UARS/FL (PLMS): Yellow/R Lights For So Many Lingering Folks_“Is Bilevel the Answer?"

[slowriter]

Very helpful mpers; thanks for taking the time to annotate these!

[mper6794]

Hi, dear folks,

Updating and refreshing : I am a UARS-PLMS case. Started therapy 2.0 years ago; lost 1.5 with CPAP and APAP.  After 7 months with BPAP and OSCAR/daily analyses, it may happen I would have reached to what do this could get. With my current EPAPmin: 7.6 and PS: 5.0 (IPAPmax:12.6) (semi-quantitatively determined), flagged FL pretty much zero daily, on both p95 and Max columns, still remain some unflagged RERA’s, which I used to counting daily.

You guys may agree: OSA sufferers count AHI, we, UARS sufferers, count respiratory-driven arousal/awakenings. In my case, I have to count also PLMS-driven and other cause-driven arousals/awakenings as well, fortunately somewhat under control these days. I am currently on Valerian 1060mg and supplements, lithium 5mg, and sporadically Clonazepam 0.4mg when anxiety get a little too much high. 
Elsewhere, only in threads closely related to FL/RERA/UARS, I have been trying to learn and eventually pass some experience I may have acquired during those 7 months, back and forth between literature and waveforms from my own and others, here and in other blogs.

Main purpose of this check in is raising a question, which has to do with the rationale with this thread: would it be worth FL/RERA/UARS-sufferers moving as soon as possible to BPAP, rather than stay long on APAP?

About one month ago, when revisiting what happened overnight, while moving from APAP (EPR:3.0) to BPAP (PS:4.0), I realized that not only pretty much all FL gone way, but also there was a complete rearrange on respiratory patterns. There were sudden changes on the E:I ratio and MV, as well as on the expiration limb of the FR, which was plagued by flow reductions, seen as a ratty aspect, distinct from the flat top of the inspirations. This could reflect well on the aerophagia I faced at the time, with the APAP (Pmin: 8 to 10.8).

I am aware this would be well known for many here, but for me, still learning day after day, was a rather surprising, particularly when I started seeing same happenings and patterns in similar cases posted here. Then, I have quickly gathered data from some three more fellows here, with regard to E:I ratio and PS, while moving from APAP to BPAP (see attached hereinbelow).

What has come out was a pattern of APAP/BPAP blow-up expiration time, overnight, followed by a complete rearrange of the I:E median ratio. Such blow-up, based on the four cases I have analysed, appears to be proportional to the ultimate tailored PS of each one. It appears the higher the tailored PS, the larger the effect, which, in fact, could be expected?.

However, what has looked far more important for me, if we look the phenomenon backward, would be the potential detrimental and deleterious effects of APAP respiratory pattern, with a I:E ratio close to 1:1, on account of decreasing expiratory time. “Normal I:E at rest and while asleep is 1:2 or less. On great effort (exertion) I:E is 1:1”. Therefore, I have concluded that while on APAP, trying to tame FL under higher Pmin’s, would be analog to entering in a rush rather than into the night to sleep.

Now, a question for you guys, with longer term experience in historic cases, and which has been intriguing me: even we consider that APAP could treat FL/RERA/UARS, would it be possible for individual waiting too long to get acquainted with the machine, without some risks?

All the best

[mper6794]

...on my updating, forgot of the most important: how do i feel on my scale 1.0 to 5.0? Well, i wish It were better; 90% of nights above 4.0, not counting other good things: no nightmares, nocturia, panic wakeups, somewhat better architeture, better blood in general. That is, so-so...
Good luck

[mper6794]

Hi, folks
I have been asked to update my semi-quantitative method, empirical, aiming at fine-tuning and quickly obtaining tailored PS and EPAPmin. It looks fair this request. While revising posts above, it looks indeed it would deserve more clarifications.
Please, find attached a summary of the method. Any doubt, please, let me known.

all the best
MP

[slowriter]

I don't know; I think if there's value to this sort of analysis, it should be straightforward to express it in the form of an example spreadsheet, with formulas, and that you (or someone else who is following) should do that.

And I also think, per other feedback, expecting people to manually count RERAs and such is impractical. Even I won't do that. So to simplify it.

A reasonable alternative, for example, might be using the UF flags.

[mper6794]

Thanks, Slowriter
Today Will follow more details of the method; origin, more rationale, etc
GL

[mper6794]

Hi, folks, sheepless (to encourage or discourage you!    )

The semi-quantitative approach I been suggesting for you guys to use to quickly fine-tuning and determine your tailored EPAPmin and PS, while in bilevel machines, came across some 2.5 months ago in my historic (see attached).

I wish I knew this approach this before. I took me some 6 months to get my fine-tuned EPAPmin and PS. Today, after realizing on the quick, overnight, response of median RR, both to P.S and EPAPmin, I could do this within some 15 days.

First thing to know is having and proxy of your normal RR: could do this as simple as put your hands on your stomach, count BPM and multiply by 0.89 (literature); sleep studies, etc.

