Physiologic and histologic determinants of gas exchange during induction of oleic acid pulmonary edema.

Five anesthetized mongrel dogs were studied during the induction of acute oleic acid pulmonary edema to determine the influence of cardiac output (Qt), extravascular lung water (ETV), and the degree of alveolar flooding on pulmonary gas exchange. Ot and ETV were measured by thermal dye dilution techniques, alveolar flooding was assesed by histologic studies, and gas exchange was quantitated by the multiple inert gas elimination technique (MIGET). Estimates of the inert gas venous admixture [(Qva/ Qt) IG%] were obtained at different experimental stages from the MIGET data to provide an index of overall gas exchange impairment. Pulmonary edema was produced by the intravenous (IV) infusion of oleic acid (0.08 mL/kg). Measurements of Qt, ETV and (Qva/Qt) IG% were made prior to lung injury and at 40, 80, and 120 minutes after injury. After death the lungs were inflated and frozen. Thirty cores of lung parenchyma (2 mL each) were obtained for histologic assessment of alveolar flooding. In the early phase of edema formation (0 to 80 minutes), (Ova/Qt) IG% increased as ETV increased. After 80 minutes, ETV stabilized and further changes in (Qva/ Qt) IG% were then primarily determined by changes in Qt (r = .94). The histologically assessed degree of alveolar flooding correlated well with ETV at the 120-minutes stage (r = .85). However, by use of multivariate analysis, the addition of the histologic information did not appreciably improve the prediction of gas exchange in acute oleic acid pulmonary edema.