4882.

MARCH 24, 1917.

The Lumleian LecturesON

MODERN ASPECTS OF HEART DISEASE.Delivered before the Royal College of Physicians of London,

BY G. A. SUTHERLAND, M.D. EDIN.,F.R.C.P. LOND.,

PHYSICIAN TO THE HAMPSTEAD AND NORTH-WEST LONDON HOSPITAL;PHYSICIAN TO THE PADDINGTON GREEN CHILDREN’S HOSPITAL.

LECTURE IL1Dedivered on Vlarch 15th.

DISTURBANCE OF CARDIAC RATE.MR. PRESIDENT AND GENTLEMEN,—The second great dis-

order of the heart is characterised by a disturbance of therate, which in the vast majority of cases means an accelera-tion, and in the minority a retardation, of rate. An increaseof the heart’s rate, as compared with the normal standardof adult life, may be found under various conditions, bothphysiological and pathological. Thus in infancy and childhoodthe heart beats more rapidly, and may be presumed to do soin order to meet the demands of the growing organism. In

many forms of general disease an increase in the cardiacrate is part of the general disturbance, just as a rise in tem-perature is. The increase is not probably of much import-ance in itself and does not, as a rule, lead to any specialsymptoms.

Acccleration of Cardiac Action.In connexion with actual disease. of the heart, writers in

the past have noted the frequent occurrence of a rapidcardiac action, and they have speculated widely as to thecauses of this increase. As a rule the symptom, especiallyif progressive, has been ascribed to increasing feeblenessof the myocardium and cardiac failure. The writers do notseem to have considered very fully what the results of apersistently rapid action are on a previously damaged heart.Yet this question is one of great practical importance inconnexion with prognosis and treatment. The old termsI I failure of compensation" and "broken compensation"

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conveyed no information of any value because the actualprocess at work was unknown. These descriptive terms arenow known to apply to conditions of cardiac failure broughtabout in many cases by an increase of cardiac rate, or, to bemore precise, by the weakening effect which the rapid ratehas on the efficiency of the left ventricle.

It may be allowed that there is a certain range of altera-tion in the cardiac rate, above and below the normal, whichin all probability has no important effect on the heart andleads to no symptoms. As regards an increase, if we take75 beats per minute as the normal, an increase up to 100-that is, of 25 beats-will not probably be productive of anydefinite effect on a healthy heart. Similarly, a reduction ofthe rate to 50-that is, of 25 beats, will not of itself affectthe efficiency of the heart. It is outside these limits thatwe find symptoms beginning to appear which are to betraced to the heart-rate. It is not only from the symptomsthat we can infer that the rate is affecting the heart’sefficiency; there are also definite changes in the heartitself, for example, dilatation, and evidences of a deficientcirculation, for example, congestion of the liver, which mayfollow as a direct result of an excessively rapid action of theheart.

If we take 100 beats per minute as our limit for cardiacefficiency we shall find that every increase of 10 beats maymake a difference in the efficiency. Such an increase

certainly makes a difference in the strain thrown upon theheart, so that we may express the increase as being a 10 percent., 20 per cent., or 50 per cent. added strain to the heart,according to the number of heart beats above 100 added perminute. Although the ventricular contractions are weakeras compared with those of the normal or slower rate, noperceptible changes may follow at first. Working at anincreased rate the ventricle eventually suffers because of theloss or diminution of its normal resting time (diastole) whenfresh energy is built up. It may be that for a time a doubling1 Lecture I. was published in THE LANCET of March 17th, 1917, p. 401.No 4882.

of the ventricular rate allows of the circulation being main-tained at its former level, or even in some ways of beingimproved, but the continuance of such a rate will eventuallytell on the ventricular power. If we adopt the terma"rest power " and reserve power " as applied to the heart,it will naturally be the reserve power which is diminishedfirst.

It will probably be found that a continuous rate of120, 130, or 140 will always tend to affect the ventricularastion eventually. An 80 per cent. increase (rate of 180) willbe sooner productive of serious results. These will ariseeven in hearts which have been previously healthy, butnaturally they will be manifested sooner in hearts which are

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diseased. There are certain factors which have to be takeninto account in estimating how a diseased heart will beaffected by a marked increase of rate-that is, above thestandard of 100 beats per minute. (1) The age of thepatient. In the young an increase of rate is not so patho-logical or so productive of injurious effect as in adult lifeand old age. (2) The state of the myocardium of the leftventricle. A healthy myocardium will I I carry on " success-fully, when a diseased myocardium would show signs <stress. (3) The amount of strain already thrown on theventricle from associated disease in other parts-for example,the presence of valvular lesions. (4) An associated irregla-larity of rhythm. The diastolic filling of the ventria6,already defective by reason of the arrhythmia, may -1}eseriously interfered with by the shortening of the diastole.The effect of the cardiac irregularity may thus be mu 1enhanced by an increase in the rate. (5) The suddennsgof onset of a great increase of rate may disturb 1)Ieventricular action much more than if the process bad beenslow and progressive. This is well shown in some forms oftachycardia, when the heart has no time to accommodate-itself to the excessively rapid action which sets in abruptly.

I During the course of a general infection (rheumaticfever) or during active carditis an increase of cardiac ratemay be regarded as a normal reaction. It does not, as a.

rule, demand any special treatment, because it is usuallymoderate in degree and a temporary disturbance. The classof case in which a rapid rate may be said to be injurious isthat in which, in the absence of any general cause or localcardiac inflammation, there appears to be a permanentlyirritable or excitable focus in the heart. From this focu9-start numerous impulses which, while causing frequent con-tractions in the auricles, unimportant in character, may alsocause an excessive rate of ventricular contractions. Undet-these conditions the increase of rate does not cease while thepatient is asleep, although it may be less pronounced, and ’itmay be considerably augmented by excitement or by physicalexertion. The reserve power of the heart is certainlydiminished in all such cases, and according to the degreeand persistence of the increased rate the rest power may beencroached on. This subject will be further referred to whenwe deal with the question of therapeutics.

