Recompression & O2 Toxicity

[rmediver2002]

That's quite logical, and maybe it is that simple. Certainly the risk/benefit analysis seems to be that obvious. But I guess I was under the impression that at levels approaching 3.0, even with varying individual tolerance, the great majority of people would be seizing. And that doesn't seem to happen in practice in these chambers, and that's what I can't figure...

I am just curious if you had a reference for that information or could recall where you had heard a finite level for toxicity occuring?

 

[Rick Murchison]

Crush the bubbles - pressurize to sixty feet.
Get rid of the nitrogen - drop nitrogen PP to zero in the breathing gas and introduce no other inert gas - breathe 100% oxygen.
As for oxtox, here's an experiment at 3.1 ATA, and a chart attempting to come up with some kind of "human average" based on 10% of the vic... uh, participants having a tox event.
So, on the one hand we see a variability of anywhere from 5 to 150+ minutes before having any problems at 3.1 ATA, while on the other we see an average 75 minutes where 10% have problems at 3 ATA.
It's a Risk vs Rewards thingie
Rick

 

[Tom Smedley]

A grand mal seizure at 60 feet in water leads mostly to drowning and maximum pucker index for those who must manage it.

A grand mal seizure at 60 feet in a dry chamber is just another seizure and the management is much simpler.

As has been said - the benefit outweighs the risk.

 

[Saturation]

The recreational standard is one that minimizes the incidence of CNS O2 tox. to an insignifigant amount.

The NOAA standard 1.6 is also very conservative. NOAA also has a table to compare time of exposure and level of exposure. (higher PPO2 / lower exposure rate)

The evidence supports us being able to tolerate higher levels of O2.

The bolded item above is key.

You can find the issue very well discussed in diving medicine texts such as Bove or Bennett and Elliott.

Above P02 3.0, the risk for convulsions rises exponentially [3.0 is roughly the knee of the curve], and this is why 3.0 is used as the maximum exposure for humans. However, that cutoff was established by the scientists who did it, and one can argue for extending it a touch to 3.1, or .2, .3 etc., because in the end, the threshold occurs through varying shades of grey. Lambertsen at U of Penn did much of the core work back in the 1970s.

The NOAA limits for CNS exposure clock has very little basis in science, at best its faulty interpretation of the medical literature. If safety were the major concern, its far better to reduce the absolute P02 exposure than to spend even a few minutes at the maximum P02 of 1.6.

 

[ianr33]

Crush the bubbles - pressurize to sixty feet.
Get rid of the nitrogen - drop nitrogen PP to zero in the breathing gas and introduce no other inert gas - breathe 100% oxygen.
As for oxtox, here's an experiment at 3.1 ATA, and a chart attempting to come up with some kind of "human average" based on 10% of the vic... uh, participants having a tox event.
So, on the one hand we see a variability of anywhere from 5 to 150+ minutes before having any problems at 3.1 ATA, while on the other we see an average 75 minutes where 10% have problems at 3 ATA.
It's a Risk vs Rewards thingie
Rick

Interesting. The above would seem to indicate that a diver that accidentally switches to pure O2 at 70 feet (rather than 50% ) actually stands a pretty good chance of getting away with it ( for a modest amount of deco anyway) Not something I plan on ever finding out though.

 

[Saturation]

Interesting. The above would seem to indicate that a diver that accidentally switches to pure O2 at 70 feet (rather than 50% ) actually stands a pretty good chance of getting away with it ( for a modest amount of deco anyway) Not something I plan on ever finding out though.

The chances are not good, unfortunately, errant diver has to be watched very closely by his buddy.

See the post above about the 'off effect' or better known as the off 02 effect. Once the high P02 is breathe, there is still a good risk of convulsing even, after realizing the error, diver breathes the right mix or backgas or ascends to the shallows.

 

[Sideband]

Air breaks.

Joe

 

[beezwax]

Thanks everyone for all the info! My impressions regarding the 3.0 threshold were only derived from conversations with other divers who have much more experience than I do but who are by no means experts in hyperbaric medicine. From what I've read here it sounds like the average human O2 tolerance is much higher than I'd believed.

Rmediver, you also mentioned that divers in a recompression chamber are at rest. This is actually one of the speculative reasons I had as to why there seems to be less toxing in a chamber compared to in-water exposure. [Again, keep in mind this is just a bunch of divers sitting around in a pub solving dive problems, not expert opinion.] We came up with:

1) In chamber the diver is warm and sitting or supine, so his/her METs are minimal. With less metabolic activity, oxygen uptake must occur at a slower rate.
2) The diver in chamber has experienced a DCS event, so is therefore saturated with nitrogen at the start of treatment. The nitrogen levels of this diver in/out of solution are certainly greater than average folks at 1 ata, and presumably still greater than a diver in water who is decompressing at the end of a dive but who is not yet bent. Pure O2 obviously creates a steep pressure gradient for N2 in the system, and the oxygen will spend more time pulling nitrogen out of the saturated diver in chamber before arriving at its own toxic exposure level.

Is there any science to support either of these theories?

 

[H2Andy]

sort of ... according to the NOAA Manual, immersion, cold, activity, and stress
all contribute to ox tox hits. no one really knows why. the reason is probably
that the more oxygen the body needs to stay warm and keep up with energy
requirements, the more o2 it will be absorbed into the bloodstream from the
lungs, the more danger of toxicity.

in the chamber, being dry, warm, at rest, and hopefully more relaxed, the
ox tox threshold is not as critical.

your ideas are interesting, and make logical sense, but i don't know that anyone really knows

 

[Charlie99]

In a chamber O2 tox can occur, but is pretty rare. I have seen more O2 hits at 40 FSW during surface decompression using oxygen than during treatment tables.

During treatments the patient is at rest, is being observed continuously, and are taking periodic air breaks.

Surface decompressions using O2 - 40 FSW 100% O2

Were there any air breaks during the 40fsw surface deco?