Deep Stops Increases DCS

[UWSojourner]

It is an extremely zealous individual who will on the one hand try to sell the idea that VPM controls bubbles and on the other hand also try to sell the idea that bubbles don't matter. And further that direct measurements of bubbling in divers are all flawed and meaningless "noise".

I have no formal medical training (well, I got some CPR training once ), so I just want to provide references to Neal Pollock's comments made last year in an identical "debate". They're pertinent because it's the perspective of yet another qualified researcher and because Ross posted references to Pollock several times on this forum as if somehow there was another researcher out there who holds his views. That's nonsense.

Links to Dr. N. Pollock's comments (and a few quotes with each):

#294
"Intravascular bubbles are not the perfect measure, but they provide insights that certainly are not discounted in the scientific community. Similarly, they should not be discounted in the diving community."

#305
"Unfortunately, Ross, I do not believe that our core positions are in agreement. The differences are much greater than simply semantic."

#313
"It is not valid to talk about microbubbles in the bloodsteam as different from microbubbles in any other tissue."

#318
"Everyone would like to find the holy grail, but the important thing is the process. Cogitate, hypothesize, test, revise as needed, repeat. If the research community had any reason to believe the genesis of bubbles was wildly different between blood and non-blood tissue, we would probably have some evidence at this point. We do not."

#333
"... a fundamental element that is common to all bubble models of decompression ...Not one of them measures bubbles. Not one. There is theorizing and hand waving, but no measures. Despite this, the near-religious fervor is often felt."

#356
"Bubbles are a clear indicator of decompression stress. Getting off the bottom (that is, skipping the deep stops) can reduce tissue loading in intermediate and slow tissues. No matter what is done at depth, prolonging shallow stop time is effective at reducing VGE in individuals predisposed to develop them. Other strategies might work, but I am most impressed by those based on credible evidence. I call prolonged shallow stops really cheap insurance."

#375
"The impact of deep stops is not that they target some different physical reality. It is actually quite simple; the extra time spent deep allows more inert gas uptake in the relatively undersaturated intermediate and slow tissues. This is simply a loading problem that subsequently produces a higher degree of decompression stress. If there is less uptake at depth, ascent to a relatively shallow stop has much less risk. The idea that deep stops controlled bubble growth is one of the armchair arguments that has not lived up to human testing ... As with all the protocols we developed and subsequently saw fail, it is time to respect the data over the hand-waving."

#390
"The story is advancing nicely. Simon [Mitchell] has provided a number of solid references that describe some of the relevant current understanding ... Read, learn, decide for yourselves."

There were other posts that can be found by reading around the posts referenced.

 

[rossh]

It is an extremely zealous individual who will on the one hand try to sell the idea that VPM controls bubbles and on the other hand also try to sell the idea that bubbles don't matter. And further that direct measurements of bubbling in divers are all flawed and meaningless "noise".

No, your trying to play both side now, and pretend they are the same... no.

Quoting Neal all out of context, is not helping.


Tissue (extra vascular) micro-bubbles which are the things deco models are concerned with, where are DCS problem exists, are not intra-vascular micro-bubbles (VGE). Plain simple logic says they are not the same. Medicine has no evidence either way. Medicine can't explain how or why there is such a huge variance in VGE between individuals. Until these mysteries are at least partially solved, any attempt to put meaning on VGE is misguided, or invalid.

.

 

[Dr Simon Mitchell]

Correlated to what??

Correlated to each other of course. You have expended a lot of effort trying to say that VGE don't matter because it is tissue bubbles that cause DCS and that numbers of VGE do not predict numbers of tissue bubbles. There are multiple inaccuracies in this thesis, but the one addressed by the recent study is the VGE vs tissue bubbles one. Ross: the study shows that VGE correlate with tissue bubbles. Does that make it clear enough? That is what the study demonstrates. Therefore, if bubble models result in greater numbers of VGE then they almost certainly result in a greater tendency to form tissue bubbles. You cannot separate VGE and tissue bubbles as you have been trying to do.

You have also expended considerable energy criticizing the aggressive decompression. The decompression stress required to produce a range of VGE from 0 - 5 which could then be correlated against presence or absence of tissue bubbles is what it is, and is irrelevant to the interpretation of the study's main finding. They could have done a more gentle decompression resulting in 0 VGE in all rabbits, or an even more aggressive exposure resulting in grade 5 bubble in all rabbits; but what use would that have been??? They needed a range of VGE to perform the correlation between VGE and tissue bubbles. All of your commentary on the decompression and why the rabbits died is completely irrelevant and demonstrates a fundamental lack of understanding of the goals of the study.

All rabbits absorbed to same volume of gas....

It is hardly worth debating for the reasons I point out above, but I do have to point out that this is an unsustainable assumption. Gas uptake is dependent on factors other than just depth / time exposure.

