Recompression & O2 Toxicity

[beezwax]

by acute you mean CNS toxicity? and i guess chronic is pulmunar oxygen
toxicity?

I think that's right-- acute resulting from the level of exposure (elevated PO2) whereas chronic resulting from the duration of exposure (as in chamber). But I'm at the edge of my knowledge here too. Seems like they produce different physiological harms-- seizure on one hand, permanent lung damage on the other.

 

[Rick Murchison]

I think that's right-- acute resulting from the level of exposure (elevated PO2) whereas chronic resulting from the duration of exposure (as in chamber). But I'm at the edge of my knowledge here too. Seems like they produce different physiological harms-- seizure on one hand, permanent lung damage on the other.

"Pulmonary" oxygen toxicity is indeed the chronic oxygen problem, but it is probably poorly named - I prefer "whole body" or "organ" oxygen toxicity, as long term exposure (not necessarily in a chamber - a hospital room will do) to elevated oxygen levels (theoretically anything above .5 ATA) can do damage to organs, not just the lungs. Given enough oxygen over enough time the body just sort of starts shutting down. In addition to pulmonary problems things like kidneys and liver and pancreas etc start dropping off-line; you can actually die from it.
It's only a concern along the very outside edge of the technical diving envelope and in some commercial diving. Most of us can just take care to avoid CNS oxtox and the chronic exposures will automatically be avoided.
Rick

 

[Rick Murchison]

Could someone explain the relationship between CO2 toxicity and O2 toxicity to me?

While I don't think the exact cause of CNS oxtox is known, it is known that hemoglobin's ability to fully saturate with oxygen and so blood's ability to carry more oxygen is improved by higher levels of CO2, which would seem to mean that more oxygen will get to the tissues with higher CO2 levels around. Whether that is the only factor that predisposes one to CNS problems at high PPO2 exposures is doubtful, but it is certainly one of 'em.
Rick

 

[H2Andy]

it is known that hemoglobin's ability to fully saturate with oxygen and so blood's
ability to carry more oxygen is improved by higher levels of CO2

wow, that's weird... you would think the opposite would be true: the more
CO2 binding to the hemoglobin, the less O2 that will get a chance to bind

the body is a weird place

 

[Rick Murchison]

wow, that's weird... you would think the opposite would be true: the more
CO2 binding to the hemoglobin, the less O2 that will get a chance to bind

the body is a weird place

CO2's ability to take up vacant sites on hemoglobin is a convenient transport mechanism that helps keep the pH change effect of elevated CO2 levels down somewhat - but O2 will readily displace it if it's around (unlike CO, which is a real pain to get rid of). On a tangential issue this may help explain why CO2 problems at depth can be so much more severe than at the surface for the same amount of exertion - you have so much oxygen in the breathing gas there are fewer vacant Hemoglobin binding sites for CO2 transport, so (1) the efficiency of the CO2 transport system is affected, and (2) the blood's pH is affected more at a given CO2 level. I have no idea if there's any clinical data to back up these thoughts, but they do all sort of fit together into a probable theory, don't you think?
Rick

 

[H2Andy]

interesting...

more O2 means less ability for the body to remove CO2, so the higher your O2 mix,
the worse you make your CO2 retention problem

i'm way over my head here

 

[Rick Murchison]

interesting...
more O2 means less ability for the body to remove CO2, so the higher your O2 mix,
the worse you make your CO2 retention problem
i'm way over my head here

As I say I have no idea if there's any clinical study to back that up, but it does make sense. Add the fact that all that extra oxygen lets you work harder longer without as much lactic acid buildup - and therefore with less fatigue AND more immediate CO2 production from the same exercise, and...
Rick

 

[beezwax]

Rick, tell me if I'm understanding this correctly... CO2 and O2 both readily bind to hemoglobin in our bloodstream. If CO2 is present at higher levels, such as by being generated through diver exertion, then more will bind to the hemoglobin as the body attempts to maintain a stable blood pH and CO2 level by transporting this excess to the lungs and out via respiration. If, however, elevated levels of O2 are also present because of the breathing mix, these O2 molecules will tend to bump the CO2 molecules and bind to the hemogoblin instead because it has a greater affinity toward O2 (and/or prevent the CO2 molecules from binding in the first place for the same reason). Thereby driving or keeping the CO2 back in free circulation, pushing down blood pH, and increasing the risk of CO2 tox. And, I suppose, if the CO2 actually causes more O2 to fully bind with or saturate hemoglobin, then it simulatneously increases the risk of O2 tox. I have no idea what I just said, but it sounds like a double whammy.

 

[Thalassamania]

yes to the acute vs chronic

CO2 and O2 DO NOT both READILY bind.

CO and O2 READILY bind.

CO2 weakly binds.

This is refered to as the HALDANE EFFECT.

Hemoglobin with oxygen on it does not bind C02 as well as Hemoglobin without
oxygen. This makes makes sense, in the body when oxygen is used up carbon dioxide binds more easily to hemoglobin. In the lungs, when hemoglobin gets more oxygen, carbon dioxide binds less well to hemoglobin and is released.

If you give someone with a lot of C02 in their body high oxygen, then the oxygen binds to their hemoglobin and, since C02 does not bind as well to oxygenated hemoglobin it is released into blood. If a lot of C02 was bound to hemoglobin there will get an increase in C02 in the blood.

for details see: http://www.calgaryhealthregion.ca/clin/rt/EdDay_2004Nov/ControlOfBreathing2.pdf

 

[beezwax]

First of all, Thalassamania, let me just say welcome to scubaboard! Your input and many years of experience will be much appreciated here. I read the .pdf link you provided, and would be completely lying if I said I understood more than half of it. It appears to be a powerpoint presentation for people in the medical field who do not need terms or variables in equations to be explained. For example, regarding CO2 retention we are told:

PaC02=k (V02xR)/VE x 1/1-VD/VT
– decrease VE - increase paC02
– increase VD - increase paC02
– increase R - increase paC02
– increase V02 - increase paC02

What is VE, or VD, or R?

But the section concerning the CO2 increase resulting from 100% O2 was helpful to me. They identified three reasons:
1) loss of hypoxic drive
2) increased V/Q mismatch
3) haldane effect

The loss of hypoxic drive I understand-- that's the lack of oxygen-deprivation distress I mentioned earlier due to higher PO2 gas mixes. And the haldane effect is what we have just been discussing-- CO2 vs O2 binding to hemoglobin, when how and why. But I'm not entirely clear on this V/Q mismatch thing. For starters, what are V and Q? I understand that it is referring to hypoxic vasoconstriction, where blood vessels in areas with poor ventilation tend to constrict. So bumping up O2 can relieve this and "create areas with poor ventilation, but good blood flow." Does that just mean extra O2 simply boosts circulation and that draws out CO2 buildup from areas that previously were poorly ventilated?

It's interesting, this presentation you linked to focuses on elevated CO2 levels for COPD patients, folks with emphysema and such, and their recommendation is to use the LEAST amount of O2 possible in treatment. Obviously that is not the thinking for DCS recompression patients who are nitrogen saturated.