Not such a goodknight

[dsm]

Must say how interesting this thread has been. So much to learn & comprehend.

The issue of pCO2 levels & stage of sleep, & relation to CAs seems to me one of the most complex area of the SA & SDB spectrum.

Now to go clear my brain so it can cope with the ingestion.

Tks

DSM

[christinequilts]

RG: this is what I was looking at on Pam's hypnograph's. In the dark blue boxes I highlighted the CA's seen at the bottom. Directly above those square boxes indicating Centrals there is an X which represents the arousal. If you follow that up to the Sleep Stage chart, you will see "WAKE" at the top. Every time you end up there you are awake, maybe not where you can remember the event. And as you go down on that chart you see R for REM, stage1-4 etc.

See I look at those same events as being something woke her up completely and then she had a central apnea as she went back to sleep. Overall, looks like some sleep onset centrals in the beginning (first cluster) and then two post arousal/awake centrals. My understanding is that any time you transition through the sleep stages, you have central apnea, if your current O2/CO2 needs don't meet the current needs.

[christinequilts]

and with all due respect Christine, I think you are incorrect in lumping all categories of Central apnea seen as CSR or even CSA into one. It is simply not the case.

See, I see you doing the same thing- that all central apneas are bad, that they indicate something wrong that must be fixed, that they must be avoided at all cost, when they are a natural part of breathing. They only become a problem if they are over a certain number per hour, usually 5-10. Even if significant centrals are seen on a diagnostics PSG, they are not always an issue- if they go away with CPAP, then there is a good chance they were mislabeled obstructive events, which you're PSG results that you've shared shows.

Further, I've never lumped all types of central apneas in one category. I've always maintained there are different types. I definitely differentiate between clinical significant centrals and insignificant one (aka- normal fluctuations in breathing).

If every central results in an arousal, then why did my first PSG show 528 central apneas & only 21 awakenings & 77 arousals? According to you're calculations, I should have had 400 or so more arousals and/or awakenings, right? Thankfully I didn't get the same memo on centrals=arousal or awakenings as you seem have received

The point you miss here, is if you were having that many CA's, I'd bet you were never making it to deep sleep or REM? My guess is you probably never got past Stage2 with those number of events.

I didn't miss the point at all- you're jumping to conclusions based on very little data and making assumptions once again, just like you do when you think you see a possible central on someones nightly xPAP reports. That PSG showed my sleep architecture percents were not that bad, considering: Stage 1 19.6%, Stage 2 43.7%, Stage 3/4 15.2% and REM 21.6%. You do have to take into account they let me sleep for 10 hours, otherwise the results would have been very different (more REM towards morning). At that time, my normal sleep pattern was 10-12, even 14 hours, with an afternoon nap and wondering why TAS would schedule chats at such a late hour of 9pmEST for people with SA. That study also showed significant Alpha Intrusion, and like I said, there were times the sleep staging line looks more like an EGG reading, with bouncing from stage I to awake. I'm pretty sure if they reevaluated it today, they would also note significant CAP, but that wasn't something they looked for 4 years ago.

Last time I checked there were 3 or more different Central Apnea categories of Central Apnea. What is it they use to classify the different classes? If not mistaken, one form is if you have >10 per hour Centrals and 5 per hour Obstructive, then your primary disorder is CSA Central Sleep Apnea Syndrome.

There are a lot of different classifications of CSA, depending on who you talk to. There is Primary, Secondary, Idiopathic, ect. One thing you have to be careful with is having a few central apneas is not the same as having CSA. Just as I have a few obstructive apneas, but I don't meet the guidelines to be Dxed with OSA. Its not even the number of events per se that trigger a CSA DX, but the ratio of central events to obstructive.

One time you say your understand there is difference between having a few central apneas, then you turn around a few paragraphs later and confuse it with CSA. I'm not sure what the issue is Snoredog?:

But as I understand it, having a few CA's seen during sleep does not indicate you have CSA, does not indicate you have CSR, does not indicate you are having Post-arousal CA's or if they happen during the beginning of sleep on-set CA's. Then there are pressure induced CA's. In my case, I can make those happen at will if I wanted to.

yet later you say:

They say CA is rare. I disagree, there seems to be more and more people popping up here with the syndrome. If it were so rare why is it so many people including yourself have it? I have it, you have, I seen RG's 420 reports before she has it. RG doesn't use an AdaptSV and I bet she feels she doesn't need it (but I bet she would like to try it just like me).

