General UARS Discussion

[-SWS]

This whole area of SDB is a moving target and it is hard enough for us lay people to work through the complexities. Being a technical researcher I have enjoyed working through the mechanical & algorithmic aspects of the machines but issues like this get difficult when we read one persons view of UARS (Krakow) then get told he has it all wrong.

Sorry about all those technical researcher hardships.

[-SWS]

As a side note, there are plenty of white papers published by Dr. Guilleminault since 2004. You can click on Dr. Guilleminault's name in this recent white paper to yield much of his published work on Pubmed:
http://www.ncbi.nlm.nih.gov/pubmed/1923 ... d_RVDocSum

Similarly you can click on Dr. Krakow's name in this recent paper to yield his work:
http://www.ncbi.nlm.nih.gov/pubmed/1921 ... d_RVDocSum

While Dr. Krakow has plenty of well-respected white papers regarding nightmares, insomnia, post-traumatic stress, anxiety, etc., my hunch is the bulk of his UARS white papers and research may be down the road. He definitely has his sights set on UARS. And I think if he can somehow manage to find a way to empirically prove that all flow limitations are directly associated with UARS, he will literally turn all of medicine on its ear. Most researchers who acknowledge UARS as a condition, seem to require flow limitations that generate Respiratory Effort Related Arousals as minimum UARS criteria. Dr. Krakow simply requires flow limitation without the RERAs.

Why do I think scientific proof of Dr. Krakow's unique UARS theory has the capability to turn all of medicine on its ear? Because I think that would mean that episodic UARS is about as ubiquitous in the human population as the common headache. I think we all have flow limitations from time to time. Thoughts?

[dsm]

SWS

Is there a link to a Krakow quote where he reiterates that "all flow limitations are directly associated with UARS" -- I was sure I read it somewhere just in the past couple of days but now can't find a quote supporting what I thought I read which basically agrees with your point - have we got it wrong ?.

I came across these quotes from him but they appear to support UARS as related to but different. He mentions FLs & RERAS as common to UARS.

Cheers

DSM

QUOTE From the Krakow thread linked to earlier....
>>
2.Initial Response Followed by UARS Emergence. This was one of the first clues to the problem of titrations in general and UARS components in particular. Many patients reported this initial great response, lasting a few weeks or months, and then a gradual or sudden deterioration. When they returned to the lab, the pressure needed to be raised to eliminate "new" or "emerging" UARS. I'm of the belief that it is nearly impossible to get a perfect titration the first time, because the body needs to go through many adjustments. Having adjusted, the pressure almost always needs to be raised or lowered. At Stanford, the model in 1993 was full night diagnostic, followed by full night titration, and then retitration 30 days later.

3. Good FL numbers. It's not so much good numbers; it's normalized airflow, because it is not so easy to count UARS events. Still, you can find a way to count flow limitation events, and you certainly want to reduce them as much as possible. There are data from Rapoport's group that suggests that an RDI consisting only of UARS (FLs, RERAs) in the range of 15 to 20 is clinically significant, so a number lower than this level should be and usually is the minimum to shoot for. In our lab, we occasionally get some patients below 5, but it's the lab environment, which I think in and of itself prevents the "perfect" titration.
<<

>>
1. AHI. It's true that the AHI is all that Medicare wants to see, but if the sleep doc wants to build the case for the patient an RDI is critical to submit as well. If the RDI is greater than 15, then it meets AASM criteria and that carries weight (not a guarantee).

2. Pinning down the UARS diagnosis. It sounds like a UARS diagnosis was not made with advanced respiratory monitoring (as in, "...strongly suspected to have UARS..."). Again, this would be a lot stronger if esophageal manometry, pressure transducer, or EMG intercostal sensors confirmed the UARS diagnosis.
<<

[-SWS]

Doug, I just reviewed some of Dr. Krakow's old posts. What a trip down memory lane. I think he starts his earlier posts clearly equating flow limitations and UARS with comments like these:

most of these cases, assuming all other factors have been properly managed, reflect the persistence of flow limitation (aka upper airway resistance syndrome)

which means that you measure apneas, hypopneas and flow limitations (also known as RERAs or UARS).

