UARS: A Critical Link to Optimizing PAP Therapy Results

[rested gal]

I believe that the current quantitative data in most of the machines I’ve dealt with represent incomplete data

I agree. I'm not sure if attempts to get rid of all flow limitations by looking at the very limited data at home would work at all in most cases. Nor, apparently, could it be accomplished in most cases with a cpap or autopap even if a person could see the inspiratory curve the way it is shown in a PSG.

As I understand it, it's not only the higher IPAP pressure; but also, for many people apparently it would take a much greater difference than usual between IPAP/EPAP (inhale/exhale pressures)...if totally eliminating flow limitations is the goal.

Recalling what Dr. Krakow mentioned in his initial post in this thread:

Should you be able to produce the same results with CFLEX, APAP, etc? Presumably so, except for one “large” difference. You cannot generate the same gradient or gap between IPAP and EPAP with any of the other devices. And, in our clinical and research experience, we are using gaps of 4 to 12 cm of water in our patients. My personal bilevel settings are 21/12.5 for a gap of 8.5.

In our prescriptions for bilevel, I would venture that the average gap is in the 5 to 6 range with tremendous variation, including some with a gap of only 2 or 3. Those with a lower gap requirement would likely do as well on FLEX or APAP, but to repeat, the large majority of our patients have a gap of 4 or greater.

Of course, so much about any kind of xpap therapy is a tradeoff. If increasing IPAP to the point that all flow limitations disappear were to consistently cause aerophagia to a painful degree, a person might prefer to back down some. Likewise, if high pressure caused a significant (a few wouldn't worry me) number of centrals that didn't subside as the nights went by and the body got used to the change.

Even with a bilevel machine and with software, I doubt that most people could simply tweak themselves at home into "no flow limitations" settings. Without a PSG bilevel titration where the repiratory curve can be readily seen as the IPAP is increased, it would be a great big guess, at best.

The information from our machines at home can't show the picture we'd need to see -- to know when the goal (no flow limitations) was accomplished. That would take a PSG (polysomnogram) hookup in a sleep lab.

I'm a dyed-in-the-wool dial twirler...lol...but even I would hesitate to go cranking the IPAP up, up, and up...and trying to go by how I felt the next day. If I were going to go all out in pursuit of knocking out flow limitations completely, I'd definitely want to be hooked up to PSG in a sleep lab.

I suspect it would take a LOT of IPAP to do that for me. I also suspect (wuss that I am about pain, and having experienced extremely painful areophagia at times even using a bilevel at moderate pressures) that aerophagia would make me decide the tradeoff wasn't worth it.

Or, to put it another way:

If the goal is normal breathing, then the question should be at minimum, “will normal breathing yield normal sleep?”

I don't think I'd be able to get normal sleep if IPAP were raised high enough to round out my inspiratory curve. I think aerophagia would hit first. But, I can't really know that. Maybe it wouldn't take as much "extra" pressure as I guesstimate, having seen the histogram of my usual inspiratory wave form. The wakeups I think I'd experience from aerophagia would not result in "normal sleep" for me.

But this is all speculation on my part. Without trying it during a PSG bilevel titration, there's no way to know.

Sad to say, it’s also apparent that many of you do not believe you can rush back to a sleep lab and get a great bilevel titration.

Cost -- whether paying out of pocket or trying to convince insurance to pay for another study -- is what would stop many, I think. Even if people wanted to give it a try and were confident that the lab would do that kind of bilevel titration.

[Snoredog]

I'd set EPAP to where I know my apnea is taken care of, then bump IPAP by 4-6 cm higher or using 4-6 cm pressure support. I have EncorePro at least I could see something coming from it.

[Snoredog]

-think something is going on here with the database, posts are running together.

[rested gal]

That's a very interesting thread, Snoredog. Thanks for the link!

One caution, plea...whatever you want to call it... if anyone goes there to read it, that's a message board that was created by sleep techs for sleep techs. It's not an apnea support board for "cpap users" like cpaptalk is. There's no law that a "cpap user" can't post there, but I really don't think that would be a good idea.

Read that board, sure. But I don't think it's a good idea for a cpap user (ok, ok...."patient"!!) to post questions over there. That's a place for techs to discuss things with each other and....well, I just figure they'd like to get away from having to explain things to patients. They probably have to answer enough questions in their night-to-night work.

I've lurk-read there for several years, but I would never, never, ever post there. I just wouldn't.

[Guest]

Hi,

I had checked with the sleep-lab....My doctor said that if one's titration pressure increase too fast in a short time that can cause central apnea and this cause distortion!!!!!

