General UARS Discussion

-SWS wrote:[

2) All FL should be targeted for elimination---not just the ones accompanied by RERA's and/or PES criteria (again a novel view)

Well, the creators of the Autoset were saying this in 1998...
http://thorax.bmj.com/cgi/content/full/53/suppl_3/S49 (registration for papers older than 2006 is free)

Copyright © 1998 BMJ Publishing Group Ltd & British Thoracic Society.
Thorax 1998;53(Suppl 3):S49-S52 (October)
Intelligent CPAP systems: clinical experience
H Teschlera, M Berthon-Jonesb
a Ruhrlandklinik, Abteilung Pneumologie- Universitätsklinik, Tüschener Weg 40, D-45239 Essen, Germany, b ResMed, 82 Waterloo Road, North Ryde, NSW 2113, Australia


AutoSet algorithm: elimination of silent inspiratory airflow limitation
Montserrat and colleagues4 and Condos et al3 have shown that reducing the CPAP pressure by as little as 2 cm H2O below the optimal level produces silent inspiratory airflow limitation with partial collapse of the upper airway and typically a fourfold increase in oesophageal pressure swings. It seems reasonable to assume that the cost in side effects of increasing the titration pressure by 2 cm H2O will be outweighed by the benefit of the 75% reduction in work of breathing. The AutoSet system therefore titrates not only to eliminate apnoeas and snoring, but also further increases the mask pressure in the presence of flattening of the inspiratory flow-time curve, suggestive of unresolved silent inspiratory airflow limitation.17

ozij wrote:

-SWS wrote:[

2) All FL should be targeted for elimination---not just the ones accompanied by RERA's and/or PES criteria (again a novel view)

Well, the creators of the Autoset were saying this in 1998...
http://thorax.bmj.com/cgi/content/full/53/suppl_3/S49 (registration for papers older than 2006 is free)

I think it's worth noting that the flow-limitation (pressure response) strategies actually need to differ between any unattended APAP algorithm and a manually-attended PSG titration. The unattended single-channel APAP algorithm has absolutely no way to differentiate a perfectly benign series of flow limitations from those accompanied by Respiratory Effort Related Arousals (RERAs). Additionally, the occurrence of APAP-measured FL is typically used to ascertain and strategically avoid collapsible Pcrit designated by that highly generic Starling Resistor model commonly employed by APAP algorithms.

Dr. Krakow very clearly called his own views about using a vast BiLevel PS to round out both the inspiratory and expiratory flow curves as a "working theory".

While I'm still extremely skeptical that aggressively treating FL unaccompanied by any arousals makes sense, I think the idea of using a large BiLevel PS to address Respiratory Effort Related Arousals makes enormous sense (completely absent of any undesirable pressure-related side effects, of course). A larger BiLevel PS literally decreases the Work Of Breathing (WOB). That scientific term WOB is literally about "respiratory effort". If you decrease the WOB, then you clearly also decrease "respiratory effort". And how might clinicians plausibly decrease RERA's? By decreasing the respiratory effort or work of breathing.

Hence using BiLevel PS to decrease RERA's by decreasing respiratory effort or WOB makes enormous sense to me. I think Dr. Krakow's on the right track by using a significant BiLevel PS to address RERA's----as long as undesirable pressure-related side effects do not occur and the RERA's are, indeed, nicely addressed.

I would also point out that since UARS-related WOB/respiratory-effort is directly associated with "upper airway resistance" that also affecting easy reductions in nasal impedance probably makes great sense toward reducing the "work of breathing"----and thus presumably reducing the required PS setting on a BiLevel machine. In my own way of analyzing, managing to achieve a lower feasible BiLevel PS may also minimize the potential for any undesirable pressure-related side affects associated with either high IPAP or vast PS.

If I recall, Dr. K. seemed to indicate that the observations involved in that working theory suggested that the pressure support needed to be individually customized for each patient. Some seemed to do better with high PS, others with low (2 or 3). And that falls outside present views of PS, too, I think, since I understand that bilevel titrations generally start off with a spread of 4 cm.

