Oxygen toxicity at Altitude

[newt]

Hi Dr. Deco,
I am a anesthesiologist who just completed his basic nitrox course. We dive here at 4-8000 ft, and have to adjust our times on the standard tables. (for example, a 58 foot dive would be adjusted to 72 feet) I understand this because we are basicly offgassing in a rarefied atomsphere and can come down with the bends easier. The issue becomes more difficult when we are talking about oxygen toxicity. Should we adjust our tables for greater depth (and a greater a.t.a.) when we are calculating our oxygen load?
On one hand I would say no because the a.t.a. would not change with altitude- you should probably use the actual depth.
On the other hand, since we breathe a much lower partial pressure of oxygen than you do at sea level, maybe we are more susceptable to oxygen toxicity and should use the altitude adjusted tables.
But what makes you susceptable to oxygen toxicity? Low antioxidants in the body? Low seizure threshold? Or do we know?

 

[RichLockyer]

If anything, the lower PO2 at the surface would reduce the likelyhood of tox, but as far as what causes/triggers it... ya... it's not totally devoid of voodoo.
Research has indicated that as long as we stick with a max of 1.4, we should be unlikely to encounter any problems.

 

[Dr Deco]

Hello newt:

Altitude Diving

The reason that one needs to adjust the dive table at altitude is traceable to the reduced ambient pressure. Tables to prevent nuclei growth (in the old days, it would be “to prevent bubble formation”) are based on the ratio between bubble internal pressure and external (hydrostatic) pressure.

Sine he external (barometric) pressure is reduced at altitude, this necessities a readjustment of these “bubble-ambient” relationships. It is for this reason that tables are adjusted. They are adjusted to give the appearance of a greater depth to increase the bubble-to-surface ratio. Tables could be calculated solely for use at altitude and a depth correction would not be required.

Oxygen Toxicity

Because the depth correction is for surfacing ratio only, it does not imply that there is a greater pressure, and thus there is not a greater risk of oxygen toxicity.

It is unclear as to what causes oxygen toxicity. Evidence points to the accumulation of many metabolites in the tissues.

Dr Deco :doctor:

Readers, please note the next class in Decompression Physiology :1book:
http://wrigley.usc.edu/hyperbaric/advdeco.htm

 

[newt]

Thank you, I also read your old posts under "Oxygen toxicity and altitude" search. I think I got it pretty well down, although I don't know if I would be more suceptable to long-term toxicity. If I look at it from a tissue level, really the Hemaglobin brings in most of the oxygen, and the partial pressure of the serum is only a minor component. I think I'm not going to worry about it.
:newbie:
But I may take some Vit C and E...

 

[wetdoc]

newt posted :

But I may take some Vit C and E...


One good article about this topic is available in full text ( pdf ):
Supplementation of antioxidants prevents oxidative stress during a deep saturation dive.
The Tohoku Journal of Experimental Medicine
http://www.jstage.jst.go.jp/article/tjem/203/4/353/_pdf

Abstract:
http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=15297742

From Buenos Aires, Omar Sanchez , Wetdoc.

 

[Jaap]

Hi

I investigated the issue of O2 toxicity when me and a friend were thinking about bringing some small O2-rebreathers to Lake Titicaca in Peru at approx 3800m alt.

I found out that it could be a risky thing to do, but I didn't put that much effort into the research.


Here are two abstracts:


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High altitude dives from 7000 to 14,200 feet in the Himalayas.

Sahni TK, John MJ, Dhall A, Chatterjee AK.

Department of Medicine, Indian Naval Hospital Asvini, Colaba, Bombay.

Indian Navy divers carried out no-decompression dives at altitudes of 7000 to 14,200 ft (2134-4328 m) in the Nilgiris and Himalayas from May to July 1988. Seventy-eight dives on air and 22 dives on oxygen were carried out at various altitudes. The final dives were at Lake Pangong Tso (4328 m) in Ladakh, Himalayas, to a maximum of 140 feet of sea water (fsw) [42.6 meters of sea water (msw)] equivalent ocean depth in minimum water temperature of 2 degrees C. Oxygen diving at 14,200 ft (4328 m) was not successful. Aspects considered were altitude adaptation, diminished air pressure diving, hypothermia, and remote area survival. Depths at altitude were converted to depths at sea level and were applied to the Royal Navy air tables. Altitude-related manifestations, hypoxia, hypothermia, suspected oxygen toxicity, and equipment failure were observed. It is concluded that stress is due to effects of altitude and cold on man and equipment, as well as changes in diving procedures when diving at high altitudes. Equivalent air depths when applied to Royal Navy tables could be considered a safe method for diving at altitudes.
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1: J Appl Physiol. 1975 Feb;38(2):279-81. Related Articles, Links


Relative susceptibility of altitude-acclimatized mice to acute oxygen toxicity.

Hall P, Schatte CL, Fitch JW.

The influence of hypoxic acclimatization at altitudes of 0, 5,000, or 15,000 ft on the relative susceptibility to acute oxygen poisoning was determined in 288 adult female mice. After acclimatization periods of 1, 2, 4, or 8 wk, the mice were exposed to oxygen at high pressures (OHP) of 4, 6, or 9 ATA and the times to convulsion and death recorded. A factorial analysis of variance indicated that altitude and OHP level had inverse, log-linear effects on both parameters. The duration of acclimatization progressively decreased the time to death. The onset of convulsions and death was independent of body weight. There were significant interactions on the measured parameters between various combinations of altitude, OHP level, and duration of acclimatization. While alterations in the metabolism of gamma-aminobutyric acid and high-energy compounds are common to both hypoxia and hyperoxia, the most plausible explanation of the results relates to the decrease in buffer base induced by hypoxic acclimatization which might have caused CO2 potentiation of OHP symptoms.

Undersea Biomed Res. 1991 Jul;18(4):303-16.