Oxygen solubility and half times

[padiscubapro]

Originally posted by DivingDoc
The basis for my thinking there was some lifetime exposure limit was that I have a friend whose financee has had horrendous disfiguring mouth and jaw surgery due to squamous cell CA. 2/3 of her jaw and part of her tongue was removed. After a bone graft implant, she developed a wound infection requiring removal of the graft. She had had previous radiation therapy, which was thought to contribute to the poor wound healing and infection.

When I suggested they might consider HOT, my friend told me that she had had some previously and was told she had reached the limit and couldn't have any more.

I accepted this, since at the time, she was being treated by Dr. Marx in Miami, an oral maxillofacial surgeon who has written many of the protocols for HOT.

Anyway -- are you aware of any possibility of pulmonary oxygen toxicity that could be incurred by diving Nitrox 2-3 dives per day for a week, staying within suggested limits on computer?

Elaine

I am not aware of any problems even someone exceding NOAA daily limits.. I am a RB diver and do most of my dives at a PO2 of 1.3 and my decos at 1.6.. on average I get 5 - 6 hours diving a day for my entire trip (it would be quite difficult for an OC diver to get theses exposures).. This exceeds NOAA limits considerably and I have never noticed any symptoms.. If any, the effects of very high PO2s (my 1.6 decos) seem to be less as the week goes on.. On the first day or 2 of diving when I am decoing on 100% I get the normal "snotty" type congestion as the week progresses it gets less and less.. I am not recommending anyone break noaa limits its just my personal observations... My last trip I did 10 straight days with depths to 210 which followed only a 1 day break for flying where I previously had 6 consecutive diving days down to 300..

 

[DivingDoc]

Originally posted by Dr Deco
Dear DivingDoc:

I must admit that I am at a loss to explain why Dr Marx eliminated retreatment. I am only aware of the possibility that fibrotic tissue could be forming in the lungs. This would be indicated by pulmonary function tests.

I do not have any figures or info on Nitrox diving, but I have not heard of any problems with that mix for the time limits mentioned. [Pure oxygen for decompression is entirely another matter.]

Dr Deco
:doctor:

OK, here's the reason for my asking all my questions: Last week, I went on a SCUBA diving trip with my husband and son. We did a total on 12 dives, not counting one shore dive, over a period of 7 days, taking the 5th and 7th days off (the 5th for relaxing and off-gassing and sightseeing and the 7th for no-fly time). Most days, the first morning dive was deeper (6-100 feet) and the second dive was shallower (45-60 feet). On two evenings, we did shallow night dives. We were doing our Nitrox certification and after the 2nd day, when we first tried the Nitrox, we felt so well that we used Nitrox for every dive after that ( EANx32 for first dive and EANx36 for second morning dives and for night dives).

I have a history of asthma, but am very well controlled and usually do not get exercise induced bronchospasm as long as I take my regular preventer medsa (Advair 250/50), even when exercising in air conditioned air and without bronchodilator pretreatment.

For a week prior to the trip, I augmented my regular medication to Advair 500/50, just in order to have bullet-proof control, and I felt great, with inspired air going deep down into the last recesses on a deep breath and no hint of any delay or tightness on forced expiration.

On the dives, I felt great -- if anything, breathing even more freely at depth than at the surface. However, after the 2nd dive on the 4th day, I felt somewhat short of breath. It did not feel like asthma -- more like a decrease in pulmonary compliance. There was no associated wheezing or choughing, and no response to bronchodilator. My upper airways felt a bit irritated -- a burning feeling. I wondered if swimming head down on my descent and to sneak up on fish lying under coral ridges had something to do with it, as I do have a history of mild GERD.

Anyway, I took the next day off diving (which was scheduled as a free day anyway), lay by the pool and read a book. Gradually, the symptoms subsided and I was fine the next morning. I did 5 more dives (2 each morning and another night dive), all using Nitrox as above. Again, at depth, I felt like I was breathing especially well. But after the last dive, I again had the same sensation of being SOB.

After coming home, I went to the office on Thursday (having flown back on Wed) and while there, checked my O2 sat with an oximeter. It was 94-97% on room air. I have continued to improve over the 5 days I've been back, even though I returned to my usual dose of Advair at 250/50. Yesterday, I again checked my O2 sat and it was 95-97% on RA. My Peak Flow today was 450 (my personal best is around 475).

Do you have any explanation for this phenomenon? I was wondering whether asthmatics might be more sensitive to the irritant effects of hyperbaric O2 or what?

