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Chronic oxtox

3K views 34 replies 9 participants last post by  jasondrake 
#1 ·
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I've been diving nitrox for a while and read piles of bumf on oxygen toxicity, acute and chronic. Pulmonary exposure seems to be a limiting factor in deco scheduling on extreme technical dives, with various methods of calculating maximum allowable exposure over a dive, series of dives and weeks of dives. I understand that oxygen is potentially damaging to lung tissues and why. However, I had a long conversation with a doctor fried who works in the ITU in Glasgow (asked to remain nameless) who tells me that they regularly have ill patients on pure O2 (realistically 90% due to masks etc) for many days 24hrs a day. No air breaks etc. I asked if this was damaging their lungs and he said sure, a bit, but nothing to worry about and certainly nothing permanent. He laughed, as did a colleague, when I explained the diving line on chronic oxtox. Long term exposures to high F02's seem the norm in hospitals.

Any thoughts?
 
#2 ·
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In hospital they have different methods of delivering oxygen mask, nasal tube, tent etc each give different FO2 eg a nasel tube gives, IIRC, FO2 of 40% ish.

As to exposure times diving increases your susceptability to CNS toxicity for reasons not completely understood but one of which, very relevant here, is exercise level. A seriously ill patient obviously is not doing any where near the exercise level of even a relaxed diver decoing on a blob.

Divers have had tox events at 1.2 Bar (Comex diver working) yet bent divers are regularly treated at 2.8 bar with an almost zero incidence rate in pots. Though some do report "fried" lungs as an after effect from the pulmonary effect.

As for pulmonary exposure, ppO2 of 0.9 bar for 24 hours gives a UPTD count of 1100 which is well within limits even if continued for a few days [OTU of 4000 produces in 50% of people a reduction in vital capacity of 50%, plus pain. IIRC]. Again the relaxed state of the patient would increase their tolerance. The patient once taken off a mask would probably be suffering some effects from the exposure including pain and decreased breathing efficiency but as they are stuck in bed and probably on pain medication these side effects are very acceptable especially given the alternatives - seriously ill or dead.

Its possible your friends didnot realise the effect that being at pressure and underwater has on the sport and commercial diving fraternities. Toxing is often fatal underwater and is not uncommon whereas its very possible your friends wont have seen an OxTox event. Plus finishing a dive with lungs fried from pulmonary effects hurts. And for people doing this for fun or work is unacceptable.

So bottom line we have different degrees of acceptable exposure cos we are after different experiences.

Scotty

Edit: missing 0 in "OTU of 4000 produces in 50% of people a reduction in vital capacity of 5%, plus pain. IIRC" 5% -> 50%
 
#3 ·
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As it goes the effects of O2 both CNS and pulmonary are fairly well documented, in a hospital the risks of pulmonary are offset against the benifits. The one far outweighs the other.

There have been a significant number of tests done for CNS in chambers which is where the max value of 1.6 PO2 comes from. The biggest threat comes from people who have been working fairly hard at depth as the surface they think that they will be OK to raise the PO2 to 1.6 for deco, wrong, they have a high level of CO2 in there system, the body thinks I need more O2 and so increases the percentage of 02 in the system. Bang, a hit. This for me is why I set a max O2 of 1.5 on deco, and why I will never use 100% o2 on deco, I have a family I would like to see grow up.

Lastly, pulmonary, for the most part will take care of itself provided you watch your PPO2 level, and overall O2 clock during a repetative dive series. All that will happen is you will grow older quicker.

Andrew
 
#4 ·
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<font color='#0000FF'>Thoughts? yes, I've got a couple.

The first one - and I'm not having a go at you Jason, it happens a lot - is that a weekend nitrox course or two seems to mislead many people to believe they are then equipped with a broad understanding of the myriad effects of oxygen biochemistry; a subject you could study from now "until the 12th of never" and still not get to the end of it (I've been doing it for the past six years and will continue to do so far at least another 2 & 1/2 years in my current job).

My PhD topic was about oxidative-damage in biological systems,  particularly in terms of proteins (which make up the largest percentage of the dry weight of your body), so as you can imagine I've read quite a lot on the biochemical effects of oxygen, 99.99% of which you won't find in any diving related texts (I've posted a couple of oxy-facts below).

