COLUMBIA LIBRARIES OFFSjTE 
 
 HEALTH SCIENCES STANDARD 
 
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 1916 
 
 28768 
 
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THE DIAGNOSIS AND TREATMENT OF 
 HEART DISEASE . 
 
thf: 
 DIAGNOSIS AND TREATMENT 
 
 OF 
 
 HEART DISEASE 
 
 PRACTICAL POINTS FOR STUDENTS AND 
 PRACTITIONERS 
 
 BY 
 
 E. M. BROCKBANK 
 
 M.D. (Vict.), F.R.C.P. 
 
 HON. PHYSICIAN, ROYAL INFIKMARY, MANCHESTKR 
 CLINICAL LECTURER ON DISEASES OF THE HEART, DEAN OF CLINICAL INSTRUCTION, 
 « UNIVERSITY OF MANCHESTEK 
 
 SECOND EDITION 
 WITH ILLUSTRATIONS 
 
 PAUL B. HOEBER 
 
 67-69 EAST FIFTY-NINTH STREET 
 
 NEW YORK 
 
 1916 
 
[Printed in England] 
 
PREFACE TO SECOND EDITION 
 
 The demand for a second edition of this small work has 
 enabled me to alter and add to it considerably. I hope 
 it will prove even more useful now to students and 
 practitioners than it did in its original form. It could 
 have been improved further had not National affairs 
 distracted attention from teaching matters. 
 
 E. M. B. 
 
 PREFACE TO FIRST EDITION 
 
 (Entitled " Heart Sounds and Murmurs, Their 
 Causation and Differentiation.") 
 
 In this small work I have attempted to put simply, 
 clearly and in convenient pocket-book form for clinical 
 reference the elements of cardiac auscultation for the 
 use of students. I have repeated myself a good deal 
 with the object of making an argument or explanation 
 as complete as possible in the one place and thereby of 
 avoiding turning backwards and forwards. 
 
 E. M. B. 
 Manchester, 1911. 
 
CONTENTS 
 
 SKCTION PAOE 
 
 1. PRI LIMINARY CONSIDERATIONS - - - 1 
 
 Anatomy and Physiology. 
 
 II. K'uUTiNE Examination - - - - 6 
 
 What patients complain of — The arterial pulse : 
 how to feel it : varieties : tension : wall of 
 artery — Venous pulse — Inspection of patient : 
 general : the neck : the praecordia — Palpation : 
 cardiac impulse and apex- beat — Percussion : 
 routine method : cardiac dulness — Auscultation. 
 
 III. The Heart Sounds - - - - 29 
 
 The first sound and its variations— The second 
 sound and its variations — Rhythm of sounds: 
 tic-tac rhythm : cantering rhythm, bruit de 
 galop. 
 
 IV. Heart Murmurs - - - - 48 
 
 Timing — Changes in the valves which lead 
 to murmurs : obstruction : incompetence — 
 Physical causes : fluid veins : vibration of cur- 
 tains: blood changes, hsemic murmurs — Changes 
 in the different valves which cause murmurs : 
 auriculo-ventricular valves, stenosis, dilatation, 
 ulceration : semilunar valves — Crescendo mur- 
 mur — Murmurs with heart sounds— Absence of 
 heart sounds with normal valves— Influence of 
 mobility of curtains on sounds, 
 
 V. Aheas of Audibility of Heart Murmurs - 65 
 
 Situation of valves — Influence of change of 
 position on murmurs. 
 
 VI. Conduction and Transmission of Murmurs 68 
 
 Conduction — Transmission, 
 vii 
 
Vill CONTENTS 
 
 SECTION PAOE 
 
 VII. Special Characteristics of the Different 
 
 Valvular Murmurs - - - 72 
 
 Mitral murmurs — Rheumatism in childhood : 
 nodules — Crescendo murmur — Tricuspid mur- 
 murs — Aortic murmurs — Posture murmur — 
 Pulmonary murmurs. 
 
 VIII. H.EMic Murmurs - - - - 89 
 
 Cardiac — Vascular: bruit de diable. 
 
 IX. Exocardial Sounds - - - - 91 
 
 Pericardial — Cardio-respiratory. 
 
 X. Septic Endocarditis, Pericarditis, Angina 
 
 Pectoris - - - - - 93 
 
 Septic, malignant, or ulcerative endocarditis — 
 Pericarditis, simple, serous, purulent — Adherent 
 pericardium — Angina pectoris. 
 
 XL Cardiac Irregularity resulting from Dis- 
 turbances OF Stimulation - - 98 
 
 Electrocardiogram — Tachycardia : apprehen- 
 sive heart : paroxysmal tachycardia — Slow 
 pulse : bradycardia —Heart-block — Irregular or 
 intermittent pulse : premature systole, extra- 
 systole — Sinus arrhythmia — Auricular fibrilla- 
 tion — Auricular flutter. 
 
 XII. Treatment of Cardiac Disease - - 107 
 
 Before muscle failure : general : diet : exercise : 
 drugs — Cardiac muscle failure : rest in bed : 
 diet : sleep : drugs — Drugs acting on the heart 
 muscle : digitalis : strophanthus : cafifein : 
 strychnine - Vessel dilators — Treatment of 
 special forms of heart disease : mitral valve : 
 aortic valve : alcoholic heart failure : angina 
 pectoris. 
 
 Index - - - - - - 118 
 
PRACTICAL POINTS IN THE 
 
 DIAGNOSIS AND TREATMENT OF 
 
 HEART DISEASE 
 
 PRELIMINARY CONSIDERATIONS 
 
 AXATOMY AND PHYSIOLOGY. 
 
 Anatomy. — The heart is a conical-shaped organ with 
 the great vessels attached to its base ; it is about the 
 size of its owner^s clenched fist, and lies obliquely in 
 the thorax, inclined from above downwards, forwards, 
 and to the left, with one-third (the base) to the right 
 and two-thirds to the left of the mid-sternal line. 
 
 The anterior aspect of the heart is formed almost 
 entirely by the right ventricle, right auricle, and infun- 
 dibulum or conus arteriosus ; only a suiall part of it, 
 namely, the apex and about half an inch along its left 
 margin, is formed by the left ventricle. The tip of the 
 left auricle just comes to the surface behind the second 
 interspace. It is covered by lung all over except in 
 the mid-sternal line, and a triangular space formed by 
 the mid-sternal line, a line from the fourth chondro- 
 sternal articulation to the junction of the fifth costal 
 cartilage with its rib, and the line of liver dulness, the so- 
 called area of superficial cardiac dulness (see p. 26). 
 
 1 
 
^ HEAUT DISEASE 
 
 Surface anatomy. — The upper limit is behind the 
 second costal cartilage. Its right side extends half an 
 inch beyond the right edge of sternum. Its apex or its 
 limit to the left is in the fifth intercostal space two and a 
 half inches beyond the left edge of the sternum ; in adult 
 males this is about one inch below and three-quarters 
 of an inch to the sternal side of the nipple. Its lower 
 limit is about the sixth rib, where the heart lies in con* 
 
 Fig. 1. 
 
 A., Aorta ; A.V., aoriic valve ; i»/., mitral valve ; P. A., pulmonary artery ; /'. V., pul- 
 monary valve ; li.A,, right auricle ; & F., septum ventriculorum ; S. F.C., superior 
 vena cava; T.r., tricuspid vrlve. (Cunningham.) 
 
 tact with the diaphragm. In children the heart may be 
 rather higher and its apex farther out in the chest. 
 
 N.B. — The ni'pi)le in men, normally situated ahoni 
 4 inches from the mid-sternal line, may be nearer than 
 this to the sternum if the chest is not well developed. 
 An apex-beat outside the vertical nipple line, therefore, 
 need not necessarily indicate disease. In children the 
 
ANATOMY 3 
 
 apex-beat may be farther out and up in relation to the 
 nipple than it is in man. The nij^ple in women is use- 
 less as a point which has definite position. 
 
 The surface lines or landmarks which are of use in 
 the examination and note-taking of thoracic affections 
 are : 
 
 The mid- sternal line down the middle of the sternum. 
 
 The lateral sternal lines down the right and left edges 
 of the sternum. 
 
 The parasternal lines midway between the lateral 
 sternal lines and 
 
 The mid-clavicular lines, which are lines drawn per- 
 pendicularly from the middle of the collar-bones or 
 midway between the middle of the suprasternal notch 
 and the top of the acromion. 
 
 The nijpjple line in the normal adult male is practically 
 the same as the mid-clavicular line, the nipple being 
 situated about four inches from the mid-sternal line. 
 
 The axillary lines, anterior, mid, and posterior, running 
 perpendicularly downwards through the anterior, mid, 
 and posterior regions of the axilla. 
 
 The scaptdar lines, through the angles of the scapulas. 
 
 Nervous mechanism of the heart-beat.— The stimu- 
 lation of the heart for its beating is carried on by 
 means of a special form of tissue, partly nervous and 
 partly heart muscle in structure, which occurs in aggre- 
 gations or nodes, and connecting or end fibres. 
 
 (1) The sino-auricular node is in the subepicardial 
 tissue at the junction of the superior vena cava and the 
 right auricular appendix. This node is the most highly 
 developed aggregation of the neurQ-muscular tissue, and 
 it initiates the stimulus and sets the pace and rhythm of 
 
4 HEART DISEASE 
 
 the heart. It is believed to receive fibres from the vagus 
 and sympathetic nerves. From it the stimulus passes, 
 in some way not fully understood, through 
 
 S.A. node 
 
 A . V. node 
 A V. bundle 
 
 Fig. 2. — The Cardiac Nervous Mechanism. 
 
 S.A. node, Siuo-auricular node; A.V. node, aiiriculo-ventricalar node (Tawaia) 
 A.V. bundle, auriculo-ventricular bundle. The connection between the S.A. 
 node and the A.V. node is indefinite. It may be through the contracting 
 auricular niu.scle. 
 
 (2) The auricular walls to the aiiriculo- ventricular node, 
 which lies m the right side of the auricular septum. 
 From this a.v. node the stimulus is carried by 
 
 (3) Hie auriculo-ventricular hundle {a.v. bundle) to the 
 ventricles. This bundle divides in the interventricular 
 
NERVOUS MECHANISM O 
 
 septum into two branches^ which ultimately spread out 
 in the subendocai'dial tissue of right and left ventricles 
 as Purkinje's fibres. The papillary muscles are said to 
 be the first part of the ventricles to receive the stimulus 
 to contract. 
 
 It is not known how the stimulus from the sino-auri- 
 cular node traverses the auricles. It is probably carried 
 by the muscle fibres^ regular and complete contraction 
 of which is essential for the regular contraction of the 
 ventricles. At any rate, irregular and incomplete con- 
 traction of the auricles results in irregular contraction 
 of the ventricles. In a marked condition of auricular 
 disease, in which the wall is dilated, and in which the 
 muscle is in a state of over-excitability and is making 
 constant incomplete attempts to contract (see Auricular 
 fibrillation and Flutter), there is an extreme degree of 
 irregularity in the ventricular rhythm. 
 
 Whilst the stimulus for the heart beat arises normally 
 in the sino auricular node, and is rhythmic or regular in 
 origin, in abnormal conditions, functional or organic, it 
 may arise in other parts of the nervous mechanism, or 
 be arrhythmic or irregular in origin. Thus it not un- 
 commonly starts in the auricle or ventricle causing the 
 condition known as premature systole (q.v.), or pre- 
 mature stimuli may leave the sino-auricular node A\dth 
 the same result. 
 
 If the nervous tissue of the heart be changed struc- 
 turally by disease, or become unduly irritable, irregu- 
 larity in the action of the heart results, giving rise to 
 conditions (i^. v.) known as premature systole, heart-block, 
 auricular fibrillation, and paroxysmal tachycardia. 
 
II 
 
 ROUTINE EXAMINATION 
 
 What Patients with Heart Disease complain of. 
 
 Patients suffering from the worst forms of heart disease 
 may feel perfectly well, and have no complaint of any sort. 
 Their cardiac weakness may only be discovered during 
 the course of an examination for life insurance, or for 
 some illness not connected with the heart. As a rule, 
 however, they do complain of one or more subjective 
 symptoms, chiefly shortness of breath, palpitation, and 
 pain. 
 
 1. Shortness of breath, especially after only slight 
 exertion, as on going up a flight of household stairs or 
 up a short hill. In more severe conditions the patient 
 may be awakened from his sleep with a sensation of 
 breathlessness and tumultuous action of the heart — a 
 very distressing condition. 
 
 2. Palpitation, or unusual action of the heart, which 
 attracts its subject^s attention. The quick action with 
 a "throbbing" sensation in the neck resulting from 
 emotional or muscular overaction is commonly met with, 
 and generally described as palpitation. It may be met 
 with in normal as well as diseased hearts. A " flutter- 
 ing" or " tumbling" sensation is often felt. This, how- 
 
ROUTINE EXAMINATION ' 
 
 ever, in its slighter forms may be present wlien the heart 
 is quite sound, and be due to functional disturbance of 
 the regular stimulation of the heart. In disease, Avhen 
 the heart is enlarged and its action forcible, this symptom 
 is often most distressing*, especially when it wakens the 
 patient up out of his sleep with a smothering feeling. 
 
 3. Pain (1) over the praecordia, made worse by exer- 
 tion or increased quickness of beat, is met with chiefly in 
 cardiac enlargement due to valvular disease or adherent 
 pericardium. There is much tenderness to the touch in 
 these cases. 
 
 Or (2) shooting down the arms, especially the left 
 arm, or in the shoulder or up the neck, in aneurysm or 
 angina pectoris. There is oft^n also a sense of suffoca- 
 tion or of gripping of the heart, mth apprehension of 
 impending death, in anginal cases while the pain is 
 present. 
 
 N^.B. — Pain in the upper arms, especially in the left 
 arm J w up the haclc of the nech, may he the first indication 
 of aneurysm of the arch of the aorta. 
 
 The Cause of the Cardiac Pain. — The pain is one form 
 of referred pain. The heart, developmentally, is asso- 
 ciated with the first eight dorsal segments and nerves, 
 and painful impressions arising in it are usually referred 
 to the first and second dorsal nerves. The cutaneous 
 distribution ^of these nerves is the inner aspect of the 
 arm as far down as the elbow, and anginal pains which 
 arise from disease at the base of the ventricles, or first 
 part of the arch of the aorta, are referred to the shoulder 
 and down the arm. 
 
 HsemoPPhag'e from mucous surfaces may be com- 
 plained of by patients with mitral disease, especially 
 
8 HEART DISEASE 
 
 mitral stenosis. Epistaxis, haemoptysis, haematemesis, 
 and bleeding from the ears, have been present in cases 
 under my care. The heart must therefore always be 
 carefully examined in all cases of mucous membrane 
 haemorrhages. 
 
 Dropsy. — In heart disease dropsy affects the legs in 
 the first place, and is improved by rest in bed. In 
 looking for oedema pressure should be applied deliber- 
 ately, for about five seconds, over the face of the tibia 
 near the ankle, and als o over the sacrum . Slight degrees 
 of it will be overlooked unless this care be taken. 
 
 Coug^h from congestion of the pulmonary mucous 
 membrane is a frequent consequence of disease of the 
 mitral or tricuspid valves. 
 
 The Arterial Pulse. 
 
 N.B. — The pulse should be examined at the com- 
 mencement of the investigation of any heart affection. 
 
 Much valuable information can be obtained in heart 
 affections by an intelligent feeling of the radial pulse 
 with the fingers. The sphygmograph is an. interesting 
 instrument, and gives instructive information when you 
 know the kind of tracing you ought to get and the 
 proper way to get it. But even to one experienced in 
 its use it gives but little information which escapes the 
 practised fingers. 
 
 The best way to feel the radial pulse is to use two 
 hands for the purpose. One hand is to steady the 
 patient's wrist, by holding his hand so as to allow the 
 delicate application of three fingers of the other hand 
 to the artery, as it runs over the end of the radius. 
 The thumb, to further steady matters, should be placed 
 behind the patient's wrist. All three fingers should be 
 
THE PULSE 9 
 
 placed closely together over the end of the radius, so 
 that the artery can be pressed against it, and not against 
 the less resisting soft tissues. The index finger should 
 be applied firmly as close to the base of the metacarpal 
 bone of the thumb as possible to obliterate the junction 
 of the radial artery with the palmar arch, and prevent 
 any wave coming round that way. The ring finger is 
 used to tell when the pulse in the artery is beating or 
 not, and the fourth finger to apply pressure over the 
 artery and estimate the amount of force necessary to 
 obliterate the pulse in the radial artery. In this way 
 changes in the tension of the bloodvessel can be very 
 accurately estimated witli a little practice and knowledge 
 of the normal condition of aifairs. 
 
 Another useful icay of feeling the jndse is to grip the 
 lower end of the radius between the forefinger and 
 thumb of one hand, with the finger applied firmly over 
 the artery close up to the base of the metacarpal bone 
 of the thumb to cut oif the palmar arch anastomosis 
 pulse, and then to apply the first and second fingers of 
 the other hand to the radial artery as before. In either 
 method all three fingers must occupy as little space as 
 possible, so that they can manipulate the artery as it 
 runs in front over the end of the bone. 
 
 It is sometimes instructive to feel the pulse by gripping 
 the wrist Avith the hand in such a way that the palm of 
 the observer will lie over both radial and ulnar arteries 
 and feel their pulsation, at the same time elevating the 
 patient^s forearm so that there is a considerable stretch 
 of perpendicular artery. In this way the water-hammer 
 or Corrigan^s pulse is best developed, both arteries slap- 
 ping their pulse wave against the palm of the hand, and 
 its simulation by a low tension pulse of cardiac dilata- 
 tion reduced to a minimum, 
 
10 HEART DISEASE 
 
 No apology need be made for giving such details of 
 good methods of feeling the pulse, for by their adoption 
 an accurate estimate of changes in the pulse tension 
 may be more easily made, and variations from the 
 normal m other ways more easily recognized than if less 
 deliberate methods be adopted. 
 
 Congenital abnormalities in the anatomy of the radial 
 arteries may occur, and must be allowed for. Thus the 
 radial artery may be of smaller size than normal in one 
 or both wrists, and make pulse-feeling rather difficult. 
 
 Comparison of the two radial arteries. — Inequality in 
 the pulse wave of the two radial arteries may occur, and 
 be due to — 
 
 1. Congenital causes. 
 
 2. Pressure on the artery somewhere on the proximal 
 side of the wrist (with a thoracic aneurysm or new 
 growth). 
 
 3. Changes in the wall of the artery (atheroma). 
 
 4. Obstruction in the lumen of the vessel (embolism 
 or thrombosis). 
 
 The points to bs noticed in feeling the radial pulse 
 
 are, the rate, volume, regularity, tension, condition of 
 the vessel wall, aud the comparison between the two 
 radial pulses. 
 
 Pulse-pate. — In counting a pulse-rate, it is to be 
 remembered that the result does not always indicate 
 the rate the heart is beating at. It generally does, 
 but in one form of heart disease — namely, auricular 
 fibrillation — in which the rhythm and force of the 
 ventricular systole is extremely irregular and uneven, 
 
THE PULSE 11 
 
 many of the ventricular beats, which are considerably 
 increased in number, are so feeble that they do not 
 transmit a pulse wave to the radial artery. Therefore, 
 when the radial pulse is irregular in rhythm and size of 
 wave, and increased in frequency above the normal, the 
 stethoscope should be applied to the heart whilst the 
 pulse is being- counted. 
 
 A quick pulse in heart disease practically always 
 means either 
 
 1. Some dehility of the heart muscle — that is, inability 
 to do the extra work thrown on it by the abnormal 
 condition by its usual number of beats. It often means 
 some giving way of the heart muscle, that is, cardiac 
 muscle failure, but not necessarily so ; or 
 
 2. An abnormal excitability of the nervous mechanism 
 which causes an abnormally increased number of stimuli 
 sent to the ventricles. 
 
 These points will be referred to again under the 
 headings tachycardia and irregular pulse. 
 
 An abnormally slow pulse in heart disease — that is, a 
 rate below 50, especially one below 30 — frequently means 
 some pathological change in the auriculo-ventricular 
 {a.-v.) bundle, which impedes the conduction of stimuli 
 from the auricular nervous mechanism. (See Brady- 
 cardia.) In this case the auricles will be contracting 
 more frequently than the ventricles. 
 
 A certain but small number of persons have a heart- 
 rate below 50 with auricles contracting as slowly as the 
 ventricles. 
 
 The volume of a pulse, that is, whether it is large and 
 full or small and empty, depends chiefly on the amount 
 of blood propelled by the ventricle into the aorta at each 
 systole. 
 
12 HEART DISEASE 
 
 Small and empty pulses. — In mitral disease the pulse 
 is often small and empty, because in stenosis less than 
 the normal amount of blood enters the left ventricle 
 during its diastole, and in incompetence some reguEgi- 
 tates into the auricle. In either case an abnormally 
 small amount passes from the ventricle into the aorta 
 with each beat. Furthermore, when the ventricles in 
 mitral disease are contracting Avith increased rapidity, 
 irregularity in rhythm, and inequality in force, only a 
 considerably reduced amount of blood has time to pass 
 into the left ventricle for it to contract on. 
 
 With marked aortic stenosis the pulse is a small one, 
 and there is delay in its transmission to the wrist. 
 
 A large and full pulse is met with when there is an 
 abnormal amount of blood expelled from the ventricle 
 into the aorta, and this is met with in cases of dilatation 
 of the left ventricle with hypertrophy. In dilatation 
 without adequate compensation the pulse often lias a 
 soon-full, soon-empty, or slapping character, which may 
 simulate very closely a Corrigan\s or water-hammer 
 pulse iq.v.). 
 
 Reg'Ularity. — Normally the heart, and therefore the 
 pulse-beats, follow each other regularly in rhythm and 
 uniformly in character. It is very common, however, 
 to meet with irregularity in rhythm and varying character 
 of heart-beat and pulse-wave, not only when the heart 
 is diseased, but also when it is quite sound. 
 
 In healthy children the heart may be irregular, its 
 rate varjnng with inspiration and expiration. A similar 
 irregularity in rhythm is often met with in nervous 
 people. 
 
 The commonest form of irregularity in adult life is 
 the so-called missed beat, in which a heart-beat and a 
 
PULSE TENSION 13 
 
 pulse-wave apparently drop out. What happens is that 
 the heart gives a premature and weak contraction^ which 
 does not create a pulse-wave. (See Premature or extra 
 systole.) This frequently occurs in normal hearts as the 
 result of digestive disturbances. 
 
 The other extreme is met with in certain forms of 
 heart disease when scarcely two successive beats of the 
 heart and pulse are regular in rate or uniform in char- 
 acter. The beats occur in a most irregular way (delirium 
 cordis), and with more or less greatly increased rapidity. 
 Sometimes the pulse-rate is uncountably fast. (See 
 Intermittent pulse and Auricular fibrillation.) Between 
 these two extremes lie varying degrees of irregularity. 
 
 Tension. — increased tension is an important indica- 
 tion of pathological processes taking place in the system, 
 the most important of which are arteriosclerosis and 
 interstitial nephritis. It may be the first physical sign 
 of these diseases, and when it is present the urine must 
 be examined carefully by boiling and acidulation — the 
 most delicate test for albumen. The specific gravity of 
 the urine will probably be low, and often only a very 
 faint trace of albumen is found, or none at all. 
 
