects of venous congestion and over-distension of the 
 right side of the heart, are present, the first element in 
 the mental calculation will be the severity of the symptoms. 
 But recoveries are witnessed in conditions apparently so 
 desperate that if it is the first time the patient has suffered 
 from a similar complete break-down of compensation, 
 the case must not be pronounced absolutely hopeless. The 
 number of times severe symptoms have arisen and the 
 readiness with which they have been provoked become 
 the most important considerations. If the patient has had 
 similar attacks previously, and if a very slight cause has 
 been sufficient to induce them, the danger is very great, 
 and the chance of even temporary recovery is a poor one. 
 
196 heart disease. 
 
 Treatment. 
 
 The first stage of mitral stenosis is attended with few 
 symptoms, and rarely calls for treatment. So long as the 
 narrowing of the orifice is only moderate, compensation 
 appears to be easily effected, and the patient suffers little 
 or no inconvenience. The fear is that once the flaps of 
 the valve have begun to adhere, the adhesion will extend 
 and gradually narrow the fissure between them. If this 
 could be prevented by any means, the treatment effecting 
 it would be of extreme value. We have no power, how- 
 ever, of directly influencing the process of adhesion, and 
 can only endeavour to obviate causes tending to keep up 
 or excite inflammation of the valves. Every possible pre- 
 caution should be taken against rheumatism, which is 
 extremely prone to attack the damaged valves ; and slight 
 rheumatism, which might be neglected in a sound in- 
 dividual, should receive attention in a patient suffering 
 from mitral stenosis of however small degree. Unduly 
 high pressure in the arterial circulation will react on the 
 valves by giving rise to high intra-cardiac pressure, and 
 stress upon them will tend to keep up or revive irritation. 
 Over-eating and drinking, again, and constipation, giving 
 rise to accumulation of impurities in the blood, will have 
 a like tendency. Precautions based on this knowledge 
 should therefore be inculcated upon the patient. 
 
 Bronchitis and other affections of the lungs will increase 
 the resistance in the pulmonary circulation and the strain on 
 the right ventricle, and should be specially guarded against. 
 
 As the narrowing of the orifice progresses, or when 
 the affection is found on examination to have reached 
 the second stage, and when symptoms such as breathless- 
 ness and cardiac pain or oppression or weight are readily 
 induced, or are more or less constantly present, or when 
 haemoptysis has occurred, the precautions suggested above 
 
MITRAL STENOSIS. 197 
 
 should be urged more emphatically. Mercurial purgatives 
 will then be of service, and rest in the recumbent position, 
 and, if necessary, confinement to bed for a time should be 
 ordered. Strychnia and iron, with nitroglycerine or nitrites 
 and stimulants, may be prescribed, but digitalis should 
 not be given unless there are symptoms of right ventricle 
 failure, and not then until after free purgation ; on no 
 account should it be given for a long period. 
 
 The rules for exercise will be the same as in other 
 forms of valvular disease. Sufferers from mitral stenosis 
 of slight or moderate degree are perhaps more liable to 
 do themselves harm by imprudent exertion than the 
 subjects of mitral incompetence, as they are often not 
 checked by breathlessness, but persist in overtaxing their 
 strength till severe pain in the heart, or perhaps an attack 
 of haemoptysis is induced. At an advanced stage of the 
 disease exertion may prove suddenly fatal, but never while 
 the patient is free from serious symptoms ; more commonly 
 it is by overthrowing the compensatory balance already 
 inclined to the wrong side, and so aggravating the existing 
 venous stasis, or by detaching a thrombus, which gives 
 rise to embolism, that effort or excitement proves injurious 
 and ultimately fatal. Haemoptysis is rarely considerable, and 
 seldom requires any other treatment than rest and aperients. 
 
 When from neglect of precautions, or from overtaxing 
 of strength by unavoidable duties, or from depressing 
 emotions, or from the advance of the disease, decided 
 symptoms of right-ventricle failure have supervened, such 
 as great weakness, cough, dyspnoea, with evidences of 
 venous stasis in swollen jugulars and enlarged liver, and 
 dropsy, then energetic measures will be required. These 
 will be mainly such as will relieve the venous engorge- 
 ment and the overloaded right ventricle and auricle, 
 smart purgation by calomel or blue pill and colocynth, 
 followed, if necessary, by salines. 
 
198 HEART DISEASE. 
 
 When the symptoms are very urgent, venesection may 
 be of striking service, and in certain cases there is no 
 other treatment that will take its place and avail to 
 avert a speedy fatal termination. 
 
 The indications will be, not a full bounding pulse, but 
 the opposite — a small, weak, irregular pulse, many of the 
 beats being scarcely perceptible ; the heart, on the other 
 hand, more especially the right ventricle, will be beating 
 violently, epigastric pulsation being very marked, while 
 the apex beat is scarcely perceptible. The liver will be 
 enlarged, and perhaps pulsating, and the jugulars will be 
 full and pulsating. The contrast between the powerful 
 right ventricle impulse and the small, weak, irregular pulse 
 is very striking, and is one of the most important indica- 
 tions for venesection. The sufferer will be in a state of 
 dyspncea, though not always of an agonizing kind, and 
 not always compelling him to sit up ; the face may 
 be dusky and the lips blue, but it may also be pale with 
 a red patch of injected capillaries on the cheeks. 
 
 The narrowed mitral orifice constitutes a fixed obstacle, 
 which keeps up an unremitting backward pressure in the 
 pulmonary circulation, and makes it difficult or impossible 
 for the right ventricle to overcome the paralyzing over- 
 distension to which it is subjected. Venesection lessens 
 the amount of blood arriving by the veins, and gives the 
 right ventricle a chance of recovery, so that it can again 
 contract down more or less efficiently on its contents. 
 
 Venesection does not, however, dispense with the 
 necessity for relieving the portal circulation by purgation. 
 Stimulants which without these measures afford no relief, 
 and may indeed do harm, will then be of the greatest 
 service, and digitalis and like remedies will find their 
 opportunity. 
 
 When the symptoms are less urgent or venesection is 
 objected to, seven or eight leeches applied over the liver 
 
MITRAL STENOSIS. 199 
 
 may be of service, and in hospital patients, where rest and 
 care and proper nourishment make such an enormous 
 difference in the influences acting on the patient, leeches 
 will usually be sufficient. 
 
 The administration of digitalis in the early stages of 
 the disease is seldom if ever called for ; it is only when 
 there are symptoms of right ventricle failure, and then 
 only after free purgation and, if necessary, venesection 
 have been employed, that it should be prescribed. Up 
 to a certain point in such cases its influence is often most 
 beneficial, but sometimes it fails to relieve, and even 
 appears to aggravate the symptoms. If continued too 
 long in cases where it has been of signal service, un- 
 favourable effects may supervene, marked by slowing of 
 the pulse, a sense of precordial oppression, and by coupled 
 heart-beats, the first of which alone reaches the wrist, the 
 second being unaccompanied by an aortic second sound. 
 
 In many cases the coupled heart-beats with two beats 
 of the heart to one beat of the pulse at the wrist can be 
 induced at will by the administration of digitalis. 
 
 Digitalis, therefore, must be employed with caution in 
 mitral stenosis, and its effects should be carefully watched. 
 Under no circumstances should it be prescribed unless the 
 patient is under observation, and it should rarely be given 
 for a long period of time. 
 
 Nitro-glycerine and other vasodilators may sometimes 
 be given with good effect for many weeks or even months 
 in conjunction with general tonics, such as iron, quinine, 
 and nux vomica. 
 
CHAPTEK XIII. 
 
 VALVULAE DISEASE OF THE EIGHT SIDE OF 
 THE HEAET. 
 
 TRICUSPID INCOMPETENCE AND STENOSIS — PULMONIC INCOM- 
 PETENCE AND STENOSIS — SYSTOLIC PULMONIC MURMURS 
 WHICH DO NOT INDICATE STENOSIS. 
 
 Primary tricuspid valvular disease is rare, aud for the 
 most part is congenital. 
 
 Tricuspid regurgitation is so common when the right 
 ventricle is overdistended by violent exertion (the so- 
 called safety-valve action) that it may be looked on as 
 physiological ; it is not usually attended with a murmur. 
 Tricuspid incompetence, again, with or without a murmur, 
 is an early and almost constant effect of back pressure 
 through the lungs when there is serious valvular disease 
 of the left ventricle. In both instances the cause of the 
 regurgitation is dilatation of the right ventricle, temporary 
 or permanent, as the case may be. 
 
 The tricusjnd valve may, however, be damaged during 
 intra-uterine life, or more rarely in childhood or adolescence 
 by endocarditis of rheumatic origin, or, where serious 
 valvular disease of the left ventricle exists, may undergo 
 thickening and contraction from chronic inflammation set 
 up by the irritation and undue strain caused by protracted 
 high pressure in the pulmonary circulation. 
 
 The murmur attending tricuspid regurgitation is systolic 
 
TRICUSPID INCOMPETENCE. 201 
 
 in time and is usually blowing in character, having its 
 maximum intensity about one-third of the distance between 
 the left edge of the sternum and the vertical nipple line. 
 It is usually audible outwards towards the apex, and 
 sometimes at the apex itself, where it may be mistaken for 
 a mitral murmur. Such a murmur, when constant and 
 not occasional only, may be looked on as indicative of 
 definite tricuspid insufficiency, with probably actual change 
 in the valvular flaps and chordae tendineae. A musical 
 tricuspid systolic murmur may sometimes be heard over 
 a limited area, but it seldom has any important significance. 
 
 It is not, however, from the character of the murmur, 
 or from its presence, that conclusions as to the degree of 
 tricuspid incompetence are to be drawn. More important 
 information is gained from the condition of the veins of 
 the neck and from enlargement of the liver. The veins 
 of the neck are more or less distended according to the 
 degree of regurgitation, and the external jugulars may 
 attain even the size of the little finger. Frequently they 
 will fill from below when emptied by pressure. 
 
 Pulsation is usually present when there is much regurgi- 
 tation, and is often very conspicuous. It is sometimes seen 
 to be double, the contraction, first of the auricle, then of 
 the ventricle, sending a reflux wave along the jugulars. 
 At times the pulsation in the internal jugular vein is so 
 marked, and extends so high, that at first sight it may be 
 taken for the carotid throb of aortic regurgitation ; but it 
 is of course easily extinguished by light pressure. 
 
 The effect of tricuspid incompetence, causing damming 
 back of the blood in the inferior vena cava, is felt by 
 the liver, which gradually becomes much congested and 
 enlarged, and eventually may pulsate as the reflux becomes 
 considerable. 
 
HEART DISEASE. 
 
 Tricuspid Stenosis. 
 
 Tricuspid stenosis is of rare occurrence, and is usually 
 associated with mitral stenosis. It seldom, if ever, occurs 
 as an isolated valvular lesion. It is in most cases the result 
 of an attack of endocarditis affecting mitral and tricuspid 
 valves simultaneously, and is rarely a congenital affection. 
 
 The most characteristic physical sign, when it can be 
 recognized, is a presystolic murmur, audible in the tricuspid 
 area, but it is not always present, and when present is 
 not easily distinguished from a concurrent mitral presystolic 
 murmur. In many cases in which tricuspid stenosis has 
 been diagnosed from the symptoms during life and found 
 on post-mortem examination, and when consequently the 
 presystolic murmur has been carefully and perseveringly 
 sought for over a long period, it has been impossible to 
 recognize and distinguish it. There can be no doubt, 
 however, that the murmur has been frequently heard and 
 recognized. Another important physical sign of tricuspid 
 obstruction is distension of the jugular veins with little 
 or no pulsation. Mackenzie* of Burnley has obtained 
 graphic records of jugular pulsation, and describes an 
 auricular and ventricular type : when the right side of 
 the heart is distended, the double jugular pulsation — the 
 first wave auricular and the second ventricular — is frequently 
 very distinct. But if the tricuspid valves are contracted 
 and rigid and the orifice narrowed, the ventricular wave is 
 cut off, while the auricular may be present. If, however, 
 the auricle is paralyzed by over-distension, the auricular 
 wave may also be missing. 
 
 When any considerable degree of tricuspid stenosis 
 exists, the symptoms of embarrassment of the circulation 
 and of venous back pressure are present in a marked 
 degree. When it supervenes on mitral stenosis it is 
 
 * Edin. Hosp. Reports, 189A, vol. ii. 
 
AFFECTIONS OF PULMONIC VALVES. 203 
 
 possible that it has a beneficial effect in postponing the 
 supervention of and limiting the degree of tricuspid re- 
 gurgitation, but this is doubtful. The symptoms are 
 usually severe. Cyanosis and dyspnoea are prominent 
 features, and cedema of the legs is commonly present. 
 
 The Pulmonic Valves. 
 
 Disease of the pulmonic semilunar valves is rare, and 
 of the two conditions, insufficiency and stenosis, the former 
 is the more uncommon. 
 
 Pulmonic insufficiency gives rise to a diastolic murmur, 
 best heard in the left third intercostal space, and conducted 
 downwards. It must, however, be borne in mind that the 
 murmur of aortic regurgitation is also frequently heard 
 at this spot, so that before venturing on a diagnosis 
 of pulmonic regurgitation, it must be ascertained, not 
 only that the pulmonic second sound is impaired, but 
 also that the carotid throb and collapsing pulse are 
 absent, and that the aortic second sound is unimpaired. 
 No special train of symptoms can be attributed to 
 pulmonic regurgitation. 
 
 Pulmonic stenosis is nearly always a congenital defect, 
 and as it is fully discussed in the chapter on Congenital 
 Malformations, little need be said here. The murmur to 
 which it gives rise is systolic in time and usually loud and 
 rough, varying in intensity. It is most distinct in the 
 third left space, about three-quarters of an inch from 
 the margin of the sternum, but it is conducted along the 
 branches of the pulmonary artery and is often audible over 
 the whole cardiac area and far beyond, sometimes over the 
 entire chest, front and back. Pulmonic stenosis is often 
 associated with some other congenital defect, such as a 
 perforate interventricular septum or patent foramen ovale. 
 When the last-named condition exists cyanosis is, in the 
 
204 HEART DISEASE. 
 
 majority of cases, present in a more or less pronounced 
 degree, or is easily induced by exertion. 
 
 Systolic pulmonic murmurs are very common without 
 change in the orifice or valves. 
 
 A pulmonic murmur may be present in a patient 
 suffering from anaemia and disappear as the blood regains 
 its normal character ; it is then properly termed " hseniic." 
 
 Again, a murmur in this situation may be induced by 
 severe or protracted exertion, and last for some hours or 
 days. There will probably be at the same time indica- 
 tions of dilatation of the right ventricle, though it is not 
 easy to explain how this could give rise to the pulmonic 
 murmur. 
 
 A third variety of systolic murmur in the pulmonic 
 area, which may be loud and rough, and often varies 
 greatly in the same subject and without obvious cause, 
 or especially on change of position, is not unfrequently 
 met with in adolescents of both sexes, which cannot be 
 attributed to anaemia or to dilatation of the right ventricle. 
 It is not indicative of temporary weakness or organic 
 unsoundness of heart, nor is it incompatible with capacity 
 fur vigorous and sustained exertion, as boys and men in 
 whom it is present can play football and train for races 
 with impunity. Its presence may be made a pretext for 
 rejecting candidates for the army on medical grounds, but 
 I have known many men in whom such a murmur was 
 present go through arduous campaigns without breaking 
 down. I have never known such a murmur develop into 
 actual heart disease ; on the contrary, it usually disappears 
 in adult life, except now and then in women. 
 
 The causation of such a murmur is apparently as 
 follows. Usually the conus arteriosus of the pulmonary 
 artery is covered by the thin edge of the overlapping left 
 lung. In the cases under consideration the covering by 
 lung is incomplete, and a part of the conus comes into 
 
PULMONIC MURMURS. 205 
 
 contact with the chest wall, and during systole is flattened 
 more or less against the chest wall. An eddy is thus 
 formed in the current of blood rushing into the pulmonary 
 artery, which gives rise to a murmur. Evidence in support 
 of this explanation is afforded by the fact that the murmur 
 usually disappears when the patient is told to take a deep 
 breath and hold it, as a cushion of lung is then brought 
 over the conus arteriosus between it and the chest wall. 
 The result is the more striking if the murmur haprjens to 
 be loud and vibratory. 
 
CHAPTEE XIY. 
 CONGENITAL MALFORMATIONS. 
 
 VARIETIES OP CONGENITAL MALFORMATIONS — RELATIVE 
 FREQUENCY OF OCCURRENCE — OF SINGLE AND COMBINED 
 DEFECTS — PHYSICAL SIGNS — SYMPTOMS — CYANOSIS — 
 CAUSE OF CYANOSIS — DIAGNOSIS — PROGNOSIS. 
 
 Some of the most important varieties of congenital mal- 
 formations of the heart and great vessels are — 
 
 1. The heart consisting of two or three cavities, the 
 interventricular or interauricular septum, or both, being 
 absent. This is of rare occurrence. 
 
 2. Incomplete interventricular septum, usually taking 
 the form of a perforation in the upper third of the 
 septum. 
 
 3. Patent foramen ovale. 
 
 4. Persistence of patent ductus arteriosus. 
 
 5. Stenosis of the pulmonary orifice due to constriction 
 of the trunk of the vessel itself, or of the infundibular 
 portion of the right ventricle, or to the adhesion or 
 malformation of the valves. 
 
 6. Transposition of pulmonary artery and aorta. 
 
 7. The aorta and pulmonary artery may both arise from 
 the same ventricle. 
 
 8. Malformations of the aortic, tricuspid, or mitral 
 valves are not of common occurrence. In most cases, where 
 the tricuspid valve is found to be affected at birth, the 
 probabilities will be that it has been damaged by endo- 
 carditis occurring during foetal life. 
 
CONGENITAL MALFORMATIONS. 207 
 
 Pulmonic Stenosis. — Of these varieties by far the most 
 common is stenosis of the pulmonary orifice. Of 181 cases 
 of congenital malformation collected by Peacock, in 90 
 more or less contraction of the pulmonary orifice was 
 present, and in 29 others the orifice or trunk of the vessel 
 was obliterated.* 
 
 The narrowing may be due to constriction of the conus 
 arteriosus above the valves, or to adhesion between the 
 cusps of the valves. The artery may be very small and 
 ill developed and the valves present but impervious. 
 
 The most common varieties of congenital heart disease, 
 after pulmonic stenosis, are deficiency of the interventricular 
 septum and patency of the foramen ovale. 
 
 Deficiency of the interventricular septum usually takes 
 the form of a perforation in the upper third of the 
 septum, in the undefended or membranous space, so called 
 because normally the septum here only consists of two 
 layers of endocardium. It is rare as an isolated lesion, but 
 is not uncommon in association with other malformations 
 which give rise to unequal pressure in the two ventricles. 
 For instance, it is frequently found coexisting with pul- 
 monic stenosis, in which the pressure in the right ventricle 
 is in excess of that in the left. Not unfrequently in such 
 cases the right ventricle is greatly hypertrophied and the 
 septum is deviated to the left, and in some cases the aorta 
 arises wholly or in part from the right ventricle. 
 
 Patency of the foramen ovale may occur in connection 
 with pulmonic stenosis ; but this cannot be always attributed 
 to excess of pressure in the right auricle, as it is sometimes 
 found as an isolated lesion; and also cases are recorded 
 in which the foramen was found closed, though excess of 
 pressure must have existed in the right auricle. 
 
 The ductus arteriosus may remain patent in consequence 
 of some obstruction to the passage of blood through the 
 
 * Peacock, "Malformations of the Human Heart," p. 193. 
 
208 HEART DISEASE. 
 
 lungs or systemic vessels ; not infrequently a patent ductus 
 arteriosus occurs in association with a patent foramen 
 ovale, the patency of both being due to similar causes : 
 hence the two may be found together with, and as a direct 
 result of, pulmonic stenosis. 
 
 In a case recently under my care at St. Mary's Hospital, 
 patency of the ductus arteriosus existed as an isolated 
 lesion. 
 
 Transposition of Pulmonary Artery and Aorta. — The aorta 
 may arise from the right ventricle, and the pulmonary 
 artery from the left. The ductus arteriosus will usually 
 remain patent. The aorta and pulmonary artery may both 
 arise from the same ventricle. In a specimen in the St. 
 Mary's Hospital Museum, both aorta and pulmonary artery 
 arise from the right ventricle. The interventricular septum 
 is absent in the upper third, so that there is free com- 
 munication between the two ventricles. The right ventricle 
 is greatly dilated and hypertrophied and the left very 
 small. The pulmonary artery is very small and ill 
 developed, and its lumen is only about 2 mm. in diameter. 
 
 In spite of this the child from which the specimen was 
 taken lived to the age of three months, though cyanosed 
 and dyspnoeic from birth, and very poorly developed. 
 
 Physical Signs. 
 
 In pulmonic stenosis a loud, rough, systolic murmur is 
 usually to be heard over the precordial region with its 
 maximum intensity at the level of the nipple, midway 
 between the nipple and the sternum. It will be conducted 
 along the branches of the pulmonary artery so that it 
 will be heard over a large area on both sides of the chest ; 
 but it will be heard more distinctly on the left side of the 
 chest between the base of the heart and the clavicle than 
 over the aorta. In association with this the right ventricle 
 will usually be hypertrophied. 
 
CONGENITAL MALFORMATIONS. 209 
 
 Deficiency of the interventricular septum may give rise 
 to a systolic murmur whose seat of maximum intensity 
 is, according to Roger and Potain, in the fourth left space 
 half an inch above the nipple ; but as this defect commonly 
 coexists with pulmonic stenosis, such a murmur would 
 probably be masked by that due to the pulmonic lesion. 
 A murmur that may occur in cases of deficient inter- 
 ventricular septum, and which I look upon as diagnostic, 
 is one quite different in character to any that occur in 
 the usual forms of valvular disease. It is harsh and loud, 
 but its great peculiarity is that it never ceases, becoming 
 suddenly louder and higher pitched with the systole, 
 and subsiding into a continuous rumble during diastole, 
 reminding one of the kind of noise of varying intensity 
 made by a knife-grinder's wheel when a knife is being 
 sharpened. 
 
 Patent foramen ovale. — There is no known auscultatory 
 or other physical sign by which a patent foramen ovale 
 can be diagnosed. Peacock quotes one case of patent 
 foramen ovale without other defect, in which the patient, 
 a girl, lived to the age of sixteen, when she died of 
 pulmonary tuberculosis. There was no cyanosis, and till 
 she began to suffer from tuberculosis there were no 
 symptoms other than those of general debility. In a 
 case under my care the patient was a man, who died at 
 the age of thirty from bronchitis. There was no marked 
 cyanosis during infancy, there were no special symptoms 
 of morbus cordis, and no cardiac murmurs ; the patient 
 was, however, dull and of sluggish intellect, but could 
 take long walks without seeming distressed in any way, 
 or appearing the worse for it. During the fatal attack 
 of bronchitis cyanosis developed, attended with torpor. A 
 noteworthy point was that the cyanosis deepened during 
 sleep, and there was no spontaneous waking up, and the 
 patient was roused with difficulty. Eventually the torpor 
 
2io HEART DISEASE. 
 
 and cyanosis deepened into fatal coma. At the autopsy 
 the only cardiac lesion found was a patent foramen ovale. 
 
 Patent Ductus Arteriosus. — This usually is found asso- 
 ciated with other lesions of which it may be difficult to 
 differentiate the physical signs. I have recently, however, 
 had under my care a case, already referred to, in which 
 patency of the ductus arteriosus existed as an isolated 
 lesion The only physical sign was a soft blowing systolic 
 murmur of moderate intensity audible over most of the 
 cardiac area, most marked in the third left intercostal 
 space ; it diminished in intensity towards the clavicle and 
 towards the aortic area, but was very distinct at the apex. 
 There was no cyanosis, and there were no symptoms 
 directly attributable to the condition, but the child died of 
 diarrhoaa and vomiting. It was 7 months old. 
 
 Symptoms. 
 
 The child suffering from a serious congenital affection 
 of the heart is usually irritable and fretful, and may be 
 subject to fits. The fingers and toes are clubbed, and the 
 extremities cold. He may be always cyanosed to a varying 
 degree, or only become cyanosed on exertion. There will 
 usually be constant shortness of breath, and paroxysms of 
 dyspnoea may occur, in which cyanosis becomes so intense 
 that the extremities become almost black. He will remain 
 stunted in growth and backward in development, intel- 
 lectually as well as physically. The symptoms will of 
 course vary, according to the nature of the lesion. They 
 will be most marked in a case of severe pulmonary stenosis, 
 and may, as has already been seen, be entirely absent in a 
 case of uncomplicated patent foramen ovale. 
 
 Cyanosis. — In many instances of congenital malforma- 
 tion of the heart, the most marked and striking feature is 
 the cyanosis of the patient ; hence the various forms of 
 
CONGENITAL MALFORMATIONS. 21 i 
 
 congenital heart disease have been grouped together under 
 the names morbus cceruleus, or blue disease, by English, 
 and cyanose, or maladie bleue, by French authors. 
 
 The explanation of the cause of this peculiar discolora- 
 tion is still a matter of dispute. Senac, Corvisart, Gintrac, 
 and others attribute it to the mixture of arterial and 
 venous blood in the heart or great vessels, owing to defec- 
 tive septa or patent ductus arteriosus. Cruveilhier at- 
 tributed it to venous congestion. It has been proved, 
 however, that cyanosis may exist without the intermixture 
 of currents of blood, also that complete intermixture may 
 take place without the occurrence of cyanosis. 
 
 It is obvious, therefore, that neither of these explana- 
 tions are sufficient. Stille, with a view to determining the 
 cause of cyanosis, collected 77 cases of congenital morbus 
 cordis in which cyanosis was present. In 53 instances 
 the pulmonary artery was constricted or impervious, or 
 its orifice was obstructed in some way. He came to the 
 conclusion, therefore, that cyanosis was due to venous 
 congestion usually dependent on obstruction at the orifice 
 of the pulmonary artery, or on some other cause giving 
 rise to obstruction to the venous return. This is clearly 
 not a complete explanation, as there is often no cyanosis 
 in cases of morbus cordis in adults where the venous 
 congestion is extreme. Peacock makes another important 
 suggestion, that deficient aeration of the blood is a con- 
 tributory cause of cyanosis ; he says, " where only a small 
 proportion of the blood is submitted at one time to 
 aeration in the lungs, the whole mass must be of a dark 
 colour, consequently the hue of the surface will be pro- 
 portionately dark." This is especially the case in pulmonic 
 stenosis, and Stille's statistics, which show that pulmonic 
 stenosis is the commonest cause of cyanosis, afford strong 
 support to this view, that aeration of a small proportion 
 only of the blood is the essential cause of cyanosis. 
 
HEART DISEASE 
 
 Diagnosis. 
 
 Though in severe cases it is usually easy to arrive 
 at a diagnosis of congenital heart disease from a history 
 of cyanosis and dyspnoea since birth, with the clubbing 
 of the fingers and toes, it is difficult and in many instances 
 impossible to be certain of the exact nature of the 
 malformation. 
 
 Where with a history of cyanosis and paroxysms of 
 dyspnoea since birth we find a loud, rough, systolic murmur, 
 with its maximum intensity on the left side at the level 
 of the nipple, midway between the nipple and sternum, 
 together with a hypertrophied right ventricle, we may 
 be fairly certain that pulmonary stenosis is the main 
 lesion; but whether a patent foramen ovale or perforate 
 interventricular septum, or patent ductus arteriosus, is 
 present as well, it will often be impossible to decide. 
 
 Prognosis. 
 
 The lesion is in this case stationary, and not pro- 
 gressive, but the malformations being widely different, 
 the effect they have on the duration of life will vary 
 considerably. 
 
 1. In cases of moderate constriction of the pulmonary 
 artery without other malformation, for which hypertrophy 
 of the right ventricle is sufficient to compensate, there 
 will be no cyanosis, and the patient may live many years 
 without serious inconvenience, except on violent exertion. 
 
 2. In cases where the foramen ovale is open the 
 pulmonary stenosis is usually greater, and hence the 
 duration of life will probably be less ; but out of 20 cases 
 which Peacock collected, 11 lived to the age of 15 years 
 and over, 1 living to the age of 57. 
 
 3. Where with pulmonary stenosis the interventricular 
 
CONGENITAL MALFORMATIONS. 213 
 
 septum is also deficient, the prognosis is much less 
 favourable, for not only must the pulmonary constriction 
 be considerable to have given rise to this deficiency, but, 
 further, in such case the aorta usually arises in part from 
 the right ventricle. Of 64 such cases collected by Peacock, 
 only 14 survived the age of 15. If, however, the degree 
 of pulmonic stenosis is slight and the perforation in the 
 septum small, life may be prolonged, and two patients are 
 now living, at the age of 30 or upwards, in which I believe 
 this condition to exist ; one has borne a child. 
 
 4. Where the pulmonary artery is impervious, the 
 duration of life rarely exceeds a few months, though of 28 
 such cases of Peacock's, 3 lived to the age of 9 or 10, and 
 1 to 12 years. 
 
 In a case under the care of Dr. Cheadle in St. Mary's 
 Hospital in 1902, a child lived to the age of 14 months with 
 an impervious pulmonary artery and a heart consisting of 
 only two cavities, an auricle and ventricle. It was cyanosed 
 and dyspnoaic from birth. 
 
 5. Transposition of the main arteries, or arrest of 
 development, so that the heart consists of two or three 
 cavities only, is usually incompatible with life for any 
 long period after birth, but 4 cases are recorded by Peacock 
 where with one ventricle only and two auricles persons 
 lived to the ages of 11, 16, 23, and 24 years respectively. 
 
 6. Patency of the foramen ovale uncomplicated by any 
 other defect may not of itself give rise to any serious 
 symptoms; doubtless in most instances where the opening 
 is valve-like it will become closed before adolescence is 
 reached. Where it persists or allows of extensive leakage, 
 any lung affection, such as bronchitis, which tends to 
 increase the pressure in the right side of the heart and 
 cause a flow of non-aerated blood from the right to the 
 left auricle, will be especially dangerous and liable to 
 prove fatal. 
 
CHAPTER XY. 
 
 PROGNOSIS IN VALVULAR DISEASE 
 (GENERAL). 
 
 the nature op the lesion : the relative danger 
 attaching to each particular lesion — sudden 
 death: the valvular diseases in which it is 
 liable to occur — the extent of the lesion — 
 the stationary or progressive character of the 
 lesion as influencing prognosis. 
 
 In cases of heart disease, prognosis is of special im- 
 portance, since a patient who knows that he is suffering 
 from some affection of the heart immediately dreads the 
 worst. It is always necessary to allay his fears as far 
 as possible, as these in themselves tend to aggravate the 
 danger attending the disease. In some cases this may 
 be done with absolute confidence ; in others, the appre- 
 hensions may be only too well founded ; in others, again, 
 the issue may be uncertain and may be dependent on other 
 conditions than the state of the heart. It will be most 
 important in all instances that the medical attendant should 
 form a definite idea of the probable effect the heart disease 
 will have in shortening life, so that he may guide the 
 patient and his friends in making arrangements on which 
 the welfare of the family may depend. 
 
 The following are the points which should specially be 
 considered in regard to prognosis : — 
 
 1. The valve affected and the relative danger attaching 
 to the particular lesion. 
 
RELATIVE DANGER OF VALVULAR LESIONS. 215 
 
 2. The extent of the lesion. 
 
 3. The stationary or progressive character of the lesion. 
 
 4. The degree of soundness and vigour, functional and 
 
 nutritional, of the muscular substance of the heart, 
 of the arterial walls, and of the tissues generally. 
 
 5. The age of the patient. 
 
 6. The family history, especially in regard to whether 
 
 there is any hereditary tendency to heart disease. 
 
 7. The habits and mode of life of the patient. 
 
 8. The presence or absence of other diseases — such as 
 
 anaemia, bronchitis, renal affections — as compli- 
 cations. 
 
 The Relative Danger attaching to the Different 
 Valvular Lesions. 
 
 According to Walshe, the valvular affections stand in 
 the order of relative gravity as follows : tricuspid regurgi- 
 tation, mitral regurgitation, mitral constriction, aortic 
 regurgitation, pulmonary constriction, aortic constriction. 
 Tricuspid regurgitation, however, as has already been said, 
 is rarely primary, but usually occurs as a result of obstruction 
 to the transit of blood through the lungs either from disease 
 in these organs, or from valvular disease in the left side of 
 the heart. It is therefore an effect of serious valvular 
 lesions of the left side of the heart, and can scarcely be 
 regarded as a cause of the fatal termination. 
 
 My own experience would lead me to modify Walshe's 
 arrangement somewhat, and to give this order of relative 
 danger : aortic incompetence, mitral stenosis, aortic stenosis, 
 mitral incompetence. Aortic incompetence is most rapidly 
 fatal when it comes on late in life at a period when com- 
 pensatory hypertrophy is established with difficulty, more 
 especially when due to degenerative change in the valves. 
 In childhood and early adolescence, mitral stenosis is often 
 more serious than aortic incompetence, owing to the 
 
216 HEART DISEASE. 
 
 progressive nature of the lesion and to imperfect develop- 
 ment of the left ventricle. It is, however, difficult to 
 estimate with any accuracy the relative danger of different 
 valvular lesions, as so many other factors must he taken 
 into consideration in prognosis. 
 
 Sudden Death. 
 
 One of the first questions to be discussed is the liability 
 to sudden death in heart disease. In the mind of the 
 general public, disease of the heart and sudden death are so 
 closely associated that the mention of the one immediately 
 suggests the other, and in a nervous patient, a pain or a 
 sense of weight or oppression in the cardiac region, easily 
 exaggerated by the concentration of his attention upon the 
 heart, will make him think the end is near. 
 
 It is therefore of the greatest importance that we should 
 know with certainty, in what form of heart disease sudden 
 death is liable to occur, and be able in cases where no such 
 danger exists to say so with confidence. It must be under- 
 stood that the sudden death under consideration is such as is 
 meant by the familiar phrase " dropping down dead," with 
 little or no warning, the individual having been up to the 
 moment in apparent health, or so far well as to be able to go 
 about his duties, or at any rate not suffering from dropsy or 
 other serious symptoms of cardiac embarrassment. 
 
 In all forms of heart disease, when the effects on the 
 circulation have become very decided, and such symptoms 
 as engorgement of the lungs, with dyspnoea, dropsy, effusion 
 into the pleural cavities, albuminuria, have set in, the final 
 struggle may come on abruptly and end speedily. This, 
 however, is not the mode of death which is the special 
 dread attending heart disease. 
 
 Walshe, in speaking of the different forms of valvular 
 lesions, says that only one causes sudden death, namely, 
 aortic incompetence. 
 
SUDDEN DEATH. 217 
 
 In a paper read before the Harveian Society in 1866, 
 I gave as the conclusion at which I had arrived that 
 " sudden death is a contingency which may almost be left 
 out of consideration in valvular disease, except in aortic 
 regurgitation." This would still express very nearly my 
 individual experience. As will be shown in the part of this 
 book on the structural changes in the wall of the heart, 
 there are other conditions more likely to give rise to 
 sudden death than aortic regurgitation. Here, however, we 
 are considering only the valvular lesions. 
 
 As individual experience is not altogether a trustworthy 
 guide, some years ago Sidney Phillips, at my request, 
 went through the post-mortem records of St. Mary's 
 Hospital of four hundred cases in which the heart had 
 undergone marked change, in order to see what light they 
 threw on the question of heart disease and sudden death. 
 Of these, 151 were cases of valvular disease, 204 examples of 
 changes in the wall of the heart. Of aortic regurgitation 
 there were thirty-eight cases. Three were brought to the 
 hospital dead, a fourth died in the hospital suddenly during 
 convalescence from acute rheumatism. In six more the 
 final symptoms came on abruptly and were rapidly fatal, 
 one dying within twenty-four hours of his admission to the 
 hospital, another within two days. There were eleven 
 examples of aortic stenosis without one sudden death in the 
 sense of the patient being overtaken by death while in 
 apparent health or free from symptoms arising from heart 
 disease. 
 
 Of mitral stenosis there were fifty-three instances. One 
 patient only was brought in dead, a young girl who was 
 picked up in the street. From the condition of the lungs 
 there was no doubt that she must have been suffering 
 severely from symptoms due to the heart affection. 
 
 Of mitral insufficiency there were forty-nine cases. 
 Of these, two may be said to have died suddenly, but 
 
218 HEART DISEASE. 
 
 both had serious symptoms and were under treatment in 
 hospital, and in both the pericardium also was universally 
 adherent. 
 
 In three more a final attack of dyspnoea set in abruptly 
 and proved rapidly fatal. 
 
 These numbers are not given as representing with 
 anything like accuracy the proportion of sudden deaths in 
 the different forms of valvular disease, but they afford 
 confirmation of the opinion formed from personal experience 
 that aortic insufficiency is the only form of valvular disease 
 attended with danger of sudden death. 
 
 The Extent of the Lesion. 
 
 In a previous chapter the indications by means of which 
 the extent of the lesion may be estimated, have been 
 discussed. A certain limited amount of information on 
 this head is obtained from the character of the murmur. 
 Further help is derived from the pulse, and still more 
 from the amount of hypertrophy and dilatation which the 
 heart has undergone in consequence of the lesion. A 
 valvular murmur, accompanied by dilatation or hypertrophy 
 or both, is attended with greater danger than a similar 
 murmur not so accompanied ; not, however, because the 
 hypertrophy and dilatation add new elements of danger, but 
 because the valvular change causing the murmur has given 
 rise also to mechanical difficulty when these changes are 
 present, whereas their absence shows that it has given rise 
 to no serious obstacle to the circulation. 
 
 It must be understood, however, that when hypertrophy 
 and dilatation are taken as a measure of the valvular lesion 
 it is in the absence of any evidence of functional inefficiency. 
 Where, in addition to the disease of the valves, there is 
 degeneration of the muscular substance of the heart, this 
 will give rise to further dilatation. Still, however, the 
 
PROGNOSIS ACCORDING TO ETIOLOGY 219 
 
 amount of dilatation may be taken as expressing the 
 relation between the mechanical difficulty and the power of 
 the heart to cope with it. Naturally the more extensive 
 the lesion, as estimated by the changes in the heart, the 
 more serious the prognosis, because the compensatory 
 balance has been established with difficulty and is more 
 easily upset. 
 
 The Stationary or Progressive Character of the 
 Lesion as influencing Prognosis. 
 
 A given state of valve existing— a certain degree of 
 obstruction or incompetence— it will be obvious that the 
 future of the patient will be very greatly influenced by the 
 question whether the morbid process which has damaged 
 the valve is still in progress, or has come to a standstill. 
 In the one case, where the change has reached its 
 maximum, we know what we have to deal with — the 
 hypertrophy and dilatation give an approximate idea of the 
 functional imperfection ; they compensate it or they do not, 
 and the prognosis varies accordingly : in the other there 
 can be but one course and issue, a gradual or swift aggra- 
 vation of symptoms, unless indeed sudden death interferes. 
 
 Such a difference exists arising out of the character of 
 the pathological process by which the valve is affected. 
 Speaking generally, the question is whether the valvular 
 change has had its origin in an acute inflammatory 
 attack or is the result of a chronic degenerative process. 
 Fortunately the distinction is for the most part easy. 
 
 In the chapter on the aetiology of valvular disease the 
 various causes of lesions of the valves and orifices have 
 been enumerated and briefly discussed. They are, acute 
 endocarditis, chronic endocarditis, and degenerative changes 
 in the valves, rupture of valve, dilatation of the orifice. 
 
 Acute Endocarditis. — When the valvular lesion can be 
 
HEART DISEASE. 
 
 traced definitely to an attack of acute endocarditis, there 
 is this favourable element in the prognosis, that the lesion 
 once established is not progressive. If the lesion was slight 
 it remains slight, and does not increase in severity after 
 the endocarditis has subsided; consequently the dilata- 
 tion and hypertrophy of the heart will be small, if indeed 
 they are appreciable ; if the lesion is extensive, the dilata- 
 tion and hypertrophy which will follow are proportionate. 
 Hence we are able to arrive at a definite conclusion as to 
 the extent of the lesion, and give an approximate idea as 
 to the probable effect it will have in shortening life, and 
 say how far exercise and exertion can be allowed. The only 
 exception to be made will be in cases of mitral stenosis, 
 where the orifice may become gradually further narrowed 
 after the initial damage has been done, owing to cicatricial 
 contraction of the inflammatory products. 
 
 Chronic Endocarditis. — The fatal feature about this 
 chronic inflammatory or degenerative change in the valves 
 is, that once begun it is inevitably progressive. The heart 
 and system may have accommodated themselves to a degree 
 of obstruction or regurgitation, but this does not remain 
 the same; slowly or rapidly the valvular lesion will in- 
 crease, and with it the obstacle to the due transmission of 
 the blood through the heart. This takes place at an age 
 when the heart is little able to adapt itself to change or to 
 meet the increasing difficulty, and is, moreover, itself liable 
 to structural decay ; further, the cause which has worn out 
 the valves, the excessive resistance in the peripheral circu- 
 lation giving rise to unduly high tension in the arterial 
 system, is probably still in operation. 
 
 Before, however, we take so serious a view of any given 
 case in which a valvular murmur has been developed late 
 in life, and accept it as necessarily indicative of progressive 
 disease, we ought to make sure that it is due to degenera- 
 tive changes, and not to mere roughening of the valve. To 
 
PROGNOSIS IN RUPTURE OF A VALVE. 221 
 
 prove the former we ought to have evidence of actual 
 damage to the valve, either in the shape of symptoms 
 traceable to functional inefficiency or of modifications of 
 the physical signs. It is common in elderly people to find 
 a mitral or aortic systolic murmur develop, which persists 
 for years without any symptoms of heart disease, due to a 
 slight roughness or rigidity in the case of the aortic valve 
 which sets up vibrations ; or, in the case of the mitral valve, 
 to a little thickening or want of pliability which prevents 
 an accurate apposition of the flaps of the valve, but does 
 not allow of any appreciable regurgitation. 
 
 Rupture of Valve. — Eupture of a valve is of rare 
 occurrence and is always a serious lesion. The valve 
 affected is usually the aortic, and the sudden and severe 
 strain on the heart, which has no time to accommodate 
 itself to the altered conditions of the circulation, leads to 
 dilatation of the left ventricle and the consequent onset 
 of severe symptoms when the rupture of a cusp is com- 
 plete. The accident is usually accompanied by sudden 
 pain in the chest, and the patient may be seized by a 
 syncopal attack, which will at once prove fatal. The 
 early symptoms may, however, not be very severe. The 
 patient may appear to progress favourably for a time, but 
 dyspnoea and other symptoms of cardiac embarrassment 
 will soon set in, for the accident usually takes place at a 
 time in life when degenerative changes are already be- 
 ginning to take place in the walls of the heart, and it is 
 incapable of undergoing sufficient hypertrophy to com- 
 pensate for the valvular lesion. Hence the ultimate cause 
 of death, if the patient survives, is a gradual stasis of the 
 circulation, the premonitory indications being a rapid 
 increase in the size of the liver, with dilatation of the 
 right ventricle following on that of the left, and later 
 the onset of oedema of the extremities. It may be some 
 weeks or months after the accident before the fatal 
 termination ensues. 
 
222 HEART DISEASE. 
 
 Dilatation of the Orifice. — (a) The Aortic Orifice. — The 
 aortic orifice is less liable to dilatation than the mitral, 
 owing to the strong fibrous ring surrounding it. When 
 dilatation does occur, it usually takes place comparatively 
 late in life as a part of a general dilatation of the aorta due 
 to degenerative changes in the Avails of the vessel or its 
 orifice : it is therefore progressive in character and the 
 prognosis is unfavourable, more especially as these same 
 degenerative changes may lead to the production of 
 aneurysm. 
 
 Syphilitic disease of the aorta, invading the orifice and 
 valves and giving rise to incompetence, carries with it a 
 grave prognosis. 
 
 (b) The Mitral Orifice. — Speaking generally, mitral re- 
 gurgitation, established by means of dilatation of the left 
 ventricle, in the young, or as a result of acute febrile 
 conditions or anasmia, is, under favourable conditions, 
 curable. When it is secondary to aortic disease, the 
 prognosis necessarily merges in that of the primary lesion. 
 When it occurs as a result of protracted high tension or 
 a kidney disease, it may be temporarily curable by suit- 
 able treatment, but will be liable to recur. 
 
 In later life and old age it may be gradually and 
 imperceptibly established without any obvious cause for it, 
 and it is difficult to diagnose between dilatation of the 
 orifice and changes such as gradual thickening and contrac- 
 tion of the valves. It is in such cases, however, very 
 slowly progressive, as a rule. 
 
CHAPTER XVI. 
 
 PROGNOSIS CONTINUED — AGE, SEX, HEREDITY — EFFECTS OF 
 HIGH ARTERIAL TENSION — HABITS AND MODE OF LIFE 
 OF THE PATIENT — ANAEMIA — THE CIRCUMSTANCES 
 UNDER WHICH PROGNOSIS MAY HAVE TO BE MADE : (1) 
 IMMEDIATELY AFTER ACUTE ENDOCARDITIS ; (2) WHEN 
 THE VALVULAR LESION IS SLIGHT AND HAS GIVEN RISE 
 TO NO STRUCTURAL CHANGES IN THE HEART ; (3) WHEN 
 COMPENSATORY CHANGES HAVE TAKEN PLACE BUT NO 
 SYMPTOMS OF EMBARRASSMENT OF THE CIRCULATION 
 ARE PRESENT ; (4) WHEN SYMPTOMS OF FAILURE OF 
 COMPENSATION HAVE SET IN; (5) IN ADVANCED 
 VALVULAR DISEASE WHEN SEVERE SYMPTOMS OF 
 CARDIAC FAILURE HAVE SUPERVENED. 
 
 Age. — Little need be said with regard to age as affecting 
 the prognosis of heart disease. Late in life, degenerative 
 processes are almost invariably in operation, and the hyper- 
 trophy which is needed, in order that the effects of valvular 
 affections may be neutralized, is established with difficulty ; 
 moreover, compensatory hypertrophy, which has served its 
 purpose for twenty or thirty years, may at the end of this 
 time be undermined by fatty or fibroid degeneration of 
 the cardiac walls. 
 
 Childhood. — In early childhood, the outbreak of rheumatic 
 endocarditis is always a matter of grave prognostic signifi- 
 cance : firstly, because it is so frequently accompanied by 
 pericarditis, which may prove fatal at the time of the attack 
 
224 HEART DISEASE. 
 
 or leave the heart permanently hampered and disabled by 
 pericardial adhesions ; secondly, because, even though the 
 heart escapes serious damage from the first attack of either 
 peri- or endocarditis, both are extremely liable to recur. 
 Further, it would appear that when a valvular lesion of 
 some severity is established, the heart cannot both answer 
 the demand for hypertrophy and keep pace with the active 
 growth of this period of life, so that the child is liable to 
 remain small and stunted, with clubbing of the fingers and 
 toes, and to be generally backward in development. 
 
 Sex. — It is a remarkable fact that mitral stenosis is very 
 much more common in women than in men. The post- 
 mortem statistics previously referred to, show that out of 53 
 cases of mitral stenosis, 38 were in females, and only 15 in 
 males, which is approximately a proportion in accord with 
 the experience of most observers. No satisfactory explana- 
 tion of this predominance has yet been given. 
 
 On the other hand, aortic insufficiency is more frequently 
 met with in men, which again is borne out by the same 
 statistics, as out of 36 cases, 30 were males, and only 6 
 females. This appears to be explained by the occupation 
 and mode of life of men ; in my own experience, however, 
 aortic regurgitation has been much more common in boys 
 than in girls at a period of life long before the influence of 
 occupation would begin to operate. 
 
 When valvular disease has been established in childhood, 
 girls are, according to my experience, more likely to break 
 down at the trying period of puberty than boys, and, speak- 
 ing generally, the compensatory changes in the heart 
 walls are less perfectly effected in the female than in the 
 male. 
 
 Hereditary Tendencies.— In no class of cases is it more 
 necessary to inquire into the family history than in diseases 
 of the heart. It is more particularly in affections of the 
 muscular walls that a family tendency to heart disease is 
 
PROGNOSIS IN HIGH TENSION. 225 
 
 seen, which may take the form of fatty degeneration, 
 or of fibroid change secondary to high arterial tension. 
 I have known a family in which three out of four brothers 
 died suddenly before reaching the age of fifty-five from 
 disease of the heart or aorta, and other examples almost 
 equally striking ; similar histories must be known to most 
 medical men of large experience. It is not, however, only 
 a special liability to structural degeneration of the heart at 
 a certain age which is important. In any valvular affection, 
 and at any stage, the constitution of the patient is an 
 element in the prognosis which must be kept in view. We 
 have to take into account, not simply the cardiac lesion 
 and the functional derangement of the circulation caused 
 thereby, but also the behaviour of the system under this 
 disturbing influence and its power of endurance, and in a 
 short-lived family we cannot have the same confidence in the 
 tissues as in a family noted for longevity. More than once 
 in my own experience, a prognosis based upon the state of 
 the heart has been falsified through failure of general con- 
 stitutional power. 
 
 Effects of High. Tension in the Circulation. — High 
 tension in the arterial system, frequently a hereditary 
 condition, may in itself be a cause of chronic valvular 
 disease in later life, as has been already stated in discuss- 
 ing the causes of chronic endocarditis. It increases the 
 shock of every closure of the aortic valves, and renders 
 necessary more powerful contraction of the left ventricle to 
 drive on the blood, and thus increases the stress on the 
 mitral valve and its tendinous cords. The unremitting' 
 strain thus imposed on both aortic and mitral valves is 
 more injurious than the occasional strain due to violent 
 muscular efforts. Hence, when there is high arterial 
 tension in addition to valvular disease, it will greatly tend 
 to aggravate the mischief already effected, and will con- 
 tribute a grave addition to the unfavourable elements of 
 
 Q 
 
226 HEART DISEASE. 
 
 prognosis, unless carefully watched and relieved by diet 
 and treatment. 
 
 Habits and Mode of Life of the Patient. — These have a 
 very important bearing on the prognosis. Violent efforts 
 or sustained exertion impose a great strain on the valves 
 of the heart ; vicissitudes of temperature tax its power of 
 accommodation to different conditions of circulation, while 
 unfavourable hygienic influences tend to malnutrition and 
 degeneration. The man, therefore, who must labour with 
 his hands, who is exposed to all weathers, whose food is of 
 inferior quality and sometimes insufficient in quantity, who 
 breathes impure air and indulges perhaps in strong drink, 
 who seeks advice only when he can no longer toil, and 
 abandons all precautions as soon as he leaves the hospital, has 
 far less chance of long life than the man who can seek advice 
 early and has adequate means to carry it out. There can be 
 little probability of existing compensation being maintained, 
 or of rejjarative hypertrophy being established under such 
 circumstances. The first condition of recovery from the 
 effects of disease, the removal of the cause which gives 
 rise to these effects, is wanting. Conversely, protection 
 from adverse influences which have precipitated the access 
 of symptoms, together with rest, warmth, good food, and 
 care, may reverse an apparently hopeless forecast, as is not 
 unfrequently seen in the all but miraculous recoveries 
 which take place in hospitals. In the same way, persistence 
 in habits of eating and drinking, which may lead to valvular 
 disease, directly, by overloading the blood with impurities, 
 which give rise to high arterial tension, or indirectly, through 
 gouty inflammation, will affect the prognosis unfavourably, 
 while obedience to rules of diet carefully laid down and 
 supervised as to their effect will incline the balance to the 
 opposite side. 
 
 Anaemia. — Ansemia, as is well known, is very common 
 at the period of adolescence, and especially in girls ; and 
 
PROGNOSIS IN ANEMIC SUBJECTS. 227 
 
 its effects may be most prejudicial. About middle age, 
 essential or pernicious anaemia may complicate heart disease, 
 and in at least two instances which have come under my 
 observation, has been the real cause of death which was 
 attributed to the state of the heart. 
 
 But, in addition to primary anaemia, a deterioration of 
 the blood is a common and almost inevitable result of heart 
 disease when this reaches a point at which it begins to 
 affect the circulation. The slow movement of the blood 
 through the systemic capillaries and through the lungs, 
 whether due to deficient vis a tcrgo, as in aortic disease, or 
 to venous stasis in mitral disease, prevents those active 
 changes from taking place by means of which the blood is 
 constantly purified and renewed. Absorption of food, again, 
 will be more or less hindered by the languid movement of 
 the blood in the gastro-intestinal mucous membrane, and 
 by the congestion of the liver, which result from obstruction 
 to the return of blood to the heart. 
 
 Anaemia, therefore, existing at a time when prognosis is 
 called for, and especially a tendency to recurring anaemia, 
 is a serious element in the forecast. 
 
 Anaemia, however induced, has always a detrimental 
 influence on the heart. It may of itself, aided by the high 
 arterial tension which often accompanies it, give rise to 
 dilatation of the left ventricle and leakage of the mitral 
 valve ; it will, therefore, tend to aggravate such dilatation 
 as has already been produced by valvular disease, while 
 it will retard compensatory hypertrophy by impairing the 
 quality of the nutritive material supplied. It is also 
 often attended with palpitation of the heart, and will 
 add to the liability of the valvular disease to this distress- 
 ing and sometimes dangerous symptom. 
 
 Anaemia, again, may of itself give rise to oedema, and it 
 will precipitate the occurrence of dropsy when a tendency 
 thereto exists from the nature of the cardiac lesion. 
 
228 heart disease. 
 
 The Circumstances and Conditions under which 
 a Prognosis may have to be made. 
 
 1. We are frequently asked, during convalescence 
 after acute endocarditis — sometimes, indeed, before trie 
 attack has subsided — how far the heart is likely to be 
 ultimately affected. This is a question to which no 
 prudent man will give a definite reply. It is impossible 
 at this time to appeal to the changes in the walls and 
 cavities of the heart for guidance, as there has been no 
 time for their development. The cardiac murmurs are not 
 trustworthy guides, as a systolic apex murmur, or some- 
 times an aortic murmur, which has developed in the course 
 of acute rheumatism, may disappear afterwards. If, however, 
 aortic regurgitation is actually established, the prognosis 
 is serious, although no definite opinion can be formed as 
 to the probable rate of progress. 
 
 2. When the lesion is one of old standing we may have 
 an individual in apparent health and vigour, scarcely con- 
 scious of any inconvenience arising from derangement of 
 the circulation even on exertion, but in whom the discovery 
 of a valvular murmur has been made. There is no modifi- 
 cation of the pulse, the murmur accompanies and does not 
 replace the sound with which it is associated, and there is 
 no marked hypertrophy or dilatation of the heart. In such 
 a case the valvular change is slight and unimportant, and 
 of present danger there is none. 
 
 With regard to the future of such a patient, everything 
 depends on the question whether the existing state of the 
 valves is an old-standing, permanent condition traceable to 
 a long past attack of rheumatic endocarditis, or is just the 
 beginning of mischief, such as chronic valvulitis, or atheroma, 
 which will go on increasing. In the former case the patient 
 may live to old age and weather all storms of illness and 
 hardship ; in the latter, if we take as an illustration the most 
 
PROGNOSIS WHEN COMPENSATION IS GOOD. 229 
 
 serious form of disease, aortic regurgitation, he will probably 
 not live more than four or five years, though a definite 
 judgment as to the course and duration of the affection can 
 only be formed after repeated and careful examination at 
 long intervals. 
 
 3. In another case, while no symptoms are present, 
 there is hypertrophy or dilatation of the heart, or both. 
 Here the presence of structural changes testifies to the 
 existence of mechanical difficulty due to obstruction or 
 regurgitation, and shows that the valvular lesion is real : 
 there will almost certainly be some corresponding modifi- 
 cation of the pulse, and although compensation has been 
 established, the equilibrium may be disturbed by causes, 
 which would have no effect on the normal heart, and once 
 overthrown will not be very easily restored. While, there- 
 fore, under favourable circumstances, the health may remain 
 unaffected for many years, an illness of any kind, and 
 especially an attack of bronchitis, may be attended with 
 dangerous disturbance of the circulation. 
 
 In such a case, again, it is of the utmost consequence 
 whether the valvular disease is stationary or progressive : 
 should it be progressive, the prognosis will necessarily be 
 grave, though much will depend on the seat and character 
 of the valvular lesion. The age, sex, general constitutional 
 vigour, and family history must be taken into account, as 
 also the position in life and habits of the patient. 
 
 4. In another patient, symptoms of embarrassment of 
 the pulmonary or systemic circulation are present, habitual 
 shortness of breath on slight exertion, violent or irregular 
 action of the heart on slight provocation, which does not 
 readily subside, pain or a feeling of oppression in the 
 precordial area, incipient oedema about the ankles and 
 perhaps albuminuria with a thick deposit of pink or high- 
 coloured urates in the urine ; further evidences of im- 
 perfect compensation are also found in the pulse, in the 
 
230 HEART DISEASE. 
 
 enlargement of the liver and fulness or pulsation of the 
 veins of the neck. 
 
 Here danger is never far off and may be imminent, 
 though by suitable precautions it may be guarded against 
 and warded off for years. Speaking generally, there is 
 less probability of prolonged life and comfort after such 
 symptoms have set in, in aortic than in mitral disease. 
 There are more chances of obviating the effects of obstruc- 
 tion by compensatory changes than of making up for failure 
 of vis a tcrgo. As a rule, the earlier in the course of 
 valvular disease symptoms supervene, the more serious is 
 their significance. 
 
 5. In another case we are called upon to give a prognosis 
 when grave consequences of a valvular disease have already 
 been developed. The occurrence of these serious symptoms 
 may have taken place in spite of compensatory changes in 
 the shape of hypertrophy of the right or left ventricle or 
 both, as the case may be, or for the want of them ; we 
 must therefore consider whether by opportunity for the 
 restoration or establishment of compensation and by suitable 
 treatment a working equilibrium can be attained. The 
 most important question will be whether the symptoms 
 have been brought on by any temporary or removable 
 cause, such as over-exertion, exposure, anxiety, recent acute 
 illness, pulmonary disease such as bronchitis, antenna, or 
 debility or the like, or whether there is no recognizable 
 cause for their appearance. In the latter case, the prognosis 
 is far more serious, as some degenerative change in the 
 cardiac walls or organic weakness of the heart or system 
 generally, or possibly some further complication in the 
 shape of adherent pericardium, is to be apprehended. ' A 
 working man admitted into hospital will almost certainly 
 recover, only however to break down again when he resumes 
 his occupation, and is again exposed to the injurious 
 influences which brought on the symptoms of compensatory 
 
PROGNOSIS WHEN COMPENSATION HAS BROKEN DOWN. 231 
 
 failure. A patient in easy circumstances may by care 
 maintain for a long time the statum quo, but lie will not 
 easily retrace downward steps taken in spite of all favouring 
 conditions. The character of the valvular change loses none 
 of its importance, the only hope of prolonged immunity from 
 further consequences of failing or obstructed circulation will 
 be the absence of any tendency to aggravation of the lesion 
 in the valve. Subject to this the soundness of the patient's 
 organs and tissues and the tenacity of life exhibited by the 
 family history will be elements of great consequence. 
 
 6. When we are called upon to form an opinion of the 
 chances of recovery of a patient who is suffering from 
 advanced dropsy, with severe pulmonary congestion and 
 extreme dyspnoea, then indeed the stationary or progressive 
 character of the lesion has no longer any bearing on the 
 immediate issue of the case. If the symptoms have been 
 gradually increasing in severity without any apparent cause, 
 and the dropsy has crept on from the legs and invaded 
 the trunk, and the dyspnoea is extreme even while the 
 patient is at rest in bed, then there is little hope of recovery. 
 If, on the other hand, the access of severe symptoms is 
 traceable to over-exertion or a chill or intercurrent pulmo- 
 nary trouble, such as bronchitis, then there is a hope that 
 suitable treatment may for a time restore the compensatory 
 balance, provided that there is evidence of a certain degree 
 of vigour and force in the cardiac impulse, more especially 
 in that of the right ventricle. If it is a second attack of 
 this kind, there will be less chance of recovery, and any 
 complication, such as kidney disease, will diminish mate- 
 rially this chance. The occurrence of a pulmonary apoplexy 
 at this stage, or of thrombosis of the veins of the leg, will 
 be of very serious import, rendering the prognosis as regards 
 the prolongation of life, even for a short period, almost 
 hopeless. 
 
CHAPTER XVII. 
 TREATMENT (GENERAL). 
 
 TREATMENT OF VALVULAR DISEASE IN GENERAL — PROPHY- 
 LACTIC MEASURES — GENERAL RULES, IN CASES WHERE 
 LESION IS NOT OP SERIOUS EXTENT, AS TO EXERCISE, 
 CERTEL AND SCHOTT TREATMENTS, CLIMATE, CHOICE OF 
 RESIDENCE, DIET, STIMULANTS — TREATMENT WHERE 
 LESION IS OF MORE SERIOUS NATURE AND HAS GIVEN 
 RISE TO MARKED HYPERTROPHY AND DILATATION OF 
 THE HEART — PRECAUTIONS TO BE TAKEN — SELECTION 
 OF WINTER RESORT — REST IN BED— DIET— STIMULANTS 
 — EMPLOYMENT OF DRUGS— TREATMENT OF VENOUS 
 CONGESTION — VENESECTION — TREATMENT IN AORTIC 
 DISEASE. 
 
