Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1977;55:195-199

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Figueras, J.
Right arrow Articles by Weil, M. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Figueras, J.
Right arrow Articles by Weil, M. H.

Circulation, Vol 55, 195-199, Copyright © 1977 by American Heart Association


ARTICLES

Increases in plasma oncotic pressure during acute cardiogenic pulmonary edema

J Figueras and MH Weil

Colloid osmotic pressure (COP) was measured in 95 patients with clinical and radiological evidence of acute cardiogenic pulmonary edema. Fifty patients who were admitted for coronary observation but in whom acute myocardial infarctin was excluded, and 21 patients who had sustained acute myocardial infarction without evidence of left ventricular failure served as controls. Significantly higher values of COP, total plasma protein, and hematocrit were observed in patients with pulmonary edema. Increases in COP during pulmonary edema were best explained by transudation of hypooncotic fluid into extravascular spaces. Following treatment of pulmonary edema in 76 patients with furosemide, morphine, and oxygen, pulmonary edema was reversed in 65 patients. Reabsorption of hypooncotic fluid from extravascular sites with a significant decline in COP, total protein and hematocrit followed reversal of pulmonary edema. No significant changes in these parameters were observed in patients who failed to respond to therapy. These observations implicate filtration of hypooncotic fluid from the intravascular compartment during onset of cardiogenic pulmonary edema and reabsorption of hypooncotic fluid into the intravascular compartment during reversal of pulmonary edema.