Managed to blog on a couple of topics this week; the latest seems to be interesting for people.
Air Breaks
Air Breaks
Air Break Myth...
- Thread starter Doppler
- Start date
Please register or login
Welcome to ScubaBoard, the world's largest scuba diving community. Registration is not required to read the forums, but we encourage you to join. Joining has its benefits and enables you to participate in the discussions.
Benefits of registering include
- Ability to post and comment on topics and discussions.
- A Free photo gallery to share your dive photos with the world.
- You can make this box go away
PfcAJ
Contributor
Adding air breaks does stop people from toxing, apparently. If people who are using this technique don't have toxic events when crossing the 100% (or 500%, or more) threshold, what do you use to explain the reason they don't have issues? WKPP guys routinely undertake massive o2 exposures and are thus far without issue (when following the prescribed gas break guidelines).
Personally, I think the NOAA limits are shenanigans. Nothing happens when 100% is reached, and you can tox well below it.
Personally, I think the NOAA limits are shenanigans. Nothing happens when 100% is reached, and you can tox well below it.
LiteHedded
Contributor
nedu seems to think they help
Warning: the below post is made by someone not remotely qualified to hold an opinion on this subject. I have never even done a dive which put me over about 50% on the CNS exposure clock:
Steve, I think that it is missing in your article is that we don't seem to know very much about the rate of decay of the CNS exposure clock, and so people play it conservatively and discount it entirely by saying that providing the exposure occurs within a 24 hour total window. But we know that the CNS exposure does decay, and it seems that the higher the level of exposure, the faster the decay, which suggests that air breaks at very high exposures are worthwhile, even if we cannot measure the benefit.
I have certainly heard lots of anecdotal stories about people doing deco on pure O2 and "felt" something coming on, and then switching to air or their lowest bottom mix, and the sensation receding. However, in theory their oxygen exposure is still accumulating, albeit at a much lower rate (say 0.32 ATA instead of 1.6 ATA).
I have also heard anecdotal suggestions that higher partial pressures of other gases in a breathing mix may help reduce the onset of oxygen toxicity (I remember John Chatterton trying to tell me that this was why he believed so few people toxed on "deep air" - but that is another point entirely).
Steve, I think that it is missing in your article is that we don't seem to know very much about the rate of decay of the CNS exposure clock, and so people play it conservatively and discount it entirely by saying that providing the exposure occurs within a 24 hour total window. But we know that the CNS exposure does decay, and it seems that the higher the level of exposure, the faster the decay, which suggests that air breaks at very high exposures are worthwhile, even if we cannot measure the benefit.
I have certainly heard lots of anecdotal stories about people doing deco on pure O2 and "felt" something coming on, and then switching to air or their lowest bottom mix, and the sensation receding. However, in theory their oxygen exposure is still accumulating, albeit at a much lower rate (say 0.32 ATA instead of 1.6 ATA).
I have also heard anecdotal suggestions that higher partial pressures of other gases in a breathing mix may help reduce the onset of oxygen toxicity (I remember John Chatterton trying to tell me that this was why he believed so few people toxed on "deep air" - but that is another point entirely).
techintime
Contributor
Late comer to the discussion, but anyway...
The article at the beginning of the thread has its logic backwards...these charts (like any other) are guidelines based on experience that seem to work. The only way to get a useable chart is to simplify a large number of variables, apply some assumptions, add a best-guess safety factor, and come up with some generic rules that work "nearly all of the time". Hence, just because the guidelines give no credit for an airbreak, does not mean that the airbreak has no effect. The chart is a simplified best guess, not biological reality. Hence, if air breaks (periodic reduced PPO2) have a track record of working, then stick with it no matter what the oversimplified chart says about it.
The article at the beginning of the thread has its logic backwards...these charts (like any other) are guidelines based on experience that seem to work. The only way to get a useable chart is to simplify a large number of variables, apply some assumptions, add a best-guess safety factor, and come up with some generic rules that work "nearly all of the time". Hence, just because the guidelines give no credit for an airbreak, does not mean that the airbreak has no effect. The chart is a simplified best guess, not biological reality. Hence, if air breaks (periodic reduced PPO2) have a track record of working, then stick with it no matter what the oversimplified chart says about it.
