How fast is O2 tox?

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TheRedHead:
Charlie made a good point about gas. And you have to consider the depth of the hard bottom. Could you rescue someone at 140 feet with narcosis?

I generally tend to obsess on things when I'm narced, so if I went down with the thought of "go get the OOA diver", I'm pretty sure it would happen.

I know if I'm deep enough, I can check my SPG at least 6 times a minute and not remember what it said. :cool:

Terry
 
BigTuna:
An important rescue matter is that the toxing diver's airway could be locked closed with a spasm. If that happened, moving him to the surface could result in a lung overexpansion injury. There seem to be several options for dealing with this, such as:

- Wait until the convulsions stop before raising the victim.
- If the victim can be raised to a depth with lower PO2 such that the pressure reduction is minimal, do so and hold him there until convulsions stop.
- Interrupt the airway lock with a force applied to the chest, perhaps with a Heimlich maneuver.

Are there expert recommendations on this?
I was thinking about this as I typed my response above. I have been around or with several people having seizures of differing origins and providing air or oxygen was never an issue even though the seizure events lasted, in some cases, for a couple of minutes. I don't recall that there was any indication of a fully obstructed airway either.

I've not been around anyone that was having a seizure caused by O2 toxicity. It would be good to hear from someone that has experience in dealing with seizures based on O2 toxicity. Is an obstructive larygospasm a normal or common event with this type of seizure?
 
Bagging somebody in a tonic-clonic seizure can be challenging, but I'm with jbd; I haven't encountered anybody who appeared to have laryngospasm. Airway obstruction during seizures, in my experience, is far more likely to be due to the tongue, which is a very effective blocker of inspiration, but generally not of expiration. Of course, there's always a brief lag between seizure onset and the provision of oxygen, even when they seize in the ER, so maybe we're just not trying to bag them during the phase of spasm. But that delay would occur underwater as well.
 
Fortunately, I have not been around anyone who has toxed underwater, so this is not a real world experience. Ironically, I was reading an article about a public safety diver who toxed (and died) on a deep water recovery. His PO2 was well above 2% and the biggest issue (in reading the article) was that he didn't analyze his mix.

However, based on my training, this is what I know:


Web Monkey:
Does anybody know how long it takes for O2 toxicity to cause seizures for any particular PO2? Is it an immediate effect, as in any given person has a threshold and will have a seizure when it has been reached, or does it take a significant amount of time to build up?

The rate of development for Oxygen Toxicity can be influenced by a number of conditions including procedures, drugs and environment. One of the most significant physiological factors may be the production and retention of carbon dioxide (it increases the cerebral blood flow). This can happen if someone is over-exerted, breathing shallow(er) or has insufficient CO2 removeal from a closed circuit scuba unit. In some Navy studies, it has been noted that thermal stress also appears to play a significant role in the predisposition of Oxygen Toxicity. Thus, a diver with a more rapdily cooling core temperature may become toxic at a gaster rate than someone who does not drop in temperature as quickly.

Furthermore, individual tolerance to elevated oxygen levels can be modified by physiological variables and medications. Simple drugs like insulin and sudafed may increase your susceptability as well as decrease a PO2 limit where one becomes toxic, hasten the onset where one becomes toxic, or increase the severity to where one may become toxic. I remember reading in one of IANTD's Nitrox Magazine articles where Tom Mount discussed the safety of taking pseudoephedrine (Sudafed) while diving deep. Furthermore, the physician's desk reference indicated that side effects of pseudoephedrine may include nausea, heart palpatations, irritability, headache, dizziness, drowsiness .... and seizures.

Thus, to answer your questions because there are too many variables between human beings (from personal metabolism to external environmental conditions), it is impossible to predict when one person may become oxygen toxic versus another person.

This uncertainty encourages conservative exposure limits. For enriched air (or air) diving a maximum exposure limit would appear to be conservative while allowing a cushion for oxygen partial pressure increases due to changes in a dive plan. Perhaps 1.4 would be acceptable if depth will be carefully controlled. On the other hand, I know a lot of seasoned divers who would testify to diving safely (and continuously) at 1.6

Web Monkey:
For example, say someone is diving EAN 36@ 95', which gives a PO2 of 1.4, then sees a diver in distress (OOA, etc.) at 130', which would be a PO2 of 1.78, if the first diver went down to 130' to assist the second diver for a couple of minutes, and then do a normal ascent to the surface with both divers, how probable would it be, or how long would it take for an O2 hit to occur?

What about the same situation, but going down to 150'? (PO2 of 2.0)

The real question is: Would going significantly beyond your maximum PO2 for a short time be likely to create 2 victims, or a successful rescue?

