Dear madmole and Dr Thomas:
This certainly was a busy thread when I finally had time to look at it. Here are a couple of comments if anyone is still left.
[1.] Carbon dioxide does indeed contribute to the gas in decompression bubbles, but its concentration is generally very low in comparison to nitrogen (or helium). In diving, carbon dioxide partial pressure in the tissues is quite trivial. In altitude depressurizations, however, CO2 can play a very large role since all gases have relatively small partial pressures.
During WWII, one explanation for exercise-induced DCS was referred to as the work theory. Here, musculoskeletal work increased the concentration of carbon dioxide, contributed gas to bubble growth, and increased the incidence of DCS.
This theory was countered by the strain theory of E. N. Harvey. According to this concept, musculoskeletal activity generated low-pressure regions within the tissues and generated micronuclei. This concept is in use today by many barophysiologists (but certainly not by all).
[2.] Nitrous oxide will most certainly cause laboratory animals with incipient (sub clinical DCS) to develop more severe problems of decompression sickness. I have not heard of an instance where nitrous oxide has effected an exacerbation of DCS in humans. It is certainly a possibility, however.
[3.] Xenon could be used as a decompression gas with respect to its slower uptake than nitrogen. I would suspect that it is of no real value since it is an anesthetic at atmospheric pressure. Decompression could be accelerated on the surface more by breathing oxygen and some kinetic activity (to increase blood flow).
Dr Deco
:doctor: