What is the deepest you have been on pure O2?

[Lorenzoid]

It's my understanding that there is also a time factor involved along with the depth factor, and probably many more factors than that, including individual physiology--and this contributes to unpredictability just like we have unpredictability in decompression. How many minutes spent at a given depth matters, though I believe the relationship is not well understood. The conservative "rule" is that a diver should spend zero minutes below whatever MOD they have calculated based on whatever PPO2 they believe is safe for what they're doing.

 

[Doppler]

Once again we need to return to the basic concept... the oxygen depth (the partial pressure the gas delivers), which we express 1.2, 1.3, 1.4, 1.5 bar etc, DOES NOT constitute oxygen dose... To be able to judge the "safety" of any particular oxygen partial pressure, we also have to consider TIME...

In short: DEPTH + TIME = DOSE

NOAA's guidelines suggest 45 minutes for an oxygen depth of 1.6 bar/ata; 120 minutes for 1.5 bar/ata, 150 minutes for 1.4 bar/ata, etc.

To suggest that a PPO2 of 1.6 bar is more "dangerous" than 1.4 without supplying the rest of the equation shows a misunderstanding of the issue.

Certainly the limits at 1.6 are very much more appreciable, but three hours at 1.4 is more dangerous that 10 minutes at 1.6... all things being equal.

To answer the OP's original question, My peers and I have regularly and routinely breathed a gas delivering a PPO2 of 1.6 bar with no ill-effects. However, one needs to be aware of the risks of this practice AND one needs to UNDERSTAND what the NOAA limits mean.

**** covered in any worthwhile technical diving program.

 

[Akimbo]

I have spent well over 100 hours decompressing on pure in the water at 20' and several more times that at 60' on pure O2 in a chamber. The recommended limit was 2.0 ATA most of my career. Doppler's comments are very important to understand rather than assuming you are going to convulse at 1.61 ATA. This thread has a fairly complete discussion on the subject:

Oxygen Toxicity Limits & Symptoms

Edit: I have had two friends over the years that were ex-SEALs. They both told me that they have been to 60-65' in the water on pure O2 rebreathers under adverse conditions. I also saw divers in the North Sea using 3.0 ATA in the water during the 1970s.

 

[karstdvr]

Once again we need to return to the basic concept... the oxygen depth (the partial pressure the gas delivers), which we express 1.2, 1.3, 1.4, 1.5 bar etc, DOES NOT constitute oxygen dose... To be able to judge the "safety" of any particular oxygen partial pressure, we also have to consider TIME...

In short: DEPTH + TIME = DOSE

NOAA's guidelines suggest 45 minutes for an oxygen depth of 1.6 bar/ata; 120 minutes for 1.5 bar/ata, 150 minutes for 1.4 bar/ata, etc.

To suggest that a PPO2 of 1.6 bar is more "dangerous" than 1.4 without supplying the rest of the equation shows a misunderstanding of the issue.

Certainly the limits at 1.6 are very much more appreciable, but three hours at 1.4 is more dangerous that 10 minutes at 1.6... all things being equal.

To answer the OP's original question, My peers and I have regularly and routinely breathed a gas delivering a PPO2 of 1.6 bar with no ill-effects. However, one needs to be aware of the risks of this practice AND one needs to UNDERSTAND what the NOAA limits mean.

**** covered in any worthwhile technical diving program.

Good answer. Important to remember other intangibles like CO2 build up from the work of the dive, and medications that lower the convulsion threshold, for example

 

[Kevrumbo]

Simon Mitchell M.D. Ph.D, on a Bikini Atoll charter 29Jun to 11July2013, gave an interesting lecture on re-examining the efficacy of deepstops based on a NEDU study (Study Conclusion: Controlling bubble formation in fast compartments with deep stops is unwarranted for air decompression dives) with some of his as of yet unpublished data & analysis. He also kindly provided "pro bono" adjunctive Intravenous treatment -Plasmalyte with Ibuprofen drip- after my IWR (In-Water-Recompression) session for a type I pain only Right Arm DCS hit on Day 8 out of 9 scheduled dive days at Bikini. His lecture and the NEDU study got me to re-think about utilizing deep stops when using Deep Air or light Trimix -i.e. on non-Standard Bottom Mixes.

Probable cause of my DCS was a slow tissue accumulation of N2 which finally approached critical surfacing M-values by Day 4 -experienced "niggles" post-Dive#1 but which went away on descent of Dive #2- and further exacerbated on Day 8 by aggressive Scootering (right hand is my trigger handle hand) & deco bottle manipulation of four 11L/AL80 tanks at depth and at the surface post-dive. Used 20/20 trimix and Air top-off for the second dive -only two deco dives a day- with 50% & 100% O2 deco gases in 11L tanks, and using the Ratio Deco Method. Depth ranges were 36 to 57 meters; Bottom times 40 to 70 minutes on open circuit double 11L backgas & a 11L stage tank for all dives.

