Deep Stops Increases DCS

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You asked for a discussion about you. but it breaks the TOS rules - I'll try to be gentle.


consensus_2.jpg


The peer position, and its discussion is quite clear - a balanced - unbiased - no preference - cautious approach.


Did you keep to that balanced approach? NO. see below. You seem to make every effort to push one side of this argument to the exclusion and detriment of all else. And have actively downplayed the opposing views and test that were included the Workshop. You display a one sided view on deep stop efficacy - contrary to the in the workshop position, with no new evidence to support that..

Ross,

I asked you for evidence to support your claim my peers had rejected ideas related to this discussion and articulated by me at the 2008 workshop, not a diatribe on your opinions about whether you think my arguments are valid or balanced. Obviously you have no such evidence, which is no surprise to me because it is simply not true. My "view on deep stop efficacy" is entirely consistent with those of the vast majority of my scientist peers, and with the "workshop position"; it did say there was conflicting evidence. Or am I not allowed a view that favours one side of that conflict? I might add that this view was distilled largely on the basis of the arguments I saw presented at that workshop.

The workshop also had a section on VGE and how to interpret them, but you don't follow that advise either. Your agenda to make VGE the primary measure (in the public view), is not accepted by expert researchers in the field.

What agenda to make VGE a primary measure? All I have done in relation to VGE is prevent you rewriting related aspects of the pathophysiology of DCS in your attempt to defend a commercial product. I would have thought that your next post on VGE might have been an apology for wasting so much time and bandwidth on that particular effort after reading this post: Deep Stops Increases DCS

Simon M
 
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If ISS is a good indicator of DCS risk, what tools are available to a typical Tec Diver to compare ISS across different algorithms/settings?

Answer: MultiDeco.

In MultiDeco, press this button:

btn_supersat.png



It has a real time display of Supersaturation and tissue pressures. You can see in an instant how much real stress exists. You can see what pressure levels the model is making its decisions on. It shows surface decay details too. These features are built in to MultiDeco, and lets anyone cross check the plan against the theory of risk.


kw_compare_ss_170(2).png



The "ISS" is the area under each of the brown lines. You can visualize that stress amount.



Sadly these charts do not have as many pretty colors as a heatmap :(


Heatmaps do not show supersaturation as they claim. Instead they compare plans, with no actual display of total values. They show red when real risk can be quite low and harmless. They try to create danger between all kinds of successful dives, where none exists.


.
 
You asked for a discussion about you. but it breaks the TOS rules - I'll try to be gentle.


consensus_2.jpg


The peer position, and its discussion is quite clear - a balanced - unbiased - no preference - cautious approach.


Did you keep to that balanced approach? NO. see below.
I think you have a skewed idea - or representation - of how science works.

  1. A workshop isn't the end-all, the final decision of how facts are. On the contrary, it's where scientists meet to discuss their different interpretations of what available data means
  2. A "peer position" is what all the peers agree on given their different opinions and interpretations of what the data mean. This is a sound principle, since it statistically gives the most reliable interpretation of the data. On the other hand, it means that progress is slow, since there are different interpretations and sometimes it's the outlier opinion which is the most correct
  3. Scientists aren't bound by any consensus. On the contrary, scientists have an obligation to argue their opinion about what is right. Scientific progress isn't a democracy, it's an elitocracy. So unless a scientist has been convinced that their previous position was wrong, they are expected to pursue the truth the way they believe is right. Ever heard of Galileo?
And finally, fakery is the one deadly sin in science. A scientist caught in fakery will be stripped of their standing and may easily lose their job, never ever working in science again. Ever heard of Andrew Wakefield? So being repeatedly accused of fakery is extremely insulting to anyone working in science and a clear personal attack.
 
Ross,

We have had quite a long debate about the significance of VGE in this thread after I pointed out that the Split group recorded consistently high VGE grades after decompressions from trimix dives using VPM. In an attempt to lessen the negative implications for VPM your position has been that VGE don't matter because DCS is caused by tissue bubbles and that the propensity to form tissue bubbles is somehow unlinked from the propensity to form VGE. You have claimed that VPM selectively protects from tissue bubble formation. Let me remind you of some of your statements:




Can I remind you of one of the things I said to you?



You might want to look the following (just published) paper up... For clarity, "autochthonous bubbles" are tissue bubbles and the pulmonary artery actually carries venous blood so the bubbles in it are VGE.

Bernaldo de Quirós, Møllerløkken A, Havnes MB, Brubakk AO, González-Díaz O, Fernández A. Bubbles Quantified In vivo by Ultrasound Relates to Amount of Gas Detected Post-mortem in Rabbits Decompressed from High Pressure. Front Physiol. 2016 Jul 21;7:310. doi: 10.3389/fphys.2016.00310. eCollection 2016.

