Deep Stops Increases DCS

[ajduplessis]

What would you do differently? Can you be a little more specific about how you would design a study on this subject ?

I would compare apples with apples and stop blowing smoke up others a$$es.

 

[Nasser]

I would compare apples with apples and stop blowing smoke up others a$$es.

That's too general a statement.

In diving terms what do you mean? please give me an example of how you would specifically set up the study (or at least give broad strokes) what do you not like about the way it was conducted - specifically ?

 

[shoredivr]

It's interesting how new research is greeted with rudeness, and how even though all these questions have been answered again and again on the RebreatherWorld thread, there is some kind of disconnect when one's cherished beliefs are challenged.

 

[ajduplessis]

Do you think the profiles generated represents typical deep stop within the VPM model?

 

[Nasser]

Do you think the profiles generated represents typical deep stop within the VPM model?

I don't know... what's typical for you?

Don't want to get into the whole answering a question with a question thing, but I actually think that if you and other experienced technical divers "in the field" have problems with the NEDU study - or any other study for that matter - then you could be in a good position to give constructive feedback on how to improve these studies and the research. Given that we now have some of the Scientists and Hyperbaric physicians chiming in, perhaps you could offer up some specific suggestions on how they can improve these experiments ? How would you set it up?

let's get some dialogue going... I would be very interested in hearing your ideas and their responses to your suggestions. I'm sure we could learn a few things in the process.

 

[boulderjohn]

I would hope that anyone who has the scientific background necessary to question the validity of the study's methodology would also have the scientific background necessary to suggest the way the study should have been conducted instead and explain why.

As I mentioned earlier, when a study is designed, it frequently has to have certain artificial constraints put upon its methodology in order to isolate the specific factor being tested. If you don't do that, you may have too many variables at play to identify which variable is having what effect.

As an additional point, when one is trying to be convincing about one's challenges to study methodology, it is best to use terms that persuade one's audience that one has the scientific credentials needed to make such a challenge. "Blowing smoke up people's asses" is not a phrase usually associated with quality scientific discourse.

 

[Dr Simon Mitchell]

"Blowing smoke up people's asses" is not a phrase usually associated with quality scientific discourse.

Thank you.

Since the last few posts on this thread have focussed on methodology of the NEDU study, it is an appropriate time to reprise a post by David Doolette from RBW (forgive the cross post) which explains / justifies the methods in some detail. People seem interested, so here it is.

The Navy Experimental Diving Unit (NEDU) “deep stops” study (Doolette DJ, Gerth WA, Gault KA. Redistribution of decompression stop time from shallow to deep stops increases incidence of decompression sickness in air decompression dives. Technical Report. Panama City (FL): Navy Experimental Diving Unit; 2011 Jul. Report No.: NEDU TR 11-06) was undertaken to determine if deep stops decompression schedules, such as those prescribed by bubble decompression models, are more efficient that the traditional shallow stops schedules prescribed by “Haldanian” models. More efficient in this context means a decompression schedule of the same or shorter total decompression time has less risk of decompression sickness (DCS) than an alternative schedule. Theoretical analysis at NEDU and by others had suggested this might be the case, and bubble models were being considered for calculating air decompression tables to replace the Standard Air Decompression Table that had been in the U. S. Navy Diving Manual since 1959, but this big change required a test.

To be clear about the purpose, methods, and outcome of the study, we need to be clear what is meant by decompression efficiency. The purpose of a decompression schedule is to reduce the risk of DCS to some acceptably low level. The cost of a low risk of DCS is time spent decompressing; efficiency relates to this cost/benefit trade off. In comparing two decompression schedules, if one could achieve the same target level of DCS risk with a shorter total decompression time than the other, the shorter schedule is more efficient.

With this definition in mind, one way to test if a deep stops schedule is more efficient than a shallow stops schedule would be to show that a deep stops schedule has the same (or less risk) than a longer shallow stops schedule. However, this is not a good scientific design because you are varying two things, stop depth distribution and total decompression time , and you will not know which was responsible if the result does not show deep stops to have lower risk. A better scientific design is to compare a deep stops schedule and a shallow stop schedule that have the same total decompression time and see which is riskier - only one thing is varied, the stop depth distribution, and any difference can be attributed to that alone. This latter is the method we used.

