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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
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