-7?etardatioit of Cardiao Action.A slow rate of the heart, slower, that is, than 40 beats per

minute, may also have, if prolonged, an injurious effect onthe circulation. The ventricle does not suffer in itself, bttunder certain conditions it fails to maintain a sufficientsupply and pressure of blood in different organs, more

especially in the cerebral centres. A total bradycardia-that.is, a slowing of the heart-rate which starts at the sinus nodeand is continued through the heart-beat-is not usually ofclinical importance. The pathological slowing, which ix

important, will be found dealt with and explained under th-aheading of I Heart-block" in the current literature. Itforms a particularly illuminating chapter in the history ofthe successful analysis of disturbances in the cardiac rhythmand rate. Gaskell found that by clamping the junctionaltissues which form a bridge between the auricles andventricles he was able to form a barrier or block, so that onlya certain number of impulses passed through. According’tothe amount of pressure exercised, only every second or thirdor fourth impulse was able to pass, and the ventricularaction was slowed accordingly. This is known as partialheart-block. By raising the pressure still more he was ableto form a complete barrier or block, so that no impulses atall reached the ventricle from above. This is known as

complete heart-block. When this happens a latent and un-suspected action of the ventricle comes into play, as shown

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, by- its .starting .a. rhythm .a.n<&Igrave;- rate of its own, at first, rather’irfegilar, but tending soon to settle down to a regular beatat a rate much below normal. So that below the junctionaltissues, in some part of the ventricular wall, there lies a.

centre, usually dormant, capable of impulse formation anddischarge and of starting ventricular contractions.

’ The clinical bearing of these facts has been very thoroughlyworked out by Mackenzie. He showed that in disease

partial heart-block is frequently produced through lesions oftlie,junctional tissues. The conducting bridge of the junc-tional tissues becomes a barrier to the impulses descendingfrom above, and only a certain number get through at

regular or irregular intervals, so that the rate and regularityof the ventricular contractions bear no fixed relation to the

auricular rate and regularity. The ventricular rate isinfluenced by the rate at which impulses are able to passthe, barrier. The clinical proof of these conditions can bedemonstrated very clearly, by, means of graphic records. Itwould appear, further, that .partial heart-block may resultnot only from damage to the junctional tissues, but from anexcessive number of stimuli descending from above andexhausting the powers of conductivity of normal junctionaltissues. The bridge becomes blocked from excess of traffic.This is manifested in the clinical conditions of auricularJl&ugrave;tter and auricular fibrillation. The conducting tissues arestimulated to such an extent that they are incapable oftransmitting all the impulses reaching them. The conditionof partial heart-block . is bhu3 seen to be proved in experi-- mental physiology ; it is also demonstrable in various formsof cardiac disease and disturbance, and it is capable ofbeing induced by means of drugs in the treatment of heartdisease, as will be described later in dealing with digitalistherapy.

’ Complete heart-block is the result of organic disease

affecting the junctional tissues to such an extent that noimpulses reach the ventricle from above. The idio-ventri-oular rhythm and rate which then develop, or which, maydevelop, are apt at first to lead to attacks of syncope because.of,the prolongation of some of the diastolic pauses. After atime the action becomes more regular, the rate is usuallyabout 30, and symptoms.,of ventricular inefficiency maydisappear. The site of origin of this rhythmic action of,the ventricles is now reasonably assumed to be in some

part of the auriculo-ventrioular bundle in connexion withthe ventricles. One thing marks it out as different fromall the other abnormal rhythms which have been con-

sidered. When a new rhythm, has been started -from someabnormal focus we have found that the rate was alwaysfaster than normal. As the result of complete heart-blockthe new rate of the ventricles -is always slower than thenormal rate. The new. rate, although slow, may allow of .a..sufficient number of ventricular contractions to ensure the,- maintenance of the circulation, at perhaps a lower levelthan formerly. The important point about the new rhythm.is that it should be regular. If the intervals between thebeats are too prolonged the pressure in the cerebral vesselsfalls, and unconsciousness and even convulsive movementsfollow. These conditions are seen clinically in the symptom-complex which is known as StokesTAdams’s disease. If theventricular rate falls below. a certain level the intervalsbetween the beats are so prolonged that death ensues.

Relation of DistaPbanoes to-Sulpra-ventri(Jular TisS1lOS.The disturbances in rhythm and :rate which we have been

considering have come to occupy a most important place inconnexion with the etiology of cardiac weakness and cardiacfailure. We have already stated that these disturbances tendto affect injuriously the efficient action of the left ventricle.It is interesting to note, further, that every form of dis-ordered action of the heart, be it an irregularity of rhythmor an excessive rate, or a diminished rate, is always supra-,ventricular in origin. That is to say, these disturbances ariseoutside of the contractile muscle of the ventricles, except,perhaps, the ventricular extra-systole. There may be other

exceptions to this, but so far as is at present known they ’,,must be extremely rare. Clinically, we find that the abovegeneral statement holds good. The supra-ventricular tissues,as previously defined, are the sino-auricular node, certain

puts of the auricles, the auriculo-ventricular node, and theauriculo-ventricular bundle. In health these tissues regulatethe rate and rhythm which are designed to lead up toefficient ventricular contractions. In diseased conditions ofthe heart disturbances in these tissues may lead, and do 1(,-a,l,

