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abdominal viscera exists, a careful physical examination of the chest, and a jealous inquiry into the history of the case is needed, in order to ascertain that the displacement is not due to any former or existing disease, but is attributable to congenital malposition.
Displacement of the heart as a consequence of disease is of frequent occurrence. It has been already shown how disease within the heart or its membranes may cause the organ to occupy a higher or a lower position than natural in the chest, or to extend further to the right or left than natural; but disease external to the heart and its membranous covering may prove even more effective in producing displacement. The attachments of the heart are such as to admit of the organ being elevated or depressed by external pressure, or being drawn or pushed to one side or the other; and the extent to which this alteration of position occurs is sometimes quite remarkable.
The causes external to the heart which operate in producing displacement of that organ upwards are ascites, ovarian dropsy, and various abdominal tumours which push up the diaphragm, and at the same time force up the heart; but the same result may be brought about by enlargement of liver or spleen, or by the pressure of the gravid uterus. In some few instances a similar displacement may be produced by the upward traction exerted on the heart as a result of the cicatrization of tuberculous cavities in the upper part of the lung, or of the contraction of pleuritic exudation.
The cause which most frequently forces the heart downwards is emphysema of both lungs; but it must be remembered that hypertrophy and dilatation of the right side of the heart are constant accompaniments of extensive emphysema, and that epigastric pulsation may be due to that cause more than to displacement the result of external pressure. Tumours of whatever character, developed in the upper part of the chest, may also exercise a downward pressure.
Pleurisy and pneumothorax are the forms of disease which operate most powerfully in driving the heart out of its position towards the one side or the other; and their effect is most conspicuous when the disease exists on the left side, and the heart is driven towards the right. Hydrothorax or dropsical effusion into the pleura generally occurs on both sides of the chest, and, therefore, fails to displace the heart sideways; but intra-thoracic tumours, and emphysema on one side of the chest, may, and do sometimes, have that effect. Great diminution in the bulk of the contents of one side of the chest, whether induced by the pressure and subsequent absorption of pleuritic fluid, or by the contraction of one lung, consequent on tuberculous disease, is sometimes productive of lateral displacement of the heart towards the affected side, partly as a result of the hypertrophic development of the other lung, which pushes the heart over towards the opposite side, but possibly also in some measure as a result of the traction exerted on the heart during the contraction of the pleuritic exudation.
In all cases of displacement of the heart, the sounds will be heard loudest and the impulse will be felt strongest over that portion of the chest walls under which the heart lies, and it is by these signs and by the dulness on percussion in that situation, and by the absence of all these signs in the position ordinarily occupied by the heart, that we are enabled to ascertain the fact of its displacement, and judge of the direction in which it has taken place.
The effects of displacement of the heart cannot be separated from the effects of the disease to which the displacement is due, and the treatment of displacement is in like manner that of the disease by which it is caused. It should be understood, however, that the action and sounds of the heart are not seriously affected by its displacement. Its action, although accelerated, is usually regular, and its sounds remain clear.
FIBRINOUS CONCRETIONS IN THE HEART-EMBOLISM.
FIBRINOUS concretions within the heart are formed under two very different conditions, and are productive of very different results. Sometimes they result from the slow deposition of fibrin on the valvular apparatus, or on other parts of the heart, as described in the section on endocarditis; sometimes apparently from the coagulation of the blood, especially in the right cavities of the heart. The one form of concretion is quite independent of any retardation of the circulation, and is associated with a hyperinotic condition of the blood, and probably, also, with some local irritation; the other is almost exclusively observed
towards the close of life, when the circulation is becoming languid, or when from any serious cause any obstruction exists to the current of the blood through the heart.
The cardiac disturbance and valvular murmurs ordinarily produced by the slow deposition of fibrin on the valves have been already described in the section on endocarditis, and it is only necessary further to remark that this variety of fibrinous concretion is sometimes productive of mischief elsewhere than in the heart, and gives rise to a singular set of symptoms which have been recognised as resulting from “embolism.” To Dr. Kirkes we are indebted for having directed attention to this fact, and for having pointed out that portions of these concretions may become detached, and carried with the current of the circulation to different parts of the body, producing plugging of the arteries, and local arrests of the pulmonary and systemic circulations, serious cerebral disturbance, and paralysis. * But, inasmuch as the slow deposition of fibrin from the blood almost always takes place on the left side of the heart, it follows that in these cases the detached portions of the concretions are usually conveyed along the systemic circulation, and are ultimately arrested by the systemic capillaries; and the points at which experience has shown that plugging of the vessels is most likely to occur, are in the brain, spleen, kidneys, and liver. In a remarkable case, which recently occurred in St. George's Hospital, under the care of my colleague, Dr. Page, the vessels of all these organs were found plugged with fibrin, resulting from the detachment of fibrinous concretions from the left cavities of the heart.