 The treatment of valvular disease of the heart has been 
 foreshadowed in the consideration of its prognosis. What- 
 ever influences have been seen to affect unfavourably the 
 condition of the circulation and of the patient, such must 
 be averted or counteracted, and injurious tendencies arising 
 out of the particular lesions of the valves must be combated. 
 The order also in which the therapeutic methods and 
 resources employed for the above ends must be discussed is 
 dictated by the arrangement adopted in the consideration 
 of the prognosis. 
 
 One of the most important prophylactic measures is the 
 prevention, as far as possible, of the ill effects on the heart 
 of a recently established valvular lesion. When an attack of 
 endocarditis has subsided, leaving behind it some valvular 
 lesion, the exercise of caution and care will prevent undue 
 
TREATMENT OF VALVULAR DLSEASE. 233 
 
 cardiac dilatation, which might prove rapidly fatal or 
 cripple the heart seriously in the future. 
 
 The patient should be kept in bed, or confined to his 
 room for some weeks, or perhaps even months, according 
 to the degree of severity of the lesion, cases of aortic 
 incompetence requiring the longest period of rest. The 
 object of protracted rest is to allow time for the necessary 
 compensatory hypertrophy of the cardiac walls to take 
 place. In many cases, more especially when pericarditis 
 accompanies the endocarditis, as it frequently does in 
 children, the heart is left dilated and weakened after the 
 subsidence of the attack, so that the risk from premature 
 exertion will be doubly serious, and the period of rest 
 required afterwards will be proportionately longer. 
 
 In children, in whom the joint manifestations of rheu- 
 matism are usually slight, while the heart is frequently 
 attacked, the heart should be examined from time to time 
 if there is the slightest suspicion of rheumatism, such as 
 fugitive pains in the joints or limbs, with rise of tempera- 
 ture, still more if there are obvious manifestations such as 
 rheumatic nodules ; for the onset of pericarditis or endo- 
 carditis is often very insidious, and serious mischief may 
 result before it is detected, if the child is allowed to go 
 about as usual. 
 
 When the lesion is established, and sufficient rest after 
 the attack of endocarditis has been allowed, the next 
 question to be settled will be, how far the patient may live 
 his ordinary life, or what rules must be laid down for his 
 future conduct, and what precautions should be taken. 
 Everything will of course depend on the nature and the 
 degree of severity of the lesion, and in discussing the treat- 
 ment the less severe class of cases will be first considered, 
 in which there is no evidence in the shape of marked cardiac 
 dilatation or hypertrophy that the lesion is considerable. 
 
 Exercise. — Almost the first question will be as to the 
 
234 HEART DISEASE. 
 
 rules to be laid down with regard to exercise and exposure 
 to changes of temperature. These will necessarily vary 
 according to the character and seat of the lesion, but not 
 so only — the constitution, strength, habits, and disposition 
 of the patient will also have to be considered. One man 
 is timid and apprehensive ; he will scarcely move out of 
 doors lest he should overtax his heart, or eat a sufficient 
 meal for fear of palpitation, or go away for change of air 
 lest he should die away from home. He must be encouraged 
 or even compelled to take exercise. Another is only too 
 ready to ignore the state of his heart, and will run or row 
 or swim or take part in violent games ; he must be warned 
 against imprudence, and it may be necessary to forbid such 
 forms of exertion as are liable to be indulged in to excess. 
 In another, an eager temperament and impetuous disposition 
 may reside in a weakly frame, and ordinary duties and an 
 average amount of work may be done with injurious energy 
 and haste. It is not possible, therefore, to draw up definite 
 regulations applicable to all cases. To make the restrictions 
 imposed too severe will in one person directly injure the 
 sufferer's health; in another, will make him unnecessarily 
 depressed and miserable ; in a third, will provoke revolt and 
 lead to rash and dangerous violation of all rules. The 
 principle on which recommendations must be based will be 
 to interfere as little as possible with the avocation, habits, 
 and mode of life of the patient, as long as these are not 
 injurious, and especially to allow a maximum of exercise 
 in fresh air compatible with safety. 
 
 Nothing can be worse than to debar all patients who 
 are found to have valvular disease from games and vigorous 
 exercise, and to forbid them to go upstairs or to walk 
 uphill, and on no cases do I look back with greater satis- 
 faction than on those, and they have not been few, in which 
 I have liberated boys and girls from such orders. In the 
 class of cases under consideration, supposing a sufficient 
 
THE CERTEL TREATMENT. 235 
 
 time to have elapsed after the acute attack in which the 
 valvular affection was established for the necessary 
 compensatory changes to take place, a girl may be allowed 
 to take long walks, to play lawn tennis, to ride, cycle, 
 swim, and dance, and a boy to play cricket and racquets, 
 to hunt, box, and fence, provided that these exercises are 
 not attended with undue breathlessness and distress, and 
 that they are entered upon gradually and practised with 
 moderation and discretion. On the other hand, football, 
 paper-chases, long house-runs, training for races of any 
 kind, are scarcely permissible. 
 
 While discussing the question of exercise the (Ertel 
 and Schott methods may be described. 
 
 The (Ertel Treatment consists in systematic, graduated 
 muscular exercise carried out at a certain elevation, about 
 two thousand feet above sea-level. The patient is required 
 to walk a certain distance up a gentle ascent each day, the 
 distance and pace being gradually increased. At the same 
 time the diet is carefully regulated, and the amount of 
 fluids ingested is strictly limited. The object of the treat- 
 ment is : firstly, to stimulate the heart by muscular exercise, 
 carefully adjusted to the capacity of the patient, so as to 
 bring about hypertrophy of its walls ; secondly, to diminish 
 the volume of blood in circulation by restricting the amount 
 of water consumed, and increasing the amount eliminated. 
 (Ertel claims that this treatment is successful in cases of 
 fatty heart uncomplicated by disease of the coronary arteries, 
 in cardiac dilatation, and in valvular disease, even when 
 compensation has broken down, and dropsy with other 
 evidence of venous congestion is present. 
 
 In cases of valvular disease, in which compensation has 
 completely given way, this treatment is certainly not 
 advisable, nor in many instances would it be possible ; but 
 where compensation has been established after a recent 
 valvular lesion, or has been restored by rest and suitable 
 
236 HEART DISEASE. 
 
 treatment, or where it is maintained with some difficulty, 
 gentle climbing exercise in fresh and pure and somewhat 
 rarefied air will certainly do more to develop further com- 
 pensatory hypertrophy of the heart, than mere walking on 
 the level, which has not the same beneficial effect on the 
 circulation, and where the air is not so pure or invigorating. 
 
 It is more especially in cases of fatty infiltration of the 
 heart without fatty degeneration of the cardiac muscle, 
 arising from overeating and drinking and insufficient 
 exercise, that this treatment by dieting and systematic 
 muscular exercise may be of real service. At the com- 
 mencement of the treatment, great caution should be 
 observed as to the nature and amount of exercise. The 
 patient should only be allowed to walk a certain distance 
 up a gentle slope, and each day the distance may be 
 gradually increased. By this means, and by the limitation 
 of the fluids ingested, the superfluous adipose tissue is 
 gradually got rid of, and the tone of the heart muscle is 
 restored. Not infrequently this treatment is employed as 
 a sequel to the Nauheim methods. 
 
 The Schott Treatment. — The treatment by baths and 
 exercises by the method of Schott, of Nauheim, may be 
 of service in suitable cases. The waters of Nauheim 
 are remarkably rich in free carbonic acid gas, as well as 
 in mineral constituents, the chief of which are chloride 
 of sodium, and chloride of calcium, and carbonate of iron. 
 At the beginning of the treatment the baths should 
 contain about 1 per cent, of chloride of sodium, and 
 1 per 1000 of calcium chloride, and should be free from 
 carbonic acid gas. The bath at first should last from six 
 to eight minutes, and should be of the temperature of 
 92° to 95° Fahr. As time goes on the proportion of 
 solids in the bath should be increased, also the duration 
 of the bath, while the temperature is gradually lowered. 
 Eventually, baths containing free carbonic acid gas, and 
 
THE SCHOTT TREATMENT. 237 
 
 about 3 per cent, of sodium chloride and 3 per 1000 of 
 calcium chloride, may be taken. Baths can be artificially 
 prepared in imitation of those at Nauheini, the essential 
 ingredients being the chlorides of sodium and calcium 
 and the free carbonic acid gas. 
 
 The exercises consist of a series of simple movements of 
 each limb and of the trunk made against slight resistance, 
 so that every muscle of the body, as far as possible, is in 
 turn brought into play. The movements should be made 
 slowly and systematically, and a short interval of rest should 
 be interposed between each ; they should be stopped if the 
 patient experiences any distress in breathing or discomfort, 
 but may be proceeded with again as soon as he is rested. 
 The movements consist of flexions, extensions, adductions, 
 abductions, and rotations of each limb in turn, and of 
 flexion, extension, and rotation of the trunk. 
 
 The effects produced on the circulation and the heart, 
 whether by the baths or exercises, are similar ; the pulse 
 frequency is diminished, its volume and force are increased, 
 and the area of cardiac dulness in cases of cardiac dilata- 
 tion is diminished, while the apex beat recedes and comes 
 nearer to the normal position. 
 
 Such are the immediate results which appear to indicate 
 an improvement in the contractile power of the heart and 
 a reduction of its dilatation ; but these are not permanent. 
 
 Similar temporary results may, indeed, be obtained in a 
 normal individual as the immediate effect of a simple hot 
 or cold bath without any saline constituents. 
 
 Too much importance is attached by advocates of the 
 Schott treatment to the percussing out of the area of 
 cardiac dulness and to the diminution it is said to undergo 
 after each bath, more especially when the so-called 
 auscultatory method is employed. This method lends 
 itself very much to the imagination, and is absolutely 
 untrustworthy. A shifting inwards of the apex beat is of 
 
238 HEART DISEASE. 
 
 importance, but in cases of dilatation from over-exertion 
 a similar inward movement of the apex may sometimes 
 be effected by making the patient walk rapidly two or 
 three times across the room. It is also probable that the 
 diminution of percussion dulness is due, not so much to 
 fluctuations in the size of the heart as to encroachment by 
 the lungs on the cardiac area, due to deeper respirations 
 taken while the patient is in the bath. It does not there- 
 fore follow that, because the area of cardiac dulness diminishes 
 after a bath, the heart was previously dilated. Moreover, 
 accurate delineation of the outline of the heart by per- 
 cussion is in many cases impossible, and even in the mere 
 percussing out of the area of superficial cardiac dulness 
 there may be many difficulties and sources of error in the 
 adult, from the solid nature of the chest walls and the 
 thickness of their coverings, from an emphysematous con- 
 dition of the lungs, or from pleuro-pericardial adhesions. 
 It is difficult, therefore, to attach any real value to the 
 remarkable diagrams of the cardiac dulness " before " and 
 " after " the bath, published in quantity by the enthusiastic 
 advocates of this treatment, and one is compelled to 
 question their accuracy if not their honesty. Even if they 
 approximate the truth, they are worth nothing if there is 
 not other evidence of improvement in the general condition 
 of the patient and in the symptoms and physical signs of 
 the affection from which he is suffering. The treatment 
 cannot, of course, cure a valvular lesion, but it may give 
 beneficial results in suitable cases. But it is rather in 
 cases of cardiac dilatation from loss of tone after influenza, 
 or some depressing disease, and in cases of functional 
 and neurotic heart disease, than in actual valvular disease, 
 that it is satisfactory. The change of air and scene, the 
 sedative effect of the baths, the enjoined rest after each 
 bath, the quiet, uneventful life, the early hours and regular 
 meals, together with freedom from excitement and worry, 
 
GENERAL HYGIENIC TREATMENT. 239 
 
 and the satisfaction engendered by " taking a cure," will 
 be among the most important factors which contribute to 
 its success in this class of cases. 
 
 Exposure to Change of Temperature. — As regards exposure 
 to vicissitudes of temperature and to changes of weather, 
 we have to bear in mind that the subjects of valvular 
 disease have, in most cases, already manifested a suscepti- 
 bility to the effects of cold and wet, or an inherited 
 predisposition to rheumatism. One of the things, therefore, 
 most to be feared and guarded against, is another attack of 
 rheumatism. Flannel or woollen underclothing of some 
 kind should be worn next to the skin winter and summer, 
 and standing or sitting with wet feet or in damp clothes, or 
 lying down on the grass after games, involving the risk of 
 getting chilled after perspiration, must be forbidden. But 
 we must not go to the other extreme and cultivate an undue 
 susceptibility to cold by excessive care. The patient need 
 not be kept indoors by rain or cold, or forbidden to get into 
 a perspiration. Excessive precautions defeat the object for 
 which they were enjoined, and it is easy to reduce the 
 power of resistance to changes of temperature until the 
 slightest exposure is attended with risk. While, however, 
 the primary aim ought to be to maintain and confirm such 
 hardihood as the constitution possesses or is capable of, 
 there are cases in which safety consists in flight from too 
 severe a climate, or from a situation or soil conducive to 
 rheumatism. There is full opportunity for the exercise of 
 judgment in deciding how much may be dared and how 
 soon the patient must yield. 
 
 Climate. — Climate may do much to influence the course 
 of heart disease. On a priori grounds, we should say that a 
 mild, dry, bracing and equable climate, in which the patient 
 could have a maximum of exercise in the open air, would be 
 the best ; but, independently of the question where these 
 desiderata are to be found, all such general statements have 
 
240 HEART DISEASE. 
 
 to be qualified to meet the idiosyncrasies of individuals ; 
 the great majority of our patients, moreover, are tied down 
 by circumstances to a particular spot, and the most important 
 practical problem usually is how to make the best of a given 
 neighbourhood. 
 
 Choice of Residence. — If the choice of a residence is open 
 we should direct the patient to seek a gravelly or sandy 
 soil at a moderate elevation, where the rainfall is below and 
 the sunshine above the average, and the water not hard ; 
 conditions best realized — in England — in Kent, Surrey, and 
 Sussex. The exposure of the house should be to the south, 
 and there should be protection from the north and east. 
 The immediately surrounding country should not be too 
 hilly, and especially the house itself should not be on 
 the top of a steep hill, making every walk necessarily end 
 in an ascent. There would be danger, some day or other, 
 of dilatation or other ill effect from the exertion after a 
 longer or more tiring walk than usual or when out of sorts. 
 It must always be borne in mind that the good results 
 obtainable from the best climate may be neutralized by 
 faults of detail in the placing or construction of a house. 
 
 Diet.— About food little need be said. Excess should 
 be avoided, but, subject to this condition, the diet may be 
 liberal and varied. It is important, however, that there 
 should be a due proportion of farinaceous and vegetable 
 articles of diet; when the food is highly nitrogenized, as 
 when it consists largely of meat, imperfectly oxidized waste 
 accumulates in the blood, and this is a great cause of 
 resistance in the capillary circulation, which constitutes a 
 serious addition to the work imposed upon the heart, and 
 puts a continued strain upon the compensation by which it 
 adjusts itself to the imperfect state of the valves. This 
 recommendation is specially important in the case of 
 constitutions disposed to gout, since the valves may be 
 further damaged by gouty inflammation. Habitual excess 
 
GENERAL HYGIENIC TREATMENT. 241 
 
 of food beyond the requirements of the system will have 
 the same effect. 
 
 The food, again, should be divided into three fairly 
 equal meals, and not taken in excessive quantity at dinner, 
 or at breakfast and dinner. If the nourishment for the 
 twenty-four hours is consumed at one huge repast, the blood, 
 in the long interval, is drawn upon for the nutrition of 
 the tissues and for the supply of the secretions and its 
 volume being reduced, the vessels are depleted; the 
 products of digestion are then rapidly absorbed, the amount 
 of blood is increased, and the vascular system is rapidly 
 filled and perhaps overcharged. Wide variations in the 
 volume and pressure of the blood are thus liable to result, 
 and are harmful to the patient. 
 
 When its valvular apparatus is unsound, or its structure 
 is impaired, the heart does not easily adjust itself to such 
 extremes, and, if it so far effects this that no particular 
 discomfort is experienced, the increased work thrown upon 
 a weak organ cannot fail to be injurious in the long run. 
 A very large meal, again, must distend the stomach, and the 
 diaphragm may be pushed up and hindered in its action so 
 as to embarrass the heart directly by pressure, and indirectly 
 by interference with respiration. A dilated stomach by 
 upward pressure may so embarrass a heart which is dis- 
 eased as to give rise to irregularity of rhythm, anginoid 
 pains, and even syncopal attacks, one of which may prove 
 fatal. 
 
 Stimulants. — Strict moderation must be observed in the 
 matter of alcoholic drinks ; in comparatively few cases are 
 they necessary, and if taken they should be taken only as 
 part of a substantial meal. Their effects as excitants of the 
 heart may, to some extent, be neutralized by the relaxation 
 of the peripheral vessels which they induce, but their general 
 tendency is to interfere with due metabolism and elimina- 
 tion, and to bring about degeneration of structure. 
 
 R 
 
242 HEART DISEASE. 
 
 Unduly high arterial tension, from whatever cause, must 
 be combated. Its injurious effects have been already pointed 
 out. The regulations as to diet and drink have for one of 
 their objects the prevention of high blood-pressure. When 
 this condition exists from inherited tendency, or from gout 
 or renal disease, it must be kept down within safe limits by 
 suitable eliminants. 
 
 Regulation of Bowels. — It is always important to take 
 measures against constipation. Accumulation of fsecal 
 matters in the large intestine, with the associated flatulent 
 distension, will more or less embarrass the heart, both by 
 direct pressure upwards of the diaphragm and indirectly by 
 interference with respiratory movements. Palpitation, again, 
 is a frequent result of constipation, and both the effort 
 required to unload the bowel and the different pressure on 
 the abdominal veins before and after a large evacuation put 
 stress upon the heart. A further ill-result is the retention 
 of toxic matters in the blood, which provoke resistance 
 in the capillaries and tend to the production of high 
 tension. 
 
 Anaemia. — While everything is done to maintain the 
 general health, special precautions must be taken to guard 
 against anaemia. We have seen that it may itself give rise 
 to dilatation of the left ventricle, which is a most serious 
 aggravation of valvular disease. Valvular disease, moreover, 
 tends to deteriorate the blood in so far as it interferes with 
 its free movement through the glands and tissues generally, 
 and to produce antenna. It does not follow that we are to be 
 always giving iron or other reconstituent tonics, but it is a 
 valid reason for careful choice of residence and for frequent 
 change of air, and for attention to and treatment of the 
 earliest indications of anaemia. 
 
regulation of exercise. 243 
 
 Treatment in Cases of Severe Valvular Lesion. 
 
 When the presence of dilatation and hypertrophy in- 
 dicate that the damage to the valve has been such as to 
 interfere perceptibly with transmission of the blood through 
 the heart, while the principles with regard to exercise remain 
 the same, some modification in their application will be 
 necessitated. Each form of valvular disease gives rise to a 
 certain kind and degree of interference with the efficient 
 pumping of the blood through the heart, lungs, and system, 
 which tends to the production of results injurious to health, 
 and in the long run dangerous to life. We must not Avait 
 for the recognition of such tendencies till they are forced 
 upon our attention by the appearance of symptoms ; they 
 can always be foreseen, and they may often be prevented. 
 Again, it must be borne in mind that when valvular disease 
 of any importance, as indicated by changes in the walls and 
 cavities, exists, the heart has to some extent lost the power 
 of responding to sudden calls for variations in the rate or 
 force of the circulation ; more than this, its power of re- 
 covering itself after disturbance is impaired. The com- 
 pensation effected by hypertrophy is efficient only for 
 ordinary purposes, or within certain limits more or less re- 
 stricted. When the muscular pressure on the veins all over 
 the body, which attends vigorous exercise, brings the blood 
 in increased quantity to the right cavities of the heart, it 
 cannot be sent on against the resistance in the pulmonary 
 circulation, which results, as we have seen, from most forms 
 of valvular disease. Even in health there is a period of 
 breathlessness before the right ventricle succeeds in driving 
 the blood through the lungs as fast as it arrives from the 
 system, when we begin to run, and in disease, this breath- 
 lessness is more readily provoked and is easily exag- 
 gerated to painful dyspnoea ; the distended condition of 
 the right ventricle and auricle, which is induced by 
 
244 HEART DISEASE. 
 
 exertion in health, and which acts as a reservoir for the 
 blood till it can be delivered to the lungs by the increased 
 action of the heart, may already exist in disease, so that 
 the provision for the emergency is already exhausted, and 
 there is no margin left for severe exertion. 
 
 While, therefore, we avoid unnecessary and injurious 
 restrictions on exercise, sudden and violent exertions must 
 be forbidden, and it must be understood that anything 
 which gives rise to painful breathlessness is injurious. A 
 patient, however, will often, by beginning gradually, arrive 
 at a rate of walking which attempted at first would have 
 been impossible, and may eventually, by the exercise of 
 similar caution, mount with ease an incline which would 
 otherwise have brought him to a standstill. So long as the 
 equilibrium of the circulation is not disturbed, there is no 
 particular danger in going uphill. The danger arises from 
 the fact that on coming to an ascent, the tendency is to 
 maintain the same pace as on level ground until we are 
 checked by shortness of breath. The sufferer from heart 
 disease cannot afford to do this. What would be a mere 
 fugitive inconvenience to a man in health may be a risk 
 and injury to him. If, however, he will exercise a little 
 foresight and slacken his pace immediately on coming to an 
 incline, he may afterwards gradually increase it again within 
 certain limits and so climb hills. The same conclusions apply 
 to stairs. So long as the subject of a valvular affection 
 can go upstairs quite comfortably, there is no objection 
 to his doing so ; and if by ascending them quietly he 
 avoids breathlessness, this need not be forbidden even when 
 symptoms are already manifest. Sometimes he can go up 
 backwards without distress, when to take them step by step in 
 the ordinary way is difficult. But there comes a time when 
 stairs must be avoided as far as possible, and when the 
 patient must be carried up or must live on one floor. This 
 will especially be the case when not mere breathlessness 
 
SELECTION OF WINTER RESORT. 245 
 
 but faintness is produced by slight exertion, and the patient 
 feels giddy or has dimness or temporary loss of vision, or 
 weakness and trembling of the knees after going uphill or 
 upstairs. It is in aortic disease that such symptoms are 
 most likely to be experienced, but they may occur whenever 
 the left ventricle is greatly dilated or is weak from any 
 cause. 
 
 Age.— In applying any rules for the management of 
 valvular disease of the heart, a great difference will be made 
 between the young and those who have reached or passed 
 middle age. After a certain period of life, varying greatly 
 according to constitution and habits, there is a liability to 
 dilatation of the heart on exertion, and this condition, 
 attended at once by symptoms and leading to a speedy 
 fatal issue, is often brought about by an imprudent effort 
 independently of any pre-existing affection of the valves. 
 The risk of such an event is indefinitely increased when 
 dilatation, attendant on valvular lesion, is already present ; 
 or when the tendency thereto has only been neutralized 
 by compensatory hypertrophy. The ventricle is tried by 
 chronic overwork, and the nutrition of the increased amount 
 of muscular tissue in the walls is maintained with difficulty, 
 the heart is consequently more ready to break down under 
 stress. We may, therefore, allow a boy to play cricket, or 
 the young of either sex to play lawn tennis, to boat, or 
 even swim in moderation, provided always that no distress 
 of breathing or tendency to syncope is induced, while a 
 corresponding amount of exertion would be altogether for- 
 bidden at middle age. 
 
 Under no circumstances, and at no age, must fatigue be 
 carried to the point of exhaustion. There is less chance of 
 recovery from the effects of overtaxed endurance than from 
 those of a brief violent effort. 
 
 Selection of Wintering or Holiday Place. — In deciding upon 
 a place for temporary change of air for a patient suffering 
 
246 HEART DISEASE. 
 
 from valvular disease, we must be guided very much by the 
 previous experience of the patient. In some cases a trip by 
 sea will be of the greatest service, but this could be recom- 
 mended only to good sailors. A winter in Egypt, Algiers, 
 or Rome may be good in others, or, if this is not practicable, 
 a few months on the south coast of England, at places 
 where exercise can be taken without much up and downhill. 
 In summer the seaside is most generally useful ; but some 
 people tell us it does not suit them, that it makes them 
 bilious. This is often a mere temporary effect, which quickly 
 passes off, or it may be a result of the constipation, which 
 is common. In all cases constipation must be provided 
 against. 
 
 When change of air is recommended, great caution must 
 be exercised in sending patients suffering from heart disease 
 to any considerable height, such as 5000 or 6000 feet. The 
 effects of the reduction of atmospheric pressure cannot be 
 foreseen ; paljDitation is often set up which is absolutely 
 intractable without removal to a lower level, and this is 
 sometimes difficult. One reason for this may possibly be 
 the expansion of the gases in the stomach and intestines, 
 permitted by the diminution in the atmospheric pressure 
 at high altitudes. Every year people arrive in the 
 Engadine with unsuspected heart disease, which is revealed 
 or perhaps developed by palpitation and dyspnoea, render- 
 ing a hasty retreat imperative. On the other hand, in a 
 case in which the absence of dilatation and hypertrophy 
 shows the valvular lesion to be slight and the patient is 
 capable of all ordinary forms of exercise without suffering, 
 high altitudes will usually give rise to no inconvenience or 
 danger. 
 
 Moderate heights, say 2000 or 3000 feet, are usually 
 well borne, even when there is decided valvular disease, 
 and graduated exercise at such elevations is systematically 
 employed as a means of improving the tone and vigour of 
 
NECESSITY OF COMPLETE REST. 247 
 
 the muscular walls of the heart, and of removing fatty 
 deposit which may have taken place upon its surface and in 
 its substance. 
 
 Complete Rest in Bed. — Eest is, in many cases, an im- 
 portant part of the treatment, and when the state of the 
 patient demands it, rest in bed is of the greatest service ; 
 but one of the questions calling for the greatest exercise 
 of judgment is to decide when absolute rest is necessarv. 
 There are circumstances in which a month or six weeks in 
 bed will prolong life for as many years. On the other hand, 
 the disturbance of compensation and the supervention of 
 symptoms often date from some slight injury which has 
 confined the patient to his couch or to the house for a 
 month or two. Even when severe symptoms are present, 
 to insist upon confinement indoors is sometimes to add to 
 the suffering of the last few months of life without adding 
 to its duration. When the onset or exacerbation of 
 symptoms is distinctly attributable to work persisted in 
 from necessity, as in the case of most hospital patients, or 
 from courage and defiance of pain, as we sometimes see ; 
 or when the aggravation is due to imprudent exertion or 
 exposure, or to some intercurrent pulmonary complication 
 or other illness, there can be no hesitation in ordering rest. 
 The doubt arises in cases in which the effects of valvular 
 disease are gradually creeping on, and the increasing 
 breathlessness and evening oedema are the direct result of 
 the obstruction to the circulation and of failing compensa- 
 tion. Under such circumstances it is difficult to decide 
 when to interfere. The patient will say he is worse in bed 
 than up, that he cannot lie down, but has to be propped up 
 by pillows ; that he cannot and dare not sleep, and that if 
 he drop off into a dose he wakes up in indescribable fright 
 and distress. His attendants, it is true, may tell us that he 
 has had more sleep than he supposes, but all the same the 
 nights are long and miserable, and it is no light matter to 
 
248 HEART DISEASE. 
 
 condemn a sufferer, who has looked and longed for morning, 
 to a couch which, in his experience, is associated with his 
 worst moments. Not uncommonly, however, after sleepless 
 tossing till early morning, with inability to lie down, 
 quiet sleep may come, and the sufferer may slip down 
 into a comfortable position in which he gets real repose, 
 and sometimes after twenty-four or forty-eight hours in 
 bed, relief is experienced, which reconciles the patient to 
 the confinement. We must be guided by results and by 
 our knowledge of the patient. 
 
 A similar difficulty frequently confronts us in advanced 
 stages of heart disease, especially when attended with 
 dropsy. The patient implores us to be allowed to sit up, 
 and in paroxysms of dyspnoea he is compelled to do so and 
 to throw his legs out of bed and let them hang down. It 
 is an unequivocal dictate of experience, not easily accounted 
 for by theory, that the heart in disease is often relieved by 
 an upright posture of the body and a dependent position of 
 the legs. Such is the case, not merely because in dropsy 
 the swollen abdomen and thighs make it impossible to sit 
 well forward in bed when the legs are raised, but because 
 in some way the position facilitates the action of the heart, 
 it may be by taking off the pressure of the abdominal 
 viscera from the diaphragm, or by allowing blood to 
 gravitate from the right auricle into the vena cava inferior 
 and abdominal veins, or it may be in consequence of a 
 physiological diminution of the arterial tension which, 
 according to Dr. Oliver, attends the erect position. There 
 are few medical men of large experience who have not seen 
 instances in which the sufferer has not gone to bed for 
 months, but has slept all this time in an armchair with 
 some support contrived for the head. On the other hand, 
 our results are better when the patient can be kept in bed ; 
 there is a better chance of removal of dropsical effusion and 
 of recovery generally in the recumbent position. While, 
 
STIMULANTS. . 249 
 
 therefore, we do not carry too far our resistance to a 
 patient's entreaties to be allowed to sit up in a chair for 
 a part or the whole of a day, recognizing, also, that a few 
 days or weeks of life may be dearly purchased if it is at the 
 expense of increased suffering, it is our duty sometimes, 
 and especially when there is a chance of recovery from 
 the existing complications, to exercise firmness in keeping 
 the patient in bed in spite of great temporary distress. 
 
 There is less uncertainty with regard to exposure to 
 cold, though in an advanced stage the patient often 
 complains of subjective heat, and throws off his coverings, 
 or insists on the window being opened on the coldest day 
 to satisfy his want of air. External cold contracts the 
 arterioles of the surface, and increases the resistance in 
 the systemic circulation, and it should be prevented from 
 reaching the sufferer. The open window, however, may be 
 permitted, on condition that the patient is efficiently pro- 
 tected. The play of cool, fresh air on the face, and a deep 
 draught of it into the lungs, are indescribably refreshing. 
 The cold and livid lower limbs in aggravated dropsy appear 
 to be almost insensible to changes of temperature, but they 
 should none the less be carefully covered. 
 
 Diet. — Little need be said about nourishment. The 
 patient may have whatever he can eat and digest, but his 
 appetite will leave deficiencies, which must be supplied 
 partly by liquid food of different kinds, and partly of pre- 
 parations of pounded meat, fish, or chicken. 
 
 When dropsy is present the use of common salt and 
 of chlorides in general should be restricted as far as pos- 
 sible, for the reasons given in the chapter on dilatation, 
 page 308. 
 
 Stimulants. — Alcoholic stimulants afford valuable help, 
 and will be required more or less in every case of 
 severity. At first a small quantity of any wine which suits 
 the patient may be taken with food, and frequently a little 
 
250 HEART DISEASE. 
 
 spirit in hot water at night will help to procure sleep. 
 Ultimately stimulants, especially spirits, may have to be 
 given freely; but great caution must be exercised in the 
 early periods, since the struggle against the encroach- 
 ments of the malady is often very long and trying, and if 
 the good effects of alcohol are exhausted by abuse of it, 
 the patient is left without resource when the time of greatest 
 need arrives. As to the actual amount required, I should 
 consider about six ounces of brandy per diem the maximum 
 likely to be useful in the most urgent cases. This should 
 be reached very gradually from two or three ounces, and 
 whenever an emergency has led to an increase of the 
 allowance, it should be reduced when the occasion has 
 passed. We must, above all, be careful not to be misled by 
 the patient's demands. He is conscious of relief from the 
 stimulant, and not unnaturally asks for it whenever the 
 oppression or depression becomes severe ; but it is easy to 
 pass the limits of usefulness, and to produce a feeling of 
 depression which is only reaction from an excess of alcohol. 
 
 In larger quantities than six ounces the effects become 
 uncertain, and I have often seen improvement from diminu- 
 tion of a dose which seemed to be imperatively required. 
 
 Drugs. — When symptoms have arisen requiring the em- 
 ployment of medicinal treatment, the first question to be 
 considered is whether the heart can be relieved, in any 
 degree, of work to which it is no longer equal. It is very 
 rarely that this is not the case, and not uncommonly a 
 lessening of stress upon the heart is sufficient of itself to 
 restore the circulatory equilibrium. A diminution in the 
 volume of the blood by eliminants of various kinds, removal 
 of portal congestion and of distension of the abdominal veins 
 by purgatives, which will relieve the right side of the heart 
 and lower the arterial tension, are among the measures most 
 generally useful and most commonly required. 
 
 The fatal result is reached through various secondary 
 
TREATMENT BY DRUGS. 251 
 
 consequences, the prevention or removal of which postpones 
 the final issue, and not only does this, but also relieves 
 suffering. These consequences, therefore, must be studied, 
 and it will be necessary to revert to the modes of death from 
 valvular disease of the heart and to consider the tendencies 
 thereto which we have to counteract. Leaving out of con- 
 sideration thrombosis, whether systemic or pulmonary, which 
 will best be averted by the prevention of stagnation of 
 blood in the heart, heart disease tends to the arrest of the 
 circulation in two different ways — by failure of propulsion 
 through the arteries and by damming back in the veins. 
 It is not to be understood that one or other of these 
 tendencies is alone in operation in any given case ; the 
 rule is that both are present, as has been already seen. 
 While, however, in most cases of valvular disease which 
 have proceeded so far as to give rise to serious symptoms, 
 the double effect on the circulation — the damming back in 
 the veins and the imperfect propulsion through the arteries 
 — is recognizable, one or other will be a primary tendency, 
 and will predominate, and the treatment must be directed 
 to the rectification of the tendency which is most concerned 
 in placing life in danger. By far the more common is 
 venous stasis, since it not only follows directly from both 
 forms of mitral disease, but may also be a secondary result 
 of aortic disease, and it gives rise to a characteristic train of 
 phenomena. Inadequate arterial supply is of itself more 
 likely to cause sudden death than to produce symptoms. 
 
 With venous obstruction the liver will be enlarged and 
 greatly congested, perhaps pulsating, and one of the first 
 objects of treatment is the relief of this engorgement of the 
 liver. Thereby relief will also be afforded to the nausea 
 and sickness dependent on the congested state of the 
 gastro-intestinal mucous membrane, and also to the over- 
 distended right side of the heart, which is constantly 
 receiving from the liver, which acts as a kind of reservoir, 
 
252 HEART DISEASE. 
 
 more blood than the right ventricle can transmit through 
 the lungs. The means to be employed for the purpose are 
 chiefly aperients, and all purgatives will have the desired 
 effect in a greater or less degree ; but it is not a matter of 
 indifference what drugs we employ. The best results are 
 undoubtedly to be obtained, according to my experience, 
 from purgatives, in which calomel or other mercurial 
 preparation is a constituent, such as calomel and compound 
 jalap powder, calomel, blue pill, or grey powder, with 
 colocynth and hyoscyamus, followed or not by salines. 
 Hydragogue cathartics of greater violence may be necessary 
 in some cases, but the effect on the liver and heart is not 
 proportional to the degree of purgation, and the relief of 
 dropsy is not due simply to the amount of liquid carried off 
 by the intestinal surface, but is frequently the effect rather 
 of the diuresis which follows improvement in the circulation. 
 Digitalis is often useless, and appears only to add to the 
 embarrassment of the heart- and to produce sickness, until 
 the way has been cleared for its operation by a mercurial 
 purge, and where its good effects on the heart seem to be 
 expended, a fresh start will often follow a calomel and 
 colocynth pill. 
 
 A troublesome, watery diarrhoea, which is not unfre- 
 quently present, is no contra-indication for purgatives, but, 
 on the other hand, constitutes a distinct call for a decided 
 aperient. It is due to the passive congestion of the gastro- 
 intestinal mucous membrane which results from the obstruc- 
 tion in the portal system, and is relieved by free secretion 
 from the mucous surface and from the liver. 
 
 Venesection. — But the venous obstruction may reach a 
 point which it is out of the power of purgatives to affect. 
 The lower edge of the liver is at or near the level of the 
 umbilicus (or this organ may be prevented from swelling by 
 cirrhosis), the right cavities of the heart are almost paralyzed 
 bv over-distension, which, with regurgitation through the 
 
VENESECTION. 253 
 
 tricuspid orifice, reduces the trausmissiou of blood through 
 the lungs to a minimum, and the left ventricle receiving 
 little blood has little to forward into the arterial system. 
 The pulse is weak, small, irregular, both from the irregular 
 action of the heart usually present, and from some of its 
 beats not reaching the wrist. Unless the circulation is to 
 come to a standstill the right side of the heart must be 
 promptly relieved of the over-distension which is the imme- 
 diate cause of the threatened arrest, and this can be most 
 quickly and effectually done by venesection. The with- 
 drawal of a few ounces of blood (8-16) so far reduces the 
 pressure in the right auricle and ventricle when the latter 
 is checked at the very beginning of its systole by resist- 
 ance which it is unable to overcome, that it regains com- 
 mand over its contents, and is once more able to drive the 
 blood through the lungs. Nothing can be more striking or 
 satisfactory than the effect of bleeding from the arm under 
 such conditions. The face may be livid and bedewed with 
 cold sweat, the extremities blue and cold, but as the blood 
 flows warmth and colour will return, the dyspnoea will be 
 relieved, and the pulse will improve. The condition of the 
 right ventricle is of critical importance when venesection 
 appears to be required. If it is weak and degenerated, 
 and unable to take advantage of the relief afforded by the 
 withdrawal of blood, the desired result does not follow. We 
 ought, therefore, for bleeding to be successful, to have a 
 powerful right ventricle impulse heaving the left costal 
 cartilages, and perhaps the lower end of the sternum itself, 
 and felt below the costal margin. 
 
 In some cases, where the circulation is so nearly at a 
 standstill that blood will not flow from the vein when 
 opened, a hypodermic injection of ether or strychnia in the 
 precordial region may cause the blood to start flowing, and 
 save the patient from impending death. 
 
 Very frequently, especially in hospital patients, the 
 
254 HEART DISEASE. 
 
 desired relief may be obtained by leeches, and I have 
 usually selected the region of the liver for their applica- 
 tion, not of course with the idea of taking blood from this 
 organ, but because there is, as a rule, local pain here which 
 is relieved : six or eight may be applied at a time. The 
 abstraction of blood will be followed up by a mercurial 
 purge and digitalis. Brandy and other stimulants may be 
 given at the same time ; there is nothing inconsistent in 
 helping the oppressed organ at the same time that it is 
 being relieved from the special difficulty with which it has 
 to contend. 
 
 When, as in aortic incompetence, a spasmodic and 
 imperfect supply of blood is the cause likely to lead to 
 arrest of the circulation, there is no such conspicuous train 
 of symptoms. There may be precordial pain, dyspnoea, 
 syncopal attacks, etc. ; but since a momentary failure of 
 the circulation in the vital nerve centres is fatal, sudden 
 death may occur before the warnings of danger have 
 arrested attention. Such warnings are sudden attacks of 
 faintness and dimness of vision, giddiness, anginoid pains, 
 sudden weakness and trembling of the knees. 
 
 In this condition, measures suitable for the relief of 
 venous stagnation would be fatal. We cannot resort to 
 bleeding ; purgation must be employed with caution. The 
 treatment must rather be directed to stimulation of the 
 failing heart, by drugs such as strychnine, ammonia, and 
 ether, together with good, easily digested, nourishing food, 
 and alcohol regularly administered in small quantities. 
 Vascular dilators, such as nitro-glycerine and nitrite of 
 amyl and sodium nitrite, or perhaps erythrol, or mannitol 
 nitrate, the effects of which are more lasting according 
 to Bradbury, may be of great service in cases in which 
 the incompetence is due to degenerative change and not 
 to endocarditis, especially where anginoid pains are a 
 prominent symptom. 
 
VENESECTION. 255 
 
 Digitalis may sometimes be of great service, but its 
 effects are not constant, and may be unfavourable, or may 
 become so after a period of marked benefit. The reasons 
 for the apparently uncertain and inconstant results of 
 digitalis in aortic incompetence will be discussed in the 
 next chapter. 
 
CHAPTER XVIII. 
 TREATMENT BY DRUGS. 
 
 use and abuse op digitalis — substitutes foe digitalis 
 — the group op cardiac tonics of the digitalis 
 type— their physiological action : therapeutic 
 effects— use of digitalis in aortic stenosis, in 
 mitral incompetence, in mitral stenosis. 
 
 Use of Digitalis. 
 
 It is too commonly taken for granted that the existence of 
 valvular disease constitutes an immediate indication for 
 the administration of digitalis. But to make the discovery 
 of a murmur the signal for giving digitalis is fatal to 
 anything like precision in treatment, and may deprive the 
 sufferer of the advantage to be derived from this remedy 
 when it is really needed. The special indications for its 
 use are frequency, weakness, and irregularity of pulse, and 
 oedema of the extremities, with scanty, turbid, concentrated 
 urine. When these are absent, it is rarely of service ; but 
 even when these symptoms begin to show themselves 
 gradually or occasionally on slight provocation, it will be 
 well to combat them at first with strychnine, iron, quinine, 
 and general tonics, rather than resort at once to digitalis, 
 the salts of potash and any suitable vegetable diuretic 
 being employed to promote secretion of urine. When the 
 use of digitalis is called for, the most trustworthy evidence 
 of its beneficial effects will be increase in the amount 
 
THE CARDIAC TONICS. 257 
 
 of urine secreted, with an improvement in the tone and 
 vigour of the pulse, as well as a more regular and less 
 hurried action of the heart. When there is no response 
 in the form of diuresis, the pulse and general symptoms 
 must be carefully watched lest harmful effects should 
 arise. 
 
 Digitalis may be given in combination with mix vomica 
 or strychnia, or with caffein, or with ammonia or ether, 
 or various other drugs, according to circumstances, which 
 cannot be minutely laid down. In most cases it will be 
 advisable to give a mercurial purge before its administration, 
 and to repeat this from time to time. 
 
 In cases where there is high arterial tension, the 
 exhibition of a mercurial purgative from time to time is 
 especially important, and it may be well to give with the 
 digitalis some vaso-dilator such as spiritus setheris nitrosi, 
 liq. trinitrin, erythrol tetranitrate, etc., to counteract the 
 tonic effects of the digitalis on the arterioles and capil- 
 laries. As alternatives to digitalis, strophanthus, conval- 
 laria, caffein, spartein, cactein have been advocated. 
 
 Convallaria has been extensively tried, but either its 
 effect or its preparation is uncertain, and it does not 
 appear to be of great service. 
 
 Strophanthus may be a most useful alternative when 
 digitalis produces sickness, and may even succeed where 
 digitalis has failed. It is claimed for strophanthus that its 
 tonic action is mainly confined to the heart, and that it 
 does not cause contraction of the arterioles and thus in- 
 crease the peripheral resistance in the same way as digitalis. 
 
 Caffein is said to increase the solids in the urine, 
 which would make it a useful complement to digitalis, 
 which promotes a flow of water. It is also a cardiac 
 stimulant. In my hands it has often been a most useful 
 accessory to digitalis, diuresis and general improvement 
 setting in promptly on the administration of 5 gr. doses of 
 
258 HEART DISEASE. 
 
 citrate of caffein three times a day in addition to digitalis, 
 which had failed to produce any decided effect without 
 it. I have not, however, found that caffein alone is an 
 efficient substitute for digitalis. 
 
 Theobromine and diuretin, the latter of which is a sodio- 
 salicylic compound of theobromine, are powerful diuretics, 
 and have a similar stimulant action on the heart to caffein ; 
 they may be used with advantage in cases of cardiac 
 dropsy, and sometimes succeed where caffein fails. 
 
 Digitalis and its congeners, which contribute the most 
 important group of cardiac tonics, possess special interest, 
 and merit a separate discussion, since they not only 
 render important service in the treatment of disease, but 
 furnish one of the best illustrations of the relation between 
 physiological and therapeutic action. Digitalis, the best 
 known and longest employed, as well as the most important 
 of them, will be taken as the general representative of 
 the class. Their physiological action will first be briefly 
 mentioned. 
 
 Their Physiological Action. 
 
 The physiological action is a stimulation of the muscular 
 fibres of the entire cardio-vascular system, giving rise, on 
 the one hand, to more deliberate and powerful action of the 
 heart, and on the other to tonic contraction of the arterioles 
 and capillaries. After death from the poisonous effect of 
 digitalis, the arterioles are narrowed to an impervious 
 thread, and the ventricles of the heart are found firmly 
 contracted upon themselves, and empty. The drug apj)ears 
 to act directly upon the muscular structures, and not 
 through an intermediate influence upon nerves ; we have 
 not, therefore, in considering the effects upon the heart, to 
 discuss the question whether they are produced by in- 
 hibition of the sympathetic or stimulation of the vagus. 
 
action of digitalis. 259 
 
 Their Therapeutic Action. 
 
 There are various ways in which the physiological 
 action thus briefly sketched may come to the aid of the 
 circulation when the transit of blood through the heart is 
 hampered by valvular or other disease. Besides the more 
 complete expulsion of their contents by the energetic con- 
 traction of the ventricles, which will help to fill the 
 arterial side of the circulatory system, there will be im- 
 proved suction action during diastole, which will tend to 
 withdraw from the veins the blood which has been dammed 
 back and remains stagnating in the liver and abdominal 
 venous plexuses. Another effect is that not only are the 
 force and effectiveness of the systole increased, but the 
 general vigour of the heart is renewed, through the in- 
 creased physiological rest resulting from the relative pro- 
 longation of the diastolic period, which gives opportunity 
 for nutritive repair of the cardiac muscular fibres, and for 
 the reaccumulation of energy expended in the systole. 
 
 The primary effect of the tonic contraction of the 
 arterioles will be to increase the resistance in the peripheral 
 circulation, thus throwing more work upon the heart ; and 
 it is conceivable that the arterio-capillary contraction may, 
 under certain conditions, more than neutralize the increased 
 force of the ventricular systole, as, for example, when the 
 cardiac muscular fibres have undergone serious degenera- 
 tion, and, as a matter of observation, this is found some- 
 times to be the case. For the most part, however, the 
 disease, and especially valvular disease, which has given 
 rise to the necessity for cardiac tonics, will have brought 
 about considerable hypertrophy of the muscular walls of 
 the heart without any corresponding hypertrophy of the 
 muscular walls of the vessels. The balance of advantage, 
 therefore, when the contractile energy of both heart and 
 vessels is increased, is largely on the side of the heart, 
 
260 HEART DISEASE. 
 
 its muscular fibres having greatly increased in number 
 and size. 
 
 It might seem, again, that the contraction of the 
 arterioles would more or less intercept the vis a tergo in 
 the veins which is already lacking, as is often manifested 
 by the presence of cedema. If, however, we bear in mind 
 that the contraction affects not only the arterioles but the 
 capillaries also, it will be evident that the narrowing of 
 these channels will give rise to increased rapidity of the 
 current of blood within them which will carry to the 
 venules the propulsive force communicated by the heart 
 better than a sluggish and irregular movement through a 
 network of flaccid, dilated and bulging capillaries. This 
 more rapid onward flow of the blood will again favour the 
 taking up of fluid effused into the inter-cellular spaces. 
 
 It would seem that the effects just enumerated ought to 
 be of equal service in all forms of heart disease, excepting 
 structural degeneration of the walls, and certainly in all 
 forms of valvular disease. As a matter of observation, how- 
 ever, such is not found to be the case. In one valvular 
 disease, mitral incompetence, all observers agree that 
 digitalis is of the greatest possible service ; in another, 
 mitral stenosis, there is almost equal concurrence of opinion 
 that this remedy is not of the same benefit, and, indeed, 
 that it is capable of doing harm and of aggravating the 
 bad effects of the disease. In aortic incompetence orjinions 
 are divided, some maintaining that the cardiac tonics in 
 general and digitalis in particular are injurious, others 
 that they are helpful. The same may be said of aortic 
 stenosis. 
 
 It appears to me that an explanation of this difference, 
 if it can be arrived at, will make our comprehension of the 
 beneficial effect more clear, and render our employment of 
 these remedies more precise. 
 
 The question of the effects of digitalis is often argued 
 
DIGITALIS IN AORTIC DISEASE. 261 
 
 on theoretical grounds ; but it must be pointed out that it 
 is upon experience and not upon theoretical considerations 
 that the conclusion just stated as to the difference in its 
 remedial influence is based. Long before the physiological 
 action of digitalis was ascertained, it had been noted that 
 this remedy was not always beneficial in its action, and was 
 sometimes obviously injurious, and much was said by old 
 writers as to intolerance of the drug and especially as to its 
 cumulative effects. When mitral stenosis was not distin- 
 guished from incompetence of this valve, the varying 
 effects of digitalis must have been most perplexing, and, 
 indeed, incomprehensible. 
 
 In aortic regurgitation failure of compensation is 
 manifested in two distinct ways, and there are two different 
 modes of death. In one, the effect is defective propulsion 
 of blood into the arterial system, manifested by faintness, 
 giddiness, and sudden weakness of the legs, sometimes by 
 anginoid pain ; death is by syncope ; in the other, there is 
 obstructive backworking through the lungs and right heart, 
 giving rise to venous obstruction and dropsy, exactly as in 
 mitral insufficiency. There are, in effect, aortic physical 
 signs with mitral symptoms. 
 
 We have in this, it appears to me, an explanation of the 
 different views as to the influence of digitalis in aortic in- 
 sufficiency. When the tendency indicated by the symptoms 
 is defective propulsion with failure of arterial blood supply 
 to the brain, the effects are uncertain and even doubtful. 
 While sometimes apparently beneficial for a while, a 
 frequent result is the production of irregularity of the pulse 
 with aggravation of the symptoms, and occasionally of 
 vomiting attended with rapidly increasing weakness of the 
 heart's action. Cases are met with, indeed, in which there 
 is grave reason to suspect that it has precipitated a sudden 
 fatal termination. 
 
 When, on the other hand, the symptoms are due to 
 
262 HEART DISEASE. 
 
 secondary dilatation of the left ventricle not adequately- 
 neutralized by hypertrophy, with or without mitral regurgi- 
 tation, and to the effects of this upon the pulmonary 
 circulation and right ventricle, we have exactly the same 
 opportunity for the beneficial influence of digitalis in 
 reinforcing the right side of the heart, and the same 
 favourable results as in mitral regurgitation. The effects, 
 indeed, are sometimes much more striking, and the removal 
 of dropsical effusion more rapid. I have observed, however, 
 that not uncommonly patients suffering from serious aortic 
 insufficiency, after recovering from the mitral symptoms, die 
 suddenly from failure of the left ventricle, and this whether 
 the digitalis has been continued or left off, and sometimes 
 before the patient has begun to get up and move about. 
 
 Aortic stenosis, like aortic incompetence, leads up to a 
 fatal termination in two ways — directly, by limiting the 
 supply of arterial blood, and indirectly, by giving rise to 
 back pressure in the pulmonic and venous circulation, 
 through secondary mitral incompetence. It is only when 
 symptoms arise from the latter that digitalis is useful. 
 In the earlier stages the left ventricle may be injured if 
 stimulated to drive its contents through a narrowed orifice. 
 More relief is often obtained by relaxing the arterioles 
 by means of nitroglycerine, deducting thus the arterio- 
 capillary resistance from the total work with which the 
 heart has to contend. 
 
 Mode of Action of Digitalis in Mitkal 
 Eegukgitation. 
 
 Mitral regurgitation, being the disease in which the 
 action of the cardiac tonics is almost always beneficial, a 
 study of the conditions presented may enable us to arrive 
 at some comprehension of the way in which the good effects 
 are brought about. 
 
DIGITALIS IN MITRAL INCOMPETENCE. 363 
 
 What takes place in mitral regurgitation is as follows : 
 The regurgitation into the left auricle dilates this cavity 
 (there may be some hypertrophy of its muscular walls, but 
 no compensatory influence of any consequence is gained 
 thereby) and at the same time drives back the blood which 
 is flowing to the left auricle and ventricle by the pulmonary 
 veins. The obstruction in the pulmonary veins necessarily 
 gives rise to resistance to the onward flow through the 
 capillaries, to overcome which increased pressure is required 
 in the pulmonary artery, and therefore greater driving 
 power on the part of the right ventricle. From this results 
 hypertrophy of the right ventricle, which is the great 
 compensating agency by which the leakage of the mitral 
 valve is more or less perfectly neutralized. If the blood 
 pressure in the pulmonary veins could be maintained at 
 such a point as to be greater than the pressure in the aorta, 
 there would be no reflux into the auricle durina; the con- 
 traction of the ventricle, even were the mitral valve 
 completely destroyed; but, however powerful the action of 
 the right ventricle, this can never be absolutely the case. 
 The walls of the pulmonary capillaries and veins and of 
 the left auricle, are too weak to resist such a distending 
 force, and moreover the suction action of the left ventricle 
 during diastole will always temporarily reduce the pressure 
 in the left auricle. 
 
 Another change in the heart resulting from mitral 
 regurgitation must be noticed. This is, a dilatation of the 
 left ventricle, produced by distension of this cavity during 
 the defenceless diastolic period, by the high pressure in the 
 pulmonary veins and left auricle. It involves some con- 
 secutive hypertrophy of the ventricular walls. 
 
 These familiar and elementary explanations are enume- 
 rated in order once more to emphasize the fact that the 
 work of compensation for mitral regurgitation falls upon 
 the right ventricle, and that, when systemic venous 
 
264 HEART DISEASE. 
 
 stasis and other late effects of mitral regurgitation show 
 themselves, it is because the right ventricle is beaten 
 by the resistance in the pulmonary circuit and can no 
 longer keep up adequate pressure in the left auricle. 
 
 Applying now our knowledge of the physiological 
 effects of digitalis, we shall see that the favourable results 
 of its administration are due almost entirely to reinforce- 
 ment of the right ventricle. On the left side of the heart 
 and in the systemic circulation there will be produced a 
 certain degree of arterio-cajjillary contraction, with slight 
 increase in the peripheral resistance and in the intermediate 
 arterial tension, and a more deliberate and energetic action 
 of the left ventricle in systole, which makes room for a 
 large volume of blood in diastole, while the elastic rebound 
 at the end of systole exercises a better suction action on the 
 contents of the distended left auricle. The hypertrophy 
 of the ventricular walls, which will more than neutralize 
 the increase of resistance in the peripheral circulation, and 
 the greater capacity of the cavity would, in the absence of 
 regurgitation into the auricle, result in the projection of 
 a larger charge into the arteries at each systole. The effect 
 of this is undoubtedly good, but the regurgitation into the 
 left auricle is a set-off against it, and this will be increased 
 with the increase of resistance in the arterial system. So 
 far, however, as these good effects on the left ventricle and 
 systemic circulation are concerned, they would be much 
 more conspicuous in aortic regurgitation than in mitral 
 regurgitation, since the ventricle is stronger and its 
 capacity larger, and yet we do not find that digitalis is 
 more useful in this affection, but very often the contrary. 
 
 Looking now at the effects upon the right side of the 
 heart and the pulmonary circuit, there may or may not be 
 contraction of the arterioles and capillaries in the lungs 
 with increase of resistance. This could, however, in any 
 case only be slight, while the ventricular walls being 
 
DIGITALIS IN MITRAL INCOMPETENCE. 265 
 
 greatly hypertrophied, increase of vigour in their con- 
 traction will at once raise the blood pressure in the entire 
 pulmonary circulation and in the left auricle. Improved 
 pressure in the left auricle, as has been seen, will fill 
 the left ventricle better during diastole, will resist reflux 
 through the mitral orifice in the systole, and so will 
 increase the amount of blood thrown into the aorta. 
 
 It is here that the beneficial influence of digitalis really 
 comes in. As has been before stated, the neutralization of 
 the effects of mitral regurgitation is almost entirely the 
 work of the right ventricle, and it is by increasing the 
 efficiency of its compensatory action that digitalis is of 
 service. Additional evidence of this is, on the one hand, 
 the fact that relief of over-distension of the right side of 
 the heart by venesection or leeches and purgation is an 
 important corroborative measure, in many cases absolutely 
 essential to the result, and, on the other hand, that digitalis 
 fails when the right ventricle is seriously degenerated or 
 hampered by pericardial adhesions. 
 
 Among the conspicuous favourable results of the ad- 
 ministration of digitalis is diminished irregularity of the 
 pulse. This is entirely due to the higher blood pressure 
 in the left auricle, and the more regular supply of blood to 
 the ventricle. Mitral incompetence is the one among the 
 valvular affections which is specially liable to give rise to 
 irregularity of the pulse. This will be understood from 
 the following considerations. The left auricle is exposed to 
 the respiratory variations of pressure which its thin walls 
 resist only imperfectly. When, therefore, these variations 
 are exaggerated, as when the breath is held or when there 
 is dyspnoea from bronchitis or asthma, the amount of blood 
 carried on into the left ventricle will vary, and the pulse 
 will be more or less irregular. During inspiration the 
 negative pressure will tend to keep the auricle dilated, and 
 to prevent it from contracting properly, so that the ventricle 
 
266 HEART DISEASE. 
 
 will not have a full charge of blood, and its systole will be 
 brief and abortive. During forced expiration the auricle will 
 be compressed, and its contained blood will be forced on 
 into the ventricle, with opposite consequences. In mitral 
 regurgitation a further effect will be that the negative pres- 
 sure of inspiration will encourage the reflux into the auricle, 
 while the positive pressure of expiration will oppose it. 
 In this way — the ventricle sometimes being imperfectly, at 
 other times perfectly, filled, sometimes sending back more, 
 sometimes less, of its contents into the auricle — we have 
 ample explanation of irregularity of the pulse. Now, the 
 lower the internal blood-pressure in the auricle and pul- 
 monary veins, the greater will be the effect of variations of 
 external pressure, and the higher the pressure within the 
 auricle, the more independent it will be of pressure from 
 without. It will be seen, therefore, how digitalis steadies 
 the action of the heart and renders the pulse more regular. 
 
 Effects of Digitalis in Mjtkal Stenosis. 
 
 If we examine the effects of digitalis in mitral stenosis, 
 we may perhaps see why they are less certainly favourable, 
 and sometimes clearly unfavourable. In an uncomplicated 
 case the left ventricle is neither dilated nor hypertrophied, 
 and the arteries generally are already small and contracted. 
 No obvious advantage can be seen in further contraction 
 of the arterioles, and, in point of fact, the symptoms are 
 somewhat relieved by causing them to dilate. No great 
 improvement in the output of blood, again, is to be gained 
 by more vigorous contraction of the walls of the left 
 ventricle, as they are not specially strong, and the cavity is 
 small. But it would seem that increased vigour in the 
 contraction of the right ventricle should have the same 
 good effect here as in mitral regurgitation, and marked 
 beneficial influence is indeed very commonly observed if 
 it is judiciously administered when the right ventricle is 
 
DIGITALIS IN MITRAL STENOSIS. 267 
 
 beginning to give way. The conditions, however, are 
 different, and if given in the early stages of mitral stenosis 
 it may do actual harm. In mitral regurgitation the 
 increased amount of blood driven by the right ventricle 
 into the pulmonary artery, by raising the pressure in the 
 pulmonary circulation, antagonizes the reflux into the 
 auricle, so that more blood finds its way into the left 
 ventricle, whereas in mitral stenosis the blood cannot be 
 forced through the constricted mitral orifice beyond a 
 certain rate of speed, and if the right ventricle is stimu- 
 lated to contract more than is required for this, it 
 encounters an insuperable obstruction, and becomes em- 
 barrassed in its action, its energy being uselessly expended. 
 A common result is irregularity in the beats, accompanied 
 by a sense of precordial oppression, and not infrequently 
 the heart-beats are in couples, the first of which alone 
 reaches the wrist, the second having no aortic second 
 sound. 
 
 In many cases of advanced mitral stenosis, in which 
 there is fair compensation, the coupled beats can be pro- 
 duced at will by giving digitalis. The second of the two 
 beats is evidently a supplementary systole of the right 
 ventricle : there is a right ventricle impulse felt over the 
 lower left costal cartilages, while the apex beat is scarcely, 
 or not at all, perceptible. At the second of the coupled 
 beats both right ventricle sounds are heard, while the aortic 
 second sound is absent, and if there is a systolic mitral 
 murmur as well as the presystolic, it is audible only with 
 the first of the two beats. When compensation has broken 
 down and there are pulsation of the veins in the neck, 
 oedema of the extremities, and other evidence of secondary 
 tricuspid regurgitation, digitalis may be given, oftentimes 
 with marked benefit, but its effects should be carefully 
 watched, and it should not be persevered with too long if 
 good results do not follow. 
 