Even slower on the draw than techintime 
but some of the physiologic basis of air breaks:
Inspired pO2 as low as 0.6 ATA can induce the vasoconstriction that doppler described above. The vasoconstriction is thought to be a result of the binding of nitric oxide (an endogenous vasodilator) by reactive oxygen species (aka free radicals) that are produced during hyperoxia. Less nitric oxide = more vasoconstriction. There are several enzymes that are involved in the synthesis of nitric oxide: endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) are two. eNOS is produced by vascular endothelieum (the lining of the blood vessels). nNOS is produced in nervous tissue.
Tissue blood flow is reduced during hyperoxia and remains so until the hyperoxic condition is removed.
Hyperoxia also produces an initial reduction in cerebral blood flow (CBF), but CBF increases after a period of time. This is thought to be related to upregulation in the production of nNOS. Increased CBF coupled with the increased arterial pO2 that happens during oxygen decompression increases the risk of CNS oxygen toxicity.
An air break reduces the arterial pO2 within a minute or two. Reduced arterial pO2 decreases the risk of CNS oxygen toxicity. It's not known how long it takes the cerebral blood flow to return to a pre-hyperoxia condition; in fact, when I was talking with our director, who's one of the world's leading experts on the subject, he said he'd need to remind one of our scientists (another leading expert) to try this out on some rats and see what happens! However, it's well-established that the air breaks during, say, the deep phase of a treatment table 6 are sufficient to significantly decrease the risk of CNS O2 toxicity.
but some of the physiologic basis of air breaks: Inspired pO2 as low as 0.6 ATA can induce the vasoconstriction that doppler described above. The vasoconstriction is thought to be a result of the binding of nitric oxide (an endogenous vasodilator) by reactive oxygen species (aka free radicals) that are produced during hyperoxia. Less nitric oxide = more vasoconstriction. There are several enzymes that are involved in the synthesis of nitric oxide: endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) are two. eNOS is produced by vascular endothelieum (the lining of the blood vessels). nNOS is produced in nervous tissue.
Tissue blood flow is reduced during hyperoxia and remains so until the hyperoxic condition is removed.
Hyperoxia also produces an initial reduction in cerebral blood flow (CBF), but CBF increases after a period of time. This is thought to be related to upregulation in the production of nNOS. Increased CBF coupled with the increased arterial pO2 that happens during oxygen decompression increases the risk of CNS oxygen toxicity.
An air break reduces the arterial pO2 within a minute or two. Reduced arterial pO2 decreases the risk of CNS oxygen toxicity. It's not known how long it takes the cerebral blood flow to return to a pre-hyperoxia condition; in fact, when I was talking with our director, who's one of the world's leading experts on the subject, he said he'd need to remind one of our scientists (another leading expert) to try this out on some rats and see what happens! However, it's well-established that the air breaks during, say, the deep phase of a treatment table 6 are sufficient to significantly decrease the risk of CNS O2 toxicity.
OP
Even slower on the draw than techintime
Inspired pO2 as low as 0.6 ATA can induce the vasoconstriction that doppler described above. The vasoconstriction is thought to be a result of the binding of nitric oxide (an endogenous vasodilator) by reactive oxygen species (aka free radicals) that are produced during hyperoxia. Less nitric oxide = more vasoconstriction. There are several enzymes that are involved in the synthesis of nitric oxide: endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) are two. eNOS is produced by vascular endothelieum (the lining of the blood vessels). nNOS is produced in nervous tissue.
Tissue blood flow is reduced during hyperoxia and remains so until the hyperoxic condition is removed.
Hyperoxia also produces an initial reduction in cerebral blood flow (CBF), but CBF increases after a period of time. This is thought to be related to upregulation in the production of nNOS. Increased CBF coupled with the increased arterial pO2 that happens during oxygen decompression increases the risk of CNS oxygen toxicity.
An air break reduces the arterial pO2 within a minute or two. Reduced arterial pO2 decreases the risk of CNS oxygen toxicity. It's not known how long it takes the cerebral blood flow to return to a pre-hyperoxia condition; in fact, when I was talking with our director, who's one of the world's leading experts on the subject, he said he'd need to remind one of our scientists (another leading expert) to try this out on some rats and see what happens! However, it's well-established that the air breaks during, say, the deep phase of a treatment table 6 are sufficient to significantly decrease the risk of CNS O2 toxicity.
Thank you for taking the time to read and respond... Can you flesh out with a little more detail what you mean by the "deep phase" of a table 6 run.
The article taught me that women don't have logic filters.
Similar threads