The symptoms in these cases necessarily vary, according as there happens or does not happen to be any co-existent endocarditis or other active inflammation, and also according to the function of the organ the circulation of which is arrested. Softening of the brain and hemiplegia are two of the most frequent results of this form of mischief, when the fibrin is detached, as it usually is, from the left side of the heart; local pulmonary congestion is its immediate consequence when the fibrin is detached from the right cavities of the heart. In either case death is almost inevitable. In some instances disintegration of the fibrinous concretions takes place, and the disintegrated matter, finding its way into the circulation, causes symptoms analogous to those observed in cases of pyæmia, in addition to the special symptoms referable to the disturbance of the organ or organs in the vessels of which the detached fibrin is impacted. These, however, are exceptional cases.
* Med.-Chir. Trans. vol. xxxv.
+ See ‘Post-mortem and Case-book' for February 21st, 1862, in the museum of St. George's Hospital, under the name of Jones.
We are indebted to Dr. Richardson for directing our attention to the other form of fibrinous concretion, which is not the effect of slow deposition of fibrin from the blood, but results from the coagulation of the blood itself.* It is most commonly observed on the right side of the heart, and more frequently commences in the right auricle than in the right ventricle. The coagulated blood forms mechanical adhesions to the walls of the cavity, and, as its quantity increases, portions of the coagula extend through the auriculo-ventricular opening, causing obstruction to the onward flow of blood into the ventricle, preventing the valves from closing the opening, and thus producing reflux of blood into the auricle. Unlike the concretions which result from slow deposition from the blood, these concretions when first formed are more or less blood-stained, of gelatinous consistency, and entangled in, rather than attached to, the structure of the heart; but they speedily lose their colour, and become firmer, more consistent, and opaque, and contract adhesions, either mechanical or organic, to the walls of the cavity in which they are seated. Externally they are grooved by the continued passage of the blood, or, if they have contracted adhesions to the walls of the cavity, they are indented externally by the surrounding structures, and in their centre are perforated in consequence of the current of blood having made its way through them. Their structure is usually laminated, and not unfrequently their centre is softened and is found to consist of disintegrated fibrin.
The symptoms which result from this form of fibrinous concretions in the heart, are necessarily obscure. Primarily there may be nothing more than suddenly occurring cardiac dyspnea, with violent palpitation, and feeble and irregular pulse, faintness, gasping respiration, lividity, twitching of the muscles, and all the usual evidences of obstruction to the circulation on the right side of the heart, and to the return of blood from the systemic capillaries. But, after a time, wandering or actual delirium ensues, and, when the clot extends into the ventriclė through the
* Richardson on the “Coagulation of the Blood.
I A case which remarkably illustrates these facts occurred under my care in St. George's Hospital, in the year 1857, and is reported in ‘Trans. Path. Soc. Lond.,' vol. ix, p. 99.
auriculo-ventricular opening, a tricuspid murmur may be set up; and if portions of the clot become detached, and are carried with the blood into the pulmonary artery and produce obstruction or plugging of that vessel, symptoms of pulmonary distress and intense congestion of the lungs at once supervene. The patient ordinarily dies from syncope or from coma, sometimes preceded by convulsions.
Whether recovery ever takes place from this form of fibrinous concretion, is a question which cannot be satisfactorily answered, inasmuch as its occurrence would at once preclude the possibility of verifying the existence of concretion. But, inasmuch as these concretions usually accompany some otherwise serious malady, or are formed in the later stage of a patient's existence, when the circulation is becoming languid, it is scarcely possible to conceive that treatment can avail to produce their reabsorption. When there is reason to suspect their formation, stimulants should be resorted to, and alkalies, especially ammonia—which has been shown by Dr. Richardson to possess a remarkably solvent power-should be freely administered. Dry cupping between the shoulders might also prove serviceable in relieving congestion, and therefore should be employed.
Whilst discussing the symptoms of fibrinous concretions in the heart, and the “ embolism "* which their detachment sometimes produces, it may be well to append a few remarks respecting the formation of fibrinous coagula in the arteries. Fibrinous coagula may form in the vessels at the spot where they are found after death, quite independently of local inflammation,t but, except as the result of inflammation of the vessel, coagulation in the small arteries is rare. In the larger vessels, however, extensive fibrinous coagula are often formed in connection with aneurismal dilatation, and occasionally it happens that some portions of the coagula escape from an aneurismal sac, and are carried with the blood into the smaller vessels, where they produce plugging and obstruction just as when they are detached from the heart. In a practical point of view, the fact of the existence of this source of embolism is of the greatest moment, inasmuch as it renders necessary the
* A term derived from cußodov, a plug, and applied to the plugging of the vessels produced by fibrinous concretions, whether formed in the vessels or detached from the heart, and carried with the blood to the point at which obstruction takes place.
† A remarkable case of this sort, which occurred in St. George's Hospital, was reported by me in the 'Med. Gazette' for 1847, vol. ii, p. 187. A similar case was reported by Dr. Dickinson in vol. xii, p. 81, of. Trans. Path. Soc. of London.'