Abstract
Patients with chronic congestive heart failure without evidence of hypertension or renal disease were studied to determine the role of the kidney in the formation of cardiac edema. These patients tended to have an inadequate cardiac output by the catheter method utilizing the direct Fick principle, and a low renal blood flow by the para-amino hippurate method. The filtration rate by the inulin technique was reduced only about half as much as the renal plasma flow, frequently giving filtration fractions higher than those reported in any other condition. This indicates a high intraglomerular pressure, which was probably caused by efferent arteriolar constriction. Stud-ies of Na filtration, excretion and reabsorption show that the retention of salt resulting in edema is caused by the low filtration rate, and is not due to increased reabsorption of salt. The renal blood flow was reduced to about l/5 normal when the cardiac output was approx. half normal, indicating a specific diversion of blood away from the kidney. It is suggested that a similar shunting of blood from the kidneys may be important in those patients who have a normal renal blood flow and normal cardiac output at rest, but who develop evidence of heart failure and edema on exertion. When the cardiac output becomes inadequate to meet the demands of exercise, blood may be diverted from the kidneys to other parts of the body whose metabolic needs are greater. The reduction in renal blood flow had no relation, to the venous pressure, but was correlated with the reduction in cardiac output, indicating that it is a "forward failure" phenomenon and not due to "backward failure" or increased hydrostatic pressure in the veins.

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