Topics: UARS obstructions, 420e, etc.

General Discussion on any topic relating to CPAP and/or Sleep Apnea.
-SWS
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Topics: UARS obstructions, 420e, etc.

Post by -SWS » Mon Apr 11, 2005 10:08 pm

Below is a response I posted on TAS discussing UARS-specific hypopneas and apneas versus "classic" hypopneas and apneas that are most often attributed to typical OSA. The former airway closures are specifically believed to be associated with a lateral airway collapse from extreme negative pressure whereas the latter classic obstructions are most often attributed to a sagging palate. These are not the only two airway-obstruction or SDB etiologies by any stretch of the imagination! This particular discussion only compared the UARS airway failures versus the typical soft-palate sourced OSA airway failures, specifically focusing on the UARS case.

That discussion also touched on the 420e's IFL1 and IFL2 triggers in much the same way as we have discussed here in the past. I apologize in advance to those who do not like posts that are technically complex. My assumption is that there are at least a few members here who will find this UARS discussion either relevant or interesting.

Before posting the UARS part of that discussion, here's alink to the entire thread. The UARS portion of that discussion follows:
-SWS on TAS wrote:Mountainwoman, early PB 420e marketing literature touted IFL1 and IFL2 as being special functional parameters aimed at UARS. Yet IFL1 and IFL2 are merely on/off switches for the two algorithmic triggers dealing with: 1) flow limitation runs, and 2) hypopneas that are concomitant with flow limitation runs (respectively). Interestingly, the other "modern" AutoPAP models also trigger on flow limitations, they also aggresively trigger on concomitant hypopneas, and they tend to very cautiously treat (via proactive techniques) non-concomitant hypopneas for fear of pressure-inducing central apneas.

So what's the difference with the 420e design relative to UARS, then? My hunch is that the difference lies in how very aggressively the 420e will trigger on and elevate pressures when flow limitations are detected (via the IFL1 trigger). So aggressively, that more than a few 420e users have had to turn IFL1 off. There are actually two ways to turn IFL1 off: 1) within the environs of the Silver Lining 3 software, or 2) directly from the 420e's LCD control panel (by setting "FL" to 0 versus 1). There is no way to turn IFL2 off from the 420e's LCD control panel, however. In my way of thinking that probably implies that IFL1 must be turned off more often than IFL2. The 420e can be very pressure-aggressive relative to attempting to eliminate flow limitations which are believed to be associated with UARS.

Yet flow limitations can occur for an entire variety of reasons, many of which are not associated with UARS. Some UARS patients receive adequate elimination of their upper airway restrictions via air pressure, and yet others do not. When a UARS patient does happen to receive efficacious treatment from air pressure therapy, that implies the UARS patient's upper airway resistance was successfully eliminated via PAP's inflation of the elastic portions of the upper airway. Yet it is entirely possible that upper airway impedance can be high for rigid structural reasons entirely unrelated to soft tissue. In this latter UARS case, PAP inflation of the upper airway will not completely (if at all) alleviate UARS symptoms---assuming the UARS diagnosis adheres to the most common etiology attributed to UARS.

That most commonly accepted etiology of UARS entails exactly that which the acronym implies: Upper Airway Resistance Syndrome. Specifically this most commonly accepted UARS etiology entails extreme flow limitations that result from extremely high impedance in the upper airway---most often nasal impedance. The etiological distinction doesn't stop there, however. Because the upper airway is so severely flow-restricted, the diaphragm must create extreme negative pressure on inhalation in order to draw in an adequate volume of air necessary for normal respiration. When the diaphragm creates this excessive negative pressure, it can not only be measured all the way into the esophagus, but the UARS patient is typically pestered with negative-pressure-based cortical arousals throughout the night. The UARS specific etiology of sleep disordered breathing actually stops there for some patients. However, if the UARS sourced negative diaphragm pressures are of an extreme magnitude, then the airway itself can start to laterally collapse during inspiration, much as a paper straw collapses when you try to draw a very thick milk shake through it. If that lateral airway collapse is only partial, then a UARS-specific hypopnea tends to result. If that lateral airway collapse is a total collapse for adequate duration, then a UARS-specific apnea results. These UARS-specific hypopneas and apneas are quite different than the classic etiology of hypopneas and apneas that entail simple sagging of the soft palate.

