New Baseline PSG - What to expect?

[DreamDiver]

They want to do a new baseline PSG, since my original baseline in 2007 does not seem to include any information about what percentage of my apneas were central or otherwise. What centrals I had in studies thereafter were deemed non-essential since they tend to clump at the beginning and end of sleep events.

I'm guessing I'll have considerably fewer apneas than I had at my 2007 baseline even without the machine because my body is used to a certain pattern of breathing. Does that seem right? If so, what if my baseline shows almost no apneas? I generally don't have any for the first mask event. I'm concerned that once again, I'm going to get misdiagnosed because of 'over-efficiency' of the system.

EDIT: Plus I don't think they were counting 'RERAs' back then - or if they were, they called it something else.

I could use some feedback on this.

[Slinky]

Hopefully, it will be a full night PSG and not a split-study. I almost never have any events my first sleep cycle as well.

[SleepingUgly]

They want to do a new baseline PSG, since my original baseline in 2007 does not seem to include any information about what percentage of my apneas were central or otherwise. What centrals I had in studies thereafter were deemed non-essential since they tend to clump at the beginning and end of sleep events.

I'm guessing I'll have considerably fewer apneas than I had at my 2007 baseline even without the machine because my body is used to a certain pattern of breathing. Does that seem right? If so, what if my baseline shows almost no apneas? I generally don't have any for the first mask event. I'm concerned that once again, I'm going to get misdiagnosed because of 'over-efficiency' of the system.

EDIT: Plus I don't think they were counting 'RERAs' back then - or if they were, they called it something else.

I could use some feedback on this.

Are you talking about a new diagnostic PSG or a titration? If the former and you'll be sleeping without CPAP, I'm not sure why they would not see you at your baseline. I've never seen or read anything to suggest that there is some residual effect of previous CPAP use, but I could be wrong.

Not all labs score RERAs, so you might want to check of whether they do. Personally I would not want a split-night study. I want them to examine me in REM as much as possible to get at any possible REM-dependent SDB.

I don't remember your history, so I don't remember about your misdiagnosis. Wasn't there something about an MSLT in all this, testing for narcolepsy? (Sorry for my bad memory and difficulty keeping people straight). If you have apnea, and during the night's PSG you are without CPAP, they really shouldn't do an MSLT on you because they won't be able to differentiate narcolepsy signs from those of sleep deprivation associated with your untreated respiratory events.

[echo]

...and if CAs or complex / mixed apnea are your major concern, doesn't it make sense to do a PSG under xPAP conditions? ... since many times (?) then tend to appear after therapy is started? On the other hand a baseline PSG could make sense if you completely doubt the first one.

I tend to agree with SleepingUgly, there's no reason to suggest that a PSG without the xPAP will be less effective or efficient due to successful xPAP therapy. Although I did have one (stupid) sleep doc say that the effects of cpap therapy last a few days, that's the same guy that told me to go to 4cm when i complained of mouth breathing and refused to give me a FFM .

Is this study going to be at a different clinic? Do you trust them more? The 'studies you had thereafter' - I assume they were all with some sort of xPAP?

If I remember correctly you have the CMS pulse-ox (50F? it's because of your posts I got mine!). Have you ever tried it on a night with no xPAP? Just to see how bad your desats are ? At least then you can put your mind at ease that's you're having some sort of event(s) and you'll sleep better (well in one way at least!) during the PSG.

Good luck dreamdiver, I know you've also had a real rough time getting the right treatment. I know exactly how frustrating this process must be for you.

[DreamDiver]

Are you talking about a new diagnostic PSG or a titration? If the former and you'll be sleeping without CPAP, I'm not sure why they would not see you at your baseline. I've never seen or read anything to suggest that there is some residual effect of previous CPAP use, but I could be wrong.

Not all labs score RERAs, so you might want to check of whether they do. Personally I would not want a split-night study. I want them to examine me in REM as much as possible to get at any possible REM-dependent SDB.

I don't remember your history, so I don't remember about your misdiagnosis. Wasn't there something about an MSLT in all this, testing for narcolepsy? (Sorry for my bad memory and difficulty keeping people straight). If you have apnea, and during the night's PSG you are without CPAP, they really shouldn't do an MSLT on you because they won't be able to differentiate narcolepsy signs from those of sleep deprivation associated with your untreated respiratory events.

New baseline. They won't be doing a split night.

I have centrals only. That much is what the S9 is showing. When I titrate below 10.4, AHI rises. When I titrate above 10.4, again - AHI rises. So I know I should be on xPAP. However, they are all centrals, and I do have periodic breathing.

I can't seem to find my baseline report. I'll have to call the old sleep center to get that, I think. But I've reviewed the two titrations I've had. They're almost all centrals. Why on earth didn't they dig further the second titration if they knew I was having trouble and they knew it was almost all centrals?

