Diving too carefully?
- Thread starter Ben Field
- Start date
Neal, Thank you for the paper abstracts and details.
I am in agreement with all of the above.
But I do wish to point out for other readers, that it did not provide an answer the pertinent question: a location distinction between tissue micro-bubbles (extravascular, autochthonous formation), vs VGE microbubbles (intravascular formation).
That's OK. I respect that.
Simon Mitchell
Well-Known Member
Ross,
I'm not sure what you mean by "location distinction", but (obviously) VGE are found in the venous blood, and tissue bubbles are found in tissue. But that is not really the discussion we have been having. If "other readers" wish to understand this issue they will find the pertinent information here:
http://www.ccrexplorers.com/showthread.php?t=18348&p=178383&viewfull=1#post178383
The most important points are:
It is incorrect to imply that tissue bubbles cause DCS and VGE don't.
It is incorrect to imply that VGE and tissue bubbles are somehow a result of separate processes and (similarly) that there is no relationship between them.
Neal has given an answer on this matter at least 3 times now:
npollock said:
Simon M
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Simon Mitchell
Well-Known Member
Hello Mik,
The first bed of tiny blood vessels (capillaries) that the venous blood encounters is the lung capillary bed where gas exchange takes place (carbon dioxide is eliminated and oxygen is taken up). Once the oxygenated blood leaves the lungs it passes to the left side of the heart and is pumped around the body in the arteries.
We have known for some time that these tiny blood vessels are efficient at removing VGE that arrive in the venous blood. This is obviously a good thing for us because it prevents these small bubbles entering the arteries and distributing around the body to various organs. Unfortunately, this "filtering"system can be bypassed in several ways. The one many divers are familiar with is the patent foramen ovale (PFO). This is a communication between the venous and arterial circulations in the heart itself and it can allow VGE to be "shunted" (a term used in this context to imply that VGE are getting from the veins directly into the arteries). The association between the presence of large PFOs and certain forms of DCS (cerebral, spinal, inner ear, skin) strongly indicates that this process of shunting VGE from veins to arteries can be harmful.
Another path by which VGE can cross into the arterial system is in the lungs themselves. This phenomenon is much less well understood or researched in the diving context than PFO. However, it seems there may be blood vessels in the lungs that are larger than the capillaries, and that these vessels can open up and allow blood (and any VGE present) to bypass the lung capillary beds which would have otherwise filtered out the bubbles. These vessels are called pulmonary shunts. In some people they may be open at rest, and we have seen them provoked into opening by the same things that provoke blood to cross a PFO (valsalvas, lifting, straining etc). But by far the most potent stimulus for their opening seems to be exercise. One study found pulmonary shunts in over 90% of exercising "normal" subjects. There are some in the diving medicine community who believe that such shunts account for close to all cases of those forms of DCS known to be associated with PFO, but which occur in subjects without PFO. This is unproven however.
You cannot easily test yourself for a pulmonary shunt, and there would almost certainly be nothing you could do about it if you found that you did shunt VGE by this pathway (except try to avoid high VGE grades [which is what some of Neal's work is about] and probably avoid exercise for a number of hours following diving).
Simon M
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Ben Field
All IMVHO obviously...
So you are at the coast and your tanks are empty, I invite you to join us tomorrow bashing flatties or a 10mtr reef and you would purposefully buy a Trimix dil?!
FWIW, Your Sorb supplier is robbing you blind if you pay £25+/kilo!
Firstly I am surprised anyone gives credibility to anything written online, I thought it was universally accepted everyone online is nonsense?
Anyway, I was expressing an opinion (which I stand by) "Divers in general should MTFU and use the right gas for the dive"
I think that's a legitimate concern. I see alot of Air use when Nitrox card is owned but not used for cost or laziness reasons and I see alot of Trimix abuse for bragging rights. In general "we" (as divers) should Man Up and accept no face is lost doing an Air Dil dive when it is the optimal choice rather than going out of our way to create a trumped up reasons to say we've used Trimix to sound like a big hard nut- I 100% have seen this.
The average diver is not on these forums I realise so if I went Irvine it would have no effect, they also only have 1 dil bottle and don't bank gas, that's for the hardnuts and regulars, the average diver is not a regular, he/she dives occasionally and buys gas to suit the dive- or Not IMVHO.
