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immediately beneath the endocardium and the pericardium are usually attacked before the intervening tissue; and the muscular structure towards the apex of the heart before that which is seated towards the base. Hence it is that in an atrophied and softened beart, extraordinary thinning of the ventricular walls is generally observed towards the apex, and that when rupture of the heart takes place, as it does sometimes in connection with this condition of the tissue, the laceration most frequently occurs in that situation.

The physical signs of softening of the heart are nearly identical with those of attenuated dilatation. The area of percussion dulness is unchanged, unless the heart be hypertrophied or dilated, or large masses of fat be deposited on its surface; the impulse is weak or imperceptible, the apex beat indistinct and often invisible; the action of the heart is sometimes regular, more frequently irregular and intermittent; the first sound is short, feeble, and toneless—sometimes inaudible—the first systolic silence prolonged; the second sound clear and relatively loud and prolonged. If the left ventricle be more affected than the right, the first sound will be heard louder, and of fuller tone at the right than at the left apex, and the second sound both louder and clearer at the second left costal cartilage than at the corresponding position on the right side. The pulse is weak and unequal, both in force and rhythm; it is often slow, and when, as sometimes happens, every alternate pulsation is imperceptible at the wrist, it may not exceed 24 or 28 in a minute. If endocardial murmurs occur, they are referable to coexistent valvular disease, and not to mere atrophy or softening of the heart.

The general symptoms are quite in accordance with what theoretical considerations would lead us to anticipate. In the earlier stages of the disorder, the heart may perform its functions tolerably, the physical signs may be so little altered as not to attract attention, and the patient may not be conscious of ill health, or even of local discomfort. By degrees, however, he begins to complain of languor and disinclination to active exertion. He is pale, and easily put out of breath, irritable, peevish, and low spirited; he sometimes suffers from pain or uneasiness at the heart, with fluttering, giddiness, loss of memory, and temporary loss of sight; there is a constant tendency to sigh, without any emotional cause to explain it; the pulse is very weak, sometimes regular, more commonly irregular both in force and rhythm; the tissues of the body become soft and flabby, the digestive organs are easily deranged, excessive flatulence is a frequent source of trouble, and the bowels are usually torpid. As the disease proceeds, the breathlessness increases, until the patient is unequal to the slightest exertion; paroxysms of dyspnoea resembling asthma supervene, and are often accompanied by serious oppression or acute pain in the cardiac region ; orthopnea is an occasional, but by no means constant symptom; distressing palpitation or fluttering of the heart occurs on the slightest excitement, and whenever the chylopoietic viscera are deranged, or the stomach is distended with flatulence; and, on some of these occasions, attacks of giddiness and coma occur, during which the patient may fall to the ground insensible.

In most instances these attacks are of a syncopal nature, and of very brief duration, their immediate cause being a deficiency in the supply of blood to the brain, consequent on the feebleness of the heart's action ; but in some cases they are of an apoplectic character, accompanied by stertorous breathing, and followed by paralysis, the immediate cause of the seizure being an outpouring of blood into the brain, consequent on an atheromatous condition of the vessels, which leads to brittleness and rupture whenever anything occurs to check the venous circulation, and so induce stagnation in the cerebral capillaries. But inasmuch as in these cases the strain on the vessels is due to venous obstruction and capillary distension, and not to the unwonted force of the cardiac propulsion or arterial action, the smaller vessels usually give way; so that the quantity of blood effused is seldom large, and if paralysis ensues, it is not generally of long duration.* Unlike what happens in cases of apoplexy connected with hypertrophy of the left ventricle, and excitement of the arterial circulation, the patient when attacked is pale, and has a feeble pulse, and presents more or less lividity of the lips—symptoms which ought to serve as indications of the true nature of the disorder.

* In a case of this sort, in which I had the opportunity of inspecting the brain after death, there were six clots in different parts of the brain, each of a different date and in a different stage of discolorization. The patient, a gentleman, aged forty-six, had fallen into pecuniary difficulties, and consequently had been subject to great anxiety during the last eighteen months of his life, and during the last nine months he had experienced five slight apoplectiform syncopal seizures, followed by temporary loss of power. In three out of the tive attacks the insensibility was only of a few minutes' duration and the loss of power was so slight that he went to his office on the following day. On the other two occasions he was nearly a week before he had entirely recovered power, and on the sixth and last occasion, an enormous quantity of blood was effused, and he died within twenty minutes from the commencement of the attack. The previous attacks had been so slight that they were pronounced by his medical attendant to have been attacks of “serous apoplexy,” but the post-mortem examination revealed the existence of six clots, one corresponding to each of the apoplectic seizures. Three of the clots were on the surface of the hemispheres, very small and quite discolourised. The vessels were atheromatous, and here and there calcified, and the heart was soft and flabby, and, under the microscope, presented wellmarked evidence of fatty degeneration.

In extreme cases of cardiac softening, ædema of the feet and ankles occurs; the pulse may be rapid, or may fall to 26 or 30 in a minute, owing to the failure of certain systoles of the heart to communicate a pulsation to the radial artery,* and the breathing may be alternately quick and slow, or even gasping. Sometimes, as in a case related by Dr. Stokes,t it may observe a peculiar rhythm, the respirations gradually increasing in force and duration, until they attain a prolonged gasping character, and then as gradually decreasing until they are no longer perceptible and the patient apparently has ceased to breathe, and may be almost regarded as dead, when, after a lengthened interval, a faint inspiration takes place, and a fresh series of gradually increasing and then decreasing inspirations occur.

