Summary (So that those uninterested can stop reading early!):

An analysis is presented implying that the usually cited 'inert gas'
mechanism is unlikely to account for the observed phenomenon of
O2 narcosis.  The hypothesis is presented that O2 narcosis is
more like acute CNS ox tox in its underlying mechanism/s.

--

I have avoided touching the subject of 'O2 narcosis' until I had
more facts, (and apologise to those individuals who are offended
by 'speculative' posts), but the article Mike Rodriguez's recent
post refers to (URL quoted below) reminded me of a question about
O2 narc I've had brewing for a while:

Has anyone got a physiological basis for the phenomenon (widely
reported, and therefore not to be easily discounted) of O2 narc?

Important anti-flaming note: I'm NOT saying that O2 narc doesn't
happen, nor that O2 isn't equipotent with N2 in its subjective
narcotic potential in diving (But: see quote from Richard Pyle,
below.)  I AM saying that if this is so it is not due to a simple
"inert gas" effect, but is instead more likely to involve cerebral
vasoconstriction, hypercarbia, free radicals (or some combination
of these) and is therefore more alike in mechanism to (sub)acute
ox tox than N2 narc.

The usual short answer has to do with the "inert gas" chemical
properties of oxygen being comparable to those of other gases
known to impair neurological processes at various concentrations.
(See a quoted text of a short thread on techdiver late 12/98,
quoted below)

None of these other gases are metabolised by the tissues, so
(after a period of time which depends on many factors) the arterial,
tissue and venous partial pressures tend to be equal.

Such a simple approach is not appropriate for oxygen, but is never-
theless (unfortunately) typical of articles such as that in
http://divermag.com/archives/dec96/divedoctor_Dec96.html

The correct approach to use for oxygen is to first note that one
of the characteristics of haemoglobin is its non-linear binding
to oxygen, such that at relatively low pO2 (~ 0.15 bar) it is pretty
much saturated, and further increases in pO2 (within the diving-relevant
(non-hyperbaric therapy) range up to 1.4-1.6 bar) result in only
moderately increased arterial oxygen content, by means of O2 dissolved
in plasma.

So... we have:
1. arterial O2 content (but not pO2) only modestly affected by
inspired/arterial pO2 (~0.15 - 1.4 bar)

2. cerebral metabolic rate hopefully ticking along normally

If the usual coupling of cerebral metabolism to cerebral bloodflow
is maintained ( <- assumption, and known to be GREATLY affected
by pCO2), we get:

3. basically the same arterio-venous difference in oxygen content

Conservation of mass then means that the cerebral venous O2 content
is pretty much unchanged by inspired pO2 (again, within the limits
specified above), and therefore the venous pO2 is unchanged.
(This is not just me bulls****ing: it is a phenomenon known as the
'oxygen buffer' effect of haemoglobin.)

Plugging typical numbers into the above gives a brain venous arterial
pO2 ~ 40mmHg, which increases to perhaps 60 mmHg over the range
of inhaled/arterial pO2 specified above.  (I've left out the math here:
those who know this stuff don't need it spelled out, but the words
"Fick Principle" will be a clue to the initiated)

Now, here's the Odd Thing: The tissues (including brain cells)
are pretty much in equalibrium with their _venous_ blood gas values,
not arterial.  In other words, by increasing the inspired pO2 to
values commonly used in advanced rec & tech diving, the brain tissue
pO2 has not changed by anywhere nearly enough to have an "inert gas"
effect.

So: how is 'O2 narcosis' explained?

While the above analysis rules out an "inert gas" mechanism for O2 narc,
brain tissue O2 has increased by nearly 50%, almost certainly enough
to have significant physiological effects:

- vasoconstriction (? -> reduced local glucose delivery)
- free radical production (as noted in a thread on rebreather, free
radical scavengers are already present, but their activity is tuned
to the normoxic rate of free radical production)

For a variety of reasons mild hypercarbia is common (universal?) during
diving.  CO2 retention will be synergistic with the second of these, since
it will decouple brain O2 uptake/perfusion and increase brain tissue O2,
but will tend to offset the first.

It would be interesting to test this hypothesis with a hyperbaric
chamber, variable inhaled gases, a really good test for narcosis (ie.
involve a person expert in neuropsychiatric evaluation) and (preferably)
a jugular bulb venous sampling catheter.  Does anyone know of this
experiment being done?  Any volunteers?  Can someone lend me a chamber?

Odd Observations and Notes

#1: CNS O2 tox, regardless of its actual cellular toxic mechanism,
becomes far more likely when brain tissue pO2 finally rises as a result
(usually) of very high pO2 (~ 2 - 3 bar), which result in sufficient
dissolved oxygen in the arterial blood that the entire cerebral metabolism
can be supplied by dissolved O2. This means that venous haemoglobin remains
fully saturated, cancels the effect of the 'O2 buffer' role of haemoglobin,
and the venous blood oxygen increases from its normal value (~75% sat,
pO2 = 40mmHg).