That is the question that needs to be solved..... what causes some subjects to transport / convert the same volume of gas into a different states, where, why and how?

You are trying to reframe the debate, probably in an attempt to obfuscate the main outcome which was that VGE do correlate with tissue bubbles.

In the test they killed some rabbits by skipping a bunch of deco, and found venous bubbles. Big deal. Doesn't add anything to the knowledge. I have to think the researchers were hoping to see a lot more than they did.

You are exhibiting an inability to comprehend the study.

Simon, please stop trying to tell the public that bubble models manage VGE - they do not.

I have never said this. You, on the other hand, have said multiple times that bubble models somehow magically control tissue bubbles whilst allowing high numbers of VGE. This latest study demonstrates the implausibility of this claim.

Please stop trying to tell the public that tissue bubbles are venous bubbles - they are not.

My point is and always has been that their numbers are linked. If there are high VGE, then high tissue bubbles are more likely. If there are low or no VGE, then fewer or no tissue bubbles are likely. That is exactly what this latest study shows.

No deco model in use today, bothers with tracking VGE... there is no point - it adds nothing to the equation.

Of course a deco model doesn't "track VGE". How could it?? However, a number of models have been tested against VGE production across a range of representative profiles, and adjusted on that basis. Most notable, the Canadian Navy tables which are in widespread use.

VGE are everywhere in almost all tech dives, and half of all recreation dives, yet they remain harmless, for at least 99.95% of the time. Obviously they are not a source of wide spread trouble. Yet you seem to want to over emphasize the value of VGE based on no science that supports that conclusion.

How many more times must I tell you that there is an extensive body of scientific literature demonstrating that "shunting" (transfer) of venous blood (and any VGE present) direct from veins to arteries (thereby by-passing the lung capillary bed which normally filters VGE out) appears to be involved in causation of the majority of cerebral, spinal, inner ear, and cutaneous DCS cases. VGE in high numbers can also cause cardiopulmonary DCS. Given that these are the most important DCS variants that have the potential for death or long term harm I think that having a goal of minimising VGE by whatever practicable means is sound. If you really do not know this, then I would suggest you read the following:

Ignatescu M, Bryson P, Klingmann C. Susceptibility of the inner ear structure to shunt-related decompression sickness. Aviat Space Environ Med. 2012;83:1145-51.

Klingmann C, Benton PJ, Ringleb PA, Knauth M. Embolic inner ear decompression illness: correlation with a right-to-left shunt. Laryngoscope. 2003;113:1356-61.

Mitchell SJ, Doolette DJ. Pathophysiology of inner ear decompression sickness: potential role of the persistent foramen ovale. Diving Hyperbaric Med 45, 105-110, 2015

Cantais E, Louge P, Suppini A, Foster P, Palmier B. Right-to-left shunt and risk of decompression illness with cochleovestibular and cerebral symptoms in divers: case control study in 101 consecutive diving accidents. Crit Care Med. 2003;31:84-8.

Wilmshurst PT, Byrne JC, Webb-Peploe MM. Relation between interatrial shunts and decompression sickness in divers. Lancet. 1989;2(8675):1302-6.

Germonpre P, Dendale P, Unger P, Balestra C. Patent foramen ovale and decompression sickness in sports divers. J Appl Physiol. 1998;84:1622–6.

Wilmshurst P, Bryson P. Relationship between the clinical features of decompression illness and its causes. Clin Sci (London). 2000;99:65-75.

Gempp E, Blatteau J-E, Stephant E, Louge P. Relation between right-to-left shunts and spinal cord decompression sickness in divers. Int J Sports Med. 2009;30:150-3.

Wilmshurst PT, Pearson MJ, Walsh KP, Morrison WL, Bryson P. Relationship between right-to-left shunts and cutaneous decompression illness. Clin Sci (London). 2001;100:539–42.

Mitchell SJ, Doolette DJ. Selective vulnerability of the inner ear to decompression sickness in divers with right to left shunt: the role of tissue gas supersaturation. J Appl Physiol 106, 298-301, 2009

Torti S, Billinger M, Schwerzmann M, Vogel R, Zbinden R, Windecker S, et al. Risk of decompression illness among 230 divers in relation to the presence and size of patent foramen ovale. Eur Heart J. 2004;25:1014-20.

Moon R, Camporesi E, Kisslo J. Patent foramen ovale and decompression sickness in divers. Lancet. 1989;1:513-4.

I hope this does not become yet another attempt, to do an end run around the peer review process, and play voodoo scary hyperbole games with VGE on the public That would be a disgraceful abuse of privileged.

David has dealt with your ridiculous interpretation of "the peer review process". You demand peer reviewed evidence from us for all our positions (which by and large we have), yet you almost never have any supporting your claims. The majority of times when you cite scientific studies you selectively quote or misinterpret them. Quite frankly Ross, you have repeatedly demonstrated yourself incapable of properly interpreting the scientific literature, most explicitly in relation to the latest paper we have been discussing (see, in particular Deep Stops Increases DCS). You are doing everyone a disservice, and all in the defence of a commercial product. If you want a definition of "disgraceful abuse of privilege" .... well.....