RERAs. Just to be clear RERAs (respiratory effort-related arousals) are essentially the same as FLEs (flow limitation events).

A reminder that for all practical purposes, the following three terms are interchangeable:
· UARS (upper airway resistance)
· Flow limitation
· RERAs (respiratory effort-related arousals)

the optimal pressure has not been identified to adequately titrate out all the flow limitations (aka UARS).

To reiterate, the algorithms dealing with flow limitation (UARS) on these machines have not reached the state of "rocket science."

While I'll admit there's some wiggle room in those statements for lovers of debate, I also think Dr. Krakow atypically equates flow limitations with UARS---including his zero-tolerance comments that aim to eliminate all flow limitations regardless of lacking measured arousals. I don't think those strong virtual equations of flow limitations being tantamount to UARS are in agreement with the rest of the UARS-embracing medical community.

But Dr. Krakow seemed to eventually modify his own views just a bit regarding flow limitations in relation to normal sleep (or perhaps he finally shared reservations he always had):
viewtopic.php?f=1&t=26896&p=243501#p243501

In some of my earlier posts, I raised the question about what is normal sleep, and I offered the hypothesis that a normal sleeper might have little or no daytime sleepiness. Recently, we started looking at patients who claim they are normal sleepers, and in the first 3 individuals we tested all of them had significant flow limitations and flow limitation events (with arousals). They also had sustained flow limitations. Would I expect to see this in a normal? No. In hindsight, we probably lowered our guidelines just enough to let these people into the protocol.

One patient reported excellent sleep quality, yet he said he could doze off occasionally during the afternoon. Another said she slept great all through the night, but she started off the day with one cup of coffee. A third reported minimal sleep symptoms but was on a medication that might confound the results.

In sum, we looked at 3 people who said they were normal sleepers and they came close to meeting our standards, but not close enough. Still, they had flow limitations, and my bet is that if treated, they would see a reduction in sleepiness, caffeine use or perhaps some other improvement in function.

My point is that flow limitations probably do not equate to UARS but they come close, meaning that if you look hard and long for people who think they are normal sleepers, I think you will discover that many of them are not.

I think he's a good guy, by the way. And I really do think some very good UARS research is in front of him. However, another area where I think his views diverge with Dr. Guilleminault's relates to whether UARS is a separate and unique SDB condition than OSA. As with many doctors, Dr. Krakow seems to think UARS is part of the same disorder, but simply on the lower end of the continuum regarding degree of airway closure. Dr. Krakow thus contends that UARS is not at all mutually exclusive of apneas and hypopneas. As it turns out, that view actually makes for a more universal correlation between FL and UARS. In other words, that view can more easily support the contention that FL and UARS are essentially the same.

By contrast, I believe that Dr. Guilleminault and his thought-camp contend that UARS may very well be a separate condition than OSA. Unlike Dr. Krakow, that camp seems to think that UARS may be associated with hyper-reactivity to an increased inspiratory load (related to increasing upper airway resistance). Conversely they suspect that more severe airway closures associated with frank obstructive apneas may be associated with the opposite: hypo-reactivity to an increased inspiratory load (also related to increasing upper airway resistance). That view more easily lends to mutual exclusivity, since subscribers suspect the UARS patient's airway is overly sensitive and overly reactive, thus causing very early-stage RERA's. But that the obstructive apnea patient's airway may be essentially dulled or blunted to those same afferent signals, thus allowing for a more complete airway closure and late-stage blood-gas related arousals. Not only are the proposed disturbance mechanisms different, but they can plausibly be mutually exclusive: over-reactivity resulting in afferent-related RERA's typical of UARS, versus under-reactivity eventually resulting in a more severe airway collapse and blood-gas related arousals typical of obstructive apnea.




Opposing UARS views in 1999:

Upper Airway Resistance Syndrome Is a Distinct Syndrome

Upper Airway Resistance Syndrome Is Not a Distinct Syndrome

And that lack of consensus about UARS carries on to this day. That's science hard at work on one very mysterious SDB problem.

[dsm]

SWS

As you have highlighted many times, this is an evolving science & people's views from as little as 12 months ago could be quite different today, just as I am sure yours are, mine certainly are.

