The Lettsomian Lectures on Diseases and Disorders of the Heart and Arteries in Middle and Advanced Life [1900-1901]

by J. Mitchell Bruce

LECTURE III.

Mr. Vice-president and Gentlemen,—In this, the concluding lecture of the series, I will attempt to deal with the applications of the facts and considerations which I submitted to you on the two previous occasions when I had the honour to address you. I trust that what I then laid before you proved to be of some interest. Let us see now whether it is practically useful. However much the etiology and pathology of the diseases and disorders of the heart and arteries in middle and advanced life may deserve study as matters of natural history, we should be disappointed if they could not be turned to account in prognosis and treatment. These are the subjects I propose to discuss this evening.

Now, prognosis and treatment, to be rational and useful, have to be based on as full and as correct a diagnosis as knowledge permits. The present disposition is to fall short of this; to rest content with an incomplete diagnosis. We say that the patient's "heart is dilated," that he has "arterial degeneration," that there is "fatty degeneration." But you will remember that we have found that cardiac dilatation may be present in every kind of cardio-vascular degeneration; that the arteries are naturally enlarged and thickened after middle life, and that we refused to call these changes morbid. Clearly, therefore, a purely anatomical diagnosis of this sort is insufficient. If you are asked what the prognosis is of fatty degeneration of the heart, you answer that you must first be told whether syphilitic or gouty disease of the coronary arteries, or strain, or alcoholism, or phosphorus-poisoning or anæmia is the cause of it. When you are planning the treatment of dilatation of the heart you first determine whether the dilatation is a result of the stretching of a sound heart by overfilling during muscular effort, or of the insufficient emptying of failing chambers with degenerated and feeble walls. Obviously what we ought to determine in these instances and in every instance is the origin of the disease. The ultimate diagnosis to be reached for practical purposes is the etiological diagnosis.

Is this possible? Does our knowledge of the nature, characters and course of these cardio-vascular affections enable us to say, after investigating a case, what the kind of the pathological change is that constitutes the disease, or in what respect the physiological mechanisms are disordered? Can the cause of these degenerations of the heart and arteries be determined in each instance? How is the practitioner to proceed to do so? What method might be followed with advantage in making a complete diagnosis of heart disease in older subjects?

A man of 60 consults us about his heart. He says that it has caused him a good deal of concern lately. More specifically he describes a sense of oppression behind the sternum as often as he exerts himself, and palpitation with consciousness of irregular cardiac action when he goes to bed. We inquire for other familiar cardiac symptoms, such as pain, angina, fluttering, faintness, giddiness, and a sense of impending death. We find that one or more are present occasionally, and that they have increased in number and degree during the last few months or years. Perhaps cough, nocturnal orthopnœa and dropsy may be beginning to give trouble. The next part of the inquiry relates to the patient's previous history from childhood upwards. Which of the acute diseases has he had? Acute rheumatism, chorea, scarlet fever, typhoid, diphtheria and influenza must be mentioned individually, and in women the nature of any puerperal disease from which they may have suffered. Gout, irregular gout, gravel, eczema, sick headache, asthma must be inquired after with the same minuteness, and so must syphilis. We next hear an account of any accident which the patient may have met with, such as a blow, or a fall from a horse or a carriage. This brings us naturally to question him about his occupation and modes of relaxation and amusements—whether active or sedentary, regular or irregular, their characters otherwise, and their direct effects, including strain. More difficult to elicit is a correct account of the patient's habits—in respect of food, stimulants and tobacco, and his manner of life generally. As I said in my first lecture, this is an inquiry which the family practitioner has an opportunity to carry out much more successfully than the hospital physician or consultant. The family practitioner has known for years of his cardiac patient's work and worries; it may be of his large eating, of his secret drinking, of the history of syphilis in earlier years. It is always well also to inquire after a family history of gout, rheumatism and heart disease. A list of questions like this sounds far more formidable than it is in reality. A few minutes suffice to arrive at the truth. We already have a pretty fair notion what we have to deal with, whether strain, gout, syphilis, tobacco, an old rheumatic lesion, or a combination of two or more of these.

We next proceed to physical examination, beginning with the pulse and arteries, and passing on to the heart and associated structures. The characters of the præcordial impulse—particularly the seat of the apex-beat and the strength of the impulse—are closely (I might almost say laboriously) investigated. We must never yield to the temptation to disregard weakness or absence of the impulse. Like many other negative signs it is apt to be overlooked. Then the præcordial dulness is mapped out by means of light percussion. Finally, auscultation reveals to us the presence or absence of murmurs and the characters of the sounds—in the standing and recumbent postures, and, if necessary, after a little exertion. The relative loudness of the first and second sounds over the different parts of the præcordia is particularly worthy of note.

Now let us suppose that we have found a mitral systolic murmur. We ask ourselves whether it is structural or whether it is functional, that is, due to relaxation and dilatation of the ventricular walls. If structural, with which (if any) of the diseases elicited in the man's previous history would it correspond? Most probably with gout or glycosuria. Thus we attempt to connect the lesion with its cause, and the cause with its effects, and have reached the ultimate diagnosis. So with other valvular murmurs: for example, an aortic diastolic murmur proves to be related to syphilis. If there be no murmur audible, we naturally think of dilatation with failure, or of enlargement from strain, from Bright's disease, from arterial sclerosis, from emphysema, from an insufficient or impure blood-supply in the coronary arteries, from disordered innervation, or from some rarer cause, such as adherent pericardium; and then, with these associations in our minds, we review once more the patient's history, and generally succeed in our diagnosis.