 Nocturnal polyuria. — There will, however, generally 
 be obtained a history of nocturnal polyuria as well — 
 that is, the necessity of getting up regularly at night 
 two or three times to pass a considerable amount of 
 urine. In making this point, it must be ascertained how 
 much fluid is drunk late at night, for many men take 
 half a pint at least of nightcap fluid, such as whisky 
 and water, hot milk, or plain hydropathic hot water; 
 but this will rouse them only once in the night as a rule, 
 and generally early in the morning. Further, the in- 
 creased frequency of micturition in small amounts caused 
 
14 HEART DISEASE 
 
 by an irritating prostate must not be confused with high 
 tension polyuria. 
 
 Increased tension may be caused by absorption of 
 toxins from the alimentary canal without there being 
 any primary interstitial nephritis. This condition may 
 last for years, with its attendant discomforts. 
 
 In mitral stenosis the pulse, though small, is often one 
 of considerable high tension. 
 
 The distinction between hardness of the wall of the 
 artery and increase of arterial tension must be borne in 
 mind. Either may be present without the other, or 
 both may be present together. 
 
 Abnormally low tension is rather more difficult to 
 make out. It is present in debilitated states in children 
 who are subject to fainting attacks with no definite 
 ascertainable cause. 
 
 The condition of the wall of the artery must be 
 made out by rolling it under the fingers against the 
 end of the i*adius. When this is done, a normal artery 
 can scarcely be felt at all after the pulse-wave has been 
 obliterated, whilst a diseased one feels more or less hard, 
 like w piece of string when there is fibroid degeneration 
 of the middle coat, or like a hard calcareous tube (pipe- 
 stem artery) with marked atheromatous degeneration. 
 Movements of the fingers in the long axis of the end 
 of the radius will reveal any annular deposits of cal- 
 careous material. 
 
 Venous Pulse. 
 
 The venous pulse affords valuable information in heart 
 disease, especially of the condition of the right side of 
 the heart. The only vein in which it can be observed is 
 the jugular vein, between the tlioi*acic attachments of 
 
THE VENOUS PULSE 
 
 15 
 
 tlie sterno-mastoid muscle. When there is ohstructioR 
 to the flow of blood from the right auricle into the 
 ventricle, the jugular veins are distended, and stand out 
 
 ■r. a. 
 
 V. V. 
 
 R 
 
 E. C. 
 
 P. 
 
 Fig. 3. 
 
 V. a. , Auricular form of venous pulse 
 V. v., Ventricular form of venous pulse. 
 R., Radial pulse. 
 £. C, Electrocardiogram. 
 
 P. , Phonoscope tracing showing heart sounds and murmur 
 a., Auricular wave ; v., ventricular wave ; c, carotid waves. 
 I. and II., first and second heart sounds. '1 second intervals of time. 
 
 prominently, but often there is no visible distension, 
 let alone pulsation, of the veins. 
 
 With obstruction to the large veins in the chest there 
 will be distension of the veins in the neck but no 
 pulsation. 
 
16 HEART DISEASE 
 
 The venous pulse cannot be felt by the finger like 
 the arterial pnlse^ but requires a special recording ap- 
 paratus for its investigation. For the use of this clinical 
 polygraph considerable experience and practice is neces- 
 sary. Its application is consequently limited to hospital 
 practice or to the work of a few specialists. Whilst it 
 gives information which helps in the understanding of 
 the conditions present in heart disease, especially con- 
 cerning' the condition of the auricles and the relative 
 number of auricular and ventricular contractions, it 
 does not as often afford much assistance in treatment 
 beyond that gained by other and more manifest evidence 
 of cardiac muscle failure. 
 
 Jugular pulse waves. — The common form of jugular 
 pulse tracing is known as the auricular form, and shows 
 three waves. The first, or the auricular (a.) wave, is 
 caused by auricular systole; the next and smaller wave 
 is called the carotid (c.) wave, and is probably caused 
 by the pulse-wave in the carotid artery being trans- 
 mitted through the jugular vein to the surface ; and the 
 last, or ventricular (?;.) wave, is caused by the rebound 
 of blood in the filling auricle against the closed tricuspid 
 valve (Fig. 3, V. a). 
 
 In the other form of venous pulse, known as the ven- 
 tricular venous pulse, there is no a. wave, the v. wave 
 predominating. In this case there is no contraction of 
 the auricle, this organ being paralyzed and acting 
 merely as a reservoir (Fig. 3, V. v). 
 
 The jugular pulse, then, gives information as to what 
 is going on in the right side of -the heart chiefly. It is 
 recorded synchronously on paper by means of a poly- 
 graph with the radial pulse, or occasionally with the 
 apex-beat, and for its interpretation some time standards 
 
THE VENOUS PULSE 17 
 
 and a pair of compasses are necessary. The time 
 standards are the following : 
 
 The radial pulse follows one-tenth of a second, and the 
 carotid pulse one-twentieth of a second after the onset of 
 ventricular systole, Avhich in its turn is preceded by auric- 
 ular systole by one-fifth of a second. Before the tracings 
 are taken, the two recording pens are moved up and down 
 across the paper to mark the relative positions of the 
 venous and arterial pulses at the same moment of time, 
 and to give the "oi^dinate^^ for accurate measurement. 
 A time-recorder constantly marks intervals of one-fifth 
 (two-tenths) of a second. When a tracing is completed, 
 the distance between the ordinate for the artery tracing 
 and the beginning of the upstroke of its pulse-wave is 
 measured accurately with the compasses. The stretch 
 between the points of the compasses is then decreased 
 by a distance exactly equal to a one-tenth of a second 
 interval on the time- marker. The compasses are now 
 applied to the venous pulse, one limb being placed accu- 
 rately on its ordinate, and the other on the tracing, 
 where it will fall exactly where the carotid wave ought 
 to be developing. This spot is then marked as the rise 
 of the c. wave. Each successive c. wave is marked 
 out by resetting the compasses to a space equal to the 
 distance between the commencement of the upstroke of 
 the arterial pulse tracings, and measuring successive 
 complete pulse-waves along the venous tracing from the 
 originally marked a. wave, marking each a. wave as 
 before. The auricular wave ought to begin two-tenths 
 of a second before the c. wave. 
 
 General Inspection in Cases of Heart Disease. 
 
 The general inspection should always be carried out 
 with the patient facing a good natural daylight, as 
 
 2 
 
18 HEART DISEASE 
 
 artificial light destroys the delicate changes in shades 
 of colour, especially the yellow of jaundice, which are 
 such important indications of the health. Whilst 
 patients suffering from heart disease, even in its most 
 serious forms, may look " the picture of health,'^ with a 
 general natural freshness of complexion, there are cer- 
 tain signs in the face and general aspect pointing to 
 cardiac disease which are visible to the eye of a skilled 
 observer. 
 
 The g'eneral sig'ns are those of shortness of breath 
 on slight exertion, or even without any, inability to 
 breathe in any but the erect position (orthopnoea), oedema, 
 — especially swelling of the legs and dependent parts. 
 Marked throbbing, with short and sudden pulse-waves, 
 in the carotid or other arteries, may be seen, and gener- 
 ally means aortic regurgitation, but a quickly acting 
 dilated heart may cause similar appearances. Distension 
 of the veins of the neck with or without visible pulsation 
 may be present. 
 
 In the face, in addition to signs of the general dis- 
 tress, there may be seen, but not always, some special 
 changes. 
 
 Mitral stenosis often gives rise to a high colour, 
 localized more or less to the malar eminences of the 
 cheeks, and due to dilated veins (ven^ stellatas). An 
 exactly similar condition is met with in people who have 
 been exposed to the weather, and a somewhat similar 
 condition, and one which often deceives the student, is 
 met with in myxoedema. Here, however, there is a 
 peculiar yellowish, waxy appearance of the rest of the 
 face. 
 
 In aortic disease, when it is severe, there is generally 
 
INSPECTION 19 
 
 much pallor, from the tendency which incompetence of 
 the valve has to empty the blood vessels rapidly, and 
 often also marked '^ lines " running from the nose to the 
 outer angle of the mouth. 
 
 Capillary pulsation may be seen if looked for care- 
 fully over the forehead ; but to see this properly it is 
 generally necessary to make a small patch of blush by 
 rubbing the forehead with the back of the finger-nail. 
 
 Cyanosis. — When the cardiac muscle, especially that 
 of the right heart, fails, the pulmonary circulation 
 cannot be carried on effectively, with the result that the 
 venous blood is imperfectly oxygenated. It then collects 
 in the systemic circulation, and is seen in the skin and 
 mucous membranes as a bluish discoloration, or cyanosis. 
 Cyanosis is most marked in dependent parts, the lobes 
 of the ears, the fingers and toes, but it is well seen in 
 the face. This form of cj^anosis is the result of a deficient 
 force pumping blood through the lungs. 
 
 With heart disease of long standing, especially of 
 congenital origin, the fingers and toes are often clubbed 
 as well as purple. 
 
 A hluish, ashy grey appearance is, however, often met 
 with in chronic bronchitis and emphysema with the heart 
 working well. This is due to inability of the lungs to 
 expand freely and oxygenate the blood properly. 
 
 In congenital heart disease there is generally a very 
 deep red, purple, or bluish aspect. When congenital 
 heart disease is met with in people over puberty, espe- 
 cially over twenty, as it occasionally is, it is almost 
 always due to pulmonary stenosis. Other congenital 
 heart lesions generally terminate in childhood, but I saw 
 one adult of thirty-one who died from the effects of a 
 
20 HEART DISEASE 
 
 congenital septum in the auricle, which simulated mitral 
 stenosis. How he lived as long as he did was a wonder. 
 
 Jaundice is also often present. For this to be de- 
 finitely established the conjunctivae under the upper 
 eyelids must be examined^ the yellow discoloration so 
 often seen in the exposed parts not being due to bile 
 pigments. 
 
 Anxiety. — In angina pectoris or severe intrathoracic 
 aneurysm there is often an appearance of extreme 
 anxiety, and, if the pain be present, of great distress. 
 
 The attitude is fixed and immobile as though move- 
 ment of any sort were feared, in marked contrast to the 
 excited movements of hysterical angina. 
 
 Inspection of the Neck. 
 
 Arterial pulsation. — Pulsation or throbbing of the 
 carotid arteries, varying in degree, will often be seen, a 
 thin neck favouring its visibility. In the majority of 
 cases of slighter degree it means nothing abnormal, merely 
 a favourable position of the arteries for their pulsation to 
 reach the surface. Even when marked it may be due 
 simply to nervous overaction of the heart. With aortic 
 regurgitation it reaches its highest development, when 
 the throbbing of a soon-full, soon-empty vessel is very 
 striking. The frontal artery may also be seen to throb 
 in aortic incompetence, but a visible pulse wave in any 
 exposed artery may occur without any heart disease 
 being present. In dilatation with hypertrophy, the 
 carotid arteries may pulsate in a way very suggestive of 
 an aortic pulse. 
 
 The condition of the veins must be noted, distension 
 indicating oljstruction to the return of blood to the right 
 
INSPECTION 21 
 
 auricle, or to its flow through the right side of the heart. 
 The jugular veins are often seen to be very full, and if 
 examined carefully between the attachments of the 
 sterno-mastoid to the clavicle and sternum pulsation in 
 them may be seen and felt. A transmitted impulse 
 from the carotid artery must be discriminated from true 
 venous pulsation. 
 
 The direction in which blood flows to fill the veins is 
 important. If a stretch of vein be emptied between two 
 fingers the vein will fill from below upwards if there 
 is tricuspid regurgitation, and from above downwards 
 when auricular distension alone or venous obstruction 
 is present. 
 
 Any general swelling of the neck, if present, must be 
 noted, as it is generally a sign of serious intra-thoracic 
 disease or venous obstruction. 
 
 Inspection of the Pr^cokdia. 
 
 Inspection of the preecordia must never be omitted, as 
 it gives most valuable information in disease. A side or 
 tangential view should be taken if the direct inspection 
 is negative, pulsation being sometimes seen by it, and 
 not otherwise. 
 
 The normal cardiac impulse may be invisible, and 
 negative observation may mean nothing abnormal. 
 The anterior and mid-axillary regions should be most 
 carefully examined, as the impulse is often surprisingly 
 far out in disease. 
 
 Diffuse pulsation between the mid-clavicular line and 
 the sternum generally means disease of the right ven- 
 tricle, and widelj^ spread pulsation, outwards as well, 
 means enlargement (dilatation with hypertrophy) of 
 both ventricles. Auricular pulsation is never seen. 
 Pulsation over the base of the heart generally indicates 
 
22 HEART DISEASE 
 
 aneurysm of the arch of the aorta. The impulse of a 
 forcibly beating normal heart may extend outwards to 
 the nipple line. 
 
 Bulging of the prcecordia is generally best seen in 
 children, whose chest walls give easily in front of 
 enlarged hearts. When limited to intercostal spaces it 
 often indicates pericardial eifusion. 
 
 Systolic retraction of the interspaces may be seen ; it 
 is often diffuse, and means adherent pericardium or 
 great cardiac enlargement, the contraction of the heart 
 causing negative pressure in the thorax, and consequent 
 retraction of the intercostal spaces. 
 
 Palpation. 
 
 Palpation is a very valuable method of cardiac diag- 
 nosis, and should always be practised. The hand must 
 be warm, and must be placed over the region of the 
 apex-beat below and within the nipple line. As much of 
 the hand as possible should be laid over the praecordia, 
 from the sternum outwards, with the region of the distal 
 interphalangeal joints about where the impulse is ex- 
 pected. As the prgecordia are often very tender, a 
 light touch must always be used. 
 
 Cardiac Impulse. — When the impulse is felt by the 
 hand, the outermost limits of it to the left should be 
 determined by the pad of one finger applied in the inter- 
 costal spaces. This gives very accurate information as 
 to the area of heart dalness, which will be further in- 
 vestigated later by percussion. If the impulse cannot 
 be felt in the lying position, let the patient sit up and 
 lean forward, but not to the left ; also try the effect of a 
 deep expiration and the holding of the breath after- 
 wards. 
 
palpation' 23 
 
 N.B. — The heart often extends surprisingly far into the 
 axilla, and mistakes in diagnosis result from want of 
 attention to this fact. 
 
 An absent cardiac impulse may mean thick chest 
 walls^ with too much adipose tissue, an intervening rib, 
 emphysema, feeble heart action, or pericardial effusion. 
 
 The normal apex-heat has characters which must be 
 learned by experience. It is produced by systolic con- 
 traction and elongation of the heart, the elongation 
 being communicated to the chest wall by the apex of 
 the left ventricle. It is limited in area to that of about 
 half,a crown, and is moderately forcible and abrupt. 
 
 In disease it may no longer be an apex-beat from the 
 left ventricle, but becomes a diffuse impulse from the 
 anterior surface of the right ventricle. 
 
 A distinction should therefore be drawn between the 
 apex=beat and the cardiac impulse. 
 
 In hypertrophy of the heart the impulse is slow, 
 heaving, and stronger than normal. 
 
 In dilatation of disease, or feeble action in debility, it 
 is quicker, feebler, and more slapping, than in health. 
 
 In mitral stenosis the accentuated first sound can be 
 distinctly felt, and should be a definite indication of 
 what will be heard on auscultation ; a thrill may be felt. 
 
 In pulmonary valve lesions an accentuated second 
 sound may sometimes be felt in the second left inter- 
 costal space, and in aneurysm of the aorta the aortic 
 second sound may be felt as a diastolic shock. 
 
 Thrills arising within the heart are caused by pal- 
 pable vibrations set up in the diseased valves of the 
 heart and carried to the surface of the chest. They 
 arise at a rigid and narrowed orifice, with altered curtains, 
 
24 HEART DISEASE 
 
 and may be systolic or diastolic in rhythm. The sensa- 
 tion of liquid being sprayed against the hand, or of a 
 cat purring^ is conveyed l)y them. 
 
 Systolic thrill is met with (a) at the apex of the heart 
 in regurgitation through a mitral or tricuspid valve 
 made incompetent by stenosis ; 
 
 (b) At the base in obstruction due to an atheromatous 
 aortic valve. A pulmonary thrill is extremely rare.- 
 
 Diastolic thrill is met with (a) at the apex, with blood 
 entering the ventricle through a stenosed mitral or 
 tricuspid valve. 
 
 Regurgitation through an incompetent aortic (or pul- 
 monary) valve may cause a thrill over the ventricles. 
 
 (h) At the base a diastolic thrill is extremely rare. 
 
 A crescendo thrill is felt with a crescendo murmur. 
 The rhythm of this, as usually taught^ is presystolic or 
 auricular systolic — that is^ just before the systole of the 
 ventricle. As will be seen later, the rhythm is probably 
 early ventricular systolic. 
 
 Pericardial friction may be felt, and simulate a rough 
 thrill, but it has not the character of sprayed liquid, 
 but more that of two rough surfaces rubbing together. 
 
 Peecussion. 
 
 Liyht iwrcussion gives the best results, and should be 
 cultivated. Changes of resonance can be best appre- 
 ciated by the sensation of touch aiding that of sound. 
 Apart from this, the pra^cordia in subjects of heart 
 disease are often exquisitely tender, and most patients, 
 especially in private practice, prefer gentle methods. 
 After locating the outermost limits of the cardiac im- 
 pulse by palpation, the heart should be percussed in a 
 routine way, and always from resonance to dulness. 
 
PERCUSSION 25 
 
 The most delicate results are obtained by very light 
 percussion in an intercostal space, thus avoiding the 
 sounding-box of a rib, and by quick contrasts brought 
 about by two strokes in one place followed quickly by 
 two in another not more than half an inch away. 
 
 Note the results by measurement from the mid-sternal 
 line, the normal distance in an adult being about three 
 and a half inches from it. 
 
 Routine method of percussing* out the heart 
 dulness. — 
 
 N.B. — It is very important to follow regularly a 
 definite method of percussion in the examination of the 
 heart. 
 
 1. Limit to the left. — Percuss horizontally along the 
 line of the normal apex-beat from the axilla inwards. 
 If the heart is enlarged or displaced, begin to percuss a 
 couple of inches farther out, and follow along its changed 
 horizontal line. 
 
 2. Limit to the right. — First locate the liver dulness 
 (about the sixth rib) by percussion downward in right mid- 
 clavicular line. Then take a line one inch above this and 
 percuss inwards towards the sternum. It is very unusual 
 to get' any distinct line of dulness to the right of the 
 sternum in health, although the right auricle extends 
 half an inch in this direction, the ribs and sternum acting 
 as a sounding-box. When the right auricle is enlarged 
 or the heart displaced to the right, dulness will be 
 found. 
 
 3. Limit uijwards. — Percuss in a line one inch to the 
 left of the sternum. Dulness will be found about the 
 third rib. 
 
 4. The limit downwards is the upper limit of the liver 
 and diaphragm against which the heart lies. 
 
26 HEART DISEASE 
 
 Superficial or absolute cardiac dulness is obtained 
 over the small triangular part of the heart which is un- 
 covered by lung^namely, that bounded by the mid- 
 sternal line, a line running from it at the level of the 
 fourth left costal cartilage to the union of the fifth rib 
 with its costal cartilage, with its base line at the level 
 of the diaphragm (sixth rib). 
 
 The dulness obtained over this part of the heart with 
 no intervening lung is more marked than that ob- 
 tained over the deeper-seated part of the heart. Its 
 determination is not important, unless it is to note the 
 encroachment of an emphysematous lung towards the 
 middle line. 
 
 Deep cardiac dulness is usually that sought for on 
 percussion of a heart. Its limit is that of the heart in 
 the chest. The more lung tissue in front of the heart, 
 the less absolute is the dulness obtained. With much 
 emphysema it may be impossible to get any dulness 
 at all. 
 
 Practical points — in health. — There should be no 
 dulness to the right of the sternum, to the left of the left 
 mid-clavicular line, or above the third rib on a line one 
 inch to the left of the sternum in the adult. 
 
 In disease. — 1. Dulness to the right of the sternum 
 means enlarged right auricle or displaced heart. Do 
 not forget the possibility of a congenital development of 
 the heart on the right side. 
 
 2. Dulness to the left of the mid-clavicular line m^ans 
 dilatation of the left ventricle or great dilatation of the 
 right ventricle, or displacement of the heart to the left. 
 
 3. Dulness below the fifth costal space, in the region of 
 the nipple line, means hypertrophy of the left ventricle. 
 
AUSCULTATION 27 
 
 In hypertropliy of the right ventricle pulsation of this 
 ventricle can be felt under the costal arch, close to the 
 xiphisternum. 
 
 4. Dulness to the left of the left mid-clavicular line 
 and helow the fifth interspace means dilatation and 
 hypertrophy of the left ventricle or of both ventricles. 
 
 5. Dulness above the third rib, due to cardiac changes, 
 means pericardial effusion. The whole cardiac dulness 
 in this case is pear-shaped, with the base of the pear 
 downwards, and the cardiac impulse, when it is felt, is 
 sometimes well within the outer limits of dulness. 
 
 Diminished cardiac dulness means emphysema or 
 pneumothorax. 
 
 Extrinsic causes of displacement of the apex-beat. 
 
 — The whole heart, and consequently the apex-beat, may 
 be displaced by other causes than those which arise 
 within the heart itself or within the pericardium. 
 
 The heart may be pushed out of place — 
 
 (a) By intrathoracic causes, such as fluid or air in the 
 pleural cavities, new growths or aneurysm. 
 
 (b) Abdominal causes, ascites, or new growths, which 
 push up the diaphragm. The apex-beat is generally 
 pushed up and out by ascites. 
 
 The heart may be pulled out of place by shrinking of 
 the lung, especially in an upward direction, as by 
 phthisis of the upper part of the left lung. 
 
 Auscultation. 
 
 A wooden stethoscope gives the most delicate results 
 in auscultation, but a binaural, with its flexible rubber 
 tubes, is often more convenient. The use of both may 
 
28 HEART DISEASE 
 
 be cultivated Avith advantage. Nothing should be 
 allowed to rub against the stethoscope, otherwise very 
 alarming auscultatory phenomena will be heard. 
 
 N.B. — Theprsecordia are often exquisitely tender in heart 
 disease, and the stethoscope chest-piece must be applied 
 with this in mind. 
 
 Localize the apex^beat. Before using the stethoscope^ 
 it is of the utmost importance to find the apex-beat of 
 the heart, or the outermost limit of the heart to the left. 
 Unless this be done, murmurs, especially the crescendo 
 murmur heard only at the apex of the left ventricle as 
 a rule, may be overlooked. 
 
 The proper way to use a stethoscope, whether 
 binaural or monaural, and with the patient in or out of 
 bed, is to place one hand on the patient's shoulder ^ and to 
 use the other for moving the stethoscope from place to 
 place. This not only prevents the examiner from adopt- 
 ing the unbusinesslike and objectionable habit of keeping 
 one hand in his pocket, but it also maintains the proper 
 distance-relationship between the examiner and the 
 patient, and facilitates the timing of murmurs by the 
 carotid artery. 
 
Ill 
 
 THE HEART SOUNDS 
 
 It is important to bear in mind the anatomy and 
 mechanism of the normal valves in studying the changes 
 ill the normal heart sounds which are met with in 
 disease. 
 
 THE FIRST SOUND 
 
 The first sound is produced by the act of closure of 
 the normal mitral and tricuspid valves (auriculo- 
 ventricular or a.-v. valves) by the contraction of the 
 normal ventricles. 
 
 No sound is heard whilst the blood is passing through 
 the a.-v. valves into the ventricles. 
 
