Deep Stops Increases DCS

[ajduplessis]

It appears that no one knows quite where that sweet spot is...
yet
But according to at least 2 of the most expert opinions on this thread, it appears that 40/80 is a very good start.

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.

 

[Dr Simon Mitchell]

Aspects of this post have been dealt with by others.

For an unbiased look and review of VGE and it role in DCS, readers might like to see this paper:

Venous gas embolism as a predictive tool for improving CNS decompression safety

This is by a research group with many years of work, studies and papers in the topic of VGE.

The Brubakk / Norwegian group have indeed been interested in VGE for many years and have published extensively on the subject. If one reads the cited paper holistically (as opposed to scouring it for cherry-picked quotes that appear to support a particular position) it becomes very clear that Alf Brubakk and his team consider VGE (and particularly VGE that cross into the arterial system) to be extremely important in the pathophysiology of neurological DCS. They have taken this position for many years and to try to infer that they support your suggestion that VGE are unimportant (if that is what you are doing) would be a gross misrepresentation of their views.

As they say in the paper, "This illustrates that having detectable bubbles yields only a 4% chance of developing DCS. Even when using high bubble grades as test criterion, the positive predictive value is low..."

See above about cherry picking. You could also have quoted:

"...measurement of VGE could be considered as the gold standard for validating decompression procedures..." or "...it seems reasonable to suggest that the formation of venous gas emboli (VGE) and their effects on the endothelium may be the central mechanism leading to central nervous system (CNS) damage".

VGE does not predict DCS.

David has comprehensively dealt with this claim here: Deep Stops Increases DCS

Normal tissue DCS is theorized to grow from "extra vascular" bubble growth. This is your standard everyday DCS risk, and its what all deco models try to control and regulate - tissue bubbles - type 2 DCS.

No one in the world of diving science or medicine believes your particular version of DCS pathophysiology. Yes, some forms of DCS may be caused by formation of bubbles in tissues themselves. However the strong positive correlation between the presence of a large PFO (which allows blood to get from veins to arteries) and the most feared forms of neurological DCS (type 2 DCS in the traditional terminology) clearly implicates VGE that cross from veins to arteries in the causation of these events.

Bubble models work with tissue micro-bubble growth - not VGE.

Impossible. VGE arise from supersaturated gas that the capillary blood only acquires as it passes through tissues. It is also possible (and indeed has been demonstrated) that some VGE actually ARE tissue bubbles that have ruptured into the capillary (see here):

RBCs = red blood cells in a capillary. a = a bubble that you can see rupturing into the capillary from the tissue.

Either way, VGE are inevitably a barometer of gas supersaturation conditions in tissues through which the venous blood has passed. Therefore, to infer that bubble models can allow large numbers of VGE to form (as they appear to do) whilst magically protecting tissues in some sort of separate process is nothing short of ridiculous.

The DAN PFO workshop report describes issues of PFO / shunts and gives good summary suggestions.

However, one aspect of a PFO / shunt has been overlooked.... A PFO recirculates blood - unfiltered blood, that still contains high levels of inert gas. This will lead to an effective increase in [correction by author inserted] inert tissue pressure, and as a result, we probably do not off gas as fast as planned.

This has not been overlooked. It was specifically addressed by our paper in the DAN PFO Workshop which I linked to previously and which you cite. It clearly states in the edited transcript:

"I should briefly mention the extent to which we could expect PFOs shunting from right to left to disturb inert gas exchange to a point where it might disadvantage a diver. We do not believe that disturbance of nitrogen elimination is a plausible explanation for the significance of a PFO in DCS. Dr Eldridge may comment on this but he published a paper in 2011 in which he showed that even in a group of subjects where the PFOs were mostly spontaneously shunting, the shunt fraction was about 1.5%. This would not significantly impair nitrogen elimination".

