Any reported cases of Ox Tox between 1.4 and 1.6?

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Considering that fewer and fewer chamber reportedly accept divers, I suspect that at most diving locations there are more ERs "nearby" than chambers.
This is the truth. We've lost a lot of them over the past few years. There are entire regions of the country that are without facilities that will treat emergent hyperbaric indications.

Best regards,
DDM
 
This is the truth. We've lost a lot of them over the past few years. There are entire regions of the country that are without facilities that will treat emergent hyperbaric indications.

Best regards,
DDM
Is there something that we as a community can do to help with this?
 
Is there something that we as a community can do to help with this?
Thanks for asking! The Undersea and Hyperbaric Medical Society is raising awareness of this issue nationally. Individuals can contact their local, state, and federal government representatives.

Best regards,
DDM
 
Thank you, certainly more approachable thru explicit terms.

So this paper/concept begins by assuming the tissue/venous system is subject to "inherent unsaturation," even under a 'steady state' (stated as such; the equations are static)

Eq. 1 is defined based on this assumption (perhaps prematurely?)

Pw = PB - (PtisN2 + PtisO2 + PtisCO2 + PtisU + PH2O) [Eq. 1]

But we know that total tissue gas pressure is the sum of gas partial pressures (Dalton's Law?)
PB = (PtisN2 + PtisO2 + PtisCO2 + PtisU + PH2O) [Eq. 0?]

Eq. 0 already accounts for whatever the PtisO2 happens to be. No Pw 'oxygen window' term is required to explain that for a low PtisO2, PtisN2 will be a higher proportion of total tissue (bubble) gas pressure. PB will not be "unsaturated"--it will be equilibrated to ambient pressure, which for tissue/veins is actually slightly above ambient/'barometric' pressure (it's why we bleed..)

So why do we need to explicitly invent a Pw, and why do we think arterial oxygen pressures change this?

Eq. 2 is folded into Eq. 1 to generate Eq. 3, which removes PtisN2 and now weirdly implies that PbubN2 depends on PAO2, but not on PB, the ambient pressure, which was "canceled out" in the operation. I don't think this can be right.

I am not sure this is valid algebra. For one, ambient pressure in the arteries is probably not actually the same term as the ambient pressures in the tissues, veins, or lungs, and perhaps not so simply canceled out.

Eq. 2 (as used) doesn't help the Eq. 3 rationale on pure oxygen either, regardless of depth or ppO2:

PtisN2 = PAN2 = PB - PAO2 - PACO2 - PH2O [Eq. 2]
PtisN2 = PAN2 = 1.6 - 1.6 - ~0 - ~0 = 0 [6 metres / 20 ft]

PtisN2 = PAN2 = PB - PAO2 - PACO2 - PH2O [Eq. 2]
PtisN2 = PAN2 = 1.3 - 1.3 - ~0 - ~0 = 0 [3 metres / 10 ft]

The result in both cases of "PtisN2 = 0" certainly changes what happens to the algebra used to make Eq. 3.

The relevant part of Eq. 2 is to prevent inspired PAN2, especially when staying deeper. Not sure I follow or agree with the rest of the maths (Eq. 3 ...)

I don't see how the math actually justifies that maxing out the PAO2 itself while on oxygen (by staying deeper) magically "vacuums" more nitrogen out of the tissues. But keeping bubbles smaller, or from forming at all makes sense.

Maybe there is a more decompression-relevant treatment of the gas dynamics somewhere... might need to include explicit rate equations, and separate and distinct terms for the pressures of various spaces/compartments.
 
Another way to try to express this oxygen window concept might be just to think higher ambient pressure simply means more pN2, something like:

6 metres / 20 ft:
1.6 atm = PtisN2 + PtisO2 + PtisCO2 + PtisU + PH2O
1.6 atm = PbubN2 + ~0 + ~0 + ~0 + ~0
1.6 atm = PbubN2

vs.

3 metres / 10 ft:
1.3 atm = PtisN2 + PtisO2 + PtisCO2 + PtisU + PH2O
1.3 atm = PbubN2 + ~0 + ~0 + ~0 + ~0
1.3 atm = PbubN2

And this kind of looks interestingly simple--will the pN2 then have a higher gradient when deeper, simply because it is equilibrating against no counter-gradient? 1.6 atm > 0 atm pN2? We didn't need to put metabolism or arterial levels of other gases into any equations for that

But this too probably over-simplifies decompression.

And we were talking about bubbles, in theory, so: higher ambient pressure > smaller bubbles at higher pressure > same number of inert molecules (regardless of depth?)
 
Thank you, certainly more approachable thru explicit terms.

So this paper/concept begins by assuming the tissue/venous system is subject to "inherent unsaturation," even under a 'steady state' (stated as such; the equations are static)

You need to read all the foot notes too:
“There have been a few measurements that are pertinent to the oxygen window (l,9,12,18)”

Those references included in vivo measurements
 
To TL;DR my previous posts looking into the equations...

If 'oxygen window' just means: 'there is little oxygen in the venous blood that will add to the total venous gas pressure for off-gassing purposes,' then that's great, and it doesn't really depend on arterial oxygen pressures at all--that's a separate compartment.

I don't think it means that arterial ppO2 by itself changes this, nor that maxing out your arterial ppO2 is beneficial as an isolated term. I don't see valid math for that--it looks more like a mis-applied concept while simply trying to minimize input ppN2.

I'm guessing this actually has been tested? For example run deep air deco dives, then compare nitrogen off-gassing rates when breathing either a) 100% oxygen or b) 50/50 heliox.

If a maxed out input arterial ppO2 itself mattered for the 'oxygen window' effect, then you would expect to see that nitrogen off-gassing was better on 100% oxygen, compared to 50/50 heliox. And that might start to violate Dalton's Law

Alternatively, run deep heliox dives like 10/90, then compare helium off-gassing on 100/00 oxygen vs 50/00 nitrox.

Is this in one of the other studies?
 
-it looks more like a mis-applied concept while simply trying to minimize input ppN2.
Pretty much this. Which is why it shouldn't be referred to anymore. It belongs in the trash heap of misunderstandings of yesteryear along with stuff like acclimatizing to narcosis.
 
It seems like both of you are trying to say that the physiology outlined in these papers doesn’t exist?

I can’t find any newer studies saying that hey this effect we’ve measured in vivo doesn’t exist can you guys point them out.
 
you would expect to see that nitrogen off-gassing was better on 100% oxygen, compared to 50/50 heliox.
No, because the oxygen window does not influence the rate of off-gassing. This is unequivocally stated by the authors of the O2 window papers.
 

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