In the various forms of valvular disease we meet with numerous examples of dilatation. In aortic incompetency during diastole blood enters the left ventricle from the unguarded aorta and from the left auricle, and the amount of blood at the termination of diastole subjects the walls to an extreme degree of pressure, under which they inevitably yield: in time they augment in thickness, and we have the typical eccentric hypertrophy of this condition.
In mitral regurgitation a certain quantity of the blood which should have been driven into the aorta is forced into the auricle from which it came, dilating it; and then in the diastole of the ventricle a larger amount is returned from the auricle, and with increased force, by the hypertrophied walls of this chamber. In mitral stenosis the left auricle is the seat of greatly-increased tension during systole, and dilates as well as hypertrophies; the distension too may be enormous. Dilatation of the right chamber is very common, and is produced by a number of conditions, which were considered under Hypertrophy. All circumstances which permanently increase the tension of the blood in the pulmonary vessels will cause it—mitral stenosis, emphysema, etc. The dilatation seems easily produced, but the accompanying hypertrophy may hold it in check for years. We may here refer to the extreme distension of the right chambers in pneumonia, particularly when the consolidation is extensive. The passive dilatation may be very great and the walls much thinned, and we see the same in states of asphyxia. Valvular lesions of the right heart are not frequent causes of dilatation. When the causes which bring about the dilatation act suddenly, the degree of distension may be great, and there is much more difficulty in the establishment of compensation, as in rupture of an aortic cusp.
2. Impaired nutrition of the heart-walls from degeneration or inflammation may lead to such a diminution of the resisting power that dilatation readily occurs.
In fevers the loss of tone due to parenchymatous degeneration or myocarditis may lead to a condition of acute dilatation which may prove fatal. It is a well-recognized cause of death in scarlatinal dropsy,65 and may occur in rheumatic fever,66 typhus, typhoid, erysipelas, etc. The myocarditis accompanying acute endo- or pericarditis may lead to dilatation, especially in the latter disease. The cavities are usually large in fatty degeneration or infiltration from the relaxed and atonic state of the walls. In anæmia, leukæmia, and chlorosis the dilatation of the chambers may be considerable. In fibroid degeneration the wall generally yields where the process is most advanced, as at the left apex. The impaired nutrition in coronary disease may lead to dilatation. Under any of these circumstances the walls may yield with normal blood-pressure, or if increased tension is present the effect is the more readily produced.
65 Goodhart, Guy's Hospital Reports, Series iii. vol. xxiv.
66 Samuel West, Barth. Hospital Reports, xiv.
Pericardial adhesions are usually spoken of as a cause of dilatation, acting by traction from without, and we generally find in a case of extensive and firm union considerable hypertrophy and dilatation. In this condition there is usually some impairment of the superficial layer of muscle which may permit of over-distension.
MORBID ANATOMY.—Usually the condition exists in two or more chambers, and is associated with hypertrophy, the appearances of which have already been described. It is more common on the right side than on the left. Perhaps the most general dilatation which we see is in cases of aortic incompetency, in which all the cavities may be enormously distended. In mitral stenosis the left auricle is often trebled in capacity, and the right auricle and ventricle also are very capacious. The former may contain eighteen to twenty ounces of blood. In many chronic affections of the lungs the right chambers are chiefly affected. Dilatation with thinning is often the result of an acute process met with in the fevers. The walls may be very much thinner than normal, almost membranous, and the dark color of the blood may show through with distinctness. When the distension of one ventricle is very great, there may be a distinct bulging of the septum toward the other side. The shape of the organ is altered, and when the right chambers are chiefly affected it is more globular in shape. Distension of the left auricle may render it visible in the front of the heart, and the appendix may be prominent. The right auricle when enormously enlarged, as in some cases of pneumonia, in emphysema, and in leukæmia, may form a large mass occupying a considerable space in the antero-lateral part of the thorax. The walls in dilatation with thinning are flabby and relaxed, and collapse at once when cut, but in dilatation with hypertrophy they are firm, especially those of the right ventricle.
The auriculo-ventricular rings are often dilated, and there may be an inch and a half, or even two inches, of increase in the circumference. Thus, the tricuspid orifice, the circumference of which is about four and a half inches, may admit freely a graduated heart-cone of over six inches, and the mitral orifice, which is about three and a half inches normally, may admit the cone to five and a half inches or even more. Great dilatation is always accompanied with relative incompetence of the valves, so that free regurgitation into the auricles is permitted. The orifices of the cavæ and of the pulmonary veins may be greatly dilated.
The muscle-substance varies much in appearance according to the presence or absence of degenerations. The endocardium is often opaque, particularly in the auricles. The microscopical examination may show marked fatty or parenchymatous change, but in other instances of dilatation and heart failure in eccentric hypertrophy there may be no special alteration noticeable. I fully agree with Niemeyer's assertion, "that it is not possible by means of the microscope to recognize all the alterations of the muscular fibrillæ which diminish the functional power of the heart."67 We know too little as yet of the changes in the ganglia of the heart in these conditions: as centres of control they probably have more to do with cardiac atony and breakdown than we generally admit. Degeneration of them has been noted by Putjakin68 and others.