Counter intuitive diving physiology question that must surely have a sensible answer

[Bubbletrubble]

This is an excellent question.
If someone is really listening to a lecture on DCS pathophysiology/treatment and understands the basics of bubble growth, this kind of question should pop into his head.

To round out the above discussion related to post-dive oxygen administration...

I think Kern's comments can be a little misleading, although he did point out the predominant factors in bubble growth dynamics. It's more complicated than that. FWIW, there have been animal studies which demonstrate measurable bubble growth in tissue during the initial stages of post-dive oxygen administration. A few different hypotheses have been offered to explain this phenomenon. TSandM alluded to one of them (O2 diffusion into a bubble which exceeds inert gas diffusion out of the bubble). As TSandM mentioned, researchers still know embarrassing little about DCS pathophysiology.

The OP asked why O2 administration at the surface does not worsen the diver's DCS symptoms. In searching for an answer, it's very easy to get caught up in the math/physics underlying bubble growth dynamics and various other biological processes (inflammation cascades, ischemia/hypoxemia, etc.). Unfortunately, the average diver lacks the scientific training to make sense of it all. One thing to bear in mind is that the clinical benefits of breathing 100% O2 at the surface may not be solely due to the decreased amount of inert gas (nitrogen) inhaled. In certain contexts, O2 is known to have direct cardiovascular effects -- some potentially good, some potentially bad. Reading up on the vasoactive effects of oxygen, you'll learn that hyperoxia can give rise to reactive oxygen species which decrease bioavailability of nitric oxide and result in vasoconstriction (good or bad depending on the location/type of blood vessels involved). O2 administration can also potentially increase the oxygen dissolved in blood plasma. It's a relatively tiny effect compared to the oxygen-carrying capacity of hemoglobin in the blood, but given the possibility of the diver being hypoxic/ischemic, every little bit might help the overall clinical picture.

If talk of M-values and inflammatory signal transduction makes your head spin, then focus on the real reason we administer oxygen as first aid treatment for DCS -- it just works. There's at least one study (Longphre et al., UHM. 2007, 34:1) out there, investigating a large number of DCS cases, that demonstrates a better outcome for people who received normobaric O2 administration following the dive. From a treatment perspective, this is all that really matters. Discussion of M-values and possible inflammatory cascades is purely theoretical and/or speculative. Empirical evidence trumps any theoretical or mathematical discussion.

I realize that this probably doesn't sound like a satisfying explanation. It's not meant to be.
It seems like the more you learn about something, the more you realize you don't know.

FWIW, I really hate it when a teacher/instructor/professor/scientist attempts to dismiss a student/audience member with a question by giving a hand-waving/theoretical answer (unless that type of answer was specifically sought by the person posing the question). My BS detector goes into full-alert mode at that point. This happens all the time in scientific post-talk Q&A sessions. I'm not always sure if it's due to the scientist lacking social skills, purposefully overstating the results of the work, or just trying to BS his/her way out of the question. (Just to clarify, I don't think any participant in this thread has done that.)

 

[Bombay High]

What I was originally taught (22 years ago) kept changing over the years.

The answer (as I now see it) is that although you surface , reducing ambient pressure (thereby increasing bubble size) you are also
1 - taking away the N2 source by breathing pure O2
2 - Also increasing the rate of diffusion, increasing the gradient between the 100% intake to the N2 offgassing.

Obviously the better solution would be to stay at 6 metres and breathe pure O2

I have to say that the bubble models make a hell of a lot more sense to me than the Haldanean model we were originally taught.

My hunch is that we are still a way away from concrete answers.

 

[Agility]

One document I am reading is Understanding M-values By Erik C. Baker, P.E. It expresses M-values in FSW and tells me, for example, the M-value (DSAT RDP) for the 480 half-time compartment is 43.4 FSW.

Another document is "Assessing dive profile safety by using A Combined Decompression Model" by Steve Burton C.Eng, Mark Ellyatt. This document gives M-values in bars and gives me 1.32 bars for the 480 compartment (DSAT RDP)

Ignoring the weight of salt, they seem to be about the same pressure. And I believe they are telling me that the limit for surfacing the 480 minute compartment is 1.32 bars for the maximum tolerated overpressure.

So that means that the maximum inert gas pressure that cells in the 480 minute compartment can tolerate at the surface is 2.11 bars (1.32 + .79). Is that correct? Or is it 2.32 bars?

If I understand Baker's paper correctly the Mo value gives you the tolerated inert gas pressure at sea level, which would be 1.33 bars for the 480 minute compartment, meaning, that at this pressure you can ascend to the surface without the gas coming out of solution.
The pressure graph (figure 1) shows that the 1 bar for atmospheric pressure has already been considered and must not be added (again).