Extravascular lung water as a function of the magnitude of pulmonary artery pressure in the septic pig

Using a model of sepsis by which PAP can be manipulated, we generated two groups of pigs receiving similar bacterial doses while varying the PAP. The group with severe PHT uniformly developed fulminant pulmonary edema. The group with moderate PHT did not develop significantly elevated EVLW. The bacterial dose or rate was unrelated to the outcome. We conclude that our data support the hypothesis that pulmonary microvascular pressure can play a major role in the pathogenesis of septic pulmonary edema, either primarily or by exacerbating a coexisting pulmonary capillary permeability lesion. Our data are consistent with others and suggests that if a means of aborting the increased pulmonary hypertension early in sepsis could be developed, the increased EVLW in sepsis might be lessened. Once increased EVLW has occurred, however, there is no evidence that lowering the PAP results in any clinical improvement.