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Ok, Doc(s), here's another one for ya. What's the latest on the subject of O2 narcosis?
The last I heard, a few years ago, there was significant division in both the diving community and the scientific community over this. Disputes included everything from defining narcosis to how it is physically affecting you and whether it is relavant to sport divers and even technical divers.
I gave up on it. The most I got out of it was that it sounded like O2 narcosis does exist, their not exactly sure why, and it's not relavant to PPO2's less than 1.6 (therefore not to divers). I don't know if this is right or not, but I've seen doctors and divers quible and argue on both sides of the subject.
I'll try to dig some stuff up I had so I can ask some decent questions.
Have at it!
PS. Here's an article by Dr. David Sawatzki where he argues against O2 narcosis, or at least the lack of scientific data on the subject. It appears as though it was written in Dec. 1996, so it could be out of date.
I cannot place where I saw it but I saw a chart that listed the
"narcotic potential" (based on solubility in some specific solution) of various gases. Oxygen was listed closely to Nitrogen with others, such as Argon, Helium, Hydrogen, and Krypton or Neon
occupying various positions on the list. I also recall reading
somewhere that one of the difficulties of testing its narcotic effect is that O2 becomes toxic at certain levels (as we all know).
I'm going to post some of the stuff I have about 02 narcosis for everyone to look at. This will be most of what I've collected, and I'm sure it will be quite long. I will try to simply put the web pages if I can, but for some of this, I've lost the web pages so I just pasted it here.
Like I said, I had given up trying to figure out what the truth was as there seemed to be contradictory evidence on both sides. I suppose someone with a better medical vocabulary and understanding than I would have a mucho better chance of figuring it all out.
Excerpt from Eddie Brian.....
Narcotic Properties of Oxygen
Based on study of animals and humans, oxygen is a narcotic gas. Based on lipid solubility, oxygen should be twice as narcotic as nitrogen, as oxygen is twice as soluble (see table). However, as several individuals have pointed out, the increase in tissue partial pressure of oxygen is limited as the oxygen is metabolized. This means that for any given increase in the inspired partial pressure of oxygen, the change in tissue partial pressure is less.
Study of the narcotic properties of oxygen is limited by oxygen seizures; so study of oxygen narcosis in humans have been limited to lower partial pressures where "narcosis" is more subtle and difficult to test for. In animals, treatment to suppress seizures allows exposure to very high PO2's, and exposure to 11 ATA O2 produces anaesthesia in mice.
1. In humans, testing for psychomotor performance indicates that 1.65 ATA O2 is about equal to 6.3 ATA N2 in narcotic effect.
2. Measurements of change in brain PO2 under hyperbaric conditions are limited in number, and also limited to animal studies. In animals, exposure to 2.34 ATA O2 produced a brain PO2 of 291 mmHg (1 ATA = 760 mmHg)
3. Assuming a normal partial pressure of CO2 of 40 mmHg, alveolar PO2 would be 1738 mmHg, so the ratio between alveolar and brain PO2 is 219/1738 = 0.17, which means that the rise in brain PO2 is only about 1/6 the rise in inspired PO2. If we now apply the correction for lipid solubility, (twice as soluble/narcotic), oxygen should be about 1/3 (0.17 x 2 = 0.34) as narcotic. This takes into account both the lipid solubility and the change in brain PO2. In the human study cited above, oxygen was 1.65/6.3 = 0.26 as potent as nitrogen. The calculated (0.34) and measured (0.26) values are in reasonable agreement.
Taken from Undersea Biomedical Research, Vol 5, No. 4 December 1978 Hesser, Fagraeus, and Adolfson
Oxygen would appear to be the answer to all our problems, the more the better. Hmmm perhaps not. Oxygen is toxic, narcotic, can cause temporary bends and is a vasoconstrictor. What does this mean to us as divers? Oxygen is potentially twice as narcotic than Nitrogen. The upside being that at the partial pressures of oxygen within which we normally operate (0.21 to 1.6), oxygen narcosis is not a relevant issue. Nitrogen, which is breathed at far higher partial pressures, is the over riding concern. The vasoconstricting affects of oxygen are well documented. There is some evidence that the resultant reduction in perfusion (blood flow) may reduce off gassing by as much as 20%, this however only manifests as a problem at PO2's in excess of
I've gotten a couple (out of a couple hundred) emails from ZPlan users requesting that O2 be considered narcotic as an option in future versions. I'll probably chuck it in, just because it's a trivial computation, but this got me thinking about the whole O2 narcosis issue, and I'd be interest to hear some informed opinions.
While I certainly realize that there's a fair amount of research that indicates O2 may very well be narcotic, my current thinking is that the whole issue is basically irrelevant anyway. Here's why:
 O2 is theoretically about as narcotic as N2, so as you dial down your PN2 in a Nitrox, the narcotic potential of O2 increases accordingly, so for Nitrox/Air it's a totally moot point.
 Narcosis is not usually considered a problem by most divers in the Nitrox (well, EANx) depth ranges. So again, it's a meaningless concern for Nitrox.
