Lung irritation - PO2 vs. FO2

[Atticus]

I apologize if this has been asked before; a brief search did not turn anything up.

My diving buddy believes that lung irritation is as much a function as FO2 as it is PO2. I don't understand his logic, and wanted to ask the diving doctors to a straight answer.

My buddy is taking an EMT course and is using the statement that a patient (out of the water) will experience lung irritation breathing 100% O2 as the basis for his argument.

It seems to me that everything I've read points to PO2 and time exposure as being the source of lung irritation. I don't understand how the presence of other inert gasses can benefit the lungs.

Can someone straighten this out for us please?

 

[dlegros]

FO2 is the fraction (percentage) of oxygen, so at 1bar, room air, FO2 = 0.21

ppO2 = FO2 x Absolute Pressure, so for the above conditions, ppO2 = 0.21 x 1 = 0.21bar.

Pulmonary oxygen toxicity occurs when ppO2 >360mmHg (0.48bar) for at least 6 hours.

So you would need to breath FO2 0.5 at 1bar, FO2 0.25 at 2bar etc.

So your buddy is correct in stating that it is dependant on both.

I hope this makes sense as it is 1am nearly, all my patients are asleep and I would like to be asleep as well

HTH

Dom

 

[Atticus]

To restate the question -

My buddy is under the impression that breathing 100% at 20' is more harmful than breathing 80% at 33', even though the partial pressures are (rougly) the same. His argument is that the presence of inert gasses in the breathing mix (ie: lower fraction of O2) somehow protects the lungs.

What I have read indiciates that pulmonary affects are the result of the partial pressure of O2 (ata * fo2) and time. This is as written in just about every nitrox training manual.

 

[dlegros]

Sorry if I misunderstood you before, my brain is always a little sluggish on nights!

I would agree with you that the relative concentration of inert gases should have no bearings.

The evidence on pulmonary ox-tox seems to point towards the role of high ppO2 causing free-redical formation and I can't see what effect inerts could have on this process.

Hopefully Dr Deco will have some good info for us

Dom

 

[billboardbob200]

My understanding is that breathing high FiO2 oxygen (100%)causes similar problems as breathing high ppO2 oxygen say 30% @ 1.3 atmos. the principle as I believe some on stated is the formation of a super oxide where the oxygen takes on a negative charge and combines with water to produce hydrogen peroxide (H-O-O-H) which dissociates to produce 2 OH radicals the active ingredient in drain cleaner an hence the damage. I attach a link for more info


http://members.tripod.com/tjaartdb0/html/oxygen_toxicity.html


Hope this helps

 

[Atticus]

Thanks for the replies. I appreciate the information, and this is inline with what I have come to believe as well. I don't know that anything will convince my buddy; he says "well, those are just theories...".

*Sigh*

 

[Dr Deco]

Dear dlegros:

Nitrogen and Pulmonary Oxygen Toxicity

If one reads the current Bennett and Elliott book, one would derive the impression that there is no effect of dilution on pulmonary toxicity. Little is said.

There does appear to be some effect of inert gases when rats or mice are used as the subjects. This can only be noted if the duration of exposure is long. It is possible that the effect and duration already brings them into the realm of permanent, irreversible pulmonary fibrosis.

One of the first to raise this question was an assistant of mine when I was at Ocean Systems in New York. Peter Belizi asked about the effect of the addition of nitrogen. Arterial gas sampling (arterial oxygen), lung weights (edema) and histological examination all indicated that nitrogen was protective, in rats, anyway. The rats were taken to the point where they were close to death, but the ones in nitrogen-oxygen did better than those in oxygen also. The partial pressure of oxygen was kept constant.

This was repeated using only air and pure oxygen and lifetimes of the mice were measured. This is shown in the attachment. One needs to enlarge this to view it better. Again, the partial pressure of oxygen is a constant, but the oxygen is diluted in some cases.

The study was repeated using other inert gas diluents and the same prolongation of life was found.

Therefore, for relatively short durations, the effect of dilution is not observable. If the administration is kept up (on rats and mice anyway), dilution will postpone problems.

Dr Deco :doctor:

References :book2:
1. PJ. Belizi and MR Powell. Amelioration of chronic pulmonary oxygen toxicity by inert gas dilution. 48th Annual Meeting, Aerospace Medical Association, Las Vegas, (1977).
2. MR Powell and MP Spencer. The Pathophysiology of Decompression Sickness and Doppler-detectable Gas Bubbles. Final Technical Report, O.N.R., Contract #N00014-73-C-0094, (1980).
3. MR Powell, HD Fust. The Influence of Inert Gas Concentration on Pulmonary Oxygen Toxicity. In: Proceedings, VII Symposium on Underwater Physiology, Undersea Medical Society, Bethesda, MD, (1980).

 

[Atticus]

This is exactly what we were looking for. I don't think it has resolved our difference of opinions, but it's real data that we can talk about instead of just conjecture.

Dr. Powell - I'd just like to say thank you for all the time and energy you put into answering our questions on SB.

 

[dlegros]

Atticus once bubbled...
Dr. Powell - I'd just like to say thank you for all the time and energy you put into answering our questions on SB.

Here here!

Thank you for the info, I'll have to have a look in our main library when I'm back on days.

The information I posted came out of our "collection" of journal articles (About 20 filing cabinets of toxicology articles and letters).

The Ox-tox file only had about 5 articles in it so thanks for the further references.

Any ideas on the protective mechanism provided by nitrogen?

Thanks again

Dom

 

[Dr Deco]

Mechanism - - -

It is independent of the type of inert gas, and the effect is probably physical.

It has been proposed that it delays what is known as absortion atelectasis. This is the collapse of an alveolus because the oxygen is utilized by metabolism.

Dr Deco
:doctor: