Deep Stops Increases DCS

[lowviz]

...//... 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), ...//... 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. ...

Dr. Doolette,

First, thank you so much for sharing your expertise with those of us trying to follow all of this.

The idea of tissue bubbles breaking into vascular tissue seemed a bit of a stretch for me until you quoted the size range. If I remember correctly from one of my more notable BME courses, vascular tissue is rich with both structure and pores that are highly dependent on where you are in the vascular system. A quick external check of the literature (I no longer have access to the really good search engines) quickly supported this: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2792116/

So, if we are talking about pore sizes and microbubbles of not just the same order of magnitude, but literally the same size -it now appears to be not just reasonable, but expected...

 

[scubadada]

I second that! Thank you Dr. Doolette and Dr. Mitchell!

....and UWSojourner

I've learned a tremendous amount from this thread, some of it about decompression

 

[DavidFL]

I second that! Thank you Dr. Doolette and Dr. Mitchell!

+1

 

[shoredivr]

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

Dr Doolette thanks for this summary.

 

[rossh]

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

Hi David,

I would think and expect your last paragraph is probably correct. But it's not the issue.

I accept that VGE exist while concurrently, there is gas pressure stress in the tissues, and concurrently, the probable formation of (extra vascular) tissue micro-bubbles. They all happen concurrently but separately, for one connected reason - gone diving.

The implied connection Simon wants to make, is that all bubbles are one contiguous event. Of course it also fits perfectly the anti bubble model / anti deep stop agenda.

But I don't think the existing sketchy science supports that. I think we need to treat both micro-bubbles types as separate events, because they come and go for different reasons and at different times. The Bennett Elliot describes how VGE can form on the endothilium. Various sources suggest micro nuclei exist in our system that can also be the basis of VGE growth.

The literature describes DCS as tissue events, not intra vascular events. All models in use today, theorize about tissue bubbles, not circulation bubbles.

****

Simon suggests that VGE are tissue bubbles that some how escaped into the circulation.

But we also think the well perfused regions will remain in a dissolved stated, particularly if supersaturation stresses are lower (deep stops). So no bubbles there. We think DCS form in poorly perfused areas, so how does this extra vascular micro-bubble get transported to the circulation system, all in one piece? Makes no sense.

If VGE were actually tissue bubbles that "escaped", then how do we get away with no injury 99.95% of the time? Makes no sense again.

******

I'd love to get the answer to these problems. So far most of the testing has been by gross profile abuse, to force enormous bubbles and huge DCS events or death. But that does not say much useful. It just more misguided noise to the hyperbole.

What we need is info on trouble free dive conditions.

.

 

[Shearwater]

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 agree completely. Ross's persistence in claiming black is white is amazing. It is also a huge disservice to the diving community. If it is done in the interest in his own income over the good of the diving community, which is my opinion, then it is also shameful.

Bruce

 

[rossh]

I agree completely. Ross's persistence in claiming black is white is amazing. It is also a huge disservice to the diving community. If it is done in the interest in his own income over the good of the diving community, which is my opinion, then it is also shameful.

Bruce

I'm interested Bruce. You seem to hide behind the curtain and pull the strings on a lot of this and remain silent.

Are you in favor of fake profiles, meaningless pretty graphs with no dimensions, meaningless stress measures that have no proven basis. Deliberate hyperbole of unrelated science. Gross exaggeration of tests and consequences?

Because that is what your friends have been up too, for years to prop up this one side argument. Do you think that is science? Do think our future deco should be determined on such shabby, public persuasion, no peer reviewed, conjecture?

I certainly do not think the above is acceptable, and I hope that you - president of a successful dive computer company, would demand far better than has been offered so far.

.