Support Level: If the air pressure at "support level" is too low will cause apnea and this support level needs to be high enought to open up the airway. A crucial point to have low apnea.

Resistant Level: If the air pressure at the "resistant level" is too low will not be able to given full treatment. As the air pressure increases for most of the auto-pap the pap algorithm play a main part in order to sense whether is the air pressure is able to delivered succefully, in this case THREE tries, if not sucessful the auto-pap will reset to start all overall again.

So this the algorithm that expalined but nothing been emantioned about the anxiety and round curve in bipap as yet.

Mckooi

[track]

Great post RG, seems Bi-level works by allowing you to stop where CA's may start to kick in and as we know they are not a problem only an indicator of unstable sleep.

Are you thinking you would still have difficulty with aerophagia if EPAP was limited to where it just eliminated apnea (and avoided CA's) that the higher IPAP would still contribute to aerophagia?

For me (without medical insurance) cost of a PSG would be a deciding factor, purchasing a Bipap Auto would be more economical way to go, afterall I've had several titrations and they haven't been able to hit that magical mark yet.

I would be more inclined on spending $1225 for a new Bipap auto then blowing $5000 on another PSG.

I agree with RG that aerophagia plays a big part in shaping pressure. I have for all practical purposes given up trying to find the point where apneas stop when sleeping on my back(because of aerophagia) so I have restricted myself to side sleeping at a lower pressure.

I think sometimes we focus too much on cpap therapy and put all the responsibility on cpap in our attempts to feel better during the day. One should not just focus on AHI or cpap factors. There are so many other factors that go into good sleep that can be controlled by our daytime activities. The amount of exercise, our diet, minimizing stress. cessation of smoking, amount of drinking, being over medicated, quality of bed, etc etc.

[krousseau]

I am going to start a new thread on aerophagia

[BarryKrakowMD]

This topic keeps coming up, but I've not heard anyone mention the relationship between leg jerks (periodic limb movement disorder) and air swallowing. When an SDB patient also suffers from PLMD, they kick, wake up and swallow the air. In our clinical experience more than 50% of patients with aerophagia have PLMD, and when it's treated most of them report a decrease or elimination in aerophagia. Now here's a big surprise (coming from me), we also see a reduction in aerophagia when we switch patients from CPAP to bilevel, but not as much as I would like to see, and not as much as those people whose aerophagia was caused by leg jerks. Last, I've seen a few patients where the ENT doc stated the patient had an anatomical susceptibility to aerophagia, but there was no treatment that worked for them.

[krousseau]

PEEMD??? Periodic Epiglottal/Esophageal Movement Disorder-can I have naming rights or is it already taken?

Are there any numbers to indicate how much the Repironics under reports FLs? For example ithe machine/Encore reports 10 FLs-is the total really more like 20, or 30?

[track]

Interesting...just the other day I was thinking I haven't had those violent jumps when I first go to sleep or the restless leg like I used to have prior to starting cpap about a year ago......but maybe these are things an individual can't judge for themself.

[krousseau]

Bump-thought it was worth keeping on Page 1 for one more round.

[johntee]

I'm not sure if attempts to get rid of all flow limitations by looking at the very limited data at home would work at all in most cases. Nor, apparently, could it be accomplished in most cases with a cpap or autopap even if a person could see the inspiratory curve the way it is shown in a PSG.

As I understand it, it's not only the higher IPAP pressure; but also, for many people apparently it would take a much greater difference than usual between IPAP/EPAP (inhale/exhale pressures)...if totally eliminating flow limitations is the goal.

Great thread! I'm wondering if I've found my "Eureka" moment...
A question about this idea of using BiPAP to successfully control events that are not being adequately controlled via CPAP or AutoPAP --

I've noticed (thanks to JSkinner's wonderful Encore Pro Analyzer) that the pressure I need to best control Apneas is about 5cm. (I start to get some Centrals if I go alot higher.)
Meanwhile, I seem to need 9cm to best control Hypopneas.
And 8cm for Flow Limitations, and 11cm for Snores (neither of which occur in great quantities), so let's just focus on the 5cm for Apneas and 9cm for Hypopneas...

I've been wondering for a few weeks if there was just a lack of a single setting that would adequately treat my events, each of which seemed to need varying numbers.

Do you think a BiPAP, say set to 5cm Exhale and 9cm Inhale pressure, would prevent the Apnea events (without creating Central events) while also addressing the Hypopnea events?

