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Bible Encyclopedias
Heart Diseases
1911 Encyclopedia Britannica
or "HEART DISEASES ( see 13.132). - The study of disease of the heart entered on a new phase in the second decade of the 20th century as a result of the researches of the Scottish physician, Sir James Mackenzie (b. 1853). His work, which first made a public appearance in 1902 with his Study of the Pulse, and later was embodied in Diseases of the Heart (1908) and Principles of Diagnosis in Heart Affections (1916), followed three. lines. In the first place there were new observations on the rhythm of the heart itself; secondly there were observations and conclusions regarding the meaning of heart failure and its recognition; finally the importance of the early signs of disease as opposed to its later manifestations was emphasized.
Mackenzie showed that by making tracings from the neck as well as from the wrist it was possible to obtain information regarding the activity of all the chambers of the heart. The neck tracings gave a wave when the auricles contracted. This was caused by a reflux of blood up the jugular veins; following this came the ordinary pulse beat in the carotid artery, which lies close to the jugular vein and so can be recorded by the same tambour. Thereafter a third wave in the vein indicated the muscular tightening-up of the organ at full systole.
The three waves were named respectively a (auricular), c (carotid) and v (ventricular). Normally the a wave occurs 1 / 5 sec. before the c wave. The tracing which shows these waves is a continuous line and thus it is difficult to determine in the first instance which wave is which. This difficulty can be overcome by putting an ordinary pulse tracing on the same piece of paper. The carotid pulse occurs 1 /10 sec. before the radial pulse. Thus the wave occurring in the composite tracing 1 /10 sec. before any beat in the wrist pulse tracing is the c wave. It is then easy to determine the other waves.
This work led to the differentiation of cardiac irregularities - a subject which had been shrouded in mystery. It was much facilitated by the discovery of the string galvanometer or " electrocardiograph." This instrument depends for its working on the oscillations of a special string between the poles of a magnet. Currents are set up when the heart beats, separate currents for auricles and ventricles, and these cause the string to move. Its movements are photographed onto a moving plate in such a way that a line tracing is produced. The nomenclature of electrocardiograms differs from that of pulse tracings in that the a wave is called the p wave, the c wave the r and the v wave the t wave. (It must be noted, however, that the tracings are produced. in entirely different ways and therefore there is no real comparison between these waves.) There are several " leads " to the electrocardiograph - i.e. the patient may have a hand and a foot in the salt pails which constitute its terminals or he may have both hands.
The electrocardiograph confirmed Mackenzie's findings and enabled them to be extended. In this work Thomas Lewis, who had assisted Mackenzie, played a great part and was able to clear up some points which had not been fully understood. Thus the discovery of the fact that in a certain irregularity of the heart the auricles of that organ are no longer beating is due to Lewis. He named the condition " auricular fibrillation." The following types of irregularity are described by Mackenzie: - Youthful Irregularity. - The pulse varies with the breathing. It is quickened by inspiration and slowed by expiration. When the breath is held the irregularity disappears. This condition is occasioned by the vagus nerve which exercises a slowing influence on the heart. It is common in young persons and is of no evil significance. Extra Systoles. - These are the popular " missed beats." They are not, however, missed beats at all, but beats which occur out of their normal time. The so-called " auricular extra systoles " are produced by the whole heart, both auricles and ventricles taking part; the " ventricular extra systoles " are produced by the ventricles only, the auricles beating at their normal time. These beats occur too soon and so the heart is not fully charged with blood. In consequence, the beat may not be discernible at the wrist. The heart pauses after the beat to recover itself. There is then a big beat. Extra systoles in the absence of signs of cardiac failure may be ignored.
Paroxysmal Tachycardia: Auricular Flutter
In this condition a period of abnormal rhythm suddenly occurs. The pulse rushes off and the patient is pulled up and feels a soft fluttering in his chest.
A tracing shows that the auricles are beating more rapidly than the ventricles, only a few of the beats being followed by ventricular contractions. The auricles may achieve very great speed, even 200 beats a minute. The condition, as a rule, ends suddenly.
