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Date: Tue, 1 Oct 1996 19:32:30 -0700 (PDT)
From: Peter Heseltine <heseltin@hs*.us*.ed*>
To: Richard Pyle <deepreef@bi*.bi*.ha*.or*>
cc: techdiver@terra.net
Subject: Re: Figure deco on the fly was Fwd: Real Life Scare
Rich,

A long answer to my short question, but since you brought it (them) up;

On Tue, 1 Oct 1996, Richard Pyle wrote:

> > Long, long ago, Peter Heseltine wrote:
> > 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?

Oxygen consumption rate. The Navy terms this a flow-rate (according to my
notes) because they were writing specs for all rebreathers. Note this
might be *more* than an injection of 3 L/min. It depends on the plumbing
and how much gas is already in the system, which is why the requirment
that the concentration not fall below 20%.

> 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?

> 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


> 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?

> 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.

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. 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

> 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. 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.

> 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)

> 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?

Not with your 1): As you've just pointed out, hypoxia is not insidious

> 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.

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
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. It's a lot easier to add O2
than to deal with a high pPO2 in the bag.
>
> > 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. ;-)

And as Kevin is saying right now, but what the fuck does Peter know
about this anyway? :-]

Mahalo

-peter

     *******************************************************************
     * Peter Heseltine, M.D., F.A.C.P.                                 *
     * Professor of Medicine                                           *
     * University of Southern California        LAC+USC Medical Center *
     * Tel: 213/226-6705                       1200 North State Street *
     * Fax: 213/226-2479                    Los Angeles, CA 90033-1084 *
     * Eml: heseltin@hs*.us*.ed*                                   USA *
     *******************************************************************


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