Remembering that the purpose of a decompression schedule is to reduce the risk of DCS, the definitive way to evaluate a schedule is to conduct many man-dives, following the schedule exactly, and count the incidence of DCS; the incidence of DCS is an estimate of the risk and the more man-dives the more confidence there is in this estimate. To compare two schedules, dive both, and count which results in more DCS. Contrary to what has been suggested in this thread, it is meaningless to compare the decompression efficiency of two schedules that are very unlikely to result in DCS – imagine conducting a thousand man-dives on each of two schedules with no DCS occurring, all you have learnt is both schedules are very low risk, and probably quite inefficient.

So this is the experiment. In the wet pot of the NEDU Ocean Simulation Facility, where we can precisely control depth, time, water temperature, divers’ workload (all things that influence DCS risk), divers undertook two different profiles. Both profiles were to 170 fsw for 30 minutes during which time the divers exercised on cycle ergometers, followed by 174 minutes of decompression stops during which divers were at rest. The water temperature was 86 °F (30 °C) and dives wore only swimsuits and t-shirts and became cold during decompression. Divers were submerged and breathed surface supplied air throughout. More on all these conditions later. The only difference between the two profiles was the distribution of the total stop time among stop depths. The shallow stops schedule had stops of (fsw/minutes): 40/9; 30/20; 20/52; 10/93. The deep stops schedule had stops of (fsw/minutes): 70/12; 60/17; 50/15; 40/18; 30/23; 20/17; 10/72.

We planned to conduct 350 man-dives on each schedule, but to protect the diver-subjects from unnecessary risk, we also had several rules by which the experiment would stop early. We had stopping rules if both schedules had unexpectedly high or low risk, which were likely to result in severe DCS or an inconclusive result, respectively. We never came close to these (the figure presented in an earlier post is misinterpreted). We were also to stop if, at an interim analysis, we saw a statically significant higher incidence of DCS on the deep stops schedule than the shallow stops schedule, and this is what happened. At approximately the mid-point of the experiment we had 10 DCS out of 198 man-dives on the deep stops schedule and 3 DCS out of 192 man-dives on the shallow stop schedules. Incidentally, we also measured venous gas emboli (VGE) and these were higher on the deep stops than the shallow stops schedule. As Simon pointed out in a post, this is, in statistical terms, only moderately strong evidence that the deep stop schedule was riskier than the shallow stops schedule. So why did we stop? Because it is very strong evidence that the deep stops schedule is not better and, because deep stops better was the only result of any consequence to the U. S. Navy (shallow stops are the status quo).

I want to talk about the schedules we tested in some detail, because these have been the source of a lot of confusion and misdirection in various forums. Clearly they do not look like technical diving schedules - they are not, they are deep air decompression schedules. In selecting the test pair of schedules, there were two principal criteria. First, they had to result in some DCS so there was something to compare. Second, they had to be long, so that they could have substantially different stop depth distribution, i.e. the deep stops schedule should require a substantial amount of time at deep stops, so any deep stops effect (good or bad) can manifest. There is no point in testing, for instance, two 90-minute decompression schedules where one has five or ten minutes of time spent at deeper stops – I would happily move five or ten minutes around in a 90-minute schedule and not expect it to make a any detectable change in my risk of DCS. Remember that the purpose of a decompression stop (deep or shallow): we stop to limit gas supersaturation and thereby limit bubble growth, and we stay to washout inert prior to moving to the next stop. The staying is important, the amount of gas washout that occurs in the course of one, two, or five minutes is relatively inconsequential.

