what do we know about high ppO2's?

Gene_Hobbs

We just recently updated this section of our "suggested reading list" after several requests for places to start in the RRR.

As for the 1.6 limits, some good history of this is described in the DAN Nitrox Workshop Proceedings. Lang (ed). 2001 (available here). There is also some GREAT discussion from Ed Thalmann on how the USN picked their limits for testing of deco models in there.

Lanphier EH (ed). Unconscious Diver: Respiratory Control and Other Contributing Factors. 25th Undersea and Hyperbaric Medical Society Workshop. UHMS Publication Number 52WS(RC)1-25-82.Bethesda: Undersea and Hyperbaric Medical Society; 1982; 160 pages. RRR ID: 4278

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"Oxygen is addictive and deadly. Everyone who uses it will eventually die" --RW Hamilton, PhD 1991

teksimple

Do you mean considering the existence of O2 DCS? As far as I know in both empirical and theoretical studies O2 has never been treated as an inert "bendable" gas because higher animals have an O2 transport mechanism that would never be outperformed by any inert gas transport mechanism. In case that it were, the clinical manifestation could be a gas embolism, but not DCS. Case in point: Oxygen rebreather divers cannot be bent by oxygen, but can be embolized by it. It is conceivable that latent inert gas saturation in such divers (from breathing 78% inert gases at the surface prior to the dive) could cause manifestation of DCS, but it would not be from the oxygen.

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apitkin

Hmmm.

In medicine, never say 'never'. Especially when it relates to a poorly understood theoretical framework for a complex physiological process.

Oxygen transport in humans is very sophisticated, but it has evolved to work in only one direction: from lungs to tissues. Its performance in this direction is extremely effective, including its delivery of high PO2s to the brain to cause CNS toxicity. I'm not saying it can't work in the opposite direction, but if it does I would expect it to be much less effective.

There is no specific 'inert gas transport mechanism'. Just simple passive diffusion, albeit in a complex environment. What is not well understood is the connection between the bubbles and the clinical symptoms.

Could oxygen bubbles form within humans? I don't know, but I would certainly not rule it out. Theoretically it seems unlikely, but so did circulation of the blood until William Harvey came along. Would oxygen bubbles cause symptoms? I would say very unlikely, but not impossible.

Experimental evidence of the existence of oxygen bubbles would, I think, be very difficult to obtain. Inert gas bubbles are difficult to detect outside the bloodstream, and their composition would extremely challenging to ascertain. However, these physiology scientists are fiendishly clever people and I wouldn't be surprised if someone came up with an ingenious technique to do so.

One of the things that makes DCI (and diving medicine generally) so interesting is that the more you know about it, the less you understand it.

Andy

Genesis

One has to take the various empirical evidence on high PO2 exposures in the proper context, then apply whatever "discount" factor you want to them in the view of a CCR, or you're asking for trouble.

Specifically, high PO2 exposures in OC divers are not the same as high PO2 exposures in a CCR diver. Why? Because an OC diver only experiences the maximum PO2 on bottom gas at maximum depth. Everywhere else, he experiences less.

On OC, as you switch to the 50% EANx at the 70' stop, you get a 1.6 exposure. But it only lasts a few minutes. You move up to the next stop, and the exposure drops.

Now the 20' stop is typically significant, but it really is the only "long" exposure. And - surprise - that's where people fit on OC, usually.

A CCR is entirely different. Whatever PO2 level you dive at is maintained through the entire dive. Is this relavent? I think it is. Add to that the potentiation of hits by CO2 and the potential for trouble goes way up.

So for me, I've decided that I will dive with a bottom PO2 of no more than 1.2. Typically, I cut it back even further, and dive around 1.0, and deco at 1.4. Yes, this means I'm not on pure O2 until I'm at 15', but that's ok. The few extra minutes of decompression that this imposes on me is, IMHO, worth it for the additional safety margin.

I've been ok with a 1.4 PO2 for the OC limit and the traditional view (50% switch at 70', O2 at 20') for deco on OC, but on a CCR, for the above reasons, I believe more caution is advised.

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teksimple

See my post here

Vitally challenged divers don't post, but they can conceivably get oxygen bends

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Sutty

How about keeping an experimental animal in pure O2 environment at 0.2Bar, flushing continually to denitrogenate the animal and the environment. Compress to 2Bar for a while, then rapidly decompress to 0.2bar again and look for symptoms. Could even then sacrifice animal and do histology at 0.2bar to look for bubbles - would need a hypobaric chamber with a human occupant to do the last bit but not impossible - the astronauts lived at hypobaric pressures I understand. If done with some small animals like tadpoles may even be able to microscope into the pressure chamber to examine their tails for bubbles after adding anaesthetic or poison to the chamber.

Neil

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abowie

Agreed.

I don't know either although I'm still looking.

For a bubble to form the venous PO2 would have to be high enough to exceed the magical M value. I suspect that you'd be fitting long before that happened.

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Andrew Bowie

Rebreather-friendly Buddy

abowie

Nasty man! At least you have implied a difference between the two.

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Andrew Bowie

Rebreather-friendly Buddy

Sutty

It doesn't necessarily have to form in tissues that are at venous PO2, although probably not much difference at very high PO2s anyway.

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Sutty

One is (hopefully) reversible

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