Having CENTRAL SLEEP APNEA, as a diagnosis, is rare. Having a few central apneas during the night isn't, its very common & is completely NORMAL. Big difference there, IMHO. Simple enough concept. Why do I have it? Who knows, I've managed to collect a herd of zebras in my medical charts...what I wouldn't do for horses instead, it sure would make life easier. Nothing I've seen has indicated RG has 'it', nor has she ever claimed to have 'it' and even you have stated you do not have CSA.

I wouldn't say having a few central apneas means they are necessarily pressure induced, as you seem to be saying in the first quote either. You would have to look at the full PSG to determine the cause, IMHO. Remember, a few central apneas are perfectly normal and not all will have a reason.

Then if your breathing pattern is distinct with regular waxing and waning such as seen with Cheyene-Stokes Respiration associated with Congestive Heart Failure (CHF) you have the most severe form CSA.

There are some people with have CSR that don't have CHF, so having CSR doesn't necessarily make it more serious then other types of CSA. What makes CHF CSR more troublesome is the CHF part of it.

Then there is what seems to be the newest classification, that is CSA combined with OSA then it is thought you have Complex Sleep Disordered Breathing or CSDB. Now what is it they use there to classify that type? Think they use a combination of "Mixed" apnea to help classify that type. We all know a Mixed apnea is a combination of both.

We don't all know 'Mixed is a combination of both'. Mixed apnea means an apnea that starts out as a central then converts to an obstructive, when the airway collapses because there is nothing going through it to hold it open. It is not having both central and obstructive apneas separately. CompSA is something different, under current guidelines- the person starts with obstructive events pretty much primarily on DX PSG, but when xPAP is applied, significant and persistent centrals appear. Its not just a few, its a lot- 5 per hour minimum, but some feel the number of residual centrals per hour needs to be even higher, especially in light of the possibility of pressure induced centrals. Some have added cases like mine, with pure CSA that has high persistent residual central AHI with all forms of treatment, including BiPAP ST, to the CSDB category too, though I try to make a point to note I have CSA/CSDB, not 'typical' CSDB. You can find the Medicare guidelines for CompSA- I've posted links to it enough times in the past- its pretty straight forward.

Then as I learned from SAG recently in Pam's discussion there are Post-Arousal CA's. I already knew there were on-set CA's from a discussion of Wally's reports.

I'm glad you're aware of post arousal CA- I've tried several times to point them out to you, but you never wanted to listen. The last time I took the time to engage you in a conversation on centrals and have meaningful debate, you choose to attack with stupid & hurtful comments.

I also disagree with the theory we are always given that they are neurological. While that may be true if you had damage to your spine and/or brain and the signal doesn't make it there. They say it is the mid-brain or brain stem as the cause. But that should be easy to rule out with today's MRI imaging...If you show absolutely no damage to the spine and/or to the brain and you are still having those, I think you can rule out most of the neurological cause debate. Is it the neurological signal that is broken or is it the limit switch? Are the stretch receptors in the lungs neurological?
While CA may be a neurological "function" I don't see it as a dysfunction. One of the chemoreceptors that play a part in respiration is the stretch receptors in the lungs. Does it not sound logical that if those receptors could play a part when pressure induced CA's are seen from artificial pressure?

The cause for centrals is still up in the air. Finding the cause is difficult, because it isn't the same for everyone, someone could even have multiple causes. The article that related it to being an electrical problem versus OSA being a plumbing problem was a good description. Though being neurological also doesn't mean that there is a problem in the brain or spine- it can mean there is neuropathy some where along the line, or nerves, between the muscles that control breathing, the sensors that read O2/CO2 levels, & the brain, etc. MRI's don't show everything either- they are not a real picture, like an x-ray is of a bone. MRI's are a computer generated graphic based on the information it receives. It would only show if there is a structural problem...I'm sure you've replaced plenty of electrical parts that looked great but didn't work no matter what you did to them.

I said it before and I'll say it again, I don't see Central Apnea (CA) as a problem by themselves. I see CA as indicator something is wrong with respiration. Stabilize respiration and they should go away on their own.

