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> 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.
Depending on how rigorously you are defining the word "know" (none of us
really *knows* - in the strictest sense - what actually causes DCS, let
alone why O2 alleviates symptoms), I will offer these two suggestions:
1. If, indeed, DCS symptoms are largely the result of gas-filled bubbles
within our blood and tissues (at least initially after the onset of symptoms,
which is when the O2 is usually administered), then breathing 100% O2 at the
surfaces will very quickly reduced the concentration of N2 in the blood (due
to the large N2 gradient across the alveolar membranes). With a reduced
concentration of N2 in the blood, the PN2 gradient from the insides of the
bubbles to the surrounding blood/tissues increases sharply. This increases
the rate at which N2 molucules move from the insides of the bubbles to the
surrounding blood (and out the lungs). While it may be argued that O2 will
diffuse into the bubbles due to a reverse gradient, it wouldn't offset the
movement of N2 out of the bubble, because the concentration of free-dissolved
O2 in the blood is reduced due to metabolism and binding by hemoglobin.
(Besides, O2 in the bubble would be more likely to diffuse out at the site of
tissue damage/circualtion blockage for reasons associated with # 2 below). In
any case, I think it is safe to say that with N2 removed (or greatly reduced)
from the blood, bubble shrinkage would result. Bubble shrinkage should reduce
symptom severity (especially immediately following the onset of symptoms).
2. I suspect that many, if not most, of the DCS symptoms we experience
are proximally the result of tissue hypoxia (especially for neurological,
or "Type II" symptoms). Flooding the blood with O2 can help deliver O2 to
these hypoxic tissues, thus alleviating symptoms.
> 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.
I see where you're going with this. I don't think the presence of O2,
per se, prevents DCS. I think it can help thwart symptoms (as in # 2
above). And because it is metabolized and bound to hemoglobin, its
free-dissolved concentration is proportionally lower than what it would
be for N2 or He (i.e., the total gas load in the blood is lower, and the
gas available for bubble growth is less). However, there are other
factors associated with O2 that can (theoretically) work against you. For
example, high PO2 leads to vasoconstriction, which means reduced
perfusion. This can theoretically lead to reduced N2/He elimination
efficiency from the tissues.
> 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.
My hunch is that the main advantage of doing the 10-foot stop time at 20
feet is that, because of the increased ambient pressure, bubble diameters
are smaller. Smaller bubble diamters lead to proportionally greater
internal bubble pressures (due to surface tension effects on the bubble).
This leads to steeper gradients across bubble membranes, which means
faster gas elimination from bubbles.
> 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?
I hope my tome above makes sense in this concept. The real aswer, as
always, is: "nobody really knows".
Aloha,
Rich
Richard Pyle
Ichthyology, Bishop Museum deepreef@bi*.bi*.ha*.or*
1525 Bernice St. PH: (808) 848-4115
Honolulu, HI 96817-0916 FAX: (808) 841-8968
"The views are those of the sender and not of Bishop Museum"
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