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Circulation, Vol 68, 164-169, Copyright © 1983 by American Heart Association

ARTICLES

Pulmonary edema formation with myocardial infarction and left atrial hypertension: intravascular and extravascular pulmonary fluid volumes

RA Slutsky, WW Peck and CB Higgins

The response of pulmonary blood volume (PBV) and extravascular lung water (EVLW) was examined by indicator-dilution techniques in 14 "open chest" dogs, seven that underwent coronary occlusion (group 2) and seven that served as controls (group 1). Data were obtained in a control stage (control stage 1) 45 min after coronary ligation (control stage 2), and 90 min after the left atrial pressure had been increased to approximately 35 mm Hg with a left atrial balloon. In group 2 animals, EVLW increased after coronary ligation without a marked change in left atrial pressure (6.9 +/- 0.4 to 8.2 +/- 0.5 ml/kg mean +/- SD; p less than .05) and increased to 20.1 +/- 1.4 ml/kg after the production of left atrial hypertension (p less than .005 vs control and vs coronary ligation). In the control dogs, EVLW was unchanged 45 min after the initial data had been collected (7.1 +/- 0.7 to 7.0 +/- 0.8 ml/kg). After the production of left atrial hypertension in these dogs, EVLW rose (14.8 +/- 1.2 ml/kg; p less than .005 vs control stage 1 and control stage 2, p less than .01 vs group 2 dogs). PBV did not change significantly with ligation and increased similarly in both groups during left atrial hypertension. We conclude that coronary ligation can increase EVLW, independent of microvascular hydrostatic pressure. During the production of left atrial hypertension there was greater transcapillary fluid flux in group 2 dogs at matched levels of left atrial pressure elevation. This may be due to an alteration in the permeability of the pulmonary capillary membrane during myocardial infarction and provides a partial explanation for the occasional disparity between left heart dynamics and the chest radiograph in acute myocardial infarction.

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