Does an APAP Recognize UARS?

[SleepySandy]

This is something I should be able to figure out. I've done research, but I can't find a definite answer. So, I've given up and need to ask.

In addition to OSA, I have UARS. I'm working from this general definition of UARS: Increased upper airway resistance in this disorder does not lead to cessation of airflow(apnea) or decrease in airflow(hypopnea), but instead leads to an arousal secondary to increased work of breathing to overcome the resistance.

I've been wondering if an APAP can recognize UARS events. If it does, what's it looking for? Does anyone know?

[-SWS]

I've been wondering if an APAP can recognize UARS events. If it does, what's it looking for? Does anyone know?

Well, the medical community has been batting around and debating the etiologies/existence of UARS for years. If that UARS presentation entails either lesser flow limitation, snore, or both, then an APAP should at least in theory be able to recognize UARS.

But then that question or debate of UARS etiology arises. If that upper airway impedance is soft-tissue based, then inflation of the upper airway via CPAP/APAP should help. However, if that upper airway impedance is purely based in structurally rigid type problems, then airway inflation via CPAP/APAP may not help one bit with that type of UARS.

That's my interpretation only. Please bear in mind that I'm a patient, and not a medical expert.

[Snoredog]

I've been wondering if an APAP can recognize UARS events. If it does, what's it looking for? Does anyone know?

Well, the medical community has been batting around and debating the etiologies/existence of UARS for years. If that UARS presentation entails either lesser flow limitation, snore, or both, then an APAP should at least in theory be able to recognize UARS.

But then that question or debate of UARS etiology arises. If that upper airway impedance is soft-tissue based, then inflation of the upper airway via CPAP/APAP should help. However, if that upper airway impedance is purely based in structurally rigid type problems, then airway inflation via CPAP/APAP may not help one bit with that type of UARS.

That's my interpretation only. Please bear in mind that I'm a patient, and not a medical expert.

[-SWS]

I love that whole description, Snoredog. I personally think there are several possible etiologies that can and do lead to excessive upper airway resistance. Sleep science is sooooooo under-researched...

[sleepyred]

I have UARS and was put on a straight cpap. And I was very lucky to get that. My doc saw that I had micro arousals in my breathing but not enough for my insurance company to say Okay to a cpap. He sent me home with what I'm assuming was an APAP that recorded data and he was amazed at the results and that I slept so well (for the 1st time in years!) He appealed the insurance company and now I am a happy cpaper. But I don't have OSA, but have RLS.

Sleepyred

[StillAnotherGuest]

Defending the position of "There's Nothing Mysterious About UARS" today will be Stil... no, slee..., no delt..., no... ahh, whoever.

Borrowing a response from another post, because I basically want to make my responses bigger than they really are...

I think a fairly definitive assessment of UARS can and should be made through physical exam and PSG, and in the end, there shouldn't be too many questions left on the table for any given UARS patient. BTW, "upper airway" refers to anything north of the vocal cords, so all the structures involved in apnea and hypopnea also participate in UARS. If there is a fixed "upper" upper airway obstruction, this should easily be identified by any good ENT guy, and then the surgical approach opens up (or maybe FF alternatives).

UARS is not that hard to identify in even the most basic of sleep labs. Increasing effort seen in the thoraco-abdominal belts, flattening in the sum channel, concomitant snoring, flow limitation in the pressure transducer (even if the sleep laboratory is not using pressure transducers in the diagnostic, they're definitely using them in intervention), and the use of suprasternal notch pressure transducers are all diagnostic aids in identifying UARS...

Is there really such a thing as an unresponsive flow limitation? If such a "fixed" obstruction exists (and in re: prevalence, we're talking about a subset of a subset), we have to consider what it is actually unresponsive to. Saying it's exclusively pressure ignores the equally dynamic force in "pressure" therapy, which is flow. Pressure gradient seen because of fixed obstruction can be largely, if not completely, overcome by flow. Just because an obstruction is not affected mechanically by pressure does not mean it is not affected whatsoever.