The final test pair of schedules was the result of hundreds of hours of analysis and even a workshop attended by many people working in the field of decompression (acknowledged in NEDU TR 11-06). The shallow stops schedule was calculated using the VVal-18 Thalmann Algorithm. This algorithm was developed at NEDU for air and constant PO2-in-nitrogen rebreather diving and about 1500 man-dives were conducted during its development (NEDU TR 11-80, NEDU TR 1-84, NEDU TR 8-85). VVAl-18 Thalmann Algorithm is still very much in use, it runs in the U. S. Navy Dive Computers, desktop decompression software, and was used to calculate the MK 16 MOD 0 and MK 16 MOD 1 N2-O2 decompression tables in the U. S. Navy Diving Manual. For a 170 fsw / 30-minute bottom time air decompression dive VVal-18 requires the 174 minutes of decompression stops given above for the shallow stops schedule. Although this particular schedule was not tested during the development of Val-18, many deep, long air dives were, and lengthy air decompression was required. Many U. S. Navy dives are conducted with the diver working on the bottom and, because wet suits are often used, cold during decompression. This combination makes for a lot of required decompression because blood flow is increased, and therefore inert gas uptake is relatively fast, during the working bottom time, and blood flow is decreased, and therefore inert gas washout is relatively slow, when divers are at rest and cold during decompression. U. S. Navy decompression algorithms are designed to account for this worst case situation and tested under these condtions. Just to clarify some comments in this thread about the effects of cold, cold can increase the required decompression time, but cold does not cause DCS.

It has been suggested in this thread that 174 minutes decompression is 100 minutes too long for a 170 fsw / 30-minute dive – well, of course, you can do 74 minutes of decompression if you want, if you accept a high risk of DCS. In fact, 74 minutes is close to the time required in the new Air Decompression Table in the U. S. Navy Diving Manual Revision 6 (2008): 170 fsw / 30 minutes requires 88 minutes of air decompression stops, which has an estimated risk of DCS of about 6% (NEDU TR 09-05), but this exceptional exposure schedule is for emergency use only (this dive is required to be planned using the lower risk oxygen decompression schedule). Why didn’t we test this schedule? It is not long enough to allow meaningful redistribution of time to deep stops.

Now the deep stops schedule. This was calculated using a model called BVM(3) (Gerth & Vann Undersea Hyperb Med 1997;24:275-292). BVM(3) is a Bubble Volume Model, and models in this class (Mike Gernhardt’s TBDM is another example) model the growth and dissolution of bubbles using the equations that describe exchange of gas between tissue and blood (a feature of most decompression models) and the equations that describe diffusion of gas between spherical bubbles and surrounding tissue (the characteristic of this class). BVM(3) output is the estimated risk of DCS for a dive profile, and this risk is a function of bubble volume and duration in each compartment. BVM(3) is used in conjunction with an exhaustive search algorithm to find the optimum decompression schedule (under the model). This can be done two ways. First, you can specify a total decompression stop time, and an exhaustive combinations of stop depths and times (that add to the total) are tested to find the schedule that gives the minimum estimated risk. Second, you can specify a target risk, and the first step is repeated with different total stop times, searching for the shortest schedule that just reaches the target risk. We used the first step, and specified 174 minutes total stop time (the VVal-18 total stop time) and had the model find the optimum distribution of that time, which resulted in the deep stops schedule specified above. Actually, we examined hundreds of candidate schedule pairs until we decided on the 170 fsw / 30-minute dive.

To interpret our results, I have to describe some “Decompression 101” theory, so this may a bit basic for a lot of you, and for brevity I am going to confine the description to diving on a single gas (e.g. air diving, as in the experiment) although it is possible to extend to multiple gas. The purpose of a decompression stop is to limit bubble formation and allow washout of tissue inert gas. Deeper stops are generally controlled by faster exchanging (short half time) compartments and shallower stops by relatively slower exchanging (long half time) compartments. Bubbles form and grow only while tissue is supersaturated and shrink when tissue is undersaturated. In a supersaturated tissue, at a deeper stop (compared to a shallower stop) less bubbles form, they will grow less rapidly, they will dissolve more quickly, and in some circumstances inert gas washout can be faster. This is all good stuff and the motivation for deep stops. However, the NEDU results indicate that emphasizing these effects in fast tissues by doing “deep stops” is not as important as previously thought, because our shallow stops schedule, in which fast tissues had substantial supersaturation, resulted in very few cases of DCS. So why did the deep stops schedule result in more DCS? We looked at the supersaturation predicted in a range of half-time compartments. In fast compartments, the deep stops schedule resulted in less, and less prolonged supersaturation than the shallow stops schedule. However, iIn slow compartments, gas washed out slowly or continued to be taken up during deep stops, so that later in decompression, the deep stop schedule resulted in more, and more prolonged, supersaturation than the shallow stops schedule. The increase in supersaturation in the slow compartments was greater than the decrease in fast compartment. There is a principal, Occam’s Razor, that roughly means “the simplest answer is the preferred one”. The simplest answer here is that the greater supersaturation (and by extension greater bubble formation and growth) is responsible for the greater incidence of DCS on the deep stop schedule. In other words, the cost of doing the deep stops outweighed any benefit. And remember, “any benefit” was slim, because there was very few DCS in the shallow stops schedule.