Just to be clear, what this means is that at rest, even with a large PFO, about 1.5% of blood bypasses the lungs through the PFO. Marlowe Eldridge was in the audience, along with other relevant experts such as Richard Moon and Fred Bove, and nobody challenged our conclusion on this matter. Moreover, if one reads the Eldridge paper, it seems that during exercise the volume of blood shunted across the PFO remained constant as the cardiac output (amount of blood the heart was pumping) increased, and therefore the % of blood bypassing the lungs progressively falls. At moderate exercise it was about 0.3%. Thus, in a diver exercising even lightly, the fraction of blood bypassing the lungs will be even less than 1.5%.

You may recall that I specifically brought this issue to Doug Ebersole's (a diving cardiologist) attention, in your presence, in question time after his presentation at Tek Dive USA. You may also recall that he dismissed the issue as unimportant.

Here is the summary slide from the Dr. Neal Pollock presentation on Decompression Stress at the TekUSA 2016.

Note the salient points: VGE does not equal DCS. It can be a relative, but NOT an absolute indicator of stress, and needs to be used cautiously.

It is intellectually unfair to infer that Dr Pollock is sympathetic to your views on the unimportance of VGE (which seems to be your intent in citing him); especially as he has dedicated a substantial portion of his academic career to studying them. You also failed to point out that his slide states "lowest grades practical should be the goal". I have little doubt that by "lowest grades practical" he had grades lower than 3 or 4 in mind.

[/QUOTE]

 

[kensuf]

From the link "WKPP extreme exposure correlations and calibrations", sounds to me that he looked at what the WKPP was doing and then compared and tweaked RGBM to what he was getting reported as the profiles in use on the WKPP.

WKPP used decoplanner and cut tables by the makers of decoplanner.

Decoplanner didn't exist when the doppler studies were being conducted on WKPP divers. Most of the guys were using DECOM (straight ZHL-16) for cutting tables, and then the "classical" RD (not this new-fangled mumbo-jumbo) to tweak the profiles, but a few also had access to tables generated by Hamilton.

I'm getting caught up on this thread, I had been ignoring it for various reasons, but I'll post something about the doppler study later on today.

 

[rossh]

Impossible. VGE arise from supersaturated gas that the capillary blood only acquires as it passes through tissues. It is also possible (and indeed has been demonstrated) that some VGE actually ARE tissue bubbles that have ruptured into the capillary (see here):


Either way, VGE are inevitably a barometer of gas supersaturation conditions in tissues through which the venous blood has passed. Therefore, to infer that bubble models can allow large numbers of VGE to form (as they appear to do) whilst magically protecting tissues in some sort of separate process is nothing short of ridiculous.

So in order to make your point, you use a photo from an animal study, where the ascent and ceiling violations were so gross, that it caused death, and allowed for a dissection of tissue that showed honking great bubbles..


And now you want us to think (scare), that humans suffer this every day, on a grade 4 VGE, but not a grade 2 VGE dive ???? i.e. a 10 minute difference in deco time. Hmm... sounds like BS Simon.

I don't think anyone is going to be convinced by this gross exaggeration and trickery you are playing at.


Simon, Find some literature that actually supports your extra vascular microbubble growth == intra vascular VGE growth in normal everyday diving?? Because almost every diver has VGE, your theory therefore implies that every diver suffers this breakout condition. It doesn't ring true Simon.

And while we are at it, explain how VGE can be reduced by a good pre-dive shake, or a nice warm bath, or how a Breath hold diver can make grade 4 bubbles.. etc. etc..

You may recall that I specifically brought this issue to Doug Ebersole's (a diving cardiologist) attention, in your presence, in question time after his presentation at Tek Dive USA. You may also recall that he dismissed the issue as unimportant.

I did a follow up with him the next day, without your interference.... makes a world of difference.



.

 

[kensuf]

Decoplanner didn't exist when the doppler studies were being conducted on WKPP divers. Most of the guys were using DECOM (straight ZHL-16) for cutting tables, and then the "classical" RD (not this new-fangled mumbo-jumbo) to tweak the profiles, but a few also had access to tables generated by Hamilton.

I'm getting caught up on this thread, I had been ignoring it for various reasons, but I'll post something about the doppler study later on today.