I wonder what Dr Krakow's views on this topic might be right now but, I see that if he saw a close correlation between UARS & FLs (this is our 'opinion', without his endorsement (perhaps words in his mouth)), then a humble pleb like me when reading his views might see UARS as closely related to a condition just above hypopneas. A limitation of airflow not serious enough to qualify as an obstructive event be it hypop or osa. Is the UARS condition out on its own ?, I wouldn't know, it may be when one considers the potential for heart damage, but this point seems to be still open to debate.

There was a doctor who posted in that Krakow thread about how he had been on a sleep study & was told he didn't have OSA or SA but was convinced his daytime drowsiness was likely to be fixed by xPAP therapy. He went on it and started to notice a distinct improvement over time. What I see in a man like him is someone who has an instinct for working out what might work or him then proving it. Some folk may have wanted to give him a hard time because their 'classic' view of OSA / SA said he had no basis for believing xPAP would help him because his AHI was below 5 despite how he felt during the daytime. I believe he ended up on Bilevel.

Anyway, this is a very interesting line of discussion (or debate - as per dictionary ).

DSM

[-SWS]

I wonder what Dr Krakow's views on this topic might be right now

I don't know. But I know his UARS and FL views are guaranteed to be vastly more complex than mine. That's for sure. But that alone wouldn't distinguish his as an unusual medical researcher. His ability to summarize his own highly complex medical paradigm in a way that virtually everyone can clearly understand is one incredibly rare and special skill IMHO. And I think his ability to think outside the established scientific box and potentially synthesize new paradigms make him a novel and highly valuable researcher as well.

There was a doctor who posted in that Krakow thread about how he had been to a sleep study & was told he didn't have OSA or SA but was convinced his daytime drowsiness was likely to be fixed by xPAP therapy. He went on it and started to notice a distinct improvement over time. What I see in a man like him is someone who has an instinct for working out what might work or him then proving it.

I absolutely agree. While I personally don't yet see compelling evidence to make me agree that flow limitations and UARS are as tightly correlated as Dr. Krakow suspects, we can clearly see that Dr. Krakow and his clinical team are looking very hard for other measurable indicators of UARS----besides the usual benchmarks such as FL, RERA's, negative esophageal pressure, etc. I honestly think that's research at it's best.

With that said, I was so glad to see that his prolific research and published papers continue in the key areas of dreams, post-traumatic stress, anxiety, nightmares, cognitive behavior therapy, etc. I personally feel that much-needed line of inquiry may very well yield important benefits to a larger affected population than even that of UARS. And IMHO that area of sleep research would sustain an enormous loss if it were missing Dr. Krakow's prolific key contributions.

[WearyOne]

Again, so glad, SWS, this had been brought up in a separate thread. Just last week, I decided I'd had enough of still feeling bad all the time and have started the ball moving to find the answer (sleep-related or otherwise) even if it eventually involves another sleep study to look at possible non-breathing-problem issues. I intend to have a long sit-down with the sleep doc after (if not before) my overnight pulse/ox (which still hasn't been set up yet, unfortunately).

My original sleep doc has left, which isn't bad because I like the new one better! But when the "old" doc went over my sleep study and titration, I noticed the "MH Index" had been crossed out and "ReRa" written in. He said those were ReRa's, another name for UARS.

RERAs are the pathognomonic events that define the upper airway resistance syndrome (UARS), which is manifested by the hypersomnolence that is the result of frequent RERAs. http://acronyms.thefreedictionary.com/RERA

1. AHI. It's true that the AHI is all that Medicare wants to see, but if the sleep doc wants to build the case for the patient an RDI is critical to submit as well. If the RDI is greater than 15, then it meets AASM criteria and that carries weight (not a guarantee).

My sleep center did RDI instead of AHI. On my sleep study, my RDI was 19; my AHI was 4.7. So, technically, I guess if they had only gone by AHI, I may not have insurance-qualified for cpap! (Desats went down to 85%, baseline averaged 92.5.) Titration comment "...9.0 cm eliminated OSA and RERAS and maintained..." Only had one REM cycle, though. (Sleep study had a total arousal index of 31.6, 18.6 of which were respiratory related. I know a lot more now and intend to find out what those other arousals were/are.)

