NEDU Study

[UWSojourner]

Of course you like it.... it's a one sided nonsense measure, that always favors the shallow profile..... junk science... which is why you let Kevin make it up and use it.... so you can avoid being blamed for it later on.

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See this post (or just go back 6 posts) as your comment was already addressed.


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Integral supersaturation is not that difficult. Supersaturation is necessary for bubble formation. More bubbles are formed with higher supersaturation pressures. More bubbles are formed with longer supersaturation exposures.

Integral superaturation just sums up (supersaturation exposure) x (time your exposed) for the entire dive and surface period until supersaturation is no longer present.

It's just an index of decompression stress for dives of the same run time.

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For example, a CCR 270ft 20min 10/70 1.2 1.6@20ft dive produces the following index of decompression stress for 4 different profiles -- VPM-B+2, GF20/90, GF30/88, GF50/82 (all dives have the same run time):

You can see that the profile recommended by VPM-B produces the most decompression stress. As Dr. Pollock stated, this is simply a loading problem. The diver diving VPM-B+2 incurs about 25% more deco stress at the surface than does a GF30/88 diver.

You can see why VPM-B might incur more deco stress exposure if you look at the peak GF chart below. The fact that VPM-B "sags" below the other profiles during the deeper portion of the dive is an indication of its recommended deep stops. Those deep stops delay effective off-gassing and continue on-gassing in intermediate and slow tissues.

Hope that helps.

 

[rossh]

Integral superaturation just sums up (supersaturation exposure) x (time your exposed) for the entire dive and surface period until supersaturation is no longer present.

It's just an index of decompression stress for dives of the same run time.

There is no proper definition or reference on how to apply this formula as a stress measure like this. No reference or baseline to decide what is big, small, allowed, off scale, invalid, reversed, non-calculating, etc.... Corrections and limits, boundaries? Who knows? Other known data - none. Should overlapping data be summed or not? Is supersaturation pressure stress a linear or exponential measure?

eg... (40 ATA/mins) could be a 4 ATA for 10 minutes which is deadly, but 0.1 ATA for 400 minutes is harmless (weekend ski trip). Obviously the simplistic formula above, is not enough


Kevin is in brand new territory.

And this measure always favors the shallow profile side.... how convenient.

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[rossh]

In a recent discussion on the same subject David Doolette told him:

I doubt there is a single scientist working in the area of decompression research who does not believe that the sizes and profusions of intravascular and extravascular bubbles are proportional, and that a decompression procedure that results in many VGE also results in many extravascular bubbles.

As for the rest of your post Ross, the diagrams are impossible to interpret and don't depict what you claim they depict. You have previously avoided engaging in discussions about criticisms of them. I doubt there is much value in further debate and I am happy enough at this point to just let people decide who to believe on this subject.

Simon

David's quote above, does not excuse or permit you to deliberately mix and confuse intra-vascular (VGE) with extra vascular (tissue) microbubbles. He simply points out they will both occur in decompression.

The occurrence of two independent events, at similar times, does not make them the same thing. I would expect a hyperbaric doctor to never make such a basic mistake.

It's the deliberate but invalid combining them into one thing, that is then used to confuse people into how bubble models operate. It creates a false impression of bubble model theory and performance.

Bubble models limit ascent based on theoretical levels of extra-vascular micro bubbles (tissue bubbles), not intra-vascular VGE. Dissolved gas models also limit on tissue values, and not VGE.

VGE is not DCS, and does not predict DCS... that is the latest consensus position of your peers: peer position.



*****


I'm sorry that you can't understand basic supersaturation charts Simon. I guess you therefore can't understand the nedu tests validation chart either? Or are you just pretending to be obtuse?

These formula and supersaturation chart displays, are the basis of decades of decompression papers and testing, and its how the nedu test validates it findings too.

These charts clearly show the opinion based position and interpretations of the nedu test to tech profiles and VPM-B connections, have been wrong all along.

Bad luck for you....
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[igor p]

Igor, since you're looking for accuracy, I think the idea that VPM, GF30/x, and GF20/x should be grouped under the "deep stop" banner should be considered inaccurate. I've said this before, but GF in almost ANY configuration accomplishes the "shallower stop" goal when compared to VPM.

To illustrate, consider a CCR dive to 270ft 20min 10/70 1.2 1.6@20. If you use VPM-B+2 then GF20/90, GF30/88, and GF50/82 all match the run time.

