So there's no S curve (you know it's an S because the shape looks like an S, right? because "more time spent at the optimal oxygen window", so you spend a lot of time on the high pO2 that follows a gas switch) anymore. Why do you then pop out the article on which it's built?
UTD Ratio deco discussion
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Gotta correct myself as I just found The Extended Oxygen Window Concept for Programming Saturation Decompressions Using Air and Nitrox , so there should be such thing as a "vacancy" ?
@Duke Dive Medicine or @Dr Simon Mitchell, anyone able to give a hand? (Sorry about the excessive tagging you're receiving Simon! ) Did I skim too fast over the articles? I am aware PLoS is not necessarily the most respected journal out there.
@Duke Dive Medicine or @Dr Simon Mitchell, anyone able to give a hand? (Sorry about the excessive tagging you're receiving Simon! ) Did I skim too fast over the articles? I am aware PLoS is not necessarily the most respected journal out there.
Kevrumbo
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("S-curve" aka similar to a Sigmoid Function.)
Because there is no advantage to utilizing a S-curve profile to sit at 21m for any greater length of time than necessary with a deco gas that has an inert gas percentage of 50% (Eanx50).
To truly take advantage of the full efficiency of the "Oxygen Window", you would have to switch to 100% Oxygen at 18m -->as in a Table 6 Treatment in a dry Recompression Chamber. Obviously not advisable for in-water decompression procedures (unless you're Brett Gilliam).
Practical and Simpler Oxygen Window Explanation in Decompression:
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Hello again Mikeny9,
I am beginning to understand where your discomfort with "giving up" bubble model or RD style deep stops originates. You appear to hold the idea that deep stops protect the neurological tissues and shallow stops protect the less important musculoskeletal tissues as an article of faith. I have never taken a UTD course but I presume you have been told this as part of your training. There are 2 points I would like to make about this:
First and most importantly, you are assuming that neurological tissues are fast, and that they are injured in DCS by the formation of bubbles within the tissue itself. Both assumptions are probably flawed in at least some circumstances. Indeed, there is strong evidence that neurological DCS is caused in many (and perhaps the majority of) cases by venous bubbles that cross into the arterial circulation either via a PFO or a pulmonary shunt. The majority of these bubbles almost certainly come from slower peripheral tissues which are the ones you put at risk by emphasising deep stops. This claim is corroborated by the findings of essentially all the relevant studies to date which demonstrate higher bubble grades when deep stops are emphasised. The obvious point being that in setting out to protect neurological tissues by emphasising deep stops, you may paradoxically be creating a higher risk of neurological injury by causing greater venous bubble formation in slower tissues. It is notable that the NEDU study, which is the only one to have used clinical DCS as an outcome measure, did not show that DCS cases in the deep stops arm were restricted to mild symptoms. Neurological cases were distributed across both the deep stop and shallow stop groups.
Second, I would respectfully like to point out that you are holding onto this notion in the absence of any evidence that it is valid, and in the face of a growing body of evidence (which admittedly involves fitting an evidence jigsaw puzzle together because no one study is definitive) that suggests it is probably wrong. If your "belief" does indeed come from what you have been told on UTD courses as I suspect, then I really do think it is worth reflecting on the pedigree of that information.
I anticipate you will want to come back to the argument that you can "have your cake and eat it too" by indulging your passion for deep stops and then compensating with longer shallow stops and oxygen decompression. Something along the lines of:
I reiterate that it would certainly be possible to run such a regimen to an acceptable level of safety. But in doing it you will never be able to escape the question of whether your safety could have been even better if you did the same length of decompression, but with less deep stops and more shallow high PO2 stops. The currently available data is suggesting that this would be the case, and it does not support the idea that the deeper stops in the range prescribed by bubble models or RD are helping you.
Finally, I would like to pick up on these comments:
I think you are clearly wrong on this point. The final conclusions are indeed worded appropriately cautiously. But the discussion makes it crystal clear that the authors consider the poor outcomes in the deep stops dives are a consequence of bubble formation in slow compartments, which occurs because of an apparently unnecessary emphasis on protecting fast tissues with deep stops. This is backed up with illustrative analyses of supersaturations in typical fast and slow tissues. One example of relevant text reads:
The present results indicate that this reduction of initial gas supersaturations in fast compartments (produced by deep stops) does not manifest in reduced DCS incidence. On the contrary, DCS incidence was higher after the tested deep stops schedule than after the shallow stops schedule, an indication that the large ascent to the first stop in classical schedules is not a flaw that warrants “repair” by deeper initial stops. Figure 5C illustrates that deep stops result in greater and more persistent gas supersaturation in relatively slow compartments on subsequent ascent than during the comparable period in the shallow stops schedule. This results from continued uptake of inert gas into these slow
compartments during the deep stops. Gas supersaturations in slower gas exchange compartments late in the decompression are in accord with the present results from the tested dive profiles. The observed higher VGE scores and DCS incidence following the deep stops schedule than following the shallow stops schedule must be a manifestation
of bubble formation in slower compartments.
