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> >"Blow & Go", I think, refered to "blowing" the BC full of air
> >and "going"
> >to the first decompression stop as quickly as possible.
>
> That still does not alter the INERT composition of the contents
> of the lungs - it will equal to that of the latest breath + a
> small quantity added due to offgassing.
Hi Esat,
Yes I know, but the discussion didn't have anything to do with the fact
that the inert gas partial pressure in the alveoli is proportional to
depth. "Blow and Go" was a term used to describe the practice of rapid
ascents from the bottom to the first "required" decompression stop
("required" according to compartment-based models). This practice seems
like a real winner from a compartment-based perspective, because it
maximizes the inert gas gradient across the alveolar membranes while
"theoretically" preventing the formation of bubbles (because as we all
know - bubbles don't exist in our bodies until we exceed the
M-values...yeah right)
The discussion was about the fact that looking only at dissolved gases
(and not gas-phases gases), decompression schemes proposed by
compartment-based models are fundamentally sub-optimal.
> Rich, as I proceeded to elaborate below, from the standpoint of
> real body modelling, Haldane & most compartment models R most
> probably inadequate. Notice the caveat 'if Haldenian is
> accepted, then t1/2=5, ' etc. At no instance did I equate tissue
> with compertment and, provided that t1/2 of compartments are
> being discussed, one has to look at the values used in the
> models.
I know, and I apologise. I saw what you had written, but I was running
late this morning and didn't have time to go back and edit the message -
I left it in to get across to the techdiver subscribers.
> That is most probably correct it you assume that the rate of
> ongassing of blood is solely driven by ppINERT alveolar.
> However, I would propose that, at that level, one has to look at
> the difference of
>
> ppINERT alvolar mediated loading of blood & the unloading due
> to blood yielding some
> of its INERT at the tissues as it is SSAt to INERT relative to
> them.
Agreed.
> I am not in the position to extrapolate from what I know. Deeper
> stops
> would have the presumed benefit of regulating offgassing in a
> parallel
> compartment model.
My favorite theoretical explanation of the deep stops is that they allow
time for off-gassing from intravascular BUBBLES into the surrounding
tissue, and therefore minimize bubble growth during the initial ascent
(keeping bubbles below a threshold radius). However, since I am also not
in a position to extrapolate from what I know, I'll make it clear that
the only thing I "know" is that I have consistently felt better after
decompression dives whereon I included deep stops, than after dives
following compartment-based profiles. And my n-value is pretty damn big.
> >But level of supersaturation may NOT be the main determinant of
> >DCI
>
> Agreed & actually I would love to discuss that with you (private
> Email).
Anyone else have comments? Karl? Are you on the list? (If so, you should
have gotten two copies of this message). Do you have an opinion on this
discussion? I apologise if you didn't want to get dragged in, but I'd
really like your thoughts.
> Wow - an agreement!
Yeah, it was weird for me too ;-)
> No No No.... I can't take this, not to big A's in row!!!!!
Well, we can't agree on EVERYTHING!
> >Maybe, matbe not. Let's take off our lab coats, put the
> >theorizing on hold for a while, and go out and see what happens
> >in the real world,
> >shall we?
>
> Pyle let's not rehash the IWR article & the reponses back &
> forth.
Sorry....I coudn't resist....:-)
But I wanted to make sure you understood Eric Maiken's point that the
advantages of "compression" (in addition to O2) go BEYOND a simple
interpretation of Boyle's law. Bubble physics is a complicated subject,
but from what I am learning, it's EXTREMELY useful to our understanding
of how to optimize decompression. In a nutshell for the case in point: A
bubble will shrink or grow as a function of the gradient between the ppINERT
inside the bubble and outside the bubble (dissolved in blood & tissues)
This is an oversimplication. Giving O2 to a DCI victim on the surface
establishes a gradient from the bubble to the blood, but giving O2 to a
DCI victim at, say 1.4ATA ambient pressure, establishes a much larger
gradient from the bubble to the surrounding tissues, not only because the
ppINERT inside the bubble is greater due to boyle's law, but ALSO because
other aspects of bubble physics (surface tension, etc.) lead to a
non-linear (increasing) internal bubble pressure.
Your suggestion (if I read it right) that compression is only useful
because it shrinks bubble radii, therefore allows more blood flow to
potentially anoxic tissues -- is missing a more important aspect of the
value of compression (which also happens to relate to the
theoretical value of deeper inital decomrpession stops)
> >It's only clear from what's actually happening in the real
> >world.
>
> I have yet to see evidence that there exists a causal, note word
> causal, b/ DCS & bubbles.
Fair enough. Anybody else care to comment here?
> Yeah, for all of our non-knwledge, yes. But again the issue of a
> causal relationship between 'bubbles' & DCI (bends type) remains.
Do you see a "causal" relationship between inert gas loading and DCI?
I'm not sure I do.
Aloha,
Rich
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