In summary it is the extreme negative diaphragm pressures that are required in order to overcome the extreme upper airway impedances that cause both cortical arousals and obstructive airway events. A UARS patient might have: 1) UARS events only, 2) UARS events coupled with UARS-based lateral-airway-collapsing apneas and/or hypopneas, 3) UARS events coupled with classic soft palate apneas and/or hypopneas, 4) UARS events coupled with both types of apneas/hypopneas, 5) UARS events coupled with any sleep disordered breathing and/or other concomitant sleep disorder known to modern medicine. In addition we said that the UARS-based upper airway restrictions may be soft-tissue related and thus air pressure responsive, or perhaps related to hard or dense structure airway characteristics, and thus likely nowhere near as air pressure responsive as the soft-tissue case.

Add to that the fact that many MDs simply diagnose UARS if the patient's sleep events are exclusively/predominately flow limitations and/or hypopneas, and you likely have several failing airway etiologies attributed to UARS. When you put all the above UARS-related "ifs", "ands", as well as "buts" together, my very strong hunch is that the ability to achieve a total of four therapeutic combinations relative to IFL1 and IFL2 just may lend those diagnosed with UARS an edge in finding suitable/comfortable therapy. If a UARS patient happens to have air-pressure-unresponsive UARS events coupled with classic soft-palate-related apneas and/or hypopneas (which are generally very air pressure responsive) then that patient may fare better with IFL1 turned off and IFL2 turned on----or quite possibly with both IFL1 and IFL2 turned off. The conjecture being that there are very likely quite a few combinational sleep disordered breathing etiologies related to UARS, and the ability to experiment with IFL1 and IFL2 combinations is in and of itself an experimental advantage for UARS patients in general.
Again I apologize if you view this topic as being too complex or otherwise inappropriate for this message board.

Disclaimer: I am not a medical professional or expert by ANY stretch of the imagination.


_____________________________________________________________________________________________

Update- October 27, 2010: as of this writing, UARS is considered a controversial diagnosis within sleep science; and there is not yet an adequately understood underlying etiology for UARS. Here is a more recent discussion about UARS (note conflicting opinions at end of following post): viewtopic.php?f=1&t=40009&st=0&sk=t&sd= ... 15#p349995
Last edited by -SWS on Wed Oct 27, 2010 3:42 pm, edited 1 time in total.

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ozij
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technical info

Post by ozij » Tue Apr 12, 2005 1:05 am

Hi -SWS
I think it takes anyone less than an hour of dedicated browsing on the forum to discover that "this -SWS poster is one of the most technical posters around". (Except for when he lets his sense of humor through).

At that point anyone can say "Yippee! I'm going to learn something new; I have something to chew on"
Or They can say: "Oh no, I don't want to read that boring stuff" at which point they can and should skip to some other topic.

I am of the "yippee" persuasion. Your technical info has helped me a lot towards understanding the ins and outs of my (beginning) therapy. Anyone who doesn't like your topics can just avoid them - which is true for other topics as well - that's what the topic headings are there for.

Thanks for your efforts! Please keep on those posts - and you really shouldn't feel the need to apologise.

And now - I'm off to some hearty chewing.
O.

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Mikesus
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Post by Mikesus » Tue Apr 12, 2005 4:42 am

SWS - Good Stuff!

Question. In your opinion, how does the Remstar Auto algorithm compare? It seems to me that the multiple controller approach would be a bit more accurate as it would be able to try to determine the cause of the obstruction and if there is no response wait it out and stop raising the pressure, vs the potential runaway conditions that would appear to exist if the IFL switches are not set properly. Not trying to belittle that method, but to me it seems strange that a manufacturer would allow a machine to be overly responsive when there are methods that could stop it.

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Post by snoozin' » Tue Apr 12, 2005 10:52 am

I too am interested in how the RemStar auto might differ, as that is the machine I am currently using. Per the copy of my sleep study which I got, it seems as if most of my events are more UARS or similar, rather than the usual OSA/hypopneas because of soft palate obstructions.
Debbie

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rested gal
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Post by rested gal » Tue Apr 12, 2005 11:57 am

Excellent info, SWS. I poured over that thread on the other message board and am so glad you've posted it here as well!

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Hugh Jass
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Post by Hugh Jass » Thu Apr 14, 2005 8:52 am

I have two interesting documents (one particular to UARS), that my MD gave me several months ago.

I'll leave it available for download for a couple of weeks for anyone interested.

http://ca.geocities.com/thefoisys/uars.pdf
http://ca.geocities.com/thefoisys/SRBDAug1999.pdf

Let me know if it doesn't work, and I can PM you.