And is the science really all that exact in precisely lining up FL, EEG, and O2 in the lab? Isn't there a bit of wiggle room for judgment by the tech? For example, even though I am sure there are clear guidelines, could it be that some FLs might be scored RERAs by one tech and not by another?

jnk wrote: could it be that some FLs might be scored RERAs by one tech and not by another?

I personally get the distinct impression that there's an enormous challenge with clinicians correctly and uniformly scoring RERA's throughout the field.

And I think that just may be the crux of why Dr. Krakow is essentially suggesting: "Let's ditch that dysfunctional status-quo UARS/FL protocol reflected in DSM-IV and ICSD.... Rather, start indiscriminately treating all FL as if they were UARS, and your patients---on whole---may have the significantly improved results that we think our patients are having."

Then he goes on to suggest using vast BiLevel PS as a very plausible way to treat "work of breathing" problems that are related to upper airway resistance. Very novel thinking in my opinion. Not at all UARS status-quo.

-SWS wrote:

jnk wrote: could it be that some FLs might be scored RERAs by one tech and not by another?

I personally get the distinct impression that there's an enormous challenge with clinicians correctly and uniformly scoring RERA's throughout the field.

And I think that just may be the crux of why Dr. Krakow is essentially suggesting: "Let's ditch that dysfunctional status-quo UARS/FL protocol reflected in DSM-IV and ICSD.... Rather, start indiscriminately treating all FL as if they were UARS, and your patients---on whole---may have the significantly improved results that we think our patients are having."

Then he goes on to suggest using vast BiLevel PS as a very plausible way to treat "work of breathing" problems that are related to upper airway resistance. Very novel thinking in my opinion. Not at all UARS status-quo.

I think your way of putting that hits the nail squarely on the head.

Some may call that approach "treating UARS" while others call that approach "tweaking PAP therapy for OSA." A distinction without a difference, in practice, in my opinion. A UARS, treated by any other name, would rest as sweet.

Nevertheless, I hope all such research continues to get at the bottom of exactly what is happening and how best to treat it.

It is interesting to me that many international researchers refer to OSA as a syndrome--Obstructive Sleep Apnea-Hypopnea Syndrome. Maybe one day General UARS can order that it henceforth be called OSAHFLAS--Obstructive Sleep Apnea-Hypopnea/Flow-Limitation-Arousal Syndrome. Or maybe: BBANSTS: Bad Breathing At Night Sleepy/Tired Syndrome.

Am I being a bit reductionist? I never know.

You know what this thread needs? Some GRAPHS!

jnk wrote:If I recall, Dr. K. seemed to indicate that the observations involved in that working theory suggested that the pressure support needed to be individually customized for each patient. Some seemed to do better with high PS, others with low (2 or 3). And that falls outside present views of PS, too, I think, since I understand that bilevel titrations generally start off with a spread of 4 cm.

Agreed---that Dr. Krakow never suggested that vast BiLevel PS should be indiscriminately employed.

Rather, his zero-tolerance flow-limitation policy suggests that it's really residual FL that should be indiscriminately targeted for elimination. That very plausibly may be accomplished with little or no PS at times(that gap between IPAP and EPAP). However, that zero-tolerance flow-limitation policy will quite often require an unusually big cannon by the way of a vast BiLevel PS.

jnk wrote:Some may call that approach "treating UARS" while others call that approach "tweaking PAP therapy for OSA." A distinction without a difference, in practice, in my opinion.

This may be one point where we can politely disagree. I think the term "tweak" for a whopper of a BiLevel PS value may actually short-change what is a pressure-aggressive and novel treatment method for residual FL. I don't think very many clinicians were previously employing that vast PS to treat residual FL. And in my opinion, it deserves to be underscored for the novel and pressure-aggressive suggestion that it is rather than relegated to the more routine category of "tweaks".

I think it's highly plausible as a treatment method. IMHO it deserves prominent discussion as a novel and potentially viable way to treat Work of Breathing (WOB) or Respiratory Effort that is related to upper airway resistance. On-whole it may be the wrong way to treat UARS (or FL associated with excessive upper airway resistance). But it may very well be a treatment method that the entire sleep industry should very strongly consider adding to their repertoire of viable treatment methods for daytime somnolence associated with residual FL: discriminately and aggressively employing a significant BiLevel PS to decrease upper-airway-resistance associated WOB.

