Diving too carefully?

Why it is so implausible is that if it is that rare, we have only one public case over all the years of diving, so how many cases may those experts have seen? None? One? So basically they may be experts but not for cardiopulmonary DCS.

It's not that hard to believe. Of course there will be other cases of cardiopulmonary DCS that aren't publicly discussed, for a start there is the minor issue of patient confidentiality. Another very plausible explanation is that only deaths end up in the media or in (public) coroner's publications. Not everything that happens to divers ends up on a dive forum (thank goodness), and just because it isn't there doesn't mean it hasn't happened! A quick read of any medical description of DCS will include the signs/symptoms of cardiopulmonary DCS - I'm pretty confident it exists, and has occurred more than once. The existence of cardiopulmonary DCS isn't some sort of weird conspiracy theory!

Deralie
 
Why it is so implausible is that if it is that rare, we have only one public case over all the years of diving, so how many cases may those experts have seen? None? One? So basically they may be experts but not for cardiopulmonary DCS.

There must be some cover-up. They colluded in choosing an outrageously unlikely diagnosis for some mysterious ulterior motive.

Come on. They may not have seen many cases of cardiopulmonary DCS but they have seen more than you or Ross. Most diving physicians have. And they have the medical training, specialist experience and knowledge of diving medicine to be able to weigh the differential diagnosis and come to that conclusion.

There is no conspiracy. Just agreement between experts. Does that make it fact? No. But I would place more money on their explanation than one of yours.
 
There must be some cover-up. They colluded in choosing an outrageously unlikely diagnosis for some mysterious ulterior motive.

Come on. They may not have seen many cases of cardiopulmonary DCS but they have seen more than you or Ross. Most diving physicians have. And they have the medical training, specialist experience and knowledge of diving medicine to be able to weigh the differential diagnosis and come to that conclusion.

There is no conspiracy. Just agreement between experts. Does that make it fact? No. But I would place more money on their explanation than one of yours.
I never gave any explanation.
 
Ross, seriously, do you have the necessary medical training to second guess multiple medical doctor's opinions on the cause of this man's death? I don't understand why it seems so implausible to you that different people's bodies' physiology respond differently to nearly identical stimulus. Regardless of what your "math" says, everyone's bodies are different, and it doesn't necessarily mean that someone's circulatory system is defective simply because they got bent.

I have been on multiple dives where I have seen one member of the dive team exhibit symptoms of decompression sickness while following the same exact profiles as the rest of the team, for no obvious reason. It just happens!


Hi Randy,

But how may divers have you seen collapse and die after doing a normal deco? You see, that's an enormous difference from a dive team member getting a bit of DCS. It is expected that we can experience a little DCS from time to time, because we all have a some variance and differences within us and in procedure and preparation, etc. We have reasonable explanations of the physics and physiology process for these deviations.

But this victim was off the scale. We have no reasonable explanation of the physics / physiology process here. The Doctor involved is unable to provide any explanation of the rare event. Nothing. His only suggestion was normal processes and "massive" VGE, but gave no validation of how this off scale deviation could occur.

In the absence of any supporting theory or explanation of the physics / physiology process for this victim, I seriously doubt the "massive" VGE claim is correct.

To your question about training - I am asking the trained expert and professional in the science, to provide us with a reasonable and plausible explanation of the physics / physiology process for this victim. The expert did after all, offer his opinion to the coroner inquest so its a matter of public record.
 
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Hello Ross,

I suppose this focus you have adopted on debating a single case of cardiopulmonary DCS is a welcome respite from trying to defend the undefendable position that VGE, even at high grades, are harmless. In that regard, as meaningless as it is in the context of the overall debate, I can understand why you are doing it.

rossh said:
I am asking the trained expert and professional in the science, to provide us with a reasonable and plausible explanation of the physics / physiology process for this victim.

