Increasing intracranial pressure with air causes air embolism, not neurogenic pulmonary edema.
In an effort to duplicate a previous model of neurogenic pulmonary edema (NPE), we maintained intracranial pressure (PIC) at 20 Torr below mean arterial pressure in six closed-chested dogs anesthetized with alpha-chloralose and urethan. This was accomplished by infusing 1) isotonic saline (NS), 2) a gas mixture of 80% helium and 20% oxygen (HeO2), or 3) 100% carbon dioxide (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 helium in expired gas during HeO2 infusion and confirmed by Doppler recordings. We conclude that increasing Pic with air produces the physiological changes of air embolism; this is not a satisfactory model for investigating NPE.
D000818:Animals; D004285:Dogs; D004618:Embolism, Air / Q000209:etiology*; D006439:Hemodynamics; D007427:Intracranial Pressure; D008176:Lung Volume Measurements; D011652:Pulmonary Circulation; D011654:Pulmonary Edema / Q000209:etiology*; D011655:Pulmonary Embolism / Q000209:etiology; D011669:Pulmonary Wedge Pressure; D012126:Respiratory Dead Space; D013355:Subdural Space; D014655:Vascular Resistance