Simon M
I am beginning to understand where your discomfort with "giving up" bubble model or RD style deep stops originates. You appear to hold the idea that deep stops protect the neurological tissues and shallow stops protect the less important musculoskeletal tissues as an article of faith. I have never taken a UTD course but I presume you have been told this as part of your training. There are 2 points I would like to make about this:
First and most importantly, you are assuming that neurological tissues are fast, and that they are injured in DCS by the formation of bubbles within the tissue itself. Both assumptions are probably flawed in at least some circumstances. Indeed, there is strong evidence that neurological DCS is caused in many (and perhaps the majority of) cases by venous bubbles that cross into the arterial circulation either via a PFO or a pulmonary shunt. The majority of these bubbles almost certainly come from slower peripheral tissues which are the ones you put at risk by emphasising deep stops. This claim is corroborated by the findings of essentially all the relevant studies to date which demonstrate higher bubble grades when deep stops are emphasised. The obvious point being that in setting out to protect neurological tissues by emphasising deep stops, you may paradoxically be creating a higher risk of neurological injury by causing greater venous bubble formation in slower tissues. It is notable that the NEDU study, which is the only one to have used clinical DCS as an outcome measure, did not show that DCS cases in the deep stops arm were restricted to mild symptoms. Neurological cases were distributed across both the deep stop and shallow stop groups.
Second, I would respectfully like to point out that you are holding onto this notion in the absence of any evidence that it is valid, and in the face of a growing body of evidence (which admittedly involves fitting an evidence jigsaw puzzle together because no one study is definitive) that suggests it is probably wrong. If your "belief" does indeed come from what you have been told on UTD courses as I suspect, then I really do think it is worth reflecting on the pedigree of that information.
I anticipate you will want to come back to the argument that you can "have your cake and eat it too" by indulging your passion for deep stops and then compensating with longer shallow stops and oxygen decompression. Something along the lines of:
I reiterate that it would certainly be possible to run such a regimen to an acceptable level of safety. But in doing it you will never be able to escape the question of whether your safety could have been even better if you did the same length of decompression, but with less deep stops and more shallow high PO2 stops. The currently available data is suggesting that this would be the case, and it does not support the idea that the deeper stops in the range prescribed by bubble models or RD are helping you.
Finally, I would like to pick up on these comments:
I think you are clearly wrong on this point. The final conclusions are indeed worded appropriately cautiously. But the discussion makes it crystal clear that the authors consider the poor outcomes in the deep stops dives are a consequence of bubble formation in slow compartments, which occurs because of an apparently unnecessary emphasis on protecting fast tissues with deep stops. This is backed up with illustrative analyses of supersaturations in typical fast and slow tissues. One example of relevant text reads:
The present results indicate that this reduction of initial gas supersaturations in fast compartments (produced by deep stops) does not manifest in reduced DCS incidence. On the contrary, DCS incidence was higher after the tested deep stops schedule than after the shallow stops schedule, an indication that the large ascent to the first stop in classical schedules is not a flaw that warrants “repair” by deeper initial stops. Figure 5C illustrates that deep stops result in greater and more persistent gas supersaturation in relatively slow compartments on subsequent ascent than during the comparable period in the shallow stops schedule. This results from continued uptake of inert gas into these slow
compartments during the deep stops. Gas supersaturations in slower gas exchange compartments late in the decompression are in accord with the present results from the tested dive profiles. The observed higher VGE scores and DCS incidence following the deep stops schedule than following the shallow stops schedule must be a manifestation
of bubble formation in slower compartments.
Simon M
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You have changed. Thanks for copying that information, btw.
Did anyone else read it, because I did, and I'll tell you a couple of things that seemed odd to me.
