Deep Stops Increases DCS

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99.95% of have no issues with VGE.... there is no crisis to be solved... this gives you time to go do a real proper test to discover what and where VGE really come from, why there is such a huge variance.
I would again ask you to provide a plausible hypothesis for why bubbles in the blood are fundamentally different from bubbles in spinal fluid, or epithelial, or connective tissue fluids. If those bubbles are not connected at all, there has to be a physical-chemical reason for that.

If no plausible hypothesis can be formed, Occam's razor strongly suggests that all those bubbles are governed by the same mechanisms and thus are connected.
 
... and all stumbling around, trying to make sense of something vague and almost useless. Trying to put or invent meaning for matters that can't yet be relied upon.


If you take a look at history, this has been tried several times before. Spencer had a go in the 70's, got nowhere, and they were doing mauch faster plans and more VGE than we do today.


Until these mysteries are at least partially solved, any attempt to put meaning on VGE is misguided, or invalid.

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Oh come on. Spencer's M values were incorporated into DSAT/PADI RDP and have become among the most utilized computer and table algorithms. These have proven to be safe and effective. I have 1150 dives on DSAT, so far, so good.
 
Oh come on. Spencer's M values were incorporated into DSAT/PADI RDP and have become among the most utilized computer and table algorithms. These have proven to be safe and effective. I have 1150 dives on DSAT, so far, so good.

We have not made any more sense of VGE than in his day - vague - approximate, and not very accurate. But I admit I have not really studied the DSAT history. As you say, his "M" values are used.... not his VGE values. M values are supersaturation values. The most reliable measure and predictor of stress in the compartment tissue pressure model. Not VGE.

David Doolette "There is broad (universal?) agreement that modelling tissue gas uptake with a range of exchange rates - as we do for instance with a collection of compartments with mono-exponential gas exchange - captures the essential processes, at least crudely."

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This basic description is OK from a generalized wide angle point of view. But once the specific of the dive situation is added, some extra description is needed. The above described the on gassing, but missed the off gassing side of the equation during the dive and surface.


"Tissues that are at a lower tension will continue uptake until they reach saturation or the pressure is reduce below their tension pressure.


In ascent, this also applies in the opposite direction. Tissues on/off gas towards the inspired pressure line, which is always less than the divers ambient pressure. Hence while holding a stop, any tissue that is faster than the current ceiling limiting one, will be off gassing. A tissue that drops its pressure below the ambient line, contributes no further stress to the dive. This occurs in all dive profile patterns - shallow and deep. Any tissue that on gassed from the deeper stop, but also has a faster time than the current limiting one, will no longer have any influence on the ascent.


"If you have two dives of equal length where one moves to shallower depth faster, it will have less saturation than the one which holds a deep stops"



Whilst true, it is a hypothetical situation. Real dive models all get longer for the same dive and deeper stops, because of internal gas tracking changes. All models have this ability built in now.

But, this extra on gas, may not change the actual decompression limit or required time by any significant amount. A deco model sets it limits based on the maximum value of any one discrete cell limit values. If during the course of the dive, no significant change in cell pressure is observed, at the time that cell becomes limiting then deco times may change only slightly.

In the case of deep vs shallow stops the difference in gas load is actually quite minor. The cells have been subjected to typically 30 mins of full depth (7?) ATA differences. When it comes to the ascent, and the different in stop types, the extra pressure changes are small in the tissue, when compared to the depth exposure just carried out. i.e deep stop add very little extra to the overall gas volume.


This graph compares two profiles: with / without deep stops, and examines the resulting stress changes.

kw_deep-stop-effect.png


It hard to see much difference at all. That's because the deep stop changes are tiny compared to the effects of the bottom time segment. In this sample, it adds about 12% to the deco time.


You can see in the pure deep stop comparison:

  • Fast cells have half the decompression stress in the deep stop dive.
  • Fast cell time surface pressure not affected by deep stops.
  • The most affected slow cell in deep stop (#9), at surface time, only rose 4kPa .
  • The surface stress / off gas has risen by an average of 4kPa across whole ascent.

The real world affect of a deep stop approach, is to significantly decrease in-dive stresses, but only increase surface stress and required deco time by a small amount.