CHAPTER XIX. 
 STRUCTURAL CHANGE IN THE HEART. 
 
 HYPERTROPHY — CAUSES OP HYPERTROPHY OP THE LEFT 
 VENTRICLE, OF THE RIGHT VENTRICLE — PHYSICAL SIGNS 
 — SYMPTOMS— PROGNOSIS— TREATMENT. 
 
 The muscular walls of the heart are liable to changes of 
 various kinds, some of which constitute diseases which 
 shorten life and give rise to much suffering. Of these 
 structural alterations, some are common — hypertrophy, 
 dilatation, fatty degeneration, fibrosis ; others rare — cancer, 
 syphilitic gumma, abscess, aneurysm. We shall concern 
 ourselves mainly with those which are comparatively 
 frequent; the others, obscure as well as uncommon, are 
 very seldom recognized during life, and a diagnosis is only 
 made when an exceptionally clear case comes under the 
 notice of an exceptionally acute observer. 
 
 Even when the common and familiar affections — hyper- 
 trophy, dilatation, and degeneration — only are taken into 
 consideration, we find ourselves on much less secure ground 
 than when dealing with lesions of the valves. The latter 
 we can localize with great confidence ; and knowing, partly 
 by experience, partly by the application of mechanical 
 principles, their effects and tendencies, we can, by making 
 out how far such effects are manifest, form an opinion as to 
 the probable course of the symptoms and as to the future of 
 the patient. On examination after death, again, we can 
 understand the connection between the lesion and the 
 
STRUCTURAL CHANGE IN THE HEART WALLS. 26c, 
 
 symptoms, and can follow the sequence of secondary 
 changes in the heart and vessels which are set up by the 
 original valvular defect. In the case of structural changes, 
 on the contrary, the diagnosis cannot be made with the 
 same precision, and we are often left in some degree in the 
 dark even by a post-mortem examination. In one patient 
 fatty degeneration has apparently proved fatal at so early 
 a stage that the naked-eye characters of the condition are 
 scarcely perceptible, and it is only by the microscope that 
 its existence is definitely established ; in another the 
 change has proceeded so far that the fingers sink into the 
 pale greasy walls, and the muscular fibres have almost 
 disappeared, so that it is scarcely conceivable how the 
 heart has been able to impress any movement whatever 
 011 the blood, or how life has been sustained through the 
 intermediate stages of disintegration. So with regard to 
 dilatation, there is no fixed relation between the degree of 
 enlargement of the cavities and thinning of the walls found 
 after death and the interference with the circulation 
 observed during life. One man will live for years with 
 a heart which has reached the extreme limits of dilatation, 
 while another succumbs when it is but moderately advanced. 
 If, therefore, we could make out with great exactness the 
 dimensions of the heart, the size of its separate chambers, 
 and the thickness of their respective walls, which is no easy 
 task, we could not on these grounds alone compare one case 
 with another, and decide upon the relative danger. 
 
 Many other considerations of extreme importance will 
 come into the estimate — the functional vigour of the 
 muscular walls as well as their thickness, the liability to 
 palpitation, the state of the great and small vessels, the 
 degree of peripheral resistance, the presence or absence of 
 reflex irritation of the heart from gastric or other derange- 
 ment. The question of prognosis thus becomes extremely 
 complicated, and is beset with uncertainty. An element of 
 
270 HEART DISEASE. 
 
 chance or luck even comes in — the subject of advanced 
 disease is at the mercy of the slightest accident; many a 
 patient lives for years with a dilated or fatty heart who 
 would be killed by an attack of influenza, or by a powerful 
 emotion, or by tripping over a stone or a mat. A serious 
 obstacle to the attainment of the minute and definite 
 knowledge which alone is of real use in arriving at a sure 
 prognosis in structural disease of the heart, is the fact 
 that a large proportion of the cases occur in private and 
 consulting practice, and comparatively few come under 
 observation in hospital. It is difficult, therefore, to keep 
 such cases in sight and to watch their progress, and seldom 
 possible to obtain a post-mortem examination to confirm 
 the diagnosis. 
 
 While, however, the great difficulty of prognosis and 
 diagnosis in structural diseases of the heart is acknowledged, 
 it is of the utmost consequence that such approximation to 
 a forecast of the prospects of life as is possible should be an 
 object of serious endeavour. The cases are numerous, far 
 more numerous at and after middle age than those of 
 valvular disease, and everything which has been said as to 
 the importance of prognosis in general applies here. An 
 early recognition of these changes, indeed, is often of 
 greater service to the subject of them than in the case 
 of valvular affections, since it reveals also the tendencies 
 which are in operation, and often at a time when they can 
 be successfully combated by treatment. 
 
 Too commonly, however, no attempt is made to recog- 
 nize the existence and extent of degeneration or dilatation. 
 The symptoms due to derangement of the circulation force 
 themselves upon the attention of the medical man, but no 
 murmur being detected, the only diagnosis ventured upon 
 is that of "weak heart," a vague term which covers the 
 entire ground, from temporary functional debility to disease 
 inevitably and imminently fatal. Such a diagnosis reacts 
 
STRUCTURAL CHANGE IN THE HEART WALLS. 271 
 
 unfavourably upon the mind of the observer who rests upon 
 it, and makes him less exact and trustworthy, while it may 
 be full of danger to the patient. 
 
 These considerations alone would justify an attempt to 
 render the prognosis of structural diseases of the heart 
 more definite, but a study of these affections from the 
 point of view of prognosis also leads to closer observation, 
 and to the recognition of the importance of details which 
 do not force themselves upon the attention so long as 
 diagnosis in the ordinary and limited sense of the word 
 only is the object. 
 
 A further justification of the prominence given to prog- 
 nosis is that the grasp of all the facts of the disease and 
 of the individual case, which is necessary to the formation 
 of a just forecast of the result, is the best guide for 
 treatment, whether this may demand chiefly patience and 
 caution, or must be energetic and prompt. Prognosis is 
 not merely a well-instructed conjecture as to the ultimate 
 issue, it is a deliberate judgment as to the processes and 
 tendencies of the disease, and as to the constitutional 
 soundness and strength of the patient. The foresight 
 relates to the dangers which attend the attack, to the 
 course it will run, and to the influences and contingencies 
 which make for or against the sufferer. To this there has 
 only to be added a knowledge of the therapeutic measures 
 by which the tendency to death or structural injury can 
 be antagonized, and by which the patient can be guided 
 and helped, together with skill, courage, and promptitude 
 in applying it, and we have all the requisites for successful 
 treatment. 
 
 Treatment, therefore, will form a natural sequel and 
 corollary to prognosis. 
 
272 HEART DISEASE. 
 
 HYPEETEOPHY. 
 
 This condition of the heart will not detain us long. The 
 prognosis of cardiac hypertrophy, like the symptoms, is that 
 of its cause, and the character and degree of hypertrophy 
 are important, not so much in themselves or on account of 
 danger likely to arise out of them, but as indicating the 
 existence of some condition which has given rise to the 
 increase in thickness and contractile power of the muscular 
 walls of the heart, and which is serious, possibly, in pro- 
 portion to the hypertrophy which it has provoked. 
 
 Causes of Hypeeteophy of the Left Venteicle. 
 
 The causes which give rise to hypertrophy must be 
 enumerated. The left or right ventricle may be affected 
 alone or predominantly, or both may have undergone 
 change. The causes which bring about hypertrophy of 
 the left ventricle are, in the first place, valvular diseases, 
 stenosis, or insufficiency of the aortic valve, or mitral 
 insufficiency. With these we are not now concerned, 
 as they have been fully discussed in the chapters on the 
 respective valvular lesions. Next in frequency will be 
 protracted high arterial tension. When high pressure in 
 the systemic arteries is recognized, and especially when 
 there are evidences of its having been habitual for some 
 time, such as large, thickened, tortuous, radial and temporal 
 arteries, or a dilated ascending aorta, the underlying con- 
 dition to which it is due must be identified. The causes of 
 high arterial tension and the mechanism of its production 
 have been dealt with in Chapter II., so they will only be 
 briefly enumerated here. They are renal disease, gout, 
 diabetes, lead poisoning, excessive nitrogenous diet, consti- 
 pation, alcohol, tobacco, and, above all, a hereditary predis- 
 position. 
 
 Left ventricle hypertrophy, again, may in rare instances 
 
HYPERTROPHY. 273 
 
 have no other assignable origin than adherent pericardium, 
 a condition which is difficult to diagnose, and with regard 
 to which prognosis is, as a rule, unfavourable if the heart is 
 much enlarged. 
 
 If hypertrophy is at any time produced by a mode of 
 life entailing sustained muscular exertion, it is physio- 
 logical and not pathological, and has no claims on our 
 attention ; unless, indeed, the initial change has been 
 dilatation caused by violent and sustained effort, such as 
 racing, the hypertrophy being secondary to this ; but even 
 here it is the dilatation and not the compensatory process 
 which has to be considered. 
 
 Causes of Hypeetrophy of the Eight Ventricle. 
 
 Hypertrophy of the right ventricle, as of the left, has 
 its most common cause in valvular disease — in this instance 
 chiefly mitral stenosis or insufficiency ; — and after valvular 
 disease, in conditions which give rise to obstruction in the 
 pulmonary circulation. 
 
 Emphysema and bronchitis are the lung affections 
 which most frequently give rise to hypertrophy of the 
 right ventricle, but the hypertrophy is rarely dissociated 
 from dilatation, which is the primary effect of the obstruc- 
 tion in the pulmonary capillaries. Collapse of a portion 
 of the lungs, contraction of a lung from pleural adhesions, 
 fibroid phthisis, or any condition which throws a consider- 
 able area of lung surface out of gear, will to a certain 
 degree give rise to overwork and consequent hypertrophy 
 of the right ventricle. 
 
 Hypertrophy of the Left Ventricle. Physical Signs. 
 
 The Pulse. — The pulse will be that of the condition which 
 has given rise to the hypertrophy. When this has been 
 high arterial tension due to renal disease, gout, lead poison- 
 ing, pregnancy, etc., the character of the pulse will be as 
 
 T 
 
274 HEART DISEASE. 
 
 follows : The artery will be full between the beats, will not be 
 easily flattened under the fingers, and can be followed some 
 distance up the forearm like a cord. The pulse wave will 
 not have a violent ictus, but will rise gradually and subside 
 slowly, and as it makes little impression on the fingers 
 it is sometimes described as weak, but when the attempt 
 is made to arrest the wave very firm pressure is required. 
 When the cause of the hypertrophy has been valvular 
 disease, the character of the pulse will be as described in 
 the chapters on the particular lesion. 
 
 The Heart. — On inspection, there may or may not be 
 recognizable bulging over the cardiac area ; the impulse is 
 not extensive or violent in uncomplicated cases; the ajDex 
 beat, if visible, is seen below the normal point, frequently 
 in the sixth, sometimes even in the seventh, space, and is 
 probably also displaced somewhat outwards ; it is a cir- 
 cumscribed gentle heave. Occasionally one or more of 
 the intercostal spaces above and to the inner side of the 
 apex line may be seen to be retracted, but this is very 
 rare, and is never so well marked in hypertrophy without 
 valvular disease as it may be seen in aortic regurgitation. 
 
 By palpation, which is always an extremely important 
 part of the physical examination of the heart, the apex 
 beat is further defined, and is felt as a powerful but 
 deliberate thrust in the space, sometimes distinctly lifting 
 the adjacent ribs. The more the fingers are pressed into 
 the space, the more distinctly is the thrust recognized. 
 When the flat of the hand is laid over the cardiac region, 
 a general heaving impulse can usually be felt, but when 
 the left ventricle is alone or mainly affected, it is not very 
 conspicuous. As a rule, no impulse is felt to the right 
 of the sternum except when the aorta is dilated, in which 
 case pulsation may be felt when the fingers are thrust into 
 the second and third spaces near the sternum. It must 
 be added that sometimes neither apex beat nor impulse 
 
HYPERTROPHY. 275 
 
 can be seen or felt when the hypertrophy is considerable. 
 Mostly this is in deep-chested individuals with large, over- 
 lapping lungs, but occasionally hypertrophic enlargement 
 takes a direction which carries the heart away from the 
 chest wall. 
 
 Percussion maps out more or less accurately the enlarge- 
 ment of the heart downwards and to the left. This 
 demarcation should be done with extreme care, but it 
 must not be taken for granted that the outline drawn 
 on the surface corresponds exactly with that of the organ, 
 or gives a trustworthy idea of its size. To say nothing 
 of the difficulty of defining deep dulness, the heart may 
 enlarge backwards instead of laterally. The results of 
 percussion must be correlated with all the other evidence 
 as to the size of the heart. 
 
 Auscultation, besides teaching the character and in- 
 tensity of the sounds, must be made to contribute to the 
 information on this point by careful noting of the seat of 
 maximum intensity of the sounds in the apex region. 
 
 The left ventricle first sound as heard at the apex is 
 longer and of lower pitch than in a normal state of the 
 heart ; either the mass of muscle enters into contraction 
 more slowly, and the muscular tension being less sudden 
 yields a duller sound, or the thickness of the walls masks 
 the sound produced by the sudden tension of the valves and 
 tendinous cords. The aortic second sound, heard at the 
 apex, is usually louder than normal, and is often heard at 
 or near the apex more distinctly even than in the right 
 second space. 
 
 The systole is usually somewhat prolonged. The first 
 sound may be reduplicated, due to the two first sounds, 
 produced by the right and left ventricles respectively, not 
 coinciding. This indicates that the left ventricle is no 
 longer quite equal to the extra work imposed upon it, and 
 marks the supervention of a tendency to dilatation. 
 
276 BE ART DISEASE. 
 
 At the base of the heart the left ventricle first sound 
 is less distinct than at the apex, and is frequently inaudible, 
 while the accentuation of the second sound is rendered 
 more evident by the absence of the first. When this sound 
 is not only accentuated but low-pitched and ringing, it 
 indicates that the root of the aorta is more or less dilated, 
 and the sound will be heard for some distance to the right 
 of the edge of the sternum. 
 
 The sounds of the right ventricle undergo no modifica- 
 tion of sufficient importance to require notice. 
 
 Symptoms. 
 
 Various symptoms are described as resulting from 
 hypertrophy of the heart — discomfort from the violence 
 of the impulse, or actual pain in the region of the heart, 
 tenderness on pressure in the neighbourhood of the apex, 
 throbbing sensations in the head and neck, pulsatile noises 
 in the ears, or audible pulsation in the carotid and other 
 arteries. The action of the heart may be unduly frequent, 
 or too easily excited, or abrupt and irritable, or irregular 
 with falterings and bounds, which are very disturbing to 
 the subject, and the heart may be prone to palpitation. 
 There may be a sense of respiratory oppression, with sigh- 
 ing and desire to fill the chest with air. 
 
 Some of the symptoms are simply the result of the size 
 of the heart and of the vehemence of its beat ; others are 
 due, not to the hypertrophy itself, but to its cause, whether 
 in the valves or in the vessels, or to external influences 
 which have given rise to it ; others, again, are common to 
 various affections of the heart, functional or organic, 
 besides hypertrophy. They have no such direct or definite 
 bearing on prognosis as would warrant a discussion of their 
 significance, though a sustained frequency of the pulse is 
 an unfavourable sign. 
 
hypertrophy. 277 
 
 Prognosis. 
 
 The question of prognosis in relation to hypertrophy 
 mostly resolves itself into this : whether the compensation 
 which it establishes is adequate and efficient, and how far 
 it promises to be durable. The danger that the hyper- 
 trophy may go beyond the requirements of the occasion 
 which has called for it does not, in my opinion, need 
 consideration. 
 
 Compensation is efficient when there are no symptoms 
 of embarrassment of the circulation, and when the heart 
 responds to all ordinary calls upon it without undue short- 
 ness of breath or respiratory distress. The effects of exertion 
 are an important criterion, due allowance being made for 
 the greater liability to breathlessness which is natural to 
 some individuals, or is produced by bodily conformation or 
 which results from a sedentary mode of life. 
 
 But the sounds of the heart usually give notice when 
 it is overtaxed by the resistance to the onward movement 
 of the blood. The interval between the first and second 
 sound may be prolonged, the systole requiring more time 
 than under ordinary circumstances to complete itself. So 
 long as the normal proportion between the systolic and 
 diastolic pauses is not disturbed, there is no indication that 
 the heart is unequal to its work or is suffering from the 
 stress put upon it : but when the systolic interval between 
 the first and second sounds is lengthened at the expense 
 of the diastolic, so that the sounds are equidistant, the 
 period of repose and reconstitution of the muscular fibres 
 of the ventricle is shortened, and their nutrition must in 
 time suffer. During systole the blood is squeezed out of 
 the walls of the heart, and it is during the diastolic 
 relaxation that it obtains free access to the cardiac fibres. 
 
 Another evidence that the heart is yielding to the strain 
 of overwork is reduplication of the first sound. That is, 
 
278 HEART DISEASE. 
 
 as has been already said, due to want of synchronism 
 between the two ventricles in the act of contraction, or 
 rather in arriving at that point in their contraction when 
 their valves and tendinous cords and muscular walls are all 
 made tense. This reduplication is at first very slight, the 
 two sounds are separated by the briefest possible interval, 
 and are distinct one from the other only at one spot, just 
 to the inner side of the apex; elsewhere there is only a 
 slurring or prolongation of the first sound. Later the 
 sounds of the right and left ventricles are quite distinct, 
 and the duplex first sound is recognized over a considerable 
 area, usually in the direction of the ensiform cartilage, but 
 sometimes upwards. One variety of the cantering rhythm 
 or bruit de galop is produced by this doubling of the first 
 sound, where the successive sounds are one-one, two. Some- 
 times the dislocation of the ventricular first sound is so 
 considerable that it is a task of extreme difficulty to identify 
 the sounds of the heart at all, and associate them with the 
 systole or diastole respectively so as to say which is first 
 and which second. The most striking and confusing 
 examples are met with in aortic stenosis and pericarditis. 
 The prognosis becomes serious when the first sound is broken 
 up in any considerable degree. 
 
 But when the cardiac hypertrophy has been brought 
 about by high arterial tension, whether associated with 
 renal disease, or lead poisoning, or other cause, there must 
 be taken into consideration the possibility that the power- 
 ful heart may rupture diseased vessels in the brain, and 
 if the arteries are conspicuously degenerated it is better 
 for the patient that the heart also should undergo some 
 degree of degeneration; and sometimes this takes place, 
 so that the patient escapes cerebral haemorrhage, and lives 
 longer, though he succumbs in the end to cardiac failure. 
 
hypertrophy. 279 
 
 'Treatment. 
 
 Treatment for hypertrophy, as such, appears to be 
 out of place. The functional vigour and energy of the 
 overgrown and overstrong heart could no doubt be re- 
 duced by various means — low diet, enforced rest, and 
 such drugs as aconite — but unless it is clear that the 
 hypertrophy has gone beyond the requirements of the 
 condition which has given rise to it, the advantage of this 
 procedure would be more than doubtful. Even in the 
 attempt to relieve the incidents of hypertrophy, palpita- 
 tion, throbbing sensations in the chest, prsecordial oppres- 
 sion, the employment of direct cardiac depressants is rarely 
 of service, and is at times attended with danger. In aortic 
 stenosis, for example, I have known aconite, given with a 
 view of quieting tumultuous action of the heart, so far 
 reduce the contractile energy of the left ventricle that it 
 was no longer able to cope with the obstruction, and death 
 quickly followed from cardiac asthenia, the pulse becoming 
 imperceptible, the extremities livid, and the surface of 
 the body cold and damp. This would be less likely to 
 occur where the cau3e of the hypertrophy was obstruction 
 in the peripheral circulation, as the arteries and capillaries 
 are relaxed by such agents as depress the action of the 
 heart. 
 
 The treatment of the chief causes of hypertrophy, aortic 
 disease and high arterial tension, have already been dis- 
 cussed elsewhere, so that what we have to consider here is 
 not the treatment of hypertrophy or its causes, but treat- 
 ment suggested by the hypertrophy. We shall recognize, 
 for example, the necessity of diminishing the volume and 
 improving the quality of the blood by appropriate diet 
 and hygiene, and, if necessary, by tonics. We shall recog- 
 nize, also, the desirability of diminishing the resistance to 
 the onward movement of the blood in the arterio-capillary 
 
280 HEAkT DISEASE. 
 
 network by care in diet again, by aperients, and by 
 eliminants of various kinds. In some cases, the resistance 
 in the peripheral circulation may be further lessened with 
 advantage by the physiological relaxants of the arterioles 
 and capillaries, such as nitroglycerine and the nitrites. By 
 these means the work thrown upon the heart is reduced, 
 and, if necessary, the heart may be strengthened by such 
 remedies as strychnine and digitalis. 
 
 All these measures are specially required when the 
 hypertrophy is no longer quite equal to the task which it 
 had originally been developed to perform, and reduplica- 
 tion and other modifications of the sounds are present. 
 It is now that the incidents of hypertrophy, palpitation 
 and the like, are most commonly complained of, and they 
 will be best alleviated or removed by the measures just 
 sketched, by relieving the heart of work on the one hand, 
 and by helping it on the other. 
 
CHAPTER XX. 
 DILATATION. 
 
 ETIOLOGY — VALVLLAR DISEASE, EXERTION, STRAIN, RENAL 
 DISEASE, ACUTE BACTERIAL INFECTIONS— PHYSICAL 
 SIGNS— SYMPTOMS — PROGNOSIS — TREATMENT. 
 
 The word " dilatation " requires no explanation as applied 
 to the cavities of the heart. Individual cavities may be 
 dilated, as, for example, the left auricle in mitral stenosis 
 or regurgitation, the right ventricle in pulmonary emphy- 
 sema or mitral disease ; but when spoken of as a form of 
 heart disease, dilatation usually means dilatation of the 
 left ventricle, mostly with, but sometimes without, dilata- 
 tion of the right ventricle. Together with the expansion 
 of the cavity of the ventricle there may be more or less 
 thickening of its walls, representing an attempt at hyper- 
 trophy, compensatory of the dilatation itself, or of the 
 difficulty in the circulation which has led to it. The walls 
 of the heart may have an approximately normal thickness, 
 which will really imply a certain degree of hypertrophy, 
 or they may be distinctly thinned. The parietes may have 
 a normal colour, consistence, and structure, or they may 
 be pale, flabby, and degenerated, or dense and tough from 
 fibroid substitution. But even more important than the 
 anatomical condition is the physiological or functional 
 condition, the special characteristic of which is that the 
 ventricle does not complete its systole, but only expels a 
 portion of its contents. 
 
282 HEART DISEASE. 
 
 Dilatation of the heart may be contrasted with hyper- 
 trophy rather than compared with it. Hypertrophy is 
 compensatory and an evidence of vigour ; dilatation is, for 
 the most part, a confession of failure on the part of the 
 heart muscle and an aggravation of other causes of inter- 
 ference with the circulation which may be in operation. 
 In hypertrophy the augmented mass and increased strength 
 of the muscular walls enable the ventricles to complete 
 their contraction in the face of difficulty. The result of 
 dilatation is that the ventricles habitually fail to expel 
 the whole of their contents. Very frequently it is only a 
 very small proportion of the blood which is projected into 
 the great arteries. In well-marked cases the chambers of 
 the heart are always full, and little blood being received 
 and expelled, there is a stagnation in the auricles and 
 ventricles. It has seemed to me that the imperfect empty- 
 ing of the ventricles has not always been fully realized as 
 the special feature of dilatation, but it will be seen that if 
 a dilated ventricle launched the whole of its contents into 
 the arterial circulation, the amount being much larger, the 
 rate of movement of blood would be greatly accelerated, 
 whereas the contrary is the case. 
 
 A distinction must be drawn between the dilatation 
 due to inherent weakness of the muscular walls of the 
 heart and that attending valvular disease. 
 
 Etiology. 
 
 Valvular Disease. — The dilatation attending aortic re- 
 gurgitation belongs to a different category from primary 
 dilatation, as has already been shown, and, instead of 
 aggravating the difficulties of the circulation, it is a part 
 of the compensatory arrangement. It is clear that if a 
 certain proportion of the blood projected into the aorta at 
 each systole returns to the ventricle during diastole, it is 
 
DILATATION. 283 
 
 an advantage, and indeed a necessity, that the capacity of 
 the ventricle should be increased, so that, in spite of the 
 reflux, a normal amount of blood may remain in the arteries 
 and be distributed to the tissues. The dilatation, however, 
 in aortic regurgitation is accompanied by hypertrophy 
 which enables the ventricle to contract perfectly, so that 
 the characteristic of dilatation — the partial and imperfect 
 emptying of the ventricle — is not present. 
 
 It is probable, again, that the dilatation of the left ven- 
 tricle met with in mitral regurgitation may have a similar 
 compensatory effect. It would seem to be an advantage, 
 since some of the blood regurgitates into the auricle, that 
 the ventricle should contain sufficient to allow for this, and 
 yet discharge a due amount into the aorta. In dilatation con- 
 secutive to mitral regurgitation, moreover, there is a certain 
 degree of hypertrophy, and the systole is carried through. 
 The dilatation of mitral regurgitation stands, then, on a 
 totally different footing from primary dilatation. 
 
 The mode of production of dilatation of the heart is 
 highly complex ; it is usually understood to be the result 
 of a gradual yielding of the walls of the ventricles, either 
 from their own inherent weakness or from undue resistance 
 to the onward course of the blood. It is often supposed also, 
 when dilatation exists, that it is an established and more or 
 less unvarying or progressive condition. Both these ideas 
 require modification. 
 
 Exertion. — All violent or protracted exertion is attended 
 with temporary dilatation of the heart, which may go so far, 
 even in strong and healthy persons, as to give rise to tempo- 
 rary murmurs. Loud murmurs so produced may be heard at 
 the apex, over the tricuspid area and over the pulmonic area, 
 in individuals who have no evidence of cardiac weakness 
 at the time, and who develop no valvular or other cardiac 
 disease for many years afterwards. A personal friend always 
 had a loud, systolic, pulmonic murmur after hunting, which 
 
284 HEART DISEASE. 
 
 sometimes, when there had been a severe run, lasted two or 
 three days. It is, again, not very uncommon for young and 
 strong men to return from climbing in Switzerland with 
 more or less dilatation of the heart, which may persist for 
 weeks. This is usually when little exercise has been taken 
 during the year, and considerable ascents or very long 
 walking excursions have been made without sufficient 
 preliminary training. Boat-races no doubt give rise to 
 temporary dilatation, and it may be met with as a result of 
 training for races. It might, perhaps, be better to speak of 
 distension of the cavities of the heart in these instances, 
 rather than of dilatation. 
 
 In violent exercise the pulse in becoming extremely 
 frequent also becomes extremely soft and short; the 
 arterioles and capillaries are relaxed in order to facilitate 
 the rapid movement of the blood which is necessary to 
 supply fuel and oxygen to the muscles during exertion, and 
 the arterial tension is low. The resistance to be overcome 
 by the ventricles is thus reduced to a minimum, which 
 diminishes the liability to over-distension. 
 
 But the circumstances which are capable of producing 
 a temporary distension of the ventricles in a sound and 
 vigorous state of the organ will be competent to give rise to 
 dilatation when it is weak and flabby, and when other 
 conditions are present which tend to dilatation, and it is 
 more likely that the weakly ventricles give way from time 
 to time under stress and fail to recover perfectly, than that 
 the yielding is gradual and continuous. 
 
 Overstrain and Degenerative Change. —Acute dilatation of 
 the heart is more common than is generally supposed. 
 
 In a very large proportion of the cases admitted into 
 hospital suffering from symptoms due to cardiac dilatation, 
 there has been an acute aggravation of the affection from 
 work or exposure, and under treatment a considerable dimi- 
 nution in the size and capacity of the heart is commonly 
 
DILATATION. 285 
 
 observed. But cases occur in which there is ground for 
 supposing that dilatation has been induced at once in a 
 heart not previously affected. The following are examples 
 selected as illustrations. 
 
 A gentleman at the age of 70, in vigorous health and 
 capable of any ordinary amount of exercise, overtook a 
 labourer pushing a heavily laden wheelbarrow uphill, who 
 had to stop and rest every few yards. Proud of his strength, 
 he told the man to stand aside, and himself wheeled the 
 barrow for some distance at a good pace. He lost his breath 
 and found that he did not recover it as he expected, but 
 that he continued to pant and to be conscious of violent 
 action of the heart, accompanied by a sense of oppression in 
 the chest. He got home with difficulty, the least exertion 
 was attended with shortness of breath, and he could not 
 rest at night. After a few days he sent for his medical man, 
 when the physical signs of dilatation of the heart were found 
 to be present. Mitral insufficiency was quickly established, 
 and when I saw him considerable dropsy existed. He died 
 shortly afterwards. 
 
 A gentleman, aged about 55, remarkably strong and 
 active, who was said to have had a slight attack of pleurisy 
 shortly before, ran quickly up a long flight of stairs in the 
 City. On arriving at the top he was found gasping for 
 breath, unable to speak and scarcely able to stand. He was 
 soon sufficiently recovered to be sent home, and a few days 
 later he was brought by his medical attendant to my con- 
 sulting-room, chiefly in order that I might aid in enforcing 
 the rest and care which were considered necessary. The 
 patient admitted that he was weak and soon out of breath, 
 but declared that he was quite equal to business. The 
 pulse was irregular in force and frequency, the apex beat of 
 the heart diffuse, devoid of the impulse or thrust, and dis- 
 placed downwards to the sixth space and outwards beyond 
 the nipple line, and the other physical signs of a considerable 
 
286 HEART DISEASE. 
 
 degree of dilatation were present. With great reluctance 
 a certain amount of rest and treatment was submitted to, 
 and the heart and pulse became stronger and steadier, and 
 the apex beat came in towards its normal situation about an 
 inch. 
 
 Two months later the patient ran down from a committee- 
 room in the House of Commons for a bag of papers which he 
 had forgotten, and back again. An attack of the same kind 
 as that just described came on, and this time lasted longer. 
 The evidences of dilatation of the left ventricle were more 
 marked, and oedema of the ankles soon came on. The 
 patient was kept in his room, and as far as practicable 
 at rest in bed or on a couch. Improvement was again 
 obtained, but much more slowly than before, and as my 
 visits were the chief restraint upon him, after a brief 
 attendance at short intervals, further consultations were 
 put off indefinitely. 
 
 Within a few days the exertion of going downstairs and a 
 serious imprudence in diet brought on a return of symptoms, 
 and the osdema of the lower extremities was shortly compli- 
 cated by thrombosis of the deep femoral vein of the left side, 
 which extended along the iliac vein to the vena cava and 
 down the right iliac and femoral veins. A tedious illness 
 followed, which finally proved fatal by extension of the 
 thrombosis to the renal veins, the heart itself appearing to 
 improve somewhat. 
 
 Another case was that of a boy who was admitted into 
 St. Mary's Hospital with extreme dilatation of both ven- 
 tricles. He had had no previous illness, but had been 
 underfed. Most Londoners will be familiar with the ap- 
 pearance of lads in the scanty attire of the cinder-path, who 
 are making use of the streets as a training-ground for 
 races, usually in the dusk of the evening, after working 
 hours ; perhaps, also, this time is chosen to avoid police 
 interference. I have myself often been astonished at the 
 
DILATATION. 2S7 
 
 pace and endurance of these athletes-under-difficulties. The 
 patient had been training in this way, and had persevered in 
 spite of shortness of breath, till severe symptoms set in. He 
 died soon after admission, and the ventricles were found to 
 be enormously dilated. 
 
 Renal Disease. — A certain degree of dilatation of the left 
 ventricle usually occurs at the onset of acute renal disease, 
 under the combined influence of the resistance in the 
 peripheral circulation and of the enfeeblement of the heart. 
 
 It is very striking in watching the course of a case of 
 what is commonly termed "large white kidney," in which 
 the patient survives the dropsical stage and the kidney 
 tends to approximate that of the " contracted granular." 
 At the outset the heart is greatly dilated, the apex beat is 
 not palpable, and the first sound is short and feeble. The 
 pulse is only of moderate tension, as there is little force in 
 the cardiac systole. After the lapse of about six months the 
 dropsy may all subside, and the pulse will then be found to 
 be one of higher tension with the vessel in a state of 
 hypertonias. The heart will have, to a great extent, re- 
 covered from its dilatation, and will have undergone very 
 marked hypertrophy, and the apex beat will be easily felt 
 and forcible. The patient will then be liable to die from 
 ursemic convulsions as in chronic interstitial nephritis. 
 
 In cases which are from the outset of the type of 
 " granular kidney," associated with very high arterial 
 tension, dilatation of the heart is seldom met with, though 
 the hypertrophy of the left ventricle is often enormous. 
 This is what one would expect, as here the increase of the 
 peripheral resistance and of the strain on the heart is 
 gradual, so that the heart has time to hypertrophy, to 
 cope with the extra work thrown on it, whereas in acute 
 nephritis a severe strain is suddenly put upon it which it is 
 unable to meet, and thus dilatation of the left ventricle 
 occurs. 
 
288 HEART DISEASE. 
 
 Acute Bacterial Infections. — In acute rheumatism and 
 chorea there is usually a certain degree of cardiac dila- 
 tation, which is often extreme in cases of acute pericarditis. 
 Attention has been called to this in the chapter on peri- 
 carditis, so it will not be further discussed here. In pneu- 
 monia the right ventricle is especially liable to become 
 dilated under the combined effects of the extra strain 
 thrown on it by the obstruction to the flow of blood through 
 the lungs and the damage to the cardiac muscle by the 
 action of the bacterial toxins. 
 
 Influenza is a common cause of cardiac dilatation which 
 is liable to be overlooked and to be a source of trouble after 
 the acute illness has subsided, as the patient is apt to go 
 about and resume his ordinary avocations too soon after 
 the attack, and increase or perpetuate the dilatation. 
 
 Undue exertion at an early period after any acute 
 bacterial infection, e.g. enteric fever, is liable to induce 
 cardiac dilatation, as the heart muscle will have suffered 
 a varying degree of injury from the toxins evolved by the 
 micro-organisms, and will not be able to stand any extra 
 strain, even if it has not given out during the illness itself. 
 
 Psychological Influences. — Another cause of dilatation of 
 the heart is anxiety. The influence of prolonged mental 
 depression upon the heart, as experienced by the sensation 
 of aching, oppression, and weight which attends grief and 
 anxiety, which were considered to point to the heart as the 
 seat of emotion generally, is indicative of an injurious effect 
 upon this organ. The combination of overwork, excitement, 
 worry, and trouble, often met with in City life, esjDecially 
 on the Stock Exchange or in mercantile or financial circles 
 during a commercial or financial crisis, is responsible for 
 many cases of cardiac dilatation among men, and domestic 
 anxieties — grief on account of children who have died or 
 given trouble, etc., — may have the same effect among 
 women. 
 
DILATATIOX. 289 
 
 Injudicious Regime. — Among the special causes of dila- 
 tation of the heart — acting, no doubt, on pre-existing 
 tendencies — which have come under my notice, are inju- 
 dicious hydropathic treatment, the so-called Banting method 
 of reducing obesity, and inhalation of the fumes of Himrod's 
 powder for the relief of asthma. 
 
 In one case a gentleman suffering from dyspeptic 
 symptoms, probably due to cardiac weakness and consequent 
 sluggish circulation in the abdominal viscera, underwent a 
 routine treatment by baths, wet cold packs, and compresses, 
 under which attacks of dyspnoea came on and oedema set 
 in. He had previously been under the care of competent 
 observers, who had not found any serious degree of dilata- 
 tion. The dropsy advanced in spite of treatment, and when 
 I saw the patient it was considerable, and the physical 
 signs gave evidence of extreme dilatation and thinning of 
 the left ventricle. Death occurred suddenly during a 
 paroxysm of dyspnoea. 
 
 Another patient came straight to my consulting-room 
 from a hydropathic institution, where he had undergone 
 vigorous treatment for digestive and liver derangements, 
 attributed to long residence in India. He was very anaBinic, 
 and breathless ; the heart was greatly dilated and its action 
 irregular, and there was incipient oedema. Fortunately he 
 recovered. 
 
 One of the most extreme cases of dilatation I have ever 
 met with was in the case of a lady who had undergone an 
 amateur course of Banting treatment for obesity. She had 
 lost some of her fat, but had become extremely breathless, 
 so that to walk across a room or put on an article of 
 clothing with the assistance of her maid caused her to pant 
 and gasp for breath in a very painful way. The pulse was 
 weak, small, and very irregular; no impulse or apex beat 
 could be felt, and the size of the heart, as mapped out 
 according to the deep dulness, was incredibly large, had not 
 
 u 
 
290 HEART DISEASE. 
 
 the results of percussion been confirmed by the sounds 
 being audible over the entire area of dulness, and, later, by 
 a feeble apex beat in the seventh space near the mid-axillary 
 line. Apparently habitual high arterial tension had been 
 exaggerated by an exclusively nitrogenous diet, and, under 
 it, the ventricle had given way. 
 
 It may, perhaps, be well to add that in the treatment of 
 obesity by beefsteak and copious draughts of hot water 
 there has not been, according to my experience, increase of 
 arterial tension, but the reverse. 
 
 The following case is the most serious of several attribu- 
 table to Himrod's powder : — 
 
 In December, 1883, I saw, with Dr. Andrews, of Hamp- 
 stead, a gentleman, aged about thirty-six, apparently of 
 sturdy constitution, who, after an attack of bronchitis, 
 suffered from severe nocturnal attacks of asthmatic dyspnoea. 
 A month at Hastings had apparently restored his health ; 
 but, after a fortnight of work in London, his nocturnal 
 asthma and shortness of breath were as bad as ever. For 
 the asthmatic attacks he had inhaled immoderately the 
 fumes of Himrod's powder, obtaining relief for the time, 
 but with disastrous after-effects. The whole house was 
 reeking with the odour of the fumes at the time of our 
 consultation. Dr. Andrews had witnessed the rapid develop- 
 ment of the condition of the heart which existed. The 
 area of cardiac dulness was greatly increased ; no apex beat 
 was recognizable ; there was a doubtful systolic murmur 
 (mitral) in the region of the apex, a loud systolic murmur 
 (tricuspid) near the ensiform cartilage, and a faint systolic 
 aortic murmur. Tricuspid incompetence was further dis- 
 tinctly manifested by great enlargement of the liver, and 
 by marked jugular pulsation. There was nothing in the 
 patient's habits, or mode of life, or previous history which 
 was at all calculated to give rise to dilatation of the heart, 
 and I had the less hesitation in attributing it to the 
 
DILATATION. 291 
 
 solanaceous fuines, from having seen similar effects in other 
 cases. In about a fortnight, after free purgation by calomel 
 and the administration of digitalis, the patient was much 
 better, free from asthma, and able to walk upstairs, while 
 the liver had gone down to its usual size. The heart 
 remained very large, gave no defined apex beat and only 
 a diffuse general impulse, while a high-pitched mitral 
 murmur, a louder tricuspid murmur of low pitch, and a 
 faint aortic murmur, all systolic, were audible. The action 
 of the heart was curious ; now and then there was a sudden 
 bump against the palm of the hand placed over the right 
 ventricle, and it was found that the beats of the heart were 
 in pairs, only the first of which was accompanied by a 
 systolic apex murmur, the second having a loud first and 
 second sound, but scarcely reaching the pulse. With 
 both beats the loud tricuspid murmur was present. The 
 improvement continued, so that the patient resumed his 
 duties before the end of January, and attended regularly to 
 business through the month of February. In March came 
 another relapse which led to dropsy, and the patient died 
 early in April. Fortunately an examination of the body 
 was permitted, notes of which are as follows : — 
 
 There was much oedema of the legs and right arm, 
 but no fluid in the abdomen. The heart was enormous, 
 measuring six inches and a half from base to apex, and 
 sixteen and a half in circumference. It was flabby, 
 pale, fatty looking, not lacerable. The right auricle was 
 greatly dilated and very thin, the wall being translucent 
 at one part ; the appendix was filled up by solid clot and 
 stained black by blood. The tricuspid orifice took four 
 fingers easily ; there was no roughness. The right ventricle 
 was enormously dilated, and would almost have held a 
 duck's egg ; the walls were thin, soft, and flabby, the valve 
 stained black ; the flaps were thin and the cords delicate. 
 The pulmonary artery and valves were normal. The left 
 
292 HEART DISEASE. 
 
 auricle was not at all dilated, the appendix contrasting with 
 the right, and compared with the other cavities curiously 
 small. The mitral orifice would admit two fingers. The 
 left ventricle, like the right, was enormously dilated, and 
 looked as if it would hold a fist : the walls were thin, 
 mottled, and flabby, but not lacerable ; the papillary 
 muscles were small, the mitral valve and cords quite 
 normal, and remarkably free from thickening. The aorta 
 was very small and the valves normal. 
 
 Physical Signs. 
 
 The pulse in advanced dilatation of the heart is usually 
 irregular in rhythm and unequal in force of beat, and is 
 sudden, short, unsustained, and usually easily compressed. 
 The artery at the wrist may be large or small ; it will be 
 specially large when there has been antecedent high tension 
 which has dilated the arteries. The significance of a pulse 
 of this character is not absolute, as all these characters may 
 be present when there is no recognizable change in the 
 walls, cavities, or valves of the heart, apparently from 
 disordered nervous influence only. The pulse, again, need 
 not be irregular in advanced dilatation of the heart so long 
 as the patient is in repose and the breathing is tranquil 
 and easy. The regularity, however, is easily disturbed by 
 exertion or effort, or by bronchitis, or merely by deep 
 breathing. In moderate and slight dilatation the pulse 
 may be regular, but, while irregularity is the rule, there is 
 no such constant relation between the degree of regularity 
 or irregularity of the pulse and the amount of dilatation of 
 the heart as to make one diagnostic of the other. 
 
 The Heart. — In the examination of the heart, inspection 
 and particularly palpation will be of the greatest importance. 
 The visual examination will be directed to the situation and 
 character of the apex beat and to the impulse of the right 
 
DILATATION. 293 
 
 ventricle. Retraction or bulging of the intercostal spaces, 
 elsewhere than at the visible apex beat, will be noted. 
 
 The apex will be displaced outwards and downwards, 
 and it may be visible over a large area. Very commonly it 
 cannot be seen at all, and the point of maximum apparent 
 impulse does not necessarily belong to the true apex. The 
 right ventricle impulse will be diffuse, if recognizable at all, 
 and as a rule it is inconspicuous. 
 
 Palpation in most cases of dilatation furnishes informa- 
 tion which contributes more to precision of idea as to the 
 actual state of the heart than any other branch of physical 
 exploration. The right hand should be applied closely 
 over the entire cardiac region, the palm over the right 
 ventricle, the fingers, spread out and close together alter- 
 nately, over the apex region. Distinct impulse over the 
 right ventricle, while it indicates more or less obstruction 
 in the pulmonary circulation, indicates also some degree 
 of vigour in this ventricle available for compensatory 
 work. A mere vibration has a converse significance. The 
 first object of attention, however, will be the identification 
 of the point of maximum impulse in the apex region, and 
 a careful estimation of the area over Avhich the apex beat 
 extends, and of its force and character ; whether, for 
 example, it is a mere concussion of the chest wall or a 
 more or less distinct thrust at any point. Sometimes the 
 word "slapping" is employed to describe the impulse or 
 apex beat characteristic of dilatation. Further exploration 
 will be made by pressing the fingers into the intercostal 
 spaces around and beyond the point of maximum impulse, 
 and it must be borne in mind that this impulse may not 
 be the real apex beat, but the impulse of the right 
 ventricle. Sometimes impulse is detected much above the 
 normal situation, in the fourth space perhaps as far 
 outwards as the anterior axillary fold or behind it, or it 
 may be concealed by the female mamma. It may be the 
 
294 HEART DISEASE. 
 
 left edge of the right ventricle resting on the inter- 
 ventricular septum which is here felt, or a part of the 
 rounded apex of the left ventricle. According as the apex 
 is capable of giving a distinct thrust or communicates only 
 a diffuse shock, and, according as the beat is well-defined 
 and steady, or vaguely felt over a considerable area, will 
 be the estimate of the degree of dilatation and of the 
 thickness or thinness of the heart wall. Not unfrequently 
 neither impulse nor apex beat can be detected, or the 
 impulse is so vague that it cannot be localized ; unless 
 this is due to overlapping lung, it indicates great weakness 
 of the muscular walls of the heart. 
 
 By deep percussion the outline of the heart can be 
 more or less accurately mapped out. It is more rounded 
 in the apex region than normal, and the area of dulness 
 is greatly extended to the left. When no impulse of any 
 kind can be felt we may have to depend entirely on 
 percussion for information as to the size of the heart. I 
 have found continuous deep dulness outwards as far as 
 the mid-axillary line and downwards to the seventh space, 
 shown to be cardiac by the intensity of the sounds at 
 the extreme limits, and, when the heart had gained strength, 
 by an apex beat recognizable by palpation at the farthest 
 point. 
 
 Auscultation. — The characteristic modification of the 
 sounds of the heart produced by dilatation is that the left 
 ventricle first sound becomes short ; usually it is also 
 sharper than normal. Probably from this change in the 
 character of the left ventricle first sound it is almost 
 always audible in the aortic area, contrasting in this 
 respect with hypertrophy. It is audible also to the left of 
 the apex beat. When no impulse or apex beat can be 
 felt, the sounds, and especially the first, must be made 
 use of to ascertain how far to the left, the left border 
 and apex of the heart have been carried by the dilatation, 
 
DILATATION'. 
 
 295 
 
 and in what degree the enlargement is due to dilatation 
 or hypertrophy. Percussion, of course, maps out the deep 
 dulness, and shows approximately the limit of the heart 
 and its extension to the left, but the point of maximum 
 intensity of the sounds and the area over which they are 
 audible will corroborate or correct the idea formed as to 
 the size of the heart from percussion, and percussion yields 
 no information whatever as to the kind of enlargement, but 
 leaves it to be supplied by the character of the sounds on 
 auscultation. 
 
 Not uncommonly dilatation of the left ventricle gives 
 rise to a systolic apex murmur, obviously due to mitral 
 incompetence. This is induced by imperfect accomplish- 
 ment of the constriction of the orifice, which is part of the 
 normal contraction of the ventricle, and which co-operates 
 with the curtains of the valves in preventing regurgitation 
 into the auricle. Mitral valvular disease is attended with 
 precisely the same combination of conditions — incompe- 
 tence of the valve and dilatation of the ventricle — and 
 of physical signs — a systolic murmur and displacement of 
 the apex beat with increased cardiac dulness. The prog- 
 nosis is different in the two cases, and it is therefore 
 important to distinguish between them. This cannot 
 always be done by means of physical signs alone, but they 
 may give important information. 
 
 The presence of the left ventricle first sound and its 
 peculiar character in primary dilatation, and its partial or 
 complete replacement by the murmur in a valve lesion will 
 sometimes be of service in differential diagnosis. The 
 age of the patient, and the history of the case, will be of 
 great help, and the mode of onset of the symptoms and 
 their causation should be carefully inquired into. If the 
 patient is middle-aged and the symptoms date from some 
 imprudent over-exertion, the presumption will be in favour 
 of primary dilatation. If there is a history of acute 
 
296 HEART DISEASE. 
 
 rheumatism, there will be little doubt as to the diagnosis, 
 especially if the patient be a child or young adolescent, 
 and there is evidence of compensatory hypertrophy of the 
 right ventricle. 
 
 There is nothing in dilatation of the cavities of the 
 heart to affect specially and directly the second sound, but, 
 in proportion as this condition of the ventricles impairs 
 the propulsive energy of the systole the second sound will 
 be enfeebled, and the aortic second sound is usually weak 
 as compared with the left ventricle first sound. The 
 relative loudness of the sounds therefore enters into the 
 considerations from which may be calculated the efficiency 
 of the ventricle. 
 
 Very important information is often supplied by 
 observation of the intervals between the first and second 
 and the second and first sounds, the short and long pauses 
 respectively. When, with dilatation of the left ventricle 
 there is resistance in the arterioles and capillaries, which 
 is very commonly the case, the interval between the first 
 and second sound may be prolonged, and as this marks 
 the duration of the systole it shows that the ventricle is 
 endeavouring to cope with the difficulty and to complete 
 its contraction. The short or systolic pause may be so 
 prolonged as to equal the diastolic or long pause, and the 
 sounds thus become equidistant, the first also having 
 become short and sharp ; the only difference between the 
 sounds is one of emphasis or of pitch, and it is often 
 difficult to say which is which. The sounds may be 
 compared, when the heart is acting slowly, to the ticking 
 of a clock ; when rapidly, to the puffing of a distant 
 locomotive. 
 
 On the other hand, the first and second sounds may be 
 approximated, and as we cannot suppose that a dilated and 
 enfeebled ventricle completes its systole in a shorter time 
 than normal, the only possible explanation is, that it is 
 
DILATATION. 297 
 
 quickly brought up short by the resistance in the arterial 
 system and expels but a small proportion of its contents. 
 This abbreviation of the systolic pause is therefore a serious 
 indication of failure of the ventricles, and when carried to 
 an extreme, so that the second sound follows the first 
 immediately and almost seems to overtake it, is significant 
 of immediate danger. 
 
 In two successive attacks of symptoms due to dilatation 
 of the heart, when the degree of dilatation appears to be 
 exactly the same, a difference in the length of the systolic 
 interval is sometimes the chief, if not the only, point 
 which makes a difference in the prognosis. The first and 
 second sounds are spaced in the first attack, which is sur- 
 vived, and approximated in the second, which proves fatal. 
 
 Symptoms. 
 
 The symptoms which attend the earlier stages of 
 dilatation are extremely varied and often very vague. An 
 imperfect and fluctuating supply of blood to the brain will 
 give rise to impairment of bodily and mental energy, and 
 to irresolution and vacillation of purpose ; the memory is 
 liable to fail, especially in regard to recent events, and 
 the power of sustained attention and consecutive thought 
 is diminished. The frame of mind will often be despondent, 
 and the temper may be irritable. There may be attacks of 
 giddiness or faintness. Sleep is usually disturbed, and some- 
 times almost absent, and, whether the nights are good or bad, 
 there may be slumber at any period of the day, the patient 
 dropping off to sleep even over his morning newspaper. 
 For the same reason, viz. the irregular and imperfect blood 
 supply and the back pressure in the veins, digestion and 
 the action of the liver will be deranged. The appetite 
 is bad, and food is followed by discomfort and by flatulent 
 distension, which latter again reacts on the heart, and gives 
 
298 HEART DISEASE. 
 
 rise to oppression, or palpitation, or irregular action. The 
 bowels are usually torpid. The urine is deficient in amount 
 and high coloured, and there is often an habitual deposit 
 of urates. Turbidity of the urine day after day, whatever 
 the food and drink, or weather, or mode of life, should 
 direct attention to the state of the circulation. 
 
 There is no one, and scarcely any combination, of the 
 symptoms enumerated, however, which may not occur 
 independently of weakness and dilatation of the heart, 
 especially in states of system attended with high tension ; 
 and it would be waste of time to attempt to disentangle 
 those directly due to the state of the heart from those 
 which are merely accidentally associated with it. 
 
 The special symptom which calls attention to the heart 
 as the probable starting-point of a number of ailments is 
 breathlessness on slight exertion, but even this may be 
 produced by other causes — by anaemia, for example ; after 
 middle age, pernicious ansemia may often give rise to 
 extreme breathlessness, which may excite a suspicion of 
 heart disease. High arterial tension alone, which has not 
 yet given rise to dilatation, simple debility, sedentary habits, 
 with a tendency to corpulence, may also cause shortness of 
 breath. These facts are mentioned in order to warn against a 
 too ready inference that dilatation of the heart exists simply 
 because the breath is short. An interesting fact in connec- 
 tion with breathlessness due to dilatation of the heart is 
 that it is often relieved by exercise of the voice. I have 
 met with several instances in which a clergyman has 
 climbed into the pulpit with the utmost difficulty, and has 
 not only preached a sermon comfortably, but has been 
 all the better for it. A sense of breathlessness coming on 
 during repose, and inciting the patient to make frequent 
 deep inspirations, is usually a symptom of nervous depres- 
 sion, and has no necessary relation to heart disease. Eor 
 the most part, as the disease advances, symptoms arise 
 
DILATATION. 299 
 
 which are indicative of back pressure in the systemic 
 veins, a gradually advancing cedema of the legs, congestion 
 of the lungs, etc. 
 
 In an extreme case the patient will be dropsical, oedema 
 invading the thighs, loins, and abdominal parietes, as well 
 as the legs, and there may be fluid in the abdomen, and 
 perhaps in one or both pleural cavities. The feet and legs 
 will be cold and pale, or purple and livid, especially if hang- 
 ing down ; the hands also will be cold, and are often crimson 
 or purplish, and the nails of a deep or dusky tint, instead of 
 a bright pink. A white patch on the hand, produced by 
 pressure, is very slowly invaded by returning colour. The 
 sufferer is probably unable to lie down in bed, and is 
 propped up by pillows, or he must have his legs down, 
 and therefore spends day and night seated in his chair. 
 Remarkable exceptions, however, are met with in this 
 respect, some sufferers, while extremely ill, being able to 
 lie down without distress. The face is pale, and perhaps 
 puffy, especially under the eyes, with injected capillaries 
 over the cheeks, and wears an expression of distress, and 
 the eyes are watery. The lips are pale or bluish ; the 
 breathing is more or less laboured, even in repose, and 
 the sufferer constantly supplements his reflex respiration 
 by voluntary deep breaths. When he speaks it is in 
 fragmentary sentences, and with evident effort and aggrava- 
 tion of the respiratory distress. The least movement brings 
 on shortness of breath, which is often painful, even to 
 witness. The pulse is frequent, irregular, and probably 
 greatly deficient in tension. The urine will be scanty, of 
 a deep colour, and high specific gravity ; it most commonly 
 throws down a copious deposit of brickdust lithates, and it 
 may contain albumen, the amount of which may vary from 
 day to day. The appetite will be bad, and there may be 
 nausea ; the tongue may be furred, the bowels constipated 
 or irregular. One of the most distressing symptoms is 
 
300 HEART DISEASE. 
 
 sleeplessness, and when, after hours of Aveary shifting of 
 position, the sufferer is overcome by fatigue and drops off, 
 he has painful dreams, and wakes suddenly in affright and 
 suffocation for lack of voluntary help to his respiration. 
 The longest and best sleep will be obtained while sitting 
 in a chair, and sometimes by day rather than in the night. 
 
 The jugulars will be found full, but not, as a rule, greatly 
 distended or pulsating forcibly. The liver will be enlarged, 
 coming down sometimes as low as the umbilicus, and extend- 
 ing across the epigastrium into the left hypochondrium. It 
 will often be jogged by the right ventricle, but does not 
 usually exhibit true expansile pulsation. The jugular dis- 
 tension and pulsation, as was pointed out by Mackenzie of 
 Burnley, may be greatly exaggerated by pressure on the 
 enlarged liver. There may be fluid in the peritoneal or 
 pleural cavities, more commonly not, and there will, in most 
 cases, be physical signs of cedema and congestion of the 
 lungs ; occasionally the percussion note may be good and 
 the entry of air free and unattended with adventitious 
 sounds of any kind to the very base of both lungs. 
 
 Peognosis. 
 
 We may consider first the most serious case where the 
 symptoms present are such as have just been described. We 
 are called upon to answer the question, Has the patient a 
 chance of recovering from the condition described, or will 
 he die ? 
 
 The first element in the judgment to be formed will be 
 the urgency of the symptoms, and special importance will 
 attach to two of the series — the nausea and loss of appetite 
 and the sleeplessness — from the effects which they have 
 on the patient's strength. Frecpient vomiting of food is of 
 very grave import, not only because the patient does not 
 get the benefit of the nourishment, but because it shows 
 
DILATATION. 301 
 
 that the stasis in the abdominal circulation has reached a 
 point which interferes seriously with the digestive secre- 
 tions. Attacks of faintness and of extreme exhaustion, or 
 of severe dyspnoea, are also of serious import. 
 
 It is not always when the dropsy is excessive that the 
 condition of the patient is worst. From the late appearance 
 or entire absence of dropsy in fatty degeneration of the heart, 
 in aortic disease, and mitral stenosis, it would appear that a 
 certain degree of pressure in the arterial system is required 
 to co-operate with the back pressure in the venous system 
 for the full development of dropsical effusion; and when 
 the osdema remains moderate in amount, while other 
 symptoms — such as breathlessness, faintness, and muscular 
 weakness, the latter especially — indicate great cardiac 
 inefficiency, it may be because the left ventricle propels 
 the blood with very little force. Degeneration may be a 
 factor in the case. A frequent, short, unsustained pulse 
 and heart-beat, without much oedema, may thus indicate 
 a more grave condition than extreme dropsy. Long- 
 continued excessive frequency of the pulse is an un- 
 favourable sign. 
 
 The urgency of the symptoms being about the same, a 
 greater degree of dilatation, as indicated by a more extended 
 area of dulness, by marked displacement of and diffuseness 
 and weakness of the apex beat, will add gravity to the prog- 
 nosis. A further unfavourable indication will be approxima- 
 tion of the first and second sounds. 
 
 When the symptoms and physical signs have been well 
 weighed, the first question to be asked in view of prognosis 
 is whether there has been any adequate exciting cause of 
 the symptoms. If there has been recognizable over-exertion 
 or excitement, or grave anxiety- — any mental or bodily 
 strain — or if there has been a chill, giving rise to bronchitis 
 or other affection of the lungs, or deranging seriously the 
 liver and digestive organs, it may be hoped by means of 
 
302 HEART DISEASE. 
 
 rest and treatment to undo the ill-effects and restore the 
 balance. If, on the other hand, the symptoms have crept 
 on gradually without traceable cause of the kind mentioned, 
 and especially when due care has been exercised, and there 
 has been no habitual error of regimen or neglect of bowels, 
 the probabilities are that the symptoms are the outcome of 
 conditions which cannot be reversed — of radical inherent 
 weakness of the heart. 
 
 The previous mode of life, active or sedentary, careful 
 or imprudent, and especially the habits with regard to 
 alcoholic stimulants, will have a very important bearing on 
 the probable issue of the attack, as will also the general 
 soundness and the absence or existence of disease of any 
 other important organs, especially of the kidneys and liver. 
 The patient's cheerfulness, hopefulness, and courage under 
 his sufferings, or his despondency, will make powerfully for 
 or against him, not only as direct influences, but because the 
 state of mind is often an index of the state of the system. 
 
 Another inquiry of great prognostic weight will be as 
 to the patient's family history. It is through this that we 
 obtain an idea of his vital tenacity, of the trustworthiness 
 of his tissues, and of the special liabilities to cardio-vascular 
 degeneration. There are few tendencies which run more 
 strongly in families than those which are manifested in 
 the heart and vascular system, whether to high arterial 
 tension with the effects on the vessels and heart, which 
 follow from this, or to dilatation and weakness, or to 
 degeneration, and a prognosis, otherwise not unfavourable, 
 might have to be instantly revised on learning that the 
 father, an uncle, or a brother, had died at about the patient's 
 age from heart disease. Finally, the response to treatment 
 will speedily afford an indication of the utmost value. 
 
dilatation. 303 
 
 Treatment. 
 
 Mild Cases. — In view of the tendency to dilatation in 
 acute rheumatism and influenza, and after any acute 
 bacterial infection when the heart muscle has been more 
 or less damaged by toxins, a period of rest, with avoidance 
 of any undue exertion, is advisable after any acute illness. 
 Loss of tone of the cardiac muscle, with a certain degree of 
 dilatation of, and, it may be, irritability of, the heart, is 
 especially liable to occur after an attack of influenza, and 
 is frequently associated with mental depression and loss 
 of nerve tone. This class of case is usually much benefited 
 by the " Schott " treatment of baths, as the daily routine, 
 enforced period of rest, the sedative effect of the baths, the 
 change of air and scene, with absence of excitement and 
 mental exertion, is highly beneficial. It is by no means 
 essential that the patient should go to Nauheim, as the. 
 treatment can be carried out at his own home or at various 
 bathing stations in England, e.g. Bath, Buxton, Harrogate, 
 and other places, or, if the patient wishes to go abroad, at 
 numerous other health resorts ; in France, for instance, as 
 pointed out by Huchard, at Chatel Guyon, Salins Moutiers, 
 Koyat, etc., and at various places in Germany. This hydro- 
 therapeutic treatment is usually only necessary in cases 
 in which there is an element of neurosis, cardiac irritability, 
 or mental depression, Avhen the psychological element must 
 be taken into consideration. 
 
 In slight cases of dilatation and loss of tone, a complete 
 holiday from work, with change of air to a bracing climate, 
 will usually suffice. Mild cardiac tonics may be given, 
 and gentle exercise taken, the duration of which should 
 be gradually increased day by day. At first, rest in the 
 recumbent position for at least half an hour before meals 
 should be insisted on. 
 