- The linked info makes statements about the 1/2 times of Buhlmann that are factually incorrect
- It proposes a method of calculating a ceiling that is nothing like what a Bulhmann algorithm would do. The technique is entirely based upon 1/2 times of compartments (of which the chosen compartments do not exist in Buhlmann) while Buhlmann actually calculates using pressure. I know there is a relationship between the 1/2 times and the pressure because you can calculate the "a" and "b" coefficients for Buhlmann using the 1/2 time and the a and b coefficients allow you to pin down the slope and intersection of the pressure gradient relative to a given absolute pressure. The big problem with only using the 1/2 times, however, is that the allowable supersaturation of the tissue group is entirely ignored. That comes across to me as being a glaring mistake that draws the entire procedure into doubt.
- It states flat out that the fast tissues are controlling for the ascent and gives a reason for that which is incomplete and inaccurate. Given what I said above I suspected that fast tissues wouldn't even show up on the radar so I threw together a spreadsheet this morning (I'm home sick for the last few days so I needed something to do anyway). The spreadsheet simulates unmodified (pure) Buhlmann and I only did it for nitrox. Nevertheless on any single-exposure Nitrox dive, even ones that are unrealistically long and regardless of the mix the fast tissues are LITERALLY never controlling for the ascent. They don't even calculate a ceiling. Literally Never. It's always the slower tissues that show up as over their saturation limits (ie, exceeding their M values).
- As an aside to the above, I verified the model against the PADI RDP when I was testing it and it lead to some interesting insights about the RDP as well. I would highly recommend that everyone make a spreadsheet like this. Anyone who took any degree of math should be able to throw one together fairly easily. It took me about an hour and an hour of testing to make sure it was right. The model I made didn't account for ascent/descent rates and it doesn't calculate the length of deco stops but it does calculate a ceiling. The ceiling is never 66%. Never. On the most unrealistic scenarios (very deep and very long on air) it will calculate a ceiling at about 50%. On realistic dives the ceiling maxes out at about 25% on air. On Nitrox it's less than 20%.
- In the tradition of Mythbusters I decided to find settings that WOULD create a 66% ceiling at a diveable depth. It can be done but it would require an exposure of over 40 hours at 66m of depth on air. Using 32% Nitrox the model will not resolve a ceiling of 66% at any achievable depth in a human lifetime.
- I also noticed one or two typos in the RD manual, and one in particular, that can cause confusion until you realize it is a typo. It seems like it's not finished yet.
I would urge people to verify these conclusions for themselves.
R..
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It might be easier to put that spreadsheet up here, so that people can check it, instead of having them redo the work.
I'm concerned about posting it on an open forum. It's just a model I made to give me a perspective on the 66% rule. It's not good enough to use as a planning tool and I'm worried that someone will download it and use it for cutting a table that subsequently gets them hurt.
I will, however, share a link with you to a document that should make the implementation straight forward. http://www.diveresearch.org/download/Publicaties/Haldane en bellen 2006.pdf
It's a good paper, albeit in need of a readability edit, and almost everything you need to understand to make a model of Buhlmann in a spreadsheet is on pages 7/9. You'll also need the actual 1/2 times, which can be found in Erik Baker's paper about understanding M values.
If your math is any better than mine then you should be able to use the information on pages 9 and 10 to unscramble the previous equations and allow the spreadsheet to predict the NDL's as a function of depth, time and mix. I got stuck on it though (probably because I'm sick today
) and gave up before I had it.
R..
I will, however, share a link with you to a document that should make the implementation straight forward. http://www.diveresearch.org/download/Publicaties/Haldane en bellen 2006.pdf
It's a good paper, albeit in need of a readability edit, and almost everything you need to understand to make a model of Buhlmann in a spreadsheet is on pages 7/9. You'll also need the actual 1/2 times, which can be found in Erik Baker's paper about understanding M values.
If your math is any better than mine then you should be able to use the information on pages 9 and 10 to unscramble the previous equations and allow the spreadsheet to predict the NDL's as a function of depth, time and mix. I got stuck on it though (probably because I'm sick today
) and gave up before I had it.R..
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Kevrumbo
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Re-calculate your spreadsheet again, using Table 1 in Imperial US or Table 2 in Meters from p.5 of Eric C. Baker's Understanding M-values:
Use Buhlmann's tissue compartments of 1b, 2, 3, 4 and 5 corresponding to Half-Times (HT) of 5, 8, 12.5, 18.5, and 27 minutes respectively (roughly similar to UTD's chosen interpretation Fast Tissue HT's of 5, 10, 15, 20 and 30 minutes). Use the Mo -values listed for each tissue compartment in the table (either column schedule A, B or C).