As a side-note, I recall reading that excessive WOB alone, during sleep, is viewed by some researchers as sufficient to leave COPD patients feeling tired or fatigued the following day.

If so, are we really surprised that Dr. Krakow's obstructive SDB patients also seem to feel more refreshed the following day---- since he very methodically decreases their WOB associated with upper airway resistance? And that daytime improvement may plausibly be irrespective of measured frank arousals during sleep IMHO.

-SWS wrote: . . . This may be one point where we can politely disagree. . . .

I like it when you disagree with me; that's when I learn the most. And frankly, I've never seen you be impolite with anyone, -SWS, even a few times when I've secretly wished you would be. Indeed, it is your presence in this thread that has allowed me to feel safe trying to play doctor's advocate. It's hard to learn this stuff, when, as DSM says, it is a moving target. It seems to be a nebulous area in more ways than one.

If you don't mind my asking, what's your take on the likelihood of a UARS sufferer becoming an OSA sufferer if left untreated? And what about those patients who are being told they have both, as seems to be what some docs are telling patients, according to some posts I've read on this board?

On page 6 of the topic Dr. Krakow started: (BILEVEL PAP Therapy Pearls: Clearing the First Hurdle)

viewtopic.php?p=243359#p243359
-SWS wrote: I don't think significant numbers of clinicians today frequently and readily accept such large PS values toward achieving rounded I and E curves as described below:

BarryKrakowMD wrote: Using a zero tolerance attitude about flow limitation, Dom titrated me to 18/14 (which we both thought insane since I’d been using APAP of 8 to 12 and rarely 10 to 14), and I titrated Dominic to 20 over whatever. It was around 4 am, and the assigned sleep tech kept saying, “are you sure that’s flow limitation?” My response, “I’m not sure, but it’s not rounded, so keep increasing until it rounds,” which it did at IPAP of 20.

From that point forward I started using bilevel at pressures around 14/10 and fairly rapidly worked my way up to 18/10…”and loving it!” to quote the immortal secret agent Maxwell Smart. Now, I'm at 21/12.5.


"Keep increasing until it rounds" LOL!!!!

jnk wrote:You know what this thread needs? Some GRAPHS!

I agree!!!

Given that my normal AWAKE breathing is slightly "flow limited" ....


This graph was first posted on page 3 of the "Bilevel Pearls" topic:
viewtopic.php?p=239799#p239799

The line labeled PTAF/CPAP that runs through the top of the letter W's (for "Wake") shows the flattened-on-top waveform of my flow limited breaths. The label called "chest" should be down farther, on the line that runs through the bottom of the W's.

Well, it's a jagged looking flattening in this closeup. But the point is, the breath waveform is not smooth and round. My usual breaths are "flow limited." Which is the reason I have to turn off IFL1 on a 420E autopap -- but that's a whole different story.

Anyway, flow limited breathing seems to get me through life, and through sleep with any-kind-of-PAP-treatment. Effective treatment with moderate pressures that leave me refreshed and well rested. And without trying to round out every last flow limitation.

I don't think I'd much like being titrated "until it rounds." Even though I do have a mask and a homemade strap that could take whatever IPAP pressure Dr. K's titration protocol could throw at it. IPAP 20? 25? 30? Have at it.

SWS wrote: that zero-tolerance flow-limitation policy will quite often require an unusually big cannon by the way of a vast BiLevel PS.

No kidding!

jnk wrote:
<snip>It's hard to learn this stuff, when, as DSM says, it is a moving target. It seems to be a nebulous area in more ways than one.

If you don't mind my asking, what's your take on the likelihood of a UARS sufferer becoming an OSA sufferer if left untreated? And what about those patients who are being told they have both, as seems to be what some docs are telling patients, according to some posts I've read on this board?

It's also hard to understand it when a lot of it just zips right over my head!

I am one of those who's sleep doc said I had both, actually more UARS (or RERA's, as he termed it), than AHI.

I'm I correct in understanding that something other than straight CPAP might be more beneficial for UARS? The tech had a dickens of a time titrating me because every time she tried to bump it up, I'd start to wake up and she'd have to back off and start again much slower. That makes me think I might be one of those that would do worse on a machine with changing pressure (other than CFlex). Any thoughts?

