Deep Stops Increases DCS

[rossh]

Some forms of DCS (such as musculoskeletal pain) are almost certainly caused by tissue micro-bubbles. However, more serious neurological forms of DCS (cerebral, spinal and inner ear) have been strongly linked to the presence of a patent foramen ovale whose only plausible contribution to the process is to allow VGE to cross into the arterial circulation and distribute to these organs. VGE may also cross pulmonary shunts and contribute to these forms of DCS in divers without PFO. Thus, VGE would seem to be very important in the pathophysiology of serious DCS.
Simon M

Yes, agreed. Some people do have defects in the circulatory system, that allows a bypass of both VGE and unfiltered blood (re: inert gasses not removed), to recirculate through the system. They are at much higher risk I believe. I would argue that its not appropriate that these people to be doing high stress deco dives. These people will need to add an enormous margin of safety to the dive plan, and they are still at a much higher odds of taking a hit. Sadly, these people were just not built right for doing deco.

On the other hand, the work of the Split team showed that small amounts of VGE are recirculated regularly within many of us. A forceful cough was enough to send the VGE micro-bubbles across the lung in one study. Another study showed that strong post dive exertion (ie: dragging the dive gear back up to the car after a dive), that was enough for temporary bypass in the lung in 50% of the subjects.

So given that post dive heavy exertion is common, one has to think many of us experience some form of small recirculation many times. Which makes me think that we humans have some inbuilt tolerance for this condition, and its not as threatening as it sounds.

Would you care to explain to me exactly how tissue microbubbles and VGE are unlinked in respect of deco models, especially given that VGE must form in tissue microvessels which are part of (wait for it) ....the tissue.
Simon M

No. What I ask of you, is to provide some reference or study to back up your claim that VGE and DCS tissue micro-bubbles are one in the same? Because last time I checked, such a connection does not exist.

As I understand it, the theory is that VGE will form on micro-nuclei or particle seeds, that are present on the endothelium, or in cavities in the endothelium, all within the venous system. But I have not seen any papers that show that VGE come from the same place that tissue DCS forms.

Do you have a new paper or study to show that confirms VGE and tissue micro-bubble DCS is the same thing? If you can provide that, then I will let you off the hook on this topic.

However, if you cannot then that would be making stuff up, and creating associations that are not valid or proven. For someone in your position, that is not a good practice.

 

[Kevrumbo]

Again, with respect to the academic (?) debate between Ross & Simon on the efficacy/efficiency of VPM and bubble models in general, the practical application of the Nedu conclusion for the non-military/non-commercial Sport/Recreational Technical Diver is to simply extend your O2 deco profile at 6m as needed -whether you're using a Bubble/Dual Phase Model Algorithm like Ross' Multideco VPM, or Buhlmann GF's with shortened shallower Deep Stops (or no deepstops at all). This is strategically prudent especially if you're doing multiple deco dives per day for a week or more while using high fractional N2 content bottom mixes like deep air. . .

 

[Dr Simon Mitchell]

So given that post dive heavy exertion is common, one has to think many of us experience some form of small recirculation many times. Which makes me think that we humans have some inbuilt tolerance for this condition, and its not as threatening as it sounds.

Clearly, VGE entering the arterial circulation can be tolerated to some extent, depending on when they enter the arteries, and where they distribute to. For example, if they distribute to a critical sensitive tissue like the inner ear when the inner ear tissues remain supersaturated with inert gas, then the bubbles will grow as supersaturated inert gas diffuses into them and will be more likely to cause problems. Bubbles distributing to non-sensitive tissues or tissues that are not supersaturated with inert gas may cause no problems at all. I'm not entirely sure what point you are making. It is clear from the association between serious neurological DCS and right to left shunt that VGE are important in a signficant proportion of cases.

No. What I ask of you, is to provide some reference or study to back up your claim that VGE and DCS tissue micro-bubbles are one in the same? Because last time I checked, such a connection does not exist.

