Increases in plasma oncotic pressure during acute cardiogenic pulmonary edema.
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.
D000208:Acute Disease; D000328:Adult; D000368:Aged; D001798:Blood Proteins / Q000378:metabolism; D003102:Colloids; D005260:Female; D005665:Furosemide / Q000627:therapeutic use; D006331:Heart Diseases / Q000150:complications*; D006400:Hematocrit; D006801:Humans; D008297:Male; D008875:Middle Aged; D009994:Osmolar Concentration; D009997:Osmotic Pressure; D010949:Plasma; D011654:Pulmonary Edema / Q000188:drug therapy / Q000503:physiopathology*
D001798:Blood Proteins; D003102:Colloids; D005665:Furosemide