up to disordered and impaired ventricular-action. Someforms of supra-ventricular disturbances if reproduced in theirentirety in the ventricles would make efficient ventricularaction impossible. Thus, if a condition of auricularfibrillation spread unchanged to the ventricles, efficientaction of the latter would cease at once and a fatal termina-tion would ensue. As a matter of fact, sudden death doesoccur from ventricular fibrillation, and it is now believedthat sudden death under chloroform anaesthesia is due toventricular fibrillation. By a process of blocking of certainof the impulses at the junctional tissues-partial heart-block-a diminished number of them reach the ventricleswhich are thus able to carry on the circulation. To expressthis in another way, impulse formation and impulse dischargemay develop at a dangerous rate-dangerous, that is to say,if it spread to the ventricles-but the conducting tissues failto develop the same rate of conductivity, and the ventricularaction is successfully carried on.The disturbances referred to above arise in the heart and

as a result of disease of the heart. Other injurious influ-ences arising from without may reach the heart through thenervous system and produce similar disturbances. They havefirst of all to pass through the defences of the supra-ventri-cular tissues, where they are often so modified that anythreatened danger to the ventricles is removed. We mayregard the vagus and the accelerator nerves as always onguard and controlling the functions of the supra-ventriculartissues for the benefit of the ventricles. So that it wouldappear that the ventricles are partially protected by thesupra-ventricular tissues from disturbances which may arisein the heart itself or which may reach the heart fromwithout.! " Soldier’s Hea1.t." ,

Amongst the varieties of disordered action of the heartthe war has brought into prominent notice is one which isknown as the soldier’s heart " or I the irritable heart ofsoldiers." " It is in no sense comparable to the conditions wehave been discussing and for this reason. The disorderedaction of the heart which occurs in heart disease is the resultof definite changes in the muscular tissues of the heart, thesupra-ventricular tissues more especially, which have arisenfrom inflammatory or degenerative lesions. -The disorder is

primarily cardiac in origin. On the other hand, the disorderin the case of the soldier’s heart is essentially not cardiac inorigin ; it is the result of disturbance or disease in otherparts of the system, which react on the heart and modify itsaction. This is shown in many ways. In the first place, wedo not find any signs of organic heart disease to which thesymptoms may be referred. The symptoms themselves arenot such as can be definitely associated with any known formof heart disease, but they resemble closely those present inpatients suffering from a ’’ neurotic heart." Again, we findmany other changes present which are not traceable to thecardiac condition, but clearly to a common cause. It is notthe heart alone but the whole vascular system which isaffected, and it is not affected in the way which we see asthe result of heart disease. There is a loss of tone or powerin the whole cardio-vascular system.As regards the primary cause of the disturbances opinions

still differ. Physical stress and strain, anxiety, sleeplessness,infective disease, preceding illness, and toxaemia have allbeen assigned the first place, and possibly each will be foundto play a part if a sufficient number of cases be taken. What-ever the primary cause of disturbance one cannot fail to notein the patients the presence of nervous irritability andinstability, that general condition which for want of a betterterm we call neurasthenia. It would appear likely from thesymptoms in oases of "soldier’s heart" that the cardiacphenomena do not proceed from the heart primarily, butfrom a disturbance of the power and action of the heartarising in the nervous centres which act on the heart. In an

interesting analysis of 40 cases of "soldier’s heart" JohnParkinson found that in about half the cases the same dis-ability had been present to some extent in the civil occupa-tions pursued before the war. As he expresses it, "thesemen are the subjects of a cardiac difability which is un-masked by the exertion required of a soldier." Thisdisability, whether constitutional or acquired, does not comeinto the category of organic heart disease. On the otherhand, if certain symptoms persist-for instance, tachy-cardia-the effect on the heart may be as exhausting as ifthe tachycardia had been primarily cardiac in origin.

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, DILATATION OF THE HEART.

Dilatation of the heart, of one or more of its chambers,has long been recognised amongst the changes associatedwith valvular disease. The view taken was ’that dilatationwas a sign of weakness, a sign that the heart was yielding tosome stress or strain more than it could effectively deal with. IAnother form of dilatation recognised was that in which the Icondition developed suddenly, usually in a heart previouslydiseased, and was accompanied by an increase in the oldsymptoms or the development of fresh ones. This wascalled acute dilatation of the heart, and the patient wassubjected to treatment for the reduction of the dilatation.As we read the clinical reports of such cases it seems clearthat the sudden onset of dilatation was usually the result ofsome strain thrown on the heart, and was associated withthe presence in the heart of a disordered action of rate or

rhythm, or both. We must not, therefore, assume off. handthat the dilatation was the primary condition, or that it wasdue to some essential weakness of the myocardium.

Results of Experimental Researon.The whole subject of dilatation, which in its most

important aspect means dilatation of the left ventricle, isadmittedly one of great difficulty. It deals with the

qualities of tonicity, contractility, and relaxation in thecardiac muscular tissues. On the physiological side Starlingand his co-workers have recently promulgated some newviews on this subject.They state that the ventricles cannot dilate unless fluid I

enters them. The view that there is such a condition as

muscular dilatation, leading to a filling of the ventricles bysuction, does not seem to receive physiological support. Ifblood does not enter the heart the ventricles do not dilateat all during diastole, and may become smaller with eachsystole until they are empty. This is not the result ofincreased tonicity of the heart, but is purely a mechanicalresult of absent or deficient venous inflow.