Auricular Fibrillation
In this condition the patient suddenly becomes very unwell. His feet may swell and his liver dilate. He becomes breathless on exertion and may have much cyanosis. The pulse is often rapid and is always markedly irregular. There are small and big beats but no two beats are of the same length. Moreover the irregularity does not disappear on exertion as does that caused by extra systoles - a useful means of distinguishing the conditions. The cause of the trouble is a fibrillation of the auricles which are no longer contracting. In tracings the a wave and in electrocardiographs the p wave is absent. The condition points as a rule to grave cardial mischief; it frequently occurs in mitral stenosis, - narrowing of the orifice of the mitral valve. In this disease a. rough murmur is heard just before systole of the heart and is caused by the rush of blood through the narrowed orifice under the compul sion of the contracting auricles. When, however, auricular fibrillation begins this compulsion is removed and then the pre-systolic murmur is no longer heard. A curious point, too, is that patients who have suffered from attacks of angina pectoris before auricular fibrillation began seldom so suffer after its appearance. The condition is amenable to treatment. Mackenzie advises that digitalis is the drug for auricular fibrillation and that it must be exhibited in large doses, 15 miniins four times a day, until the pulse slows down. Thereafter the drug must be stopped or, rather, given in small doses sufficient to maintain the slowing. The results of this treatment in favourable cases are remarkable.
Heart Block. - Stanley Kent and the junior His showed that there exists in the heart a neuro-muscular mechanism whereby stimuli pass from a node of tissue situated on the sinus venosus (and so known as the sino-auricular node), where they arise, to the auricles and ventricles. The means of their passage is the auriculo-ventricular bundle, a strand of fibres of neuro-muscular type which bifurcates and supplies a branch to each ventricle. In cases of disease this bundle may be affected and so the passage of stimuli be prevented. Thus the auricles and ventricles will be dissociated from each other.
Partial Heart Block occurs when the dissociation is not complete. In this condition only alternate stimuli may pass (" 2-I block ") or only every third stimulus. The patient is apt to suffer fainting attacks and also a condition known as the Stoke Adams syndrome. This occurs when a period of more than 18 seconds elapses before a stimulus passes. It is characterized by a convulsion, by stertorous breathing and by the bringing-up of frothy expectoration. As the disease causing the block advances the dissociation becomes more complete and then, curiously enough, the ventricle takes on its own rhythm and beats regularly at about 40 to 50 beats per minute. The fainting attacks now pass away.
Complete Block. - Auricle and ventricle beat separately without relation to one another. The ventricular rate is slow (40 to 50). The auricular may be fast or normal. The patient may go on for a long time with this dissociated rhythm.
Block is not always caused by disease of the bundle. Certain infections and certain drugs may cause it temporarily. Treatment is not of much avail, but if the condition is diagnosed much may be done to prevent ill-effects from exercising their full force.
The main cardiac arrhythmies was elucidated by Mackenzie, Lewis and others. This work has now been accepted throughout the whole medical world. Lewis has pursued further the electrocardiographic study of arrhythmia and has recently suggested differentiation between " homologous " and " heterogenous " rhythms.
A type of the former is the youthful irregularity; of the latter the extra systole auricular flutter and auricular fibrillation.
Not less momentous than the researches on cardiac irregularities was Mackenzie's contribution to the subject of heart failure. He pointed out that the study of valvular disease had been largely a study of sounds heard through the stethoscope. It was the habit of the profession to relate an abnormal sound to a supposed gross abnormality of structure - e.g. a broken valve and to make a prognosis on this supposition. This method led to many mistakes and even to abuses, for time had shown that patients with murmurs of various kinds might yet be well able to carry on active lives and even to live to old age without any symptoms of distress. It seemed therefore to be necessary to discover some more sure ground of diagnosis than that existing.
Mackenzie asked himself the question: " What is it that I am afraid of when I examine the patient?" The answer evidently was: " Heart failure." Thus a new direction was given to the assessment of the significance of cardiac symptoms. These symptoms were no longer to be accepted and read in terms of the post-mortem room. They were to be put to the test of their relationship with failure of cardiac power, that is to say of the myocardium or heart muscle.
