Topics: UARS obstructions, 420e, etc.

[rested gal]

Shoot. I would've sworn that "Guest" was WillSucceed getting accidentally "guested".

Is that you, Will? You fascinating thing, you!

[dsm]

Hi SWS,

I am very new to CPAP & doing my best to understand the differences between CPAP APAP & BiPAP. I have an AUTO (RemStar) set in CFLE mode but in 2 weeks will begin trying it out out AFLE mode. I am hoping the 4 weeks of straight CFLE will help me better appreciate the differences in using AFLE mode.

I gather that the BiPAP/VPAP machines are highly sensitive re IFL1 & IFL2 thus My questions are ...

Would a RemStar BiPAP offer a better level of therapy over a RemStar AUTO for a normal (typical case) CPAP user ?

Are the modern AUTOS starting to outpace the more sophisticated functionality previously associated with BiPAP/VPAP machines ?

Cheers

DSM

[WillSucceed]

Rested Gal wrote:

Shoot. I would've sworn that "Guest" was WillSucceed getting accidentally "guested".

Is that you, Will? You fascinating thing, you!

Not me, Pumpkin! Although, you get full marks for the guess -you know how I love to hate C-Flex! LOL

PS, thanks for the compliment... I've been called many things, but this is a first for 'fascinating.'

[rested gal]

DSM, unfortunately -SWS took a leave of absence from the message boards. That kind gentleman helped so many people for so many years...we all miss him sooo much on the apnea message boards!

-SWS's farewell to the message boards:
Jun 16, 2005 subject: Bon Voyage!

None of us come even close to what he knew and understood about the techie aspects of these machines. At the risk of getting egg all over my face, I'll venture this - just my opinion - about a couple of things you brought up...

I gather that the BiPAP/VPAP machines are highly sensitive re IFL1 & IFL2

Those are "flows" that are sensed by the PB 420E autopap. I don't think that kind of sensing is done at all by bi-level machines like the BiPAP and VPAP III. Bi-levels are not going to change the pressures they are set to deliver (the single IPAP or inhale pressure and the single EPAP or exhale pressure.) Since bi-level machines are not going to change either of those fixed pressures, they have no need (or ability) to sense changes in air flow other than to recognize when an inhalation begins.

Some bi-levels can give data about volume of air a person is taking in/breathing out, and respiration rate (number of breaths per minute) but as far as sensing flow characteristics as in the PB 420E's sensing of "IFL1 and IFL2", I don't think bi-levels do anything even approaching that. They'd have no need to. Bi-levels are not going to change pressure depending on what the airflow is doing (other than needing to know when a person starts to inhale.)

Would a RemStar BiPAP offer a better level of therapy over a RemStar AUTO for a normal (typical case) CPAP user ?

I don't think one could say either machine would necessarily offer better treatment over the other -- for a "normal (typical case)" OSA patient. For the typical OSA sufferer, with no underlying pulmonary condition or other health condition that would make breathing out difficult, both types of machine have their own unique "comfort" features.

The autopap offers the chance to use lower pressures than the prescribed pressure much of the night, as well as adjusting automatically to any pressure need changes in the future (weight loss or gain, change of medications being used, etc.) The bi-level offers an exact setting to be used for exhaling which feels "good" to most people.

An autopap with C-flex can give somewhat that kind of comfort too, but not to the extent that a bi-level can if a person's pressure absolutely must be rather high almost all the time. The real value (to me) of a trial on autopap would be to see if that "high" pressure really was needed most of the night....might not be needed much at all.

Are the modern AUTOS starting to outpace the more sophisticated functionality previously associated with BiPAP/VPAP machines ?

Well, I'm not so sure I'd consider the bi-level machines (BiPAP and VPAP and PB's 425 to be more sophisticated than Autopaps in the first place. With the exception of ResMed's combo auto/bi-level (the CS 2) I'd think autopaps are far more "sophisticated" and complicated than bi-level machines in general. When you think about what an autopap has to do - sensing from air flow what's happening to a person's throat and deciding what to do about it, that takes some pretty darn sophisticated calculations.