Here let me recount the significance of the principal signs and symptoms which I detailed to you in my last lecture, considered in the reverse order on this occasion, some of which are of real value in differentiating the causes of cardio-vascular degeneration. To begin with negative facts: a mitral pre-systolic murmur is never significant of a degenerative lesion. Secondly, when we meet with an aortic diastolic murmur, whether alone or along with an aortic systolic murmur, we may safely conclude that we have to deal with something more than atheroma produced by regular or irregular gout and associated metabolic disturbance, cardio-vascular disease of nervous origin and alcoholic or tobacco heart, even if there be evidence of the presence of one or more of these in the case. Aortic incompetence developed in later life is the result of syphilis, or of acute or chronic valvular strain; but, of course, many instances of this lesion met with after the age of 40 can be traced to juvenile endocarditis of rheumatic or other origin. Always a serious lesion, aortic incompetence due to syphilis, or to syphilis and strain, is particularly grave, as being so frequently associated with coronary disease and consequent myocardial degeneration—fatty or fibroid, acute softening, and sudden fatal failure. A fully-developed basic systolic murmur, audible over the aortic area and manubrium and along the course of the carotid, is a very common sign of atheroma of the aortic arch and valves and great vessels in association with regular or irregular gout, diabetes, corpulence and allied disorders of nutrition. It is also one of the physical signs of syphilitic and traumatic affections of the aorta and aortic valves and of remote endocarditis. Further, these lesions are so often accompanied by similar degenerations in the coronary arteries and consequent myocardial degeneration, that the basic systolic murmur ought at least to raise the suspicion of this in the observer's mind. An ill-developed basic systolic murmur is not uncommon in alcoholism, chronic Bright's disease and nervous strain, but it is difficult to dissociate from anæmia. A fully-developed systolic murmur audible in the mitral area, I mean independently of ventriculo-auricular leakage in cardiac failure, is usually traceable to early endocarditis of rheumatic or other origin, rarely to injury, including ordinary juvenile strain of the valves or walls, or to Graves's disease. But in some instances it is unquestionably due to valvular atheroma and attendant sclerosis, caused by gout or other disturbances of metabolism, including the effects of free living; and in these instances the observer must not overlook the possible association of coronary disease and fatty degeneration. If a systolic mitral murmur prove to be somewhat indefinite and affected by posture, cubitus and effort, to vary under observation from day to day, and to disappear under treatment, it is of no more value to us in differential diagnosis than that it signifies relaxation and weakness, or disorderly action, of the left ventricle, consequent on any one of the recognised causes of failure or disturbance of the heart, including the different cardiac poisons, overwork, anæmia, acute disease, poverty and the like, and this whether in a heart previously sound or previously enlarged or previously the seat of valvular disease. An accentuated ringing second sound in the aortic area, or more extensively, is of great value in the diagnosis of arterial tension and of aortic atheroma or of both, but it is associated with far too many different causes to be of much use in differential diagnosis. It should suggest a most careful search for Bright's disease. Slight reduplication of the first sound is common over the heart strained in youth and the heart degenerated by alcoholism and metabolic disorders, but everyone knows that it is not unusual in a variety of other conditions, healthy and morbid. On the other hand, the bruit de galop, or cantering rhythm of cardiac sounds—definite doubling of the first sound followed by loud, accentuated, ringing second sound—is practically pathognomonic of Bright's disease, and is one of the most valuable, because one of the most ominous, of physical signs in connection with the cardio-vascular system. A normally-sized heart with irregularity, increased frequency, and a variable systolic murmur in the mitral area, is characteristic of tobacco poisoning. A heart enlarged on both sides, and acting irregularly without murmur, is (apart from cardiac failure) suggestive of strain in early life.

Cardiac symptoms taken individually are of less diagnostic value than signs. No symptom is pathognomonic. Palpitation is a nearly universal phenomenon of cardiac disease and disorder. Faintness and actual faints are not uncommon in cases of early cardiac strain, gouty heart, and nervous disturbances. Angina we meet with, you will remember, in regular and irregular gout, tobacco heart, strain (especially strain after 40), and in syphilis and alcoholism, whilst pseudo-angina is extremely common in nervous women: thus angina is of less diagnostic value than might have been expected. A high-tension pulse I have found most often in Bright's disease, in juvenile strain, and in cardio-vascular affections of nervous origin; a low tension pulse in connection with alcoholic and tobacco poisoning, and with senile strain.

When we review these facts, I think we are entitled to conclude that the physical signs and symptoms carefully determined by clinical investigation may be confidently employed, along with the patient's previous personal history, and the history of his present illness, to differentiate from each other the causes of cardio-vascular degeneration in individual cases. And, further, that they inform us of the seat of at least some of the lesions, valvular, parietal and vascular. A little trouble, patience and attentive observation are all that are required to reach a complete or working diagnosis. Now we may approach the great practical subjects of prognosis and treatment with some confidence.