Regards
Trying is the first step towards failure.

Guest

Post by Guest » Fri Apr 15, 2005 1:21 pm

Mikesus wrote:SWS - Good Stuff!

Question. In your opinion, how does the Remstar Auto algorithm compare? It seems to me that the multiple controller approach would be a bit more accurate as it would be able to try to determine the cause of the obstruction and if there is no response wait it out and stop raising the pressure, vs the potential runaway conditions that would appear to exist if the IFL switches are not set properly. Not trying to belittle that method, but to me it seems strange that a manufacturer would allow a machine to be overly responsive when there are methods that could stop it.
Mike, I suspect the Remstar Auto likely addresses air-pressure responsive flow limitations as good as any AutoPAP. For all intents and purposes, the multiple controller approach is implemented by the other AutoPAP models as well. That is because they each: 1) must detect/differentiate sleep events, 2) provide different pressure response routines based on sleep events (versus a universal and indiscriminate pressure response routine for all detected events), and 3) Make a pressure response priority call when these differentiated sleep events either concur or simply overlap in pressure response time windows.

The 420e's tendency to over trigger on flow limitations is interesting. My first take was that this had to be a flaw or oversight. However, my second thought is that PB does not want to relinquish the real-time resources toward a more robust pressure-response "sanity checking" routine than they already have. Because the IFL1 can be turned off directly from the LCD control panel (whereas IFL2 cannot), PB is full aware of this particular response. Yet they opt not to relinquish it. Rather, they implicitly leave the assessment of possible IFL1 over triggering to human eyes. I'm sure they intended those eyes to be therapists' versus the end user. The first Remstar RG bought was from a woman who also experienced pressure runaway. The Spirit has experienced pressure runaway as well. The potential for APAP to pressure-runaway with under specific circumstances seems to be an Achilles Heel in my opinion.

My hunch is that PB would have to beef up physical resources to accomplish even more algorithmic tasks then they currently do. That implies the possibility of more accommodation for IPS, more heat transfer, more physical form factor at worst. At best it implies additional development cost to overhaul the design toward accomplishing quite a bit with the same real time constraints. More guesswork and pondering on my part than anything else, however. I would love to see all AutoPAPs capable of detecting and correcting pressure runaway scenarios. I think the 420e suffers IFL1-based pressure runaway so much because it is so very pressure aggressive with flow limitations.

-SWS
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Post by -SWS » Fri Apr 15, 2005 1:35 pm

I'm just seeing how many times I can get automatically "guested" in one day (me above).

Thanks for the input, everybody. Thanks for the links, Hugh. I was able to retrieve the first document, but not the second.

UARS is a difficult condition to directly diagnose with PES or indirectly diagnose with flow-based cues and other observations. Supposedly it is under diagnosed, presumably because of diagnostic equipment shortcomings. Many patients cannot sleep with a PES transducer in their throats, therefore most sleep labs don't use PES diagnostics.

UARS is caused by severe upper airway impedances, which in turn cause the diaphragm to create extreme negative pressure during inhalation. I can't help but wonder if most UARS patients aren't susceptible to UARS-based sleep deterioration, in large part, because they are more sensitive to sensory-based cortical arousals than the rest of us. Severe nasal restriction is supposedly statistically prevalent. Yet the UARS diagnosis is not. Most UARS patients do not significantly desaturate. They suffer from poor sleep based on cortical arousals that occur when their measured esophageal pressures are extreme. The question is how many nasally congested individuals in the general population also suffer extreme negative pressures, yet are not cortically aroused? Or perhaps the better question is how many are cortically aroused, suffer poor sleep, and don't receive proper UARS screening or diagnosis?

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Hugh Jass
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Post by Hugh Jass » Fri Apr 15, 2005 1:43 pm

The link to the second document has been fixed.

Didn't realize the URL was case sensitive...
Trying is the first step towards failure.

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ozij
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"file damaged"

Post by ozij » Fri Apr 15, 2005 9:11 pm

Hi Hugh,
Thanks for the correction - however....
Adobe Acrobat 6 says - for the corrected second link - that the file is damaged.
O.

