Deep Stops Increases DCS

[JohnnyC]

I'm so glad Ross is participating in this and other threads on other sites. Should pretty much clear up any "What software shoud I use" questions people may have.

The sad thing is that Multi-Deco is probably the best planning software on the market. If Ross would just stick to programming, there would be no issue. Like kensuf said, if he just stuck to being neutral on the subject, things would be fine.

 

[rossh]

So you cannot comment authoritatively on the decompression requirements of 20 kg anaesthetized pigs. So how can you make the the following statement dismissing the relevance of the Swan et al. study to everyday diving?

I don't see a solution to the the pertinent issue in your answer. It does not provide a reasonable explanation for the dismissal of my human graphs. The 2 to 3 hours of human deco that has been missed, is a huge amount. How much is that in pig deco?

The point being, the Dr. Swan pig test showed what happens in gross failure mode. It also showed a bubble in the middle of a major muscle group, but we do not typical get injured in this region. The pig test is not relevant for what we need to know about VGE.

We want to know what happens for 99.95% of the diving experience - where, how, why do VGE grow, and why such huge variance between individuals, under normal dive conditions. As confirmed below in the new rabbit test, that important information is not available.

Read the paper. That is exactly what the results say. Despite what you consider to be a catastrophic decompression a substantial proportion of the rabbits had low VGE including 2/14 with NO VGE. The decompression imposed on these animals produced a good even spread of VGE. You could have exposed them to a human style dive and probably none of them would have produced VGE. What use would that have been when you are trying to correlate different levels of VGE against tissue bubbles?
Simon M

The animals probably died from pulmonary DCS - we know about that - we know how to avoid it.... it's a procedural matter. The remaining living ones were probably severely injured, but that was not investigated in the test. It does demonstrate something new though: that EB grade 4-5 VGE, has an indicative range from harmless, to death in 5 minutes. Really highlights the (non) reliability of VGE.


Some exerts from the test paper:


"The main finding from this study was that EB bubble grade measured in vivo by ultrasound correlated to mortality and to gas score determined PM..."

So....... skipping all the deco stops, in combination of producing high VGE, can result in death (pulmonary DCS).... But we knew that already.



"This study has focused in lethal decompression, which is rare among human divers except for the most severe accidents, thus the application of these results in human clinical medicine might be limited. On the other hand, studying diseases in their most extreme expression might be helpful to detect better pathophysiological mechanisms of the disease that might not be detected otherwise. The results from the present experiment should be considered carefully due to the low number of individuals studied, but the results suggest a strong relationship between fatal decompression and high loads of gas emboli in NZW rabbits.This relationship remains unclear in less severe decompression cases in human divers (..."


The study is focused on the disease conditions (DCS), in sever mode.... not VGE origins under normal harmless mode.



"Another limitation to our data is that there are to our knowledge no studies available today that describes where decompression induced vascular bubbles do originate from, ..... and whether there are specific tissues or organs that are more “bubble-producers” than others..."


The study paper confirms..... The central piece of information we need to identify - the origins and reasons for variance of VGE, was not studied, and remains elusive and unknown. Until then..... reliance on VGE would seem to be futile.


.

 

[DavidFL]

Would they? If I remain silent, then who is to challenge the fake profiles, phony graphs, over-inflated science and hyperbole and the agenda that is operating outside the peer review system.

Trust me ... *IF* these guys can come up with a proper new model, it will be in MultiDeco.

.

In my view, the frequently repeated list (above) doesn't need continuous noise (as opposed to silence)
1. fake profiles? It's the internet; these are the forums that everyone who is posting and reading have chosen to communicate in. If you don't like the rules, please feel free to stop participating. The profiles are documented; the experimental design was reviewed; how can the profiles that were conducted be accurately described as fake?
2. phony graphs? I find the graphical representations on both sides of this discussion provocative and useful.
3. over-inflated science and hyperbole? As opposed to no-science, no experimentation, no data, no graphs, just internet text chat?
4. operating outside the peer review system? I've seen this charge convincingly answered on multiple occasions in multiple forums. Making the same charge over and over again despite externally verifiable evidence that answers the charge is just noise.

