NEDU Study

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"...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.

Your objection does not apply to the situation we're discussing -- decompression diving.. The diver is obviously exposed to far more than the minimal supersaturation pressures you reference.

And your objection tends to work against you (i.e. against VPM). If we modified the simple integral supersaturation calculation to reflect this threshold supersaturation idea, then we'd simply disregard compartments that never exceeded a certain threshold supersaturation. So, for example, if the supersaturation pressure never exceeded, let's say, 400mb in a compartment we'd not allow that compartment to contribute to the integral supersaturation since, as you point out, there is some level that is harmless.

I've gone through that exercise and it invariably hurts VPM-B and tends to put more distance between VPM and GF which is why I never decided to actually show it. It's just one more thing you could object to and, as you note, VPM-B is already shown to have higher supersaturation exposure due to the deep stops.

The reason it hurts VPM-B is because the deeper stops allow more on-gassing in the intermediate and slow compartments. That additional on-gassing causes more compartments to exceed the threshold sooner. So you might find yourself using, for example 12 compartments in the integral supersaturation calculation for VPM-B, but only 10 for GF. Not for every profile obviously, since at some point all the compartments exceed the threshold just due to the dive being more substantial.
 
Your objection does not apply to the situation we're discussing -- decompression diving.. The diver is obviously exposed to far more than the minimal supersaturation pressures you reference.

And your objection tends to work against you (i.e. against VPM). If we modified the simple integral supersaturation calculation to reflect this threshold supersaturation idea, then we'd simply disregard compartments that never exceeded a certain threshold supersaturation. So, for example, if the supersaturation pressure never exceeded, let's say, 400mb in a compartment we'd not allow that compartment to contribute to the integral supersaturation since, as you point out, there is some level that is harmless.

I've gone through that exercise and it invariably hurts VPM-B and tends to put more distance between VPM and GF which is why I never decided to actually show it. It's just one more thing you could object to and, as you note, VPM-B is already shown to have higher supersaturation exposure due to the deep stops.

The reason it hurts VPM-B is because the deeper stops allow more on-gassing in the intermediate and slow compartments. That additional on-gassing causes more compartments to exceed the threshold sooner. So you might find yourself using, for example 12 compartments in the integral supersaturation calculation for VPM-B, but only 10 for GF. Not for every profile obviously, since at some point all the compartments exceed the threshold just due to the dive being more substantial.


10 vs 12.... not a valid comparison then. The ZHL model gas tracking structure being used throughout here, is strictly a parallel cell design, with each cell as an independent stress. These cells cannot be summed together to create one large over all stress.

Models that are designed for serial or interconnected cell use (adding cells), have typical 3 or 4 cells max. These are widely spaced cells to prevent the overlap or duplication of information. These typically have further controls or multipliers to equalize or normalize values to a common base.


Your method does none of those. Your summing of 10 vs 12 is clearly not a valid or equalized method. What you do now, is without control, or validation. It is one big junk number.


My 4 ATA diver death situation, vs the weekend skier situation, highlights exactly the problems that your simplistic method creates. The same value for both conditions, but obviously the ski condition is harmless. However, your simple method has no way to differentiate the two, it does not recognize the good from the bad. It does not place any weight on the deathly situation, or eliminate the safe condition.

Stress in ascent occurs under elevated ambient pressure, but it has no weighted corrections to normalize values in the method.

The majority of your big number on the surface, comes from the harmless lower stress end, and therefore obliterates any important differences that occur at the early high stress end.

With these kinds of inbuilt errors and obfuscations, this simple method is not useful.





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

The universally accepted measure of stress in a parallel design, is the peak value of each discrete cell at any given time. It does not permit the averaging or summing of these.

.
 
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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.



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.



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.



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.



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.



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.


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 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


None of this excuses you from mixing the two together.... or to confuse the theory of bubble models and operation.

The true origins of VGE are still unknown, so you should not be making claims about the location and method that they form.

.
 
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10 vs 12.... not a valid comparison then. The ZHL model gas tracking structure being used throughout here, is strictly a parallel cell design, with each cell as an independent stress. These cells cannot be summed together to create one large over all stress.

Why not, exactly, Ross? How did the expert NEDU study authors get away with summing cells in a parallel model then?

It is one big junk number.

You no doubt wish that this were true, but unfortunately its not.

My 4 ATA diver death situation, vs the weekend skier situation, highlights exactly the problems that your simplistic method creates.

No it doesn't, It is a reductio ad absurdum argument. Your weekend skier example has supersaturation and time parameters nothing like those seen in diving.

However, your simple method has no way to differentiate the two, it does not recognize the good from the bad. It does not place any weight on the deathly situation, or eliminate the safe condition.

Yes it does. We have a hard outcome study (the NEDU study) that shows a higher rate of DCS in divers exposed to greater integral supersaturation where the contributory parameters of supersaturation and time are close to those used by UWSojourner in his comparisons and nothing like your harmless weekend ski trip.

Simon M
 
None of this excuses you from mixing the two together.... or to confuse the theory of bubble models and operation.

I don't need to be excused from anything Ross. I have described to you the widely accepted pathophysiological paradigm around venous bubbles in DCS, and provided references to the relevant literature. I have provided quotes from other experts specifically on this topic. All of it backs what I say. You just keep quoting your own idiosyncratic version of the story, which no one else supports.