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gracie97
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Post by gracie97 » Sun Jul 24, 2005 4:00 am

I can't help but wonder if most UARS patients aren't susceptible to UARS-based sleep deterioration, in large part, because they are more sensitive to sensory-based cortical arousals than the rest of us. Severe nasal restriction is supposedly statistically prevalent. Yet the UARS diagnosis is not. Most UARS patients do not significantly desaturate. They suffer from poor sleep based on cortical arousals that occur when their measured esophageal pressures are extreme. The question is how many nasally congested individuals in the general population also suffer extreme negative pressures, yet are not cortically aroused? Or perhaps the better question is how many are cortically aroused, suffer poor sleep, and don't receive proper UARS screening or diagnosis?
[/quote]

Reviving this wonderful thread on UARS and autopaps (which is going to take me a few more readings to fully digest)...

Is APAP runaway, then, a more common problem for UARS patients than OSA patients?

I've read that UARS is now theorized to be the primary condition underlying fibromyalgia (FMS) and that almost all FMS suffers have UARS (and consequent significant alpha intrusion). Both are far more prevalent in women than men.

Despite the fact that alpha intrusion has long been linked to FMS, my casual observation from contact with many FMS sufferers is that they are rarely referred for sleep dx/tx.

Nasal congestion peaks in the very early morning (3 - 5 a.m.) hours due to biochemical fluctuations. That may be one reason why UARS is not often suspected and diagnosed.

Although I have UARS (and a great deal of alpha intrustion), I was seldom aware of having any problem with breathing during waking hours. It was only after I read about UARS and paid attention to my breathing ability during frequent awakenings in early morning that I became aware of upper airway problems.

Although my OSA is quite mild, the sleep doctor hypothesized that I have significant UARS on the basis of severe alpha intrusion and hence suggested a trial of CPAP.

At three weeks into CPAP treatment but still losing much sleep to problems with only/first interface (Breeze) and other sleep problems, so far it seems to be helping my chronic pain (chronic daily complex migraine that is thought to be very closely related to FMS and in fact causes many of the same symptoms).
Started CPAP on 7/1/2005
Mild apnea
Plus upper airway resistance syndrome with severe alpha intrusion

Guest

Post by Guest » Sun Jul 24, 2005 9:42 am

Your question about UARS and apap runaway is addressed in a lot of threads by -SWS among others. This discussion also lead me to switch to the PB420E with the benefit of experimenting with the IFL1 and IFL2 settings, after experiencing runaways with the REMstar Auto w/C-Flex.
When you put all the above UARS-related "ifs", "ands", as well as "buts" together, my very strong hunch is that the ability to achieve a total of four therapeutic combinations relative to IFL1 and IFL2 just may lend those diagnosed with UARS an edge in finding suitable/comfortable therapy. If a UARS patient happens to have air-pressure-unresponsive UARS events coupled with classic soft-palate-related apneas and/or hypopneas (which are generally very air pressure responsive) then that patient may fare better with IFL1 turned off and IFL2 turned on----or quite possibly with both IFL1 and IFL2 turned off. The conjecture being that there are very likely quite a few combinational sleep disordered breathing etiologies related to UARS, and the ability to experiment with IFL1 and IFL2 combinations is in and of itself an experimental advantage for UARS patients in general.
Was not aware of link between UARS and Fibromyalgia, from which I also suffer. Very, very, very interesting.

(By the way I've poured over literally all of -SWS posts, and continue to learn from them each time I go back. He also had many posts on the talkaboutsleep forum. Pure genius!

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ozij
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Post by ozij » Sun Jul 24, 2005 10:18 am

Guest,
Do you mind making up a name for yourself so we can distinguish you from other "Guest"s? You don't have to register, but if you use it consistently, at leat we'll know we're speaking to the same person.

By the way, before I decided to register, I used "Fascinated" as my name, since I was fascinated by -SWS's discsussions with Derek....

Please?

O.

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Mask: AirFit™ P10 Nasal Pillow CPAP Mask with Headgear
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And now here is my secret, a very simple secret; it is only with the heart that one can see rightly, what is essential is invisible to the eye.
Antoine de Saint-Exupery

Good advice is compromised by missing data
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Fascinated2

Post by Fascinated2 » Sun Jul 24, 2005 10:23 am

Certainly!

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ozij
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Post by ozij » Sun Jul 24, 2005 11:21 am


Thanks
O.

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Mask: AirFit™ P10 Nasal Pillow CPAP Mask with Headgear
Additional Comments: Machine: Resmed AirSense10 for Her with Climateline heated hose ; alternating masks.
And now here is my secret, a very simple secret; it is only with the heart that one can see rightly, what is essential is invisible to the eye.
Antoine de Saint-Exupery

Good advice is compromised by missing data
Forum member Dog Slobber Nov. 2023