If anyone should be bored enough to be interested, I could probably do a synopsis from my thesis introduction on "the superoxide theory of oxygen toxicity". In the meantime, for anyone with a smattering of scientific knowledge (or a lot of perseverance) I can recommend leafing through "Free Radicals in Biology and Medicine" by Halliwell and Gutteridge.

Chee-az
Steve
~~~~~~~~~~~~~~~~~~~~~~~~~~~
Some Oxygen facts:

it is oxygen (in the form of oxygen free radicals or reactive oxygen speces: ROS) which has been implicated as a (or the)causitive agent in: aging, many forms of cancer, Alzheimers disease, Motor Neurone disease, muscular dystrophy, huntingdons corea, AIDS,  etc etc.....

The only reason we can exist in this 21% O2 atmosphere is that we possess numerous oxygen detoxifying systems,

Once upon a (pre-historic) time, the release of oxygen into the atmosphere wiped out over 90% of all life on earth
 
#6 ·
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I understand why my thread had no relevance to acute cns toxicity, but it's the pulmonary bit that baffles me.  I've done a bit more than the standard weekend course, and have a biology degree although obviously not as specialised as what Steve W has done. It's because I've studied (and even carried out god help me) some 'science' that I have absolutely no faith in scientific statistics, published or not.

I appreciate that the environments of a diver and a patient are wildly different and very significant. Thats kind of why I posted.I was just interested that a guy who's done 10 years of medical exams and spent 10 years administering oxygen to people, while closely observing their cardio-respiratory health, feels that fear of oxygen lung damage while diving is a joke. This guy has a profound understanding of cardiorespiratory physiology, gas physiology and  so many other ologies that I coudn't keep up. I personally prefer to follow the advice of those who 'do' over what the books say. But this time I've no idea. Mind you I've smoked so much crap over the years that my lungs are probably beyond salvage anyway.
 
#7 ·
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can I ask a question here?

AIUI CNS tox is the main cause of concern for those diving and is therefore important to manage your 'dose' over time / course of dives - Pulmonary Tox is covered in the manuals but really only for 'completeness' of info as it is not a major cause of concern for divers as it requires very long exposure times that we just don't suffer.

Or am I just plain wrong?
 
#8 ·
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A very interesting thread this......With some excellent, and very well informed posts.  I'm certainly no expert on cardiorespiratory physiology but I have done some diving...... The primary "risk" associated with high PPO2 oxygen exposure is that of oxtox.  The effect of CNS oxygen toxicity in diving is.....drowning.  An O2 hit can result in a convultion which will *drown* you.  That is the difference between hyperbaic medicine, where patients are regulrly exposed to PPO2'sof 2.8 bar or whatever, and diving, where we like to set a max ppO2 of 1.6 bar at deco and a much lower limit for the "working" portion of the dive.  You can tox in a chamber quite "safely". Tox in the water and you need a really switched on buddy team to help you out.
 
#9 ·
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This really is Steve W's field, but, my understanding, and this comes from floating about on the periphery of the field is that over the last few years it has been discovered that by subjecting the body to high PPO2's i.e. breathing O2 at pressure has led to some fairly miraculous results in certain diseases, and in the treatment of burns, there is some research currently in Cancer Research with surprising results.

O2 itself is fundimentally toxic, it is what causes us to age, but Steve W can add more to this line.

What Bob say's is correct, for diving we are concerned with CNS toxisity, this can cause a seizure and thus drowning. This being said, damage can be caused to the lung tissues due to low presures of O2 but as long as we are aware of this and pay it respect we can ignore it for diving.

Andrew
 
#10 ·
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On a slightly different note, does steve w or anyone else know if any studies have been done on the in interaction of acute cns oxtox and nitrogen narcosis. Nitrogen at high pp obviously has  a 'soporific' effect on the nervous system, and high oxygen pp seems to have kind of the opposite. (twitchy lips and spasms etc) I'm sure the areas of biochemical effect are probably different and complex but could one counteract the other? For intance at 70metres on air could the high levels of nitrogen delay the onset of acute cns? I'm not suggecting anyone tries this but has anyone ever had an O2 hit while diving deep on air?
 
#12 ·