 In the Helium-addition depth ranges, PO2 is fundamentally limited by toxicity concerns, and thus any O2-enduced narcosis is constrained by the fact that your MOD limits the FO2.
 In the trimix/heliox range, the selected PO2 is likely to be the same, or less, than that selected for the Nitrox range, so the O2 narcotic potential is a relative constant, and amounts to only a small fraction of your total END.
For example, let's say we're doing a trimix dive and wish to dial in our END and PO2, and fill the gap with Helium, and we want a max END of 130ft and a max PO2 of 1.4.
At 130fsw on air, your PO2 is about 1.0 and your PN2 is about 3.9, for a total "narcotic partial pressure" of 4.9 (assuming O2 is narcotic). Sticking with a max PO2 of 1.4, and a max PN2 of 3.9, the difference *at any depth* in narcotic potential for an END of 130fsw, if you assume O2 is narcotic, is .4 P(total narcotic gas), which is about 10 feet of Equivalent Air Depth. And for 10ft of EAD, I'll bet most divers will opt for the deco advantage of the additional .4 PO2.
So basically, like I said, I think the whole O2 narcosis issue is
irrelevant to actual diving, and best left for academia. Sad part
is, it's easier to put the "O2 is narcotic" switch into the software
than to include this long-winded explanation as to why I didn't.
The Meyer-Overton principle can be used to predict the anaesthetic properties of gasses and predicts that oxygen should be approximately six times as narcotic as nitrogen, I believe. However this is not seen in practice. Why?
There are two good reasons.
Firstly, unlike nitrogen, oxygen is not inert and there is a gradient between the blood and the tissues because it is used up by the body's metabolism, while nitrogen is not and its partial pressure is the very much the same throughout the body as in the inspired gas.
Secondly, it is a stimulant countering the depressant - narcotic - effects of the other (inert) inhaled gasses.
i) The pressure gradient;
The partial pressure of oxygen in normal breathing air of 0.21 bar is 158.8 torr. On inspiration the breathing gas is diluted with saturated water vapour with a partial pressure of 47 torr so its pp in the bronchi is 112 torr (0.15 bar). Because air in the lung is affected by dead space and by venous return of carbon diaoxide when it reaches the alveolus the ppO2 is 105 torr (0.14 bar). In the arterial system it is about 97 torr (0.13 bar). Across the capillary bed it is considerably further reduced to about 35 torr (0.05 bar).
But it does not stop there! In the tissue fluid the partial pressure of oxygen is further reduced to about 20 torr (0.026 bar). The oxygen then arrives at, and crosses, the cell membrane. In the cytosol it is about 10 torr (0.013 bar) whereas within the mitochondria, which is where all the energy producing reactions (cellular respiration) takes place it is only in the region of 6 torr or 0.008 bar in normal healthy tissues. YES 0.008 bar! Clearly oxygen is so powerful the body needs it in only very small amounts to generate all the energy it needs. (See the attachment. from McGilvery, Bichemistry a Functional Approach.; I am trying to add it but need to change the format.)
If the partial pressure of oxygen in the tissues varies from this low level the normal chemical reactions producing the body's energy either cease or go out of control. Consequently an hypoxic inspired ppO2 of less than 75 mmHg or 0.1 bar is unable to support life and partial pressures above 1.8 bar are toxic.
ii) Oxygen as a stimulant
This is the realm of the biochemist and is extremely complex but suffice it to say that there are many stages in cellular respiration resulting in oxidative phosphorylation and generation of the energy molecule ATP. This battery of enzymes acts like the controls of a car but can be damaged by poisons, temperature and biochemical changes within the cell, such as changes in acidity (H+ concentration).
Cyanide kills by blocking the mitochondrial enzyme at the very end of this long biochemical chain, which is the only biochemical reaction that uses molecular Oxygen itself. Cyanide poisoning produces a fatal tissue hypoxia through starving it of energy even though Oxygen may be present and freely available in higher than normal quantities.
So how can we explain oxygen toxicity? Too much oxygen causes damage to the lungs and mucous membranes after prolonged periods of exposure (whole body or pulmonary toxicity). This can easily be explained as a chronic inflammation, whatever the biochemical mechanisms. (Although these are likely to be the same as those producing CNS toxicity and related to the hydrogen ion). It is easy to speculate that it does not take much to raise the intra-mitochondrial oxygen partial pressure above the normally low value of 0.008 bar when breathing any enriched nitrox mix as oxygen is being supplied to the tissues in quantities far in excess of the body's metabolic needs.
In general if the inspired partial pressure of Oxygen exceeds 1.8 bar CNS toxicity will eventually be produced in all subjects leading to grand-mal convulsions, which must be avoided in divers at all costs.
Possible explanations of CNS oxygen toxicity
1) Build up of toxic chemicals
Most of the enzymes involved in cellular respiration (oxidative phosphorylation) have sulphydryl groups, which are very sensitive to oxygen. If the cellular pp O2 even approaches half a normal atmosphere these enzymes are deactivated by the formation of disulphide bridges and, as with cyanide poisoning, intracellular respiration slows or stops even though more than enough oxygen is present. Unlike cyanide poisoning, however, CNS Oxygen toxicity is not complete and can rapidly be reversed.