 Anatomy of the auriculo-ventriculap valves. — 
 
 1. The fibrous^ inelastic valve curtains, two in the left, 
 or mitral, valve ; and three in the right, or tricuspid, 
 valve. From the edges of the curtains run tendinous 
 cords (chordee tendineae) to — 
 
 2. The musculi papillares, which arise from the muscle 
 of the ventricular wall. 
 
 3. Muscular fibres around tlie orifice of the valves. 
 It used to be taught that these were arranged as circular 
 fibres, but recent observations suggest that in addition 
 to some circularly disposed fibres the spiral muscle 
 
 29 
 
30 HEART DISEASE 
 
 fibres of the ventricle are attached to the fibrous valve 
 ring in such a way that when they contract they help to 
 diminish the valve orifice. 
 
 Mechanism of the closure of the auriculo- ventri- 
 cular valves. — 
 
 1. When blood is passing from auricle into ventricle 
 the valve curtains lie against the ventricle wall and 
 offer no impediment to its flow. 
 
 2. As the ventricle fills the blood floats the edge of 
 the curtains of the valves into such a position that — 
 
 3. The curtains are locked in competent apposition at 
 the very onset of ventricular systole (v.s.), when the papil- 
 lary miiscles are said to contract^ and before the intra- 
 ventricular blood-pressure has reached its maximum. 
 
 4. At an early phase of v.s. the " circular " muscular 
 fibres contract, and so reduce the areas of the orifices of 
 the valves . that the curtains, when in apposition, com- 
 petently close the valve orifices. 
 
 5. The force with which the ventricle contracts is 
 determined by the resistance of the arterial circulation, 
 and for this to act with maximum efficiency the valves 
 must be competent. The greater the resistance to its 
 contraction, the more vigorous is the systole of the 
 ventricle, within certain limits. 
 
 Causation of the normal first sound. — The first sound 
 of the heart is caused by — 
 
 1. Vibration, or tension, set up in the curtains of the 
 mitral and tricuspid (a.-v.) valves by the force of intra- 
 ventricular blood-pressure which closes the valves. This 
 is the dominant factor in the causation of the first sound. 
 
 2. Muscle vibration, or tension, in the contracting walls 
 of the ventricles. 
 
FIRST SOUND 31 
 
 3. Arterial tension. There must be a certain amount 
 of pressure in the arteries to afford that resistance 
 which is necessary for the ventricles to contract with 
 a certain degree of deliberation and force. 
 
 There is a considerable degree of elcisticity in forces 
 2 and 3. 
 
 The valve curtain note is of higher pitch than the 
 muscle note, but the sound cannot be resolved into its 
 component parts by the ear. 
 
 iSTo sound is heard whilst blood passes through the 
 normal open valves into the ventricles. 
 
 The Mitral sound louder than the Tricuspid sound, 
 
 — The left side of the heart, though more deeply seated, 
 is the predominant partner in the causation of the 
 first sound, because the blood-pressure which acts in 
 closing and maintaining competent its valves is two or 
 three times greater in the left ventricle and the aorta 
 than in the right ventricle and pulmonary artery. This 
 suggests that the valves of the left side of the heart 
 close with twice or thrice the tension of the valves of 
 the right side. 
 
 Location of the apex-beat. — The importance of 
 localizing the apex of the heart as accurately as 
 possible by palpation or percussion, or b}^ both 
 these methods of examination, has been referred to 
 under the section on Auscultation. This point 
 cannot be emphasized too much, for, unless the 
 stethoscope be placed over the left ventricle, sounds or 
 murniurs produced at the mitral valve may he entirely 
 overlooked. 
 
 When the heart is enlarged and the right ven- 
 tricle is dilated, the true apex of the heart (the 
 apex of the left ventricle) may not come to the 
 
82 HEART DISEASE 
 
 surface, but by finding the outermost limit of the 
 heart to the left we get as near to it as possible, 
 and reduce possible errors to a minimum. 
 
 Characteristics of the first sound. — The normal first 
 sound is dull and deliberate, and is imitated by the 
 sound nhbj as compared with the higher pitched, 
 shorter sound produced at the semilunar valves, imitated 
 by the sound vjj. To produce this sound, tension in the 
 curtains of the closed a.-v. valves and in the contracting 
 muscle of both ventricles, and the blood-pressure in 
 the arteries must be normal 
 
 There is some degree of elasticity in the papillary 
 muscles acting on the a.- v. valves, like sailors holding 
 the ropes of a flapping sail, which probably prevents 
 sudden, inelastic tension of the curtains, and produces 
 a note of lower pitch than that developed at the rigid 
 inelastic curtains of the semilunar valves, which may, to 
 continue the simile, be compared with a flapping sail 
 fixed to the rigid sides of the ship. 
 
 To summarize, then, the first sound is produced by 
 tension of the a.-v. valve curtains and of the ventricle 
 muscle of the right and left sides of the heart, and is a 
 double compound sound, though it is caused chiefly by 
 the mitral valve and left ventricle. 
 
 Time. — It is important to note that the first sound is 
 developed at an early phase of v.s., and only occupies 
 the first part of this event. 
 
 A first sound can therefore he continued, ov followed, by 
 a murmur produced at a later phase of v.s. (in a manner 
 to be described later) through defects at the same valve 
 orifice tchlch allow of ^regurgitation of blood into the 
 auricle during the coniph'tion of v.s. (systolic murmur). 
 
FIRST SOUND 33 
 
 Distinctness. — The distinctnes.s witli wliich tXm normal 
 fimt sound of the heart can be heard over the pra^cordia 
 depends on — 
 
 (1) The thickness of the structures ivhich intervene 
 between the heart and the stethoscope. Thus^ much 
 adipose tissue in the chest wall will diminish the sound, 
 as also will an emphysematous lung pushing forwards 
 over the heart, or pericardial fluid displacing the apex. 
 
 (2) The force of the contractimj ventricle. A forcibly 
 contracting ventricle, as in nervous palpitation, or after 
 exertion, makes the sounds so loud that they can be 
 heard by the subject himself, or by an observer at a 
 short distance from tlie chest, without the help of any 
 conducting medium. 
 
 On the other hand, a feebly heating normal heart, as 
 in debility, or syncope, or '^ fainting," gives rise to a 
 correspondingly feeble first sound. 
 
 Modifications of the Fiest Sound. 
 
 Departures from the normal condition of the valve 
 curtains, cardiac muscle and blood-pressure which pro- 
 duce the normal first sound, will modify the character 
 of the sound, or produce additional audible signs. 
 
 I. — Chang-es in the valve curtains may modify the 
 sound. — 
 
 1. Weakening or absence of the sound. — The curtains of 
 the valve may be more or less stiffened by disease so that 
 they can only close slowly or that they cannot close at 
 all. The sound will then be modified, or it will not be 
 heard at all. 
 
 2. Production of Tnurmtirs. — When the curtains are so 
 diseased that they are unable to move and close the 
 
 3 
 
34 HEART DISEASE 
 
 valve, they not only no longer produce a sound, but they 
 may cause the development of a murmur of incompe- 
 tence. This new sign will be referred to fully later. 
 
 3. Accentuated sounds. — When thickened by disease, 
 but still able to close more or less competently, the 
 curtains may come together with a snap or markedly 
 accentuated sound. Such an unusually sharp and 
 accentuated first sound is best heard in a. v. stenosis. 
 
 4. Perforation of the curtains through ulceration may 
 lead to the production of a murmur with or without 
 a first sound, according to whether the valve is or is 
 not too much diseased to produce a sound. 
 
 II. — Changes in the muscle of the ventricle may 
 
 modify the first sound in two ways : 
 
 1. Thickening, or ti'tie hypertrophy, with slower, more 
 deliberate and more forcible contraction of the heart 
 muscle, and a less sudden development of tension in the 
 curtains, as compared with normal, gives rise to a note 
 which is of lower pitch, more lengthy duration, and is 
 dull or muffled, as compared with the normal first sound. 
 
 The thickened ventricular wall probably aids further 
 in the production of this dull sound by hindering con- 
 duction of the valve tension element of the sound. 
 
 2. Thinning of the wall, as in dilatation of the ven- 
 tricle, on the other hand, owing to the quicker and less 
 efficient contraction of the heart muscle and more in- 
 elastic production of curtain tension, causes a note which 
 is more abrupt and slapping and of higher pitch than 
 the normal sound. The unusually thin walls of the 
 ventricles probably facilitate the hearing of the valve 
 tension element of the sound. 
 
 In marked cases of dilatation of the ventricles the 
 sound heard is probably mostly one of valvular tension. 
 
FIRST SOUND 35 
 
 the papillary muscles contributing to tliis effect ])y losing 
 their elastic pull on the valve curtains. 
 
 3. Any structural changes in the walls of the ventricle 
 which (a) diminish the force of contraction , such as myo- 
 carditis, fatty degeneration or infiltration, will diminish 
 the loudness of the first sound ; or 
 
 {})) Any changes which diminish its ela,sticity, such as 
 fibroid degeneration^ will accentuate the sound. 
 
 III. — Changes in blood-pressure also have an effect 
 on the heart sounds. A high pressure, generally asso- 
 ciated with some muscle hypertrophy or increased force 
 of heart-beat causes a more vigorous ventricular con- 
 traction and a louder sound than a low blood-pressure, 
 Avhich tends to weaken the sounds. 
 
 IV. — An association of two or more of the above- 
 mentioned factors which modify the first sound of the 
 heart, a condition frequently met with in heart disease, 
 will cause more marked changes in it. 
 
 A weak or absent first sound will result from — 
 
 1. Changes in the valve curtains which interfere with, 
 or do away with altogether, the development of tension 
 in them at the onset of v.s. The valve curtains may 
 become so thick and stiff, forming a permanent funnel- 
 shaped passage, that they are immovable, and cannot be 
 closed or thrown into tension. No valve sound is then 
 heard, a murmur of regurgitation or incom'petence taking 
 its place ; a murmur of obstruction is also generally 
 heard during the passage of blood in the proper direction 
 through the valve. 
 
 2. Feehle action of the heart, as in debilitated states, 
 after continued fever, or during faintness. 
 
36 HEART DISEASE 
 
 3. Pericardial effusion, when there is a fair amount 
 of fluid present. 
 
 4. Diminution of the hlood-pressure. 
 
 Accentuation of the first sound. — The term ac-cen- 
 tuation is generally applied to the first sound heard in 
 abnormal conditions, in which, however, the valve curtains 
 are either normal, or not diseased enough to aifect their 
 mobility. 
 
 1. The tone is clearer, sharper, shorter than normal. 
 Such an accentuated sound is heard with dilated ven- 
 tricles, in which there is a more sudden stretching of 
 the valve curtains owing to the weak, inelastic condition 
 of the papillary muscles. It is also heard when the 
 hlood-jyressiire is increased. 
 
 2. The dull, prolonged, and thudding note of ven- 
 tncular hypertropliy is much muffled in its conduction to 
 the surface by the thickened ventricular wall. 
 
 3. When the thickened, almost cartilaginous valves 
 of a.'V. stenosis come together, they produce an abrupt 
 and accentuated sound which is characteristic of this 
 form of valvular disease. 
 
 4. When a heart is lying in contact with a stomach 
 distended with air or gas, the sounds may have a peculiar 
 " tympanitic " ring, which disappears when the flatulent 
 distension passes off. 
 
 Reduplication of the first sound. — Normally the 
 ventricles contract synchronously, and give rise syn- 
 chronously to the sounds which blend into what we 
 hear as the single first sound. We often hear, however, 
 the single first sound replaced by two sounds — that is, 
 by reduplication or doubling. An excellent imitation of 
 the single or double first sound can be made by striking 
 on the forehead by two fingers synchronously, and then 
 
FIRST SOUND 37 
 
 with varying interval between the contact of the two 
 fingers with the forehead. 
 
 The distinctness of the double first sound may vary 
 from a slight degree which has been imitated by the 
 sound truj) to one in which the two component sounds 
 are quite separate (ter-up). These variations can be well 
 imitated Avith the fingers on the forehead. 
 
 The explanation of a double first sound which is 
 usually given is want of synchronism of ventricular 
 contraction generally due to abnormalities of blood- 
 pressure in the two circulations. If one ventricle has 
 more work to do than in the normal condition of affairs, 
 it is said that it will reach that part of its systolic phase 
 at which the first sound is produced earlier than does 
 the other ventricle, and so produce the double first sound. 
 
 This explanation of reduplication of the first 
 sound of the heart is not without objection. To 
 begin with, the blood-pressure in the left ventricle 
 and the aortic circulation is two or three times as 
 great as that in the right ventricle and pulmonary 
 circulation ; but, on the other hand, the wall of the 
 left ventricle is correspondingly thicker, and there- 
 fore more powerful than that of the right ventricle. 
 If the blood-pressure in one of the circulations is 
 increased, one of two things results : 
 
 1. More muscle is developed — compensatory 
 hypertrophy — to deal with this increased pressure, 
 and therefore this ventricle is enabled to start on 
 level terms with the contraction of the other ven- 
 tricle ; or — 
 
 2. Dilatation of the ventricle and muscle in- 
 capacity results, with dilatation of the valve and 
 consequent regurgitation. This safety-valve action 
 
38 HEART DISEASE 
 
 relieves the increased pressure on the overworked 
 muscle, and again takes away any handicap as 
 between the ventricles. 
 
 Physiology teaches us that normally the left side 
 of the heart commences its contraction about one- 
 fiftieth of a second before the right, but this 
 difference is imperceptible to the human ear. 
 
 It seems to me that we may have another explana- 
 tion of the double first sound when it occurs with 
 actual or relative weakness of the papillary muscles 
 of one or both ventricles. The intraventricular 
 blood-pressure is at its highest after the contraction 
 of the papillary muscles, which occurs at the earliest 
 phase of v.s. ; but whilst the papillary muscles 
 maintain their systolic contraction as long as that 
 of the ventricle persists, in the normal condition of 
 affairs, it seems quite possible in disease of the 
 ventricle muscle, or in abnormal pressure in the 
 ventricles — such as is met Avith in an increased 
 arterial tension — for the papillary muscles to fail 
 after their initial contraction, but before the systole 
 of the ventricle is completed, and allow the valves 
 to fly back and to be put suddenly into a state of 
 secondary tension by the stretching of the musculi 
 papillares and the chordas tendineas. At any rate, 
 it is in conditions which cause increased arterial 
 pressure, and in muscle failure of the ventricle with 
 or without abnormal blood-tension that we get the 
 double first sound. 
 
 Clinical sigriificance of double first sounds. — 
 1. Functional causefi. — Doubling of the first sound 
 may not have any pathological significance — that is, it 
 may be heard with no organic lesion. It may occur at 
 
SECOND SOUND 39 
 
 the end of full expiration and the beginning of inspira- 
 tion on deep breathing. 
 
 2. 07'ganic causes. — A double first sound may be a 
 physical sign of severe disease in which increased arterial 
 tension develops, or in which the heart muscle fails. 
 In this latter case the rhythm of the cardiac cycle is 
 altered, and the first sound follows the second abnormally 
 quickly (see Rhythm of Sounds of the Heart and Bruit 
 de Galop, p. 45). 
 
 Doubling of the first sound is not a special sign of any 
 form of valvular disease. 
 
 THE SECOND SOUND 
 
 The second sound is produced by the act of closure of 
 the normal aortic and pulmonary valves by the intra- 
 arterial blood-pressure. 
 
 No sound is heard whilst blood passes through the 
 normal open semilunar valves into the aorta or j)uliTion- 
 ary artery. 
 
 Anatomy of the semilunar valves. — The semilunar 
 valves at the aortic and pulmonary orifices consist of 
 fibrous, inelastic valve curtains, three in each valve. 
 These curtains are attached by their bases to the fibrous 
 ring of the valve orifices, which also contains a little 
 elastic tissue. 
 
 There is nothing in the semilunar valves to compare 
 with the musculi papillares or the chordae tendineae of 
 the a.-v. valves. 
 
 Mechanism of the closure of the semilunar valves. — 
 
 1. Whilst blood is being driven into the aorta and 
 
 pulmonary artery the curtains of the semilunar valves 
 
 are closely apposed to the wall of the vessels so as to 
 
40 HEART DliSEASE 
 
 offer no resistance to the flow of blood through the 
 valve. 
 
 2. The curtains of the valves are locked in competent 
 apposition when the pressure in the large arteries is 
 greater than the driving force of the ventricles. 
 
 Causation of the normal second sound.— The second 
 heart sound is caused only by tension^ and has no muscle 
 element in it. 
 
 No sound is heard whilst blood passes through the 
 normal open valves into the large arteries. 
 
 The rlosure of the semilunar valves is brought about by 
 an elastic force — namely, the contraction of the muscle 
 fibres and the elastic tissue of the walls of the aorta and 
 pulmonary artery. It is important to remember this, 
 because loss of elasticity in the wall of the large arteries 
 through vascular sclerosis modifies the sound. 
 
 N.B. — This force, which may be called the systolic 
 contraction of the aorta or pulmonary artery, is at its 
 maximum in its earliest phase, and not at a later 'period, 
 as in the case of ventricular contraction. 
 
 This elastic force gives rise to one act of curtain 
 tension and one sound in each of the two valves. 
 This action may be compared to the single sound 
 which can be made when an inelastic object — e.g., 
 a hammer (the column of blood in the arteries) — is 
 brought suddenly against an inelastic resistance — 
 e.g., an anvil (the valve curtains) — by an elastic 
 force — e.g., the muscles of the arm governed by the 
 will (the elastic structures in the arterial wall). 
 On the other hand, if the inelastic hammer is 
 allowed to fall by its own weight on the inelastic 
 anvil, a double sound of primary and rebound 
 impact will result. The importance of this point 
 
SECOND SOUND 41 
 
 will be seen when we speak of reduplication or 
 doubling" of the second sounds. 
 
 The normal second sound^ then^ is a compound .sound, 
 being caused by the closure of the aortic and pulmonary 
 valves ; but as the blood-pressure in the aorta is two or 
 three times as great as that in the pulmonary artery, 
 the aortic valve probably contributes chiefly to its 
 causation. On the other hand, the deeper situation of 
 the aortic valve must be borne in mind. 
 
 Any second sound heard over the carotid arteries is 
 aortic in origin. 
 
 Characteristics of the second sound. — Normally the 
 second sound has definite characteristics of pitch and 
 duration. It is sharper and shorter than the first sound, 
 being imitated by the sound tip, as compared with ubb 
 of the first sound, and suggests valve tension only as its 
 causative agent. 
 
 Time. — The second sound is developed at the very 
 outset of v.d., and therefore it can be followed by any 
 abnormal sound which may be produced at a defective 
 valve during the remainder of v.d. (diastolic murmur). 
 
 Distinctness. — The conditions which affect the audi- 
 bility of the normal first sound — namely, thickness of 
 intervening structure, force of heart-beat — will also 
 affect that of the normal second sound. 
 
 Modifications of the Second Sound. 
 
 Modifications of the condition of the semilunar valve 
 curtains, of the elasticity of the arterial wall, and of the 
 blood-pressure, will modify the second sound, much as 
 similar changes modify the first sound. 
 
42 HEART DISEASE 
 
 I. — Changes in the valve Curtains may modify the 
 sound. — 
 
 1. Weakening or absence of the sound. — The curtains 
 of the valve may be so stiffened by disease that they 
 cannot close at all or can only close slowly. The sound 
 will then not be produced at all, or it will be modified. 
 
 2. Production of Murmurs. — When the curtains are so 
 diseased that they are unable to move and close the 
 ^alve, they not only no longer produce a sound but they 
 may cause the development of a murmur. This new 
 sign will be referred to fully later. 
 
 3. Accentuated sounds. — With the curtains diseased, 
 but still able to close competently, the sound of closure 
 is more accentuated, and may be followed by a murmur. 
 
 4. Perforation or injury to a curtain may occur in 
 aortic disease after unusually severe and sudden exer- 
 tion. Some sound of tension, followed by a murmur 
 of incompetence, is then heard. 
 
 II. — Changes in the wall of the artery. — 
 
 1. Loss of elasticity from atheromatous degeneration 
 of the middle coats leads to a more abrupt a(;centuated 
 sound of tension. 
 
 2. When the above change is followed by dilatation 
 of the artery (especially of the aorta), the second sound 
 is often of a peculiar ringing character, which may be 
 the first sign of the condition of the aorta. 
 
 III. — Changes in the blood-pressure affect the second 
 sound very markedly, accentuating it when it is ab- 
 normally high (increased tension), and diminishing it 
 when it is abnormally low. 
 
 A feeble or weak second sound will be heard when 
 
SECOND SOUND 43 
 
 the arterial blood -pressure is abnormally low, and is 
 generally associated with a weak first sound. 
 
 The second sound may be ahseyit altogether if the 
 valve curtains are so stiffened by disease as to be unable 
 to come together during v.d., or to be thrown into a state 
 of tension sufficient to produce a sound. 
 
 Accentuation of the second sound. — Physiologically, 
 this occurs at the end of deep inspiration and the begin- 
 ning of the following expiration, and can be brought on 
 by holding the breath. 
 
 In disease it is very common to hear the aortic second 
 sound accentuated when arterial tension is high, especi- 
 ally in Bright^s disease, and the pulmonary second sound 
 in congestion of the leseer circulation, especially in mitral 
 regurgitation. 
 
 Accentuation of the second sound is often associated 
 with accentuation of the first sound in these conditions. 
 . Ringing Sound. — In one condition in which there is an 
 abnormally large amount of blood just above the valve — 
 aneurysm of the aorta — the second sound has a peculiar 
 accentuated ringing sound, which may be the only aus- 
 cultatory sign of aneurysm of the first part of the 
 aorta. 
 
 Effect of Thickened Curtains on the Sound. — ^^[ormally 
 the edges of the cusps of the valves which come into 
 contact on closure of the valve are very fine and uni- 
 formly smooth, and no sound of impact is caused from 
 the way in which they are ^' floated " into apposition 
 before the final locking in competent closure. If the 
 edges of the cusps of the valve be thickened or calcareous 
 whilst the cusps are still capable of coming into compe- 
 tent apposition, an accentuated sound may be produced 
 by the impact of these cusps. 
 
44 HEART DISEASE 
 
 Reduplication of the second sound. — A double second 
 sound is usually said to mean asynchronous closure of the 
 aortic and pulmonary valves, and to be due to a higher 
 blood-pressure in one of the circulations which induces 
 abnormally early closure of the valve of the artery in 
 question. 
 
 [A fallacy in this teaching suggests itself at once 
 — namely, that as the pressure in the aorta is 
 normally twice or thrice that in the pulmonary 
 arter}^, we should get reduplication of the second 
 sound normally. 
 
 It is not the amount of pressure in the large 
 arteries, then, that determines the time of closure 
 of the semilunar valves. They close when the 
 pressure in the arteries is greater than that in their 
 corresponding ventricles ; so if asynchronism of 
 closure of the semilunar valves is to occur, it must 
 be because one ventricle takes longer to drive blood 
 into its artery than the other, not because there is 
 abnormal pressure in the aorta or pulmonary artery. 
 Thus, a dilated ventricle may be pumping blood 
 into its artery for a longer time than the other 
 ventricle, or a badly filled ventricle (often met with 
 in mitral stenosis) may pump its blood into the aorta 
 sooner than the normal or dilated right ventricle. 
 In both these cases double second sounds would be 
 heard. 
 
