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softening and disintegration of the fibrinous deposits, both of which are rare occurrences. But it often arises concurrently with or during the progress of pericarditis, and then seriously aggravates the patient's danger.

Its more remote prognosis is of a far more serious nature. So delicate and so nicely adjusted is the valular apparatus of the heart, that any damage it sustains must necessarily interfere with the due maintenance of the circulation. To overcome the obstruction which the mischief occasions, the heart contracts more forcibly than natural, and as the damage is permanent, the increased labour of the heart is permanent also, and hypertrophy of the walls or dilatation of its cavities are necessarily produced, the relative degree of hypertrophy or dilatation being dependent on the firmness and contractility of the muscular tissue. Of course the rapidity with which the disease runs its course will depend in some measure upon the irritability of the heart, the state of the lungs, the habits of the patient, and other collateral circumstances, but, cæteris paribus, it will bear a tolerably constant relation to the degree of impediment offered to the circulation. The more serious the mischief the greater the obstruction to the blood's current, the quicker will hypertrophy and dilatation result, and the sooner will the effects of these lesions be perceived. When the obstruction is slight, though sufficient to induce distinct murmur, the patient may go on for many years with little or no palpitation or apparent cardiac disturbance, or he may suffer constantly from slight palpitation, or may be troubled with it only when the heart's action is augmented by mental excitement, gastric derangement, or active exercise. But if the obstruction be great, no long time will elapse before the patient's sufferings will become very serious. After a few months, or, possibly, two or three years, severe palpitation or dyspnea will ensue, and the heart, struggling to overcome the resistance, will become gradually more and more dilated or hypertrophied, until, when it is unable any longer to fulfil its functions, the blood will begin to be arrested in its passage through the lungs, and cough and severe dyspnea will result. Then will follow the terrible array of symptoms connected with an impeded pulmonary cir. culation—a loading of the capillaries with dark-coloured, imperfectly aerated blood, coldness and lividity of the extremities, blueness and lividity of the lips and face, congestion of the liver and other internal organs, and, as a natural consequence, dropsical effusion into the cavities of the chest, into the abdomen, into the pericardium, and into the cellular tissue of the body. Nor will these fearful changes occur without producing a proportionate amount of suffering. Excessive palpitation, with præcordial pain and anguish, paroxysms of dyspnea threatening suffocation, orthopnea, constant restlessness and impossibility of sleep_these are among the inevitable consequences of such an embarrassed state of the vascular and respiratory systems, and are the symptoms immediately preceding death.

Endo-pericarditis, or inflammation both of the internal and external surfaces of the heart, is not an unfrequent occurrence, though it certainly is less common than has been represented by some authors. Taking rheumatic endo-pericarditis alone, I met with 27 examples of it at St. George's Hospital, amongst 114 cases of recent rheumatic heart disease, 12 of the other cases being instances of pericarditis alone, and 75 of endocardial affection alone. * I cannot refer to the same number of non-rheumatic cases, and cannot speak with equal certainty as to the date of the endocardial mischief; but I have notes of ten cases of endo-pericarditis, among fifty-four cases of non-rheumatic cardiac affection, twelve of the other cases being instances of pericarditis alone, and thirty-two of endocarditis alone. If the relative frequency of the various affections shown by these figures would hold good over an extended series of cases, it would appear that endocarditis, relatively to pericarditis, is more frequent in rheumatic than in non-rheumatic cases.

There is nothing distinctive in the general symptoms of endo-pericarditis, and even the physical signs are often uncertain, inasmuch as the sound of pericardial friction may for a time obscure or render undistinguishable the valvular murmurs induced by endocarditis, whilst in certain cases the effusion of a large quantity of liquid in the pericardium may not only weaken any existing valvular murmur, but may even excite one, and sustain it for many days.

The treatment of these cases is the same as that of pericarditis and endocarditis, and must be varied according to the nature of the disease from which the attack originates.

The prognosis is usually more unfavourable than in cases of pericarditis or endocarditis alone, and, as already pointed out in reference to those diseases, it varies, cæteris paribus, with the nature of the primary disease.

* For full statistical details respecting rheumatic diseases of the heart, see my work On Rheumatism, Rheumatic Gout, and Sciatica,' ed. iii, pp. 257-284.

Little is known of acute carditis, except on a very limited scale, in connection with endo-pericarditis ; for although some few cases are on record in which inflammation of the walls of the heart has resulted in abscess or purulent infiltration of its tissue, with bulging, or even perforation of the part affected, still such cases have never been diagnosticated during life, and their clinical history has yet to be determined. The general symptoms appear to have been those which are met with in pyæmia and other forms of blood-poisoning.




