Effect of afterload reduction on plasma volume during acute heart failure |
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Authors: | R J Henning M H Weil |
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Affiliation: | 1. From the Institute of Critical Care Medicine, the Shock Research Unit and the Department of Medicine, University of Southern California School of Medicine Los Angeles, California, USA;2. From the Los Angeles County/University of Southern California Medical Center Los Angeles, California, USA;3. From the Center for the Critically ill, Hollywood Presbyterian Medical Center, Los Angeles, California, USA |
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Abstract: | Previous investigations in our unit indicated that acute cardiogenic pulmonary edema is associated not only with an increase in left ventricular end-diastolic pressure and pulmonary arterial wedge pressure but also with a relative increase in colloid osmotic (oncotic) pressure and peripheral hemoglobin concentration. This combination of changes suggested that acute congestive heart failure with pulmonary edema, unlike chronic congestive heart failure, is associated with a contraction of intravascular blood volume. In this study, plasma volume changes were measured before and during the treatment of acute cardiogenic pulmonary edema in 14 patients with arteriosclerotic heart disease. The plasma volume measurement in all 14 patients before the initiation of treatment was either normal or decreased. After treatment with the alpha adrenergic blocking agent phentolamine, the plasma volume increased rather than decreased when measured 4 and 12 hours after the initiation of treatment. During this time colloid osmotic pressure and peripheral hemoglobin concentration progressively decreased. These findings suggest that acute cardiogenic pulmonary edema is associated with the extravasation of large quantities of plasma water from the intravascular compartment into the interstitial compartment and contraction of the intravascular plasma volume. The treatment of acute cardiogenic pulmonary edema is associated with the return of hypo-oncotic fluid from the interstitial compartment back into the intravascular compartment with expansion of plasma volume and reduction of colloid osmotic pressure and hemoglobin concentration. |
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Keywords: | Address for reprints: Robert J. Henning MD University of Southern California School of Medicine Center for the Critically III Hollywood Presbyterian Medical Center 1300 North Vermont Avenue Los Angeles California 90027. |
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