Pam

jnk wrote:what about those patients who are being told they have both, as seems to be what some docs are telling patients, according to some posts I've read on this board?

I think everyone in the medical community agrees that FL is not at all mutually exclusive of apneas and hypopneas. Then the big disagreement seems to enter the picture when doctors try to figure out just what the etiology of those problematic FL events might be, and whether they all deserve to be called UARS.

However, when you get to sleepy or fatigued patients who have almost exclusively FL (or even exclusively FL)---then I think many practicing doctors will understandably say "That must be UARS." I think there's a possibility that those FL-exclusive patients may be divided into two etiological categories (see below).

jnk wrote:If you don't mind my asking, what's your take on the likelihood of a UARS sufferer becoming an OSA sufferer if left untreated?

I think one of those proposed etiologic categories are the patients fitting Dr. Guilleminault's classic definition of UARS. I think those patients will almost always present RERA's associated with a hyper-reactive airway etiology. I think that etiology is probably mutually exclusive of latent airway arousal activity associated with apnea. I think those UARS patients are not likely to develop frank OSA or apneas.

However, I truly think there's a second etiologic category of patients who also suffer problems with excessive upper airway resistance. While the shared etiology between these two patient phenotypes is clearly high upper airway resistance, I think this second patient type lacks the hyper-reactive airway etiology typical of Dr. Guilleminault's description of classic UARS. But these patients may also initially present exclusively FL events. They may or may not present RERA's as a result of excessive respiratory effort. But if they lack that hyper-reactive airway etiologic component, then these patients clearly have a much higher probability of going on to presenting frank apneas typical of OSA.

In the medical field, doctors seem to be referring to both airway-resistance associated phenotypes as UARS patients. And yet I believe one of those etiologies entails low probability of OSA progression while the other entails a much higher probability. I think that latter patient phenotype shows up at the doctor's office all the time. And yet I think that latter phenotype is virtually remiss from classic UARS medical literature. I think we essentially have the classic UARS phenotypes mixing with that latter phenotype (lacking the hyper-reactive airway portion of the etiology).

Since both UARS phenotypes essentially have problems with respiratory effort or WOB that is related to excessive upper airway resistance, the treatment methods are going to largely overlap. But I think we can expect one of those etiologic phenotypes to be at greater risk of progressing onto frank OSA---much more than we would ever expect of that first hyper-reactive UARS phenotype.

If that second phenotype suffers daytime symptoms despite having no RERA's---and genuinely symptomatically improve with Dr. Krakow's treatment method of decreasing WOB----then research dollars may be well spent taking a closer look at the sustained biochemical-related pathophysiologic effects associated with WOB itself (rather than merely looking at RERA's and other classic UARS benchmarks for that second proposed patient phenotype)..

Great flow of discussion folks - very insightful - am enjoying this.

One comment I want to add re using PS the way Dr Krakow does. I tried doing this myself on my PB330 knightstar back in 2006. I set a gap of 7 CMs

Epap was 8 & ipap was 15. I ran that for 3 months & at the time was pretty well comfortable with it. Then I got my hands on a Vpap III that showed the nightly data & was shocked to see, at those same settings (8/15) 40+ AHI + lots of hyperventilation. I very quickly adjusted epap to 10 & that greatly reduced the AHI & then with further adjustments I got the lowest AHI readings when I dropped Ipap to 13. Also, the hyperventilation dropped away. I later did a new sleep study in early 2007 & was given a cpap titration CMs of 12 but told to stay with 13 if that was working well.

The reason I was on 15 CMs at all was that the sleep lab transcribed my original titration (which turned out to be 13) into a 15. So I managed to work out for myself what worked & the next sleep study confirmed it.

Now I know that Dr Krakow was chasing Flow Lims when running up the PS - but I just have this instinctive reservation about merrily pushing up PS in a Bilevel (vs an ASV machine). I know there is a contradiction in this attitude as my ASVs (both brands) regularly go up to 20 CMs Ipap (with epap at 10) & I don't believe I always know this is happening except, with the Vpap Adapt SV it causes mask leak/squeaks that then wake me (as they often do). I tend not to get these pressure induced leak/squeaks with the Bipap AutoSV (else I sleep through them). The machine data for both models shows I get a lot of leaks.

