Well, the hard thing has been elucidating the mechanism through which bubbles do tissue damage. One theory is that it is simple ischemia -- the bubbles serve as emboli, blocking small blood vessels and depriving the tissues downstream of their blood supply. Unfortunately, this doesn't explain why some people can have high-grade bubbling without symptoms, and it also doesn't do a very good job of explaining why simply going on oxygen often relieves symptoms fairly immediately. So it has been considered that the air/liquid interface in the bubble may serve as a surface to activate immune modulators like complement -- studies have been done which have been inconsistent, some showing this occurs and some showing it does not. I believe there is also some interest in whether the interface can serve as a site for leukocyte adhesion and activation, as well.
I talked to some NEDU folks a couple of years ago, and they said they were also pursuing purely intracellular mechanisms of DCS -- Is the high nitrogen tension, or are intracellular bubbles interfering with cellular function?
The bottom line is that the precise physiological mechanisms of DCS really are not well understood. It's clear that keeping nitrogen offgassing tidy and controlled will vastly reduce the chance of symptoms. But the occurrence of DCS in divers whose profiles seem to be normally acceptable is really proof that there are more variables than we are currently taking into account.
awap, as I understand it, M-values are assumed maximum overpressure gradients that will be tolerated by a given compartment before bubbling occurs. These are assumed or empirically derived, and the decompression algorithm uses this value to determine where the diver needs to stop. Pure dissolved gas models (Buhlmann-type) use the M-values alone, along with tissue half-times and the information on depth and time, to calculate ascent profiles. Bubble models, although they also use the same kind of maximum tension limits, also consider bubbles, usually assuming that microbubbles exist before and during the dive, and making assumptions about critical radius (above which the bubble will expand, and below which it will collapse). Bubble models tend to create profiles where first stops are deeper than the pure dissolved gas models.
To my knowledge, there are no good, sizeable studies comparing people running dissolved gas models with people diving bubble models to see if there is any significant difference in DCS between them, and if so, on which profiles it occurs. The bottom line is that both work well in the majority of cases, if the divers stick to their plan. This kind of research is extremely hard to do, because the low prevalence of DCS means you have to put a lot of people through a lot of dives to get people with symptoms (and not many people want to dive profiles that are likely to cause them!) Doppler monitoring has been substituted for symptoms as a measure of decompression stress, but as noted, it isn't a perfect proxy.
For people who find this kind of discussion interesting, I would highly recommend Mark Powell's book, Deco for Divers. The book is highly readable and has very little math, and draws together information I spent a couple of years finding and wading through on line -- it's well worth the investment in money and time.
