Ox Tox

PeteS

Well that's a risk/benefit thing. 1.3 bar PPO2 is fine for me, but if your O2 consumption is not average, is your risk of Ox Tox higher or lower than average?

Maybe there is no answer that is available at this time. I guess that all the research was done on OC systems, and that there was never any need to look at metabolised O2 consumption as a factor.

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Pete S.

http://www.steggle.co.nz

Every silver lining has a cloud

jasondrake

It seems to me that O2 metabolism will be a factor. OxTox is almost certainly a result of higher than normal ppO2 acting on the CNS biochemistry. So the ppO2 at the CNS cell membranes is key. ppO2 at the CNS will be a function of ppO2 at the lungs and ppO2 in the blood. ppO2 in the blood will increase over time as long as the ppO2 in the lungs is greater than the metabolism of O2. So increased metabolism of O2 will have some reducing effect on ppO2 at the CNS. Whether this is significant who knows.
And there are so many factors that could it even be calculated accurately?
Day to day and minute to minute changes in our metabolism, blood pressure, etc. makes fine tuning your personal ppO2 tolerance impractical. What works in the morning might tox you in the afternoon. Like narcosis, which is so unpredictable we just assume it'll be asignificant risk below a certain depthand so we make broad rules to avoid it.
Better to stay within general safe limits. What works works.

nigelh

I'm not very convinced.

The problem I see is that clearly the direct ppO2 in the nervous tissue is not a factor as this is one of the best oxygenated and most thoroughly perfused parts of the body so it will be effectively in the fastest of 'compartments' and certainly nowhere near the 'safe for up to three hours' type of statistics we get from the largely empirical CNS tables.

There has to be a chain of reactions to get a delay like that and I can't see how actual gross oxygen metabolised will effect that. I still suspect that CO2 is the demon king here. I have stated elsewhere that if we had an explanation of the freediver's samba, the shallow water blackout, again blamed on oxygen but in my opinion wrongly, we might understand CNS and have a lot more insight into rebreather accidents.

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nigelh

UWSojourner

Give me your opinion on something. I usually run a setpoint of 1.2. My setpoint bobbles around 1.2-1.27ish.

My question is, How close to the true PPO2 do you think my displays are?
For you, when you set at 1.3, how close to the true PPO2 do you think you are?

I'd be interested in anyone's response, or if there is a study out there containing direct, independent measurement that would be great.

nigelh

Naturally I can't comment on yours exactly but I assume the sensors are within their 5% fsd temperature tolerance, since the normal 2% fsd is at constant temperature and a rebreather from calibrate to dive is hardly constant temperature, so plus/minus 0.1bar. (fsd = full scale deflection = 2 bar)

Then the tracking of the control loop may be good if I'm stooging round a wreck at pretty constant depth but if I'm playing SBs and going up and down a lot not going to be so accurate. Try this dump of me learning to use a scooter and getting depth control totally base over apex.

Over all my 1.3 is probably 1.3 but excursions to 1.5 and 1.1 can't be ruled out but won't be very long. However I admit that the way the CNS curve runs 20 seconds at 1.4 is not paid back by 20 seconds at 1.2, the higher numbers run the clock faster.

We have the problem with ECCRs that our control loop can only adjust upward. There is no mechanism to pull the loop ppO2 down other that wait for the diver to breath it off. Naturally this happens a lot faster if we are running good MLV but even so a sudden descent will cause it to spike a bit. The biggest spike on my plot is caused by a 12->19m descent in about a minute just after an ascent so I suspect it wasn't anything like MLV.

When I say I can live with 1.3 it's this whole scenario that I mean. I'm afraid I'm one of the old codgers who were taught 1.6 was the limit, 1.5 if you're working hard and don't exceed 2.0 or else. When I look at reported incidents all but very few ox-tox cases are at high levels. Somebody breathes the wrong mix or has a calibration error or bad sensors and their tox would be predicted even on my old training. I'm quite prepared to roll back the limits to 1.6 max 1.3 good but watching the ratchet try to click further down annoys me. If we try to run too far from the oxygen limits and deco limits and into the Comex hardworking diver tables we start doing such long hangs that we are more at risk. We do not do our deco in a dry bell or on a habitat style platform, we are often dangling on a string from a DSMB with a boat trying to watch us drift.

I'm sorry. I've rambled and rather drifted off the question. I just hope I went in the direction it was aimed in.

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nigelh

UWSojourner

Not trying to annoy you. I'm new to this game ( less than 2 yrs ) and just trying to figure things out. At this point I'm not doing a lot of deco time (about 30 min is max so far) so maybe your situation is different.

Thanks for the response. It looks like you are diving an inspiration? Can you give me an idea of what that calibration procedure looks like?

For example, my cal procedure looks like this: 1) cal my O2 analyzer in air and tune to 20.9, 2) analyze O2 cylinder, 3) if O2 cylinder less than 0.98, adjust handset to indicated % otherwise just use 98%, 4) run O2 over Meg sensors via the head-only procedure and, when stabilized, calibrate. For the Shearwater its 1-point calibration. No altitude Rebreather diving yet.

babar

also, don't forget the role of co2 in ox-tox. We do know from various studies done at university of pennsylvania, that co2 retension greatly lowers the threshold for toxing.
helping a troubled student, carrying his bottles and yours, 100% o2 on deco, alittle co2, and... Bam, there it is.

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Babar
Evolution Plus
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dteubner

THIS IS NOT TRUE AT ALL. THe ppO2 in the CNS is the same as the PPO2 in the lungs. If you are diving a ECCR increased O2 consumption will make the solenoid fire more often and use more O2 out of the tank but will have NO EFFECT on various body partial pressures which will be roughly whatever the set point is.

The partial pressure of oxygen in the CNS varies with the partial pressure of oxygen in the inspired gas, it has nothing to do with oxygen consumption by the whole body.

Dave T

jasondrake

Are you sure?
I appreciate that the ppO2 in the CNS will always roughly approximate the inspired ppO2.
And I suggested that metabolism of O2 will probably not be significant.
But should the metabolism of O2 outstrip the transfer of O2 into the blood via the lungs, the ppO2 in the tissues will drop some. So metabolism can be a factor, albeit an almost certainly insignificant one.

dteubner

Yes, I'm sure.

The metabolism of O2 cannot "outstrip the transfer of of O2 into the blood via the lungs". The blood which is seen by the CNS comes straight from the lungs without going to any other tissue. The blood passing through the lungs fully equilibrates with the oxygen in the alveoli on each pass. End of story.

The partial pressure of O2 in that blood is given by the formulae:-

PAO2=FIO2(Pambient-47)-PaCO2/R

Where
PAO2 = arterial partial pressure of O2 - in mmHg
FIO2 = fraction of inspired oxygen
Pambient = ambient pressure (in mmHg)
47 = saturated vapour pressure of water at 37 degrees
PaCO2 = arterial partial pressure of CO2 - in mmHg
R = constant - the respiratory quotient - ususally 0.8

PaO2 = PAO2-Aa gradient

where
PaO2 = arterial partial pressure of O2 - in mmHg
Aa gradient = constant difference between alveolar and arterial blood - usually 10-15mmHg

There is nothing in the equation about VO2 (whole body oxygen consumption).

In fact, given that higher VO2's mean higher CO2 production, and that CO2 retention is likely to be a precipitant of O2 toxicity, higher VO2's MAY be more likely to be assosciated with O2 toxicity via a very indirect and not causal route.

Dave T