 

[DivingDoc]

Originally posted by padiscubapro


I am not aware of any problems even someone exceding NOAA daily limits.. I am a RB diver and do most of my dives at a PO2 of 1.3 and my decos at 1.6.. on average I get 5 - 6 hours diving a day for my entire trip (it would be quite difficult for an OC diver to get theses exposures).. This exceeds NOAA limits considerably and I have never noticed any symptoms.. If any, the effects of very high PO2s (my 1.6 decos) seem to be less as the week goes on.. On the first day or 2 of diving when I am decoing on 100% I get the normal "snotty" type congestion as the week progresses it gets less and less.. I am not recommending anyone break noaa limits its just my personal observations... My last trip I did 10 straight days with depths to 210 which followed only a 1 day break for flying where I previously had 6 consecutive diving days down to 300..

Interesting. But I am unfamiliar with some of your acronyms. What is an "RB diver" .... an "OC diver"?

You don't use Nitrox at those depths, do you? More likely Trimix?

ET

 

[The Iceni]

Diving Doc,

The article you quote is a very good attempt to account for both types of oxygen toxicity in practice.

I believe it is generally accepted that pulmonary or whole body oxygen toxicity is exposure dependent and reasonably predictable from individual to individual and over time with the same individual. Advanced deco computers, such as the HS Explorer, include calculations for it. The same, however, cannot be said about CNS Oxygen toxicity, which is highly variable. Indeed the British Royal Navy long ago abandoned any attempts to screen out susceptible subjects in their diver-training programme.

To quote from the article

“The NOAA limits for CNS oxygen toxicity (normal, single exposure) are plotted in Figure 2. These limits are based on research by Drs. F.K.Butler and Edward D. Thalmann, U.S. Navy Experimental Diving Unit, and by Drs. Christian J. Lambertsen and Russell E. Peterson, Institute for Environmental Medicine, University of Pennsylvania. These limits take operational safety into consideration and have been widely adopted by the technical diving community.”

Indeed the NOAA limits appear to be accepted by many, but these limits are now frequently ignored by British amateur technical divers. Many more like myself and Mr Padiscubapro question the usefulness of these figures simply because sensitivity to CNS oxtox is so variable. My worry is that the actual cause of CNS oxtox has not been firmly established and there is considerable ignorance of the subject generally. Oxygen is still the "devil gas".

My hypothesis, as stated in my earlier posts, is that carbon dioxide (i.e. acidity) AND high oxygen partial pressures together within the brain are the culprits and and the variability is seen only when the Hb of the local VENOUS blood is close to saturation. If the research conducted by Butler et al. was based in chambers, and their divers were not exercising to produce excess carbon dioxide it is hard legitimately to extrapolate their findings to exercising submerged divers on bichemical grounds alone.

You asked what OC and RB meant;- Open circuit scuba and closed circuit or rebreather equipment.

As for the use of Trimix as opposed to Nitrox, it seems to me not to matter a jot. What matters is the pp O2. In the case or CC it is always close to the set point on the dive (e.g. 1.3 bar) and may exceed 1.6 bar during spikes. In OC it depends on mix and depth alone, peaking only at the deepest part of the dive or during accelerated decompression. Therefore in CC oxygen exposure is usually greater.

As you report, most feel less fatigued on Nitrox. I most certainly do.

I was interested to learn of your symptoms of breathlessness. It is a shame you were not able to record your PEFR or pulse oximetry during your vacation pre and post dive. I suspect the flight home would have affected these somewhat. However, as you must know, regardless of the fact that you do not suffer from symptomatic exercise or cold-induced asthma, as an asthmatic your airways are more sensitive to ANY assault. The dryness of the gas mix being one of many.

You most certainly did not reach anything like the accepted limits for pulmonary oxygen toxicity in normal healthy subjects so I postulate that your sympoms were more likely to be due to bronchospasm than fibrosis, but who knows? Does you treatment include an inhaled steroid? I am not familiar with the US names but suggest an inhaled steroid could be helpful in future.

As ever, this article is for discussion purposes only and is not a recommendation for the treatment of any individual.

 

[DivingDoc]

Originally posted by Dr Paul Thomas
Diving Doc,

Indeed the NOAA limits appear to be accepted by many, but these limits are now frequently ignored by British amateur technical divers. Many more like myself and Mr Padiscubapro question the usefulness of these figures simply because sensitivity to CNS oxtox is so variable. My worry is that the actual cause of CNS oxtox has not been firmly established and there is considerable ignorance of the subject generally. Oxygen is still the "devil gas".