 It is, however, quite possible for an increase in 
 the blood-pressure of the aorta or pulmonary artery 
 to give rise to a double second sound by causing a 
 rebound of tlie column of blood which throws the 
 semilunar valves into sound-producing tension, such 
 a rebound being due to a want of elasticity in the 
 
TIC-TAC RHYTHM 45 
 
 vessel wall which frequently accompanies increased 
 tension. In this case there would be a comparatively 
 inelastic force closing the valve, and with this re- 
 bound a double sound would result in the manner 
 described on a previous page (p. 46).] 
 
 The rhythm of the first and second sounds is of 
 very great importance in the diagnosis of the condition 
 of the heart muscle, and may be referred to here. 
 
 In a normal heart beating seventy- five times per minute 
 the whole duration of a cardiac cycle is 0*8 second. Of 
 this time OS is occupied by v.s. and 0-5 by v.d. As the 
 
 M 
 
 1 — \ — iA» r I I r ^ r 
 
 V5 ■ VD ' 
 
 Fig. 4. — Khythm of Noiimal Sounds of a Heaiit beating 
 75 PER Minute. 
 
 YS equals three-tenths ; VD, iive-tenths ; auricular systole, one-tenth 
 second. All the figures are thus spaced except Figs. 5 and 6. 
 
 first and second sounds occur at the beginning and end 
 respectively of v.s., it follows that there is a longer 
 interval between the second and first than between the 
 first and second sounds in the proportion of 5 to 3. This 
 relative duration of the intervals between the heart 
 sounds is maintained, and can be recognized in hearts 
 
 1 — r — I — J" — 1 — [■ — I — r I r — ] — \ — I — I — I — I — r 
 
 VS VD V5 VD 
 
 Fig. 5.— Tic-Tag RhytHxM. 
 
 Space between first and second and second and first sounds equal. 
 Diastolic rest much shortened. 
 
 beating rapidly — 120 to 130 per minute. When the 
 
46 HEART DISEASE 
 
 time intervals between the sounds become equal — tlie 
 so-called "tic-tac" or "embryocardial" rhythm; or when 
 the second sound follows too quickly on the first sound, 
 and there is a proportionately longer pause between the 
 second sound and the following first sound, it is most 
 probable that there is some lesion of the cardiac muscle 
 (see later, p. 47). 
 
 u 
 
 "1 — J — I — I — I — J — » — J — I — I — I — J — I — J — ? — I — r 
 
 VS. VD. 
 
 Fig. 6. 
 
 Space between second -and -first sounds too short. Diastole 
 comparatively prolonged. 
 
 Cantering' rhythm, or Bruit de galop. — In its slighter 
 degrees, reduplication of the first or second sounds of 
 the heart is not readily recognized by the beginner, but 
 familiarity with the peculiar characteristics of the ab- 
 normal sound can be obtained by practising, as de- 
 scribed previously (p. 36), its imitation by the finger tips 
 on the forehead. The more marked degrees of redupli- 
 cation are easily recognized, and the only difficulty is to 
 
 P 
 
 T—] — ! — I — I — r—] — I — I T ^ I — I — I — » — I — 
 
 V5. V.O. VS. VD. 
 
 Fig. 7.— Bruit de Galop. 
 
 Double first and single second sound, and single first and double 
 
 second. 
 
 determine which of the sounds is doubled — a difficulty 
 which is removed by timing them by the carotid artery. 
 The carotid pulse follows the onset of ventricular systole 
 at an inappreciable interval of only 0*05 second. There- 
 
BRUIT DE GALOP 47 
 
 fore any sounds which are synchronous with the carotid 
 pulse are synchronous with ventricular systole, and any 
 which are not are synchronous with ventricular diastole 
 (see Timing of Murmurs). 
 
 When reduplication is marked, and one of the three 
 sounds is accentuated, the rhythm suggests the simile of 
 a cantering or galloping horse ; hence the name which 
 is often applied to the condition. It may be phonetically 
 represented by the sounds luh terup, luh ferup, or terup 
 tup, temp tup. Any one of the three sounds may be the 
 most accentuated. 
 
 Whatever pathological significance reduplication of 
 the first or second sounds of the heart may have when 
 the sounds maintain their relative distance from each 
 other, the prognosis is much icorse ivhen the first 
 sound, whether single or double, /b//oi«.9 mo7-e closely on 
 the second, whether single or double, thari it ought to. 
 This means that the ventricles are not getting their 
 proper amount of diastolic rest, and that we have almost 
 certainly to deal with a severe affection of the cardiac 
 muscle — cardiac muscle failure, either temporary or 
 permanent — and effective measures of treatment must 
 be undertaken at once. An invariable symptom in true 
 bruit de galop is dyspnoea on slight exertion. 
 
IV 
 HEART MURMURS 
 
 Hitherto we have been considering conditions in which 
 the vdlve curtains, even if altered structurally, have 
 beeu able to meet properly and to competently obliterate 
 the orifice they guard with or without modification of 
 the normal sound produced by the closure of the valve. 
 The valve also has offered no resistance to the passage 
 of blood through it in the normal direction of flow 
 through the heart. 
 
 MupmuPS. — In disease, however, it frequently happens 
 that the valve is so changed that it either ohstructs the 
 flow of blood in the normal direction through the heart 
 or allows the blood to pass back in the wrong direction 
 (to regurgitate), setting up sound-producing vibrations 
 in the blood itself or in the valve curtains, or in both, and 
 giving rise to new or adventitious signs — " murmurs " 
 or " bruits " — instead of, or in addition to, the ordinary 
 sounds, and these are heard over the heart. 
 
 Timing of murmurs. — In determining the valve at 
 which a murmur is caused, it is essential to know the 
 phase of the cardiac cycle during which tlie murmur is 
 produced. 
 
 It is of the utmost importance to time all murmurs, for 
 by so doing inexcusable and serious errors in diagnosis 
 
 48 
 
HEART MURMURS 41J 
 
 are avoided. It is often impossible to feel any apex- 
 beat, or, when it is possible, we may want to place a 
 stethoscope over it Therefore, the best way to time a 
 murmur is to keep a thumb on the carotid pulse, which 
 follows 0'05 second after the onset of v.s. 
 
 One-twentieth of a second is inappreciable to the 
 ordinary observer, but the radial pulse is O'l second after 
 the carotid pulse, and this is appreciable ; for instance, 
 the crescendo murmur, as a rule, is not more than 
 O'l second in duration. 
 
 We may say again here that any niuruiur which is 
 
 Flo. 8. — AiisoMiTE Stenosis OF Fig. 9.— Absolutk Stenosis 
 
 Semilunar Valve THJiouiiH of Mitual Valve through 
 
 TliICKENIX(J OF CUII'I'AINS OF THICKENING AND ADHESION 
 
 Valve : Vkutical Section. of Cusrs of Valve Cuktains : 
 
 Viewed Transversely. 
 
 synchronous with the carotid pulse is v.s. in rhythm, 
 and any one not syncronous is v.d. in rhythm. The a.v. 
 crescendo murmur is an exception to this rule (see p. 79). 
 
 Changes in the Valves which lead to the Pkoduction 
 
 OF Murmurs. 
 
 Broadly speaking, these changes result in the valves 
 becoming obstructive or incompetent. 
 
 1. Valvular obstruction. — ^Through thickening of the 
 curtains the lumen of the valve is diminished, causing 
 obstruction to the free passage of blood through it in 
 the normal direction of the circulation (Figs. 8 and 9). 
 
50 HEART DISEASE 
 
 In most of these cases of obstruction there is a greater 
 or less degree of adhesion of the curtains to each other 
 where they arise from the fibrous ring of the valve which 
 correspondingly diminishes the free-way, and causes the 
 condition known as valvular stenosis, and generally, but 
 not always, a murmur of obstruction. 
 
 Valvular stenosis may be actual or relative. 
 
 Actual stenosis is the term applied Avhen the valve 
 orifice and its fair-way is actually narrowed by disease. 
 
 Relative stenosis is the term applied when the lumen 
 of the valve remains normalj but the cavity beyond it, 
 
 Fig. 10. — Relative Stenosis of Fig. 11. — Dilatation of a.-v. 
 
 Semilunar Valve, Akteiiy Valve Ring: Normal Cuu 
 
 T.EINO dilated : VaLVE OrI- TAINS UNABLE TO MEET 
 
 FICE NOIIMAL IN SiZE. ACROSS THE DiLATED OrIFICE. 
 
 into which the blood passes from the valve, is abnormally 
 large or dilated. Such a condition is only met with 
 practically in connection with the semilunar valves and 
 the aorta and pulmonary artery beyond them (Fig. 10). 
 A stenosed valve, actual or relative, may, but does not 
 always, cause a murmur during the passage of blood 
 through it in the normal direction of flow through the 
 heart. 
 
 2. Valvular incompetence. — Here the curtains are 
 unable to prevent regurgitation of blood through the 
 valve in the opposite direction to that of the normal 
 
HEART MURMURS 51 
 
 course through the heart, and during this regurgitation 
 a murmur is heard. 
 
 Such incompetence may arise in two ways : 
 
 (1) The valve curtains are normal j but the orifice is 
 dilated — that is, the area of the orifice is rendered 
 abnormally great through stretching of the structures 
 which normally limit it. This condition is met with 
 chiefly in stretching of the circular muscular fibres 
 around the orifices of the a.-v. valves (Fig. 11). 
 
 (2) The valve curtains are diseased and unable to meet 
 competently across the orifice of a valve, which, as the 
 result of the disease, is generally of diminished lumen, 
 or actually stenosed (see Figs. 8 and 9). 
 
 Failure of the circular muscular fibres may be present 
 along with disease of the valve curtains. 
 
 Murmurs then can arise through — 
 
 {a) Ohstruction to the normal fiow of the blood through 
 the heart; or 
 
 {})) Incompetence of a valve to prevent the regurgitation 
 of blood in the reverse direction to the normal flow. 
 
 The Physical Causes op Cardiac Murmues. 
 
 There are two chief physical causes of cardiac murmurs 
 — fluid veins and vibration of valve curtains. Changes 
 in the viscosity of the blood also may have some in- 
 fluence. 
 
 1. Fluid veins. — When a stream of blood is driven 
 through an orifice which is of relatively small area com- 
 pared with that of the mass of blood into which it passes, 
 sound-producing currents, or eddies of blood, are pro- 
 duced which are more intense when there is a greater 
 disproportion between the moving column and the mass 
 
52 HEART DISEASE 
 
 into which it passes and when the driving force is 
 increased. 
 
 Such a method of producing a murmur can l)e imi- 
 tated by blowing through the pursed-up lips, the lips 
 remainino' ri"'id. 
 
 For the development of a fluid vein it is necessary that 
 some degree of -stenosis, absolute or relative, should exist. 
 
 (a) In Absolute Stenosis there is an actual narrowing 
 of the valve orifice with the cavity beyond (that is, in 
 relation to the direction of the stream of blood causing 
 the murmur) of normal or abnormal size. 
 
 The most typical conditions in which this absolute 
 stenosis is met with are those of mitral and aortic 
 stenosis. In these conditions the valve orifice is more 
 or less narrowed by adhesion of the cusps of the valves, 
 with some thickening of the non-adherent portions of the 
 valves (see Figs. 8, 9, and 12). 
 
 Tricuspid and pulmonary stenosis also occur, though 
 not so commonly. 
 
 (Ij) In Relative Stenosis the valve orifice remains 
 normal in area and the cavity beyond is pathologically 
 dilated. It occurs only at the aortic and pulmonary 
 valves. Theoretically, it might occur at the a.-v. valves 
 if the ventricles be much dilated, and so account for rare 
 a.-v. diastolic murmurs heard in cardiac dilatation. But 
 in practice relative stenosis is only important at the 
 semilunar valves. 
 
 The fluid vein murmur is of a smooth, soft, blowing 
 character, and probably not transmitted as widely as 
 when there is valve vibration as well. 
 
 Stenosed valves are also often incompetent as well as 
 obstructive, when regurgitation of blood through the 
 narrow opening will cause a murmur of fluid-vein origin, 
 and probably also of valvular vibration origin. 
 
HEART MURMURS 53 
 
 It must be remeriib(3red tlitit vvlieri there is obstruction 
 to the flow of blood through a valve, the cavity of the 
 heart behind the valve (in relation to the normal direction 
 of blood-flow) is often imperfectly emptied, and therefore 
 contains blood for the development of a fluid-vein re- 
 gurgitant murmur. 
 
 It must also be borne in mind that the curtains of a 
 valve which adhere to each other and cause absolute 
 stenosis may be thrown into vibration by the stream of 
 blood and alter the character of the murmur [see next 
 subheading (2)]. 
 
 2. Vibration of the valve curtains.— (1) Ohstruction 
 murmurs may be produced by the blood throwing the 
 rough, stiffened curtains into sound-producing vibration 
 as it passes over them in its direct passage through the 
 heart. 
 
 (2) The regurgitation of hlood over similarly diseased 
 curtains throws them into vibration and produces a 
 murmur. 
 
 Tj-ie sound-producing vibration of the valve thus caused 
 is analogous to that of a flag fluttering in the wind. 
 
 Vibration murmurs are of a rougher, more vibratory 
 character than those produced by a fluid vein. 
 
 Not uncommonly a tag of fibrous tissue attached to a 
 valve is thrown into rapid vibrati »n by the blood-stream, 
 and produces a musical murmur without causing any 
 symptoms of heart disease ; and it may be pointed out 
 here that the loudness of any cardiac rnurmur is not 
 necessarily an indication of the severity of the lesion, 
 the " bark '^ of a murmur often being worse than its 
 '' bite.'' 
 
 N.B. — It is the condition of the cardiac muscle, not 
 of the valve, that determines prognosis. 
 
54 HEART DISEASE 
 
 Thrills, — In marked cases we can feel the vibration 
 murmur as a "thrill/' typical instances of which are 
 the thrills met with frequently in mitral and aortic 
 stenosis. 
 
 3. Murmurs due to chang-es in the blood — Haemic 
 murmurs. — In marked cases of ana3mia a systolic mur- 
 mur, usually called a " haemic murmur/' is frequently 
 heard over the heart, with its point of maximum intensity 
 generally in the pulmonary valve region. 
 
 It used to be thought that the actual blood change — 
 namely, the diminished number of red corpuscles per 
 cm., especially if the total blood volume be abnormally 
 great, as in chlorosis — gave rise to the sound. There is, 
 however, no satisfactory proof that endocardial murmurs 
 can arise as a consequence of diminished viscosity. They 
 are probably of valvular origin, and arise in one of 
 two ways : 
 
 (1) Begurgitation through the mitral valve, which has 
 been rendered incompetent by the circular muscular 
 fibres of the valve partaking in the condition of ven- 
 tricular weakness not uncommonly met with in severe 
 anasmia; in other words, mitral incompetence through 
 valvular dilatation, the curtains remaining normal. This 
 murmur is best heard at the apex of the heart. 
 
 (2) III relative stenosis of the pulmonary valve, which 
 is brought about by dilatation of the artery in its first 
 part immediately beyond the valve, the valve orifice 
 remaining normal. Such a condition of dilatation can 
 be made out in the post-mortem room. This murmur 
 is best heard over the region of the pulmonary valve. 
 
 iV.jC?. — Murmurs caused in the above-mentioned ways 
 are all diminuendo in character, dying aicay with the force 
 which jyToduces them. 
 
11 K ART MURMUR 8 55 
 
 Changes in the Different Valves wiircii (Iive Rise 
 
 TO Murmurs. 
 
 It will make things clearer if the changes in the 
 different valves which give rise to murmurs be now 
 considered. 
 
 1. Auriculo-ventricular valves — («) Actual stenosis. 
 
 — This results from thickening and adhesion of the valve 
 curtains, which consequently oppose the passage of 
 blood from auricle to ventricle ; and if the forces moving 
 the blood, especially that of auricular systole, are strong 
 enough, which is not always the case, a diastolic murmur 
 will be heard. Sometimes vibrations are thus produced 
 
 Fig 12. — Two Dkgrke.s of Adhesion of Mitral Cuktaiks 
 CAUSING Stenosis. 
 
 in the valve curtains, and these can be palpated at the 
 apex as a diastolic thrill. 
 
 The degree of stenosis varies, and may be so extreme 
 as to narrow the orifice of the valve from an area 
 admitting three finger-tips to one scarcely admitting the 
 tip of the little finger only — the so-called button-hole 
 orifice (see Figs. 9 and 12). 
 
 The musculi papillares and chordae tendineae participate 
 more or less in this thickening and rigidity, and may in 
 consequence fix the edges of the valve curtains in a 
 funnel-shaped structure, and prevent the normal move- 
 ments and co-aptation of the curtains during v.fi. 
 
56 HEAET DISEASE 
 
 The process which causes this sclerosis is generally 
 of a chronic, slowly progressing nature, mostly set up 
 in childhood, and often without symptoms to attract 
 attention. 
 
 As a result of these changes the valve, in addition to 
 being obstructive, is very often incompetent, allows oi 
 reguryitafion, and creates a systolic murmur during v.s. 
 
 The presence of vegetations on the valves without 
 adhesion, which occurs in acute endocarditis, will ob- 
 struct the flow of blood from the auricle to the ventricle, 
 and may cause a diastolic murmur. They generally 
 
 FfG. 13. — Vegetations ox ]\1itral Vai.ve (closed) which prevent 
 Competent Closuiie, and which obstruct tjie Flow of Blood 
 through the Open Valve. 
 
 There is no adhesion of the curtains and no true stenosis. 
 
 make the valve incompetent, and give rise to a .systolic 
 murmur of regurgitation. 
 
 Confusion of terms.' — The terms ohstrudion and 
 stenosis (referring here to actual, not relative stenosis) 
 are often rather loosely used as meaning the same condi- 
 tion of a valve. Whilst all forms of absolute stenosis 
 obstruct the flow of blood throuo-h the valve, a condition 
 may occur in which, through marked roughening or the 
 presence of vegetations on the curtains without adhesion 
 of the curtains, the normally unhindered flow of blood 
 through a valve may be obstructed and an a.-v. diastolic 
 murmur result (see Fig. 13). 
 
HEART MURMURS 57 
 
 The latter condition would be really one of obstruc- 
 tion, but hardly one of absolute stenosis, this term 
 generally implying* absolute narrowing of the blood-way 
 through the valve caused by adhesion of the curtains or 
 nodular excrescences stiffening the valves 
 
 {h) Valvular dilatation. — Here the deficient factor in 
 the closure of the valve is the inability of the muscular 
 fibres round the valve ring to reduce the orifice of the 
 valve during v.s. to an area which the curtains, remain- 
 ing normal, can competently close. In consequence, a 
 systolic murmur of regurgitation is caused during v.s. 
 This condition results from cardiac muscle failure (see 
 Fig. 11). 
 
 The musculi papillares may also be unable to contract 
 and hold the edges of the curtains down. In this case 
 the curtains bulge into the auricle and probably become 
 incompetent. 
 
 (a) and [h). — As the result of acute endocarditis the 
 valve curtains may become affected with vegetations, 
 which impede the flow of blood from auricle to ven- 
 tricle and prevent competent closure of the valve during 
 ventricular systole ; and at the same time the muscle 
 element of the valve may, as a result of coincident myo- 
 carditis, fail and cause enlargement of the ring of the 
 valve. In such a condition a systolic murmur is almost 
 certain to be heard, and possibly a diastolic murmur 
 also. 
 
 Cardiac dilatation with no murmur, — It must be 
 noted that cardiac muscle failure, leading to dilatation 
 of the heart, may occur, and yet no systolic murmur 
 of valvular incompetence be heard. In these cases the 
 circular and spiral muscular fibres of the valve ring 
 
58 HEART DISEASE 
 
 must be more resistant to stress and strain than the rest 
 of the ventricular muscle, and are not stretched at all, or 
 only to a slight degree which the valve curtains can 
 make good and so prevent regurgitation. We shall then 
 have no systolic murmur of regurgitation, only an 
 accentuated or reduplicated fij-st sound. 
 
 Ulcerative erosion of curtains. — Valvular incompe- 
 tence may result from ulcerative endocarditis eroding 
 holes through the valve curtains and thus allowing of 
 regurgitation; but such a condition would be impossible 
 to recognize clinically. It would probably occur with 
 changes in the edges of the valve curtains, which would 
 themselves create incompetence. 
 
 2. Semilunar valves. — The changes which lead to 
 valvular murmurs at the aortic and pulmonary orifices 
 are practically the same as those above described at the 
 a.-v. valves, with the difference that there are no musculi 
 papillares and practically no muscular or elastic element 
 in the valve ring. The rhythm of the murmurs is, how- 
 ever, different. Thus, at a stenosed semilunar valve the 
 obstructive murmur is systolic in rhythm and the 
 regurgitant murmur diastolic, whilst at a stenosed 
 auriculo-ventricular orifice the obstructive murmur is 
 diastolic and the regurgitant systolic. 
 
 The aortic obstructive murmur, being always caused 
 by the great force of ventricular systole, is much more 
 regularly heard than the mitral obstructive murmur. 
 The obstructive aortic murmur may be accompanied 
 by a thrill palpable over the aortic area. 
 
 N.B. — A systolic murmitr at the auriculo-ventricular 
 valves, or a diastolic inurinur at the semilunar valves, 
 per se, only means incompetence of these valves. The 
 
HEART MURMURS 59 
 
 rhytlim of these )tiitrmws gives no information whatever 
 rr-v to the caicse of the incompetence — that is, whether this 
 is due to stenosis or dilatation. The means of deter- 
 mining this point will be referred to later. 
 
 The Crescendo mupmup. — So far we have dealt with 
 murmurs which, however they may be caused, have a 
 common feature — namely, they are diminuendo in char- 
 acter, and die away with the force which creates them. 
 
 There is, however, another murmur which, instead of 
 dying away, increases in force until it is abruptly cut 
 short at its maximum intensity by an accentuated first 
 sound. It is therefore a crescendo murmur. In addition 
 to this, it has another essential characteristic — namely, 
 it rises in pitch progressively with its increase in vigour, 
 and is at its highest pitch and maximum force when it is 
 abruptly terminated by the accentuated first sound. 
 
 This t3^pe of murmur is only produced at a stenosed 
 auriculo-ventricular valve, and almost always at the 
 mitral valve. A tricuspid crescendo murmur is very 
 rare. A crescendo murmur, then, has three essential 
 features : 
 
 (1) Increasing force, (2) Bising pitch, and (3) Abrupt 
 termination hy an accentuated first sound at its maximuin 
 of force and highest pitch. 
 
 Such a murmur, except the terminal abrupt first sound, 
 can be imitated closely by blowing, with increasing force, 
 through the lips pursed up to produce a low-pitched 
 whistling sound, and closing the lips whilst doing this. 
 In this way the sound represented by oo-ip is created. 
 It can also be imitated by blowing through a piece of 
 drainage tubing and obliterating the lumen of the tube 
 with the fingers or teeth whilst doing so. The rising 
 pitch characteristic of the murmur can only be caused 
 
60 HEART DISEASE 
 
 afc an orifice Avliich is he Ing progressively closed during 
 the prodicction of the murmur. 
 
 Causation of the Crescendo murmur. — It is usually 
 taught that this crescendo murmur is caused immedi- 
 ately before the onset of c.s-. by systole of the auricle_, 
 and therefore it is called a presystolic or auricular 
 systolic murmur. The auricle is . supposed to contract 
 with a crescendo force^ and to terminate its contraction 
 abruptly at its maximum of effort. During this con- 
 traction blood is forced through the stenosed mitral 
 valve and produces the murmur. How the rising pitch 
 
 Fig. 14. 
 