Now look at the supersaturation-time chart below for that dive.

View attachment 399260

Anyone can see looking at this chart that the decompression stress of GF20/90, GF30/88, and GF50/82 are far closer than between VPM-B+2 and GF20/90. In fact about 80% of the "gain" obtained by switching from VPM-B to GF50/82 is also enjoyed by GF20/90.

You see the same thing looking at peak GF by depth:

View attachment 399262

Clearly, this chart also shows the 3 GF profiles are more closely related to each other than any of them are to VPM. The large VPM-B "sag" on the line represents the deeper stops that cause the need for the high surfacing gradient factor (i.e. the high surfacing GF is the "cost" of the continued on-gassing, delayed off-gassing, during the deeper stops).

So in the spirit of being correct, it makes more sense to group VPM-B, bubble models, and ratio deco together under the label "deep stop". The others should be under the shallower stop label. That would put deep stop practices at about 22% and shallower stop practices at 78%. My guess is that Bruce actually has a better handle on the pulse of dive practices than this relatively small poll given his business and contacts, but even that poll puts deeper stop practices in a clear minority.

Again, just for the sake of accuracy.

Just for the sake of accuracy I was talking about % that were inaccurate. Beside that.what you wrote was just intention of fogging view on Bruce desinformation and I am not interested in. You can keep your disertation for you.
What I wrote is/was accurate.

 

[UWSojourner]

And this measure [integral supersaturation] always favors the shallow side.... how convenient.

That's a pretty damning admission. You're saying that VPM will always produce profiles that expose the diver to more of what makes bubbles (i.e. supersaturation). I know there have been studies that did show VPM produced more bubbles, but I'm surprised to hear you admit it.

So you know VPM produces MORE of what divers would like to minimize for any particular dive. So the logical question a diver should ask is (and I've asked it before here) what benefit is VPM-B providing that would make it reasonable to incur more exposure to supersaturation?? In other words, if you're going to be exposed to 30% more of what your trying to minimize, what are you getting from VPM-B in return?

The answer used to be "I protect my fast tissues". But the NEDU study showed that protection of fast tissues was not the defining characteristic of a safer profile. So what can you point to now that makes the additional supersaturation exposure a good trade?? Complete this sentence: I think its reasonable to expose myself to 30% more supersaturation for the same dive time because _________________________??????

 

[rossh]

The answer used to be "I protect my fast tissues". But the NEDU study showed that protection of fast tissues was not the defining characteristic of a safer profile. So what can you point to now that makes the additional supersaturation exposure a good trade?? Complete this sentence: I think its reasonable to expose myself to 30% more supersaturation for the same dive time because _________________________??????

"...the measure is a meaningless one, that is obviously invalid as used here, and the 30% is a junk number...."


eg... (40 ATA/mins) could be a 4 ATA for 10 minutes which is deadly, but could also be 0.1 ATA for 400 minutes that is harmless (weekend ski trip). Obviously the simplistic formula above, is not enough.

.

 

[Dr Simon Mitchell]

eg... (40 ATA/mins) could be a 4 ATA for 10 minutes which is deadly, but could also be 0.1 ATA for 400 minutes that is harmless (weekend ski trip). Obviously the simplistic formula above, is not enough

EXCEPT that we have a hard outcome study that shows greater DCS in divers exposed to greater integral supersaturation where the contributory parameters of time and depth are close to those used by UWSojourner in his comparisons and nothing like your harmless weekend ski trip.

 

[Michael Guerrero]

Ross has stated in another thread that when these threads get started, "sales go up." The motive is pretty clear to me at least.

Subsurface is free, does Buhlmann and VPM-B, and works on Mac, Linux, and Windows.

 

[PfcAJ]

David's quote above, does not excuse or permit you to deliberately mix and confuse intra-vascular (VGE) with extra vascular (tissue) microbubbles. He simply points out they will both occur in decompression.

The occurrence of two independent events, at similar times, does not make them the same thing. I would expect a hyperbaric doctor to never make such a basic mistake.

It's the deliberate but invalid combining them into one thing, that is then used to confuse people into how bubble models operate. It creates a false impression of bubble model theory and performance.

Bubble models limit ascent based on theoretical levels of extra-vascular micro bubbles (tissue bubbles), not intra-vascular VGE. Dissolved gas models also limit on tissue values, and not VGE.