I am always transparent about where my training and expertise lies Ross; it is a good habit to have. My expertise, as I have acknowledged many times in the past, is in clinical diving medicine and in the pathophysiology of DCS. I am expert in recognising patterns of dysbaric disease and in formulating rational diagnoses based on the clinical presentation of symptoms, and (at least to some extent) in rationalising such data against the findings of pathological examinations. Based on the clinical presentation of symptoms and the pathological findings at autopsy, I and multiple other similarly qualified experts agreed that this was cardiopulmonary DCS caused by VGE. On the pathophysiology side the diver must have formed more VGE than expected after this dive; indeed, sufficient to produce his demise. Variability in VGE production after dives is a well recognised phenomenon and we assume that this diver (and other similar cases before him) were at the far end of a bell shaped curve whose extremes are (apparently) not properly predicted by your theoretical physical modelling (and indeed, not fully understood).

One of the things that my extensive experience in clinical diving medicine has taught me is that devastatingly serious DCS, including fulminant versions with multi-organ involvement (and occasionally death), can occur after technical dives on which nothing has gone wrong; that is, where decompression has been completed properly and where your models would not predict the event. Such cases have occurred multiple times (including divers without obvious 'defective circulation' as you call it) and there are members on this board who I know have seen (and in one or two cases treated) such divers. Your implied stance in respect of the case we have been debating (that everything must conform to your modelling or it can't be real) is therefore simply unsupportable.

Finally, my true expertise is not in gas modelling, though as you know, I work closely with people who are expert (at a global level) in this field. Their advice is that we should not accept at face value your claim that causation of the index case by VGE is implausible. I would be interested to know whether your personal analysis of the dive(s) is at the level of "it could not have happened because the prescribed decompression was completed" (in which case I would refer you to the above paragraph) or if you have made a more sophisticated evaluation of the dive which would allow you to draw such a conclusion? If the latter, could you explain that evaluation? How much gas needs to be present in the venous blood to cause pulmonary DCS? How much gas was available in this diver? On that basis, can you rule out the possibility that the problem was caused by VGE?

Simon M
 
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Of greater relevance to the actual debate about whether VGE can cause harm:

Ross, you selectively cited a DCIEM report that did, indeed, focus on the development of their table using the Kidd-Stubbs model. Remember....

rossh said:
But I would prefer that people read the report by the DCIEM that explains all this in full context. The link is here: download

Because your simplistic interpretation of the reasons Simon, is well... not accurate.

Your implied position was that since this report did not contain much in the way of reference to Doppler testing of the DCIEM schedules, that they were not really interested in VGE as an outcome measure in the testing of their profiles.

What you failed to mention was that this report did not really provide "full context" as you claimed; there was a subsequent plethora of publications describing their testing program which used Doppler measurement of VGE levels, and in which profiles which consistently produced high grade were rejected. You can choose from any of:

1 Nishi RY, Kisman KE, Buckingham IP, Eatock BC, Masurel G. XDC digital decompression computer: assessment of decompression profiles by ultrasonic monitoring, phase I: 36 - 54 msw. Report. Downsview (ON, CAN): Defence and Civil Institute of Environmental Medicine; 1980. 46 p. Report No.: 80-R-32.

2. Nishi RY, Kisman KE, Eatock BC, Buckingham IP, Masurel G. Assessment of decompression profiles and divers by Doppler ultrasonic monitoring. In: Bachrach AJ, Matzen MM, editors. Underwater Physiology VII. Proceedings of the 7th Symposium on Underwater Physiology. Bethesda (MD): Undersea Medical Society; 1981. p. 717-27.

3. Nishi RY, Eatock BC, Buckingham IP, Masurel G. XDC digital decompression computer: assessment of decompression profiles by ultrasonic monitoring, phase II: 30 - 75 msw. Report. Downsview (ON, CAN): Defence and Civil Institute of Environmental Medicine; 1981. 43 p. Report No.: 81-R-02.

4. Nishi RY, Eatock BC, Buckingham IP, Ridgewell BA. Assessment of decompression profiles by ultrasonic monitoring, phase III: no-decompression dives. Report. Downsview (ON, CAN): Defence and Civil Institute of Environmental Medicine; 1982. 26 p. Report No.: 82-R-38.

5 Nishi RY, Lauckner GR, Eatock BC, Hewitt JT. Oxygen decompression techniques for compressed air diving using the XDC-2 decompression computer programmed with the Kidd-Stubbs 1971 model. Report. Downsview (ON, CAN): Defence and Civil Institute of Environmental Medicine; 1984. Report No.: 84-R-19.

