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Date: Mon, 12 Jan 1998 16:01:06 -0500
From: Ben Greenhouse <b.greenhouse@ut*.ca*>
To: "William M. Smithers" <will@tr*.co*>
CC: "techdiver@aquanaut.com" <techdiver@aquanaut.com>,
     rebreather@nw*.co*
Subject: Re: Surface O2 and DCS...
William:

    I am not sure about this, but it is an educated guess.  For starters, an
increased PO2 will increase the pressure gradient across the alveolar
tissues. This will result in an increased rate of uptake of O2 by the
blood.  The absence of Nitrogen in the breathing mixture will increase the
pressure gradient across the alveoli in the other direction.  In this
manner, I imagine that breathing 100% oxygen would seem to actively "pull"
Nitrogen out of the blood stream relative to when breathing air.  This
phenomenon would work in the same manner in the various tissues, but to a
lesser extent for Oxygen as it is used up, and hence the gradient drops.  I
think that you might have been referring to this when you said "filler" gas,
but I wasn't positive.

    I was thinking of all sorts of other ways that high PO2s could increase
the rate of offgassing, using pH values and Bohr effects etc until I
realized one important thing.  I have a typical human oxygen equilibrium
curve infront of me, and our blood becomes saturated with oxygen at a PO2 of
around 120 mmHg (oxygen bound to hemoglobin, and dissolved in hematocrit).
Now unless my math is wrong....  100% oxygen at sea level is at a PO2 of 1
atm, which is equal to 760mmHg.  Even a normoxic mixture has a PO2 of around
160mmHg.  This would indicate to me (again unless my math is wrong) that
breathing gases with higher PO2s will allow for no physiological or
biochemical mechanisms of increased gas exchange since no more oxygen can
physically get into our systems.  This would then suggest (I think) that
perhaps the only way high PO2s contribute to decompression is as a "filler"
gas.

    In addition, my above speculation on high PO2s increasing the pressure
differential at the tissues must not be true since no more O2 can get into
the system.  I believe however that it would still be true at the gas
exchange surface in the lungs.  Also, the _rate_  of exchange of O2 could
increase due to the high PO2 in the lung.

You may have thought of all that before, but if not, I hope it helps.

Ben

William M. Smithers wrote:

> Anyone know exactly why it is that breathing 100% O2
> at the surface sometimes cures minor type 1 hits, and helps
> significantly with Type 2 hits?
>
> I am assuming there's more to it than simply eliminating
> the Nitrogen from the breathing mixture.
>
> If so, this might have implications for normal deco,
> as halftime-based models only consider the partial-pressure
> of the dissolved N2 and He, not the partial pressure of
> inspired O2, which it would seem has beneficial effects on its
> own.
>
> For example, if you combine your 10/20ft stops at 20ft,
> using Buhlmann, you get no deco advantage, despite
> the elevated PO2 of 1.6 at 20ft.  Why?  on 100% O2,
> your inspired PN2 and Phe are zero at any depth, so the algorithm
> effectively says it makes no difference what your PO2
> (or depth) is - the partial pressure of N2 and He can't fall
> below zero on the inspired side.
>
> So naturally the question arises: is O2 at higher partial
> pressures really only beneficial as a "filler" gas, as
> compartment-based models would suggest, or does it actively
> contribute to decompression?
>
> -Will
> --
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