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J Appl Physiol 63: 2380-2387, 1987;
8750-7587/87 $5.00
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Journal of Applied Physiology, Vol 63, Issue 6 2380-2387, Copyright © 1987 by American Physiological Society

ARTICLES

Role of oxygen in the production of human decompression sickness

P. K. Weathersby, B. L. Hart, E. T. Flynn and W. F. Walker
Naval Medical Research Institute, Bethesda, Maryland 20814.

In the calculation of decompression schedules, it is commonly assumed that only the inert gas needs to be considered; all inspired O2 is ignored. Animal experiments have shown that high O2 can increase risk of serious decompression sickness (DCS). A trial was performed to assess the relative risks of O2 and N2 in human no-decompression dives. Controlled dives (477) of 30- to 240-min duration were performed with subjects breathing mixtures with low (0.21-0.38 ATA) or high (1.0-1.5 ATA) Po2. Depths were chosen by a sequential dose-response format. Only 11 cases of DCS and 18 cases of marginal symptoms were recorded despite exceeding the presently accepted no-decompression limits by greater than 20%. Analysis by maximum likelihood showed a shallow dose-response curve for increasing depth. O2 was estimated to have zero influence on DCS risk, although data variability still allows a slight chance that O2 could be 40% as effective as N2 in producing a risk of DCS. Consideration of only inert gases is thus justified in calculating human decompression tables.


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