 Severe Cases, — In the treatment of advanced symptoms 
 
304 HEART DISEASE. 
 
 due to dilatation of the heart, we have to deal at the same 
 time with defective propulsive power on the part of the 
 ventricle, and damming back of blood in the venous system 
 — the former being the primary and principal difficulty — 
 and the indications are to relieve the ventricles of work and 
 give them strength, and at the same time to deplete the 
 venous engorgement. 
 
 This last object must, indeed, be taken first. 
 
 Venesection, the most effectual means of relieving the 
 right side of the heart, is rarely applicable in acute dilata- 
 tion. It is conceivable that under some pulmonary com- 
 plications resulting from chill, the engorgement of the 
 right ventricle and auricle might be such as to make blood- 
 letting the less of two dangers ; but, the initial fault being 
 weakness of one or both ventricles, we cannot trust the 
 heart to adjust itself to a rapid change of any kind, and 
 the right ventricle may not be in a condition to take 
 advantage of the relief afforded it. Usually, however, the 
 venous engorgement is developed slowly, and the indica- 
 tions for venesection do not arise. 
 
 The application of six or eight leeches over the liver is 
 safer, and it will usually effect all that can be done by 
 direct abstraction of blood. The indication for this local 
 bleeding is enlargement of the liver, and, when this is 
 considerable, it rarely fails to afford striking relief. Fre- 
 quently, for example, the patient, who has previously 
 been tortured by sleeplessness, will sleep at once aud some- 
 times for a night or two afterwards. The reason for selecting 
 the hepatic region for the application of the leeches is 
 simply that pain and tenderness felt there are relieved; 
 it is not supposed that blood is drawn from the liver, or 
 that the same amount abstracted elsewhere would not be 
 equally efficacious. The leeches should be followed by a 
 hot fomentation, which, besides encouraging the bleeding, 
 will bring blood to the surface. When the liver is not 
 
DILATATION. 305 
 
 enlarged, and especially if the right ventricle impulse and 
 sounds are weak, there is no advantage to be gained by- 
 leeching. 
 
 Concurrently with the application of leeches a purgative 
 will be given, which will deplete the portal system at the 
 same time that the leeching depletes the systemic veins. 
 Afterwards this will be the principal means of keeping down 
 the venous engorgement. In a large majority of cases, 
 indeed, we have to depend entirely upon purgatives for this 
 purpose, as abstraction of blood by any method is inadmis- 
 sible. It is not a matter of indifference what purgatives are 
 employed. The object of a purgative is not simply to carry 
 off as much fluid as possible and so drain the tissues. This 
 may be the case, perhaps, in ascites from cirrhosis of the 
 liver ; but in heart disease of any kind, and especially in 
 dilatation, much more is to be gained by rectifying the 
 balance of the circulation : the kidneys will then often 
 resume their function and remove the excess of liquid. 
 
 Purgatives, then, may be made to contribute to this ; and 
 before considering them further we must refer to the first 
 object of treatment, the relief of the heart from work and 
 the increase of its vigour. Of these we can be much more 
 sure of the first than of the second ; we can more easily and 
 certainly diminish the resistance in the arterioles and 
 capillaries than we can lend strength and efficiency to the 
 action of the heart, and, without removing the obstruction 
 in the peripheral circulation, it might only do harm to 
 incite the heart — weakened as its structures are — to greater 
 effort to overcome it. Mercurial purgatives have this effect 
 of diminishing arterio-capillary resistance and of lowering 
 arterial tension, and therefore of relieving the heart. This 
 is a fact of clinical experience and observation, and its 
 explanation is a matter of secondary importance, but the 
 hypothesis by which, as it seems to me, it is best explained, 
 is that mercury influences the liver metabolism and promotes 
 
 x 
 
306 HEART DISEASE. 
 
 the elimination of impurities which, when retained in the 
 blood, give rise to resistance in the capillaries. But, 
 whatever the explanation, the fact that the arterial tension 
 is notably lowered by mercurial aperients is one which is 
 confirmed by daily experience. It is remarkable how 
 frequently the statement recurs in works on heart disease 
 that other remedies often fail to act until a dose of calomel 
 or other mercurial preparation has been given. 
 
 Mercurial purgatives, then, have the double effect of 
 depleting the portal system, which relieves the enlargement 
 of the liver and the distension of the right side of. the heart, 
 and of diminishing the resistance in the peripheral circula- 
 tion, and so relieving the left ventricle of stress. Very 
 commonly the best of testimony as to the beneficial character 
 of the result is given by refreshing sleep. The disadvantage, 
 if such it be, that less fluid is carried off than by hydragogue 
 cathartics is often compensated by an increased flow of 
 urine ; and elaterium, gamboge, pulv. jalap, co., and the like, 
 when repeated, give rise to great exhaustion. 
 
 Calomel, then, or blue pill or grey powder, should be 
 given in doses of from 1 to 5 grains, according to the 
 urgency of the case, with colocynth and hyoscyamus or 
 rhubarb, followed by some mild saline. After one or more 
 full doses at the outset, a moderate dose may be given 
 every third or fourth night. The acid tartrate of potash 
 will often co-operate beneficially, both by its action on the 
 bowels and on the kidneys. 
 
 The heart being relieved of work may be urged to more 
 vigorous contraction by digitalis, strophanthus, spartein, 
 squills, caffein, convallaria, apocyanum, the special heart 
 tonics, with which strychnine may usually be combined with 
 advantage. In a case of extreme suffering, digitalis may 
 be given with ammonia, ether, and nux vomica ; in a more 
 chronic stage, with iron, strychnine, and perhaps nitric or 
 hydrochloric acid. Sometimes an effect can be obtained 
 
DILATATION. 3"7 
 
 by giving diuretin or caffein in a cachet, at the same time 
 with digitalis in a mixture, when singly neither seems to 
 be efficacious. Squills, again, may be given with digitalis 
 as in the well-known pill with mercury, or in some liquid 
 combination. Next to digitalis stands strophanthus, which 
 is a most valuable alternative when digitalis seems to 
 produce sickness, as is sometimes the case, or when it fails 
 to exercise a favourable influence on the heart. Sulphate 
 of spartein I have seen to be of great service when digitalis 
 and strophanthus appeared to have exhausted their influence. 
 Of convallaria I have little to say. Apocyanum has, in one 
 or two cases, seemed to carry off dropsy in a remarkable 
 way, but one patient died suddenly when apparently just 
 well. 
 
 It is not necessary to go into greater detail with regard 
 to these remedies. Throughout a case of the kind the 
 medical man has to fight, so to speak, with both hands, and 
 continuous watchfulness will be necessary to meet the 
 vicissitudes which occur, and many changes in method 
 may be required, while the same principles are held in 
 view. 
 
 The prognosis, as has been said, will be greatly influenced 
 by the response to treatment. This will be energetic, 
 especially in the matter of purgatives, in proportion as the 
 symptoms are urgent, and if no favourable effect is produced, 
 the prospect of recovery is very poor. Very commonly 
 improvement takes place up to a certain point, and then 
 progress seems to come to an end. This is a trying stage 
 both to the patient and to the medical man. Change of 
 remedies and new combinations must be tried, both in 
 regard of the aperient and of the tonic, not frequently and 
 capriciously, but with careful study of the results and due 
 allowance of time for obtaining them. Sometimes it does 
 good to suspend all medicines for a few days and start 
 afresh. When the oedema of the legs is considerable, it may 
 
3oS HEART DISEASE. 
 
 be of the greatest service to drain the fluid from the legs. 
 The good result of removing an ascitic accumulation, 
 should this be present, may be still more striking. Even 
 a moderate amount of effusion in the pleural cavity, such 
 as we should not think of dealing with under ordinary 
 circumstances, should be aspirated. A straw may turn the 
 balance either way, and a very slight obstacle may prevent 
 the heart from regaining control over the circulation. It 
 is not always desirable to postpone the removal of fluid till 
 the particular conjuncture described arrives ; it may be an 
 urgent necessity at a very early period. Usually, however, 
 it is prudent to give remedies a chance before resorting to 
 puncture or paracentesis. As regards the method of drainage 
 to be employed, Southey's tubes are, in my opinion, much 
 the best, whether for oedema or ascites, but particularly 
 in case of ascites, as the too rapid removal of the fluid 
 is inadvisable. 
 
 Dropsy. — It has been found that in Bright's disease with 
 oadema and ascites the dropsical fluids are rich in chlorides. 
 Normally, the proportion of chlorides in the blood and 
 urine is a stable quantity, and any excess of chlorides 
 ingested is eliminated in the urine. In Bright's disease 
 there is usually deficient elimination of salts in the urine 
 and an excess in the blood. It is argued, therefore, that 
 when the kidneys are diseased, and there is defective 
 elimination of salts, the accumulation of salts, more 
 especially chlorides in the blood, favours the production 
 of dropsy. Widal, indeed, claims that he can in certain 
 cases of Bright's disease provoke or abolish dropsy at will, 
 simply by the administration or withholding of sodium 
 chloride in the diet. Though this is not altogether proved 
 in the case of cardiac dropsy, it is advisable, in view of these 
 observations, to eliminate from the diet common salt and 
 other chlorides, as far as possible. 
 
 The feeding of the patient through the long course of 
 
DILATATION. 309 
 
 treatment will be a task of extreme difficulty. We have 
 to contend with nausea and distaste for food amounting to 
 disgust ; sometimes the sufferer positively cannot swallow 
 anything requiring mastication. The object to be held 
 in view is to keep down the volume of the blood while 
 maintaining its quality. A small amount of solid or semi- 
 solid food should be taken about every three hours. When 
 the patient is not too ill to take his meals at the accustomed 
 times it is a great encouragement to him to be allowed to 
 do so, and he may then eat what he can of fish, fowl, tender 
 meat, and milk puddings. When the appetite is small 
 the regular meals may be supplemented by intermediate 
 nourishment, such as a beaten-up egg, a little milk, or 
 perhaps a small cup of beef-tea, or a little beef or chicken 
 jelly, or meat extract. Soups and jellies have the dis- 
 advantage of containing little proteid and much liquid, 
 and many extractives and salts, but they are stimulants 
 to the flagging heart. Potted meat sandwiches are a great 
 resource, and the pulp of raw beefsteak can be given in this 
 form, disguised by cooked meat or concentrated gravy. A 
 German method of treatment is to feed patients suffering 
 from cardiac dropsy entirely on raw ham. 
 
 The amount of fluid must be restricted as far as possible, 
 especially that taken with food. Stimulants are usually 
 necessary, but should be kept within limits known to 
 and defined by the medical man. The patient is under 
 a great temptation to resort to them for the relief of 
 faintness, exhaustion, and nausea. Cream of tartar drink 
 may be taken to quench thirst between meals, and in some 
 cases a copious draught of hot water once or twice a day 
 will run through the system rapidly and wash out the 
 organs and tissues without augmenting permanently the 
 volume of the blood or adding to the dropsy. When this 
 is tried it must be ascertained definitely that the amount 
 of urine is correspondingly increased. 
 
3 io HEART DISEASE. 
 
 A question which arises in almost every severe case is 
 whether the patient must be urged to remain in bed or 
 allowed to get up. Bed is undoubtedly the best place for 
 him at first, during what may be called the crisis of the 
 attack, for many reasons ; the rest and warmth protect the 
 heart from the strain of exertion and changes of temperature. 
 On the other hand, the dyspnoea is usually worse in the 
 recumbent posture, even with the shoulders raised, and may 
 be intolerable unless the legs are allowed to hang down ; 
 not unfrequently it is simply impossible for the patient to 
 remain in bed. A suitable chair, therefore, is necessary, 
 with support for the elbows, shoulders, and head, which 
 can be taken advantage of in turn in the frequent 
 changes of position to which the patient has recourse to 
 ease his breathing or elude discomfort, and the quickness 
 and ingenuity of the medical man or nurse in devising 
 expedients may greatly alleviate his sufferings. A bed 
 table or other form of support, upon which the patient may 
 rest his arms or elbows and head when leaning forwards 
 while sitting in his chair, will often be useful. A patient 
 will frequently sleep better in this position than in any 
 other. Perhaps the most common state of things is that 
 the patient is up during the day, and tries to spend more 
 or less of the night in bed. When he cannot at once 
 bear to go to bed at night, he may undress and sit in his 
 chair wrapped in blankets near the bed, when he will 
 often, after a time, be able to lie down and sleep. 
 
 Small doses of morphia may be given hypodermically 
 to enable the patient to get a little sleep and relief from 
 his sufferings. Little benefit can be expected at this stage 
 from the administration of cardiac tonics which will have 
 been freely given at an earlier period. The heart is past 
 recovery, and all that can be done is to treat symptoms 
 as they arise and give temporary relief as far as is possible. 
 
CHAPTER XXI. 
 
 STRUCTURAL CHANGE IN THE RIGHT 
 VENTRICLE. 
 
 PHYSIOLOGICAL DILATATION — HYPERTROPHY AND DILATA- 
 TION — DEGENERATION OF THE MUSCULAR WALLS. 
 
 Dilatation and hypertrophy of the right ventricle are 
 perhaps the most common of all the structural changes 
 to which the heart is subject. Some primary dilatation 
 accompanies all severe exertion, and when the exertion 
 has been inordinate it may be considerable and persist for 
 some time, but unless the muscular fibres have undergone 
 degeneration from age or abuse of alcohol, or a sedentary 
 life, or from recent febrile disease, or diphtheria, there is a 
 wonderful power of recovery. If over-exertion is habitual 
 the dilatation will be neutralized by hypertrophy. In all 
 cases of valvular disease of the left ventricle or of lung 
 disease, such as bronchitis, emphysema, etc., which give 
 rise to obstruction in the pulmonary circulation, dilatation 
 and hypertrophy of the right ventricle follow as a necessary 
 physiological result, as has already been explained in a 
 previous chapter. 
 
 Dilatation and hypertrophy of the right ventricle are 
 thus, for the most part, pathological in name only, and are 
 really compensatory adjustments which neutralize more or 
 less perfectly the effects of valvular or other disease of the 
 left side of the heart, and when compensation is effectual 
 become an indication of the degree of severity of the 
 original disease. 
 
312 heart disease. 
 
 Physical Signs and Symptoms. 
 
 Hypertrophy or Dilatation of the right ventricle carries 
 the apex of the heart to the left and increases the hori- 
 zontal dimensions of the heart. The apex beat may be 
 found at or beyond the vertical nipple line, not unfre- 
 quently in the anterior or even mid-axillary line, when 
 there is also enlargement of the left ventricle. The cha- 
 racter of the apex beat depends more on the left ventricle 
 than the right, but with much dilatation of the right 
 ventricle it is usually diffuse. The area of cardiac dulness 
 will be increased, and, on percussion, it may be found that 
 the area of dulness extends to the right or considerably 
 beyond the right margin of the sternum and upwards to 
 the second rib, in consequence of the dilatation of the 
 right auricle, which usually coexists with the dilatation 
 of the ventricle, which is evident from its pulsation in the 
 epigastrium. 
 
 The degree of hypertrophy is estimated by the force of 
 the right ventricle impulse as communicated to the hand 
 applied over the lower left costal cartilages and the 
 epigastrium, and also by the degree of accentuation of the 
 pulmonic second sound. It is the degree of hypertrophy 
 which is of vital importance, as on this depends the 
 efficiency of compensation. 
 
 The symptoms usually associated with the changes in 
 the right ventricle just described are pulmonary congestion, 
 venous stasis, and dropsy, but these are not so much the 
 effects of dilatation of the right ventricle as the final results 
 of the original disease of the left ventricle or lungs, which 
 the right ventricle has been unable to combat efficiently. 
 
 It has seemed to me that our ideas of the effects of 
 disease of the right ventricle have been too much based 
 upon a study of the symptoms which attend affections of 
 this ventricle secondary to disease of the left ventricle or 
 
HYPERTROPHY & DILATATION OF RIGHT VENTRICLE. 313 
 
 its valves, which therefore are really attributable to the 
 original disease. 
 
 Undoubtedly the supervention of dilatation of the right 
 ventricle and of reflux through the tricuspid orifice allows 
 back pressure to be brought to bear upon the veins, but 
 this only intensifies pre-existing effects and symptoms, and 
 makes no change in their character. 
 
 We are perhaps justified in assuming that the venous 
 back pressure, to which insufficiency of the tricuspid valve 
 will give rise, will in some degree produce the same results, 
 whatever the state of the left side of the heart, and whether 
 or not the tricuspid regurgitation has been caused by 
 obstruction in the pulmonary circulation; but the condi- 
 tions are fundamentally different when the tricuspid reflux 
 is primary. It is not impossible, for example, that a sound 
 and strong left ventricle may come to the aid of the right 
 ventricle, just as the right ventricle so constantly comes 
 to the aid of the left, notwithstanding the great length of 
 the systemic as compared with the pulmonic circuit and 
 the weak blood pressure in the systemic veins. The pressure 
 which will cause the blood to spurt for two or three feet 
 in venesection might carry a current through the capillaries 
 of the lungs aided by the respiratory movements and the 
 valves of the pulmonary artery. 
 
 It has, moreover, seemed to me that weakness of the 
 right ventricle — the left ventricle being in a normal con- 
 dition — has in some cases given rise to symptoms due 
 rather to inadequate supply of blood to the left side of the 
 heart than to damming back of blood in the veins. I have, 
 for example, met with several instances of primary tricuspid 
 regurgitation, either as a constant condition or coming on 
 under very slight provocation. When any effect of this 
 has been traceable it has not been breathlessness on 
 exertion, but tendency to syncope. Perhaps this is what 
 we ought to expect, since the occurrence of tricuspid 
 
314 HEART DISEASE. 
 
 regurgitation in the breathlessness of violent exertion has 
 been regarded as a safety-valve action, by lowering the 
 pressure in the pulmonic circulation. A difference of 
 symptoms ought to attend mitral and tricuspid insuffi- 
 ciency, one giving rise to turgescence and high pressure 
 in the pulmonary circulation, the other to deficient supply 
 of blood and low pressure. If mitral disease produces 
 pulmonary symptoms, tricuspid disease may well produce 
 systemic symptoms. 
 
 In a few cases which have come under my notice, in 
 which the right ventricle has appeared to be predominantly 
 or almost exclusively affected by asthenia or degenera- 
 tion, the effects have been similar to those of tricuspid 
 regurgitation. 
 
 A master in a public school, who had been accustomed 
 to vigorous exercise, received a severe blow on the chest. 
 He had for some time great pain in the cardiac region, 
 and when he walked he soon felt faint. When I saw him 
 some time after the injury he had had slight but distinct 
 syncopal attacks. On examination, no valvular disease 
 was present, and the heart was of normal size. There was 
 a fair apex push in the normal situation, and the left 
 ventricle first sound and the aortic second sound were 
 normal in character. JSTo right ventricle impulse, how- 
 ever, could be detected, and its first sound and the pulmonic 
 second sound were very weak. 
 
 What had happened exactly cannot be stated, but from 
 the contrast between the action and sounds of the two sides of 
 the heart, it seemed as if the right ventricle had been in some 
 way injured, and that its contractile energy was impaired. 
 
 The patient regained the power of taking exercise, and 
 with this the sounds of the right ventricle became normal. 
 
 A patient, aged 72, who had never had a day's illness 
 in his life, consulted me in 1879, complaining of failing 
 vigour, giddiness on running to catch a 'bus, tendency to 
 
HYPERTROPHY &° DILATATION OF RIGHT VENTRICLE. 315 
 
 fall asleep in the day. He was constipated ; the pulse, 
 which was not more than 60, was sometimes tense, some- 
 times soft. The heart sounds generally were weak, the 
 aortic second accentuated. In April, 1881, symptoms, 
 which had previously been relieved, returned, and it was 
 now found that over all parts of the right ventricle, and 
 even over the pulmonic area, there was absolute silence. 
 No impulse or apex beat could be detected, but at the apex 
 the sounds were normal ; the aortic second sound was 
 accentuated. The pulse was 72, a little irregular, but fair 
 in force and length. A month later he was much better. 
 The pulse was 60, fair in strength and length ; the left 
 ventricle sounds were good, the right ventricle sounds 
 faintly audible. From this time neither the right ventricle 
 first, nor the pulmonic second sound were ever at any time 
 audible. The pulse varied considerably both in frequency 
 and in tension, but it was usually well sustained, indicating 
 considerable vigour of the left ventricle, and the left 
 ventricle sounds were good. He had from time to time 
 severe fainting attacks, which sometimes threatened to 
 prove fatal. He was always worse when the bowels were 
 not kept freely open. In June, 1883, the pulse is described 
 as large, full, and tense ; the aortic second sound was 
 accentuated at the apex and in the right second space ; 
 there were no right ventricle sounds whatever. Towards 
 the end of 1884, when not under my care, the bowels were 
 allowed to get confined, and he fell into a condition of 
 torpor, with incontinence of urine and faeces. He recovered 
 from this condition after free purgation, and was again able 
 to go about, though his mental faculties were impaired 
 and he was childish ; but in November, 1885, thrombosis 
 of the left middle cerebral artery took place, giving rise to 
 hemiplegia and aphasia, of which he died. 
 
 The entire absence of right ventricle sounds in this 
 case was very remarkable, and I cannot doubt that there 
 
3l6 HEART DISEASE. 
 
 was a very feeble action of this ventricle. As it seemed to me 
 impossible that the pulmonary circulation could be main- 
 tained without its aid, I formed a very unfavourable 
 prognosis ; and when this was belied I watched the case 
 with extreme care, first to make sure that my observation 
 was not at fault, and next in order that I might arrive at 
 some comprehension of the problem presented by the facts. 
 The conclusion appeared to be unavoidable that the left 
 ventricle was carrying on the circulation through the 
 lungs; it was throughout capable of maintaining high 
 tension in the arteries. The amount of blood passing 
 through the pulmonary vessels under these conditions and 
 reaching the left auricle would be easily influenced, and 
 would vary greatly, and the fluctuating supply of blood to 
 the left ventricle would account for the varying character 
 of the pulse. 
 
 One of the most serious effects of weakness of the right 
 ventricle is met with in disease of the mitral valve. When 
 the mitral valve is incompetent, or from thickening and 
 shrinking of the curtains and tendinous cords becomes 
 stenosed, the right ventricle is for a time the rampart by 
 which the reflux of blood is arrested, or increased pressure 
 in the left auricle is maintained to promote a more rapid 
 flow through the narrowed orifice. When we hear an apex 
 murmur telling of mitral regurgitation or stenosis, the 
 murmur itself gives no trustworthy information as to the 
 severity of the lesion. We gather this mainly from the 
 effects upon the right ventricle. The first of these is 
 accentuation of the pulmonic second sound, indicating 
 increased pressure in the pulmonary circulation, and fol- 
 lowing on this hypertrophy of the right ventricle, by means 
 of which the obstruction to the passage of blood through 
 the lungs is overcome. It is by the augmented strength 
 of the right ventricle that the mitral leakage or obstruction 
 is neutralized and a working equilibrium established. The 
 
HYPER TROPHY & DILA TA TION OF RIGHT VENTRICLE. 3 1 7 
 
 greater the regurgitation or stenosis the greater the amount 
 of hypertrophy required to compensate for it. The change 
 in the right ventricle thus becomes, together with the 
 accompany in g changes in the left ventricle, a measure of 
 the regurgitation or stenosis. 
 
 When, therefore, we detect a mitral murmur, we at once 
 examine the right ventricle in order to gather from its con- 
 dition information as to the amount of reflux or obstruction 
 which is not yielded by the murmur itself. This is specially 
 the case when symptoms of failing compensation have set 
 in. But if the right ventricle is in a state of degeneration 
 or great weakness, as may be the case in lesions established 
 late in life, these indications fail us altogether. The 
 absence of dilatation and hypertrophy, instead of denoting 
 comparatively slight regurgitation or stenosis, shows that 
 the right ventricle is incapable of coping with it. There is 
 no right ventricle impulse, and the pulmonic second sound 
 instead of being accentuated is weak, while dropsy and other 
 evidences of serious stasis and back pressure in the venous 
 system are prematurely developed for lack of hypertrophy 
 or compensatory effort on the part of the right ventricle. 
 
 Under these circumstances the prognosis is extremely 
 srrave. The risrht ventricle is unable to come to the aid of 
 the left, the mechanism of compensation makes default, 
 and the back pressure bears at once upon the venous 
 system. The fulcrum for some of our most efficacious 
 therapeutic measures is missing. We dare not open a vein 
 however great the respiratory embarrassment and cyanosis ; 
 the effect of leeching over the liver is less certainly good, 
 and a dose of calomel is not well borne. Eecovery is rare, 
 and twice it has happened in my experience that during 
 apparent convalescence, when an unfavourable prognosis 
 seemed to have been belied, the patient has died suddenly 
 when beginning to walk about, and the right ventricle has 
 been found degenerated at the autopsy. 
 
3i 8 HEART DISEASE. 
 
 Similar conditions result from time to time from adhesion 
 of the pericardium. The right ventricle suffers proportion- 
 ately more than the left from pericarditis, as its walls are 
 relatively very thin, and when the muscle is damaged by 
 myocarditis the ventricle readily dilates. Again, the right 
 ventricle is much more hampered by adhesion of the peri- 
 cardium than the left, partly because its superficial area is 
 relatively large, but chiefly because of the thinness of its 
 walls ; and when the adhesions are general, and especially 
 if there is also adherence of the pericardium to the chest 
 wall and diaphragm, efficient contraction of this ventricle 
 must be impossible. Cases are not uncommon in which 
 there is valvular disease, mitral or aortic, but from the size 
 of the heart, the position and character of the apex beat 
 and impulse, the persistence of sounds in spite of the 
 murmurs, there are grounds for concluding that the valvular 
 lesion is not very severe. There is, however, a premature 
 development of symptoms. Under such circumstances, we 
 may often confidently infer adhesion of the pericardium 
 when it cannot be demonstrated with any certainty by 
 physical signs. This has already been discussed in the 
 chapter on adherent pericardium. 
 
 The right ventricle is undoubtedly sometimes the cause 
 of sudden death, and when the heart is embarrassed or 
 stopped by pressure upwards of the diaphragm by a dis- 
 tended stomach or colon, it must be on the right ventricle 
 that the pressure takes effect. This part of the heart rests 
 upon the diaphragm, and will be directly compressed when 
 it is pushed up. Probably it is the diastole which is 
 mostly interfered with, and it would seem that the proper 
 expansion and filling of the ventricle must be impossible 
 when the pressure upon it is such that the heart is carried 
 up bodily by the diaphragm, especially when the ventricle 
 is dilated and over-distended. A melancholy illustration 
 of this occurred in my experience in the case of an eminent 
 
HYPER TROPHY &> DILA TA TION OF RIGHT VENTRICLE. 3 1 9 
 
 artist. He was suffering from mitral stenosis and regurgi- 
 tation, and had overthrown the compensation established by- 
 hypertrophy of the right ventricle by serious imprudence in 
 the form of over-exertion and exposure undertaken to remedy 
 the effects of overwork. There was an extreme degree of dis- 
 tension of the right side of the heart, with tricuspid regur- 
 gitation, and he suffered from sleeplessness and dyspnoea, 
 so that his misery was insupportable, and life was despaired 
 of. The application of leeches over the liver, which was 
 enormously swollen, and the administration of calomel, at 
 once gave him sleep, and by a repetition of the leeches and 
 regular employment of mercurial aperients, with the usual 
 heart tonics, he so far recovered as to be able to leave his 
 room, and his convalescence seemed to be assured. 
 
 One morning, after a hearty breakfast in bed, the nurse 
 was about to wash his face and hands as usual, but he 
 impatiently bade her give him the basin, and stand aside. 
 He sat up in bed with the basin between his knees, and 
 when the time came for washing his face, bent forwards over 
 it. The pressure upwards of a full stomach caused by this 
 movement brought the weak right ventricle to a standstill, 
 and the patient fell back dead. 
 
 One cannot help being reminded, in relating this incident, 
 of the rough and ready, but effectual, way in which a man 
 is brought to who faints after the severe exertion of a 
 boat race. He is seated on the ground, and his body is 
 bent forcibly forwards, so that his head almost comes to the 
 ground between his knees, or, if he has fallen forwards over 
 his oar, it is done while he is in the boat. The modus 
 operandi of the remedy is pressure on the distended right 
 heart, and, when emetics are resorted to in bronchitis, which 
 has gone on to the production of cyanosis, the good effect is 
 due, not only to the emptying of the bronchial tubes, but 
 to unloading of the right auricle and ventricle by compres- 
 sion in the act of vomiting. 
 
CHAPTER XXII. 
 DISEASE OF THE CORONARY ARTERIES. 
 
 ATHEROMA OE SCLEROSIS — ENDARTERITIS — THROMBOSIS — 
 EMBOLISM — ANEURYSM. 
 
 Disease of the coronary arteries is very common, and is of 
 the first importance, inasmuch as they constitute the sole 
 blood supply to the heart, and obstruction to the flow of 
 blood through them from disease of their walls may be a 
 cause of sudden death, or give rise to degenerative change 
 in the cardiac muscle which eventually occasions heart 
 failure. 
 
 Atheroma or sclerosis is the commonest affection of the 
 coronary arteries. The terms " atheroma " and " sclerosis " 
 are employed indiscriminately to denote the same affection, 
 though, strictly speaking, atheroma etymologically means 
 " a gruel-like condition," and sclerosis " a hardening." 
 
 Probably this confusing nomenclature has originated 
 from the presence in the aorta of patches of softening and 
 ulceration, whereas arteries when affected are hard, firm, 
 and inelastic to the touch. Hence the term " atheroma " 
 is commonly employed to denote degenerative changes in 
 the aorta, and " sclerosis " similar changes in the smaller 
 arteries. Pathologically, however, and to a great extent 
 etiologically, the conditions are identical. 
 
 The general question of atheroma is discussed in a later 
 chapter. For the present we are chiefly concerned with 
 the effect on the heart of degenerative changes in the 
 coronary vessels. 
 
DISEASE OF THE CORONARY ARTERIES. 321 
 
 Morbid Anatomy. — The coronary arteries are thickened, 
 inelastic, and hard. Their lumen may be partially 
 obstructed by small whitish, opaque projections, so that on 
 section they have the appearance of a signet ring, with the 
 signet turned inwards, or the lumen may be almost 
 occluded by a uniform thickening which involves the whole 
 
 FlO. 19a. — SECTION OP CORONARY ARTERY SHOWING ADVANCED SCLEROSIS. A, 
 GREATLY THICKENED INTIMA ; B, INTERNAL ELASTIC LAMINA ; C, MUSCULAR 
 COAT ; D, ADVENTITIA. AT X THE MUSCULAR COAT IS ALMOST DESTROYED, 
 AND PATCHES OF CALCIFICATION ARE SEEN IN THE DEGENERATED TISSUE 
 BENEATH. 
 
 circumference. On microscopic examination of a section 
 through one of these projections, it is seen to consist of a 
 swelling immediately beneath the endothelium, which is 
 pushed inwards ; externally it is usually limited by the 
 internal elastic lamina. The muscular coat beyond this 
 may be atrophied from pressure, or may in advanced disease 
 be involved in the degenerative process and to a great 
 
 Y 
 
322 HEART DISEASE. 
 
 extent destroyed. The swelling is seen to consist of 
 amorphous non-staining debris, in which may be distin- 
 guished strands of hyaline degenerated tissue, and small 
 atrophic nuclei of cells which vary greatly in number in 
 different stages of the disease. ( Vide Fig. 19a.) Frequently 
 calcareous patches are present from deposit of lime salts 
 in the degenerated tissue. 
 
 The condition would seem to suggest necrosis of the 
 subendothelial tissue either from toxic influences or from 
 imperfect nutrition, followed by swelling of the necrotic 
 tissue and a futile attempt at repair, the latter being 
 evidenced by the presence of the cellular infiltration, which 
 appears to consist of atrophic connective tissue cells. 
 
 Huchard regards endarteritis obliterans of the vasa 
 vasorum, which may be due to a variety of causes, as the 
 most important etiological factor in this primary necrosis. 
 Some consider that proliferation of connective tissue cells 
 beneath the endothelium is the first stage in the process, 
 occurring as a result of irritation due to intermittent strain, 
 or to some toxic substance, and that necrosis of this newly 
 formed tissue follows. Be this as it may, the important 
 point is, that narrowing of the lumen of the coronary 
 arteries and its branches results, and consequently obstruc- 
 tion to the flow of blood through them ; moreover, even in 
 the absence of pronounced obstruction, the rigidity and loss 
 of elasticity in the vessels and the presence of calcareous 
 plates in their walls seriously impair the circulation in 
 the heart. Hence may result sudden death, angina pectoris, 
 and various degenerative changes in the heart muscle 
 described in the following chapters. 
 
 Endarteritis obliterans of syphilitic origin, or possibly 
 due to other toxins, may affect the coronary arteries. 
 
 In this affection there is active proliferation of the cells 
 of the endothelium which is not followed by degenera- 
 tive changes, so that there is uniform thickening of the 
 
DISEASE OF THE CORONARY ARTERIES. 323 
 
 vessel with narrowing of its lumen, and actual obliteration 
 may ensue in some of the smaller branches of the coronary 
 artery. It is frequently accompanied by periarteritis or 
 thickening of the adventitia. 
 
 Thrombosis. — This usually occurs in association with 
 sclerosis of the coronary arteries, the diseased condition of 
 the vessel wall and the narrowing of its lumen contributing 
 to the result. Obstruction at the mouth of the coronary 
 artery from atheroma of the aorta involving its orifice, or 
 from a thrombus attached to a diseased aortic valve, may 
 also be a contributory factor. Slowing of the blood stream 
 in a failing heart is also an important cause. 
 
 Infarction. — There are anastomoses between the main 
 trunks of the coronary arteries, but there are no anasto- 
 moses between the smaller branches after they have entered 
 the myocardium. The intramuscular branches are there- 
 fore "terminal arteries" in Cohnheim's sense of the word, 
 and infarction results when they are occluded by thrombosis 
 or embolism. 
 
 Infarcts of the heart are not typically wedge-shaped, as 
 in the kidney or lung, but are somewhat irregular in 
 outline, those I have seen being oblong, tapering at the 
 distal end. They are usually anaemic, of a pale yellowish 
 colour, sometimes surrounded by a zone of hyperemia. 
 Microscopically they show coagulation necrosis of the 
 portion of muscle cut off from its blood supply. They 
 may break down and give rise to an aneurism or to rupture 
 of the heart, or they may be gradually absorbed and 
 replaced by fibrous tissue. 
 
 Thrombosis of one of the main trunks of the coronary 
 artery may be a cause of rapid death. Cases are, however, 
 on record which show that thrombosis of a large branch 
 may occur without causing death. This may be explained 
 by the fact that there are anastomoses between the main 
 branches of the coronary arteries, and if the thrombosis is 
 
324 HEART DISEASE. 
 
 gradual in onset, sufficient time may elapse for efficient 
 collateral circulation to be established. Much will, of course, 
 depend on the size of the thrombus and its situation, and 
 whether or not it blocks the mouth of an anastomosing 
 branch. 
 
 There are no characteristic physical signs or symptoms 
 by which thrombosis of the coronary vessels can be 
 diagnosed. 
 
 It is probably of much commoner occurrence than is 
 generally supposed, and it is possible that it may cause 
 attacks of angina pectoris or precordial pain, and be 
 responsible for a certain proportion of cases of sudden 
 death which are put down to other causes, such as fatty 
 degeneration of the heart, etc. A systematic investigation 
 of the coronary arteries throughout their course is not 
 commonly made at post-mortem examinations, and my 
 attention was drawn to the subject in investigating a case 
 of Bright's disease in which the heart was enormously 
 hypertrophied, where I found two infarcts in the wall of 
 the left ventricle, with extensive thrombosis of two branches 
 of ihe left coronary artery. The thrombosis was not evident 
 till I laid open the walls of the vessel throughout their 
 course in searching for an explanation of the infarcts. The 
 patient died from uraemia, and not from the coronary 
 thrombosis, which from the microscopic appearances of the 
 infarcts had apparently taken place some little time 
 before. 
 
 Embolism. — This is far less common, according to Welch,* 
 than thrombosis. It may occur in pernicious endocarditis 
 from detachment of a fragment of an affected valve, or 
 possibly in atheromatous degeneration of the aorta, from 
 detachment of a portion of a thrombus adherent to the 
 diseased surface. Embolism of the coronary arteries gives 
 rise to results similar to those of thrombosis described 
 * Allbutt's " System of Medicine," vol. vi. p. 281. 
 
DISEASE OF THE CORONARY ARTERIES. 325 
 
 above, namely, sudden death or infarction, according as a 
 main branch or an intramuscular branch is affected ; but 
 whereas death due to thrombosis may be preceded by pre- 
 monitory symptoms from the more gradual nature of the 
 onset of thrombosis, death due to embolism must, when it 
 occurs, be absolutely sudden. 
 
 Aneurysm of the coronary arteries is rare. It may 
 result from local weakening of the vessel by atheroma or 
 syphilitic disease, or from acute softening of the arterial 
 wall due to lodgment of septic emboli on its inner aspect 
 in pernicious endocarditis. 
 
 Huchard* gives an account of eleven cases which he has 
 collected from international literature. In all except two 
 the aneurysms were associated with atheromatous degenera- 
 tion of the coronary vessels. In the remaining two the 
 patients were young, 21 and 22; the aneurysms were 
 multiple ; pyrexia was present in one case of obscure origin, 
 in the other the patient had suffered from malarial fever. 
 In nine of the cases sudden death occurred from rupture of 
 the coronary aneurysm. 
 
 In the St. Mary's Hospital Museum is a specimen with 
 thirteen small aneurysms of the coronary artery of embolic 
 origin, from a case of pernicious endocarditis in a girl aged 
 ten. 
 
 There are no symptoms or physical signs by which 
 aneurysm of the coronary arteries can be diagnosed during 
 life. They must, however, necessarily impair the circulation 
 in the heart, and most commonly they rupture and cause 
 sudden death. 
 
 * " Mai. du Coeur," vol. i. pp. 232 et seq. 
 
CHAPTER XXIII. 
 AFFECTIONS OF THE MYOCARDIUM. 
 
 ACUTE MYOCARDITIS — FIBROID CHANGE — ETIOLOGY AND 
 MORBID ANATOMY — SYPHILITIC AFFECTIONS OF THE 
 MYOCARDIUM — PHYSICAL SIGNS AND SYMPTOMS OF 
 FIBROSIS —DIAGNOSIS— PROGNOSIS — TREATMENT. 
 
 Acute interstitial myocarditis occurs most commonly in 
 association with pericarditis or endocarditis. It is not 
 simply due to direct extension of the inflammatory process 
 from the pericardium or endocardium along the connective 
 tissue network to the subjacent muscular substance, but, 
 as Poynton * has shown, in rheumatic pericarditis and 
 endocarditis there is usually a general "carditis," a term 
 suggested by the late Dr. Sturges, and implying inflam- 
 mation of the heart throughout its substance. 
 
 Morbid Anatomy. — The inflammatory changes are usually 
 best marked in cases of subacute pericarditis that prove 
 fatal. On microscopic examination, the nuclei in the inter- 
 stitial tissue are seen to be increased in number owing to 
 exudation of leucocytes between the muscle fibres and pro- 
 liferation of the connective tissue cells. In pernicious 
 endocarditis large masses of micrococci, surrounded by an 
 inflammatory zone of polynuclear leucocytes, may some- 
 times be seen in the substance of the heart wall as shown 
 in the illustration (Fig. 20), where the muscle fibres in 
 the neighbourhood are destroyed and broken up. The 
 
 * Med. Chi. Trans., May, 1899. 
 
ACUTE MYOCARDITIS. 
 
 327 
 
 muscular fibres are affected iu varying degree, those near 
 the surface, as a rule, more than those in the deeper layers. 
 Of some, nothing will remain but a mass of granular 
 material ; others have lost their striation, and are swollen 
 and opaque; others are in a state of cloudy swelling, and 
 some may appear to be little altered. The changes will 
 be more marked and general in proportion to the duration 
 and severity of the inflammation. 
 
 FIG. 20. — SECTION OP HEART MUSCLE FROM A CASE OF PERNICIOUS ENDO- 
 CARDITIS, SHOWING ACUTE INTERSTITIAL MYOCARDITIS. MASSES OF 
 MICRO-ORGANISMS ARE SEEN AT A, A, A, AND THERE IS 'WIDESPREAD 
 INFILTRATION OF POLYNUCLEAR LEUCOCYTES WITH DESTRUCTION OF 
 MUSCLE FIBRES. 
 
 Physical Signs. — In the early stages, acute myocarditis 
 gives rise to no definite physical signs or symptoms by 
 which its existence can be diagnosed with any degree of 
 certainty. When present, the physical signs will be those 
 indicative of progressive cardiac dilatation or asthenia, or 
 of both combined. The signs of cardiac dilatation will be, 
 increase in the area of cardiac dulness with displacement of 
 the apex beat downwards and outwards, and weakening of 
 
328 HEART DISEASE. 
 
 the first sound, the impulse becoming, at the same time, 
 diffuse and tapping in character. The signs of cardiac 
 asthenia will be feebleness or loss of the apex beat, with 
 weak and short heart sounds, and a frequent, short, and 
 easily compressible pulse. When acute myocarditis occurs 
 in association with pericarditis of rheumatic origin, the 
 cardiac dilatation is rapid and considerable, and signs of 
 cardiac weakness and embarrassment appear early in the 
 course of the disease. 
 
 Prognosis. — The prognosis depends on the extent to which 
 the cardiac muscle is affected by the inflammatory process. 
 Myocarditis is, however, almost invariably associated with 
 pericarditis or endocarditis, affecting the prognosis in these 
 affections very materially. This has already been referred 
 to in the chapter on pericarditis, where the prognosis of 
 the combined affections is fully discussed. After the acute 
 attack has subsided, the muscle fibres which have been 
 destroyed are replaced by fibrous tissue, which leads to 
 serious weakening of the heart wall. Consequently, the 
 heart will be liable to break down under any unusual 
 exertion, and the various symptoms associated with fibroid 
 changes in the heart walls may set in at a later period. 
 
 Treatment. — There is no special treatment beyond that 
 for the pericarditis and rheumatism usually associated 
 with it. 
 
 Cloudy Swelling. — Under the head of myocardial in- 
 flammation are included the changes in the cardiac muscle, 
 known as " cloudy swelling," or albuminoid degeneration, 
 which occur in certain diseases attended by high and pro- 
 longed fever, such as septicseinia, pneumonia, enteric fever, 
 scarlet fever, rheumatism, etc. Cloudy swelling is not 
 confined to the heart, but is found at the same time in the 
 liver, kidney, and spleen, and appears to be due, mainly, 
 if not entirely, to toxins evolved by the micro-organisms 
 which are responsible for the disease. The changes differ 
 
CLOUDY SWELLING. 329 
 
 from those found in acute interstitial myocarditis just 
 described, inasmuch as they are mainly confined to the 
 muscular fibres. 
 
 Morbid Anatomy. — The interstitial tissue is not as a 
 rule affected, though some cellular exudation may be 
 present, the changes being chiefly manifest in the 
 muscle fibres. These are swollen, their striation is indis- 
 tinguishable, and they are rendered opaque by the fine 
 granules which pervade their substance and obscure their 
 nuclei. The granules are composed of an albuminoid 
 material, soluble in acetic acid, after treatment with which 
 the muscular fibres seem to almost regain their normal 
 appearance. The condition of cloudy swelling is frequently 
 followed by fatty degeneration of the muscle fibres, if the 
 fever is prolonged or the toxaemia is severe. 
 
 Physical Signs and Symptoms. — The physical signs and 
 symptoms are those of progressive cardiac asthenia. The 
 first sound of the heart becomes gradually weaker and 
 shorter, and the apex beat more and more feeble till it is 
 scarcely perceptible. There is seldom any marked dilata- 
 tion of the ventricles in the earlier stages, as is the case 
 in the interstitial myocarditis of rheumatism. The pulse 
 is increased in frequency, easily compressible, and often 
 markedly dichrotic. 
 
 Prognosis. — The prognosis is that of the disease to which 
 the cardiac condition is secondary. 
 
 Treatment. — Stimulants such as brandy or ether may be 
 necessary, together with strychnine, which is usually more 
 effective when given hypodermically. Sometimes digitalis 
 in small doses is of benefit during convalescence, but it 
 should not be given while fever is present, as the damaged 
 muscle fibres are not in a condition to profit by increase of 
 tone, and the increase of peripheral resistance would entail 
 more work on the heart. 
 
33° HEART DISEASE. 
 
 Fibroid Change in the Heart Walls. 
 
 Two main varieties of fibroid change in the heart wall 
 may be distinguished — 
 
 (1) A substitution of fibrous tissue for muscle fibres 
 which have been damaged or destroyed by disease. 
 
 (2) A patchy or diffuse fibrosis of the heart associated 
 with marked degenerative changes in the coronary vessels. 
 The question as to whether this fibroid change is a direct 
 result of disease of the coronary vessels, or whether it is the 
 result of a chronic interstitial inflammation, or whether 
 some of these cases should be classified in Group I., will 
 be discussed later. 
 
 Etiology. — 1. In the process of repair, cicatricial fibrous 
 tissue may take the place of muscle fibres destroyed by 
 acute myocarditis due to some acute bacterial infection, 
 by gummata, or by acute softening the result of embolism 
 or thrombosis of branches of the coronary arteries. 
 
 Huchard * gives a remarkable illustration of areas of 
 dense fibrosis in the heart wall, produced experimentally by 
 Mollard,f by repeated inoculations of diphtheria toxin, 
 the fibrous tissue having been formed in the process 
 of repair to replace the muscle fibres which have been 
 destroyed by the toxin. This important experimental 
 evidence shows that acute toxaemias may be responsible, if 
 the patient recovers, for areas of dense patchy fibrosis, which 
 later on may give rise to apparently unaccountable symptoms 
 of myocardial weakness. In a very extreme case of fibrosis 
 of the heart, which I mounted for the St. Mary's Hospital 
 Museum, and which is figured in the text (Fig. 21), about 
 two-thirds of the heart wall consists of dense fibrous tissue. 
 The endocardium was also of a dense white opaque colour, 
 
 * " Maladies du Cceur," vol. i. p. 214. 
 
 | " Sclerose du Myocarde," Ann. de VInstitut Pasteur, 18D7. 
 
FIBROSIS OF THE MYOCARDIUM. 331 
 
 and the mitral valve were thickened and rigid, though there 
 
 FIG. 21.— HEART SHOWING AN EXTREME DEGREE OF FIBROSIS 
 OF THE WALLS AND ENDOCARDIUM. 
 
 was no actual loss of substance. The coronary arteries were 
 patent, and not rigid or thickened. The heart was dilated, 
 
332 HEART DISEASE. 
 
 but not hypertrophied. Microscopically, the white opaque 
 tissue, of which the bulk of the heart wall consists, was seen 
 to consist of very dense old fibrous tissue, in which here and 
 there were seen muscular fibres isolated from their fellows, 
 some in a fair state of preservation. The vessels were not 
 obliterated or markedly narrowed. The condition suggests 
 that this cicatricial fibrous tissue has replaced muscular 
 fibres destroyed at one time by a severe toxaemia, possibly 
 the result of acute endocarditis, with accompanying myocar- 
 ditis. The heart was obtained from a woman aged 61, who 
 was brought in dead to St. Mary's Hospital, having suc- 
 cumbed to a sudden syncopal attack. Unfortunately, 
 therefore, no history could be obtained. 
 
 2. Weigert drew attention to what he considers an im- 
 portant cause of fibroid changes in the heart wall, namely, 
 sclerosis of the coronary arteries. He states that when the 
 cardiac circulation is slowly interfered with by sclerosis of 
 the coronary arteries, atrophy of the muscle fibres takes 
 place without destruction of connective tissue, and that 
 the shrunken and atrophied fibres are gradually replaced 
 by fibrous tissue. 
 
 Huchard * also considers that obliterative lesions or 
 endarteritis of the coronary arteries are the most common 
 cause of patchy fibrosis, or, as he terms it, of "sclerose 
 dystrophique." He holds that the fibrosis is the result of 
 a primary degenerative change in the muscle fibres due to 
 their deprivation of nutriment, and that this necrosis of 
 the muscle fibres sets up an irritative proliferation in their 
 neighbourhood, with resulting formation of fibrous tissue. 
 He gives illustrations f of patchy fibrosis in the heart 
 wall with obliterated vessels in their neighbourhood, and 
 states that " there is never well-marked sclerosis without 
 accompanying endarteritis." % 
 
 * "Maladies du Cceur," vol. i. t Ibid., pp. 215, 240, 241. 
 
 X Ibid., p. 242. 
 
FIBROSIS OF THE MYOCARDIUM. 333 
 
 He considers that a diagnosis can be made between chronic 
 myocarditis and what he terms " sclerose dystrophique." In 
 both affections symptoms of myocardial weakness will be 
 a prominent feature, namely, dyspnoea on exertion, feeble- 
 ness of the apex beat and the first sound, enlargement of the 
 area of cardiac dnlness, and perhaps congestion of the bases 
 of the kings from dilatation and back working. Certain 
 symptoms, however, will be peculiar to "sclerose dystro- 
 phique," for inasmuch as it is due to sclerosis of the cardiac 
 vessels, there will be evidence of vascular degeneration else- 
 where, or of high arterial tension, which is usually associated 
 with it, namely, thickening of the radials, dilatation of the 
 aorta, tortuous degenerated brachials, and possibly cerebral 
 haemorrhage may occur. 
 
 In addition, there may be angina pectoris from the 
 narrowing of the coronary arteries. 
 
 Lindsay Steven,* in a paper on the subject, gives a 
 series of twenty-one cases of cardiac fibrosis, which bear 
 out Weigert's observations, and in a later communication, f 
 discussing the difficult question as to why obstruction 
 to the coronary circulation should in some cases give rise to 
 fatty degeneration and in others to fibrosis, comes to the 
 following conclusion : — 
 
 " In cases where the main coronary artery is slowly 
 obstructed, and at last completely occluded at its origin, 
 generalized fatty degeneration is likely to occur, and the 
 cause is similar to that in profound anaemia, namely, 
 deterioration in the supply of blood to the whole organ. 
 
 " When smaller branches are slowly obstructed but the 
 main branches remain patent, slight fatty degeneration 
 may result with localized fibrosis." 
 
 He bases his conclusions on a study of twenty-one cases, 
 in nine of which fatty degeneration was present as well as 
 fibrosis. In nearly all his cases the heart was hypertrophied, 
 * Journal of Path, and Bact., 1894. f Lancet, 1887, vol. ii. 
 
334 HEART DISEASE. 
 
 nd in nine there was chronic interstitial nephritis and in 
 seven atheroma of the aorta. 
 
 It is easy to conceive, and we have ample evidence that 
 sclerosis of the coronary arteries may give rise to fatty 
 degeneration and atrophy of the muscle fibres by interference 
 with their nutrition, but it is difficult to understand how it 
 can give rise to fibrosis, though the two conditions are 
 undoubtedly very frequently associated. Huchard considers 
 that the narrowing of the coronary arteries causes death of 
 the muscle fibres supplied by its terminal branches, and 
 that this necrobiosis sets up an irritative inflammation in 
 the adjoining areas. 
 
 Some authors consider that fibroid change in the heart 
 is the result of chronic inflammation. Bristowe applied 
 the term "cirrhosis" of the heart to this condition, and 
 Friedreich and Lancereaux speak of chronic interstitial 
 myocarditis as responsible for cardiac fibrosis. 
 
 Gibson * includes under the head of chronic myocarditis 
 all conditions in which there is general or local increase of 
 fibrous tissue in the myocardium. Among the causes he 
 
 includes — 
 
 (1) Factors modifying the condition of the blood, e.g. 
 lithoemia, glycsemia, and faulty conditions of the blood 
 arising from defective metabolism. 
 
 (2) Infective diseases such as enteric fever, also 
 syphilis. 
 
 (3). All changes in the coronary arteries, whether affecting 
 their walls or lumen. 
 
 Huchard considers that a true chronic interstitial 
 myocarditis is rare, if, indeed, it occurs, as he holds that 
 destruction of muscle fibres precedes fibrosis, and that this 
 is most commonly dependent on sclerosis of the coronary 
 vessels. 
 
 In examining hypertrophied hearts from cases of 
 * "Diseases of the Heart and Aorta," p. 681. 
 
FIBROSIS OF THE MYOCARDIUM. 335 
 
 Bright's disease, in which there was slight diffuse interstitial 
 change or fibrosis, I have found that the most marked 
 change was in the muscle fibres, namely, swelling, absence 
 of staining, and breaking up of the nuclei (karyorhexis), as 
 in Fig. 22, at the poles of which in the muscle fibres were 
 granules of brown pigment, similar to those seen in brown 
 atrophy of the heart. In these cases death had occurred 
 from cerebral liEeinorrhage, and not from heart failure. 
 
 In other cases of hypertrophied hearts associated with 
 
 FIG. 22. — SECTION OP MUSCLE FROM HYPERTROPHIED HEART, SHOWING 
 SWELLING, LOSS OP STAINING REACTION, AND BREAKING UP OF NUCLEI, 
 WITH DEPOSIT OF GRANULES OF BROWN PIGMENT AT THEIR POLES. 
 
 high arterial tension and general arterio-sclerosis, not attri- 
 butable to Bright's disease, in which death occurred from 
 heart failure, I have found similar changes in the muscle 
 fibres, with areas of patchy fibrosis, as seen in Fig. 23. 
 These would come under Huchard's category of "sclerose 
 dystrophique," as they were associated with atheroma of 
 the coronary arteries and general arterio-sclerosis. 
 
 Possibly, in some cases of cardiac fibrosis associated with 
 atheroma of the coronary arteries, destruction of muscle 
 
336 HEART DISEASE. 
 
 fibres and substitution of fibrous tissue for them occurs at 
 an earlier date than the degenerative changes in the 
 vessels, as a result of some acute toxsemia. Later on the 
 vessels are affected, and sclerosis of the coronary arteries 
 takes place, which would tend to cause fatty degeneration 
 in muscle fibres previously undamaged, and thus explain 
 the presence of fibrosis and fatty degeneration side by 
 
 
 / t ' 
 
 I ■ 
 
 J - 
 
 
 
 :^J«< 
 
 
 FIG. 23. — SECTION OF HEART WALL, SHOWING AREA OP FIBROSIS ASSOCIATED 
 WITH ATHEROMA OF THE CORONARY ARTERIES. 
 
 side in the same heart, as drawn attention to by Lindsay 
 Steven. 
 
 It is probable that syphilis is an etiological factor in a 
 certain proportion of cases, fibrosis resulting either from 
 cicatrization of gummata, or possibly occurring in association 
 with endarteritis and periarteritis of the coronary vessels. 
 
 The illustration (Fig. 24) is a striking instance of 
 fibrosis associated with extreme narrowing of the smaller 
 
FIBROSIS OF THE MYOCARDIUM. 337 
 
 branches of the coronary arteries, the lumen of which was 
 almost obliterated. The specimen came from a woman 
 aged 37, who died suddenly. The heart was hypertrophied, 
 and the aorta was atheromatous, but there was no kidney 
 disease. The age of the patient and the condition of the 
 vessels, which is that of endarteritis obliterans, strongly 
 suggest syphilis as the cause. 
 
 Syphilitic affections of the heart wall are not very 
 
 
 
 
 '•— /j® 
 
 FIG. 24. — SECTION OF HEART WALL, SHOWING FII5R0SIS ASSOCIATED WITH 
 ENDARTERITIS OBLITERANS PROBABLY OF SYPUfLITIC ORIGIN. 
 
 common, but are doubtless frequently overlooked. Sidney 
 Phillips,* in a paper on this subject, recorded twenty-five 
 cases described by various authors, together with some 
 which had come under his own observation. In the majority 
 of these cases gummata were the lesions found, and the 
 diagnosis was only made on the post-mortem table. 
 
 Physical Signs and Symptoms. — In cases associated with 
 coronary sclerosis and general vascular degeneration, the 
 
 * Lancet, 1897, vol. i. p. 223. 
 
 Z 
 
338 HEART DISEASE. 
 
 patient, usually middle-aged or elderly, may complain of 
 breathlessness, palpitation, precordial oppression, or of 
 anginoid pains. He will usually be a man who lias lived 
 well, or who has led an arduous and strenuous life. The 
 arterial tension will be high and the radial vessel thickened 
 somewhat. The heart will be hypertrophied to a varying 
 degree. There will usually be breathlessness on exertion, 
 and possibly slight oedema of the legs, which subsides after 
 a night's rest in bed. The pulse may be irregular, and 
 the arterial tension moderate or low, because of the failing 
 power of the heart. A sudden syncopal attack may prove 
 fatal before any symptoms of a nature to cause anxiety 
 have arisen. This is especially liable to occur in cases 
 where there is marked narrowing of the coronary arteries or 
 rigidity due to degenerative changes, and the sudden death 
 is to be attributed to this cause and resulting ischemia of 
 the heart rather than to the fibroid changes in the cardiac 
 muscle. Cerebral haemorrhage is liable to occur, as degene- 
 rative changes are frequently present in the cerebral vessels. 
 Cheyne-Stokes respiration may develop in association with 
 this, and is often pronounced and persistent. 
 
 In other cases there may be distressing dyspnoea at 
 night of the type of uraemic asthma. 
 
 When cardiac fibrosis is the result of cicatrization after 
 damage to the muscle by some severe toxaemia, there may be 
 at a later date dilatation of the heart, for which there is no 
 apparent cause ; dropsy may set in, with engorgement of the 
 lungs and other symptoms of back working and right 
 ventricle failure, and the condition of cardiac fibrosis is not 
 suspected during life. 
 
 Diagnosis. — As may be gathered from what has been 
 previously said, the diagnosis of this condition is one of 
 considerable difficulty, and is to a great extent a matter of 
 inference during life, and can only be determined with 
 certainty by a post-mortem examination. When, however, 
 
FIBROSIS OF THE MYOCARDIUM. 3j9 
 
 in association with evidence of vascular degeneration, the 
 heart is hypertrophied, and there are breathlessness, anginal 
 pains, a tendency to syncopal or apoplectiform attacks, 
 with a failing pulse, one may suspect fibrosis ; but there are 
 no characteristic features by which this can be diagnosed 
 from other degenerative changes in the heart muscle. 
 
 Prognosis. — This is necessarily unfavourable, inasmuch 
 as cardiac fibrosis is usually associated with degenerative 
 changes in the vascular system as a whole, and in the 
 coronary and cerebral vessels in particular. Because of 
 the associated sclerosis of the coronary arteries, death may 
 result from sudden syncope without previous warning, or 
 anginal attacks may set in, one of which eventually proves 
 fatal. Cerebral haemorrhage is liable to occur, giving rise 
 to hemiplegia, and is frequently associated with Cheyne- 
 Stokes respiration of a pronounced and distressing type. 
 This may develop in the absence of cerebral haemorrhage, 
 and is always of serious prognostic significance. 
 
 Frequency or irregularity of pulse usually are un- 
 favourable indications, if persistent, and not due to reflex 
 causes; but in one case in which irregularity was present 
 to a marked degree, with breathlessness on exertion and 
 slight cedeina of the legs, the patient, after a month's rest 
 in bed, regained his health, and by care in his mode of 
 life survived for six years, though the pulse remained 
 irregular all the time. Eventually he succumbed to a 
 sudden syncopal attack. 
 
 In another case, apparently similar at the outset, the 
 patient, three months after he sought medical advice, had 
 an attack of cerebral hsemorrhage, associated with Cheyne- 
 Stokes respiration. He began to recover some power in 
 the affected side, but a month later had another attack of 
 cerebral hemorrhage, which proved fatal. 
 
 Possibly, in fibrosis associated with syphilitic endarte- 
 ritis, the prognosis is more favourable if an early diagnosis 
 
34° HEART DISEASE. 
 
 could be made and suitable treatment carried out, but this 
 is scarcely possible in the majority of cases, and even on 
 careful microscopic examination post-mortem it is difficult 
 to be sure of a syphilitic origin. 
 
 According to the statistics of the cases collected by 
 Sidney Phillips, gummata usually give rise to no definite 
 physical signs or symptoms, and death is liable to occur 
 from a sudden syncopal attack, or possibly rupture of the 
 heart. Aneurysm of the heart may be a result of a gumma, 
 or, in the most favourable cases, cicatrization, with a result- 
 ing patch of fibrosis. 
 
 Apart from syphilis, the cases in which the prognosis is 
 most favourable are those in which the fibrosis is the result 
 of cicatrization after damage to the heart muscle by acute 
 myocarditis. It is probable that in many cases no symptoms 
 arise until later on in life, when possibly degenerative changes 
 may set in in the previously undamaged muscle, associated 
 with sclerosis of the coronary vessels. In other cases, 
 Avhere the lesion is severe, cardiac dilatation may result, 
 for which there is no apparent cause, and which resists all 
 treatment, and it is only on careful microscopical examina- 
 tion of the heart muscle post mortem that the explanation 
 is manifest. 
 