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So if no-one has ever had a deep air cns hit and lived, and there's no way that a pathologist could tell if a cns hit occurred from looking at a soggy corpse, then do we know if it's ever happened?

( a bit like when diving death stats. say someone had a heart attack at depth and drowned. I understand, again from this mystery doctor mate, that there is no way to tell at all if someone had a heart attack prior to death after they are dead. The heart damage etc. from normal post-mortem decay looks the same as that from the attack. So where do the stats. come from or does the examiner just fill in the blanks with the most likely cause. And if so then what value are incident report statistics?. Sorry, bit of a tangential rant there.)

I feel you'r dismissal of any relationship between inert gas narc. and cns oxtox is a bit hasty. I've never read anything (and I've looked) or spoken to anybody who can adequately explain the mechanism of either. Narcosis, like anaesthesia and sleep, are an almost complete mystery to medical science. They can produce measurable, repeatable effects from known causes but can't fill in the bit in the middle. And cns oxtox understanding seems little better. I agree it's probable that they are acting independantly but I'm interested if anyone's ever tested it. For instance morphine and amphetamines act in different ways on different bits of your biochemistry but they sure as hell have an impact on each other, producing a combined not an independant overall effect.
 
#13 ·
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I have spent about the last 7 months studying this, go away and learn some more, there is no relationship between O2 CNS and Nitrogen narcosis (I have not mentioned in any way other gasses than nitrogen), when you get a report that a diver was seen to convulse and sink, then it turns out he has drowned then one can fairly safely assume he took a CNS hit which caused the convulsion. Whatever, it is a tragic way to go, and we have the information and tools to minimise the risk as much as possible.

As for actual research, then yes there has been research, this is in the field of hyperbaric medicine, and the possibilities of keeping patients at high PPO2's in a chamber, but this is not directly for diving, we are just getting the benefit of research done. I have people I know who use the systems I sell doing just this research. Belive me, when I go as far as to state something then as far as the information I have, which has to be reasonable for me to go that far, I am making a correct statement. Argue with me by all means, but do not tell me I dismiss something out of hand.

If you want information on the research done, e-mail me offline and I will forward to you the links to the relevant papers.

Andrew
 
#14 ·
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Just re-read this thread, I was getting a bit "ranty" - sorry

Matt

GI3 obviously does not have children, anybody trying to hold a 6M stop in the channel will know that on a bad day this is not always that easy. On top of which, the reality is the washout rate varies little from 80 to 100% O2. Added to which if I dive on a wreck at 60M I want to have a while to take a look around, to do this you need to track you O2 clock if  deco on 100% O2 at 6M my clock would be running like a bast**d I would rather spend a few more minutes on deco. Depending on which software you look at, the time between 80 and 100% for a 60M dive for 30 minutes is 4 minutes where as the CNS percentage goes from 44% to 79%.

For those who want to check, this is 18/30 bottom mix, 50% from 21M and 80 or 100% at 6M 30 minute bottom time, and including deep stops.

Andrew
 
#15 ·
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[b said:
Quote[/b] ]GI3 obviously does not have children
Wrong

[b said:
Quote[/b] ]anybody trying to hold a 6M stop in the channel will know that on a bad day this is not always that easy.
wrong

[b said:
Quote[/b] ]On top of which, the reality is the washout rate varies little from 80 to 100% O2
Wrong

[b said:
Quote[/b] ]Added to which if I dive on a wreck at 60M I want to have a while to take a look around, to do this you need to track you O2 clock if  deco on 100% O2 at 6M my clock would be running like a bast**d I would rather spend a few more minutes on deco.
Wrong

[b said:
Quote[/b] ] Depending on which software you look at, the time between 80 and 100% for a 60M dive for 30 minutes is 4 minutes where as the CNS percentage goes from 44% to 79%.
GIGO [Garbage In Garbage Out]

Scotty
 
#16 ·
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Bored,,,,,