The effect of this re-statement was an increased interest in such subjective symptoms as breathlessness and pain. These symptoms, it was remarked, vexed the patient as a rule when he attempted exertion, at which times one or other might make its appearance. The breathlessness seemed to be due to an excitation of the respiratory centre by lack of oxygen - weak circulation; the origin of the pain was more obscure. Mackenzie, however, called attention to the fact that in cardiac pain there is present as a rule an area of tenderness or hyperalgesia on the left side of the chest, below or surrounding the nipple. This is clearly a " referred " tenderness and corresponds to similar areas found in the skin of the abdomen in cases of visceral disturbance, e.g. gall-stone colic or appendicitis. The view was therefore formulated that the cardiac pain represented an effort of the heart to deal with large quantities of blood, that organ being incompletely prepared for its task. Thus the pain pointed to a weakness of the heart muscle.
The upshot of this work was a system of relating such findings as a murmur to the general state of the patient. Thus, if a murmur was heard and it was found that the individual was also breathless or suffered from marked pain and that these subjective symptoms were increasing, a tendency to myocardial exhaustion might be inferred.
If on the other hand the murmur was unaccompanied by symptoms its presence was not to be regarded as of so serious a character. This applied specially to systolic murmurs occurring at the moment of the cardiac beat and replacing the first sound. It applied also, however, to the two murmurs which are generally regarded as betokening organic disease, the presystolic murmur of mitral stenosis and the diastolic murmur of aortic disease.
In connexion with the presystolic murmur Mackenzie pointed out that when auricular fibrillation occurred this sign disappeared, leaving however a mid-diastolic murmur, which is also frequently found in mitral stenosis. The disappearance of the murmur is occasioned by the failure of the auricle to beat. In the case of aortic disease the accompanying hypertrophy of the heart is an important additional sign of muscle damage, even though the cause of the hypertrophy is by no means clearly understood.
Evidently the value of this method of determining the degree and progressive character of heart failure must lack in value without some system of correction and test. Mackenzie early apprehended this difficulty and set himself to supply the want. He conceived that in the last issue the proof of the danger or otherwise of a symptom is the after-life of its possessor. Consequently while still a young man he undertook the laborious task of following up a large number of patients during a long period of years.
The test was continued for some 20 years and its results then published in a series of books and monographs. A great many symptoms had been recorded in the first instance and their after-histories were therefore, when revised collectively, a commentary on the prognosis of heart affections of a unique kind, both as respects content and value. It was found that certain symptoms which had an evil reputation had not at all interfered with healthy life - an example is the systolic murmur met with in toxic persons; these murmurs are very frequent and the irritable type of hearts in which they appear is also a commonplace of the consulting-room. Mackenzie named the general condition " X-disease," because its exact nature was doubtful.
Another dreaded symptom which proved more or less without harm was the missed beat or extra systole. Another, the so-called caput medusae or group of injected venules seen on the margin of the ribs of many persons. Still another was the tendency to occasional palpitation or heavy beating of the heart after an acute illness.
On the other hand it was found that persons suffering from auricular fibrillation, attacks of true anginous pain (angina pectoris), from the curious cardiac rhythm known as pulsus alternans because every alternate beat is smaller, and from various forms of dyspnoea, tended to succumb at more or less early periods. In some cases, for example auricular fibrillation, much could be accomplished by proper treatment (digitalis); in others, for example pulsus alternans, little or nothing could be achieved.
This body of evidence is now at the disposal of the medical profession and constitutes a contribution of enormous value.