Bi-levels only have to push one single pressure into you, no matter what; and drop the pressure to another lower single pressure for exhalation. At that point, the bi-level just "sits there" at the lower pressure, waiting for an inhalation to start again. Not very complicated considering everything that autopaps have to do to treat people effectively by sensing changes in air flow patterns and deciding what to do.

Even the "ST" bi-levels with the capability of setting a "timed" mode for backup breaths to kick in if a person has centrals and needs a "nudge" to remind the brain to take a breath...even those do not have to do the kinds of calculations autopaps do for us, every minute, every night.

Just my non-techie two cents. I could be very wrong! Gawd, how we miss -SWS!!

[dsm]

Thanks as always RG.

I followed that ok (so I believe ). The difference does beggar the question
"Why are BiPaps/Vpaps so much more expensive than APAPs ?".

Is it the issue of volume sales of APAP vs these others ?

Cheers

DSM

[ozij]

Gawd, how we miss -SWS!!

Me too.
O.

[ozij]

Bi-levels are not going to change the pressures they are set to deliver (the single IPAP or inhale pressure and the single EPAP or exhale pressure.) Since bi-level machines are not going to change either of those fixed pressures, they have no need (or ability) to sense changes in air flow other than to recognize when an inhalation begins.

RG, I think this is a case of easier said than done. I have no idea what this capability to "recognize when an inhalation begins" entails, but it has to be very exact. Otherwise you get what happened to WillSucceed with the cflex - an utimely reaction that was worse than unhelpful.

The fact that Bi-paps can have so many setup options (I am basing this on mails by their users, e.g. freqenseeker, not on experience) means that whatever computing stuff is done in them is pretty sophisticated as well.

For all we know, bi-paps could be using air flow charaterisitics as data for them to decide how to react, thought their reaction is not a automatic adjustment of pressure.

"Why are BiPaps/Vpaps so much more expensive than APAPs ?".
Is it the issue of volume sales of APAP vs these others ?

I would guess at a number of other possible reasons:
1. Bi-paps have been around longer, and it could be that originally their electronic boards and chips were much more expensive than the ones in use today.
2. They probably include development price as well - they were the first "sensing and reacting" machines - probably path breakers for the autos
3. Another guess - they might need more expensive and sophisticated mechanics - since they have to change pressure immediately, and not gradually.

I never cease wondering at the fact that the computer I use today (even the one I used 15 years ago) is many many many more times sophisticated than the one used in the Eagle that landed on the moon....

My 2 cents...
O.

_________________

CPAPopedia Keywords Contained In This Post (Click For Definition): cflex, APAP

[Janelle]

The two pdf articles seem to be identical. Only the file name is different. Is this a booboo or they ARE the same?

[kyethra]

I have a couple of related questions that I am hoping someone can help me out with. I read the linked article. I noticed that 1) it did not discuss Narcolepsy and how to differentiate UARS from narcolepsy without measuring esophogial pressure. 2) Exactly what are the differences between catathrenia (nocturnal groaning) and UARS? Could it be that Catathrenia does not have impaired breathing?

To return to my issue about distinguishing UARS from Narcolepsy-- I know this is probably something that should seem obvious to me, but it isn't. Narcolepsy can also cause a high level of arousals and fragmented sleep, along with Excessive Daytime Sleepiness. I assume that UARS would not affect REM onset because that is not mentioned and that is the only way of distinguishing it?

I have had three sleep studies in the last six months. The first one was the traditional kind- got off all of my meds except birth control, zyrtec, sudafed (got special permission for that one), and flonase. And then I had a MSLT the next day. According to the MSLT I am narcoleptic- rapid onset REM, about five mins. I also had 2 min onset REM during the night sleep study. During that sleep study I had excessive REM and Delta Sleep. I also exhibited a lack of REM paralysis (an issue I have always had and known about annecdotally for quite a while), and a strange thing I do where I move my head from side to center and back rythmically and reapeatedly while lying supine, and also mild PLMD. This sleep study also picked up on what they thought was obstructive sleep apnea.

So a couple of weeks later I went in for a titration study for CPAP the sleep apnea. I was getting back on my meds at that point- including my hydroxyzine which I had to get off of for the study. During the titration study I had absolutely no REM sleep. I also had a very low Apnea and Hypopnea index despite the way they kept cranking the machine up. So the doctor said he wanted to put me on a pressure of 5 but he made a mistake and wrote the scrip for 15 and then later changed it to ten. I tried CPAP for two months.

