My DCS Hit

[rossh]

Dr. Neal Pollock:
"The impact of deep stops 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.”

Dr. David Doolette:
"The U. S. Navy has some very successful probabilistic models in which the risk of decompression sickness is a function of the time integral supersaturation (ISS) in all compartments. “ This is in contrast to Ross calling ISS “fake science”.
Excellent Doolette presentation. See minute 34:30-38:50.

Dr. Simon Mitchell:
Presentation here is excellent.
Clearly Dr. Mitchell does not believe the dive under question can be used as a validation of deep stops. See this post.

...
This is a pretty good group of experts who clearly have a better grasp on science than Ross.

.


UWSojourner is trying to validate HIS junk science version of ISS, by implying some connection to the real science measures... again.


1/ The work David Doolette refers to is their use within pDCS and probabilistic use. They have strict controls on scope and how they use it. They use only 3 cells only, almost no overlapping cells, all within the context of one model.

But the Kevin Watts home made invented version of ISS, uses all 16 overlapping cells, and then you add it up to one giant useless number.... Then you try to cross compare models..... Your version of ISS is worthless noise... and nothing more than eye candy to trick people with... something you have a long history of doing. It seems this is a pretty good group of experts who clearly have a better grasp on science than Kevin Watts (UWSojourner).



2/ Neal Pollock's point is frivolous, because ALL dives on gas the slow tissues, including your "new deco" method. How much real difference is there? About 2 or 3 minutes of extra bottom time only. That's all it is. This entire argument can be nullified by a 2 minute change in bottom time..... see here

He made a mistake too (or is being quoted out of context) ... deep stops lower supersaturation, and excess supersaturation is what causes tissue microbubble growth .... that's basic decompression theory.


3/ Dr. Mitchell is one who initiated this campaign 5 years ago, so he is not going to have an independent opinion on this topic. His video that you refer too, uses a fake model concept and has no breathing O2. He uses invalid interpretations of the Nedu test that are provably wrong. He co-mingles intra-vascular and extra-vascular bubble formations to falsely bolster his arguments. And numerous other mistakes that have been discussed before.

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

Now if you have finished with the distractions and diversions, then can we get back to the topic. What caused Don's mid water spinal DCS hit to occur? I have put forward and shown how the supersaturation pressure were too high. Can any one dispute that with a valid argument?

.

 

[UWSojourner]

The work David Doolette refers to is their use within pDCS and probabilistic use. They have strict controls on scope and how they use it. They use only 3 cells only, almost no overlapping cells, all within the context of one model.

But the Kevin Watts home made invented version of ISS, uses all 16 overlapping cells, and then you add it up to one giant useless number.... Then you try to cross compare models..... Your version of ISS is worthless noise...

Dr. Doolette
"It is true that the raw integral supersaturation is not calibrated, but this does not detract from it's utility for comparing similar profiles, such as Kevin has done here, or I did in NEDU TR 11-06."

See this link where Dr. Doolette corrected Ross on this issue 4 years ago.

See this link for a response to Ross's "idea" that deep stops are inconsequential to the overall level of decompression stress (ISS).

 

[rossh]

Dr. Doolette
"It is true that the raw integral supersaturation is not calibrated, but this does not detract from it's utility for comparing similar profiles, such as Kevin has done here, or I did in NEDU TR 11-06."

See this link where Dr. Doolette corrected Ross on this issue 4 years ago.

See this link for a response to Ross's "idea" that deep stops are inconsequential to the overall level of decompression stress (ISS).

.


So... you have no valid information about the worth of YOUR home invented version of ISS.. You just made it up. No details of what any of it means, no connections to stress, no validity what more or less of anything actually means. No way to determine good, bad or indifferent stress or saturation levels.... No testing or calibrations, not verified it can actually tell you anything worthwhile. No peer review or paper to read.

The NEDU use of ISS in pDCS modelling....is NOT what you have done. Stop trying to hide behind that.

Your version of ISS is a giant made up fallacy... intended to trick people with a meaningless bar graph.... We can see why you might engage in such a dishonest trick on the public, because you are not a scientist and it its too easy to get trapped eating your own dog food.


But really alarming, is how Dr. Mitchell uses your sham measure and promotes it too. I guess Dr. Mitchell prefers coercing the public with junk. i.e. a fait accompli.


Nice to know the central justification for your side's arguments, is some junk measure you cooked up at home.


