.i ?^s (I rrJt ijth m in . 9 from the junction of the right auricular appendix and superior vena cava towards the inferior vena cava (see Fig. 1). The tissue of the node, consisting of a network of small spindle- shaped muscle cells, richly supplied by the nerves of the heart which enter in this region, lies therefore at the mouth of the Sup VfN» Cava 5lN0-AUftlCULAR Node Sulcus TerminaliSl AuRicuLO Vent Bundle LEftBrahch FoRAMtN Ovale >vuriculo-veht. Node CoPONARv Si M o T« ICOSPIO Vaive I Nt VCNA Cava Aorta T Branch Fig. 1. A diftgrain of a human heart. The walla of inferior vena cava, right auricle and right ventricle have been i)artial]\' removed to exjiose the septa. The position of the sino-auricular node, in which the heart beat commences, i.s shown, as are also the position of the auriculo-ventric-ular node and the course of the auriculo -ventricular trunk and its branches. The last-named structures convey the contraction wave from auricle to ventricle. superior vena cava and is embedded in the wall of the right auricle. The contraction which commences in its neighbour- hood spreads through the walls of both auricles and is transmitted by a special band of tissue, which will receive subsequent description, to the ventricles. The orderly 10 Chapter II. rhythm of the whole heart takes its origin in this node, to which I have consequently applied the term heart's " pace- maker." In the normally acting adult heart, the pacemaker sends forth waves of contraction at rates which average 72 per minute, and, the separate beats being evenly spaced, the systoles follow each other in a regular order or rhythm. The pacemaker is under the control of the vagi, or inhibitory nerves of the heart, and these normally restrain this stimulus producing centre, holding it, as it were, in leash. Destruction of the nerves, more especially that of the right side, or the administration of atropine, which paralyses the nerve endings in the heart, raises the rate at which the heart beats follow each other. In the human subject, the probable limit to which the rate may rise as a result of this denervation is 150-160 per minute. In many subjects under special conditions, the vagus curbs the heart excessively, and this over-action of the nerve may be constant or rhythmic. There consequently results either a uniform pulse slowing or a waxing and waning of heart rate. Let us deal with the uniform slowing first, for it is a subject with which we are only briefly concerned in these chapters. Pronounced slowing of the whole heart is com- paratively rare ; the lesser grades of slowing, most of which are probably of vagal origin, slowing to 50 or 60 beats per minute, are not uncommon and are especially prominent in athletes and in association with increased arterial pressure, pregnancy, jaundice, aortic stenosis, convalescence from the acute fevers and less frequently with other conditions. Pulse slowing of this degree has no great significance, and it is- common to meet with people who enjoy perfect health and in M hom during rest the pulse rate lies habitually between these limits. Periodic or varying disturbances, which influence the rhythm of the heart at its source and produce a greater or Sinus arrhythmia. 11 lesser degree of arrhythmia, are more important, though only the commoner varieties of such irregularity need to be described. In Fig. 2, a diagram of a characteristic sinus arrhythmia is given. I shall refer to similarly constructed diagrams in succeeding chapters. The figure is arranged so that each narrow black rectangle (^4) represents a single co-ordinate beat of the auricle, and so that each broad black rectangle ( V) represents a co-ordinate ventricular contraction. Where an II I I III I I Fig. 2. A diagrammatic representation of the action of a heart affected bj' sinus arrhythmia. The contractions of auricle and ventricle are represented by the thin and broader black rectangles, A and V respec- tively. The auricle contracts at the beginning of each cycle, and sends its impulse, indicated by an oblique line, to the ventricle, which responds. The irregularity consists of a waxing and waning of rate, in which auricle and ventricle participate equally. auricular contraction is followed by a ventricular response, an oblique line is drawn, joining the corresponding rectangles. The slope of the oblique line indicates the time interval between the contractions of auricle and ventricle. All such diagrams read from left to right. In the present example, a sinus irregularity, the whole heart is affected, so that each ventricular contraction is preceded by an auricular systole at the usual interval. The irregularity consists of a gradual waxing and waning of auricular rate ^hich is repeated periodically, and which is followed exactly by the ventricle. 12 Chapter II. Bespiraiory irregularities . It is well known that young adults manifest a very appreciable irregularity of the heart and pulse action when they breathe deeply (Fig. 3). The pulse quickens when the chest is inflated, and slows when the chest is emptied. But in young adults and in the aged also there is no respiratory variation of pulse rate, which the finger can Fig. 3. A sphygmographic curve from a normal subject, breathing deeply. There is an increase of pulse rate during inspiration and a decrease during expiration. I m 1 1 1 n r » ■ I • (I 11 Fig. 6. A gross sinus arrhythmia of rare type ; a long pulse cycle accompanies each expiration. In this, as in all similar figures, the top line represents time in fifths of seconds. discover, while the breathing is natural. On the contrar}'-, a percef)tible degree of natural respiratory irregularity of the pulse, characterised chiefly by one or more longer pauses during the expiratory period (Fig. 4 and 5), is not uncommon in young children, and sometimes it is sufficiently prominent to attract immediate attention. Irregularity of a very similar Sinus arrhythmia. 13 ^ -^ * — Si s >■ * i."^ ■- o ffl "- >- y O i .0 ^ §_, ^ op .3 cS ss ^ iH .2 ^'■ is o "S — -- cS "k ■~ o X -^ S il .^ c 5 OJ « "3. Mtc .S * c5 s-c u >«j 5 ^ c -f^ © S «x ? i H C y. o" J •y; '- — ® o i Xl >.* +2 J^x CS >. o G .^•? r o •2 o *i r' -d © .ii fi S o % ©^ u © *i -3 c 2 !S « a: ^ C c£ o o ^ (5 c8 © is 3 o © © c © ■^ 3 r— i r* o c8 ^ b< -*-* 3 ,, , -►i O c5 I>; m •+i d is f-^ ^ to © J' 3 ■_^ •; >> to ■p to c t^ s "S C8 o © l-( b cc -0 ki U) E? 14 Chapter II. kind is found frequently at the age of puberty, and it is also seen on rare occasions in the adult (a striking though rare example of the last is shown in Fig. 6). All these irregularities are of vagal origin. Sinus irregularities ivhich bear no relation to respiration. While the vagal irregularities of heart rhythm generally show a respiratory relation, disturbances of similar origin occur where there is no association between the changes and the several acts of breathing. These disorders of the heart mechanism fall into three main categories. They are : — (1) Sudden and prolonged cessation of the whole heart beat usually associated with syncope ; it is a rare condition and requires but a passing notice in this general survey. (2) Relatively abrupt and profound slowing of the whole heart (to 20 or 40 beats per minute), accompanied by an indepen- dent lowering of blood-pressure. This disturbance is often responsible for attacks of faintness or actual loss of con- sciousness. I have met with it frequently in soldiers invalided for the condition known as " irritable heart." It is, I believe, the commonest cause of fainting attacks in men and women. (3) Phasic variation of pulse rate, in which a retardation and subsequent gradual acceleration of the whole heart occurs ; the change is spread over ten, fifteen or more seconds and may be repeated regularly or may occur from time to time ; it is associated with the administration of heavy doses of drugs of the digitalis group, but may be seen apart from them (Fig. 7) ; it is an uncommon type of irregularity. (4) An irregularity of the whole heart of mild degree, in which shorter and longer pauses are mingled indiscriminately. It is not infrequent, and is almost always combined with a general reduction of pulse rate. It may be found in quite young and apparently healthy children (Fig. 8) and is also encountered in young adults in whom no other cardiac sign Sinus arrhythmia. 15 Is apparent. It is specially frequent in patients who have rheumatic heart disease and who are under the influence of digitahs ; it is accentuated when the heart slows after it has quickened in response to exercise. Tliese sinus irregularities, like those which are related to respiration, are all due to alterations of vagal tone, Th£ recognition of sinus irregularities. Sinus irregularities are usually recognised with ease. It may be said that the great majority of pulse irregularities which occur before the end of the first decade are of this kind, and most of them are respiratory. When there is the definite and stated relation to respiration, no further evidence is required ; in most instances of sinus irregularity, this relation is present, but if it is absent, it becomes established if the breathing is deepened ; a gradual Avaxing and waning of rate is always highly suggestive, if not conclusive. The radial beats and apex pulsations correspond ; the heart sounds are simply modified according to the incidence of the ventricular contractions. The radial beats are full, and the apices of the several pulsations maintain an almost constant height in arterial curves (Fig. 4, 5 and 8). Vagal irregularities are all abolished by any factor whicli notably increases the average pulse rate. Thus they disappear with exercise, with fever, or shortly after the administration of atropine. Atropine also cuts short or prevents standstill of the heart and the profound slowing described on the previous page. The prognostic significance of sinus irregularities. The commoner forms of sinus irregularity (excluding those which may be responsible for syncope and the true, phasic variation of pulse rate) are of little prognostic value, Thev are so frequent in patients who present no other sign 16 Chapter II. of cardiac disturbance, either at the original examination or subsequently, that they are to be regarded either as slight exaggerations of a normal phenomenon (respiratory irregularity) or as evidences of a mild and insignificant instability of tonic inhibitory nerve action.* Their importance lies chiefly in possible confusion Avith other forms of heart irregularity. They should not be allowed to influence the habits of those who exhibit them ; they neither suggest nor require special therapy. * Occurring in children, this irregularity has obtained without reason an unenviable reputation, on account of its supposed relation to tuberculous meningitis. ( n ) Chapter hi. HEART-BLOCK. Definition. An abnormal heart mechanism, in which there is a delay in, or absence of, ventricular responses to the auricular impulses. The nature of heart-block. Under normal circumstances the ventricle depends, for its stimulus, upon impulses which are sent down to it from the regularly contracting auricle. Each auricular systole transmits a stimulus to the ventricle and this stimulus travels from auricle to ventricle along a narrow neuro- muscular tract, the auriculo- ventricular bundle. This band of tissue starts in the right auricle near the coronary sinus* and proceeds forwards and downwards to the membranous septum of the ventricle (Fig. 1), where it divides into two main branches on either side of the septum. The main branches subdivide and are connected to the ventricular musculature through the complex network of cells named after Purkinje. The sequence in which the chambers of the heart normally contract is diagrammatically illustrated by Fig. 9. 18 Chaj3ter III. When from any cause the function of the tissues uniting auricle and ventricle is impaired, a disturbance of this sequential contraction is engendered. The grades of disturbance which human hearts manifest are numerous. There may be a mere prolongation of the interval which separates the commencements of auricular and ventricular systole (the As-Vs interval, as it is termed). Such a con- duction defect is illustrated by Fig. 10 ; the thin lines become more oblic^ue in the diagram, and a gap is left between the end of auricular and the beginning of ventricular systole. Fig. 9. Fig. 10. Fig. 9. A diagram representing normal heart action. The auricle contracts first and transmits an impulse (the oblique line) to the ventricle. The ventricle responds and commences to contract immediately at the cessation of auricular systole. Fig. 10. A diagram illustrating the eaiiiest stage of heart-block. An interval appears between the end of auricular and the commencement of ventricular systole. There is delay in the transmission of the impulse from auricle to ventricle (indicated by the increased obliquity of the line which joins the rectangles in the diagram). Where the grade of heart-block is higher, the ventricle may fail to respond to occasional auricular impulses ; a condition commonly designated by the term " dropped beats." This form of heart-block is rarely a simple phenomenon ; it is almost always complicated by variations in the lengths of As-Vs intervals over the period of disturbance. The relation of chamber contractions may be studied in Fig. 11. A " dropped beat " or ventricular silence produces a pause of exceptional length and^ this pause breaks the natural Heart-block. 19 rhythm of the ventricle. Where there is no associated variation in the As-Vs intervals, the long ventricular cycle is necessarily equal to that of two regular cycles. But this is rarely the case ; the " dropped beat " is foreshadowed by a progressive increase of the preceding As-Vs intervals (Fig. 11, 1, 2 and 3). Moreover, the As-Vs interval which follows the silence is generally curtailed (Fig. 11, 4). These changes in the conduction intervals shorten the long cycle and consequently diminish the grade of ventricular dis- turbance. The exact manner in which the changes happen is of importance and requires closer study. Consider the first three As-Vs intervals of Fig. 11; as illustrated by the obliquity of the lines, the interval gradually widens, but it widens in a peculiar manner. The increase of the second interval Fig. 11. The second stage of heart-block, to which the term " dropped beats " is applied. Up to the point where the chief disturljance occurs, the gaps between the auricular and corresponding ventricular contractions widen out. The impulses travel to the ventricle with increasing difficulty. The fourth auricular contraction stands isolated, it yields no response ; a ventricular contraction is " dropped." Following the ventricular pause, the As-Vs interval is short, for the tissues have rested, but it again widens as successive cvcles follow. I I I I I Fig. 12. A diagram of 2 : 1 heart-block, in which alternate ventricular beats are " dropped." c 2 \ 20 Chapter III. over the first is greater than the increase of the third over the second. The result is a decrease of the interventricular period directly preceding the ventricular silence. The ventricle quickens to the point of the disturbance. The shortening of the As-Vs interval following the pause, and the subsequent prolongation of it, produces a similar quickening of the ventricle after the disturbance. The primary and secondary accelerations of ventricular rate, before and after the disturbance, help to identify the disorder in many cUnical cases of heart-block. As the grade of heart-block rises, and ventricular silences become more frequent, relatively simple ratios are established between the auricular and ventricular rates. When the ventricle beats at only half the rate of the auricle, because alternate impulses are ineffective, the con- dition is spoken of as 2 : 1 heart-block (Fig. 12). 