You've said that before, but yet you still make alarmist type post whenever a few random possible central apneas show up. You're saying one thing, but doing the opposite.

SAG has shown PSG's here with CSR where the AdaptSV does just that stabilizes respiration and the CA's disappear.

That has been my personal experience too, at least with CSA & periodic breathing. It not only stabilized my breathing, but it also helped significantly reduce my AI & CAP. It is a wonderful machine, but it is not for everyone- there has to be significant residual centrals for it to work. If someone only has a few, it really isn't going to do much and may be even worse, especially if they need a pressure higher then 10 to prevent obstructive events. And to burst your bubble, I still have centrals every night, not sure the exact number, but I do know I make the Adapt the work every night to keep my breathing stabilized. I still didn't make it to single digit AHI on my Adapt titration.

When I had my first PSG with NO CPAP, I had 32 CA's per hour. I also had 27hr spontaneous arousals. I had a AHI of 72 per hour. I also had a combination of Mixed apnea. They put me on CPAP most of those went away. Continued use of CPAP I would still be waking up like I wasn't getting enough pressure and still having apnea. I had 3 more PSG's I still had CA's with CPAP. I still woke up dead ass tired. Still do today.

What, your PB autoPAP doesn't prevent you from being tired? Maybe its not the centrals that are causing the problem, since you've said its eliminated them.
I'm willing to bet that at least some of the centrals scored on your original PSG were mislabeled obstructives. The fact they were dealt with by CPAP indicates that. How many central apneas per hour have they seen on subsequent PSG?

I have mixed apnea. I have central apnea. Do I think I have CSA? no. Do I think I have CSR? obviously not. Do I think I have CSDB simply because I have a few mixed apnea? Absolutely not. As far as I'm concerned I don't have any of those main categories of CA. Since mine don't take place during sleep onset, I don't feel I have that either. I don't have detailed enough reporting to even rule out post-arousal CA.

Do you mean 'Mixed Apnea', as in apneas that start our as centrals then convert to obstructive or 'mixed apnea', as in having primarily obstructive events with a few centrals? They are different things, as I noted above. What do your PSG's show? What stage sleep did you have centrals in? Awakenings at least will be noted, so you can see if it looks like the centrals happened after an awakening.

But what I do know from my OWN experience, is that nearly all auto's on the market today will confuse CA's for obstructive which can only increase them in frequency.

That's your experience- those machines didn't work for you, but it doesn't mean they won't work for someone else with similar issues. The VPAP II STA was terrible for me, almost as bad as if I wasn't using a BiPAP ST at all, yet I never told others VPAP's were bad & should be avoided. Not that I ever wanted to use another VPAP II or III if I could help it. For most people who need BiPAP ST, the type doesn't matter thankfully. A few of us end up not matching with certain brands of machines, that doesn't mean it won't work for others. Some people like Pepsi more then Coke, neither work for me.

Today they do, in fact the sensors are sensitive enough to detect changing CO2 levels.

None of the machines detect CO2 levels- that is only done in sleep labs. Not even the Adapt monitors or detects changes in CO2 level. Show me one xPAP that monitors CO2?

If you have off-the-shelf obstructive apnea, that seems easy to take care of. But how many patients with off-the-shelf obstructive apnea are not like me? Like RG? like yourself? and just don't know it, they were told "don't worry about those they will go away on their own".

But is telling everyone they need to eliminate every single possible central event any more helpful? Telling them their machine is worthless, that their doctor doesn't know anything and they need to use the same machine as you if they 'want to see the light' any more helpful? You make it sound like having any central events is as bad as having the plague. Yeah, its nice if we can get the number of either obstructive or central events as low as possible, but at what cost? Wouldn't it be nice to never sneeze again too? But how many allergy meds are you willing to take and are you willing to live in a bubble to avoid anything that might make you sneeze? An occasional sneeze is a pretty normal occurrence, as is an occasional central apnea.