6. Lauckner GR, Nishi RY, Eatock BC. Evaluation of the DCIEM 1983 decompression model for compressed air diving (Series A-F). Report. Downsview (ON, CAN): Defence and Civil Institute of Environmental Medicine; 1984. 31 p. Report No.: 84-R-72.

7. Lauckner GR, Nishi RY, Eatock BC. Evaluation of the DCIEM 1983 decompression model for compressed air diving (Series G-K). Report. Downsview (ON, CAN): Defence and Civil Institute of Environmental Medicine; 1984. Report No.: 84-R-73.

8. Lauckner GR, Nishi RY, Eatock BC. Evaluation of the DCIEM 1983 decompression model for compressed air diving (Series L-Q). Report. Downsview (ON, CAN): Defence and Civil Institute of Environmental Medicine; 1985. Report No.: 85-R-18.

At various places in this thread you (and others) have promoted the notion that VGE represent 'decompression stress' and that this is an index of tissue gas washout. As I pointed out in an earlier post, you have bordered on insinuating that high VGE = decompression stress = high inert gas washout = good. This is incorrect. What the authors of these DCIEM reports mean by decompression stress, is an index of the probability of decompression sickness.

To quote from the senior author:

"All the data show that, in general, the incidence of decompression illness is higher when many bubbles are detected and that the incidence of is low when few or no bubbles are detected. Thus for the purposes of evaluating decompression profiles, dives which produce many bubbles in the majority of the divers can be considered stressful with a higher risk of symptoms and should be avoided. Conversely, dives which produce few or no bubbles in the majority of divers can be considered safe. We can speak of 'decompression stress' rather than decompression illness as the end-point for evaluating dives and need not give divers symptoms to know whether or not a dive profile is safe."

Nishi RY. Doppler and ultrasonic bubble detection. In: Bennett PB, Elliott,DH, editors. The physiology and medicine of diving. 4 ed. London: W.B. Saunders; 1993. p. 433-453.)

Would you care to revise your claim that VGE can be ignored?

Simon M
 
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Hi Randy,

But how may divers have you seen collapse and die after doing a normal deco? You see, that's an enormous difference from a dive team member getting a bit of DCS. It is expected that we can experience a little DCS from time to time, because we all have a some variance and differences within us and in procedure and preparation, etc. We have reasonable explanations of the physics and physiology process for these deviations.

But this victim was off the scale. We have no reasonable explanation of the physics / physiology process here. The Doctor involved is unable to provide any explanation of the rare event. Nothing. His only suggestion was normal processes and "massive" VGE, but gave no validation of how this off scale deviation could occur.


Ross, as someone who got royally - not 'a little' - bent on a dive that fell well within your physics and physiology parameters, I have to say that you're now starting to become offensive.

Sometimes, the human body does things we'd all rather it didn't. It's not Simon Mitchell's responsibility to explain why one person's physiology didn't match your theoretical model. It's your responsibility to explain why your model doesn't match the physiology.

Until you can, or at least until you can hold an argument without resorting to bleating, whining, and denigrating anyone who doesn't agree with you, you would serve yourself well by keeping your fingers away from the keyboard.

Sent from my iPad using Tapatalk HD
 
Hello Ross,

I suppose this focus you have adopted on debating a single case of cardiopulmonary DCS is a welcome respite from trying to defend the undefendable position that VGE, even at high grades, are harmless. In that regard, as meaningless as it is in the context of the overall debate, I can understand why you are doing it.
M


For 99.99% of the diving world, VGE is seemingly harmless Simon. The random nature of VGE and the personal variance amongst individuals means some a portion of divers is always diving with high grade VGE. That includes millions of NDL divers too.


How can you overlook the fact that high grade VGE (venous gas emboli) exist in divers everyday, and apparently cause no harm Simon?


(Note to readers: we are discussing VGE, and not tissue micro-bubbles. The two are not the same thing.)