It's also odd that all hypopneas are labeled obstructive on the titrations below. I thought hypopneas were by definition an open airway phenomenon. There seems to be less and less I can actually understand about hypopneas. It makes me wonder about how my old machine used to score many more hypopneas. They look a lot like the low end of a cheyne-stokes pattern to me. I imagine it might not look too different to a machine with a simpler detection algorithm. Maybe the way the S9 grades hypopneas is the reason why I'm seeing less of them on the S9 than I did on the M-Series. Maybe the ends of my more obvious cheyne-stokes episodes were being logged as hypopneas on the M-Series. The S9 makes no distinction between central and obstructive hypopneas. There has got to be a definitive text on hypopneas somewhere that isn't in Greek or Sanskrit. If someone has a link to that, I'd be grateful.

2007 Titration


2008 Titration

Have you ever tried it on a night with no xPAP? Just to see how bad your desats are ? At least then you can put your mind at ease that's you're having some sort of event(s) and you'll sleep better (well in one way at least!) during the PSG.

I've used the oximeter to self-titrate. It hurts my head too much for the whole next day or two to purposefully not use CPAP, even for a nap. When I get down to about 8, I get some serious desats.

I don't trust doctors at all. At this point I'm jumping through hoops again. Unfortunately, I've been hoodwinked into believing I'll get a different result. We shall see. At some point I wonder if it would be appropriate to parade up and down in Centennial Park in downtown Atlanta with a very large placard saying "My health insurance is helping my doctor kill me, and I can't stop them."

I suspect there could be a pattern remembrance for a night or two off cpap that could affect a truer outcome of any baseline done after long-term cpap therapy. I have no proof. I'm just curious because it seems unlikely that I'd go back to 237 events a night again after a single night off cpap.

[echo]

I'm so sorry. But if you're gonna be parading around the park with a big ole placcard you can't be all THAT tired ok sorry bad joke.

I really can't answer your questions about the cheyne-stokes breathing or any of the other technical questions... but I would like to comment that since the central's appear on the titration that doing a baseline PSG without xPAP will proably just be a waste of time! It sounds like complex apnea. Just as a starting point, on old article on the Mayo Clinic website, i'm sure there's much more recent info: http://www.mayoclinic.org/news2006-rst/3608.html

Also, I'm not sure why you are confused with hypopnea's? Or maybe I don't understand your question. A hypopnea is a reduction in the airflow by a certain % with an accompanying desaturation. So it's not a complete blockage like an apnea, but a partial. I suppose that the cheyne-stokes breathing could be confused for a hypopnea because since the breath volume is reduced in the former it could appear as a hypopnea? I have no idea how the scoring algo's work though so this is all just rambling on my part.
In my PSG for example, I have nearly ALL hypopnea's and a minimum desat of no less than 90%, and yet I'm still OSA. And I also am not 100% on CPAP, but I'm not sure how bad my central's are, they appear at 11cm and higher, so I'm stuck at 10.5cm.

Now let's hope SWS or Ms Muffy will chime in.

[montana user]

My mom has been on CPAP for 8 years, and when we did her psg baseline ( this was under different lab rules where anything over 5 years, you had to "re-qualify" the patient and prove they have apnea. Thank goodness we don't have to do that anymore) so her one night off CPAP after 8 years her AHI actually raised some. The CPAP does not train the airway to stay open, so the second you fall asleep with out xpap, gravity takes over, and airway closes. Ive been on CPAP for just over a year now and the second I fall asleep without my mask, I snort, wake up, and head to bed with CPAP.

The hypopneas as someone described was correct. It is a partial blockage of the airflow. It blocks enough of the airway that it causes the O2 saturations to drop. You need a 4% drop on O2 to count it as a hypopnea. It used to be the same way for an obstructive, but now we don't need a desat in O2 to count it as obstructive as long as the flow is flat.

Complex sleep apnea is one that we did not like. The higher the pressure to fix the apnea, the worse the apnea gets. A night techs worst nightmare. Before they came out with the auto SV CPAP's there was really nothing we could do. Now we can treat it! most insurance companies require that you prove CPAP and Bi-level do not work. Auto SV machines are very expensive, and I'm sure the insurance companies don't want to buy one if they don't have to.

I know how it sucks to sleep without your CPAP, but hopefully they will get the results they are looking for and get your treatment adjusted if need be!!!

[unadog]

Part of the question is how his PSG looks for centrals while they are titrating him on a CPAP, I think, rather than how obstructives
look without a CPAP. I say that because of other discussions DD and I have had.

The question, then, is what is causing the centrals. In my case, I have a primary sleep disorder - sleep apnea. And a secondary sleep disorder - pain - that causes fragmented sleep.

So as I have better quality sleep, and then am able to stretch, and exercise a bit, and when I get my pain under control, my sleep is less fragmented due to pain, I have deeper sleep and fewer arousals, and hence fewer centrals.

That is a bit of a "feedback loop.". In my case, I can also go the other way, and spiral out of control. A bad night or inadequate sleep increases my pain levels the next day. The pain, in turn, makes it harder to fall asleep and to stay asleep the next night. The arousals lead to centrals, which make deep sleep impossible. Higher pain levels also requie more pan meds, which can themselves cause centrals and fragment sleep. And so it goes.

[kteague]

I have been on PubMed's site looking with no luck for an article I saw last week about if after cpap there is any residual benefit. The study said at there could be at least the first night.