Abstract: The pathophysiological mechanism of decompression sickness is not fully understood but there is evidence that it can be caused by intravascular and autochthonous bubbles. Doppler ultrasound at a given circulatory location is used to detect and quantify the presence of intravascular gas bubbles as an indicator of decompression stress. In this manuscript we studied the relationship between presence and quantity of gas bubbles by echosonography of the pulmonary artery of anesthetized, air-breathing New Zealand White rabbits that were compressed and decompressed. Mortality rate, presence, quantity, and distribution of gas bubbles elsewhere in the body was examined postmortem. We found a strong positive relationship between high ultrasound bubble grades in the pulmonary artery, sudden death, and high amount of intra and extra vascular gas bubbles widespread throughout the entire organism. In contrast, animals with lower bubble grades survived for 1 h after decompression until sacrificed, and showed no gas bubbles during dissection.


The pubmed link is here: Bubbles Quantified In vivo by Ultrasound Relates to Amount of Gas Detected Post-mortem in Rabbits Decompressed from High Pressure. - PubMed - NCBI

"wishful thinking of some around here to bundle it all together"?

"another fake problem to justify more fake answers"?

Simon M


This continued effort to incorrectly merge intra vascular and extra vascular bubbles together as one, and then plays tricks on the public about VGE, continues.

It ignores the advise of experts that VGE are a secondary indicator only, that VGE do not predict DCS, and are at best a relative indicator only, that has to be applied cautiously.

You repeat your attacks on VPM because it was used in a study to perform exactly as it was asked , and it it performed flawlessly.

You quote a new animal study, where they drove the subjects to death with a direct ascent, found bubbles as expected post-mortem. But adds nothing to any of your points above. (8 ATA, 45 mins, direct ascent).


Do you have any science that properly identifies (or refutes) extra vascular bubble growth, under normal safe decompression condition, that then some how transport themselves to the intra vascular system?

.
 
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This continued effort to incorrectly merge intra vascular and extra vascular bubbles together as one, and then plays tricks on the public about VGE, continues.

It ignores the advise of experts that VGE are a secondary indicator only, that VGE do not predict DCS, and are at best a relative indicator only, that has to be applied cautiously.


.

About VGE this I believe has been already discussed Deep stops debate (split from ascent rate thread) - Page 107

with several references linking VGE to DCS. Is there new data (please data coming from modeling software is imaginary unless you can show that the model is correctly interpolating between real datapoint and not extrapolating where no data exists), supporting this old (and I must add, not entirely correct) statement? Where is it published?

Cheers
 
About VGE this I believe has been already discussed Deep stops debate (split from ascent rate thread) - Page 107

with several references linking VGE to DCS. Is there new data (please data coming from modeling software is imaginary unless you can show that the model is correctly interpolating between real datapoint and not extrapolating where no data exists), supporting this old (and I must add, not entirely correct) statement? Where is it published?

Cheers

No. Its same old half truths, and vague loose approximations, that just don't add up.

The most expert recommendations on this subject, the real facts, the studies, simply do not allow for VGE to be used or promoted to the significant way that Simon wants to portray them.

.
 
You quote a new animal study, where they drove the subjects to death with a direct ascent, found bubbles as expected post-mortem. But adds nothing to any of your points above. (8 ATA, 45 mins, direct ascent).


Do you have any science that properly identifies (or refutes) extra vascular bubble growth, under normal safe decompression condition, that then some how transport themselves to the intra vascular system?
.

In an argument from ignorance, you seem to be suggesting that because, at present, there is not technology that can measure extra-vascular bubble formation in the course of a "normal" dive, that it doesn't happen. Since it is approximately the one year anniversary of having this same argument here:

Diving too carefully? - Page 40

I will repost the evidence that existed then, before the paper Simon just cited. None of these are "normal" dives although for the pig study, the profile (45 min O2 pre breathe / 4 atm air / 2 hr / no stop) was not particularly severe as it resulted in VGE grade 1 or less in 2/3rd of the animals ARTICLES | Journal of Applied Physiology

There is limited evidence, but on the balance of the available evidence, yes, extravascular and venous bubbles are the same thing. The available evidence suggests that bubbles form in the extravascular tissue and then break through the walls of the blood vessels and into the blood.

First of all, we have the photomicrographs of exactly this happening (Bennett,P.B. Fine Structure of decompression sickness. In; Schilling CW, Beckett MW eds. Underwater Physiology VI. Bethesda (MB): FASED, 1978. pp595-9), which has already been cited and the figure reproduced on this thread.