Now use this formula to figure out the NDL times (same as controlling tissue compartments) for a depth range of 30m to 45m (same as 100ft to 150ft):
t = T/ln2 * (ln [(Po - Pa)/(Pm - Pa)];
Where:
T is the Tissue Half-Time value;
Po is surface of pressure of Nitrogen given at 0.79 ATA;
Pa is ambient pressure of Nitrogen at a particular depth in ATA units:
either [0.79 * (depth fsw/33 + 1)] in Imperial US; or [0.79 * (depth msw/10 + 1)] in Meters;
Pm is the Mo -value given from the Table divided-by 33 (Imperial US) or divided-by 10 (Meters) to use as ATA units.
To find the NDL for a particular depth, look for the shortest time result in the spreadsheet for that depth and reference it back to its representative Tissue Compartment Half-Time.
You will find that the decompression controlling or leading tissue for depths 33m/110ft and deeper is the 5 Minute Half-Time Fast Tissue Compartment. . .
Generally, the faster compartments will cross into the decompression zone first and be leading (gas loadings closest to M-value lines) and then the rest of the decompression profile will be controlled by the slower compartments in sequence.
(This is just a simple Buhlmann table generating exercise showing the rationale behind UTD's conservative deepstop methodology of protecting the Fast Tissues, but isn't meant to refute the apparent paradoxical results relative to UTD's RD interpretation by the NEDU Deepstop Study in which the Fast Tissues are more tolerant of critical supersaturation earlier in the decompression profile than the Slow Tissues later shallower and upon surfacing).
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Actually Kevin, you're right to a point.
The compartments in a Buhlmann model always fill up from fast to slow. So in a very deep AND very short dive like one to 36m for 5 or 10 minutes, the fastest compartment will generate the ceiling.
However, that ceiling will be shallow and given that it would take maybe 3 or 4 minutes to ascend from that depth any related decompression obligation would clear on the ascent.
A significant ceiling on air could be generated using the fastest compartment by making a short dive to a very deep depth like 56m. That dive would generate a ceiling of 6m or so using the bare-bones model and once again, there is a very high probability that it would clear during the ascent because while the fast compartments fill quickly, they also empty quickly.
The disconnect in AG's thinking regarding the ceilings for RD is that on a significant exposure, like 150min that (a) the fast tissues are still controlling even if exposures are long, which they are not, and (b) that the ceiling can be calculated based only on the 1/2 times of the compartments, which they cannot be.
On the first point, on a 150 min exposure (the example he used in the thing you linked) depending on depth compartments 6 7 or 8 are usually controlling the ceiling. Compartment 6 is 38.3min and compartment 8 is 77 min. I haven't made the model to see which compartments control the deco at every given point throughout then entire ascent but at least leaving the bottom it would never be the fast compartments.
On the second point, he uses the 1/2 time to calculate the ceiling. He references compartments like what he is doing is pseudo-Bulhmann but that's just BS. Bulhmann calculates ceilings based upon total tissue pressure as function of time and permissible overpressure. This is depth dependent and it is time dependent. Every diver should recognise depth and time as being fundamentally important for the NDL, well, it's also fundamentally important for the ceiling once you go over the NDL.
R..
The compartments in a Buhlmann model always fill up from fast to slow. So in a very deep AND very short dive like one to 36m for 5 or 10 minutes, the fastest compartment will generate the ceiling.
However, that ceiling will be shallow and given that it would take maybe 3 or 4 minutes to ascend from that depth any related decompression obligation would clear on the ascent.
A significant ceiling on air could be generated using the fastest compartment by making a short dive to a very deep depth like 56m. That dive would generate a ceiling of 6m or so using the bare-bones model and once again, there is a very high probability that it would clear during the ascent because while the fast compartments fill quickly, they also empty quickly.
The disconnect in AG's thinking regarding the ceilings for RD is that on a significant exposure, like 150min that (a) the fast tissues are still controlling even if exposures are long, which they are not, and (b) that the ceiling can be calculated based only on the 1/2 times of the compartments, which they cannot be.
On the first point, on a 150 min exposure (the example he used in the thing you linked) depending on depth compartments 6 7 or 8 are usually controlling the ceiling. Compartment 6 is 38.3min and compartment 8 is 77 min. I haven't made the model to see which compartments control the deco at every given point throughout then entire ascent but at least leaving the bottom it would never be the fast compartments.
On the second point, he uses the 1/2 time to calculate the ceiling. He references compartments like what he is doing is pseudo-Bulhmann but that's just BS. Bulhmann calculates ceilings based upon total tissue pressure as function of time and permissible overpressure. This is depth dependent and it is time dependent. Every diver should recognise depth and time as being fundamentally important for the NDL, well, it's also fundamentally important for the ceiling once you go over the NDL.
R..
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