While titrating EPAPmin and P.S, such relations, would be useful not only to get those two, but also to know whether or not you would be heading/how far toward trigger CA’s by increasing P.S (see examples elsewhere).

This is empirical. Science wise, why increasing P.S would decrease RR? Not sure. Maybe this could be just apparent. Lowering RR would just reflect “tendencies” toward CA’s (lower/none RR at all) in the overall median; my analyses suggest heading to CA’s would occur only RR runs lower than normal RR (see attached graphs in previous post, above). Moreover, of course: more P.S, more ventilation, less need for breathing.

Why increasing EPAPmin leads to higher RR, for a certain PS? Not sure, likewise. Could be more EPAPmin, more space, more CO2 flush, need from more O2 to balance, higher RR?

This first setp on fine-tuning EPAPmin would have to be followed by approaching the best result we can get on RERA’s reduction, by cross-plotting EPAPmin x RERA’s (flagged+unflagged). A zero interception of EPAPmin+PS can be projected, which would lead to ultimate EPAPmin (see attached above).

Slowriter, I know this last step is hard manually; however, I have been doing this daily; it took me some 10 min, including discriminating between PLMS-driven and RERA-driven awakenings. I would never thrust in any machine to do this for me, as I don’t thrust for events in general. For us, UARS-PLMS, absolute majority of all these events are fake ones.

Shepless: I will return later on the medications, supplements, etc, if you think would worth.

All the best for everyone.

[sheepless]

I'm happy to be a test case, partly curious, partly thinking apap and asv haven't done it for me yet and I feel no worse and maybe a little better on vauto (to my surprise actually).

I can't say I understand your method very well and because of that my questions at this point aren't well developed. I'll throw a few out there, partly playing devil's advocate and to try to flesh this out a little. I'm not asking for academic or professional level documentation, just some additional discussion.

the plots of your self titration are so busy it's hard (for me) to get a handle on what's going on and what it means, at least quickly. in time, adding slides that isolate one or a few plots to make it easier to interpret would certainly help me.

how did you conclude ipap max should be epap min + ps?

have you experimented with other ipap max settings? do you think it's worth playing with ipap max after completing your procedure?

I'm surprised my pressures are almost always constant with vauto. is this normal for this machine or a function of the relatively tight range and capped ipap max? relatively stable pressure has it's benefits but I wonder if giving the machine some room to adjust to night to night variances would eventually be beneficial.

what are the blue dots in the plots you've done for me? it looks like only the orange/red ones are my data?

are you using rr/2 or rr x 0.89 and why? why should it be less than actual?

you've said knowing our rr is important. how is it used relative to the plotted machine data? are we trying to duplicate or get as close as possible to that value during treatment?

what are fake events if more than waking ca?

how do you identify fake vs real events, especially oa and h?

are you assuming all or some departures from the ideal flow rate curve indicate arousals? if not all, what signifies arousal? rising rr? does the literature support this (or whatever means people use to identify arousals)? aren't some arousals normal in normal sleepers?

I don't mind searching my charts for unflagged stuff (for lack of a more precise term); I just don't know exactly what to look for.

I"m sure I'll have more questions if as when I really study on your posts and graphs. for now I'm content to keep using the vauto for a while.

three things in my case that interest/concern me with respect to application of vauto and your method.

1. an apparent increase in ca and/or the csr-like periodic breathing pattern that's different than my typical periodic limb movement pattern and punctuated by events and short pauses in breathing. asv seems to resolve these.

2. higher ahi with vauto than asv. I still wonder if much the same thing you're doing with vauto can be accomplished with asv. when we're done, I'd like to try your procedure with asv.

3. my sense is that my plm is the root of all my remaining problems, there's nothing cpap can do to counter plm and that it's confounding effective titration.

I appreciate your efforts to potentially advance how plm and uars are treated, together or separately. I don't know if this experiment will work for me or not yet, but I need to do something to improve my lot, it's interesting and I'm always in favor of learning and discovery.

[WillSleep]

have you experimented with other ipap max settings?  do you think it's worth playing with ipap max after completing your procedure?

 
Sheepless that is a rack of good questions, a full rack Lol.
 
"have you experimented with other ipap max settings?  do you think it's worth playing with ipap max after completing your procedure?
 
Beyond testing options other than locking IPAP Max so that the VAuto is in CPAP mode it has been on my mind that on the VAuto there are additional settings that might be tested to help reduce the CSR type breathing produced by the high PS.  

• Trigger is often set to "High" on the VAuto to reduce CAs, though it that increases Inspiration Tidal Volume in a way that causes more CO2 washout then Medium or possibly Low might be a better setting.
    
  
• Setting TiMin and TiMax might help turn Inspiration Tidal Volume in a way that impacts CSR
    
  
• Cycle set to Low might reduce Expiration time and increase PaCO2 in a way that lowers CSR breathing patterns.      
  

 
WillSleep

[sheepless]

thanks WillSleep! after reading about it in another thread, I did bump trigger to high for one or two nights and it did reduce ca. not sure about pb. for mper, I have all timing settings set to default except ti min at 0.8 from 0.3 at his suggestion. I'll read up and experiment with those settings when mper's done with dialing in the pressures.