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Defects in Cardiac Rhythm in Relation to Cardiac Failure*

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Defects in Cardiac Rhythm in Relation to Cardiac Failure* Mr. Geo. A. Allan?Defects in Cardiac Rhythm. 333 DEFECTS IN CARDIAC RHYTHM IN RELATION TO CARDIAC FAILURE* By GEO. A. ALLAN, M.B., F.R.F.P.S.G., First Assistant to the Regius Professor of Medicine, Glasgow University; Assistant Physician, and Physician-in-Charge of Electro-Cardiograph, Western Infirmary. In the remarks which are to follow, I do not pretend to say anything that is original, and to many present the facts may not be new. One can at least say for the subject that it is very important, and deals with problems which meet the practitioner in many ways and very often. It is one which has had for me a special interest even before I began teaching clinical medicine, now nearly fifteen years ago, and needless to say, the recent advance in this department has only stimulated that interest. It may be well at the outset to define the limits of the subject, and to come to an understanding of some general facts. Failure of the circulation may be brought about in different ways, and the failure is not always on the part of the heart. The venous supply within wide limits governs the ventricular output (Starling), but the venous supply will fail if from vasodilatation the blood is retained in the abdominal blood lake, and the circulation will fail even though the heart is healthy. Such a failure will be due to vasomotor failure and not to cardiac failure. My remarks will be directed chiefly to failure of the circulation when this is due to failure on the part of the heart itself, and to a consideration of the relationship, if any, which exists between this failure and the various well recognised defects of the cardiac rhythm. The term cardiac failure, though in common use, is one which may lead to confusion. We may define it in general terms as the failure on the part of the heart to supply a quantity of blood sufficient for the ordinary needs of the individual without the production of uncomfortable symptoms. The same uncomfort- able symptoms which are present with a failing heart are those * Paper read before the Southern Medical Society, 3rd February, 1921. 334 Mr. Geo. A. Allan?Defects in Cardiac Rhythm which are produced when a healthy heart is subjected to a stress which it is not capable of meeting. Breathlessness, palpitation, pain at the heart, exhaustion and giddiness, are common to both conditions. Dropsy cannot be taken as a distinguishing factor, for it is not an essential element in cardiac failure, and death may ensue from heart failure without its presence. Nor can a standard stress be fixed which would enable us to say that a heart is failing if it is unable to meet that standard. The criterion of cardiac failure is an individual matter, and no uniform standard test can be applied to different persons. We may try to form an estimate in our own minds as to the amount of work a certain person should be able to perform without symptoms, but a much more practical method is to obtain facts which will permit us to compare his present with his previous ability to perform the same piece of work. This will allow us to judge if the circulation is tending to fail, and it is our duty to find out whether his heart is primarily or only secondarily at fault. This will? suggest a failing heart, but not necessarily heart failure. When dropsy is present the position is much simpler, but, as we have seen, it is not present in all cases. Signs of gross change in the heart only suggest that the heart is likely to be the cause of the symptoms, but they do not of themselves tell of the presence of failure. Let us consider this question for a little in the light of what we know about the reserve power of the heart. It has been estimated that the heart of a healthy man doing moderate muscular work expends about five times as much energy as when he is at rest (Krogh). In other words, his heart has a reserve of power equal to at least four times the amount required to carry on his circulation when he is recumbent. This, of course, will vary with the training of the heart muscle whether the heart be healthy or diseased. For argument let us accept these figures, one unit when resting and four in reserve, and let us consider how in gross heart disease that reserve may be used up, and so lead to actual failure. (In the diagram, A shows a constant load of one unit with a reserve of four units.) 1. There may be disease of the muscle itself. This may be due to blood - supply defective in quantity or quality (narrow coronaries or anaemia), or to direct action of bacterial toxins or in Relation to Cardiac Failure. 335 to invasion by the organisms themselves. The exact lesion does not here concern us?the muscle may be atrophic, fatty, or fibrous?in any case its efficiency is impaired, and the muscle has less reserve than a healthy heart. Let us suppose it has lessened the reserve by two units (B in diagram), though it may, of course, abolish the reserve altogether. 2. There may be constant extra load on the heart due to Diagram to illustrate the relationship of heart reserve to heart failure. A?healthy heart; B?heart with unhealthy muscle ; C?heart with extra load due to valvular disease or high blood-pressure, and compensatory hypertrophy; D?failing heart due to load and muscle damage encroaching "on reserve. disease of the arteries or heart valves. In diseases of the arteries associated with high blood-pressure the left ventricle has more work to do, and so reserve is encroached on. In the case of damaged valves similar conditions prevail. The two most important results of valve damage are obstruction at the mitral orifice and leakage at the aortic valve, the former adding load chiefly to the right and the latter to the left ventricle. Good 336 Mr. Geo. A. Allan?Defects in Cardiac Rhythm heart muscle can overcome these mechanical difficulties by being trained. It may hypertrophy, and we may say the lesion is compensated, but even then the reserve is seldom, if ever, equal to the normal reserve. In the diagram (C) I have suggested two units as the extra load with the addition to the reserve of one unit for compensatory change. 3. An important point to note is that the causes which are at work in producing arterial or valvular disease often also produce damage in the heart muscle. In the case of arterial lesions the coronary arteries are very liable to be involved in the process, and so the muscle suffers, or the muscle may be damaged directly by the primary cause. In the case of valvular disease, rheumatism and syphilis are the common causes. In both the muscle is liable to be directly attacked by the infection, and in the case of the latter the coronaries may be affected in their course or at their orifices in the aorta. When extra load is added to the work of a heart whose reserve is limited by disease of the muscle itself, it is easy to see how the remaining reserve is used or defects and how up by gradual increase in either both of these cardiac failure results. In the diagram (D) I have shown the last unit of reserve being encroached on by these two factors. In a heart of which the reserve is limited, but not used up, a certain amount of exertion is possible without the production of symptoms. If that exertion is within the limits of the person's daily requirements, he may experience no symptoms of cardiac failure; but if symptoms are produced by exertion which, say a no is If year ago, produced symptoms, then his heart failing. he is unable for any exertion without symptoms then he has cardiac failure. If these conceptions are true, or even approximately true, we must endeavour to know all the signs which are indicative of involvement of heart muscle. Frequently the patient's symptoms are the first guide, but at other times we get warning from the cardiac rhythm, and it is this aspect of the subject to which I should like to draw special attention. This object will, I think, be best attained by passing in review the commoner disorders of rhythm, and noting, first, in how far each is indicative of muscle damage, and, second, how much load each adds to the heart's work. in Relation to Cardiac Failure. 337 Perhaps I might be permitted to remind you of the nature of near the intrinsic cardiac mechanism. In the rightO auricle,' the opening of the superior vena cava, there is a small mass of tissue which differs from the muscle of the auricle, called the sino- auricular (S.-A.) node. It is supplied by branches from the sympathetic and vagus nerves. In the lower part of the right auricle, to the right of the opening of the coronary veins, there is another mass of tissue with similar nerve supply called the auriculo-ventricular (A.-V.) node from which there emerges a bundle of fibres, the auriculo-ventricular (A.-V.) bundle, and this main bundle divides into two branches which pass to the left and right ventricles and ultimately, by minute branches, connect with the muscle fibres of the ventricles through the Purkinje system.
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