This is the real question and there is no right or wrong answer. Since there are so many variables in this question, it is difficult to answer (such as, what would the new partial pressure of the rescue be? Are you comfortable going to that PP, Is this your first (enriched air) dive, is it early in the dive, etc.?) I address these types of questions in my rescue class all the time. Do you know whether or not the victim is still alive? Can you safely respond to the victim without creating 2 victims? Is someone who is on air close by? The more intimate you are with this person, the more risk you are willing to take. If it was my son, I wouldn't hesitate! Someone I met on the boat, I would be more cautious. For most people these decisions (hopefully never) will be made on the fly and a true testimony to why proper, advanced and ongoing training is necessary so you do not act in haste, but act wisely.


Diver Dennis:
Is there a quick onset though? Web Monkey had a great question, is it possible to help a diver in trouble that is over your MOD for a few minutes or is it too dangerous?

With Pulmonary Oxygen Toxicity there is not a "quick onset". It is exposure over time. With CNS Oxygen Toxicity, it is brought on by a high PO2 (or continual exposure at a P02 exceeding table time limits). An individual's susceptability could be very quick or take a bit, but the end result is inevitable. The speed is determined by the variables, many of which are near impossible to measure.

Web Monkey:
OK, now how about if there's a gas switch? Say you're on EAN36 @95', then switch to air and drop to 130?

Is O2 Tox still a possibility?

Terry

Even if you switch, you are still subject to some oxygen exposure. And, you still have some build up of Oxygen in your tissues. However, by making the switch, you would definitely lessen your susceptability to Oxygen Toxicity. The good news, if it is a radical drop in P02 (by making the switch), you would be metabolizing the 02 built up and probably not run into a CNS issue. You would still have Pulmonary 02 Toxicity issues, but I think the risk may outweigh the concern (conditions and variables, of course, being a consideration).


BigTuna:
An important rescue matter is that the toxing diver's airway could be locked closed with a spasm. If that happened, moving him to the surface could result in a lung overexpansion injury. There seem to be several options for dealing with this, such as:

- Wait until the convulsions stop before raising the victim.
- If the victim can be raised to a depth with lower PO2 such that the pressure reduction is minimal, do so and hold him there until convulsions stop.
- Interrupt the airway lock with a force applied to the chest, perhaps with a Heimlich maneuver.

Are there expert recommendations on this?

If the victim is breathing and has a regulator in his/her mouth, then moving them to a lower PO2 and ending the dive would be the best thing. Moving to a lower PO2 may end the symptoms and/or seizure. However, if the victim does not have a regulator, then drowning is the main concern and getting them out of the water is the highest priority. You can try putting the reg back in their mouth, but that may be a waste of time and effort. The proper technique is to end the dive as safely and as quick as possible without embolizing the victim (or the rescuer).
 
Hello readrs :

I have been away for a bit – as you can tell.

Tolerance

The oxygen tolerance and exposure times for increased oxygen work best in the range where time to symptoms is quite long, since there is a relatively large degree of variability from person to person. [This is true also of decompression tables; they work best with a large margin of safety.]

When one comes to very high exposures of oxygen pressure, the exposure durations are short. The large variability that is - unfortunately – inherent in oxygen tolerance becomes very important. That is why short, high exposures are very dangerous and should be avoided.

Guidelines

Ther British researchers found:

- a very large individual variation in susceptibility and time to symptom onset;
- exercise decreased oxygen tolerance compared to individuals at rest;
- immersion decreases oxygen tolerance compared to dry exposures [reductions of exposure times by a factor of four or five];
- diving in very cold (<49°F / 9°C) or very warm (>88°F / 31°C) water decreases oxygen tolerance.

Dr Deco :doctor:

The next class in Decompression Physiology for 2006 is September 16 – 17. :1book: http://wrigley.usc.edu/hyperbaric/advdeco.htm
 
All interesting reading.........
 
In the only study I know of that addressed your specific concern, participants were subjected to 3.1 ATA oxygen and the time to OxTox symptoms measured. The study ran the 3.1 ATA exposures daily for 90 days.
The earliest OxTox event occured after 5 minutes exposure. There was only one of those. On day one.
The longest a subject went without any symptoms was 155 minutes (!) There was only one of those, too. (day 39)
Most symptoms onset occured in the 30 to 60 minute range.
There was no appreciable "acclimation" over the study period - time to symptoms stayed highly variable over the whole period in every test subject.
Bottom line... I'd go after the diver in trouble in your example and not worry about an oxtox event. I'd take the rest of the day off, too.
Rick
 
https://www.shearwater.com/products/peregrine/

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