I haven't seen any proposal of a new model, "proper" or otherwise. I see a multi-year, multi-forum discussion that suggests none of the existing models have been shown by scientific methods to be 'optimum', and further suggests that people engaged in bounce technical diving should at least consider an important comparative study; a well controlled study in which no new model emerges, but one side of the comparison generated a statistically significant higher incidence of DCS.

The study was sufficient, as far as I can tell, to support a decision by the U.S. Navy not to change from one model to another. There seems to be a view that the Navy thinks it is acceptable for some percentage of its divers to be injured in routine training and peacetime operations; I don't believe it. I worked inside the U.S. Navy aviation safety program for a decade or so; I was a carrier based single seat single engine airplane pilot. Every single mishap was investigated; the "system" didn't accept the concept of a mishap that wasn't preventable; there was (and is) a continuous never-ending improvement process. The externally verifiable fact that the Navy didn't change its model helps clear away a lot of the noise in my opinion.

 

[David Doolette]

The study is focused on the disease conditions (DCS), in sever mode.... not VGE origins under normal harmless mode.

"Another limitation to our data is that there are to our knowledge no studies available today that describes where decompression induced vascular bubbles do originate from, ..... and whether there are specific tissues or organs that are more “bubble-producers” than others..."
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A problem with selectively quoting from a technical paper, and editing those quotes, is it can fail to give the correct sense of the overall meaning.

The quote actually reads (with a comma, not ellipsis), and continues:

"Another limitation to our data is that there are to our knowledge no studies available today that describes where decompression induced vascular bubbles do originate from, and whether there are specific tissues or organs that are more “bubble-producers” than others. Recent studies are attempting to detect small stationary bubbles in tissues using Dual-frequency ultrasound (Swan et al., 2011, 2014). In this regard, the total gas score estimated for each animal might underweight the pathophysiological importance of high bubble loads in a single tissue. The gas score for each tissue might be more informative for that respect."

and clearly concerns which tissues contribute to centrally detected VGE, not the intravascular or extravascular origin of VGE.

 

[EFX]

EFX, your statements about VPM reveal a more popular, but flawed, understanding of VPM, it's theory and goals. No. The theoretical "crushing" of the bubbles occurs on maximum descent.

Yes, the crushing of bubbles occurs on descent. A minor technicality. If my understanding is flawed I guess Mark Powell's ("Deco for Divers") understanding is flawed also.

VPM's deep stops have the same goal and use the same theory as the shallow stops.

I'm not comparing VPM deep stops to VPM shallow stops. I'm comparing [the protection of] VPM deep stops to bubble-blind dissolved gas models. Yes there are 16 TC's, yes we need to consider volume not just size, and yes to supersaturation constraints, and yes, and yes, and yes.

But you now should see the issue I tried to bring out here. If you simply allow part of the bubble distribution to grow, and if you don't adjust the supersaturation levels when slower and slower compartments come into play (i.e. when your exposure to supersaturation gets longer and longer), what happens? Yeah. That part of the bubble distribution just grows more and more. So, as pointed out in that post and a few after, you MUST either continually increase conservatism, pad shallow stops, or some combo of both as you increase depth and time. Otherwise you are simply increasing risk. There's not another option.

I understand you but I think you are too focused on the effects of supersaturation alone. Both VPM and B-GF are concerned with limiting SS levels to reduce bubble growth. I get that. The important thing I tried to emphasize is VPM is concerned with existing bubbles. B-GF knows nothing of these bubbles. If these existing bubbles grow to certain larger size because we ascended without deep stops then a lower level of SS gradient can cause them to grow beyond the critical size. Buhlmann's happy with the gradient; we didn't exceed the adjusted M-values but it looks like we're at higher risk for DCS.

 

[EFX]

You say this as if it's a fact, not an unproven hypothesis

Yes. I assume it to be correct until actually proven by experiments. My intention though, is not to simply say I think VPM or bubble models are necessarily valid models, but to balance out all the one sided discussion that supersaturation limits are the end all and be all of DCS risk. I posted what I thought was a glaring omission in the discussions that lower levels of SS could feed existing bubbles allowing them to grow to the point of increasing the risk of DCS.

