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> A long answer to my short question, but since you brought it (them) up; I know - that wasn't my original intent, but I'm recovering from a cold and my brain is sluggish, so the usual eloquence just wasn't flowing ;-) > > So, then, how do I reason that a setpoint of 0.7 doesn't leave enough > > margin for error for hypoxia? The answer stems from the fact that 90% of > > my concerns about diving with a rebreather have to do with what happens > > when the rebreather *fails* in some way. > > But first you digress? Actually, no - not really. I had to set the stage. > > A number of folks at the forum indicated that CO2 buildup > > can lead to blackout as insidiously as hypoxia or hyperoxia. > > My notes suggest that it can be as *fatal* as hypoxia or hyperoxia, not > that it is usually as sudden in onset as an O2 hit ir as insidious as > hypoxia. More important, it is probably a significant risk factor for O2 > toxicity. That is, hypercapnia and hyperoxia lead to CNS toxicity at lower > pPO2s Yeah, that's all fine. But the point is, we agree the real killer is the O2, not the CO2, right? > > Furthermore, if O2 continues to be injected into the loop faster than > > your body burns it up, the loop volume expands and expands until it > > maxes out on exhale (you also notice it by the fact that your buoyancy > > is changing substantially). > > I suppose that might depend on how tight you have the overpressure valve, > but the point is taken you will bubble or rise. I believe that on most > systems you could raise your FiO2 big time before you would notice a > volume change in the bag - especially at depth. Has this actually > happened to you while at depth? Is this what happens in practice? You're right about the depth thing - the volume (= buoyancy) changes are much more subtle at gereater depth, because the O2 represents a smaller fraction of the total gas at a given partial pressure. It's not that there can be a larger shift in the FiO2 without obvious signs at depth but rather, it's that a smaller change in FiO2 leads to a proportionally greater change in PO2. But in either case, the causes of too much O2 entering the loop are generally more obvious to the diver than the causes of not enough O2 entering the loop. Yes, it did happen to me once at about 250 feet. Two of the sensors had pockets of sub-setpoint PO2 gas trapped against the membrane, so the solenoid took voting logic and kept on pumping O2 into the loop. It was very obvious to me fairly quickly that the solenoid was firing far too frequently. It took me a while to figure out what was wrong, but I finally did the procedure to solve the water on the sensors, and brought all of them back on line. The PO2 peaked at about 1.6 or so, and I brought it back down with a burst of DIL. Next time it happens, it won't take me so long to figure out the solution, so the PO2 probably won't peak as high. > If I learned one thing from Ed Thalman and David Elliot, it was that O2 on > 30 - 60 mins deco at 30ft (say 1.0 ATA) is a whole lot different than O2 > breathed for 1-2 hours while you are generating CO2 exercising. I think > that it is a great mistake to assume a pPO2 tolerable while deco (usually > at rest) is not going to give you an O2 hit when used as a "hot" bottom > mix. On the other hand, deco is done at the end of the dive, after the cumulative exposure to O2 is high. If there's any truth to the time/dose concept of CNS O2 toxicity, then I could just as easily argue that the deco time is more dangerous than the bottom time because the "clock" has been ticking. Bottom line is, nobody really knows what the hell is going on, so we're all just rolling dice. The trick is to load the dice as much in our favor as reasonable. Besides, my bottom exertion level is seldom much greater than my deco exertion level, and if anything, I retain more CO2 on the deco line because I'm often catatonic and under-breathing. > Thalman really does have a point when he syas that both from a N2 and > an O2 safety point - the *only* large scale test data (3092 dives, if I > recall) are with fixed pPO2s of 0.7 and 1.2 You mean the only *published* and *controlled* data set. I have a data set of more than a couple of thousand dives of my own, mostly OC, but a growing number of CC dives. On the one hand, these weren't in totally controlled conditions. On the other hand, they were all done with me as the subject, so more accurately reflect my own personal physiology. Also, I fancy myself a rather clever chap who tends to pay attention to what has worked