My biggest reservation about Ipap greater than 15-16 is mask management & the arousals that causes. I tend to think they then become the bigger problem. Naturally there are people who really need a titration in that 18 CMs region but they surely have to me in the minority & they have the biggest challenge in finding a working mask configuration.

DSM

For me, the real progress in the industry is how it has gone from one-size-fits-all, here's-a-box-that-spits-out-10-cm type of treatment to customizable treatment. So Dr. K.'s overall approach of trying stuff to see what works for people using whatever tools were at hand makes sense to me on that level. If he was getting a lot of referrals from other sleep docs, it would make sense for him to start from the assumption that "something else" might help--diffrerent ways of titrating, different ways of using a bilevel, different approaches to measuring response. And if OSA had already been titrated away on those patients, he had to find something else to "treat." I agree that, often, going experimental can mean walking a fine line between experienced expert and mental. I've been there. But I TRULY respect the fact that he was generous enough to share what he was seeing and what he was thinking, with the world and the members of this board.

After all, in a way, this board is full of people similarly thinking outside the box in the sense of seeing what works for them in adjusting their own pressures. We adjust our pressures until we see the best numbers we can get and we feel better, often using the only channel we have--flow. And a lot of people think we're crazy to do that. They think our chasing our AHI below 5 is silly. But some of us know from how we feel that it is worth a little more pressure. Others feel no difference, and lower their pressure back down. Obviously no one wants more pressure just for the fun of it. It is only worth the pressure if we feel results along with improved numbers. But as any of us adjust our own pressures, we are basically addressing flow limitations without knowing whether they are accompanied by arousals or not.

The Respironics autobilevel seems designed to allow large increases in PS at its discretion in chasing things (depending on how it is set up). Likewise, some autos claim to raise pressures in reacting to flattening, so I don't see that as all that odd of a thing to do.

For those reasons, I guess I still don't see how the approach Dr. K. was describing (even if at times extreme) is all that different an approach from ours, when you boil it down.

Maybe what he was attempting to fix shouldn't have been called UARS. And maybe everyone he saw was merely the formerly undertitrated being responsive to the gentle rocking of the bilevel. Either way, though, at least he was able to do for some people what many of us, in principle, are trying to do for ourselves.

[The more people who disagree with the above post, the better! ]

JNK,

No disagreement here

DSM

WearyOne wrote:I'm I correct in understanding that something other than straight CPAP might be more beneficial for UARS?

Well, Dr. Krakow has a working theory that a BiLevel machine might be highly effective for UARS, if the inhale and exhale flow curves are both deliberately rounded by adequate pressure. But I think that can still be considered "experimental UARS treatment".

WearyOne wrote:The tech had a dickens of a time titrating me because every time she tried to bump it up, I'd start to wake up and she'd have to back off and start again much slower. That makes me think I might be one of those that would do worse on a machine with changing pressure (other than CFlex). Any thoughts?

That's a tough one. If your arousals were related to pressure-sensitive receptors in the airway, for instance, then BiLevel with a high IPAP pressure may plausibly cause more arousals. However, there are other arousal mechanisms---and Dr. Krakow's experimental BiLevel treatment for UARS may actually treat UARS better than CPAP in some or perhaps even many cases. I personally think the jury is still out regarding the use of BiLevel treatment for UARS.

I think if I received good UARS treatment results from CPAP, then I'd stick with that (I don't have UARS). However, if I felt there was plenty of room for improvement in my UARS treatment, then I'd probably try Dr. Krakow's BiLevel method.

jnk wrote:But I TRULY respect the fact that he was generous enough to share what he was seeing and what he was thinking, with the world and the members of this board.

I absolutely agree with that.

I still think there's even a chance that reducing Work of Breathing (WOB) associated with high Upper Airway Resistance (UAR) may yield important following-day benefits for many SDB patients---benefits that are not currently measured by classic UARS benchmarks. If so, I think that's a potentially important find. On that basis alone I personally wouldn't dismiss Dr. Krakow's current experimental BiLevel work. He may be onto something important.