If you meet diagnostic criteria for UARS (like AHI <5, RERAI >10), then we would expect some sort of improvement during titration. Or alternatively, UARS that is unresponsive to pressure therapy probably isn't UARS, or at the very least, there are significant other issues underfoot. If during titration, the underlying sleep architecture continues to be a train wreck (delayed sleep latency, increased WASO, WAFA, Stage 1, arousals and awakenings) then there is more searching to do.

...CPAP titration unto itself can be a good diagnostic tool for UARS (i.e., it disappears with pressure therapy).

...let's say there is truly a fixed resistance component in a specific case of UARS. A different strategy may be considered, for instance, utilizing a somewhat more aggressive flow-based approach (basically a pressure-support methodology) to overcome the work of breathing associated with the resistive forces. Ideally, this would take the form of some form of Proportional Assist Ventilation, but might also be accomplished through the use of bilevel support (and consider tailoring inspiratory waveforms by adjusting rise time when available), or in a rudimentary form, through the use of EPR.

One must view this strategy in the light of a very important concept. When looking at UARS under ambient conditions, the body is breathing in a "negative pressure" mode. Diaphragm drops down, negative force in the airway is generated and breath is drawn in. Unfortunately, this negative force can serve to collapse unstable airways. As positive pressure is applied, particularly bilevel, increasing positive pressure is applied during inspiration, and breathing is done in a "positive pressure" fashion. While distendable structures may be mechanically dilated, another effect is the relief of some of the Work of Breathing that would have normally be needed to overcome the forces of resistance. And relief from the negative pressure swings.

If there is a "fixed component", your ENT guy will tell you this because he can see all that stuff. Posterior airway space is inversely proportional to RERAI, so it's not like UARS, even from a "fixed" source, can hide anywhere.

Even if all else fails, you can still get a PSG and monitor with esophageal pressure and get supporting documentation, but I'd be looking in a lot of other places before I'd look there. You got 80-something other sleep disorders floating around out there, and trying to necessarily stuff a square diagnosis into a round symptom hole (besides being a backwards approach) is gonna be tough.

In response to your original question, there is another area of concern. If we believe that pressure therapy in the treatment of UARS has a Narrow Range of Therapeutic Value, which we do, and that a constellation of co-morbidity exists that serves to create an overall low arousal threshold, then anything that delivers pressure outside of your NRTV (like screwy APAP response or arbitrarily wingin' the pressure dial around) stands a good chance of making everything substantially worse.
SAG

[SleepySandy]

Some of these responses are cracking me up. Which is much needed for my tired self. Please keep the humor coming.

I didn't give a lot of background in my first post because I didn't want to muddy the waters, but based on some of the responses, I'll share more info:

I was diagnosed with both UARS and OSA via a PSG. My AHI was 14.1. My arousals were 462 total / 64.5 per hour. My titration study got my AHI down to 0.7. However, my arousals were left at 92 total / 22 per hour. My 2 studies are side-by-side in another post if you are so inclined: viewtopic.php?p=147614&highlight=#147614
The side-by-side info is on Page 2.

I'm still having debilitating fatigue, which is even considered excessive by my sleep doc. I've been trying to research the possible culprit. I'm wondering if my pressure is incorrect. While my pressure (10) got my AHI down, my arousals were still pretty high.

I'm working on a couple of assumptions here which might be incorrect. My highest arousals during my titration study were listed as "Snoring" (50 total / 12 per hour). In that same place on my initial study, "Snoring" is listed as "RERAs". I'm assuming they are referring to the same thing. And, my leap here is RERAs are UARS events. I have no idea if that's correct.

Assuming my logic is right, I've been wondering if an APAP would recognize my UARS events and indicate if my pressure is off. Maybe I should be asking if an APAP recognize my RERA events. In case they're not the same thing.

[SleepySandy]

SAG - There's much in your post my tired brain just can't sort out.

As positive pressure is applied, particularly bilevel, increasing positive pressure is applied during inspiration, and breathing is done in a "positive pressure" fashion.

