My DCS Hit

[Simon Mitchell]

I'm not letting you off the hook on this one Ross, because it is very important people understand how poor your knowledge is, or how deceptive you can be, or both.

When debating the effect of exercise on DCS risk on scubaboard you said perfusion doesn't matter.

When debating the effect of cold on DCS here you said perfusion is critical to the point where it explains the results of the NEDU study.

You have completely and utterly contradicted yourself. The actual quotes are all there. The links are all there. People can read it for themselves. You have been caught out. It is not an ad hominem attack. It is the simple truth.

The discussion on SB you refer is about increased perfusion, and how its simply not visible in typical / usual dive conditions as it lack of effect on real divers. David confirmed the same in the summary of his report.

This is barely comprehensible. Are you trying to say that increased perfusion doesn't matter in gas exchange but decreased perfusion does? And Dr Doolette certainly did not confirm anything that remotely conforms to your position.

However getting cold and shutting down circulation, and its effect with off gassing, is not in dispute. A nedu report (TR 06-07) showed how dramatic that can be.

Neither the effects of increased nor decreased perfusion on tissue gas exchange are in dispute as far as decompression physiologists are concerned. The point is that you have completely contradicted yourself on this matter. Its worse than that though. In the scubaboard thread you even gave a little lecture on how it was half times and not perfusion that determined tissue gas kinetics; seemingly completely unaware that perfusion is the principle determinant of half time:

Exciting (note: I think Ross meant "existing") model gas kinetics theory and formula, follow the concept that the individual tissue is the limiting component of the uptake / off gas rate, as represented by a tissue half time value set. Its the balance of partial pressures against the tissues density and its ability to absorb excess inert gas, represented by a half time value. That is the basic theory you will find in all current models in use (VPM-B, ZHL, VVAL and more). The parallel tissue models do not support a perfusion limit in their calculations. Same can be said for the various serial tissue model designs.

Looks like the science supports my view on this....

?????????????

Simon M

 

[rossh]

I'm not letting you off the hook on this one Ross, because it is very important people understand how poor your knowledge is, or how deceptive you can be, or both.

When debating the effect of exercise on DCS risk on scubaboard you said perfusion doesn't matter.

When debating the effect of cold on DCS here you said perfusion is critical to the point where it explains the results of the NEDU study.

You have completely and utterly contradicted yourself. The actual quotes are all there. The links are all there. People can read it for themselves. You have been caught out. It is not an ad hominem attack. It is the simple truth.



This is barely comprehensible. Are you trying to say that increased perfusion doesn't matter in gas exchange but decreased perfusion does? And Dr Doolette certainly did not confirm anything that remotely conforms to your position.



Neither the effects of increased nor decreased perfusion on tissue gas exchange are in dispute as far as decompression physiologists are concerned. The point is that you have completely contradicted yourself on this matter. Its worse than that though. In the scubaboard thread you even gave a little lecture on how it was half times and not perfusion that determined tissue gas kinetics; seemingly completely unaware that perfusion is the principle determinant of half time:

Exciting (note: I think Ross meant "existing") model gas kinetics theory and formula, follow the concept that the individual tissue is the limiting component of the uptake / off gas rate, as represented by a tissue half time value set. Its the balance of partial pressures against the tissues density and its ability to absorb excess inert gas, represented by a half time value. That is the basic theory you will find in all current models in use (VPM-B, ZHL, VVAL and more). The parallel tissue models do not support a perfusion limit in their calculations. Same can be said for the various serial tissue model designs.



?????????????

Simon M

"I'm not letting you off the hook on this one Ross, because it is very important......"

.....that I (Simon), create yet another false argument and gross distortion, and distraction to hide behind, and avoid the following from emerging again:

• Simon's whole take on nedu study has been disrupted with a full tissue supersaturation graph.
  
• Simon can't prove any connection or validity to your home grown ISS junk stress / risk measure claims.
• Simon's explanation for Don's dive is weak to irrelevant.
• Simon's can't avoid that his deco theories from the above, were put to the test in Don's dive, and failed miserably, and he tries to dodge the implications on that.
  
• Simon fails to admit that Don's dive demonstrates that fast tissues are important, and that deeper stops are essential in some cases - contrary to his 5 years of saying the opposite.
• And more.....

******


Let me fix the misquoting so you don't get more confused Simon. Then you can drop your straw man argument. I will add two words only "increased" and "reduced", to restore context to the quoted phrases.,


...on scubaboard (in a thread about the effect of INCREASED perfusion through excess activity) I said increased perfusion doesn't matter to the outcome in regular divers.