Sorry to disappoint you Nick but I see alot of divers down here, IMO there is a competitive element who should but don't use non-Trimix dil and make their lives more difficult because of it, my MTFU comment was intended to imply my frustration with that level of stupidity not preaching to the (should be) converted on CCRX.
Whatever... threads OT now anyway.
This generalization of events, is not right.
Extravascular tissue micro-bubbles can cause neurological DCS - yes.
But, Intravascular VGE does not normally make DCS. If they did, then virtually everyone would get DCS, because almost everyone has VGE, but it doesn't happen.
For VGE to actually do harm, ones needs all the conditions you just explained in the post above: to get arterialization of VGE, and a large dose of bad luck.
The literature provides: The growth of extravascular tissue micro-bubbles and intravascular VGE are two separate events. One event does not depend on the other. One event does not know the other exists. There is no known linkage between the two. It is wrong to imply that existence of one type of microbubble bubble is representative of the other. However, obviously they do both require conditions of supersaturation in inert gas to make them appear and grow, but those conditions are different.
Neal has not given a definitive answer to the question and instead choose be vague.
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AdrianSmith
New Member
Ladies and gentlemen, I give you.... The Backfire Effect.
http://rationalwiki.org/wiki/Backfire_effect
http://rationalwiki.org/wiki/Backfire_effect
Hi Adrian, Your comment is miss placed. Perhaps you don't fully understand what is being discussed.
They provided nothing to assert the position that neurological DCS micro-bubbles, and VGE micro-bubbles are the same, or indicative of each other, or concurrent, or related, or any other such relationship.
We are back where we started. Simon looks to be maneuvering to ignore the distinctions on microbubble types, and tries to merge it all into one (to pretend that bubble models are at fault). Tries to imply VGE are more dangerous than they actually are, tries to imagine they are a reliable predictor of DCS. Do you want your deco based on such blinkered ambition?
GLOC
real name: Gareth Lock!
Ross,
As I understand this, it is the level of VGE that causes DCS not VGE per se.
Maybe Neal doesn't have the concrete answers and maybe the answer has to be vague! Also judge absence of comment as an absence of knowledge. Your confrontational nature isn't helping the conversation. Neal is a nice guy (so is Simon), please don't piss them off otherwise they will not partake in these informative conversations - they don't have to and I personally am glad they are taking part on CCRx.
Regards
As I understand this, it is the level of VGE that causes DCS not VGE per se.
What is the citation for that text?
Maybe Neal doesn't have the concrete answers and maybe the answer has to be vague! Also judge absence of comment as an absence of knowledge. Your confrontational nature isn't helping the conversation. Neal is a nice guy (so is Simon), please don't piss them off otherwise they will not partake in these informative conversations - they don't have to and I personally am glad they are taking part on CCRx.
Regards
AdrianSmith
New Member
Thank you for your condescension, Ross. It seems to be par for the course for you, unfortunately.
I understand completely what is being discussed. What I see is two reputable scientists providing empirical evidence complete with published papers to back up that evidence trying to rationally discuss why your beliefs are misplaced. In response I see ad hominem attacks against them from you, cherry picking of data to support your subjective beliefs, a complete and utter lack of scientific data to support your position, and what appear to be complete obliviousness to the overwhelming body of evidence standing against your beliefs.
I would like to see you stop and read what Simon and Neal have written and consider the merits of their points rather than reading them only thinking about how to instantly rebut them, but unfortunately I don't think that will happen. The inclusion of the backfire effect is entirely appropriate in this case - you cling to your subjective, unsupported beliefs more and more tightly the more you're shown the errors in them.
I hate to break it to you but you're not Copernicus or Galileo. You're Don Quixote, and your tilting at windmills is making you look foolish. I can guarantee that I will never purchase any product you have any part in, because your refusal to be open to any idea except your own misguided ones would leave anything you do open to suspicion and distrust on my part. I suspect your intransigence has done you a huge disservice, but you can't even see that.
-Adrian
No. You haven't been paying attention. Its the presence of pulmonary recirculation defects that is the key to this - not the level. If you have no pulmonary defects, the level does not seem to matter (with the exception of the chokes - which is procedural matter).
Bennett and Elliott Chapter 10.4 - read it and summarize, including the information posted above. And a dozen more papers that I'm not going to link here - summarized.
