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

• Main Author: Tauriainen, M. Peter
• Format: Others
• Language: en; en_US
• Published: 2007
• Online Access: http://hdl.handle.net/1993/923

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.)