CPAP made me worse. It caused me to wake up repeatedly and it raised my blood pressure, gave me fatigue (I was sleepy before but no really fatigued), and left me not as well rested. We changed masks. We added heated humidity. The presure was lowered- still not working. I was also still making noise in my sleep and thrashing around.

So I found a neurologist with more experience. She had me do another titration study where I slept for a couple of hours before CPAP was introduced and where I also slept at my normal sleeping hours. According to this titration study I have no Apnea at all. No hypnonia. No indications of it whatsoever. And after the CPAP was introduced I just slept worse like I had said- it caused my sleep to be even more fragmented and to have more arousals. Even before the CPAP I was having a lot of arousals. Much more than would be explained by (and they didn't all correlate with) my PLMD. Oddly, I also didn't have any REM sleep during this sleep study either.

Normally I have a lot of dreams and REM sleep as indicated by my sleep movements and talking (since I will sometimes act out those dreams. It drives my husband batty). Another odd thing that turned up on all three sleep studies was snoring. I don't snore. At all. I never have. But I do moan/groan in my sleep every night. THe sleep centers use vibration sensors for their snore mics and not actuall audio so I think they picked up on that instead of on real snoring, especially since CPAP has no affect on it. The moaning/groaning is always on exhale for me and the respiratory patterns assosciated with it are like those assosciated with speech (sometimes its mumbling, sometimes its talking, but majority of time it is moaning and groaning). Apparently it is same period of night time when I do my head turn thing.

In both the the titration studies I did not display the head thing though, but it happens very frequently at home and during the first study. Its awfull for my hair and neck.

So my doc is going to have me use CPAP for one month now to see if that helps at all and what the data from it says. Then if it doesn't help I think the diagnosis of my narcolepsy is much firmer and I will try xyrem. I also have a history and symptoms that are suggestive of narcolepsy, but since I'm not catapletic we need to be certain.

I suspect the breathing difficulties in the original study could be allergy related-- I normally take hydroxyzine every night along with guiaphenesine in addition to my zyrtec and sudafed as well as astelin and I have also been getting allergy shots for a couple of months now which I think are starting to help.

But I find all this ambigious and I thought I would try and get more information.

[-SWS]

Kyethra, welcome to the board! I would like to come back to this thread and at least attempt to step through some of your questions (as a patient, but not as any kind of medical professional or expert). Others here may be able to do so as well. In the meantime, I would also like to get Rested Gal's recent series of UARS links and discussions added to this thread for reference (also please note: sleepydave below is this message board's very favorite StillAnotherGuest, also known as "SAG"!):

Links to UARS:

http://www.clevelandclinicmeded.com/dis ... /sleep.htm

http://www.chestjournal.org/cgi/content/full/115/4/1127

http://ajrccm.atsjournals.org/cgi/conte ... 161/5/1412

http://ajrccm.atsjournals.org/cgi/conte ... 161/5/1413

viewtopic.php?p=101358


sleepydave (RPSGT manager of an accredited sleep lab) wrote an interesting post about UARS:

New Here/Need help with Sleep Study Results

____________________________________

sleepydave
Moderator [apneasupport.org]
Joined: 05 Jul 2005
Posts: 813
Location: In the Sleep Laboratory


What's UARS?

Hi Arline!
UARS is the acronym for Upper Airway Resistance Syndrome. It is characterized by respiratory events that are not severe enough to be classified as apneas or hypopneas still cause arousals. These respiratory events can be snores or minor narrowing of the airway, but the increased negative intrathoracic pressure trying to draw air through the restricted airway, as well as the arousals, can cause the same havoc as plain old OSA.
Here's an interesting blurb that should perk your ears up:

UARS

So it's still nothing to sneeze at.
Sure, continue to gather more info, including maybe seeing an ENT. Also keep in mind that surgery of the upper airway can have some significant associated hazards, so don't make that decision lightly.
See what the CPAP results bring, then maybe go from there.

sleepydave

______________________________

(Click the red word "UARS" in sleepydave's comments to go to the ncbi.nlm.nih.gov link.)