Do Apnea events happen exclusively/predominantly on the Exhale, and Hypopneas on the Inhale? I've seen two posts in this thread that say different things --

• krousseau's post on Dec 17 suggests the forces that lead to collapse don't happen when you exhale. While split_city's response, also on Dec 17, says "the airway generally collapses either towards the end of expiration or at the end of expiration in OSA patients. This is a time when the dilator muscles around the neck are electrically quiet, leaving the airway exposed to mass loading by the surrounding tissue/fat. This is referred to as passive collapse of the airway".

Would a BiPAP give "the best of both worlds", essentially two different pressures for each breath cycle, one (Exhale) targeted at the Apneas, and one (Inhale) killing the Hypopneas? (Because none of us has a Pressure Transducer at home to see the Breath Curve, I'm ignoring for now the ultimate goal of eliminating all Flow Resistance, in favor of addressing just the major events for now -- Apneas and Hypopneas.)

[BarryKrakowMD]

I think it is a reasonable approach to find the EPAP at the lowest
number to eliminate apneas and then look for a higher number for IPAP to
eliminate hypopneas, but I would contend that this approach is still a
gross generalization of what really can prove effective. In other
words, it's just a starting point.

As I see it from clinical experience, you don't want EPAP to just
eliminate apneas, you want that curve to look normal on expiration.
Same with IPAP, you want it to look normal on inspiration.

Given the limitation of only working with data downloads and not having
access to a titration, though, I understand the conventional wisdom here
and the need to find a starting place with two bilevel settings.

But, the bigger question still remains: Is your goal still
directed at optimizing the response to PAP therapy? Occasionally, there
are individuals who get a great response just by eliminating apneas and
hypopneas. But, more commonly, you see more "great" responses in those
who have also eliminated the UARS component of their SDB.

Last, and not least, we have not discussed the factor of CAP or cyclic alternating pattern effect on the EEG. CAP is likely a critical barrier to success in a number of SDB patients, because abnormal CAP patterns will either cause direct sleep fragmentation in and of themselves or they cause respiratory instability, which in turn leads to an SDB event of some type.

Years ago, two camps argued about what UARS really indicated: the UARS camp and the CAP camp. Initially CAP proponents insisted that UARS was just a manifestation of abnormal CAP. Now, the two camps actively discuss their theories and have engendered some mutual respect for their ideas.

I only mention this point as another explanation for the greater value of the titration, because there are some SDB patients with "non-breathing" issues, such as CAP or leg jerks that impede progress in optimizing PAP therapy, and regrettably a data download won't suffice to resolve these types of issues.

[Guest]

Hi,

UARS is just one of the sleep disorder issue....many more like deviate septums, turbinates enlargement, pharlygeal, muscle tone, fat tissues, center apnea, psychological impact and many more. If one need to be fully detected of the real cause of sleep apnea there are procedures and protocoals need to be established between sleep expertise and ENT....MRI scan etc is just another part to have close look. Read the "Clete Kushida's Sleep Disorder Diagnosis and Treatment" text and you will open your eyes of how complicated the problems are. Many still in the search for real cure and solutions and none fits all in one solutions. CPAP with right setups of pressures and algoritms. sleep postures on left instead of supine, weight loss maintenace, medications and many more none still challenging espacilly adherances of each methods. But one thing is for sure as mentioned in the Kusida text....with CPAP treatment one live longer in general despite all the adherance and challenges live with cpap Any comment?

Mckooi

[ofarchesandants]

KHVN (and others) Please forgive this email if your query was answered as i'm looking at year old posts and haven't read them all yet. However what was said in Dr. Krakow''s email but not reiterated is that a primary function of bilevel in UARS is to prevent arousals caused by flow limitation. In other words the brain of someone, oh let's say like me, who does not snore and has few to no apneas and also few hypopneas, pulse oximetry that remains mostly in the high 90's but is also incredibly sleepy every day is due to a hypersensitivity of that brain to the slightest flow reduction. In other words the flow reduction is minor but the brain perceives it as a major threat, thus causing an arousal. So in that case the slightest pressure needed to prevent flow reduction would be preferable over a greater pressure that is designed merely at keeping the airway open because that greater pressure would also cause arousals. So the point here is to eliminate "AROUSALS" with the least amount of external stimuli and "NOT" to simply keep the airway open. If the airway is kept open but a high pressure is causing arousal and thus preventing adequate sleep you have not only not helped the problem but you may have made it worse.
cheers,
gregg )
(who is currently not on bipap but would love to be)