Comparing the cardiac muscle to an ordinary skeletalmuscle, Starling says the extending load is represented bythe diastolic intracardiac pressure and is dependent on theinflow; the load against which the cardiac muscle has tocontract is represented by the pressure in the aorta. In his

experiments he found that it was length of cardiac musclerather than tension which determined the energy of contrao-tion, so that there existed a direct proportion between thediastolic volume of the heart-that is, the length of its

Imuscle fibres-and the energy set free in the followingsystole. This would seem to mean that to bring out the I,maximum capacity of a healthy heart a moderate dilatationis advantageous. Fatigue is shown by the fact that, startingat a given length, the change from the relaxed to the con-tractea state is atcenuea witn a smaller production ot tenszonthan was the case when the muscle was fresh. This meansthat a tired heart must dilate in order to carry on the samework as the fresh heart, and this is what Starling found actuallyoccurred. If the condition is relieved, say by increasing thesupply of oxygen to the heart or by diminishing the load,and the muscular tissue of the heart is given an opportunityto recover, the heart may once more return to its normal size,the evolution of energy per unit length of the muscle fibreat each contraction becoming the same as before.

This is his understanding of the word tonus or tone asapplied to cardiac muscle. The term is properly employedas synonymous with physiological condition or fitness of themuscle fibre, and its measure is the energy set free perunit length of muscle fibre at each contraction of the heart.A good heart-that is, one with a good tone-will carry ona large circulation against a high arterial pressure andnearly empty itself at each contraction ; while a heart witha defective tone, as is the case when it is tired, can carryon the same circulation, but only when. its fibres at thebeginning of contraction are much longer, that is whenthe heart is dilated. In the latter case the output of bloodwill be the same as in the former, but both the systolic andthe diastolic volumes of the heart will be increased. Whenthis dilatation proceeds to such an extent that the tensionof the muscle fibres becomes increasingly inadequate inproducing rise of intra-cardiac pressure, the fatigue of theheart passes on to cardiac failure.

Clinical Siipport of Eaeperimentxl Results.Turning to the clinical side we find a good deal of

support for Starling’s experimental results. In the case of

healthy children there is a marked instability of all thecardiac functions, and dilatation of the heart is by no meansuncommon. The fluctuations in size of the heart at thisage are such as to suggest strongly that there is a self-regulating influence at work, seated in the heart, whichadjusts the size of the heart to the varying calls on itspowers. In the case of severe athletic exercises, such asrunning a race, we fiud that the heart becomes temporarilydilated, apparently in all its chambers. Here, again, wemay assume that the dilatation is the result of the strainthrown on the heart, and is called for in order to meet thedifficulties of the circulation. When an attack of paroxysmaltachycardia sets in, the patient and his heart having been,previously healthy, there is not necessarily any dilatation ofthe heart or any noticeable change except in rate. Bat whensymptoms of fatigue of the heart appear, breathlessness, &o.’,dilatation usually comes on, and this may well be an effortto render the ventricular contractions more effective. Whenthe attack of tachycardia ceases the cardiac dilatationusually subsides rapidly. The onset of auricular fibrillationis often characterised by great distress in the breathing and-a marked degree of cardiac dilatation. Usually such dilata-tion has been ascribed to weakness of the wall of the left.ventricle ; but, on the other hand, it may simply be anattempt on the part of the heart to overcome the freshdifficulties of the circulation.The point of view that dilatation is not necessarily an-

indication of weakness of the cardiac muscle, and, may be-one of the means by which the cardiac muscle meets adisturbance or difficulty in connexion with the circulation, does not imply that it. meets all difficulties in this way or.-that cardiac failure cannot occur without dilatation. As amatter of fact, we know that the contrary holds true.Clinical research may well be directed into determining,more exactly what are the underlying conditions which giverise to dilatation. Possibly it may be that in cases ofextensive degeneration the cardiac muscle has lost the powerof dilating. Starling has emphasised the fact that the

question of dilatation is closely associated with the venousinflow of the heart, the quantity and the pressure of the flow.He says that the output cf the heart is equal to, anddetermined by, the amount of blood flowing into the heart,and may be increased or diminished within very wide limitsaccording to the inflow. With a minimal inflow the venous,pressure on the two sides of the heart may be zero, and with.

increasing inflow rises at first only slightly as long as theamount of blood flowing in is not more than sufficient toexert a minimal distension on the relaxing ventricles. Withfurther increase in the inflow the venous pressure may bepositive during diastole, causing an active distension of theheart, and an increase in the rate of filling. The greaterthe arterial resistance the higher- will be the venous pressure-for any given inflow. It seems probable from these con-; clusions that while certain disturbances, such as excessive-,rate or a disordered rhythm of the heart, may tend to induceidilatation, the question of the venous inflow and pressure.has also an important bearing in determining the amount of &pound;: dilatation.! SYMPTOMS.