3:1 and 4 : 1 ratios, in which each third or fourth auricular impulse alone yields a ventricular response, are sometimes encountered, but they are uncommon. The mechanisms which have been described are all included under the term " partial heart-block." I I I I I I I I I I I I I I I Fig. 13. A diagram of complete heart-block or dissociation. Both the auricle and the ventricle beat regularly, but at independent rates. The relative positions of auricvilar and ventricular contractions are very variable. Heart-block. 21 The highest grade of heart-block is reached when no impulses are transmitted to the ventricle. When this happens, the ventricle, having completely lost the controlling influence of the auricle, beats in response to a slow and regular series of impulses which it builds up intrinsically. In " complete heart-block " or " dissociation " two entirely separate rhythms are maintained ; one starts in and controls the auricle, the other originates in and controls the ventricle. The first has the usual rate, 72 per minute or thereabout ; the last has an approximate rate of 30 to the minute. Though both are regular, the rhythms are mutually indepen- dent (Fig. 13) and the systoles of auricle and ventricle fall with varying time relations to each other. Etiological and pathological associations. Age. Heart-block may occur at any age. It has been observed in the newborn child and at almost all ages into the eighties and nineties. Its age distribution is settled by the age incidence of the diseases which produce it. Thus, it is especially prevalent amongst those whose hearts have been severely damaged by rheumatic fever or chorea, so that a special class of case is grouped between the years 10 and 35. Senile affections account for another large group of patients who suffer from this cardiac disturbance ; these patients are elderly. But the causation is so varied that no age is exempt. The distribution in a group of my own cases was as follows : — Age 10-20 20-30 30-40 40-50 50-60 60-70 70-80 80-90 Cases 7 7 5 8 3 6 5 1 Sex. As in other disturbances of the cardiac mechanism, heart-block is most prominent in the male sex. I may illustrate this by a reference to the same group, in which 33 are males and 9 are females. 22 Chapter III. Heredity. A single instance of the supposed occurrence of several cases of heart-block in the same family has been reported, but has not been substantiated. It is highly improbable that heredity plays any direct part in the affection. Relations to infective disease. Relatively, heart-block is not infrequent during the course of infective diseases, and of these rheumatic fever holds the first place ; the disturbance is usually temporary. The exact relation of rheumatic affections to acute and sub-acute inflammatory lesions of the heart is but imperfectly known, but there is a clear connection between them. Many instances of heart-block have been reported during the course of severe rheumatic fever and its complications, acute endocarditis and pericarditis. It is pro- bable that the infection of the heart is never limited to its outer or inner layer ; the middle layer or myocardium is probably always involved. My own experience leads me to think that heart-block is almost, if not quite, a common accompani- ment of acute or sub-acute rheumatism of the heart, for I have seen a number of patients in whom during the course of rheumatic fever involving the valves or pericardium, or both, dropped beats or partial heart-block in its several grades were exhibited. In other instances, temporary heart-block has appeared during short febrile attacks in patients who have been previously affected by rheumatic fever. It is certain that, being transient, it is often overlooked. Other acute infections \A'hich should be mentioned are those of the more active pus organisms, and also those of diphtheria, influenza, tyjihoid, scarlet fever and pneumonia ; heart-block in these conditions is limited to infections of severity. A large proportion of the reported cases of chronic heart-block and of those which have come under my own Heart-block. 23 observation, have belonged to two groups ; the disorder has followed single or repeated attacks of rheumatic fever, or has been the direct result of syphilis. Whether of rheumatic or syphilitic origin, whether acute or chronic, heart-block is generally but an expression of a widespread affection of the heart muscle in these patients, though the lesion may be confined to, or may fall most heavily upon, the tissues which establish functional connection between the auricle and ventricle. In a fourth of the cases in which the hearts have been secured after death the lesion has been gummatous. In a series of 38 cases of my own, 4 gave a frank history of venereal infection and 12 a history of rheumatism. The relation of heart-block to rheumatism in chronic heart affections is a peculiar one. The heart-block is often dormant or is detected only by exact instrumental methods ; it may be unmasked by the administration of drugs of the digitaUs group, for the higher grades of heart-block are produced from the lesser by these poisons. Relation to chronic degenerative processes of more obscure origin. A large number of the reported cases of heart-block have been in elderly people, and observation has shown that the responsible damage has been part and parcel of a widespread change, either in the heart alone, or in the heart and its vessels. A number of the lesions can undoubtedly be traced to syphilis or rheumatism, but the cause of a still larger number is obscure. Chronic inflammation, fibrosis, atrophy, calcification or fatty degeneration of the tissues, associated or unassociated with disease of the coronary arteries, are amongst the most frequent causes. « Heart-block as the result of digitalis administration. I have referred to the unmasking of dormant heart-block in 24 Chapter III. rheumatic heart-disease. When digitalis, or an alhed drug such as strophanthus and squills, is given in toxic doses to young patients who have rheumatic hearts, it is not uncommon to observe the severer grades of partial heart-block as a sequel. And it is known that in most of the cases which react in this manner a slight defect in the conduction of impulses from auricle to ventricle was present before the drug was taken. The added effect may be due to the action of digitahs upon the vagus nerve, for sometimes it can be removed by atropine. Heart-block may be induced in experiment by stimulating the vagus, and efforts have been made to establish a clinical group in which the heart-block is attributable to disturbed innervation. Up to the present time, there is no very clear evidence that even a temporary disturbance of this character may be initiated purely by vagal impulses ; though, as I have stated, a pre-existing tendency may be exaggerated in this manner ; if the higher and enduring grades of heart- block are ever due to derangement of the vagi, this form is so rare that it scarcely needs consideration in practice. Special morbid anatomy. It is in the main bundle, or in its auricular attachment, that the lesions responsible for heart-block are found. The kind of lesion has been spoken of already. Gummata, chronic inflammatory processes and their accompaniments, fibrosis, atrophy, and calcification are most frequently seen. Examples of tumours (fibroma and endothelioma) affecting these special tissues have been recorded. Ulceration invading the bundle (rarely), acute inflamma- tion evidenced by deposition of leucocytes (commonly), or parenchymatous degeneration of the bundle are the lesions found in hearts damaged bv acute or subacute infections. Heart-block. 25 The recognition of heart-block. The disorders of the heart's mechanism caused by heart-block, in its several grades, are readily recognised by the exact graphic methods provided by the polygraph and galvanometer. The efficacy of these instruments and the certain analysis which they provide must be evident, for heart-block produces deranged sequence in the contractions of auricle and ventricle, and the polygraph and galvanometer supply separate and clear records of the systoles of upper and lower chamber. To compare the onsets of the several systoles therefore is relatively simple when these recording devices are employed. But I speak to those to whom special methods are not available, and I hope to show that heart-block can be recognised in many of its grades by simpler means. It will be necessary to treat each grade of the disorder separately and, in this instance, to refer especially to exact measurement of the arterial pulse pauses. In many forms of irregularity such measurement is not necessary, though it may be expedient ; in the disturbance produced by heart-block it is often essential. Often the earliest manifestations of heart-block consist in a widening of the As-Vs interval (see page 18) ; this defect can rarely be identified by ordinary clinical means ; yet it may be responsible for two physical signs. It may not be known to everyone that auricular systole produces a distinct though muffled sound, and that while this sound is inaudible when the heart's mechanism is normal, it is frequently heard when the auricular and ventricular systoles are sufficiently separated. A slight widening of the As-V-'^ interval may lead to a reduplication of the first heart sound ; a more pronounced widening may result in a double second sound, for the auricular systole will then fall in early diastole. 26 Chapter III. The second sign is confined to cases of mitral stenosis and is of similar origin ; in these patients the systole of the auricle is the cause of the presystolic miirmur which characterises the valve lesion. Contraction of the auricle at an abnormal instant in diastole is accompanied by a murmur and thrill which replace the customary presystolic events. When the pulse is regular, apical thrills or rough murmurs, confined to mid- or early diastole, are physical signs which should suggest^ not alone stenosis, but also the beginning of heart-block. Single dropped beats are not difficult to detect. Take the case of a pulse, which though it seems otherwise regular, is interrupted by an occasional pause of unusual length, while examination of the apex beat reveals neither movement nor sound in the pause. If the pause is not associated regularly with the expiratory phase of respiration (see page 12) it can be attributed to a failure of the customary response of ventricle ta auricle. The length of the pause in radial tracings may be exactly equivalent to that of two rhythmic beats. More frequently (as in the radial pulse tracing of Fig. 14) it is Fig. 14. A pulse curve showing " dropped beats." The arrows, which represent the positions of the regular auricular contractions, have been accurately determined in this and subsequent figures by means of poly- graphic curves. There is, of course, a big delay between the auricular systole and the pulse beat. The heart sounds are shown diagrammatically. The arrangement of the pulse beats depends upon the lengths of the As- Vs intervals and upon the failure of response at the points marked by asterisks. Note the widening of the .4s- Fs intervals and accompanying increase of pvilse rate before and after each dropped beat. distinctly short of this, and is preceded and succeeded by slight pulse quickening. The nature of these changes has been. Heart-block. 27 considered already (page 19), and the n\echanism is indicated in the present figure by arrows showing the points at which the regular auricular systoles fall. Responses to the auricular contractions marked by asterisks have failed. With exercise the pulse accelerates and becomjes regular ; with rest the irregularity reappears and the first sign of its return is the occurrence of an unusually long ventricular pause. When dropped beats are more frequent, the irregularity takes the form seen in Fig. 15. Here each third or fourth im])ulse miscarries, and the heart and ])ulse beats arc grouped in twos and threes. Had we not the termination of this curve, the analysis of the first half could not be completed, for the picture is identical with one jiroduced by premature contractions. The clue to the true interpretation is given by the lengths of cycles 1 and 3. These are the opening beats of two groups, the first of two, the second of three pulsations. Cycles 1 and 3 are alike, they have the same duration. If beat 2 were interj^reted as an extrasystole, so also would beat 4 ; but cycle 4 is short while cycle 2 is long. In the slight shortening of cycle 4 as compared with cycle 3 we recognise the acceleration of pulse rate which follows a dropped beat. Fig. 15. Curves of heart's apex beat and pulse from a patient in whom ventricular responses failed frequently. 2 : 1 heart-block is to be suspected in any patient in whom the ventricle beats regularly and in whom the heart rate lies between 40 and 50 contractions to the minute. A sudden and exact halving of ventricular rate is always most suggestive. 2 : 1 heart-block is unstable, the ventricle c^uickening from time to time, and these changes in the rate of its response to auricle disclose the nature of the whole disturbance. Exercise abruptly doubles the ventricular rate ; with subsequent rest the raised rate falls abruptly to one half. 28 Chapter III. In mitral stenosis partial heart-block is often character- ised by peculiarities of the murmurs. They are often extremely complex. Where 2 : 1 heart-block is present two thrills and two diastolic murmurs may accompany each Fig. 16. Curves of heart's apex beat and pulse, taken during the transition from frequent " dropped beats " to 2 : 1 heart-block. The rate is reduced to exactly three-fourths the original at the change. Fig. 17. Curves showing the interruption of a period of 2 : 1 heart-block by a single resj:)onse of the ventricle to one of the series of alternate impulses which usually yield no ventricular contraction. The transition between 2 : 1 heart-block and an arrangement previously studied, namely, the loss of each third response, is shown in Fig. 16. A bigeminal or covipled action of the ventricle passes over into a slow regular action. The features which proclaim heart-block in this curve are the increase in the length of cycle b as compared to a, and the exact reduction of rate to three-fourths. The lengths of the several pauses are understood by examining the positions of the auricidar systoles which have been indicated by arrows drawn on the curve. Systoles 2a, 4a, 5a, 6a and 7a do not affect the ventricle ; and where the ventricle is silent an unusually lengthy pause is found. The arterial cycle a is brief as compared with b because the auricular impulse 4 takes longer to reach the ventricle than does impulse 5. Distiu'bance of a 2 :1 period is shown in Fig. 17. An early contraction of the ventricle is followed by a pulse cycle a which is shorter than b and the succeeding cycles. The reason of this shortening has been explained in the description of the last figure. In Fig. 17 heart-block is also evidenced by the total duration (c) of the two short C3'cles; it is equal to one and a half times that of the longer cycles (period d). In other words, c and d each correspond to three auricular cycles. Heart-block. 