INTRODUCTIONIn a preceding paper (Keefer and Resnik (1926)) we described ten patients suffering from myocardial insufficiency, in whom jaundice appeared for the first time or increased considerably if already present following the development of pulmonary infarction.It is apparent that pulmonary infarction in a patient suffering from heart failure involves more than the mere extravasation of blood into the lungs. The experimental work of Binger, Brow and Branch (1924) shows that the chief functional disturbance which occurs as a result of pulmonary embolism is the development of anoxic anoxemia, a state in which the arterial blood contains less than its normal quota of oxygen. Undoubtedly, anoxemia of a similar kind developed in the patients whose histories we have reported. While it is true that in the experiments of Binger, Brow and Branch it was only after multiple embolisms had taken place that anoxemia appeared, and that in some of our patients on the contrary only one infarct occurred, it must be remembered that the circumstances differ in the two instances. In the experiments of Binger, Brow and Branch, the animals and the lungs were normal. A considerable amount of mechanical obstruction of the pulmonary circulation must take place before the functional impairment of the lungsissufficiently great to produce anoxic anoxemia. On the other hand, it is altogether reasonable to assume that, in patients such as we have described, in whom there is already functional impairment of the lungs, due to chronic passive congestion, still further 389 JAUNDICE FOLLOWING PULMONARY INFARCTION diminution in the amount of effective pulmonary tissue may bring on anoxic anoxemia, or exaggerate the degree of anoxemia already present.There is another factor of prime importance. All the patients in whom jaundice appeared following pulmonary infarction died within a relatively short time of progressive myocardial failure. There is evidence to show that anoxemia depresses myocardial function, particularly when the myocardium is already damaged (Resnik, 1925); so that the effect of pulmonary infarction in patients with myocardial failure is not only to cause anoxic anoxemia to appear, but also to increase the degree of stagnant anoxemia, which is dependent on the development of diminished circulatory minute volume.Finally, the condition of the liver remains to be considered. Since all our patients were suffering from severe and long standing myocardial insufficiency, it is probable that at the time when pulmonary infarction developed there must have been present changes in the liver characteristic of chronic passive congestion. Since according to contemporary theories of jaundice (McNee, 1922), (Rich, 1925), it is the function of the hepatic cells to excrete the bile pigment that is brought to them by the blood stream; the functional efficiency of these cells must be kept dearly in mind.In pulmonary infarction in patients with myocardial failure, we must deal, then not only with extravasation of blood into the pulmonary tissues, ...