I did not say that VGE and tissue bubbles causing DCS are one in the same Ross. I was responding to your assertion that deco algorithms control tissue bubble formation and not VGE ("Deco models work to prevent tissue microbubble growth, not VGE"), as though the two are completely independent. You don't need references Ross, it is simple laws of physics and physiology. During a normal ascent the arterial blood, having just passed through the lungs, will have equilibrated with inert gas at Fi(inert) x Pamb (approximately); the point being the arterial blood is not supersaturated. It then passes through the tissue capillaries. This is where it may acquire a supersaturated pressure of inert gas (if the tissue is supersaturated) as the gas diffuses from tissue to blood. The degree of tissue supersaturation is totally influenced by the tissue gas kinetics and the decompression algorithm followed to that point. Thus, the decompression algorithm is influencing both the tissue inert gas pressure and thereby the inert gas pressure that is developed in the blood passing through the tissue microcirculation. This inert gas pressure (and the degree of supersaturation it represents) will have a direct influence (obviously) on the propensity for bubbles to form both in the tissue itself and in the blood vessel. The latter are the bubbles which become VGE in the blood leaving the tissue, and which we can detect.

Interpretation of the signficance of the VGE counts is complicated in multiple ways, but of relevance to this conversation: First, by the fact that by the time we count them there are VGE from tissues that are probably unimportant, mixed with VGE from tissues which almost certainly are important. Second, in most individuals we have no idea of the propensity of those VGE to shunt into the arterial circulation. Third (and I think this is one of your points), the mechansims of bubble formation in both tissue and blood are uncertain, but it may well be (for example) that bubbles form more easily in blood than tissue meaning that there would not be a strictly proportional relationship between VGE and those DCS symptoms that are caused by tissue bubbles. These factors almost certainly explain why the specificity of VGE counts as a predictor of DCS symptoms is poor. Nevertheless, you can see from the description of the origin of VGE above, that it is fallacious to claim that deco algorithms only have relevance to tissue bubbles and not VGE. The relationship between VGE and tissue supersaturation is complicated but it is undeniable, and tissue supersaturation is influenced by the decompression algorithm being followed.

Simon M

 

[rjack321]

Again, with respect to the academic (?) debate between Ross & Simon on the efficacy/efficiency of VPM and bubble models in general, the practical application of the Nedu conclusion for the non-military/non-commercial Sport/Recreational Technical Diver is to simply extend your O2 deco profile at 6m as needed -whether you're using a Bubble/Dual Phase Model Algorithm like Ross' Multideco VPM, or Buhlmann GF's with shortened shallower Deep Stops (or no deepstops at all). This is strategically prudent especially if you're doing multiple deco dives per day for a week or more while using high fractional N2 content bottom mixes like deep air. . .

Or you could cut out the deep stops starting at 75% of depth and such... And perhaps not need to extend your shallow stops as compensation. I know you like them a lot - based on some theoretical need which is not born out by recent evidence and every other agency's practices.

Its not academic, check out Kevin's heat maps from the 200ft for 30mins with EAN50 and OO2 for deco. The buhlmann profile was way better than the vpm profile in ending gas loads. Your ratio deco profile is worse than even the vpm profile he tested.

 

[Kevrumbo]

Or you could cut out the deep stops starting at 75% of depth and such... And perhaps not need to extend your shallow stops as compensation. I know you like them a lot - based on some theoretical need which is not born out by recent evidence and every other agency's practices.

Its not academic, check out Kevin's heat maps from the 200ft for 30mins with EAN50 and OO2 for deco. The buhlmann profile was way better than the vpm profile in ending gas loads. Your ratio deco profile is worse than even the vpm profile he tested.

You're right Richard, it is not academic -but an anecdotal yet still compelling extrapolation and application.

