Saturation
Medical Moderator
Efficiency?
If what this means is shortened deco time, breathing the highest pp02 with tolerable toxicity is a proven way to accelerate decompression from inert gas loads
80 vs 100% 02 at Stop 20'
In the time frame of decompression, the choice is over a risk of 02 convulsions, and less about pulmonary toxicity. Is the risk of 02 convulsions greater with pp02 of 1.6 versus 1.3 at decompression? In deco, of little consequence, so risks being equal, the higher pp02 is better. See below for explanation.
Background Info:
O2 Convulsion Studies
Since 1947, across a range of pp02 with most at pp02 > 3, no air breaks. Convulsions occurred in ~100% of subjects up to a maximum period per pp02, but on repeated trials the same subjects convulsed at different times within a maximum period. The only constant was that periods when 100% of test subjects convulsed were earlier as the pp02 rose. For example, at a pp02 of 3.5, subject 1 seized 10minutes into the exposure. All subjects seized within 60minutes. After a break rest, the test is repeated, subject 1 seizes in 5 minutes, all subjects seized within 60 minutes. After a break, test is repeated, subject 1 now seizes in 50 minutes, while all subjects seize within 60 minutes.
02 convulsions thus, do not begin at the end of a clocked period per pp02 such as made out in NOAA limits; it becomes possible immediately past a threshold pp02. When subjects convulse varies for the same individual doing the same pp02 exposure at a different time: it may be less, unchanged or more.
The plotted shape of 02 toxicity, whether convulsions or minor ones labeled in recreational nitrox as "VENTID," were X = maximum time to toxicity, Y = pp02, appears as a rectangular hyperbola. For decompression or treatment purposes experts agreed that for safety a pp02 < 3 is a trade off, at ~ knee of curve, but as the shape shows its smooth there is no sharp cut off.
The image is on the upper right of the link, image with caption xy=1 in Quadrant 1 : http://mathworld.wolfram.com/RectangularHyperbola.html
Convulsions are rarer if pp02 < 2. Tolerance to pp02 at this level is high and made even higher with normoxic breaks, such that the principle concern is not convulsions, but pulmonary toxicity.
Dr. Edmonds has > 10 years experience is using pp02 2.0 and instituted this level as the pp02 of an in-water recompression protocol.
http://www.cisatlantic.com/trimix/AQUAcorps/Bent/inwater/Edmunds.htm
A review of others is:
http://www.bishopmuseum.org/research/treks/palautz97/iwr.html
At this point, we should really refer to pulmonary toxicity as whole body toxicity, since the lungs are just a manifestation divers feel of the effects of 02 throughout the entire body.
Being such, were do _you_ draw the line on a safe pp02? Dr. Vann summarized issues ~ that haven't changed much since 1992{?}, here's a copy:
http://www.cisatlantic.com/trimix/AQUAcorps/rebreather/OxygenExposure.htm
In conclusion, its very likely convulsions ARE related to a build up of an unknown byproduct of high pp02 exposure beyond the body's capacity to repair it [ thus pp02 > 3 inevitable leads to convulsions] AND can be accelerated or work synergistically with products of exertion, such as andrenaline release and C02 build up.
NOAA Nitrox Limits
NOAA threshold of 1.4 and the exceptional threshold of 1.6 were judgments by an expert panel and used to limit bottom mix pp02. These thresholds are for "normal" diving activity [or working dives], not in the resting state of decompression. There have been rare reported seizures on these pp02, so recommendations as far back as before 1995, were to lower it to about 1.2, of which few experts disagree.
The NOAA clock is modeled after convulsion studies. However, once past a threshold pp02, the risk of convulsions is more random, thus whether the per-dive time limit is true or not is moot in regards to CNS toxicity. However, one should track their total time, in regards to whole body toxicity in technical level dives.
FWIW there were many USN studies on 02 rebreathers that are similar to the NOAA clock, and these form part of the rationale behind the per dive exposure limits for NOAA table pp02 such as pp02 of 1.6 for 45 minutes. The end point was not 02 convulsions, such as the older convulsion studies, the end point was the development of VENTID in working dives in test subjects [with some subjects actually convulsing.] Again, these limits are for working dives.