So an important question is how relevant is this result to other deep stops schedules, or put another way, is there another deep stops schedule that would have given the reverse result. Accepting the explanation that greater supersaturation is the culprit, we modeled the gas supersaturation in a range of half-time compartments for half a million different schedules, each comprising 170 fsw / 30 minutes followed by 174 minutes of decompression stops, but with different combinations of stop depths (deepest stop 100 fsw) and times. At the level of granularity we chose (5-minute blocks of time was the shortest we moved) we looked at all reasonable ‘shapes’ of decompression schedule. As it turned out, the VVal-18 shallow stops schedule resulted in near the least combined (adding together the fast and slow compartments) supersaturation. Moving a small amount of time to deeper stops resulted in no improvement, and moving any substantial amount of time to deeper stops resulted in more combined supersaturation. This would suggest that there are some schedules with a little bit of time at deep stops that are no worse than the shallow stops schedule, but most deep stops schedules will be worse. Clearly, this theoretical analysis is not proof, but it is a compelling hypothesis, and I am very confident we would not have gotten the reverse result (deep stops better) if we had tested another schedule.

So what is the relevance of this to technical diving? For that I have to speculate a bit because I am moving away from the facts of the study. First let us deal with the issue of whether this applies to helium-based breathing mixtures. Probably. Blatteau and colleagues have done a small comparison of deep stops versus shallow stops open circuit trimix decompression profiles, using VGE as an endpoint and found more VGE with the deeps stops (Proceedings of the Decompression and the Deep Shop Workshop) and there is another, as yet unpublished, similar study with similar results, although using algorithms familiar to technical divers. The more important issue is that technical divers do not do air decompression dives, they use oxygen-accelerated decompression. If decompression stops are conducted using a breathing mixture with a low inert gas fraction, then, of course, there is less gas uptake into the relatively slow compartments. The effect of this is to increase the depth at which stops become “bad” deep stops.

Simon M

 

[rossh]

Ross,

Re:

1. "shooting my foot off". I feel I am at very low risk of shooting my foot off in an argument about decompression and DCS. Having treated a number of the sort of cases (fulminant DCS) you refer to after omitted decompression I am well aware that extremely high tissue supersaturations can produce bubbling and symptoms with almost no delay. I am also aware that very low levels of supersaturation may be sustained for very long periods without the development of problems. However, these facts do not constitute a valid argument against time being important at levels of supersaturation between these extremes. Indeed, since you raised the example of surface decompression on oxygen, would you care to explain why the various tables instruct you to get the diver across the deck and recompressed within 5 - 7 minutes? If the integral of supersaturation and time didn't matter, why not come up, have a coffee and a scone, and recompress later (or even at all?). Since you're "more intelligent that to get suckered into this "integral of supersaturation and time" nonsense" I'm sure you can explain this to me.

Simon M

1/ You can read all about SurD decompression procedures in the USN dive manual (sect 9.8.3), including contingencies for missed procedures.


The point of bringing up the SurD supersaturation, is that it demonstrates there are limits to high initial supersaturation. Yes its tolerable for a brief period(3 1/2 mins), but it must be addressed immediately with O2 treatment. They are basically doing part of a re-compression treatment. They have taken a great (life threatening) risk, and then patch it up quickly with a lot of serious O2 treatment.

So your contention that the Fast tissues can be ignored, does not seem to hold true.