The discovery of physical signs of heart disturbance ordisease is always satisfactory from a diagnostic point ofview. The presence of a cardiac murmur or irregularitydoes not, however, convey much information as to the func-tional efficiency of the heart. This question is decidedchiefly by the symptoms which are complained of by thepatient, or which are brought out by testing the responseof the heart to various forms of physical exertion.Symptoms are the signals of distress sent out by the heart

,when its efficiency has become impaired. ’In cases of chronicheart disease the physical signs may persist unchanged for10 or 20 years, and the first indications of weakening of thecardiac force are to be found in the symptoms. We have.therefore come to regard .symptoms as the most reliableevidence of impaired action of the heart and circulation.Amongst the chief of these symptoms may be mentioned’i breathlessness, pain, palpitation, languor, giddiness; faintI ness, and fainting. ’

I A symptom may be unrecognised by the patient. For-

instance, breathlessness, quite apparent to, outsiders, may,have come on so gradually as- not to have attracted thepatient’-s attention. In other cases the symptom-forexample, pain-may be not only recognised, but very, much

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emphasised and exaggerated by the patient. The sensi-tiveness of the individual varies to an enormous extent, sothat while in some cases we hear of few symptoms in otherswe are met with a multiplicity of them which is embarrassing.In the one case more leading and particular questions are tobe asked, and in the other the different symptoms are to be

more minutely examined into. It has also to be recognised*%hat many of the symptoms associated with organic diseasejtue reproduced with marvellous accuracy in functional dis-turbances of the nervous system. So that in dealing withsymptoms, and in order to estimate them at their proper4alue, the important thing is to establish a clear correlationbetween the physical signs of heart disease and the symptoms"complained of or elicited by testing the response of the heartto effort. Further, as the symptoms of heart weakness areeot distinctive, one has to exclude other possible causesthan the heart. Such symptoms as breathlessness, proa-cordial pain, and palpitation may come from disturbances invarious organs and regions of the body. An enlarged liverand fainting attacks are not necessarily due to heart disease.Shortness of breath and a cardiac murmur or irregularitymay be present without organic heart disease. Chronicrenal disease and arterio-sclerosis may lead to many sym-ptoms not unlike those of heart disease. So that while inmany cases the establishment of a definite correlationbetween the symptoms and the signs’of cardiac disease maybe easy, in others care may be necessary lest we assume tooreadily from the presence of symptoms the existence ofheart disease as the cause. Patients are especially liable tofall into this error and to come with a ready-made diagnosisof .. something wrong with the heart."Symptoms are a measure of the difficulty with which the

4eft ventricle is meeting some strain thrown on its action.fatigue of the heart may be shown by symptoms only after-some unusual exertion has been made which, however, thepatient had previously been able to make without dis-comfort. A further stage-weakness of the heart--is shownwhen the patient has increasing difficulty in making anyexertion without the onset of symptoms. In Mackenzie’slanguage this implies a diminution in the "reserve powerof the heart." A further stage-failure of the heart-isreiched when symptoms are present even when the patientis resting in bed or on a chair. In Mackenzie’s languagethis means a diminution of the rest power of the heart."In connexion with heart disease, fatigue, weakness, andfailure, as defined above and as shown by the symptoms,may be regarded as milestones indicating the progressiveimpairment of ventricular action. Whatever the physicalsigns in the heart may be, a sound prognosis must take intoaccount the importance of the symptoms, and successfultreatment will be shown by the diminution or cessation ofthe symptoms.

Relative Importanoe of Signs and Synaptoms at DifferentAges.

We expect and usually find symptoms present at all ageswhen the patient is the subject of acute heart disease

(myocarditis, endocarditis, pericarditis), or of a sudden andsevere disturbance of rhythm such as auricular fibtillation.In the chronic forms of heart disease we find a markeddifference in the relative importance of symptoms andphysical signs at different ages in estimating the questionof cardiac impairment.

In the young, say up to the age of 15 years, heart diseaseis usually part of the rheumatic infection. At this periodof life the re ’.uperative powers of the heart after an acuteattack are little short of marvellous, and the symptomsmanifested or complained of are often extremely slight, orabsent altogether. Yet the heart may have been permanentlydamaged. At this age, therefore, the physical signs ofdisease are much more important than the symptoms in

forming an estimate as to how far the cardiac efficiency hasbeen or will be impaired. It is on the physical signs thatthe prognosis is to be based, so far as a prognosis can begiven during the years when rheumatic reinfection is so aptto occur. Symptoms, the result of disease in early life, maynot assume any importance until maturity is reached oreven later. Possibly the physical signs of disease may nothave altered much since childhood, but impairment of thefunctional efficiency of the left ventricle will first of all beindicated by symptoms when the physical stress of life hasbegun to tell on the previously damaged heart.

From middle life on through old age there is another largeclass of case met with-namely, those with degenerativechanges in the musculature of the heart. Here the physicalsigns of heart disease may be slight or absent, but the

symptoms are often clearly indicative of weakness in theaction of the left ventricle. The extent of the weakness canbe roughly estimated by the response which the individualmakes to effort, long before confirmatory evidence is obtainedin the form of oedema, &c.

CARDIAC THERAPEUTICS.

In acute inflammatory disease of the heart it is generallyagreed that the field of direct cardiac therapeutics isextremely limited. We employ measures to allay or removeany infective disease in the system, such as rheumatic infec-tion, and we adopt those measures which experience hasshown useful in the case of fevers generally. We do notpossess any direct means of checking disturbed action or

strengthening cardiac action when the heart is in a state ofinflammation, acute or subacute. This period is short-livedcompared with that which follows, in which the effects areshown in the form of chronic heart disease. The time atwhich the treatment of chronic heart disease begins and theform which it takes seem to vary considerably with theindividual therapeutist. In some cases whenever a cardiacmurmur is discovered digitalis is given. In others, when avalvular lesion is diagnosed from the murmur, digitalis isgiven. In others, when some change in the heart is diag-nosed as the result of a valvular lesion, digitalis is given.In others again, while valvular lesions and cardiac changesmay have been recognised, treatment is deferred until"compensation has broken down." These statements arenot based on the teaching or text-books of the day, but onthe experience gained in professional intercourse. It is not

necessary to consider any treatment which is based merelyon a cardiac murmur or a valvular lesion, but that based onfailure of compensation calls for comment.