 A, B, C, D, Progressive stages ia the obliteration of the lumen of a 
 tube in which is being produced an imitation crescendo murmur ; 
 E, F, condition of the lumen of the tube when a systolic murmur 
 continues ihe crescendo murmur, 
 
 characteristic of the murmur is imparted to it during 
 a.s. has never been explained. This, as I have said, 
 must be produced at an orifice which progressively 
 closes whilst a murmur is being produced at it ; and 
 how the auricle can at one and the same time keep open 
 and yet progressively close the stenosed valve by driving 
 blood through it has never been explained. 
 
 The Crescendo murmur is early ventricular systolic 
 in rhythm. The a.-v. crescendo murmur must, in my 
 opinion, be produced between the onset of v.s. and the 
 carotid pulse ; that is, be early v.s. or prespliygmi-c in 
 rhythm. 
 
HEART MURMURS 61 
 
 The accentujited first sound which terminates the 
 crescendo murmur is probably caused by the forcible 
 coaptation of the thickened margins of the valve, and 
 must be ])roduced at a later phase of v.s. than the 
 normal first sound. This view of the early ventricular 
 or presphygmic rhythm of the a. -v. crescendo murmur, 
 and the lateness of the first sound which terminates it, 
 has been supported by independent observers with 
 evidence obtained by accurate timing of the events of 
 the cardiac cycle in mitral stenosis with instruments 
 recording synchronously tracings of the carotid pulse 
 and of the heart sounds. 
 
 Semilunar valve cre.srendo mitrmiir. — Theoretically, a 
 crescendo murmur may be caused at a diseased semi- 
 lunar valve, with curtains which are not as mobile as 
 the normal ones, but require some greater force than 
 the cessation of the vis a teryo of ventricular systole to. 
 close them. This might be developed at a later phase 
 of ventricular diastole than that at which the normal 
 semilunar valves close, by " systole " of the artery, and 
 whilst the valves were being closed blood would re- 
 gurgitate through their gradually narrowing orifice and 
 create a murmur of rising pitch. It is very probable 
 that the short aortic diastolic " whiffs '^ are caused in 
 this way. 
 
 Murmurs accompanying heart sounds produced at 
 the same phase of the ventricular cycle. — Sometimes a 
 murmur is accompanied by a heart sound produced 
 during the same phase of the ventricular cycle. Why 
 this should be so is not always clear. 
 
 It is easy to understand how a first sound produced at 
 the a.-v. valves can accompany a systolic murmur pro- 
 duced at the semilunar valves, or if the a.-v. valves give 
 
62 HEART DISEASE 
 
 rise to a diastolic murmur, and the semilunar valves are 
 normal, a second sound will be heard with the murmur. 
 Difficulties arise, however, when both the sound and 
 murmur are produced at one of the pairs of a.-v. or 
 semilunar valves. Such an occurrence may be due — 
 
 1. To the mitral (or the aortic) valve being so affected 
 as to create a murmur of regurgitation but no sound, 
 the tricuspid (or the pulmonary) valve curtains respec- 
 tively remaining normal and producing an audible 
 sound ; or vice versa to the tricuspid (or pulmonary) 
 valve allowing regurgitation, the mitral (or aortic) valve 
 remaining normal and producing a sound which is 
 audible through the murmur. 
 
 2. To the curtains of one affected valve being in such 
 a condition that they can close with a sound and yet not 
 be sufficiently competent to prevent some regurgitation 
 and the development of a murmur after the sound. This 
 condition may be met with in incompetence from stenosis 
 or dilatation. When the murmur and sound arise at the 
 same valve during the same phase of the ventricular 
 cycle the murmur distinctly follows the sound. There 
 is one exception to this, namely, the crescendo murmur 
 which precedes the first sound, both murmur and sound 
 being caused by v.s. (p. 60). 
 
 Absence of sounds with apparently normal rigrht 
 heart valves. — It not uncommonly happens that where 
 there is apparently disease of only the mitral or the aortic 
 valves, and not of the right side valves, the murmur 
 produced at the diseased valve is often unaccompanied 
 by any normal sound which ought to have been produced 
 at the corresponding healthy valve. Thus in cases with 
 incompetence of an abnormal mitral valve, and an ap- 
 parently normal tricuspid valve, a systolic murmur of 
 
HEART MURMURS 63 
 
 mitral regurgitation may be heard, with no tricuspid first 
 sound. Or_, again, in aortic incompetence, and apparently 
 a normal pulmonary valve, a diastolic aortic murmur is 
 not infrequently heard with no pulmonary second sound. 
 These facts may mean either that the tricuspid or the 
 pulmonary valve is unable to produce a first sound of its 
 own, which is contrary to common belief, or that the first 
 and second sounds produced at the normal right side of 
 the heart have not sufficient intensity to be heard through 
 a murmur. 
 
 Incompetence through dilatation of a valve, — It is 
 
 interesting to consider why, if the curtains of an a.-v. 
 valve are normal, but through dilatation of the orifice 
 a murmur is produced, there is not always a sound of 
 tension also. There often is, but not uncommonly it 
 happens that a soft systolic murmur of muscle-failure 
 incompetence is heard with no first sound. This may 
 be explained in one of several wa3^s : 
 
 1. In a normal heart the a.-v. curtains are "floated" 
 up into apposition by the filling of the ventricle ; then — 
 
 2. At the very onset of v.s. they are competently 
 locked, and this provides the resistance for the "ex- 
 plosive" contraction of the ventricle, which throws the 
 curtains into sound-producing tension, and also causes 
 a note of muscle contraction. 
 
 3. If the valve curtains are unable to meet across a 
 dilated orifice they cannot be competently locked at all 
 by V.S., but allow blood to slip away and so prevent the 
 necessary resistance for the normal explosive contraction 
 of the ventricle and its sound-producing (curtain and 
 muscle tension) results. The more gradual tension of the 
 curtain and muscle fails to produce a first sound, a 
 murmur taking its place. In support of this contention 
 
64 HEART DISEASE 
 
 is the fact that a systolic murmur sometimes grows in 
 intensity pari passu with the abnormally slow develop- 
 ment of the maximum of v.s. 
 
 Influence of mobility of curtains on sounds. — 
 
 (a) Mitral and tricuspid valves. — It does not follow, 
 then, that Avhen a systolic murmur of regurgitation is 
 heard the absence of a first sound denotes loss of mobility 
 of the mitral or tricuspid [a. -v.) valve curtains. 
 
 (h) Aortic and pulmonary valves. — Absence of a second 
 sound when an aortic or pulmonary murmur of regurgita- 
 tion is heard does mean almost certainly loss of mobility 
 (atheroma) of the valve curtains. This is probably ex- 
 plained by the fact that the normal semilunar valve 
 curtains are thrown more suddenly into tension by the 
 pressure in the large arteries, which is at its maximum 
 at its onset, than are the a. -v. valves by the slower-acting 
 muscle of the ventricles. A leak in the semilunar valve 
 will, then, not have the same effect on the development 
 of sound-producing tension in them as will a leak in the 
 a.-v. valves. 
 
 The presence or absence of a second sound with an 
 aortic (or pulmonary) incompetent murmur, therefore, 
 gives more information as to the mobility of the valve 
 curtains than is the case with a similar condition at the 
 a.-v. valve. 
 
V 
 
 AREAS OF AUDIBILITY OF HEART 
 
 MURMURS 
 
 Situation of the valves. — Broadly speaking, the mur- 
 murs produced at the various valves of the heart are 
 
 Fig. 15. 
 
 A., Aorta ; A.V., aortic valve ; M., mitral valve ; P. A., pulmonary artery ; P.V., pul- 
 monary valve ; R.A., right auricle ; SF., septum ventriculorum ; S.V.C, superior 
 vena cava ; 7". F., tricuspid valve. (Cunningham.) 
 
 heard best at those parts of the anterior chest-wall 
 Avhich are named after the individual valves. These 
 
 65 5 
 
66 HEART DISEASE 
 
 areas are not all directly over the valves, the situation 
 of which may be stated accurately enough for all prac- 
 tical purposes to be as follows : Pulmonary valve at the 
 level of the third left costal cartilage ; aortic valve, third 
 interspace ; mitral valve, fourth costal cartilage ; and 
 tricuspid valve, fourth interspace, and in a line running 
 obliquely downwards from the third left cartilage, where 
 it joins the sternum, to the midsternal line at the level 
 of the sixth rib. 
 
 Mitral area. — Murmurs produced at the mitral valve 
 are best heard at the apex of the left ventricle — i.e., the 
 apex-beat in the fifth interspace f inch internal to the 
 mid-clavicular line, or 3 J inches from the midsternal line. 
 
 If the heart is enlarged or displaced, the apex must 
 be located as accurately as possible in its new situation 
 by the methods described previously. 
 
 The danger of using the ni'pjple as a landmarh must be 
 remembered. Thus it may be out of place in relation to 
 the midsternal line through abnormalities in the shape 
 of the chest, and in women, naturally, it is generally no 
 guide at all. 
 
 Tricuspid area. — Tricuspid murmurs are heard best 
 at, and to the left of, the lowest part of the body of the 
 sternum. 
 
 Aortic area. — The area at which experience shows 
 aortic systolic murmurs to be generally best heard is that 
 of the first intercostal space against the sternum, behind 
 the second right costal cartilage at its junction with the 
 sternum, or on the sternum at this level. This is where 
 the arch of the aorta comes nearest to the anterior chest- 
 wall, and sounds produced at the aortic orifice during 
 systole of the ventricle are conducted along the aorta. 
 
EFFECT OF POSTURE ON MURMURS 67 
 
 Diastolic aortic murmtcrs, however, may be inaudible 
 here, and are generally heard best down the left margin 
 of the sternum or over the tricuspid area. They may 
 be audible at any small area of the pra3cordia only ; so 
 an aortic diastolic murmur, when suspected, must be 
 sought for carefully, square inch by square inch, all over 
 the chest anterior to both ventricles. 
 
 Pulmonary area. — The pulmonary area is situated 
 at the junction of the third left costal cartilage and 
 sternum, or in the third left intercostal space against 
 the sternum. 
 
 Whilst the above-mentioned principles relating to the 
 area of audibility of murmurs produced at the different 
 valves hold good in most cases, it must be remembered 
 that a murmur produced at any one of the orifices, if 
 intense enough, may he heard all over the 'prsecordium 
 (see Section YI.) . 
 
 Effect of Change feom the Upright to the Lying 
 Down Position on Murmurs. 
 
 It is important to note that some organic murmurs^ 
 especially mitral systolic murmurs, are most marked when 
 the patient is lying down. They may, indeed, only be 
 heard when he is in this position, so in doubtful cases 
 examination in the erect posture only is not conclusive. 
 
VI 
 
 CONDUCTION AND TRANSMISSION 
 OF MURMURS 
 
 Conduction means the carrying of lieart sounds and 
 murmurs from their seat of origin to other parts of the 
 heart (or pr^ecordia) and into the large vessels by means 
 of the heart muscle or the blood. 
 
 Transmission means the carrying of the sounds and 
 murmurs beyond these limits by means not thoroughly 
 understood. 
 
 Conduction. — a murmur is conducted best in ttie 
 direction of ttie flow of blood which causes it. We can 
 
 get fairly close with our stethoscopes to the direction of 
 the flow of blood through the tricuspid, pulmonary and 
 aortic valves. 
 
 The tricuspid and pulmonary valves, being on the right 
 side of the heart, which forms the anterior and most 
 superficial part of the organ as it lies in the chest, are 
 nearer to the anterior portion of the chest than are the 
 mitral and aortic valves. 
 
 1. Tricuspid murmurs.— A systolic murmur ought to 
 be conducted towards the right of the sternum, the right 
 auricle, especially when dilated, extending well beyond 
 
 68 
 
CONDUCTION OF MURMURS 69 
 
 the r'lQ-ht border of the sternum. It is heard over the 
 
 o 
 
 praecordia anterior to the right ventricle. 
 
 A diastolic murmur is conducted towards the apex of 
 the right ventricle. 
 
 Both murmurs are difficult to distinguish from mitral 
 murmurs. 
 
 2. Pulmonary murmurs.— The pulmonary artery at 
 the base of the right ventricle is nearer the anterior wall 
 of the chest than the aorta^ but its divisions are deeply 
 seated within the chest. 
 
 Systolic pulmonary murmurs are audible to the left of 
 the sternum in the second intercostal space. 
 
 A diastolic pulmonary murmur is rare^ but^ when heard, 
 may be conducted down the sternum or over the right 
 ventricle. 
 
 Aortic murmurs. — Systolic murmurs are conducted 
 upwards into the large arteries, subclavian and carotid, 
 and therefore these murmurs are conducted to more 
 accessible regions than any other heart murmur. 
 
 When being sought for over the vessels in the neck, 
 care must be taken to avoid pressure on the artery, 
 otherwise a murmur will be produced from the pressure 
 itself. 
 
 They may be easily heard over the apex-beat, though 
 less distinctly there, as a rule, than at the aortic area. 
 When traced from the aortic cartilage to the apex- 
 beat over the pra3cordia they gradually decrease in 
 loudness. 
 
 Diastolic murmurs will be conducted back into the 
 left ventricle, and, as said before, may be audible any- 
 where over that part of the chest-wall lying in front of 
 both the ventricles. Their usual line of conduction is 
 down the left edge of the sternum below the level of 
 
70 HEART DISEASE 
 
 the aortic area, and they may he heard at the tricuspid 
 region only. 
 
 They may also be heard over the sternum towards the 
 pulmonar}^ area. 
 
 Mitral mupmuPS. — Systolic murmurs should be con- 
 ducted towards the sternum and left auricle, but the 
 left side of the heart is too deeply situated for their 
 conduction to be traced. They may be transmitted round 
 through the axilla to the back, and be audible at the 
 lowest part of the left scapula. 
 
 Diastolic murmurs are best heard at the apex of the 
 left ventricle, which is in the direction of the flow of 
 blood causing them. They are scarcely ever transmitted 
 into the axillary region. 
 
 Crescendo murmurs are audible, as a rule, only over 
 the apex-beat, but they are occasionally conducted more 
 or less widely over the pr^cordia. As a rule, however, 
 the terminal portion or accentuated first sound only is 
 heard away from the apex or at the back. 
 
 Transmission.— The conditions which favour the 
 transmission of cardiac murmurs are not fully under- 
 stood; but I think that there are certain factors pre- 
 disposing to a wider area of audibility. 
 
 1. Condition of chest-wall. — A thin chest-wall, with no 
 fat, in close apposition to a heart without intervening 
 lung, will tend to favour transmission. Thus a largely 
 dilated heart in a child will have its murmurs trans- 
 mitted more widely than if the same heart were in an 
 adult with thicker or more rigid chest-wall and more 
 intervening lung. The ribs may have something to do 
 with transmission of mitral murmurs, especially if one 
 be immediately in contact with the apex of the heart. 
 
TRANSMISSION OF MURMURS 71 
 
 2. The nature of the murmur — that is, if produced by 
 vihratioii of the valve — will have some effect. In my 
 opinion, such a murmur will be conducted and trans- 
 mitted more widely than one produced by the small 
 column of blood passing into a large chamber (fluid 
 vein) . 
 
 Thus a systolic mitral murmur is likely to be trans- 
 mitted further through the axillary region if it is pro- 
 duced by regurgitation through valve curtains distorted, 
 thickened_, and made nodular by chronic endocarditis, 
 and capable of being thrown into vibration by the blood- 
 stream, than if the regurgitation is through a dilated 
 orifice with normal valve curtains, such as we meet with 
 in cardiac muscle failure, or through a rigid thick car- 
 tilaginous funnel, such as is met with sometimes in 
 mitral stenosis. 
 
 But loudf vibratory murmurs are not always conducted 
 or transmitted the farthest. Thus, I have several times 
 noticed a soft systolic murmur produced at the mitral 
 or aortic orifice which was audible all over the chest, 
 and even down over the lumbar region below the ribs. 
 Several of these cases were malignant endocarditis, with 
 involvement, especially, of the aortic cusp of the mitral 
 valve. 
 
 Whilst murmurs produced at any of the valves may, 
 if intense enough, be transmitted in the opposite direc- 
 tion to their path of conduction, those produced during 
 systole at the aortic and mitral valves are the mur- 
 murs most commonly transmitted. An aortic systolic 
 murmur is frequently transmitted to the apex of the 
 heart, whilst a mitral systolic murmur is often trans- 
 mitted to the axillary region. 
 
Vll 
 
 SPECIAL CHARACTERISTICS OF THE 
 
 DIFFERENT VALVULAR 
 
 MURMURS 
 
 MiTEAL Murmurs. 
 
 Lesions of the mitral valve are the commonest of all 
 valvular lesions. 
 
 Mitral systolic murmurs vary very much in character 
 according to the condition of the curtains of the valve at 
 which regurgitation takes place. If they can be thrown 
 into vibration by the regurgitant stream of blood the 
 murmurs are more intense, harder^ rougher, and more 
 penetrating than when the leak is between normal 
 curtains which are incompetent through dilatation of 
 the valve orifice, when they are softer, more " blowing," 
 and have less carrying power. A projecting tag of 
 fibrous tissue may give rise to a loud " nmsical " murmur. 
 
 The murmur is of uniform pitch — that is, it arises at a 
 leak which is constant (in relation to each v.s.) in its 
 area whilst the murmur is being produced. In intensity 
 it fades with the cessation of v.s. — that is, it is decrescendo. 
 The mitral crescendo murnmr has characteristics peculiar 
 to itself. 
 
 72 
 
MITRAL MURMURS 73 
 
 In time it is synchronous with the throb in the carotid 
 artery. The murmur may or may not be accompanied 
 by a first sound. In either case^ if tlie murmur be not 
 transmitted round the back, the first sound will often be 
 heard where the murmur is inaudible. (Figs. 16 and 17.) 
 
 Best heard at the apex-beat, a mitral systolic murmur 
 may be conducted with diminishing intensity more or 
 less widely over the pra^cordia. 
 
 The murmur may be transmitted to varying extent, 
 according to its nature and causation, through the 
 axillary regions to the angle of the left scapula. 
 
 1 — r 
 
 Fig. 16. — First Sound, Systolic Muemur ; Double Second, Dias- 
 tolic Murmur, with a Sound-free Interval between Double 
 Second Sound and the Murmur. 
 
 Significance. — Many students think a mitral systolic 
 murmur indicates mitral stenosis, but it only means 
 regurgitation through a defective valve. It means this 
 definitely; but the actual rhythm of the murmur gives 
 no information as to the condition of the valve which 
 allows of leakage. How this is determined must now 
 be considered. 
 
 Condition of the mitral valve at which regurgitation 
 takes place. — In investigating the condition of an incom- 
 petent mitral valve the medical history of the patient is 
 of the greatest importance. Causes of cardiac muscle 
 failure such as anaemia, alcohol, increased arterial ten- 
 sion, diphtheria, etc., likely to produce mitral dilatation, 
 must be sought for. In the absence of such a cause of 
 
74 HEART DISEASE 
 
 incompetence, clinical experience and pathological find- 
 ings have shown that a mitral systolic murmur in an 
 adult who has had endocarditis in childhood means 
 regurgitation through a stenosed and incompetent valve 
 in the great majority of cases. 
 
 Rheumatism in cliildliood. — The indication of 
 endocarditis in childhood is a history of acute rheu- 
 matism, chorea, " growing pains,^' or scarlet fever, 
 and careful inquiry will show that, where mitral 
 stenosis exists in adults, nearly every one of the 
 patients will give such a history. 
 
 Cases do, however^ occur in which there can be 
 
 1 — I — I — r 
 
 Fig. 17. — Systolic Muumur avith no First Sound, accentuated 
 Second (kedui'licated in Second Cycle), 
 
 obtained no history of any aches or pains which 
 generally accompany rheumatism with endocarditis, 
 but the question about "growing pains "must always 
 be put. It is astonishing how often an adult of 
 fifty, with mitral disease, will deny having had 
 rheumatism in any form, but will remember dis- 
 tinctly severe pains as a child, which were called 
 " growing pains." They may have been bad enough 
 to interfere with school or work, but they were not 
 called rheumatic either by the doctor or by the 
 parents. 
 
 It must be remembered that in infancy the ten- 
 dency in acute rheumatism is for the joints to he less 
 involved, for there to he less pain and more endocardial 
 
EHEUMATISM IN CHILDHOOD 75 
 
 troiihle, than in older ages, in which the opposite 
 conditions tend to prevail. There may even be no 
 trivial aches or pains, and the sole indication of an 
 illness in which the slowly progressing valvulitis is 
 set up is entirely confined to the heart, with the 
 disease so insidious and slow in development that 
 even breathlessness and debility are not prominent. 
 It is probable, however, that in nearly all these 
 painless endocarditis cases there is at least some 
 debility, if it only be recognized. 
 
 A severe general affection of the heart, endo- 
 carditis, myocarditis and pericarditis may also be 
 set up and lead to changes which can not be made 
 good, and which cause death at the time or in a 
 few years. 
 
 Bheumatic Nodules are sometimes, but not com- 
 monly, seen in children suffering from acute rheu- 
 matism. They are almost always associated with 
 serious heart muscle complications, and generally 
 prognose a fatal termination before long. 
 
 The ahseyice of a ''rheiomatlc'' history need not therefore 
 exclude the diagnosis of mitral stenosis in an adult in 
 whom the regurgitation is found. 
 
 The reason ivhy the diagnosis of mitral stenosis in an 
 adult ivho has had rheumatism in childhood can be made 
 is that the simple valvulitis set up by the endocarditis 
 then is a very slowly progressing disease and only 
 causes cardiac symptoms after some years, whilst the 
 endocarditis with myocarditis and pericarditis which not 
 uncommonly complicates rheumatism in childhood and 
 causes dilatation of the valve orifice through severe 
 muscle failure and adherent pericardium, ends fatally at 
 the time or before adult life is reached. 
 
76 HEART DISEASE 
 
 Further indications of the condition of the incom^ 
 petent mitral valve. — Apart from the above evidence 
 as to the condition of the valve at which regurgitation 
 is taking place, clinical experience and pathological 
 findings show that mitral regurgitant murmurs which 
 result from disease of the valve curtains are audible more 
 widely than those which result from cardiac muscle failure 
 dilatation of the valve ring, the curtains remaining normal. 
 
 This is probably because valve vibration murmurs are 
 transmitted farther than those of fluid-vein origin, and 
 are heard in the axilla whilst the latter are not. 
 
 If an incompetent stenosed valve be so stiff and carti- 
 laginous that its curtains cannot be thrown into vibration 
 by a regurgitant stream of blood, the smooth murmur so 
 
 T 
 
 V5 ' VD "^' V5 ' VO 
 
 Fig. 18. — Systolic Murmuh, Second Sound continued by Aortic 
 Diastolic; Systolic and Diastolic Murmurs with no Sounds. 
 
 produced will not be propagated towards the axilla 
 farther than one of ordinary fluid-vein production. 
 
 Cardiac muscle failure regurgitant murmurs j as has been 
 stated before, are not transmitted into the axilla like 
 those of curtain disease. 
 
