Response of pulmonary veins to increased intracranial pressure and pulmonary air embolization

Abstract

Brain compression with subdural air causes pulmonary hypertension and noncardiogenic pulmonary edema. To see whether air emboli to the lungs rather than brain compression caused these findings, pentobarbital sodium anesthetized dogs received i.v. air infusions, subdural air infusions or brain compression from balloons inflated in the subdural space. Subdural air and i.v. air resulted in similar vascular responses. Pulmonary artery pressure (Ppa) increased 160% (P < 0.01) and pulmonary venous pressure transiently rose 13 .+-. 5 Torr (P < 0.05) without an increase in left atrial pressure or cardiac output (.ovrhdot.Q). The end-tidal partial pressure of CO2 fell 55% (P < 0.01) and the postmortem weight of the lungs increased 55% (P < 0.05). Brain compression with a subdural balloon instead of air only caused a 20% rise in Ppa and .ovrhdot.Q without pulmonary edema. Pulmonary air emboli rather than brain compression accounts for the edema and pulmonary hypertension caused by subdural air. Catheters in pulmonary veins and the left atrium showed that air emboli cause transient pulmonary venous hypertension and a reproducible form of noncardiogenic pulmonary edema.