I'm perfectly willing & able to make the choice in risking your Fast Tissues' Supersaturation without O2 deco extension, especially over 21 consecutive days of expedition deco diving high FN2 bottom mixes in a remote central Pacific Region, and essentially similar to the working gases used in the Nedu Study (Deep Air). . .

Post #329 ("Twenty-one consecutive days. . ."):
http://www.scubaboard.com/forums/te...-deep-stops-increases-dcs-33.html#post7335373

 

[rossh]

Or you could cut out the deep stops starting at 75% of depth and such... And perhaps not need to extend your shallow stops as compensation. I know you like them a lot - based on some theoretical need which is not born out by recent evidence and every other agency's practices.

Its not academic, check out Kevin's heat maps from the 200ft for 30mins with EAN50 and OO2 for deco. The buhlmann profile was way better than the vpm profile in ending gas loads. Your ratio deco profile is worse than even the vpm profile he tested.

Yes, you could do that - cut the deep stops and shorten the shallow, i.e. raw Buhlmann plans. But no one wants to do that nowdays. Instead the Buhlmann plans are all morphed with GF into longer and deeper to get them further towards deep stop model attributes. So be careful not to assume that the subtle changes of late, are actually shallow stop attributes.

Kevins heat maps used faked up model data - there is no such thing as +7. His stretched out examples are of little value.

 

[Dr Simon Mitchell]

Yes, you could do that - cut the deep stops and shorten the shallow, i.e. raw Buhlmann plans. But no one wants to do that nowdays. Instead the Buhlmann plans are all morphed with GF into longer and deeper to get them further towards deep stop model attributes.

That is what people started to do with gradient factors Ross, at a time when the belief in deep stops was at its zenith. But the truth is that the trend "nowdays" is to manipulate the gradient factors to de-emphasize deep stops to some extent. It has been acknowledged many times that nobody knows how far we should back away from what I will refer to loosely as the deep stop model (as prescribed by bubble models), but there is clear evidence in support of backing away from it to some extent.

Kevins heat maps used faked up model data - there is no such thing as +7.

Maybe not in your application, but the original description of the VPM model clearly described a range of critical radii that encompasses what has been referred to as "+7" in the various debates. This has been explicitly dealt with elsewhere. Are you seriously suggesting that VPM works on low conservatism but not high conservatism?

His stretched out examples are of little value.

If you don't like the heat maps of supersaturation patterns using VPM +7 then see the ones where he compares VPM +4 with GF 40/74 during and after decompression from a typical technical dive here:

http://www.rebreatherworld.com/show...r-dive-charts)&p=446919&viewfull=1#post446919

It is clear that the VPM profile produces the same pattern of tissue supersaturation (protection of the fast tissues whilst deep at the cost of greater slow tissue supersaturation shallow and at the surface) that appeared to explain the different outcomes in the NEDU deep stops (A2) and shallow stops (A1) dives that can be seen here:

http://www.rebreatherworld.com/show...t-rate-thread)&p=445956&viewfull=1#post445956

Simon M

 

[rossh]

Maybe not in your application, but the original description of the VPM model clearly described a range of critical radii that encompasses what has been referred to as "+7" in the various debates. This has been explicitly dealt with elsewhere. Are you seriously suggesting that VPM works on low conservatism but not high conservatism?
Simon M

Well Simon, *IF* you actually looked into the proper causes of stress and injury in the nedu study, and tried to fully explain the anomaly of the nedu test, then you would see how stretching out models and profiles to ridiculous amounts, is a foolish way to compare.

If you don't like the heat maps of supersaturation patterns using VPM +7 then see the ones where he compares VPM +4 with GF 40/74 during and after decompression from a typical technical dive here:
Simon M

Those eye candy heat maps is 90 % meaningless noise, and the important data is not visible. But they do make for good advertising and marketing technique to play tricks on people.

A proper examination of the pressures and stress can be seen in my diagrams below.