 The prognosis of mitral systolic murmurs depends 
 entirely on the condition of the cardiac muscle ; the less 
 this is affected, the better the prognosis. With a regular, 
 slow pulse the prognosis may be quite favourable; it is 
 bad with a quick, irregular pulse. 
 
 As it has been said on a previous page, a loud murmur 
 does not necessarily indicate serious disease of any of 
 the cardiac valves. 
 
MITRAL MURMURS 77 
 
 Mitral diastolic murmurs. — These are best heard at 
 the apex-beat, and are not transmitted towards the 
 axilla. They may be heard towards the tricuspid region. 
 
 Time. — They almost always distinctly follow a second 
 sound, which is frequently reduplicated, a sound-free 
 interval occurring between the sound and the mnrmur' 
 This is an important point in distinguishing them from 
 aortic diastolic murmurs with which often no second 
 sound is heard, or which follow immediately and un- 
 interruptedly on a second sound, if one be present (see 
 Figs. 16 and 18). 
 
 The reason why mitral diastolic murmurs generally 
 follow at a later phase of v.d. than aortic diastolic mur- 
 murs is that the conditions which cause them are later 
 in developing than with the aortic murmur. Thus the 
 main forces which move the blood from auricle to ven- 
 tricle^ namely, active ventricular relaxation or diastole 
 and auricular systole, are at their minimum at the 
 beginning of ventricular diastole, whereas those driving 
 blood back through an incompetent aortic valve into the 
 ventricle (elasticity of the aorta) are at their maximum 
 then. 
 
 The diastolic murmur varies from soft, blowing, to 
 hard, thrill-producing characters, and is decrescendo in 
 force. 
 
 Cause. — Mitral diastolic murmurs are almost invariably 
 due to obstruction at the stenosed valve to the flow of 
 blood from auricle to ventricle during diastole of the 
 ventricle, and often can be palpated as a thrill. 
 
 The force moving the blood through the valve is that 
 of ventricular aspiration with auricular systole helping 
 at the end of ventricular diastole when the auricle is 
 strong enough to contract. 
 
78 HEART DISEASE 
 
 A diastolic murmur does not occur in every case of 
 stenosis, probably because the contraction of the auric- 
 ular wall, which aids in its production, is often very 
 feeble or entirely absent in mitral stenosis. 
 
 A few cases have been described in which a diastolic 
 murmur was produced at a dilated mitral valve. An 
 explanation of them is difficult to find. 
 
 The Prognosis of mitral diastolic murmurs is not 
 
 good, as their presence indicates some definite obstruction 
 to the flow of blood through the heart which may lead 
 to auricular muscle failure and pulmonary and, finally 
 systemic venous congestion. 
 
 VD ^ V3 ' 
 
 Fig. 19. — Cuksoendo Murmuh (early v.s.) accentuated First Sound 
 (delayed), Accentuated Second, Pause, Diastolic Murmur. 
 
 The Mitral crescendo murmur is characterized by 
 rising pitch, increasing force, and abrupt termination 
 with accentuated first sound at its highest pitch and 
 maximum force. 
 
 It has been argued on a previous page that, judging 
 from its characteristic of rising pitch, this murmur must 
 arise at an orifice which closes whilst it is being pro- 
 duced. The sound oo-ij^, produced at the lips only, 
 demonstrates this point clearly. 
 
 The mitral valve when stenosed is often so diseased 
 that it cannot close at all during ventricular systole, 
 when an ordinary systolic murmur of uniform pitch and 
 decrescendo force is heard ; or it can only be closed 
 at a later phase of ventricular systole when a sufficient 
 
CRESCENDO MURMUR 79 
 
 amount of power has been developed to force together the 
 stiffened rim of the valve. Whilst this force is gathering, 
 blood regurgitates through the open valve and produces 
 a systolic murmur, to which a rising pitch character is 
 imparted b}^ the closing of the valve. 
 
 With the gathering* force which closes the valve the 
 murmur increases in vigour or becomes crescendo in force. 
 
 The accentuated first sound is caused by forcible co- 
 aptation of the thickened margins of the valve, and has 
 been shown to arise at an a])normally late phase of v.s. 
 
 Time. — The crescendo murmur^ therefore^ is early v.s. 
 or presphygmic in rhythm, and occurs immediately before 
 the carotid pulse. 
 
 1 — r 
 
 V5 
 
 VD ^S' V5 I VD 
 
 Fig. 20.— Accentuated Fiust acjd Doublk Second Sounds: "wiih 
 CiiESCENDO Murmur of so-called Pue-Systolic Rhythm, that 
 IS, Auricular Systolic; Systolic Murmur; Double Second, 
 Mitral Diastolic api'arently continuous with following 
 Pre-Systolic Murmur. 
 
 The crescendo murmur varies in type from a soft 
 " oo-ip " sound to one of a rougher valve vibration 
 character. 
 
 It is usually taught that this murmur is late diastolic, 
 auricular systolic, or presystolic in rhythm (Fig. 20), 
 but the manner of its causation, in my opinion, negatives 
 this. 
 
 Location. — Crescendo murmurs are usually only heard 
 at the apex of the heart, and this must he carefully located 
 and the stethoscope applied exactly over it. They are 
 
80 HEART DISEASE 
 
 rarely transmitted into the axilla, possibly because the 
 murmur is often really of a fluid-vein type and lias not 
 wide carrying powers. The accentuated first sound is 
 generally heard in the axilla and at the back. Occa- 
 sionally, however, a crescendo murmur is both conducted 
 towards the sternum and transmitted into the axilla. In 
 these cases the valve probably is made to vibrate by the 
 regurgitant current of blood which causes the murmur. 
 
 N.B. — Whilst a crescendo murTnivr always means stenosis, 
 the absence of one does not necessarily mean no stenosis. 
 
 The Association of a crescendo murmur with other 
 murmurs in mitral stenosis is important. 
 
 1. It may be the only murmui' heard in mitral stenosis. 
 
 2. It may follow a diastolic murmur (see Figs. 19, 20 
 and 21). As a rule there is a sound-free interval be- 
 tween the decrescendo diastolic murmur and the 
 crescendo murmur. Sometimes, however, there is, to 
 the ear, no interval between the murmurs^ and a con- 
 tinuous murmur apparently runs from after the second 
 sound to the accentuated first sound. This is one reason 
 advanced in support of the auricular systolic or pre- 
 systolic rhythm theory of the murmur, for it is said that 
 such an apparently continuous sound must be produced 
 by blood flowing in the same direction through the 
 valve. This argument can be used to prove that it is 
 early systolic in rhythm (see paragraph 3 below). 
 
 When the diastolic murmur is apparently continuous 
 with the crescendo murmur, it probably means that the 
 auricle is able to contract in its proper rhythm — namely, 
 just before v.s., and so keep u]) the true diastolic 
 murmur. 
 
 Very often in mitral stenosis the auricle is so dilated 
 and weakened as to he unable to contract ivith sufficient 
 
CRESCENDO MURMUR 81 
 
 force to help in cmt-nng a diastolic murmur. I believe 
 that this explains the frequent absence of this murmur 
 in mitral stenosis. 
 
 3. A crescendo murmur may he uninterruptedly folloiced 
 by a systolic murmivr. This occurs when the curtains are 
 so distorted by disease that, although their edges are 
 brought into apposition abnormally late in ventricular 
 systole (crescendo murmur), they still are unable to com- 
 pletely close the orifice, and a leak is left through which 
 blood continues to regurgitate throughout ventricular 
 systole and continues the crescendo murmur as a systolic 
 murmur (see Fig. 14, E and F). These two murmurs 
 are produced at the mitral valve by the continuous action 
 
 J 
 
 T— -I p-r \ \ ; 1 r— ! p-i — ^ 1 r—, r*— , . 
 
 Fig. 21. — CRESCExno Murmur (early v.s. Rhythm), Double Second 
 Mitral Diastolic, Sound-free Interval, then" Crescendo 
 Murmur again, followed by Systolic Murmur, etc. 
 
 The first is the commoner condition, the continuous diastolic and cres- 
 cendo murmur, depicted in the second cycle, being not so common. 
 
 of the ventricle in its successive stages of systole, and 
 are continuous, though so very dissimilar in character. 
 The impact of those portions of the thickened valve 
 curtains which can come into apposition causes the 
 accentuated first sound which delimits these murmurs. 
 
 4. A systolic murmur may change into a crescendo 
 murmur within a few heart-beats and vice tersa. When 
 the ventricle is not contracting with sufficient force 
 to close the valve, a systolic murmur of regurgitation 
 is heard. If the force of contraction be increased, as by 
 making the patient sit up in bed, the valve is then 
 closed and the crescendo murmur developed. When the 
 
 6 
 
82 HEART DISEASE 
 
 patient lies down and the extra force of ventricular 
 systole is reduced, the systolic murmur again appears. 
 To put it in another way, a systolic murmur may be 
 heard when the patient is up and about and overworking 
 the heart, Avhich is replaced by a crescendo murmur 
 after rest in bed and treatment by digitalis. 
 
 5. Crescendo, systolic, and diastolic murmurs may all he 
 heard during one cardiac cycle, with accentuated first 
 and double second sounds (see Fig. 21). 
 
 Prognosis of crescendo murmurs, — The presence of a 
 crescendo murmur means that the ventricle is contract- 
 ing well and that regurgitation through the valve is 
 reduced to a minimum, and less than when a systolic 
 murmur is heard. I look upon it as a favourable sign, 
 for it often is only heard after overworked heart muscle 
 recovers its tone through rest in bed and treatment. 
 
 Tricuspid Muemuks. 
 
 Lesions of the tricuspid valve are much less common 
 than those of its fellow valve, and are often difficult to 
 diagnose. They are, however^ often accompanied by 
 evidence of back-pressure in the pulmonary arterial 
 or systemic venous circulations, and this evidence is 
 useful. 
 
 Tricuspid systolic murmurs are best heard over the 
 heart between the apex and the tricuspid region. They 
 are similar to mitral murmurs in origin and charac- 
 teristics, but are not transmitted through the axillary 
 region. They are often hard to differentiate from 
 mitral murmurs, and often heard with them. 
 
 When a systolic murmur is heard to the right of the 
 sternum, and there is evidence of enlargement of the 
 
TRICUSPID AND AORTIC MURMURS 83 
 
 right auricle and pulmonary and general venous conges- 
 tion, it is almost certainly due to tricuspid incompe- 
 tence. 
 
 Tricuspid diastolic murmurs are similar in char- 
 acteristics to mitral murmurs, but may be conducted 
 slightly to the right of the sternum, especially with 
 dilatation of the right auricle. They are not common. 
 
 The tricuspid crescendo murmur is of similar origin 
 and characteristics to the mitral murmur of the same 
 name. 
 
 With both diastolic and crescendo murmurs there 
 would be evidence of systemic venous congestion, 
 enlargement of the liver and general oedema, and also 
 of pulmonary circulation congestion. 
 
 The prognosis of tricuspid murmurs is not good, as 
 disease of this valve impedes the return of venous blood 
 to the lungs and induces general oedema and secondary 
 cardiac muscle failure. 
 
 Aortic Murmurs. 
 
 Lesions of the aortic valve are not so common as those 
 of the mitral valve. 
 
 Aortic systolic murmurs vary in nature according to 
 their causes. In relative stenosis, due to dilatation of 
 the aorta, they ought to be of the softer fluid-vein type ; 
 but, as a matter of fact, when relative stenosis occurs at 
 this valve, there is generally some atheroma of the aorta 
 as well which affects the curtains of the valve also, 
 roughening and stiffening them more or less, and giving 
 rise to the rougher, more intense vibration murmur of 
 actual stenosis. Sometimes they are of a musical char- 
 
84 HEART DISEASE 
 
 acter, in which case a tag of fibrin may be vibrated by 
 the blood- stream. When actual stenosis exists, or Avhen 
 the curtains are much changed, a thrill can often be felt 
 over or above the aortic area. 
 
 They are best heard in the aortic area, whence they 
 are conducted into the great arteries, and are especially 
 well heard over the carotids without any pressure from 
 the stethoscope. 
 
 They may be heard down the cardiac area to the apex- 
 beat, gradually diminishing in intensity all the way. It 
 is therefore important to listen to an apex murmur over 
 different portions of the pra^cordia between the apex and 
 the aortic area. A murmur which grows in intensity 
 when followed in this way indicates an aortic (or 
 pulmonary) murmur, and one which diminishes a mitral 
 (or tricuspid) murmur. 
 
 Aortic sj'Stolic murmurs are of a decrescendo nature, 
 fading away with cessation of v.s. 
 
 If an aortic systolic murmur be due to actual stenosis, 
 the radial pulse is regularly delayed. 
 
 Time. — Aortic systolic murmurs are synchronous with 
 the carotid pulse, and should always be timed by it, 
 because a loud diastolic murmur may alone be present 
 and simulate one. 
 
 Aortic diastolic murmurs vary in intensity from a 
 loud, rough, easily audible sound to the faintest whiif, 
 which is the most difficult of all cardiac murmurs to 
 recognize. The difficulty of hearing the short faint aortic 
 diastolic murmurs is increased by the fact that they 
 may be audible only at the tricuspid region of the heart, 
 and they are very commonly overlooked. Their presence 
 may be suspected by the change in the second sound 
 when they are associated with one. The sound is no 
 
AORTIC MURMURS 85 
 
 longer distinct and clear; it is impure, and apparently 
 prolonged into a whiff or faint blow, as if the ^' bottom 
 were knocked out " of the sound (see Fig. 18). 
 
 An aortic diastolic murmur is particularly difficult to 
 hear if there be a co-existent mitral diastolic murmur. 
 
 This short diastolic murmur may be cau.^ed by a similar 
 mechanism to that which produces an a.-v. crescendo 
 murmur, and have some of the rising pitch character- 
 istic of this murmur (p. 59). The short duration of it 
 can hardly be due to inability of the contracting aorta 
 to keep up the murmur, for aortic diastolic murmurs 
 are generally more prolonged. 
 
 The important difference in rhythm hetiveen aortic and 
 mitral diastolic murmurs — namely, that the latter begin 
 at a later phase of ventricular diastole than the former — 
 has already been pointed out, and reasons why such 
 should be so given (see Figs. 16 and 18). 
 
 Condition of ttie aortic valve at wliicli regurgitation 
 occurs, — The diastolic murmur may continue a distinct 
 aortic second sound, in which case the curtains are mobile 
 and more or less normal, perhaps with dilatation of the 
 valve ring ; or there may be no aortic second sound, in 
 which case the leakage results from a stenosed valve with 
 thickened, rigid, immovable curtains. The latter form 
 of murmur is rougher than the former. 
 
 Sometimes the aortic diastolic murmur is the only 
 murmur present, and, unless it be timed by the carotid 
 artery, will very likely be mistaken for a systolic murmur, 
 especially by the student, who is inclined to look upon 
 all murmurs as systolic unless they prove themselves to 
 be diastolic. 
 
 Like all other murmurs, except the crescendo murmur, 
 they are of diminishing intensity, or decrescendo. 
 
S6 HEART DISEASE 
 
 Crescendo aortic murmurs. — The possibility of an 
 aortic diastolic murmur having some rising pitch char- 
 acter has already been referred to above and in the 
 paragraph on crescendo murmurs (p. 85). 
 
 See=saw or *' To=and-fro" murmur, — Not uncom- 
 monly the aortic diastolic murmur follows immediately an 
 aortic systolic murmur^ giving a to-and-fro characteristic 
 known as the " see-saw murmur." If the lesion be one 
 of absolute stenosis with incompetence, an aortic second 
 
 Fig. 22.— See-Saw Aoktic Mukmuk, continuous, no Sounj>s, but 
 THE Diastolic I'oiiTioN akises immediately at the End of v.s., 
 
 AND not after A SoUND-FllEE InTEUVAL, AS IN MlTllAL DIASTOLIC 
 
 MuiiMuns. 
 
 sound is rarely heard. If it be one of relative stenosis 
 with aortic dilatation or aneurysm, a sound may in- 
 tervene. 
 
 Prognosis of aortic murmurs. — Aortic systolic mur- 
 murs generally indicate actual obstruction to the flow of 
 blood from, and increase in the work done by, the left 
 ventricle. Sliglit obstruction may be easily compensated 
 by ventricular hypertrophy, and if this is adequate the 
 condition may not affect the duration of life. When 
 greater, the ventricle may be unable to respond ade- 
 quately; it fails or dilates, and the outlook is bad. 
 
 When aortic systolic murmurs indicate relative obstruc- 
 tion of the orifice with a dilated aorta or an aneurysm 
 beyond, the prognosis is serious. 
 
 Aortic diastolic m?tr//iwr.9, indicating incompetence of the 
 valve, are more serious. Slight degrees of regurgitation 
 
POSTURE MURMUR 87 
 
 may be adequately counteracted by efficient ventricular 
 hypertrophy, and may be present for years without 
 adversely affecting the health. When the leakage is 
 greater the strain on the left ventricle is very great, and 
 adequate compensation becomes impossible. The out- 
 look is then most serious, sudden overstrain of the heart 
 with fatal syncope being a common ending. 
 
 The condition of the muscle of the left ventricle is the 
 determining factor in prognosis of both forms of aortic 
 disease, as it is in all other forms of valvular disease. 
 
 Posture murmur. — A very well-marked systolic mur- 
 mur, simulating exactly an aortic murmur, is sometimes 
 heard over the manubrium sterni and base of the heart 
 in quite healthy persons who are holding the shoulders 
 well back, and probably thereby causing some pressure 
 of the collar-bone on the subclavian artery. Such a 
 murmur may be heard when the subject being examined 
 is holding his vest well up for auscultation at the base 
 of the heart. It disappears at once if the shoulders are 
 brought forward to remove the pressure. The murmur 
 is so deceptive that it may create the impression of some 
 aortic valve disease. (See also p. 67.) 
 
 Pulmonary Murmurs. 
 
 Pulmonary murmurs are very much like those pro- 
 duced at the aortic valve in nature. Structural changes 
 in the valves do not often arise in adult life, and when 
 met with then are almost always congenital in origin. 
 
 Pulmonary systolic murmur. — This is not uncom- 
 monly heard in marked anaemia, when it is caused by 
 relative stenosis of the valve orifice, the pulmonary artery 
 beyond the valve frequently dilating, for some reason or 
 other not understood, in anemic conditions of the blood. 
 
88 HEART DISEASE 
 
 It may be met with in apparently healthy persons, and 
 may mean nothing ; and it is also commonly heard in 
 mitral stenosis. It is frequently heard in Graves' disease. 
 
 A systolic murmur due to structural changes of the 
 curtains is by no means common in adult life, but is 
 more often heard in childhood. 
 
 Actual stenosis of the valve occurs as a congenital 
 deformity, but generally causes death before adult life. 
 It may be present in young adults, when cyanosis will be 
 a marked feature of the circulation. 
 
 Conduction, — Pulmonary systolic murmurs are not 
 conducted into the carotid or subclavian arteries, but are 
 conducted or transmitted over the left second intercostal 
 space well away from the sternum. 
 
 Pulmonary diastolic murmurs are very rare, but 
 when heard have much the same area of conduction, 
 down the left margin of the sternum, as the analogous 
 aortic murmur, with, however, the pulmonary cartilage 
 as the theoretical seat of maximum intensity. 
 
 Prognosis. 
 
 Prognosis in pulmonary murmurs. — If due to anaemia 
 the prognosis is that of the primary cause. If due to 
 structural changes it is bad, and subjects of pulmonary 
 valve disease rarely reach adult life. 
 
VIII 
 HiEMIC MURMURS 
 
 Cardiac haemic murmurs, which are of a soft, blow- 
 ing character, are met with in anaemic conditions of the 
 blood, and without there being any disease of the valve 
 curtains. They are systolic in rhythm, and not con- 
 ducted widely. Their causation has been much debated. 
 It is very doubtful, as has already been stated, whether 
 the diminished viscosity of the blood itself has anything 
 to do with the production of the murmur. Moreover, it is 
 important to remember that in chlorosis, in which these 
 murmurs commonly occur, there is sometimes tivo or 
 three times the normal volume of blood present, and this 
 may lead to abnormal distension of cavities and so to the 
 easier production of fluid-veins, especially at the semi- 
 lunar valve orifices. 
 
 The commonest situation for them to be heard is at 
 the base of the heart over the pulmonary cartilage and 
 in the second left intercostal space. The murmur thus 
 heard is probably due to there being relative stenosis of 
 the pulmonary valve, experience having shown that this 
 artery immediately beyond its valve is often dilated in 
 marked angemia. 
 
 A haemic murmur may also be heard over the apex 
 in severe anemia. In these cases there is generally some 
 dilatation of the ventricle, and the murmur is one of 
 valvular incompetence arising from muscle failure. 
 
 89 
 
90 HEART DISEASE 
 
 They are often heard best with the quicker hearths 
 action of the erect position, and disappear when the 
 patient lies down, or the heart's action slows. 
 
 Vascular haemic murmurs are heard over the large 
 vessels with or without slight pressure from the stetho- 
 scope. If pressure is used the constriction of the 
 vessel produces a fluid vein. 
 
 Bruit de diable- — This is best heard over the veins 
 about the attachment of the sterno-mastoid to the 
 sternum, and without any pressure from the stethoscope. 
 It is of a continuous humming or buzzing character and 
 is probably only heard in chlorosis where we have an 
 increased volume of blood, sometimes more than double 
 the normal amount, in addition to diminished viscosit^^ 
 It is possible that the continuity of the hum is due to the 
 abnormal distension of the large veins in this disease 
 forming large masses of blood into which comparatively 
 small streams pass from the tributary veins with an 
 abnormal head of pressure produced in the overfull 
 capillaries. Diminished viscosity may also contribute 
 in some unknown way to its production. 
 
 The hum can also be heard by placing the stethoscope 
 lightly over the ball of the eye, the mastoid region, or 
 on the occiput over the site of the torcular Herophili. 
 In these situations the stethoscope is close to the cavern- 
 ous sinuses of the skull. 
 
 The hridt de diahle is rarely met with in severe anaemia 
 without increased volume of blood ; in these cases, in- 
 stead of a continuous hum, the murmur over the veins is 
 of a broken, swishing, rhythmic nature. 
 
 Like true chlorosis, it is uncommon in Manchester. 
 
IX 
 EXOCARDIAL SOUNDS 
 
 These sounds are produced outside the cavities of the 
 heart. 
 
 Pericardial sounds. — Normally the smooth surfaces 
 of the visceral and parietal layers of the pericardium 
 move over each other without any audible sound^ but 
 when this membrane is inflamed, as it is in pericarditis, 
 and becomes rough, then the movement of the two 
 roughened surfaces against each other causes a sound 
 known as a pericardial rub or friction sound. 
 
 This pericardial rub varies greatly in character from a 
 very slight, almost inaudible sound to a marked, rough, 
 leathery creaking, the latter being occasionally so well 
 developed as to be palpable to the hand. 
 
 The pericardial rub frequently simulates an endocardial 
 sound, but usually is easily differentiated from it. 
 
 It is generally a double or to-and-fro sound, corre- 
 sponding roughly with systole and diastole of the heart, 
 and is well imitated by rubbing the balls of the thumbs 
 over each other and in a to-and-fro movement with vary- 
 ing degrees of pressure. 
 
 In some instances one or other parts of the sound may 
 be double, imparting to it a shuffling character. 
 
 Pericardial friction is generally best heard over the 
 base of the heart, and often can be intensified by gentle 
 
 91 
 
92 HEART DISEASE 
 
 pressure u-ith the stethoscope, wliich has for its object the 
 bringing of the two layers of the pericardium more 
 closely together. It is unchanged by holding the 
 breath, and may only be heard for a day or so. 
 
