The rules in regard to hygiene, diet, and exercise which have been given for the management of mitral disease are equally indicated in the management of pulmonary obstruction or regurgitation. Beyond this their treatment is purely symptomatic.
The treatment of tricuspid obstruction depends upon the gravity and sequelæ of the accompanying disease—viz. mitral. Stenosis of the tricuspid orifice never occurs until mitral obstruction is excessive, and the latter condition is always the predominant one.
The same rules of hygiene and diet which have already been given for mitral disease must be followed with the utmost care by those suffering from tricuspid reflux. The patient must lead a life of perfect quiet, and should live in a warm, equable climate. When occurring with mitral disease digitalis should not be omitted; for although the drug, by increasing the action of the heart, would seem to be injurious, yet it promotes ventricular contraction, and thus tends to relieve the tricuspid pressure. In tricuspid insufficiency with pulmonary emphysema this drug should be very cautiously exhibited, and its use or omission must depend upon the effects produced in each case. If the cerebral symptoms are exaggerated, it must be discontinued. The indications for the use of tonics, such as iron, quinine, strychnine, are the same and follow the same demands as in mitral disease. When venous engorgement demands prompt relief, drastic cathartics or the abstraction of a few ounces of blood from the arm will temporarily diminish the high venous tension. The treatment of the dropsy and the local oedema is the same as for similar condition occurring in mitral disease. There are many subsidiary remedies which will have to be employed for the relief of gastric, hepatic, and intestinal symptoms, which are often the most troublesome occurrences of this disease.
CYANOSIS AND CONGENITAL ANOMALIES OF THE HEART AND GREAT VESSELS.
BY MORRIS LONGSTRETH, M.D.
The questions involved in the subject of the congenital defects of the heart and its great vessels and their causes are not easy of settlement. In the first place, the seat, the extent, and the consequences of the deficiency or defect are not regular or constant. Secondly, the causes and the mode and date of their origin are involved in great obscurity. Their classification either on a purely topographical or on a purely etiological basis is almost impossible on the one hand, because the changes are so irregular and varying, and, on the other hand, because our knowledge of the primary cause or causes of the alterations is quite defective. The views which at the present time find most favor arrange the various malformations into classes according to the period of development of the foetus at which the arrest or change of tissue occurred—as it were, a chronological classification. The ideas in respect to the pathology or the pathological causes of malformed hearts have undergone great changes—changing in some degree pari passu with the mode of classification, and in great degree inducing and compelling such changes.
In early times deformed hearts were looked upon as monsters, curiosities, lusus naturæ. When a knowledge of foetal development and circulation was acquired the deformed heart was compared with the heart-formation in classes of a lower grade than mammals. Such were the beliefs of comparative anatomy and physiology that it was held that the human foetus was matured by stages from the forms found in the lowest invertebrates through the various ascending scales of the animal kingdom. This classification was, on the basis of comparative anatomy, purely anatomical. The underlying thought of such pathological teaching was that in the original ovum something was left out—an actual deficiency of parts which, when developed in the natural manner, made man different from the lower animals; or else, supposing these parts to have been originally present, there was a defect of plasticity, causing a failure of the proper adhesion of symmetrical portions. Excessive development was looked upon as a surplus of parts in the ovum, and by their growth certain of the openings of the heart were prematurely closed. In this view of the pathological alterations no expression of opinion was made how the excess or deficiency of structure was occasioned: the malformation was merely a failure of the parts to rise and pass through the various grades of development—a too rapid or a too slow growth of one or more of the various parts of the foetal heart. There was no reason assigned why the human ovum had in it deficiencies or excesses of material, and thus came to resemble in one of its parts the conditions found in lower animals.