| Summary: | This purpose of this study was to evaluate the contribution of post-dive peripheral tissue warming to the production of venous gas emboli (VGE) in divers.
Inert gas elimination from the tissues is limited by both perfusion and diffusion. If changes in diffusion are matched by corresponding perfusion (vasoactive) changes, decompression should be asymptomatic (within allowable exposure limits). Under conditions when the diffusion of inert gas from the tissues is not matched by blood perfusion, VGE will ensue. Increasing tissue temperature will decrease inert gas solubility and thus diffusion into the blood. It has been demonstrated that problems may arise during rapid changes in peripheral temperature, as often occurs post-dive, when divers previously exposed to cold water actively rewarm themselves in showers or baths. The effect of moderate rewarming, however, may be to increase the rate of inert gas elimination without the formation of VGE since increased perfusion is encouraged. The effect of mild post-dive warming was investigated.
Ten male subjects, between the ages of 21 and 29 years completed two dry chamber dives to 70 feet for 35 minutes (no decompression limit of the Canadian Forces Air Diving tables). Each dive was followed by a 30 minute head-out immersion in either a thermoneutral (28°C) or warm (38°C) bath. Non-invasive Doppler ultrasonic monitoring was then carried out at 30 minute intervals for the next 150 minutes to assess measurable VGE. Subjects did not display VGE formation in either the control or experimental conditions.
Our findings suggest that: 1) the Canadian Forces table limits (for the profile employed) provide safe no-decompression limits not compromised by mild post-dive warming, and 2) mild peripheral warming, since not bubble generating, may be a useful adjunctive therapy in the management of decompression sickness by increasing the rate of inert gas elimination. === Education, Faculty of === Curriculum and Pedagogy (EDCP), Department of === Graduate
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