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

Dive planning is all about Totals of stresses, and those can be shifted around through planning and dive conditions, among others things. Dive models control only one small part (the gas pressure stress) from the total dive stresses. ZHL has more gas pressure stress in the dive, and less on the surface. VPM has less gas pressure stress in the dive and more on the surface. They both attempt to balance up the gas pressure stresses across the dive and surface periods..

This is especially so when it comes at the cost of increased supersaturation (both in terms of peak levels and duration) in slower tissues later in the ascent.

and ...

However, these facts do not constitute a valid argument against time being important at levels of supersaturation between these extremes.

and...

3. The Haldane and Schreiner equations. A complete red herring. There is nothing wrong with them. I have no idea why you raised this.
Simon M

Because you don't seem to understand what or where this "integral of supersaturation and time" detail comes from:

You do realize that Haldane and Schreiner equations, include a time component? They are tracking pressure over time. The duration of a pressure level is accounted for within the formula. The period and sustained levels of supersaturation can be retrieved from Haldane and Schreiner equations, and all our currently used deco models address this in the same way.


But you seem to want to add a second layer of time components on top of that with "integral of supersaturation and time"? Your trying to apply a time component twice, and one is magnified against to the other. That's not right.



Here is yet another example of why "integral of supersaturation and time" is an ambiguous nonsense.

3000 kPa/mins = riding the elevator to the 30th floor and staying there 50 hours.
3000 kPa/mins = a 32% EAN dive within the NDL range.
3000 kPa/mins = a small deco dive.
3000 kPa/mins = 150 mins of normal flight in pressurized aircraft.
3000 kPa/mins = 15 mins surface transfer times for a SurD diver - serious injury / possible death
3000 kPa/mins = 40 mins of blood boiling total pressure loss for a space walker - death.

Your "integral of supersaturation and time" needs more work. In its current state it's an ambiguous nonsense.

4. The DCIEM tables. I am well aware of the pedigree of these tables. However, I challenge you to provide any evidence that they tested 170ft / 30 minute air decompression dives with human subjects working at at the same intensity as the NEDU divers, in 30 degree water and no thermal protection, with sufficient repetitions to derive an accurate probability of DCS for the 77 minute decompression profile that their tables prescribe. In other words, do they really know the risk of DCS for their decompression following a 170/30 dive performed under the conditions of the NEDU study?
Simon M

I'm sure that the old DRDC team will be very happy to see you hold their work on DCIEM tables in such low regard.

I forgot to mention, the USN when it published it latest tables, it too ignored the nedu test outcomes. The standard USN table for this dive calls for 93 mins deco.

It seems that the Naval dive command (who decide on the table sets and publishes them), they didn't take any cues from the nedu test either. The published USN tables for this dive is consistent with times from DCIEM, ZHL, VPM-B, RGM, and just about everything else.

Here we have two table sets - the DCIEM and the USN rev6, that give realistic deco times, while the nedu test used 2x (double) the required time.


You wrote above "performed under the conditions of the NEDU study". So now you have changed positions. All throughout the RBW thread you claimed the nedu test conditions were normal to regular diving. But now they have been elevated that to special conditions.


I think the astute scientist would have looked into the reasons for the nedu test anomaly, and explored and explained why the test outcomes are so far outside the normal experience. But no one involved with the test, or in recent commentary has done that. In fact all we have seen so far, is a concerted effort to hide the anomaly, to pretend it's not there, to play games with descriptions and language, and omission and Half-Truths.

5. "these are two shallow stop profiles": no they are not. They are profiles that generated tissue supersaturation patterns typical of one that emphasizes deep stops (like your own algorithm) and a one that does not emphasize deep stops. The prevention of fast tissue supersaturation early in the decompression at the expense of greater slower tissue supersaturation later in the decompression was shown to produce more DCS. Sorry Ross. That is the reality.
Simon M

The test profiles manipulated stops between 60 and 30 ft, to make them longer. I think those are shallow stops. It's also the same procedure you are suggesting now which is to push divers towards higher risk outcomes. Actual deep stops that we use, are in the 110 to 80 ft range for this dive, which were not present in this nedu test.