***********

Back to Don's dive..... do you have an explanation for his spinal DCS, using your "new, more efficient" deco method?

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[UWSojourner]

So... you have no valid information about the worth of YOUR home invented version of ISS.

Dr. David Doolette:
"Integral supersaturation (ISS)... is an index of decompression stress." Ross' criticisms do "... not detract from it's utility for comparing similar profiles, such as Kevin has done here, or I did in NEDU TR 11-06."

But really alarming, is how Dr. Mitchell uses your sham measure and promotes it too.

Dr. Simon Mitchell:
"Ross exhibits a profound level of ignorance of the inference one can (or can’t) draw from a single case of DCS ... Contrary to the way Ross has portrayed my 'advice' it has always been to cautiously back away from deep stops as prescribed by bubble models."

 

[DSix36]

As usual, Ross does himself no favors and seems incapable of making any point in a way which actually provokes thought and reasonable discourse. Using terms like "junk science", "fabrications", "made up" in referring to the work of the USN, scientists and medical professionals, who have vastly more experience and resources is sheer folly. It makes me wonder if Ross's main goal is merely to be nuisance enough to keep us talking about him, if so nice work.

To change the subject hopefully not at more of Don's expense, I'm amazed that more people have not mentioned his average (!) PO2 was 1 on a 600'+ dive. This seems to me reason enough for all the tissue trauma/DCS, stop depths and super saturation being the obvious following factors. Is there ANY profile to 600' which could possibly get you out of the water healthy with an average PO2 of 1 in a reasonable amount of time? I mean, it was practically a bounce dive, so the exposure to a higher PO2 at depth would have had the most minimal risk of tox. Isn't the point of constant PO2 diving to minimize our insert gas uptake?

Let me clarify something. My average PO2 was MUCH higher than 1.0. For the 7-1/2 minutes of my descent from the ledge to my max bottom depth, my average PO2 was about 1.0 (may have even been a bit less). I intentionally began my descent with a PO2 of .7 to help prevent too much of a spike on descent.

 

[silent running]

Let me clarify something. My average PO2 was MUCH higher than 1.0. For the 7-1/2 minutes of my descent from the ledge to my max bottom depth, my average PO2 was about 1.0 (may have even been a bit less). I intentionally began my descent with a PO2 of .7 to help prevent too much of a spike on descent.

Thank you for the clarification Don. But do you agree that your low SP was probably a factor in your hit, especially given the extra workload at depth?

 

[Bobjr]

Thank you for the clarification Don. But do you agree that your low SP was probably a factor in your hit, especially given the extra workload at depth?

I think this is a red herring - after all Po2 has nothing to do with decompression stress rather what is important is partial pressure of inert gas. Try running the ppN2+He at set points of PO2 of 1.0 vs 1.2 and you will see the effect is minimal. @10b its 2% more inert gas and @20bar/600ft more like 1%

 

[silent running]

I think this is a red herring - after all Po2 has nothing to do with decompression stress rather what is important is partial pressure of inert gas. Try running the ppN2+He at set points of PO2 of 1.0 vs 1.2 and you will see the effect is minimal. @10b its 2% more inert gas and @20bar/600ft more like 1%

Understood, but:

1) Why push the inert gas uptake envelope on a short duration bottom time dive at all, considering the lack of deco model validation at depths beyond 100m?

2) The possibility, in this case an actuality, of exertion at depth during a deep exploratory dive would also cause me to balance more to a higher PO2.

3) Excepting O2 sensor failure, don't most O2 tox events occur shallower when divers are accelerating their deco with elevated PO2's after a long dive/exposure?

4) If I read the account correctly his PO2 even went below 1 during his hard swim away from the rock to the MOD.

To be clear, while I understand that this is a discussion about profiles and the pressures they generate, my point is that less inert gas uptake would produce less saturation in the first place, and the stress of passing gas through the various tissue barriers. Less saturation equals less pressure gradient during ascent and stops, right? Or am I missing something?

 

[DSix36]

Thank you for the clarification Don. But do you agree that your low SP was probably a factor in your hit, especially given the extra workload at depth?

There are several things that could potentially be at fault for my hit. Any single one of them or any possible combination of them could have been the cause. Maybe if I would have done the dive a day early I would not have even been hit. This is deco theory instead of deco fact for a reason. I was a test rat in a failed experiment that was too small of a sample to draw any definite conclusions.

