Kitabı oku: «The Lettsomian Lectures on Diseases and Disorders of the Heart and Arteries in Middle and Advanced Life [1900-1901]», sayfa 4

Strain Before Forty

A more interesting group of cases than those which I have just discussed is composed of persons who have strained their hearts in youth or early manhood, have never been quite well since, and in middle or advanced life are at last driven to us for help. Cases of this character would furnish excellent material from which we might attempt to judge of the after-effects of excess or abuse of muscular exercise in the young. This is a tempting subject of discussion, but one far too long and much too important to be taken up casually at this time. Therefore, I will content myself with submitting to you as plainly as I can certain facts bearing on it that have come before me in my present inquiry, along with a few simple observations of a practical bearing. First, then, let me read to you the history of what I should call a typical case of the kind. A man of 69 complains that as often as he walks any distance or climbs a stair he is arrested by a distressing sense of having a bar across the lower end of the sternum, breathlessness, irregular palpitation of the heart, and a very little choking in the throat; the discomfort has lately deserved the name of pain. His heart is very large, the area of præcordial dulness being increased in all directions and measuring transversely 7 inches. The impulse is weak over the left ventricle, but definite in the epigastrium; the sounds come in couples – moderately good and very weak respectively, without murmur; and the radial artery is large and thick, with rather low pressure and irregular rhythm. It turns out that for the last 40 years these uncomfortable feelings have troubled the man more or less, and that at three different periods of his life – at 31, at 42 and at 67 – they increased so much as to incapacitate him for many months, the first time with a sudden sense of something snapping in the heart, the second time with a faint, and always, as he believes, consequent on overwork. Now this man never had rheumatism, nor gout, nor syphilis, and was always a temperate, careful liver; and he volunteers the statement that he first felt his heart at Cambridge, where he was captain of his College boat, and was tried for the University boat but felt that he was not fit for it. Belonging to this type of cardiac strain I have selected 11 cases. The heart is always found to be enlarged, and in about one-half of the cases it is irregular. It may be weak and beating at the ordinary rate, but in other instances it is increased both in force and frequency. Only in quite exceptional cases did I meet with endocardial murmurs in this group of old strained hearts; as a rule the sounds were ordinary, with a disposition to accentuation of the aortic second sound. High tension and sclerosis of the radial artery were respectively found in about one-half of the cases. The patients complain most commonly of a distressing sense of irregular palpitation of the heart, and very commonly of præcordial pain, but rarely of angina. Faintness also is sometimes mentioned. Let me hasten to add, with respect to these cases, that they do not include any instances of direct injury of the valves mechanically. Rupture or stretching of the aortic and mitral valves during exertion furnishes us with some very remarkable clinical cases; but it is with parietal strain that we are concerned now – mechanical over-stretching of the cardiac walls, which are thereafter left with but a narrow margin of the elastic and muscular reserve required by them to meet trying circumstances of any kind, particularly exertion. The subjects of dilatation of the heart from mechanical stress suffer by no means from what is commonly called "heart disease," excepting in the worst cases, but yet they feel their hearts comparatively, and it may be seriously, disabled. Naturally they associate these feelings of disability with fresh attempts at exercise or exertion, as in the case which I have just read. I pointed out in my first lecture that such exertion is not by any means connected with the patient's occupation or daily duties, but quite often occurs during unwise attempts on his part to resume at 50 the athletic exercises of his youth in order to reduce his weight, relieve his liver, or dispel gout. It is not wonderful that under such circumstances a permanently enlarged and badly-nourished heart should become embarrassed, or even seriously deranged or still further strained. I have known a man of 43, going straight from London to the Alps, have not only præcordial distress but dropsy of his legs after his first ascent in his regular holiday. Indeed, the man who has reached later middle-life with his heart enlarged by years of great bodily activity in youth, and settles down quietly on retirement, let us say from the navy, sometimes finds that ordinary exercise is sufficient to produce alarming cardiac distress and curious loss of courage, obviously due to the muscular tissue of the thickened cardiac walls having fallen quite out of condition. How instructive, for instance, is the following case: – A gentleman of 60, who has led from his boyhood upwards a life of physical activity and at the same time of temperance, and has suffered from neither syphilis nor rheumatism, but possibly from a very mild attack of gout, settles in a relaxing provincial town, continues to eat heartily, and considers that a little work in the garden is sufficient exercise for him. He increases in weight, his breath gets short, his heart flutters, and now he begins to get anxious about his health, fancying, as he says, that he has all sorts of diseases – a disposition to worry about himself which is entirely new and provoking to him. I find his heart very large and feeble, the cardiac sounds scarcely audible, and in the mitral area a well-developed systolic murmur. The patient is ordered to reduce his diet as a whole and in respect of carbo-hydrates, to return carefully to walking exercise on the level, and to take a calomel purge followed by a saline twice a week, and a mild strychnine mixture. He improves, and continues to do so; is able to walk miles without discomfort; and in the course of two months not only do I find his heart reduced in size on physical examination, but I fail to hear the apical murmur, which must have been produced by dilatation of the left ventricle. The bearing of such a case as this on the pathology, prevention and treatment of certain cases of heart disease in old subjects will be obvious to all.