29 ventricular cycle. The arrangement of the murmurs will be understood when it is remembered that the thrill and harsh murmur of mitral stenosis are produced by auricular systole and that in 2 : 1 block the auricle contracts twice as frequently as the ventricle. A more complex arrangement of murmurs is Fig. 18. Arterial and apex curves from a case of mitral stenosis, while there is a transition from dropped beats to 2 : 1 heart-block. Note the arrange- ment of the diastolic n^nrmurs and their dependence upon those auricular contractions which force blood into the ventricle. Fig. 19. Apex and radial curves in a case of complete heart-block. The heart sounds are modified bj' the auricular contractions, which are faintly audible. Where auricular and ventricular contractions begin together the first sound is exaggerated. The pure auricular sounds_are shown as dots. illustrated by Fig. 18. The ventricle beats at first in couples, and at such times the murmur occurs before the first and after the second sound of the first beat of a couple ; the second beat of the couple is accompanied by no murmur, for the single auricular contraction falUng in its neighbourhood coincides with that of the ventricle and forces no blood through the 30 Chapter III. stenosed orifice. Over the last portion of the curve 2 : 1 heart-block is present, and each cycle is accompanied by presystolic and early diastolic murmurs. In complete heart-block the action of the ventricle is phenomenally slow ; nearly all hearts which beat at rates of 35 and under are affected in this manner. The rhythm is generally quite regular. The rate is almost or c^uite unaffected by exercise, or by the administration of atropine or amyl nitrite. Each ventricular beat is accompanied by a first and second sound ; in addition, very faint muffled sounds are heard in the long diastoles. The latter are due to auricular systoles. A sign which is characteristic, and often present, is a changed character of the first and second heart sounds from beat to beat. When the auricular and ventricular contractions begin together, the first sound is intensified, and when they fall almost together the first or second sound may be reduplicated (Fig. 19). Evidences of the relatively rapid auricular contraction are generally seen in the neck ; small and regular pulsations (Fig. 20, a waves) appear by the jugular veins between the beats of the carotid (c waves). From time to time a prominent venous pulsation (Fig. 20, ajc) accompanies the intensified first heart sound, when auricular systole coincides with that of the ventricle and when as a consequence the blood cannot be ejected naturally from the auricle. A periodic waxing and waning of the venous pulsations, independent of respiration, is always highly suggestive of complete block. Traces of auricular pulsations upon the arterial curves are also evident in most of the patients from whom full pulse excursions can be obtained (Fig. 21). Where, as in the accompanying figure, the little waves on the downstrokes of the regular pulse beats show a gradual and orderly change of position, moving steadily away from the succeeding radial upstroke, the presence of complete heart-block is certain. Heart-block. 31 « »,- s ■■2-2 2 — fc. 05 © o ? © o i . • d — — I ® /^ o ■:1 Q_ C o o 4) ■*-* to o c -^ 3 ^ .S o Ji ® — _o -^ "5 ^ o SCO ^ "T^ So ^ b J> b t- 'as -a >i © -»^ '**' ® __^ ^' , 05 s 0! o '5 o bC e be « ^ 2 :; •- bo ;5 t- -^ o fc/ !«l ki ® C ^^ X -»:> -tJ +j s _g 1 3 2 _2 tH Eh [3 03 o3 15 bi S" 2 4^ 32 Chapter III. Effects on the circulation and the general symptomatology. The symptoms suffered by the subjects of heart-block are divisible into two groups. On the one side are those which are especially associated with the condition itself, and on the other are those which result from co-existing disease in other parts of the heart. For disease is rarely limited to the bundle, and generally heart-block is but a local manifestation of a more widespread process ; the local lesion is often accidental. The effects of a lesion which transects the bundle differ from those of a similar lesion in another portion of the musculature in one chief respect ; the lesion so placed produces manifest disturbance ; there is no second strand which may fulfil the functions of that which is destroyed, whereas a defect in the general mass of muscle is hidden by the response of the remaining tissue. As in disease of the nervous system, where large masses of the tissue may be destroyed without gross outward signs of damage, but where a minute morbid focus in a given situation gives rise to obvious and profound disturbance, so it is with the heart. It should be emphasised that heart-block is usually an indication of a far graver condition than simple transection of the bundle ; it is a sign of diffuse invasion of the myocardium. The symptoms produced by affections of the whole heart musculature do not lie within the scope of this book ; but it is important to state that the presence of heart-block demands an exhaustive study of the subject in whom it appears ; in all instances special attention should be directed to the fitness or otherwise of the heart as a whole. And this caution is not limited to heart-block ; it applies to all departures from the normal mechanism. The special symptomatology of heart-block may be conveniently approached from two standpoints. Heart-block of high grade is accompanied by a reduction of the rate of the heart beat, often to a half its former rate. Heart-block. 3.3 What is the effect of this retardation of heart rate upon the circulation, and what are the results of the lessened nervous control of rate which often accompanies it ? It is certain that thereby a serious burden is imposed upon the efficiency of the heart as a pump ; but nothing is more remarkable than the accommodation of the cardiovascular system to conditions which diverge widely from the normal. Dissociation of auricles and ventricles, and the consequent establishment of a slow ventricular rhythm, is followed by some degree of ventricular hypertrophy. No doubt this increase in the mass of the ventricular muscle compensates in a measure for the loss of co-ordination and of the natural rates. During the long diastoles the blood is squeezed from arteries to veins and a low^ diastolic blood pressure results ; but the blood pours equally fast from veins to heart, whose efficient chambers, receiving the extra load, expel it into the arteries. Fullness of pulse and high systolic pressure (170-200 mm. Hg.) consequently characterise the arterial system when in persistent heart-block there is no lack of healthy cardiac tissue. In evidence of the adaptability which the circulation as a whole shows to the new conditions, I may cite the case of a patient in whom, judging from the signs and symptoms, the damage to the muscle mass was but little. The patient, a man of 33 years, was known to have had a heart rate of 30 to 35, with occasional accelerations to 48, for 15 years. He was the subject of complete heart-block. There was a little hypertrophy of the heart, but no subjective symptoms. He led, when last seen, a very active business life, and passed in the street would have been judged a perfectly healthy person. There was no circulatory embarrassment, even after strenuous exertion ; he prided himself upon his sprinting power and had recently run in races. An instance of this kind offers a partial answer to the original questions ; the slow pulse of heart-block and the lost regulation of rate do not disable an otherwise 34 Chapter III. healthy heart from performing its full work. In hearts more profoundly affected, the extra burden is less readily borne, but in these it is not easy to dissociate the effects of the new mechanism from those of disease of the remaining muscle. In the second place, heart-block is responsible for a group of symptoms which arise as a direct result of excessive slowing. Reduction of pulse rate beyond certain limits, or the cessation of the arterial fio-y for a certain time, is accom- panied by grave disorders of nutrition, and the brain is an early and anxious plaintiff. The patient, who exhibits marked pulse slowing in conjunction with fits, falls into the category of Adams-Stokes' syndrome. The higher grades of heart-block, whether of persistent heart-block in which ventricular responses are frequently missed (2:1, 3:1 ratios, etc.), or of complete dissociation, are frequently accompanied by temporary periods of excessive pulse slowing or by cessation of the ventricular systole for prolonged intervals. The cause of change in the ventricular rate — the auricles continue to beat at the usual or at an enhanced rate — is not fully understood, and I do not propose to discuss it. The symptoms presented by the patient are intimately dependent upon the degree of heart slowing or upon the duration of isolated periods of asystole. When the pulse falls to 8 or 20 beats per minute, unconsciousness supervenes ; suspension of the mental functions is also produced by a single period of asystole of from 3 to 7 seconds duration. Patients who suffer from the higher grades of heart-block commonly relate a history of brief attacks of giddiness, fainting, temporary loss of consciousness and its dependent accidents. Seen in mild attacks, the subject of them is pulseless and momentarily pale. In severer seizures, where the pulse ceases for 15 seconds or more, there are additional phenomena. The blood is dammed back in Heart-block. 35 tlie venous system, increasing pallor has cyanosis added to it, the breathing deepens and becomes stertorous ; twitching of the face and upper limbs eventuates. The convulsive fit rarely spreads beyond the described area, but it may become more generalised. Urine is not passed, neither is the tongue bitten during the attacks. In most cases the condition is readily recognised by the silence of the ventricle and by the rapid undulations in the veins of the neck, signify- ing activity of the right ai. 'icle. Unexpected death is a by no means uncommon accident amongst the affected, but considering individual attacks it is rare. Death occurs after a period of status epilepticus in a number of the patients, and the status consists of repeated seizures of the forms described. As a rule the patient has no warning of an impending syncopal or epileptic attack ; though on occasion he or his medical attendant may be informed of the approaching danger by a change in the heart's action, for example, by the occurrence of unusual ventricular slowing. The sensations of the patient at the commencement of long seizures are generally similar to those accompanying a brief cessation of the heart beat, and consequently do not properly constitute an aura. The prognosis. Heart-block in itself does not kill ; those who suffer or have suffered from it mostly die with the usual symptoms of general heart failure. Let me be clearly understood in this statement. Heart-block and the Adams-Stokes' syndrome are by no means synonymous terms ; the majority of patients who exhibit heart-block never have fits. Lesser grades of heart-block are common in conjunction with rheumatic heart disease, and, as a rule, they produce no symptoms. Moreover, the disturbed mechanism is not of necessity directly fatal even in chronic heart-block of high grade. D 2 36 Chapter III. The prognosis in heart-block has to be dealt \Vith from several points of view. In the first instance, let us consider the common variety, the milder grades of heart-block such as are associated with rheumatic heart disease (prolonged As- Vs intervals or " dropped beats "). Where such heart-block is 'persistent, there are usually a number of physical signs in addition to those dependent upon the heart mechanism ; they are the signs of heart disease, muscular or valvular, in its several and universally recognised forms. Heart-block is often the least prominent phenomenon in these patients ; they often suffer from mitral stenosis. The only question that I raise is as to the manner in which heart-block affects the prognosis in these cases. It should be regarded as an evidence of myocardial damage, not necessarily limited to the bundle, but probably diffused throughout the heart. My experience of such cases is that they are serious ; in fact, most of those I have seen are dead, though they have not died of heart-block. But temporary heart-block of mild grade is not uncommon during the febrile attacks to which rheumatic heart subjects are liable ; it occurs also in pneumonia and typhoid. The appearance of this abnormal mechanism is of great importance, for it is often the sole sign which points to myocardial damage. Whenever it complicates an acute infection it consequently dulls the prognosis ; at the same time it should be understood that the normal mechanism is usually recovered. Occurring as an accompaniment of fever in a patient who has rheumatic heart disease, it should be regarded as an outward sign of an isolated injury which, if often repeated, eventually so weakens the muscle that life is no longer supported. Where the higher grades of heart-block are present, the prognosis is based upon two chief considerations. The general evidence of the integrity and fitness of the muscle as a whole should be weighed first. The fits, especially their Heart-block. 37 frequency and severity, are next taken into account ; a number of the patients are free from them ; others are in constant peril ; and it is not easy, nay it is often impossible, to predict the ultimate effects of syncopal attacks or severer crises in a given case. Those patients especially who have progressive lesions, and those in whom partial is eventually converted to complete and permanent dissociation, must pass through a time of particular danger ; for, during the passage from one grade of block to the other, fits are very common and the period of passage may not be a short one. It is useful to remember also that those who have partial heart-block are more prone to fits than those in whom the obstruction is complete. Uncertain in both incidence and effect, the fits always dictate a cautious prognosis. Regarded in its entirety, persistent heart-block of high grade is a grave condition. It is usually complicated, and then a few years generally close the scene. Nevertheless, some, and especially the younger patients, survive for many years, in comparative and absolute comfort. These are patients in whom the mass of heart muscle is comparatively healthy and in whom fits are rare or absent. The treatment. In all cases of heart-block a careful inc[uiry into the causation is to be undertaken, if it is not obvious. Syphilis as a possible cause is to be kept in mind especially. Persistent heart-block of the milder forms requires no immediate treatment, but is an indication for repeated examination of the patients who show it. As such patients usually require treatment for the general condition of the heart, constant supervision is not difficult. Digitalis medica- tion will frequently increase the grade of block. The increase of block should not deter digitalis administration, for that is 38 Chapter III. not in itself detrimental ; the drug or its allies may be given without restraint and some seem to receive benefit from it. When the abrupt onset of partial heart-block is observed, it is, as I have said, an index of active mischief. The patient should remain in bed and should be thoroughly searched for the provocative cause, which, when found, is attended to. The acute infections are suitably treated. Rheumatic patients are treated with salicylates, and scrupulous attention is paid to the hygiene of the mouth and throat. If, after the subsidence of remaining symptoms, the block remains and persists for several weeks, the patient is treated along the lines indicated in the previous paragraph. Heart-block in itself does not call for rest in bed or other interference, though a suspicion of an active or progressive lesion does. Full exposure to open air has been advocated and deserves a thorough trial. The higher grades of heart-block are usually chronic and stationary and the habits of the patient should be governed by his general fitness. Most patients of this class are up and about, and are able to undertake many of their ordinary duties ; yet it is only exceptionally that real bodily activity is either possible or permissible. Here again a suspicion that the lesion is active or progressive calls for rest and careful watching. A history or sign of syphilis constitutes an imperative demand for thorough and appropriate treatment, and in some cases success has attended the administration of mercurials and iodides or intravenous treatment. All those who have fits should be warned of the danger which they run from falls during these attacks if they do not appreciate it fully. Not a few have lost their lives by falhng heavily or in traffic and suffering mortal injury. In many cases the fits occur in groups, and additional precautions are required until such attacks cease. Most patients have brief Heart-hJock. 