I'm not really following all the technical stuff of what UARS is or isn't; all I know is I still feel rotten! Maybe UARS related or not. Maybe I'm still not getting sufficient oxygen or my heart rate is doing weird things when I sleep. Maybe it's not breathing related at all. Maybe it's not sleep-related at all. (Though I tend to think it is.)

Keep the discussion going, and please join in if you have UARS!

Pam

[-SWS]

Keep the discussion going, and please join in if you have UARS!

I'm hoping that anyone who has UARS can share absolutely anything they want to in this thread.

How did you learn you have UARS? Is yours a case of UARS with apneas and hypopneas, or without? What technique(s) work best for treating your UARS? Are there any UARS treatment techniques that worked poorly for you?

You name it! This is a general UARS chit-chat thread, and anything goes!

CALLING ALL UARS PEOPLE!
Any UARS discussion is great UARS discussion!

[WearyOne]

Do oxygen desats occur with UARS?

As I understand it, no. One of the hallmarks of UARS is that the arousals to "breathe better" (RERA -- Respiratory Effort Related Arousal) happen before the O2 has a chance to drop very much. Kind'a as if the brain was hypersensitive to the beginning of a hypopnea before that event can stay in place long to cause enough drop in O2 and get labeled "hypopnea."

In the Diagnosis section of the Medscape article -SWS linked, Drs. Gang Bao and Christian Guilleminault mention:

"Polysomnography reveals AHI < 5, oxygen saturation > 92%, and the presence of respiratory related respiratory arousals (RERAs) and other nonapnea/hypopnea respiratory events (Table 1 and Table 2)."
---
"not associated with a drop in oxygen saturation of 3% as used for the definition of hypopnea."

An AHI less than 5 and oxygen sats staying above 90% would be considered "normal" -- no "sleep apnea."

In a PSG sleep study, the presence of repeated Respiratory Effort Related Arousals (RERAs) is probably the most obvious clue that Upper Airway Resistance could be going on.

Thank you, RG, this is extremely helpful. My AHI was 4.7, RDI 19, but I did have desats down to 85%. Even though I'm still sleepy and tired most of the time, I'm not waking up with my heart pounding in my chest or with headaches, so I know cpap is helping my health, even though I obviously still have other issues going on. And before cpap, I woke up a lot, which I usually don't do anymore. But may be waking enough to mess up the sleep architechture, and not enough to remember it.

Pam

[jnk]

If a doc thinks a person may benefit from PAP therapy (or a dental device or something else) though the person doesn't meet the insurance criteria to get it, the doc can either use the measurements at hand to argue the person has a slightly different form of OSA by pointing at flow limitations or the doc can argue the person has something else with a different name. Or the doc can train the tech to fudge the numbers a little. (Isn't that the real reason for the line between sleep doc and tech--plausible deniability? ) It would be a lot easier if the diagnosis was just "SDB with accompanying fatigue/somnolence" and the issue wasn't what specific name to give it.

I'm not sure Dr. K.'s ideas are all that divergent from the rest of the researchers in the field--he has, in my opinion, simply chosen different words to communicate the ideas. I don't claim to understand much of what he says. But when he speaks of flow limitations, I think that may be merely a shorthand way of saying it involves breathing. The thing is that you only treat people who are sick, and that is assumed as understood in his discussions. It is true that in one sense everyone has flow limitations, since no one breathes perfectly. But in another sense, it is only the people whose imperfect breathing causes them fatigue or somnolence that honest docs are interested in giving treatment to.

Similar to the way a blister can turn into a callus, or the way tingling can precede numbness, it would make perfect sense to me that a throat going bad could either show up as hypersensitive or nonresponsive. Is that all part of the same process or are those two different processes? I have no problem with either way of looking at it. I guess that is why I divide up the issues of research definitions, insurance definitions, and what works in practice into three different areas of thought. When Dr. K. makes any statement about UARS that attempts to address all three realms of thinking simultaneously, he is going to sound wrong to at least two thirds of the people listening at any given moment.

So maybe we do need a General UARS to unite the realms!

I too am VERY interested in hearing anecdotal UARS stories. I like how you put it, -SWS:

I'm hoping that anyone who has UARS can share absolutely anything they want to in this thread.