Whole body toxicity is first felt by divers as burning in the chest, but its very unlikely the lungs undergo a full recovery with a normoxic break between exposures. The mechanism of action for for normoxic breaks is unclear, but it does work in delaying manifestations of whole body oxygen toxicity. Yes, you can diminish your risk of 02 convulsions by plugging normoxic breaks between you high pp02 exposure, whether its bottom mix or deco mix.
How long is recovery? Vital Capacity recovers in most people within 24 hours, it can be as long as 5 days. If DLCO is a measure of recovery, its likely full recovery is in at ~ 7-14 days. Post a recompression treatment, the return to diving period was arbitrarily set to twice that, what experts feel was enough time for residual bubbles to dissipate and for the body, such as the lungs, to recuperate.
What is there to worry about with repeated high pp02 exposures whether its from deco or high pp02 bottom mix? At minimum, accelerated deterioration of lung elasticity. Rebreather divers exposed to constant pp02 <= 1.3 have suffered month long injuries to their eyes, specifically retinas and lens, which appear to be reversible, for now. There are many others, but these two would be most noticeable to divers. FWIW changes in retina function is noticeable by electronic testing in dry dives before vision changes are noted by divers.
Take Home Message:
A resting state is key to tolerating high pp02, such as in decompression. Backgas breaks do delay toxicity and its physiologic rationale at this point is moot
There is data to suggest in water decompression can be tolerated up to a pp02 < 2.0
Divers shouldn't be lured into a false sense of security of a clock in using pp02 >= 1.4, a risk of convulsions can occur at any time in working dives
Bottom mix pp02 are safer pp02 < 1.2 and are limited by pulmonary toxicity
It probably unncessary, as time for sleep during a dive safari provides enough normoxic breaks to keep whole body toxicity at bay. But if one is engaged in doing a week long series of repeated decompression dives, tracking one's OTU is effortless .. most deco software do this. The main rationale for tracking OTUs is if remotely diver will need recompression during this period, the chamber operator can estimate just how much "frying" the bent diver's lungs are going to endure if he has pre-treatment OTU numbers in hand.
If what this means is shortened deco time, breathing the highest pp02 with tolerable toxicity is a proven way to accelerate decompression from inert gas loads
80 vs 100% 02 at Stop 20'
In the time frame of decompression, the choice is over a risk of 02 convulsions, and less about pulmonary toxicity. Is the risk of 02 convulsions greater with pp02 of 1.6 versus 1.3 at decompression? In deco, of little consequence, so risks being equal, the higher pp02 is better. See below for explanation.
Background Info:
O2 Convulsion Studies
Since 1947, across a range of pp02 with most at pp02 > 3, no air breaks. Convulsions occurred in ~100% of subjects up to a maximum period per pp02, but on repeated trials the same subjects convulsed at different times within a maximum period. The only constant was that periods when 100% of test subjects convulsed were earlier as the pp02 rose. For example, at a pp02 of 3.5, subject 1 seized 10minutes into the exposure. All subjects seized within 60minutes. After a break rest, the test is repeated, subject 1 seizes in 5 minutes, all subjects seized within 60 minutes. After a break, test is repeated, subject 1 now seizes in 50 minutes, while all subjects seize within 60 minutes.
02 convulsions thus, do not begin at the end of a clocked period per pp02 such as made out in NOAA limits; it becomes possible immediately past a threshold pp02. When subjects convulse varies for the same individual doing the same pp02 exposure at a different time: it may be less, unchanged or more.
The plotted shape of 02 toxicity, whether convulsions or minor ones labeled in recreational nitrox as "VENTID," were X = maximum time to toxicity, Y = pp02, appears as a rectangular hyperbola. For decompression or treatment purposes experts agreed that for safety a pp02 < 3 is a trade off, at ~ knee of curve, but as the shape shows its smooth there is no sharp cut off.
The image is on the upper right of the link, image with caption xy=1 in Quadrant 1 : http://mathworld.wolfram.com/RectangularHyperbola.html
Convulsions are rarer if pp02 < 2. Tolerance to pp02 at this level is high and made even higher with normoxic breaks, such that the principle concern is not convulsions, but pulmonary toxicity.
