Good post, Rich. Your rationalization works for me. And, on the BioMarine, I've got four ways to notice whether I got the right amount of peotouze. Rod On Tue, 1 Oct 1996, Richard Pyle wrote: > > Hi Pete, > > > Assuming the right flow rate up to 3.0 L/min (which is mil spec) > > How do you reason that a pPO2 of 0.7 ATA does > > not leave enough room to prevent hypoxia? > > First of all, what do you mean by flow rate of 3.0 L/min? Since we're > talking setpoints, we're talking fully closed. "Flow-rate" has tended to > be used in SemiClosedSpeak. I assume what you mean is "Can the solenoid > keep up with 3.0 L/min O2 injection?", and I suspect that for most if not > all of the fully-closed units about to come on the market, the answer to > that question is a solid "yes". > > 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. When they work, they work > great. The situations you find yourself in when they *don't* work are > the ones that you really need to train for. Now, if a rebreather fails > on you, how are you gonna die? One way is from bends, but this is easy > to cover yourself for (backup deco tables, plenty of OC bailout gas > supply, IWR rig ready to go in the boat, etc.). Another way is from > hypercapnia. A number of folks at the forum indicated that CO2 buildup > can lead to blackout as insidiously as hypoxia or hyperoxia. This stance > surprises me, because it is utterly inconsistent with my own personal > experiences. Talking to the guys who are using BioMarines, I find it is > inconsistent with their experiences as well (and you BioMarine guys can > correct me if I'm wrong on that). I'm not saying that the people who > maintain that CO2 blackout is insidious are wrong, especially in light of > the fact that they have vastly more experience than I do. However, there > is no denying that my personal experiences are not consistent with that > stance. In any case, I think essentially everyone would agree that CO2 > blackout is nowhere near as insidious as hypoxia or hyperoxia, (i.e., that > the latter two problems are likely to occur much more quickly and with > much less warning than the CO2 problems). > > O.K., so that leaves us with O2 problems -- specifically either too much, > or too little. Like I said, 90% of my concern for diving with > rebreathers is when the things fail, not when they work. Putting aside > user error for a moment (users will always be able to kill themselves > pretty easily, and that's an entirely different discussion), the > rebreather can give you a hyperoxic mix by injecting too much O2, and a > hypoxic mix by injecting insufficient O2. Let's start with the hyperoxic > problem. One way this can happen is the solenoid can jam open. As I > already explained to "John Todd", this is a problem that is immediately > self-evident to the diver, and with the right training & equipment, is > easily overcome. Another way it could happen is by injecting too much O2 > in the loop because of a flaw in the solenoid control system (electronic > hardware or software). From my experience, this problem is also often > ('though not always) failry self-evident, simply because I find it easier > to notice a solenoid that continues to fire over and over again much more > obvious than a solenoid that doesn't fire at all. 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). > > O.K., so that's two ways a rebreather system failure can lead to > hyperoxia, the former is extremely self-evident, and the latter is at > least partially self-evident. Now, how can a rebreather lead to hypoxia? > First of all, there are essentially the same two ways: the solenoid can > stick shut, or the control system can malfunction. The difference is, > failures of this type on the hypoxic side are much less self-evident. My > solenoid often doesn't fire for one or two minutes at a time. Thus, > relatively long periods of time with no solenoid injection is not > unusual. If I am task-loaded, I have found that I am *much* less likely > to notice a non-firing solenoid than I am to notice an over-firing > solenoid, for several reasons. But these are not the only ways a > rebreather can lead to hypoxia. For example, a failure in the gas > delivery system (i.e., regulators and plumbing) might easily go > un-noticed. The solenoid continues to fire, but no or insufficient O2 is > passing through it into the loop. A well-trained diver will notice this, > but it is still much subtler than the hyperoxia failure modes, and is > therefore barely self-evident. > > O.K., now lets compare how "lethal" hypoxia and hyperoxia are. I think > it's fair to say that both can lead to death in divers, and neither has > any reliable