The same mechanism also suggests why diving hyperbaric O2 exposure carries
an increased risk of neuro ox tox - specifically, exertion, deliberate
hypoventilation, equipment encumbrance, dense breathing gas etc resulting in
hypercarbia, increased cerebral blood flow -> increased brain tissue pO2.

It also (to make it explicit) explains why hypercarbia is so dangerous to
divers.  Normobaric hypercarbia doesn't cause much more than headache and
increased respiratory drive up to pCO2 of ~ 60mmHg (unconsc ~ pCO2 100mmHg).
Divers seem to be at risk at pCO2 much less than this.

#2: indirectly, the various principles noted above go a long way to showing
OBJECTIVELY why aerobically fit individuals are less at risk of DCI for any
given dive (in working this out, it helps to know that aerobically trained
muscle has a greater capacity for O2 extraction than untrained muscle).
Keep jogging, George!

#3: plugging real numbers in strongly suggests that rec/tech diving should
stick to below 1.4 bar O2 (obviously for extreme exposures (WKPP) much lower
pO2 is required during most of the dive because of pulmonary toxicity.)
I think it's likely that 'O2 narcosis' as a problem would be virtually
eliminated by reduction of inspired O2 to 0.8 - 1.0 bar. This is consistent
with a statement by Dr Richard Pyle (quoted from post to rebreather):

Date: Mon, 1 Feb 1999 16:53:53 -1000 (HST)
From: Richard Pyle <deepreef@bi*.or*>
Subject: Re: Narc Question

-- start quoted text
<snip>

- With EAN mixtures yielding a PO2 in excess of about 1.6-1.8, I have
consistently found that narcosis is more severe than it would be on air at
the same depth.

- With EAN mixtures yielding a PO2 less than about 1.6-1.8, I have
consistently found that narcosis is less severe than it would be on air at
the same depth.

<snip>
-- end quoted text
 
#4: My specialty is anaesthesia: I tweak inhaled gases and drive rebreathers
(anaesthetic circuits) all day, and advances in monitoring over the past few
years have provided the luxury of continuous, breath-by-breath analysis of
inspired and expired gases. I am able to (and do) measure venous and arterial
blood gases with insp O2 from 0.21 to 1.0 bar (drats: no chamber!), and
nothing I've ever measured has contradicted any of the above.

there is no #5, I've run out of steam :-)
(Thank heavens!)

With apologies to those individuals who will probably end up with
3 copies of this :)

Gerard Stainsby

--

Appendix:

Typical techdiver O2 narc thread: Dec 29 1998
(most headers deleted & some snips, not changing context)

<start of quoted thread>

From: <Jsuw@ao*.co*>
Subject: Narcosis Question

When determining the acceptable narcosis exposure for a dive, it seems that
only the narcotic effect of nitrogen is considered.  Oxygen is at least as
narcotic as nitrogen.  Although helium is far less narcotic than either, it
still is an inert gas with potential to have narcotic properties.  

With this in mind, why is it that only nitrogen's narcotic effects are
considered?  How can the narcotic effect of the other gases be accounted for?
Does it matter?

From: Bill Bott <aquadart@ix*.ne*.co*>

<snip 1 para>

Now as for handling O2 as a narcotic gas...  The calculations are actually
simplified!!  Calculate the PPO2 and the PPN2 for the given depth and add
the two numbers together, then subtract 1 and multiply by 33.
((PPO2+PPN2)-1)*33

From: Mike McDiarmid <mmcdiarm@ya*.co*>

There are others on this list with far more knowledge than I, but I
have been told that in determining the narcotic effect of a gas you
must consider its lipid solubility.  Oxygen has a high lipid
solubility so therefore is in fact narcotic and should be considered
when determining the END of a mixture.  He does not, or is very low,
so not a factor in the calculations.  Bill Mee, George or JJ can
answer this one better.  My apologies if I have mis-stated anything.
    Traditional teachings by the agencies do not account for the O2
content of a mixture in determining the END.  This is a mistake.  End
of subject.

From: s_lindblom@co*.co* (Steve Lindblom)

By who? Just about everyone I know considers the O2, or at least is aware
of the situation, and most of the better texts acknowledge that O2 is
narcotic. In the initial overselling of nitrox a lot of the agency texts
and promo material claimed it reduced narcosis, but I don't hear anyone
saying that anymore.

>When determining the acceptable narcosis exposure for a dive, it seems that
>only the narcotic effect of nitrogen is considered.

<End of quoted thread>

--

Mike Rodriguez wrote:
> 
> At 03:21 PM 2/25/99 -0500, H20Caver wrote:
> 
> >the narcotic effect of oxygen is,in general, a question. Specifically and
> >anecdotally, I know it to be as narcotic as nitrogen.
> 
> There's an interesting article at
> 
> http://divermag.com/archives/dec96/divedoctor_Dec96.html
> 
> arguing that O2 is *not* narcotic.  The argument seems to make
> sense, but from my own (and others') subjective experience,
> I still believe it to be at least as narcotic as N2 and I'll
> continue to treat it as such.  The article is an interesting
> read, though.
> 
> -Mike
--
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