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1 Department of Medicine, Indiana University School of Medicine; and Veterans Administration Hospital, Indianapolis, Indiana
Arterial blood gases were measured after 10 min of full-phase negative pressure breathing at a gauge pressure of 40 mm Hg. Oxygen capacity increased slightly, and oxygen saturation fell from 96.9% to 92.6% in the seated position (P < 0.05) and from 96.0% to 92.2% in the recumbent position (P < 0.05). At this transthoracic pressure differential there would be expected only an 810-mm decrease in oxygen tension resulting in a 1% decrease in arterial saturation. pH and calculated pCO2 were not altered. The physiological shunt appeared to increase as evidenced by the arterial desaturation. If blood is redistributed away from poorly ventilated regions, the redistribution is not complete during negative pressure breathing at this magnitude. Although there appears to be an increased shunting, it is quite small compared to that reported in the anesthetized dog at only 20 mm Hg. The differences are probably related to the effects of anesthesia causing a decrease in lung volume and tidal volume. Forward acceleration has been said to simulate negative pressure breathing. However, the arterial saturation at 8 g was 75%, and 8 g has been estimated as being equivalent to 28 mm Hg (3.5 mm Hg/g). Therefore, the degree of arterial desaturation during forward acceleration is more reasonably related to the hydrostatic effects than to possible negative pressure breathing effects.
Submitted on May 1, 1961
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