Symptom was acute pain Right Arm immediately upon surfacing from Dive#2 (36m ave depth for 70min on the aircraft carrier USS Saratoga) of Day 8 -on a scale of one-to-ten, the pain was a throbbing "10++". Upon re-descending to start IWR (9m depth on O2), the pain immediately reduced to 4, and further subsided to 2 after 90 minutes of O2 IWR Therapy. Additional surface breathing on O2 for two hours with IV therapy administered by Dr. Mitchell as described above.

Took four days off in between Bikini and Truk Trips, and resumed similar deep diving on the Truk wrecks 13 to 20July 2013, using Ratio Deco but with extended Oxygen deco with a slow surfacing ascent rate of 0.5m/min, monitoring for relapse/recurrence signs & symptoms of DCS (there were none).

Lessons learned: Be aware of "longish" deep stops coming off relatively high N2 bottom mixes (20/20 trimix and essentially Deep Air); and especially with consecutive dive days over the course of a week or more, consider extending O2 deco stop time with slow surfacing ascent profiles by day 3 or 4. And have an IWR plan ready if you do surface with acute type I DCS pain.

The besr practice is to take at least a day-off midweek to effectively off-gas the slow tissues. I would recommend this even for those diving lower N2 content Standard Bottom Mix Gases as well. . .

Finally, I have now bought a Shearwater Petrel Dive Computer to help monitor & track slow tissue loading, as well as CNS/Ox-tox exposure.

______________________________________________
Breathing Open Circuit Oxygen at 9meters depth for over an hour (an Oxygen ppO2 of 1.9) during an In-Water-Recompression (IWR) session last year Oct-Nov 2014, with interval relieving Air Break gas switches. The IWR was performed off the end of Truk Stop Hotel Pier lying prone & relaxed at 9m depth on a sandy bottom in 28 deg C water temp.

Three separate type I DCS incidents experienced on this trip last Oct-Nov 2014 -all were upper Right arm/Shoulder classical acute "pulsing" symptoms with increasing pain within 90min time post-dive, and occurring within three to four days of starting Open Circuit Deep Air bottom mix dives with 50% & O2 deco (two tech deco dives per day with a 3 hour SIT). Possible contributing factors were dehydration, insufficient "acclimatization" to the tropical environment, and no prior "work-up" practice deco dives to sensitize the body's immune/inflammatory response system to high FN2 saturation & resultant residual bubbles in slow tissues & venous blood vessels (first early AM deep dive with deco of that trip was SF Maru at 51m ave depth, 45min BT and over two-and-a-half hours runtime, after trans-pacific flight from Los Angeles arriving late in the night before). Also rule-out neo-vascularization of Right Shoulder Joint/Upper Arm due to previous type I DCS injury ( see above Bikini Atoll 2013).

All DCS Pain Symptoms at that time last Oct-Nov were resolved with IWR -the modified Australian Method as taught by UTD- with either 30, 60 or 90min of elective prescribed O2 breathing therapy at 9m depth (10min O2:with 5min Air Break); and then slow 0.1m/min ascent to surface (same breathing 10min O2:with 5min Air Break). Went with 60 minutes O2 time at 9m (Air Breaks do not count or accrue credit into the O2 time at 9m; on the slow 0.1m/min ascent you have to hold at depth during the 5min Air Break, so after 10 minutes and 1 meter delta of ascent on O2 you switch to Air and stay at that depth for 5 minutes). The entire IWR treatment session took three-and-a-half hours and the CNS readout on the Petrel Dive Computer was maxed out at "999". ​

_______________________________________________________
From Simon Mitchelll, MD, Ph.D ; quoted from CCR Explorer Board:

Hello,

This is an interesting topic which is open to a huge amount of misunderstanding.

First, let me make one thing very clear: I am not proposing any change to the CNS limits as currently taught to technical divers. For a start I have no data to justify such a proposal, and any change would be replacing one set of limits that are largely data free with another set that are largely data free. What I was trying to do in the presentation was to put some context on the current NOAA limits from the perspective of expedition level technical diving where we are frequently forced to exceed them during long decompressions. Let me try to explain.

One of the most common questions I get asked at high-end technical diving shows is "how do I deal with the fact that my CNS% frequently exceeds 200 towards the end of a long decompression from deep dives. Am I going to tox, or are the limits wrong"? The truth is that many such dives have been done, and adverse outcomes (seizures) seem rare so where does this leave us? The current limits were originally proposed by brilliant diving scientist Chris Lambertson, and first published by NOAA. They have become known as the NOAA limits. As best we can tell, Lambertson based them on his experience and observations, rather than on a formally accumulated database of known outcomes. Morevoer, they probably reflect his experience of working exposures / or experiments in which physical activity was maintained at a fixed depth, rather than of dives or experiments with a short period of activity deep and a long tail of shallow exposure during rest (like a real technical dive).