Nature of Compensation and Compensatory Changes.The so-called compensatory changes are the result of

efforts which the heart has made to overcome some mechanicalinterference with its efficient action. In its simplest formit is seen in the dilatation and hypertrophy of the wall ofsome chamber in arder to overcome the effect of an obstruc-tion in front, for instance, the right ventricle in mitralstenosis. We may compare this with the dilatation andhypertrophy of the stomach wall in pyloric stenosis. The

compensatory change is more complicated in the case ofaortic regurgitation with mitral regurgitation when the leftventricle has to compensate for a great loss of its systolicpower by a double valvular leakage. In the case of adherent

pericardium, when some part of the heart is fixed to thechest wall, the compensatory changes may be of a mostcomplicated kind because of the tying down of the heart.

In all of these cases great changes may take place in thesize of the heart, and they are evidently purposive anddirected solely to the carryitg on of the circulation. Howare they brought about ? It would appear that the automaticpowers of the heart are solely responsible for these changes.For they are manifested in cases in which no treatment hasbeen adopted, and they are seen more especially in youthwhen the natural recuperative and adaptive powers of theheart are much greater than in later life. In the case of avery large and hypertrophied heart we may assume that theunaided powers of nature have produced the condition, andthat the enlargement is compensatory in character. Thereis no known method of producing such a result by drugs orother treatment, and it is very doubtful whether we shallever be able to improve on it.

Condition when Compensation has Bro7zen Do7vn.Such would appear to be the nature of compensation and

compensatory changes. What is the condition when com-pensation has broken down? 2 The term "failure of com-pensation " was applied in cases where there was a more orless sudden breakdown of the heart, with marked subjectivesymptoms of distress and usually with well-defined physicalchanges in the heart. The old view was that the heart hadgiven out. Sometimes it was described as "right-sidedfailure" and sometimes as "left-sided tailure," according tothe predominance of certain signs. The aim of hopefultherapeutists was ’’ to increase the tone of the heart muscle,’’ or "to strengthen the cardiac action," or "to improve the

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contractile power of the heart," as it was variously expressed.Now, if we are not able to add one muscular fibre to theheart or to improve the contractile power of the heart inorder to prevent the "failure of compensation" it does notappear to be likely that we shall be able to do so whenfailure has set in. Yet this was what was usually attemptedin cases of "loss of compensation" and what many claimstill that they can do by means of digitalis.There may be attacks of cardiac weakness induced by over-

exertion or illness, but they are temporary and relieved byrest and do not fall within the category of failure of com-pensation. There may also be failure of the power of theleft ventricle to carry on the circulation, a primary loss ofcontractile power from exhaustion, in which case the end isnot usually far off, and treatment is of little avail. But inthe vast majority of cases of " failure of compensation " withsymptoms there is a new factor present which is of greatimportance. That factor is the development of a new andabnormal rhythm in the heart, which has interfered with thecardiac action to such an extent that a " failure of com-

pensation has been diagnosed. The abnormal rhythm is,as a rule, accompanied by a great increase in the ven-tricular rate, and this adds to the impairment of the cardiacefficiency.

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Now the importance of these two, an abnormal rhythmand a rapid action of the heart, would appear to lie in this,that they react so injuriously on the ventricular contractionsas to produce the signs and symptoms on which a diagnosisof "failure of compensation has been based. One mightsay that there has been a disturbance of the compensatoryaction of the heart, in the sense that this action is weakenedfrom the presence of a new rhythm or from tachycardia.But to say that

" compensation is lost" is to say that all islost, for the carrying on of the circulation has been dependenton the compensatory changes, and we cannot influence themdirectly. As a matter of fact, in cases coming under thisdescription we know that if the disturbing factors are removedor checked by treatment the compensatory changes will befound unimpaired and ready to carry on the circulation

efficiently. Successful treatment will depend on the recog-nition of the exact form of disturbance which has upsetcompensation and on the application of the above facts inthe employment of our chief drug in heart disease-namely,digitalis.

Direct or Indirect A ct6orr of Digitalis? ?In considering the action of digitalis a clear distinction

must be drawn between its direct and indirect action. Thefact that it has a special and direct action on the cardiacaction is universally accepted, and the method of this actionwill be diseased later on. It has also been maintained bymany that digitalis has a direct action on the kidneys, on thearterioles, and on the blood pressure, while others assert thatthis is only an indirect action due to and dependent on theincrease in the cardiac efficiency. The former view is

probably based chiefly on experimental work on animals, thedeductions from which have been appiied, without clinicalob,ervation, to the human subject under conditions of cardiacfailure. Experience has shown that conclusions of thisnature are extremely unreliable.The view that digitalis has only an indirect action on the

kidneys is now strongly supported by pharmacologists andphysicians. Cushny states that the diuresis appears toarise not from a direct action on the secretory mechanism,but only indirectly through the changes in the circulation ;the kidney shares in the general acceleration of the bloodand functions more vigorously.’’ The change in the renalactivity under digitalis is not due to any local vascularaction but to the augmented activity of the heart, whichimproves the nutrition and promotes the activity of the

kidney. At the same time, the increased power of the heartquickens the circulation in the lymphatic system, dropsicalfluids are reabsorbed into the blood-vessels, and are excretedby the kidney.These views of Cushny appear to fit in very well with the

clinical results which we obtain from digitalis. We can seesimilar circulatory changes produced in other organs of thebody-for example, the liver. In heart failure the liver isoften swollen and engorged with blood, the patient is

jaundiced, and bile appears in the urine. The condition isassumed to be one of hepatic venous congestion withdeficient excretion of bile. When the cardiac efficiencyhas been restored by means of digitalis the hepatic con-

