Oxygen and Decompression

[Octo-Danny]

I've read that oxygen should be taken under consideration while calculating tissue ongassing (not O2 toxicity), as part of the inert gases. I haven't seen any application of this neither in Buhlmann algorithms nor in Schriner's equations.
How do I take this under consideration if at all?

 

[Green_Manelishi]

how so "taken into consideration"? cumulative effect on
nervous/pulmonary (?) system?

it is a metabolised gas and to best of my recollection
is not "inert"; what your body cannot utilize is exhaled
along with CO2. some believe that O2 is narcotic in and
of itself, beyond the toxicity effect, more so than Nitr-
ogen (i am not disputing it just mentioning it) and therefore they do not subject themselves to "ean" beyond
100 ft. It becomes a trimix dive.

Nitrogen, helium, argon, krypton, neon, hydrogen etc are 'inert' (and some are narcotic as hell) because your body cannot do anything with them other than absorb and de-absorb. they just 'do their thing' while in you.

looking forward to Doc's response.

 

[Dr Deco]

Dear Octo:

Oxygen is not considered in dive calculations, since it is metabolized and is always in low concentration when compared to the inert gases (nitrogen, helium, etc). Their lack of inclusion in the models of Buhlmann and Schreiner is well noted.

The endobiotic gases (water, carbon dioxide and oxygen) comprise a very small percentage of the tissue gases. For example, the approximate partial pressures of these at body temperature are water = 47 torr, carbon dioxide = 45 torr and oxygen = 40 torr for a total of 127 torr. The partial pressure of nitrogen in the tissues at sea level will be approximately 570 torr. Table algorithms are always adjusted to take into account these gases; their influence become progressively small as one goes to deep.

The situation at high altitude is quite different, however. In this case, the role of the inert gases becomes progressively larger. In fact, the commonly known fact that “blood boils” at altitude is ascribable to these partial pressures. Even in the absence of any inert gas, these endobiotic gases will be present and contribute to bubble growth. This is not a problem for recreational divers but it is a problem for aviators and astronauts.

Dr. Deco

 

[Octo-Danny]

Dr. Deco,

my question derives from reading Bennet and Ellyot both first and forth edditiopn. It is stated there that in the past oxygen wasn't taken under consideration but now it is well known it should be.

I understand that it's not a major factor in recriational dives but should it be in long deco' dives?

 

[Green_Manelishi]

is it possible the consideration to which they refer is
the effect that "high" O2 has on the ability of your lungs to effectively 'off-gas'? by that i refer to the now-known
fact that the effective transfer of the inert gases OUT of
your system is negatively effected by long(er) periods
of breathing high O2 with the goal of reducing deco time.
therefore many of the divers doing long deco dives take
"BG" breaks every 'x' number of minutes. it 'gives the lungs a break' so to speak and when they resume the high
O2 the transfer ability is improved.

 

[Dr Deco]

Dear Readers:

I would need to take issue with the claim that oxygen reduces the outflow of nitrogen during decompression. All experience from NASA studies is that the determining factor in elimination halftime is the tissue perfusion. This is expressed as the halftime and is modified by physical activity.

In most models, the “compartment” or “tissue” halftimes are fixed and are not perturbed (= changed or adjusted by the exercise level. The first model to seriously consider a change in inert gas exchange rates as a function of activity was that of Richard Vann, PhD, at Duke University (see Bennett and Elliott, The Physiology and Medicine of Diving ). The model developed was with respect to gas bubble resolution rates.

In addition, the degree of gas exchange in the lungs is not modified to any degree by reasonable gas bubble loads in the lung capillaries. “Reasonable” in this case refers to normal recreational diving practices, and it is not to be confused with the adverse effects of long durations of omitted decompression [God forbid!].

Considerable oxygen was employed in the tables developed by Cabarrou at the DFVLR in Germany, and modifications of nitrogen exchange did not need to be made with respect to duration of oxygen breathing.

Dr Deco

 

[rcohn]

Dr. Deco,

I think I remember reading about some concerns with the affects of extended duration breathing O2 at higher pressures leading to constrictions in blood vessels, which would obviously alter perfusion. I assume this isn't an issue for NASA but could be a factor for divers doing extended decompression with a PO2 of 1.6 atm.

Any insights?

Ralph

 

[Dr Deco]

Hi Ralph:

Oxygen at higher pressures is indeed a vasoconstrictor , and it is good that you bring attention to this for tech divers. It is for this reason that I would recommend that individuals move their arms and legs while decompression. “Windmill-type” activity for the arms and bicycle kicks for the legs. This would increase the blood flow sufficiently to reduce the halftime and counter the oxygen-induced vasoconstriction.

This activity is also recommended for non-tech divers at the safety stop.

Dr Deco

 

[Octo-Danny]

To all it may concern,

As I know the oxygen affects deco in two ways. One is increaed production of CO2 and thus increase in perfusion. and the other way as is acctually decreasing oxygenation BUT ONLY in whole body toxicity while the lung begins to be rigid due to lack of enzimatic activity (Bennet and Ellyot)

Dr Deco,
I'f I'm mistaken I'd appreciate the correction.

 

[Dr Deco]

Dear Octo:

The effects of oxygen are many, but there is not an increase in metabolism. Such an increase would possibly result in an increase in carbon dioxide production, but this only occurs if there is also an increase in muscle activity. It is the activity and its associated metabolism increase that make CO2 and not the oxygen itself.

The perfusion changes are in the opposite direction from what you mentioned. Oxygen causes a constriction of the blood vessels. This can be reversed by muscle activity and the production of CO2, a dilator of blood vessels.

Oxygen is toxic to all organs of the body but manifests its presence first in the lungs and central nervous system, depending on the exposure pressure. The first is from long exposures to oxygen partial pressures of 0.5 to 2 ATA for several hours. The toxicity manifests itself as increases in fluid in the lung (chemical pneumonia), which is reversible and later, the production of connective tissue (fibrosis) that is not reversible. It is not the result of enzymatic activity, although the lack of protective enzymes (e.g., superoxide dismutase, catalase, etc) could be interpreted as an effect of enzyme lack.

The CNS form is found with oxygen pressures higher than two ATA and shorter exposures than for pulmonary toxicity. These effects are convulsions and loss of consciousness – and drowning if you are in the water by yourself.

Dr. Deco