Increasing intracranial pressure with air causes air embolism, not neurogenic pulmonary edema

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Abstract
To duplicate a previous model of neurogenic pulmonary edema (NPE) intracranial pressure (Pic) was maintained at 20 Torr below mean arterial pressure in 6 closed-chest dogs anesthetized with .alpha.-chloralose and urethan. This was accomplished by infusing isotonic saline (NS), a gas mixture of 80% He and 20% O2 (HeO2), or 100% CO2 through a trephined hole into the subdural space. Three more animals were studied with the same protocol after thoracotomy to permit Doppler examination for bubbles in the left pulmonary artery. Significant increases in pulmonary artery pressure, pulmonary vascular resistance, physiological shunt, dead space fraction and hypoxemia were recorded when Pic was elevated by HeO2 infusion but not during infusion of NS or CO2. Pulmonary gas-bubble embolism was suggested by an increase in the fraction of He in expired gas during HeO2 infusion and confirmed by Doppler recordings. Increasing Pic with air produces the physiological changes of air embolism; this is not a satisfactory model for investigating NPE.

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