Gareth,
Well, if you want to start issuing directives about comment, then go back into this thread and take a look at the personal attacks and insults Mitchell sends my way on my work, my products, my intentions, my integrity, etc, etc. What did you say the other day - play the ball, not the man? That would be a good place to begin. Mitchell is not a nice guy in the forums, he is a mean and viscous person who tries anything possible to bully his way and get rid of those who don't agree with him, or interfere with his agenda.
Neal is a nice guy, and I like his input too. He wasn't able to answer the questions I put forward.
Neal wrote: "I will give answers where I have them, and try to limit my speculation where I do not have them."
I wrote: "That's OK. I respect that. "
Anything more need to be said?
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I do not believe that I am being vague at all but am happy to let the various readers and participants in this thread decide for themselves.
There is a clear linkage between supersaturation and bubble formation. To be clear, both can occur in any tissue as a response to pressure gradients. The degree of supersaturation in a given tissue will be unique for the conditions. The formation of bubbles (or not) is in response to local conditions. VGE provide a reasonable index of decompression stress. It is clearly not perfect, since bubble formation in other tissues can lead or lag depending on the conditions.
VGE can clearly cause direct harm. This thread has already contained discussion of cardiopulmonary symptoms ("chokes") associated with intravascular bubble loads that are high enough to overwhelm the lungs filtration ability and impair effective gas exchange. This has been well demonstrated in animal studies, and we have had four cases in our lab. One of these was beautifully captured in one of our NASA studies. Very high bubble loads preceding the onset of mild but escalating symptoms of coughing, retrosternal pain, and anxiety. Rapid descent brought rapid resolution of the symptoms; it could very well have been a life-threatening situation had the fast action not been taken. Interestingly, while one otherwise healthy subject experienced these conditions, another subject completing the same exposure at the same time had no difficulties. The variability in physiological responses is impressive and sometimes frustrating, but what seeing it firsthand does is to remind you not to rely on simple explanations. What some may call vagueness, others will call prudence.
Let's talk about another aspect of vagueness for a minute. An important example for me would be a fundamental element that is common to all bubble models of decompression. Not one of them measures bubbles. Not one. There is theorizing and hand waving, but no measures. Despite this, the near-religious fervor is often felt. Here's one more - critical radii for bubble growth. Is that with a nice spherical bubble or one subject to real conditions common to the bloodstream or any other tissue that distort the shape of bubbles? What mathematical model is robust enough to calculate the impact of the infinite shape changes that a bubble can undergo? None of them. Fortunately, again, models do not have to express truth, just get close enough to an acceptable outcome to be accepted.
Please do not confuse my lack of detailed pontificating with avoiding a question. I have provided the most meaningful answer regarding bubble formation - it is driven by supersaturation; in any tissue that is subjected to the same physical laws as any other tissue (which captures all of them). The conditions are dynamic, which is why it is a waste of breath to try and describe a single picture of reality - it does not exist. Do not lose track of the fundamentals, though. Inadequate elimination of inert gas increases the likelihood of bubble formation and symptomatic DCS. High intravascular bubble grades have a stronger association than lower grades, and a much, much stronger association than zero grade VGE. Yes, bad luck probably plays some role in poor decompression outcomes, but this is almost certainly far less important than the factors we can control - dive profile, exercise, thermal status, for example - as well as some that are more subtle.
I leave it to the group to interpret the discussion. We are beginning to cover more old ground than new ground.
There is a clear linkage between supersaturation and bubble formation. To be clear, both can occur in any tissue as a response to pressure gradients. The degree of supersaturation in a given tissue will be unique for the conditions. The formation of bubbles (or not) is in response to local conditions. VGE provide a reasonable index of decompression stress. It is clearly not perfect, since bubble formation in other tissues can lead or lag depending on the conditions.
VGE can clearly cause direct harm. This thread has already contained discussion of cardiopulmonary symptoms ("chokes") associated with intravascular bubble loads that are high enough to overwhelm the lungs filtration ability and impair effective gas exchange. This has been well demonstrated in animal studies, and we have had four cases in our lab. One of these was beautifully captured in one of our NASA studies. Very high bubble loads preceding the onset of mild but escalating symptoms of coughing, retrosternal pain, and anxiety. Rapid descent brought rapid resolution of the symptoms; it could very well have been a life-threatening situation had the fast action not been taken. Interestingly, while one otherwise healthy subject experienced these conditions, another subject completing the same exposure at the same time had no difficulties. The variability in physiological responses is impressive and sometimes frustrating, but what seeing it firsthand does is to remind you not to rely on simple explanations. What some may call vagueness, others will call prudence.