 

[UWSojourner]

I'm comparing [the protection of] VPM deep stops to bubble-blind dissolved gas models ... B-GF knows nothing of these bubbles.

Your statements, of course, have the desired effect of assigning undesirable attributes to GF (i.e. blind and know-nothing), but they reveal a poor understanding of the situation.

There might be a number of ways an algorithm can "know something about bubbles", but only one that's desirable. First, as you point out, the model can develop a theoretical idea about how bubbles might develop and grow. Based on this theory, the model then develops profiles that, if the theory is sufficiently accurate, will limit bubble growth. VPM attempts to use this method.

Second, a model can be developed by observing DCS (or VGE) in divers over a range of dive profiles, gases, etc. The idea of this method is to directly observe the harmful effects (or in the case of VGE, the indicators of conditions leading to a higher risk of those effects) and develop algorithms that avoid those conditions. Buhlmann's M-Values used this method. It's a gross mischaracterization to say the M-Values, and therefore GFs which use the M-values, "know nothing of bubbles" and "are bubble-blind" when the tables developed were the result of directly observing the harmful effects of the bubbles themselves.

At the end of the day, the method that "knows something about bubbles" and "isn't bubble blind" is the one that is more successful at limiting their adverse effect on divers. Given the convergence of research providing indicators that bubble models are NOT being particularly effective at limiting bubble growth, I'd simply ask who's really blind -- the model that actually limits bubble growth, or the model that theoretically limits bubble growth but then turns a blind eye to considerable research showing that in fact the bubble models allow more bubbling?

I understand you but I think you are too focused on the effects of supersaturation alone.

Consider this EFX. A closely monitored study by the NEDU performed dives and observed the harmful effects of bubbles. The gas-content model WAS BETTER at limiting their growth and had 1/3rd the risk of the model that, in your words, "knew something about bubbles". The bubble theory did not perform better.

The NEDU's spotlight focused on supersaturation because it was the additional gas loadings during the bubble model's deep stops that caused the higher supersaturations that caused excessive bubble formation that led to a much higher incidence of DCS. So I think the focus is warranted.

A reply to your critique might go something like this. Yes we are focused on supersaturation, but really supersaturation of a certain kind. We're focused on that additional supersaturation exposure resulting from the deep stops imposed by bubble model theory. It's this additional supersaturation that the NEDU study found to be harmful to the tune of 3x the DCS rate for the bubble model divers.

 

[EFX]

This is a restatement of aspects of the attractive theory underpinning the bubble models. As uwsojouner has pointed out, there is no "crush" advantage in deep stops; after all, you have already been much deeper at your bottom depth no matter what decompression approach you subsequently use to ascend. There remains, however, the hypothetical "limiting" advantage of deeper stops that you mention, because you reduce supersaturation in the faster tissues early in the ascent. The goal (as you obviously know) is that there will be a smaller population of (assumed) bubble micronuclei that will be excited into growth by this smaller degree of supersaturation.

However, you have (probably unintentionally) portrayed this theory as fact, and there is little or no evidence that supports such a position. It is really important to understand that. I think that many divers, having been taught bubble model theory by their instructors, simply assume there must be supporting evidence. There isn't and never was. It was just an attractive theory.

It appears that I portray it as fact. See my reply to Storker. I agree there is no evidence, but lack of evidence is not evidence of lack.

Indeed, the reason this debate is taking place is that the NEDU study (the first human study with a very hard outcome) showed that protection of the fast tissues early in the ascent did not result in better outcomes. Ross claims that there were no "proper deep stops" in the NEDU study. Maybe not according to his definition (whatever that is), but the NEDU deep stops did protect the fast tissues from supersaturation compared to the NEDU "shallow stop" profile, and this did not result in a better outcome (the opposite in fact). This is clearly illustrated and discussed at the following link:

Deep stops debate (split from ascent rate thread) - Page 108

"Maybe not according to his definition (whatever that is)"... Are you kidding?! Ross has posted definitions and graphs and I've posted definitions and profiles. I've compared the deep stop profiles between VPM-B and NEDU A2 and they are fundamentally different. You simply won't admit this obvious fact. See Mark Powell's response below.

