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> Pyle :
> However, there are other factors associated with O2 that can
> (theoretically) work against you. For example, high PO2 leads to
> vasoconstriction, which means reduced perfusion. This can
> theoretically lead to reduced N2/He elimination efficiency from
> the tissues.
>
> Chuck :
> Could this not also lead to reduced delivery of N2/He to the
> tissues ? Perhaps a benefit of high O2 mixes within safe tox
> limits such as 100 dives on nitrox 32. Maybe not enough O2 !
Theoretically; yes. But by the time we get this far out into theory
(i.e., O2-induced vasoconstriction and its effects on both ongassing and
decompression) we are probably so far afield from what actually happens
in our bodies that to try to model it, or account for it on our deco
schedules would be silly. The theory is important to discuss, because it
helps us all get a slightly better handle on what might be happening to
us during decompression. But the bottom line in the practical world will,
for a long time continue to be (as Bill Hamilton says): "What works,
works."
> Pyle :
> My hunch is that the main advantage of doing the 10-foot stop time at 20
> feet is that, because of the increased ambient pressure, bubble diameters
> are smaller. Smaller bubble diamters lead to proportionally greater
> internal bubble pressures (due to surface tension effects on the bubble).
> This leads to steeper gradients across bubble membranes, which means
> faster gas elimination from bubbles.
>
> Chuck :
> I've wondered if the rate of diffusion of gas across bubble membranes
> effected by high surface tensions (slowed).
Perhaps not so much the surface tension per se, but certainly it is
slowed by the smaller surface area of smaller bubbles, and smaller
bubbles also *may* have more impervious surfactant layers. Like I keep
saying, it's all very complicated stuff. But based on my understanding,
at the depths we're talking about (10 vs 20' on 100% O2), and the bubble
sizes we're talking about (in the range that are considerably larger than
"micronuceli", but not overtly symptomatic), my money is still on the 20'
stop instead of the 10' stop.
> Is the surface tension at these interfaces caused by attraction between
> molecules of the blood or of the inert gas, or both?
I honestly do not know what's going on at a molecular level with bubble
surface tensions. A couple of those papers I cited by Yount talk about
possible effects of surfactant biomolecules that accumulate/align along
the bubble surface.
> Most likely it is a
> case of the properties of adjacent surfaces interacting to create a surface
> or interface with qualities specific to the combination rather than either
> substrate alone. This would mean that as the gases within the bubble or the
> chemistry and physics of the blood changed so would the nature of the
> interface through which these gases must pass by diffusion.
I think there is very little doubt that the manifestation of bends symptoms
is in large part dependant on the particular biochemical nature of the
diver's blood at the time of decompression. There was a guy on this list
years ago by the name of Steve Helps (went by the handle "Prime Rat") who
knew an incredible amount on this topic (I think it was his doctoral
thesis). I haven't heard from him lately.
> If oxygen is able to diffuse through tissues to parts of tissues deprived by
> reduced perfusion then so should nitrogen and helium be. There are so many
> avenues by which gases are being transported and redistributed and so many
> variable phenomena involved that there will never be a 100% reliable or
> accurate mathematical model of decompression dynamics. We will always be
> stuck with "what works" with a little bit of fudge factor thrown in.
THAT is *EXACTLY* what I think the take-home message of **ALL** of these
discussions should be!!!
> Pyle :
> I'm not sure if the unbound dissolved O2 is consumed directly, or if
> metabolic use of Hb-bound O2 frees up more Hb binding sites, to which the
> unbound O2 may bind. There are complicating factors (e.g., Bohr effect),
> but the point is that O2 is being removed (in one way or another) by
> metabolism; whereas He and N2 are not.
>
> Chuck :
> In discussions of O2 and its ability to cause DCS Hans Roverud
> assures me that the dissolved O2 is used before the Hb bound O2 is used
> as follows;
Yes, several people have confirmed for me that this is the case. I had
an argument once with a biochemist who told me otherwise. Had he not
been a biochemist, I would have discounted it outright. However, until
recent private email, I still harbored some doubt.
> In practice you do metabolize any excess of
> oxygen since the body draws from dissolved
> oxygen before calling upon that bonded to
> hemoglobin. Oxygen becomes a deco liability
> at PO2s far into the tox zone only.
>
> Chuck :
> Further input on this subject from George and others indicates that Oxygen
> can and does cause mild cases of DCS that tend to resolve quickly.
That's dangling way out on the hairly limb of speculation.....
> Every breath you take is mixed with what tidal volume of gas you
> could or did not exhale. This would keep the effective inspired mix
> from ever being a result of only the gas you are breathing, rather a
> resultant combination of what you inspired diluted by or mixed with
> some of what you had just exhaled.
Another complicating factor - yes.
> The more N2 or He you are removing from the blood at the lungs
> or the faster you are removing it the higher the fraction of that gas
> in the tidal volume remaining and mixing with the newly inspired mix.
> So the faster you remove inert gas the greater the fraction of that
> inert gas will be in your actual inspired mix.
and so on...and so forth...
> Since the alveoli hopefully do not collapse, as long as you are offgasing
> an inert gas it should be diffusing into them at all times during the
> breathing cycle as the blood passes by so that in that spanse of time between
> breaths they are still loading up with inert gas to mix with the next
> inhalation. If this is right then it is impossible to achieve 100% O2 in the
> alveoli since you are always off gassing at least CO2 (unless, of course,
> you're dead and someone has you on a DAN O2 kit).
Yup.
>
> Water vapor also exerts a partial pressure and comes into play when
> considering the actual situation within the lungs during respiration.
So many complicating factors.....
> radicals. Most of the O2 and virtually all the N2 you breath simply
> passes into and out of the respiratory tree having only gotten a little
> wet.
Hail rebreathers!
> So! Though more O2 is dissolved as ambient PPO2 rises, no
> matter how much more O2 you breath at any time during a dive
> your chemistry will not make any more radicals than it would
> while watching Bevis & Butthead in your livingroom.
I don't follow....
Aloha,
Rich
Richard Pyle
Ichthyology, Bishop Museum deepreef@bi*.bi*.ha*.or*
1525 Bernice St. PH: (808) 848-4115
Honolulu, HI 96817-0916 FAX: (808) 841-8968
"The views are those of the sender and not of Bishop Museum"
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