39 warnings of the onset of unconsciousness, and, if advantage is taken of these, less risk is incurred. A careful inquiry for causes predisposing to the fits may eUcit a history of gastro-intestinal disturbance or over- exertion, upon which it is well to act. For the fit when it is present I know of no remedy which is of avail to increase the pulse rate and restore the unconscious patient. Many drugs have been administered with this end in view, and the list includes oxygen, strychnine, strophanthine, digitalis and amyl nitrite. They appear to have no appreciable effect. Atropine is said to have abolished fits in isolated instances. As a rule it is contra-indicated. Adrenalin has recently been suggested ; I know not if it is of value. ( 40 ) Chapter TV. PREMATURE CONTRACTIONS OR EXTR ASYSTOLES. Definition. Contractions of the heart which disturb the rhythmic sequence by appearing early and in response to impulses newly formed in the musculature. The nature of premature contractions. A clear conception of disordered heart action can be attained only by those who are perfectly familiar with the normal beating. The orderly sequence of muscle movements, which constitute the normal heart cycle, is propagated, as I have already stated, from a single impulse born in the sino-auricular node. The contraction, starting from the mouth of the superior vena cava, travels rapidly through the auricle, reaches the auriculo-ventricular node and traverses this node and the bundle which is its continuation ; it is distributed in an orderly manner amongst the mass of ventricular fibres in which it ends. The normal rhythm of the heart consists of a regular sequence of such beats, so that auricle and ventricle contract in proper time relation to each other. Each stimulus elaborated at the sino-auricular node requires a certain time of preparation, and this time of Premature Contractions. 41 preparation is very constant in given circumstances. It is relatively long, reaching nearly two-thirds of .a second when the heart is beating at a normal rate. Indeed it is the time of impulse preparation which controls the rate of a normally beating heart. A second characteristic of physiological impulse formation is regular repetition. Each impulse belongs to a regular or rhythmic series. The premature contraction or extrasystole differs from the physiological beat in two fundamental respects. Firstly, the impulse which gives rise to it is formed at a phenomenally rapid rate. It is to this quality that the pathological con- traction owes its prematurity. Secondly, the pathological impulse is not one of a rhythmic series, and upon this character the usual isolation of the pathological contraction depends. Premature contractions originate abruptly, and may spring from the auricle, from the ventricle, or from the tissues which unite these two contractile structures. For ordinary clinical purposes it suffices if we remember the two chief classes of premature beat, the auricular and the ventricular. If, while the heart chambers are beating in a normal and sequential manner, a pathological impulse arises in the ventricle, the ventricular beat which it awakens disturbs this rhythm by anticipating the next rhythmic beat ; whence comes the term " premature contraction." It disturbs the sequence of ventricular contractions in a definite manner. Excepting the premature im])ulse, the ventricle is dependent for its stimuli upon the impulses which descend to it from the auricle. Consequently, after the disturbance produced by a single premature beat, the ventricle rests until a rhythmic auricular impulse reaches it. If the accompanying diagram (Fig. 22) is studied, it will be seen that for the first three cycles the ventricle follows the auricle in contraction ; a premature beat {p) is then interposed and as a consequence the oncoming auricular impulse, represented by the brokerj line, 42 Chapter IV. arrives while the ventricle is already in a state of contraction. Being in contraction the ventricle shows no response, ita muscle is in the " refractory " state. The dominance of Fig. 22. A diagrammatic representation of the disturbance produced by a premature venti-icular contraction (p). The auricle beats regularly throughout. The ventricle responds to six auricular impulses. The impulse of the central auricular systole is lost, for it falls while the ventricle is in preinature systole. The abnormal origin of the ventricular beat is indicated by the break in its centre. Note the equality in the lengths of periods a and b. c is the compensatory paiise. auricular impulses is reasserted during the succeeding cycle. Thus, the original sequence is restored by the fundamental heart rhythm which proceeds, unheedful of the disturbance. The ventricular contractions, subsequent to the disturbance^ fall at points which may be accurately anticipated ; the period of the disturbance (b) is exactly equivalent to the length of two complete cycles of the normal rhythm (a). The diastole which follows the premature ventricular beat is long ; the ventricle is waiting. The length of this diastole (c) is such as to compensate for the brevity of the diastole which precedes it, consecjuently it has been termed the " com- pensatory pause." When a premature impulse originates in the auricle the events are different. The premature contraction of the auricle, which it calls forth, is followed by a similar and x^arallel disturbance in the ventricle (Fig. 23), for the Premature Contractions. 43 ventricle responds to each auricular contraction, normal or abnormal. In all but exceptional instances too, there is a disturbance of the fundamental heart rhythm ; the premature contraction (/;) is followed by a long pause, but a b Fig. 23. A diagrammatic representation of a premature auricular con- traction. Tlie auricular rhythm is disturbed bj^ the abnonnal auricular beat (p) ; the disturbance in the ventricular rhythm is parallel, for each auricular systole yields a ventricular response. The rhythin of the whole heart is dislocated, the period a is longer than the period b. the whole period of the disturbance (6) is not equivalent, as in the case of the premature ventricular beat, to two full cycles of the normal rhythm {a). The original sequence is not restored. Etiological and pathological relations. Age. Premature beats have been recorded at all ages from a few weeks to old age. During the first decade they * are rare. Their incidence in an age table is actually heaviest between 50 and 70 years ; if the age distribution of the ])opulace is considered in conjunction with this fact, it becomes evident that they are essentially connected with advancing years. Age distribution of premature beats in 112 cases. Age 0-10 10-20 20-30 30-40 40-50 50-60 60-70 70-80 80-'J0 DO 100 Auricular 0244426101 Ventricular 2 13 8 14 20 18 , 4 2 15 12 13 18 22 24 5 1 44 Chapter IV. Sex. Premature contractions are much commoner in men than in women. In 129 subjects the sex distribution was as follows : - Sex Male. Female. Auricular . . 20 12 Ventricular. . 65 32 44 Associated conditions and provocative factors. It should be remembered that any statistics compiled to show the relations of premature contractions to associated conditions and infections suffer from a defect. Those cases which exhibit frequent and persistent premature beats preponderate in the tables ; for in these circumstances they are conspicuous, while if they are scarcer they often fail to attract attention. It is probable that the majority of people who live to middle life or advanced years are affected in this manner at some time or another. Amongst patients who attend out-patient departments or are admitted to the wards of general hospitals, frequent and persistent premature contractions are most common in those who exhibit definite symptoms and signs of cardiac disease. They are often found in association with aortic incompetence and mitral stenosis ; an even larger number of curves are collected from patients who present signs of degenerate heart muscle, as evidenced by dilatation and symptoms of muscle insufficiency in the absence of gross valve lesions. In yet another large group of patients, no evidence of functional impairment of the heart, leaving the irregularity out of consideration, can be discovered. They are not uncommon accompaniments of infectious disease ; thus, in scarlet fever and diphtheria they may cause irregularity of the child's pulse, and local pus infections are not infrequent associations. Prein ature Con tract io ns . 45 Premature auric ula r contractions. Cardiac group. Remainder. Mvoc'urclial degeneration Mitral stenosis 12 5 Bronchitis and emphysema . Puhnonary tuberculosis 2 2 Aortic stenosis 2 Dyspepsia Lumbago Exophthahnic goitre . . A])parentlj' healthy . . 1 1 1 4 19 11 Premature I'entricular contractions. Cardiac group. Bemainder. Myocardial degeneration 24 Tuberculosis (lungs and pleura) 5 Aortic disease 12 Bronchitis and emphysema 2 Mitral stenosis \:i Gallstones Angina pectoris Bright's disease and granular kidney 7 5 Gangrene of toes (senile) Epilepsy Lipoma of neck Arteriosclerosis 3 Fractured skull Acute endocarditis . . 2 Abdommal tumour Aneurism 1 Exophthalmic goitre . . Gastric ulcer . . Dyspepsia . . . . . . 1 Apparently healthy otherwise 8 67 24 Of the factors which appear to be predominantly associated with them, gross lesions of the heart stand first. Otherwise an inquiry into the habits, history and state of the patients throws but an obscure Hght upon the causation. A history of rheumatic infection is certainly common ; it was present in one-third of the cases of the above series. In young adults, excessive tobacco smoking is recognised as an exciting cause of their temporary appearance. Digitalis and its alUes are not uncommonly responsible, when the patient is under the full influence of these drugs. There are also clinical associations between premature contractions, raised arterial pressure and digestive disturbances, but these are not fully understood at the present time. Many things affect the frequency of premature con- tractions. Fatigue, subsequent to exertion, is provocative in those who are predisposed. The influence of heart rate 46 Chapter IV. is especially noteworthy. Hearts beating at 100 per minute and over are not often disturbed, and premature contractions are very rare when the heart rate exceeds 120. Fever usually rids the pulse of this form of irregularity, and so also does any cause which notably accelerates the pulse rate. Thus they are abolished during exercise and for a short period afterwards, but during the period of slow heart action which often follows exercise, they are frequent. As we shall subsequently see, this knowledge may often be used advantageously to induce premature beats in patients pre- disposed to them. Suspension of respiration for a period compatible with comfort often suflEices. The pathological beats are in evidence either in the apnoeic stage or shortly after the resumption of respiration. No factor is more potent than posture. Patients who exhibit numerous premature contractions while standing may soon lose them in recumbency, and this despite a slight decrease of heart rate in the last position. In other patients, pressure upon the abdomen may abolish them. The recognition of premature contractions. The work accomplished by premature beats is small, because the periods of rest that precede them are short. They may or may not raise the aortic valves. Accompanying the premature beat, a feeble pulsation or a prolonged pause is noted in the arterial pulse ; auscultation reveals early first and second sounds when the aortic valves are forced, but only an isolated and premature first sound if the ven- tricular pressure fails to top the arterial. The consequent grouping of sounds in threes and fours is comprehended when the nature and degree of the corresponding arrhythmia are discerned. The commonest arrangements of pulsations and sounds are described in the following paragraphs, and are illustrated by the accomjDanying diagram and tracings. Premalure Contractions Fig. 24. A diagram showing common disturbances of the arterial pulse and heart sounds when premature ventricular contractions are ])resent. (a) Normal rhythm ; (b) Occasional jiremature beat, which affects arterial pressure ; (c) Occasional premature beat, which fails to affect arterial ])ressure ; (d) Premature beat re|)lacing each third normal beat and affecting arterial pressure ; (e) Premature beat rei)lacing each third normal beat and failing to affect the arterial pressure ; (/') Premature beat re])lacing each second normal beat and affecting the arterial ])ressure ; (g) Premature beat replacing each second normal beat and failing to affect arterial pressure. The heart sounds occur in groups, and the grou})s are of four or three, according as the aortic valves are raised or remain at rest when the premature beat occurs. 48 Chapter IV. In the succeeding ])aragraphs I have sub -grouped the symptoms according as the premature beat (a) raises or {[3) fails to raise the aortic valves. 1. When a systole of a regularly beating ventricle is replaced by a premature beat, this abnormal contraction is accompanied by an early apex thrust and by (a) a weak arterial wave and two extra sounds, which together with those of the preceding rhythmic beat form a group of four (Fig. 24 h and 25) ; or by (ft) an intermission in the arterial pulse and one extra sound, forming with the sounds of the preceding rhythmic beat a group of three (Fig. 24 c). 