The possibility of the establishment of compensation in the lesions of the tricuspid valve was doubted by Romberg (Cf. Franke2) and hesitatingly admitted by Krehl (Cf. Franke2) on account of the weakness of the right auricle, which is the only cavity of the heart left to perform the task. MacKenzie1 and others have, however, described cases of tricuspid insufficiency lasting over long periods. Recently, Franke2 has cited several cases where, in the light of the literature, he believes that dilatation and hypertrophy of the right auricle and ventricle, venous congestion, and especially congestion of the liver were factors in maintaining compensation.
The clearness with which the rôle of venous congestion as an element in compensation is demonstrated makes the following case worthy of record:
—The patient, an adult white female with a long-standing heart lesion, developed ascites. There was mitral insufficiency, secondary tricuspid insufficiency, and