Effect of peripheral temperature on the formation of venous gas bubbles.

Undersea Biomed Res

School of Kinesiology, Simon Fraser University, Burnaby, British Columbia, Canada.

Published: September 1989

Temperature of the tissue affects the many components involved in the formation of tissue gas phase formation: diffusion, perfusion, and inert gas solubility. Since the effects of perfusion and inert gas solubility may be counteracting in terms of enhancing growth of gas bubbles, the optimal thermal status of divers throughout a dive remains unresolved. To elucidate the role of peripheral body temperature on gas phase formation, four subjects were exposed to a 10 degree and 40 degree C environment for 3 h on two separate occasions, after a no-stop decompression from a 12-h dive to 9.14 m (30 fsw) on air. The 3-hour exposures to either a cold or warm air environment resulted in a significant difference in mean skin temperature (P less than or equal to 0.01) with no alteration in rectal temperature. Total peripheral resistance during the 10 degree C exposure was 13.8 +/- 1.9 mmHg.liter-1.min-1 and significantly higher than that observed during the 40 degree C exposure (10.4 +/- 3.5 mmHg.liter-1.min-1). Gas bubbles in the venous return were monitored with a Doppler ultrasonic transducer placed in the precordial region, both at rest and after a deep knee bend. Venous bubbles were only detected in 1 subject following the warm air exposure, whereas 3 of the 4 subjects developed Doppler-detectable bubbles during the cold air exposure. Although both the cold and warm air exposures (3 h postdecompression) were uneventful, a hot shower taken by the subjects on completion of the cold air exposure (6 h postdecompression) precipitated mild type I symptoms of decompression sickness. These symptoms were not present after a hot shower following the warm air exposure. The present results indicate that despite the assumed greater inert gas solubility of tissues expected during cold air exposure, the decrease in the perfusion may have played a more significant role in the observed levels of detectable venous gas bubbles. Development of type I symptoms following a 12-h saturation, a 3-h cold exposure, and a subsequent hot shower suggests that a rapid rise in peripheral temperature may cause a significant rise in tissue gas tension. This increase in tension does not seem to be sufficiently reduced by increased perfusion to the tissues to prevent bubble formation.

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