2. When each third beat of the regular ventricular rhythm is replaced by a premature beat, we find a grouping of the apex thrust in threes, of which the third beat in each group is premature. The arterial beats (a) are grouped in threes,* with groupings of the apical sounds, so that two normal heart sounds alternate with a group of four sounds (Fig. 24 d) ; or (fS) are paired with groupings of the apical sounds, so that two normal heart sounds alternate with a group of three sounds (Fig. 24 e and 30). 3. Premature beats which alternate with rhythmic beats give rise to pairing of the apical thrusts (Fig. 27, 28, 32)^ and to (a) pairing of arterial beats of which the second stroke is weak, and to groupings of heart sounds in fours (Fig. 24 / and 29) ; or to (/?) halving of the rate of the arterial pulse, and heart sounds in groups of threes (Fig. 24 g and 28). To decide whether the premature beat arises in auricle or ventricle is not usually possible without suitable recording- instruments. When an occasional premature beat occurs, the indica- tions of its ventricular origin are as follows : (a) There is no disturbance of the fundamental heart rhythm. The presence * Premature beats may also be responsible for groups of three arterial beats when they replace each fourth rhj'thmic beat (Fig. 26). Premalure Contractions. 49 "irvnfwvwwmmw r\ ,y Apti" F^oiial Fig. 25. Apex and radial curves, showing a single jirematiire ventricular contraction. The intervals a and 6 are equal. ■vvv^ yrry- "(^•>»"« 't \) k. t' \t ^ \f v-~v— V- Fig. 26. Radial curve and heart sounds m a case in which })reinature ventricular contractions replace each fourth normal beat. The premature beats fail to affect the pulse. ilfT» fl f U » l » » '»«»»»1»»»»ltII»ttt H tll»»' V >»« l t» ll» »1l ( tT»»»«l'«l 'M li~y Fig. 27 and 28. A])ex and radial curves and heart sounds. The normal mechanism passes into one in which jiremature ventricular contractions, replace alternate normal beats. Fig. 27 is from a case in which mitral regurgitation was present. In Fig. 28 the intervals a and b are equal. fKV**- Fig. 29. Premature ventricular contractions replacing each second normal beat. The heart soimds are groui)ed in fours ; the pulse is of the form termed pulsus bigeminus. 50 Chapter IV. of this phenomenon may sometimes be elicited, in feehng the radial pulse, by anticipating the points at which the rhythmic beats, following the disturbance, ought to fall to carry on the original rhytlim ; but it is usually easier to detect disturbance of the rhythm than to exclude it by this method. A strip of radial curve by itself is almost always sufficient to distin- guish one from the other ; in the instance of the premature ventricular beat the full period of the disturbance is equal to two normal cycles (Fig. 25). In the instance of the premature auricular beat the full period is less (Fig. 31). (b) There is often a prominent jerk and swelling of the veins of the neck (Fig. 30) at the time of the premature ventricular beat. This is brought about in the following fashion. The ventri- cular beat, falling prematurely as it does, coincides with a rhythmic auricular contraction, so that the two heart chambers are in systole together (see Fig. 22). As a consequence of this simultaneous contraction, the auricle fails, for a single cycle, to empty itself into the ventricle, and pumps the blood back into the veins, (c) Synchronism of the premature ventricular beat and the rhythmic auricular contraction often exaggerates the corresponding first sound. When the premature beat follows pairs of normal beats or alternates A\nth normal beats, signs b and c mav be present, but a is usually valueless unless a transition from a period of disturbance to a period of normal rhythm is graphically recorded (as in Fig. 28 and 32). A com])arison can then be instituted between the lengths of the disturbed and undisturbed heart cycles. Thus, in Fig. 28 the long cycles are exactly twice the length of the short ones ; a is equal to b ; premature contractions arising in the ventricle have created an exact halving of joulse rate. In Fig. 32 the pause following the premature contraction is not compensatory ; a is longer than b (see Fig. 23). The effect of premature beats upon the auscultatory signs, when murmurs are present, are manifold ; yet most of them can be foretold if the general principles are grasped. A systolic mitral murmur will be found with the premature as well as with the rhythmic beat (Fig. 27), but it is usually short and may be absent. In aortic disease, a systolic or Premature Contractions. 51 I'ig. ."50. Curves from the neck iiiul rtulial artery. Promature ventricular contractions rei>laco each third normal beat, but do not affect the pulse. An exaggerated first sound and a prominent wave, easily visible in the neck, accompanied each premature beat ; these phenomena result from simultaneous contraction of auricle and ventricle. » < > y \^m^ Fig. 31. Apex and radial curves showing occasional premature auricidar contractions ; a is greater than b. I ■ » ■ » » T » ^lTv^/I/^ TlA ' ^ ' Fig. .32. A " bigerainy " or coupling of heart beats, resulting from ])remature auricular contractions, passing into the normal rhythin ; a is greater than b. Fig. 33. A bigeminy, resulting from j)remature auricular contraction!. The beats are paired in apical and radial curves. Aortic regurgitation was present. E 2 62 Chapter IV. diastolic murmur is present at the base of the heart when the premature beat raises the aortic valves (Fig. 33) . On the other hand, in mitral stenosis, a pres3^stolic mitral murmur is usually absent whether the premature beat is auricular or ventricular, but in the former instance, it is often replaced by a presystolic sound. The absence of the presystolic murmur in the case of the auricular beat is attributable either to weakness of the premature contraction or to its coincidence with the preceding ventricular systole. More complex heart sounds are heard when a premature beat raises the pulmonary but not the aortic valves, as sometimes happens ; the second pulmonary sound occurs, but the second aortic sound is absent. This phenomenon has been erroneously ascribed to hemisystole, the presence of the second sound of the right heart and the absence of that of the left heart being taken as evidences of activity and quiescence of the respective ventricles. The subjective phenomena ivhich accompany premature contractions. In a very large number of those affected, the disturbances of heart rhythm pass unnoticed. On the other hand pre- mature beats not uncommonly cause what patients term " palpitation." The symptom is more prominent in young subjects, especially those of female sex and those afflicted by nervous instability. When numerous, they sometimes occasion actual distress ; by calling attention to the heart, they often induce anxiety. The sensations experienced are exaggerated by depression of the general health, by fatigue and by emotion. They are often more noticed after the , patient retires for the night, after excessive smoking, after : a heavy meal, or after exertion. As a general rule the premature contraction itself passes unperceived ; the long pause which follows awakens a sense Premature Contractions. 53 of uneasiness or oppression in the chest, or a feeling of void, while the succeeding contraction of the heart is accompanied by consciousness of shock to the chest wall and frequently by a gripping in the throat. Patients in whom these sensations are vivid sometimes swallow, cough, or inspire as soon as they experience them. When a number of premature beats succeed each other at short intervals, and consciousness of them is marked, anxiety may be profound, v and faintness, coldness of the extremities and even sweating may result. The prognosis and treatment. It should be clearly understood that, in speaking of the prognostic value of premature beats, I speak of these beats without reference to the conditions with which they are associated. That when frequent and persistent they often accompany grave affections of the heart will be evident from a study of the tables already given ; but this fact does not affect the question discussed.* The associated lesions give prognostic indications of their own ; our inquiries are as to whether a heart, which presents no other sign, can be regarded as healthy and as to whether, in the case of an unhealthy heart, the prospect has an added gloom. It must be admitted that all such beats are decided evidence of a pathological condition and that the pathological process has its seat in the tissues of the heart. The presence of premature contractions is an indication of disturbance of cardiac nutrition, whether temporary or permanent, but it is an aspect that should not be allowed undue prominence, / A number of people are temporarily affected by premature ^" beats which do not reappear, while the heart manifests no sign of further damage, either at the time or afterwards. In * Some fail to grasp this point and I would enforce it by a simple illustra- tion. Scars on the tongue of an epileptic do not influence the prognosis of the disease. 54 Chapter IV. such instances it is impossible to suppose that the disturbance of the cardiac function has been more than transient or that the nature of it has-been serious. Observations and inquiry also teach that they may be present constantly and for long periods, and that those who manifest them may do so from an early to a good old age, such patients never showing any other sign or symptom of cardiac disability. It may be said, therefore, that in themselves premature beats cannot be v/ regarded as evidences of serious involvement of the heart muscle, although such involvement is often found in conjunction with them. The question can be regarded from another standpoint. The premature contractions, when present and frequent, inevitably increase the work of the heart, but the amount of the added burden is not easy to ascertain. It is probably not weighty, for where the muscle is evidently compromised and frequent premature contractions occur periodically, little change in the condition of the patient can be detected from time to time, and serious embarrassment of the circulation as a direct result of them is only suspected on rare occasions. Modern observations therefore tend to minimise the significance of these beats ; in fact, it has been taught that they may be neglected in the forecast. My own standpoint is a more guarded one. Premature contractions constitute and bear witness to defects ; there is the mechanical imper- fection and there is the evidence of altered cardiac nutrition ; \ and the more frequent the interruptions, the greater the \ . degree of such defects. Moreover, single premature beats ^' ' testify to the presence of a process which may lead to cardiac irregularities of a more serious nature. They may be precursors of grave conditions, which are considered in subsequent chapters. Premature beats, true paroxysmal tachycardia, auricular flutter and fibrillation have a common Premature Contractions. 56 pathological basis ; they are one and all the outcome of new impulse formation in the heart. While it is true that the majority of hearts which show premature contractions never exhibit profounder derangements, it is also true that these occur for the most part in hearts in which single interruptions have been common ; it follows that of hearts seen to-day, some of which show premature contractions and some of which show none, the incidence of grave irregularities will in later years be greater in the former than in the latter. I may summarise in the statement that, while premature contractions have unquestionably a relatively insignificant import, as compared to many forms of cardiac irregularity, to neglect them entirely is inadvisable. Although their detection should not be allowed, in itself, to cripple or hamper the patient A\ho is the subject of them, a re-examina- tion of such cases from time to time is recommended. The first standpoint of treatment is already indicated. The presence of premature beats does not call for a limitation of bodily exercise ; it should not prejudice the vocation or pastime of the patient. Restrictions are necessitated only where other signs render them advisable, or where some particular act or occupation is definitely known to originate symptoms of a distressful kind. The anxiety to which the beats conduce in some subjects may be materially allayed by reassurance. No drugs are known which influence their prevalence ; digitalis as a direct measure is contra-indicated. The symptoms are usually masked or considerably modified by the bromides administered in doses of from fifteen to thirty grains or more a day ; and these drugs are especially useful in tiding a nervous or excitable patient over a period of disturbance. ( ^^c ) Chapter V. SIMPLE PAROXYSMAL TACHYCARDIA. Definition. Paroxysmal tachycardia is a term which has been and still is applied to several distinct phenomena. It will be of material assistance at present if I restrict my description to the simple form and define it as a condition in which from time to time the normal mechanism is interrupted by a series of rapid and regular beats, varying in rate between 100 and 200 per minute,* the series starting and ending quite abruptly. The nature of simple paroxysmal tachycardia. It has been said that the normal pacemaker of the heart lies at the union of the superior cava and right auricle. The usual rate at which the rhythmic impulses proceed from this focus is 72 per minute in the adult. If a new centre of in:pulse formation develops in any portion of the heart wall, and this centre forces responses at a rate surpassing that of the normal rhythm, then, while it is active, the new centre dominates the movements of the whole heart. Such are the paroxysms which we are about to study ; they consist of sudden accelerations of heart rate in response to new and pathological impulses. The paroxysms may be regarded * In so defining it I have purposely excluded all accelerations of normal or sinus rhythm, for these are dependent uj)on altered innervation. I have also excluded two forins of tachycardia, which are closely related to that descriVjed in the present chapter ; one, which is regular, but in which the aiu-icular rate exceeds 200 per minute (see Chapter VI) ; the other, which is irregular (see Cha])ter VII). Simple Paro.vt/snial Tachycardia. 57 both clinically and pathologically as formed essentially of a regular series of extrasystoles. The new impulses are elaborated in a single focus, whence the regularity of the series, and this focus lies, usually or always, at a point Mhicli is removed from the pacemaker.* Fig. 34 opens with •X. V Fig. 34. A diagrammatic representation of a short paroxysm of premature auricular beats ; a paroxysm of tachycardia. The abnormal auricular beats are broken in their centres. Each yields a ventricular response. The first abnormal beat occvipies the same position in relation to preceding events as does that of Fig. 23. The short paroxysm ends in a cycle y. y is longer than .t. three normal heart beats, and the fourth auricular contraction (p) is premature. Up to this point the diagram is identical with that shown in Fig. 23t ; it differs from the earlier picture in the repetition of the abnormal contraction, five such beats following each other in rapid and regular succession. In each instance the ventricle responds. The paroxysm terminates, and its end is marked by a cycle {y) which is longer than the normal cycle {x)% ; the pause which follows a paroxysm derived from the auricle has generally the same length as that which in the same case succeeds an isolated premature contraction (see Fig. 23). * A statement which is based upon the findings of electro-cardiographic curves. t In both diagrams I have broken the auricular rectangle, to emphasise the abnormal birthjilace of the pathological contractions. % The interval {x) has been deliberately chosen at the onset of the ])aroxysm, because the restored rhythm of the old pacemaker is often slow for a few cycles. For simplicity this retardation is not figured, but it will be referred to again at a later stage. 