what do we know about high ppO2's?

jasondrake

Reading other posts about unexplained diver 'blackouts' got me thinking.

The arrival of doppler testing brought to light that exisiting deco tables were very much based on empirical testing showing symptoms of dci, and that sub-clinical or asymptomatic effects were important. Could the same apply to accepted rules/limits regarding ppO2 exposure?

What I mean is - our limit of 1.6 bar as a 'line in the sand' below which very, very few divers will 'fit' and above which the risk of fit becomes significant is based, I think, on empirical tests plotted on a graph. Essentially they stuck a bunch of lads in a pot and exposed them till they started breakdancing! Fair enough. Ramping up our ppO2 to accelerate deco is a standard practice in diving, and divers control their exposure based on accepeted guidelines. Is it possible that (usually) subclinical side-effects of high ppO2 exposures are in some cases significant? We are, after all, evolved to breathe about 0.2 bar ppO2, and divers - especially tec divers - often spend long dives breathing in excess of 1.0 bar ppO2.

Perhaps high pp02 is wreaking havok with our physiology, and a percentage of individuals will come to harm? I'm not a physiologist so specifics are beyone me, perhaps someone could suggest possibilities as food for thought? Perhaps micro-vasoconstriction in parts of the brain could cause blackouts? Perhaps blood pressure is involved?

Anyone got any thoughts?

Thanks
Jason

Mdemon

What about O2 bends? It's known that O2 makes bubbles enlarge before they start to shrink (phrased wrongly but that's the gist). We often go to O2 for a period before surfacing. OK, it's metabolised, but if you go straight from 6m to 0 then there's bubble-expanding potential there. I'd like to know if there's research on O2 bends and if ICD can occur.

jasondrake

Here's an interesting abstract:

http://stinet.dtic.mil/oai/oai?&verb...fier=ADA026855

teksimple

[quote=jasondrake;122025]Here's an interesting abstract:

Interesting, indeed. This makes sense because oxygen is a vasoconstrictor and reduces the blood flow to the brain (not unlike like caffeine or nicotine?) Probably a defense mechanism to reduce damage to tissue. The effects of oxygen vasoconstriction can be reduced somewhat by increasing the pressure, so would be interested if this short term memory loss is still observed in a hyperbaric environment. CO2 is a vasodilator so maybe a bit of that would also counteract the observed effect.

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ScubaDadMiami

I, too, am nervous about the unknown effects of elevated PPO2 over longer exposures. For this reason, I tend to run at 1.0 during my dives (compared to a lot of people that run at 1.2), and then I go to 1.2 for deco. I don't mind a few extra minutes in the water.

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Howard Packer
IANTD CCR Instructor
Miami Beach, Florida
CCRDiveTraining.com

Allan_o

What do we define as longer exposures????

ppo2 at 2,4 is what hyperbaric chambers around the world treat patients with.

The duration is 1½ hour....


/Allan

HelenM

I'm not nervous about high PO2 at all, as long as it's what I'm after. I'm more curious about the unconsidered effects of O2 - treating it as an inert before it's metabolised if that makes sense.

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Would paper take tortoise?

ScubaDadMiami

Yes, but most people are resting in chambers, and they do not repeat the exposure over long periods of time.

I just see no reason to push the exposure when the diver can stay on the conservative side at the cost of a few extra minutes of deco. Only if conditions in the water dictate a higher exposure do I move the PPO2 to a higher level during the bottom phase of the dive.

__________________
Howard Packer
IANTD CCR Instructor
Miami Beach, Florida
CCRDiveTraining.com

Allan_o

I agree with you on the resting issue, but concerning long periods of time, normal procedure in some countries is 30 treatments, 1 treatment a day, (breaks in weekend)
Some patients are given up to 60 treatments.
My guess is approx 1-5 o2 hits a year (based on approx 10-14 patients every day)
Another thing that patients are complaining about on a regular basis is myopia..

/Allan

dteubner

I don't think that we can extrapolate dry chamber experience to diving at all - there are too may differences.

I also personally believe that the Donald experiments and the NOAA recommendations have set the bar too high and that there is a real rsik of O2 toxicity in rebreather divers at 1.6 ATA.

There are likely to be facors which expose rebreather divers to higher risks of O2 toxicity than other people. For example hypercapnea (and I'm talking only mild here) can be expected to increase the risk of CNS O2 toxicity. No-one really understands what happens to CO2 in real recreational (middle aged, maybe a bit unfit, smokers) rebreather divers in the water. Many of them seem to be pissed as well if we can judge from the original thread .

O2 seizures are idiosyncratic events so we need to think about risk, which people don't seem to like doing. There was quite a good discussion about risk here - http://www.rebreatherworld.com/decom...light=roulette

I think that there is probably some absolutely safe PO2 (0.8? 1.0? 1.2?) above which the risk of an O2 seizure begins. The risk is smaller on any given dive the lower the PO2, but the more dives you do, the higher the PO2, the more likely you are to be hit.

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Dave T

Hanlon's Razor - Never attribute to malice that which can be adequately explained by stupidity.