What I see you encouraging is for people to not trust their doctors, DME or anything but what the nightly report says. But your PB autoPAP only tells you part of the story. You mention you're still 'dead ass tired' every morning, when is the last time you had a full PSG? Did they look for other reasons you may be tired? Things are changing in sleep medicine, you use the quote “someday science will catch up to what I'm saying...” in your siggy line. I chuckle every time I see that (well, most times)- my sleep doctors exact words after my split night PSG last fall was 'someday sleep medicine & technology will catch up to what your brain is doing well you're asleep, but it just isn't there yet'. Gee thanks, just what you want to hear from your sleep doc, right? He still can't explain why the Adapt not only stabilized my breathing, but also significantly improved my AI & CAP and sleep quality overall. Yet when I first posted about being Dxed with CSA & having be treatment resistant on TAS almost 4 years ago, there was someone who was fairly well respected who questioned why the heck was I listening to my doctor and even trying BiPAP ST if it left me with severe CSA still. If I had listened to him and never even tried BiPAP ST, I don't know if I would have been around to see the Adapt and benefit from it (and I don't mean around the sleep boards). I'm glad I stuck with it, even if BiPAP ST wasn't the perfect treatment for me- it was the best available. I'm glad I had knew sleep studies, even if the results were not what I wanted to hear. I know my case is the extreme, but I cringe when I see people discouraging people from at least trying to develop a trusting relationship with their sleep doctor (or finding one they can if the first wasn't right for them) and having occasional sleep studies if things still aren't going great. Sleep apnea is only a small part of the things that go bump in the night that screw with our sleep quality. Not everything has been identified or is easily quantified, like AHI, but sleep medicine is improving- we can't give up on it or get so fixated on just AHI and forget there are other reason for waking up 'dead ass tired'.

I just disagree with lumping everyone category when you see a few CA's as having your condition and that your method applies in all cases.

When have I EVER suggested someone with few central apneas was the same as my situation? What 'method' have I suggested? I've been jumping up & down to say there are different type of centrals for almost 4 years now, as has RG. In simplest terms, there are clinical significant and clinically insignificant central events. Period. 3 central apneas in one nights sleep are pretty insignificant, even 3 per hour doesn't mean much. You're the one who's been saying every central results in an arousal or awakening, no matter what. My original PSG clearly show they don't.

[rested gal]

They say CA is rare. I disagree, there seems to be more and more people popping up here with the syndrome. If it were so rare why is it so many people including yourself have it? I have it, you have, I seen RG's 420 reports before she has it.

Huh? No, I don't have Central Sleep Apnea and have never said I did. Nor do I have CompSAS (complex sleep apnea syndrome), nor even any "mixed" apneas. I have plain old garden variety OSA, and very mild at that. I have PLMD (periodic limb movements disorder) too, which I wouldn't have known about without a PSG sleep study.

The only 420E report of mine that could have given you that impression was on the third night of my sleep study when I was using my 420E while wired up for PSG data acquisition. For whatever the reason the 420E's Silverlining data ERRONEOUSLY showed 13 centrals. The PSG going on that same night showed NONE happening. Nor did I have any centrals in the PSG results done on the two previous nights -- one night without cpap, one using the lab's cpap. It's still a mystery to me why the SL data was coming up with them, when the PSG on the third night showed absolutely no centrals were occurring.

I never have had the 420E mark up anywhere near that many...not even back before I found out IFL1 and I didn't gee and haw well together and was hitting stratosphere pressures for a couple of months. I did chalk up a few scattered centrals here and there when it was spending time up at pressures of 17, 18, 19. Without any exhalation relief in the 420E, I'd say I was holding my breath in my sleep sometimes when I couldn't exhale easily up at those pressures. LOL!!

But you know, the small handful of centrals every night during the IFL1 saga were not affecting how I felt the next day...fully rested. Had I not seen the data, I'd never have had any reason to think something odd was going on with the machine and me. Thankfully, -SWS took a look at the data for me and suggested switching off IFL1. Sure made masks easier to deal with once the pressure was brought under control.

My usual two years worth of nights (not counting before I knew to turn off IFL1) with the 420E show none, zilch, nada, NO centrals. At most (until that oddity of 13 being marked) one or two Ca's would show up on my SL data once in a blue moon.

I almost never (like one tick mark, one time a year) register an "NR" on the Encore Pro data with the REMstar machines I've used.

So...I'm just plain old OSA with a touch of PLM thrown in. No centrals for me. Other than maybe occasional brief normal ones like what EVERYONE has...the normal ones that Christine has been describing so well for at least a couple of years now.

If you have off-the-shelf obstructive apnea, that seems easy to take care of. But how many patients with off-the-shelf obstructive apnea are not like me? Like RG? like yourself? and just don't know it, they were told "don't worry about those they will go away on their own".