Interesting UARS links were posted by SleepyJ in a topic at this clickable link:
Sleep Studies Forum, apneasupport.org, August 2006.

[-SWS]

I have a couple of related questions that I am hoping someone can help me out with. I read the linked article. I noticed that 1) it did not discuss Narcolepsy and how to differentiate UARS from narcolepsy without measuring esophageal pressure.

These two conditions can both entail similar daytime symptoms, but have different etiologies. Because the underlying etiologies are different between Narcolepsy and UARS, the measurement and diagnostic criteria differ significantly. Narcoloepsy is a neurological disorder adversely affecting maintenance of wakefulness during the day and quite often sleep drive/architecture during the night. By contrast UARS is a sleep breathing disorder that has to do with upper airway impedance and its potential disturbances to sleep and sometimes oxygen.

The gold standard for UARS diagnosis is esophageal manometry. Unlike UARS, narcolepsy will not cause extreme negative esophageal pressure, and therein lies one important differentiation technique between UARS and narcolepsy. Note that these two conditions are not mutually exclusive. It is thus possible, although somewhat improbable, for a patient to suffer from both narcolepsy and UARS. Regardless of improbability, when this concomitant pairing does happen, it is probably often difficult for sleep doctors to efficiently differentiate the concomitant pair in the screening process itself. I would think this statement would be especially true when narcolepsy presentations or manifestations are either subtle or atypical. However, the ensuing diagnostic process itself would ideally medically differentiate these two. Also note that narcolepsy and UARS are both currently thought to be much less statistically prevalent than common sleep apnea.

By contrast to the overnight PSG used for apnea and UARS diagnoses, the daytime MSLT is additionally employed as a means to diagnose narcolepsy. Again, narcolepsy diagnostic criteria does not entail negative esophageal pressure, or airflow reduction. Rather narcolepsy diagnostic criteria is listed below (note the dark red text delineating two alternative criteria categories):

Minimal Criteria: B plus C, or A plus D plus E plus G.

A. The patient has a complaint of excessive sleepiness or sudden muscle weakness.

B. Recurrent daytime naps or lapses into sleep occur almost daily for at least 3 months.

C. Sudden bilateral loss of postural muscle tone occurs in association with intense emotion (cataplexy).

D. Associated features include:

1. Sleep paralysis

2. Hypnagogic hallucinations

3. Automatic behaviors

4. Disrupted major sleep episode

E. Polysomnography demonstrates one or more of the following:

1. Sleep latency less than 10 minutes

2. REM sleep latency less than 20 minutes

3. An MSLT that demonstrates a mean sleep latency of less than 5 minutes

4. Two or more sleep-onset REM periods

F. HLA typing demonstrates DQB1*0602 or DR2 positivity.

G. No medical or mental disorder accounts for the symptoms.

H. Other sleep disorders (e.g., periodic limb movement disorder or central sleep apnea syndrome) may be present but are not the primary cause of the symptoms.

So in recap, to receive a narcolepsy diagnosis, patients would need to meet one of these two diagnostic criteria categories: 1) B plus C, or 2) A plus D plus E plus G. Since either category is considered a diagnostic minimum, some narcolepsy patients will manifest presentations from both of these diagnostic categories. Note that F (a genetic marker) and H are presently listed as consideration factors only.

2) Exactly what are the differences between catathrenia (nocturnal groaning) and UARS? Could it be that catathrenia does not have impaired breathing?

I don't know much about Catathrenia. However, it is a relatively newly discovered parasomnia that entails vocal-chord-based noise during expiration. It may be neurologically driven, and it may entail impaired breathing since I see CPAP proposed to treat catathrenia (mentioned both on the Internet and in your post). Note that UARS is characterized as difficulty breathing during inspiration, unlike catathrenia which entails expiratory vocalizations. My best guess is that catathrenia may entail vocal-chord-based breathing restrictions or flow limitations in some patients during inspiration as well. This postulated vocal-chord-based airflow reduction may be the premise behind experimentally using CPAP to treat catatherina. If so, catathrenia may have more in common with vocal chord dysfunction (VCD) as a nocturnal sleep-disordered-breathing condition than with UARS (which is not considered a disordered function of the vocal chords).