How did you learn you have UARS? Is yours a case of UARS with apneas and hypopneas, or without? What technique(s) work best for treating your UARS? Are there any UARS treatment techniques that worked poorly for you?

I even agree with:

anything goes!

[-SWS]

I'm not sure Dr. K.'s ideas are all that divergent from the rest of the researchers in the field--he has, in my opinion, simply chosen different words to communicate the ideas.

That might be spot on. But I see his view as almost universally correlating FL with UARS. I haven't yet been able to pick up that same message from the other UARS researchers.

But for all I know that near-universal correlation between FL and UARS may be exactly where many or most of the other UARS researchers happen to be at the present regarding their own theoretical views. Doug makes a good point that views and evidence in this field can both change very fast.

So maybe we do need a General UARS to unite the realms!

I agree! If surgery can have its own general, then it only seems fair that UARS should have a general as well. And Colonel Sanders may have to take over the battle against General Tso's spicy chicken to get this whole UARS thingie straightened out. Where the heck is General Patent and his Bull Terrier when you need to call in strategical airway support?

[jnk]

. . . I see his view as almost universally correlating FL with UARS. . . .

I would not disagree with that view of his views, as I read them. If a tired/sleepy person with flow limitations improves, subjectively, with PAP therapy, I am guessing he would call that UARS.

[-SWS]

. . . I see his view as almost universally correlating FL with UARS. . . .

I would not disagree with that view of his views, as I read them. If a tired/sleepy person with flow limitations improves, subjectively, with PAP therapy, I am guessing he would call that UARS.

And I think that's where his present theory is hoping to push the UARS envelope a bit----in a potentially positive and UARS paradigm-changing way. He seems to very strongly suspect that UARS entails even more symptomology than that which is currently being measured. He may very well be right with that theory.

[riverdreamer]

OK, this is really long, but you did ask!

I’m not sure if I might have UARS or not, but it has been suggested to me. My primary care doc sent me to a sleep study after an echo showed pulmonary hypertension, which was a complete surprise. I have had very poor sleep for the last 16 years. In my first sleep study, my anxiety about night driving, and the study itself, caused enough reflux that I had to sleep propped up. That night I had an AHI of 1.3, with an arousal index of 13.5. My lowest O2 saturation was 90%. My few apneas were centrals, the hypopneas were claimed to be obstructive. They blamed everything on GERD, and sent me away.

My primary doctor felt very sure there was more going on. I rarely have reflux, and they were blaming everything on GERD. Now, I know GERD can be silent, but my doc was not convinced, so they agreed to a second sleep study, based on the fact that I was unable to sleep flat for the first one.

The second one, I planned for how to manage the possible GERD. While I don’t think I have GERD, I do have slow transit time, and they had me going to bed before my normal bedtime. So, I ate early enough to allow digestion. I also asked to be allowed to relax for while reading, so that when I lay down, I would not be as jazzed up as I was the first time. All of that worked just fine, and as predicted, I had no GERD symptoms in my second study.

This study showed an AHI of 6.2, with 10 central apneas, the rest obstructive hypopneas. O2 sats went as low as 91%. The arousal index was 18.0. This time, even with a diagnosis of mild sleep apnea, they said I didn’t need any treatment, because during the study I slept on my back, but at home I did not. Well, this was made up out of thin air, because what I told them was that I did not sleep propped up, but that I DID sleep on my back primarily. I sent a correction letter on this issue, as I have Medicare, and that would have been the kiss of death for any treatment.

Again, my primary doctor felt very sure that I should receive treatment, and was willing to push things. Fortunately, though my sleep doctor has not been very aggressive about ensuring treatment, she has been co-operative about anything I ask for. I work in a doctor’s office, doing research, and I think she realizes I do my homework. Even with a very low AHI, I fit well within Medicare’s treatment parameters, with morning headaches, daytime fatigue, and pulmonary hypertension. So, when I insisted on CPAP, she agreed to do a titration.