Count RG out. I'm plain old OSA and PLM. Not a single central in 3 consecutive nights of full PSG. And except for the 420E mistakenly marking those 13 centrals, not enough Ca's marked in Silverlining to shake a stick at...over a two year period.

http://www.tnlc.com/Lara/laura/osa/study-Oct2005/

[dsm]

I do believe a lot of folk *wonder* if they have centrals & some become convinced of it. My 1st sleep study showed none.

But speaking for myself, I went through about 3 cycles of great results followed by a gradual declines & it bothered me enough that I started investigating xPAP in general and trying different brands & types of machines. In particular my wife had started to complain that I was stopping breathing again & the machine 'having a fit' (whining under strain).

So based on observations of my wife & some of my own logic, I wondered if I really had centrals and that this had been missed. The lack of them in my sleep study was rather glaring though. But one other factor that emerged was that my sleep clinic had written down 15 CMS when it should have stated 13 CMS for the titration & for a while I wondered if I had been experiencing pressure induced centrals in the year it took me to discover that transcription error.

The breakthrough for me came when I went BiLevel (set to 8/15) & then a greater improvement came when I changed to 10/13 based on feedback from FS SWS & others it was shortly after going to 10/13 I learned of the sleep clinics transcription error. 10/13 is clearly a sweet spot for my therapy.

Having lost a ton of weight, in feb 2007, did another sleep study - *again* no centrals of any note.

In hindsight, believe I may never have had any other than the now well understood sleep onset variety & any notions that I had been misdiagnosed were just that, notions without any solid basis.

Having seen the topic of CAs arise repeatedly, I note that many folk seem to have felt the same way I did & so it seems to me many go through an 'I wonder if I am having undiagnosed centrals' phase.

I subscribe to both CQ & RG's view that most centrals we OSA suffers experience are either normal (sleep onset) or the odd naturally occurring events, due to other momentary sleep factors.

So am saying, I suspect our own perceptions of ourselves having CAs when our sleep studies didn't show them, are perhaps exaggerated.

DSM

[christinequilts]

If you have off-the-shelf obstructive apnea, that seems easy to take care of. But how many patients with off-the-shelf obstructive apnea are not like me? Like RG? like yourself? and just don't know it, they were told "don't worry about those they will go away on their own".

Count RG out. I'm plain old OSA and PLM. Not a single central in 3 consecutive nights of full PSG. And except for the 420E mistakenly marking those 13 centrals, not enough Ca's marked in Silverlining to shake a stick at...over a two year period.

I read that comment so many times as I prepared my response to Snoredog, but I never understood why he included me in that group or you RG. Truly puzzling. I clearly don't fit that example either- 'off the shelf OSA' is not something anyone who's read more then a handful of my post would think I have-lol. Snoredog really does seem to be lumping all types of centrals together, which is what he repetitively accused me of-lol.

Can someone have a few centrals that doctor feel may go away if they are Dxed with OSA and are on xPAP? Sure, but I don't think you'll ever find a doctor telling someone not to worry about about 60+ central apneas per hour pretreatment or 30+ per hour on best available treatment- its a totally different ballgame. The difference, once again comes down to are if the centrals are likely to be clinically significant or not.

Could someone with OSA who is it not feeling resting with xPAP have other issues going during their sleep besides apnea, like I did. That's a real possibility, but that's not something any xPAP software is going to tell you, no matter how much you try to read between the lines. I don't know the prevalence of AI & CAP, though it does seem like they tend to be noted more often in people with CSA then OSA, but that's my observation. They are but 2 of countless other sleep disorders and medical issues that affect our sleep & sleep quality, which is why working with your sleep doctor and any other specialist is so important, particularly in more complex cases. In my case, they were obviosuly linked, at least that's how it seems to me.

People can become over focused on their AHI and apnea to the point they won't accept any other cause for their continued sleep issues. FQ was a great example, her first BI PSG noted AI and a possible DX of hypersomolance, but she was so focused on getting EERS, even though the study really didn't indicate it was needed. She pushed on to use an Adapt with EERS, which was totally inappropriate for her, as her continued issues indicated & second study attempted with it. Both SAG & I pointed out the AI & hypersomolance repeatably, long before SAG finally laid the cards on the table a few months ago. As far as I can tell, she never looked into the other possible causes for her continued issues, which is a real shame.