Actually, I am curious, please let me know the information on the washout rate arguament, also how can it be wrong to want to take a look around, also, I deliberatly used DecoPlanner, this is off the GUE web site, the home of DIR, so it kind of negates your garbage in garbage out arguament doesn,t it. Lastly, if you deco on 100% at 6M you have around 45 mins before your CNS O2 levels are said to have reached 100%, OK on the profile I posted it reached a max of 79% including the bottom time, if I used 80% it was half that for 4 mins extra in the water, plus I have a safety margin in terms of holding the stop. Again, explain your reasons for telling me I am wrong,

Please do not just attack me, prove me wrong, that way I can learn something, along with everybody else who reads this thread, I admit I went off on a bit of a rant, and I have appologised for that.

Andrew
 
#17 ·
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[b said:
Quote[/b] ] I deliberatly used DecoPlanner, this is off the GUE web site, the home of DIR, so it kind of negates your garbage in garbage out arguament doesn,t it
All Deco planner is is a pretty UI wrapped around a ZH 16 deco model, with a deep stop algorithem as an extra so why do you expect it to produce results based on a different deco model?

[b said:
Quote[/b] ]Lastly, if you deco on 100% at 6M you have around 45 mins before your CNS O2 levels are said to have reached 100%
The CNS clock is an inaccurate measure to control a divers exposure to  the risk of a tox event. There have been many dives done all over the world with CNS clocks in the 1000s some now in the 10,000s. There are well proven methods for minimising the risk that exposure to ppO2 > 1.2 incurs.

Scotty
 
#18 ·
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The CNS clock is an inaccurate measure to control a divers exposure........There are well proven methods for minimising the risk that exposure to ppO2 > 1.2 incurs.

Tell me about them? (not trying to be inflammatory, genuinely interested) I thought the ox clock was developed by NOAA/DAN/NASA type people and seems to be accepted by IANTD/TDI.
 
#19 ·
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There's nothing fancy about controlling your OxTox risk. Breaking to the lowest FO2 available every so often is all that is generally required. How to schedule the breaks is based on how long the oxygen deco will be. If its less than 20 minutes then generally no break required. If its longer then add a 5 minute break in the middle, as it gets even longer then the advice is to use a 12 minute on 6 minute off approach. Note time off oxygen is still counted as part of the deco time in this approach.

Some general points that go with the above approach:
Keep the ppO2 low during the bottom time < 1.4 down. Consider taking a gas break on the stop preceding a switch to a higher FO2 eg if decoing on EAN50 then consider using your back gas on the 9m stop. Physical fitness may be a component of why this method is succesfully used by some. As is the use of high FHe mixes. Some advocate the use of anti oxidents such as Vitamin E

Scotty
 
#20 ·
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While I've got all the enthusiastic and educated minds on a thread, a few more thoughts.
Oxygen Window:  Stop me when I start talking shite. I understand that the higher the ppO2 the larger the window and the greater the off-gassing advantage will be. Pure O2 at 6 metres opens the biggest window, beecause a ppO2 of 1.6 at greater depth using a 'mixed gas' will occupy part of the window with (possibly ongassing) inert gas pp. So pure O2 produces the largest outward gradient while allowing no inert gas back into the blood. So at what point does the vasocontricting effects of high ppO2s start to negate the effects of this big window? Do air breaks reverse this effect and how quickly? Does the ppO2 damage to lung tissue significantly impact on gas exchange during 'normal' dive exposure?

Isobaric Counterdiffusion: What relevance does this have to switching from a trimix to a nitrox during deco? I understand that the N2 can ongass faster than the He will offgass, causing tissue supersaturation. What does this mean in practical terms? Do any divers support the idea of using an intermediate trimix for mid-depth deco before switching to nitrox shallower?

(When will it all stop? I just wanted to see some fishes and now I'm getting excited about physics on a sunny Sunday.) A cheery quote to make me feel better :

"It is important that students bring a certain ragamuffin, barefoot, irreverence to their studies; they are not here to worship what is known, but to question it."
 
#21 ·
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[b said:
Quote[/b] ]So at what point does the vasocontricting effects of high ppO2s start to negate the effects of this big window? Do air breaks reverse this effect and how quickly? Does the ppO2 damage to lung tissue significantly impact on gas exchange during 'normal' dive exposure?
The tissues of the lung react within minutes of exposure to high ppO2's. The 12/6 regime is said to be about the most efficient use of gas by maximising off gassing via diffusion methods and limiting the changes it causes, which it is suggested, can have a negative impact on off gassing via diffusion or perfusion methods.