Supported by Davids paper and summary From the summary: "However, don’t expect the substantial differences seen in the experimental trials were extreme levels of risk factors were used." DAN tech conf 2008 p129.


When debating the effect of cold on DCS here I said REDUCED circulation (THROUGH the effect of excess cold) is critical to the point where it explains the results of the NEDU study. Which is clearly correct, as described in nedu report (TR 06-07).


See, my views are supported by the science and the reports.....


*************

All you have Simon is more stupid word play games.... to create a phony straw man argument.... which appears to be the max of your capabilities on this topic.

.

 

[DSix36]

• Simon's explanation for Don's dive is weak to irrelevant.
  Makes sense to most of us
  
• Simon's can't avoid that his deco theories from the above, were put to the test in Don's dive, and failed miserably, and he tries to dodge the implications on that.
  My dive profile was nothing like Simon has been talking about and he has said so many times
  
• Simon fails to admit that Don's dive demonstrates that fast tissues are important, and that deeper stops are essential in some cases - contrary to his 5 years of saying the opposite.
  Simon already said that fast tissues do matter (in fact all tissues matter).

.

 

[Simon Mitchell]

"Let me fix the misquoting so you don't get more confused Simon. Then you can drop your straw man argument.

...on scubaboard (in a thread about the effect of INCREASED perfusion through excess activity) I said increased perfusion doesn't matter to the outcome in regular divers.

This just keeps getting better. So you actually DO believe this!? You are doubling down on your lack of knowledge of one of the most fundamental concepts in decompression physiology right here.

Can you explain why you believe that increased perfusion and increase inert gas uptake during exercise at depth would not increase the risk in "regular divers" whereas cold, reduced perfusion and reduced inert gas washout during decompression would increase risk? What is the physiological basis for that belief?

Supported by Davids paper and summary From the summary: "However, don’t expect the substantial differences seen in the experimental trials were extreme levels of risk factors were used." DAN tech conf 2008 p129.

Utter nonsense. This quote simply means that the real world effect of a risk factor that has been intentionally exaggerated in a study will not be as big as seen in the study. It does not mean that the risk factor doesn't exist in the real world. Dr Doolette's opinion on the role of exercise and increased perfusion on risk is clearly articulated here, and it is NOT the same as yours.

See, my views are supported by the science and the reports.....

??????????????

All you have Simon is more stupid word play games.... to create a phony straw man argument.... which appears to the max of your capabilities on this topic.

No, what I have is you completely contradicting yourself by claiming that decreased perfusion explains the NEDU study results, but increased perfusion doesn't matter, and then doubling down on this claim, and your obvious lack of knowledge of the topic.

Keep going Ross. This is stuff everyone needs to see.

Simon M

 

[rossh]

All you have Simon is more stupid word play games, semantics.... to create another phony straw man argument.... which appears to be the max of your capabilities on this topic.

You never win these argument on merit. You just stomp on everyone else argument and hope they run away and hide from the barrage of attacks..

 

[silent running]

You never win these argument on merit. You just stomp on everyone else argument and hope they run away and hide from the barrage of attacks..

He either "wins" "his" "argument" by default because you won't answer direct questions, or refuse to clarify whatever position you seem to be defending. Or "he" wins because the majority of people here, on RBW and SB understand the factual basis and conclusions of the NEDU tests and other studies and citations from Simon's peers. I doubt very few people understand whatever your position is at this point anymore.

Speaking of "straw man" arguments, referring to "winning", or any argument as belonging to Simon or anyone, is the ultimate distraction/straw man tactic. We are talking about a knowledge base and the continuing enlargement of it for all our benefit. Have the courage of whatever convictions you have and argue about facts and the ideas you believe in. Personalizing any aspect of a discussion on the emerging science of decompression theory is so petty as to be pathological. Whatever ideas you want us try and understand will never be able to cut through the bizarre fog of your relentless pettiness. So please stop it and start sticking to whatever point you want to make if you really actually want to persuade anyone.

 

[Simon Mitchell]

All you have Simon is more stupid word play games, semantics....

Its not semantics Ross. It is an obvious response to the self-contradictory position you are taking on a fundamental aspect of decompression physiology, which speaks strongly to your lack of knowledge of the topic. That lack of knowledge is very relevant to readers' general appraisal of your many claims in these debates.

