Negative pressure pulmonary edema, a clinical review and study of its pathophysiology

Abstract

This experiment studied the pathophysiology of negative pressure pulmonary edema. Laser colorimetry, weight transients, hematocrit and plasma protein changes were used to determine fluid and protein flux in 3 groups of isolated blood-perfused left lower canine lung lobes. Each group (n = 12) was subjected to an initial 50 minute control period with a capillary pressure $\rm(P\sb{c})$ of 15 cm H$\sb2$O and pleural pressure $\rm(P\sb{pl})$ of $-$5 cm H$\sb2$O. Group 1 was subjected to a further 50 minutes of perfusion with the same conditions. Transpulmonary pressure was increased in the other two groups from 20 to 30 cm H$\sb2$O for 50 minutes by decreasing P$\rm\sb{pl}$ in group 2 (preferentially affecting extra-alveolar vessels) and by increasing P$\rm\sb{c}$ in group 3 (affecting alveolar and extra-alveolar vessels). There were no differences in fluid flux between initial and final filtration periods in Group 1 by laser colorimetry (0.333 vs. 0.431 ml/gm dry weight/hour). Group 2 had a significant increase in filtration during the final filtration period. Group 3 filtration also increased. Weight transients overestimated edema compared to hematocrit and laser colorimetry derived values. Filtrate to plasma protein concentrations (CF/CP) decreased in Groups 2 and 3 but did not change significantly in Group 1. No differences in CF/CP could be detected based on plasma protein concentrations. Negative pleural pressures significantly increased pulmonary fluid filtration with the majority of the increase taking place in the extra-alveolar vessels. Filtrate protein concentration changes suggest that the increased filtration appears due to increased surface area and/or increased hydrostatic forces, not from a permeability change. (Abstract shortened by UMI.)