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GASEOUS EXCHANGE AND THE EXPRESSION OF DECOMPRESSION SICKNESS

On-gassing and Off-gassing

Increased ambient pressure, as would be experienced by scuba divers descending through the water column, causes the rapid inward diffusion of gas across the alveolar membrane. Over a series of mere minutes, the alveolar membranes permit the equilibration of gas tensions in the arteries and the mixture of gas being breathed. This creates a tension gradient across the gap between the arterial and venous systems that is partially bridged by perfused tissues. Based on this model, the loading of a given tissue with gas will depend on the rates of perfusion and diffusion and the solubility of the gas in the tissue in question. During decompression, the circumstances would reverse, leading to the perfusion- and diffusion-related movement of inert gas from tissue to the venous system, which dumps its gaseous cargo in the lungs.

In most tissues, perfusion rather than diffusion chiefly regulates gaseous exchange, with exceptional tissues being comparatively nonvascularized (e.g., bone). However, the basic structure of the vasculature for a given tissue may permit diffusion to interfere with normal perfusion-dependent on-gassing or off-gassing. To explain, suppose that fatty and lean tissues closely coincide. During compression, the rate of absorption of nitrogen by the lean tissue may decrease as the inert gas diffuses from the lean tissue to the adjacent mass of fat. During decompression, by contrast, one would predict that the lean tissue would rapidly reduce its load of nitrogen. However, gas being off-loaded from the lean tissue may be partially replaced by gas diffusing from the fatty tissue, again functionally reducing the rate of gaseous exchange with respect to the lean tissue.

In another model, gas may rapidly diffuse directly from arterioles to adjacent venules, thus permitting nitrogen to by-pass the tissue being supplied by the arterioles in question. The net effect would be a reduced rate of on-gassing for the specific tissue. Again, during decompression, arterial inert gas tension should be lower than venous inert gas tension, thereby reversing the pathway of diffusion (i.e., ambient pressure would govern arterial gas tension; perfusion would govern venous gas tension). With nitrogen now diffusing from the venules to the adjacent arterioles, local arterial gas tension may not be as low as would be predicted on the basis of ambient pressure. The tension gradient between the affected tissue and the local capillaries would therefore be functionally reduced, again leading to diminished tissue-specific rates of off-gassing. It is therefore clear that tissues can violate the basic assumption guiding popular Haldanian based dive-planning instruments (i.e., that tissues exchange gases in a strictly perfusion-limited fashion). The precise contributions of such hypothetical patterns of diffusion to the expression of decompression sickness are unclear.