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> Yup, if you assume that bubbles are already present
> at the point of gas switch, because bubble formation
> is basically unrelated to decompression issues (except
> for cases of gross tension differential), the
> whole gradient-participation theory goes right to hell.
>
> In which case, it's all in the lungs, baby.
I'm not sure I follow you here.
> But it ain't so simple. The question begs: what's "gross"?
If I understand your question correctly, I believe we are talking
something on the order of 20,000 atmospheres.
> When considering tissue tension (NOT bubbles), is it really
> absolute, unrelated to the dissolved percentages of its
> component gasses?
Why would we ever consider tissue tensions for discussions of
decompression, without the context of bubbles? I don't believe there is
anything to suggest that the tissue tensions per se cause any bends
symptoms (narcosis, yes; O2 toxicity, yes; bends, I don't think so).
I suspect that what you are getting at here is:
According to compartment-based models of deco, only the combined "load"
of inert gas is considered in determining what the shallowest safe
decompression stop should be; no consideration is given to the ratio of
N2 to He (in our examples) comprising that "load".
You seem to cast doubt on this approach, and I will almost always favor
doubt cast upon purely compartment-based deco models.
The part that I don't understand, however, is that you seem to be
suggesting that abruptly switching from trimix/heliox as a breathing
gas at depth to air/nitorx as a breathing gas during ascent can lead to
spontaneous bubble formation (presumably in the blood adjacent to the
alveoli of the lungs), and such formation is more acute with more
significant gradient steepness? I can envision this process occurring
when a diver whose blood is heavily ladden with N2 abrubtly switches to a
helium-rich breathing gas; but I don't see it happening in the reverse
direction.
Exactly what aspect of the steepeness of the gradient in the former case
(He in blood, N2 in lungs) would cause bubbles to sponatneoulsy form?
Would it be the rate of diffusion across the alveolar membrane? If so,
where do the voids (bubbles) come from, exactly?
Maybe I'm just not understanding you correctly here.
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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