 When fluid develops and, by distending the pericardial 
 sac, separates the two sufaces the rub will disappear, 
 possibly to reappear with the absorption of the fluid. 
 
 The sound is not conducted away from its seat of 
 origin unless it be very loud, in which case it may be 
 transmitted slightly beyond the limits of the pr^cordia. 
 
 Cardio-Pespiratory sounds. — Occasionally sounds are 
 produced by the movements of the heart acting on the 
 lungs or pleura which may simulate endocardial or 
 pericardial sounds ; but they are, as a rule, easily 
 differentiated from the endocardial sounds because they 
 vary with the respiratory movements, and because 
 the sounds of the heart are heard as usual. 
 
 Card io= pulmonary sounds. — Respiratory sounds syn- 
 chronous with systole of the ventricle may be heard 
 when an emphysematous lung comes forward over the 
 heart and is compressed by the movements of the heart. 
 
 Such a sound may simulate an endocardial murmur, 
 but it is loudest with expiration and disappears when 
 the breath is held on full inspiration. It may also 
 resemble the creaking of a saddle. 
 
 CardiO'pleural sounds. — With inflammation of the 
 pleura over the front of a lung a sound of friction may 
 be caused by the movements of the heart pressing the 
 two pleural surfaces together. Such a sound may closely 
 simulate a pericardial rub and will not vary with inspira- 
 tion . 
 
SEPTIC ENDOCARDITIS, 
 PERICARDITIS, ANGINA PECTORIS 
 
 Septic, maligrnant, op ulcerative Endocarditis is 
 
 not uncommonly met with, especially in the practice of a 
 general hospital. It is also, unfortunately, not uncom- 
 monly unrecognized during life, as an elevated tempera- 
 ture, often in the form of rigors, and evidence of great 
 debility are the only physical signs present. The heart 
 sounds may be quite free from murmur. 
 
 In typical cases with elevated temperature, murmurs, 
 enlarged spleen, hematuria and infarcts the diagnosis is 
 straightforward . 
 
 Its presence must always be suspected when there is 
 prolonged elevation of temperature in cases of chronic 
 valvular disease. 
 
 Treatment is very unsatisfactory. In some of the 
 cases complicating chronic endocarditis the acuteness 
 subsides and the chronic condition remains much as 
 before, but the acute cases arising de novo almost in- 
 variably end fatally. Vaccine treatment by autogenous 
 vaccines where the organism can be isolated, which is, 
 however, very difficult to do, is reported to have relieved 
 a few cases, but all treatment is as a rule unavailing. 
 
 93 
 
94 HEART DISEASE 
 
 Pericapditis generally occurs as a complication of 
 rheumatic infection, but may be found in gout, cachectic 
 conditions and (N.B.) acute pneumonia. 
 
 Simple acute pericarditis results in the exudation of 
 lymph which in the most favourable cases is soon re- 
 absorbed without any permanent damage. Its presence 
 is recognized by the associated endocarditis, by some 
 respiratory distress, and by pericardial friction {q.v.), 
 which may be heard with the stethoscope. Pain is not 
 a prominent symptom, and for this reason pericarditis 
 is often overlooked. In less favourable cases the 
 inflammation may become dry and persist for a longer 
 time, clearing up eventually or leading to the formation 
 of adhesions and adherent pericardium. Dry pericarditis 
 may be felt by the hand, causing a rubbing sensation be- 
 hind the praecordia, and it can be heard by the stethoscope. 
 
 The danger to the patient in most cases is not the 
 actual pericardial inflammation itself, but the fact that 
 it is evidence of an acute inflammation of the whole of 
 the cardiac tissue — endo-, myo-, and pericardium. A 
 patient with acute pericarditis is always in danger, the 
 termination being not infrequently remarkably sudden. 
 
 Pericardial effusion. — The inflammation of the peri- 
 cardium may lead to effusion of serous fluid in greater 
 or less amount. Fluid may be suspected if a rub passes 
 off in a day or so and reappears in a few days. If it is 
 poured out in large quantity it causes increased cardiac 
 dulness, especially in an upward direction^ by distending 
 the sac into a pear-shaped body which can be made out 
 by percussion, the broad part being about the line of the 
 fourth intercostal space. The intercostal spaces of the 
 pra3Cordia may be distended. The impulse of the apex- 
 beat diminishes in intensity and is internal to the limits 
 
ADHERENT PERICARDIUM 95 
 
 of cardiac dulness. The heart sounds are muffled or 
 weakened, and the apex may be pushed up and out. 
 There is a good deal of respiratory distress, due to the 
 interference with the hearths action, which makes the 
 sitting-up (orthopnoea) position necessary. The pulse is 
 also quick, 120 or more, and there is much pallor. 
 Serous effusions tend to be absorbed in time, and opera- 
 tive interference — paracentesis pericardii — is not often 
 advisable. 
 
 Purulent pericarditis is often only recognized post 
 mortem, and its diagnosis in life is quite uncertain. 
 
 Adherent pericardium is most likely to be met with 
 before adolescence, but it is more often found in the 
 post-mortem room than diagnosed in the wards. Patients 
 in whom it is present rarely reach adult life. It may be 
 suspected when severe rheumatic inflammation of the 
 endocardium, myocardium, and pericardium has led to 
 considerable dilatation of the heart which persists per- 
 manently after subsidence of the acute symptoms, and 
 in spite of treatment by prolonged rest in bed and 
 especially by digitalis. Uncomplicated dilatation of the 
 ventricles often recovers very well after such treatment, 
 but if the inflamed pericardium covering the enlarged 
 ventricles adheres to the inflamed outer layer of the 
 pericardial sac subsequent shrinking of the muscle 
 becomes impossible. 
 
 In adherent pericardium there may be systolic retrac- 
 tion of the intercostal spaces between the left lateral 
 sternal line and the region of the apex of the enlarged 
 heart, with synchronous protrusion of the apex of the 
 heart. Such a condition, however, may be met with 
 when there is considerable cardiac enlargement with no 
 pericardial adhesion, the systole of the base of the 
 
96 HEART DISEASE 
 
 enlarged right ventricle causing negative pressure in the 
 chest which leads to retraction of the intercostal spaces 
 in front of it. When the heart is much enlarged and 
 the two layers of the pericardium are coherent con- 
 traction of the heart may pull on the diaphragm^ and 
 consequently on its attachments to the ribs in the axillary 
 and posterior regions of the chest_, causing systolic in- 
 drawing of the regions of the diaphragmatic attachment. 
 
 On auscultation a systolic murmur, indicating incom- 
 petence through dilatation of the mitral valve, will 
 generally be heard. 
 
 There are also present signs of interference with the 
 action of the heart muscle leading to back pressure in 
 the pulmonary and systemic circulations. 
 
 Pericardial adhesion may be a part of a process leading 
 to a general mediastinal inflammation which has a 
 special group of symptoms, or of a process leading to 
 inflammation of all the serous membranes of the trunk, 
 — the pericardium, pleura and peritoneum. 
 
 Angfina pectOPis is the term given to the extremely 
 distressing and painful condition which results from 
 interference with the circulation of blood through the 
 heart muscle itself by some obstruction of the coronary 
 arteries or by overworking a heart with enfeebled 
 muscle. The pain is of two kinds — a heavy, suffocating 
 feeling behind the sternum or of something gripping 
 the heart and giving rise to a sensation of impending 
 death; and shooting neuralgic pains down the arm, 
 especially the left arm, to the elbow or even to the little 
 and ring fingers, up the neck behind the ear, and into 
 the left shoulder-joint. 
 
 Diagnosis, — Angina pectoris may occur without there 
 being the slightest auscultatory evidence of any cardiac 
 
ANGINA PECTORIS 9? 
 
 disease ; when there is evidence of aortic disease, 
 atheroma, or aneurysm ; of mitral stenosis or of severe 
 cardiac muscle failure or debility. It is not uncommonly 
 fatal in its first appearance, but more often it recurs at 
 intervals over longer or shorter periods of time. It is 
 generally made worse by exertion, but it may be brought 
 on through the interference with the hearths action 
 which a stomach distended with flatulence often gives 
 rise to. 
 
XI 
 
 CARDIAC IRREGULARITY 
 
 RESULTING FROM DISTURBANCES 
 
 OF STIMULATION 
 
 Electrocardiogram. — The different phases of the 
 cardiac cycle can be timed with great accuracy by means 
 of the property which muscle has of giving rise to 
 currents of electricity by its contraction. These currents 
 are very slight, and they need the most delicate instru- 
 ments for receiving and recording them. The instrument 
 now used, the string-galvanometer, is an elaboration and 
 improvement of that originally used as a receiver in the 
 first days of transatlantic telegraphy. The principle of 
 it is that the minute current of electricity generated by 
 the muscle contraction is carried on a silvered filament 
 of rock crystal or on some suitable wire between the 
 live poles of a strong electro-magnet and according to 
 whether the current passing is + or — so will the string- 
 be deflected to the — or + pole. The movements of the 
 string are recorded by the shadow which is cast by it, 
 on a moving sensitized roll of photographic paper between 
 which and a light it also lies. The tracing is very small, 
 and has to be magnified subsequently to get the record 
 which is to be used for observation. 
 
 With a normal heart contracting, a regular type of 
 
 98 
 
RAPID HEART-BEAT 99 
 
 electrocardiogram is obtained showing movements which 
 are caused by the currents induced by contraction and 
 relaxation of the auricles and ventricles. Departures 
 from the normal rate, rhythm and method of contraction 
 of the auricles or ventricles show corresponding depar- 
 tures from the normal cardiographic tracing. 
 
 An electrocardiogram is generally taken synchronously 
 with one or more other tracings taken from the carotid 
 or radial artery or the jugular vein ; a phonoscope re- 
 cording the sounds produced in the heart may be used 
 at the same time as well. The most elaborate tracings 
 give all of these synchronously with a time record also. 
 
 The electrocardiograph is a very valuable instrument 
 for the investigation of cardiac disease, but its cost 
 (£200) and the laboratory accommodation necessary for 
 its use practically restricts its employment to hospitals. 
 
 Tachycardia means quick hearths action, over 130 a 
 minute, but its use as a term is best restricted to a more 
 rapid action which is the result of some patholoD*ical 
 change in the hearths nervous mechanism or musculature. 
 
 The apprehensive heart.— A very rapid beat is often 
 met with in a heart unaffected by disease when the 
 patient is of a nervous, apprehensive type. The so-called 
 insurance heart and the legal neurasthenic heart are 
 of this nature. I have counted a pulse of above 160 in 
 a girl who was being treated with zinc ionization for 
 oesophageal ulcer. The heart was structurally normal 
 and slowed down to its proper rate within a couple of 
 hours after the exciting experience. A rate of 130 is 
 not uncommon in insurance work. In this type of rapid 
 heart action the quickness varies even within a few^ 
 seconds. The heart may slow down almost to normal 
 after a time, or when the subject lies down, only to race 
 
100 HEART DISEASE 
 
 off again within a few seconds. The relative spacing of 
 the heart sounds is normal. The increased stimuli do 
 not originate in the heart. 
 
 In Graves' disease the pulse is often very rapid — from 
 120 upwards. I have counted it at 150 or more when 
 the patient has been excited, as by a visit to a physician. 
 The rhythm is regular, and the rate persists uniformly, 
 without slowing down to near the normal as with the 
 apprehensive heart. The rapid action is not caused by 
 abnormal conditions in the heart. 
 
 Paroxysmal tachycardia is the term given to a con- 
 dition in which the Avhole heart, auricles and ventricles, 
 jumps from about a normal rate to one of 150 or more, 
 and continues at this rate for a longer or shorter period, 
 and in spite of all attempts to slow it down by treatment. 
 Thus, I was once listening to a heart to make sure if a 
 murmur was present when it instantaneously jumped 
 from a rate of 80 to 170 a minute. It continued in 
 hospital for three weeks at this pace, in spite of complete 
 rest in bed and all drug treatment, and then stopped of 
 its own accord, and, as far as I could gather, equally 
 suddenly. I subsequently saw this case several times, 
 and during the last illness, and I thought it was one of 
 mitral stenosis ; but it proved to be one of a congenital 
 septum in the left auricle, with only a small aperture, 
 about half an inch in diameter, for the blood to pass 
 through. There was great enlargement of the liver 
 during the longer paroxysms. 
 
 The paroxysms of rapid action may last from a minute 
 or so to days or months. The rate is not materially 
 altered when the patient changes from the erect to the 
 lying position or vice versa. The stimuli to contraction 
 arise from some other j^art of the heart than the sino- 
 
HEART-BLOCK 101 
 
 auricular node, but there is one beat of the ventricles to 
 every one of the auricles. There is generally some 
 lesion in the muscle or nerve tissue of the heart. 
 
 Abnormally slow pulse. — Many healthy people of a 
 phlegmatic, stolid type have a pulse-rate below 60, and 
 a similar slow beat is often found in athletes used to 
 prolonged exertion. I have seen it in several cross- 
 country runners, and tennis or racquet players, and 
 also after acute illnesses with a high temperature. The 
 whole heart, auricles as well as ventricles, partakes of the 
 abnormal slowness. 
 
 Bradycardia is the term applied to a very slow pulse 
 (40 or less), and its use is best confined to cases in which 
 there is some pathological cause, such as heart-block 
 (q.v.), acting to produce the slow pulse. The beat of 
 the auricles is more frequent than that of the ventricles. 
 
 Heart-block means the interruption of the passage of 
 stimuli from the a.-v. node through the a.-v. bundle to 
 the ventricles, with the result that the ventricle con- 
 tracts only a fraction of the number of times stimuli 
 from the auricles try to pass to it. If the block be com- 
 plete so that no stimuli pass from auricles to ventricles, 
 the latter continue to beat a rhythm of their own, which 
 is usually about 30 per minute. In its severe forms it is 
 due to some disease, of sclerotic, calcareous, or gum- 
 matous nature, interrupting the integrity of the a.-v. 
 bundle, and the number of beats of the ventricles may 
 be reduced to 9 or 10, as in a case under my care. 
 It may be associated with epileptiform convulsions in the 
 type of disease known as Stokes- Adams disease. 
 
 Irregular or intermittent pulse — Premature or 
 extrasystole. — In feeling a pulse it is a very common 
 
102 HEART DISEASE 
 
 occurrence to find that a beat is missed, and simul- 
 taneously the patient has an unusual sensation in the 
 chest as if the heart stopped for a second and then gave 
 an extra forcible beat. To this condition the term 
 ^^ dropped beat " is often given, but it does not correctly 
 describe what has happened. If the stethoscope be 
 used whilst the pulse is being felt, a very feeble beat of 
 the heart will be heard to follow prematurely a normal 
 beat, and then a long pause comes before another normal 
 beat. This early beat is best called a premature systole, 
 as it is not an eMra systole. It may be too feeble to open 
 the aortic valve, when a feeble first sound alone is heard ; 
 or it may be strong enough to open the valve and 
 cause a slight second sound but no real pulse-wave. 
 Any accompanying murmur will be modified also in a 
 similar way. The premature systole is brought about 
 by a stimulus arising in some part of the heart other 
 than the sino-auricular node and before its proper time. 
 The premature systole form of cardiac irregularity of 
 itself, that is, provided there is no evidence of cardiac 
 muscle disease, namely, abnormal frequency of heart- 
 beat, want of diastolic rest (tic-tac rhythm), valvular 
 disease, muscle failure, need not alarm, as it is met with 
 very frequently in apparently normal hearts. A very 
 common cause is a reflex action of some functional dis- 
 order of the stomach, especially flatulence. Tobacco is 
 probably another cause, acting directly on the heart or 
 reflexly through disturbance of the digestion. A. single 
 premature sj^stole, occurring occasionally, is the simplest 
 form of the condition, and the next is a more frequent 
 repetition of the premature beat, varying to a state in 
 which beats are dropped regularly every few or more 
 (4 to 20) heart-beats, and which persists for years, or in 
 which three or four premature systoles will occur con- 
 
PREMATURE SYSTOLE 03 
 
 seciitively witli a flattering sensation. Such a condition 
 often runs in families, tending to be more persistent as 
 its subjects, often liable to sujDpressed gout, grow older, 
 when there are degenerative changes in the cardiac 
 muscle. By suppressed gout I mean a diathesis in 
 which the metabolism of food is not carried to its proper 
 end-formation of urea, but stops in a variation of the 
 sodium biurate formation of true articular gout. Sup- 
 pressed gout may lead to a variety of ailments, affecting 
 every system of the body, which develop after a period 
 of consumption of food which, though not immoderate, 
 is in excess of the demand for the body in later adult 
 years. Premature heart-beats is one of the commonest 
 of these suppressed gout manifestations. 
 
 Such irregularity generally passes off on exertion, and 
 may pass off during an acute illness, or in older people 
 may be made worse. I have seen an old patient of 
 seventy-three, whose heart had been more or less ir- 
 regular for many years, pass safely through an attack 
 of acute pneumonia in which there were very few suc- 
 cessive regular cardiac cycles for three or more days. 
 The heart seemed to roll over and over in a state of 
 delirium cordis. With convalescence the usual degree 
 of irregularity returned. 
 
 Whilst cardiac irregularity means nothing serious 
 with healthy heart muscle, it is serious when other signs 
 of muscle failure, such as breathlessness on exertion, 
 absence of diastolic rest, etc., are present. 
 
 Sinus arrhythmia. — Another form of irregularity is 
 that arising from the sinus ; it occurs chiefly in young 
 people, and may be produced by such a physiological 
 action as swallowing. Here diastole onl}^ is prolonged, 
 systole being of the normal length. 
 
 It has no evil prognostic significance. 
 
104 HEART DISEASE 
 
 AupiculaP fibrillation is tlie term given to a condition 
 in which the contraction of the auricles is so feeble and 
 indefinite that the muscle is thrown into a state of fibril- 
 lation or twitching of a very rapid nature. The auricle 
 now ceases to contract as a whole and the a. wave dis- 
 appears from a jugular tracing. In many if not all of 
 the cases there is some stretching of the muscle fibres 
 and dilatation of the cavities of the auricles, with also 
 some chronic inflammatory process of a fibrotic nature. 
 The auricular tissue becomes very excitable and re- 
 sponds to stimuli which arise with very great rapidity 
 (200 to 300 per minute)' from somewhere else than the 
 sino-auricular node_, possibly in the auricular muscle 
 itself. The conducting tissue between the auricles and 
 ventricles in the majority of cases is not damaged and 
 conducts a greatly increased number of stimuli to the 
 ventricles. These stimuli are of unequal strength and 
 catch the ventricles at phases of their cycle when they 
 cannot respond properly to any stimulus. The result is 
 usually increased frequency (90 to 150) of ventricular 
 action with extreme irregularity of rhythm and of com- 
 pleteness of contraction. The pulse becomes quick and 
 very irregular, with scarcely two beats of a similar 
 nature following successively. The irregularit}^ of force 
 of ventricular contraction may only be fully appreciated 
 by using the stethoscope at the same time that the pulse 
 is being felt. A very irregular pulse of over 1 20 in rate 
 is almost certain to be of auricular fibrillation origin. 
 Increased strain on the heart, such as is caused by exer- 
 cise, increases the number of beats and also the irregu- 
 larity of the hearths action. 
 
 Auricular fibrillation occurs most commonly in hearts 
 affected by rheumatism, but it may occur when there is 
 no evidence of this disease. In the rheumatic cases it is 
 
AURICULAR FIBRILLATION AND FLUTTER 105 
 
 very common in mitral stenosis and between the ages 
 of twenty and sixty, whilst in the non-rheumatic cases 
 its incidence is later — between fifty and seventy. The 
 quick, irregular pulse of mitral stenosis is a typical 
 example of the condition. Although the pulse is gener- 
 ally quick, it maybe slower and more regular; but there 
 will always be found some irregularity in the duration 
 of the cardiac cycle if careful measurement of the length 
 of the arterial pulse- waves be made. In a few cases 
 with impaired conduction through the a.-v. bundle the 
 pulse-rate may be below normal. 
 
 With auricular fibrillation there are generally present 
 some of the usual signs of cardiac failure and back 
 pressure on the circulation. 
 
 It may persist for several j^ears in cases of mitral 
 stenosis which react to digitalis and are carefully treated 
 and dieted ; the subjects of it may be quite able to keep 
 up aud about and follow some clerical occupation. 
 
 Aupicular flutter is the term given to a much less 
 common condition which occurs chiefly in the later 
 years of life, over fifty, when there is some senile arterio- 
 sclerosis and cardiac muscle degeneration with or without 
 valvular disease. The auricle contracts so very rapidly 
 (260 to 320 per minute) to stimuli which arise — probably 
 from some single focus in its own tissue — that it is in a 
 state of flutter. It is almost always associated with 
 some degree of heart-block, so many stimuli being unable 
 to pass through the a.-v. bundle, and the ventricle only 
 contracts one-half, one-third, or a less fractional number 
 of times of the auricular rate. It is difficult to distin- 
 guish from paroxysmal tachycardia. The ventricular 
 beating is often regular in rhythm and completeness of 
 contraction. Even when irregular, the irregularity is 
 
106 HEART DISEASE 
 
 more or less regular in its appearance. The attacks may 
 last for a few hours or for months or years; in the 
 former case they may occur from time to time for several 
 years. In one of Dr. Lewis's cases the ventricular rate was 
 160 for four years. If the ventricles take on the full 
 auricular rate the attack is very serious, causing faintness, 
 and if it should persist for more than a few hours death 
 is likely to ensue. Firm pressure on the carotid artery 
 passing on to the vagus produces a slowing of the pulse. 
 Digitalis often controls the rapidity of the heart-beat 
 very efPectively. 
 
 Further information on the cardiac affections referred 
 to in this section should be sought for in Dr. Thomas 
 Lewis\s valuable small work, '' Clinical Disorders of the 
 Heart-Beat/' or in Sir James Mackenzie's much larger 
 book on " Diseases of the Heart." I am indebted to 
 Dr. Lewis's work for some of the information in this 
 section, especially in the paragraphs on Auricular Fibril- 
 lation and Auricular Flutter — subjects which he has 
 studied very closely. 
 
XII 
 
 TREATMENT OF CARDIAC DISEASE 
 
 The treatment of affections of the heart centres chiefly 
 round the cardiac muscle, and has for its objects : 
 (1) The prevention of weakening of the muscle — that is, 
 of cardiac muscle failure — or (2), if the cardiac muscle 
 is already weakened or has failed, to bring about com- 
 pensation or prevent any further weakening. In other 
 words, treatment in heart affections may be called for 
 (a) before muscle failure, or (h) after muscle failure. 
 
 Treatment of Cardiac Affections before Muscle 
 Failure develops. 
 
 Many slight cases of valvular disease occur in which 
 there is no evidence of cardiac muscle failure. In the 
 most favourable cases the heart-rate is normal, there 
 is no shortness of breath, and the patient leads a life 
 like the average person. Slight murmurs not un- 
 commonly occur without the patient knowing of their 
 existence. No treatment is called for in these cases. 
 
 In the next class of case the lesion is a little more 
 severe, and, although the heart may stand well a quiet 
 life, there is no margin for meeting the extra demands 
 of the muscular exertion required in periods of excite- 
 ment, in going up hills or stairs quickly, or in playing 
 
 107 
 
108 HEART DISEASE 
 
 games. In other words, there is danger of cardiac 
 muscle failure developing. 
 