I am asking the trained expert and professional in the science, to provide us with a reasonable and plausible explanation of the physics / physiology process for this victim. The expert did after all, offer his opinion to the coroner inquest so its a matter of public record.

On the pathophysiology side the diver must have formed more VGE than expected after this dive; indeed, sufficient to produce his demise. Variability in VGE production after dives is a well recognised phenomenon and we assume that this diver (and other similar cases before him) were at the far end of a bell shaped curve whose extremes are (apparently) not properly predicted by your theoretical physical modelling (and indeed, not fully understood). Simon M


No description of the changes needed in physics or physiology for this extreme event. OK.

No explanation for the reasons this victim has deviated so far from normal, to cause his sudden death. OK.

Only information available is the assumption that his body made an extreme and sudden deviation, because that is needed to fit within the theory of a cause of death, which is itself poorly understood and not well documented.


******


We are getting nowhere here, so I think we have exhausted this topic for now.
 
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Ross, as someone who got royally - not 'a little' - bent on a dive that fell well within your physics and physiology parameters, I have to say that you're now starting to become offensive.

Sometimes, the human body does things we'd all rather it didn't. It's not Simon Mitchell's responsibility to explain why one person's physiology didn't match your theoretical model. It's your responsibility to explain why your model doesn't match the physiology.

Until you can, or at least until you can hold an argument without resorting to bleating, whining, and denigrating anyone who doesn't agree with you, you would serve yourself well by keeping your fingers away from the keyboard.

Sent from my iPad using Tapatalk HD

I'm sorry to hear about your troubles.

You wrote. Sometimes, the human body does things we'd all rather it didn't. .... Yes that is true. The decompression models form only a small part of the total risk. Other factors influence the result such as preparations and procedure, which are also beyond the control of deco models.

The case being discussed, was one that Simon offered up as an example for discussion.
 
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For 99.99% of the diving world, VGE is seemingly harmless Simon.

And for about 99.99% of the diving world decompression from a dive is "seemingly harmless" too Ross. That cannot be construed to mean that decompression does not cause decompression sickness.

We know from extensive datasets that low grade VGE rarely cause harm which, of course, is the basis for your observation. However, those same datasets show that high grade VGE are associated with a markedly increased risk of DCS. For example, go to your copy of Bennett and Elliott and look at Table 10.3.9 on page 518 (Ron Nishi's chapter) [1] which summarizes the DCIEM test dive database. If you look at the precordial measurement after movement panel for air diving (because this is the most common approach) it reports the results of 1726 dives which were all considered within limits.

The incidence of DCS for Grade 0 bubbles is 0.3%

The incidence of DCS for Grade 1 bubbles is 1.8%

The incidence of DCS for Grade 2 bubbles is 2.7%

The incidence of DCS for Grade 3 bubbles is 6.9%

The incidence of DCS for Grade 4 bubbles is 10.8% which is 36 times the risk for Grade 0 bubbles and 6 times the risk for Grade 1 bubbles.

That is what is called a positive dose response relationship Ross. The numbers speak for themselves. When you combine these risk data with the fact that several serious forms of DCS are strongly associated with right to left shunts, and that the only plausible explanation for such an association is that VGE are passing into the arterial circulation through the shunts, it starts to make this statement:

How can you overlook the fact that high grade VGE (venous gas emboli) exist in divers everyday, and apparently cause no harm Simon?

.....look clumsy at best, but probably a bit disingenuous coming from someone who sells a decompression planner whose schedules may result in high VGE grades more often than divers would be comfortable with [2] if they were not reassured by what you are saying. Parenthetically, to those of you who are incredulous about why I bother, that is part of the reason. There is misinformation of potential relevance to diver safety contained in various posts on this thread.

I must say that I continue to be amazed by the 180 degree U turn you have made on this whole bubble thing. In the early 2000s it was all about how bubble models control bubble formation from the beginning of ascent by imposing deep stops and how good that was, and now (after the emergence of several studies suggesting the opposite) it is now all about how bubbles are normal and harmless and we should ignore them. And please don't come back with claims that bubble models control tissue bubbles but not venous bubbles (as if that were plausible or possible). We've had that debate.

