In order to evaluate the effect of acute upper airway obstruction upon
pulmonary edema (PE) formation, we studied seven dogs that were subje
cted to inspiratory obstruction for three hours. Hypoxia was avoided b
y the administration of supplemental oxygen during the study period. S
ix dogs developed pulmonary vascular congestion, and four developed hi
stologic findings of PE. Inspiratory intrapleural pressure decreased t
o -28 +/- 4 mmHg in dogs that developed PE and to -23 +/- 2 mmHg in do
gs that did not. Transmural pulmonary artery pressure and pulmonary ar
tery wedge pressure did not increase significantly. Central venous pre
ssure during inspiration (CVPi) increased in all dogs, and CVP at end
expiration (CVPe) was significantly higher in dogs with PE. Dogs that
developed PE experienced a decrease in cardiac output and an increase
in systemic vascular resistance. Furthermore, alveolar ventilation dec
lined in dogs with PE, ultimately resulting in ventilatory failure. Pu
lmonary edema formation was not preceded by an increase in pulmonary v
ascular pressures but was associated with higher CVP, pulmonary vascul
ar congestion, and hypercarbia.