 Treatment. — This must be directed to relieving the heart 
 of work as far as possible. Moderation in food and drink, 
 and regularity of meals must be enjoined, to avoid undue 
 variations of blood pressure ; and measures must be taken 
 for the lowering of arterial tension if this be excessive. 
 For this purpose mercurial purgatives combined with colo- 
 cynth and hyoscyamus should be given once a week, or 
 oftener if required, and vaso-dilators, such as erythrol 
 tetranitrate or liquor trinitrin, should be administered, and 
 continued for a long period if necessary. Rest in bed must 
 be insisted on when warning symptoms such as breathless- 
 ness on slight exertion, or oedema of the extremities are 
 
FIBROSIS OF THE MYOCARDIUM. 341 
 
 present. Iodide of potassium is useful not only in syphilitic 
 fibrosis, but in all cases where there is general thickening 
 of the arteries and evidence of atheroma. Cardiac tonics, 
 such as strychnine, mix vomica, and arsenic, may often be 
 given with marked benefit, but digitalis and its congeners 
 are seldom indicated. 
 
CHAPTER XXIV. 
 
 AFFECTIONS OF THE MYOCARDIUM (Continued). 
 
 distinction between fatty infiltration of obesity 
 and fatty degeneration — causation of fatty 
 degeneration — symptoms — spontaneous rupture 
 of the heart — physical signs — diagnosis — prog- 
 nosis — treatment — aneurysm and new growths 
 of the heart. 
 
 Fatty Degeneration. 
 
 No form of heart disease is regarded with so much appre- 
 hension as fatty degeneration. More than any other, it 
 carries with it the danger of sudden death and the liability 
 to angina pectoris, and, although happily it is not very 
 common, it would be a most important acquisition to be 
 able to make the diagnosis with certainty at an early 
 period. 
 
 It must be understood from the first that fatty infiltra- 
 tion or the fat-laden heart of obesity does not come under 
 the designation of fatty degeneration, and it may be dis- 
 missed from further consideration with a few words. In 
 advanced life there is a tendency to the formation of adipose 
 tissue beneath the visceral pericardium, especially along 
 the course of the coronary arteries. In obese persons and 
 those addicted to alcohol, more especially beer drinkers, 
 the amount may become considerable, so that the entire 
 heart may be encased in fat, and adipose deposit may 
 penetrate between the muscular fibres. When such is the 
 
FATTY INFILTRATION OF THE MYOCARDIUM. 343 
 
 case, the heart will be hampered in its action, and a further 
 source of embarrassment will be present in fatty deposit 
 on the surface of the diaphragm and in the omentum. 
 
 Fatty Infiltration. — In fatty infiltration there is a deposit 
 of fat between the muscle fibres, which may be traced, on 
 careful examination, as a down-growth from the overlying 
 layer of fat around the heart. There is no deposit of fatty 
 material in the muscular fibres themselves, as is the case 
 in fatty degeneration. It is possible that compression of 
 muscle fibres by intervening fat may lead to atrophy of 
 some of them, and it is of course possible that there may 
 be fatty degeneration as well as fatty infiltration, but the 
 two are quite distinct processes, and are due to different 
 causes. 
 
 Distressing shortness of breath may be produced by 
 such fatty deposit and infiltration, and not uncommonly 
 there is a certain degree of oedema about the ankles and 
 along the tibiae at night, especially in hot or relaxing 
 weather. Such patients are especially liable to succumb 
 to acute infections such as pneumonia, typhoid fever, etc., 
 and usually take anaesthetics badly. The condition, how- 
 ever, is not attended with the same danger as actual 
 degeneration of the muscular fibres or with the charac- 
 teristic symptoms. 
 
 Fatty Degeneration: Morbid Anatomy. — Virchow taught 
 that in the liver the presence of fat in the cells might be 
 merely the result of physiological infiltration, but that in 
 the heart the appearance of fatty globules in the muscle 
 fibres was invariably due to a retrogressive change in which 
 there was actual conversion of the degenerated protoplasm 
 into fat. Hence the term " fatty degeneration." 
 
 In 1901 Eosenfeld * carried out a series of experiments 
 on animals, tending to show that in the heart, as in the 
 liver, the fat found in the interior of the muscle fibres is 
 
 * Gent, fur Inn. Med, 1901, p. 145. 
 
344 HEART DISEASE. 
 
 really an infiltration, and is not formed from the degene- 
 rated protoplasm, but brought from fat stores elsewhere 
 in the body and deposited in the damaged muscle. 
 
 The presence of fat in the cardiac muscle fibres, how- 
 ever, even though it be due to infiltration, and not a 
 degeneration in Virchow's sense of the term, is pathological, 
 the result of a retrogressive morbid change, and, to avoid 
 confusion, the term "fatty degeneration" will here be 
 retained to denote this condition. 
 
 In advanced fatty degeneration the heart substance will 
 be pale and softer than normal, so that the finger can be 
 readily thrust into it; the musculi papillares will usually 
 have a streaky appearance, the so-called " tabby-cat " stria- 
 tion, due to pale strands of fattily degenerated muscular 
 substance, being interspersed among healthy fibres. 
 
 Microscopically, on staining with osmic acid, it will 
 be seen that the deposits of fat are in the muscle fibres 
 themselves, and not between them. The tiny globules of 
 fat first make their appearance at the poles of the muscle 
 nuclei, but eventually the degenerative process extends 
 throughout the muscle fibre, so that it loses its striated 
 appearance, and is seen to be filled with globules of fat. 
 
 When unstained, the granular appearance of the 
 degenerated fibres might be mistaken for the condition 
 of " cloudy swelling " or albuminoid degeneration ; but 
 the distinction is readily made by treating the section 
 with acetic acid, which does not affect fat globules, but 
 dissolves the albuminoid granules, or by staining with 
 osmic acid, which gives quite characteristic appearances. 
 
 Etiology. 
 
 1. Sclerosis of the coronary arteries or obstruction of 
 these vessels by endarteritis is one of the most important 
 causes of fatty degeneration. The heart — perpetually at 
 
FATTY DEGENERATION. 345 
 
 work — cannot afford to be mulcted of its full supply of blood. 
 When, from any cause, this is defective, the wear and tear 
 of the muscular fibres, which must go on, is not repaired, 
 and their structure breaks down. Whether the fatty 
 granules and globules which are found within the sarco- 
 lemma are deposited there, or are derived from the atro- 
 phied sarcous elements, is not a matter of great consequence. 
 The important point is that the primary change is atrophy 
 of the muscle substance, the invasion of the fibres by fatty 
 matter being secondary to this and consequent upon it. 
 
 Disease of the coronary arteries, being thus a cause of 
 fatty degeneration of the heart, the existence of conditions 
 which may lead to the implication of the coronary arteries 
 or their orifices in morbid processes, will warrant a suspicion 
 that any cardiac weakness which may be recognized is the 
 result of degeneration. For example, an aortic murmur 
 coming on after middle age may not indicate serious 
 valvular lesion, but, as it is probably the result of athero- 
 matous changes in the valves or arterial walls in close 
 proximity to the orifices of the coronary arteries, there is 
 reason to apprehend that the disease may cause obstruction 
 here or may have extended to the vessels themselves, and 
 progressive weakness of the heart, were this to supervene, 
 would be attributable to degenerative change in its walls. 
 
 Acute aortitis, again, may in the same way give rise to 
 blocking of the mouths of the coronary arteries. A like 
 apprehension attaches to syphilitic disease of the aorta 
 and its valves, which is not uncommon in early middle 
 life, and especially to endarteritis obliterans affecting the 
 coronary arteries. 
 
 2. Apart from disease of the coronary arteries, there is 
 a large and varied group of causes which may give rise to 
 fatty degeneration of the heart, comprising — - 
 
 (a) Certain poisons : phosphorus, arsenic, and phlorizin. 
 
 (b) Acute yellow atrophy of the liver. 
 
346 HEART DISEASE. 
 
 (c) Acute or prolonged toxaemia of bacterial origin, e.g. 
 typhoid fever, diphtheria, erysipelas, pneumonia, and long- 
 continued suppuration. 
 
 True fatty degeneration is by no means always present 
 in these affections, and the morbid change commonly found 
 is limited to so-called " cloudy swelling," or albuminoid 
 degeneration. 
 
 (d) Carcinoma, phthisis, diabetes, and pernicious anremia. 
 Fatty change in the heart may thus be due to toxins 
 
 present in the blood, either ingested or of bacterial origin, 
 or to deterioration in the quality of the blood from morbid 
 processes elsewhere in the body. Consequently, the clinical 
 features in this group, apart from the signs of increasing 
 cardiac asthenia, do not specially point to the heart as the 
 seat of disease, but are those of the primary affection. 
 
 It is otherwise with the more serious form of fatty 
 degeneration associated with disease of the coronary arteries, 
 in which anginoid attacks and sudden death from syncope 
 are liable to occur. 
 
 It is a disputed point whether the sclerosis and narrow- 
 ing of the coronary vessels or the fatty change in the 
 muscle fibres is immediately responsible for the sudden 
 cardiac failure in these cases. 
 
 Huchard * attributes the symptoms in angina pectoris 
 entirely to the coronary sclerosis. Gibson f and Douglas 
 Powell J admit the importance of fatty degeneration as a 
 possible cause of angina and sudden syncope. Pratt, § in a 
 recent paper on the causes of cardiac insufficiency, con- 
 cludes with the somewhat sweeping statement "that there 
 is no evidence to show that fatty metamorphosis of the 
 heart produces cardiac insufficiency," adding, " that in the 
 light of our present knowledge, anatomical considerations, 
 
 * " Maladies du Cceur," vol. ii. p. 1. 
 t " Diseases of the Heart and Aorta," p. 7G; - ). 
 J Alllmtt's " System of Medicine," vol. v. p. 891. 
 § Bull. "John Hopkins Hospital," vol. xv. p. 16?. 
 
FATTY DEGENERATION. 347 
 
 especially coronary sclerosis and interstitial myocarditis, 
 must be regarded as the most common causes of heart failure." 
 
 He bases his conclusions partly on a series of pathological 
 investigations carried out by himself, and partly on experi- 
 ments on animals performed by Welch, Balint, Hasenfeld, 
 and Fenyvessy. As the fatty change in these experiments 
 was induced by phosphorous poisoning, which is an acute 
 process due to an irritant poison, whereas the fatty de- 
 generation under discussion is very slow in its onset and 
 due to deficient blood supply, this evidence can scarcely be 
 admitted. In spite also of the conclusions he draws from 
 his own observations, it is impossible to accept the statement 
 that fatty degeneration cannot be a cause of cardiac failure. 
 
 The fatty change, even if it be an infiltration, as argued 
 by Rosenfeld, and not a " degeneration " in Yirchow's sense 
 of the term, is unquestionably a serious pathological con- 
 dition, and the fat deposited in place of contractile proto- 
 plasm must necessarily impair the efficiency of the 
 muscular fibres. That it is a serious lesion is further 
 demonstrated by the fact that spontaneous rupture of the 
 heart may occur. 
 
 It is not denied that sclerosis and narrowing of the 
 coronary arteries is the most important and serious lesion, 
 inasmuch as the fatty change is secondary to and depen- 
 dent on this ; but it is impossible to determine whether 
 syncopal attacks and sudden death in these cases are due 
 to ischemia of the heart from coronary stenosis, or to in- 
 ability of the fat-laden, atrophied muscle to respond to 
 the call when extra work is thrown upon it. The latter 
 is, at any rate, quite sufficient, and it can be recognized 
 clinically. The former can only be inferred. Many of 
 the symptoms and physical signs of fatty degeneration 
 associated with coronary stenosis, as will be seen later, can 
 scarcely be ascribed directly to the vascular lesion, but are 
 significant of failing muscular power of the heart. 
 
34§ HEART DISEASE. 
 
 Symptoms. 
 
 There is little that is characteristic in the symptoms 
 unless we consider angina pectoris to be such, and definitely 
 associate it with fatty degeneration of the heart. The 
 relation between the two is undoubtedly very frequent but 
 is not constant, and angina is therefore reserved for special 
 and separate consideration. 
 
 In a large proportion of cases the subject of this affec- 
 tion has had no ailment which has led him to consult a 
 medical man when he is overtaken by sudden death during 
 exertion or excitement, or after a full meal. Or, the excite- 
 ment and exertion may be passed through safely and death 
 follow some hours later, next day even. Among the causes 
 which precipitate a sudden fatal termination, dilatation 
 of the stomach is frequent. Digestion is usually imperfect 
 from advancing years, or as a result of sluggish circulation 
 due to the state of the heart, and the tone of the muscular 
 coats of the stomach is impaired, allowing of passive dis- 
 tension by the contained gases, the products of fermentation. 
 The upward expansion of the stomach is moreover often 
 facilitated by a weak and relaxed condition of the diaphragm, 
 so that the upper line of gastric resonance can not unfre- 
 quently be traced horizontally across from the root of the 
 ensiform cartilage to the usual situation of the apex beat 
 in the fifth space. Such a condition is attended with im- 
 mediate danger when there is degeneration of the heart 
 walls, and may cause sudden death by pressure on the 
 heart, long before this would have resulted from the state 
 of the heart alone. 
 
 Rupture of the heart is one mode of termination, and 
 this may take place on very slight provocation. Some- 
 times the patient has been engaged in his usual avocation 
 up to the moment of its occurrence. In one case which 
 came under my observation, an old gentleman of quiet 
 
FATTY DEGENERATION. 349 
 
 retired habits, with nothing beyond the weakness incident 
 to age, was heard to knock at the wall against which his 
 bed was placed, and was found dead, the bedclothes 
 scarcely being disturbed. A neat slit was found in the left 
 ventricle near the apex close to and parallel with the septum. 
 In another case in which very advanced fatty degeneration 
 of the heart was found to be present at the autopsy, associated 
 with extreme stenosis of the coronary arteries, the diameter 
 of which was less than a millimetre, spontaneous rupture took 
 place during an attack of biliary colic. There had been no 
 history of attacks of angina or any warning symptoms. 
 
 The bearing of such occurrences on prognosis is direct 
 and simple. No doubt in many cases of sudden death there 
 have been warnings which the patient has ignored or has 
 not spoken of. These will sometimes be acknowledged in 
 the course of examination when they have not been 
 mentioned spontaneously. 
 
 When the course of the disease has been sufficiently 
 chronic to permit of the recognition of symptoms, which 
 in my experience is chiefly when the degeneration is 
 secondary to change in the coronary arteries, they will 
 be such as are produced by a slackening circulation, and 
 they are not so different from those attending dilatation 
 as to permit of any distinction being drawn between the 
 two conditions in an early stage, without physical ex- 
 amination. There may, perhaps, be greater fluctuations in 
 dilatation, though even in degeneration there may be great 
 temporary improvement under care and treatment. In 
 advanced stages characteristic differences make their 
 appearance. The symptoms of advanced dilatation have 
 already been described ; those attending degeneration are 
 evidences of heart failure of another kind. A noteworthy 
 point is that well-marked dropsy is rare, and probably never 
 occurs in uncomplicated degeneration. The significance of 
 this is that the special effect of the disease is defective 
 
3So HEART DISEASE. 
 
 pressure in the arterial system ; and it is to this are due 
 the syncopal, apoplectic, and epileptiform attacks, which, 
 together with the angina pectoris, are the most character- 
 istic later effects of fatty degeneration. 
 
 The syncopal attacks vary greatly in intensity. So far 
 as they have come under my observation, they have been 
 marked rather by duration than intensity, and have rarely 
 been so complete as to be attended with absence of con- 
 sciousness ; they have usually been accompanied by pro- 
 longed coldness of the extremities and of the surface. I 
 have not met with instances of sudden and complete loss 
 of consciousness and immediate recovery as in dilatation. 
 These fainting attacks are very significant, and are often 
 premonitory of fatal syncope. 
 
 The apoplectiform seizures are very remarkable, and in 
 the absence of history and without examination they are 
 not distinguishable from the apoplectic condition resulting 
 from cerebral hEemorrhage. The patient is unconscious ; 
 the respiration, if he is allowed to lie flat on his back, may 
 be stertorous — though stertor, after the teaching of Dr. 
 Bowles, ought to be eliminated from the symptomatology 
 of apoplexy — and there may be hemiplegia, but this will 
 be fugitive. Cheyne-Stokes breathing, which was first ob- 
 served in connection with fatty degeneration of the heart, 
 has not been present in the few cases which I have actually 
 seen in the apoplectiform state, while I have met with it 
 in a very large number of cases of ursemic coma and in 
 connection with serious consequences of high arterial ten- 
 sion. On examination of the pulse and heart, however, it 
 will be clear that there cannot have been sufficient pressure 
 in the arteries to rupture even the most degenerate vessel, 
 and, on the other hand, thrombosis or embolism is not com- 
 petent to produce unconsciousness of the character and 
 duration of these attacks. According to my experience, 
 the patient is never quite the same after an apoplectiform 
 
FATTY DEGENERATION. 351 
 
 attack ; lie is feebler in mind and body, and sometimes 
 increasingly liable to syncopal attacks. 
 
 The epileptiform attacks are not often violent, but re- 
 semble petit mat rather than a typical epileptic fit ; while, 
 however, the convulsion may not be so severe, there is 
 profound unconsciousness — not like epileptic coma, but of 
 a syncopal character — and the pulse may be extremely in- 
 frequent, sometimes less than twenty in the minute. In 
 my judgment, the heart failure manifested by the slow 
 pulse and the consequent arrest of the cerebral circulation 
 are the cause of the fits, and it is not the epileptiform 
 attack that affects the action of the heart. 
 
 By the time any of these forms of attack occur the 
 diagnosis of fatty heart is usually sufficiently clear ; but 
 Avhen they are associated with a very slow pulse, in which 
 the strength and volume of the pulse and the degree of 
 impulse of which the heart is capable preclude the idea 
 of fatty degeneration, they are probably to be referred 
 to the condition of Bradycardia known as Stokes-Adams 
 disease, which is discussed in a later chapter. 
 
 An important question is whether there is anything 
 characteristic in the appearance of a patient suffering from 
 fatty degeneration of the heart? A greasy state of the 
 skin with a sallow pallor of the face has been described, 
 and if such a condition has supervened upon a previously 
 healthy complexion the change would have significance, 
 but nothing of the kind is present in a large majority of 
 the cases. Many of the subjects of the disease retain the 
 look of health for a long time, and even up to the moment 
 when the heart ceases to beat. The degeneration may be 
 due to a local cause — obstruction of the coronary arteries ; 
 and, even if a tendency to general deterioration of the 
 tissues is present, the change mostly advances so much 
 more rapidly in the heart than elsewhere, that there is no 
 time for it to become conspicuous in the skin. The picture 
 
352 HEART DISEASE. 
 
 appears to have been drawn from cases of a universal 
 chronic degeneration of vessels and heart. The arcus 
 senilis again, which has been said to indicate the existence 
 of cardio-vascular degeneration, has no such significance. 
 
 Physical Signs. 
 
 The Pulse. — The most constant and significant feature 
 of the pulse is that it is short and unsustained. The size 
 of the artery at the wrist and the condition of its walls 
 may vary greatly. When the arterial coats are healthy 
 they are apt to feel extremely thin. The pulse rate may 
 be regular and about normal, or extremely irregular both 
 in force and time, and it may be frecpient or slow. A very 
 slow pulse with extreme low tension is most characteristic, 
 but then it is the most rare. 
 
 The Heart. — The physical signs may be described as 
 negative. Unless degeneration has attacked a heart already 
 enlarged the size will be normal. If the fatty change is 
 at all advanced, impulse can neither be seen nor felt, or, 
 if perceptible, it is only as a faint vibration. A heart in 
 this condition is incapable either of giving a distinct 
 push or of maintaining continuous pressure in the arteries. 
 The sounds are weak, sometimes so weak as to be almost 
 inaudible ; but except that the first is short, there is 
 nothing abnormal about them ; the intervals, again, are 
 usually normal. The very absence of physical signs, such 
 as murmur, or conspicuous modification of the sounds or 
 intervals, or disturbance of the relation between the two 
 sides of the heart, or increase of dimensions, when symptoms 
 of serious slackening of the circulation are present, and 
 especially when there have been anginal, or syncopal, or 
 apoplectic attacks, adds gravity to the case. 
 
 But a weak, short, unsustained pulse is common as a con- 
 stitutional peculiarity, or may at any period of life be simply 
 
FATTY DEGENERATION. 353 
 
 a result of general debility, and impulse and apex beat may 
 be entirely absent, and the sounds may be short and weak. 
 In young people there is no danger of such weakness being 
 taken to be indicative of degeneration of the heart, but it 
 may arouse anxiety after middle age, especially if there is 
 also irregularity in its action. 
 
 It is important to be able to distinguish between func- 
 tional weakness of this kind and weakness arising from 
 organic disease. Usually this is accomplished by making 
 the patient walk briskly. A few steps will often be suffi- 
 cient. If the heart is. sound it rises to the occasion. The 
 pulse, and beat, and sounds are all more distinct, and strong, 
 and regular, whereas the fatty heart " goes to pieces," and 
 the pulse becomes irregular and shorter than ever, or may 
 even disappear. 
 
 Until the disease is far advanced the diagnosis of fatty 
 degeneration of the heart is not easy, and is scarcely to be 
 made without more than one opportunity of examination. 
 
 Prognosis. 
 
 When the diagnosis has once been made, the prognosis, 
 for the most part, can contemplate only one result ; a fatal 
 termination is merely a question of time and circumstance. 
 Excluding cases in which death has been sudden without 
 warning, the shortest period in my experience over which 
 characteristic symptoms have extended, together with recog- 
 nized physical signs, has been about six weeks ; several 
 patients have survived the diagnosis two years before justify- 
 ing it by dying suddenly. But circumstance as well as time 
 enters into the question ; a slight effort, or a fall, a little 
 hurry or excitement, too hearty a meal, an attack of flatulent 
 indigestion or constipation, a chill, may hurry on the fatal 
 termination ; and on the other hand, judicious care may post- 
 pone it till the heart is completely worn out and conies to a 
 
 2 A 
 
354 HEART DISEASE. 
 
 standstill, or senile gangrene may result from the combined 
 effects of cardiac and arterial degeneration. 
 
 The question must be asked, Is fatty degeneration of the 
 heart ever cured or arrested ? If the fatty change which 
 may result from typhoid fever and other toxgemias is to be 
 included under the term, the answer must undoubtedly be 
 Yes. The heart may ultimately regain structural soundness 
 and functional vigour when during the fever the first sound 
 has been completely lost and the impulse has been scarcely 
 perceptible ; and when degeneration has been the result of 
 other forms of blood poisoning or deterioration, it ought to 
 be possible, and now and then to occur, that recovery of the 
 heart should follow a return to a healthy state of the blood. 
 
 Twelve years before his death I came to the conclusion 
 that a gentleman, aged at the time about 55, was suffering 
 from fatty degeneration of the heart. Spare in habit, 
 strictly moderate in eating and drinking, regular in taking 
 exercise, and a great pedestrian, he rapidly lost strength 
 without recognizable cause, became breathless on very slight 
 exertion, so that he could scarcely walk slowly a hundred 
 yards without actually stopping, either to get his breath, or 
 on account of anginoid pain. On one occasion at least, while 
 sitting in his chair he became suddenly pale and uncon- 
 scious, his head fell on his chest, and the jaw dropped. 
 With this change in his health, the pulse and heart were 
 extremely weak. He would never relinquish exercise, but 
 continued to walk, however slowly and at whatever cost of 
 pain and distress, every day, exercising great self-command 
 and measuring his strength very exactly. Little by little 
 he gained ground, and attained fair health, but was capable 
 of very little in the way of work, though never at any time 
 were his intellectual faculties at all affected. Eventually 
 he died suddenly in bed. 
 
 This case may have been an instance of arrest and partial 
 recovery, but unfortunately no autopsy was obtainable. 
 
fatty degeneration. 355 
 
 Tkeatment. 
 
 It must be acknowledged at the outset that it is not in 
 our power to modify in the least degree the condition of the 
 cardiac muscular fibre when far advanced in fatty degenera- 
 tion, and that we can do very little, if anything, to arrest the 
 progress of the deterioration when it has reached a stage at 
 which it is recognizable either through symptoms or by 
 physical signs. Even at a very early period we should 
 doubt the possibility of reversing a process which in some 
 cases is an inherited tendency to natural decay at a given 
 time of life, in others an effect of imperfect blood supply 
 due to narrowing of the coronary arteries. 
 
 If, indeed, the degeneration has been the result of acute 
 disease, such as typhoid fever, time and care will bring about 
 a restoration of the muscular fibres ; but this is not fatty 
 degeneration of the same nature as that due to coronary 
 sclerosis, but is rather a secondary consequence of the 
 condition of so-called cloudy swelling, which is a result of 
 prolonged toxaemia. 
 
 When, again, the condition is not true degeneration of 
 the muscular fibres, but a fatty heart, due to a sedentary 
 life, with privation of fresh air and neglect of exercise, 
 together with undue indulgence in alcoholic drinks and in 
 the pleasures of the table, there is not then, at any rate 
 till an advanced stage, true fatty degeneration, but a deposit 
 of fat between the muscular fibres or fatty infiltration. In 
 such cases careful dieting and graduated exercise, such as 
 the CErtel treatment, may reverse the degenerative tendency 
 and even cause a gradual absorption of the fatty tissue 
 already deposited in and around the heart as well as 
 elsewhere. 
 
 While, however, acknowledging the limitation of thera- 
 peutics in dealing with the organic change, we are not alto- 
 gether powerless to avert its consequences, and by so doing 
 
356 HEART DISEASE. 
 
 to prolong life. We see from time to time, on post-mortem 
 examination, the heart so far gone in fatty change that it is 
 scarcely recognizable as muscle, either to the naked eye or 
 under the microscope. Such change must have been long 
 in progress, and the subject of it must have lived for 
 months if not for years, while the slightest obstruction in 
 either pulmonary or systemic circulation would have brought 
 the heart to a standstill, and a shock, a fall, or an indi- 
 gestible meal, would have been fatal. We meet with cases 
 of this kind during life, in which the decay of the mental 
 and bodily powers is so slow as to be almost imperceptible, 
 or in which thrombosis of one cerebral vessel after another 
 brings the patient to a state of dementia or bed-ridden 
 paralysis from general or local cerebral softening. Or 
 the immediate cause of death may be senile gangrene. It 
 is not that results such as those just named are desirable — 
 death would be preferable were we allowed to choose — but 
 cases of the kind serve, with others, to show that prolonga- 
 tion of life is possible when the central organ of the 
 circulation can barely keep the blood in motion, and to 
 illustrate the conditions under which this is observed. 
 These conditions are a gradual diminution of mental and 
 bodily activity, together with attention to diet and regula- 
 tion of the bowels. The setting in of softening of the brain, 
 or an attack of paralysis, not unfrequently seems to put an 
 end to cardiac symptoms and to prolong life ; the sufferer is 
 no longer his own master ; he cannot undertake business or 
 go about, his food is under orders, and the action of the 
 bowels is known to others besides himself. 
 
 If, in an early stage of fatty degeneration of the heart, 
 the same command over the patient's mode of life and the 
 same knowledge of the -state of his secretions were attain- 
 able, not only might life be made longer by many years, 
 but much suffering Avhich is seen to arise out of this form 
 of disease might be averted. It is unnecessary, and it 
 
FATTY DEGENERATION. 357 
 
 would be impossible to enter into particulars with regard to 
 trie amount of work and exercise to be permitted, or trie 
 quantity and kind of food to be allowed ; the latter may, 
 and indeed in most cases must, be liberal and varied, but 
 precautions must be taken against an inordinate appetite, 
 and it is always safest to let some judicious relative or 
 attendant who knows his likings and what suits him, help 
 the patient at meals, and decide for him what dishes and 
 what quantity will be good for him, acting under the advice 
 of the medical man. 
 
 Proper regulation of the bowels is of the utmost import- 
 ance. As years increase people are apt to become less 
 observant, and to take it for granted that, so long as the 
 habitual regularity in going to stool obtains, the action of 
 the bowels is satisfactory and efficient, whereas it may be 
 that the evacuation is much too small in amount. Accumu- 
 lation thus gradually takes place, and it is not uncommon 
 for a second daily call to relieve the bowels, resulting from 
 this, to be regarded as evidence of improvement in their 
 action. The statements of patients, then, with regard to 
 this function, are not always trustworthy, and the testimony 
 of a competent observer, or inspection by the medical man, 
 is necessary. The quantity of fsecal matters which may 
 unconsciously accumulate in the colon is astonishing, and 
 the prevention of such an occurrence is essential to the 
 well-doing of a patient whose heart is organically weak. 
 For the regulation of the bowels mild aloetic aperients are 
 best, with pil hydrarg. and colocynth occasionally in small 
 doses, if there is arterial tension. Any tendency to flatulent 
 distension of the stomach must be counteracted, as far as 
 possible, by careful dieting and the administration of alkalies 
 and carminatives. Bitter tonics may be given, and massage 
 or gentle exercise is often of great service. Extremes of 
 heat and cold should be avoided, and a dry, bracing, healthy 
 spot in the country should be selected as a residence. 
 
358 HEART DISEASE. 
 
 Aneurysm of the heart is of rare occurrence, and seldom 
 gives rise to any physical signs or symptoms by which it 
 can be diagnosed during life. It usually affects the left 
 ventricle. It results from local destruction or weakening 
 of a portion of the heart wall, which may be due to break- 
 ing down of a gumma, abscess from a septic embolus, 
 softening from thrombosis, or embolism of a branch of the 
 coronary artery. 
 
 It is usually lined by laminated clot, and varies in size. 
 In one instance I have seen, the aneurysm was situated in 
 the lower half of the wall of the left ventricle, and was 
 three inches in diameter. It was completely filled up with 
 layers of laminated clot. It gave rise to no distinctive 
 physical signs or symptoms during life, and did not appear 
 to be the immediate cause of death. 
 
 New growths of the heart are rarely, if ever, primary. 
 Secondary growths are also very uncommon ; but nodules of 
 sarcomatous or carcinomatous growths in the heart wall are 
 occasionally met with secondary to growths in other organs. 
 
CHAPTER XXV. 
 ANGINA PECTORIS. 
 
 CHARACTERISTICS OP TRUE ANGINA — ASSOCIATED SYMPTOMS 
 — EXCITING CAUSES OP PAROXYSMS— ETIOLOGY AND 
 MORBID ANATOMY — DISCUSSION OP THEORIES ADVANCED 
 TO EXPLAIN THE PAIN — DIAGNOSIS — PROGNOSIS — 
 TREATMENT. 
 
 While heart disease generally is remarkable for the almost 
 entire freedom from pain — so that when patients come 
 complaining of pain in the cardiac region, it is a presumption 
 against the existence of any serious organic lesion rather 
 than an indication of any such change — there is one form 
 of pain in and around the heart, angina pectoris, which is 
 very definite and constant in its significance of disease and 
 danger. The term " angina pectoris," or pain in the chest, 
 has come to have a specialized meaning, and is commonly 
 employed to denote a complex group of symptoms associated 
 with certain grave pathological changes in the heart and 
 coronary arteries. 
 
 As an account of the distinctive features of "angina 
 pectoris " involves a discussion of the associated symptoms, 
 it will be more convenient to describe these first, and to 
 defer the consideration of the etiology and morbid anatomy 
 to a later period. 
 
 Characteristics op true Angina Pectoris : Associated 
 
 Symptoms. 
 
 In a typical attack of angina there is intense pain in 
 some part of the cardiac region, most frequently behind the 
 
360 HEART DISEASE. 
 
 sternum, with radiation down the left arm, but occasionally 
 across the upper part of the chest, in the left breast, or in 
 the neighbourhood of the ensiform cartilage. Accompany- 
 ing the pain is a sense of utter helplessness and extreme 
 fear and dread. The patient keeps still, not daring to 
 moye, and feels as if he were in the act of dying. He will 
 say afterwards that if the pain had lasted another moment 
 he must have died. In no other condition is the physical 
 agony of dying realized in the same degree. The two 
 elements of pain and sense of impending death coexist 
 in a true paroxysm of angina, and are almost equally 
 characteristic. 
 
 The pain differs in character and situation and in in- 
 tensity in different cases. Some sufferers will say it is 
 indescribable — nothing in their previous experience suggests 
 even a comparison ; others speak of the pain as severe 
 cramp in the heart, or as if the heart were gripped by an 
 iron claw ; while pain of a shooting, neuralgic character 
 sometimes intermittent, sometimes persistent, seems to 
 radiate from the chest to the left shoulder, down the inner 
 side of the arm to the forearm, and the ring and little fingers. 
 Occasionally there is a sensation as of the wrist being 
 grasped so tightly as to cause pain. With the pain in the 
 heart there may be pain down both arms or shooting up into 
 the left side of the neck, very rarely in the right arm only. 
 Occasionally the pain may be felt first in the wrist or arm 
 and seem to travel up to the chest, or may come in the inner 
 side of the arm as a kind of warning of an attack. Another 
 description of the pain is that it feels as if the sternum were 
 being crushed back to the spine, or, again, as if the whole 
 chest were being held in a vice. In other cases the pain is 
 compared to a bar of iron across the upper part of the chest ; 
 in others, again, to a ton weight upon the lower part of the 
 chest. The ramifications of the cardiac plexus and its com- 
 munications witli other nerves make the radiation of pain 
 
ANGINA PECTORIS. 361 
 
 in all the various directions enumerated comprehensible, 
 and the nerve of Wrisberg has been specially instanced as 
 explaining the pain in the left arm, but no explanation can 
 be given why in one case the pain is felt in one part of the 
 cardiac region, and has some particular character, and takes 
 a given direction down one arm or both or through to the 
 back, while in another case the seat, character, and exten- 
 sion of the pain are quite different. It is not a pressure 
 effect on the plexus outside the heart, neither heart nor 
 aorta being necessarily enlarged, and fusiform dilatation of 
 the arch of the aorta is common without anginoid pain ; 
 there can be no stretching or mechanical irritation of the 
 nerve-ramifications beneath the endocardium at all com- 
 parable to that which takes place in acute dilatation of the 
 heart. It seems to me that the pain is a danger signal 
 given by the sensory nerves of the heart. The radiation 
 of irritation giving rise to its extension takes place in 
 the spinal cord, as will be shown in the next chapter. 
 
 An interesting point is that at the end of a paroxysm 
 there is usually flatulent eructation from the stomach. 
 The attacks are therefore very commonly attributed to 
 flatulence, and distension of the stomach by food or gases 
 may undoubtedly be, and often actually is, an exciting 
 cause, but more frequently the sensation as of wind on the 
 stomach is only a part of the general commotion, and is due 
 to communicated or sympathetic irritation of the gastric 
 distribution of the vagus, the cardiac branches of which are 
 primarily implicated. The escape of gas from the stomach 
 is often a signal that the paroxysm is over rather than the 
 means of bringing it to an end. Occasionally there is a 
 vehement desire to pass urine, although the bladder may 
 at the time be empty. 
 
 The duration of the attacks is very varied ; sometimes 
 it can be reckoned in seconds. Most frequently, perhaps, a 
 paroxysm will last a few minutes, but I have known a 
 
362 HEART DISEASE. 
 
 patient sit in the same position almost through an entire 
 night, not venturing to make the slightest movement and 
 scarcely seeming to breathe, while the perspiration rolled 
 off his forehead and came through his clothes. According 
 to my experience, it is when the attack comes on in the 
 night, without provocation by exertion or exposure, that it is 
 protracted. When it is started by exertion it generally 
 ceases soon after the exertion is left off. 
 
 While it would not be justifiable to say that a patient 
 was the subject of angina pectoris unless he had had one or 
 more paroxysms of intense radiating pain, associated with 
 a sense of immediately impending death, it must be ad- 
 mitted that attacks of true angina occur which fall short 
 of the typical development. For example, when a patient 
 has been taught prudence by one or more bad attacks, he 
 may, by standing still on the first warning, or by taking 
 remedies, cut short the paroxysm, which will then have 
 been represented only by the initial pain in the breast or 
 arm without the mortal dread. It is possible, therefore, 
 that before any characteristic attack has occurred, pains of 
 a similar kind and intensity, disregarded by the patient or 
 relieved by rubbing the chest or arm, may have the same 
 significance as a fully developed paroxysm. 
 
 Again, a patient who has had attacks of true angina 
 may cease to suffer pain, but may have attacks of what he 
 calls faintness, in one of which he ultimately dies. These, 
 which have lost their title to the name angina, have an 
 equally serious significance. They are sometimes called 
 angina pectoris sine dolore. 
 
 The aspect of the patient is one of extreme anxiety or 
 alarm. He is usually pale and often livid round the mouth, 
 but it is said that sometimes the colour does not change. 
 A cold perspiration usually bursts out on the forehead, and 
 may be so copious as to drip off the face. The pulse, in the 
 rare instances in which I have had the opportunity of 
 
ANGINA PECTORIS. 363 
 
 examining it during a paroxysm, has been irregular, small, 
 and weak. In some cases it has been reported to be very 
 small from contraction or spasm of the arteries. In others, 
 again, it has scarcely been affected at all. 
 
 Exciting 1 Causes of a Paroxysm. — Great importance attaches 
 to the exciting cause of the paroxysms. In the first instance 
 they are almost always brought on by exertion. The patient, 
 while walking perhaps more sharply than usual, or uphill, 
 or against a wind, is more or less suddenly arrested by pain 
 in the chest, with a feeling as if the heart were about to 
 stop and he to fall down dead. On standing still the pain 
 gradually passes off, and he is able to resume his walk, but 
 only feebly and gently. For a while the attacks only occur 
 when provoked by exertion, but more and more easily as 
 time goes on, and they tend to become more severe. They 
 are more readily induced when a walk is taken, or any 
 imprudent exertion, such as stooping, drawing on boots, 
 pulling open a drawer, pushing up a window, is made soon 
 after a meal, especially after breakfast. External cold, 
 again, predisposes to an attack, and exercise, which can 
 be taken with impunity in mild weather, brings on a 
 paroxysm if the air is cold and damp. Attacks, again, 
 may be brought on by indigestion or constipation, appa- 
 rently either through reflex disturbance of the heart, or as 
 a result of pressure from the distended stomach or colon 
 carrying the diaphragm upwards and obstructing mechani- 
 cally the action of the heart and the expansion of the 
 lungs. 
 
 They are also liable to occur during the night, and may 
 be induced in various ways. On first lying down, the 
 contact of cold sheets may have this effect by causing 
 contraction of the peripheral arterioles, and thus throwing 
 increased work on the heart ; the exertion of undressing- 
 may predispose to an attack, or the upward pressure of the 
 abdominal viscera, on assuming the horizontal position, may 
 
364 HEART DISEASE. 
 
 embarrass trie heart. An attack may come on after sleep 
 when the vigour of the circulation has run clown, and when 
 possibly also evolution of gases in the stomach, and disten- 
 sion of this viscus or of the colon, have given rise to 
 pressure on the diaphragm. 
 
 It is clear that the great exciting cause is a demand for 
 increased effort on the part of the heart to which it is not 
 equal, or occasionally the cause may be interference with 
 the movements of the heart by a dilated stomach and colon. 
 
 Etiology and Morbid Anatomy. 
 
 The conditions of the heart associated with angina 
 pectoris are varied, but perhaps the most remarkable and 
 significant point in the relations between heart disease and 
 angina is that angina does not attend the chain of events 
 through which stenosis or incompetence of the mitral valve 
 proves fatal, and is not among the symptoms which arise 
 out of the valve lesion and its effects upon the heart. This 
 fact was duly emphasized by Walshe, in his classical work 
 on the heart, and no exception to it has occurred in my 
 experience. I have, indeed, known instances in which, 
 after attacks of angina had occurred at intervals for many 
 months, mitral regurgitation has supervened with dilatation 
 of the left ventricle, and concurrently with the establish- 
 ment of so-called mitral symptoms — pressure in the pulmo- 
 nary circulation, dilatation of the right side of the heart, 
 and dropsy — the angina has ceased. In these particular 
 circumstances Balfour's view, that the giving way of the 
 mitral valve may be an advantage to the sufferer from aortic 
 disease, is perhaps justified, or it is possible that in such 
 cases breathlessness may compel the cessation from exerti< »n 
 before the condition which gives rise to pain is reached. 
 
 Aortic stenosis may be attended with true angina, as 
 may also aortic incompetence or combination of the two 
 conditions of the aortic valve. In association with aortic 
 
ANGINA PECTORIS. 365 
 
 valvular disease angina may be met with in early adult 
 life, and may continue for many years without proving fatal. 
 The sense of impending death is, however, not so fully pro- 
 nounced in aortic cases, though the pain may be very severe. 
 
 Injury to the root of the aorta has been known to give 
 rise to ano-ina. I have had a case under observation for 
 several years, in which a severe crush of the chest gave 
 rise to a double aortic murmur and to distressing attacks 
 of angina. For a time the attacks came on very frequently, 
 even while the patient was kept in bed, and they continued 
 to occur on very slight provocation, requiring frequent 
 recourse to nitro-glycerine, which the patient took in con- 
 siderable quantity. There was scarcely any compensatory 
 hypertrophy and dilatation in this patient, and he was 
 never able to work. 
 
 In aortitis affecting the root of the aorta there is usually 
 angina, the attacks at first slight, increasing in intensity 
 and duration, and coming on more frequently as the disease 
 advances. The heart rapidly becomes weaker without notable 
 enlargement, the impulse more feeble, the sounds weak and 
 short. Both the angina and the weakness of the heart point 
 to interference with the coronary circulation, and the orifices 
 of the coronary arteries are found small and contracted by 
 the swelling of the walls of the aorta. 
 
 Gout. — Attacks of pain in the region of the heart may 
 occur in gouty subjects. Frequently they are merely reflex 
 due to gastric disturbances. True angina, when it is met 
 with, is to be attributed not directly to the gout, but to the 
 degenerative vascular lesions to which gout predisposes, and 
 which may affect the aorta or coronary arteries. 
 
 Bacterial Infections. — Angina has followed recovery from 
 plague in two cases I have seen, and was experienced on 
 slight exertion for several years, and a characteristic attack 
 of angina has been described to me as having occurred in 
 intermittent fever. 
 
366 HEART DISEASE. 
 
 Fatty Degeneration of the Heart. — In a very large pro- 
 portion of cases in which angina proves fatal the heart is 
 found, when examined after death, to be in a more or less 
 advanced stage of fatty degeneration. The fatty change may 
 be so far advanced that the fingers sink into the walls of the 
 heart on slight pressure, and scarcely any sound muscular 
 fibres can be found on microscopic examination. Sometimes 
 it may appear to be comparatively slight, and only evident to 
 the naked eye as yellow patches or strise in the ventricular 
 walls and in the musculi papillaries, but microscopic 
 examination shows widespread fatty degeneration and fat 
 globules in fibres that appear to be normal to the naked 
 eye. The heart may be normal in size or perhaps greatly 
 dilated, or there may be a considerable degree of hypertrophy. 
 The coronary arteries will invariably be found to be diseased. 
 Sometimes they can be dissected out as hard, rigid, cal- 
 careous tubes from the auricular grooves, and frequently 
 their walls are so thickened that the lumen is almost 
 obliterated. 
 
 Fibrosis. — In some instances the morbid condition 
 found is fibrosis, general or local, associated with coronary 
 sclerosis, or possibly the result of myocarditis. 
 
 There may be little or no change recognizable in the 
 wails of the heart, and the coronaries at first sight may 
 appear to be healthy, especially when the first attack has 
 proved fatal or death has supervened after a few paroxysms. 
 It is probable, however, that in such cases, on careful 
 examination, obliteration of a branch of the coronary artery 
 by endarteritis or its obstruction by an embolus or thrombus 
 will be discovered. 
 
 Angina Vasomotoria. — Angina is also met with in a 
 certain proportion of cases of high arterial tension associated 
 with general arterio sclerosis, in which the maintenance of 
 a high degree of pressure in the circulation precludes the 
 existence of any marked degree of fatty degeneration in 
 
ANGINA PECTORIS. 367 
 
 the cardiac muscle. In this class of cases the paroxysms 
 of angina appear to depend on increased arterio-capillary 
 resistance, which raises the blood pressure and throws extra 
 work on the heart. To this group the term " angina vaso- 
 motoria " may be conveniently applied to distinguish them 
 from cases in which fatty degeneration of the heart is 
 pronounced, and inherent cardiac weakness is the prominent 
 feature. The heart is hypertrophied and may be capable of 
 powerful contraction, and the circulation in the coronaries 
 may be sufficient for ordinary needs, but when the arterial 
 tension is further raised by exertion or increase of peripheral 
 resistance attacks of angina are induced. I have thought 
 it well to make special allusion to this form of angina, 
 which has been termed " vasomotoria," as the prognosis is 
 less serious, and more satisfactory results can be obtained 
 from suitable treatment than in cases in which angina is 
 associated with fatty degeneration of the cardiac muscle. 
 The attacks of angina cannot, of course, be attributed simply 
 to the high arterial tension, which is met with in an 
 extreme degree, without angina, in chronic Bright's disease 
 and various other conditions. The real underlying cause 
 will be found to be partial occlusion of the mouth of the 
 coronary arteries by degenerative changes in the aorta, or 
 sclerosis of the coronary vessels, which are results of the 
 high arterial tension. There will not, as a rule, be extreme 
 stenosis of the coronary vessels such as may be present in 
 fatty hearts, but rather thickening and rigidity, and it may 
 be calcification of their walls, the loss of contractility, which 
 must have seriously impaired the circulation in the heart 
 during life. 
 
 Conclusions. — It will be seen from a review of the above- 
 mentioned etiological factors that interference with the 
 flow of blood through the coronary arteries from disease of 
 their walls, from thrombosis or embolism, or from narrowing 
 of their orifice by atheromatous changes in the aorta, is by 
 
368 HEART DISEASE. 
 
 far the commonest cause of true angina pectoris, and is the 
 only constant pathological lesion found post-mortem. In 
 fatty or fibroid degeneration of the heart, with which angina 
 is frequently associated, sclerosis of the coronary vessels is 
 present, and in the aortic lesions to which reference has 
 been made above there is either atheromatous degeneration 
 of the aorta, which may involve the orifice of one or both 
 coronary arteries, or the coronaries themselves are diseased. 
 In cases of angina following acute bacterial infections, it 
 may be that acute arteritis is set up in the coronary 
 arteries, or in the vasa vasorum supplying them, Avhich 
 will subsequently lead to degenerative changes in the 
 coronary vessels from impaired nutrition. Of this, however, 
 we have no direct proof. Huchard,* after a very compre- 
 hensive enumeration and a masterly discussion of all the 
 possible causes of angina, sums up in the following words, 
 " II n'y a pas plusieurs angines de poitrine, il n'y a 
 qu'une seule, l'angine coronarienne." He | admits, however, 
 that in tobacco poisoning there may be attacks of true 
 angina without coronary sclerosis. These he attributes to 
 temporary spasm of the coronary arteries, 
 
 Theories advanced to explain the Pain. 
 
 Numerous theories have been advanced to explain the 
 pain of " angina pectoris." 
 
 Stretching of the Heart Muscle Fibres. — It might be 
 supposed that mechanical stretching of the muscle fibres 
 in the endeavour to overcome resistance in the circulation 
 would give rise to pain, but acute dilatation of the heart may 
 occur under various conditions without giving rise to angina. 
 
 Neuralgia. — It has been suggested that the pain might 
 
 be due to cardiac neuralgia, but the nature of the attacks 
 
 and of the exciting causes which induce them are scarcely 
 
 * " Maladies du Coeur," vol. ii. p. 13d. 
 t Ibid., p. 1U5. 
 
ANGINA PECTORIS. 369 
 
 compatible with this theory. Angina, moreover, is far 
 more common in men than women, whereas the converse is 
 the case with neuralgia. 
 
 Impairment of Contractility of the Heart Muscle. — Mac- 
 kenzie,* in a paper on the cause of angina, gives an 
 interesting series of pulse tracings, two of which, taken 
 during an attack of angina, show the presence of the " pulsus 
 alternans," that is, a large beat regularly alternating with 
 a small beat. This pulse is not necessarily associated with 
 angina, but is frequently met with in other conditions. He 
 regards the " pulsus alternans " as evidence of impairment 
 . of the contractile power of the heart muscle, and states 
 that in cases of angina, the same exciting cause — extra 
 strain on the heart — may provoke both angina pectoris 
 and the alternating action of the heart, and that both may 
 disappear with removal of the cause. He therefore con- 
 cludes that angina pectoris will be found to be associated 
 with impairment of the function of contractility of the heart. 
 
 Spasm of the Heart. — The condition of the heart during 
 the attacks has been supposed to be one of spasm, but there 
 are many objections to this view, and ideas as to what is 
 meant by spasm of the heart in the anginal paroxysm by 
 those who have employed the term have been diverse and 
 vague. If by spasm of the heart is understood tonic con- 
 traction or an unrelaxing systole, this is certainly not the 
 condition present. The heart has never been found in this 
 state after death, and in most cases is incapable of such 
 contraction from the state of its walls. No pulse would be 
 possible were the heart in a spasm of this kind, and the 
 pulse, though small and often irregular, can usually be felt. 
 It has, indeed, in some cases been apparently unaffected by 
 the paroxysm. 
 
 But by spasm may be meant an irregular and partial 
 contraction like cramp in voluntary muscles, or a fibrillar 
 * B.M.J., vol. ii. 1905, p. 845. 
 
 2 B 
 
37° HEART DISEASE. 
 
 contraction, such as is sometimes induced by faradic cur- 
 rents in muscle under experiment. The late Dr. Matthews 
 Duncan, in the last conversation I had the honour to hold 
 with him, suggested that the state of the heart in angina 
 pectoris might be like hour-glass contraction of the uterus. 
 He had at that time experienced the pain. 
 
 Views of this kind cannot be proved to be wrong, but 
 objections might be raised, and the central fact and essen- 
 tial significance of angina is that stress is put upon the 
 heart, to which, for the moment, it is unequal. 
 
 One of the main causes of such stress is resistance in the 
 peripheral circulation, or, in other words, high arterial 
 tension, and we owe to Lauder Brunton the knowledge that 
 in many attacks of angina there is an aggravation of 
 habitual high tension by a general contraction of the arteri- 
 oles. But the habitual state of the arterial circulation may 
 be one of relaxed arterioles and capillaries and low tension, 
 so that the heart has no abnormal resistance to overcome. 
 Here sudden general arterial spasm would put the heart to 
 greater stress than if the habitual tension were high, since 
 the contrast between the work demanded would be greater. 
 Huchard considers that the attacks of anginoid pain are 
 due to ischemia of the heart, either from spasm of the 
 coronary arteries, or from the relatively deficient blood 
 supply through the narrowed vessels when exertion or 
 increase of arterial tension demands increased blood supply 
 to the heart. He compares the condition of the heart to 
 that of the limbs in " claudication intermittante." 
 
 This explanation is by far the most satisfactory that has 
 yet been advanced, and the cases Huchard instances of true 
 angina occurring in patients suffering from the rare con- 
 dition of claudication intermittante are of great interest. 
 Whether actual spasm of the coronary arteries occurs must 
 be problematical, and, indeed, from the thickened, rigid 
 condition of their walls in many cases, it would scarcely 
 
ANGINA PECTORIS. 37 1 
 
 seem, to be possible. But the suggestion that the relatively- 
 deficient blood supply to the heart muscle through the 
 diseased coronary vessels induces a condition akin to cramp 
 of the heart when it is called upon to do extra work will 
 explain the occurrence of angina in all the diverse patho- 
 logical conditions of the heart with which it may be 
 associated. 
 
 We must, it seems to me, assume that it is one of the 
 arrangements by which the adjustment of internal reactions 
 to external conditions is secured. The existence of the 
 patient is threatened at the moment of the attack by arrest 
 of the heart's action, and were it not for the warning given 
 by the pain, and the cessation of exertion thus enforced, 
 the subject of this particular affection of the heart would 
 die suddenly without any warning. 
 
 Diagnosis. 
 
 Angina pectoris may be closely simulated by paroxysms 
 of pain which are not symptomatic of disease of the heart 
 of any kind, and are not attended with danger, and, as we 
 usually have to depend on the account given by the 
 patient, it is often a matter of great difficulty to distinguish 
 between true angina and merely anginoid attacks. The 
 difficulty will sometimes be aggravated by the fact that the 
 patient has carefully read up the symptoms. 
 
 The age of the subject may be of assistance in deter- 
 mining the question. Angina is very rare before the age 
 of forty-five, except in the case of aortic valvular disease or 
 aneurysm or aortitis. 
 
 Sex, again, may often enable us to exclude angina 
 without hesitation. It is extremely rare in women at any- 
 period of life in the absence of the conditions just enume- 
 rated, whereas so-called angina is a favourite complaint of 
 neurotic ladies at all ages above thirty. What is described 
 
372 HEART DISEASE. 
 
 as " spasms " by tea-drinking female out-patients becomes 
 angina among the educated and neurotic. 
 
 The appearance of the patient as ascertained from friends 
 who have witnessed attacks may be valuable evidence. It 
 does not necessarily follow that if he turns pale and has a 
 look of alarm and suffering the paroxysms are those of true 
 angina ; but if his colour and expression show no change 
 it will be evidence to the contrary. 
 
 The circumstances under which the early attacks come 
 on are very significant. With rare exceptions the pain of 
 angina is first experienced during exertion, and when it 
 gradually increases in intensity with each successive attack 
 and is provoked more and more readily, there can be little 
 doubt as to its nature. If, on the other hand, the first 
 paroxysms set in during repose, and particularly at a given 
 interval after food, or at a particular hour of the night, the 
 inference is equally strong that they are pseudo-anginal in 
 character and of gastric origin. Unless the history, onset, 
 and nature of the paroxysms are quite characteristic, and 
 confirmatory physical signs are present, we should only 
 make a definite diagnosis of angina when all possible 
 explanation of the pain can be excluded. 
 
 If we leave out of the consideration neurotic and 
 hysterical attacks, which are usually easily recognizable, 
 the cause of the spurious angina is nearly always some 
 functional derangement of the stomach, and evidences of 
 disturbance of the digestion, such as occasional attacks of 
 vomiting, habitual flatulency with eructation, will often aid 
 in establishing the distinctive diagnosis. In many cases 
 dilatation of the stomach may be demonstrable by percus- 
 sion and succussion. 
 
 A common combination is dilatation or distension of the 
 stomach and high arterial tension. Together they give the 
 nearest imitation of true angina, and if the heart be at all 
 weak a fatal result is by no means impossible in elderly 
 
ANGINA PECTORIS. 373 
 
 subjects. Such a result may be invited if the functional 
 derangement of the stomach and liver are ignored, and 
 digitalis or other cardiac tonic is given or the Schott treat- 
 ment adopted, or if the paroxysms are simply treated by 
 nitrite of amyl or nitro-glycerine. 
 
 The following case may be given to illustrate these attacks of 
 so-called "Pseudo-angina." A medical man, aged 52, consulted me 
 for sudden and agonizing attacks of pain in the prsecordial area. 
 They were so severe that he had to sit down and lean forward, and 
 was incapable of movement or speech while they lasted. He himself 
 attributed them to angina pectoris, but found that trinitrin or nitrite 
 of amyl gave no relief. He was a gouty subject, and had had several 
 attacks of acute articular gout, and some of his medical friends attri- 
 buted the anginoid pain to gout. I found, on examination, that the 
 vessels were in good condition, the arterial tension was not high, 
 there was no valvular disease of the heart, which was normal in size ; 
 and that the heart sounds were good. On examining the abdomen, I 
 found that there was enormous dilatation of the stomach, and, on 
 questioning him, ascertained that he was a heavy feeder, and was in 
 the habit of eating large quantities of meat and drinking effervescing 
 water with whisky at lunch and dinner. I also ascertained that the 
 attacks of pain did not come on after exertion or exposure to cold, but 
 usually after a full meal. Taking all these matters into consideration, 
 I came to the conclusion that the attacks were not those of true 
 angina pectoris. I enjoined moderation in diet, the giving up of 
 effervescing water, and limitation in the amount of fluids taken, and 
 prescribed a mercurial purge once a week. The attacks soon ceased, 
 and have never recurred, and though he has since had several bouts 
 of acute gout, he is now in good health, and it is ten years since the 
 attacks of precordial pain for which he consulted me. 
 
 Prognosis. 
 
 The prognosis of angina is beset with uncertainty. We 
 can never tell when the next attack will come on, or 
 whether it may not be the last. We are not, however, 
 altogether without guidance, the elements of which will be 
 an estimate of the relative predominance of the two chief 
 factors in the production of the attack — whether inherent 
 weakness of the heart wall on the one hand, or, on the other. 
 
374 HEART DISEASE. 
 
 obstruction in the circulation or other cause of embarrass- 
 ment of the heart's action. 
 
 V/hile the attacks only come on when provoked by- 
 considerable exertion or excitement, or by flatulent in- 
 digestion (not, of course, taking the patient's word for the 
 last-named cause), the hope may be entertained that by 
 care in avoiding all known occasions they may be post- 
 poned indefinitely. If, further, there is habitual high 
 tension in the pulse, as in "angina vasomotoria," this is 
 at the same time evidence of obstruction in the arterioles 
 and capillaries which may be capable of mitigation by 
 treatment, and of some degree of vigour in the heart, which 
 will usually be hypertrophied. So also will be accentuation 
 of the aortic second sound, and still more any recognizable 
 impulse or apex beat. 
 
 The patient, of course, must not take exercise imme- 
 diately after food, must never hurry or walk against a 
 wind, and even on level ground must adapt his pace to his 
 condition, and if compelled to go uphill must do so very 
 gently and circumspectly. 
 
 Angina, again, in connection with aortic valvular dis- 
 ease, may run a very protracted course. It is when the 
 pulse is soft and the heart is normal in dimensions, with 
 imperceptible impulse and weak sounds, as in fatty degene- 
 ration — when, in fact, the results of careful examination are 
 negative — that the greatest uncertainty and danger exist. 
 The occurrence of unprovoked attacks and of nocturnal 
 angina will emphasize this conclusion. 
 
 Treatment. 
 
 The primary significance of angina pectoris is, as has 
 been said, that the heart is unequal to the task of pro- 
 pelling the blood. The heart is itself always in fault, but 
 undue resistance in the vessels may play an important part 
 
ANGINA PECTORIS. 375 
 
 in the production of the pain. The first consideration' 
 therefore, when the treatment of angina is undertaken, will 
 be whether there is arterio-capillary obstruction which can 
 be removed. The pulse will be examined carefully and 
 repeatedly at different periods of the day, before and after 
 food, before and after the night's rest, before and after such 
 exercise as the patient can take with impunity. If at any 
 time the artery is distinctly full between the beats, virtual 
 tension exists, i.e. there would be tension were there adequate 
 vis a tcrgo, and it may be concluded that obstruction is 
 present in the arterioles and capillaries which probably 
 contributes to the embarrassment of the enfeebled heart, 
 the removal of which may afford relief. Not uncommonly 
 there will be found a well-marked senile pulse, with the 
 arteries large, tortuous, and thickened, full between the 
 beats, but compressible, the pulse wave being sudden and 
 unsustained. Here the loss of elasticity and expansibility 
 of the entire arterial tree will be a cause of difficulty to 
 the heart. The aortic trunk and its main branches being 
 atheromatous and refusino- to dilate Avhen the blood is 
 propelled into them, the systole encounters the peripheral 
 resistance at once just as if the vessels were a system of 
 rigid, inelastic tubes. Nothing can be done to remedy /the 
 degeneration of the arteries, but it may be possible to lessen 
 the resistance in the capillary net-work which has been a 
 chief factor in the production of the atheromatous state, 
 and which is now adding cardiac overstrain and angina 
 to previous ill-effects. 
 
 In some cases of angina the pulse has all the characters 
 of high tension without advanced disease of the vessels. 
 This will usually be in gouty subjects, and we have angina 
 which may justly be called " gouty." 
 
 Whenever high arterial tension can be distinctly recog- 
 nized in angina pectoris, there is an opening for treatment 
 which may be palliative to a very important extent, and 
 
376 HEART DISEASE. 
 
 sometimes curative. The treatment will be such as has 
 already been described in discussing high arterial tension. 
 Colchicum may be given with the mercurial aperient in 
 gouty angina, and also a mixture containing iodide and 
 bicarbonate or citrate of potash, with gentian or some 
 other vegetable bitter tonic, twice or three times a day. 
 The iodide when well borne is often of remarkable service. 
 In such cases the treatment may be pursued with con- 
 fidence and with a certain degree of vigour. The diet 
 must be strictly regulated, and the nearer it can be brought 
 to a milk and farinaceous diet without incurring distension 
 of the stomach and flatulent dyspepsia the better. Heavy 
 meals must, of course, be avoided. Elimination may be 
 furthered by a tumbler of Vichy or Evian water, or plain 
 soft water night and morning. 
 