We must be careful, however, to observe that neither unwise abandonment of wholesome exercise, nor ill-advised return to physical exertion, separately or in succession, can be regarded as the only cause of the recrudescence of cardiac distress after 40 in those who have strained their circulation in youth. Any one of the many circumstances that produce cardiac failure and dropsy in chronic valvular disease may lead to embarrassment and fresh dilatation of the simply enlarged heart: anæmia and chronic disease, the acute specific fevers including pneumonia, emphysema, granular kidney, gout, syphilis, tobacco and alcohol poisoning, as well as anxiety and worry, and in women the advent of the menopause; and I may say here parenthetically that pains at the heart in athletic youths are sometimes due to the tobacco smoking in which they often indulge socially when the exercise is finished – not to strain at all. In these cases of old cardiac strain, as in every form of chronic valvular disease and of chronic heart disease of all kinds, not only the original and permanent lesion, but the recent and probably temporary circumstance that caused the failure has to be ascertained and fully respected in connection with prognosis and treatment.

Syphilis

Syphilis appears to account for a very considerable proportion of the more serious cases of heart disease which we meet with in older subjects – excluding of course chronic valvular disease originating remotely in endocarditis. But I ought to repeat here what I have already mentioned, that syphilis as a cause of cardio-vascular lesions is very often associated with other morbific influences, particularly strain and alcohol. Of its position as the principal cause of grave disease of the valves as distinguished from the walls of the heart, originating in middle life, there can be no question. No fewer than nine out of 28 cases, of which I have private notes, were the subjects of double aortic disease; practically all the others had a loud ringing second sound over the aorta, significant of degeneration; pain of anginal type in half the cases was the prominent complaint; and two-thirds of the subjects had sclerosis of the radial artery. When we consider that syphilis does also affect the myocardium primarily; that fibroid disease, chronic aneurysm and fatty degeneration of the heart are all traceable to specific disease of the coronaries in many instances; and, finally, that many of the subjects of syphilitic cardio-vascular disease have perished before 40, the magnitude of this cause can be fully realised. I believe that the profession in general have not yet woke up, if I may say so, to the gravity of this subject. How seldom we inquire for a history of specific disease in patients coming to us with cardiac disease in middle life! To no one, as far as my reading goes, are we so much indebted for the truth on this subject as to my friend and colleague Dr. Mott. Thirteen years ago he published a paper on 21 cases of sudden death from cardio-vascular disease, and in nine of these there was a history of either actual or probable syphilis. What was of greater interest, however, at that early date, he drew attention to the association of syphilitic cardio-vascular lesions with Bright's disease in the broad acceptation of the term. Dr. Mott's work in the interval on syphilitic lesions of the arterial system of the brain has been so brilliant, and is so generally known, that it requires nothing more than this appreciative mention by me, and it saves me the trouble of an excursion into the subjects of cerebral hæmorrhage and thrombosis in connection with these lectures.

Nervous Strain

I confess that it is difficult to say much that is of real diagnostic value on the clinical aspect of cardio-vascular disorders and disease from nervous strain. As I remarked in discussing this subject from the etiological point of view, several factors come into play besides nervous excitement followed by exhaustion and their effects on the heart, great vessels and cerebral arteries; and the cases, therefore, are found to present a puzzling variety of features. Certain clinical characters are, however, common to the majority. Arterial tension is high; the radial artery is thick, sometimes markedly so; the heart enlarges; and in about one-half of the cases a systolic murmur is to be heard either in the aortic or in the mitral area, significant of chronic endocardial lesions – all readily intelligible results of cerebral strain in the light of our knowledge of the innervation of the cardio-vascular system. I have already pointed out that in some of these patients polyuria and temporary albuminuria occur along with the high tension and the increased action of the heart; but the heart may fail later on. The direct cardiac symptoms of which they complain are of the ordinary character, palpitation with accelerated cardiac frequency and pain (not angina) being the most common at first, feelings of indescribable discomfort and suffocation in the more advanced stage. A great deal that I might have had to say on the very interesting subjects of pseudo-angina, and the climacteric and pre-climacteric disturbances of the circulation in women, I am reluctantly compelled to omit from want of time.

After having reviewed, as I have attempted to do, the principal clinical characters of the disorders and diseases of middle and advanced life under their several causes, it may appear for a moment strange that the most important of all the clinical types of cardio-vascular degeneration has been mentioned only incidentally. This is chronic Bright's disease, which, from its complex pathological relations, its widespread effects on the heart and circulation and the organs that they supply, and the far greater gravity of these than those of any of the other causes which we have studied (unless it be syphilis), is a subject of endless interest to us all. Fortunately for me my immediate predecessor in this chair on the medical side, our distinguished Fellow, Dr. Samuel West, took for his subject the "Clinical Aspects of Granular Kidney," and thus relieved me of a task which he was so much better able to discharge than I. Emphysema must also be passed over with the single remark that it is a very common accompaniment both of vascular and cardiac degenerations.

I trust you do not conclude that the description which I have just given you of the clinical characters of these various disorders and diseases of the heart is in any sense complete. It only relates to the most prominent symptoms and signs as they present themselves to us in what might be called the every-day life of the patient, at a period in the history of his case precedent to failure. In all of them there may occur occasional attacks of acute embarrassment of the heart and lungs from one or more of a variety of causes, such as indigestion, excitement or over-exertion. Sooner or later, also, there occurs either cardiac dropsy – insidiously developed after increasing local distress, growing dyspnœa and "bad nights"; or Bright's disease; or cerebral thrombosis or hæmorrhage, or acute myocardial failure with angina: or the patient dies from failure of the heart in the course of some acute disease such as bronchitis or pneumonia. Neither have I considered it necessary in this lecture to dwell on some of the rarer phenomena occasionally met with, such as tachycardia and bradycardia. I may have occasion to refer to them next time in connection with prognosis.

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.