There is yet one symptom which requires notice, not so much on account of its intrinsic importance, as in consequence of the diagnostic value, which has been falsely attached to it. I refer to the existence of fatty atrophy of the cornea, constituting what has been termed “arcus senilis,” to which attention has been especially directed by Mr. Canton, in connection with fatty heart. It is as its name implies, a frequent accompaniment of old age; and as softening and fatty degeneration of the heart is also a disease to which persons advanced in years, are peculiarly liable, it is not surprising that the two lesions should be sometimes found coexisting. But in the dead-house of St. George's Hospital I have repeatedly found a well-marked arcus senilis, when the heart has been perfectly healthy, and have as frequently noted hearts thoroughly softened and fatty in persons whose eyes presented no trace of an arcus senilis. The conclusion, therefore, is inevitable, that, arcus senilis is a sign of little value in the diagnosis of fatty degeneration of the heart.

Indeed, the diagnosis of a softened or fatty heart is by no means easy, more especially if it is wished to distinguish between simple and fatty softening, and to draw a distinction between these varieties of disease, and simple or attenuated dilatation. In fact, in uncomplicated cases it is impossible during life to discriminate between them, and, even were it not impossible, it would be practically useless. They are all connected with feebleness of constitution, impaired nervous energy, and defective nutrition, and are characterised by fluttering and palpitation of the heart occurring without any increase in the area of dulness on percussion, and with feebleness of the cardiac impulse, a feeble and often irregular pulse, and shortness of and want of tone in the first sound of the heart—conditions which, whatever the precise form of atrophy in which they originate, require in each instance a similar plan of treatment.

* This was observed in an interesting case of the disease under consideration, which I saw in the year 1860, in consultation with Dr. C. J. B. Williams and Mr. Gardner. For many weeks the pulse did not exceed 28 or 30, though the heart could be heard beating 56 or 60 in a minute. A similar case occurred under my care in St. George's Hospital, in December, 1861, in the person of a woman named Cross, aged thirty-six, in Roseberry Ward.

of Loc. cit., p. 324.

The prognosis must necessarily be unfavourable, not because softening of the heart need prove rapidly fatal, but because it is a form of disease which may cause death suddenly, either from rupture of the heart, or from syncope, or from the occurrence of a paroxysm of angina pectoris, or if it does not prove suddenly fatal will in most cases run on in spite of treatment until it terminates in gradual sinking from asthenia.

Having already described the treatment to be pursued in cases of dilatation of the heart—a condition which is usually connected with softening and fatty degeneration of the muscular tissue—it is needless to recapitulate the directions concerning it. Suffice it to say, that iron in its various forms, quinine, and other vegetable bitters, digitalis, and the mineral acids, are the most efficacious medicinal agents, and that freedom from anxiety, thorough repose of mind, entire avoidance of fatigue, gentle and regular exercise in the open air, careful attention to the state of the skin, and a generous and stimulating diet, taken at regular intervals, and in moderate quantity, are the hygienic means best calculated to aid the effect of remedies, the object being to impart tone to the system, improve the condition of the blood, and so induce a more healthy nutrition of the heart. It is impossible to insist too strongly on the avoidance of all actions which are calculated to put any unwonted strain on the heart, or to accelerate its action. Weakened as that organ is, and unfit for the due performance of its function, it may yet suffice to carry on the circulation if perfect repose of mind be enjoined, and all violent bodily exertion avoided. But strong emotional feelings, or a slight straining muscular effort, either of which would make an extra demand on the energy of its contraction, might suffice to overwhelm it, and endanger life. The bowels should be so regulated, as to render straining at stool unnecessary. Stooping should be avoided, as tending to press the abdominal organs upwards, and so interfere mechanically with the heart's action; and bodily exercise, though taken regularly, should be extremely quiet, and in amount always short of producing fatigue. The paroxysmal pain in the region of the heart, and the syncopal seizures, which are apt to occur during the course of the disease, must be treated on general principles by diffusible stimulants and anti-spasmodics internally, and by warmth and counter irritation to the lower extremities.



SPONTANEOUS rupture of the heart is one of the curiosities of medical pathology, and assuredly one of the accidents least amenable to medical treatment. Occurring only under circumstances productive of structural alteration in the muscular walls of the heart, it may be regarded as a consequence of some pre-existing mischief, rather than as itself a special form of disease. Aneurism of the walls of the left ventricle, hydatids, and carditis leading to abscess and perforation, may prove occasional causes of its occurrence, but its most frequent origin is atrophy of the heart, with attenuation of the walls and fatty degeneration of the muscular fibre.* When the heart is thus weakened, or prepared, as it were, for giving way, any strong emotional paroxysm, such as sudden alarm, or a violent fit of passion; any violent straining effort, and any suddenly induced congestion of the thoracic viscera may prove the exciting cause of its occurrence. But, in some instances on record, it appears to have taken place independently of any undue cardiac excitement, and to have resulted simply from the inability of the atrophied and degenerated tissue to sustain the strain which it has had to encounter, even during the tranquil action of the heart-a strain

* Cruveilhier, in his · Anatomie Pathologique du Corps humain,' speaks of apoplectic effusion of blood into the walls of the heart as an occasional cause of rupture; and Dr. Walshe and other authors have adopted his views on the subject; but I am inclined, with Dr. Stokes, to regard the clots to which Cruveilhier refers as themselves the result of a previous partial laceration of the muscular tissue, rather than as the cause of the final rupture.

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