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

[Rhone Man]

For all the medical gurus on the board - one thing has always puzzled me about DCS.

1. We all know that DCS is caused by reducing the pressure such that nitrogen (let's keep it simple) dissolved in the tissues comes out of solution too rapidly forming bubbles.
2. We all also know that standard emergency treatment is put a bent diver on pure O2 until they can be treated in a recompression chamber. However, there are lots of well documented incidents where a diver's symptoms have resolved on O2 alone, obviating the need for chamber treatment.
3. But we are also taught that one can accelerate decompression safely by breathing pure oxygen, or highly enriched oxygen mixtures at depth, by dramatically reducing the ppN2 and accelerating off-gassing (which of course is safe at depth, because the pressure at depth will keep those little nitrogen bubbles small).

So my question is this: Why doesn't treating the bent diver with O2 at the surface make the DCS symptoms worse? You are reducing the ppN2 from 0.79 to zero - surely that should accelerate the nitrogen coming out of solution and make symptomatic bubbles worse rather than better?

[Kern]

You need to reduce the ambient pressure to force bubbles out of tissues/solution, & to grow in size. Reduction in gas fraction from 0.79 N₂ to 0, without an ambient pressure change, just reduces the amount of gas uptake by the tissues.

[Agility]

The oxygen window Oxygen window in technical diving - Wikipedia, the free encyclopedia provides the possibility to lower the sum of partial pressures in the tissues or bubbles beneath atmospheric (or ambient) pressure, thus causing bubbles (or pneumothoraces) to shrink.

[TSandM]

Kern really has the answer. There are two processes in play here. One is bubble formation and growth, and the other is gas tension related diffusion gradients. When you go on oxygen on land (or when you switch to O2 or a rich mix in the water) you increase the diffusion gradient, but you do NOT reduce the ambient pressure, so bubbles cannot grow, or cannot grow very much. You obviously will have some tendency for O2 to diffuse INTO the bubbles, as the oxygen tension around them increases, but oxygen's poor solubility and poor diffusion characteristics minimizes this.

To address another one of your assumptions, the role of bubbles in the pathophysiology of DCS is far from clear. Studies have revealed people with Grade 4 bubbling and no symptoms, and other people who are significantly symptomatic. So there is more to the process than simple bubble formation and growth, which is why people have spent a lot of time looking at immune system activation by bubbles (without really clarifying things very much, I might add.)

[Blue Sparkle]

So there is more to the process than simple bubble formation and growth, which is why people have spent a lot of time looking at immune system activation by bubbles (without really clarifying things very much, I might add.)

That sounds unusual/interesting to the un-schooled me. It sounds like you're saying it's completely unproven, but what is the theory? I get that the immune system must be (thought to be) involved somehow, but.... would you mind giving your "nutshell" version of the idea that's driving it?

(I would have posted what I though I understood as the theory and asked you if it was correct, but then I figured no point in "stating" something that's completely wrong and just confusing the issue.)

[awap]

So, the PP gradient and tissue half-time is what regulates on and off gassing rates. But ambient pressure regulates bubble growth in a tissue. How do those two parameters relate to M-values? I'm in the process of trying to understand M-values and this does have me a bit puzzled.

[TSandM]

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.

[Doppler]

So, the PP gradient and tissue half-time is what regulates on and off gassing rates. But ambient pressure regulates bubble growth in a tissue.

In addition to Lynne's excellent summary above, and her recommendation to invest in Mark's very useful reference book, you might be interested to note that if one follows the logic behind Dual-Phase decompression theory, the factors that some think drive BUBBLE GROWTH are not simply ambient pressure, but include much more complicated issues relating to bubble mechanics. You may find a quick study of Fick's Laws of Diffusion and Graham's Law (effusion) helpful.

How do those [-] parameters relate to M-values? I'm in the process of trying to understand M-values and this does have me a bit puzzled.

M-Values relate to neo-Haldanian decompression theory and not to modern Dual-Phase algorithms... Not suggesting you stop your study of M-Values but be aware that the science behind them is predicated on an assumption that maintaining tissue pressures less than the M-Value for the controlling compartment during ascent will PREVENT bubble formation. Also BE AWARE, with the aid of portable Doppler Ultra-Sound experiments on divers in the 70s and many, many times since, indications are that ALL DIVES are capable of producing bubbles in a diver's blood vessels: even a very mild sport dive during which no M-Values were exceeded.

As Lynne remarked, bubbles themselves may or may not be a major player in DCS. There have been a couple of studies that focused on the reaction of a diver's immune system to bubbles and whatever it may be that triggers the diver's complement complex. Certainly worth a search. But nothing to do with M-Values as such.

[TSandM]

Thanks, Steve. I didn't want to complicate the answer by getting into counterdiffusion issues and the effect of bubble radius on internal pressure . . . that stuff starts to make even my head spin. But there are some pretty good papers on line, if you do some searching for bubble radius and critical volumes. I have a whole binder full of papers, which I have read with varying degrees of comprehension, as my calculus is many years behind me . . .

[awap]

Thanks Lynne and Steve. I have no plans to go beyond recreational NDL diving but I am trying to better understand the processes and limits of my dive computers (Oceanics). So dissolved gas and M-values it is. The exponential on and off gassing is simple enough. But I am finding data on M-values and I am still trying to make sure I am understanding them correctly.

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?

Edit: Or am I not even in the ballpark?