You claim on this thread that the increased risk of DCS in the NEDU deep stop profile can be explained by a cold-induced reduction in perfusion during decompression which slows inert gas wash-out. Yet on another forum thread you vehemently argued that increased perfusion does not accelerate inert gas wash-in during a dive. You clearly state in this post that increased perfusion "doesn't matter to the outcome in regular divers"

I simply want you to explain why you believe that increased perfusion and increased inert gas uptake during exercise at depth would not increase the risk in "regular divers" whereas cold, reduced perfusion and reduced inert gas washout during decompression would increase risk? What is the physiological basis for that belief?

Simon M

 

[rossh]

Its not semantics Ross. It is an obvious response to the self-contradictory position you are taking on a fundamental aspect of decompression physiology, which speaks strongly to your lack of knowledge of the topic. That lack of knowledge is very relevant to readers' general appraisal of your many claims in these debates.

You claim on this thread that the increased risk of DCS in the NEDU deep stop profile can be explained by a cold-induced reduction in perfusion during decompression which slows inert gas wash-out. Yet on another forum thread you vehemently argued that increased perfusion does not accelerate inert gas wash-in during a dive. You clearly state in this post that increased perfusion "doesn't matter to the outcome in regular divers"

I simply want you to explain why you believe that increased perfusion and increased inert gas uptake during exercise at depth would not increase the risk in "regular divers" whereas cold, reduced perfusion and reduced inert gas washout during decompression would increase risk? What is the physiological basis for that belief?

Simon M

Why are you attempting to conflate and confuse two different scenarios, into one generic description?

The two conditions are diversions from the normal - one to the cold side, the other to the high exercise and hotter side. The cold one is addressed in nedu report (TR 06-07). The higher exercise example by Davids paper in DAN tech conf 2008 p129.

The cold side affects us all. But the higher exercise side takes some extreme effort to see any deviation from normal in regular divers.

The lack of correlation from higher exercise level to gas uptake is demonstrated by beginner divers, river divers, and others who swim hard. Seemingly their theoretical gas uptake increases, but they do not experience an increase in DCS. A review of DCS cases reports does not put exercise as a lead cause, but high exercise is something that a significant portion of divers do on dives.

Quite simply, experience shows for most of us, increased perfusion through increased energy use under water, "doesn't matter to the outcome in regular divers".

You may wonder why that is so, and therefore the 1:1 perfusion to on/off gas values that you seek, does not hold true. I will leave that one for you to explain.

.

 

[cathal]

Ok after 388 posts, no harm to remind us of post 57:
"To be honest most of us on this forum and others (RBW) have witnessed Ross's contributions on this topic over the years, most of us attempted to politely show him where he erred in his analysis but we were all wrong, the leading scientists in this area e.g. Doolette and Mitchell attempted to explain to him and guess what they were wrong as well. We all were met with his confirmation bias that he was right no matter what"

The reason why I posted this reminder and as Simon alluded to in an earlier post, nobody and no evidence will persuade Ross to abandon his view point, its a text book example of cognitive dissonance. Did we learn anything new from this thread diving wise? Not really but what this thread did illuminate, was the completely isolated and bizarre position Ross has taken on this subject. To the subject matter experts who helped highlight this to the dive community in general, thank you.

 

[Simon Mitchell]

Why are you attempting to conflate and confuse two different scenarios, into one generic description?

Because tissue perfusion IS one generic variable, and this comment further highlights your lack of understanding of this most fundamental aspect of decompression physiology. You are very fond of quoting the "basic science formula" for calculating inert gas uptake and elimination from theoretical tissues. But it is clear from the Scubaboard thread, and from your comments here, that you really don't understand it. One of the key variables in gas uptake and elimination (and in the formulae used to model it) is tissue perfusion (blood flow to the tissue). Increased perfusion enhances gas exchange and decreased perfusion reduces it. The formulae have no accounting for the reason perfusion changes!

So for you to come on here and say that the NEDU results are explained by a cold-induced reduction in perfusion whilst over on another forum you have vehemently argued that increased perfusion during exercise at the bottom does not increase risk is a massive self contradiction. In fact, on the SB thread your intial argument was that it is tissue half times not perfusion that primarily influence gas exchange!! but I notice you are have backed away from that now as the lights have gone on. All of this betrays a huge hole in your knowledge of a field in which you have tried to portray yourself as expert.

The cold side affects us all. But the higher exercise side takes some extreme effort to see any deviation from normal in regular divers.

The lack of correlation from higher exercise level to gas uptake is demonstrated by beginner divers, river divers, and others who swim hard. Seemingly their theoretical gas uptake increases, but they do not experience an increase in DCS. A review of DCS cases reports does not put exercise as a lead cause, but high exercise is something that a significant portion of divers do on dives.

