Treating suspected DCI with 100% O2 (is it wrong?)

chrismc

Whilst I hate to disagree with everyone, I have heard a similar comment before.

I recently went to a presentation and talk by one of the specialists at the north west uk hyperbaric chambers.

I was told that whilst 100% o2 has historically been whats taught, they are now reconsidering this.

Pure oxgen causes the blood vessels to narrow. Whilst the bubbles will be reducing, this is not immediate. Therefore there is a possibility that the blood vessels will contract to the point of a bubble causing a blockage.

However I must confess, we currently have not acted on this information, and still use pure o2 as emergency.

I will try and find some more information and contact information, if people wish to find out more. However as he is leading a major chamber, I would of thought he knew the latest information.

dteubner

It is almost always a good idea to challenge received wisdom. It is not at all a good idea to discard it because someone is "reconsidering" it.

On the evidence of this thread there are two hyperbaric specialists who are certain that 100% O2 is the first aid for DCI "period".

With all due respect this is just wrong in many many ways. Oxygen does not cause systemic blood vessels to narrow. There are not circulating arterial bubbles in most patients with DCI. Arteries get smaller and smaller as they divide so a bubble will have to stop somewhere.

If we are to reconsider the use of 100% O2 in first aid (and therefore presumably treatment) of DCI there would have to be some evidence that an alternative was better or, at the very least, a theoretical reason that actually made sense. There is no evidence and there is no good reason.

Dave T

apitkin

Thank you Dave, for putting it so eloquently.

It's always funny to see people who really don't understand the subject making assertions based on such ridiculous pseudoscience. The fact that those assertions directly contradict all the evidence and experience in a highly specialised field somehow seems to convince them even more that they are true. Diving and hyperbaric medicine unfortunately has always had more than its fair share of mavericks and quacks. It is a difficult field to do good clinical research in, so it does tend to encourage more 'inventive' points of view.

To all the anti-oxygen brigade I ask this: when you are pulled out of the water with girdle pain and you cannot move your legs because of a spinal cord hit, are you going to push the oxygen away?

Exactly. I thought not.

Andy

Nick uk.

If you get off your high horses, and read what has been writen we might be able to get somewhere. Mavericks and Quacks..........i'm neither, and unless you are an expert on hyperbaric medicine, my guess is your guessing, and if a concept is new to you doesn't nesecerally make it wrong!

The fact is that hight PpO2 for a prolonged time do cause 'capilaries' to restrict on a polmonary level and therefore inhinit the gas exchange at this level, not in the arteries, and blood stream, but in the lungs where the gas exchange takes place....during deco, for example, which is why we/i take air breaks to combat this and re-open, if you like the efficiency levels, or the all famous Oxygen Window, but there is a benefit on any deco profile from lets say 30mins + not just for the CNS but for the restriction of the capillaries.

Believe it or not.

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divechief2000@hotmail.com

dteubner

Nick,

I am a hyperbaric physician and so is Gasman. Pulmonary oxygen toxicity is not due to pulmonary capilary vasoconstriction but due to direct damage to the lung cells. Air breaks have been shown to prolong the time to measurable decreases in various lung volumes - no question - but it's not got much to do with blood flows.

Air breaks underwater are mostly to do with a (presumed) CNS toxicity benefit. You would have to do a lot of diving in a day to get to a level of exposure that you would even begin to see measureable pulmonary toxicity (about say 700 UPTD - over 8 hours at a setpoint of 1.4) Even at this level there would not be a significant decrease in gas exchange in someone with normal lungs.

There is a thing called hypoxic pulmonary vasoconstriction where blood flows to areas of the lung are not well ventilated are reduced, to help maintain good gas exchange. There may be circumstances (in diseased lungs) where high concentrations of oxygen may abolish hypoxic pulmonary vasoconstriction and paradoxically worsen gas exchange but this doesn't have much to do with diving medicine.

The question being debated in this thread (as I understand it) is "Is it wrong to use 100% O2 for the treatment/first aid for DCI"? The answer to this question is NO, absolutely and emphatically.

Dave T

Nick uk.

That goes without saying, and i hope evryone is clear on this..

As i've allready said...'if in doubt getit out' .......your O2 that is..

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divechief2000@hotmail.com

babar

Actually under hyperbaric conditions, there is some sytemic vasoconstriction, but that's not what we're talking about. I agree that 100% O2 is THE initial treatment of DCI

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Allan_o

Hi Guys.
Please correct me if im wrong here.
But dident the Hyldegaard papers show that a rat breathing 20/80 heliox for an hour at 30meters and recompressed to surface, treated with 100% O2, making larger bubblegrowth in the tissues at the initial stage of treatment (actually most of the rats died)
compared to a treatment with 50/50 heliox dident have as much bubble growth?

Still its my opinion that 100% O2 is the best first aid for DCI, but i must say that the Hyldegaard work is very interesting.

/Allan

apitkin

I vaguely remember this. Can you post the reference?

I would advise great caution in extrapolating this kind of work. For various reasons, rodents have been found to be unsuitable animal models for human DCI. This has been known for decades. Haldane used goats (these are still used in the UK) and the US Navy developed a useful model of spinal DCI in miniature swine.

Also, the pathophysiology of fatal DCI is (probably) not the same as that which causes lesser injuries, and therefore extrapolating from one mechanism of injury to another may also be invalid.

The third point is that a treatment involving 50/50 heliox will use compression to 4 ata rather than 2.8 ata with 100% oxygen, and there are possibly some types of DCI that may respond more to the pressure component of the treatment rather than the hyperbaric oxygen component of the treatment. This is irrelevant in a discussion of the best gas to breathe at the surface for first aid.

As for the best gas to breathe during recompression, that's a whole other question, and there is much discussion of it amongst experts.

Andy

saturation

At 1 ATA, 100% 02 is the preferred gas. Under high pressures, heliox has advantages due to a countercurrent exchange.

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