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You wrote:
>
>> If this 'blow&go' refers to the 'exhale maximally @ depth
>> prior to ascent' historically used in submarine escape
>> training (not used any more), I fail to see how this will
>> produce a large gradient.
>> Irrespective of the amount of exhalation, the residual gas in
>> lungs (which will be there irrespective of how forcefully one
>> expires) will have the ppINERT of the absolute pressure @ wh/
>> that breath was inhaled at.
>> Thus the percieved tisssue sat at the aforementioned depth &
>> the ppINERT of lungs post 'full exhalation' will be
>> comparable. This assumes no local airway collapse, a problem
>> of blow & go.
>
>"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.
>
>> >Yes. By Causing a large gradient(~5ata) to exist between
>> >tissue nearly
>>
>> >saturated at 260fsw (as all *fast* compartments will be after
>> >25 min) and
>> >gas cavities pressurized at the ambient 100 ft stop, you
>> >could cause a
>>
>> >population of bubble nuclei to start growing.
>>
>> According to the Haldenian concept, it takes the t1/2=5 min
>> compartment
>> 30 minutes to 'sat'. THus no 'fast', or, for that matter, no
>> compartments are saturated in 25 min @ any depth. Saturation
>> is
>> intrinsically depth based. That is a compartment saturates
>> for a
>> certain depth. I presume the implication was not that
>> saturation is
>> reached faster as depth increases.
>Why is there any validity to the notion that the "fastest
>tissue" has a
>half-time of five minutes? Just because Haldane said so?
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.
At the same time assuming that most 'fast compartments' are
saturated in 25 min can be invalid, or at least nebulous, as fast
remains undefines, as does 'tissue'.
>Methinks blood,
>for example, would have a MUCH faster half-time. But blood is
>likely NOT
>limited by diffusibility of gas molecules; it is probably more
>limited by
>how long it takes for the blood to pass through the circulatory
system.
>
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.
Just like O2 extraction from blood can be computed, INERT
xtraction by
non SSat tissues from the relatively SSat blood can be computed.
So the time it tkes for 1 complete whole body circulation of
blood
would underestimate that. That consideration does not take into
account the true (whatever it is) kinetics of gas uptake.
>When they found that straight compartment models got people
>bent, their
>solution was to increase the maximum allowable tissue tension in
>the
>faster compartments, and decrease the allowable tissue tension
>in the
>slow tissues. This meant initial stops were shallower, and
>shallow
>stops
>were longer. I'd bet if they did the reverse (lower tissue
>tensions for
>the fast compartments and higher for the slwo compartments),
>they would
>have gotten people out of the water with less decompression
>time, and
>lower incidence of DCI. Of course it would still be a weak
>model,
>because it only looks at dissolved gases.
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. In a series compartment model the outcome
would be
different. So again lack of knowledge (my) does not allow me the
luxury of that conjceture. Another point to consider is the
differences that we all think we see as a result of saw tooth
profiles. Again, & I think U said it also, a single depth dive
(that is one that proceeds principally a given depth, save for
the descent & ascent) carries less risk that saw tooths.
An addition factor to consider may the variable effects of being
closer to supersaturation and is there allowance (time &
subsaturation) for redistributing dissolved gas
>
>> Obviously the relative supersaturation that will exist upon
>> arrival at
>> 100 ft (or any shallower depth) from a deeper depth is
>> predicated on depth & duration of deeper sojourns.
>
>But level of supersaturation may NOT be the main determinant of
>DCI
Agreed & actually I would love to discuss that with you (private
Email).
>
>> We have had this discussion with Pyle. I think that ascribing
>> the value derived from IWR solely to bubble 'crushing' may be
>> an over simplification.
>
>Agreed!
Wow - an agreement!
>
>> Rapid intervention with high ppO2 appears to be the
>> principal value of IWR.
>
>Double Agreed!
No No No.... I can't take this, not to big A's in row!!!!!
>
>> The presumed benefit (depth 30 ft) is
>> preventing tissue anoxia and contribute to the prevention of
>> further bubble formation (bubble formation based on offgassing
>> of supersat
>> tissue is time dependent & continues after surfacing) by
>> assisting in
>> offgassing - a result that can be achieved by 100% surface O2.
>
>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.
Incidentally when I was referring to the Hawaiian deco method, I
was
not referring to the Hawaiian IWR, but what was published in UBR
& SPUMS while bck (88 or so) on the final rpid deep dive Hi'in
fishermen use
at the end of their dive series. I think it was Kelly that
published
it. Something like Dysbarism in Paradise????
>> Again the value of IWR from the stndpt of bubble/DCS theory is
>> not
>> clear.
>
>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.
>
>> The same result could be obtained by slower ascents. The
>> issue here is
>> the large body of 'no knowldege'. The Haldenian model is
>> based on the
>> compartment SSat ratio and its reduction. It treats the body
>> as a set
>> of discreet & independent comparments. As this is not
>> reality, it would be
>> shortsighted to not consider compartment to compartment
>> transfer of gas
>> during deco, even gas uptake by slower comparments (that R not
>> yet SSat
>> to the deco depth) while the faster ones are offgassing. In
>> addition
>> one has to wonder about diffusion & diffusion limited
>> offgassing.
>
>Well said. It would also be shortsighted not to consider the
>effects of
>the presences of gas-phase bubbles in the blood and tissues.
>
Yeah, for all of our non-knwledge, yes. But again the issue of a
causal relationship between 'bubbles' & DCI (bends type) remains.
>Aloha,
>Rich
>
Regards
Esat Atikkan
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