Tidal volume and Flow limitations

[Morbius]

I refer you to your image example from Sat Jan 08, 2022 7:31 am. Obvious severe FL, obvious increasing I-time but a clinically important arousal at 6:57:20.

Now, duty cycle has "dutifully" confirmed what your eyes just saw but I mean like "duh".

[Morbius]

Expanded RR Graph, which I think you requested:
15112728-RR.GIF

Actually I NM'ed that, but if you want to pursue that area, put up some 2 minute windows. I think that guy's problem centers around "Sleep Disaster", not "Duty Cycle".

[AmSleepnBetta]

@Morbius

Thanks for responses.

Among the obvious, my wordy efforts are not intended for clinicians like you apparently are. Many sleep fora members indicate clinicians and their patients would benefit from knowing and applying these matters. Nothing of this "so obvious" was known to me as I struggled with FL as so many do under guidance of clinicians.

As you know, very little attention is given to flow limitation, especially that not flagged by our PAP devices. Inspiration time and duty cycle are little known key indicators of those, especially unflagged limitations. Good to know you recognize and deal with flow limitations and long inspiration time for benefit of your patients

My most recent three images, 2-minute, 52-minute and 7 hour view, are from one of my better nights two and one half months into therapy in 2015. My severe apnea, TTIA up to 40% of TST and my record OA of 155 seconds, are down somewhere over two years with AHI 0.2 and FL cut to low and few by VAuto. So, yeah, the Jan 8 sleep was, relative to my sleep now, a trainwreck.

As to the January 8 post image of my RERA, the whole purpose, as usual, was to select and show a close up of relationships among the metrics Resmeds provide at the RERA. Funny you, not I, would discover my most important arousal marked by the RERA. Arousals. When first PAPing with dense OA, FL and lengthy TTIA, I once badgered forum members and advisors (pugsy? probably) for graphics showing typical arousals so I and others could learn to recognize them. Such is part of motivation to dig into and blather on about all this so trivial to you.

It is apparent you've not followed many cases I and others have tracked and the arguments about meanings and meaninglessness of RM FL.

[Morbius]

Thanks for responses.

Is that like netspeak for "I wish you were dead"?

Among the obvious, my wordy efforts are not intended for clinicians like you apparently are.

Assumption.

As you know, very little attention is given to flow limitation, especially that not flagged by our PAP devices.

Assumption.

so trivial to you.

Assumption.

It is apparent you've not followed many cases I and others have tracked and the arguments about meanings and meaninglessness of RM FL.

Assumption.

So now I'm going to make an assumption.

Your goal is to help people understand the finer points of FL. Who is your target audience? Are your explanations geared toward helping them? I mean, if a teacher isn't actually teaching anything then they're not really a teacher. And I'm also "assuming" that the lack of feedback is due to a lot of tl;dr.

OTOH maybe I'm totally wrong and everybody is going "Wow! I never knew that! That's exciting! Duty cycle is the new black!"

[Morbius]

But if discussion continues, then besides

Can you highlight those observations that are clinically relevant?

can you post how increased duty cycle represents the Second Coming of Satan?

Because increased (or even inverse) I:E Ratios (the ultimate result of +duty cycle) might not be a bad thing.

AAMOF some people think (thought) it could be quite beneficial:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2792969/

One wonders if all that arousal-free FL during SWS was a result of +duty cycle (Auto-PEEP helping to treat OSA)

Inquiring minds and all that...

[palerider]

But at the risk of "doing a palerider" I would submit that your Guide to Understanding Oscar Reports is the equivalent of a Rube Goldberg Machine-- an exceeding complex explanation for the obvious.

Oh, I don't know that I would have ever been so eloquent, or gentle, though I agree completely with your determination. It's entertaining to see you taking an amused interest in this travesty of elucidation.

[AmSleepnBetta]

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.

[Morbius]

Second, Your link, Morbius, to NIH paper about treating apnea with auto-PEEP:

Actually, the thought I was hoping to highlight from DPW was the role of FRC (which might be attained by inverse I:E ratio).

As far as Provent goes, I believe we sufficiently raked it over the coals when it first came out.

AAMOF they closed up shop a couple years ago.

BTW are you using a translator?

[Morbius]

My bumbling novice work ...

Humblebrag.

I really hate that.

[Morbius]

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...

No? What do mean "No"? You KNOW you weren't in SWS?

Other than those points, I have NFI what you're trying to say.

[Morbius]

clinicians coruscating among hoi polloi -

I only coruscate with my wife.

And even then, I need to feed her a few drinks to loosen her up.

[Morbius]

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?

Wellll, let's talk about that a little. Cause actually, in many of the examples of flow limitation you and daquill have posted, no reduction in tidal volume occurs. And indeed, that's the whole purpose of increasing duty cycle, namely preserving tidal volume.

That said, you do have one example where there is tidal volume reduction in the face of severe flow limitation, but frankly, that flow limitation is so severe I would score that as a hypopnea (at the least).

[Morbius]

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."

Yeah, trust me when I tell you, I know exactly how effective Provent is (was).

[palerider]

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.

I have never understood the confusion on some people's part where they mischaracterize a response as 'offense' when it's really "they think I'm full of shit". Do expound please. Maybe they're just trying to cast aspersions?

First, the target audience I try to serve:

You really should understand that you don't *serve* any audience. Your overly wordy attempts to sound educated are going to fly right over the heads of almost everyone that can force themselves to try and follow your twists and turns of something approximating English.

However, you *have* found a perfect target audience in dataq1 If only you two could just get together for your wankfest where it doesn't clutter up the board for the folks that have come here for help.

And no, I have no way to contact "Morbius". I'm just greatly amused by his pointing out the sieve of flaws(not just a few holes) in your verbiage.

[jimbud]

by palerider » Thu Feb 17, 2022 3:04 pm

Another candidate for the:

Accounts to put on the foe list: dataq1, mper!?, DreamDiver, Geer1, almostadoctor, sleepgeek, ajack, stom, mogy, D.H., They're often post misleading, timewasting stuff.

???

JPB