 When there is no conspicuous tension in the arteries, 
 and their walls are in a state of degeneration, and when 
 with this the walls of the heart are weak and probably 
 fatty, while the same end is held in view and similar means 
 are put in operation, great caution and watchfulness must 
 be exercised. The bowels must be made to act daily, but 
 mercurial aperients must be sparingly employed, an aloetic 
 pill or liquorice powder, or some preparation of cascara, 
 being given, if necessary, in the intervals. 
 
 When angina complicates disease of the aortic valves, 
 it is difficult to say whether arterio-capillary resistance con- 
 tributes in any way to its production, but if the pulse is 
 good it will be well to give mild mercurial aperients and 
 iodides on the assumption that such may be the case, though 
 caution must be observed in their administration. 
 
 If the pulse in the intervals between the attacks of 
 anginoid pain is small, short, easily compressible and 
 destitute of tension, no good result is to be expected from 
 eliminant treatment, and even small doses of mercury may 
 depress the patient. 
 
ANGINA PECTORIS. 377 
 
 Prominence has been given to removal of arterio-oapil- 
 lary resistance by eliminant treatment, because when called 
 for, it may yield more permanent relief than any other 
 line of treatment ; but arsenic and phosphorus may render 
 very important service, and except in cases of markedly 
 high arterial tension one or other of these should be 
 given concurrently with eliminants. A particularly useful 
 combination is arsenic with iodide of potassium and nux 
 vomica. Phosphorus seems to have a specially fa\ r ourable 
 effect in angina associated with aortic regurgitation. Bella- 
 donna or cannabis indica may be useful adjuvants in some 
 cases ; quinine and nux vomica also are often of service. 
 Nitro-glycerine or the heavier nitrites may also be required 
 habitually, though it is best when possible to reserve their 
 use for the anginoid attacks themselves. In the case of a 
 medical friend the erythrol tetranitrate appeared to be of 
 great service, enabling him to avert a fatal attack for 
 many years. 
 
 Treatment op the Attacks. 
 
 There remains to be considered the treatment of the 
 attacks themselves. Formerly brandy, various combinations 
 of ether, nitrous ether, ammonia, lavender, and camphor, 
 were the chief drugs resorted to. Inhalation of amyl 
 nitrite and the administration of nitro-glycerine or of 
 sodium nitrite or erythrol tetranitrate have now almost 
 entirely superseded these remedies. 
 
 Whatever the remedy, the patient should always carry 
 it about with him, and have recourse to it as soon as the 
 pain really sets in. The amyl nitrite is supplied in the 
 convenient form of glass capsules containing five mins., 
 enclosed in a silk bag, so that one of these can be broken 
 in a handkerchief and the vapour inhaled. Some prefer 
 to carry a small bottle of amyl nitrite about, to which 
 
37§ HEART DISEASE. 
 
 they can have recourse when the attack threatens. Nitro- 
 glycerine, however, taken by the mouth, appears to be 
 more generally useful, since, though the effect is scarcely as 
 rapid as that of inhaled amyl nitrite, it lasts much longer. 
 Erythrol tetranitrate is even more satisfactory, as its effects 
 are more prolonged than those of trinitrin. Tabloids of 
 nitro-glycerine containing one min. of a one per cent, 
 solution can be carried about, and one or two can be 
 swallowed when necessary with very little loss of time. 
 
 In most cases nitro-glycerine has a better effect than 
 amyl nitrite, though in rare instances nitro-glycerine ap- 
 pears to have no influence on the spasm to which nitrite 
 of amyl at once gives relief. In two cases of the kind 
 that I have seen, it has seemed to me extremely probable 
 that the anginoid paroxysm had its origin in the right 
 ventricle. 
 
 Occasionally when the nitrites fail we have to fall back 
 on the old-fashioned remedies, especially when the heart 
 failure is pronounced and the pulse tension is extremely 
 low. Here it may do more good to help the heart by 
 stimulants than to relieve it of work. While the paroxysms 
 of angina are for the most part brief, the agony being such 
 that it seems as if another moment must prove fatal, there 
 are at times attacks of a protracted character. When the 
 pain persists in spite of nitrites and stimulants, morphine 
 and atropine should be administered hypodermically, and 
 it is well to carry the needle into the substance of a muscle 
 where the circulation is more active than in the sub- 
 cutaneous cellular tissue. The initial dose should be small, 
 but it may be necessary to employ morphine boldly. A 
 turpentine stupe may also be applied over the region of 
 the heart, or a mustard leaf or poultice. 
 
 It must be remembered also that the nitrites give rise to 
 great frequency of the heart action which may be a source 
 of distress. We should consequently employ them very 
 
ANGINA PECTORIS. 379 
 
 cautiously wheu the augina is accompanied by a frequent 
 pulse. The nitrites have been supposed to be heart tonics, 
 but while their most prominent action is relaxation of the 
 arterio-capillary net-work they also relax the cardiac 
 muscular fibres. 
 
 As in so many other instances, the employment of nitro- 
 glycerine and the nitrites is not without its drawbacks. 
 Patients often come to rely on the immunity from pain 
 which the remedies confer and then presume upon it. 
 Liberties are taken and imprudences are committed, so that 
 not unfrequently sudden death is precipitated which might 
 with care have been staved off for years. In placing the 
 remedy in the patient's hands, therefore, emphatic words 
 of caution must be spoken and the danger must be 
 pointed out. 
 
 The instructions to be given with regard to exercise are 
 extremely important. After a very severe paroxysm, how- 
 ever provoked, rest in bed may be necessary for some days, 
 and even for a period of two or three weeks, if the attack 
 has been prolonged. The heart may be left extremely weak, 
 its action slow or faltering and irregular, and the sounds 
 scarcely audible, and sitting up or turning in bed may be 
 attended with giddiness or faintness or pain in the region 
 of the heart. When such conditions are present, time must 
 be given to the heart to recover itself, and measures must 
 be taken to relieve flatulence and constipation, which will 
 probably be associated with the other symptoms. 
 
 Under ordinary circumstances, however, the rule usually 
 applicable in heart disease holds good here. Whatever 
 exercise the patient can take without provoking an attack 
 at the time, or prostration afterwards, he will be the better 
 for. While, however, the exercise should be as regular 
 as possible, in no case is it more necessary to bear 
 in mind the fact that the capacity for exertion varies from 
 day to day, and that the sufferer from angina can do easily 
 
3§o HEART DISEASE. 
 
 one day what would be impossible for hirn on another. 
 This is one of the objections to the (Ertel methods of 
 treatment. Some of the influences which affect him we can 
 recognize, such as wind, or severe cold, or great heat, or 
 weather which is felt by people in health to be oppressive, 
 or a moisture-laden atmosphere ; others arise out of internal 
 conditions, flatulence, dyspepsia, constipation, functional 
 derangements of the liver. The patient's feelings and in- 
 clinations have thus to be taken into account, but without 
 allowing inertia or nervousness to have undue weight. 
 There is great room here for judgment and tact and per- 
 sonal knowledge of the patient's disposition. Besides the 
 caution necessary in cold and hot weather, the liability to 
 anginoid attacks on walking soon after food must be borne 
 in mind, and a period of rest after meals must be enjoined, 
 esj^ecially after that particular meal which experience in the 
 case under treatment has shown to be worst in this respect. 
 
CHAPTEE XXVI. 
 
 FUNCTIONAL AFFECTIONS (SO-CALLED) OF 
 THE HEAET. 
 
 PAIN IN PRECORDIAL REGION— SITE OF PAIN — EXPLANA- 
 TION OP REFERRED PAIN AND AREAS OF CUTANEOUS 
 HYPERALGESIA — DISORDERS OF RHYTHM OF THE 
 HEART — MECHANISM BY WHICH THE RHYTHM OF 
 THE HEART IS REGULATED — INTERMITTENT AND 
 IRREGULAR ACTION OF THE HEART — PALPITATION : 
 TACHYCARDIA. 
 
 The term " functional affections " is retained, not for any 
 merit of its own but for want of a better. Under it must be 
 discussed a variety of symptoms having the heart for their 
 centre, but which cannot be assigned to any structural 
 change. Taken all together they give rise to much actual 
 suffering, and to far more nervous apprehension and fear 
 of death than definite valvular and structural disease com- 
 bined. So much is this the case that when patients come 
 complaining of the heart, we are almost safe in concluding 
 that the heart is disturbed by some cause outside itself and 
 is not the seat of disease. 
 
 Cardiac Pain. 
 
 Pain is one of the symptoms which frequently gives rise 
 to apprehension of heart disease. Leaving out of the 
 question that of angina, which has already been discussed, 
 
382 HEART DISEASE. 
 
 its most common seat is the region of the apex, but it 
 may be felt over any part of the cardiac area, the left 
 third space being next to the apex, the most frequent part 
 in which pain is experienced. It is most commonly of a 
 dull aching character, but may be sharp and stabbing or 
 burning, and nervous women will exhaust all the epithets 
 which can be applied to pain in their description of their 
 sufferings. Tenderness on pressure very commonly accom- 
 panies the pain; it is superficial and is equally severe, 
 whether the pressure is made over a rib or in an intercostal 
 space ; it is often particularly severe in the edge of the 
 mamma when this extends into the tender area. The 
 tenderness is quite extra-thoracic, and is felt when the heart 
 is not even indirectly reached by the pressure. 
 
 Another special seat of tenderness is over the second rib, 
 about an inch from the edge of the sternum, where a branch 
 of the cervical plexus crosses the rib. Pressure here not 
 only causes pain, but may give rise to intolerable cardiac- 
 distress. 
 
 Explanation of Referred Pain and Areas of Hyperalgesia. — 
 The relationship of areas of cutaneous hyperalgesia and 
 referred pain to visceral affections has been ably demon- 
 strated by Mackenzie * and by Head,t and will explain 
 most of the above phenomena. Briefly, Head's conclusions 
 are as follows : — 
 
 As the viscera are insensitive, and from their inacces- 
 sibility to touch are incapable of developing the sense of 
 localization, the maximum pain is not felt in the affected 
 organ. A painful stimulus to an internal organ is con- 
 ducted to the corresponding segment of the cord, where it 
 comes into contact with the sensory nerves from the area of 
 the body supplied by the same segment. The sensory and 
 localizing power of the skin is enormously in excess of that 
 
 * Med. Chron., Manchester, 1892, p. 293; and Lancet, 1895, vol. i. p. 1G. 
 f Brain, 1893, pp. 1 et seq. ; and J894, pp. 339 et seq. 
 
CARDIAC PAIN. 383 
 
 of the viscera, and by a psychical error of judgment the 
 pain is referred to the corresponding segmental area of the 
 body, instead of to the affected organ. 
 
 In neuroses of the heart, hyperesthesia, or, as Head puts 
 it, hyperalgesia, of the corresponding cutaneous segmental 
 areas is a common feature, whereas in angina pectoris this 
 is as nothing compared with the widespread agonizing 
 referred pain. 
 
 According to Mackenzie and Head, in most affections 
 of the heart and aorta the cutaneous areas in which hyper- 
 algesia is present, and to which the pain is referred, are 
 those corresponding to the first, second, third, and fourth 
 dorsal segments, which comprise, roughly, all the front of 
 the chest, from the second rib to the level of the nipple, 
 the posterior and lateral surface from the level of the seventh 
 cervical to the fourth dorsal spine, and certain areas on the 
 inner aspect of the arms. 
 
 In angina pectoris, however, the distribution of the 
 referred pain differs considerably from that in other affec- 
 tions of the heart, and it would appear that the painful 
 stimulus to the heart is so severe that it sets up a wide- 
 spread and violent commotion in the cord, so that pain may 
 be referred upwards over certain cervical areas and down- 
 wards as low as the ninth dorsal segmental area. 
 
 Etiology. — Pain in the region of the heart may be due to 
 conditions of the heart itself, to dilatation or overstrain, 
 to an enfeebled and irritable state after a depressing- 
 illness, or to toxic influences, e.g. tobacco, to direct pressure 
 upon the heart by a dilated stomach or extreme distension 
 of the abdomen, to reflex disturbance from some visceral 
 derangement, or to nervous or emotional states. 
 
 Taking the last-named first, it is exemplified by the 
 sharp pain in the heart, which may be induced by a sudden 
 shock or fright, or by powerful emotion, and by the heart- 
 ache of profound or protracted grief. But, without adequate 
 
384 HEART DISEASE. 
 
 emotional influence nothing is more common than cardiac 
 pain as an expression of nervous depression. 
 
 Eeflex pains are mostly of dyspeptic origin, but may be 
 associated with uterine derangements. The pain caused by 
 direct pressure of the diaphragm, carried upwards by a 
 dilated stomach or distension of the colon or intestine 
 generally, is accompanied by oppression of the breathing, 
 and is usually felt at the base of the heart and is aggravated 
 on lying down. 
 
 Pain due to overstrain of the heart is commonly a diffuse 
 ache over the cardiac area, generally accentuated in the 
 region of the apex. 
 
 The treatment of cardiac pain will in its details vary 
 with the cause. If due to toxic influences, these should 
 be removed. If due to overstrain or dilatation, the treat- 
 ment should be on the lines given on p. 303. But in 
 all cases it is most important to be able to convince the 
 patient that there is no disease. While he has the idea 
 in his mind that he is suffering from some serious heart 
 affection, the concentration of his attention on the heart 
 will be sufficient to renew the pain, and his apprehensions 
 will interfere with the recovery of his nervous equilibrium. 
 
 If due to reflex disturbances, such as derangements 
 of the digestive organs, liver or uterus, these should be 
 rectified by suitable diet and treatment, and, as a rule, 
 tonics will be of service. 
 
 With the internal and general remedies the local 
 application of belladonna as a liniment or plaster will be 
 useful. The plaster is often more efficacious if it is applied 
 so as to afford support or to exercise pressure on the painful 
 part, and it is well, therefore, to apply it in strips. 
 Counter-irritation over the tender area by a mustard-leaf 
 or blisters is often of great service in neurotic individuals. 
 
mechanism regulating rhythm of the heart. 385 
 
 Disorders of Ehythm of the Heart. 
 
 These may be classified under the following heads ; — 
 
 1. Interniittency of the heart's action. 
 
 2. Irregularity in the force and frequency of the heart 
 beats. 
 
 3. Abnormally rapid action of the heart, which may be 
 temporary (palpitation) or continuous (tachycardia). 
 
 4. Abnormally slow action of the heart (bradycardia). 
 These will be discussed in detail under their respective 
 
 headings ; but it may be as well first to briefly refer to the 
 views held as to the mechanism by which the rhythm of 
 the heart is regulated. 
 
 Mechanism regulating the Ehythm of the Heart. 
 
 Gaskell * describes the functions of the muscular fibres 
 of the heart as rhythmicity, excitability, contractility, con- 
 ductivity, and tonicity, by virtue of which the heart is able 
 to beat and keep up the circulation independently of nerve 
 control, the vagus and sympathetic having only a moderating 
 influence upon these varied functions. 
 
 The muscle fibres at the mouth of the great veins and 
 adjoining portion of the right auricle, and the muscular 
 tissue joining the auricles and ventricles, according to 
 Gaskell, possess the greatest power of automatically creating 
 a stimulus for contraction. 
 
 The fibres joining the auricle and ventricle play an 
 important part in the conduction of the stimulus for con- 
 traction from auricle to ventricle. On applying a clamp to 
 the auriculo- ventricular groove in a frog's heart, Gaskell 
 states that, according to the tightness of the clamp, the 
 ventricle may be made to respond to every second, third, or 
 fourth contraction of the auricle. 
 
 * " Text-book of Physiology," edited by Scbafer, vol. ii. 
 
 2c 
 
386 HEART DISEASE. 
 
 Mackenzie,* in a valuable paper, calls attention to these 
 facts, and to the work of Englemann and Wenckebach on 
 disordered rhythm of the heart, and contributes a series of 
 interesting observations on the nature of the conducting 
 power whereby the stimulus is conveyed from auricle to 
 ventricle. His method of investigation is to take simul- 
 taneous tracings of the jugular and carotid or radial pulses, 
 and thus time the period which elapses between the auri- 
 cular and ventricular systole. 
 
 He attaches great importance to the function of the 
 muscle fibres connecting the auricle with the ventricle, and 
 shows that certain forms of arrhythmia, more especially 
 intermittent action of the heart and bradycardia, are pro- 
 bably due to depression of or a block in the conductivity of 
 these fibres. 
 
 Nervous Influences. — Though the rhythmic action of the 
 heart is automatic and dependent on the inherent properties 
 of its muscular fibres, the central nervous system exercises 
 an important controlling influence on the varied functions 
 of the cardiac muscle through the pneumogastric and sym- 
 pathetic nerves. Messages must constantly be passing to 
 and fro along these nerves between the heart and centres 
 in the medulla, by means of which the heart is kept in- 
 formed of the condition and requirements of the body in 
 general, and the vascular system in particular, so that the 
 force and frequency of its beat, and the degree of tonicity 
 of its muscle fibres, are regulated accordingly. 
 
 All are familiar with the extreme and distressing varia- 
 tions in the frequency of the heart beat which may be 
 induced by sudden and violent emotions of fear or anger, 
 or by intense excitement, which in certain diseased con- 
 ditions may give rise to a fatal syncopal attack by arrest 
 of the heart's action. Disturbances of rhythm may be 
 occasioned by reflex impulses transmitted from the stomach 
 * " New Methods of Studying Affections of the Heart," B.M.J., March, 1D05. 
 
INTERMITTENCY OF THE PULSE. 387 
 
 or other viscera in consequence of functional derange- 
 ments. 
 
 G-ibson,* in his excellent account of " Nervous Affec- 
 tions of the Heart," gives some interesting tracings from 
 the experimental work of Wenckebach and Cushny, which 
 show the different effects of electrical stimuli on the rhythm 
 of the heart, according to the region stimulated, and the 
 time in the cardiac cycle at which they are applied. 
 
 As one of the results of these experiments, it is demon- 
 strated that if a stimulus is applied to the heart just before 
 the normal of contraction is due, a premature imperfect 
 systole takes place, which is insufficient to transmit a 
 pulse wave to the wrist, so that a beat is dropped in the 
 radial pulse. This will explain certain forms of inter- 
 mittent pulse and irregular action of the heart. The 
 nature of the stimulus which interferes with the normal 
 automatic contraction of the heart is not always easy to 
 determine. Probably, when the intermittency is a tem- 
 porary phenomenon, it is the result of a reflex from some 
 gastric or other visceral disturbance. When persistent, 
 it may perhaps be due, not to reflex nervous influences, 
 but to a block in the conductivity of certain of the cardiac 
 muscle fibres referred to above. 
 
 Intebmittency of the Pulse. 
 
 By an intermittent pulse is meant a pulse in which a 
 beat is missing from time to time, while in the intervals it 
 is perfectly regular. The intermission may occur at regular 
 and definite periods every four, six, or more beats up to 
 twenty, or the number of intervening pulsations may vary. 
 
 It is not characteristic of any form of heart affection and 
 is rarely indicative of organic disease. An intermittent 
 pulse may be constant and habitual, and the intermission 
 
 * " Nervous Affections of the Hearf," Young Pentlaud, 1904. 
 
388 HEART DISEASE. 
 
 is then more likely to occur at definite intervals ; it may- 
 be occasional only, and may be attributable to some dis- 
 turbing reflex cause, of which flatulent dyspepsia is the 
 most common. In some cases the pulse is intermittent 
 after each meal ; or in others tea, coffee, or tobacco may be 
 the special cause of the intermission. It is common also 
 in chronic gout, and may be among the signs of fatty 
 degeneration of the heart. In case of doubt the patient 
 should be made to walk briskly for a minute or two, when, 
 if the heart is really weak and degenerated, the pulse will 
 falter, whereas, if the heart is healthy, the intermission will 
 usually disappear. Intermittency of pulse may also be 
 associated with nervous debility and hypochondriasis, the 
 pulse becoming normal again when the patient regains 
 good health. On examining the heart it is usually found 
 that the cause of the intermission is not the actual omission 
 of a heart beat, but the occurrence of a hurried and im- 
 perfect contraction which rapidly follows the last of the 
 series of normal beats, and does not transmit a pulse wave 
 to the wrist. The imperfect beat may sometimes be felt on 
 palpation ; usually only the first sound is heard on aus- 
 cultation at the apex unaccompanied by a second sound. 
 The heart beat which follows the intermission is usually 
 more powerful than normal. While it is the rule that 
 there is this feeble interposed heart beat, instances occur 
 where it cannot be heard or felt, and in which the heart 
 appears to remain quite passive. This condition will be 
 discussed further in the chapter on bradycardia. 
 
 The patient may or may not be conscious of the inter- 
 mittent action of the heart. He is more likely to be aware 
 of it when it is symptomatic of some functional derange- 
 ment than when it is habitual; he may be conscious of a 
 vague sense of discomfort or of an unpleasant sinking 
 sensation in the cardiac region during the intermission, or 
 he may feel the bump of the stronger beat which usually 
 
IRREGULARITY OF HEART'S ACTION. 389 
 
 follows the feeble and imperfect or dropped beat. In view 
 of G-askell's, Wenckebach's, and Mackenzie's work, referred 
 to above, the explanation of intermittent action of the heart 
 when persistent would seem to be that it arises from a 
 lowering of conductivity in the muscle fibres joining the 
 auricle and ventricle, so that the stimulus for contraction 
 is not regularly transmitted from auricle to ventricle. Some- 
 times this may be attributed to cardiac sclerosis, sometimes 
 there is no apparent cause. It may be met with in men who 
 enjoy vigorous health and live to a good old age. When 
 the intermittent action of the heart is only occasional, it is 
 usually traceable to some toxic cause, such as tea, coffee, 
 or tobacco, or to reflex gastric or other visceral disturbances, 
 and suitable treatment for removal of the cause should then 
 be adopted. 
 
 Irregularity of the Heart's Action. 
 
 Irregularity of the heart's action, like intermittency, 
 may be habitual or occasional. Habitual irregularity is 
 commonly present in mitral incompetence and in cases of 
 cardiac dilatation of any severity, when it is probably due 
 to the variable supply of blood to the left ventricle, as 
 explained in Chapter XI. It is occasionally met with in 
 individuals in whom there is no evidence of any heart 
 disease, and who enjoy good health and live to old age. 
 In one instance I have known the heart's action, without 
 any apparent cause, to be markedly irregular during a 
 period of at least twenty years to my knowledge in a 
 gentleman who lived to the age of seventy and enjoyed 
 vigorous health. 
 
 Irregularity associated with excessive frequency of pulse 
 is usually of serious prognostic significance, and may be an 
 incident in the final stages of paroxysmal tachycardia. 
 
 Irregular action of the heart setting in after middle life 
 
39° HEART DISEASE. 
 
 with evidence of degenerative change in the vessels is also 
 serious, as it may be due to fibroid change in the heart 
 associated with sclerosis of the coronary vessels. 
 
 Temporary irregularity of the cardiac action is much 
 more common, and may be occasioned by tobacco or strong 
 tea, by mechanical embarrassment of the heart by a dis- 
 tended stomach or colon, or by various reflex causes, such 
 as gastric and liver derangements, or emotional disturbances 
 of various kinds. 
 
 Irregularity of the cardiac action is more serious than 
 intermission, and steps should at once be taken to remove, 
 if possible, the exciting cause. When there is mechanical 
 embarrassment of the heart by a distended and dilated 
 stomach the distress at times may be severe, and there is 
 danger of a sudden syncopal attack in elderly people in 
 whom the heart has undergone degenerative changes. 
 
 Palpitation. 
 
 By palpitation is meant frequent and violent action of 
 the heart, of which the subject is conscious ; but patients 
 will sometimes say they are suffering from palpitation when 
 there is neither frequency nor violence recognizable in the 
 beat of the heart or pulse by the observer, and, on the 
 other hand, may be unconscious of extremely rapid action 
 of the heart found on examination. 
 
 With palpitation there is usually uneasiness, sometimes 
 pain, in the region of the heart, oppression of the respiration 
 with frequent deep sighs and a sense of inability to fill the 
 chest sufficiently. Often there is excitement and alarm 
 and the patient feels giddy or faint ; the face may be 
 flushed or very pale. 
 
 When the heart is acting very rapidly, many of the beats 
 may fail to reach the radial artery, so that the pulse be- 
 comes irregular. The reason probably is that the ventricle 
 
PA LPITA TIOX. 39 1 
 
 has not time to fill, and that consequently there is not 
 sufficient blood propelled into the aorta to communicate a 
 wave to the peripheral vessels. Very often the artery is 
 small and full between the beats, there being a general 
 excitement of the vascular system with spasm of the 
 arterial walls. This is particularly the case in hysterical 
 palpitation, when there will frequently also be a copious 
 secretion of pale dilute urine. 
 
 On examination, during an access of palpitation, the 
 heart may be felt to be beating violently, but when the 
 rapidity of its action is extreme a faint vibration only may 
 be communicated to the hand. On auscultation, the first 
 sound may be loud and short, followed immediately by a 
 weak second sound, or, in the case of extreme frequency, the 
 first and second sounds may be almost identical in character 
 and equidistant, resembling very closely those of the foetal 
 heart, and comparable to the puffing of a distant locomotive. 
 Etiology. — Among the causes of what may be called 
 ordinary palpitation as distinguished from tachycardia, the 
 most important is a predisposition thereto on the part of the 
 nerve centres governing the heart, which may be inborn 
 or induced by modes of life or by the various circumstances 
 which tend to lower the nervous tone or to promote nervous 
 excitability. Palpitation is much more common in women 
 than men, partly in virtue of the greater inherent suscepti- 
 bility of the female nervous system, partly from the more 
 emotional life of women, their greater confinement to the 
 house, and their less vigorous exercise ; but child-bearing 
 and over-lactation are also in themselves serious predis- 
 posing causes. In men a sedentary mode of life, exciting- 
 occupations, dissipatiou, and excesses of all kinds, over- 
 indulgence in tobacco, bring about a liability to palpitation. 
 Mitral stenosis is a form of valvular disease in which attacks 
 of palpitation are very liable to occur, the exciting cause 
 usually being gastric disturbances. 
 
392 HEART DISEASE. 
 
 Among the exciting causes are sudden violent impres- 
 sions on the nervous system of any kind — fright, an un- 
 expected noise, a startling incident taking place before the 
 eyes, a powerful emotion ; these will set any one's heart 
 beating, but in a strong and healthy person the effect is of 
 very brief duration ; where the predisposition to palpitation 
 exists they may initiate an uncontrollable attack. A similar 
 statement applies to exertion — a brisk walk uphill causes 
 the heart to act rapidly and powerfully under normal circum- 
 stances ; in a predisposed individual the action may be 
 exaggerated and protracted, so as to constitute an attack of 
 palpitation. 
 
 But the characteristic palpitation of the heart starts 
 suddenly without obvious exciting cause, while the patient 
 is sitting quietly at work or reading, or during sleep, when 
 he or she may wake up from a frightful dream which 
 appears to have brought on the attack. 
 
 There is, however, as a rule, some internal exciting 
 cause, which is most commonly gastric derangement 
 attended or not with flatulent distension of the stomach or 
 bowels. Other forms of peripheral irritation may act as 
 exciting causes, such as uterine affections. 
 
 Treatment. — To arrest an attack of palpitation it is 
 sometimes only necessary to take a dozen deliberate deep 
 breaths, and it is always well to try t this expedient before 
 resorting to drugs. The remedies of most general service 
 are combination of alkaline and carminative stimulants ; 
 bicarbonate of soda with ammonia and camphor or pepper- 
 mint water is often sufficient, but compound tincture of 
 chloroform, ether, valerian, lavender, ginger may be added 
 or substituted; in some cases bromides are required. 
 Undue acidity of the gastric contents is corrected, flatu- 
 lence is expelled, and possibly the stimulation of the 
 pneumogastric fibres of the mucous membrane of the 
 stomach may have some inhibiting influence on the heart. 
 
TA CHYCARDIA . 393 
 
 Digitalis appears to have little or no effect, but belladonna 
 may be useful, especially in combination with bromide of 
 ammonium or sodium. 
 
 For the prevention of palpitation the tone of the nervous 
 system must be raised by the usual hygienic and medicinal 
 means, namely, change to the seaside, or, better, to moun- 
 tain health resorts, exercise, fresh air, early hours, simple 
 wholesome food, avoidance of undue excitement of all kinds. 
 The emplast. belladonnas over the region of the heart 
 appears to have some influence in preventing or moderating 
 the attack, probably mainly due to the mechanical support. 
 
 Careful inquiry should be made as to any relation 
 between the taking of food and the occurrence of an attack 
 and as to the existence of functional derangements of the 
 stomach, liver, or other organs. The abdomen should be 
 examined to see if there is flatulent distention of the 
 stomach, colon, or small intestine, and suitable remedies 
 should be given for this, together with such tonics as are 
 indicated by the general condition of the patient. 
 
 TACHYCARDIA. 
 
 Attacks of palpitation, or rapid action of the heart, may 
 last a few minutes or a few hours, and are usually traceable 
 to emotional or reflex gastric disturbances, and are not of 
 great severity. 
 
 There are, however, cases in which rapid action of the 
 heart, with a pulse of 100 to 120, is a more or less perma- 
 nent condition, and others in which attacks of extremely 
 rapid action of the heart, with from 200 to 300 beats per 
 minute, set in from time to time, lasting, perhaps, for several 
 days, and eventually proving fatal. To this latter affection 
 the term " paroxysmal tachycardia " lias been applied. 
 
394 heart disease. 
 
 Etiology. 
 
 Occasionally one meets with individuals in good health 
 who have normally a pnlse of from 90 to 100. 
 
 Alcoholism in neurotic subjects may give rise to a 
 permanently rapid pulse, and I have seen two instances 
 in neurotic ladies addicted to alcohol in which a pulse of 
 100 to 120 was present for a considerable number of years. 
 A retired naval officer also consulted me from time to time 
 for some months, and when seen always had a pulse of 
 140, and there was every reason to believe that this rate 
 was maintained in the intervals between his visits when he 
 went about as usual. He was gouty, and had taken wine 
 and spirits very freely. Eventually dropsy set in, and he 
 died from heart failure. 
 
 In Graves' disease a permanent rapid pulse is one of the 
 chief characteristics associated with enlargement of the 
 thyroid, exophthalmos, etc. 
 
 In this affection the tachycardia is attributed by most 
 authors to excessive secretion by the thyroid gland. In 
 favour of this view are the clinical contrast between this 
 disease and myxoedema, the increase in the severity of the 
 symptoms when thyroid extract is administered, and the 
 improvement that has followed in some cases on removal of 
 the bulk of the enlarged thyroid. 
 
 Others consider that it is a pure neurosis, as the exciting 
 cause can frequently be traced to some profound shock or 
 emotional disturbance. 
 
 Paroxysmal Tachycardia. — This affection is characterized 
 by attacks of extreme rapidity of the heart's action, in 
 which the pulse rate may be from 150 to 250 per minute. 
 The attacks may last some days, or even weeks. They 
 may terminate fatally from syncope, or cardiac failure and 
 exhaustion, or may suddenly cease, and be succeeded by a 
 period in which the patient enjoys good health. They 
 
TACHYCARDIA. 395 
 
 may set in without any apparent cause, and post-mortem no 
 gross lesion of any kind is found in the valves or heart- 
 muscle, though there may be an extreme degree of dilatation 
 of the heart in cases in which the tachycardia has persisted 
 for a long period. 
 
 Bristowe, quoted by Huchard, gives an account of a 
 remarkable case in a boy aged 19 with a syphilitic history, 
 in which the pulse ranged from 240 to 250, then became 
 irregular, with periods in which the rate was 200 for 10 
 seconds, alternating with others in which it fell to 100. 
 This lasted for 10 days, when the pulse suddenly fell to 60. 
 Three weeks later he had a fresh attack, and the pulse rate 
 rose to 288, but fell to 84 when he took to his bed. A 
 month later he had a third attack, and the pulse rate rose 
 to 308 when he was up, but fell to 64 when he lay down. 
 This recurred on several occasions, and fifteen days later 
 he died suddenly while playing the piano. 
 
 Pathogeny. 
 
 The main cause of this affection must be some derang-e- 
 ment of the nervous mechanism controlling the heart, and 
 opinions are divided as to whether it may be due to ex- 
 citation of the sympathetic or temporary paralysis of the 
 vagus, or to some affection of the inhibitory centre in the 
 medulla. There is little to be said in favour of the theory 
 that it is due to stimulation of accelerator fibres in the 
 sympathetic. It is more probable that it may be due to 
 derangement of the inhibitory mechanism in the medulla 
 or to interference with inhibitory impulses descending from 
 this centre through the pneumogastric. 
 
 There is no evidence in support of bulbar disease as a 
 cause of tachycardia, but there are cases on record in which 
 tachycardia has apparently been due to compression of the 
 vagus in the neck by enlarged glands, growths, or cicatricial 
 
396 HEART DISEASE. 
 
 tissue. Instances of this are quoted by Huchard.* In 
 most cases of tachycardia gross lesions of the trunk of the 
 vagus can be excluded, but it is possible that its fibres may 
 be damaged after they have penetrated the myocardium, 
 (a) by compression in cardiac sclerosis ; (&) by spread of 
 inflammation in acute myocarditis ; (c) by the direct action 
 of toxins in severe toxaemias, with resulting peripheral 
 neuritis. 
 
 There is, however, no definite pathological evidence to 
 support this surmise, and paroxysmal tachycardia is not a 
 common sequela of acute toxaemias. It may be that in- 
 creased irritability of the cardiac muscle is the more 
 important factor, but little is really known as to the 
 pathogeny of this obscure affection. 
 
 Tbeatment. 
 
 In tachycardia, digitalis and the cardiac tonics gene- 
 rally, or the carminatives which are useful in ordinary 
 palpitation, appear to have little or no influence on the 
 frequency of the heart's action. Rest, mental as well as 
 bodily, and simple diet must be insisted on, and any 
 functional derangements of the abdominal or pelvic viscera 
 should be corrected. The drugs which have seemed to 
 exercise control over the heart have been bromides, in full 
 doses, and belladonna or atropine, pushed to the limits of 
 tolerance. 
 
 Huchard has found digitalis useful, and has had good 
 results in three cases with large doses of quinine. He has 
 also given ergotin with benefit. 
 
 Thymus gland has been given with the idea that it is 
 antagonistic to the thyroid, but one would only expect 
 benefit from this, if at all, in G-raves' disease. Galvanism 
 of the vagi has been tried, and sometimes a measure of 
 success has been claimed for this treatment. 
 * " Mai. du Coeur," vol. iii. p. 866. 
 
TACHYCARDIA. 397 
 
 Barr * states that lie has had satisfactory results from 
 the administration of nitrite of amyl and nitroglycerine in 
 two cases of paroxysmal tachycardia. It will be seen that 
 drugs of a widely different character have been employed 
 in the treatment of this affection, and a certain measure of 
 success has been claimed for each in individual cases ; but 
 it cannot be said that we have any certain means of reduc- 
 ing the rapid action of the heart, and a certain proportion 
 of cases defy all known methods of treatment. 
 
 * Barr, " Clin. Lect. on Paroxysmal Tachycardia," B.M.J., vol. ii. 1U04, 
 p. 109. 
 
CHAPTER XXVII. 
 
 DISORDERS OF RHYTHM OF THE HEART 
 
 {Continued). 
 
 varieties of slow pulse and their causation — the 
 condition of bradycardia known as stokes- 
 adams disease — etiology — symptoms —diagnosis — 
 prognosis — treatment. 
 
 Varieties of Slow Pulse and their Causation. 
 
 A condition of permanent slow pulse ranging from 40 to 
 60 may be hereditary and compatible with good health. 
 It is not, however, altogether free from suspicion of liability 
 to heart failure under the stress of exertion or acute illness. 
 Pathologically, it may be associated with cerebral tumour 
 or meningitis (late stages), or with certain conditions of 
 neurasthenia and with melancholia. 
 
 Extreme slowness of pulse is also met with sometimes 
 in toxic conditions, such as lead-poisoning, when it may be 
 attributed to protracted high arterial tension, or may follow 
 influenza, diphtheria, or typhoid fever, the toxins of which 
 affect the integrity of the cardiac muscular fibres. It may 
 occasionally supervene in uraemia, and in jaundice of pro- 
 longed duration. Here, again, the slowing of the heart is 
 attributable to toxic substances in the blood. It has been 
 attributed in a few doubtful cases to over-dosing with 
 digitalis and strophanthus and the like. This affection of 
 slow heart action is to be differentiated from the apparently 
 slow pulse met with sometimes in cardiac lesions, in which 
 
BRA D YCA RDIA. 399 
 
 the pulse seems to be slow because all the heart-beats are 
 not felt as a pulse at the wrist. The pulse may in such 
 cases be irregular, as well as infrequent, but cases are not 
 uncommon in which only every other beat reaches the 
 radial, the rate at the heart being, say, from 80 to 100, 
 while the pulse rate as counted at the wrist is perfectly 
 regular, but only 40 to 50. 
 
 Stokes-Adams Disease. 
 
 In addition to the above conditions in which true brady- 
 cardia is met with as an effect of various recognizable 
 influences, there is a certain clinical entity characterized 
 by a group of definite symptoms to which the name of 
 Stokes-Adams disease has been given, from the fact that 
 attention was first called to it by Adams in 1827, while it 
 was subsequently described in fuller detail by Stokes in 
 1836. 
 
 The disease is characterized by permanent slow pulse, 
 ranging habitually as low as 20, or from that to 30 or 40, 
 while there are from time to time exacerbations of the 
 infrequency associated with syncopal, epileptiform, or 
 pseudo-apoplectiform attacks. Sometimes in the later 
 stages there may be angina pectoris or Cheyne- Stokes 
 breathing. 
 
 Etiology. 
 
 The condition is almost invariably associated with senile 
 degenerative changes in the vascular system. The patient 
 is usually over 50 years of age, and the artery at the wrist 
 is large, hard, cord-like, and incompressible. The Avails of 
 the vessel are thickened, and arterio-sclerosis is the pro- 
 minent feature. Huchard, quoted by Osier, states that the 
 etiology of the condition is " la senilite arterielle," * and 
 
 * Lancet, August 22, 1903. 
 
400 HEART DISEASE. 
 
 Osier endorses this opinion, although he gives three 
 instances of the affection in young subjects in the interest- 
 ing list of clinical histories of cases under his care. 
 
 While thickening of and degenerative changes in the 
 vessels are constant and important factors in the Stokes- 
 Adams syndrome, they cannot be said to explain the brady- 
 cardia or other phenomena. 
 
 Huchard,* commenting on the frequency of arterio- 
 sclerosis and the comparative rarity of the Stokes- Adams 
 phenomena in association with it, suggests that the latter 
 may be due to relative angemia of the medulla from athe- 
 roma of the vessels supplying it. In support of this 
 explanation, he refers to experiments by Brown-Sequard, 
 Duret, and Conty, showing that anEemia of the bulb causes 
 slowing of the pulse, and he instances the slow pulse met 
 with in certain affections of the nervous system. He 
 considers that the feeble action of the heart may be a 
 contributory factor. 
 
 Impairment of conductivity of the muscular fibres between 
 the auricle and ventricle has been suggested by Mac- 
 kenzie of Burnley as an explanation of the slow pulse 
 in these cases. Gaskell has shown that in the frog's heart, 
 if a clamp is applied along the auriculo-ventricular groove, 
 the ventricle can be made to respond to every second, third, 
 or fourth contraction of the auricle or to remain quiescent, 
 according to the tightness of the clamp. Mackenzie f calls 
 attention to this, and has demonstrated, by simultaneous 
 tracings of the auricular wave in the jugulars and the 
 ventricular pulse in the carotids and radials, that similar 
 phenomena may occur in the human heart. He has shown 
 that in a case of slow pulse after influenza the ventricle 
 failed to respond to alternate systoles of the auricle, and in 
 a more extreme case of true bradycardia that the ventricle 
 
 * " Mai. du Coeur," vol. i. p. 410. 
 t B.M.J., March, 1905. 
 
BRADYCARDIA. 401 
 
 only responded to every third auricular systole. He there- 
 fore attributes the slow pulse in Stokes-Adams disease to 
 blocking of conductivity in the muscular fibres between the 
 auricle and ventricle. According to my experience, there 
 is always at least one pulsation in the jugulars between the 
 beats of the pulse. 
 
 G-ibson * has also published a tracing in which he demon- 
 strates four auricular beats to one ventricular in a case of 
 bradycardia, and he also attributes the phenomena in Stokes- 
 Adams disease to blocking of conductivity. 
 
 Maynard f has recently published an interesting case of 
 bradycardia, in which he noted two perceptible impulses of 
 the right ventricle associated with subsidiary cardiac sounds 
 interpolated between the beats of the left ventricle. He 
 concluded that these sounds and impulses were produced 
 in the right side of the heart during the diastolic pause of 
 the left ventricle. This gave rise to some criticism by 
 Gossage and Hay as to whether the assumption of an 
 independent action of the two sides of the heart was tenable. 
 I have, however, in one case, seen two or three distinct 
 right ventricle beats interposed between each systole of the 
 left ventricle. The beat of the left ventricle came at 
 irregular intervals and was very powerful, giving a good 
 radial pulse, but it did not always exactly coincide with a 
 contraction of the right ventricle. I have also seen cases 
 in which an independent beat of the right ventricle was 
 present, associated with a pulsation in the veins of the neck, 
 pointing to a right auricular contraction which had passed 
 on to the right ventricle. 
 
 Though it is not possible to demonstrate the contraction 
 of the left auricle, I think we may assume that it is present 
 in these cases, but is not transmitted to the left ventricle 
 from a block in conductivity. This would explain the 
 
 * " Nervous Affections of the Heart," 1904. (Fig. 23.) 
 t B. M.J., vol. ii. 1905, pp. 847 et seq. 
 
 2d 
 
402 
 
 HEART DISEASE. 
 
 absence of the left ventricle beat, and would not entail the 
 assumption of independent action of the two sides of 
 the heart. 
 
 The left ventricle in this class of cases is usually hyper- 
 trophied as a result of high arterial tension, and is more 
 subject to degenerative changes, and it is conceivable that 
 it would require a more forcible stimulus than the thinner 
 walled and more healthy right ventricle, or perhaps a 
 summation of stimuli, to throw it into contraction. 
 
 Symptoms. 
 Of the symptoms, the syncopal or epileptiform attacks 
 are the most frequent and the most striking. They are 
 characterized by sudden loss of consciousness without any 
 warning, in which the patient usually falls to the ground, 
 as in an epileptic fit ; but there are very rarely general 
 convulsions, usually only slight twitching of the face or 
 extremities, or perhaps none at all, the attack resembling 
 rather that of petit mal. In one case under my care for 
 two years (J. F. H. B.) the patient was a retired colonel 
 aged 74, with a pulse of 38 or 40, who had from time to 
 time epileptiform attacks with loss of consciousness of short 
 duration, in which he fell to the ground. He had no other 
 symptoms, no dyspnoea or anginal attacks, and up to 
 the day before his death he insisted on taking a daily 
 promenade in the street. 
 
 The epileptiform attacks are accompanied by a further 
 fall in the pulse rate, and it has been supposed that this 
 was a consequence of the seizures. But the sudden loss of 
 consciousness and convulsions, when they occur, are, in my 
 judgment, due to momentary suspension of the cerebral 
 circulation which results from a further fall in the pulse 
 rate, already abnormally slow. 
 
 In one case which I had the opportunity of observing, 
 loss of consciousness with slight twitching of the face took 
 
BRADYCARDIA. 403 
 
 place very frequently, and occurred on more than one 
 occasion while I was examining the heart. Each time the 
 heart-beat, previously very slow, was suspended for a long 
 interval. The attack then came on, and could be watched 
 from the first. If in the act of speaking, he suddenly 
 stopped, the expression changed, and twitchings of the face 
 and slight general movements followed. I have, however, 
 seen cases in which there was well-marked passive dilatation 
 of the stomach, and have observed a diminished tendency 
 to syncopal and epileptiform attacks when this condition 
 was treated by dieting and other measures, suggesting that 
 the exciting cause of the syncopal attacks was of reflex 
 gastric origin. 
 
 Diagnosis. 
 
 The slow pulse of Stokes-Adams disease must be differ- 
 entiated from the varieties of slow pulse enumerated at the 
 beginning of this chapter, whether physiological, due to 
 toxic substances in the blood, following on some acute 
 bacterial infection, or associated with certain diseases of the 
 nervous system. 
 
 The age of the patient, the condition of the vessels, the 
 occurrence of apoplectiform and epileptiform attacks, will 
 usually render the diagnosis an easy matter. The epilepti- 
 form attacks can be distinguished from those of true 
 epilepsy by their association with the slow pulse and by the 
 previous history of the case. The fact that no paralysis or 
 apparent ill effect results from the apoplectiform seizures 
 will readily mark them off from those due to cerebral 
 haemorrhage. 
 
 Prognosis. 
 
 This is necessarily grave, as sudden death may occur 
 from syncope, from angina pectoris, or from an apoplecti- 
 form attack followed by coma, while the epileptiform 
 
404 HEART DISEASE. 
 
 seizures involve the risk of an accident at any time. As a 
 rule, however, it does not prove very rapidly fatal, and 
 patients may survive for many months, or even years. 
 
 Tkeatment. 
 
 The condition is one in which treatment can hardly 
 be expected to effect any great improvement. Iodide of 
 potassium, nitroglycerine, and erythrol tetranitrate, which 
 tend to keep down the arterial tension and make the work 
 of the heart easier, are often of great service, and un- 
 doubtedly tend to ward off the epileptiform and apoplecti- 
 form seizures. 
 
 The frequent association of dilatation of the stomach 
 with Bradycardia must be borne in mind, and measures for 
 the relief of this condition will form an important part of 
 the treatment. Recovery may take place even when Brady- 
 cardia, indistinguishable from Stokes-Adams disease, has 
 lasted many months, and appears to be confirmed, and 
 cases are met with in which this' condition comes and goes. 
 Treatment of any gastric complication should therefore be 
 persevered with, and careful instructions as to diet should 
 be given. 
 
 A light and simple diet should be enjoined in all cases, 
 with strict moderation in animal food, if it is taken at all. 
 Hu chard advises a strict "regime lacte," as this tends to 
 keep the arterial tension low and throws least work on the 
 kidneys, and he points out that renal inadequacy is common 
 in this affection. 
 
 A certain amount of gentle exercise may be taken when 
 it is well borne and gives rise to no unfavourable symp- 
 toms, but in some cases the slightest effort is liable to 
 bring on a cerebral attack. The amount of exercise which 
 can be taken must be decided by experience in each 
 individual case. 
 
CHAPTER XXVIII. 
 
 ACUTE AORTITIS OR ACUTE DEGENERATIVE 
 LESIONS OF THE AORTA. 
 
 EXPERIMENTAL EVIDENCE — ETIOLOGY— MORBID ANATOMY — 
 PATHOGENY — PROGNOSIS — TREATMENT. 
 
 Acute aortitis, in its typical aspect, as described by Bizot, 
 is a somewhat rare affection, but in lesser degrees of severity 
 is of comparatively frequent occurrence, and has not received 
 the attention it deserves; most affections of the aorta, 
 even in acute infections, being usually loosely classified as 
 " atheroma." Bizot, in 1837, and Ranvier in 1868, gave an 
 account of the pathological, and Bucquoy and Leger, some 
 years later, of the clinical aspects of the disease. 
 
 Gilbert and Lion, in 1889, produced acute aortitis experi- 
 mentally in rabbits by inoculation of micro-organisms after 
 first injuring the aorta with a stylet. Boinet and Romary, 
 in 1898, succeeded in producing acute aortitis experi- 
 mentally by inoculation of cultures, and also of the toxins 
 only, of various micro-organisms, which in some instances 
 attacked the wall of the aorta not previously injured by a 
 stylet. They also showed that degenerative changes set in 
 rapidly in the affected subendothelial tissue. They further 
 showed that the administration to animals for some months 
 of toxic substances, such as lead and uric acid, produced 
 lesions in the intima. 
 
 Huchard,* referring to their experimeDts, gives a remark- 
 
 * " Maladies du Coeur," vol. ii. p. 270. 
 
406 HEART DISEASE. 
 
 able illustration by Boinet of a section of the aorta from 
 a case of facial erysipelas, in which typical gelatiniform 
 plaques were present on the endothelium, and chains of 
 streptococci were seen scattered through the middle coat. 
 
 Mokbid Anatomy. 
 
 The aorta is usually dilated, and may be fusiform or 
 globular in shape. On laying it open it is seen to be of a 
 patchy red or pinkish colour, and the surface is irregular 
 and uneven for a distance of about 1^ to 2 inches from the 
 aortic valves. The uneven surface is due to the presence 
 of smooth, pinkish, rose-coloured, or greyish patches of 
 varying size, termed by Bizot " gelatiniform," from their 
 opalescent appearance. The colour of these patches may 
 vary from a pale pink or grey to a deep red, the colouration 
 being mainly due to post-mortem staining from dissolved 
 haemoglobin. In cases of less severity the change may be 
 limited to one or more small yellow raised opaque patches, 
 often loosely termed atheroma. 
 
 The frontispiece, drawn from a recent specimen of 
 primary acute aortitis, well shows the appearance presented 
 by the affected aorta. 
 
 On microscopic examination of these gelatiniform 
 plaques or patches, the endothelium is seen to be swollen, 
 and beneath it are necrotic patches infiltrated with flat, 
 elongated cells, apparently due to proliferation of the con- 
 nective tissue elements. The middle and outer coats are 
 less affected, but they may be swollen and infiltrated with 
 small round cells, which, in the adventitia, are chiefly 
 conspicuous round the vasa vasorum. 
 
 Etiology. 
 
 Acute Infectious Diseases. — Acute aortitis may occur in 
 the course of scarlet fever, small pox, more rarely in measles, 
 
ACUTE AORTITIS. 4°7 
 
 and in various affections of known bacterial origin, namely, 
 typhoid fever, erysipelas, pneumonia, septicaemia, influenza, 
 rheumatism, and tuberculosis. 
 
 In young children who have died of pneumonia or septi- 
 caemia, or some acute bacterial infection, I have frequently 
 seen at the autopsy small yellow raised patches in the aorta, 
 which may be regarded as instances of acute degenerative 
 lesions due to the action of micro-organisms or their toxins. 
 
 Acute degenerative lesions of the aorta may also occur 
 in severe syphilis in the secondary stage, and also in gout 
 and lead poisoning ; but in these affections the chronic? 
 degenerative change known as atheroma is more common, 
 especially in tertiary syphilis. 
 
 Pathogeny. 
 
 The experimental results of Gilbert and Lion, and 
 Boinet and Eomary, referred to above, throw an important 
 light on the pathogeny of acute aortitis, and show that it can 
 be produced by the action of micro-organisms and their 
 toxins. 
 
 In the instances in which the vessel wall was injured 
 by a stylet, one must presume that the micro-organisms 
 effected their entry at the site of the lesion by a direct 
 frontal attack. Where acute aortitis resulted from inocula- 
 tion without previous injury to the vessel, or from ingestion 
 of toxic substances, the site of the lesion beneath the 
 intima, and the cellular infiltration round the vasa 
 vasorum in the adventitia, would seem to indicate that 
 the toxins reached the affected tissue through the vasa 
 vasorum. The immediate result appears to be necrosis of 
 the part attacked, as there are areas of swollen degenerated 
 amorphous tissue beneath the intima. Subsequently, there 
 is an attempt at repair shown by the presence of flattened 
 proliferating connective tissue cells. As the vasa vasorum 
 normally do not penetrate the middle coat, these proliferating 
 
4o8 HEART DISEASE. 
 
 cells are not vascularized, so there is no formation of 
 fibrous tissue or efficient repair, and there is a tendency to 
 the deposition of lime salts in the affected area. In many 
 instances of so-called atheroma of the aorta, as will be 
 shown later in the chapter on that affection, we find vessels 
 penetrating the media and extending down to the sub- 
 endothelial tissue, which may be an attempt to vascularize 
 newly formed connective tissue cells proliferated in the 
 process of repair. 
 
 In view of the pathological changes found, which are 
 of the nature of an acute necrosis, the term acute aortitis 
 seems scarcely suitable, and I would suggest "acute 
 degenerative lesions " of the aorta as a more suitable 
 nomenclature. 
 
 Symptoms, Physical Signs, and Diagnosis. 
 
 Throbbing of the carotids, a sense of constriction and 
 burning pain behind the sternum, a feeling of intense 
 oppression, accompanied by paroxysms of dyspnoea, have 
 been described as characteristic features of this affection. 
 The temperature is not, as a rule, raised, except as a result 
 of a primary infection of which the aortitis may be a com- 
 plication. Dilatation of the aorta frequently ensues, but as 
 an aorta previously dilated from atheromatous degenera- 
 tion may be attacked, this is not always a helpful physical 
 sign. 
 
 Angina pectoris may be a prominent symptom, as the 
 root of the aorta is very commonly affected, and the orifice 
 of one of both coronary arteries may be obstructed by swell- 
 ing of the adjacent tissues. 
 
 Huchard attaches considerable importance to dilatation 
 of the aorta, and considers that a sudden onset of severe 
 symptoms in association with this serve to render a diagnosis 
 possible. It is, however, difficult to arrive at a diagnosis 
 
ACUTE AORTITIS. 409 
 
 with any degree of certainty during life, and, in the absence 
 of angina, it can rarely be made. 
 
 An interesting account of two cases of acute aortitis was 
 published in the Lancet by Poynton.* One of these cases, 
 under the care of Dr. Cheadle, at St. Mary's Hospital, I 
 had the opportunity of observing. The following is an 
 account of the case, abridged from Dr. Poynton's description 
 in the Lancet : — 
 
 A woman aged 88 was admitted to St. Mary's Hospital, February, 
 1899, suffering from pain in the heart and vomiting. Two months 
 before admission she had suffered from attacks of precordial pain 
 extending down the left arm. These attacks, infrequent at first, had 
 during the last week become more severe, and were accompanied by 
 vomiting and faintness. There was no history of syphilis. On admis- 
 sion she was well nourished and free from pain, but shortly after- 
 wards she had an attack of pain in the left arm, with a feeling of faint- 
 ness, which Dr. Cheadle considered to be true angina pectoris. She 
 volunteered the statement that any sudden exertion was liable to bring 
 on the attacks of pain. The temperature was normal, pulse 72, but at 
 times the pulse become excited and irregular. The heart was not 
 hypertrophied ; there were no murmurs at the base, but the first 
 sound at the apex was sharp, and was preceded occasionally by a short 
 presystolic murmur. 
 
 At midnight three days after admission she had a severe attack of 
 angina pectoris, accompanied by vomiting, and she died two hours 
 later. 
 
 At the autopsy the heart was slightly dilated. The mitral valve was 
 somewhat thickened from old endocarditis, and contained a calcareous 
 nodule. Its orifice was slightly stenosed. Otherwise the heart appeared 
 to be normal. 
 
 The aorta for the first two inches was extensively diseased. The 
 intima was pinkish-red in colour, with raised patches, some of trans- 
 lucent appearance, others yellow, with a red flush round their bases. 
 A few patches resembled the condition of ordinary atheroma. The 
 appearance was that of an acute aortitis, supervening on a more chronic 
 condition. 
 
 This is well shown in the coloured frontispiece, which was drawn 
 from this specimen. 
 
 The orifice of the right coronary artery was slightly narrowed, but 
 admitted a large probe. That of the left was not affected. 
 
 Microscopical Examination — 
 
 Aorta. — The intima was swollen. The vessels were distended, and 
 
 * Lancet, 1809, vol. i. p. 352. 
 
410 HEART DISEASE. 
 
 around them was a free exudation of cells, which in places reached the 
 surface of the intima. The elastic coat was also freely infiltrated with 
 leucocytes. Where the aorta merged into the heart- wall the exuda- 
 tion could be traced beneath the endocardium of the left ventricle. 
 
 Heart Muscle. — -This showed loss of striation, extensive hyaline, and 
 fatty degeneration in many places, and the nuclei showed a feeble 
 staining reaction. In some places between the muscle fibres there 
 was a cellular infiltration and an appearance of active reaction. Some 
 of the vessels showed an increase in the thickness of the outer coat, but 
 no endarteritis or narrowing of their lumen. 
 
 Dr. Poynton points out that there was no disease of or marked 
 obstruction of the orifices of the coronary arteries to explain the 
 anginal attacks. He attaches great importance to the profound 
 changes in the cardiac muscle accompanying the aortitis, and attri- 
 butes death to cardiac failure from this cause. 
 
 Prognosis. 
 
 When the orifice of one of the coronary arteries is in- 
 volved, and attacks of angina pectoris result, the prognosis 
 is necessarily very grave. 
 
 In lesions of great severity affecting the arch of the 
 aorta, there is risk of sudden death from perforation, and 
 recently a man aged 46 was brought into St. Mary's 
 Hospital, moribund, in whom a post-mortem examination 
 disclosed the pericardium full of blood, and a minute per- 
 foration in the aorta only 1 mm. in diameter, the result of 
 an acute degenerative lesion. 
 
 In lesions of minor severity the damaged area remains 
 permanently a weak spot, and may later on in life give rise 
 to an aneurysm, or become the seat of a calcareous deposit. 
 
 Treatment. 
 
 If the affection is diagnosed, absolute rest and a light 
 non-nitrogenous diet should be enjoined. For the attacks 
 of angina, if present, nitrite of amyl or one or other of the 
 nitrites may be administered. Iodide of potassium and 
 arsenic may be given with advantage as the attack 
 subsides. 
 
CHAPTER XXIX. 
 
 ATHEROMA OR CHRONIC DEGENERATIVE 
 LESIONS OF THE AORTA. 
 
 ETIOLOGY OF GENERAL ARTERIO-SCLEROSIS AND ATHEROMA 
 — MORBID ANATOMY — PATHOGENY — DIFFERENT VIEWS 
 — PHYSICAL SIGNS AND SYMPTOMS — AORTIC INCOM- 
 PETENCE DUE TO DEGENERATIVE CHANGE— ITS DIS 
 TINGUISHING FEATURES — PROGNOSIS —TREATMENT. 
 
 Atheroma of the aorta is a degenerative change affecting 
 primarily the deeper layers of the vessel wall. The name 
 is derived from the Greek word adapt] or adtipr\, which means 
 " gruel " or " porridge," and emphasizes the fact there is 
 softening and breaking down of the diseased area. 
 
 It may be associated with degenerative changes affecting 
 the general arterial system, commonly termed " arterio- 
 sclerosis," or it may exist independently of other vascular 
 lesions. 
 
 Etiology. 
 
 Atheroma of the aorta is usually a disease of middle or 
 advanced life. Many of its causes are the same as those of 
 general arterio-sclerosis, which comprise : — 
 
 1. High arterial tension, the etiology of which has already 
 been discussed in Chap. II. Under this heading we have 
 chronic renal disease, gout, over- eating and drinking, 
 particularly excessive meat-eating, associated with defective 
 metabolism and imperfect elimination. 
 
 Heredity plays an important part, more especially in 
 
412 HEART DISEASE. 
 
 association with the last-mentioned group of cases, in which 
 the tendency to early vascular degeneration may be trans- 
 mitted through many generations. 
 
 2. In addition to high arterial tension, which involves a 
 constant undue strain on the walls of the whole arterial 
 system, and is, as has already been said, a cause of general 
 arterio-sclerosis, there is one form of intermittent strain con- 
 nected with certain occupations, which affects more par- 
 ticularly the arch of the aorta. This has already been 
 referred to in association with chronic endocarditis (p. 83). 
 The occupations in question are those of the miner, collier, 
 gravedigger, blacksmith, and hammerman, which involve 
 violent effort in a constrained and cramped position, or 
 exertion during which there is prolonged closure of the 
 glottis and fixation of the chest in holding the breath, which 
 give rise to extreme and frequent variations in the blood 
 pressure, and excessive strain on the walls of the arch of 
 the aorta. Hence dilatation of the aorta with associated 
 aortic incompetence are particularly liable to result 
 General arterio-sclerosis is usually present as well in a 
 marked degree. 
 
 3. Lead poisoning. 
 
 4. Diabetes and rheumatoid arthritis are mentioned 
 by some authors as causes of arterio-sclerosis. In diabetes 
 in young subjects I have frequently seen small patches of 
 atheroma in the aorta, and in those past middle life exten- 
 sive disease of the cerebral vessels, but in most instances the 
 diabetes proves fatal before any extensive general arterio- 
 sclerosis results. In rheumatoid arthritis and chronic, 
 joint affections thickening and hyperplasia of the vessels 
 are frequently met with. 
 
 5. Alcohol and tobacco are usually included in lists of 
 causes of arterio-sclerosis, but there is scarcely sufficient 
 evidence to prove that they are directly responsible, though 
 the wide variations of blood pressure to which they give 
 
ATHEROMA OF THE AORTA. 413 
 
 rise must have a deleterious effect apart from possible toxic 
 influences. 
 
 Among the causes of atheroma of the aorta more par- 
 ticularly, as apart from general arterio- sclerosis, are — 
 
 1. Syphilis. — This is one of the most important causes of 
 degenerative changes in the aorta, and may affect the aorta 
 alone, as in many cases of aneurysm. 
 
