Accumulated 02 following a large number of repetitive Nitrox dives over 3 days.

[doctormike]

Hi doctormike, thanks for your response. Let me digest those bits regarding the Shearwater manual and the Shearwater blog post for a bit. (I had read the manual earlier, as well as the Shearwater blog post).

I think going down the path of OTUs is not going to add clarity at this time.

The Diverite article says "Note that these air breaks are intended to forestall symptoms of pulmonary oxygen toxicity; there is no risk of seizure or other CNS manifestations in these circumstances.". This seems to buttress what I am saying (?).

Sure!

Not sure what you mean by "going down the path of OTUs"... it's just how pulmonary O2 toxicity is tracked, so it's important to know for these discussions, but not so important for practice in recreational diving. BTW, OTU is just another term for UPTD.

Also, which DiveRite article are you referring to? The one that I posted says this about CNS toxicity and air breaks:

"There are no drugs that can be used to prevent CNS oxygen toxicity. In animal experiments, the seizures could be prevented but the CNS cellular damage found after prolonged seizures still occurred. The only effective methods to prevent CNS oxygen toxicity are to limit the pO2, the time of exposure, and to give air breaks during oxygen breathing."

Not sure where your quote is from, but maybe they are referring to prolonged exposure to more limited PO2, where pulmonary toxicity might be an issue before CNS?

 

[Madacub]

did you get your questions answered?

the CNS clock has a 90min half life (in theory).
the pulmonary limits run on a 24 hour clock with no half life, and they are cumulative over multiple days as well.

and you definitely can't stay at a ppO2 of 1.4 indefinitely.

Hi rjack, thanks for following up. I don't think the questions have been (satisfactorily) answered. But I am still thinking about a couple of things.

Specifically, PO2 vs PPO2. I'll use PPO2. If someone else uses PO2, I'll look at the context. In diving, it will almost always mean partial pressure of oxygen.

I am not convinced of the answers relating to half life and and CNS. Same for my comment about safe diving practice under 1.4 ATA.

Further to my post # 229 above, here is an article referred to by the Shearwater website that says, with reference to extended periods in the hyperbaric chamber, "Note that these air breaks are intended to forestall symptoms of pulmonary oxygen toxicity; there is no risk of seizure or other CNS manifestations in these circumstances."

Alert Diver | Understanding Oxygen Toxicity

 

[GJC]

Hi GJC, thanks for your response. I don't understand part of it. You say "The pulmonary symptoms just show up first". I think it depends. If you go straight to 140 feet on EAN32, CNS will show up first. Of course you know that. So I don't understand what you wrote.

High O2 percent at high pressure causes CNS hits.

O2 in the mid range over enough time does not cause CNS hits, but does cause toxic things to happen in all cells. The pulmonary system is the first to show symptoms. At sea level if you breath 100% O2 for more than 12 or 14 hrs or thereabouts, you will start to have inflammation in your lungs and it will worsen with continued O2. If you breath 50% O2 at sea level, it will take about 24 hrs for symptoms to develop. At sea level, breathing anything less than 40% doesn't cause pulmonary symptoms even over very long periods of time.

When you dive, the OTU limits and dive computer calculations are trying to keep you from getting pulmonary symptoms. But if you dive with a high OTU accumulation, you may be more prone to getting a CNS hit on your next dive even if your dive is less than the standard 1.4 O2 pressure limit. The CNS part about lower level O2 exposure and clearance are not so clear cut.

 

[Madacub]

Sure!

Not sure what you mean by "going down the path of OTUs"... it's just how pulmonary O2 toxicity is tracked, so it's important to know for these discussions, but not so important for practice in recreational diving. BTW, OTU is just another term for UPTD.

Also, which DiveRite article are you referring to? The one that I posted says this about CNS toxicity and air breaks:

"There are no drugs that can be used to prevent CNS oxygen toxicity. In animal experiments, the seizures could be prevented but the CNS cellular damage found after prolonged seizures still occurred. The only effective methods to prevent CNS oxygen toxicity are to limit the pO2, the time of exposure, and to give air breaks during oxygen breathing."

Not sure where your quote is from, but maybe they are referring to prolonged exposure to more limited PO2, where pulmonary toxicity might be an issue before CNS?

Sorry, I quoted another article, which I correctly cited in my post 232 above. In my response to you, I meant to quote from the DiveRite article you sent me, the first line of paragrapgh 7 I think "Oxygen toxicity of the brain (CNS) is a problem of higher pO2s for shorter periods of time.". I see your point regarding limiting the time of exposure, but really, in the whole article, that is the only fleeting mention made of CNS toxicity and exposure time. Everywhere else in the article time exposure is mentioned in connection to pulmonary toxicity. Is that a fair reading? It was in that context that I said "...seems to buttress what I am saying...)

Sorry again, I had both articles open at the same time.

 

[doctormike]

Sorry, I quoted another article, which I correctly cited in my post 232 above. In my response to you, I meant to quote from the DiveRite article you sent me, the first line of paragrapgh 7 I think "Oxygen toxicity of the brain (CNS) is a problem of higher pO2s for shorter periods of time.". I see your point regarding limiting the time of exposure, but really, in the whole article, that is the only fleeting mention made of CNS toxicity and exposure time. Everywhere else in the article time exposure is mentioned in connection to pulmonary toxicity. Is that a fair reading? It was in that context that I said "...seems to buttress what I am saying...)

Sorry again, I had both articles open at the same time.

Hmmm... not sure which article, will look back, but I'm pretty sure that CNS toxicity is time and exposure (just like pulmonary toxicity). That's why it's an O2 "clock".