Let's talk about another aspect of vagueness for a minute. An important example for me would be a fundamental element that is common to all bubble models of decompression. Not one of them measures bubbles. Not one. There is theorizing and hand waving, but no measures. Despite this, the near-religious fervor is often felt. Here's one more - critical radii for bubble growth. Is that with a nice spherical bubble or one subject to real conditions common to the bloodstream or any other tissue that distort the shape of bubbles? What mathematical model is robust enough to calculate the impact of the infinite shape changes that a bubble can undergo? None of them. Fortunately, again, models do not have to express truth, just get close enough to an acceptable outcome to be accepted.
Please do not confuse my lack of detailed pontificating with avoiding a question. I have provided the most meaningful answer regarding bubble formation - it is driven by supersaturation; in any tissue that is subjected to the same physical laws as any other tissue (which captures all of them). The conditions are dynamic, which is why it is a waste of breath to try and describe a single picture of reality - it does not exist. Do not lose track of the fundamentals, though. Inadequate elimination of inert gas increases the likelihood of bubble formation and symptomatic DCS. High intravascular bubble grades have a stronger association than lower grades, and a much, much stronger association than zero grade VGE. Yes, bad luck probably plays some role in poor decompression outcomes, but this is almost certainly far less important than the factors we can control - dive profile, exercise, thermal status, for example - as well as some that are more subtle.
I leave it to the group to interpret the discussion. We are beginning to cover more old ground than new ground.
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Hi Adrian,
Not condescension, just impatience.
I have read it, and understand them.
Neal posted papers about:
Musculoskeletal activity accelerates inert gas elimination during oxygen breathing prior to decompression
DAN's Observation study update on tech diver VGE monitoring
Progress in making new Doppler to show small intravascular microbubbles before they grow into larger VGE.
Association of microparticles and neutophil activation with decompression sickness.
All that is good stuff and interesting reading. They are not new ideas, and most is long held existing theory.
But none address the pertinent questions - are extravascular and intravascular micro-bubbles one and the same? Should we allow ourselves to think of them as one? Do they form at the same time. Is one an extension of the other?
The text we have so far that is on topic, - Bennett Elliott, says no. If there is more, then lets see it please.
Attacks? What attacks? I think your just picking sides to imagine a fight going on.
I'm open to new ideas - I like good science. Is there some new model math to be added? But I'm not going to accept the junk science and twisted nonsense just to bully through some agenda.
Ross, I have not seen Simon post anywhere in this thread that bubble models are at fault. Let's not unnecessarily stir the pot. Let's please try to keep the discussion on track and avoid trying to read between the lines.
The only person I've seen arguing that they are different is you. Intramuscular or in any other tissue but blood is bad. But paradoxically, in venous blood, you appear to say they are a good thing. I say apparent position because its not always clear to me. Citing one rather old text (which doesn't actually present any primary data) is not very convincing evidence of this position honestly.
Drs Mitchell and Pollack have been much clearer about the desirability of VGE (less is better but below grade 2 is not measurably better than none). Personally I am not diving in a way to try to 'optimize' my VGE just below some fuzzy symptomatic threshold. In part because even in one subject (me) that threshold is wide, gray, and not static. I want to be on the conservative end/side of the gray zone, whereas some of the bubble models and BSAC tables sure seem to be more towards the aggressive side of the gray swath between ridiculous amounts of decompression and clinically bent.
Obviously there is a point where I would consider myself "too conservative", but adding ~10% to my deco time to conduct extended shallow stops and potentially reduce my VGE from >2 to <2 is not "too conservative" for me. The exception would be when some other issue is concurrent and I need to make a risk management decision e.g. freezing due to a suit flood, running out of deco gas.
Ross,
You missed one important element in your review of the four abstracts I included. The Swan et al. paper from Jay Buckey's group looked at both intravascular and extravascular bubbles. What they found was that the dual frequency ultrasound systems allowed them to see signals for very small (the size was not measured but indicated by the ultrasound frequency used) extravascular bubbles before they saw the larger intravascular bubbles. This work actually reinforces the common nature of bubble formation. The tool is being developed so we do not have to rely solely on intravascular bubbles to assess real-time decompression stress. This was the unit that I said we have used with a limited number of human trials in our lab. The technology is coming. Most important to this discussion, it is reinforcing the points I tried to make about how different tissues can lead or lag behind another tissue, but that the physical laws remain constant throughout different tissues.
