Until early in the nineteenth century physicians considered dropsy as a disease in itself, much as our generation deals with hypertensive cardiovascular disease. When renal, cardiac and hepatic diseases were defined, edema became merely a symptom. Starling pointed out that rise in venous pressure or fall in plasma protein would have similar effects in shifting fluid from the blood stream to the tissue spaces, and for several decades this explanation seemed to cover all cases of dropsy. High venous pressure was thought to underly the dyspnea, the proteinuria and the hepatic changes characteristic of heart failure. MacKenzie and Lewis were almost alone in their assumption that when the heart muscle failed the body would not receive its usual blood supply and that fatigue and dyspnea were due to anoxic metabolism. This view was given emphasis in Altschule's critical study1of heart failure. There the lack of correlation between symptoms