In my opinion, the single biggest cause was the total length of deco was not long enough on this particular dive on this particular day. Possibly I should have changed the entire deco curve and not just added to shallow stops to pad out the time.

 

[rossh]

Dr. David Doolette:
"Integral supersaturation (ISS)... is an index of decompression stress." Ross' criticisms do "... not detract from it's utility for comparing similar profiles, such as Kevin has done here, or I did in NEDU TR 11-06."

You deliberately cutoff David's quote where he describes some limitations and controls of their NEDU version.

Dr. David Doolette:
"It is true that the raw integral supersaturation is not calibrated,....... It is not useful for comparing widely differing profiles ...... the integral supersaturation is the core of the risk calculations, but has thresholds supersaturations and weights for each compartment."

Your home made version, has no controls, no weighted corrections... You can't explain the meaning of your version of home made ISS? Your version is not the same as David's, and your version is not the NEDU pDCS modeling version either..

You have nothing to offer for validity, other than try to hide behind a generic comment David made.. You use this homemade method because it makes biased graphs that prop up your cause.... with no valid justifications....


.

 

[UWSojourner]

You deliberately cutoff David's quote where he describes some limitations and controls... It is not useful for comparing widely differing profiles .....

Which is why I NEVER compared WIDELY DIFFERENT PROFILES. Only YOU tried to compare a ski trip to diving. The charts I posted on this thread all related to the NEDU dive profile (not widely different, right?).

I only introduced those profiles because you attempted to advance an argument that if one profile had significantly higher supersaturation in the early minutes of the decompression, then surely that was bad. And since the 600ft dive under discussion on this thread had a higher supersaturation in the early minutes of the decompression than VPM would have allowed, then you boldly proclaim a win for VPM.

The problem with your rather sophomoric argument is we have a very carefully conducted study where that pattern was not true. The NEDU profile that was statistically better than the bubble model profile also spiked the supersaturation early in the profile. The "fast compartments" had markedly higher supersaturation in the early minutes of the decompression. And yet it was CLEARLY BETTER. So you have to demonstrate why THIS profile was different. Why in THIS situation was the spike in early supersaturation bad, when in the NEDU study (and others) it proved the opposite.

PLEASE. Refer back to Dr. Mitchell's post. One dive cannot be used to conclude any general principle. Ross in his ignorance and cynicism wants to promote the view that this dive illustrated some general truth. But you have to be pretty ignorant, or biased, to buy what he's selling.

 

[Bobjr]

Understood, but:

1) Why push the inert gas uptake envelope on a short duration bottom time dive at all, considering the lack of deco model validation at depths beyond 100m?

2) The possibility, in this case an actuality, of exertion at depth during a deep exploratory dive would also cause me to balance more to a higher PO2.

3) Excepting O2 sensor failure, don't most O2 tox events occur shallower when divers are accelerating their deco with elevated PO2's after a long dive/exposure?

4) If I read the account correctly his PO2 even went below 1 during his hard swim away from the rock to the MOD.

To be clear, while I understand that this is a discussion about profiles and the pressures they generate, my point is that less inert gas uptake would produce less saturation in the first place, and the stress of passing gas through the various tissue barriers. Less saturation equals less pressure gradient during ascent and stops, right? Or am I missing something?

1-2 - its true but how much difference does 1-2% inert gas actually make - I doubt enough to be measurable for any dive given all the other variables.

3 - Yet 1.0 vs 1.2 is 20% more as an oxygen dose. I don't think there have been any documented cases of oxygen issues at 1.2 (someone will correct me if I am wrong) - but why risk it for 1-2% less inert gas. I idon'thave any data to make any conclusions about toxicity but I know of a number of cases of seizures where people have switched to the wrong gas (SCR and OC) and had problems on bottom. Human error is the biggest cause of oxygen problems so why risk it deep with lots of deco ahead of you - but shallow water where you're nearly done much less risk.

4 - again the extra exposure to intert gas is negligible.

 

[Nitrogenius]

I mean, it was practically a bounce dive, so the exposure to a higher PO2 at depth would have had the most minimal risk of tox. Isn't the point of constant PO2 diving to minimize our insert gas uptake?

Not in my book it isn't..
But maybe it is just phrased a bit off..