Other studies have shown that bubble models actually produce more bubbles than decompression approaches that do not emphasize protection of fast tissues using deep stops to the same extent, which is further corroboration of the suspicion that the theory does not play out in practice. Simon M.

And there have been studies (by DAN) that support the opposite conclusion. Mark Powell writes in Deco for Divers:

"There has been a recent study by the US Navy which appeared to show the opposite conclusion to the DAN study in terms of the benefit of deep stops. This received a lot of publicity and was seen by many as evidence that deep stops were not such a good thing. However, if you look at the US Navy study you can see that they are testing something quite different to what we have been calling deep stops and so their conclusions do not apply to this discussion. [emphasis is EFX]

The context of the above quote is from a chapter on deep stops and bubble models.

 

[Dr Simon Mitchell]

The remaining living ones were probably severely injured, but that was not investigated in the test.

Read the paper. Some animals had high VGE, some had low VGE. ALL were autopsied (including the living ones who were sacrificed after an hour). The ones with high VGE had high tissue bubbles. The ones with low VGE had low tissue bubbles. Therefore VGE and tissue bubbles were correlated. You have been trying to argue that they are not correlated and that your decompression model somehow magically protects tissues whilst allowing high VGE. Every basic principle of gas physiology deems that notion ridiculous (as we have been saying ad nauseum), and this papers demonstrates that in a clear, practical way.

Ross, there was a huge amount of circumstantial evidence that proved your notions about the relation between VGE and tissue bubbles wrong prior to this paper. The paper is a practical demonstration that confirms this circumstantial evidence. Selectively citing the limitations acknowledged by the authors is just an attempt to create noise and obfuscate the fact that this paper effectively blows you notions out of the water.

It does demonstrate something new though: that EB grade 4-5 VGE, has an indicative range from harmless, to death in 5 minutes. Really highlights the (non) reliability of VGE.

I don't know whether this is intentional deception, or simply evidence of your inability to read and comprehend the scientific literature, but either way it demonstrates why you represent such a threat to the dissemination of accurate knowledge on forums like this. What the paper says on this issue is:

"Animals with bubble grade 0–3 survived for 1h and were euthanized according to the experimental protocol. In contrast, all the animals with bubble grade 4 or 5 showed severe respiratory distress signs and died within 5 to 35min after decompression".

The study is focused on the disease conditions (DCS), in sever mode.... not VGE origins under normal harmless mode.

Some of the rabbits did have VGE at grades (0 - 2) that you would consider "normal and harmless". You do not seem to be able to comprehend that rabbits require much more provocative decompressions to produce the range of bubbling the authors were looking for than would a human.

I should also remind you that although it is not relevant to the discussion of the correlation between VGE and tissue bubbles, the concept of "normal and harmless" VGE is your own flawed construct. Yes, VGE can often occur in the absence of harm, but there is overwhelming evidence that they can be the vectors of serious neurological injury in the presence of a right to left shunt (eg PFO).

Simon M

 

[Shotmaster]

You don't stop taking on gas until you reduce the pressure by surfacing. You can't cheat physics. It is impossible to stay longer and not continue to build saturation while holding deep stops. Dissolved gas in a tissue at a higher surface tension will try to equalize as ascent (pressure is lowered) begins in those tissues. Tissues that are at a lower tension will continue uptake until they reach saturation or the pressure is reduce below their tension pressure. 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. Therefore the only way to account for this additional saturation is to add more decompression time, whether that is at a shallow water stops or on the surface. Holding a deep stop is still subsurface diving. If I hold a deep stop for a few minutes, it is no different than diving to that depth. I am becoming saturated at that pressure. The debate really hinges upon where the most efficient stops occur for stops below the surface and that minimize the incidence of DCS. I have become weary of certain "Theorists" acting as if things are fact. I can accept observed cause and effect with a high degree of reliability, but misrepresentation of "opinion" or "theory" as fact is unforgivable. I can write computer code and make things come out they way I want them to, however this does not mean that reality lines up with the computer model. The model must be verified with actual test data, not something pulled from one's head or other oriface.