58 Chapter V. How important a clear conception of this disturbance is will be evident, for the nerve control of a new centre of impulse formation is not known from analogy ; as a matter of fact, the new rhythms show only limited subordination to vagal and sympathetic control. The sites in which the new rhythms develop ar& numerous ; the abnormal focus is generally seated in the auricle, and the usual sequence of contraction is consequently maintained in the heart chambers ; but it may be ventricular and the auricle then responds reversely to the ventricular beats. The chief features of the mechanism will be sufficiently impressed by a closer examination of the commoner auricular variety. The diagram exhibits a paroxysm of five beats ; this short series displays both onset and offset. Actually the attack may last a few seconds or a week or more ; what- ever its length the mechanism is constant, but the symptoms- vary with the duration. The extreme ranges of rate in this the simple form of paroxysmal tachycardia is from 110 to 200 per minute ; during most paroxysms the heart contracts 140 to 190 times- per minute. Etiological and patJiological relations. Age. Paroxysmal tachycardia may occur at any period from childhood to old age. In a series of 45 cases, the age- distribution was as follows : — Age 10-20 20-30 30-40 40-50 50-60 00-70 70-80 Cases 4 11 7 7 7 6 3 Instances have been recorded in quite young children ; but these are rare. The highest incidence is between the ages of 20 and 30. Sex. In this series 30 males and 15 females are included. That is to say, the disorder is a good deal more frequent in Simple Paroxysmal Tachycardia. 59 men than in women. This proportion is in fair agreement with other resords, though perhaps the male element is less predominant in the whole number. Heredity has been blamed, but the evidence is insufficient to show that it has any direct influence. Relations to infective disease. In quite half the cases no history of previous illness, other than perhaps children's ailments, can be traced. Rheumatic fever is the only infection which is at all common. Occasional instances appear to have followed immediately upon malaria, measles, pneumonia and scarlet fever ; a few of the patients have been syphilitic. Associated conditions. Most cases of paroxysmal tachy- cardia show no sign of valve lesion, and in a large number of the patients there is little or no evidence of dilatation during the intervals between the paroxysms. Nevertheless many of them exhibit a limited field of cardiac response and become breathless with slight exertion. Taking dilatation, in the absence of valve lesion, undue breathlessness upon exertion and the subsequent development of more serious signs of cardiac failure as evidences of de- generation of the myocardium, I have placed nine of the patients in a corresponding group in the accompanying table. The only valve lesion which figures prominently is mitral stenosis, being present in ten of the cases. Paroxysmal tachycardia and associated conditions. Mitral stenosis . . Myocardial degeneration Arterial disease (with and without angina) Aneurism (thoracic) Renal disease and cardiac dilatation Early pulmonary tuberculosis No other signs . . 10 10 4 1 3 1 16 45 60 Chapter V. Factors promoting attacks. Exertion or emotional dis- turbance are the chief excitants of attacks in those predisposed to them, and the proportion of cases in which the history tells of paroxysms evoked in these ways is remarkably high. Flatulence, other digestive disturbances, and especially the assumption of certain postures, are also chief provocative agents. The induction of a first attack by unaccustomed effort is often responsible for their hasty assignment to overstrain, but strain is never the complete story ; probably damaged or ill-nourished muscle is in all cases the underlying mischief. Morbid anatomy. In the instances in which examination has been possible after death, the most prominent and frequent lesions have been in the walls of the heart. Fibrosis, pallor, friability, atrophy and interferences with the arterial supply are the chief naked eye changes recorded. In a fcAv cases of tachycardia nerve lesions have been found, but their association with the specific condition with which we no^^' deal is more than doubtful. The recognition of simple paroxysmal tachycardia. Whenever a patient is seen in whom excessively rapid heart action is a prominent sign, the nature of the acceleration should be determined at once ; the tachycardia may be a simple acceleration of the physiological rhythm or it may be a pathological rhythm ; in the first case it is not, in the second case it is primarily cardiac in origin. A heart rate of 180 or more in an adult is usually the result of pathological impulse formation, and especially is this the case where a heart lesion is known to be present. The rate of the ventricular beating is preserved ivhen the patient passes from the upright to the recumbent position ; it is rarely altered by more than a few beats per minute even when Siviple Paroxysmal Tachijcardia. 61 a supine position is maintained for considerable periods of time. A physical sign of the utmost diagnostic importance may be noted at the onset or offset of an attack, the increase and decrease in rate at these times is absolutely abrupt. In patients who are conscious of the rapid heart action, but in whom the offset and onset cannot be observed, the sudden change at the beginning or ending of the attack can usually be elicited by careful questioning. When tachycardia is due to a rise in the rate of the physiological rhythm, as in exophthalmic goitre, irritable heart, etc., the rate responds to posture, rest and other factors ; it is under some measure of nerve control. In palpitation, which owes its origin to quickening of the physiological rhythm, the rise of rate and the subsequent fall of rate is gradual and not abrupt. In paroxysmal tachycardia other physical signs may be present, though their significance is not so great. A prominent and palpable pulsation in the veins at the root of the neck is often present ; it may be almost aneurysmal in force. The arterial pulse is frequently irregular in force, and at the first examination may give an erroneous impression of an irregularly beating ventricle. No obser- vations are more unreliable than counts of pulse rates taken in the ordinary manner during the paroxysms ; they should always be checked at the apex beat, either by touch or hearing. The heart sounds are tic tac in character and murmurs which may have been noticed on previous occasions usually disappear while the heart rate is raised. The last sign is of value in mitral stenosis, in which such attacks are relatively common ; for the presystolic murmur is abolished. When a rough presystolic murmur is lost by a patient who develops an accelerated and regular heart action, the disappearance of the murmur is generally attributable to an abnormal rhythm. In patients who suffer periodically from tachycardia, 62 Chapter V. the presence of occasional premature beats during the periods of quiescence is extremely suggestive that the tachycardia is due to new rhythm production. The curves are illustrated by Fig. 35-37. In Fig. 35 the onset and offset of the period of tachycardia, due to m^timmrTfTT I "' • " '■' l ll»lll'WW»WT»TWWT»»»W»»WW»W»l»«HW»lTtt1tnTWIIII|ni H «I H I' H I »■■ > I> Fig. 35. ^JuJ^^^^v^J^^J^^v^^^J^O^^K^J^.J^.^^^ II II tl nil IICI II II Fig. 36. fM\iMhiJmmi^^ 1 1 I I 9 III at Fig. 37. Fig. 35 to 37. Three radial curves, taken from separate cases of paroxysmal tachycardia. In Fig. 35 a short and complete paroxysm is shown. In Fig. '3(i and 37 the terminations of longer paroxysms are seen. Note the abrupt onset and offset of the paroxysms, the pauses in which they terminate, the irregularity of the slow periods and the regtilarity of the fast periods. abnormal impulse formation at a new auricular focus, is shown. The slow periods to left and right of it are irregular, for premature contractions interrupt them The terminations of two long paroxysms are shown in Fig. 36 and 37. The Simple Paroxysmal Tachycardia. 03 noteworthy features of such curves are several. The changes from the slow to the fast and from the fast to the slow ventricular rates are quite abrupt. Following each paroxysm is a relatively long pause, and this forms the first of a series of ])auses in a period of retarded rate. The rate at the actual termination is almost always slower than the average rate during the periods of quiescence ; quickening, which is best seen in Fig. 36, occurs directly after the termination. The slow rhythm is interrupted by occasional premature con- tractions ; usually these may be shown by special methods to have the same point of origin as the paroxysm. Symptomatology of paroxysmal tachycardia. Broadly speaking, the less frequent the attacks, the longer do they last. In a given patient, the duration of attacks is fairly constant, so that the paroxysms are similar from time to time. Paroxysms of a few seconds duration are not nncommon ; attacks w^hich last for several hours are the most frequent ; those of a fortnight's duration are rare ; the attacks may be of any intermediate length. Paroxysms of accelerated heart action of longer duration and of the form considered in the present chapter are unknown (see succeeding chapter). The symptoms accompanying paroxysms of tachycardia of the kind considered are variable both in their nature and in their degree. They are intimately dependent upon the duratidh of the attack, the heart's rate during it, and upon the capacity of the heart muscle. Amongst those in whom the attacks are brief, it is not uncommon to find that a patient is entirely oblivious to the rapid heart action when it occurs, and this is more especially the case when the subject is elderly and of the phlegmatic type ; or he may be conscious of transient attacks only when his attention is specifically s s ^ cc -i-i j:: c ^ fl Nj -l^ *'^ 60 fll c8 ^ oT _S 1^ ^ t, -^ X! •- '3 X tn iD cu c6 -G CO Q C i-^ -^ G 5, fcC ^ p ■"^ C "^ Is © ca ;» ^ ^ cS > ^ «) b "G o| 33 ^ 0) C 5^ ce ?r' ;^ s 5d o 03 -^ r; CD S -2 t- fl CO £; t3 h <6 'C 5j_, ce o aa l; ® -t^ "o .^ cS 03 oc t8 _c bb ^ 'w ^ be o .£P C ^ So" qj 5, c8 ^ fl ^ p ^ -»^ ■5 Sb c3 c S^ ■^ 4) ce !-. ^ 33 '^ bb g i ® o h © s i S « <: < Ph P5 Of etiological factors, rheumatism is predominant, as we have seen ; a history of other infections, " influenza " amongst them, is given by many patients, but the influence of these infections is imperfectly understood. The heavy figures mark the rheumatic group. Ai(ricular FihriUation. 89 An idea has been prevalent in the past that dilatation of the heart may itself lead to gross irregularity of the organ, such as is here described. This idea is fanciful. Dilatation does not produce irregularity, but irregularity, when associated with rapid ventricular action, may dilate an injured ventricle. Morbid anatomy. That valve lesions are present in a number of the cases is obvious from the bedside examinations ; enlargement of the whole heart is common, and dilatation or hypertrophy of the auricles is more frequent than the valve lesions which might be held to account for them. The most constant structural alterations which are found are discovered by histological examination of the heart muscu- lature. Usually it shows a more or less intense grade of subacute or chronic inflammatory change progressing to fibrosis, and the auricles are conspicuously affected. A diffuse fibrosis, accompanied by leucocytic infiltration and atrophy of the neighbouring muscle cells, is the most frequent change. Such is the tale told by the microscope, but it does not justify us in holding that the inflammatory reaction is the cause of the disturbance. We examine the hearts of those who die, and most die with all the classical signs of heart failure. Many of the microscopic lesions are to be regarded as the result of infections producing heart failure rather than fibrillation. Similar lesions are found where fibrillation has never occurred ; and hearts which have shown this disorder may not present the lesions described. The recognition of auricular fibrillation. Auricular fibrillation gives rise in a clinical case to two series of phenomena — the one dependent upon the virtual paralysis of the auricle ; the other dependent upon the irregularity of the ventricle. It will be convenient to study the ventricular signs first. The irregularity varies in form according to 90 Chapter VII. * B a C tt 5 T. c +- ,( , ib c _CB +i « _o o -C a2 _c o K 7. H 2- ■r. ^ <_ x cc ^ c=^ S c ■i ^ ^ "C < 1 1^ o ^•^ o 7^ ^4 uriciihtr FibriUation . 91 ? n 92 Chapter VII. the rate of the contractions. When the heart is beating- rapidly at 100-160 per minute, the grade of disorder is maximal. The pulse supplies indifferent news of the ventricu- lar rate, many pulsations fail to reach it (such beats are- marked with asterisks in Fig. 46). The pulse is a medley of beats of many sizes (Fig. 45), an intimate mingling of changing pauses ; now the beats are almost uniform in strength and spacing ; now feeble pulsations chase along^ rapidly ; now the pulse is lost ; now it returns with increased vigour. Feel the pulse and the nature of the disease is disclosed ; the more turbulent the pulse, the more certain is the evidence. It is when the rate is slow that close attention and more experience are often asked, for with slower rate the- disorder is less pronounced ; all the heart beats now reach the wrist and the irregularity comprises minor variations in the length of diastole (as in Fig. 48) ; it may then escape notice, and a heedful examination, concentrating upon its presence or absence, alone brings it to discovery. Short pulse curves reveal the irregularity on all but rare occasions. The nature of the arrhythmia is such that the heart action is never quite regular, and seldom do two beats of a precisely similar character or length lie adjacent. No two whole strips of curve are alike ; the cycles bear no simple length relation one tc^ another. Proportion between the force of an arterial pulse and the length of rest preceding it is often lost (Fig. 45 and 46) ; a strong beat succeeds a brief diastole and a weak beat succeeds a long one. When the pulse is slow, only beat to beat measurement may disclose the irregularity. The fully developed disorder of the ventricle is readily appreciated at the apex. The heart sounds are modified ;. they vary in intensity and the variation runs hand in hand with the strength of the beats. First and second sounds are present with each systole which yields arterial pulsation (Fig. 45) ; a first sound stands isolated when the pulse beat is- Auricular Fibrillation. 