[Snoredog]

If you have off-the-shelf obstructive apnea, that seems easy to take care of. But how many patients with off-the-shelf obstructive apnea are not like me? Like RG? like yourself? and just don't know it, they were told "don't worry about those they will go away on their own".

Count RG out. I'm plain old OSA and PLM. Not a single central in 3 consecutive nights of full PSG. And except for the 420E mistakenly marking those 13 centrals, not enough Ca's marked in Silverlining to shake a stick at...over a two year period.

I read that comment so many times as I prepared my response to Snoredog, but I never understood why he included me in that group or you RG. Truly puzzling. I clearly don't fit that example either- 'off the shelf OSA' is not something anyone who's read more then a handful of my post would think I have-lol. Snoredog really does seem to be lumping all types of centrals together, which is what he repetitively accused me of-lol.

Can someone have a few centrals that doctor feel may go away if they are Dxed with OSA and are on xPAP? Sure, but I don't think you'll ever find a doctor telling someone not to worry about about 60+ central apneas per hour pretreatment or 30+ per hour on best available treatment- its a totally different ballgame. The difference, once again comes down to are if the centrals are likely to be clinically significant or not.

Could someone with OSA who is it not feeling resting with xPAP have other issues going during their sleep besides apnea, like I did. That's a real possibility, but that's not something any xPAP software is going to tell you, no matter how much you try to read between the lines. I don't know the prevalence of AI & CAP, though it does seem like they tend to be noted more often in people with CSA then OSA, but that's my observation. They are but 2 of countless other sleep disorders and medical issues that affect our sleep & sleep quality, which is why working with your sleep doctor and any other specialist is so important, particularly in more complex cases. In my case, they were obviosuly linked, at least that's how it seems to me.

People can become over focused on their AHI and apnea to the point they won't accept any other cause for their continued sleep issues. FQ was a great example, her first BI PSG noted AI and a possible DX of hypersomolance, but she was so focused on getting EERS, even though the study really didn't indicate it was needed. She pushed on to use an Adapt with EERS, which was totally inappropriate for her, as her continued issues indicated & second study attempted with it. Both SAG & I pointed out the AI & hypersomolance repeatably, long before SAG finally laid the cards on the table a few months ago. As far as I can tell, she never looked into the other possible causes for her continued issues, which is a real shame.

[StillAnotherGuest]

The only 420E report of mine that could have given you that impression was on the third night of my sleep study when I was using my 420E while wired up for PSG data acquisition. For whatever the reason the 420E's Silverlining data ERRONEOUSLY showed 13 centrals. The PSG going on that same night showed NONE happening. Nor did I have any centrals in the PSG results done on the two previous nights -- one night without cpap, one using the lab's cpap. It's still a mystery to me why the SL data was coming up with them, when the PSG on the third night showed absolutely no centrals were occurring.

Not, not, not! (Ooops! Thought we were doing the argyle thing again!)

We did try to look at the comparison of the two. From the post over there:

Is It The Apple or The Chicken?

"Actually, the NPSG picked up all the events and then some. It picks everything up, and then the scorer must decide what is significant and what is not. Guess the 420 does the same thing, now that I think about it.

Based on the download from the 420e, here's where the AutoPAP was ticking off events. There appeared to be a group of centrals, if I am reading this thing correctly, at about 2.25-2.75 hours into the study:



Looking at the NPSG, I think these are some of the events the 420e was calling CAs, or at least hypopneas:



A hypopnea has 50-80% reduction from baseline, apneas beyond that, so a couple of these things I wouldn't have a problem calling apneas. They still had some flow limitation quality, so we stuck with hypopneas. For that reason, and also because they appeared to have some almost central quality to them. A reduction in response to some brief hyperventilation. And I say this because this is what was happening immediately prior to this:



PLMs. Leg kicks that generated arousals, brief periods of hyperventilation followed by normal breathing. And this is what I really thought would mess up the 420 algorithm. Didn't as much as I thought it would. Perhaps with IFL1 off, it didn't react as severely as it could have. The pressure waves were all pretty much flow-limited, and it does look like the 420 did respond somewhat, figuring some of these were hypopneas.