and what hasn't worked, so I alter my protocol both in response to what the USN and other experienced types tell me, as well as what I experience in the real world. I had a long & interesting conversation with Dr. Max Hann at the Hruska and Lessre BBQ. He's a *REALLY* sharp guy when it comes to deco. I asked him a lot of questions about my ideas of deep stops & such, and my impression from him was that I'm not as far off my rocker as I used to think I was. In other words, my data, which has led me to practices that include deep stops, and repetative 300-400 foot dives in a single day, and other things formerly or presently regarded as ultimate no-no's, might not be as far off the mark as the uninitiated might assume. > > I've been exposed to higher than 7.0 in a chamber, 3.5 in heavy work > > situations underwater, hours at 2.8 in a chamber, etc. - all with zero > > signs of CNS symptoms. It's a time/dose thing, > > I think it depends on your ability to neutralize those O2 radicals. A lot of people think that - but again, we're drifting back into theoretical discussions here. These are good, but must be balanced with real-world experiences. > SOme > days may be better than others and your actual paPO2 may not rise quite as > expected in reponse to a brief FiO2 exposure, but Thalman and Elliot both > agreed that exposure to pPO2s greater than 1.6 resulted in "regular and > unacceptable" CNS toxicity. I think its worth heeding there advice. To go > by the seat of your pants on this one may be to drop a load of crap on > your head. Yup, I think you're right. That's why I'm leaning to dropping the setpoint down to 1.3 (or maybe even 1.2). But preventing spikes above setpoint is an issue of training and discipline, not physiology. > > Hypoxia, on the other hand, has a relatively sharp limit - somewhere > > around 0.08-0.12 or so for blackout (range measured in hudredths of an > > atmosphere). There is very little margin for error here - when the PO2 > > gets low > > (Ed: try 0.16 ATA! 0.09 is iguana-thingy survival O2) O.K. - that supports my argument even better - I was being liberal against my own argument, but if you want to make it 0.16, that supports my initial point even more. (incidently, to further illustrate how I am a freak of nature, my own hypoxia tests have had me down to 0.05atm before I made a *conscious* and *deliberate* decision to "pull the rip cord". I started noticing obvious symptoms at about 0.15 or so.) > > I am fairly convinced that hypoxia is 1) operationally less self-evident, > > 2) is more "absolute" in when it happens, and 3) is less recoverable than > > hyperoxia is on a rebreather. Do we agree on that? > > Not with your 1): As you've just pointed out, hypoxia is not insidious When did I point that out in my previous post? I suggested it above in this post - but that was sitting down with zero exertion. At any work load, I would say that hypoxia *IS* insidious - very much so - both physiologically and, as my point 1 above was, operationally on a rebreather. > True, but what we are really arguing about here is what setpoint is a > better safety zone between too much and too little. If you accept the USN > upper limit of 1.3 ATA, then 1.3 is closer to 1.6 than 0.7 is to 0.2. But EXACTLY, and my point is that I have come to my own conclusion that I want to leave a much wider berth to hypoxia than to hyperoxia. > what *really* needs to happen is to get trained so that by reflex you are > looking at your primary and secondary pPO2 meters within the time frame > that you could breath the loop down to <0.2. No arguments here. > It's a lot easier to add O2 than to deal with a high pPO2 in the bag. That's irrelevent - the response to an out of range situation in either direction is to go immediately to OC, and secondarily correct the loop gas concentrations. It's also irrelevent because we're talking about probabilities of noticing that there is a problem in the first place. Correcting the problem is easy as long as you catch it before it is too late. My only point (which I could have and should have made in a single paragraph) is that: The killer problems on a rebreather (ignoring human error) are the system failures that lead to insidious problems - specifically O2 out of range problems. And of the O2 out of range problems, hypoxia gives me more major willies than hyperoxia for a variety of phyiological and operational reasons. Therefore, I believe the optimal setpoint on a closed circuit rebreather is above 1.0, and probably in the 1.2-1.4 range. Aloha, Rich
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