physiologically self-evident warning. At the hyperoxic end, > the limit is unclear. Some say 1.3, some say 1.4, some say 1.5, some say > 1.6, the French commercial guys (I'm told) decompress routinely at 1.9. > 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, where the time factor is > usually at least a few minutes. In any case, the limit is at best a grey > zone of probabilities, with a range measured in tenths of an atmosphere. > 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 we black-out -- period. The time facter is always very short. > Furhtermore, hyperoxic symptoms (the CNS ones, anyway) are not especially > damaging per se - it's the subsequent drowning that gets you. With a full > face mask and an atentive partner, you can survive an O2 convulsion > relatively unscathed. With hypoxia, however, we're talking major loss of > brain cells if we're lucky, and death in any case that the problem is not > immediately identified and corrected. > > 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? > > If so, then we would put hypoxia above hyperoxia on the scale of > insidious nasties that can happen on a rebreather dive. > > Now, in my over-use of the word "insidious" above, I am emphazizing the > non selef evident nature of such failures. The more time between the > occurence of a rebreather failure and the point at which the failure leads > to death, the more likely a diver is to "catch" the failure and correct it. > > On the rebreather I use, I find it takes about 30-45 minutes for my body > to burn a loop full of gas at a PO2 of 1.4atm down to about 0.12atm - > lets' say that's about 0.1 atm every 3 minutes or so. If my setpoint is > 0.7, that means I have only about 15 minutes to "catch" a failure that > leads to hypoxia. My diving partner John burns O2 at least twice as fast > as I do, so if he was running a setpoint of 0.7, he would only have about > 7 or 8 minutes instead of 15-20. > > Alright, so I've wasted a lot of bandwidth and haven't exactly spelled > it out very clearly, so let me try to summarize: > > Rebreather failures are what get you. Hypoxia is scarier than > hyperoxia because it kills you directly, is harder to notice > operationally on a rebreather, and is not really a function of > increasing probability (more of an absolute cut-off). The best thing to > do is to choose a setpoint that maximizes your probability of survivial > for both hypoxic and hyperoxic failures. Given the relative > characterisitics of each type of failure, I prefer to leave a wider berth > between my setpoint and hypoxia, than my setpoint and hyperoxia. > > For me, the best midpoint between the two failure extremes is in the > range of 1.2-1.5atm. As stated in my original post, 0.7 does not allow me > enough margin for error on the hypoxia side. > > > It's odd to find myself advocating more O2 - or > > a higher pPO2 - but I count 0.7 ATA as three > > times what you are breathing in Hawaii right > > now. (This assumed you're not doing a 100% O2 > > surface break to get over your jet lag ;-) > > If the rebrether was 100% immune to failure, I'd be inclined to agree > with you. For me, it's not about finding the phyiologically optimal PO2 > to inspire it's about maximizing the probability of surviving the dive. > > > Seriously, the Navy upper limit of 1.3 ATA was > > just that. Remember that your reason for going > > higher than 0.7 or 1.2, better nitrogen load, has > > not been validated as a means to prevent DCI. > > (Remember the look on Ed Thalman's face). > > Rememebr, lower PN2 was only part of my reasoning. Besides, I'm not sure > if you and I got the same message from Thalman. To me, he was saying > that the models don't reflect what's going on - a message I have been > preaching for years. He was not saying that there is no correlation > between inspired PN2 and probability of DCI on a given dive profile. > > > While an O2 hit can occur almost instantaneously > > on exposure to a high pPO2, most occurred after "some > > minutes. So I reason that if it's like other phsyiology, > > exposure to 1.3 for several hours is a lot more risky than > > say a 20 min deco at rest on 1.4. > > But hypoxia does occur almost instantaneously on exposure to low PO2 in > essentially *all* cases, so that's what you REALLY need to guard against. > > > I think I'll stick at 0.7 for sport stuff and > > leave the hotter pPO2's to you guys in the > > Twilight Zone :-)) > > That's your call. ;-) > > Aloha, > Rich > -- > Send mail for the `techdiver' mailing list to `techdiver@terra.net'. > Send subscription/archive requests to `techdiver-request@terra.net'. >
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