The true origins of VGE are still unknown, so you should not be making claims about the location and method that they form.
They are known well enough for the purposes of this discussion. The only place that supersaturated gas for formation of venous bubbles can come from is the tissues through which that blood is passing. Therefore, the bubble numbers in the venous blood leaving a tissue will be proportional to the gas supersaturation in that tissue, and therefore to the propensity for bubbles to form in the extravascular compartment of that tissue. The processes are not unlinked.

In the past I have shown you electron micrographs of extravascular decompression bubbles rupturing into capillaries. You really hated that because it would imply that all venous bubbles come from the extravascular tissue (the antithesis of what you are trying to claim). Most of us suspect that at least some bubbles form in the capillaries themselves at the venous end of the capillary beds, but it really doesn't matter because what I said in the above paragraph simply must be true.

Simon M
 
I would just like to step in to say that the argument that Ross' fear that the sales of ' v-Planner might suffer as a result of this change of thinking is not a valid point because the sales of his Multi-Deco, which works very nicely to plan dives in Buhlmann with whatever GFs you want, should do very well.I have been very convinced by the arguments raised by Dr. Mitchell and Dr. Doolette and no longer use VPM, but I do use Multi-Deco for dive planning. According to a past thread on this topic, so does Dr. Mitchell.


This is what I'm doing as well.

in my last deco dives I used 70/40 for a same dive profile where I used previously VPM-B+3 ( same dive location ), I don't know if it was a coincidence but I felt less tired/sleepy with the 70/40 plan, it could had been other factors prior to dive, who knows.

I used VPM-0 on shallower-shorter Deco dives, with good results as well.

I will keep using Multi-Deco but with the recommendations of Dr. Mitchell, with 70/40 which I think it has a balance between the two algorithms theories.
 
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Does any investigation body like DAN or other have data collected of how many DCS had produced the different Algorithms taking out the ones with diver errors like ascending to fast to the next STOP in the day to day diving world ?
 
Does any investigation body like DAN or other have data collected of how many DCS had produced the different Algorithms taking out the ones with diver errors like ascending to fast to the next STOP in the day to day diving world ?
The largest database likely resides with DAN Diving Medical Research Projects — DAN | Divers Alert Network. Results have been said to be coming soon for quite a while. Though I don't know the details, I would imagine the vast majority of dives are recreational rather than technical. Some results from the DAN Project Dive Exploration component have been published Diving Medical Research Projects — DAN | Divers Alert Network Between 1999 and 2002, there were 10 cases of Type I DCS and 16 cases of Type II DCS reported. I contributed about 275 dive profiles to PDE between 2006 and 2010 when I was diving a Cochran computer as my backup. I am not optimistic that we will ever have the information that would be needed to demonstrate any difference in the risk of DCS between the many commercially available decompression algorithms and the various adjustments that can be made to them. Information, like that contained in much of this thread, probably gives us the best guidance in choosing a decompression algorithm.

Database of Dive Exposure and Dive Outcomes
DAN has obtained data from the U.S. Navy, Duke University, Project Dive Exploration (including DAN Europe's Dive Safety Lab) and the Institute of Nautical Archaeology. Data are being converted to a format that will be used as a reference database for calibration and evaluation of decompression algorithms. Divers using one of many compatible dive computers may contribute their electronic dive log data to PDE.
Database of Dive Exposure and Dive Outcomes
Study information is coming soon. For more information, contact DAN Research.
 
There are a number of problems associated with using information from people who were bent while doing dives outside of a formal study.

The most obvious is that you really don't know for sure what actually happened in the dive. If you are lucky enough to get the exact computer profile, you can know a lot, but that is apparently rare. When a friend of mine got bent after a dive we did (well after, including after a driving ascent to altitude), I provided a precise profile of our depths and times for DAN. DAN told him that it is rare that they get that kind of information. There is a possibility, though, that what I sent was not accurate. We were using Ratio Deco, with no computer. I used what I had written in my wet notes for our profile, and I am pretty sure it is indeed what we did. On the other hand, when two other friends got bent using Ratio Deco, one of them was using a computer in gauge mode as a bottom timer, and when they checked the profile, they learned that what they thought they did was not what they actually did.

There is another factor leading to problems that is rarely, if ever, mentioned in places like this--how do we know the person actually had DCS? We know that someone somewhere diagnosed it as DCS, and usually the diver was treated for it. That does not mean the diver had it. In a thread several years ago related to DAN and its sometimes tenuous relationship with hyperbaric chambers, some documents were released that suggested that a lot of people get treated in chambers when they don't really have DCS. A lot of times they have symptoms that might, for example, be related to a physical injury, and those symptoms will resolve themselves in a couple of days whether those days were spent getting a series of chamber treatments or just resting. A little over a month ago I finished a technical dive in really rough seas, and I wrenched my shoulder holding onto the ladder while it was being slammed by waves while I was wearing all my gear. I might easily have decided that pain in my shoulder was DCS-related and gone in for treatment, and I might have been given a chamber ride.
 
I guess they shall enforce turning your DC in ( if you have one ) when you go for a chamber ride, that way data can be compiled and discern the obvious divers mistakes from almost normal ascents and stops.

Of Course there is the physiological part where not everybody is necessary equal, but at least the information can be trended and compared.
 
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