During the titration they started me out at 4, and moved up very slowly. I know it may be hard to titrate with a low AHI, as the events they look for are not constant. Anyway, they titrated me up to 7, and at that point I fell into an excessively long period of slow wave sleep. They considered that a success, even though I had excess slow wave sleep in both of my two prior studies. I only spent 3 minutes in REM at that pressure, but they ran out of time, so considered me titrated.

That night I still had an arousal index of 14, not much reduced from the other studies. They do not call these respiratory arousals, but I wonder if this is accurate or not, given everything else they have been off about. The O2 sats stayed up at 97%, a nice shift! Anyway, I woke in the morning still experiencing a great deal of pain (usual) but my mind was clear. NOT USUAL!!! I was hooked.

As I said, the sleep doctor hasn’t given me anything I didn’t ask for, but she does respond if asked. When I asked for a prescription that allowed me some choice, she wrote one allowing my choice of any CPAP or APAP, and the pressure that I was titrated to (7) or an auto setting of 4-15. My DME was willing to give me an auto, so that is what I took. My medications change frequently, and I wanted as much flexibility as possible.

I started out with the recommended auto pressure of 4-15, but quickly found that was not doing it. I was having higher AHI than during my study, including much higher AI, and I figured it just wasn’t moving fast enough to correct the apneas. I moved the lower setting up to 7, where I was titrated. Over the last month, I have bumped it up to 8.4, watching how things go. For a couple of weeks, I have had lung issues after a chemical exposure that caused serious inflammation in my lungs and sinuses. I am thinking that made things worse, but it is also a common experience for me, at least at lower levels, as I am very sensitive to inhaled chemicals and fragrances. So I can expect to have periods of respiratory tract inflammation.

What I am seeing is that each time I bump the bottom pressure up, I do better for a while, and then slowly the AHI seems to creep back up. I see the sleep doc for my follow up on Thursday, and I don’t want to push it too high before talking with her, so that she will document compliance for Medicare. I’m just wondering how normal this is, to see the needed pressure keep creeping up. My 95% is running slightly above 9. The apneas seem to respond to pressure increases, but because the events, whether hypopnea or apnea, are pretty isolated, the pressure goes back down, another event occurs, and the cycle repeats.

Once I am out from under scrutiny, I will push it up again and see what happens, but in the meantime, I am wondering what it might mean. Is this just the usual process of adapting? It sounds like this might happen in UARS. I am wondering if I might need a different machine to effectively handle this, or do I just need to keep experimenting with my pressure? I understand the whole A-10 thing with Resmed. It doesn't seem to be impacting me, as so far my pressure isn't getting over 10 very often. I was wondering more about the Bi-pap, and if that really is better for these issues. Mostly my pressure is not changing a lot, and I am not aware of it bothering me when it does.

I am seeing big improvements. No more repeated awakenings in the night, where I might be awake for as long as an hour. No multiple trips to the bathroom during the night. No repeated dozing off in the afternoon, and no more fear of doing so in the car. The headaches are much reduced. My brain is beginning to think again. My body is still tired, but I do have other illnesses, and I don’t know if or when that might change. I haven’t had the pulmonary artery pressure re-measured. It does seem like there is a lot of improvement, and I am comfortable with my machine, I just want to be sure I get as much improvement as possible.

I know nobody has THE answer, but I thought I would throw my info into the mix.

[dsm]

<snip>

I'm not sure Dr. K.'s ideas are all that divergent from the rest of the researchers in the field--he has, in my opinion, simply chosen different words to communicate the ideas. I don't claim to understand much of what he says. But when he speaks of flow limitations, I think that may be merely a shorthand way of saying it involves breathing. The thing is that you only treat people who are sick, and that is assumed as understood in his discussions. It is true that in one sense everyone has flow limitations, since no one breathes perfectly. But in another sense, it is only the people whose imperfect breathing causes them fatigue or somnolence that honest docs are interested in giving treatment to.

<snip>

JNK, very well put. On re-reading the Krakow POVs (right through), I feel the same. Krakow, as with anyone who tries to simplify explanations, clearly runs the risk that someone who wants to make a point, may misrepresent or misinterpret one of his comments when he may have a good argument as to why he explained the point the way he did. Such translation is challenging.

I have asked him if he is willing to chime in here on this thread & I hope he does. But, he is a very busy man.

DSM