In the description already given of valvular disease in connection with endocarditis, it has been shown that the valves are often damaged by the deposit of fibrin on their surface or edges. But it must not be inferred that valvular disease is invariably referable to the deposit of fibrin, or that it is always, or even generally, of inflammatory origin. Not only may fibrin accumulate on the valves, as the result of slow deposition from the blood, but malnutrition and chronic textural degeneration may take place in the valvular apparatus, just as in the other tissues of the body. It is especially prone to do so in the rheumatic and gouty diathesis, and in patients who are labouring under Bright's disease of the kidneys ;* but it is often met with in after-life in persons whose kidneys are sound, and in whom it is impossible to trace the existence of a rheumatic or gouty diathesis. Hence the conclusion seems inevitable, that chronic disease of the valves may result from other forms of constitutional derangement than those above enumerated, which prove its most frequent source.

Whatever their precise character, these chronic changes in the valves are not accompanied by any special or distinctive symptoms during life. It is not even known whether they necessarily give rise to palpitation, or occasion any uneasiness in the cardiac region ; and it is quite certain that physically the murmur which results from chronic disease

* In proof of this refer to · Med.-Chir. Trans.,' vol. xxxi, pp. 183-213.

is undistinguishable from that produced by active inflammation. Pathologically, too, the results eventually may be much the same, whether the mischief began in active inflammation, or in slow deposition of fibrin, or in chronic degeneration of structure. In either case, the valves may ultimately become thickened, opaque, and puckered, and may be rendered rigid by the presence of atheromatous or calcareous matter; or they may yield under pressure, and become thinner than natural, or may even become cribriform or perforated ; * or they may be ruptured or undergo ulceration; or their surface may be rendered irregular, or their edges beaded by the deposit of fibrin from the blood; or one segment of a valve may adhere to another segment of the same or some other valve, or two or more adjoining valves may cohere. In each of these cases, the disease may be of such a nature as to offer obstruction to the onward flow of blood, or to admit of regurgitation through the valves ; and an obstructive or a regurgitant murmur will be the result.

So, again, with regard to the apparatus connected with closure of the valves. The valves themselves may be sound, but the papillary muscles may become diseased and inoperative, or the tendinous chords ulcerated, ruptured, contracted, or shortened, or the structure of the columnæ carneæ may degenerate, and their action may become inefficient. In all these cases regurgitation may take place which is not to be distinguished from that which occurs in connection with other forms of disease.

The same holds good with respect to the orifices of the heart. The valves may be sound, but the orifices which they guard may be roughened by calcareous or atheromatous deposit, or may be so much dilated that the valves may prove ineffective to close them, and may admit of regurgitation. In these cases, again, an obstructive or a regurgitant murmur may be produced which is clinically undistinguishable from a murmur resulting from valvular disease.

And yet again, the valve may be defective, not in consequence of active inflammation, or of slow degeneration, but as a result of congenital malformation. In these cases, as in the others, murmurs may exist which will not present any distinctive feature, and which during life can be attributed to their true cause only by reference to the circumstances under which they occur.

Clinically, however, the precise form of lesion is of little importance ; * It is doubtful whether this cribriform reticulated condition of the valves may not be referable to congenital malformation.

the practical question is, whether the disease, whatever it may be, is of such a nature as to offer obstruction to the onward flow of blood, or to admit of regurgitation. If it is not, it is impossible with any certainty to diagnose its existence during life; whereas, if it leads either to obstruction or regurgitation, the existence of such obstruction and regurgitation can be readily ascertained by the aid of the stethoscope, though the precise form of disease which produces the murmur must remain a matter for conjecture.

In all cases in which a permanent endocardial murmur exists, obstruction or regurgitation is unmistakeably indicated, and whether the disease from which it originated was of an acute or chronic character, is perfectly immaterial. Chronic disease of the valves leads as surely to cardiac hypertrophy and dilatation as acute disease has been shown to do.*

The practical question is as to the degree of impediment which is offered to the circulation, and especially to the pulmonary and systemic venous circulation, in consequence of the valvular obstruction or regurgitation. The greater the impediment to the cardiac circulation, the more rapid, cæteris paribus, will be the progress of hypertrophy and dilatation of the heart; and the greater the interference with the pulmonary and systemic venous circulation, the more distressing will be the symptoms, and the more rapidly fatal the consequences which ensue. If the injury to the valves be slight, and especially if it be of such a character as not to interfere primarily with the pulmonary or systemic capillary circulation, the patient may go on for many years unconscious of palpitation and of other apparent cardiac derangement; whereas, if it be excessive, and more especially if it be of a nature to impede the circulation through the lungs, or to induce congestion of the systemic capillary circulation, it may speedily give rise to fearful suffering which will terminate only with the patient's death.

It is needless to recapitulate the characteristics of the murmurs which occur at the different orifices of the heart. They have been fully described in a previous chapter, as have also the peculiarities of the radial pulse, by which they are severally accompanied.t But other changes occur in the physical signs to which it is necessary to refer. Thus, valvular disease, though not primarily and immediately productive of alteration in the position and extent of cardiac dulness, on percussion, yet after a time proves so indirectly, by inducing hypertrophy

* See Part ii, cap. ii, p. 108.

Part i, cap. iv, pp. 52-6 and 101-3.

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