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.

 

[David Doolette]

. Even breath-hold divers can make grade 4 VGE from a single breath of air (UHM 2016, Vol. 43, No. 4 – VENOUS GAS EMBOLI AFTER BREATH-HOLD DIVES)

It is mischaracterization of this interesting paper to suggest it shows VGE formation from a single breath of air. In fact, the VGE were detected after the diver conducted 14 breathhold dives to a maximum depth of 42 msw, and for a total time underwater of 32 minutes. VGE result from the same stresses as when breathing compressed gas: increased arterial gas pressures, build-up of gas partial pressures in the tissues, supersaturation of those tissues on ascent, and bubble formation in the tissues (extravascular, and maybe in the venous end of the capillaries) from where they make their way out into the venous blood where they can be detected.

 

[RainPilot]

Thanks Ken glad for the info. I suspect I know who the "best decompressor there is " was who cut short. Different strokes for different folks I guess.

 

[C Dub]

Beyond the interesting character you are referring to, has there been any research on level of vascularity/fitness as it relates to decompression/VGE/tendency to experience DCS?

 

[kensuf]

Beyond the interesting character you are referring to, has there been any research on level of vascularity/fitness as it relates to decompression/VGE/tendency to experience DCS?

I don't know, and although I am not a decompression scientist, I believe it's generally accepted that perfusion and diffusion are two key components for driving on-gassing and off-gassing rates.

 

[Dr Simon Mitchell]

So in order to make your point, you use a photo from an animal study, where the ascent and ceiling violations were so gross, that it caused death, and allowed for a dissection of tissue that showed honking great bubbles..

No, I used the photo in order to demonstrate a part of my point, which is that the propensity to form bubbles in tissue capillaries (VGE) and bubbles in tissues are not unlinked as you are trying to imply.

And now you want us to think (scare), that humans suffer this every day, on a grade 4 VGE, but not a grade 2 VGE dive ???? i.e. a 10 minute difference in deco time. Hmm... sounds like BS Simon.

I'm not quite sure what you are trying to say here Ross.

Simon, Find some literature that actually supports your extra vascular microbubble growth == intra vascular VGE growth in normal everyday diving?? Because almost every diver has VGE, your theory therefore implies that every diver suffers this breakout condition. It doesn't ring true Simon.

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.

I don't think anyone is going to be convinced by this gross exaggeration and trickery you are playing at.

I guess I've been able to "trick and exaggerate" my way around my academic colleagues who asked me to write the following textbook chapters / sections on decompression sickness pathophysiology which contain all the things I am saying here.

FRANCIS TJR, MITCHELL SJ. The pathophysiology of decompression sickness. In: Brubakk AO, Neuman TS (Eds). Bennett and Elliott’s Physiology and Medicine of Diving (5th ed). London, Harcourt Publishers, 530-556, 2003

FRANCIS TJR, MITCHELL SJ. Pathophysiology of decompression sickness. In: Bove AA (Ed). Bove and Davis’ Diving Medicine (4th ed). London, Saunders Publishing, 165-184, 2004

BENNETT MH, MITCHELL SJ. Hyperbaric and Diving Medicine. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J (eds). Harrison’s Principles of Internal Medicine (19th ed). McGraw – Hill, Chapt e477: 2015

MITCHELL SJ. Decompression sickness - Pathophysiology. In: EDMONDS C, BENNETT MH, LIPPMANN J, MITCHELL SJ (eds). Diving and Subaquatic Medicine (5th ed). Florida, USA, Taylor and Francis, 125-140, 2015

And while we are at it, explain how VGE can be reduced by a good pre-dive shake, or a nice warm bath, or how a Breath hold diver can make grade 4 bubbles.. etc. etc..

David has dealt with your misinterpretation or (?deliberate) misrepresentation of the breath hold paper. Nevertheless, although there is a lot of potentially interesting discussion that could be framed around these questions, I don't quite see what this has to do with the issue we are debating.

I did a follow up with him the next day, without your interference.... makes a world of difference.

Yes, and....??