In most dives one can not see a huge difference if a lower PO2 is used for the deep/working portion of a dive vs. a higher one.
Hence I mostly use a PO2 of 1.0 for such phase of the dive (be advised my max dive depth is around 350'ish)..
The difference kicks in during the decompression phase.. Here I usually go even up to 1.4..
So the point of constant PO2 diving is not to minimize inert gas uptake but to get rid off it as efficiently as possible..
Maybe that's what you meant though..

And yes certainly the low PO2 during ascent was also a contributing factor.
The thing is nobody (except the holy grail ross) is able to pinpoint the incident to any single contributing factor..
Way too much has been far from optimal at that dive..

 

[Nitrogenius]

.Dr. Mitchell is one who initiated this campaign 5 years ago, so he is not going to have an independent opinion on this topic.

LOL
The only one who made it a "campaign" is you ross!

 

[silent running]

1-2 - its true but how much difference does 1-2% inert gas actually make - I doubt enough to be measurable for any dive given all the other variables.

3 - Yet 1.0 vs 1.2 is 20% more as an oxygen dose. I don't think there have been any documented cases of oxygen issues at 1.2 (someone will correct me if I am wrong) - but why risk it for 1-2% less inert gas. I idon'thave any data to make any conclusions about toxicity but I know of a number of cases of seizures where people have switched to the wrong gas (SCR and OC) and had problems on bottom. Human error is the biggest cause of oxygen problems so why risk it deep with lots of deco ahead of you - but shallow water where you're nearly done much less risk.

4 - again the extra exposure to intert gas is negligible.

Thanks for the reply. I understand the part about the differences in those PO2s inert gas uptake being small and that there were other problems with the profile.

To be more precise, considering it is the inert gas passing back out of tissues into the blood stream as the pressure gradient increases which causes the injury in the first place, and that deco models are less and less validated the deeper you go, and that the CNS clock has even less validation, why not do 1.2? There was no O2 tox in the 29,000 USN RB dives at 1.3, which I'm guessing were mostly working dives. There's a lot of things we don't know about gas exchange, the feedback mechanisms within the body, bubbles and the different kinds of surfactants, the way they aggregate, or don't, etc. The one thing we certainly know is that decompression stress and injury comes from inert gas going in and coming out of tissue.

O2 tox from switching is a non issue for CCR, so no mistakes are possible, except diving MCCR and letting your PO2 drop and your inert gas uptake rise...

 

[rjack]

The problem with your rather sophomoric argument is we have a very carefully conducted study where that pattern was not true. The NEDU profile that was statistically better than the bubble model profile also spiked the supersaturation early in the profile. The "fast compartments" had markedly higher supersaturation in the early minutes of the decompression. And yet it was CLEARLY BETTER. So you have to demonstrate why THIS profile was different. Why in THIS situation was the spike in early supersaturation bad, when in the NEDU study (and others) it proved the opposite.

I'll nibble... This one is different because:
1) it was not done with air diluent, and while the He vs N2 uptake issue is still a bit subject to debate perhaps the He on-gassing and offgassing rates were sufficiently aggressive that the supersaturation spike was more symptomatic for Don than it was is the NEDU study

2) It was such a short bounce compared to the work & time at depth in NEDU that the dissolved model did not fully capture the magnitude of the gas uptake. I.e. on a less bounce-like dive intermediate tissues become controlling and slow down the ascent sooner. But on a very short BT dive those intermediate tissues were not controlling to the same degree. Which combined with the GFs of 60/90 "allowed" for too shallow of an initial ceiling. So if Don had perhaps spent 5mins at 600ft the model would have been a better fit to how his body was on/off gassing.

 

[silent running]

Not in my book it isn't..
But maybe it is just phrased a bit off..

In most dives one can not see a huge difference if a lower PO2 is used for the deep/working portion of a dive vs. a higher one.
Hence I mostly use a PO2 of 1.0 for such phase of the dive (be advised my max dive depth is around 350'ish)..
The difference kicks in during the decompression phase.. Here I usually go even up to 1.4..
So the point of constant PO2 diving is not to minimize inert gas uptake but to get rid off it as efficiently as possible..
Maybe that's what you meant though.

Not to detour too much but from multiple internet dive term definitions:

"In recreational diving terminology, in a bounce dive the diver descends directly to the maximum depth, spends very little time at maximum depth and ascends directly to the surface, preferably at an ascent rate recommended by the decompression model used, and making any necessary decompression stops. In commercial diving a bounce dive is any surface oriented dive, in which the diver is decompressed to surface pressure at the end of the dive and does not transfer to a hyperbaric habitat where the diver lives at pressure between dives and only decompresses at the end of a tour of duty. The duration of bottom time is not relevant in this usage.[15]"

My NAUI MOD 1 course described the idea of constant PO2 diving as providing the optimal gas mix for any depth by maintaining a constant PO2 and thereby minimizing inert gas uptake to minimize decompression obligation. You can find this on the TDI site, APD etc.