 2. Bacterial Infections. — These have already been 
 enumerated and their modes of action discussed in the 
 chapter on acute aortitis. It is doubtful how far they 
 should be included among the causes of chronic degenera- 
 tive change, with the exception of tuberculosis, and, perhaps 
 of rheumatism, but it is difficult to draw a hard-and-fast line 
 between acute and chronic infections. It is possible that 
 many instances of so-called atheroma of the aorta found in 
 later life may be the result of an acute degenerative lesion 
 of an early date, in which calcification or imperfect repair 
 has taken place. 
 
 Morbid Anatomy. 
 
 In the earlier stages the inner aspect of the arch of the 
 aorta is studded with opaque, yellowish elevations, smooth 
 on the surface, and varying in number, size, and shape. 
 Later on, ulceration of the endothelial surface may take 
 place, and irregular ragged ulcers result, or calcification of 
 the diseased areas may occur, which may be so extensive 
 that a portion of the aorta is converted into a rigid, in- 
 elastic, calcareous tube. 
 
 The arch of the aorta is most commonly affected, but the 
 abdominal aorta may be attacked as well, or independently, 
 or the whole of the thoracic and abdominal aorta may be 
 diseased. 
 
 Microscopic Examination. — Microscopically, in a section 
 from one of these irregular yellow swellings, the endothelium 
 is seen to be pushed forward by a mass of non-staining 
 
414 
 
 HEART DISEASE. 
 
 necrotic material, in which may be distinguished elongated, 
 
 spindle-shaped connective tissue cells with atrophic small 
 nuclei, strands of swollen fibrous tissue, and in the deeper 
 layers, elastic fibres and smooth muscle fibres, the latter 
 undergoing hyaline degeneration. (Vide Fig. 25.) In 
 more advanced cases, fat droplets, crystals of cholestrin, 
 and areas of calcification may be present. 
 
 The degenerative process appears to start in the intima 
 
 ^ :. mBt&fcM M j)?w ■?>'•■• ■ 
 
 ■ ',■•'.•. .-.. . - - i-'j", ,; '-^y 
 
 
 p), 
 
 til 
 
 mm 
 
 
 FIG. 25. — SECTION OF WALL OF AOUTA, SHOWING EXTENSIVE ATHEROMA 
 AFFECTING THE MEDIA AS WELL AS THE INTIMA. 
 
 immediately beneath the endothelium, the adjacent layers of 
 the media being next affected, or sometimes simultaneously. 
 
 While this holds good for arteries of lesser size, in the 
 aorta the seat of the primary degeneration may be at some 
 point in the deeper layers of the media, particularly in 
 aneurysm, as will be pointed out later in the chapter on 
 this affection. 
 
 The vasa vasorum in the adventitia are usually thickened, 
 
ATHEROMA OF THE AORTA. 
 
 415 
 
 and may be entirely obliterated in places as the result of 
 endarteritis, as in Fig. 26, taken from a case of advanced 
 atheroma of the aorta in a man with a syphilitic history. 
 Sometimes they are congested, and in their neighbourhood 
 are extensive areas of round-celled infiltration. The cells 
 are of the type of lymphocytes, and the appearance suggests 
 
 ■& ■■ ■' -''■■'- 
 
 '■' ',*'.< if^'i '>'"'< -'w ':;• ^ v -x :. 
 "ft; / -& \&K && x V 
 
 
 
 
 ?W/. ' >"'>« 
 
 
 ■- • :~Wr 
 
 
 •'•" 
 
 FIG. 2G. — SECTION OF ADVENTITIA OF THE WALL OF THE AORTA, SHOWING 
 ENDARTERITIS OBLITERANS OF THE VASA VASORTJM. A, VESSEL COM- 
 PLETELY OBLITERATED. (X 80.) 
 
 that they are called up from the lymphatics as a first line 
 of defence in the tissues against toxins exuding from the 
 vessels. In addition to these lymphocytes, there may be 
 periarteritis and proliferation of connective tissue cells, 
 which is the second line of defence by the tissues. Whereas, 
 normally, no vessels can be detected in the middle coat of 
 the aorta, frequently, in cases of atheroma, numerous small 
 
416 HEART DISEASE. 
 
 vessels, offshoots from the vasa vasorum, can be seen 
 scattered through the media, penetrating in some cases 
 to the intima. Sometimes areas of round-celled infiltration 
 are present in the neighbourhood of these vessels, and the 
 middle coat is extensively disorganized and broken up. 
 (Vide Fig. 21.) 
 
 
 *~»<zi: 
 
 
 
 
 FIG. 27. — SECTION OP MIDDLE COAT OF AOKTA, SHOWING NUMEROUS NEWLY 
 FORMED VESSELS. 
 
 Pathogeny. 
 
 Different views are held as to the pathogeny of this 
 condition. Some hold that the primary change is a cell 
 proliferation in the sub-endothelial connective tissue, as a 
 result of irritation due to strain or some toxic material in 
 the blood stream, and that subsequently degeneration of 
 this newly formed tissue takes place. 
 
 Thoma taught that the thickening of the intima is a 
 secondary or compensatory process to make good the loss 
 of tissue sustained by the media. 
 
 Neither of these views are satisfactory. On micro- 
 scopical examination the most constant feature in atheroma, 
 
ATHEROMA OF THE AORTA. 4*7 
 
 even in its earliest stages, is the presence of amorphous, 
 necrotic, non- staining materal. The attempt at cell pro- 
 liferation is feeble, and one never sees true fibroblasts with 
 large healthy nuclei, which take the stain well, among the 
 newly-formed cells ; the nuclei are small and atrophic, and 
 the half-starved cells seem to have given up the attempt to 
 form new fibrous tissue. 
 
 The areas of atheromatous tissue do not always fit 
 into depressions in the media, as suggested by Thoma. 
 In the section of the atheromatous coronary artery in 
 Fig. 19, p. 321, it will be seen that the whole of the 
 intima is extensively diseased, and the media is only 
 affected at the point where calcification has taken place, 
 that is, where the disease in the intima is most advanced. In 
 aneurysm it is true that definite atrophy and thinning of 
 the media and a depression on its inner aspect can be made 
 out. Here it is probable, as will be shown later in the 
 chapter on aneurysm, that focal necrosis in the inner half 
 of the media may be the primary change, but the condition 
 is different to that which obtains in atheroma of the smaller 
 vessels. It is contrary to experience that nature should 
 attempt to repair a weak spot by evolving a mass of useless 
 necrotic material, which is what is suggested by those who 
 hold that the atheromatous tissue is compensatory and 
 secondary to degenerative change in the media. 
 
 A third and more satisfactory theory is that the primary 
 change is a degeneration or necrosis of the sub- endothelial 
 tissue in the intima and deeper layers of the media. This 
 may be due, among other causes, to the cutting off of nutri- 
 ment by obliterative lesions of the vasa vasorum, as shown 
 in Fig. 26 in the case of syphilis. 
 
 Huchard * attributes all forms of arterio- sclerosis and 
 atheroma to endarteritis obliterans of the vasa vasorum, and 
 sums up his conclusions as follows : — 
 
 * " Maladies du Cceur," vol. i. p. 163. 
 
 2 E 
 
4i8 HEART DISEASE. 
 
 " 1. Arteriosclerosis or atheroma is a dystrophic sclero- 
 sis of the walls of the vessels consecutive to endarteritis 
 obliterans of their nutrient arteries. According to H. 
 Martin, atheroma of a vessel furnished with vasa vasorum 
 is invariably preceded by endarteritis of its nutrient vasa 
 vasorum. 
 
 " 2. In the evolution of general arterio-sclerosis we can 
 distinguish two periods anatomically : (a) development of 
 endarteritis of the vasa vasorum ; (b) disorders of nutri- 
 tion, which are a consequence of this, and lead to general 
 arterio-sclerosis on the one hand, and visceral sclerosis on 
 the other. Clinically, the first period is usually latent, but 
 the second, that of disordered nutrition, gives rise to 
 symptoms more or less distinctive." 
 
 Huchard * meets the objection that the vasa vasorum 
 cannot be traced to the intima, and scarcely even penetrate 
 the media, with the statement that it is for this very 
 reason, namely, that the intima is most distant from the 
 source of nutriment, that the degenerative change com- 
 mences in the sub- endothelial tissue ; the endothelium 
 itself, being nourished by the general blood stream, does 
 not usually suffer. 
 
 That the more delicate endothelium of the vasa vasorum 
 may be affected by toxins in the blood, and endarteritis 
 result, leading to obliteration of these vessels and conse- 
 quent atheroma of the aorta, is shown in Fig. 26, and has 
 already been demonstrated by Mott t in the case of 
 syphilis. 
 
 It is possible that other toxins also, e.g. lead and uric 
 acid in gouty subjects, may act in the same way, but I do 
 not think that obliteration of the vasa vasorum is invariably 
 responsible for all degenerative lesions of the aorta. 
 
 It is probable that, in some cases, the areas of focal 
 
 * "Maladies du Cceur," vol. i. p. 158. 
 
 t Allbutt's " System of Medicine," vol. vi. p. 311. 
 
ATHEROMA OF THE AORTA. 419 
 
 necrosis in the subendothelial tissue or deeper layers of 
 the media may be directly due to the destructive action 
 of toxins reaching these tissues through the vasa vasorum. 
 These toxins may be — 
 
 (a) Of bacterial origin. 
 
 (b) Metallic, e.g. lead. 
 
 (c) Antogenetic, the result of imperfect metabolism, as in 
 cases of high arterial tension or gout. 
 
 The explanation of the presence of cellular elements, 
 which have the appearance of atrophic fibroblasts, would 
 seem to be that they are the result of an attempt at repair 
 by proliferation of connective tissue cells, which fails because 
 efficient vascularization cannot take place, since the vasa 
 vasorum are too far distant to throw off capillary loops, 
 which would have to traverse the media before they reached 
 the newly formed tissue. Thus the newly formed fibroblasts 
 are incapable of forming new fibrous tissue, and themselves 
 degenerate in turn, 
 
 In some cases, however, numerous vessels can be seen 
 penetrating the media and reaching almost down to the 
 intima. This is well shown in Fig. 27. Here, I take it, we 
 have an attempt at vacularization of newly formed tissue in 
 the media. 
 
 This could scarcely occur if the primary lesion, causing 
 focal necrosis, was obliteration of the vasa vasorum, but 
 might ensue if the necrosis was an acute process due to the 
 destructive action of toxins conveyed through the vasa 
 vasorum, and was followed by an efficient attempt at repair 
 when the causative toxaemia had subsided. 
 
 Strain, whether intermittent or continuous, is an im- 
 portant etiological factor in degenerative lesions of the 
 aorta, more especially in relation to aneurysm, as will be 
 seen later. 
 
 Conclusions. — Atheroma is a focal necrosis of the sub- 
 endothelial tissues of the intima or the adjacent layers of 
 
420 HEART DISEASE. 
 
 the media, due either to the destructive actions of toxins 
 conveyed by the vasa vasorum or to loss of nutriment from 
 obliteration of the vasa vasorum by endarteritis. 
 
 The cellular elements are the result of an attempt at 
 repair by proliferation of connective tissue cells, which fails 
 because efficient vascularization is impossible. 
 
 The explanation of atheroma due to intermittent strain 
 associated with arduous occupations, if we admit that strain 
 alone can produce atheroma, may be that it is in part due 
 to impaired nutrition of the deeper layers of the media, 
 because the condition of over-tension and stretching of the 
 aorta interferes with the passage of nutritive fluids through 
 its walls, and in part to mere mechanical overstrain. 
 
 Physical Signs and Symptoms. 
 
 Atheroma of the aorta in its early stages does not give 
 rise to any characteristic physical signs or symptoms. The 
 degenerative process, however, is commonly not confined to 
 the aorta, but is associated with general arterio-sclerosis, 
 evidence of which will be found in the thickened, rigid, 
 uneven radials, the tortuous, irregular, and prominent 
 brachials, which are thrown into curves at each beat of the 
 heart. In the case of syphilis and acute toxaemias, the aorta 
 alone may be affected. The aorta frequently becomes 
 dilated from the yielding of its weakened walls. Some- 
 times there may be dulness to the right of the sternum, and 
 slight pulsation, but this is seldom apparent except in the 
 case of aneurysm or local dilatation. The most trustworthy 
 sign of dilatation is the alteration in the character of the 
 aortic second sound as heard at the aortic cartilage. This 
 becomes low-pitched, musical, or clanging in character, and 
 appears to be prolonged. 
 
 The aortic orifice may be stretched so as to give rise to 
 aortic incompetence from imperfect apposition of the valves, 
 
ATHEROMA OF THE AORTA. 421 
 
 or the aortic cusps may be damaged as a result of strain, 
 and be involved in the degenerative process, becoming 
 thickened, more or less rigid, and incompetent. 
 
 This form of aortic incompetence differs greatly in its 
 characteristics from that due to acute endocarditis, dis- 
 cussed in a previous chapter. 
 
 Here the aortic valves have become incompetent, usually 
 as a result of high arterial tension with which the degenera- 
 tive change is commonly associated, and to which it is 
 secondary. The amount of regurgitation is slight ; the 
 diastolic murmur is accompanied by a low-pitched, loud, 
 ringing, second sound ; the pulse is not markedly collapsing ; 
 the artery can be felt between the beats, and is usually 
 thickened. 
 
 The arterial tension, though somewhat reduced, remains 
 high in spite of the leakage, because the abnormally great 
 peripheral resistance, the original cause of the high tension 
 in the circulation, is unaltered, and the heart is usually 
 hypertrophied, and acting powerfully. Moreover, in this 
 class of cases, the amount of regurgitation is seldom very 
 great. I have found the blood pressure, estimated by 
 Riva Rocci's instrument, to range from 140 mm. to 190 
 mm., as contrasted with a blood pressure of 90 to 120 mm. 
 in cases of aortic regurgitation due to acute endocarditis, 
 in which, for reasons given in Chapter II., the mean blood 
 pressure is usually low. 
 
 It is the indiscriminate classification of cases of aortic 
 incompetence in which the valves have given out as a result 
 of strain and high arterial tension, with the totally different 
 group in which the valves have been rendered incompetent 
 by acute endocarditis, and to a great extent destroyed, 
 that has given rise to so much discrepancy of opinion 
 as to the mean blood pressure or arterial tension in aortic 
 regurgitation. 
 
 Aneurysm. — One of the most serious results of atheroma 
 
422 HEART DISEASE. 
 
 of the aorta is local weakening of its wall, which may lead to 
 the formation of an aneurysm. 
 
 Occlusion of Coronary Arteries. — Atheromatous change in 
 the neighbourhood of the orifices of the coronary arteries 
 may partially occlude one or both of them, and give rise to 
 angina pectoris, or to fibroid change in the heart wall. 
 
 Prognosis. 
 
 Inasmuch as atheroma is a degenerative change, is 
 usually progressive, and may give rise to aneurysm, dilata- 
 tion of the aorta, aortic incompetence, and impair the nutri- 
 tion of the heart by occlusion of the coronary vessels, the 
 prognosis is necessarily grave. As regards the duration of 
 life, much will depend on the nature of the secondary 
 change in the aorta to which the atheroma gives rise, and 
 on the influences to which the patient is exposed. 
 
 Treatment. 
 
 When atheroma of the aorta is associated with general 
 arterio-sclerosis and high arterial tension, as is most com- 
 monly the case, treatment must be directed to lowering the 
 latter, so that a minimum amount of strain may be thrown 
 on the great vessels and heart. 
 
 Alcohol, tobacco, stimulants of all kinds, should be for- 
 bidden. Strict moderation in diet should be enjoined, and 
 meat, game, and soups should be eschewed as far as possible. 
 In some cases a strict milk diet may be advisable for a time. 
 Undue exertion and excitement should, as far as possible, be 
 avoided, but gentle walking exercise may be taken. Mild 
 mercurial purgatives should be given once or twice a week, 
 and these may be supplemented, if necessary, by a morning 
 draught of a sulphated mineral water such as Hunyadi, 
 Janos, Apenta, Friedrichshall, and the like. 
 
 Vaso-dilators, trinitrin, or erythrol tetranitrate should 
 
ATHEROMA OF THE AORTA. 423 
 
 be administered if the blood pressure is high, as they tend 
 to lower the arterial tension by diminishing the peripheral 
 resistance. Iodide of potassium may be given in addition, 
 often with marked benefit. 
 
 When there is reason to believe that the degenerative 
 change in the aorta is the result of syphilis, iodide of 
 potassium should be freely administered for a long period, 
 either alone or in combination with mercury. 
 
CHAPTEE XXX. 
 ANEUEYSM OF THE AECH OF THE AOETA. 
 
 MORBID ANATOMY — ETIOLOGY — PATHOGENY — RELATIONS 
 OP THE AECH OF THE AOETA — PHYSICAL SIGNS AND 
 SYMPTOMS — ANEURYSM (1) OF THE INTEA-PEEICAEDIAL 
 POETION OF AOETA ; (2) OF ASCENDING AOETA ; (3) OF 
 TRANSVERSE PART OF ARCH ; (4) OF DESCENDING AORTA 
 — DIAGNOSIS — PROGNOSIS — TREATMENT. 
 
 An aneurysm is a pulsating tumour in connection with 
 the interior of an artery. It is caused by the bulging or 
 giving way, under the blood pressure of a portion of the 
 wall of an artery weakened by injury or disease. It may be 
 saccular, fusiform, or cylindrical in shape, according to the 
 extent and area of the arterial wall which gives way in 
 the first instance. 
 
 Morbid Anatomy. 
 
 A cylindrical or fusiform aneurysm is merely a general 
 dilatation of the vessel in some part of its course. 
 
 A saccular aneurysm is caused by the giving way of a 
 circumscribed portion of the vessel wall as the result of 
 some morbid process affecting the deeper layers of the 
 media. This weak spot gradually bulges and yields more 
 and more under the blood pressure. The dilated portion is 
 termed the sac, and the orifice by which it communicates 
 with the interior of the vessel is termed the mouth of the sac. 
 
 The intima can usually be traced for a varying distance 
 on to the interior of the sac. 
 
ANEURYSM OF THE ARCH OF THE AORTA. 425 
 
 The media is greatly thinned ; the muscular fibres are 
 atrophied and compressed, and have, to a great extent, 
 disappeared ; the elastic fibres are stretched and have lost 
 their elasticity, and may be rnptured in places. The 
 adventitia is thickened from formation of new fibrous tissue, 
 so that the wall of the sac consists mainly of the thickened 
 adventitia, with which may be incorporated adjacent struc- 
 tures to which it becomes adherent. 
 
 As the aneurysm increases in size and the mouth of the 
 sac becomes relatively small in comparison with its interior, 
 the circulation of blood in the sac becomes sluggish, 
 and layers of laminated clot are deposited on the diseased 
 walls. 
 
 The so-called dissecting aneurysm is not, strictly 
 speaking, a true aneurysm. In this condition there is a 
 rupture of the intima and of a portion of the media, through 
 which the blood penetrates the media and tears its way 
 downwards in its substance for a varying distance, some- 
 times finding its way back again into the interior of the 
 vessel at a lower level. 
 
 Etiology. 
 
 Age. — Aneurysm is a disease of middle and advanced 
 life, but is met with also in young adults. 
 
 Sex and Occupation. — It is far more common in men than 
 in women, which seems to point to hard work and laborious 
 occupations as a factor in its production. It is frequently 
 met with in soldiers and miners ; the prolonged and severe 
 exertion to which the former are subjected in campaigning 
 and forced marches, together with the restraint on the free 
 play of the chest wall by arms and accoutrements, the 
 arduous nature of the work of the latter, and the constrained 
 and cramped position in which they have to work, have been 
 
426 HEART DISEASE. 
 
 held to account for its common occurrence in men following 
 these occupations. 
 
 Atheroma of the aorta, a comprehensive term, in ordinary 
 parlance, for degenerative lesions of the aorta, of whatsoever 
 origin, is one of the commonest causes of aneurysm. Its 
 etiology has already been discussed in the last chapter, but 
 as extensive and widespread atheroma of the aorta is of 
 common occurrence without aneurysm, it is clear that 
 certain factors must be more particularly concerned in the 
 production of the latter. These are — 
 
 I. Affections which give rise to circumscribed or focal, 
 rather than general, lesions of the aorta. 
 
 II. Conditions of varying and high blood pressure 
 within the aorta. 
 
 Among the former are — 
 
 (a) Syphilis. — This is unquestionably one of the most 
 important factors in the production of aneurysm, and about 
 this opinion is almost unanimous. Welsh found a history 
 of syphilis in 50 per cent., Frankel in 47 per cent., and 
 Huchard in 43 per cent, of cases of aneurysm of the aorta. 
 Drummond of Newcastle considered that in a large pro- 
 portion of cases of aneurysm in miners, attributed to strain, 
 syphilis was mainly responsible, and this may be so, in 
 soldiers, in whom, also, syphilis is very common. 
 
 It seems probable that syphilis may produce focal lesions 
 of the aorta in two ways — 
 
 (1) In the secondary stage by a toxic action on the 
 vessel wall similar to that of acute bacterial infections. 
 
 (2) In the later stages, by setting up endarteritis obli- 
 terans of the vasa vasorum of the aorta, at one or more 
 points, and thus depriving its wall of the necessary nutri- 
 ment, with resulting slow necrosis and degenerative change 
 in the deeper layers of the media in corresponding circum- 
 scribed areas. 
 
 (b) Acute Bacterial Infections.— These I would suggest 
 
ANEURYSM OF THE ARCH OF THE AORTA. 427 
 
 as causes next in importance to syphilis. I am aware that 
 they are not generally recognized etiological factors, but 
 the experimental results of Boinet and Romary, detailed in 
 Chapter XXVIII., afford strong support to this view, which 
 has also certain pathological evidence in its favour. As 
 already explained, it is probable that the toxins evolved by 
 the micro-organisms reaching the aorta through the vasa 
 vasorum give rise to areas of focal necrosis in the deeper 
 layers of the media. Efficient repair does not take place, 
 and a weak spot in the vessel wall results, which in later 
 life, possibly some years after the primary lesion, when 
 other factors have given rise to high arterial tension and 
 increased blood pressure in the aorta, may become the site 
 of an aneurysm. 
 
 Huchard * holds that whereas gout, atheroma, syphilis, 
 alcoholism, and malaria, which may set up focal degenera- 
 tion in the media, are predisposing causes, the supervention 
 of some acute bacterial infection is commonly the immediate 
 cause of aneurysm. In support of this, he instances the 
 development of an aneurysm in syphilitic and gouty sub- 
 jects, which he has observed subsequent to a severe attack 
 of influenza. 
 
 (c) Toxins other than Bacterial. — Lead poisoning, which 
 
 is a common cause of general arterio- sclerosis, can seldom 
 
 be traced as a factor in aneurysm. We have little direct 
 
 evidence as to the part played in the production of aneurysm 
 
 by alcohol, or organic poisons such as may result from 
 
 imperfect metabolism in gouty and plethoric subjects. 
 
 Fischer f of Bonn has, however, recently published an 
 
 account of experiments in which he was able to produce 
 
 aneurysms in rabbits by repeated injections of adrenalin 
 
 or digalen, and in the light of these it is possible that 
 
 a variety of toxins may be etiological factors in aneurysm. 
 
 * " Mai. du Cceur." vol. ii. pp. 372, 373. 
 
 t Dent. Med. Woch., October 26, 190.5, pp. 1713 et seq. 
 
42S HEART DISEASE. 
 
 These experiments will be referred to in more detail 
 later on. 
 
 Gkoup II. Varying Conditions of High Blood Pressure in 
 the Aorta. — The strain to which the walls of the arch of 
 the aorta are subjected by the varying conditions of the 
 blood pressure within is greater than in any other vessel. 
 
 The blood, as it is forcibly expelled from the ventricle at 
 each systole, rapidly expands the aorta, and impinges on 
 the dome of the arch by which it is deflected. The respira- 
 tory variations of the blood pressure are also very consider- 
 able. The pressure is raised in inspiration, and in occupa- 
 tions which involve severe effort in cramped positions, 
 frequently with the glottis closed, the strain imposed on 
 the walls of the arch must be greatly increased. Strain on 
 the vessel wall, more especially intermittent strain due to 
 fluctuations in the blood pressure, which occur in these 
 arduous occupations, such as those of the miner, collier, 
 soldier, is unquestionably an important etiological factor in 
 aneurysm. 
 
 I have seen two cases of spontaneous rupture of the 
 intrapericardial portion of the aorta in which there was no 
 patch of atheroma or indication of previous disease. The 
 aorta was greatly dilated and stretched in both instances, 
 and its walls were about the thickness of ordinary brown 
 paper. One was in a man aged 42, who was brought in 
 dead to St. Mary's Hospital ; the other was in a boy aged 20, 
 with pneumothorax on the left side. The rupture in this 
 case occurred when the boy was apparently convalescent, 
 three months after the onset of the pneumothorax. 
 
 Pathogeny. 
 
 The interesting paper of Fischer of Bonn already re- 
 ferred to throws much light on the pathogeny of aneurysm. 
 He describes how he has been able to produce aneurysm 
 
ANEURYSM OF THE ARCH OF THE AORTA. 429 
 
 of the aorta in rabbits experimentally by repeated injections 
 of adrenalin. 
 
 Josue had previously produced arterio-sclerosis and 
 atheroma in rabbits by injections of adrenalin, and his 
 results have been confirmed by other investigators, includ- 
 ing Fischer, who describes his results with adrenalin as 
 follows : — 
 
 " The first alterations are circumscribed areas of necrosis 
 of the smooth muscle fibres of the media. Dilatation of the 
 aorta with straightening out of the elastic fibres, which 
 normally have a wavy outline, is the next change. The 
 thick elastic lamella? are approximated, and the more 
 delicate elastic fibres between them disappear. In most 
 cases calcification of the necrotic area sets in early, so that 
 a compact lamina of lime salts is found in the media, and 
 the elastic fibres in the neighbourhood are torn and 
 destroyed. I have thus demonstrated that this process 
 differs materially from human arterio-sclerosis, and that a 
 primary necrosis of the muscular fibres and the elastic 
 lamella? of the media is the cause of it. I have therefore 
 given to this condition the name ' arterio-necrosis.' " 
 
 Fischer has also shown that various toxic substances 
 besides adrenalin can produce this condition of arterio- 
 necrosis in rabbits, but not aneurysm, which apparently 
 requires, in addition, the increased blood pressure induced 
 by the administration of adrenalin. He has produced a 
 typical aneurysm of the aorta in a rabbit by twenty-one 
 intravenous injections of adrenalin (1 in 1000), in doses of 
 0*3 to 0*5 ccm., and in one instance, a dissecting aneurysm of 
 the aorta after twenty-three similar injections of adrenalin. 
 He has also succeeded in producing aneurysm by repeated 
 injections of digalen, a preparation of digitalis which would 
 have similar effect to adrenalin in raising the blood pressure. 
 He found that the arch of the aorta was most commonly 
 affected first, and next in sequence, the thoracic aorta. 
 
43o HEART DISEASE. 
 
 This experimental evidence would seem to point to a 
 focal lesion of the deeper layers of the middle coat of the 
 aorta as the primary lesion or predisposing cause, and to 
 undue increase of the blood pressure within its walls as the 
 exciting cause of aneurysm. 
 
 It is remarkable that in chronic interstitial nephritis, in 
 which the blood pressure is higher, perhaps, than in any 
 other affection, aneurysm is comparatively rare. The ex- 
 planation of this would seem to be (1) that, as the rise in 
 blood pressure is gradual, the vascular system has time to 
 adapt itself to the increased strain by hypertrophy of its 
 muscular coat, and is, moreover, maintained in a condition 
 of hypertonus ; (2) that the disease does not tend to produce 
 a focal lesion in the aorta. Mac William* has demonstrated 
 that in contracted arteries, the range of pulsatile expansion 
 is much less than in relaxed vessels, and that there is a 
 greater tendency to elongation and tortuosity, and con- 
 sequently to dilatation of relaxed vessels subjected to strain. 
 The maintenance of a condition of hypertonus is therefore 
 protective against aneurysm. 
 
 In the arduous occupations which have been referred to 
 above as predisposing to aneurysm, there is no protective 
 hypertonus of the vessels ; the strain is intermittent, and 
 not constant, and may take place when the aorta is relaxed 
 and more or less defenceless, so that the conditions are 
 more favourable to aneurysm. It is, however, doubtful 
 if this can result from strain alone, in the absence of 
 a previous focal lesion of the vessel wall. The impor- 
 tance of a focal lesion as a factor in aneurysm is clearly 
 demonstrated in syphilitic lesions of the aorta, in which 
 no rise of blood pressure above the normal appears to 
 be necessary to dilate the weakened area and give rise 
 to aneurysm. 
 
 * Properties of Arterial and Venous Walls, Proc. Boy. Soc, vol. lxx. 
 p. 151. 
 
ANEURYSM OF THE ARCH OF THE AORTA. 431 
 
 Anatomical Belations of the Arch of the Aorta. 
 
 Before discussing the physical signs of aneurysm, we 
 must call to mind the 'position and chief relations of the arch 
 of the aorta, as many of the symptoms and physical signs 
 of aneurysm are directly dependent on pressure effects of 
 the dilated portion of the vessel on the adjacent structures. 
 
 The aorta, as it emerges from the left ventricle behind 
 the pulmonary artery, and overlapped by the appendix of 
 the right auricle, takes an oblique course upwards, to the 
 right and forwards, to the level of the upper border of the 
 second right costal cartilage ; this, anatomically, is termed 
 the ascending aorta, but in discussing aneurysm it will be 
 more convenient, clinically, to include under this head, the 
 portion of the aorta from the pericardium to the origin of 
 the innominate. The most important relations of the 
 ascending portion of the arch with reference to the symptoms 
 to which aneurysm of this part may give rise, are, the vena 
 cava superior on the right or outer side, and the root of the 
 right lung posteriorly ; but, as there is free and extensive 
 movement of this portion of the aorta at each cardiac systole, 
 and provision is made for this, the surrounding structures 
 are not in very close relation to the vessel : hence pressure 
 symptoms will not arise till the aneurysm has attained a 
 considerable size. It must not be forgotten that part of 
 the aorta lies free in the pericardial cavity for a short 
 distance from its origin ; aneurysms of this intra-pericardial 
 portion, more especially of one of the sinuses of Valsalva, 
 are liable to rupture and cause sudden death before any 
 physical signs or symptoms arise which would lead one 
 to suspect their presence. 
 
 The second or transverse part of the arch of the aorta 
 has a direction backward and to the left, and comprises the 
 portion of the vessel between, and including the orifices of 
 
432 
 
 HEART DISEASE. 
 
 the innominate and left snb-clavian arteries. This portion 
 has little freedom of movement, and lies in close relation to 
 several important structures, pressure on which may early 
 
 r l'hyroid gland 
 
 Right vagu 
 
 Re.c u rrent 
 
 Left vayiis 
 -Left phrenic 
 Ihoracic aurt 
 
 fig. 28. — relations of akcu of aorta. From Gray's Anatomy. 
 
 give rise to characteristic symptoms. Behind it lie the 
 trachea, oesophagus and thoracic duct : interposed between 
 
ANEURYSM OF THE ARCH OF THE AORTA. 433 
 
 it and the trachea just above the bifurcation is the deep 
 cardiac plexus ; the left recurrent laryngeal nerve also 
 curves round it and ascends towards the trachea on 
 its posterior surface. In front the left vagus and left 
 phrenic nerves and the two superficial cardiac nerves from 
 the sympathetic and pneumogastric respectively, cross its 
 anterior surface which, from its oblique course, looks to the 
 left as well as forwards. Above is the left innominate 
 vein ; from its upper aspect are given off the innominate 
 and left carotid and sub-clavian trunks. Below is the 
 bifurcation of the pulmonary artery, the left bronchus, and 
 the left recurrent laryngeal nerve as it winds round the aorta. 
 
 The third or descending part of the arch completes the 
 curve downward and backward. It descends behind the root 
 of the left lung to lie to the left of the body of the fourth 
 dorsal vertebra. 
 
 As has been shown in the brief sketch of the course 
 and relations of the arch of the aorta, the ascending portion 
 is near the surface of the chest and accessible to physical 
 examination, has no attachments to surrounding structures, 
 and enjoys considerable freedom of movement. Aneurysm 
 here often attains to considerable size before it begins to 
 give rise to any symptoms from pressure on surrounding 
 organs, so that the first indication of its presence may b e 
 a pulsating tumour visible on the chest wall to the right 
 of the manubrium. 
 
 The transverse portion of the arch, on the contrary, is 
 deeply placed, is more or less firmly fixed in position, and 
 is in such close relation to various important structures, that a 
 projection from its surface cannot elude or be eluded by the 
 surrounding parts. Hence aneurysm of this portion of the 
 aorta before it attains any great size, usually gives rise 
 to symptoms from pressure on adjacent structures, of which 
 a brassy cough and cracked voice, or tracheal breathing 
 .and difGculty of deglutition, may be the indications. 
 
 2 F 
 
434 HEART DISEASE. 
 
 I have consequently been led to divide thoracic aneu- 
 rysms into two classes, namely Aneurysms of Physical Signs 
 and Aneurysms of Symptoms, from the predominance of 
 physical signs and symptoms respectively, the former 
 term applying to aneurysms of the ascending aorta and 
 first part of the arch, the latter to aneurysms of the trans- 
 verse and descending portions of the arch. 
 
 Physical Signs of Aneurysm in general. 
 
 The most important and conclusive physical sign is 
 pulsation at some part of the chest wall where it is not 
 normally present. We must of course make sure that it is 
 not due to the heart or great vessels being simply un- 
 covered or displaced, as for example by the mediastinum 
 being dragged to the right in consequence of retraction of 
 the right lung, or by deformity of the chest wall bringing 
 the heart or aorta into contact with the chest wall in some 
 unusual situation. The pulsation may or may not be 
 visible ; when obscure it may sometimes be made more 
 perceptible by pressing firmly on the part and watching 
 the hand which is making the pressure ; sometimes it can 
 be seen by standing behind the patient and looking over 
 his shoulders ; it may be recognizable only during expira- 
 tion ; in doubtful cases the pulsation may sometimes be 
 rendered evident by placing the small end of a wooden 
 stethoscope on the spot, one half resting on a rib, the other 
 pressed into the interspace, when the stethoscope will be 
 tilted. 
 
 Pulsation when visible may be a localized protrusion 
 or a general heave. Generally speaking it is best felt by 
 placing the palm of the hand flat on the pulsating area, but 
 it may be necessary to press the fingers well into the 
 intercostal spaces. In estimating the significance of pulsa- 
 tion, whether in a tumour within the cavity of the thorax, 
 
ANEURYSM OF THE ARCH OF THE AORTA. 435 
 
 or in a tumour which has made its way through the chest 
 walls, there must be taken into account, not only the 
 degree of its force or violence, and the extent of the area 
 over which it is felt, but also its character, that is, whether 
 it is distinctly expansile in some or all directions, or is 
 simply firm and thrusting without marked expansion. In 
 the former case the pulsating tumour will feel soft, and 
 there will be no laminated fibrin lining supporting its 
 wall ; in the latter case this will probably be present. 
 These conditions have an important bearing on the probable 
 progress of the aneurysm, and consequently on the question 
 of prognosis. 
 
 A characteristic vibratory thrill may be present, and is 
 best felt by the palm of the hand pressed lightly on the 
 tumour. Another point to be ascertained in the process of 
 palpation is the presence or absence of a diastolic shock. 
 This is a sharp vibration or shock, felt at the end of the 
 true pulsation, synchronous with and due to the same cause 
 as the second sound of the heart, viz. the recoil of the 
 elastic walls of the aorta from the distension caused by the 
 systolic injection of blood. This diastolic shock is the most 
 absolutely pathognomonic of the signs of aneurysm ; pulsa- 
 tion may be communicated to a tumour, or a malignant 
 growth may itself be pulsatile, but there is no diastolic 
 shock under such conditions. 
 
 The fingers may have to be pressed into intercostal 
 spaces to recognize pulsation when an aneurysm of the 
 ascending aorta is just projecting from under the right edge 
 of the sternum ; usually it is best felt at the end of expira- 
 tion, when the border of the lung is withdrawn from over 
 the vessel. It must be borne in mind that pulsation can 
 often be made out in two or three spaces close to the right 
 of the sternum, when the aorta is dilated from protracted 
 high tension, or from incompetence of the aortic valves : it 
 is when it is felt in one space only, and for a certain 
 
436 HEART DISEASE. 
 
 distance beyond the edge of the .sternum, that it may be 
 accepted as significant of aneurysm. More rarely can 
 pulsation to the left of the manubrium be detected in this 
 way in cases of aneurysm of the transverse portion of the 
 arch. 
 
 The tracheal tug should be sought for while carrying out 
 the examination by palpation. To detect this, the trachea 
 is put gently on the stretch, by the fingers, which are 
 placed just beneath the cricoid cartilage : if present a 
 distinct short tug on the trachea is felt with each cardiac 
 systole, superimposed on the slower up and down movements 
 in respiration. It is a very important sign, but not 
 absolutely conclusive, and in particular it does not help to 
 distinguish between a sacculated projection from the aorta, 
 and a general dilatation of the arch. A slight shock or 
 communicated pulsation may sometimes be felt even in 
 cases where there is no disease of heart or aorta. 
 
 Percussion. — When pulsation is distinct the evidence to 
 be obtained by percussion is of secondary importance. 
 Dulness around the pulsating area will merely serve to 
 indicate the extent of the aneurysm. When pulsation is 
 obscure, or absent, deep dulness on percussion over a certain 
 area may corroborate and reinforce other indications of 
 aneurysm, and be of great diagnostic value ; such may be 
 especially the case when the aneurysm is in the transverse 
 or descending part of the arch, and is comparatively small : 
 very slight physical signs may be then of great importance 
 in the interpretation of the symptoms present ; the area of 
 dulness in such a case would probably be situated to the 
 left of the manubrium and over the left half of the manu- 
 brium itself. 
 
 Auscultation. — Of the auscultatory indications, by far 
 the most important is a low-pitched, musical second sound, 
 which, when well marked, is loud and ringing. It is coinci- 
 dent with the diastolic shock, and when a rigid stethoscope 
 
ANEURYSM OF THE ARCH OF THE AORTA. 437 
 
 is employed in auscultation the shock and sound will be 
 felt and heard together. The significance of this ringing, 
 low-pitched second sound is greater, the more remote its 
 point of maximum intensity from the aortic valves — when, 
 for example, it is heard far out in the right chest, and 
 especially when it appears to the left of the manubrium : 
 a reinforcement and change in character of the second 
 sound in the course of the aorta can scarcely be due to any 
 other cause than a dilatation or aneurysm. 
 
 This aneurysmal second sound is not simply an accentua- 
 tion or intensification of the normal aortic second sound ; 
 the pitch is lower from the fact that the wall of the sac 
 constitutes a larger area of resonating membrane than the 
 tube of the aorta. The second sound is not produced by a 
 click of the semi-lunar valves or by their sudden tension, 
 but by the sudden tension of the walls of the aorta and 
 valves together, as a vibrating membrane. When the 
 aortic valves are incompetent, the aneurysmal second sound 
 is impaired, but rarely extinguished. 
 
 The difference in the character and mode of production 
 of the aortic and the aneurysmal second sound may be 
 illustrated by suddenly putting on the stretch a small 
 length of linen (say three inches of the border of a pocket- 
 handkerchief) and comparing the sound thus produced with 
 that which is generated when a portion double the length 
 is similarly put on the stretch. In the latter instance the 
 sound is lower pitched, of greater volume, less sharp in 
 character than in the former, and corresponds to the 
 aneurysmal second sound. 
 
 A murmur may or may not be heard in aneurysm. 
 When present over a pulsating area, it adds nothing to the 
 value of other physical signs, since a tumour pressing upon 
 the aorta, or one of its branches, may give rise to a murmur, 
 and its absence does not detract from their significance. 
 Sometimes when no murmur is heard over the aneurysm 
 
438 HEART DISEASE. 
 
 itself, one may be heard on the distal side of the sac, 
 caused by pressure on the aorta beyond it or on some of 
 its branches. A murmur may be a sign of great value 
 when, being absent over the aortic area, it is developed in 
 the course of the arch and becomes audible over, or to the 
 left of, the manubrium. 
 
 The auscultatory signs resulting from pressure on the 
 root of one or other lung, will not be discussed here, but 
 mention must be made of tracheal breath sounds conducted 
 to the manubrium by means of an aneurysm in contact with 
 the trachea ; these may be heard over this bone loudly 
 and distinctly before serious pressure is produced by the 
 aneurysm on the trachea. 
 
 The Pulse. — An aneurysm may give rise to characteristic 
 modification of, or difference between the two radial pulses. 
 
 The sac of an aneurysm is readily distended, and has 
 little contractile power or elastic recoil, and its interposition 
 in the course of the aorta will impair and delay the pressure 
 or pulse-wave which is transmitted with great rapidity at 
 each systole of the heart throughout the arterial system. 
 
 The combined effect on the pulse-wave will be, firstly to 
 delay it, secondly to diminish its height, thirdly to cause 
 its duration to be longer, and its subsidence more gradual 
 and slower than normal. 
 
 As a further consequence, the artery will also be con- 
 stantly full between the beats, as the sac acts like a black- 
 smith's bellows — being, in fact, a reservoir of blood. 
 
 These points are well illustrated by the sphygmographic 
 tracings appended (Figs. 29 and 30). 
 
 It is obvious that if the aneurysm is situated in the 
 ascending aorta, it will affect both pulses alike, and as there 
 will then be no standard of comparison, such modification of 
 the pulse, if it exist, will be of no great help in diagnosis. 
 Moreover, the modification of the pulse is not, as a rule, so 
 striking as to attract attention. 
 
ANEURYSM OF THE ARCH OF THE AORTA. 439 
 
 Difference between the two radial pulses is, however, 
 frequently one of the most important physical signs in 
 diagnosis of aneurysm, and may be present in the earlier 
 stages, before pulsation is visible. 
 
 Difference between the pulses may arise : (1) From 
 partial blocking of the mouth of one of the main branches 
 of the aorta given off from an aneurysmal sac by projection 
 into it of a portion of fibrin from the organized deposit on 
 the walls of the sac. (2) From pressure on the innominate, or 
 one of the sub-clavian arteries by an aneurysm ; one of these 
 
 Walter Bioadbent,/eci't. 
 
 FIG. 29.— LEFT KADIAL PULSE IN ANEURYSM OF ASCENDING AORTA INVOLVING ORIFICE 
 OF INNOMINATE ARTERY. 
 
 FIG. oO.— RIGHT RADIAL PULSE IN SAME CASE. 
 
 vessels may even be involved in the sac and run in its walls, 
 so that its lumen becomes partially or totally obliterated. 
 For instance, the right radial artery may be smaller than 
 the left, and the pulsation in it weakened or altered in 
 character, or entirely absent, from pressure of an aneurysm 
 on the innominate artery, or from obstruction of its orifice. 
 More frequently it is the left pulse which is affected, either 
 by the interposition of an aneurysm between the origin of 
 the innominate and the left sub-clavian artery, or by the 
 
44° 
 
 HEART DISEASE. 
 
 latter being given off from the aneurysmal sac itself. In 
 such a case the left radial pulse will present all the 
 characters of the aneurysmal pulse above described, while 
 the right radial pulse will be unaffected, and the difference 
 between the two pulses may be very marked, as will be seen 
 in the tracings (Figs. 31 and 32). It is important, however, 
 to remember that difference between the pulses at the wrist 
 may arise from other causes than aneurysm. The calibre of 
 the radial arteries on the two sides may be different ; some- 
 times the radial artery is smaller in one arm than the other, 
 
 FIG. 31. — LEFT RADIAL IN ANEURYSM OF AORTA INVOLVING ORIFICE 
 OF LEFT-CLAVIAN. 
 
 FIG 32— EIGHT RADIAL IN SAME CASE, UNAFFECTED. 
 
 and the ulnar artery larger by way of compensation. Or 
 the radial artery may turn round prematurely to the dorsal 
 aspect of the limb, being represented at the wrist only by 
 a small branch, the superficialis volse. A real difference 
 between the two pulses may be caused by pressure of a 
 tumour on any part of the arterial channel of which the 
 radial is a branch — sub-clavian, axillary, brachial. Again, 
 the orifice of the innominate or of the left sub-clavian may 
 be partially occluded by a calcareous deposit, the result of 
 atheromatous changes. 
 
 In a case that was under my care at St. Mary's Hospital 
 in 1893, the difference in the character of the two radial 
 pulses was so marked and so typical of aneurysm that there 
 
ANEURYSM OF THE ARCH OF THE AORTA. 44 1 
 
 seemed to be no escape from a diagnosis of aneurysm of 
 the transverse part of the arch involving the orifice of the 
 left sub-clavian {vide tracings Figs. 33 and 34). The patient 
 was fifty-eight years of age, and was admitted for shortness 
 of breath and severe pain in the precordial region. The 
 heart was hypertrophied, and there was a double aortic 
 murmur. There was no pulsation visible over the aortic or 
 pulmonic area, and no dulness on percussion. There was, 
 in fact, no other physical sign of aneurysm, except the 
 
 FIG. 00.— LEFT RADIAL PLLSE, IN CASE WHERE ORIFICE OF LEFT SLB-CLAVIAN 
 WAS OBSTRUCTED BY ATHEROMA. 
 
 FIG. 34. — RIGHT RADIAL PDLSE. 
 
 marked difference in the pulses, though the severe pain 
 in the chest and paroxysms of dyspnoea were symptoms con- 
 sistent with, and in favour of aneurysm. At the post-mortem 
 no aneurysm was found, but the orifice of the left sub-clavian 
 artery was about one-half occluded by a thick calcareous 
 plate projecting across it. The aorta was also dilated and 
 atheromatous, and the aortic valves were incompetent. 
 
 Delay of Pulse. — One of the most characteristic differ- 
 ences between the two radial pulses which may be present 
 in aneurysm is the apparent delay in one, when they are 
 both felt at the same time. If one is affected by the 
 interposition of the aneurysmal sac, the rise in pressure is 
 more gradual, and reaches its maximum later ; and as this 
 is what is felt as the pulse, it will be delayed as compared 
 with that of the other side. 
 
442 HEART DISEASE. 
 
 The Carotid Arteries. — It must be borne in mind also 
 that an aneurysm may affect pulsation in the carotids in 
 the same way as in the radials. For, the orifice of the 
 left carotid may be involved in the sac, or may be parti- 
 ally occluded by a plug of fibrin, and it is obvious that 
 whatever affects the innominate artery will similarly affect 
 the right sub-clavian and right carotid. The blocking of 
 one carotid, partial or complete, or a difference between the 
 pulsation in the carotids on either side, corresponding to 
 that already noted in the radials, will be important con- 
 firmatory evidence of aneurysm. 
 
 The Heart. — It has been asserted by some authorities 
 that aneurysm gives rise to hypertrophy of the heart. That 
 this is not the case has been conclusively shown by Dr. 
 James Calvert,* in a paper based on an analysis of 124 cases 
 of aneurysm collected by Dr. Oswald Browne. In 68 of these 
 cases aneurysm existed without giving rise to any hypertrophy 
 of the heart. It is, however, true that cardiac hypertrophy 
 is not infrequently found in association with aneurysm, but 
 it may almost invariably be explained by causes other 
 than aneurysm, such as arterio-sclerosis or prolonged high 
 arterial tension due to kidney disease or other causes. 
 
 The heart may be displaced by aneurysm of the ascending 
 aorta, or of the transverse part of the arch, so that the apex 
 beat may be found below and outside its normal position, 
 but this should not be mistaken for hypertrophy. More 
 frequently the apex beat is displaced upwards : its position, 
 and the extent to which the heart is displaced, will vary 
 according to the size, shape, and situation of the aneurysm. 
 
 The physical signs that have been discussed thus far are 
 mainly those directly dependent on the aneurysm itself, 
 produced in and by it, and not on indirect or pressure effects 
 of the aneurysm on adjacent structures, which will now be 
 considered. 
 
 * Trans. Med. Chir. Soc, 1891). 
 
aneurysm of the arch of the aorta. 443 
 
 Pressure Effects of Aneurysm on Adjacent 
 Structures. 
 
 1. Ths Great Veins. — An aneurysm may compress and 
 cause obstruction to the flow of blood through one of the 
 large venous trunks, the vena cava superior, or the right 
 or left innominate veins. 
 
 A sudden and complete block of the vena cava superior 
 from thrombosis, or from compression by sudden extension 
 of the aneurysm, may give rise to oedema of the head 
 and neck and upper extremities, with a cyanotic appear- 
 ance, the face being enormously swollen and disfigured, 
 while severe dyspnoea is produced by oedema of the fauces 
 and larynx. This, however, is an extremely rare event, 
 only one example having come under my observation. 
 Usually, the pressure takes effect gradually, and collateral 
 venous channels are developed which carry the blood from 
 the tributaries of the superior vena cava to the inferior, and 
 obviate the effect described. Some of these are external, 
 in the form of large tortuous veins crossing the clavicles, 
 descending the surface of the chest, sometimes continued 
 down the abdomen. A remarkable instance of this is 
 shown in the photograph (Fig. 35) taken from a case of 
 aneurysm of the first part of the arch, which was under 
 observation for upwards of six years. The mass of dilated 
 veins, some of which were of the size of the finger, on the 
 surface of and below the tumour, was a striking feature. 
 Below the mamma many of these veins disappeared, pre- 
 sumably anastomosing with the intercostal veins, but three 
 large tortuous veins continued downward to anastomose 
 apparently with the right epigastric veins. The direction 
 of the current of blood, which should always be carefully 
 ascertained, was found to be downwards. Other channels 
 of communication, in which the azygos veins take part, are 
 deep seated and not open to observation. The proportion 
 
444 HEART DISEASE. 
 
 of superficial and deep collateral venous circulation varies 
 greatly in different cases. 
 
 The jugulars are distended, and an important point 
 is that they are not emptied even partially by a deep 
 inspiration, as is the case, more or less, when the veins 
 of the neck are full from back pressure in the systemic 
 venous system in mitral disease, or in emphysema and 
 bronchitis. 
 
 FIG. 35. — TOBTOOOS DILATED VEINS ON SURFACE OF LARGE ANEURYSM OF 
 ASCENDING AORTA. 
 
 Again, there is no true jugular pulsation such as is 
 present in venous reflux from the tricuspid incompetence 
 which supervenes as a result of dilatation of the right 
 ventricle in mitral disease or emphysema. There may, 
 however, be apparent pulsation in the veins caused by the 
 subjacent carotid. 
 
 There may be pressure on the azygos vein which passes 
 up behind the root of the right lung to open into the 
 
ANEURYSM OF THE ARCH OF THE AORTA. 445 
 
 superior vena cava just before it enters the pericardium. 
 This, does not appear to give rise to any characteristic 
 physical signs or symptoms, probably because of the free 
 anastomosis with the lumbar veins, which enables the blood 
 to return without difficulty via the iliac veins and inferior 
 vena cava. 
 
 Even more interesting than obstruction of the vena cava 
 is obstruction of one or other of the innominate veins. The 
 discovery of a one-sided distension of the external and 
 anterior jugulars, not disappearing in deep inspiration, 
 especially if associated with dilatation of the veins of the 
 upper extremity, is not unfrequently the first step towards 
 the diagnosis of an aneurysm which might otherwise have 
 eluded detection for some time. In such a case the col- 
 lateral enlargement of veins is also one-sided. 
 
 2. Pressure on the Root of the Lung. — Pressure on the 
 right or left bronchus will cause diminished entry of air to 
 the corresponding lung, with characteristic alteration of the 
 breath sounds. When the bronchus is obstructed without 
 pressure on the pulmonary veins, the resonance will not 
 be impaired, or will be only slightly modified. Eesonance 
 on percussion in association with silence on auscultation 
 (pneumothorax, of course, being excluded) are highly 
 characteristic of obstruction of a bronchus. The collap>se 
 of lung which eventually ensues will give rise to some 
 falling in of the intercostal spaces, and impairment of 
 resonance. 
 
 Pressure on the pulmonary veins may occur, giving 
 rise to congestion of the lung tissue. As a rule, however, 
 they escape compression in spite of their unresisting 
 structure, probably because they are protected by the 
 bronchi which usually suffer first. One case, nevertheless 
 has come under my notice in which the lung was found at 
 the autopsy to be in a semi-gangrenous condition from this 
 cause. The aneurysm was a large one, about the size of 
 
446 HEART DISEASE. 
 
 two fists, affecting the ascending aorta and extending back- 
 wards, and compressing the root of the right lung as well 
 as presenting on the chest wall as a pulsating tumour. 
 
 3. Pressure on the cilio-spinal branches of the sympa- 
 thetic may cause dilatation or contraction of the pupil on 
 the corresponding side according as the dilator fibres are 
 irritated or destroyed by compression. 
 
 4. Pressure on the left recurrent laryngeal nerve will 
 cause paralysis of the left vocal cord. 
 
 The right recurrent laryngeal nerve is seldom affected 
 by aneurysm of the aorta, since it winds round the right 
 sub-clavian artery ; occasionally it may be subjected to 
 pressure by the sac of an aneurysm of the transverse part 
 of the arch involving the orifice of the innominate, or by 
 extension upwards of an aneurysm of the ascending part 
 of the arch. 
 
 5. Pressure on the trachea, oesophagus, and thoracic 
 duct may be caused by an aneurysm of the transverse or 
 descending part of the arch. 
 
 There remains for discussion one symptom, namely pain, 
 which is usually, at some period in the history of an 
 aneurysm, a conspicuous feature. 
 
 Pain is very rarely absent, though it differs greatly in 
 character and intensity in different cases. A feature 
 common to aneurysmal pain of all kinds and in any 
 situation, is the aggravation of it by exertion. 
 
 Pain may be the sole symptom, and may be of itself, 
 without corroboration by physical signs, sufficient for a 
 diagnosis of aneurysm. 
 
 Aneurysm at the very root of the aorta within the cavity 
 of the pericardial sac, or aneurysm of the sinuses of Valsalva, 
 may give rise to pain of anginoid character. It may 
 indeed cause true angina by extension of disease from the 
 sinuses of Valsalva along the coronary arteries, or by 
 obstructing the openings of these vessels and consequently 
 
ANEURYSM OF THE ARCH OF THE AORTA. 447 
 
 giving rise to degeneration of the walls of the heart. It 
 is not always possible to distinguish between anginoid 
 pain due to aneurysm in this situation and true angina; 
 the sense of impending death is not as a rule so marked 
 a feature of the attacks, and the pain often radiates down 
 both arms instead of along the left only ; occasionally 
 it shoots down the right arm only. In angina, there may 
 be no physical signs of disease in the great vessels ; in 
 aneurysm there will be the ringing second sound, and 
 frequently a diastolic murmur, but rarely, dulness nn per- 
 cussion or recognizable pulsation. 
 
 In aneurysm of the ascending aorta, there is usually 
 deep-seated pain of a vague kind which may be very severe 
 while the aneurysm is extending, and may become quiescent 
 when it has ceased to enlarge. It is usually aggravated 
 by certain positions, relieved by others, so as to constrain 
 the patient to a particular decubitus, different in different 
 cases without obvious reasons. Pain in the right shoulder 
 or scapular region may indicate backward extension of 
 an aneurysm of the ascending aorta which is not revealed 
 by physical signs. 
 
 Pain again attends the process of penetration of the 
 chest wall, though it need not be severe. When the 
 barrier of the ribs is overcome and the aneurysm projects on 
 the surface of the chest, there is often relief, not only from 
 the pain attending the pressure forward on the thoracic 
 parietes, but from deep-seated pain. 
 
 A remarkable pain sometimes attends aneurysm in this 
 situation, located in the tip of the right shoulder, and at 
 the occipital insertion of the trapezius. When very severe, 
 I have found the trapezius muscle in a state of spasm, and 
 the head slightly rotated ; but pain may be present when 
 the muscular spasm is slight. Apparently the cause is 
 reflex irritation of the spinal accessory nerve. 
 
 There is nothing specially remarkable about the pain 
 
448 HEART DISEASE. 
 
 attending aneurysm of the transverse part of the arch, 
 though it is often severe. It is when the descending part 
 of the arch, or the thoracic aorta is the seat of aneurysm, 
 that pain may be the sole symptom. The vessel is firmly 
 held down to the vertebral column by the intercostal 
 arteries ; erosion of the bodies of the vertebras takes place, 
 and the intercostal nerves may be reached. Lancinating 
 pain is then experienced of an extremely severe and per- 
 sistent character before the aneurysm has reached a size 
 which permits of its recognition by physical signs. 
 
 Thus far we have enumerated the general physical sign s 
 and symptoms to which aneurysm of the arch of the aorta 
 may give rise. We shall now proceed to group these 
 together around the various clinical types of aneurysm of 
 which they are severally characteristic. 
 
 Classification of Aneurysms of the Aech of 
 the Aoeta. 
 
 For clinical purposes we may divide aneurysms of the 
 aorta into four groups, according to their anatomical 
 situation — 
 
 (1) Aneurysm of the intra-pericardial portion of the 
 aorta ; 
 
 (2) Of the ascending aorta as far as the origin of the 
 innominate ; 
 
 (3) Of the transverse part of the arch ; 
 
 (4) Of the descending part of the arch. 
 
 (1) Aneurysm of the Intra-pericardial Portion 
 of the Aorta. 
 
 The favourite site of an intra-pericardial aneurysm is 
 one of the sinuses of Valsalva. As there are no adjacent 
 structures to support the sac and contribute to its wall, 
 it usually ruptures into the pericardium before it attains 
 
ANEURYSM OF 1NTRA-FERICARD1AL PART OF AORTA. 449 
 
 any considerable size. Should the aneurysm, however, 
 extend towards the pulmonary artery or superior vena 
 cava, its sac may become adherent to their wall, so that 
 rupture is deferred for a time, eventually taking place, 
 as a rule, into one of these vessels. 
 
 Physical Signs and Symptoms. — Angina pectoris may 
 be present if the aneurysm involves the orifice of one of 
 the coronary arteries, but frequently no physical signs or 
 symptoms are present, and sudden death occurs from 
 rupture of the aneurysm into the pericardium before any 
 suspicion as to its presence has been aroused. 
 
 It may so happen that the sac of the aneurysm 
 compresses the superior vena cava and obstructs the 
 return of blood to the heart through this vessel, thus giving 
 rise to characteristic symptoms. 
 
 An interesting instance of the latter condition occurred in a case 
 under my care at St. Mary's Hospital in 1893. The patient, a man 
 aged 30, was admitted suffering from shortness of breath and pain of 
 an anginoid character. On examination, the heart was found to be 
 hypertrophied, and there was evidence of aortic and mitral incompe- 
 tence. The veins of the neck were distended and full, and it was 
 noted that they did not empty on deep inspiration. This seemed to 
 indicate that some tumour pressing on the superior vena cava, possibly 
 aneurysm, was the cause of the obstruction to the return of blood to 
 the heart. The liver was not enlarged, and there was no oedema of 
 the extremities, so that it was clear there was no obstruction to the 
 return of blood by the infei*ior vena cava. There was, however, no 
 other definite evidence of aneurysm at the time of his admission, but 
 on February 19th, a month later, he had an attack of severe pain in the 
 region of the heart, and became very pale and almost pulseless ; he 
 rallied from this state of collapse, and in the evening vomited a little 
 blood. Signs of pericardial effusion were present, and it was thought 
 that a small rupture of the aneurysm into the pericardium had taken 
 place. 
 
 He died four days later, becoming suddenly very pale and falling 
 back dead in bed. At the autopsy the pericardium was found to be 
 full of blood and recent clot, and there was also pale firm clot of older 
 date due to the haemorrhage four days before death. 
 
 There was a small aneurysm on the outer aspect of the aorta about 
 one and a quarter inch above the valves, bulging into and partially 
 embedded in the superior vena cava just below the point where it 
 
 2 G 
 
450 HEART DISEASE. 
 
 entered the pericardium. This had ruptured, and caused the sudden 
 death. 
 
 Eupture op an Aneurysm into the Pulmonary 
 Artery. 
 
 A considerable number of cases of this incident have 
 been recorded. In 1840 * Thurnam recorded five cases ; 
 in 1897 f Lamplough published a case which came under 
 his observation, and gave a brief summary of fifteen cases 
 which he had been able to collect, six of which had been 
 published in the Transactions of the Pathological Society. 
 In 1899 Sir William G-airdner published a case in the 
 Glasgow Hospital Reports, and in 1900 % Michell Clarke 
 recorded a case. We have, therefore, although the con- 
 dition is rare, a sufficient number of cases recorded for 
 diagnostic data. 
 