Now, since the cluster of hypopneas occurred right after the group of PLMs, you gotta kinda wonder if they were simply a response to more PLMs. The frequency of the PLMs has dropped off somewhat, but I think you can make an easy case for a few more PLMs, with the resultant breaths just happening to be flow-limited.

We can talk about this now, give thought to what has happened, and reconsider therapies. But that's the occasional problem you run into with an AutoPAP and a tick on a graph. What's that tick really mean?

So the problem is, without directly tying into the 420 transducer, there's no real good way to know what it was actually seeing. I used PTAF2 transducers, which are in widespread use, pretty much considered to be a good transducer, and I felt our data to be quite good. I had considered tying directly into the 420, but if a circuit board got smoked there definitely would have been a HostileGal around.

With no true apnea, tho, why the 420 was thinking it saw cardiac oscillations is beyond me.
Maybe next time..."

(back to our show)
Right. So the important thing there is that 420 is thinking cardiac oscillations if it's ticking off centrals.
SAG

[tangents]

I've learned so much from this post, and don't want to see it turn into another mud slinging thread. Christine, you entered this post with a personal attack against Snoredog. You say to him:

The last time I took the time to engage you in a conversation on centrals and have meaningful debate, you choose to attack with stupid & hurtful comments.

yet you have chosen to attack him over and over in this thread. I'll read your opinions about OSA, CA, and all things apnea, but I'll skip over your opinions about Snoredog, thanks. And I'll be truly sorry if this thread becomes another witch hunt.

Thanks, everybody, including Christine, MrPaul, RestedGal, Snoredog, SAG, dsm, and any I've missed, for taking the time to share your knowledge so that a newbie like myself can begin to understand what's going on whilst I sleep.

Cathy

[Snoredog]

I've learned so much from this post, and don't want to see it turn into another mud slinging thread. Christine, you entered this post with a personal attack against Snoredog. You say to him:

The last time I took the time to engage you in a conversation on centrals and have meaningful debate, you choose to attack with stupid & hurtful comments.

yet you have chosen to attack him over and over in this thread. I'll read your opinions about OSA, CA, and all things apnea, but I'll skip over your opinions about Snoredog, thanks. And I'll be truly sorry if this thread becomes another witch hunt.

Thanks, everybody, including Christine, MrPaul, RestedGal, Snoredog, SAG, dsm, and any I've missed, for taking the time to share your knowledge so that a newbie like myself can begin to understand what's going on whilst I sleep.

Cathy

[tangents]

Snoredog said:

I READ that 2nd line of that 420e report "Apnea/CA" (the 13 events) as Apnea OR CA's. that "slash" between Apnea and CA is "OR". so items scored in line 2 of that 420e report can be either Apnea or a Central Apnea to me.

I thought Apnea/CA meant Apnea with Cardiac oscillations? Now that I think about it, maybe that would be Apnea/CO?

Educate me, please?

Thanks,
Cathy

[Snoredog]

Snoredog said:

I READ that 2nd line of that 420e report "Apnea/CA" (the 13 events) as Apnea OR CA's. that "slash" between Apnea and CA is "OR". so items scored in line 2 of that 420e report can be either Apnea or a Central Apnea to me.

I thought Apnea/CA meant Apnea with Cardiac oscillations? Now that I think about it, maybe that would be Apnea/CO?

Educate me, please?

Thanks,
Cathy

[rested gal]

SAG, it's been awhile since I looked at that infamous SL report. Seeing that screenshot reminds me...

WAS WAS WAS !!!




And speaking of excuses...

I had considered tying directly into the 420, but if a circuit board got smoked there definitely would have been a HostileGal around.

SillySag, you know better than that!

For one thing, that's not the only machine I've got.

For another, TaperGal is used to taking risks.

And for a third thing... well, I'm used to smoke.



'Course, you and your good techs only had about a bajillion other things to do, the week of the rebel invasion. (thanks, again!)

[Snoredog]

A hypopnea has 50-80% reduction from baseline, apneas beyond that, so a couple of these things I wouldn't have a problem calling apneas. They still had some flow limitation quality, so we stuck with hypopneas. For that reason, and also because they appeared to have some almost central quality to them. A reduction in response to some brief hyperventilation. And I say this because this is what was happening immediately prior to this:

yes but I think even you will agree that these machines use much different selection criteria in classifying what an event "is" than what gets used in the sleep lab during any manual scoring method.

