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Posted by MHK on October 16, 2001 at 10:08:14:

In Reply to: Re: BillP, tleemay, GI III et al: I need your help. posted by Eins on October 15, 2001 at 22:12:29:

There are basically two primary theories with respect to tracking a diver's suseptibility to a DCI *hit*. Most in-water computer's tend to use some derivative of the Buhlman algorithm. Buhlman developed this algorithm is the late 1950's and early 1960's and he, in essence, built upon the earlier Haldane model [ circa 1908]. The underlying premise of the Buhlman model focuses on tracking, or maybe a better way to put that is, limiting the saturation of nitrogen. Buhlman proposed to do this by tracking hypothetical tissue groups, and the ability of different tissue groups to tolerate higher amounts of nitrogen before reaching the tolerated amount. He referred to this saturation point as an M-value. In other words, the maximum tolerable amount that a given hypothetical tissue group can accumulate before showing signs of DCI. If your buddy is shown a underwater dive computer these M-values are generally shown via a pixal and is used by most diver's as the time to ascend. By in large if the pixals are in the green area, a diver generally hasn't reached the saturation point, or M-value. If the pixals are in the yellow, that means a diver is nearing the theoretical M-value, or aturation point, and is suggested to ascend. And if the pixals are in the red, that generally means that a diver has reached a supersaturation point and should complete a decompression stop prior to surfacing as he has already passed the M-value and if he ascended he would likely { based upon the statistical sampling of the Buhlman studies] show signs and sypmtoms of DCI.

So in short the Buhlman model basis his statitical analysis on the *tissue loading* of Nitrogen [ N2] and it's relationship to a hypothetical M-value. If you need a technical explanation for your buddy it's that the Buhlman model ascent criteria is based upon a founding principle that the diffusion of an inert gas into a tissue is inversely related to the square root of the molecular mass [ a.k.a. density] of the gas. So Buhlman primarily focused on the notion that nitrogen loads up tissue groups and by controlling the amount of N2 in the tissue you can control, via statistical sampling, the on set of DCI. By Buhlman's own admission, see Buhlman, A.A. Decompression/Decompression Sickness. Berlin:Springer-Verlag, 1984, he recognizes that bubble formation occurs and may account for DCI, but he does not address that aspect in his studies.

More recent theoretical models utilize gas kinetic theories and statistical free phase bubble growth approaches along with a theoretical tissue saturation approach. While these theories are not new by any means, they do seem to be gaining in popularity in the last 10 years. For example in the early 1950's Behnke coined the term * silent bubbles* and Hill produced a model that later became the Varying Permeability Model [ VPM]. Hill postulated that by minimizing the formation and growth of bubbles by advanced * thermodynamic* calculations of decompression tables. Hill was an earlier pioneer in the notion of *deep stops* which was directly in conflict with the U.S. Navy's notion that you ascend as quickly as allowable and then long shallow stops to allow off gassing. Had in not been for the invention of Doppler's, which proved Hill's theory, no one would have accepted Hill's theory since it was outrageous at the time. Even today you still see MANY eductaors in decompression theory arguing that you should ascend as quickly as allowable and then pull long stops at 15'. Deep stops remain controversial as we speak.

In short, there still exist debate within the decompression theory scientific community between the benefits of using a disolved gas buildup approach -v- a free phase bubble growth.

The two most commonly accepted bubble models are the VPM and the RGBM [ Reduced Gradient Bubble Model] by Wienke. The RGBM theory is by in large an dextension of the VPM that included repetitive and multi-day diving. The underlying theory behind bubble models is that they try to limit the total volume of gas that forms bubbles, as opposed to the tissue loading models that control tissue stauration via the M-value. Therein lies the major difference between the two theories and once that concept is understood your buddy will be in a better position to compare the prevailing theories. He'll of course need to become fluent in lipid solubility issues, gradient and 02 windows, which I'll discuss if requested but is beyond the scope of this analysis. I've limited this analysis to a comparative discussion of tissue models -v- bubble models.

The following studies you'll need to become proficient in:

B. Hills Decompression Sickness [ 1977]. This is one of the more easily read studies.

D.E. Yount, D.C. Hoffman, On The Use of a Bubble Formation Model.. This really talks about the mechanics of developing a computer algorithm but you can't write an algorithm unless you understand the theory..

B.R. Wienke, Basic Decompression Theory and Application. For me Weinke is VERY technical, but if you can grasp his calculations Weinke is the best.

And of course, the Buhlman study that I noted in my text.

This is intended to be an generic over view and I'll be happy to answer follow up's but as I've noted I'm not playing sematics or word games...


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