PpO2 time limits on deep air

[The Iceni]

Hi folks,

Jumping up from the back, as ever, I think the most important feature of CNS oxygen toxicity is its unpredictability.

Given the inevitable fatal consequence when using a standard regulator - as opposed to a full face mask - it seems obvious to me that the risk of such an incident should be avoided at all costs, however rare.

I think it worthwhile mentioning that there are at least a couple of well recognised variables that affect a subject's susceptibility to CNS oxygen toxicity.

The first is submersion, (i.e. it is seldom seen in dry chamber dives at the lower pressures it manifests during underwater diving).

The second is CO2 retention.

In the treatment of DCI patients (and their attendants?)are routinely exposed to long periods of high pp O2 (2.8 bar I believe) without problem, dry in a chamber. There have air breaks but I would be interested to learn the incidence of CNS toxicity during such treatment.

Carbon dioxide retention increases a diver's susceptibility.

Numerous theories abound but, as yet, I gather the mechanism is unclear, whether it is simply biochemical or an abnormal physiological response.

 

[Dr Deco]

Dr Thomas:

CNS Oxygen Convulsions

During several years that I was at IAPM in Seattle, I participated in some chamber oxygen treatments. In the more than 2,00 treatments of 90 minutes at a pressure of 2.0 to 2.4 atm, no one ever experienced a convulsion. Nor did any patient ever mention any of the other signs and symptoms of CNS toxicity (ringing in the ears, twitching of the lips or eyelids). Air breaks were given, but many patients are exposed in monoplace chambers that do not afford the easy ability to produce air breaks. Thus, the incidence is quite low, but it is not zero.

All of these were quiescent individuals. I was taught that activity elevated carbon dioxide that in turn elevated brain blood flow; this was responsible for CNS problems in active divers. It would require considerable activity to raise arterial CO2 levels and elicit an autoregulatory response in the brain, however.

Dr Deco :doctor:

 

[rcohn]

Dr Deco once bubbled...
Adaptation

I have seen some lab evidence that CNS effects are mitigated when individuals breathe an inert gas diluent. Thus you might get a bit more time with air than with pure oxygen – but I would not count on it in the water.

My understanding is that it may be the opposite. The tolerance limits are higher for 100% O2 (breathed a shallower depths of course) than for mixed gasses. The CO2 loading is less at the shallower depths which may be the reason. The US Navy allows much higher exposure limits for the rebreather divers on 100% O2 than for mixed gas diving. There was a paper on the web describing the statistical analysis of the O2 exposure data, but the site that had it is gone.

Another factor that allows higher exposures for the 100% O2 rebreather divers is that they don't completely purge the loop of N2, providing a greater safety margin. Obviously this will not be the case for open circuit scuba.

Ralph

 

[The Iceni]

Dr Deco once bubbled...
Dr Thomas:

CNS Oxygen Convulsions

I was taught that activity elevated carbon dioxide that in turn elevated brain blood flow; this was responsible for CNS problems in active divers. It would require considerable activity to raise arterial CO2 levels and elicit an autoregulatory response in the brain, however.

Dr Deco

I quite agree Dr Deco, which is why I am convinced it must be a biochemical, rather than an aberrant physiological response.

This is a summary of an earlier post of mine discsussing theoretical possibilities for the causes of CNS oxygen toxicity;-

1) Build up of toxic chemicals

If the cellular pp O2 is exceeded respiratory 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.

The increasing concentrations of harmful chemical bi-products such as lactic acid with its powerful hydrogen ion damage all sensitive tissues including the lungs and brain.

2) Destabilisation of nerve cell membranes

Enzymes located within nerve and muscle cell membranes are also damaged leaving the nerve fibres no longer able to generate a stable "resting potential". In addition the complex mechanisms normally keeping the various gates closed is damaged producing a generalised excitability.

3) Reduction in stabilising neurotransmitters.

Gamma Amino Butyric Acid (GABA) is an INHIBITOR within the brain. It has been shown that the enzymes responsible for the production of such inhibiting neurotransmitters are also 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

In the presence of a localised pp O2 equivalent to an inspired PO2 over 3 bar the haemoglobin (and myoglobin) remains 100% saturated with oxygen and the carbaminohaemoglobin buffer is completely deactivated leading to a subsequent localised rise in acidity in brain tisues which may be sufficient to trigger the ensuing fit in an already sensitised brain.

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.

5) Stress

Stress, cold and subsequent adrenaline release predisposes to fits, a warm relaxed diving environment lessens the likelihood of fits.

Any fundiing available for a research project?

I thought not!;-0

 

[Dr Deco]

Dear Paul:

You have made a good case. It seems a reasonable possibility.

Dr Deco :doctor:

 

[padiscubapro]

rcohn once bubbled...


My understanding is that it may be the opposite. The tolerance limits are higher for 100% O2 (breathed a shallower depths of course) than for mixed gasses. The CO2 loading is less at the shallower depths which may be the reason. The US Navy allows much higher exposure limits for the rebreather divers on 100% O2 than for mixed gas diving. There was a paper on the web describing the statistical analysis of the O2 exposure data, but the site that had it is gone.