Another aspect of the cardiological problem, which was brought into prominence by the war, is the so-called " nervous or irritable heart." Attention was first called to this condition in 1915, when it was found by the British army medical authorities that a very large number of soldiers were being sent to hospital and being invalided out of the service on account of heart disease. The extent of the mischief was so great that it was rightly concluded that some inquiry was called for and application was made to the Medical Research Committee to take the matter in hand. Sir James Mackenzie, Dr. Thomas Lewis, Capt. Thomas Cotton and Dr. R. M. Wilson were appointed to study the cases. At a later date a committee consisting of Sir Clifford Allbutt, professor of medicine at Cambridge, the late Sir Wm. Osler, professor of medicine at Oxford, and Sir James Mackenzie was constituted, and a separate hospital, Mount Vernon, Hampstead, was set apart for soldiers with heart complaints. This hospital had on its staff, in addition to the above mentioned, Dr. Thomas Parkinson of the London hospital, Professor Francis Fraser now at St. Bartholomew's hospital, Professor Meakins now of Edinburgh University, Dr. Nigel Drury and others. A very prolonged and careful research was carried out.
The symptoms of the condition were found to be breathlessness on exertion, pain over the praecordium, exhaustion and giddiness and fainting In addition palpitation was often complained of, as also were headache, lassitude, coldness of the extremities and irritability of temper. The signs, as opposed to symptoms, were increased heart rate, raised blood pressure in patients up and about, diffusion of the apex beat and irregularity of the heart's action. The temperature was frequently raised to 99.5° F. or to Ioo° F., such elevations being of a fleeting character. Respiration rate was also raised on exertion and tremor was the rule.
Lewis, who directed the research, gave to this picture the name of " Effort Syndrome " and wrote of it in an early publication: " A generalization which has been shown to approximate to the truth in respect of the exaggerated rise of heart rate, blood pressure and leucocyte count in response to exercise is that the rise in patient and control are identical, if the exercise is sufficient to produce in patient and control the same degree of respiratory distress." In short these patients responded to stimuli in an excessive manner. The first method of dealing with them was an attempt to sort them out by means of graduated exercises and for this purpose an instructor was obtained. It was soon found that capacity varied a good deal but that it could be increased in certain instances by a judicious use of the exercises. It was soon discovered that the predominant etiological factor in the clinical histories of the cases was infection of one kind or another. In 558 patients the history of onset was definitely dated from rheumatic fever or chorea in 68 instances (or 12%), from dysentery in 14 instances, from typhoid fever and diarrhoea in 14 instances, from pneumonia, pleurisy and bronchitis in 25 instances, from pyrexia of unknown origin (trench fever in all probability) in 28, and from miscellaneous infections such as diphtheria, scarlet fever, syphilis and pus infections in 30 instances. In all these the first symptoms of the malady were definitely noticed during convalescence from the disease in question. The percentage covered is thus 33. But this by no means exhausts the importance of infection, for of the 376 cases which remain there was a history of rheumatic fever in 57 cases, of repeated joint pains in 8 cases, and of pleurisy, pneumonia, syphilis and other maladies in many more. Moreover, any intercurrent infection always had the effect of greatly increasing the severity of the symptoms. Further work in other hospitals has only increased the tendency to regard this malady as an extra-cardial one and to assign its cause to infection or, in a few instances, to gastro-intestinal troubles, shock and so on.
That irritable heart or " nervous heart " is found in civilian practice is certain, and that it constitutes a large proportion of socalled heart disease cases is equally beyond doubt. That it is not heart disease at all is becoming increasingly evident. Indeed the vital and even revolutionary part of this work lies in the fact that symptoms which have been associated with one kind of mechanism of origin are now seen to be capable of production by another kind of mechanism. In other words, breathlessness on exertion and cardiac pain may occur in the absence of any damage to the heart.
