Liver Function in Congestive Heart Failure

Jaundice, varying from a slight yellowish tinting of the sderae to a pronounced general icterus, is a common occurrence in congestive heart failure. A review of the literature leaves one with the impression that it is seen most frequently in patients with long standing congestive heart failure, particularly in failure associated with mitral and tricuspid valvular disease and in failure associated with auricular fibrillation. It repeatedly has been shown that the jaundice occurring in the course of congestive heart failure is due to an increase in serum bilirubin (1, 2, 3, 4, 5, 6, 7, 8). Matthes (9) in his "Differential Diagnosis" noted that jaundice in congestive heart failure is often characterized by its sudden appearance. Schottmiiller (10), Eppinger (3), and Libman (11), noted that the sudden appearance of the icterus was often associated with pulmonary infarction. Resnik and Keefer (12, 13) after a clinical and experimental study of jaundice following pulmonary infarction conclude that "anoxemia may depress the function of livers already damaged to such an extent that the bilirubin content of the blood strikingly increases." They note that in every case of 'cardiac' jaundice there is anatomical and functional impairment of the liver cells. They agree with.Fishberg (6) that patients with congestion of the liver may have only a slight increase in serum bilirubin. Conversely, patients may have a high serum bilirubin and their livers may be barely palpable. The size of the liver may not give a correct idea of either its anatomical or functional impairment. Eppinger (3) showed that there is an increased blood destruction and bilirubin formation in congestive heart failure. Resnik and Rich (14) were unable to obtain conclusive evidence that local extravasations of