Another factor that allows higher exposures for the 100% O2 rebreather divers is that they don't completely purge the loop of N2, providing a greater safety margin. Obviously this will not be the case for open circuit scuba.

Ralph

Ralph,
You are dead wrong about the purging.. on an oxygen rebreather it is a paramount issue to completely purge the loop of ALL inert gasses.. Its typical to do at least 4 full purges of the loop before decending and periodically purge the loop as time progresses..

You are now probably thinking... Why???

The answer is simple oxygen rebreathers have NO means of monitoring PO2, so on mass flow injection the injection rate is constant but your PO2 will be dropping as inert gas comes out ofyou into the loop..
On a manual oxygen rebreather it is typically flown with minimum loop volume and oxygen is added when it gets difficult to breathe, again offgassing of inert gas presents a problem.. You can go hypoxic at shallow depths (granted it would need fairly long exposures but thats what they do)

This can be seen dramitically with CCR divers that have gone to depth and have built up a deco obligation.. I'll flush my loop at my 20 ft stops to run my unit as an o2 rebreather.. upon a good flushing I'll get a 1.6, but after 5 mins or so I'm down to a 1.3 and its time to flush again... The rate at which the flushing is necessary decreases with time(as you offgas).. by 30 minutes the PO2 drop is not that bad for my typical profiles..

 

[rcohn]

padiscubapro, I realize you're an "expert", but according to the United States Navy, an organization with some experience in pure O2 rebreather diving, you're dead wrong.

18-24 U.S. Navy Diving Manual—Volume 4
18-7.1 Purge Procedure. Immediately prior to entering the water, the divers shall carry
out the appropriate purge procedure. It is both difficult and unnecessary to eliminate
nitrogen completely from the breathing loop. The purge procedure need only
raise the fraction of oxygen in the breathing loop to a level high enough to prevent
the diver from becoming hypoxic, as discussed in paragraph 18-2.2. For the MK
25 UBA, this value has been determined to be 45 percent. For further information
on purge procedures, see paragraph 18-7.4.

CHAPTER 18 — Closed-Circuit Oxygen UBA Diving 18-25
18-7.4 References for Additional Information. The following references provide information
on the LAR V purge procedures:
! Purging Procedures for the Draeger LAR V Underwater Breathing Apparatus;
NEDU Report 5-84
! Underwater Purging Procedures for the Draeger LAR V UBA; NEDU Report
6-86
! MK 25 UBA (LAR V) Operation and Maintenance Manual; NAVSEA SS600-
AJ-MMO-010, Change 1, January 1, 1985

From a paper no longer available online:http://groups.google.com/groups?q=v...UTF-8&selm=8plruc$2sh$1@nnrp1.deja.com&rnum=1

"Another important factor in evaluating the risk of CNS toxicity of
these new Navy O2 exposure limits (Table 4 and Fig. 6) is the actual
FIO2 to which the diver is exposed. The recommended FIO2 is not 1.0;
the Navy recommends that divers carry out only one fill and empty
procedure to wash out lung N2. Butler and Thalmann(19) have shown that
this procedure will produce an FIO2 of 0.74. If this procedure is
followed, the model predicts that the probability drops to <1% at every
depth for the times noted in Table 4. The probability of developing CNS
O2 toxicity from breathing nearly pure O2 at 30 fsw for 80 min is about
4%. If the recommended lung washout procedure is followed to fill the
breathing apparatus, resulting in an FIO2 of 0.74, the probability of
toxicity after 80 min is less than 0.1%. If all current recommendations
are followed, Navy limits are safe. "

Where is Rainreg when we need him?

Ralph

 

[subocean]

The US Navy has exceptional exposure ppo2 limits up to 1.8 with NavSea approval required above 1.6 for extraordinary circumstances. Anything higher than that was probably tested on dogs, but hasn't been published in any operations manual and only happens by accident. An MD friend of mine got a shot of pure O2 at 160 fsw in a chamber. Afterwards, he reported concentration problems that lasted about 6 months. Perhaps he just got used to it.
What kind of full face mask are we talking about? Demand only? The possibility of flooding during a convulsion seems high without a constant flow of pressure. As a commercial diving expert witness/investigator, I have examined several deep O2 hits that have been complicated by near drowning in a "dry" helmet. The negative damages experienced by the divers were life changing; not something to shrug off.
As for 240 on air with a 1.73 ppO2, with a very short bottom time I imagine you can get lucky on occassion, but if you try that every day for a living, you will get hurt. Likewise, deep air narcosis can be unpredictable from day to day for reasons unknown.

 

[BRW]

These days, surprised anybody even dives
deep air on OCs or RBs. Helium based mixes
(bottom gas or diluent) are far safer, more
deco efficient, and everybody feels better
topside -- for any ppO2. Is being appreciated
even by USN.