We are getting nowhere here, so I think we have exhausted this topic for now.

Ah, finally something we can agree on.

Simon M

References:

1. Nishi RY, Brubakk AO, Eftedal OS. Bubble detection. In: Brubakk AO, Neumann TS (eds). Bennett and Elliot's Physiology and Medicine of Diving (5th ed). Edinburgh, Saunders Publishers 2003: 501-529.

2. Ljubkovic M et al. High incidence of venous and arterial emboli at rest after trimix diving without protocol violations. J Appl Physiol 2010;109:1670-4.
 
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Thank you for the references.


Your implied position was that since this report did not contain much in the way of reference to Doppler testing of the DCIEM schedules, that they were not really interested in VGE as an outcome measure in the testing of their profiles.
Simon M


I did not imply there is no VGE testing, or they were not interested ... that again is YOUR twisted interpretation Simon. You are arguing against yourself Simon.


The fact that they use a half way point, means that when real world variations in VGE are applied, many divers will have VGE scores that exceed this mid point.



The Kidd Stubbs model which is at the center of the DCIEM tables, is a dissolved gas deterministic design. It is not a VGE model. Yes they fine tuned the parameters to match the testing and experience, as happens to every model. They openly publish it's a more conservative approach, which is what the DCIEM tables are.


Yes I like this model, and I have dived it many times in deco, including some pretty big dives. They have sensible approach to repeat dives. The heliox tables are interesting too: the overall run time is too fast for most, but they have deep stop tendencies with many profiles commencing with a sequence of 1 or 2 min stops.



At various places in this thread you (and others) have promoted the notion that VGE represent 'decompression stress' and that this is an index of tissue gas washout. As I pointed out in an earlier post, you have bordered on insinuating that high VGE = decompression stress = high inert gas washout = good. This is incorrect. What the authors of these DCIEM reports mean by decompression stress, is an index of the probability of decompression sickness.
Simon M



Except the reliability of this "....an index of the probability of decompression sickness. " is weak to non existent in the real world. Millions of dives every year exceed the values used in the DCIEM tables, and do not receive an injury.



To quote from the senior author:

"All the data show that, in general, the incidence of decompression illness is higher when many bubbles are detected and that the incidence of is low when few or no bubbles are detected. Thus for the purposes of evaluating decompression profiles, dives which produce many bubbles in the majority of the divers can be considered stressful with a higher risk of symptoms and should be avoided. Conversely, dives which produce few or no bubbles in the majority of divers can be considered safe. We can speak of 'decompression stress' rather than decompression illness as the end-point for evaluating dives and need not give divers symptoms to know whether or not a dive profile is safe."

Nishi RY. Doppler and ultrasonic bubble detection. In: Bennett PB, Elliott,DH, editors. The physiology and medicine of diving. 4 ed. London: W.B. Saunders; 1993. p. 433-453.)

Would you care to revise your claim that VGE can be ignored?

Simon M


No. This simple fact is - we have all been ignoring VGE. We plan a dive based on dissolved gas content, and supersaturation limits, we dive it, and we accept what ever VGE that produces. No one knows what their VGE number is after a dive. I bet 95% of the diving world doesn't know that VGE exists in almost every dive we do.

VGE is a secondary measure, that is indirectly proportional to the primary measure of gas content and saturation, but VGE level is affected by other influences such as profile shape, and individual variances in hydrophobic sites and differences in venous endothilum and others variances.

The primary measure of gas content has proven to be reasonably accurate and consistent across the population, while VGE is proven to be grossly inaccurate.

Why do they try to use the inaccurate measure of VGE in testing? The answer is in the ethics of testing. The desired end point result measure of deco testing is to force DCS, but ethics prevents science from deliberately creating harm this way. So testing is reduced to use the VGE surrogate measure, and just accept that it's not a true measure of DCS probability. Any good paper will state something to that affect in its introduction.
 
I must say that I continue to be amazed by the 180 degree U turn you have made on this whole bubble thing. In the early 2000s it was all about how bubble models control bubble formation from the beginning of ascent by imposing deep stops and how good that was, and now (after the emergence of several studies suggesting the opposite) it is now all about how bubbles are normal and harmless and we should ignore them. And please don't come back with claims that bubble models control tissue bubbles but not venous bubbles (as if that were plausible or possible). We've had that debate.