What is bilevel pressure? Is that the pressure from a BIPAP? I thought a BIPAP was pretty much like a CPAP except on exhalation it has a much lower pressure. Can that matter for UARS?

anything that delivers pressure outside of your NRTV (like screwy APAP response or arbitrarily wingin' the pressure dial around) stands a good chance of making everything substantially worse.

It doesn't feel like things can be worse than they already are. I'm sure they could be. But it doesn't feel like it. However, please elaborate on the "screwy APAP response" comment.

[StillAnotherGuest]

Well, so far you've gotten rid of 80% of the arousals and 95% of the respiratory events by AHI, and yet you still say

My fatigue is completely debilitating. I'm much more tired than I was before my first sleep study.

I think that you have to strongly consider that one or more entities is underfoot. A good start would be to get a hold of those histograms and examine the medications to try to figure out if the thing you're trying to fix is the thing that needs fixing.

I'm working on a couple of assumptions here which might be incorrect. My highest arousals during my titration study were listed as "Snoring" (50 total / 12 per hour). In that same place on my initial study, "Snoring" is listed as "RERAs". I'm assuming they are referring to the same thing. And, my leap here is RERAs are UARS events. I have no idea if that's correct.

I think they are referring to the same thing in re: snoring arousals and RERAs, but there's no such thing as a UARS event. And by definition, you don't have UARS. UARS needs AHI <5 and RERAI >10, and your AHI is 14+ with a bunch of desats. Your interpretation, if that was transcribed correctly, said:

what was most impressive was the frequency of relative airflow limitation that was terminated by an arousal/snore as is seen with upper airway resistance syndrome (UARS).

Cause here's why you have to be a little careful with this. There is a connection between UARS and the functional somatic syndromes (which might offer an explanation for debilitating fatigue) but having a bunch of flow limitations mixed into a positive OSA PSG don't make it UARS.

BTW, was position accounted for in the study (like AHI worse when supine, or RERAs only when lateral, etc.)?

Maybe I should be asking if an APAP recognize my RERA events.

Some algorithms respond to flow limitations. But a RERA is actually a neuro event (an arousal) so technically, they can't directly address them.

What is bilevel pressure? Is that the pressure from a BIPAP? I thought a BIPAP was pretty much like a CPAP except on exhalation it has a much lower pressure.

BiPAP is a brand name of bilevel. Bilevel provides a base therapeutic pressure (EPAP) and then adds support to inhalation (IPAP). BTW, this is the opposite of EPR in the ResMed machines, which has a base therapeutic pressure and then reduces support in exhalation.

please elaborate on the "screwy APAP response" comment.

One good way would be to select an algorithm that's overly aggressive in event identification and confuse it with a high rate of arousals and sleep fragmentation.

Another BTW, if we consider what happened upon application of CPAP (Total Sleep Time reduced from 430 to 251 minutes, Total Wake Time increased from 78.5 to 155 minutes, and Sleep Efficiency reduced from 84.6% to 61.7%), and consider the possibility that this is still happening, just imagine what would happen if you do have a NRTV and exceeded it with an APAP. (I can hear the wheels turning. Yeah, maybe you already have). Or maybe you simply exchanged one problem (OSA and high arousal rate) for a different one (exceptionally poor sleep efficiency}.

It doesn't feel like things can be worse than they already are.

Again, fixing 80-95% of your OSA issues and you're still at rock bottom? Time to open up some more options. Get the histograms, we can take take a look at event and sleep stage location, and let's see the medication list.
SAG

[SleepySandy]

Hi SAG

Thanks for responding again.

You put things in quite a different perspective when you say:

Well, so far you've gotten rid of 80% of the arousals and 95% of the respiratory events by AHI

I've been focusing on the remaining arousals because I'm still so tired. I hadn't looked at it the other way around. I guess I should look at the positve side.

I think that you have to strongly consider that one or more entities is underfoot. A good start would be to get a hold of those histograms and examine the medications to try to figure out if the thing you're trying to fix is the thing that needs fixing.

I'm working on getting the histograms. I'm hoping to have them this week. I absolutely agree that my medications may be contributing to some of this and need to be examined. I'm just a little reluctant to post them on a public forum.