Simon wrote: "The prevention of fast tissue supersaturation early in the decompression... "

Ahh... no. The A2 profile has a high supersaturation in the fast cells. The premise you made, was not tested.




See the A2 profile - it has 110 kPa supersaturation in the fast cells, and the real deep stops models only has 65 kPa. To make that high initial supersaturation the A2 profile has to be a shallow stop profile, because that's the only way to generate high initial supersaturation. A2 then goes on to extended time shallow stops (60 to 30 ft) which are so long that supersaturation almost vanishes.

Conversely real deep stops, from real models, do actually protect the fast cells, and keep a low consistent supersaturation across the ascent.

2. "to trick the public into a false belief": Why on earth would I or any of the other scientists involved in this debate want to do that?
Simon M

I don't know what's wrong with you Simon. But you sure do ignore a great deal of basic math that contradicts your positions. Add to that the coercions and half truths that you use, and anything else to avoid the criticisms.....

Your a tech diver with plenty of experience. You know that fiddling the shallow stops at 60 to 30 ft, is not the same as a deep stop model. But still you persist with this unjustified nonsense explanations.

 

[rossh]

Hello Kev,

The bubble models and the deep stop approach were originally promoted on the basis that they were more successful at controlling bubble formation. The attempts to evaluate this notion in decompression dives in humans that I am aware of have shown that gas content models (or decompression procedures that have backed off deep stops to some extent) actually produce less bubbles when measured after surfacing. Neal Pollock presented some fascinating work they have been doing at the inner space event at a NOAA / AAUS rebreather diving forum I attended last week. Hopefully this will find its way into the literature at some point soon. In any event, the more we investigate it, the more the "control bubbles by deep stopping" concept appears to need reconsideration. What this is suggesting is that the bubbles are coming from the slower tissues that absorb more inert gas during the deep stops. It also implies that the faster tissues that deep stops attempt to protect from supersaturation are less prone to bubble formation when they become supersaturated. You are seeking a physiological explanation for this, and while I can't be definitive, I would suggest that it makes sense that a tissue washing inert gas out quickly might be less prone to bubble formation and growth than a tissue with slower inert gas kinetics where the supersaturation persists for longer (there's that time integral again).

Simon M

Here we go again.

VGE (Venous Gas Embolii: circulatory micro-bubbles detected with Doppler) is NOT DCS.. VGE in NOT an indicator of impending DCS. DCS is normally from tissue micro-bubbles, which are not VGE. Deco models work to prevent tissue microbubble growth, not VGE. VGE has been with us since Spencer first documented them in early 70's. Virtually every diver, including NDL dives, will experience some form of VGE, because VGE is supersaturation generated - something that is present in every dive we do.

But still you try to link these two aspects of deco on a 1:1 basis. More trickery... again.

 

[Dr Simon Mitchell]

1/ You can read all about SurD decompression procedures in the USN dive manual (sect 9.8.3), including contingencies for missed procedures.

I have supervised and dived many SurD procedures Ross, both in the military and commercial fields. I know how they work.

The point of bringing up the SurD supersaturation, is that it demonstrates there are limits to high initial supersaturation. Yes its tolerable for a brief period(3 1/2 mins), but it must be addressed immediately with O2 treatment. They are basically doing part of a re-compression treatment. They have taken a great (life threatening) risk, and then patch it up quickly with a lot of serious O2 treatment.

So your contention that the Fast tissues can be ignored, does not seem to hold true.

Nobody said that fast tissues can tolerate extreme supersaturation Ross. This is an absurd extention of my argument. Did you not read the bit where I wrote:

"I am well aware that extremely high tissue supersaturations can produce bubbling and symptoms with almost no delay. I am also aware that very low levels of supersaturation may be sustained for very long periods without the development of problems. However, these facts do not constitute a valid argument against time being important at levels of supersaturation between these extremes"

Moreover, as I pointed out previous (and while on the subject of shooting oneself in the foot) the SurD scenario can easily be turned back at you by asking "if peak supersaturation (without a time integral) is all that matters as you imply with your graphs, then why bother to hurry across the deck in a SurD procedure?" The diver has arrived on the deck alive and symptom free despite the high peak supersaturation. If time doesn't matter, why rush? The truth is that time obviously does matter, especially when you are close to a dangerous level of supersaturation. How much less supersaturation does there have to be before time suddenly and magically stops mattering Ross?