Simon M


Ha. see what Simon did here .....

He is trying to merge two types of micro-bubbles: tissue micro bubble into venous gas emboli. He wants (needs) to trick you into thinking its the same. Then he makes up bubble model theory and history to suit himself. Don't get fooled by his semantics.


****


VGE have been with us forever, and theory states they grow in the venous system from dissolved gas. Note its the veins, and not the tissue. These do not make DCS in normal people.

Tissue microbubble are thought to grow in the tissue, from doing deco too fast, and are the ones that create DCS.

Deco models math is built to control the growth of the tissue micro-bubbles - not VGE. Bubble models have always assumed the presence of small tissue micro-bubbles and controlled the ascent to limit the growth (its the core of the model).


*****

Why does Simon rely so heavily on playing tricks on you? Why can't this guy tell it straight up or truthfully? Why all the semantics, and deliberate effort to distort the facts?
 
rossh said:
Millions of dives every year exceed the values used in the DCIEM tables, and do not receive an injury.

.....and you know this how? Didn't you just say...

rossh said:
No one knows what their VGE number is after a dive.

.... and I'd speculate that you don't have a system in place to prospectively survey outcomes for those millions of dives.

And as for this:

rossh said:
Why does Simon rely so heavily on playing tricks on you? Why can't this guy tell it straight up or truthfully? Why all the semantics, and deliberate effort to distort the facts?

Whatever Ross. People can either believe the diving science literature (which I have attempted to represent accurately here), or they can believe you.

Simon M
 
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I hate the personal attacks, but I feel it necessary to weigh in on some of the drift in the discussion.

Grade I and II VGE were tolerated within the limits of the DCIEM tables not because they were any kind of "half way point," but because they have less association with symptomatic DCS than grade III and IV VGE do. The 0-IV Spencer scale is ordinal, not interval or ratio. In other words, the width of each grade bracket is not fixed. Conceptually, the width of grade I and II categories is narrower than the higher grades. The best way to demonstrate this is to look at what two-dimensional echo imaging has done for scoring. Grades I and II and comparable with Spencer. Grade III has a and b subgroups in our studies (this is not yet widely used by others), and grade IV has a, b and c subgroups, and it can be argued that grade V makes the fourth subgroup. The grade III threshold is not a half way point, it is the point at which a substantial degree of decompression stress is becoming apparent.

Bubbles form in tissues; blood is just one tissue. The reason we have more experience with intravascular bubbles is because our current technology is best at identifying moving bubbles, that is, those in the bloodstream. New technologies are in development to improve our ability to assess extravascular bubbles, most promising is dual frequency ultrasound, but there is good evidence accumulated over 30 years that bubbles develop in many tissues. Efforts to suggest that intravascular bubbles are somehow a completely unique thing does not make sense.

Bubbles are a secondary measure of decompression stress, but a point that was lost is that the primary measure is symptomatic DCS, not gas content. While it is true that the vast majority of divers have not been scanned for bubbles post-dive, it is a greater truth that no divers have their total gas content measured. Decompression algorithms predict gas uptake and elimination across a range of theoretical tissue compartments. This is not a primary measure. This is a mathematical estimate. We use the mathematical predictions to guide our activity, but it is a foolhardy individual that believes that any dive computer algorithm knows what is happening at the tissue level.

Incorporating sufficient conservatism to ensure the decompression safety of all divers is impractical, there are too many differences between individuals and even in their experience on the same dive (think about differences in buoyancy control, fitness, relaxation, etc.), but to blindly rely on any algorithm is not smart. Adding safety buffers where reasonable makes good sense. Getting out of the water a few minutes faster does not make one a better diver, sometimes it is just a thing, and other times it can be a mistake.