The Bennett and Elliott chapter does not state that the process of bubble formation is fundamentally different in different tissues, and the best evidence we have also supports a fairly consistent formation process. I think it is time for a new question.
You missed one important element in your review of the four abstracts I included. The Swan et al. paper from Jay Buckey's group looked at both intravascular and extravascular bubbles. What they found was that the dual frequency ultrasound systems allowed them to see signals for very small (the size was not measured but indicated by the ultrasound frequency used) extravascular bubbles before they saw the larger intravascular bubbles. This work actually reinforces the common nature of bubble formation. The tool is being developed so we do not have to rely solely on intravascular bubbles to assess real-time decompression stress. This was the unit that I said we have used with a limited number of human trials in our lab. The technology is coming. Most important to this discussion, it is reinforcing the points I tried to make about how different tissues can lead or lag behind another tissue, but that the physical laws remain constant throughout different tissues.
The Bennett and Elliott chapter does not state that the process of bubble formation is fundamentally different in different tissues, and the best evidence we have also supports a fairly consistent formation process. I think it is time for a new question.
Simon Mitchell
Well-Known Member
rossh said:
Ross,
Seriously, misquoting a chapter that I wrote in an debate with me is never going to pass muster. Yes, we described intravascular bubbles and tissue bubbles separately in the chapter, but that is just the way the material is organised. The chapter does NOT say that these bubbles are the result of separate processes, and it does NOT say VGE don't cause harm whereas DCS is caused by tissue bubbles. In the latter regard, you ask about new science.... it is probably germane to point out that a substantial body of the evidence linking DCS to PFO (and therefore most likely to VGE that have crossed the PFO) has emerged since that chapter was written. If it was written again today this mechanism would be emphasised further, particularly in relation to inner ear DCS.
Bubble formation (both VGE and tissue bubbles), as Neal points out, is linked to a common process which is gas supersaturation in the tissues through which the blood is passing. In that sense tissue bubbles and intravascular bubbles (VGE) are related. Arterial blood is not supersaturated when it enters a tissue, so the gas that drives VGE formation in the blood as it passes through the tissue must have come from the tissue. This same tissue supersaturation is what would drive any extravascular bubble formation in the tissue itself. Can you not see that? It is also clear that both intravascular bubbles (VGE) and tissue bubbles can ultimately cause injury, and some tissues seem most likely to be injured by tissue bubbles, some by intravascular bubbles (usually VGE that have entered the arterial circulation), and some (potentially) by both mechanisms.
Neal has provided an unsurprising 4th answer to your question:
Can I also point out after a long and difficult debate about cardiopulmonary DCS, that Neal has described a case that occurred in a fit healthy subject who also did not have the gas load your "model math" would predict was necessary for sufficient VGE formation to cause cardiopulmonary DCS. I don't want to go back to that argument, but I also think, in the interests of medical accuracy, it is important that this is pointed out. I do not want divers assuming that cardiopulmonary DCS cannot occur unless there is omitted decompression etc (as you claimed), because this could result in incorrect field diagnoses and choice of first aid measures if they relied upon the information you have provided.
Simon M
Michael Thornton
Rebreather Enthusiast
Neal, Simon, Ross I was wondering if I could get some simple definitions of a few terms:
DCS vs Symptomatic DCS. How are you deciding to use one term vs the other? If bubble presence or pressure related stress does not necessarily equal DCS but symptoms do at what point do you call it or consider it DCS? (Is it always the same definition for all of your research)
I thought I had been told that successful treatment is how you can diagnose as DCS with the most confidence. If someone is not treated what methods are you using to diagnose as DCS especially if they lived and/or no autopsy was performed?
Thanks in advance.
Sent from my iPhone using Tapatalk
DCS vs Symptomatic DCS. How are you deciding to use one term vs the other? If bubble presence or pressure related stress does not necessarily equal DCS but symptoms do at what point do you call it or consider it DCS? (Is it always the same definition for all of your research)
I thought I had been told that successful treatment is how you can diagnose as DCS with the most confidence. If someone is not treated what methods are you using to diagnose as DCS especially if they lived and/or no autopsy was performed?
Thanks in advance.
Sent from my iPhone using Tapatalk