Hello readers:
Sorry readers; I was away for several days at a NASA conference and did not get the these posts.
Dive Warm and Decompress Cold
This is the opposite of the warm shower or hot tub. It occurs in some cases and has been found to produce a greater incidence of DCS than would be expected. A change in the blood flow in the extremities and a slowing of the elimination of dissolved nitrogen is thought to be the problem.
There does not exist much information/data on this, but experience from non-recreational divers [military and commercial] is that it is a bad idea to dive warm and decompress cold. While the tables are computed on the bases of halftime compartments that do not change, the truth is that they do indeed change. The NASA system of decompression is passed in part on an exercise prebreathe that speeds the elimination of dissolved nitrogen from the tissues. The compartments are not only blood flow dependent and changeable.
Jacuzzi and DCS
This is a topic that arises about twice a year. In principle one would expect that this would help with inert gas elimination. In a [very] small study referenced below, cold diving and a warm exposure produced a problem. The study was not large, but it does indicate that possibly it is best to wait several hours before a hot Jacuzzi and take only warm, not hot, showers following a dive.
Always remember, that muscle stress and strain is a very big factor in nuclei generation. A long walk to the Jacuzzi might be the worst part of the whole procedure.
Dr Deco :doctor:
References :book3:
Mekjavic IB, Kakitsuba N.Effect of peripheral temperature on the formation of venous gas bubbles. Undersea Biomed Res. 1989 Sep;16(5):391-401.
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 with no alteration in rectal temperature.
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-hour post decompression)
were uneventful, a hot shower taken by the subjects on completion of the cold
air exposure (6 h post decompression) 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.