Deep Stops Increases DCS

[leadduck]

The experts only indcated that incorporating rediculouisly long stops such as 20min and more (way beyound what anyone will consider acceptable) inceases your potential risk to DCS more than if you did not.

Where did you read that? Most of this discussion is about how the findings of the NEDU study and others suggest that usual ascent profiles with deep stops such as generated by VPM-B are inefficient in terms of DCS risk.

 

[rossh]

In the summer and fall of 1998 a number of tests were conducted on five WKPP divers after bottom times ranging from 120 minutes to 150 minutes at 285' average depths. The studies were overseen by L.B. Johansen and J.M. Chimiak, my recollection was this was done for NEDU.

Data collection included Doppler readings and blood draws. For the most part, the divers had used a standard ZHL-16B (think GF 100/100) generated decompression schedule with the addition of manually inserting deeper stops into the schedule. As an example, let's say the first scheduled stop per tables was 190', stops would have been inserted at 230, 220, 210, and 200.

As to the best of my recollection, only one of the divers abbreviated (cut short) his decompression schedule by reducing his 20' and 10' stops to only 3 hours, effectively shaving off about 30-40 minutes of oxygen time. There may have been another that did the same. I'll give you a single guess as to who did that.

There are some things to be clear on. One is that the majority of the divers that conducted the dives for the bubble study were using standard neo-Haldanian tables, with the addition of deep stops -- for the most part, the tables were cut with DECOM (ZHL-16b). Two, only one of the divers cut his shallow stop shorter, but even then he still did three hours on Oxygen before getting out of the water. Three, the diver that cut his 10' stop short was an avid fitness advocate and had a high VO2Max and muscle vascularity -- this helped him out with decompression due to a high perfusion rate (note: this is my opinion). Four, to the best of my knowledge, the data and schedules from the dives were never shared with anyone that was developing decompression algorithms.

I remember hearing the story about this from someone close to the matters at the time. I understand some of the divers had very high VGE, much to the amazement of the Nedu people. I think one of the divers even wrote about this in an old usenet mail list.

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[rossh]

Read my post Ross. Bubbles breaking into capillaries is only one "possible" way in which a propensity for tissue bubble formation and VGE MUST be linked. The other more important and irrefutable issue is that the capillaries acquire their supersaturated gas from the tissues. Thus, what is going on in the tissue capillaries is a direct reflection of what is going on the tissues. If a diver is forming greater numbers of VGE then there must be a concomitant propensity for greater numbers of bubbles to be forming in tissues. David has alluded to these same processes independently in his post 1006 above.

"....tissue bubble formation and VGE MUST be linked..."


By linked?? Do you mean because tissues are supersaturated in ascent, they off gas into the blood stream, and regionally that blood stream could become supersaturated too ? Leading too VGE that grow on the endothelium, or crevices within, or other places.

That is not a "must be linked". That is a consequence of one thing leads to another.

The context of the "must be linked" term you use here, is obfuscation and semantics.

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I restate my original point. The primary and only reliable measure of stress we have, is tissue pressure stress calculated by a array of cell half time /gas tracking systems. But VGE come and go on a different schedule, for different reasons, and they are at best, a secondary indicator only.

This reverse stress condition that you are implying (VGE is equal to tissue stress), is not true, and simply cannot be relied upon.


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This reverse stress indicator has been tried several times over the years by others... none have taken hold.


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[KenGordon]

Ross, is your position that bubbles in the blood do not matter, or at most are secondary? That the 'tissue stress' is what matters?

Have experiments been done in animals where bubbles are introduced directly to the blood without the whole hyperbaric exposure thing?

 

[ajduplessis]

Where did you read that? Most of this discussion is about how the findings of the NEDU study and others suggest that usual ascent profiles with deep stops such as generated by VPM-B are inefficient in terms of DCS risk.

The commercially available VPM-B models does not generate profiles as those used by the study. The profile used by NEDU is an absurd extrapolation dreamed up by the creators. Not sure about you or Simon, but my air dives to 170 feet with VPM does not even come close to this joke.

I don't care how much sugar, scientific data or other junk you add the profile above. It represents a multi level dive with an average depth significantly deeper/longer that the other. This is then called deep stops and further associated with VPM which it clearly is not.

I stick to what I have said before.
You cant compare fudge to apples claiming the fudge looks like an apple.........

 

[leadduck]

I restate my original point. The primary and only reliable measure of stress we have, is tissue pressure stress calculated by a array of cell half time /gas tracking systems.

No, the primary and only reliable measure of stress we have are VGE counts and DCS incidence in real dives. If a model, such as VPM, predicts bubble distributions that don't match real world bubbles such as VGE, the reason is simply that the model is poor.
In the case of VPM, I think it's for two reasons: the main mechanism of VGE (other tissues offgasing into blood) is missing in the model (in VPM all tissues are independent and don't off-gas into each other). So you can't expect VPM to predict bubbles in blood.
Secondly, the bubble model parameters haven't been calibrated by experiments. So you can't expect VPM to predict bubbles in other tissues well either.