93 missing (Fig. 46). If a systolic mitral murmur is present, it •accompanies each ventricular contraction (Fig. 49), except Avhere the rate is fast, for here it is apt to vanish. Aortic murmurs obey the general rule, their presence or absence is <'ont rolled by the efficiency of the respective beats (Fig. 47). The inactivity of the auricle is responsible for special .alterations of the heart sounds in patients who have stenosis of the mitral orifice. It is customary to allude to disappear- ance of presystolic murmurs when the auricle fibrillates, but this statement is not exact. The change in the characters of the murmurs at the onset of fibrillation is oftentimes impres- sive, but it varies according to the heart rate and the degree ■of stenosis. If there are short presystolic murmurs while the heart beats regularly, these murmurs usually vanish when fibrillation begins ; and more especially if the rate during fibrillation is rapid. If the presystolic murmur is long and rough, a murmur of similar character is preserved ■during fibrillation. But its time relations are altered. Attention should concentrate upon the position of the second sound at the apex. When the auricle is fibrillating, the diastolic murmur has a fixed time relation to this sound. If the heart is rapid, the murmur begins early in diastole and fills the whole gap to the first sound of the succeeding beat (Fig. 48) ; if the heart rate is less rapid, the murmur maintains its relation to the second sound but falls short of the succeeding first sound during the longest ventricular pauses (Fig. 46^?) ; if the heart rate is slow, a long, though varying, interval separates the end of the murmur and the next first sound ; the murmur is then confined to early diastole (Fig 50). The whole series of murmur arrangements may be observed in a single case which exhibits different heart rates from time to time. The reason of the changes will be clear when the pressures and mechanism are considered. The diastolic murmurs of mitral stenosis are dependent upon the 94 Chapter VI I. rate of flow through the constricted orifice, and the rate of flow is controlled by the difference of pressure in auricle and ventricle at any given moment. Now although the auricular pressure exceeds the ventricular during the whole of diastole, the excess is greatest at two phases, namely, when the auricle is in contraction and directly after the opening of the auriculo-ventricular valves. When the auricle contracts in normal fashion, mitral diastolic murmurs are in chief evidence at flrst in late and afterwards in early diastole ; they are found in early diastole when the auricle is virtually paralysed, especially when, the heart rate being slow, stasis raises the ventricular pressure during the last phases of diastole. Auricular fibrillation is recognised clinically by the nature of the ventricular action, but its detection is aided, as we have seen, by other signs. It is possible, too, to^ formulate a few general rules, which serve as useful guides in identifying it. When the ventricle beats irregularly at a rate surpassing 120 per minute, the irregularity is almost always of this nature. When an irregular ventricular action accompanies signs and symptoms of serious heart failure, it is probably the result of auricular delirium, and the proba- bility is increased if the heart rate is much accelerated. In patients in whom the heart is irregular, but in whom the heart rate is not much accelerated and in whom signs of heart failure are absent or few, a test may be applied which is of considerable value. Moderate exercise augments the ventri- cular rate, and this is so whether fibrillation is present or not ; but there is a striking contrast in two given cases of irregularity of which one is due to auricular fibrillation, while the other has a different cause (.'.e. premature beats, partial heart-block, etc.). In fibrillation the pulse becomes more irregular with its acceleration, while in the remainder the pulse steadies. When premature beats are present, a sufficient acceleration of ventricular rate to abolish them temjjorarily Auricular Fibrillation. 95 may often be induced by several quick changes from the recumbent to the sitting posture ; this is not so where fibrillation is concerned. Reversely, as the pulse slows subsequent to exercise, the irregularity of fibrillation decreases, while other forms of irregularity become more prominent. Fever similarly raises the ventricular rate and during the febrile stage the disorder of fibrillation persists and is often augmented in degree. Finally, the persistence of the irregularity, which is due to fibrillation, needs emphasis. In most cases it is continuous from the time of observation until death. The other irregularities are present from time to time, so that there are intervals of regular ventricular action each hour or each day. The general symptomatology. The symptoms comj^lained of by patients in whom the auricles fibrillate are various, being dependent mainly upon the concomitant conditions. For the most part, they are the symptoms of degenerate and failing heart muscle, and these do not require reiteration at the present time. The symptoms which are now our special concern are those which appear to be the special effects of fibrillation itself. Patients who possess the persistent disorder often experience occasional fluttering in the chest and neck and may be conscious of irregular heart action. They are more prone to shortness of breath, exhaustion and other symptoms of over-taxation of the heart than are those with similar valve lesions and a like degree of cardiac dilatation* ; but it is not always easy to allot these superadded symptoms to precise causes ; they are in part the result of the graver myocardial condition which consorts with fibrillation ; they are in part due to the actual turbulence and embarrassment * On the other hand they seem pecuharly exempt from angini,. 96 Cha^pter VIL of the ventricular movements.* We know that the heart is taxed by its disorderly action, but it cannot be stated that any symptom, such as cyanosis, conspicuous dyspnoea, noticeable venous engorgement or dropsy, is the direct outcome of fibrillation ; for cardiac failure and these, its classical accompaniments, are to be found where there is no fibrillation, and instances of fibrillation are common in which these symptoms have not developed. The symptoms, as has been stated, are provoked by the interplay of two factors, namely, the inherent muscle defect and the extra burden of disordered action ; while the signs of failure are proportioned to the degree of muscle damage, the whole of this symptomatic scale is raised by rapid heart action. In the healthy hearts of animals it is a general rule that fibrillation of the auricle produces a fall of arterial and a slight rise of venous pressure, but at the same time it is accompanied by a decrease in the heart's dimensions, a usual phenomenon when the rate is increased. The heart accommodates itself to the new conditions in a few moments ; the arterial pressure rises and the venous pressure falls, so that they almost recover their previous levels and the blood flow is maintained in a wellnigh perfect fashion. But if the heart has been damaged, the effect is both profound and lasting and in place of decrease of heart volume, an increase may occur. So it is in patients. Patients may experience paroxysmal fibrillation at intervals of a month or perhaps a year ; many of them pass through their attacks with little or no sensibility of them ; neither can any sign, other than the disordered action, be discovered during their progress. Yet similar crises give rise in other patients to profound and serious disturbance, breathlessness, pain, cyanosis and further indications of increasing dilatation of the heart. In these, the severest cases, the symptoms * The heart embarrassment is the result of ventricular irregularity and especially rapid action ; the virtual )miralysis of the auricle is withovit appreci- able effect on the general circulation. Aiiriculdr Fibrillation. 97 resemble those of long eoiitiuued paroxysms of regular tachycardia. Between the mild and most extreme reactions is the intermediate. The variation in the reaction is great, and, as I have said, is largely attributable to the grade of underlying heart mischief. But there is another and equally important factor in the human subject ; it is the grade of the ventricular disorder during the attack. Just as the muscle defect varies in its degree, so also does the burden imposed upon it ; thus it is found that little reaction is shown in paroxysms of relatively slow ventricular action, while amongst those with grave disturbance the ventricular rate is usually rapid. Influence upon thrombosis and iiifarction. If a series of diseased hearts is examined at autopsy, ante-mortem clots are found in much the heavier percentage in those auricles which during Hfe exhibited fibrillation. The virtual paralysis of the auricles, and the consequent stagnation of blood in them, definitely predisposes to thrombosis in the appendices. Yet in mitral stenosis haemoptysis, the result of lung infarction, appears to be no commoner where fibrillation exists than where the natural rhythm is preserved. The explanation seems to be that although fibrillation aids the formation of clots, the passivity of the auricular walls safeguards the detachment of these clots. In paroxysmal fibrillation I have observed a coincidence between embolism of lungs and brain and the resumption of the normal auricular contractions. Presumably, clots formed during the period of auricular fibrillation are detached if and when the heart resumes its natural mode of beating. Remarks upon diagnosis. The diagnosis, often suggested for cases w hich exhibit fibrillation of the auricles, is still that of the accompanying 98 Chapter VII. valve lesion, though I am strongly of opinion that it is no longer warrantable. A diagnosis should include either the outstanding feature of the pathology, or it should be chosen that it may become associated with some specially beneficial form of treatment. In these patients a chronic affection of the myocardium is the essential lesion ; while the relations of the cardiac disorder to digitalis medication are so peculiar that the named disorder of the heart always brings this drug to mind. But I wish to refer but briefly to this question of termin- ology under the present heading, which I have chosen to emphasise a common and avoidable diagnostic blunder ; this comes from want of true appreciation of the mechanism in these cases. In discussing the signs associated with fibrillation, I have spoken of the modification of diastolic murmurs in mitral disease. A murmur, which originally occupies the full diastole of the shorter cycles, is replaced as the heart slows by an early diastolic murmur which is maximal in the region of the apex. It is the last murmur which so frequently misleads the physician and suggests to him an insufficiency of the aortic valves. It is said that in some cases of aortic regurgitation the character- istic bruit is confined to the apex, but this is far less common than has been supposed, and an erroneous conception •of its frequence has arisen from inclusion of many of the cases to which I now refer. When mitral stenosis and auricular fibrillation are present in the same patient, and the lieart rate is sloiv, an early diastolic murmur, most clearly audible at the apex but often audible around and above it, is an expected sign. A diagnosis of aortic reflux is never justifi- able when the heart is grossly irregular and slow, unless unequivocal signs of it are present apart from such a murmur. Uncomplicated aortic valvular disease and fibrillation of the auricles is a comparatively rare clinical picture. The Auricular Fibrillation. 99 combination, yielding a purely apical murmur, is so far an undescribed condition. Close attention to the character and accurate timing of the adventitious sound is often helpful. The early diastolic murmur of mitral stenosis is relatively soft in quality and it usually begins a little later than the second sound. The absence of a waterhammer pulse and of a murmur at the aortic cartilage should indicate the mitral valve as the probable seat of mischief. The prognosis. As in all other kinds of heart irregularity, the prognosis is largely governed by the remaining symptoms and signs, and in any individual case an estimate is formed, which includes consideration of the past history, the presence oe absence of serious symptoms, the presence or absence of enlargement, of valve lesion, renal disease, etc.. But fibrilla- tion gives an added significance to the case. It is, as I have said, in itself an evidence of muscular damage, and of serious muscle damage. It loads an already defective muscle with an extra and appreciable burden. In most cases it heralds cardiac failure, temporary or terminal, so that few patients survive its onset for more than ten years. There are well authenticated instances in which it has persisted for a longer period, but they are few. The most valuable intrinsic sign is the rate of the ventricular action, a persistent rate of 120 or over is of serious omen, and according as the rate is maintained above this count, so the outlook becomes graver. Rates of 140 and over are rarely maintained for many months, rates of 160 do not continue for many weeks. An extremely important consideration is the reaction to treat- ment. As we shall see, a large number of these cases react to cardiac drugs ; in many, more especially the rheumatic group, the rate can be controlled, being reduced and maintained within limits which spare the heart excessive taxation of H 2 100 Cha-pter VI I. its strength. In dealing with a jjatient who has a given heart rate, the prognosis, in so far as it is affected by the fibrillation, does not depend so much upon the heart rate first observed as upon the heart rate which persists under treatment. At the same time, the prognosis is more grave for a given rate, when treatment is required, than when this rate is maintained in the absence of remedies. The treat7)ient. There is no ailment in which such success can be achieved, no other cardiac disorder which may be so speedily benefited, as the well-managed case of auricular fibrillation. In no other affection can the medical attendant point with more thorough confidence to the effects of his remedies. As a direct result of active treatment the moribund may be restored and many years may be added to their lives. Auricular fibrillation is the condition to which drugs of the digitalis group almost exclusively owe their Avell-founded reputation. The guide to the physician is the rate of the heart beat, an index which rarely fails him. Auricular fibrillation is an absolute indication for the administration of a member of the digitalis group, whenever the heart rate exceeds 100 while the patient is at rest. In most of these patients the drug acts as a specific, impeding the passage of impulses from auricle to ventricle and thus reducing the ventricular rate. If the heart rate does not fall as a result of rest, and if it does not fall when digitalis or an allied drug has been properly administered, no other remedy is known which is of service in reducing the heart rate. In young people, and especially those who have been affected by rheumatism or chorea, an absolute control of the rate is almost always established and maintained. The treatment consequently consists of the administration of such doses as will keep the heart rate within reasonable limits. Auricular Fibrillation. 