Sorry again for stepping away from the thread, I was out diving for the past 4 days.
There's never been science that "bunked" the oxygen window in the first place.
Of course, I never said there was. What I did say was that it was never "debunked." If it was never "bunked," then there could never be any science that "debunked" it right? Therefore, saying it's been "debunked" simply isn't true.
Isn't even UTD stepping back from it in UTD-RD 2.0 ?
No, it still exists in UTD RD 2.0.
UTD RD 2.0 -if I understand
@mikeny9 correctly- now does the S-curve something like: 3,3,4,4,6. (More weighted toward the 9m stop)
This is incorrect. For a 15 minute spread between 70' and 30', the old RD would use 4, 4, 2, 2, 3. The new UTD Rd 2.0 it would now be 3, 3, 2, 2, 5.
GUE still does (?) the straight linear progression: 4,4,4,4,4.
This is true from my understanding among GUE friends.
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?
There is still an S-curve, as I mentioned above. The difference in the RD 2.0 is in the extra time stolen from the middle of the "S." Previously, it was distributed between the 70' and 60' stop, and now it is all added to the shallower 30' stop.
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.
Paradoxically creating higher risk of neurological injury only in the situations where a PFO or pulmonary shunt exists? If one has been tested for those, with negative results, wouldn't the statistical chance of a type II hit caused by bubble formations in slow tissues be statistically reduced?
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.
Is there any research which suggests that type II hits come from slow tissues, other than when in the presence of pulmonary shunts and PFOs?
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.
I believe any issues with fast tissues might lead to a more serious type II hit. The problem I have with the study, respectfully, is the conditions and healthy subjects participating in the test were probably not as at risk to this type of DCS than a typical, not as healthy, recreational decompression diver. Put another way, the typical recreational decompression diver could be more at risk to a type II hit, decompression schedules aside, than a Navy diver. I'd rather err on the side of protecting fast tissues, knowingly accepting the risk of saturating the slow tissues, and attempt to clean up the slow tissues with more decompression time and/or oxygen-based decompression.
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.
Respectfully, I don't agree the discussion makes it "crystal clear." The discussion you pointed out refers to the higher VGE scores in the deep stops arm due to the supersaturation of the slow tissues in the deep stops. However, no where does it discuss the importance of fast compartments as they compare to slow compartments. The authors did not conclude that protecting slow tissues was equally or more important than protecting fast tissues, otherwise wouldn't a similar statement be found inside the conclusion? They concluded only that protecting fast tissues was "unwarranted." Might I point out, the conclusion is in the scope and conditions the test was performed, e.g. the types of subjects, the depths, times, and types of gases inspired, all of which are not very standard to the typical recreational decompression diver. If anything, this conclusion should lead to further hypotheses and subsequently more scientific tests.