VGE is not DCS, and does not predict DCS... that is the latest consensus position of your peers: peer position.



*****


I'm sorry that you can't understand basic supersaturation charts Simon. I guess you therefore can't understand the nedu tests validation chart either? Or are you just pretending to be obtuse?

These formula and supersaturation chart displays, are the basis of decades of decompression papers and testing, and its how the nedu test validates it findings too.

These charts clearly show the opinion based position and interpretations of the nedu test to tech profiles and VPM-B connections, have been wrong all along.

Bad luck for you....
.

.

I didn't even have to make it halfway through the very first page of that document to find the line about bubble scores being correlated with DCS....

 

[Dr Simon Mitchell]

David's quote above, does not excuse or permit you to deliberately mix and confuse intra-vascular (VGE) with extra vascular (tissue) microbubbles. He simply points out they will both occur in decompression.

The occurrence of two independent events, at similar times, does not make them the same thing. I would expect a hyperbaric doctor to never make such a basic mistake.

They are not independent events and it is you that is making the mistake. Bubbles forming in the tissue capillaries are effectively forming in the tissue (the capillary bed is part of a tissue) solely in response to the supersaturation conditions prevailing in that tissue (the arterial blood entering the capillaries is not supersaturated and only acquires supersaturated gas from the tissues). It follows that the predilection for bubbles to appear in the venous blood leaving a tissue is directly related to the supersaturation driving bubble formation within the extra-vascular compartment of the tissue.

It's the deliberate but invalid combining them into one thing, that is then used to confuse people into how bubble models operate. It creates a false impression of bubble model theory and performance.

You are the one deliberately confusing people. You are trying to claim that the number of venous bubbles bears no relation to the number of tissue bubbles. You are trying to rewrite a basic pathophysiological paradigm in order to accommodate the real world observation that divers using VPM for deep decompression dives form lots of venous bubbles. It is your goal therefore, to deprecate the relevance of venous bubbles. This is unbelievably cynical of you in my humble opinion, given that you sell a bubble model, and I am not the only one who feels that way.

David Doolette has told you:

I doubt there is a single scientist working in the area of decompression research who does not believe that the sizes and profusions of intravascular and extravascular bubbles are proportional, and that a decompression procedure that results in many VGE also results in many extravascular bubbles.

Neal Pollock has told you:

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

Yet here you are attempting to contradict multiple experts in the field in an attempt to defend a decompression model you sell.

Bubble models limit ascent based on theoretical levels of extra-vascular micro bubbles (tissue bubbles), not intra-vascular VGE.

I would be interested in seeing a reference that says exactly that if you have one. Other bubble modellers do not seem wedded to this idea. In his book Technical Diving in Depth p156 (and even though it was published before we understood the importance of PFO and the obvious role of VGE in that scenario), Bruce Wienke appeared to grasp the concept in saying:

The moving Doppler bubble may not be the bends bubble, but perhaps the difference may only be the present site. The propensity of venous gas emboli may reflect the state of critical tissues where decompression sickness does occur.

Dissolved gas models also limit on tissue values, and not VGE.

Of course, the dissolved gas calculations are based on theoretical tissues, but that does not advance your argument at all. But contrary to your claim the vast majority of dissolved gas models have subsequently been tested against VGE production, including the DCIEM tables.

VGE is not DCS

Largely correct. Nobody has ever said they are per se, although it seems clear they can cause DCS either by impacting in the pulmonary circulation in large numbers (the chokes) or by crossing a PFO and being distributed to important tissues in the arterial circulation.

and does not predict DCS

Half correct. High VGE grades are clearly associated with a higher risk of DCS which is why they are used as an outcome measure in just about every decompression study performed in the last decade. It is true that VGE grades do not predict DCS accurately enough to be used as a diagnostic tool.

that is the latest consensus position of your peers: peer position.

I am fully aware of "the consensus position of my peers" and have never said anything inconsistent with it. You, on the other hand frequently misinterpret it. For example, it is ironic that as evidence that VGE are inconsequential / irrelevant you link to a paper written by a group of researchers who routinely use VGE as a decompression stress research tool, which describes their consensus on how to use and interpret VGE in decompression research.

Just as a reminder, Neal Pollock has hold you:

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

I'm sorry that you can't understand basic supersaturation charts Simon.

I have told you in previous posts why these charts cannot be usefully interpreted in the context of the present discussion. You have shown no in interest in correcting them.

Simon M