ZHL has more gas pressure stress in the dive, and less on the surface. VPM has less gas pressure stress in the dive and more on the surface. They both attempt to balance up the gas pressure stresses across the dive and surface periods.

Here we are getting close to the nub of the matter. The problem is that this "balance" you speak of does not seem to produce the correct (or even neutral) physiological result. Indeed, 10 or so years ago many of us (including you obviously) assumed that the "less gas pressure stress in the dive and more on the surface" approach of bubble models would produce a safer decompression. There was only theory to support this of course, and now, as real evidence from formal human studies has emerged, we are having to revisit this assumption. It seems as though the optimum approach is not defined by "less stress on the dive and more on the surface" approach. Indeed, it is probably somewhere in the opposite direction, but how far exactly nobody knows.

Because you don't seem to understand what or where this "integral of supersaturation and time" detail comes from:

You do realize that Haldane and Schreiner equations, include a time component? They are tracking pressure over time. The duration of a pressure level is accounted for within the formula. The period and sustained levels of supersaturation can be retrieved from Haldane and Schreiner equations, and all our currently used deco models address this in the same way.

But you seem to want to add a second layer of time components on top of that with "integral of supersaturation and time"? Your trying to apply a time component twice, and one is magnified against to the other. That's not right.

Hmmm. Ross, I honestly have to say that this is a real worry. You seem genuinely confused between tools (those equations) that allow prediction of what supersaturation is in a tissue over time, and consideration of the physiological consequences of that supersaturation. At the simplest level what we are saying is that exposure to a certain range of supersaturation is almost certainly more harmful the longer you are exposed to it. It is nothing to do with factoring in time twice.

Here is yet another example of why "integral of supersaturation and time" is an ambiguous nonsense.

3000 kPa/mins = riding the elevator to the 30th floor and staying there 50 hours.
3000 kPa/mins = a 32% EAN dive within the NDL range.
3000 kPa/mins = a small deco dive.
3000 kPa/mins = 150 mins of normal flight in pressurized aircraft.
3000 kPa/mins = 15 mins surface transfer times for a SurD diver - serious injury / possible death
3000 kPa/mins = 40 mins of blood boiling total pressure loss for a space walker - death.

Your "integral of supersaturation and time" needs more work. In its current state it's an ambiguous nonsense.

Did you not read the bit where I said:

"I am well aware that extremely high tissue supersaturations can produce bubbling and symptoms with almost no delay. I am also aware that very low levels of supersaturation may be sustained for very long periods without the development of problems. However, these facts do not constitute a valid argument against time being important at levels of supersaturation between these extremes"

I'm sure that the old DRDC team will be very happy to see you hold their work on DCIEM tables in such low regard.

Actually, I'm sure that they would agree with everything I said. There is nothing wrong with their work; it is your interpretation of it that is flawed. I have discussed this issue with David. You are operating under misapprehension that the schedules prescribed by the DCIEM table right across the range of profiles are "iso-risk". Put another way, you are assuming that their conservative risk acceptance and reasonably comprehensive testing of many DCIEM schedules to confirm compliance with their risk acceptance means that ALL their schedules are associated with relatively low risk. The 170 for 30 schedule is at the very extreme of their air diving / air deco limits and is a profile that would be very unlikely to ever be used by a group with oxygen deco or SurD capability. It is effectively an extreme exposure schedule and will be associated with a higher risk of DCS than their more commonly used schedules in the shallower depth range. The point is that you can't refer to the DCIEM schedule for this dive as evidence that the NEDU profiles were way longer than they needed to be, especially when you factor in the exposure to work and temperature change in the divers in the NEDU profiles.

I forgot to mention, the USN when it published it latest tables, it too ignored the nedu test outcomes. The standard USN table for this dive calls for 93 mins deco.