Dr. Edmonds has > 10 years experience is using pp02 2.0 and instituted this level as the pp02 of an in-water recompression protocol.
http://www.cisatlantic.com/trimix/AQUAcorps/Bent/inwater/Edmunds.htm
A review of others is:
http://www.bishopmuseum.org/research/treks/palautz97/iwr.html
At this point, we should really refer to pulmonary toxicity as whole body toxicity, since the lungs are just a manifestation divers feel of the effects of 02 throughout the entire body.
Being such, were do _you_ draw the line on a safe pp02? Dr. Vann summarized issues ~ that haven't changed much since 1992{?}, here's a copy:
http://www.cisatlantic.com/trimix/AQUAcorps/rebreather/OxygenExposure.htm
In conclusion, its very likely convulsions ARE related to a build up of an unknown byproduct of high pp02 exposure beyond the body's capacity to repair it [ thus pp02 > 3 inevitable leads to convulsions] AND can be accelerated or work synergistically with products of exertion, such as andrenaline release and C02 build up.
NOAA Nitrox Limits
NOAA threshold of 1.4 and the exceptional threshold of 1.6 were judgments by an expert panel and used to limit bottom mix pp02. These thresholds are for "normal" diving activity [or working dives], not in the resting state of decompression. There have been rare reported seizures on these pp02, so recommendations as far back as before 1995, were to lower it to about 1.2, of which few experts disagree.
The NOAA clock is modeled after convulsion studies. However, once past a threshold pp02, the risk of convulsions is more random, thus whether the per-dive time limit is true or not is moot in regards to CNS toxicity. However, one should track their total time, in regards to whole body toxicity in technical level dives.
FWIW there were many USN studies on 02 rebreathers that are similar to the NOAA clock, and these form part of the rationale behind the per dive exposure limits for NOAA table pp02 such as pp02 of 1.6 for 45 minutes. The end point was not 02 convulsions, such as the older convulsion studies, the end point was the development of VENTID in working dives in test subjects [with some subjects actually convulsing.] Again, these limits are for working dives.
Whole body toxicity is first felt by divers as burning in the chest, but its very unlikely the lungs undergo a full recovery with a normoxic break between exposures. The mechanism of action for for normoxic breaks is unclear, but it does work in delaying manifestations of whole body oxygen toxicity. Yes, you can diminish your risk of 02 convulsions by plugging normoxic breaks between you high pp02 exposure, whether its bottom mix or deco mix.
How long is recovery? Vital Capacity recovers in most people within 24 hours, it can be as long as 5 days. If DLCO is a measure of recovery, its likely full recovery is in at ~ 7-14 days. Post a recompression treatment, the return to diving period was arbitrarily set to twice that, what experts feel was enough time for residual bubbles to dissipate and for the body, such as the lungs, to recuperate.
What is there to worry about with repeated high pp02 exposures whether its from deco or high pp02 bottom mix? At minimum, accelerated deterioration of lung elasticity. Rebreather divers exposed to constant pp02 <= 1.3 have suffered month long injuries to their eyes, specifically retinas and lens, which appear to be reversible, for now. There are many others, but these two would be most noticeable to divers. FWIW changes in retina function is noticeable by electronic testing in dry dives before vision changes are noted by divers.
Take Home Message:
A resting state is key to tolerating high pp02, such as in decompression. Backgas breaks do delay toxicity and its physiologic rationale at this point is moot
There is data to suggest in water decompression can be tolerated up to a pp02 < 2.0
Divers shouldn't be lured into a false sense of security of a clock in using pp02 >= 1.4, a risk of convulsions can occur at any time in working dives
Bottom mix pp02 are safer pp02 < 1.2 and are limited by pulmonary toxicity
It probably unncessary, as time for sleep during a dive safari provides enough normoxic breaks to keep whole body toxicity at bay. But if one is engaged in doing a week long series of repeated decompression dives, tracking one's OTU is effortless .. most deco software do this. The main rationale for tracking OTUs is if remotely diver will need recompression during this period, the chamber operator can estimate just how much "frying" the bent diver's lungs are going to endure if he has pre-treatment OTU numbers in hand.