But VGE come and go on a different schedule, for different reasons, and they are at best, a secondary indicator only.
This reverse stress condition that you are implying (VGE is equal to tissue stress), is not true, and simply cannot be relied upon.

The main cause for VGE are tissues offgasing into blood; therefore VGE is a very good indicator of overall tissue supersaturation. DCS only show up for high tissue supersaturaion in sensitive tissues; that's the reason why you can predict only a DCS probability from the VGE bubble count.

 

[ajduplessis]

If a model, such as VPM, predicts bubble distributions that don't match real world bubbles such as VGE, the reason is simply that the model is poor.

Incorrect statement because you dont continuously record or measure VGE scores. These are recorded post dive making your statement and conclusion poor at best.

This is also funny coming from someone that used the words "imaginary bubbles" when references bubble models.

 

[Diver0001]

The commercially available VPM-B models does not generate profiles as those used by the study. The profile used by NEDU is an absurd extrapolation dreamed up by the creators. Not sure about you or Simon, but my air dives to 170 feet with VPM does not even come close to this joke.

View attachment 379502

I don't care how much sugar, scientific data or other junk you add the profile above. It represents a multi level dive with an average depth significantly deeper/longer that the other. This is then called deep stops and further associated with VPM which it clearly is not.

I stick to what I have said before.
You cant compare fudge to apples claiming the fudge looks like an apple.........

That was my initial reaction when I first saw that study too. They choose an algorithm that by all forms of logic created a multi level dive as opposed to a dive with some deep stops.

The heat maps finally convinced me to change my perspective on this.

The most important thing you can look at to understand what's going on here are the heat maps. The heat maps make it entirely clear what is ACTUALLY happening in a bubble model, which is that in a bubble model a LOT of stress is being put on avoiding supersaturation in the fast tissues early in the ascent while giving lower priority to the resulting continuation of on-gassing in slower tissues. The heat maps for both the algorithm they used to test with and VPM showed the exact same tendency.

With this insight it becomes abundantly clear that the claims of all bubble models that deep stops early in the ascent will allow the diver to shorten the shallow stops later in the ascent are simply incorrect. Deep stops may or may not have a function but it's not the function that the makers of these algorithms claim and in fact, what shows up is that making deep stops, while perhaps not damaging in and of themselves, should be compensated for by making longer shallow stops, not shorter ones.

This can clearly be demonstrated by making heat maps for the same algorithm at different levels of conservatism. One would think that a "more conservative" setting on an algorithm will result in a heat map showing "safer" ascents. In bubble models, in fact, the exact opposite occurs. VPM, for example (and I know Ross didn't like hearing this but he cannot deny the facts) show heat maps that are "safer" at LOWER levels of conservatism and that VPM, if it had conservatism settings that were as high as the model NEDU used, would most likely create equally bizarre ascent schedules. This is not to pick on VPM, by the way. Any bubble model would do the same.

So don't get too hung up on the model they used or the fact that they used an extreme conservatism setting to set that dive. In fact, using a very high conservatism setting makes it immediately evident to the reader that something is wrong with that ascent.... and the thing that is wrong are the (up to that point in time) untested assumptions about the effect of deep stops on the shallower stops that followed.

R..

 

[Dr Simon Mitchell]

That is not a "must be linked". That is a consequence of one thing leads to another.

That is not a tautology. That is saying the same thing twice in a different way.

Don't be silly Ross, "one thing leads to another" is a link by anyone's definition.

Yes, arterial blood arrives in a tissue un-supersaturated. If the tissue it enters is supersaturated then the tissue off-gases into the blood making it supersaturated too. In fact, you could think of it like this if it helps.... at any snapshot in time the blood contained in tissue capillaries is effectively part of that tissue, and its gas supersaturation will reflect that of the extravascular compartment of the tissue. That is why you cannot claim that VPM protects or models (or whatever you want to call it) the extravascular compartment only, while the blood is something separate and somehow unlinked.

You may remember this diagram which helps illustrate these things:

 

[kensuf]

With this insight it becomes abundantly clear that the claims of all bubble models that deep stops early in the ascent will allow the diver to shorten the shallow stops later in the ascent are simply incorrect. Deep stops may or may not have a function but it's not the function that the makers of these algorithms claim and in fact, what shows up is that making deep stops, while perhaps not damaging in and of themselves, should be compensated for by making longer shallow stops, not shorter ones.

One thing that's interesting to note, the original concept of "Pyle Stops" had those deep stops being added to the total bottom time for decompression calculations. So for a 30 minute dive to 150', with Pyle Stops added at 90' and 60', a person would shift to either the 35 minute or 40 minute decompression schedule, depending on how long those stops were. This means that when conducting "Pyle Stops" the original way, you're actually going to be lengthening your shallow stops, not shortening them.