 The treatment in these borderland cases must be 
 directed to helping the heart muscle to keep up with its 
 work. It must be saved from the influence of adverse 
 forces acting directly on it, chiefly muscular over- 
 exertion, and indirectly or reflexly from the nervous 
 and alimentary systems. 
 
 Mental excitement, which tends to quicken the action 
 of shaky hearts, must be avoided, and a proper amount 
 of sleep should be secured. 
 
 Diet. — In the alimentary system the diet should be so 
 ordered as to avoid the development of flatulence in the 
 stomach which tends to excite an abnormal heart. This 
 is most surely brought about b}' the avoidance of too 
 much starch and sugar food, and especially by not 
 taking these foods with the heavy meals of the day in 
 which flesh foods are consumed. It is surprising what 
 a difference the dyspeptic feels when he takes a meal 
 consisting only of fish or meat, green vegetables, toast, 
 and even potatoes, as compared with when he takes in 
 addition even small amounts of " sweets " in the form of 
 milk pudding, or any other pudding made with starch 
 and sugar. The discomfort of the second type of meal 
 arises partly from the greater amount consumed at it, 
 and partly from the flatulence which such a proteid and 
 starch meal produces. The carbohydrates and fats 
 should be taken at breakfast in the form of porridge, 
 toast, brown bread, butter, fat bacon, milk, or cream. 
 Tea, coffee, or cocoa with mixed meals comprising partly 
 flesh foods are very liable to cause flatulence. 
 
 The hoiveh should he kept regular, using, if necessar}"-, 
 some simple non-irritant aperient, two of the best of 
 
TREATMENT OF MUSCLE FAILURE 109 
 
 which are cascara, or the pill of colocynth and hyoscy- 
 amus in two and a half grain or larger doses. Purga- 
 tion must be avoided, and saline aperients often cause 
 considerable gastro-intestinal disturbance. 
 
 Exercise should be encouraged, but this must be well 
 within the capacity of the heart. The pulse-rate should 
 not be raised too high by it, and should subside to the 
 normal rate within reasonable time after resting. Short- 
 ness of breath should especially be avoided. Too much 
 is being done if the patient cannot take his food and 
 sleep properly. Golf is a useful form of exercise if taken 
 leisurely and in moderate amount, but not if played too 
 vigorously or too long. 
 
 Medicinal treatment in these cases is directed 
 towards keeping the heart from getting overstrained, 
 and should be of a general nature calculated to keep the 
 whole body in as healthy a condition as possible. The 
 digestion should be helped if necessary by stomachic 
 mixtures, tincture of nux vomica, or strychnine, being 
 specially useful ; and the blood should not be allowed to 
 become anaemic, arsenic and iron preparations being 
 used for this purpose. 
 
 Treatment of Cardiac Muscle Failure. 
 
 Rest in bed. — As the muscle failure is the result of 
 overwork, the first indication for its treatment is rest, 
 and the only way to secure this properly is to keep the 
 patient in bed altogether, even using the bed-pan for the 
 bowels. It is no use letting the patient get up and lie 
 on the couch. The exertion of dressing is considerable, 
 and any exertion increases the heart-rate considerably 
 in muscle failure. The saving of the work of the 
 heart which complete rest in bed, as compared with the 
 
110 HEART DISEASE 
 
 " up and about ^' condition, insures, can be seen by a 
 simple arithmetical sum. There is frequently a difference 
 of 20 and 30 beats per minute between the two condi- 
 tions in cardiac debility — that is, 1,200 to 1,800 an hour, 
 or 14,000 to 20,000 per twelve hours. To save the heart 
 this work means good progress on the upward journey. 
 It is astonishing to those seeing it for the first time how 
 complete rest in bed, without any drugs, in cases of 
 general oedema from muscle failure, especially if due to 
 alcoholic poisoning, will lead to elimination of the fluid 
 by spontaneous diuresis. It is not uncommon to see 
 patients, who on admission pass only 20 ounces of urine 
 a day, begin, after three or five or so days in bed, to 
 pass 50, 100, 150, or 180 ounces per day with almost 
 visible shrinking to normal bulk. 
 
 Diet. — The diet in cases of cardiac muscle failure 
 must be on the same lines as that ordered in the earlier 
 stages of heart affections. It suits the patients best to 
 be kept more rigidly to flesh foods. The lighter forms 
 of flesh foods are the best. No duck, goose, salmon, 
 pork, veal, or high game, should be allowed. Made-up 
 dishes with rich gravy, and sauces or soups thickened 
 with flour and burnt fats are all very productive of 
 flatulence. 
 
 It is also important to keep the diet as free from fluid 
 as possible, so as to try and promote the absorption of the 
 excess of fluid which tends to remain in the tissues. 
 
 The bowels must be kept acting daily, without purging, 
 but with fluid evacuations if there is oedema present. 
 When the liver is enlarged, some blue pill is useful. It 
 can be given in the form of Pil. diuretica (Guy^s pill) 
 three times daily, or else in larger single doses, 3 grains 
 at night twice or three times a week. It should be 
 followed in the morning by a saline aperient. 
 
TREATMENT OF MU8CLE FAILURE 111 
 
 Sleep. — One of the most distressing results of severe 
 cardiac muscle failure, especially with much enlarge- 
 ment of the heart, is inability to sleep restfuUy, or even 
 to sleep at all. This is due in great part to the tumul- 
 tuous contraction of the big heart, and, with aortic in- 
 competence, to throbbing of the carotid arteries as well. 
 These movements are so marked that they constantly 
 disturb the patient, and even if sleep comes from ex- 
 haustion it is not restful and sooner rather than later 
 the patient wakes up in a fright with a sense of suffo- 
 cation. There is no chance of sleeping in any but the 
 sitting position, and not uncommonly only when the 
 trunk and head incline forward. In the worst forms 
 bed is impossible, and an armchair the only resort. 
 
 In milder cases a glass of hot whisky and water may 
 help, and the addition of a drachm of ethyl nitrite when 
 there is any high tension will give some relief. Chloral 
 and bromide are useful in the more advanced stage, and 
 the former drug can be given without any fear, as it is 
 not really depressant to the heart. Even if chloral were 
 depressant, no harm would be done to a vigorously over- 
 acting heart. Chloralamide may also be tried ; par- 
 aldehyde is useful, but it is objectionable to take. 
 Unfortunately, very often none of these drugs help 
 matters, and then morphia must be used. When given 
 hypodermically in quarter-grain doses with y^jj grain 
 of atropine some restful sleep may be obtained. Alcohol 
 may help towards securing sleep. 
 
 Drug's. — The medicinal like the general treatment of 
 heart failure is primarily directed towards strengthening 
 the muscle and removing the oedema, and the groups of 
 drugs used for these purposes, with their most useful 
 members, are — 
 
112 HKART DISEASE 
 
 1. Drugs acting on the cardiac muscle — digitalis, 
 strophanthus, and caffein citrate. 
 
 2. Drugs acting as vessel dilators — the nitrite group, 
 especially sodium and ethyl nitrites. 
 
 3. Diuretics — digitalis, caffein citrate, theobromine 
 iand sodium salicylate, theocin sodium acetate. 
 
 Drugs acting on the Cardiac Muscle. 
 
 Dig^italis is the most useful drug in the treatment of 
 heart disease. It slows the heart by prolonging diastole, 
 and it also tends to raise the blood-pressure. Its indica- 
 tion is cardiac muscle failure, and not any special 
 valvular disease. It may also act well in muscle failure 
 from degeneration, fatty or fibroid, but its use in these 
 conditions must be carefully watched. 
 
 If digitalis will do good it can almost always be 
 tolerated, but sometimes it disagrees from personal 
 intolerance of the drug before an^^ question of over- 
 dosage arises, and causes nausea, vomiting, and looseness 
 of the bowels. True overdosage may cause cardiac 
 irregularity or coupling of the heart-beats, which will 
 return to normal after discontinuance of the drug and 
 treatment in bed alone. 
 
 When digitalis has been given for some time the urine 
 often becomes diminished in amount before nausea 
 appears — a warning to stop its use. 
 
 A watery extract, especially the freshly prepared infu- 
 sion (one to two drachms three times daily) is the best ; 
 but it is very convenient to prescribe it in granule form 
 (_i_j. milligramme of digitalin), people with mitral disease 
 and secondary muscle failure, especially, sometimes taking 
 one every morning with great advantage for years. If 
 it is desired to push the drug a granule may be given 
 
DIGITALIS AND STROPHANTHUS 113 
 
 twice or three times daily. The tincture in ten to fifteen 
 minim doses three times daily is also useful. 
 
 Digitalis acts best in cardiac muscle failure and 
 dilatation of the ventricles from overwork in which 
 there are signs of back pressure or oedema so often 
 associated with mitral disease or alcoholism. Whilst it 
 often acts well in cases with a quick irregular pulse 
 associated with auricular fibrillation and with some 
 oedema, it is impossible to tell definitely whether it will 
 act or not. No instruments can supply us with this 
 knowledge. It is also useful in aortic incompetence 
 with ventricular dilatation, provided the pulse is above 
 80 when the patient is in bed. 
 
 Cases of valvular disease in which the heart is beating 
 slowly (70 to 80) and regularly, and there is no shortness 
 of breath, do not need digitalis. A simple general tonic 
 like nux vomica is enough, with a healthy mode of life 
 and a diet which will avert flatulence. 
 
 Digitalis must be used with caution in hearts which 
 give evidence of senile decay, fatty degeneration, or 
 cardiosclerosis, but when so used is often invaluable. 
 If it is desired to use it with high tension, which it 
 increases, some vessel dilator should be given at the 
 same time. An excellent prescription for high tension 
 is a grain and a half each of sodium and potassium 
 iodides, a quarter to half a grain of sodium nitrite and 
 water to half an ounce three times a day. 
 
 If digitalis does not act on the cardiac muscle other 
 drugs, in my experience, are unlikely to do so, but 
 strophanthus or caffein citrate may be tried. 
 
 Strophanthus acts on the heart like digitalis, but it 
 does not raise the blood-pressure. It may be useful; 
 therefore, if there is a tendency to high tension, which 
 digitalis will emphasize, and also in cases which cannot 
 
 8 
 
114 HEART DISEASE 
 
 tolerate digitalis. The new tincture is much stronger 
 than the old one and the dose is 2 to 5 minims. 
 
 CafFein citrate stimulates the heart by increasing the 
 frequency of its beat and decreasing diastole. Its 
 diuretic effect helps. But there are only a few cases 
 which will react to it and not to digitalis and strophan- 
 thus. Two to three grains in water thrice daily is a 
 sufficient dose. 
 
 Strychnine or nux vomica even in large doses, in my 
 opinion, is not of any real value as a heart muscle stimu- 
 lant and restorative. These drugs act as tonics — that is, 
 they tend to stimulate the stomach and to enable it to 
 start the processes of digestion of food better. With 
 improved digestion there is improved absorption of food 
 and consequent improvement of the whole system, in- 
 cluding the heart. 
 
 Vessel Dilators. 
 
 The nitrites are most useful drugs whenever high 
 tension is present, as indicated by the condition of the 
 radial pulse or by dyspnoea of the asthmatic or 
 paroxysmal type. For prolonged treatment of high 
 tension a mixture containing sodium nitrite (one quarter 
 to half a gi'ain), with small doses of iodides of potash 
 and soda (of each one and a half grains), in half an ounce 
 of water, three times a day is most valuable. For more 
 rapid relief the solution of ethyl nitrite is very effective. 
 Many heart cases are liable to attacks of dyspnoea at 
 night and these are relieved by a teaspoonful of ethyl 
 nitrite solution in a little water, followed immediately by 
 a tablespoonful of whisky in hot water. The ethyl 
 nitrite is very volatile, must be kept in well-stoppered 
 bottles, and must not be given in hot water. 
 
TREATMENT 115 
 
 Diuretics. 
 
 If digitalis fails to remove dropsy, and there is no 
 nephritis, theobromine and sodium salicylate (gr. x. t.d.s. 
 for an adult) often will. Theocin sodium acetate 
 (gr. V. t.d.s.) is also often useful. 
 
 Complete rest in bed on light diet is one of the best 
 diuretics, especially in alcoholic cardiac muscle failure 
 with general oodema. After four or five days the urinary 
 output begins to go up rapidly, with gradual decrease in 
 the oedema. Guy^s pill, or Pil. diuretica, consisting of 
 a grain each of powdered digitalis leaves, powdered 
 "squill, blue pill, and extract of hyoscyamus, given three 
 times a day, is a most useful method of treating these 
 cases. The diuresis that follows its administration is 
 often very marked. 
 
 Treatment of Special Forms of Heart Disease. 
 
 Mitral disease. — Mitral stenosis with more or less 
 incompetence is the most common form of heart disease 
 in adult life. Its presence may not be suspected and 
 may only be recognized when an examination is made 
 for some purpose not connected with a suspicion of any 
 heart trouble, as, for instance, a life insurance proposal. 
 Such people lead an active life like their fellows with 
 perfectly sound hearts. In these cases the leakage is 
 small and has no bad effects. 
 
 Many other cases in which there is evidence of cardiac 
 weakness, quickened heart-rate, breathlessness, especially 
 on exertion, but without oedema, can get about quite 
 comfortably for years with the help of digitalis ; when 
 the drug acts it acts well, and a granule of ^\-ij grain of 
 Nativelle^s digit alin, given daily at breakfast- time, or 
 
116 HEART DISEASE 
 
 one of 7; Jo grain given three times daily, has kept people 
 on their legs for years. Such patients must, however, 
 rest as much as possible in the day-time. 
 
 The drug can be used as long as it does not cause 
 nausea, or does not slow the pulse below 70. With 
 oedema present digitalis still acts well, but rest in bed 
 is necessary in addition. 
 
 The quick, irregular heart of auricular fibrillation met 
 with in these cases is often considerably steadied by this 
 treatment, especially if oedema be present, but if there 
 are no back-pressure symptoms it is often very disap- 
 pointing to find that no treatment whatever improves 
 the condition. The only thing to be done is to give 
 cardiac and general sedatives, especially the bromides. 
 These are as difficult cases to deal with as any in cardiac 
 disease. 
 
 All patients taking digitalis must be watched carefully, 
 as the drug is cumulative in its action, and if given for 
 too long a time may slow the pulse too much, and produce 
 coupling of the beats and gastro-intestinal symptoms. 
 
 Aortic disease. — This disease does not contra-indicate 
 digitalis if there is any muscle failure. It can be safely 
 given, and should be given, even in extreme regurgita- 
 tion, provided the pulse-rate does not slow down 
 below 80. 
 
 Alcoholic heart failure, with oedema, and with or 
 without valvular incompetence, does splendidly on the 
 rest in bed alone, a diuresis coming on which clears off 
 the oedema. Digitalis, especially the infusion, acts at 
 its best in these cases, and soon strengthens the heart 
 muscle and hastens the diuresis. Rest in bed is, how- 
 ever, also essential for this action of the drug. 
 
TREATMENT OF ANGINA PECTORIS 117 
 
 Angfina pectoris. — During an attack one of the vessel 
 dilators, the nitrites, must be used. In the milder cases 
 they will relieve the pain. Many patients carry amyl 
 nitrite capsules in their pockets and inhale the drug 
 during the attack. In less severe cases a trinitrin tablet 
 is carried, and taken if there are threatenings of pain. 
 In the most severe cases it is necessary to give a hypo- 
 dermic injection of morphia. 
 
 Between the attacks treatment is directed to removing 
 calcareous deposits from the arteries of the heart and 
 to preventing any further deposition of them. Phos- 
 phoric acid is very useful for this ; twenty minims of 
 the dilute acid with infusion of calumba and spirits of 
 chloroform, given three times a day after food for some 
 weeks, has been followed by great freedom from attacks. 
 
 If the disease occurs in people below forty-five or fifty, 
 syphilis must be suspected. The Wassermann reaction 
 should be done, and, if positive, treatment with mercury 
 inunction and iodide of potash instituted; salvarsan is 
 dangerous in these cases. 
 
 When there is evidence of cardiac muscle failure with 
 dilatation of the heart this must be treated carefully by 
 approved measures. The question of exercise in people 
 liable to angina pectoris is a very important matter. 
 Only that which cannot throw a strain on the heart 
 should be allowed, and golf is not such an exercise. 
 
INDEX 
 
 Alcoholic heart, treatment, 116 
 Anatomy, 1, 2 
 Angina pectoris, 96 
 
 , treatment, 117 
 
 Anxiety, 20 
 
 Aortic disease, face in, 19 
 
 , prognosis, 86 
 
 , treatment, 116 
 
 Aortic murmurs, 66, 83 
 
 , crescendo, 86 
 
 , diastolic, 85 
 
 — — , see-saw, 86 
 
 , systolic, 83 
 
 Aortic valve, condition of, 85 
 Apex - beat, displacement of, 
 27 
 
 in disease, 23 
 
 , localization, 27, 28 
 
 , normal, 23 
 
 Apprehensive heart, 99 
 
 Arterial pulse, 8 
 
 , visible, 20 
 
 Artery wall, condition of, 14 
 
 Auricular fibrillation, 104 
 
 flutter, 105 
 
 Auriculo-ventricular valves, dila- 
 tation, 57 
 
 , stenosis, 55 
 
 Auscultation, 27 
 
 A.-v. bundle, 4 
 
 A.-v. node, 4 
 
 Blood pressure, changes in, 35, 
 
 42 
 Bradycardia, 101 
 Breath, shortness of, 6 
 Bruit de diable, 90 
 
 Caffein citrate, 114 
 Cardiac dilatation without mur- 
 mur, 57 
 Cardiac dulness, 26, 27 
 Cardiac impulse, absent, 23 
 
 , inspection, 21 
 
 , palpation, 22 
 
 Cardio-pleural sounds, 92 
 Cardio-pulmonary sounds, 92 
 Cardio-respiratory sounds, 92 
 Complaints, patients', 6 
 Conduction of murmurs, 68 
 Congenital heart disease, 19 
 Cough, 8 
 Crescendo murmur, 59 
 
 , aortic, 85 
 
 , causation, 60 
 
 , location, 79 
 
 , mitral, 78 
 
 , prognosis, 82 
 
 , rhythm, 60 
 
 , semilunar valve, 61 
 
 , time, 82 
 
 , with other murmurs, 80 
 
 Cyanosis, 19 
 
 Diet, 108, 110 
 DigitaUs, 112 
 Dropsy, 8 
 Dyspnoea, 6 
 
 Electrocardiogram, 98 
 Endocarditis, malignant, 93 
 
 , septic, 93 
 
 , ulcerative, 93 
 
 Exercise, 109 
 Exocardial sounds, 91 
 
 118 
 
INDEX 
 
 119 
 
 Fluid veins, 51 
 Friction, pericardial, 24 
 
 General signs of heart disease, 18 
 
 Haemic murmurs, 54 
 
 , cardiac, 89 
 
 , vascular, 90 
 
 Haemorrhage, 7 
 
 Heart - beat, nervous mechan- 
 ism, 3 
 Heart-block, 101 
 Heart dulness, limits, 25 
 Heart rhythm, irregularities, 98 
 Heart sounds, bruit de galop, 46 
 
 , cantering rhythm, 46 
 
 , embry ©cardial rhvthm, 46 
 
 , first, 29 
 
 , rhythm, 45 
 
 , second, 41 
 
 Inspection, general, of neck, 17 
 , of praecordia, 17 
 
 Jaundice, 20 
 
 Medicinal treatment, 109 
 Mitral disease treatment, 115 
 Mitral murmurs, diastolic, 77, 78 
 
 , systolic, 72, 76 
 
 Mitral stenosis, face in, 18 
 Mitral valve, 66 
 
 , condition of, 76 
 
 Murmurs, and heart sounds, 61 
 
 , area of audibility, 65 
 
 , causation, 48 
 
 , conduction, 68 
 
 , physical causes, 51 
 
 , timing, 48 
 
 , transmission, 68 
 
 Murmurs, aortic, 69, 83 
 
 , crescendo, 70, 78 
 
 , haemic, 54 
 
 , mitral, 70, 72 
 
 , posture, 87 
 
 , pulmonary, 69, 87 
 
 , tricuspid, 68, 82 
 
 Muscle, cardiac, importance of 
 condition of, 53 
 
 Neck, inspection of, 20 
 Nervous mechanism, 3 
 Nipple, line, 2 
 
 , position of, 2 
 
 Nitrites, 114 
 
 Node, auriculo-ventricular, 4 
 
 , sino-auricular, 3 
 
 Nodules, rheumatic, 75 
 
 Obstruction, valvular, 50 
 
 Pain, 7 
 Palpation, 22 
 Palpitation, 6 
 Percussion, methods, 24 
 Pericardial adhesion, 95 
 
 effusion, 94 
 
 friction, 24, 91 
 
 sounds, 91 
 
 Pericarditis, 94 
 
 purulent, 95 
 
 serous, 94 
 
 Pericardium, adherent, 95 
 Polyuria, nocturnal, 13 
 Posture, effect on murmurs, 
 
 67 
 Posture murmur, 87 
 Praecordia, bulging, 22 
 Premature systole, 101 
 Pulmonary valve, 67 
 Pulmonary murmurs, 87 
 
 prognosis, 88 
 
 Pulse, abnormalities, 10 
 
 , arterial, 8 
 
 , feeling of, 10 
 
 , intermittent, 101 
 
 , irregular, 101 
 
 , jugular, 15, 16 
 
 , radial, 10 
 
 , rate, 10 
 
 , slow, 101 
 
 , tension, 13 
 
 , varieties, 12 
 
 , venous, 15 
 
 Rest in bed, 109 
 Retraction of interspaces, 22 
 Rheumatism in childhood, 74 
 
120 
 
 INDEX 
 
 Rheumatism in childhood, his- 
 tory of, 74 
 
 , nodules, 75 
 
 Routine examination, 6 
 
 Second sound, causation, 40 
 
 , characteristics, 41 
 
 , modifications, 33 
 
 , reduplication, 44 
 
 , variations, 42 
 
 Semilunar valves, 58 
 
 , anatomy, 37 
 
 , mechanism, 37 
 
 Sinus arrhythmia, 103 
 Sounds, absence, 62 
 Stenosis, 50, 56 
 
 , absolute or actual, 50, 
 
 52, 56 
 -, relative, 50, 52 
 
 Stethoscope, use of, 28 
 Strophanthus, 113 
 Strychnine, 114 
 Surface lines, 3 
 Systole, premature, 101 
 
 Tachycardia, 99 
 
 , paroxysmal, 100 
 
 Tension, high, 13 
 
 , low, 14 
 
 Thrills, 23, 54 
 Tic-tac rhythm, 45 
 Tricuspid murmurs, 82, 83 
 
 , prognosis, 83 
 
 Tricuspid valve, 66 
 Treatment, 107 
 
 Valves, auriculo-ventricular, 29 
 
 , dilatation, 63 
 
 , incompetence, 50 
 
 , mobility, influence 
 
 on 
 
 sounds, 64 
 — , obstruction, 50, 56 
 — , semilunar, 39 
 — , situation, 65 
 — , stenosis, 50 
 — , ulceration, 58 
 -, vegetations on, 56 
 
 Veins, condition of, 20 
 Vibration of valve curtains, 53 
 
 H. K. LEWIS & CO., LTD., 13G COWER STKKtT, LOtiDOS, W.C. 
 

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