My point is simple: We know inert gas exchange is what causes DCS and stresses the body in coping with it. Managing those stresses is the goal of a deco model, but what we don't know about inert gas exchange as it actually happens in the body is vastly more than what we do know. And clearly there is still a high degree of variability between individual physiologies, so the margin of error is yet another unknown and can be very slim. People still get bent on recreational dive profiles(!) Thus, I think it wise to err on the side of minimizing inert gas uptake to whatever degree possible by using 1.2 or higher. I'm more scared of getting bent than of O2 tox. In my mind, it's a case of knowns and unknowns. Obviously it's a personal decision and there are no perfect solutions...

 

[UWSojourner]

I'll nibble... This one is different because:
1) it was not done with air diluent, and while the He vs N2 uptake issue is still a bit subject to debate perhaps the He on-gassing and offgassing rates were sufficiently aggressive that the supersaturation spike was more symptomatic for Don than it was is the NEDU study

2) It was such a short bounce compared to the work & time at depth in NEDU that the dissolved model did not fully capture the magnitude of the gas uptake. I.e. on a less bounce-like dive intermediate tissues become controlling and slow down the ascent sooner. But on a very short BT dive those intermediate tissues were not controlling to the same degree. Which combined with the GFs of 60/90 "allowed" for too shallow of an initial ceiling. So if Don had perhaps spent 5mins at 600ft the model would have been a better fit to how his body was on/off gassing.

I'm a little concerned by your response that you might be under the impression I'm arguing that GF60/90 is a valid model for a 600ft dive. I'm not. To my knowledge we don't have much of a dataset for 600ft bounce dives.

My argument is that Ross cannot say the lack of deep stops is what caused the DCS. Since his argument was "Look at the early supersaturation spike!", I simply pointed out that we have a closely controlled study where an early spike in the fast tissue compartments was not harmful.

It MAY be that for this dive the higher supersaturation early in the dive was a problem. But the DCS could also have something to do with the pain he experienced on the bottom, or the ascent rate, or that he dove to 400ft 2 days prior, or the hard breathing at the bottom, or [fill in the blank], or simply random luck. And so your points, too, may very well be true. With a data sample of 1 we can speculate, but we just don't know.

 

[Bobjr]

My argument is that Ross cannot say the lack of deep stops is what caused the DCS.

Unfortunately (since it open a door for more stupidity) the one thing you can say is that there was not enough decompression done deep.

 

[rjack]

I'm a little concerned by your response that you might be under the impression I'm arguing that GF60/90 is a valid model for a 600ft dive. I'm not. To my knowledge we don't have much of a dataset for 600ft bounce dives.

My argument is that Ross cannot say the lack of deep stops is what caused the DCS. Since his argument was "Look at the early supersaturation spike!", I simply pointed out that we have a closely controlled study where an early spike in the fast tissue compartments was not harmful.

It MAY be that for this dive the higher supersaturation early in the dive was a problem. But the DCS could also have something to do with the pain he experienced on the bottom, or the ascent rate, or that he dove to 400ft 2 days prior, or the hard breathing at the bottom, or [fill in the blank], or simply random luck. And so your points, too, may very well be true. With a data sample of 1 we can speculate, but we just don't know.

No I understand there is no validated model for a 2min dive to 600ft. I was merely guessing on why bounces, especially bounces 4x deeper than the NEDU test dives, might be substantively different and not fit a dissolved gas model. I.e perhaps the NEDU N2 supersaturation spike was better tolerated because it was a different inert.

The intermediate tissue loadings accumulated by something like added Pyle stops might not have increased DCS risks overall like the deeper profile did with NEDU because of their shorter duration than the deeper NEDU stops, which really added up to a lot of time. I guess if I were taking Don's example dive and going to repeat it tomorrow (I'm not) I would probably reduce the GFs to 40/70. And slow down getting up to the first ceiling. I'd probably still get bent though.

Agree that there's a whole lot of arguing about 1 data point and everyone wants a takeaway message which just doesn't exist.