Another odd thing that turned up on all three sleep studies was snoring. I don't snore. At all. I never have. But I do moan/groan in my sleep every night. THe sleep centers use vibration sensors for their snore mics and not actuall audio so I think they picked up on that instead of on real snoring, especially since CPAP has no affect on it. The moaning/groaning is always on exhale for me and the respiratory patterns assosciated with it are like those assosciated with speech (sometimes its mumbling, sometimes its talking, but majority of time it is moaning and groaning). Apparently it is same period of night time when I do my head turn thing.

I personally suspect that it is possible for PSG snore detectors to score false positives, based on vocalizations in the correct frequency and amplitude range. You certainly have a lot of things going on with your sleep, Kyethra. Most or all of your sleep symptoms seem neurological (narcolepsy, PLM, catathernia, etc.) rather than pulmonary (UARS, obstructive apnea). Hope others may be able to shed some light to help you out as well. Just a reminder that I'm not a doctor and most of us aren't. Good luck!

[jrgood27]

I have an OSA diagnosis, but have similarities to UARS patients - all hypops, no snoring, no desats. I have fibromyalgia and frequent migraines, hypoT, low cortisol.

What I'm wondering - Someone hypothesized that UARS patients maybe are more likely to have cortical arousals - that is why their sleep ends up being disturbed by pressure issues.

Well, I've been trying and failing at APAP for over 6 months. Even after I take a sleep aid and use the machine for 6 hours I feel awful when I wake up.

I'm wondering if it's possible to have cortical arousals in response to the APAP changing pressures.

Would it be better for someone like me to have straight CPAP.

Any ideas?

Jenny

[rested gal]

Jenny, it's certainly possible that pressure changes while an APAP goes about its work could cause cortical arousals for some people.

I'm not a doctor, but if it were me, I'd give that a try for awhile... changing the APAP's operation mode to CPAP. Quite a few people choose to run their APAPs in CPAP mode. Perhaps that would work better for you. Worth a try.

What machine do you have and what pressure range have you been using for the past month or so?

Are you comfortable with your mask?

[-SWS]

Jenny, I agree that it does not hurt to try fixed pressure, looking for improvements in sleep. Also, you asked whether APAP's changing pressures can adversely impact sleep. My own opinion is that, indeed, some people are definitely better off with CPAP modality than APAP. By contrast, I happen to be one of those people who is just slightly better off with APAP modality than CPAP. One size definitely does not fit all when it comes to xPAP therapy as the saying goes on this and other message boards.

However, you did mention fibromyalgia, which is now classified as a sleep disorder in its own right (as well as being classified as a connective tissue disorder and also as an autoimmune disorder). Recall that fibromyalgia entails alpha wave intrusions that are highly disruptive to sleep. And, of course, fibromyalgia also results in significant daytime fatigue and other symptoms related to cognitive dysfunction. At least that is my understanding as a family member of a fibromyalgia patient.

[jrgood27]

Thanks RG and SWS, I'm going to give straight CPAP a try. I have an S8 Vantage and was using it with a very wide range (5.6 to 18) to titrate.

When I saw my pulmonoligst last and brought him my smart card he said the pressure wasn't going above 7.0. So I lowered the top pressure to 9 and that didn't seem to help.

I haven't found the perfect mask situation. The Activa was the most comfortable and quietest (of 6 or so masks I tried), but I'm prone to chipmunk cheeks and couldn't get my chin strap or UMFF or taping my mouth to work.

So got myself a F&P 432 and having trouble getting it to seal without pulling the straps so tight that it's very uncomfortable. Too bad b/c it stops the chipmunk cheeks.

I didn't ask about alpha intrusion. I don't want to know. I'm hoping if I can treat my apnea, the fibro symptoms will abate. That's my hope anyway. Since my breathing problems came long before the fibro. And there is some research linking UARS and FM.

I haven't used the machine for more than 3 weeks in a row. It's tough to resign yourself to feeling even worse and more unrested than you already do.

So RG, what do you think - at this point do I just need to pick a mask and make myself use it for a long period of time even if it's difficult and makes life harder for a while. I still feel hopeful that I can do this somehow. I mean that's what everyone says - just stick with it.

You know what I need is one good night. When I wake up the next day and actually feel a little bit better. That would give me something to go on.

Thanks for listening.
Jenny