Pulmonary arterial shunting in man during forward acceleration

¹ Acceleration Section, Aerospace Medical Laboratory, Wright Patterson Air Force Base, Dayton, Ohio

The arterial blood gases were determined during forward acceleration 90° to the acceleration vector at 6 g and 8 g breathing room air and at 8 g breathing 100% oxygen. Arterial saturation fell to 84% at 6 g and 75% at 8 g. Prebreathing O₂ for 15 min prior to acceleration with continued inhalation during the acceleration plateau only partially corrected the undersaturation to 86% at 8 g. Recovery was not complete in 3 min unless O₂ therapy was used. Whole blood carbon dioxide content was depressed at 6 g and 8 g on room air, but this was corrected by O₂ inhalation. However, during the recovery period while breathing oxygen the carbon dioxide content was depressed. pH was reduced and pCO₂ elevated slightly during each acceleration period. Since cardiac output and alveolar ventilation have been reported to be essentially unaltered during forward acceleration at these magnitudes, the observed effects must represent substantial alterations in the individual ventilation to blood flow ratios throughout the lung, with approximately 50% of the cardiac output shunted through totally nonventilated areas at 8 g. There also must be some inadequately perfused or nonperfused peripheral areas, as evidenced by the fall in CO₂ content and pH and the accumulation of a substantial O₂ debt previously reported during acceleration.

Note:
With the Technical Assistance of Alice M. Caton and Justin L. Taylor, Jr.

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