This is where it gets interesting because activity status and depth have significant implications for risk of oxygen toxicity; largely because these factors influence the tendency to retain CO2, and CO2 retention in turn is a major risk factor for CNS oxygen toxicity. When we exercise at depth during breathing of a dense gas, there is a tendency (stronger in some people than others) to retain CO2. I have written at some length about this elswehere (the RF3 Proceedings freely available on line are a good place to start) and so I won't explain this in detail here. However, the increased work of breathing imposed by dense gas, the respiratory apparatus, and exercise blunts the normal increase in ventilation of the lungs which is how we get rid of CO2. If we don't ventilate the lungs enough, and therefore don't get rid of the CO2 we are producing, then body CO2 levels rise (CO2 retention). When CO2 levels rise, this markedly increases the circulation of blood through the brain, and therefore results in a higher delivery of oxygen to the brain tissue. Not surprisingly, this increases the toxicity of oxygen.

This brings me back to the question I am often asked at dive shows about high CNS percentages during decompression. The tendency to retain CO2 should be less when resting at shallow depths breathing a less dense gas. This would imply that the NOAA CNS limits are less likely to be strictly relevant to a diver resting on deco than a diver exercising at depth. On this basis, I have always been tempted to answer the question about risk during deco along those lines, and to suggest that having a CNS percent of "200" is probably not as significant in the resting deco phase of the dive as it would be if you were exercising at depth. Indeed, there is likely to be a substantial difference in risk between these two scenarios, even though the CNS% is the same. However, I was never confident in giving this answer simply because no one had ever checked for CO2 retention during resting decompression during long rebreather dives. In theory, it should be much less likely than at depth because the divers are at rest and not breathing a dense gas. But one or two of the risk factors for CO2 retention are still present during deco; not least of which is breathing through a device that does increase the work of breathing.

Thus, on a recent expedition to Bikini atoll we monitored 18 divers during two dives by measuring their end tidal CO2 immediately on arrival at the surface and before they left the water. Unfortunately there is currently no means of monitoring end tidal CO2 during the decompression itself which is why we chose this strategy. To cut a long story shortish, there was no obvious tendency for the divers to be retaining CO2 during resting shallow decompression. Their surfacing end tidal CO2 values were not different to control values made at rest on the boat 2 hours after the dive. One diver surfaced with a slightly higher than normal value after one dive.

This study suggests that there is no general trend to CO2 retention during shallow resting decompression, and this would support the notion that limits primarily targeted to oxygen exposure during activity at depth are probably not as relevant to the shallow resting decompression phase of the dive. This provides some reassurance that allowing the limits to exceed 100% during deco is not overtly irresponsible, but it does not of course, provide any guarantees that seizures will not occur under these circumstances. Clearly such events are still possible.
[Study Abstract: End tidal CO2 in recreational rebreather divers on surfacing after decompression dives. - PubMed - NCBI ]

Thus, my answer to the question "how do I deal with the fact that my CNS% frequently exceeds 200 towards the end of a long decompression from deep dives. Am I going to tox, or are the limits wrong" is now slightly more informed. I can say that there is evidence to believe that the limits are almost certainly less relevant to shallow resting decompression than they are to the deep working phase of a dive. That does not mean that divers are "tox proof" during decompression because they aren't. But this does provide some measure of reassurance that the high CNS percentages we see on deco do not have the same implications they would have if we were working at depth with the same percentages. I hope you can understand the subtleties of this.

We should continue to teach the currently limits because they have provided a useful benchmark, and entry level technical divers do need some guidelines. Moreover, the NOAA limits may well have sharper predictive power of problems during activity at depth. For example, you probably don't want to be exercising hard when breathing 1.3 ATA for more than 180 minutes (CNS 100%). But there is now reason to believe that the risk (for most people most of the time) of a problem at the same CNS% during resting shallow deco is probably less.

Hope this helps.

The paper has been accepted for publication in Aviation Space and Environmental Medicine. I will let you know when it is available.

Simon M

http://www.ccrexplorers.com/showthread.php?t=17617

PPO2 Exceptional Exposure Table

We removed the Exceptional Exposure Oxygen tables from the NOAA diving manual 4th editon because there was fear that if the general public saw them printed that they might take it as an endorsement to use them.

The NOAA exceptional exposure limits are set for extreme emergencies only and are not for routine use. IE: should be used for life saving only.

These are for a working dive meaning with lite exertion. Remember that there are a variety of factors that come into oxygen toxicity, and crossing the 1.6 atm 45min line does not guarantee convulsion, it also does not guarantee it won't.