Many, as you know, attribute O2 toxicity to the generation of superoxide radicals. Perhaps the individual's internal supply of antioxidants has to do with susceptability to O2 toxicity. Even the PADI Nitrox course manual suggests that vitamin E may be somewhat protective, presumbly due to it's antioxidant status and lipophilicity (therefore, it's ability to cross the blood-brain barrier). Admitedly, this is based on scant evidence. The following article may be relevant:

Aviat Space Environ Med 1998 May;69(5):480-5

Use of cytochrome-P450 mono-oxygenase 2 E1 isozyme inhibitors to delay seizures
caused by central nervous system oxygen toxicity.

Whelan HT, Bajic DM, Karlovits SM, Houle JM, Kindwall EP.

Dept. of Neurology, Medical College of Wisconsin, Milwaukee 53226, USA.

BACKGROUND: The neuronal origins and mechanisms of central nervous system oxygen
toxicity are only partly understood. Oxygen free radicals are felt to play a
major role in the production of CNS oxygen toxicity because of the interactions
of free radicals with plasma membranes producing lipid peroxidation. The
cytochrome P-450 monooxygenase system IIE1 isozyme is important in the brain.
This led to trials of P450 monooxygense inhibitors for prevention of oxygen
toxicity. Diethyldithiocarbonate (DDC) proved to be the most promising agent in
this class; 21-aminosteroid lazeroid compounds have been successful in
experimentally limiting pulmonary oxygen toxicity. This led to our trying to
prevent neuronal oxygen toxicity by the use of 21-aminosteroid and six other
drugs during hyperoxia. METHODS: In our experiments, mice were placed in an
oxygen-filled hyperbaric chamber in paired experiments. One pre-treated mouse
and one control mouse were exposed simultaneously to assess the efficacy of
drugs in preventing seizures caused by hyperbaric oxygen at 5.1 atmospheres
absolute. Time to seizure was observed through a port hole in the hull of the
hyperbaric chamber. RESULTS: DDC, 21-aminosteroid and propranolol produced
significant delays in the onset of seizures (p < 0.001) with no observable side
effects; 1-aminobenzotriazole and disulfiram produced much shorter delays in the
onset of seizures caused by hyperbaric oxygen and also had unacceptable side
effects.

PMID: 9591618 [PubMed - indexed for MEDLINE]

My hypothesis, as stated in my earlier posts, is that carbon dioxide (i.e. acidity) AND high oxygen partial pressures together within the brain are the culprits and and the variability is seen only when the Hb of the local VENOUS blood is close to saturation. If the research conducted by Butler et al. was based in chambers, and their divers were not exercising to produce excess carbon dioxide it is hard legitimately to extrapolate their findings to exercising submerged divers on bichemical grounds alone.

I've heard you state this before, and also read that divers who retain CO2 are more likely to suffer from O2 Tox, but am unclear on the possible mechanisms.

You asked what OC and RB meant;- Open circuit scuba and closed circuit or rebreather equipment.

Thanks -- I'm still a pretty novice diver, having just got my AOW and my Nitrox certifications -- only 21 dives under my belt so far.

As for the use of Trimix as opposed to Nitrox, it seems to me not to matter a jot. What matters is the pp O2.

It may not matter with respect to O2 toxicity, if the same fiO2 were used, but you are going to be pretty narked at 240 fsw if you use a high percentage of Nitrogen, and even air with 21% O2 would produce a pO2 in inspired air of over 1.7 at that depth-- beyond safe limits. Therefore, I should think that in general, some sort of trimix with <21% O2 and part of the Nitrogen replaced by Helium would be safer at that depth.

As you report, most feel less fatigued on Nitrox. I most certainly do.

Yes -- invigorated, even.

I was interested to learn of your symptoms of breathlessness. It is a shame you were not able to record your PEFR or pulse oximetry during your vacation pre and post dive. I suspect the flight home would have affected these somewhat

However, as you must know, regardless of the fact that you do not suffer from symptomatic exercise or cold-induced asthma, as an asthmatic your airways are more sensitive to ANY assault. The dryness of the gas mix being one of many.

Agreed, but though there are many theoretical problems associated with asthma and diving, the increased mobidity in asthmatic divers has not been borne out by empirical data. See the following links:

http://thoracic.org/chapters/state/california/adobe/asthma.pdf

http://www.ymcascuba.org/ymcascub/asthmatc.html

You most certainly did not reach anything like the accepted limits for pulmonary oxygen toxicity in normal healthy subjects so I postulate that your sympoms were more likely to be due to bronchospasm than fibrosis, but who knows? Does you treatment include an inhaled steroid? I am not familiar with the US names but suggest an inhaled steroid could be helpful in future.