Without oxygen, anaerobic respiration takes place and the concentration of harmful chemical bi-products such as lactic acid with its powerful hydrogen ion (H+) increase, damaging all sensitive tissues including the lungs and brain.
2) Destabilisation of nerve cell membranes
Enzymes located within nerve and muscle cell membranes are responsible for ion transport the most important of which is ATP phosphokinase. The nerve resting potential is generated by the energy dependent active exchange of potassium and sodium ions against an electrical gradient through gated channels. On stimulation by a neurotransmitter such as adrenaline, the nerve action potential is generated by a sudden opening of these gates and the reversal of polarity for a very short period.
Clearly damage to these intracellular enzymes leaves the nerve fibres no longer able to generate a stable "resting potential". In addition the complex mechanisms normally keeping the various gates closed is also damaged. So the leaky membranes tend to cause the nerves of the brain to fire off at-will rather than when instructed to do so, causing an electrical storm;- a grand-mal convulsion.
The warning features of oxygen toxicity, such as facial muscle twitching, represent a generalised instability of all nerve (and muscle) cell membranes; just waiting for that one nerve cell in the brain to fire off and act as a trigger for all the rest.
3) Reduction in stabilising neurotransmitters.
Gamma Amino Butyric Acid (GABA) is an INHIBITOR within the brain and acts against the stimulants such as adrenaline, noradrenaline, serotonin and dare I say it amphetamine!!
It seems that the enzymes responsible for the production of inhibiting neurotransmitters such as GABA are damaged by high levels of oxygen much more than those producing the stimulant neurotransmitters leading to a generalised excitability.
4) The carbaminohaemoglobin buffer and raised CO2
Excess carbon dioxide is harmful because in solution it produces carbonic acidic, a source of those extremely harmful hydrogen ions;
H20 + CO2 <-> H2C03 <-> H+ + HC03-
In order to prevent this, most of the CO2 in the blood is normally mopped up by the haemoglobin in venous blood to form inert carbaminohaemoglobin.
When the equivalent of 100% Oxygen or more is breathed, I surmise little haemoglobin is involved in oxygen transport as enough is directly transported to the tissues in simple solution. In excess oxygen permanently, and preferentially, occupies the available sites on the haemoglobin molecule which are no longer free to mop up "acidic" CO2 molecules but enough normally do remain to do the job. In the presence of an inspired PO2 over 3 bar, however, the haemoglobin remains 100% saturated with oxygen and the carbaminohaemoglobin buffer is completely deactivated leading to a subsequent rise in acidity in the blood and brain which may be sufficient to trigger the ensuing fit in an already sensitised brain.
This becomes particularly apparent when the inspired pp CO2 exceeds 6%.
As an aside, the carbaminohaemoglobin buffer is normally involved in respiratory control but this mechanism is destroyed by prolonged exposures to high oxygen or carbon dioxide partial pressures. This is why experienced (free) divers are able to breath-hold for much longer than normal subjects.
It is obvious that excessive work and breath holding predispose to fits by increasing the partial pressure of CO2 and acidity, while hyperventilation is protective because it reduces it.
Stress, cold and subsequent adrenaline release predisposes to fits, a warm relaxed diving environment lessens the likelihood of fits.
The way I see it is that oxygen is just as narcotic as all gas molecules at the level of the cell membrane itself but in practice this effect is countered by the low partial pressures seen there together with the fact that it is not inert and acts as a stimulant in several ways, to reverse any narcotic effects it would otherwise produce.
I suspect, in practice these effects are near enough EQUAL AND OPPOSITE at the pressures recommended for normal scuba diving otherwise we could not dive using scuba!
If that didn't confuse I'll have to try harder!
Last edited by The Iceni; August 16th, 2002 at 06:37 PM.
Although we tend to use Pascals and Kilopascals more and more physiologists and doctors traditionally worked in Torr (named after Torcelli the inventer of the vacuum manometer/barometer). As-near- as-damn-it a torr is one millimetre of mercury.
Blood pressure is always recorded in mmHg.
1 atmosphere is about 760 mmHg. So the partial pressure of oxygen in normal breathing air is 0.209 bar or about 159 torr.
(please don't ask about bars and millibars!)
Hydrochloric acid is found in the stomach and some oxides of nitrogen are also found in parts of the body but I am not so sure about Nitric Acid, which is an extremely powerful non-organic acid.
While there are many acidic molecules in the body, nitrate - the anion of nitric acid - is not one of them, as far as I know.
The question of oxygen narcosis seems to appear every so often in this FORUM. Dr Thomas gave a nice, complete answer and analysis. Since oxygen is metabolized, the partial pressure at the cellular level is not very high. I guess in the final analysis, that is why oxygen is not really very narcotic.
As far as the “acid question” is concerned, I believe what we are speaking about is nitric oxide (used in the body for signaling between cells) and not nitric acid (not used in the body at all).