Regarding Morbius and PR's several immediately preceding posts, a one time mainly off topic and sometimes in kind reply:
With sparklers, flash bangs and barbs sieved out the gravamem is, as I acknowledge from time to time, that my posts are mostly verbose, often unclear and missing targets. Mea culpa. I must do better but have said that before and this plodding old man will make fresh efforts. Snide remarks and insider codings are easy. It's difficult for me to be brief and clear making points for unserved people who likely know less than the little I know about my topic--a topic and its treatment so obvious to you, Morbius and PR.
Thank you for that remainder, Morbius, and BTW, did PR assign you a mission here, where his embarrassing early-thread dicta (e.g., "there is no connection between flow limitations and tidal volume") are being read too widely? Clicks 8,300 and up 3,200 in 5 days, more than doubled in 2 weeks for this obscure subject. Yeah, many no doubt were "tl:dr" (too long, didn't read). I've never looked at my low clicks until being amazed at their sudden increase here, quadrupling mostly in 3rd and 4th forum pages this year.
Dataq1's thread raised a vital, little addressed topic I've studied a bit. Still having much to learn I have shared the learning process which seems to offend you and PR. This is still a more or less free country, you don't need to disturb that "density" (gravamem) so "all yours" or an "inquiring" mind" reading and sniping here, Morbius.
Other matters the sieve retained:
First, the target audience I try to serve:
They are any PAP using persons--yes, even wannabes and clinicians coruscating among hoi polloi --who are troubled by inspiratory flow limitation (IFL), AHI below 1.0 with unrestful sleep. Frequently I make clear this novice's narrow work is in the IFL-UARS range below scoreable apnea and hypopnea. Most targeted readers have long struggled trying to understand their unidentified problem.
It seems patent those many, less-troubled readers who did not think "tl:dr" have read and shared this thread amazingly, have found something useful, found something to talk to their sleep specialist about, to look into or change. So, job done, but wish I were able to do more.
Second, Your link, Morbius, to NIH paper about treating apnea with auto-PEEP:
As you wrote and I partly agree, "increased or even inverse I:E ratios . . . . might not be a bad thing" but somewhere not involving my IFL work area. Apnea? Other, besides ICU ventilators?. Warfarin for rats, good. Appropriate monitored dosages of Warfarin for needful humans, good, otherwise likely lethal. Warfarin, good in places, bad others.
Morbius, you've been hoisted by your own petard
https://www.phrases.org.uk/meanings/hoi ... etard.html. Your example of useful, "good" flow limitation (PROVENT), with I/E inversion (apparently), to treat obstructive apnea has little if any direct relevance to my IFL work and its related detection and assessment tool: I-flow limitation and excess work of breathing as shown by duty cycle ratio and evaluative criteria. See the latter here
https://erj.ersjournals.com/content/33/5/1068.long
My bumbling novice work is about filling lung alveoli against air resistance, the auto-Peep about keeping that filling at end of expiration. "Corking" (flow limiting) the filled alveoli bottles. Yeah, it can be good to patch or stop leaks and deflation, but if the lung isn't filled with air, what's the point?
A quotation from your offtopic NIH item
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2792969/ about a doctor's laudable study about treating OA with auto-PEEP:
"Second: How effective is this form of therapy? The data from the current study would suggest that expiratory nasal resistors do reduce apnea severity although this effect was variable and modest. The overall AHI fell from 24.5 to 15.5 at 30 days with only 10 of 24 patients with an AHI >10 off therapy having an AHI of <10 on therapy. In addition, there was not a statistically significant decrement in ODI (3% or greater falls in SaO2), minimum SaO2 level, or a change in sleep architecture. If we believe that obstructive sleep apnea leads to its adverse consequences as a product of either sleep disruption or intermittent hypoxia, neither seem to improve with this form of therapy. Thus we need to interpret decrements in AHI with caution."
"Third: Why do some patients respond so well to this therapy while others do not respond at all? If you look at Table 2, subject #203 started with an AHI of 35.7 (severe sleep apnea) and consistently had an AHI <10 with PROVENT in place. On the other hand, subject #316 at baseline had an AHI of 9 (mild sleep apnea) which increased to 20.2 after 30 days on therapy. Although some of this can be explained by night to night variability in apnea severity, this is unlikely to be the total explanation."
Fourth: Need I repeat myself? That 52 minute view was not, nothing I' ve posted in this thread was intended for clinicians here or anywhere else nor should it be. Cases and posts of many frequenting these forums, with their unidentified sleep fragmenting IFL and UARS, could wish some of my thinking were applied by their clinician.
Fifth: Morbius, you wrote "One wonders if all that arousal-free FL during SWS was a result of +duty cycle (Auto-PEEP helping to treat OSA)" No, I was PAPing with a Resmed Autoset without C-collar then, no doubt sleeping left lateral until supine at OA and then, most likely, lateral with neck flexed--based on later evidence connecting position to apnea and FL.