[b said:
Quote[/b] ]Isobaric Counterdiffusion: What relevance does this have to switching from a trimix to a nitrox during deco?
Bugger all in normal diving

[b said:
Quote[/b] ]Do any divers support the idea of using an intermediate trimix for mid-depth deco before switching to nitrox shallower?
Lots do this for deco reasons on deep dives 80m+ where they might be using 3 deco gases. Some add He to all their deco gases except 100% cos experience is suggesting that it helps with deco. Though at present this is suggested to be of real benefit for very deep and/or dives close to saturation levels.

Scotty
 
#22 ·
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[b said:
Quote[/b] (Mark Scott-Simons @ April 24 2003,15:27)]Divers have had tox events at 1.2 Bar (Comex diver working) yet bent divers are regularly treated at 2.8 bar with an almost zero incidence rate in pots.
Agree with your sentiments Scotty, but on double extensions we get 85% + patients with symptoms of oxygen toxicity in the pot.
 
#24 ·
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<font color='#0000FF'>Blimey, this thread is all over the place, but going back to Jason's earlier point about CNS ox tox hit and N2 narcosis, my understanding (have no data at this point)  is that the increased O2 concentration won't counteract the N2 effects due to their different diffusion constants.

Also, given that the level of oxygen toxicity is not 'set in stone' (1.4 or 1.6 for recreational diving, around 2.0 for Navy divers)  I don't believe it is quite as much of a threat as narcosis which can cause death with or without an O2 hit, primarily via interference with transmission of neuronal signals i.e. it will eventually stop them, extract from a diving doctor web site, my comments in parentheses:
"N2 is generally incapacitating (ie paralysing !) at about 10 bar (90M, ppN2 = approx 7.8), where it produces an anesthetic effect resembling that of 30% nitrous oxide at sea level". compare that to ppO2 in air at 90M = 2.09 approx, which Navy divers are expected to cope with.  see here for a handy pdf file

I think most nitrox divers will probably already have been taught that this is due to N2 in the fatty tissues (myelin sheath) which insulates the nerve/neuron, correct functioning of this insulation is essential for nerve impulses to propagate. see here for info on neuronal signals and how they work

Going back to my earlier post I just wanted to point out that O2 may be wonderful for deco or in your EAN mix, but I was concerned that there was a bit of misunderstanding creeping in about the seriousness of oxygen's general effects on your body (ie in the style of Michael Jackson).

Chee-az
Steve

BTW, there have been some interesting experiments on longevity, several studies have shown that animals live longer when their cellular respiration is restricted (ie reduced mitochondrial activity) this is believed to be because of the natural production of oxygen free radicals by the mitochondria during normal activities. The down side of this is that reduced cellular respiration was achieved by a very very  low calorie diet: eat less - live longer...  

bah! gimme curry and death !
 
#25 ·
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The light that burns twice as bright....

Think I might have read about that. Didn't a mouse (or some expendible mammal) which got restricted food intake, lower than that thought to be necessary,  live longer than the one with all the pies? I'm sure some prof. who did it started starving himself to test it on humans. Would make sense. Critters with very slow metabolisms tend to be longer lived. eg turtle vs mouse. But the downside is you can't break any landspeed records while your alive.

Despite all the evidence to the contrary, some perverted part of me still believes somewhere that narcosis should suppress acute oxtox. Just coz.
I might get some mice and build a mini-pot. Will post results.
 
#26 ·
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<font color='#0000FF'>Papers I've read regarding "caloric restriction & increased life span" have studied: yeast species, several different species of flies, mice, rats , gerbils, and primates so it's pretty widespread.
Limiting calorie intake has also been shown to reduce one of the intracellular biomarkers of aging, (protein carbonyls)whilst excess calories increased them, a little playing with the title and results of the paper means you could (in a Mary Poppins sty-lee) call this "Oh....Supra-calorific-carbonyl-manipulation ...."
 I was a bit "four-parts-susan" the day I shoehorned that description into one of my reports

Steve

PS Don't forget to apply for a Home Office licence for your intended study  
 
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