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"guess would be since CO2 is a metabolic product,rather than a major component in either mix,there should be no difference,unless breathing one gas or the other causes a metabolic change which produces more CO2.or results in a significant change in breathing patterns.I'm unaware that either of these occur in either air or trimix.This is just a bit of deductive reasoning,however,not fact.Anyone have any of those laying around?Bob?" Since it was a generic 'Bob' [I think that's Robb Wolov], I'll dispense some easy biochem as well. CO2 production is thought to be independent of ppO2, but metabolic rate dependent - There is no direct relationship between ppO2 inhaled & CO2 that evolves (O18 tagged inhaled gas would appear in CO(18)2 with a delay). Hold your snide comments about CO2 production will be zero irrespective of the ppO2 if organism is dead - Let's keep this to alive humans. As CO2 production is related to metabolic rate, respiratory rate may appear to govern it. In reality an increase in metabolic rate &/or increased CO2 trigger increased respiratory rate. Interestingly that appears relatively inelastic for ppO2 irrespective of the ppO2. Now here one has to crank in ---> very high ppO2 ===> vasoconstriction thus increased local CO2 levels, which may counteract vasoconsriction. In addition Haldane effect, that is drop in CO2 transport by RBC's when enough Hb remains as HbO2 due to dissolved O2 being primary source of O2 for metabolism, reduces CO2 transport - local increase in CO2. A vasodilatory effect. CO2 in blood, which is what produces the physiol 'stimuli' will be found as HCO3- (and the various dissociation/association products, which are pH dependent), CO2 and HBCO2. As depth increases CO2 retention will increase. Both circulatory parameters & the phychem of CO2 need be considered. Assuming that circulatory rate remains unchanged & gas is normoxic ---> At any depth n, the extraction of O2 from blood (dissolved + HBO2), with HbO2 saturation remaining relatively constant with depth (nitpicking about a few 0.000m%) will be driven first by dissolved O2. The more dissolved O2 available for given O2 requirement, the more the Hb will remain as HbO2. Thus the lower the HbCO2 transport ability of RBC's The other problem is ventilatory. Viscosity of gases increase with pressure - read depth. This introduces a ventilatory CO2 issue. Obviously using a 'less dense' breathing gas will reduce the overall ventilatory work & potentially reduce the CO2 produced by that ventilatory work. But the actual ability of CO2(g) to 'move' in lungs will not change as its viscosity increase would remain the same irrespective of the reduced viscosity of the inhaled gas (Gas dynamicists - jump in here). If the microlayer of lung air at the border where pulmonary gas exchange is occuring has high CO2(g) because of that gases inability to move, the whole system will back up. So looks like the bottom line is CO2 retention will increase with depth. I think Bennett showed that. It also follows from the actual paucity of free CO2 in blood. It is all bound. Which is what causes thinks like pH shifts and ventilatry responses. I think also that U of Penn did a series of studies in the early 70's with their 5000 ft equivalent ~2000 ft chamber dive. Robb - comments appreciated - I'm wearing Au plated asbestos - and being politically incorrect. Regards Esat Atikkan
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