Quite simply, experience shows for most of us, increased perfusion through increased energy use under water, "doesn't matter to the outcome in regular divers".

What lack of correlation? What review of DCS cases? What experience? Show me one published report whose conclusions agree with what you are saying here. I can show you plenty of cases where exercise at depth may have been a risk factor, but cases are meaningless. More importantly, I can show you a mass of experimental evidence that exercise at depth increases the risk of DCS, and that exercise accelerates inert gas exchange in tissues (readers can see the SB thread). David summed it up here.

Ross, you disgust me. In order to try to cover your tracks after doubling down on massively incorrect and self-contradictory claims in an internet discussion you manufacture a narrative that seeks to downplay an important risk factor for DCS (exercise at depth) that is quite correctly taught to divers all over the world. You think nothing of the potential consequences of this sort of behaviour on the knowledge base of divers trying to optimise their practice. This is another neon lights warning that your knowledge is poor and nothing you say in these debates can be accepted at face value.

Simon M

 

[moose_grunt]

I may have missed it in the neverending argument, but I'm actually more interested in Don's experience. If you don't mind sharing, how are you doing, Don? What treatments have you gone through and how are you responding?

Jim

 

[rossh]

My claims are not contradictory.

The cold reduces perfusion and consequently is sufficient to interfere with inert gas exchange causing slower off gas. That's documented many places.

While the increased exercise and perfusion, is in-sufficient to make a difference above normal in regular divers doing everyday dives. Sure, taken to the extreme under testing conditions, a bigger gas uptake is evident, but not in normal diver activities.

In that SB thread: "Does higher RMV cause higher DCS risk?" I challenged you to produce some evidence or trend lines, case reports, showing that regular divers suffered injury from high exercise, but you were not able to provide these.

Therefore one must assume that Regular divers do not exhibit a susceptibility to injury from increased perfusion from exercise. Therefore increased perfusion through increased energy use under water, "doesn't matter to the outcome in regular divers". In any case, as I said in the SB thread, deco models have no ability to make an adjustment for changed perfusion.

These claims are backed by science reports and observations of real divers. Why are you being disgusted with reality Simon?


Also if the nedu truly thought there was a gas uptake difference from exercise induced increased perfusion, then it would use an adjusted formula in its gas uptake tracking during exercise assisted testing. But they don't.



*******

Simon wrote: "tissue perfusion IS one generic variable"

You on the other hand Simon, seem to expect a nice linear relationship between perfusion and gas uptake. But its not so. As David said in that piece "These tissue inert gas kinetics seem to be modified by diffusion..." .

When you figure out the balance between perfusion and diffusion for tissue gas exchanges, under all conditions, then you will have a far better model basis to work from.


.

 

[Randy Thornton]

While the increased exercise and perfusion, is in-sufficient to make a difference above normal in regular divers doing everyday dives. Sure, taken to the extreme under testing conditions, a bigger gas uptake is evident, but not in normal diver activities.

Ross, this statement doesn't ring true with me. Surely, exercise on any type of dive whether they be "everyday dives" (not sure what this means exactly) or big dives would create more gas uptake. When we exercise, the heart beats faster, creating greater circulation and greater gas intake. How can that rule not apply to virtually any situation when we increase exercise underwater. More gas = more nitrogen = greater DCS risk.

I don't understand your reasoning.

 

[Mr fish]

Ross, this statement doesn't ring true with me. Surely, exercise on any type of dive whether they be "everyday dives" (not sure what this means exactly) or big dives would create more gas uptake. When we exercise, the heart beats faster, creating greater circulation and greater gas intake. How can that rule not apply to virtually any situation when we increase exercise underwater. More gas = more nitrogen = greater DCS risk.

I don't understand your reasoning.

think you need to add time , from what iv seen posted risk is sort of the same up to a point , after that the risk gets bigger,

seems to be around 45mins for the jump in risk , could be v wrong tho, dont want to steep on toe,s like.

 

[emmbee]

The awkward breathing caused significant on/off changes to Don's dive explanation, is so lame. If there was any real world truth to that, then it would be common for the same injury in many divers, which it is not. Don's dive was unique in that he ascended a very long distance before stopping, and suffered an over pressure injury before he reached the surface - no rocket science required here. It was lucky he had the courage to do some IWR, as it probably bought him some valuable time to reach the chamber.

Face it guys. On big dives, fast tissues do matter, deeper stops do work, and are essential in some cases.


Microbubble studies show that real size / volume changes are affected by additional surfactant and surface tensions considerations, giving bubble skin permeability and bubble size changes. Your simple description is insufficient to describe bubble mechanics in decompression. There are numerous papers on the topic by Yount, Wienke and others.