 

[jgttrey]

Further to my post # 229 above, here is an article referred to by the Shearwater website that says, with reference to extended periods in the hyperbaric chamber, "Note that these air breaks are intended to forestall symptoms of pulmonary oxygen toxicity; there is no risk of seizure or other CNS manifestations in these circumstances."

I don't believe that is a correct statement of the context of the quote. What is being discussed in the Alert Diver article is using O2 while waiting to get to a chamber, not while in it. CNS hits are not a risk at that point because you're at 1 ATM (PO2=1.0). Air breaks have some relevance in that context for pulmonary risk, but not CNS. That's what the article is discussing. Here's the full quote, underlined:

"Divers suffering decompression illness may also be at risk of oxygen toxicity during the treatment they receive. Pure oxygen at sea-level pressure (normobaric oxygen), often provided as first aid during evacuation, is well tolerated for up to 24 hours. However, because divers will most likely be treated with hyperbaric oxygen as well, air breaks should be considered in extreme circumstances when access to hyperbaric treatment is delayed. Generally, such air breaks will occur as a matter of course as the injured diver eats, drinks and goes to the bathroom. Note that these air breaks are intended to forestall symptoms of pulmonary oxygen toxicity; there is no risk of seizure or other CNS manifestations in these circumstances. Air breaks should not be used when transport times are shorter than a few hours."

 

[rjack321]

Further to my post # 229 above, here is an article referred to by the Shearwater website that says, with reference to extended periods in the hyperbaric chamber, "Note that these air breaks are intended to forestall symptoms of pulmonary oxygen toxicity; there is no risk of seizure or other CNS manifestations in these circumstances."

Alert Diver | Understanding Oxygen Toxicity

Well as someone who has had CNS symptoms in a chamber which were ameliorated during the airbreak and returned afterwards - I can tell you that CNS effects in a chamber are absolutely possible. In a Table 6 treatment you have an hour+ at a ppo2 of 2.0 afterall.

Plus you misunderstood that paragraph is talking about being on surface O2 (ppO2 =1) for extended periods of time <before> hyperbaric treatment. It is advising against planning for air breaks in that circumstance.

"Divers suffering decompression illness may also be at risk of oxygen toxicity during the treatment they receive. Pure oxygen at sea-level pressure (normobaric oxygen), often provided as first aid during evacuation, is well tolerated for up to 24 hours. However, because divers will most likely be treated with hyperbaric oxygen as well, air breaks should be considered in extreme circumstances when access to hyperbaric treatment is delayed. Generally, such air breaks will occur as a matter of course as the injured diver eats, drinks and goes to the bathroom. Note that these air breaks are intended to forestall symptoms of pulmonary oxygen toxicity; there is no risk of seizure or other CNS manifestations in these circumstances. Air breaks should not be used when transport times are shorter than a few hours"

 

[BRT]

Hmmm... not sure which article, will look back, but I'm pretty sure that CNS toxicity is time and exposure (just like pulmonary toxicity). That's why it's an O2 "clock".

If CNS toxicity was time and exposure we could get hits after long shallow dives at say, 1.0 PPO2. I don't think there is any record of that happening.

 

[Madacub]

High O2 percent at high pressure causes CNS hits.

O2 in the mid range over enough time does not cause CNS hits, but does cause toxic things to happen in all cells. The pulmonary system is the first to show symptoms. At sea level if you breath 100% O2 for more than 12 or 14 hrs or thereabouts, you will start to have inflammation in your lungs and it will worsen with continued O2. If you breath 50% O2 at sea level, it will take about 24 hrs for symptoms to develop. At sea level, breathing anything less than 40% doesn't cause pulmonary symptoms even over very long periods of time.

When you dive, the OTU limits and dive computer calculations are trying to keep you from getting pulmonary symptoms. But if you dive with a high OTU accumulation, you may be more prone to getting a CNS hit on your next dive even if your dive is less than the standard 1.4 O2 pressure limit. The CNS part about lower level O2 exposure and clearance are not so clear cut.

Thank you for this.

"But if you dive with a high OTU accumulation, you may be more prone to getting a CNS hit on your next dive even if your dive is less than the standard 1.4 O2 pressure limit." Where did you learn this? I'm not a technical diver, so I don't need too many details, but sometimes I like a little bit.....

"The CNS part about lower level O2 exposure and clearance are not so clear cut" Just for clarity of my understanding, may I restate as "The CNS part about lower PPO2 exposure and safe diving are not so clear cut in cases of high OTU accumulation"? Does that match what you are saying? Please clarify if not.

 

[Madacub]

I don't believe that is a correct statement of the context of the quote. What is being discussed in the Alert Diver article is using O2 while waiting to get to a chamber, not while in it. CNS hits are not a risk at that point because you're at 1 ATM (PO2=1.0). Air breaks have some relevance in that context for pulmonary risk, but not CNS. That's what the article is discussing. Here's the full quote, underlined:

"Divers suffering decompression illness may also be at risk of oxygen toxicity during the treatment they receive. Pure oxygen at sea-level pressure (normobaric oxygen), often provided as first aid during evacuation, is well tolerated for up to 24 hours. However, because divers will most likely be treated with hyperbaric oxygen as well, air breaks should be considered in extreme circumstances when access to hyperbaric treatment is delayed. Generally, such air breaks will occur as a matter of course as the injured diver eats, drinks and goes to the bathroom. Note that these air breaks are intended to forestall symptoms of pulmonary oxygen toxicity; there is no risk of seizure or other CNS manifestations in these circumstances. Air breaks should not be used when transport times are shorter than a few hours."

Good point. To both you and rjack.