Hemodynamic and regional blood flow response to captopril in congestive heart failure

T. Barry Levine, Maria Teresa Olivari, Jay N. Cohn

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29 Scopus citations

Abstract

In 19 patients with moderate to severe congestive heart failure the over-all hemodynamic response to captopril was compared with its effect on regional blood flow. Ninety minutes after administering a single dose of captopril (25 to 150 mg), right atrial pressure decreased from 6.1 ± 6.1 to 3.2 ± 5.1 mm Hg (p < 0.001), pulmonary artery pressure from 33.1 ± 8.3 to 26.5 ±9.1 mm Hg (p < 0.001), pulmonary capillary wedge pressure from 22.4 ± 6.2 to 15.2 ± 7.4 mm Hg to (p < 0.001), mean arterial pressure from 77.2 ± 8.0 to 66.5 ± 13.7 mm Hg (p < 0.001), and systemic vascular resistance from 1,630 ± 503 to 1,233 ± 443 dyne-s-cm-5 (p < 0.001), and cardiac index increased from 2.0 ± 0.6 to 2.4 ± 0.7 l/minute/m2 (p < 0.001). Despite the significant increase in cardiac index there was no increase in either hepatic blood flow (203 ± 212 to 142 ± 101 units, N.S.) or forearm blood flow (2.2 ± 0.9 to 2.2 ± 1.0 ml/100 g per minute, N.S.) after captopril. Similarly, the global reduction in systemic vascular resistance was not accompanied by a reduction in either hepatic vascular resistance (0.93 ± 0.90 to 0.83 ± 0.69 units, N.S.) or forearm vascular resistance (41.3 ± 18.4 to 34.9 ± 12.4 mm Hg/ml/100 g per minute, N.S.). The over-all improvement in hemodynamics that is seen when captopril is given to patients with severe heart failure does not apply uniformally to all vascular beds. The heterogeneous response reflects the variable vasoconstrictor part played by the renin-angiotensin system in regulating flow to individual regional circulations.

Original languageEnglish (US)
Pages (from-to)38-42
Number of pages5
JournalThe American Journal of Medicine
Volume76
Issue number5 PART B
DOIs
StatePublished - May 31 1984

Bibliographical note

Funding Information:
From the Cardiovascular Division, University of Minnesota, Minneapolis, Minnesota. This study was supported in part by NIH Grant HL22977 from the National Heart, Lung, and Blood Institute. Requests for reprints should be addressed to Dr. T. Barry Levine, University of Minnesota Hospitals, Box 79, Mayo Memorial Building, Minneapolis, Minnesota 55455.

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