.

You want to talk about what the people who created VPM published?

You repeatedly asserted that surface supersaturation was not relevant. Could you explain then why VPM specifically includes a model for post-surfacing bubble modelling?

You said that pressure * time calculation was invalid. You suggested pressure squared * time may be a better option. Could you explain then why VPM's critical volume algorithm computes the former?

Or are you trying to say that VPM is wrong?

Cheers,

Matthieu

 

[rossh]

You want to talk about what the people who created VPM published?

You repeatedly asserted that surface supersaturation was not relevant. Could you explain then why VPM specifically includes a model for post-surfacing bubble modelling?

You said that pressure * time calculation was invalid. You suggested pressure squared * time may be a better option. Could you explain then why VPM's critical volume algorithm computes the former?

Or are you trying to say that VPM is wrong?

Cheers,

Matthieu

Matthieu

You are quoting me out of context, in both points. Don't be a Simon. We don't need more stupid irrelevant distractions. Keep to the context please.

.

 

[rossh]

Ross, this statement doesn't ring true with me. Surely, exercise on any type of dive whether they be "everyday dives" (not sure what this means exactly) or big dives would create more gas uptake. When we exercise, the heart beats faster, creating greater circulation and greater gas intake. How can that rule not apply to virtually any situation when we increase exercise underwater. More gas = more nitrogen = greater DCS risk.

I don't understand your reasoning.

Randy, look around you.

Do you see a trend in diving, where the active people get bent more often? Do beginner divers, clumsy divers, river divers, self propelled cave divers, and anyone else who got caught in a strong current... do these people get bent far more often than the lazy / easy going dive sites? Answer NO.

It doesn't matter what theoretical math relation you have... the realistic situation is... the increased exercise and it associated increased perfusion, does not matter to the outcome of normal divers. And why is that?

The simplistic "More gas = more nitrogen = greater DCS risk." is relevant to dive size / depth.

But the point here is whether the exercise perfusion changes make a difference. Clearly there are bigger issues and influences at play.

.

 

[David Doolette]

Also if the nedu truly thought there was a gas uptake difference from exercise induced increased perfusion, then it would use an adjusted formula in its gas uptake tracking during exercise assisted testing. But they don't.
.

Apparently I have been wasting a lot of my time producing these reports!
Doolette DJ, Gerth WA, Gault KA. Addition of work rate and temperature information to the augmented NMRI Standard (ANS) data files in the "NMRI98" subset of the USN N2-O2 primary data set. Technical Report. Panama City (FL): Navy Experimental Diving Unit; 2011 Jan. 92 p. Report No.: NEDU TR 11-02.
Doolette DJ. Addition of work rate and temperature information to the augmented NMRI standard (ANS) data files in the "he8n25" subset of the U.S.N. primary data set. Panama City (FL): Navy Experimental Diving Unit; 2017 Sep. Report No.: NEDU TR 17-10.
Doolette DJ, Gerth WA, Gault KA. Probabilistic decompression models with work-induced changes in compartment gas kinetic time constants [abstract]. Undersea Hyperb Med 2010;37:294.

 

[rossh]

Apparently I have been wasting a lot of my time producing these reports!
Doolette DJ, Gerth WA, Gault KA. Addition of work rate and temperature information to the augmented NMRI Standard (ANS) data files in the "NMRI98" subset of the USN N2-O2 primary data set. Technical Report. Panama City (FL): Navy Experimental Diving Unit; 2011 Jan. 92 p. Report No.: NEDU TR 11-02.
Doolette DJ. Addition of work rate and temperature information to the augmented NMRI standard (ANS) data files in the "he8n25" subset of the U.S.N. primary data set. Panama City (FL): Navy Experimental Diving Unit; 2017 Sep. Report No.: NEDU TR 17-10.
Doolette DJ, Gerth WA, Gault KA. Probabilistic decompression models with work-induced changes in compartment gas kinetic time constants [abstract]. Undersea Hyperb Med 2010;37:294.

Thank you David,

But you did not use these methods in the "no deep stops test" from 2006, where thermal stress was a major component of the test.. Perhaps Nedu has learned some new thing about thermal effects since then. Shame these cannot be applied retro-actively.

.

 

[jason drake]

Ross,

I am becoming confused and agree we should stop posting out of context. So, could you please answer yes or no to some basics?
For calculating decompression profiles:
Does surface saturation matter?
Does perfusion matter?
Does exercise matter?

Thanks for your time,

Jason Drake