Thus it became necessary to re-investigate these symptoms. Numerous attempts have been and are being made. At one period, about 1919, a chemical theory held first place in interest. It was suggested that breathlessness was due to a lack of " buffer " salts in the blood. The idea was that the blood contains various salts and notably acid phosphate of soda, which are capable of absorbing either an excess of acid or of alkali. Thus the action of the buffer salt is comparable to that of a sponge. It was suggested that these cases of nervous heart were deficient in buffer salts and so lacked the means of preventing alterations in blood quality. This view was supported by a great deal of very delicate work but it has scarcely found general acceptance. An alternative view has recently been suggested to the effect that the blood lacks oxygen. It is pointed out that a general condition of venous stasis exists and that on this account a smaller quantity of blood passes through the lungs in a given time. The oxygen intake is lowered. In consequence during effort there is no great reserve of oxygen for use in the muscles and so more rapid and forcible breathing is rendered necessary in order to increase the supply. The stimulus here is not an excess of waste products but a lack of oxygen. Curiously enough there appears to be some ground for supposing that oxygen want is not in any sense synonymous with excess of carbonic acid gas. In the absence of sufficient oxygen the blood does not become less but rather tends to become more alkaline. This subject, however, is at present being further investigated. The researches of Haldane of Oxford and Barcroft of Cambridge must be mentioned in connexion with it.
The oxygen want is probably secondary to a nervous disturbance whereby the circulation is upset. In fact the evidence available at present points to an effect of the toxins of disease on the nervous system, and more especially on the involuntary nervous system. This system regulates the action of the heart and also the tone of the circulation. The smaller arteries are under its control and recent work, following that of Roy, suggests that even the capillaries may be supplied with nerves. It is, moreover, related in an intimate way to certain of the ductless glands and notably the supra-renals which produce adrenalin. The work of Gaskell has furnished a new conception of this system and it is now possible to recognize two main branches - the true sympathetic, the action of which on the heart is accelerator, and the vago-sacral sympathetic or parasympathetic, the action of which on the heart is inhibitor. It can easily be seen that any disturbance of the relationship existing between these branches of the involuntary nervous system must react not only on the efficiency of the heart and of its responses to calls for increased effort but on the integrity of the whole circulatory tree. In point of fact the tendency to stasis or stagnation in many " nervous heart " cases is explicable only in terms of this nervous system.
In the same manner the origin of " cardiac " pain in these cases is probably to be related to the nervous system. How exactly the pain arises still remains in dispute. Enough that the pain is often excited by effort and tends to diminish if effort is abandoned. The fact that it usually disappears if the auricles of the heart begin to fibrillate has suggested to some workers that distention of those chambers by blood may act as the exciting cause.
The fact of immediate importance is that breathlessness, pain, palpitation, giddiness, exhaustion and the other symptoms of this series cannot be taken as of themselves indicating heart failure. They may all be present and yet the heart may be active and sound. Cardiologists have thus been compelled to reconsider the evidence on which a grave prognosis may be founded and have come to appreciate the great difficulties which beset their paths. Indeed the tendency has become apparent to regard serious heart mischief in a patient showing symptoms of the kind mentioned as the exception rather than the rule.
Nevertheless certain guides are available which should enable a reasonable opinion to be formed. If for example a patient has been suffering from a degree of limitation of the field of effort for a considerable period and if this degree is not exceeded it can be inferred that, whatever injurious agent is present, whether it be organic disease or a poison, the mischief is stationary. There is no " failure " in the true significance of that term. If moreover a sharp restriction of the field of effort is accompanied by signs of febrile illness and if the restriction is removed as the fever subsides a grave view need not be taken. But if a marked restriction occurs without evident cause this points in all probability to a weakening of the heart muscle. Again if dilation of the organ takes place and is progressive, or if auricular fibrillation supervenes, heart failure may be confidently diagnosed. In the last issue heart failure would seem to be always a muscle problem. The ultimate importance of extracardial factors is thus their influence on the burden which the heart is called upon to support. The heavier that burden and the weaker the organ (e.g. on account of organic disease) the earlier may failure be expected to show itself.
Heart Flutter
The most recent contribution to the study of heart disease is that of Dr. Thomas Lewis on the nature of auricular flutter and auricular fibrillation. Lewis followed the experiments of Mayer in 1908 and of Mines in 1913. These workers used the contractile bell of the jellyfish and later rings of muscle cut from the ventricles of turtles and the auricles of teleostean fishes. The experiments were repeated in 1914 by Mines and Garvey. on rings of muscle cut from the ventricles of the dog.