I would think it is pretty easy for these machines to establish what your baseline airflow is. How many breaths in the lab does it take to establish that base line?

But most autopaps don't use that manual scoring criteria as found in the lab where the more expensive, more accurate detection equipment is usually found, they use much wider based criteria than manual scoring methods, they may only see a 30% or 40% reduction in flow in determining what that even might be and start responding. So you might use a 50% reduction in flow where the machine's algorithm may use only 30-40%.

This can obviously be seen for example in any Remstar EncorePro help screens. There they may describe a hypopnea as needing only 40% reduction in flow lasting >10 seconds to be scored as a hyponea (vs. manual needing 50% >10 seconds along with a 3-4% drop in SAO2).

I'm sure they are basing that different scoring criteria based upon knowing how that detection circuit responds.

I'm sure these manufactures of these machines also do their own parallel testing in the lab just as you have done, but I suspect they may even use more sensitive equipment than even you are equipped with. If their machine got tested and compared to manual scoring and it was found that it was only 10% accurate at detecting apnea, I'm sure any manufacturer would want to voluntarily improve on that.

[christinequilts]

I guess other people are use to me being quiet and mild mannered, like I had been in the past, pre-VPAP Adapt days when I honestly didn't have the energy to argue. Other people are allowed to make snarky comments in nearly every post and get away with, but when I call a spade a spade, its suddenly a problem?

I have tried over the past how many years, as has RG & SAG and others, to help explain what centrals are and what they are not calmly and rationally. I entered this thread because it had shifted to a subject I happen to know a little something about- central sleep apneas. I'm tired of hearing centrals must be avoided at all cost when what is being pointed out are a few random, insignificant centrals in someone with OSA.

Snoredog, if you don't want to debate, can we come to an agreement, much like SAG & FQ did?

• Can we agree that not all centrals are a problem?
  
  A few random centrals on PSG or xPAP data may be insignificant?
  
  Not all centrals cause arousals or awakenings? and per SAG, may even be less likely to then obstructive events, thanks to those lovely snorts you guys (& gals) with OSA make?
  
  Centrals can be sleep onset or post arousal? And be perfectly normal?
  
  Having an occasional central apnea is not rare, it is perfectly normal part of breathing?
  
  Being diagnosed with Central Sleep Apnea is rare?
  
  Mixed sleep apnea is an apnea that begins as a central but concludes as an obstructive. It is not having both obstructive and central events separately?
  
  That CompSA or CSDB is generally characterized by Dx of OSA on initial PSG, which appears to go away with titration only to be replaced with persistent residual central AHI of 5 or more, which are not pressure induced centrals?
  
  Central apneas are not the only thing that can cause someone to feel tired or less refreshed after a nights sleep with xPAP?
  
  Centrals can have a lot of different causes? But neither you are I are ever going to figure out the cause of them?
  
  CO2 comes into play in some centrals?
  
  All stages of sleep are important, none of them are 'just going through the motions' of sleep? And our percent of time in various stages changes throughout life? (particularly with stage 3/4 decreasing as we age?)
  
  autoPAPs try to avoid causing centrals in different ways, which may work better for different people. No one machine is right for everyone, just as no one mask is right for everyone?
  
  ResMed's current autoPAPs don't work for you any better then their VPAP II STA worked for me? But that doesn't mean either machine is flawed and not perfectly fine for other people who may or may not have similar apnea issues respectively?
  
  Some people do have pressure induced centrals, which should be avoided if they can? But that they are not the end of the world?
  
  That the Adapt is a pretty cool machine? I would love to have conversations with you on how I understand it, based on my personal experience and what I've read. I'm not claiming to understand it totally by any means, but I can share with you what happens when I do Y and that it does X when I do Z. I've tried to engage you in a conversation about how it actually increases pressure when it senses a central apnea, which I know, seems so wrong (but feels so right )
  
  That no xPAPs detects or monitors CO2 levels?
  
  That no one should wear argyle socks?

All points are up for debate Snoredog- that's all I've every tried to do. Are there any you would like to add or change?

Maybe if we ask SAG really nice, he can post what obvious pressure induced centrals look like on PSG versus non-pressure induced in someone with OSA? Pretty please SAG?