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Research Article Free access | 10.1172/JCI105679

Systemic and Renal Hemodynamics in Oliguric Hepatic Failure: Effect of Volume Expansion

Felix E. Tristani and Jay N. Cohn

Medical Service, Veterans Administration Hospital and the Department of Medicine, Georgetown University Medical Center, Washington, D. C.

*

Received for publication 17 March 1967 and in revised form 24 July 1967.

This study was supported in part by U. S. Public Health Service Research Grant HE-0978501 from the National Heart Institute and a Grant-in-Aid from the Washington Heart Association.

Address requests for reprints to Dr. Jay N. Cohn, V. A. Hospital, 50 Irving Street, N.W., Washington, D. C. 20422.

Find articles by Tristani, F. in: JCI | PubMed | Google Scholar

Medical Service, Veterans Administration Hospital and the Department of Medicine, Georgetown University Medical Center, Washington, D. C.

*

Received for publication 17 March 1967 and in revised form 24 July 1967.

This study was supported in part by U. S. Public Health Service Research Grant HE-0978501 from the National Heart Institute and a Grant-in-Aid from the Washington Heart Association.

Address requests for reprints to Dr. Jay N. Cohn, V. A. Hospital, 50 Irving Street, N.W., Washington, D. C. 20422.

Find articles by Cohn, J. in: JCI | PubMed | Google Scholar

Published December 1, 1967 - More info

Published in Volume 46, Issue 12 on December 1, 1967
J Clin Invest. 1967;46(12):1894–1906. https://doi.org/10.1172/JCI105679.
© 1967 The American Society for Clinical Investigation
Published December 1, 1967 - Version history
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Abstract

Systemic and renal hemodynamics were studied by indicator dilution techniques before and after infusion of 500 ml of dextran 40 in 21 patients with renal failure developing in the course of decompensated cirrhosis.

Cardiac index was directly correlated with total blood volumes. Renal blood flow was low and renal vascular resistance elevated in 13 of 15 patients. Renal vascular resistance was directly related to total systemic nonrenal vascular resistance. Two patients with the highest cardiac outputs in the group were oliguric with high renal blood flow.

Plasma volume expansion increased cardiac output in 19 of 21 patients and increased renal blood flow in 12 of 14. The patients were divided into two groups on the basis of control cardiac index. Those with lower cardiac index had lower blood volumes and responded to dextran with a 73% increase in cardiac output, a 148% increase in renal blood flow, and a rise in renal fraction. Those with high control cardiac index had significantly higher blood volumes and responded to dextran with only a small average rise in cardiac output and renal blood flow.

Systolic arterial pressure was less than 100 mm Hg in 12 patients. When compared to the normotensive subjects, this hypotension was characterized by a lower vascular resistance, a tendency for a lesser rise in renal blood flow after volume expansion, and a more rapid demise.

The prompt circulatory improvement after volume expansion in many of these patients indicates that functional plasma volume depletion may be an important factor in the renal vasoconstriction of oliguric hepatic failure. In an attempt to sustain volume expansion, reinfusion of ascitic fluid was accomplished in four patients. Normal renal blood flow was maintained during reinfusion and a diuresis always occurred, but the response usually was not maintained after the infusion was terminated.

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