 Physical Signs and Symptoms. — The immediate symptoms 
 of rupture are, sudden pain in the chest with severe dyspnoea, 
 followed by cough, sometimes with expectoration of blood- 
 stained mucus. The attack does not, as a rule, prove 
 rapidly fatal, but the patient may survive some weeks or 
 several months, when definite physical signs and symptoms 
 will usually develop. The earliest fatal termination in 
 Lamplough's cases was in two weeks. The longest survival 
 one year. 
 
 The most characteristic physical sign is a continuous 
 roaring murmur, audible over the second and third left 
 intercostal spaces. The murmur is loud and vibratory, its 
 maximum intensity being systolic in time. 
 
 A vibratory thrill may sometimes be felt on palpa- 
 tion over the pulmonic area, and was present in 6 per 
 cent, of Lamplough's cases. Pulsation is not present. 
 
 * Trans. Meil. Chi. Soc, vol. xxiii. p. 323. 
 t B. M. J., 1897, vol. ii. p. 392. 
 % B. M. J., 1900, vol. ii. p. 1701. 
 
ANEURYSM OF INTRA- PERICARDIAL PART OF AORTA. 451 
 
 Subsequently, symptoms of dilatation of the right ventricle 
 develop, and as this gives way, enlargement of the liver, 
 tricuspid incompetence, and dropsy supervene, with en- 
 gorgement of the lungs, and the patient dies with all the 
 symptoms of right ventricle failure. 
 
 I11 a case recently under tlis care of Dr. Lees at St. Mary's Hospital, 
 the patient was a man aged 49, who, ten months before admission, 
 was suddenly seized with pain in the chest and severe dyspnoea. Three 
 months after this attack, ascites and oedema of the legs set in. He was 
 tapped for ascites seven times. On admission to St. Mary's Hospital, 
 ten months after the onset of symptoms pointing to rupture of the 
 aneurysm into the pulmonary artery, there was dyspnoea, slight 
 cyanosis, dropsy, and ascites. Over the second and third intercostal 
 spaces to the left of the sternum there was a well-marked vibratory 
 thrill, but 110 actual pulsation. Over this area was a ceaseless, loud, 
 roaring murmur, varying in intensity and most marked over the third 
 left space. There was some hypertrophy of the left ventricle and 
 great dilatation of the right. He died five weeks after admission. 
 Post-mortem there was found to be a perforation in the aorta about 
 half an inch in diameter, which opened into the pulmonary artery, 
 obliterating one of the cusps of the pulmonic valve. 
 
 Rupture of an Aneurysm into the Superior 
 Vena Cava. 
 
 An interesting series of twenty-five cases, which they 
 have collected from various sources, is recorded by Pepper 
 and Griffiths.* Death frequently occurs in a few hours' 
 time, but the patient may survive some months. The 
 shortest period in which death occurred was six hours ; the 
 longest survival, seven months. One case is said to have 
 recovered. 
 
 Physical Signs and Symptoms. — The immediate symptoms 
 are sudden onset of severe dyspnoea, cyanosis, turgescence 
 of the veins of the neck, rapidly followed by tense oedema 
 of the neck and face. There is usually little or no actual 
 pain. The dyspnoea, cyanosis, and oedema of the neck 
 and face persist ; distended veins make their appearance 
 * American Journal of Medical Sciences, 1890, vol. 100, p. 329. 
 
452 HEART DISEASE. 
 
 on the front of the chest from collateral circulation 
 established between the internal mammary and the inter- 
 costal and superficial epigastric veins. In course of time 
 (from two to five weeks) a murmur develops, audible over 
 the aortic area. The murmur may be systolic in time, or 
 continuous, or a double murmur, systolic and diastolic, may 
 be present. Pulsation over this area may make its appear- 
 ance at a considerably later date, and is present in about 
 50 per cent, of cases. A thrill is felt in the majority of 
 cases, but not in all. 
 
 The following case, which was under the care of Dr. Cheadle, at 
 St. Mary's Hospital, in 1903, is of exceptional interest in that it was 
 under observation from the onset of symptoms till death, some four 
 months later, and a correct diagnosis was made on the day of admission. 
 
 Thomas M., aged 59, admitted to St. Mary's Hospital, March 28th, 
 1903. 
 
 History.— Was well till the evening before admission, when he 
 suddenly, while in bed, became very short of breath and cyanosed. 
 This was rapidly followed by swelling of the neck and face. There was 
 no history of any previous symptoms pointing to aneurysm or affection 
 of the heart. 
 
 On admission next morning he was very cyanosed and short 
 of breath. The neck was swollen, brawny, and tense, somewhat 
 resembling the condition of angina Ludovici, and did not pit on 
 pressure. The face was also swollen, more especially the right side. 
 The veins in the neck were full and distended. There was no pulsa- 
 tion visible, and no murmur was audible over the pulmonic area. 
 
 In the course of a week distended tortuous veins made their appear- 
 ance on the front of the chest, and later all over the back above the 
 scapulae. The current of blood was downwards. 
 
 After three weeks a soft, blowing systolic murmur became audible 
 over the aortic area, which gradually increased in intensity and became 
 more prolonged. It remained soft and blowing and never became 
 continuous, though the diastolic interval was very short. 
 
 A month after admission the oedema of the face and neck had, to 
 a great extent, subsided, but the cyanosis persisted : the veins over the 
 chest and back were very prominent, forming a diffuse network over 
 the whole of the upper part of the front of the chest. The right 
 internal jugular vein was thrombosed and filled with firm clot. The 
 dyspnoea was less severe, and he was so much better that he insisted 
 on going home. 
 
 He was readmitted three weeks later with severe dyspnoea, 
 cyanosis, and oedema of the right arm and right side of the chest. 
 
ANEURYSM OF INTRA-PERICARDIAL PART OF AORTA. 453 
 
 The murmur over the aortic area was louder and more prolonged. 
 He became noisy and delirious at night, and his mental faculties were 
 much impaired. Slight pulsation became evident over a localized area 
 in the second right intercostal space. He died on May 10th, four and 
 a half months after the onset of symptoms. 
 
 At the autopsy an aneurysm was found springing from the ascend- 
 ing aorta about one inch from its origin. The sac of the aneurysm was 
 about three inches in diameter, and the pericardium was stretched over 
 its upper aspect. There was a communication between the aneurysm 
 and the superior vena cava about half an inch in diameter. The 
 sac of the aneurysm was firmly united to the vena cava by adhesions, 
 and there was no leakage into the pericardial cavity. The superior 
 vena cava was greatly dilated, being nearly an inch in diameter, and 
 its walls were greatly thickened. The right internal jugular vein 
 was thrombosed, and occupied by firm adherent white clot. The left 
 innominate vein was stretched over the front of the sac of the aneurysm, 
 and its lumen was entirely obliterated. The right innominate and sub- 
 clavian veins and the left sub-clavian and internal jugular veins were 
 patent and free from clot. The azygos vein was greatly enlarged. 
 The aorta was atheromatous. 
 
 KUPTURE OF AN ANEURYSM INTO THE AURICLES. 
 
 Cases are on record in which an aneurysm has ruptured 
 into one of the auricles. In one case of rupture into the 
 left auricle, described by King,* sudden dyspnoea, cough, 
 and cyanosis supervened, and death took place in fifteen 
 minutes. In another case, described by Ewart,f no 
 symptoms were traceable to the perforation. 
 
 A case of rupture of an aneurysm into the right auricle 
 is also recorded by Ewart,| and another by Norman Moore,§ 
 in neither of which were any characteristic symptoms 
 present. 
 
 (2) Aneurysm of the Ascending Aorta beyond the 
 Pericardium, or Aneurysm of Physical Signs. 
 
 Under this head are comprised aneurysms which involve 
 the ascending aorta between the pericardium and the orifice 
 
 * Transactions of the Pathological Society, vol. 26, p. 37. 
 
 t Ibid., vol. 31, p. 90. J Ibid., vol. 31, p. 95. 
 
 § Ibid., vol. 31, p. 82 
 
454 
 
 HEART DISEASE. 
 
 of the innominate artery. As has already been stated, the 
 name, "aneurysm of physical signs," has been given to 
 aneurysms affecting this part of the aorta, since, from the 
 nature of its anatomical relations, pressure symptoms do not 
 readily arise, and frequently the first definite indication of 
 the existence of an aneurysm is the appearance of an area 
 of pulsation on the chest wall, usually in the second left 
 
 FIG. 3G. — ANEURYSM OF ASCENDING AORTA WHICH RUPTURED INTO RIGHT 
 PLEURAL CAVITY AT A. 
 
 intercostal space. Dulness or impaired resonance on per- 
 cussion may be present before pulsation is visible, but 
 dulness alone is not sufficient evidence of aneurysm, and 
 pulsation may sometimes be recognizable in the second and 
 third left intercostal spaces close to the sternum, when the 
 aorta is dilated as in aortic incompetence. When pulsation 
 is present, a diastolic shock may sometimes be felt on 
 palpation over the tumour, and on auscultation the second 
 sound is usually ringing in character and low pitched. 
 
 If the sac extends outwards, there will be evidence of 
 
ANEURYSM OF THE ASCENDING AORTA. 455 
 
 pressure on the superior vena cava, shown by distension 
 and fulness of the veins on both sides of the neck ; if it 
 extends backwards, there may be symptoms of pressure on 
 the root of the right lung. 
 
 Pain in the neighbourhood of the aneurysm is usually 
 present in varying degree, being most severe, as a rule, 
 when the tumour is being pressed up against the chest wall 
 and is beginning to erode the ribs. 
 
 An aneurysm in this situation may attain very great 
 size, sometimes being as large as a child's head. Usually 
 it enlarges in the direction of the blood current, that is, 
 towards the wall of the thorax, on reaching which it may 
 erode the overlying ribs, and gradually force its way 
 through them as they undergo atrophy from the pressure. 
 It may rupture at any stage, sometimes into the right 
 pleural cavity (vide Fig. 36). 
 
 It may also rupture into the lung, giving rise to 
 haemoptysis, which may be profuse and terminate fatally. 
 If the perforation is small or at the base of a sacculus, 
 it may become occluded by clot and the haemorrhage be 
 arrested, but attacks of haemoptysis are liable to recur from 
 time to time as the clot is dislodged. Sometimes the 
 perforation is permanently closed by the development of 
 adhesions. Frequently the lung tissue is compressed and 
 adherent to the sac of the aneurysm, so that when a per- 
 foration occurs there may be little leakage at first. In one 
 case, from which I put up a specimen for the St. Mary's 
 Hospital Museum, there were no less than three separate 
 perforations, and there was a history of recurrent attacks 
 of haemoptysis at intervals for over two years. 
 
 The patient was a man aged 59. The first attack of 
 haemoptysis occurred in December, 1900, the next in 
 April, 1902, a third in September, a fourth in October, 
 the patient dying in November, 1902. In the third attack 
 10 ozs., and in the fourth 20 ozs. of blood were coughed 
 
456 HEART DISEASE. 
 
 up. At the autopsy there was a large aneurysm involving 
 the whole of the arch of the aorta, spreading out in a fan- 
 like shape. There were two perforations on the outer 
 aspect of the ascending part of the arch into the right 
 lung, which were occluded by layers of laminated clot. 
 The adjacent lung tissue was compressed, and adherent to 
 the sac of the aneurysm over the bases of the perforations, 
 which it helped to seal up. The perforations were about 
 one-third of an inch in diameter. On the outer aspect of the 
 descending portion of the arch was a third perforation into 
 the left lung, which was engorged with blood, and it ap- 
 peared that the recent attacks of haemoptysis were due to 
 leakage from this source. 
 
 Aneurysm of the ascending aorta is, however, compatible 
 with life for a considerable number of years, as the cases 
 appended will show. 
 
 Case 1. — Harriet H., aged 46, was admitted to St. Mary's Hospital 
 in May, 1887, with the history that three years before she had noticed 
 a small lump in the upper part of the right side of the chest. For a 
 year previous to this she had felt pain in the chest of varying severity. 
 
 On admission, there was a small pulsating tumour about the size of 
 a hen's egg just below the inner end of the clavicle immediately to the 
 right of the manubrium. 
 
 The aneurysm had already made its way through the chest wall by 
 erosion of the upper right costal cartilages, and was partially outside 
 the thoracic cavity. There were some enlarged veins on the front of 
 the chest wall, but the jugular veins were not markedly distended. 
 Thei'e was no evidence of pressure on the air passages, or the recurrent 
 laryngeal nerve. The second sound was accentuated and somewhat 
 low pitched, but was not ringing in character or typical of aneurysm. 
 After some weeks, she left the hospital, and was readmitted again in 
 1891, when the aneurysm had increased considerably in size, but she 
 did not remain long in hospital. In September, 1892, she was again 
 admitted. The aneurysm had then attained an enormous size, reaching 
 upwards above the clavicle, and merging below the right mamma into 
 a mass of dilated veins. The tumour was now firm and resistant, and 
 the pulsation was scarcely perceptible, showing that a large amount of 
 laminated clot had been deposited within the sac : there was no diastolic 
 shock. The radial pulse on both sides was greatly modified, and the 
 right was smaller than the left. 
 
 The jugulars on both sides were much distended, and did not empty 
 
ANEURYSM OF THE ASCENDING AORTA. 457 
 
 on deep inspiration. The current of blood in the dilated veins was 
 downwards,, and they apparently anastomosed with the superficial epi- 
 gastric and intercostal veins, showing that the vena cava superior was 
 obstructed by pressure of the aneurysm, and that some of the blood 
 normally returned by the superior vena cava was finding its way back 
 to the heart by a devious route through the vena cava inferior. A 
 photograph of this patient is given (Fig. 35). 
 
 The tumour measured 7 inches across, 9 inches long, and was about 
 19 inches in circumference. 
 
 She remained in hospital six months, and died at home eighteen 
 months later. Unfortunately, an autopsy was not obtainable, but it 
 was ascertained that she had not died suddenly ; that is, from rupture 
 of the aneurysm, but from some intercurrent pulmonary complication. 
 She had thus survived nine or ten years from the first appearance of 
 the aneurysm. 
 
 Case 2. — Lydia W., aged 40, first came under observation at 
 St. Mary's Hospital about fifteen years ago. When first admitted, the 
 aneurysm was so small that the diagnosis was difficult, more especially 
 as she was also suifering from aortic incompetence in slight degree. 
 Pulsation on the surface of the chest wall was not visible, but could be 
 made out on firm palpation in the second and third right intercostal 
 spaces. The aortic second sound was, however, low pitched and booming 
 in character, and typical of aneurysm. While she was in hospital, the 
 aneurysm steadily advanced, and pulsation soon became obvious. She 
 suffered from pain and respiratory distress, and from attacks of palpita- 
 tion and epistaxis. Treatment by pressure and iodide of potassium 
 failed to arrest the progress of the aneurysm at this stage, and it was 
 found necessary to keep her in hospital for eighteen months on account 
 of the severity of the symptoms. 
 
 The aneurysm had greatly increased in size, and at the end of this 
 period pulsation was visible in the second and third spaces as far out as 
 the anterior axillary line with a corresponding increase of dulness on 
 percussion. The administration of iodide of potassium, which had been 
 discontinued, was now resumed in large doses, and consolidation rapidly 
 took place. The tumour from being expansile became firm, showing 
 evidence of the deposition of laminated clot on its inner surface. All 
 her symptoms had greatly ameliorated, and she left comparatively well. 
 
 The reasons for this improvement, in spite of increase in the size of 
 the aneurysm, seemed to be the following : When she came in, there 
 was a small sac with a relatively large orifice communicating with the 
 aorta, so that the current of blood swept through it, distending it more 
 and more, and not allowing of the deposition of clot within the sac. 
 When she left, conditions had changed ; there was now a large sac with 
 a relatively small mouth, so that the main current of blood rushed past 
 the orifice instead of through the sac, and allowed of the formation of 
 layers of laminated clot upon its walls. 
 
 She has come up to the hospital from time to time since, and when 
 
458 HEART DISEASE. 
 
 last seen, in 1905, slie said she did not feel any special inconvenience 
 from the aneurysm. There was then a pulsating tumour about the size 
 of a hen's egg in the second and third right intercostal spaces, not pro- 
 jecting very much above the surface of the chest wall. A general heave 
 was communicated to the chest wall around this area, and pulsation 
 could be felt by deep palpation in the second and third spaces as far 
 as the anterior axillary line, over which area there was dulness on 
 percussion. 
 
 On palpation over the aneurysm, a well-marked diastolic shock was 
 felt. The aortic second sound was low pitched and ringing, and a 
 diastolic murmur was also audible. 
 
 There was no evidence of pressure on the superior vena cava, no 
 difference in the pulses, no affection of the vocal cords. The pulse 
 wave was forcible and sudden in character, but was sustained instead 
 of collapsing, and presented the characters of the pulse of aortic incom- 
 petence scarcely modified by the aneurysm. 
 
 This is practically a case of cured aneurysm. The walls of the sac 
 have become thick and strong from deposit of laminated clot within 
 and chronic inflammatory changes without, and there is little chance 
 of rupture. She has now survived fifteen years from the onset of 
 the aneurysm, and seldom has any symptoms to remind her of its 
 existence. 
 
 (3) Aneurysm op the Transverse Part of the Arch. 
 Aneurysm op Symptoms. 
 
 The name, aneurysm of symptoms, has been given to 
 aneurysms affecting the transverse part of the arch because, 
 as a rule, characteristic and important symptoms early 
 arise which engender a suspicion of aneurysm some time 
 before the physical signs are at all demonstrative of its 
 existence. 
 
 Most of the symptoms which may arise have already 
 been enumerated under the head of " Pressure Symptoms ; " 
 but, for the sake of clearness, it will be necessary to briefly 
 discuss them here. 
 
 The symptoms will vary, and one or other of them will 
 present themselves according as the aneurysm is situated 
 in the convexity or concavity of the arch, or upon its 
 anterior or posterior surface. 
 
 1. Pressure on the Left Recurrent Laryngeal Nerve. — 
 
ANEURYSM OF THE ARCH OF THE AORTA. 459 
 
 As this nerve winds round the aorta, an aneurysm on any 
 aspect of the aortic arch may press upon it or stretch it, 
 giving rise to characteristic symptoms. 
 
 One of these is the " cracked " voice, which is so pecu- 
 liar as to be almost diagnostic. 
 
 Not infrequently the patient will come up to the throat 
 department, or consult a throat specialist, complaining of 
 hoarseness and alteration of voice ; or, if he happens to have 
 a cough, he may have also noticed that the sound made 
 when he coughs has an altered, brassy character. There is 
 not, as a rule, dyspnoea unless there is in addition pressure 
 by the aneurysm on the trachea or one of the bronchi. On 
 examination of the larynx, it will be found that these 
 symptoms are due to paralysis of the left vocal cord. 
 
 The paralysis that results from pressure on the recurrent 
 laryngeal nerve is that of the abductors of the larynx, so 
 that the left vocal cord will be seen fixed and motionless in 
 the median line in the position of phonation. This may be 
 the first, and the only suspicious symptom of aneurysm, but 
 it is very significant when present, as nothing except a 
 tumour pressing on the recurrent nerve in some part of its 
 course can give rise to one-sided laryngeal palsy, and of 
 such tumours, by far the commonest is aneurysm. The 
 right recurrent laryngeal nerve may be compressed by the 
 sac of an aneurysm involving the innominate artery, as is 
 illustrated in the second case described later on. 
 
 2. Pressure on the Trachea, (Esophagus, and Thoracic Duct. 
 — Symptoms arising from pressure on these structures may 
 be the earliest indications of an aneurysm on the posterior 
 surface of the arch, or of a saccular aneurysm extending 
 posteriorly. 
 
 Pressure on the trachea may give rise to slight dyspnoea, 
 but this, as a rule, is only marked when there is in addition 
 paralysis of one of the vocal cords. Auscultation of the 
 limo-s will show the modification of the breath sounds 
 
460 HEART DISEASE. 
 
 known as tracheal breathing. Rupture of the aneurysm 
 into the trachea may occur as illustrated in Fig. 37, and 
 give rise to profuse and fatal haemoptysis. 
 
 The tracheal tug, already described, will as a rule be 
 recognizable before the pressure gives rise to dyspnoea. 
 
 Pressure on the oesophagus will cause difficulty in 
 swallowing, and it has happened ere now that adventurous 
 persons seeking to ascertain the cause of some obscure 
 oesophageal obstruction by passing a bougie, have un- 
 expectedly done so by passing it through the sac of an 
 aortic aneurysm. Many cases are on record of spontaneous 
 rupture into the oesophagus with resulting profuse and 
 fatal hseniaternesis. 
 
 Pressure on the thoracic duct gives rise to no very 
 definite symptoms, but causes impairment of nutrition by 
 obstructing the flow into the general circulation of lymph 
 and products of digestion absorbed from the lacteals. 
 
 Pressure on the ciliospinal branch of the sympathetic 
 may cause dilatation or contraction of the left pupil according 
 as its fibres are irritated or destroyed. 
 
 3. Pressure on the Root of the Left Lung. — If the 
 aneurysm is on the concavity of the arch, or the sac extends 
 downwards, it may give rise to symptoms arising from 
 pressure on the root of the left lung, already described 
 above. The most marked of these will be diminished entry 
 of air on the affected side. 
 
 Difference between the Radial Pulses. — Difference between 
 the pulses is especially liable to occur in aneurysms in- 
 volving this portion of the aortic arch, since the innominate 
 or left sub-clavian may be given off from the sac or be 
 compressed by it, or the sac may be interposed between the 
 two vessels. 
 
 Physical Signs. Pulsation. — Usually some of the 
 symptoms above described precede the appearance of pulsa- 
 tion on the chest wall. If the aneurysm is situated on the 
 
ANEURYSM OF THE ARCH OF THE AORTA. 
 
 461 
 
 posterior aspect of the arch, visible pulsation may be absent 
 throughout the course of the disease. More commonly, if 
 the aneurysm attains any considerable size, it gives rise to 
 an obscure general heave of the manubrium best appreciated 
 by laying the palm of the hand on the part. When it 
 
 J — 
 
 
 FIG. 37. — ANEURYSM OF THE TRANSVERSE PART OP THE ARCH WHICH 
 RUPTURED INTO THE TRACHEA AT X. (FRONT VIEW.) 
 
 springs from the anterior aspect of the arch, the sac may 
 present as a pulsating tumour in the second or third left 
 intercostal space close to the margin of the sternum. 
 Sometimes pulsation in the sac may be felt by pressing the 
 finger down behind the sternal notch, before it is evident 
 on the chest walls, but care must be taken not to mistake 
 a dilated aorta for an aneurysm. 
 
462 HEART DISEASE. 
 
 Dulness on percussion over the manubrium sterni, and 
 immediately to the left of it, may often be made out before 
 pulsation is visible, and when occurring in conjunction with 
 some of the characteristic symptoms, is a valuable sign, 
 though the possibility of its being due to enlarged glands 
 or other mediastinal tumour, must be borne in mind. 
 
 On auscultation, tracheal breathing may sometimes be 
 heard over the manubrium, conducted by an aneurysm in 
 contact posteriorly with the trachea and anteriorly with the 
 chest wall. 
 
 The aortic second sound may be reinforced, that is, may 
 be louder and more distinct to the left of the manubrium 
 than in the normal situation, and occasionally may be 
 audible in the left supra-scapular space. 
 
 A systolic murmur is sometimes heard over the course of 
 the aortic arch to the left of the manubrium, though no 
 murmur is audible in the aortic area. 
 
 Course of the Disease. — -An aneurysm in this situation on 
 account of the important structures in immediate relation 
 with it usually gives rise at an early stage to one or other 
 of the symptoms enumerated above. It is only when it is 
 situated on the upper and anterior aspect of the arch, and 
 attains a considerable size, that physical signs such as 
 dulness over the manubrium sterni, and to the left of it, 
 or pulsation in the second left intercostal space may precede 
 the appearance of symptoms. It never attains the great 
 size sometimes seen in aneurysms of the ascending aorta, 
 and usually proves fatal at a much earlier period. 
 
 If it is situated posteriorly and extends backwards, it 
 may ulcerate through the trachea, and rupture into it 
 when quite small, as seen in Figs. 37 and 38. 
 
 In this case the aneurysm was situated on the posterior 
 aspect of the arch, and was only about the size of a plover's 
 egg when it ruptured into the trachea. 
 
 It may ulcerate through and rupture into the left 
 
ANEURYSM OF THE ARCH OF THE AORTA. 
 
 46- 
 
 bronchus or the oesophagus, or it may rupture into the left 
 pleural cavity, left lung, or posterior mediastinum. 
 
 Death may occur from pulmonary complications caused 
 by pressure on the trachea or root of left lung. 
 
 The two following cases illustrate the predominance of 
 
 a. Sac of aneurysm ; b. Innominate artery ; c. Left carotid ; d. Left 
 sub-clavian. 
 
 FIG. 38.- 
 
 -ANEURYSM OP TRANSVERSE PART OP THE ARCH WHICH RUPTURED 
 INTO THE TRACHEA. (SIDE VIEW, SHOWING SAC.) 
 
 synrptorns over physical signs in the early stages of the 
 disease, and the rapidity with which it may progress and 
 cause death from pressure on the respiratory passages and 
 other important structures. They are also especially 
 interesting, clinically, from the number and variety of 
 symptoms and physical signs which developed during the 
 
464 HEART DISEASE. 
 
 course of the disease. In the second of these two cases 
 the right vocal cord was paralyzed, as the right sub-clavian 
 artery was embedded in the sac of the aneurysm which 
 had involved the orifice of the innominate artery. 
 
 Cask 1. — The patient, a strong-looking-, well-nourished man, aged 
 54; was admitted to St. Mary's Hospital in November, 1894, complaining 
 of cough and shortness of breath ; his lips were rather blue, and his 
 face was congested. His chest was somewhat barrel-shaped, and the 
 cardiac dulness was masked by emphysema : rhonchi were audible over 
 both lungs. At first sight the case looked like one of simple emphysema 
 and bronchitis. On careful observation it was noticed that the left 
 external jugular vein was much more distended than the right, and 
 did not empty on deep inspiration ; the veins in the left arm were full 
 and distended, and a large tortuous vein was also visible running across 
 the front of the left shoulder, from the external jugular to the cephalic 
 vein, in which the current of blood was downwards. 
 
 The carotid artery on the left side was difficult to see, and pulsation 
 in it could scarcely be detected ; in the right carotid pulsation could be 
 seen and felt without difficulty. 
 
 The pupils were unequal in size, the left being larger than the right. 
 
 The left side of the chest was noticed not to move so well in respira- 
 tion as the right, and on auscultation the entry of air was not so good. 
 The percussion note was good on both sides. Tracheal breathing could 
 be heard over the manubrium, and for a short distance on either side 
 of it. 
 
 These indications seemed to point to a tumour which pressed on the 
 trachea and left bronchus, compressed the left innominate vein hinder- 
 ing the return of blood through it to the heart, interfered with the flow 
 of blood through the left carotid, and also stimulated a branch of the 
 sympathetic, causing dilatation of the left pupil. 
 
 A tumour which would do this could scarcely be anything else than 
 an aneurysm of the aorta. In support of this, it was found that there 
 was marked tracheal tugging. There was, however, no difference in 
 the radial pulses, no affection of the vocal cords, and there was no area 
 of pulsation to be detected on the chest wall. At the end of five weeks, 
 slight pulsation could be made out in the second left intercostal space 
 at the end of expiration, and there was a small area of dulness to the 
 left of the manubrium. 
 
 While the patient was under observation, the left pupil was seen 
 to alter frequently in size, being sometimes smaller, sometimes larger 
 than the right. 
 
 Rest and treatment failed to improve his condition, and on January 
 17th, seven weeks after admission, he had a severe attack of dyspnoea, 
 sweating profusely, and becoming cyanosed. He was bled ten ounces 
 from the arm, which relieved him considerably for a time. 
 
ANEURYSM OF THE ARCH OF THE AORTA. 465 
 
 Six days later he had another similar but more severe attack of 
 dyspnoea, and this time inspiration was harsh and crowing, as if there 
 was some laryngeal spasm, so that tracheotomy was contemplated, but 
 was not deemed advisable. Venesection gave no relief, but inhalation 
 of chloroform stopped the laryngeal stridor. He had several attacks 
 of dyspnoea during the day, and became much exhausted. He died 
 suddenly in the evening. 
 
 At the autopsy, an aneurysm about the size of a small cocoa-nut 
 was found at the upper and posterior aspect of the transverse part of 
 the arch where it crossed the trachea. The trachea at its bifurcation, 
 and the left bronchus were compressed by the tumour, and the oeso- 
 phagus was displaced to the left. 
 
 The left innominate vein was stretched over the sac, and its lumen 
 was almost obliterated. A portion of the aneurysmal sac extended up 
 behind the left common carotid artery, which was flattened and com- 
 pressed by it. 
 
 The left sub-clavian artery was not involved in the aneurysm. 
 
 Case 2. — Aneurysm affecting the anterior portion of the transverse 
 part of the arch close to the origin of the innominate artery. 
 
 Samuel B , age 27. This patient came to the Throat Depart- 
 ment of St. Mary's Hospital complaining of hoarseness and attacks of 
 difficulty in breathing. On examination of the larynx, it was found 
 that the right vocal cord was paralyzed : aneurysm being suspected, he 
 was sent up to the wards. On admission, his dyspnoea was very severe, 
 his face was flushed and swollen, and when he was able to speak, his 
 voice was noticed to be cracked and hoarse, and his inspiration was 
 wheezing. He stated that he had been quite well till about six weeks 
 previously, when he had a sudden attack of difficulty in breathing, 
 which was considered to be croup and was treated as such. He also 
 complained of a troublesome cough and difficulty in swallowing. 
 
 On inspection of the chest, on both sides large veins were seen over 
 the front, in which the current of blood was downwards, carrying blood 
 from the veins of the neck to the intercostal veins. The external 
 jugulars on both sides were full and distended ; and it was evident that 
 the vena cava superior was occluded by pressure. 
 
 The pulse was absent in the right wrist, and in the right sub-clavian 
 and carotid. 
 
 Examination of the chest showed dulness on percussion over the 
 manubrium, and to the right and left of it for a short distance. 
 
 There was diffuse but faint pulsation over this region, best felt in 
 expiration, and a loud ringing second sound was audible. 
 
 Over the front of the right lung there was absence of respiratory 
 murmur and of vocal resonance, with normal resonance on percussion, 
 a condition which was clearly due to pressure on the root of the lung. 
 Posteriorly in the suprascapular region tubular breathing could be 
 heard on both sides ; over the bases the entry of air was good. 
 
 The pupils were unequal, the right being smaller than the left. 
 
 2h 
 
466 HEART DISEASE. 
 
 This was his condition on admission. He got gradually worse., in 
 spite of rest in bed and treatment. Iodide of potash;, ergot, and opium 
 were administered ; venesection was practised for the relief of pain, and 
 was effectual at the time, but the relief only lasted two or three days. 
 He died suddenly two months after admission. 
 
 At the autopsy an aneurysm the size of a large fist was found spring- 
 ing from the anterior wall of the arch, close to the origin of the in- 
 nominate. The communication between the aneurysmal sac and the 
 aorta was about the size of a shilling. The origin of the innominate 
 artery was involved in the sac, and was not recognizable ; the right 
 sub-clavian was patent but small, it ran up the posterior wall of the sac, 
 arising from it by a valvular opening. The right carotid contained a 
 plug of coagulated fibrin, but there was a small passage by the side of 
 the clot. The left carotid and sub-clavian came off beyond the sac and 
 were not interfered with. 
 
 The vena cava superior was flattened out on the front of the sac, 
 and was discoverable with difficulty, but it was not completely oblite- 
 rated : the right innominate vein was quite destroyed ; the left was 
 flattened out, but the lumen was not entirely obliterated. 
 
 The trachea was compressed by the tumour, as were also the bronchi 
 leading to the upper lobes of both lungs, more especially on the right 
 side. The mucous membrane of the trachea was ulcerated. The oeso- 
 phagus was also indirectly pressed upon, the trachea intervening between 
 it and the sac. The right recurrent laryngeal nerve was compressed, 
 and also the right vagus, which was involved in the adhesions round 
 the aneurysmal sac. 
 
 Here the symptoms caused by the pressure effects of the 
 aneurysm on the important structures surrounding it, 
 occupied a more prominent position in the history of the 
 case than the presence of abnormal pulsation on the chest 
 wall, which was at no time well marked. The first symptoms 
 were laryngeal, caused by pressure of the aneurysm on the 
 right recurrent laryngeal nerve. The presence of the 
 abnormal veins on the chest wall, and the absence of 
 pulsation in the right carotid and radial vessels were 
 striking features. The full jugulars, the distended veins on 
 the front of the chest in which the current of blood was 
 found to be downwards, pointed to some obstruction of the 
 superior vena cava, and these phenomena, together with 
 the paralysis of the right vocal cord, and disturbance 
 of circulation in the rio;ht carotid and radial, would have 
 
ANEURYSM OF THE DESCENDING AORTA. 467 
 
 been sufficient, even in the absence of pulsation on the 
 chest wall, to enable one to come to a diagnosis of 
 aneurysm. 
 
 (4) Aneurysms op the Third or Descending Part of 
 
 the Arch. 
 
 The descending aorta is deeply seated, lying to the left 
 side of the bodies of the fourth and fifth dorsal vertebrae. 
 The only important structures in immediate relation are 
 the oesophagus and thoracic duct, which lie to the right of 
 the aorta. Pressure symptoms are consequently not, as a 
 rule, characteristic, and as the aneurysm rarely comes to 
 the surface, physical signs are usually ill-marked. There 
 may, however, be dysphagia from pressure on the oesophagus, 
 and a not uncommon termination is rupture of the aneurysm 
 into the oesophagus. Frequently the only symptom com- 
 plained of is pain in the back, a pain radiating down the 
 left arm or round the left side of the chest : there may 
 be no other physical signs or symptoms present. The pain 
 is due either to irritation of a spinal nerve, when it may 
 radiate round the left side of the chest, or to erosion of 
 the vertebrae, when smartly tapping the affected vertebra 
 sometimes increases the pain. Diagnosis is in most cases a 
 matter of considerable difficulty. 
 
 The aneurysmal sac may, however, enlarge in such a 
 direction as to press on the root of the left lung and the 
 recurrent laryngeal nerve. In one case, where the patient had 
 been sent to the hospital for chronic laryngitis and attacks 
 of paroxysmal dyspnoea, the left vocal cord was found to be 
 paralyzed, and there were signs of pressure on the left 
 bronchus, which seemed to point to aneurysm of the trans- 
 verse part of the arch. At the autopsy, however, an 
 aneurysm was found involving the aorta to the left of the 
 bodies of the fourth and fifth dorsal vertebrae and adherent 
 
468 HEAR! DISEASE. 
 
 to thein, and to the lower part of the body of the third 
 dorsal vertebra. 
 
 In the accompanying illustration (Fig. 39), a large 
 aneurysm of the descending aorta is shown, which compresses 
 the oesophagus, and is adherent to the dorsal vertebrae 
 from the fourth to the eighth. 
 
 Diagnosis. 
 
 Little need be said here under this head, as the 
 symptoms and physical signs characteristic of aneurysm 
 have been fully discussed. It must, however, be borne in 
 mind that a solid tumour in the mediastinum, such as a 
 malignant growth, or enlarged mediastinal glands, may 
 give rise to many of the pressure symptoms produced by 
 aneurysm. Any mediastinal tumour may compress the 
 great veins, the trachea, cesophagus, thoracic duct, the root 
 of the lung, or may even involve the recurrent laryngeal 
 nerve or sympathetic. In conjunction with symptoms pro- 
 duced by pressure on one or other of these structures, there 
 may be an area of dulness over, and to one or both sides of 
 the manubrium sterni. Pulsation will, as a rule, be absent, 
 and there will not be the modification of the aortic second 
 sound which is common in aneurysm. Oases may neverthe- 
 less occur in which pulsation is communicated from the 
 arch of the aorta to a tumour intervening between it and 
 the chest wall, and there is a diffuse general heave of the 
 upper part of the thorax. If, on palpation, a diastolic 
 shock is felt, all uncertainty will be at an end, as this 
 could only be present in aneurysm. 
 
 On pressing the fingers down into the intercostal spaces 
 a sense of resistance will be imparted by a solid tumour, 
 and no true expansile pulsation will be felt. An aneurysm 
 will sooner or later tend to present as a pulsatile swelling 
 in one of the intercostal spaces, while the growth of a solid 
 
ANEURYSM OF THE DESCENDING AORTA. 
 
 469 
 
 tumour will be indicated only by extension of dulness on 
 percussion, without extension or localization of pulsation. 
 The history of the onset of the disease will be of service, 
 
 FIG. 39. — ANEURYSM OF DESCENDING AORTA. 
 
 and usually careful observation of the progress of the case 
 will soon clear up all doubt. 
 
 It will be seen that a tumour in the mediastinum is 
 most likely to be confused with aneurysm of the transverse 
 part of the arch. 
 
47o HEART DISEASE. 
 
 Aneurysm of the descending aorta may closely simulate 
 spinal caries, when it compresses the spinal nerves and 
 begins to erode the bodies of the vertebrae, and, as has 
 already been stated, pain may be the only symptom to 
 which it gives rise. The absence of rigidity of the spine 
 will usually serve to exclude spinal caries, but the cause 
 of the pain may be difficult to ascertain. If dysphagia is 
 present in addition, this will be a help to diagnosis, but 
 it may be impossible to diagnose with any certainty the 
 existence of an aneurysm of the descending aorta, or that 
 of an intra-pericardial aneurysm. 
 
 In doubtful cases an X-ray screen or photograph may 
 be of great service. 
 
 Prognosis. 
 
 The prognosis varies according to the situation of the 
 aneurysm and the direction in which it extends, according 
 to its shape, whether fusiform or sacculated, according as 
 it increases rapidly or slowly in size. 
 
 When situated in . the intra-pericardial portion of the 
 aorta, it usually proves fatal by sudden rupture before it 
 attains any considerable size. The vessel at this part lying 
 free in the pericardial sac, there are no surrounding struc- 
 tures which the aneurysm can appropriate for its support, 
 and there is also considerable up-and-down movement of 
 the rest of the aorta. These conditions favour rapid extension 
 and rupture of the aneurysm. 
 
 As the physical signs and symptoms are so indefinite, it 
 is difficult to make an early or certain diagnosis, but where 
 evidence points to the presence of an aneurysm in this 
 situation, the condition of the patient is one of imminent 
 danger, and little can be done to arrest the progress of the 
 aneurysm. 
 
 When situated in the ascending portion of the arch 
 above the pericardium, the aneurysm may attain an 
 
PROGNOSIS IN ANEURYSM. 47 1 
 
 enormous size, and the patient live for some years without 
 experiencing much inconvenience from it, especially if the 
 aneurysm extends forwards, and makes its way through the 
 chest wall. While the aneurysm is eroding the chest wall 
 and making its way through, there may be considerable 
 pain which will disappear later, but, the resistance offered 
 by the chest wall in front being overcome, the pressure 
 on deep-seated parts will be diminished. 
 
 If the aneurysm extends backwards, the prognosis is less 
 favourable, as serious complications may arise from pressure 
 on the root of the lung or the vena cava, or perhaps on the 
 pneumogastric nerve. 
 
 When it involves the transverse portion of the arch, to 
 the danger of the aneurysm per sc must be added the 
 danger of pressure effects on the important structures in its 
 neighbourhood. Death may occur suddenly from rupture 
 into the trachea or elsewhere, or, more slowly, from asphyxia 
 and pulmonary collapse due to pressure on the trachea or 
 on the root of one or other lung. If, however, the aneu- 
 rysm extends forwards instead of backwards, and comes 
 to the surface of the chest wall, the prognosis is less un- 
 favourable. 
 
 With regard to the shape of the aneurysm, if it is of 
 the sacculated variety, it may extend rapidly at first, and 
 perhaps prove fatal by rupture at an early period ; as it 
 continues to enlarge, however, the mouth of the sac will 
 become relatively small compared with the size of the 
 tumour : thus less blood enters the sac, and the circulation 
 in it is slowed. These conditions favour the deposition of 
 fibrin, so that the progress of the aneurysm may be checked, 
 or a spontaneous cure result. In fusiform aneurysm the 
 progress of the aneurysm is usually slow ; but little can 
 be done to arrest it, as the blood sweeping through the 
 whole of the sac gives little chance for the deposition of 
 fibrin on its walls, and washes it away when deposited. 
 
472 HEART DISEASE. 
 
 Tkeatment. 
 
 Iii the treatment of aortic aneurysm the object to be 
 attained is to keep down the blood pressure, to render the 
 circulation as slow and equable as possible, to diminish the 
 volume of blood, and to increase its coagulability. We 
 shall thus reduce the strain on the walls of the aneurysm 
 to a minimum, and favour the coagulation of blood in the 
 sac. For this purpose the most important measure is rest ; 
 the patient should be kept in bed for six weeks or two 
 months. It may be necessary to allow him to use a commode 
 when the bowels act, as the straining attending the use of 
 the bed pan may give rise to more effort than sitting up, 
 but he should not get out of bed for any other purpose. 
 Excitement of any kind must be avoided. Next in impor- 
 tance to rest is feeding. The amount of liquid taken with 
 meals should be reduced to a minimum, 40 or, if practicable, 
 30 ounces only being taken in the 24 hours. Soups, game, 
 salt fish, rich sauces, beer, and tea should be forbidden, and 
 meat should be used in moderation, as extractives, rich 
 foods, and excess of nitrogenous matter may lead to the 
 retention of toxic materials in the blood, which give rise 
 to increase in the peripheral resistance by their vaso- 
 constrictor action. The food should not be bulky, that is, 
 should not include too much farinaceous matter, such as 
 potatoes, rice, etc. ; the amount of food taken at each meal 
 should be about the same, and should not be excessive, so 
 as to avoid the extremes of repletion or depletion, and the 
 varying rapidity of the circulation which would result were 
 some meals copious and others small. The reduction of 
 the volume of blood favours the repair of aneurysm in two 
 ways — it lessens the distension of the entire vascular system, 
 and therefore the internal pressure in the sac, and the rate 
 of flow of blood is diminished ; further, the blood being 
 inspissated, fibrin is more readily deposited. 
 
TREATMENT. 473 
 
 There is one drug which undoubtedly has a favourable 
 influence on aneurysm, namely, iodide of potassium. This 
 should be given in gradually increasing doses, till 20, 30, 
 or 40 grains are taken three times a day. Its precise mode 
 of action has been much discussed ; chemically it has a 
 solvent influence on fibrin, and cannot therefore be supposed 
 to favour its precipitation on the wall of the sac ; neither 
 can the good effects of this drug in aneurysm be ascribed 
 to its action on the aneurysm as a remote effect of syphilis. 
 It is probable that it co-operates with the rest and diet, 
 firstly, by its depressing influence on the action of the 
 heart ; secondly, by promoting diuresis, and thus helping 
 to drain off water and inspissate the blood. 
 
 • Aperients may have to be taken to obviate constipation, 
 which would have a very injurious influence, and it may 
 be necessary to counteract restlessness and assist sleep by 
 bromides or opiates. Morphia may also be required for the 
 relief of pain. 
 
 Sibson gave ergot in large doses in cases of aneurysm, 
 and it could be easily demonstrated that the pulsation 
 diminished in an aneurysm which had perforated the chest 
 wall, and that its volume was lessened. This he attributed 
 to the contraction of muscular fibres in the wall of the 
 sac, but such fibres are non-existent. The cause was un- 
 doubtedly diminished output of blood by the left ventricle, 
 due to limitation of its diastole by the ergot. 
 
 Venesection may be of the greatest service when there is 
 severe pain. It usually affords immediate relief by lowering 
 the tension within the aneurysm, and it may also so lessen 
 the amount of blood in circulation as to afford a chance of 
 fibrin being deposited. Surgery does not find much oppor- 
 tunity in the treatment of thoracic aneurysm, but ligature 
 of the right sub-clavian and carotid arteries when the in- 
 nominate is involved, or of the corresponding vessels on the 
 left side when the origins of the left carotid and sub-clavian 
 
474 HEART DISEASE. 
 
 were implicated, has, in some instances, led to consoli- 
 dation of the sac, by reducing the flow of blood through 
 it. Other expedients have been tried, such as the intro- 
 duction of coils of fine wire into the sac, passed in through 
 a trocar, or the action of galvanic currents, with the object 
 of the formation of a coagulum in the sac, but the results 
 have not been encouraging. A risk sufficient in itself to 
 prevent resource to either of these proceedings, except in an 
 absolutely desperate case, is the possibility of a clot formed 
 around the pole of a galvanic battery, or on the coils of 
 wire, being carried into the carotid or vertebral arteries, 
 and giving rise to a cerebral embolism. 
 
 Injections of a solution of gelatine into the buttock, 
 with a view to increasing the coagulability of the blood 
 and the tendency to clotting in the sac, have been prac- 
 tised, but the good results claimed in some cases are open 
 to suspicion, and fatal cases of tetanus from imperfect 
 sterilization of the gelatine employed have been recorded, 
 so that this method of treatment is not to be recommended. 
 Increase in coagulability of the blood can be more safely 
 and efficiently effected by limitation of the amount of 
 fluids, and by the administration of chloride or lactate of 
 calcium in doses of from 10 to 15 grains two or three times 
 a day. A milk diet may, to a certain extent, contribute 
 to this object, as milk contains a considerable proportion 
 of lime salts. It is also beneficial in that it contains no 
 extractives or toxic materials, is non-stimulating, throws 
 least work on the kidneys, and is slightly diuretic. 
 
 Satisfactory results from treatment can only be hoped 
 for if the aneurysm is saccular, with a relatively small 
 neck to the sac, so that the circulation in the sac is slug- 
 gish, and a chance is afforded for the deposition of fibrin 
 on its walls. The deposit of layers of laminated clot will 
 afford support to the walls of the aneurysm, and help to 
 prevent its further extension, and will also tend gradually 
 to exclude the blood from it by occluding the sac. 
 
INDEX. 
 
 Adherent pericardium, 45 
 
 Age, as affecting hypertrophy, 101 
 
 , prognosis, 142, 194, 220, 223 
 
 ■ , treatment, 245 
 
 Alcohol, 241, 249, 412 
 Ansemia, 87, 164, 227, 242, 298 
 Anatomical relations of aorta, 431 
 
 • of heart, 2 
 
 Aneurysm of ascending aorta, 453 
 
 , classification of, 448 
 
 of descending aorta, 467 
 
 , dissecting, 415 
 
 , etiology of, 425 
 
 of heart, 358 
 
 from infective embolus, 78 
 
 , intra-pericardial, 448 
 
 , pathogeny of, 428 
 
 , physical signs of, 434 
 
 , pressure, effects of, 443 
 
 , prognosis in, 470 
 
 , pulse in, 438 
 
 of transverse part of arch, 458 
 
 , treatment of, 472 
 
 Angina pectoris, 322, 348, 359, 449 
 
 , diagnosis of, 371 
 
 , etiology of, 364 
 
 ■ , prognosis in, 373 
 
 , spurious, 372 
 
 ■ , treatment of, 374 
 
 vasomotoria, 366 
 
 Aorta, anatomical relations of, 431 
 
 , aneurysm of, 424 
 
 , atheroma of, 411 
 
 , rupture of, 428 
 
 Aortic area, sounds over, 16 
 
 incompetence, 123, 421 
 
 , blood pressure in, 22, 421 
 
 , from degenerative changes, 
 
 137, 421 
 
 , etiology of, 122, 136, 421 
 
 , physical signs in, 123 
 
 , symptoms in, 140 
 
 with stenosis, 98, 145 
 
 , treatment of, 146, 254 
 
 Aortic second sound, accentuation of, 
 
 95 
 
 Aortic second sound in aneurysm, 437 
 ■ in dilatation of 
 
 aorta, 137, 421 
 Aortitis, acute, 405, 413 
 Apex beat, absence of, 10 
 
 , displacements of, 10 
 
 , murmurs at, 14 
 
 , sounds at, 13 
 
 Apoplectiform seizures, 350, 402 
 Apoplexy, pulmonary, 180 
 Arterial tension, 20 
 
 . high, causes of, 27 
 
 ■ ■ , , effects of, 169, 272, 
 
 278,367, 411,430 
 , , treatment of, 171, 
 
 305, 423 
 Arterio-sclerosis, 28, 320, 411 
 Atheroma of aorta, 411 
 
 of coronary artery, 321 
 
 Auricle, left, 4 
 
 , , in mitral incompetence, 
 
 158 
 
 , , stenosis, 176 
 
 , , rupture of aneurysm into, 
 
 453 
 
 , right, 2 
 
 , , rupture of aneurysm into, 
 
 453 
 Auscultation, 13 
 
 B 
 
 Balfour, 87, 364 
 Barlow, 62 
 
 Baths, brine, 236, 303 
 Blood pressure, 22 
 
 , estimation of, 23 
 
 Bradycardia, 351, 398 
 
 C 
 
 Caffein, 257 
 Calcification of aorta, 413 
 
 of coronary artery, 322 
 
 of valves, 82 
 
 Capillary pulsation, 122 
 
476 
 
 INDEX. 
 
 Cardiac aneurysm, 358 
 
 dilatation, 281 
 
 duluess, 4 
 
 hypertrophy, 272 
 
 movements, 6 
 
 muscle, properties of, 385 
 
 Cheadle, 60, 62, 409 
 
 Childhood, rheumatism in, 60 
 
 Chorea, 31, 58, 168 
 
 Claudication intermittente, 370 
 
 Climate, 239 
 
 Cloudy swelling, 328 
 
 Clubbing of fingers, 210 
 
 Compensation, 108, 228 
 
 Congenital malformations of heart, 
 
 206 
 Coeruleus morbus, 211 
 Cole, 59 
 
 Convallaria, 257 
 Coronary arteries, affections of, 320 
 
 D 
 
 Danger, relative, of valvular lesions, 
 215 
 
 Death, sudden, 216, 322, 338, 348, 
 362, 403, 449, 470 
 
 Diastole, shortening of, 14, 296 
 
 Diastolic shock, 435 
 
 Diet in angina pectoris, 376 
 
 in aneurysm, 472 
 
 in atheroma of aorta, 422 
 
 in bradycardia, 404 
 
 in valvular disease, 249 
 
 Digitalis, 256 
 
 in aortic disease, 261 
 
 in mitral incompetence, 262 
 
 ■ stenosis, 266 
 
 Dilatation of aorta, 137, 421 
 
 of heart, 281 
 
 in pericarditis, 34 
 
 , etiology of, 282 
 
 of left ventricle in aortic re- 
 gurgitation, 134 
 
 in mitral regurgi- 
 tation, 159 
 
 of right ventricle, 310 
 
 in pericarditis, 34 
 
 Diuretin, 258 
 
 Ductus arteriosus, patent, 210 
 
 E 
 
 Effusion, pericardial, 30, 35 
 Embolism, 71,78, 324 
 Endarteritis, 322, 415, 417, 426 
 Endocarditis, acute, 56 
 , chronic, 82 
 
 Endocarditis, malignant or per- 
 nicious, 67 
 Epileptiform attacks, 351, 402 
 Erythema marginatum, 63 
 
 nodosum, 63 
 
 Exercise, 233 
 
 , graduated, 235 
 
 Exercises resisted, 237 
 
 F 
 
 Fatty degeneration of heart, 342 
 
 infiltration of heart, 343 
 
 Fibrosis of heart, 330 
 First sound, modification of, 13, 93, 
 187 
 
 in mitral stenosis, 183 
 
 in cardiac dilatation, 294 
 
 , reduplication of, 14, 95 
 
 Fischer, 427, 429 
 Foramen ovale, patent, 209 
 Friction, pericardial, 32 
 Functional affections of heart, 381 
 
 G 
 
 Gairdner, 174 
 Gibson, 334, 346, 387 
 Gout, 365, 372, 418 
 Graves' disease, 394 
 
 II 
 
 Etemic murmurs, 112, 164 
 Hpemoptysis in aneurysm, 455 
 
 in mitral stenosis, 189 
 
 Head, 382 
 
 Heart, aneurysm of, 382 
 
 , examination of, 7 
 
 , movements of, 6 
 
 , muscle properties of, 385 
 
 , relations of, 2 
 
 sounds, modification of, 13, 93 
 
 Heredity as affecting prognosis, 224 
 
 in vascular degeneration, 27, 
 
 411 
 
 High arterial tension. Vide Arterial 
 
 Tension. 
 Huchard, 322, 325, 330, 334, 346, 
 
 368, 395, 404, 417, 427 
 Hydropericardium, 52 
 Hypera2inia passive of lungs, 157 
 Hypertonus, arterial, 26. 439 
 Hypertrophy of heart, 272 
 , etiology of, 272 
 
 in aortic incompetence, 
 
 104, 135 
 
INDEX. 
 
 477 
 
 Hypertrophy of heart in aortic 
 
 stenosis, 103, 116 
 in mitral incompetence, 
 
 107 
 of right ventricle, 106, 273 
 
 Impulse, cardiac, 7 
 Infarct, pulmonary, 179 
 
 of kidney, 71, 77 
 
 of spleen, 71, 77 
 
 Induration, brown, of lung, 157 
 Inspection, examination by, 7 
 Intermittency of pulse, 3S7 
 Irregularity of pulse, 389 
 
 in aortic lesions, 136 
 
 in dilatation, 292 
 
 in mitral incompetence, 
 
 115 
 Interstitial myocarditis, 334 
 Interventricular septum incomplete, 
 
 207 
 
 Janeway, 23 
 
 Jugular veins, distension of, 9, 201, 
 
 202, 444 
 , pulsation of, 9, 201, 230, 
 
 300, 400, 401 
 
 K 
 
 Kidney, infarct of, 71, 77 
 
 Lauder Brunton, 370 
 
 Laryngeal nerve, recurrent, pressure 
 
 on, 446, 459, 465 
 
 , relations of, 433 
 
 Leeches, use of, 43, 254, 304 
 
 Lees, 35, 43, 451 
 
 Liver, enlargement of, 11, 161, 189, 
 
 201, 230, 252, 300 
 
 , nutmeg, 181 
 
 , pulsation of, 12, 161, 189 
 
 M 
 
 McAlister, 164 
 
 Mackenzie, 9, 202, 369, 382, 3S6, 400 
 MacWilliam, 430 
 
 Malformations of heart, congenital, 
 206 
 
 Mitral area, sounds over, 13 
 
 incompetence, 151 
 
 , effects on heart of, 106, 
 
 259 
 
 , digitalis in, 172, 262 
 
 , etiology of, S5, 151, 164, 
 
 282 
 
 , pulse in, 98, 154 
 
 , prognosis in, 161 
 
 , symptoms in, 161 
 
 , treatment of, 170, 264 
 
 stenosis, 174 
 
 , digitalis iu, 199, 266 
 
 , effects on heart of, 106, 
 
 175 
 
 , etiology of, 174 
 
 , morbid anatomy, 175 
 
 , pulse in, 98, 181 
 
 , prognosis in, 193 
 
 , stages of, 184 
 
 , symptoms in, 189 
 
 ■ , treatment of, 196, 266 
 
 Morphia in angina pectoris, 378 
 
 in aneurysm, 473 
 
 in aortic regurgitation, 149 
 
 in pericarditis, 43 
 
 Murmurs, aortic systolic, 111, 112 
 
 ■ , diastolic, 112, 421 
 
 , Flint Austin, 125, 193 
 
 , bseniic. Tide under Hsernic 
 
 , presystolic, 125, 183, 193 
 
 , pulmonic, 203, 208 
 
 , retarded systolic, 157 
 
 , systolic, mitral, 152, 295 
 
 , tricuspid, 200 
 
 Myocarditis, acute, 326 
 
 ■ , chronic, 330, 334 
 
 Myocardium, affections of, 326, sq. 
 
 , fatty degeneration of, 343 
 
 , fibrosis of, 320 
 
 , syphilitic disease of, 336 
 
 N 
 
 Nauheini, 236, 303 
 Nerves, cardiac, 386 
 Neuroses of heart, 381 
 Nodules, rheumatic, 39, 62 
 " Nutmeg " liver, 181 
 
 O 
 
 Occupation as affecting prognosis, 
 
 226 
 CErtel treatment, 235 
 Osier, 399 
 
47 8 
 
 INDEX. 
 
 Pain of angina pectoris, 360 
 
 , cardiac, 3S1 
 
 , , causes of, 383 
 
 Paine, 32, 58 
 Palpation, 9 
 Palpitation, 390 
 Paracentesis, pericardii, 35, 44 
 Paroxysmal tachycardia, 394 
 Peacock, 207 
 Percussion, 12 
 Pericardium, adherent, 45 
 
 , new growths of, 55 
 
 , tuberculosis of, 54 
 
 Pericarditis, acute, 30 
 
 in Bright's disease, 44 
 
 , suppurative, 51 
 
 Phillips, 217, 237 
 Pneumopericardium, 53 
 Poynton, 32, 35, 58, 409 
 Pressure, blood, 21 
 Prognosis in aneurysm, 470 
 
 in angina pectoris, 373 
 
 in aortic incompetence, 141 
 
 stenosis, 119 
 
 in dilatation, 300 
 
 in endocarditis, acute, 63 
 
 , pernicious, 8L 
 
 in mitral incompetence, 161 
 
 stenosis, 193 
 
 in pericarditis, 42 
 
 in valvular disease (general), 214 
 
 Powell, Douglas, 346 
 
 Pulmonary artery, rupture of 
 
 aneurysm into, 450 
 Pulmonic area, sounds over, 16 
 
 incompetence, 203 
 
 stenosis, 203, 208 
 
 second sound, accentuation of, 
 
 94, 184 
 Pulse in aortic incompetence, 96, 
 
 127, 132 
 
 stenosis, 96, 117 
 
 incompetence with stenosis, 
 
 130, 133, 145 
 
 , collapsing, 127 
 
 , Corrigan's, 127 
 
 , delay of, in aneurysm, 441 
 
 — : — , , in aortic incompetence, 
 
 129 
 
 in mitral incompetence, 97, 154 
 
 stenosis, 97, 181 
 
 , intermittency of, 387 
 
 , irregular, 389 
 
 , , in aortic disease, 1 30 
 
 , ,in mitral disease, 154, 182 
 
 Pulsus alternans, 369 
 
 bisferiens, 130 
 
 Pseudo-angina, 373 
 
 R 
 
 Retraction of intercostal spaces, 8 
 
 46 
 Residence, choice of, 240 
 Rosenfeld, 343 
 Rupture of aneurysm, 450, 460 
 
 of aorta, 428 
 
 of heart, 348 
 
 of valve, 137 
 
 Rhythm of heart, disorders of, 385 
 
 S 
 
 Schott treatment, 236, 303 
 Second sound, reduplication of, 95 
 Sensory areas cutaneous, relation of, 
 
 to visceral affections, 382 
 Serum, antistreptococcic, 82 
 Sex as affecting prognosis, 224 
 Sinus of valsalva, 448 
 Sounds of heart, 13, 93 
 Steven, Lindsay, 333 
 Spygmograph, 20 
 Spygmomanometer, 23 
 Spartein, 257 
 Stomach, dilatation of, 318, 357, 392, 
 
 404 
 Strnphanthus, 257 
 Stokes-Adams disease, 399 
 Syj)hilis as cause of aneurysm, 420 
 
 — of atheroma, 413, 415, 417 
 
 of chronic endocarditis, 83 
 
 of myocardial fibrosis, 336 
 
 T 
 
 Tachycardia, 393 
 Tenderness, praecardial, 382 
 Thrill in aneurysm, 435, 450 
 
 in mitral stenosis, 183 
 
 Tracheal tug, 436 
 Treatment in aneurysm, 472 
 
 in angina pectoris, 374 
 
 in aortic incompetence, 146, 261 
 
 stenosis, 121, 262 
 
 in atheroma, 422 
 
 in bradycardia, 404 
 
 in dilatation of heart, 303 
 
 in endocarditis, acute, 65 
 
 , pernicious, 81 
 
 in fatty degeneration, 355 
 
 in functional affections of heart, 
 
 384, 392 
 
 in mitral incompetence, 170, 202 
 
 stenosis, 196, 266 
 
 in pericarditis, 43 
 
 , GErtel, 235 
 
INDEX. 
 
 479 
 
 Treatment, Scliott, 236, 303 
 
 in valvular disease (general), 
 
 232 
 Tricuspid area, 15 
 
 incompetence, 200 
 
 stenosis, 202 
 
 Valvular lesions, changes in heart 
 
 in, 100 
 . estimation of extent of, 
 
 91 
 
 , etiology of, S4 
 
 . pulse in, 96 
 
 Valvular lesions, prognosis general 
 
 in, 214 
 
 , treatment of, 232 
 
 Vaso-rlilators, uses of, 122, 149, 199, 
 
 254, 377, 422 
 Venesection, 150, 252, 304, 473 
 Vena cava superior, pressure on, 443, 
 
 449 
 , rupture of aneuiysni 
 
 into, 451 
 
 W 
 
 Walshe, 101 
 Water-hammer pulse, 127 
 
 THE END. 
 
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