Simon M

 

[Patoux01]

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

Hence why everyone but you seems concerned about VGE? (recalling the various studies that have already been posted here)

 

[DavidFL]

#294
"Intravascular bubbles are not the perfect measure, but they provide insights that certainly are not discounted in the scientific community. Similarly, they should not be discounted in the diving community."

No, your trying to play both side now, and pretend they are the same... no.

Quoting Neal all out of context, is not helping.


Tissue (extra vascular) micro-bubbles which are the things deco models are concerned with, where are DCS problem exists, are not intra-vascular micro-bubbles (VGE).

Please cite the peer-reviewed references that support your statement, directly above, which is directly and specifically contradicted by Dr. Pollock's posting and, more specifically, by his peer-reviewed citations in the same posting.

The links in UWSojourner's post have the context. That particular link to a posting by Dr. Pollock has an extensive citing of peer-reviewed references.

 

[Storker]

Tissue (extra vascular) micro-bubbles which are the things deco models are concerned with, where are DCS problem exists, are not intra-vascular micro-bubbles (VGE). Plain simple logic says they are not the same.

I'd really love to hear a plausible hypothesis for why bubbles in blood are fundamentally different from bubbles in other body fluids. Please enlighten me about the physical and chemical differences between those two kinds of bubbles. Because I'll be darned if I can invent a plausible explanation for why they are not related.

Don't feel that you have to dumb things down; I can follow arguments at least up to chem major level.

 

[scubadada]

MultiDeco is good software. Ross was nice enough to point out, a few pages ago, the graphical representations of the dive to me, I had not discovered them myself. I think it's time that Ross exited the scientific discussion, he is in well over his head. We all have the information as it currently exists, we can make our own decisions and use the software and computer settings to make out plans.

 

[Dr Simon Mitchell]

Here we go AGAIN.

Tissue (extra vascular) micro-bubbles which are the things deco models are concerned with, where are DCS problem exists

Tissue bubbles may be the cause of some cases of DCS, but a substantial proportion of cases of serious DCS (arguably the majority) are caused by VGE. Take spinal DCS for example which is the most prevalent feared form of the disease. There are 3 pathophysiological mechanisms recognised:

1. VGE crossing a venous to arterial shunt and embolising the spinal cord circulation (see commentary and references in my post above!!!)

2. VGE causing coagulation in the spinal veins.

3. Tissue bubbles.

You are attempting an agenda-driven re-write of DCS pathophysiology with absolutely no basis in science for doing so. There is not a SINGLE textbook in the world that agrees with your version of this.

(tissue bubbles) are not intra-vascular micro-bubbles (VGE).

No, of course, although one possible source of VGE is tissue bubbles rupturing into capillaries. But the main point is that if VGE are high this must indicate a greater tendency to produce tissue bubbles in the tissues whose capillary beds were the site of VGE formation.

Medicine has no evidence either way.

We have just been discussing a paper that effectively proves it.

Quoting Neal all out of context, is not helping.

Neal's quotes are spot on in context, made in a virtually identical debate on another forum. Despite him correcting your misquoting of him and his providing all the correct answers, you just charged on with the same old inaccurate message.

Simon M

 

[rossh]

Hence why everyone but you seems concerned about VGE? (recalling the various studies that have already been posted here)

... 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.

.

 

[rossh]

Here we go AGAIN.



Tissue bubbles may be the cause of some cases of DCS, but a substantial proportion of cases of serious DCS (arguably the majority) are caused by VGE. Take spinal DCS for example which is the most prevalent feared form of the disease. There are 3 pathophysiological mechanisms recognised:

1. VGE crossing a venous to arterial shunt and embolising the spinal cord circulation (see my post above!!!)

2. VGE causing coagulation in the spinal veins.

3. Tissue bubbles.

You are attempting an agenda-driven re-write of DCS pathophysiology with absolutely no basis in science for doing so. There is not a SINGLE textbook in the world that agrees with your version of this.

No, of course, although one possible source of VGE is tissue bubbles rupturing into capillaries. But the main point is that if VGE are high this must indicate a greater tendency to produce tissue bubbles in the tissues whose capillary beds were the site of VGE formation.


We have just been discussing a paper that effectively proves it.



Neal's quotes are spot on in context, made in a virtually identical debate on another forum. Despite him correcting your misquoting of him and his providing all the correct answers, you just charged on with the same old inaccurate message.

Simon M

Simon: 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.

When we have that information, then we can act and adjust accordingly.

Currently, its this second guessing, and changing things around, all based on vague / weak / no understanding of VGE.

Go do the homework... then we can fix it - if anything needs fixing at all.

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





.