NOAA OXYGEN
EXCEPTIONAL EXPOSURE LIMITS
PO2 Minutes

2.8 5
2.4 10
2.0 30
1.9 45
1.8 60
1.7 75
1.6 120
1.5 150
1.4 160
1.3 240

As you can see the exceptional times allow you a fairly large margin to use this method for an "escape." The table is NOT linear. Note that exceptional exposures are DANGEROUS and can only be done once in a day. . .

Joel Silverstein

​

 

[Remy B.]

How long were your deep stops Kevin ?

 

[Kevrumbo]

How long were your deep stops Kevin ?

Initially used Ratio Deco Method Deep Stop Profile at 75% and 50% ave depth, for two and four minutes respectively (along with Nitrox50 intermediate deco S-curve profiles emphasizing the high ppO2/"Oxygen Window" at 21m & 18m). Operational ave depth ranges were from 45m to 51m on Deep Air or 20/20 Trimix.

On the Truk Oct-Nov 2014 type I DCS hits and subsequent IWR sessions: Pain immediately -on a scale of 1 to 10- reduced from a "10+" to a "4" upon descent passing 6m and settling down at 9m depth. After the three-and-a-half hour IWR session, it was an dull "achy" 2 and the next morning just general musculo-skeletal sore & stiffness. But was always falling "behind the 8-ball" on that trip last year; seems like I couldn't effectively eliminate the inert load and was becoming susceptible to later DCS hits on that limb (probably due to repeated & previous acute type I DCS Pathology & injury neo-vascularization/inflammation).

2.0 ATA (or slightly over 9m depth) in my opinion is a good compromise IWR pressure that's not as OxTox risky as going in-water deeper to 20m & starting a prescribed standard USN Chamber Table 6 profile for instance; And yet 2ATA is still deep enough for relief of most simple type I DCS musculo-skeletal limb/joint pain-only symptoms. By Boyle's Law, this is relatively equivalent to reducing pathological bubble size by roughly 20%, and of course squeezing inert gas volume by 50%. (For acute type II DCS/AGE -IWR is not recommended- There better be a dry Hyperbaric Recompression Chamber ready for use nearby).

On last return Truk trip Jan 2015, compensated for slow tissue residual N2 loading by extending O2 deco stops an extra ten to twenty minutes, but with an uncomfortably high CNS OxTox figure result of 300 to over 500 max as tracked by the Petrel dive computer on 30/85 GF. No acute DCS symptoms were experienced on this last trip.

See:
http://www.scubaboard.com/forums/te...-deep-stops-increases-dcs-33.html#post7335373

 

[Remy B.]

I'm in the middle of my AN. and it mention about a 1 to 2min stop at 50% of the max depth of the dive, but this is as for user decision and precautionary, the tables and software does not show the 50% actually, any particular reason you started at 75% and for longer periods ?,

 

[Kevrumbo]

I'm in the middle of my AN. and it mention about a 1 to 2min stop at 50% of the max depth of the dive, but this is as for user decision and precautionary, the tables and software does not show the 50% actually, any particular reason you started at 75% and for longer periods ?,

The particular reason . . .well, again my "acute attending personal Hyperbaric Physician" who treated me in Bikini Atoll 2013 understood and explains it best on my behalf:

Originally Posted by Kevrumbo

Simon, I'm simply not willing to risk bubble nucleation & formation in my Fast Tissues for the sake of not loading/supersaturating my Slow Tissues later on in the deco profile (per indication of those "heat maps" by UW Sojourner); essentially a "Robbing Peter to pay Paul" dilemma.

And yes, I have plenty of time and an 11L Alu full of O2 to clean-up those Slow Tissues. . .

Originally Posted by Simon Mitchell
-
Hello Kev,

I guess this is the sticking point. It is an article of faith for you that allowing fast tissues to supersaturate early in a profile that places less deep stops in your ascent is harmful, and there is probably nothing I can do to change your mind on that. However, I must point out that you only believe that because someone has told you it is so. It is an attractive theoretical assumption that many people believe(d) in the absence of any confirmatory data. The point is, that there is now data that challenge the idea. As UWSojourner's heat maps have illustrated the NEDU deep stops profile did reduce fast tissue supersaturation compared to the shallow stops profile, but this did not result in better outcomes. If tight control of fast tissue supersaturation early in the ascent is as important as you believe, why did the profile with the best control of fast tissue supersaturation early in the ascent produce the highest DCS rate?

Anyway bud, if you do what you say you are going to do and significantly pad your shallow oxygen decompression it may not matter too much what you do earlier. Just don't have a seizure please!

I hope you have a fabulous trip. I may have mentioned I am going back with Pete Mesley in November 2015.

Simon

 

[Divetech99]

Kevrumbo, thanks for sharing your experiences. On hindsight, in future deco dives, would you still run with GF of 30/85 or would you go with a more conservative GF like 35/75 or something else?