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I am not as dismissive about the small changes in Deco time. I have also been highly skeptical of the deep stop theory and never adopted it. I could never find any empirical evidence to substantiate the theory more than a bunch people who are not scientists coming up with their own deco models. Since I am not a Naval or commercial diver avoiding DCS is a high priority. The expense of a chamber ride and potential loss of income are not worth playing close to the edge. So pardon me if I am skeptical. I had a good friend almost lose his life after a weekend of relatively shallow diving (40-45 fsw) and 24 hours later doing a military freefall sky dive at work. He was severely bent and almost didn't survive. Like many who follow the universally accepted don't fly for 12-24 hours after diving he waited 24 hours only to find out the hard way "you don't know, what you don't know". It was a huge wake up call. I have been studying decompression science ever since. First to try and understand what happened, and second to find out more. My increased knowledge has allowed me to confidently continue to do some deco diving when warranted. I also only do it now with ideal conditions.

I think everyone's time can be better spent studying the science and make maximum use of the data that does exist. You yourself said you are bouncing VPM off of other models. That is not really science.

You should use your skills and take a look at temperature. One of the things in deco modeling which I believe can have a major impact on DCS avoidance are highlighted in the studies done which revealed huge differences in DCS rates when the descent and bottom time are cold and the ascent and decompression are warm versus being warm during descent and bottom time and cold during ascent and decompression. Temperature plays such a major role in gas activity it cannot be overlooked. If you look at a typical diver, we are generally warm at the beginning of a dive and cool down as the dive progresses, with maximum heat loss occurring towards the end of the dive, just when being warm would be most beneficial to decompression of the slow tissues. I think taking a closer look at this issue can shed some light on why doing the same dive without problems one day and then having DCS on the same dive on a different day happen beyond just being de-hydrated. When we get cold the vessels in the extremities constrict the flow of blood as the body protects the core and the extremities get colder. So you have two things happening, first, the reduced blood flow reduces the efficiency of off loading gas, second, the lower temperature reduces the pressure gradient in the tissues. I for one will be looking at how to do better thermal management on dives where I know I will get cold.
 
99.95% of have no issues with VGE.... there is no crisis to be solved... this gives you time to go do a real proper test to discover what and where VGE really come from, why there is such a huge variance.
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OK, I am curious, can you please point me to the data that shows that 99.95% of divers that present with DCS have no issue with VGE? I don't think that any such data exists of course..but hey I may be wrong. If there is no data I don't understand why and how you can make such a statement
 
One of the things in deco modeling which I believe can have a major impact on DCS avoidance are highlighted in the studies done which revealed huge differences in DCS rates when the descent and bottom time are cold and the ascent and decompression are warm versus being warm during descent and bottom time and cold during ascent and decompression. Temperature plays such a major role in gas activity it cannot be overlooked.
I remember reading a story from a Finnish diver who was bent like a pretzel and hardly survived after having his drysuit flooded during a dive in one of the flooded mines in Finland. I'll be darned if I can find the link, but IIRC he did his required deco, but since he was freezing his arse off during deco he didn't offgas properly and nearly lost his life
 
Oh come on. Spencer's M values were incorporated into DSAT/PADI RDP and have become among the most utilized computer and table algorithms. These have proven to be safe and effective. I have 1150 dives on DSAT, so far, so good.
between PADI and Pelagic (Oceanic et all computers) DSAT is the most well real world tested for recreational diving. However I don't know of many that would choose it for technical diving
I remember reading a story from a Finnish diver who was bent like a pretzel and hardly survived after having his drysuit flooded during a dive in one of the flooded mines in Finland. I'll be darned if I can find the link, but IIRC he did his required deco, but since he was freezing his arse off during deco he didn't offgas properly and nearly lost his life
Interesting you bring up thermals in this discussion, DCIEM tables were extensively tested with extreme cold exposure... using VGE as as primary indicator.
 
...discover what and where VGE really come from, why there is such a huge variance.

Ross, for goodness sake please try to get your head around this. We know that VGE must inevitably be a reflection of the supersaturation state (and likelihood of bubble formation) in tissues that blood passes through. We knew this before the recent study and that recent study starkly demonstrates it in a practical way. Who cares whether that supersaturation state causes VGE to originate from micronuclei in the blood, in crevices on endothelium, or rupture from the tissues in the blood. WHO CARES???

99.95% of have no issues with VGE.... there is no crisis to be solved...

So remediable hazards aren't worth addressing just because they don't cause a problem all the time?? It is enough to know that VGE are almost certainly vectors of the most devastating forms of DCS. Who cares if those forms of the disease are relatively uncommon. If practicable decompression protocol adjustment / choice can reduce the numbers of these vectors, why would we not make that choice.???

Its 2016, and we know not much more about VGE than Spencer did in 1975 when he first discovered them.

Absolutely wrong. We know a lot more about their role in DCS. Every one of those studies I cited above was published between 1975 and 2016.

Simon M
 
Well, Ross certainly knows how to dig a hole deeper and deeper.
 
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