 

[Shotmaster]

Ross,

You should take a step back and figure out how to work with the science, before you destroy what credibility you have left. Stop attacking people. There is no doubt that you are highly skilled in software. However, having seen your posts here, and the rebreather sites among others, it is evident that you have just enough knowledge to fool the average diver into thinking you are an expert, but not intelligent, experienced, and well informed divers, much less the real experts. My observation is that they have been trying to guide you down the path of enlightenment, being extremely civil and even kind to you while you have savagely attacked and impugned them personally and professionally. I think if they really wanted, they could destroy you. You should be thankful they have not done so. My hat is off to Dr. Doolette and Dr. Mitchell for their patience, and wisdom. They have shown themselves to be true gentlemen. You should take a lesson from them, it would serve you well.

 

[PfcAJ]

40/70 is much like VPM-B+3, in many ways. Its not quite the same but close enough to not matter. Factor in real world ascent rates. One thing is for sure - 40/70 is a lot closer to VPM-B, than the ZHL where it came from.

So yes, all this noise and fuss about DIR practices, DIR classroom theory, (conveniently blamed onto VPM), and when the expert smoke clears, the recommendation is almost,but not quite the same as a VPM-B+3 in many situations.


Simple Definition of hypocrisy

• : the behavior of people who do things that they tell other people not to do : behavior that does not agree with what someone claims to believe or feel

Again, are you REALLY trying to tell me that VPM-B+3 is close to 40/70? I'm looking at two profiles right now and they aren't.

220', 40min, 15/55 bottom gas, 35/25, 50%, 100% as deco gases.

VPM stops at 150ft with 4mins of time before hitting the 35/25 bottle.
40/70 stops at 130ft with 1min of stop time.

What do you think is happening during those 4 VPM minutes?

Additionally, VPM shows 43mins of oxygen time.
40/70 gives 58mins.

So here we are stopping earlier and getting out of the water with 15mins less oxygen time than with 40/70. Bananas. VPM+3 is more like 20/90 for that profile.

Your assertion that they're "close enough not to matter" is absolute nonsense. You should really be ashamed, Ross.

 

[David Doolette]

I accept that VGE exist while concurrently, there is gas pressure stress in the tissues, and concurrently, the probable formation of (extra vascular) tissue micro-bubbles. They all happen concurrently but separately, for one connected reason - gone diving.

The implied connection Simon wants to make, is that all bubbles are one contiguous event. Of course it also fits perfectly the anti bubble model / anti deep stop agenda.

But I don't think the existing sketchy science supports that. I think we need to treat both micro-bubbles types as separate events, because they come and go for different reasons and at different times..

Bubbles, irrespective of their location, come and go for the same reasons: they form to relieve gas supersaturation and they dissolve while the surrounding tissue has a lower gas partial pressures than inside the bubble. The Swan et al. paper I just cited and linked illustrates the time course of intravascular and extravascular microbubbles come and go at the same time.

The literature describes DCS as tissue events, not intra vascular events. All models in use today, theorize about tissue bubbles, not circulation bubbles..

No, we do not know exactly how DCS occurs, but the literature hypothesizes different manifestations of DCS as occurring from intravascular and extravascular bubbles. It is irrelevant that models of which you are aware are incomplete in this regard.

Simon suggests that VGE are tissue bubbles that some how escaped into the circulation..

No, Simon suggested this was one origin of VGE. The literature I reviewed in my earlier post supports that point of view

But we also think the well perfused regions will remain in a dissolved stated, particularly if supersaturation stresses are lower (deep stops). So no bubbles there. We think DCS form in poorly perfused areas, so how does this extra vascular micro-bubble get transported to the circulation system, all in one piece? Makes no sense..

No, DCS is thought to occur in both well- and poorly-perfused tissues, given appropriate conditions, that is why we have a range of compartment half-times in decompression algorithms. The VGE detected in the central venous blood arise from all the body tissues. Presumably those VGE which originate from extravascular tissue are those bubbles which formed adjacent to the capillaries. A poorly-perfused tissue has relatively fewer capillaries (not none).

If VGE were actually tissue bubbles that "escaped", then how do we get away with no injury 99.95% of the time? Makes no sense again..

The presence of bubbles either in the vasculature or in extravascular tissue does not inevitable lead to DCS. However, the more bubbles there are, the more likely they are to form at (extravascular) or impact (intravascular) a DCS-site.