gestion and swelling subside and bile is again freelyexcreted. We do not say that in such cases digitalis actsas a cholagogue, or assume that it has any direcc action onthe liver, although its action here is probably exactly thesame as on the kidneys. Similarly, when the clouded brainis cleared, the oedematous lungs are relieved, and thestomach and intestines are freed from their congestion, wedo not consider that digitalis has a special action on thesetissues.Another fact to be remembered is that digitalis has not

been found to be efficient as a diuretic save in cases of cardiacdropsy. Its employment for diuretic purposes may be i-aidto be confined to cases of cardiac disease with dropsy.Those who accept the view that digitalis is a diureticbecause of its direct action on the kidneys must be preparedto show that there is some special condition present in thekidneys peculiar to cardiac dropsy. No such condition isknown, and, in fact, in many cases when the congestion ofthe kidneys has been relieved the kidneys are found to beperfectly healthy.

Diuretic Action of Digitalis Alone and Combined withTAeocine.

In many cases we can say with confidence that the dropsywill disappear when digitalis has restored efficient cardiacaction. We do not understand fully the underlying causesof oliguria in cardiac cases, any more than we know theexact mechanism of cardiac oedema, but we can observe

sequences in the treatment of dropsy. In my experiencethe diuretic action under digitalis is often of a sluice-gatecharacter, in which some holding back influence has beenremoved and the excess of fluid is poured out through thekidneys. The time at which this is secured is more or less

synchronous with the recovery of ventricular efficiency, andin the most typical cases this comes soon after the cardiacrate has been lowered. If, on the other hand, the cardiacrate has been and continues normal, and no appreciablechange in the cardiac efficiency takes place under digitalis,we do not usually find much evidence of a diuretic effect.

In some cases we do not get the expected diuretic actionof digitalis, even although it may have been effective in

relieving the other symptoms. Something additional seemsto be required to "tip the balance" and make the kidneysact. This may be accomplished by such means as a sharppurge or dose of mercury, or by partially relieving the dropsyby Southpy’s tubes, or it may be brought about by some suchtrifling alteration as a change of posture, as Mackenzie

points out. He finds that "the kidney functions, when thereis dropsy, are peculiarly unstable," and this is probably thecommon experience.

It will also be found that the caffeine series of prepara-tions, when used along with digitalis, are at times veryeffective in inducing diuresis. I cannot specify the exactunderlying renal conditions which are present. It has

appeared to me that the theocine-digitalis combination hasproved specially suitable in cardio-renal cases- that is, whenboth heart and kidneys are diseased. A most efficient pre-paration is theocine-sodium-acetate, and the action is oftenvery striking. Unlike that of digitalis it begins almost atonce, and may start within an hour of the first dose. If noeffect is manifested within 24 hours or after 40 grains it isof little use continuing the drug. Theocine appears to actmost effectively in combination with digitalis and after thepatient has taken a sufficient amount of digitalis to affectthe heart. While digitalis alone may procure a diureticeffect theocine alone is not usually effective if the dropsy isessentially cardiac in origin. The action of theocine is noaccidental one, for it can be repeated in the same case, andits effect is so prompt that the element of chance can beexcluded.The diuretic action of digitalis in cardiac dropsy can only

be estimated properly when the kidneys are healthy and’merely disturbed in their function from circulatory weakness.-If renal disease is present other factors may come into playwhich cannot at present be estimated. The diuretic effectunder digitalis is not usually started until after 48 hoursfrom the commencement of treatment. This of itself is

suggestive of an indirect rather than a direct diuretic action.Mackenzie has noted in some cases the onset of diuresis within48 hours of the administration of digitalis and before anyeffect on the heart was perceptible. He thinks "it is

probable that the beneficial effect produced by the drug isT, f 9.

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due to its diuretic effect rather than to its action on the heart.’’ We have already considered some ditficlllties in the way of accepting this view. In several of his cases chronic renal disease was present so that thtiy were not suitable fordeciding the question at issue. Accepting his facts as tothese exceptional cases, we may otfer another explanationthan the one he has given. Digitalis, amongst its other

effects, has an irritant action on certain tissues which ismore pronounced in some people than in others. Thusdiarrhoe may follow quickly from the use of quite moderatedoses. CIBhny points out that digitalis may act as an.irritant to the renal epithelium, as the appearance of bloodand albumin in the urine of animals after large doses ofdigitalis shows. Mackenzie usually begins treatment withfull therapeutic doses of digitalis, and the irritant action ofthe drug may h tve told on the kidneys before the cardiacaction has had time to take effect. Such an action wouldnot bring digitalis into the category of diuretic drugs,although it might explain the early diuretic effect in some. cases of cardiac dropsy.

Action of Digitalis on Arterioles and Blood Pressure.It was formerly held by pharmacologists, as the result of

experimental work, that digitalis contracted the arterioles inanimals and raised the blood pressure. These statementswere accepted by clinicians as applicable to the employmentof therapeutic doses of digitalis in man for heart disease.Further, warnings were given that owing to this action caremust be taken in certain forms of heart disease lest it shouldreact injuriously on a weakened heart. More recent pharmaco-logical investigations have shown that digitalis has no suchaction on the blood pressure, which is affected only by theincreased efficiency of the cardiac contractions. Cushnypoints out that there is a balanced action between theincreased force of the heart’s contractions and the tone ofthe vasomotor system. An auameated efficiency ia cardiaccontraction would lead to a rise in blood pressure providedthat the blood- vessels remained unchanged in calibre. Butas the output of the heart increases the vessels relax in pro-portion and the flow of blood is accelerated. This compen-satory action arises in the vasomotor centre, and as long asit persists the blood pressure does not rise.