The experiments were as follow: If a ring of muscle was stimulated at a given point in its circumference by means of a single shock, a wave of excitation is set up. This wave develops two " crests "; one goes round the ring in one direction, the other in the other direction. Necessarily they meet at a point. The whole ring has now become involved by the wave and has passed into a state of excitation. It has become " refractory," that is to say that for the moment it is no longer excitable by further shocks.
When therefore the waves of excitation meet one another on the circumference of the ring, movement is brought to an end. In Lewis's words: " like two waves of flame, two waves of excitation meeting do not override: each crest forms an impassable barrier." The ring of muscle remains in this state of excitation (which is nearly though not quite synchronous with the state of contraction) for a period and then recovers. It recovers in the order in which it has become involved, that is to say it begins to be " responsive " again at the spot where the primary shock was applied. The responsiveness travels round the ring in two waves just as the excitability did. When the crests of these second waves meet the ring has returned to its original condition. It is wholly responsive.
Lewis uses the analogy of a prairie fire which can spread only in those directions in which unburnt grass awaits it. If, therefore, for any reason a portion of the ring of muscle happens to be " refractory " or in a state of excitability when a fresh shock is given only one wave of excitability may be able to travel. The fire, so to speak, is stopped by a patch of outburnt grass. Recovery of this refractory area may, however, have taken place before the new wave gets round to it. In that case the wave will continue to circulate, for when it returns to its starting point that starting point will have recovered its responsiveness. It is, indeed, as if the grass had grown again on the face of the prairie by the time the fire got back to it.
This curious condition of affairs is spoken of as a " circus movement " and it is in these circus movements that this investigator believes he has discovered the secret of auricular flutter and auricular fibrillation. For some reason the normal wave of excitability which should pass over the muscle of the heart is replaced by a wave travelling in a circle over the surface of the auricle. This wave follows, it would appear, the same circular path which it has mapped out for itself and then returns again to its starting point. Here it meets muscle which has so far recovered as to be responsive once more, and thus the wave keeps on travelling round and round. Subsidiary waves are sent out, like tributary tongues of fire, over the muscular surface and the auricle beats at the rapid rate which is characteristic of the clinical condition.
Lewis has been able to induce fluttering of the auricles experimentally in dogs and has been able to prove that this is the same condition as that encountered in the human subject. " Flutter," he declares, " consists essentially of a continuously circulating wave." The path taken by this wave is not always the same for each animal. In the dog an artificial flutter may last for hours; in man flutter may last not hours but years. A " single wave continuously circulating for seven years," Lewis pointed out, " may seem to be a remarkable conclusion; nevertheless, it is one we are now bound to accept." It is evident that the permanence or impermanence of this circulating wave of excitability depends on the fact that the crest of the wave always finds recovered and so responsive muscular tissue in front of it-to revert to the analogy, the advancing crest of the fire always finds new-grown grass to burn. There is thus present, in auricular flutter, a " gap " of recovered or responsive muscle between the refractory or excited portions and the crest of the oncoming wave of excitability. This gap moves round and round the ring just as the wave of excitability does. The grass in fact grows up as quick as it is burnt down-there is always a patch of it for the flames. Upon the continued presence and integrity of this gap the permanence of the flutter depends. So long as the gap is there the wave will circulate; so long as there is grass the fire will burn. But if the gap could be closed the flutter would-must-stop at once.
The same description applies to fibrillation except that the circus movement here is less well defined in its quality and the wave motion more diffuse. It will be seen that the experimental work has led to the door of the sick-room, so to speak, and that Lewis's view of the " gap " is probably justified: " it is a gap which will command the attention of many workers in the near future, for upon our power to influence its length, our success in treating flutter and the closely allied condition, fibrillation, will very largely depend." (R. M. Wi.)
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Chisholm, Hugh, General Editor. Entry for 'Heart Diseases'. 1911 Encyclopedia Britanica. https://www.studylight.org/encyclopedias/eng/bri/h/heart-diseases.html. 1910.