I think they are referring to the same thing in re: snoring arousals and RERAs, but there's no such thing as a UARS event. And by definition, you don't have UARS. UARS needs AHI <5 and RERAI >10, and your AHI is 14+ with a bunch of desats. Your interpretation, if that was transcribed correctly, said:

what was most impressive was the frequency of relative airflow limitation that was terminated by an arousal/snore as is seen with upper airway resistance syndrome (UARS).

Cause here's why you have to be a little careful with this. There is a connection between UARS and the functional somatic syndromes (which might offer an explanation for debilitating fatigue) but having a bunch of flow limitations mixed into a positive OSA PSG don't make it UARS.

It's transcribed correctly. Now I don't even know what to think. When I had my appt. with my sleep doc, he did say it's UARS - he even went into a very lengthy explanation of the physical mechanics of UARS and how the body has to work harder to breathe when the airway narrows and how that extra work is what causes the arousals. I will admit he lost me for a while, particularly when he made a comparison to a garden hose. I think he was trying to make it easier to understand, but he really didn't.

BTW, was position accounted for in the study (like AHI worse when supine, or RERAs only when lateral, etc.)?

I don't know yet. My summary results don't have any positional information. I requested a copy of all of the data from my sleep study. I'm assuming there's more than the histograms. I'll let you know when I have the information.

consider the possibility that this is still happening, just imagine what would happen if you do have a NRTV and exceeded it with an APAP. (I can hear the wheels turning. Yeah, maybe you already have).

Nope. I haven't. I don't have an APAP. I'm still on CPAP and just hunting for information.

Again, fixing 80-95% of your OSA issues and you're still at rock bottom?

Yep. And it is really, really hard. My sleep doc thought it was weird, too. He ordered a bunch of blood tests. I got a call about those yesterday. As I expected, they were all normal. I did request a copy of the bloodwork report along with my sleep study - basically, I requested my whole file.

I really appreciate all of your input.

Sandy

[StillAnotherGuest]

I absolutely agree that my medications may be contributing to some of this and need to be examined. I'm just a little reluctant to post them on a public forum.

The problem with "them" is that besides being notorious REM suppressants (not a big deal), "they" can also destroy sleep architecture and generate tons of arousals (a big deal). Not all of "them", however.

just imagine what would happen if you do have a NRTV and exceeded it with an APAP. (I can hear the wheels turning. Yeah, maybe you already have).

I don't have an APAP. I'm still on CPAP and just hunting for information.

I know, what I mean is, maybe even 10 is too much and you're outside of your NRTV. Don't assume anything yet.

BTW, "NRTV" is another acronym I made up. I'm not sure if I really like it yet, I keep getting images of NASCAR Television in my mind. Go #24.
SAG

[blarg]

I absolutely agree that my medications may be contributing to some of this and need to be examined. I'm just a little reluctant to post them on a public forum.

Consider sending SAG a pm of your medication list. Click on the "PM Me" icon under one of his posts. Only he'll be able to see the list then.

[SelfSeeker]

Hi Sandy,

I saw this post as I wanted to see what is written here about UARS.

So to your original question:

I've been wondering if an APAP can recognize UARS events. If it does, what's it looking for? Does anyone know?

I do not think there is anything for UARS to regognize in the sense of an event.

I think events as simple as flow limitations will cause UARS to arose you.

If I understand it properly UARS is more to do with neurological events that sense the slightest decrease in Oxygen. Which aroses you so you wake up. Over and over again.


AHI may not show a problem but "RDI" on other lab software reports -- Respiratory Disturbance Index -- a count of "events" that are happening.

Depends on how all the various things are read on PSG and which criteria are being used.

To you and your body and health it makes a difference.

I think AHI is being used by insurance so less money has to go out for testing, supplies etc.

I have question thought:

If even flow limitaitons disturbe the sleep, should the pressure not be higher to prevent any kind of collapse from even starting?

Would a stright auto at a higher pressure (not high enough to cause centrals) be better?