Cushny’s conclusions have been supported clinically bythe investigations of Mackenzie and his pupils. In what is

perhaps the most important form of disease in this con-

nexion-namely, auricular fibrillition-they found that noestimate of the blood pressure could be made, as it was

constantly changing. In cases with a regular rhythm theycould detect no appreciable effect upon the blood pressure.Digitalis and the bt.ood pressure is still a subject of interestto senior students because of its value for examination pur-poses. but after the examination is passed the student maydismiss the subject and rest assured that its value to himfrom the clinical and there neutic point of view is negligible.

"SOLDIER’S HEART."1

BY ADOLPHE ABRAHAMS, M.D. CANTAB.,M.R.C.P. LOND.,

TEMPORARY CAPTAIN, R.A.M.C.; OFFICER IN CHARGE OF MEDICAL

DIVISION, THE CONNAUGHT HOSPITAL, ALDERSHOT

IN considering the subject of heart affections as they areencountered in soldiers it will be desirable in the outset to

say a few words about the term "soldier’s heart," whichhas now acquired an accepted position in our nomenclatureof diseases, one which certainly appears to supply a definiteneed in corresponding to a definite condition, but, unfortu-nately, also one which is employed with so much abuse thatit is impossible not to regret that such a term should everhave been introduced. We ought to restrict its applicationto patients who are suffering from cardiac affections, or, atany rate, cardiac symptoms due in some way to militaryservice. 10 this sense soldier’s heart would be an occupationdisease, as we speak of miner’s nystagmus, scrivener’s

palsy, or housemaid’s knee. But whereas there exists a

special group of cases which in mv opinion corresponds tosuch a restriction, even though the exact determining causeis still a subject for contention, the term is applied indis-

A paper read before the Connaught Hospital Medical Society.

criminately to a large variety of symptoms which are evidentin men who happen to be tempurarily khaki-clad and mostof which have nothing whatever to do with the heart, nor,for that matter, with military service.And this reminds me to refer briefly to that question-

begging epithet which is so conveniently employed in thesedays, D.A.H. (disordered action of the heart). Now,whatever words of depreciation may be considered suitableto apply in the case of the aforementioned soldier’sheart" these fade into insignificance when you select thosecondemnatory enough for its blood-relation D.A.H. I donot hesitate to say that I have seen men complaining ofsymptoms referable to every disease above the umbilicussent in as D.A.H., and I am not at all sure that a certainnumber below this anatomical landmark have not beenincluded. But even if one eliminates those cases of so-calledD.A.H. which pass the first portal re-labelled N.Y.D. (not yetdiagnosed) and are finally discharged as N. A. D. (no appre-ciable disease), what exactly does an honest attempt to usethe words involve? What precisely is orderly action of theheart and when does chaos usurp the place of cosmos in thecirculatory world T And in the second place is it not absurdat this stage of our knowledge of the etiology of disease toimagine that a diagnosis of tachycardia is a diagnosis, orthat it is sufficient to say that a pulse is irregular or inter-mittent without taking the trouble to see what is the natureof the irregularity and if, ac a matter of fact, its existence isof the slightest consequence ?

In recalling to your memory the copious literature whichhas already appeared on the subject of ’’ soldier’s heart’’during the last couple of years, I would suggest to youthat a large variety of different conditions have been atvarious times described as if they were all the same thing.And I think the best way to support this proposition is toenump.rate a representative collection of the causes whichhave been advanced.

First and foremost very naturally is the endeavour toascribe all cases to exertion. Here, then, is our old friend" strained heart" or I athlete’s heart " in modern form. To

adapt the condition to military circumstances such featuresare introduced as marches with weights, shoulder-straps,and the other paraphernalia of service and service kit. Thesubject of heart-strain I will postpone to consider later indetail.As a sort of corollary to this school there is another which

presupposes the existence of a great deal of latent un-

suspected cardiac disease which only.manifests itself in con-sequence of the strain. physical or mental, or both physicaland mental. of military life.To other authorities the condition is due to a tox&aelig;mia. If

microbic influence is demanded-well, organisms are so easilyintroduced, from the teeth, for example, or from the fooditself, and even if you are deprived of organisms there arealways toxins to fall back upon. And if toxins likewise aredenied, there are perverted products of metabolism. and someauthors blame the excessive protein diet of the soldier.Another large group of authorities attribute the condition

to the thyroid gland. rhe majority of these think there ishvper-thyroidism. though a few believe the secretion to benormal in quantity, but of pathological qualitv. The soldier’sheart to this school is simply larval Graves’s disease.At Ifast every other week somebody writes to the medical

journals explaining " soldier’s heart" to be due to excessivecigarette-smoking, and considering the almost universal pre-valence of this vice such an opinion has at least the supportof reasonableness.Recently "soldier’s heart" has been attributed to

deficiency of buffer-salts in the blood, and such an

explanation is not without its inconvenience in view ofthe difficulty in technique in estimating these salts. moreespecially as I will be impertinent enough to hint that themajority of us are more than vague as to what a buffer-saltis. what it does. and why its absence should produce symptomsof cardiac disease.

, One turns next to an entirely different interpretation of’’soldier’s heart’’ in introducing the school which supports apsvchical origin. Its disciples see no necessity to invoke theexistence of any organic pathological cause. In fact. theysee no necessity to suppose the existence of any sign of heartdisease. Thev point out that the symptoms, although equallyfamiliar in genuine heart trouble, are quite easily or at leastspeciously, explainable on a non-organic basis and that a