101 It does not necessarily follow that a patient \\'ho has fibrillation should lie up. But where the heart rate exceeds 100 it is advisable, and the patient should remain in bed until his reaction to digitalis, or a similar drug, has been thoroughly- investigated. Further treatment in bed is decided upon according to the general condition, and according to the tolerance and reaction to digitalis. In treating cases with digitalis, it is found that in some the rate is unaffected ; these are chiefly patients of the non-rheumatic group and those in whom a very excessive ventricular rate is not found. In most patients, and in almost all where a high ventricular rate obtains, a reaction is speedily forced. These latter may be divided into three classes : the first, those in whom the reaction is a permanent one ; these are patients in whom the rate remains slow though digitalis is omitted : the second, those in Avhom the reaction is permanent when small doses are subsequently administered : the third, those in whom persistent high dosage is required to maintain control. As a routine, the tincture or fresh infusion of digitalis is given, for it is a safe and most potent remedy. The tincture is given to adults in doses of from 10 to 15 minims three or four times a day (the infusion in 1 to 1^ drachm doses) ; if the reaction does not begin within four or five days, the dosage may be increased until symptoms of nausea, diarrhoea, headache or pulse slowing appears. It usually happens that the desired fall of heart rate first comes just before or at the tiiiie when other signs of intoxication are manifested ; if these persist for several days the drug must be reduced or omitted, whether the rate has fallen or not. The dosage is also to be reduced if the heart rate falls, and the reduction is continued so long as the heart rate remains below 00. The quantity may be diminished to nothing in many cases ; often 5 minim doses eventually 102 Cha'pter VII. suffice. Usually the full reaction is obtained after six or eight drachms of the tincture or an equivalent quantity of infusion has been given. Whenever the rate has reached 60 or 80 per minute, the drug is stopped, and it is given again only if the heart rate begins to accelerate once more. The appearance of coupled heart beats (Fig. 50) is always a sign of danger : whenever they appear the digitalis must be discarded. I have seen more than one case of unexpected death, attributable to continued dosing with digitalis after this stage is reached ; it must be remembered always that digitalis is a poison, and that it has other actions than the simple reduction of heart rate. In most instances where the patient has reacted, the drug can be stopped without the rate re-accelerating so long as he remains in bed. When he rises from bed a renewal of the small dose (5 minims) may be necessary. In other cases the result is less satisfactory and heavier dosage must continue. The administration of digitalis in small or moderate doses ma}^ be continued beneficially for years in some patients. It sometimes happens that a patient is peculiarl}^ intolerant to digitalis, and that, M'^here a reaction is expected, a dosage of 15 to 20 minims of the tincture cannot be reached or maintained sufficiently long, without nausea or other discomforting symptoms supervening. The dose should be diluted and given directly after meals. Strophanthus (in its new B.P. strength) or squills may be tried, starting with doses of 10 minims of the tinctures. These drugs are pushed in the same manner, but though they are less apt to induce nausea or vomiting, and while diarrhoea is the chief disturb- ance produced by them, they are less reliable than digitalis. In some of these cases, too, recourse may be had to intravenous injections of strophanthin. Auricular Fibrillation. 103 When a patient who has fibrillation is first seen, and the heart beats persistently at 170-200 per minute, the condition is urgent and heavy doses of digitalis (20 to 30 minims) should be employed. The intravenous injection of strophanthin is also valuable at such times. Two, or not more than three, doses of 1/250 of a grain, each in 40-60 minims of saline, are given at intervals of two hours. The reduction of rate begins almost at once, and heart rates of 90 or 80 are reached in from 6-12 hours. The remedy should be employed cautiously and its adoption must be confined to the urgent case which belongs to the rheumatic group or to similar cases in which medication by the mouth has been hindered by the onset of gastro-intestinal symptoms. The treatment of the case of auricular fibrillation in the patient who is up and about is guided mainly by the rate of the heart and the urgency of the patient's symptoms. The disorder is generally persistent, and most hospital patients eventually leave their beds and return to their former occupations. But even where the pulse rate is persistently low and symptoms are few, excessive exertion should be avoided ; heavy manual labour, strenuous games and sports should form no further part in the daily life. If the pulse rate quickens readily, if drugs are constantly required to maintain a low ventricular rate, and especially if breathlessness or precordial uneasiness are easily induced, further restrictions are necessary. All patients of the female sex should be specially warned of the strain and danger of pregnancy. Regular meals, consisting only of a sufficiency of sohd and sustaining food, preferably dry, early hours, a placid existence, the avoidance of public buildings and all places and seasons in which influenza and bronchitic troubles are contracted, and, lastly, scrupulous attention to the hygiene of the teeth and throat, are sound directions in this as in other serious heart maladies. 104 Chapter VI I. Belladonna, its ally hyoscyamus and their extractives should be avoided. Their customary action is to increase the rate of the ventricle in this condition. In cases of urgency, or where the patient's life may be considerably prolonged by surgical operation, general anaes- thetics may be employed. But where there is any hesitancy to perform an operation, apart from the cardiac condition, the presence of fibrillation should countermand* it. Paroxysmal fibrillation. Most auricles Avhich develop fibrillation maintain this mechanism to the end of the chapter ; it is essentially a chronic and at last a terminal malady. But from time to time transient attacks are seen, and in some patients paroxysms of fibrillation lasting a few hours, days or weeks are noted. The affection, when it takes this form, is generally classed as paroxysmal tachycardia. In my discussion of paroxysmal tachycardia I have excluded it, desiring to deal, as I did, mth the simpler mechanism alone. The frequence of the paroxysmal affection may be gauged approximately by comparisons. Of the 152 cases of auricular fibrillation included in the table on page 88, in only 16 was the disorder temporary and recurring. Paroxysms of regular tachycardia appear to be more common ; while the 16 irregular tachycardias were being collected, simple and regular paroxysms were seen in 45 patients. The symptoms of paroxysmal fibrillation have been spoken of already. They may be inconspicuous or profound. When the rate of ventricular response is rapid (160-200 per minute) the symptoms are those of simple tachycardias at similar rates, though they are on the whole more severe. The prognosis is reasoned in the manner stated for regular paroxysms ; the management and symptomatic treatment of Auricular Fibrillation. 105 the attacks are similar in the two. A few words are necessary upon digitalis medication. Drugs belonging to this group have been known, not infrequently, to excite fibrillation in those predisposed. They are therefore contra-indicated in paroxysms of short duration and in those which produce few symptoms. When a paroxj^sm of fibrillation is prolonged and lasts for fourteen days, the fibrillation must be regarded as permanent and may be treated as is the persistent condition. In urgent paroxysms, where high ventricular rates prevail, digitalis medication may be adopted with advantage ; the dosage should be arranged for a speedy reaction. The drug affords quick relief, though by its use the duration of the attack may be prolonged. Acute Fibrillation. Fibrillation of the auricles sometimes intervenes during the course of acute infections and continues for a few moments, hours or days. I have witnessed attacks of this kind in severe tonsilhtis, acute cholecystitis, acute appendi- citis, infective endocarditis and x^ericarditis, and others have been reported in scarlet fever and in pneumonia. ( 106 ) Chaptee Vlll. ALTERNATION OF THE HEART. Definition. A condition in which the left ventricle, while beating regularly, expels larger and smaller quantities of blood at alternate contractions. The mechanism in alternation of the heart. Alternation in the size of pulse beats, so that each alternate beat is large and each alternate beat is small, is of obscure origin. The contractions of the ventricle are regular, and each is preceded at a normal interval by a contraction of A .I'.l Fig, 51. A diagrammatic representation of alternation of the heart. The auricular and ventricular beats are placed regularly and in order, but alternate ventricular contractions are weak. the auricle (Fig. 51). The disturbance is dependent upon an anomaly of the ventricular systoles, whereby at each alternate systole of the left ventricle a greater or lesser quantity of blood is thrown into the systemic arteries. In Alternation of the Heart. 107 the figure, I have represented this anomaly by varying the size of the ventricular rectangles. The hypothesis is that a variable number of the ventricular fibres contract during the systoles. Etiological and pathological relations. Alternation of the pulse is seen in two classes of patient. First, it occurs in those in whom the heart rate is unduly accelerated and more especially as an accompaniment of paroxysmal tachycardia. Associated with paroxysmal tachycardia, it has etiological and pathological relations in common with the last named disorder ; its prognostic signifi- cance is in these circumstances negligible, depending as it does chiefly, if not entirely, upon acceleration of the heart rate. It may be regarded almost as a physiological reaction to the increased frequency of the heart beat. Secondly, it occurs when the heart rate lies within normal limits and at such times it is a sign of considerable import. Seen in elderly subjects and pre-eminently in the male sex, it consorts especially with angina pectoris, high arterial pressure, renal disease, and a fibrotic or fatty myo- cardium. It has been seen in pneumonia during the pre- critical stage, and also in patients under the influence of large doses of digitalis. Alternation of the heart is encountered in experiment under similar circumstances, namely, when the heart rate is extremely rapid, or w^hen the organ has been injured by the intravascular injection of poisons. Whenever it occurs, there is reason to believe either that a tolerably healthy heart muscle is carrying an excessive burden, or that a diseased or poisoned muscle is struggling to perform work of which it is barely capable. In the remainder of this chapter, I shall allude to pulse alternation as an accompaniment of heart rates which are 108 Chaptei- VI 11. not high. When the heart is disposed to alternate, the actual alternation is unmasked by anything which imposes a fresh and added strain upon that organ. Thus it is often made manifest by a slight acceleration of pulse rate ; and, in the earlier stages of its development, it is frequentl}^ exposed by a single premature beat ; in the last named circumstance it follows immediately upon the extrasystole, and continues for a varying number of heart cycles. It is an affection of advancing years, its heaviest incidence being in the fifth, sixth and seventh decades ; it is much commoner in men than in women. Dr. White, of Boston, \ylio has collected seventy-one cases in eight months, considers it is as frequent as fibrillation of the auricles ; certainly it is a common disorder, generally passing unobserved. •••■<••<•• Fig. 52. Alternation of the pulse. Each alternate beat is strong and each alternate beat is weak. Apf II I I I I t ^ I d *^a2- Fig. 53. Apex and radial curves and heart sounds in heart alternation. The curve is taken at a faster rate than the last and shows the slight variation in pulse pauses. As opposed to the jjicture when premature beats are present, the stronger beat is followed by the longer pause. The recognition of pulsus alternans. It is unfortunate, but true, that most instances of pulsus alternans cannot be recognised other than by Alternation of the Heart. 109 instrumental means. There are patients in whom it affects the pulse continuously, and in A\'hom alteration in the force of alternate pulse beats is perceptible to the finger* ; but such cases are rare, and the feel of the pulse should never be trusted. Examination of the apex beat gives little assistance, for the heart beats with regular rhythm and the differences in the force of ventricular systoles and the intensity of the heart sounds are inappreciable. The systolic pressure of the large beats is several milli- metres higher than that of the small beats ; by nicely regulating the pressure in the armlet of the sphygmomano- meter, the small beats may be hindered from passing and the pulse rate below the armlet is thus halved. It is a sign of such importance and is so readily overlooked, that it should be sought deliberately whenever there is reason to suspect the possibility of its presence. Thus it is wise to examine all cases of angina pectoris, all cases of high blood pressure and all elderly subjects in whom affection of the heart is suspected, or renal disease is known to exist, with a specific object, namely, to determine its presence or absence. It should be looked for, too, in all elderly people in whom premature beats are frequent. If such methods are adopted it will not often escape detection. It is so frequently confined to the few cycles which follow a premature beat that, in any class of the patients mentioned, it is important to obtain a curve which contains such a beat. This may often happen at the first examination. The patient should remain standing, for premature beats are more frequent in this posture, and if he has come some distance, it is well that the examination should proceed at once, since premature beats are more conspicuous at such times. It should be remembered too, that a held breath may * The separation from a dicrotic pulse is easy ; for where the latter is jiresent the beating of the pulse is at twice the rate of the ventricle. 110 Chapter VIII. evoke a premature beat and the opportunity of detecting alternation in this manner should not be lost. Single premature beats are usually followed by a pulsa- tion of exceptional size, for the heart puts out more than its usual quantum of blood. It is the pulse which succeeds this tall beat which shows the first sign of alternation ; it is less forcible than that which succeeds it. In Fig. 54 a regular pulse is interrupted by a single premature contraction (p) ; it is followed by the usual pause and this is succeeded by a tall pulsation (Z) ; the next beat s'^ is small, it is followed by a taller beat l^. The small beat s'^ is, as I have said, the earliest sign of the condition, and it may be the sole sign. In the ' I - 9 * m V 1 / I W t ^ 9 1 V W ^ 9 9 V 9 'V ¥ t 9 ) t W