It seems that the Naval dive command (who decide on the table sets and publishes them), they didn't take any cues from the nedu test either. The published USN tables for this dive is consistent with times from DCIEM, ZHL, VPM-B, RGM, and just about everything else.

Here we have two table sets - the DCIEM and the USN rev6, that give realistic deco times, while the nedu test used 2x (double) the required time.

Same comment as above. The USN 170 / 30 profile is an extreme exposure dive that is unlikely to ever be used. If used for whatever reason, the master chief responsible will accept the fact that the risk is greater than 6% (as David points out in the commentary that I cross posted above), and maybe much greater if the dive is hard working and cold.

You wrote above "performed under the conditions of the NEDU study". So now you have changed positions. All throughout the RBW thread you claimed the nedu test conditions were normal to regular diving. But now they have been elevated that to special conditions.

I have always said that this was a hard working dive with realistic thermal stress conditions. There is no change of positions. The debate was around your ridiculous contention that all the problems were cold induced injury from the "freezing" conditions.

I think the astute scientist would have looked into the reasons for the nedu test anomaly, and explored and explained why the test outcomes are so far outside the normal experience. But no one involved with the test, or in recent commentary has done that. In fact all we have seen so far, is a concerted effort to hide the anomaly, to pretend it's not there, to play games with descriptions and language, and omission and Half-Truths.

Actually Ross, exploration and explanation of results is exactly what the astute scientists involved in this project did. The fact that you don't like what they found is unfortunate for you, but it is of enormous potential importance to the diving community.

Simon wrote: "The prevention of fast tissue supersaturation early in the decompression... "

Ahh... no. The A2 profile has a high supersaturation in the fast cells. The premise you made, was not tested.(with more commentary and graphs)

This was addressed in detail in the RBW thread here:

Deep stops debate (split from ascent rate thread) - Page 108

The NEDU study was not A2 vs all those other profiles you have graphed; it was between A2 and A1. A2 protected the fast tissues compared to A1, but A1 still had better outcomes. If protecting the fast tissues was the crucial component of decompression safety one would have expected the opposite result.

Simon M

---------- Post added March 2nd, 2015 at 08:32 AM ----------

Here we go again.

Indeed. I can keep repeating the facts Ross, and I promise I will do so if you continue peddling this idiosyncratic interpretation of DCS pathophysiology that appears only in your self-justifying on-line posts. To be clear, several key elements of what Ross claims here cannot be found in any of the major references on this subject.

VGE (Venous Gas Embolii: circulatory micro-bubbles detected with Doppler) is NOT DCS

We all know that.

VGE in NOT an indicator of impending DCS.

Not a reliable indicator would be a more accurate description. Certainly there is a higher risk of "impending DCS" when venous gas emboli (VGE) grades are high.

DCS is normally from tissue micro-bubbles,which are not VGE

Some forms of DCS (such as musculoskeletal pain) are almost certainly caused by tissue micro-bubbles. However, more serious neurological forms of DCS (cerebral, spinal and inner ear) have been strongly linked to the presence of a patent foramen ovale whose only plausible contribution to the process is to allow VGE to cross into the arterial circulation and distribute to these organs. VGE may also cross pulmonary shunts and contribute to these forms of DCS in divers without PFO. Thus, VGE would seem to be very important in the pathophysiology of serious DCS.

Deco models work to prevent tissue microbubble growth, not VGE.

Would you care to explain to me exactly how tissue microbubbles and VGE are unlinked in respect of deco models, especially given that VGE must form in tissue microvessels which are part of (wait for it) ....the tissue.

VGE has been with us since Spencer first documented them in early 70's. Virtually every diver, including NDL dives, will experience some form of VGE, because VGE is supersaturation generated - something that is present in every dive we do.

This is almost certainly because the technology to detect microbubbles in tissue has lagged behind the technology to detect microbubbles moving in blood. We are still only just getting there with respect to tissue bubbles.

But still you try to link these two aspects of deco on a 1:1 basis. More trickery... again.

I'm not sure what you mean by "1:1 basis" but I can assure you that it is not "trickery", unless you are accusing every major text book in the world of being complicit in my subterfuge.

Simon M