CO2 retention and air consumption

[The Iceni]

Originally posted by DivingDoc
Paul wrote:
Not quite sure that I see why it follows that Nitrox divers would have more CO2 due to the Haldane effect. I would accept that Nitrox divers might have more CO2 due to a slight suppressive effect of the higher pO2 level.

I am talking straight biochemistry here. Yes indeed, there is no reason to suppose that Nitrox divers have considerably more CO2 on board - all things being equal - but they will have relatively more oxygen on board, particularly if the pp O2 is set at 1.4 bar for the bottom. This excess oxygen will displace the CO2 that would otherwise be bound to haemoglobin - as carbaminohaemoglobin - so for any given CO2 load there will be proportionately more free and therfore active CO2 molecules to act at the cellular level. It is well known that in an oxygen partial pressure of 3 bar CNS oxygen toxcity is very likely. I do not believe it is simply coincidental that at these pressures the haemoglobin of venous blood remains 100% saturated with oxygen so very little CO2 is mopped up by the haemoglobin to form inactive carbaminohaemoglobin.

This phenomenon is well known and is named the Bohr effect. Reference to the haemoglobin dissociation curve will confirm this.

I believe this is also why CO2 is implicated in acute CNS oxygen toxicity - too much CO2 competes with the oxygen bound to haemoglobin and myoglobin releasing the oxygen in its biochemically active form to add to the dangerously high levels of oxygen already present.

I am much less inclined to believe this is solely to do with the autoregulation of cerebral blood flow.

 

[Dr Deco]

Dear Paul and DivingDoc:

I would put my money on autoregulation. I would suspect that the amount of oxygen that can be added to highly metabolic brain tissue is increased more by increased perfusion than by a shift in the oxygen-binding curve. Since most additional dissolved oxygen is carried in physical solution at elevated partial pressures (but in low numbers of molecules), a high flow is necessary to maintain the high partial pressures.

I do not have any experiemntal data on one over the other, however.

Dr Deco :doctor:

 

[The Iceni]

Dr Deco once bubbled...
Dear Paul and DivingDoc:

I would put my money on autoregulation. I would suspect that the amount of oxygen that can be added to highly metabolic brain tissue is increased more by increased perfusion than by a shift in the oxygen-binding curve. Since most additional dissolved oxygen is carried in physical solution at elevated partial pressures (but in low numbers of molecules), a high flow is necessary to maintain the high partial pressures.

I do not have any experiemntal data on one over the other, however.

Dr Deco :doctor:

I can see where you are coming from Dr D, but the manifestation of an acute toxic reaction is explosive, ie. certain events take place that increase the rate of those events - positive feedback. My intuition tells that autoregulation (negative feedback) does quite the opposite and cannot be an explosive event, rather a relative change. Thus it can only be one part of the story.

I agree, considerable research is needed before this can be answered with any certainty. However what is certain is that both free oxygen and free carbon dioxide are biochemically active (as are those free radicals we keep hearing about.)

Not so when they are bound to haemoglobin. As you know, even the venous haemoglobin is fully oxygenated at an inspiratory partial pressure of 3 bar O2, when a CNS hit is almost a certainty.

I therefore surmise that the more free haemoglobin there is for any given inspiratory pp O2 (or pp CO2 ) the lower the number of free O2 (and CO2) molecules will be available at the level of the tissues of the brain. We know this to be the case as an acute CNS event is less likely when their partial pressures are low as both are known to predispose to such events.

Any money out there for a research project?