I work in one of the labs where we take studies of decompression to the end point of symptoms, working with both diving and astronaut applications. We do not treat VGE but we have a much higher expectation of DCS as VGE scores climb. We have been doing this for a lot of years and have developed some insight. I will include two abstracts from the latest work we reported. The first assessing decompression risk associated with astronaut extravehicular activity (spacewalking) that was presented at the Aerospace Medical Society meeting in May:

Aerosp Med Hum Fact 2015 - 2143040
AMBULATION INCREASES DECOMPRESSION SICKNESS IN ALTITUDE EXPOSURE
N.W. Pollock1,2, M.J. Natoli1, S.D. Martina1,2, J. Conkin3, J.H. Wessel III4, M.L. Gernhardt5
1 Center for Hyperbaric Medicine and Environmental Physiology, Duke University Medical Center, Durham, NC 27710; 2 Divers Alert Network, Durham, NC 27705; 3 Universities Space Research Association, 3600 Bay Area Blvd, Houston, TX 77058; 4 Wyle Science, Technology & Engineering Group, 1290 Hercules, Houston, TX 77058; 5 NASA Johnson Space Center, 2100 NASA Parkway, Houston, TX 77058
INTRODUCTION ***8211; Musculoskeletal activity accelerates inert gas elimination during oxygen breathing prior to decompression (prebreathe), but may also promote bubble formation (nucleation) and increase the risk of decompression sickness (DCS). The timing, pattern and intensity of musculoskeletal activity are likely critical to the net effect. The NASA Prebreathe Reduction Program (PRP) combined oxygen prebreathe and exercise preceding a 4.3 psi exposure in non-ambulatory subjects (a microgravity analog) to produce two protocols now used by astronauts preparing for extravehicular activity (CEVIS and ISLE). Additional work is required to investigate whether exercise normal to 1 G environments increases the risk of DCS over microgravity simulation. METHODS ***8211; The current studies replicate the CEVIS protocol, each with single exceptions. Experiment 1 (E1) added controlled ambulation (stepping in place) at ground level (undersaturated inert gas state) and at 4.3 psi (spacesuit pressure; supersaturated state) instead of remaining non-ambulatory throughout. Experiment 3 (E3) restricted ambulation to preflight only. The metabolic output was matched between trials. Study endpoints included symptomatic DCS. Decompression stress was also evaluated with circulating bubbles identified with aural Doppler ultrasound (Spencer 0-IV ordinal scale). Fisher Exact Tests compared groups (significant at p<0.05). RESULTS ***8211; Data collection is complete for E1 (21 person-trials [16 male, 5 female]; 4/20 DCS, 6/21 peak grade IV bubbles) and ongoing for E3 (13 person-trials [11 male, 2 female]; 1/13 DCS, 2/13 peak grade IV bubbles). DCS was significantly greater in E1 vs. CEVIS (0/45 DCS, 3/45 peak grade IV bubbles) trials (p=0.0036). DCS did not differ between E3 and CEVIS (p=0.1121) or E1 and E3 (p=0.1980). Similarly, peak grade IV Doppler-detected bubbles were more frequent in E1 vs. CEVIS trials (p=0.0138). Grade IV bubble peaks did not differ between E3 and CEVIS (p=0.1899) or E1 and E3 (p=0.2110). CONCLUSION ***8211; Decompression stress and sickness at spacesuit pressure is increased by mild ambulation conducted in both undersaturated and supersaturated states. However, preliminary data do not establish an increased risk with mild ambulation conducted in the undersaturated state alone.



The second piece of work was presented at the Undersea and Hyperbaric Medical Society meeting in June, a meeting that was discussed earlier in this thread. We have spent a lot of time monitoring technical divers over the last six years, with two-dimensional echo imaging of the heart to look for bubbles post-dive as a centerpiece:

FIELD DIVE MONITORING: BUBBLE PRESENTATION IN RECREATIONAL-TECHNICAL CLOSED-CIRCUIT REBREATHER TRIMIX DIVING
Pollock NW1,2, Wiley JM1, Kernagis DN2, Clarke NW1, Mackey MN1, Martina SD1. 1Divers Alert Network, Durham, NC 27705; 2Duke University Medical Center, Durham, NC 27710.
INTRODUCTION: Recreational-technical diving has grown markedly over the past 20 years, particularly with closed-circuit rebreather (CCR) use. Divers increasingly rely on dive computer algorithms to manage their decompression profiles, many of these promising to control bubble formation, but there is little or no human testing. We evaluated decompression stress in recreational-technical CCR dives conducted beyond 40 msw.
METHODS: Observational studies were conducted on multi-day, deep recreational CCR trips. Divers controlled all their own diving activity. Subject monitoring included high resolution two-dimensional echocardiographic imaging (GE Vivid q) at 20 min intervals for two hours post-dive. Bubble loads were scored on a semi-quantitative ordinal scale (0, I, II, IIIa, IIIb, IVa, IVb, IVc, V). Grades were recorded for both right and left heart, each in three conditions: rest; following three full engagement arm movements; following three full engagement leg movements. Scores are reported as the highest of the three conditions for a given scan. Data presented as mean±SD with ranges, as appropriate.
RESULTS: We summarize five research trips; capturing a total of 287 open water CCR dives conducted by 55 individuals (41 male, 14 female) (48±8 y, 27.2±4.0 kg·m-2 body mass index). Maximum dive depth was 73±17 (40-157) msw (238±56 [131-515] fsw) and total run time 103±32 min. Right ventricular gas emboli (RVGE) were observed in all but one individual, with peak non-0 grades following 80% of dives and peak IIIa-V grades following 39%. Left VGE were observed in 33% of subjects and after 13% of all dives, peaking at grade IIIa-IIIb in five cases. Decompression sickness symptoms were noted in two cases.
CONCLUSIONS: Reflecting substantial decompression stress, high grade RVGE, LVGE, and symptomatic DCS indicate that further evaluation of decompression procedures employed by recreational-technical divers is warranted.



Intravascular bubbles are not the perfect measure, but they provide insights that certainly are not discounted in the scientific community. Similarly, they should not be discounted in the diving community. They are not found after all dives and they do represent a factor that can be modified by changing dive practice. Those wanting firsthand insight should participate in structured monitoring studies. I say structured because it is a commitment to get a reasonable picture. It is not a 'one scan and done effort.' The time can be well spent, though. It is not uncommon to have someone feeling cocky about their bubble-free diving before they participate, then to learn that the bubble grades they reach indicate that the decompression procedures they employ were not as perfect as they thought. An honest, objective understanding of your own reality is powerful; it can lead to decisions that may increase personal or team safety. I see that as a very good thing that can support a long and injury-free diving career.

I am always happy to discuss decompression and diving safety, but only focusing on the facts - the knowns and the unknowns - not the personal attacks.
 
Ditto.

Neal, Thank you for providing this. Unfortunately for the majority of divers, access to peer-reviewed journal information is hard to come by, especially in a timely manner (Rubicon does host a significant amount of work but this is normally limited to 2 yrs post-publication although certain articles such as the UHMS unconscious diver study was made available). I have access to a certain amount of work through my own research and it is a real shame to see so much stuff locked away in the 'vaults' where the lay diver can't get access.

Ross, I am not sure how much access you do have to journals but if there is any way you can get (more) access, I would.

Regards
 
Thank you Neal.

Now please stick around and bring an end to Mitchell twisting the facts and saying what ever he pleases.
 
Ditto.

Neal, Thank you for providing this. Unfortunately for the majority of divers, access to peer-reviewed journal information is hard to come by, especially in a timely manner (Rubicon does host a significant amount of work but this is normally limited to 2 yrs post-publication although certain articles such as the UHMS unconscious diver study was made available). I have access to a certain amount of work through my own research and it is a real shame to see so much stuff locked away in the 'vaults' where the lay diver can't get access.

Ross, I am not sure how much access you do have to journals but if there is any way you can get (more) access, I would.

Regards

I have access to some, subscribed to others. Neal alreday sent me those papers a while ago.


So, removing the descriptive differences and little semantic differences, between Neal and I, what I have said is substantially correct.
 
Thank's Neal! Mabe I missed - Is your study based on monitoring divers ended or still ongoing project as long run study?

Igor P

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The field dive monitoring project with technical divers is ongoing. Because the work is observational (we monitor but do not control the exposures) it takes a long time to fill out the picture.
 
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