Second, there is considerable evidence that bubbles do not form readily in blood, or inside blood vessels. The key paper, and one that summarizes the earlier evidence, is Lee YC, Wu YC, Gerth WA, Vann RD. Absence of intravascular bubble nucleation in dead rats. Undersea Hyperb Med 1993;20:289-96. In these experiments, dead rats were opened up and the inferior vena cava, a large vein that returns blood to the heart, was exposed. Two ligatures (loops of thread pulled tight to squeeze the vessel closed at each point) were put on the vena cava to isolate a section of this vessel and the blood inside it from the rest of the circulatory system. The rats where then exposed to high hyperbaric air pressure for many hours so that the blood and extravascular tissues take up gas by diffusion (in the same manner as the gel experiments that underlie VPM), and then decompressed. No bubbles form in the sections of vena cava isolated from the rest of the circulatory system. (Several related experiments were performed that demonstrate that the isolated sections of vena cava can produce bubbles if gas nuclei are added, but not in the native blood.) However, bubbles form profusely in the blood-filled sections of vena cava that are outside the ligatures and still connected to the tissue microcirculation. The tissue microcirculation is comprised of the small blood vessels (principally capillaries) that are inside, and considered part of, the tissue. So the bubbles come from the tissue. One possible location of the bubble formation is inside the tissue microcirculation, but that requires the assumption that the environment inside tissue microcirculation is different to that inside the large veins. Occam's Razor (which has also already been invoked on this thread) leads to the conclusion with fewer assumptions, favoured by the authors, that the bubbles form in the extravascular tissue, and rupture into the microcirculation.

In summary, the available evidence in the scientific literature suggests intravascular bubbles arise in the extravascular part of the tissue - they are the same thing. However, it is plausible that bubbles do form inside, and at the venous end of, the tissue microcirculation, and one day evidence may arise to support this possibility (we do see gas bubbles inside the microcirculation, and such a picture has been posted on this thread, but it is not clear if the bubbles formed there or migrated in from the tissue). However, as has been pointed out on several occasions, if bubbles do form inside the tissue microcirculation, they form in response to the same tissue supersaturation that exists less than a bubble diameter away on the other side of the blood vessel walls. Most decompression models / algorithms have compartments as their basic structure. These compartments represent the extravascular tissue and the blood in the microcirculation, precisely because over the time course of processes relevant to decompression, there are not important gradients of gas partial pressures across the regions represented by a compartment. Thus, if bubbles form separately in the extravascular and intravascular parts of the tissue, their dynamics will be closely linked - perhaps not identical, because of different physical properties of the blood and extravascular tissue, but linked. For instance, there are probably more nucleation sites in extravascular tissue than in blood, and therefore more bubbles might form in extravascular tissue than in blood, but the dynamics will be linked. Evidence for this linkage is provided by a paper already cited on this thread (Swan JG, Wilbur JC, Moodie KL, Kane SA, Knaus DA, Phillips SD et al. Microbubbles are detected prior to larger bubbles following decompression. J Appl Physiol 2014;116:790-6) These authors used a dual-frequency ultrasound (DFU) technique that can be tuned to detect bubbles of particular size (1-4 microns in this study), is capable of detecting smaller bubbles than those detected by the B-mode ultrasound used to detect VGE, and can be used to detect bubbles both in the blood and in extravascular tissues. This paper showed that, in pigs, following decompression from hyperbaric air exposures, the number of DFU-detected microbubbles of a particular size rises and then falls before larger VGE are detected. A reasonable interpretation is that the DFU-detected microbubbles are the precursors of the B-mode-detectable VGE - i.e. the number of DFU-detected microbubbles decreases as they grow (by diffusion and coalescence) larger than the size for which the DFU is tuned to detect, eventually getting large enough to be detected by B-mode ultrasound. Importantly, the authors made simultaneous DFU measurements inside veins and in extravascular tissue, and the dynamics of the intravascular and extravascular microbubbles were the same - i.e. the number of DFU-detected microbubbles in the extravascular part of the tissue and in the venous blood rise and fall at the same time - demonstrating a linkage between the magnitude and time course of extravascular and intravascular bubble formation.

I doubt there is a single scientist working in the area of decompression research who does not believe that the sizes and profusions of intravascular and extravascular bubbles are proportional, and that a decompression procedure that results in many VGE also results in many extravascular bubbles.

David Doolette
 
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Quoting from one of my favorite movies "Gentlemen, what we have here is a failure to communicate!"

What I see is essentially a computer programmer, telling some of the most respected, leading scientists in the field of decompression science, that have actually done human testing, that he knows more about how the body reacts to compression and decompression than they do, because he created software and a new algorithm!

Down South we have a saying "That dog won't hunt". I think it applies here.
 
I meant to say this for a long time after reading a couple of threads on RBW and here.
After this long thread, I think it is time for me and I hope many of those reading and getting useful info, to thank Dr @Simon Mitchell and Dr @David Doolette.

They spend liberally their time with discussion well below their par, without gain just for our benefit and for the only reason they cannot stand to see misinformation spread in our community.

[joke]
... for me to come on these threads and strongly articulate opinions that are at odds with those widely held by my scientific colleagues would rapidly result in a perception that I am a nutcase. Why would I do that?
Simon M

Simon, in fact you being a physician, are preventing harm to all of us providing better information and the current state of understanding on decompression. Please allow me a joke: in a sense you are a nut case :wink: you are undermining your customer base because if successful in better educating us you will prevent DCS!
[/joke]

Cheers and thanks to both of you :clapping:.
 
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