270ft 20 mins 10/50 CCR 1.2: VPM-B +4, GF 40/75, GF 65/65


Your "Integral of supersaturation and time", or mb/mins is a inverted measure - remember? Don't shoot your foot off Simon. The diagram shows VPM has the lowest stress and is the better choice.





Driving, flying and skiing have less stress than scuba diving, and the diagram shows that - because mb/min is a inverse measure - low is bad, high is good. But in reality, "Integral of supersaturation and time" and the way you try to apply it as some overall measure, is junk science.

It is clear that the VPM profile produces the same pattern of tissue supersaturation (protection of the fast tissues whilst deep at the cost of greater slow tissue supersaturation shallow and at the surface) that appeared to explain the different outcomes in the NEDU deep stops (A2) and shallow stops (A1) dives that can be seen here:
Simon M

That's just plain wrong. The fast cells are NOT protected by A2 profile, and A2 does not represent deep stops.






Note how the A2 has little in common with VPM-B. Nedu A2 does NOT represent a deep stop profile from a supersaturation of tissue pressure perspective.

Note how the A2 is much closer to a GF 65/85 plan with extra extended (multilevel type) shallow time. The A2 is far closer to GF profile, with extra time added shallow.






Note the similarities: A2 (the high risk profile), looks very much like this GF 65/85 profile with some extra shallow time added on.



**************

In summary Simon, many of your points are dead. You keep claiming the nedu test represents deep stop profiles when it obviously does not. You make comparisons of conditions, that did not exists. You draw conclusions from assumptions that are not possible. You ignore that the nedu A2 high risk profile is actually a shallow profile. You dismiss the basic math and graphs that clearly show your position is invalid. You use junk science to promote your position. And you push people towards the very conditions that generated the high risk profiles.

 

[Remy B.]

Sorry to interrupt I just want some clarity if any of you is so kind, just trying to understand, I have read, and read and read again, what D Doolette report said and others in this very interesting thread, with my null knowledge in diving and less in Deco's, why the NEDU study try to compare one theory to another but modifiying the other to an extend that it is out of his own original parameters, then say that the study was based in Cost/effective, while in the Navi your most valuable asset is your man, so if it cost a lot to bring him to surface it just cost a lot, but you still bring him safe out of the water no matter how much it cost, I also don't understand as the effectiveness can't be comparable if they didn't compare original theory against original theory, what did I miss ???

Did at the end the Navy change their mind of what theory to follow ?, or the Navy keep using what they have been using on Air dives ???

 

[boulderjohn]

I have to admit that much of this discussion is beyond my level of understanding, but as someone who does decompression dives, I think it is quite important, and I am struggling to follow along as best I can. I sense that others are in my booties. (Actually, Converse All Stars, but I digress.) I just did the calculations of my gas needs for an upcoming dive and dropped the tanks off for filling. I want to use the best profile for my ascent, and I think a lot of other readers have the same wish.

Although I am not a scientist, I have co-authored an educational guide book explaining how to best incorporate scientific investigation (essentially labs, but really more than that) into the high school science curriculum, so I at least have a clue about scientific processes. As I have written in this thread already, I understand that it is important to isolate the factor in a process that is being studied from other factors so that it is clear what part of a process is doing what. In a successful process with many factors, it would be a mistake to assume that all factors must be part of that success. It is possible that one factor is either unimportant or is actually detrimental to a process that would be even more successful without it.

I also understand that in this case, some people are critical of how the NEDU study was set up with that regard. In a previous post, I challenged someone who felt that way to say how it should have been done instead. He did not reply.

So I would like to repeat the challenge to the more scientific-minded people reading this thread. Let's start from scratch. Let's say you want to do a good, sound investigation of the efficacy of deep stops. You want to make sure that you are studying the efficacy of deep stops and not some other part of the entire decompression process. How would you do it? what would you do differently from the NEDU study, and why would you do it that way? Please be specific.

Please note that this challenge is not coming from someone sitting clearly on one side of the fence. It is a genuine question from someone who wants to know the answer.