Advair 500/50 consists of 500 mcg of fluticasone (a potent inhaled corticosteroid) and 50 mcg of salmeterol per inhalation. It's made by Glaxo -- don't know what it's called in England. Believe me, I know how to manage asthma -- I am an MD and board certified in both Internal Medicine and Allergy and Clinical Immunology. Half my practice for the last 20 years has been treating asthma.

But I wasn't postulating fibrosis, as that is not reversible. Clearly, whatever was causing my dyspnea was reversible. However, as I said, it did not "feel" like asthma and did not respond to bronchodilators. When I checked an oximetry, I was still feeling somewhat dyspneic, yet my O2 sat was OK. It simply felt like my lungs were "stiffer" -- no apparent obstruction to air flow. Interstitial edema? -- that should have caused some hypoxia unless it was mild.

All this is pure speculation, but I wish I knew what happened and whether it was related to the Nitrox or not.

I've attached some related abstracts.

 

[The Iceni]

Hi again Diving Doc,

Many, as you know, attribute O2 toxicity to the generation of superoxide radicals. Perhaps the individual's internal supply of antioxidants has to do with susceptability to O2 toxicity. Even the PADI Nitrox course manual suggests that vitamin E may be somewhat protective, presumbly due to it's antioxidant status and lipophilicity (therefore, it's ability to cross the blood-brain barrier).

Admitedly, this is based on scant evidence.

. . . RESULTS: DDC, 21-aminosteroid and propranolol produced
significant delays in the onset of seizures (p < 0.001) with no observable side effects;

21 aminosteroid - anti-inflammatory?

As for viatmin E. It has now been shown to be less protective than aspirin in the prevention of thrombosis. As you confirm, convincing evidence is sadly lacking.

I've heard you state this before, and also read that divers who retain CO2 are more likely to suffer from O2 Tox, but am unclear on the possible mechanisms.

I have offerd to send you my thinking. I am not making a statement I am speculating on the basis of known biochemistry! Send me an email; paul@gippingvalleypractice.co.uk and and I'll explain.

--------------------------------------------------------------------------------
As for the use of Trimix as opposed to Nitrox, it seems to me not to matter a jot. What matters is the pp O2.
--------------------------------------------------------------------------------
It may not matter with respect to O2 toxicity,

I thought that was what we were discussing, Elaine.

Advair 500/50 consists of 500 mcg of fluticasone (a potent inhaled corticosteroid) and 50 mcg of salmeterol per inhalation. It's made by Glaxo -- don't know what it's called in England. Believe me, I know how to manage asthma -- I am an MD and board certified in both Internal Medicine and Allergy and Clinical Immunology. Half my practice for the last 20 years has been treating asthma.

Apologies. Sorry if you think I was "teaching my granny to suck eggs". My comments were posted for the benefit of the non-medical reader.

Interstitial edema? -- that should have caused some hypoxia unless it was mild.

I can accept that - oxygen as an irritant will cause cell membrane damage, whether superoxide, free radicals or H+. I believe oedema is the initial, reversible, stage of tissue inflammation - as with asthma, fibrosis being the irreversible longer term complication in pulmonary toxicity.

All this is pure speculation, but I wish I knew what happened and whether it was related to the Nitrox or not.

I suppose a questionnaire study of asthamatc Nitrox divers is indicated.

I am glad someone is looking into the biochemical mechanisms of CNS oxtox and research is being done. I am no longer a researcher - no money in it!

 

[padiscubapro]

Originally posted by DivingDoc


Interesting. But I am unfamiliar with some of your acronyms. What is an "RB diver" .... an "OC diver"?

You don't use Nitrox at those depths, do you? More likely Trimix?

ET

The inert gas doesn't make a difference.. Its just that inert.. its the PP of O2 thats important..

I generally don't exceed NOAA single exposure limits unless I am doing real long decos on 100% o2 (then I take "air" breaks), but usually exceed daily limits..

an "oc diver" is open circuit /conventional scuba
a "rb diver" is a rebreather diver.. There are 2 types semi sclosed aka SCR and closed circuit aka CCR

I use a CCR which maintains a set PO2 which does not vary with depth.. so If I have my PO2 set for 1.3 its maintained at all depths where an OC diver and SCR diver the PO2 will vary at depth and only be the max when deepest, so O2 exposure is considerably less.

The dives to 210 were done with air as diluent (with a setpoint of 1.3 my nitrogen loading is higher than an OC diver)... no He available, the previous dives to 300 were done on trimix...

I also load up on antioxidents myself, vitamin E and C especially.. I figure it can't hurt...