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1 Department of Physiology, State University of New York at Buffalo, Buffalo, New York
Use of a recompression chamber permitted simulation of breath-hold dives to 33 ft of sea water (2 atm abs). Four normal subjects made such dives during rest and mild exertion while delivering alveolar gas samples at frequent intervals by a partial-rebreathing procedure. The course of alveolar gas exchange differed greatly from that in ordinary breath holding. Oxygen uptake remained at near normal levels until ascent owing to the maintenance of alveolar Po2 by increased ambient pressure. Reversal of CO2 transfer occurred during descent, and little CO2 moved in the normal direction until ascent. Greater uptake of oxygen and retention of CO2 in the body led to lower final values of both alveolar Po2 and Pco2 than in comparable breath holding at the surface. Hyperventilation made possible longer dives with harder work, and in these the Po2 reached very low values on ascent. One subject showed a final Po2 of 24 mm Hg with evidence of reversed O2 transfer. Acute hypoxia on ascent is a likely cause of drowning in breath-hold diving.
Submitted on October 17, 1962
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