[DreamDiver]

... since the central's appear on the titration that doing a baseline PSG without xPAP will proably just be a waste of time! It sounds like complex apnea. ...

I agree. However, I'm not the doctor, as is so often pointed out every time I go to the doctor.

Also, I'm not sure why you are confused with hypopnea's? Or maybe I don't understand your question. A hypopnea is a reduction in the airflow by a certain % with an accompanying desaturation. So it's not a complete blockage like an apnea, but a partial. I suppose that the cheyne-stokes breathing could be confused for a hypopnea because since the breath volume is reduced in the former it could appear as a hypopnea? I have no idea how the scoring algo's work though so this is all just rambling on my part.

If the machine doesn't have built-in oximetry, all they can do is estimate when hypopneas occur. Now I understand what's missing: the oximetry component. The algorithm used by our machines can really only estimate what might be a hypopnea because it's only working on data from the last x number of breaths sans oximetry. So in the case of M-Series machines vs. S9, it's entirely possible that the algorithm used to detect 'hypopneas' in breathing patterns on the M-Series really is detecting and misinterpreting Cheyne-Stokes breathing.

In my PSG for example, I have nearly ALL hypopnea's and a minimum desat of no less than 90%, and yet I'm still OSA. And I also am not 100% on CPAP, but I'm not sure how bad my central's are, they appear at 11cm and higher, so I'm stuck at 10.5cm.

AND

The hypopneas as someone described was correct. It is a partial blockage of the airflow. It blocks enough of the airway that it causes the O2 saturations to drop. You need a 4% drop on O2 to count it as a hypopnea. It used to be the same way for an obstructive, but now we don't need a desat in O2 to count it as obstructive as long as the flow is flat.

See, that's just it. In the titrations above, they show central and obstructive hypopneas as possibilities, but they're all in the obstructive category both times. I don't get how they can create two columns - obstructive and central - if there really is only one column somewhere between central and obstructive.

The CPAP does not train the airway to stay open, so the second you fall asleep with out xpap, gravity takes over, and airway closes. Ive been on CPAP for just over a year now and the second I fall asleep without my mask, I snort, wake up, and head to bed with CPAP.

In my case, the training would be central, since gravity is not a factor. It makes sense that if all they check is whether there is breath and not airway patency via COS and/or FOT, there is truly no logic to the system. Under that method, anything over a certain number of seconds is going to look obstructive. I question the several 'obstructive' apneas they found in my case because there are only a couple and they're always over thirty seconds. I want to at least check for COS in the original flow and mask pressure graphs for those examples to discover whether they really are appropriately marked as obstructive. In other words, I question the original reading.

Part of the question is how his PSG looks for centrals while they are titrating him on a CPAP, I think, rather than how obstructives
look without a CPAP. I say that because of other discussions DD and I have had.

The question, then, is what is causing the centrals. In my case, I have a primary sleep disorder - sleep apnea. And a secondary sleep disorder - pain - that causes fragmented sleep.

Yes - pain. Just trying to find a position to sleep in that isn't painful is, at this point, theoretical. This need to go from CPAP to BiPAP to SV when the data clearly show periodic breathing and all centrals on the S9 seems outrageous to me. They make you spend more money in labs and extra machines than you would if they just put you on the SV to begin with. And it ends up costing the insurance more in the long run because you first buy the CPAP, then a biPAP, then an ASV and have multiple labs in between. The whole system not only keeps me in pain longer, it prolongs the path to recovery and restorative sleep. They've never found stage three or four sleep in any of my studies. My apneas are predominantly central - and apparently always have been. I don't look forward to the aftermath headache from a baseline study. I'm not convinced they'll find anything that says I should be on SV.

I have been on PubMed's site looking with no luck for an article I saw last week about if after cpap there is any residual benefit. The study said at there could be at least the first night.

Thanks, kteague. I'd thought I'd read something like that on the forum too, especially with regards to centrals, but I couldn't be sure.

I'm Eeyore tonight, I guess. I'll get back to sleep in a little while. That should help. Thanks for letting me vent.

[echo]

... since the central's appear on the titration that doing a baseline PSG without xPAP will proably just be a waste of time! It sounds like complex apnea. ...

I agree. However, I'm not the doctor, as is so often pointed out every time I go to the doctor.

Yeah, I know what you mean.

Also, I'm not sure why you are confused with hypopnea's? Or maybe I don't understand your question. A hypopnea is a reduction in the airflow by a certain % with an accompanying desaturation. So it's not a complete blockage like an apnea, but a partial. I suppose that the cheyne-stokes breathing could be confused for a hypopnea because since the breath volume is reduced in the former it could appear as a hypopnea? I have no idea how the scoring algo's work though so this is all just rambling on my part.

If the machine doesn't have built-in oximetry, all they can do is estimate when hypopneas occur. Now I understand what's missing: the oximetry component. The algorithm used by our machines can really only estimate what might be a hypopnea because it's only working on data from the last x number of breaths sans oximetry. So in the case of M-Series machines vs. S9, it's entirely possible that the algorithm used to detect 'hypopneas' in breathing patterns on the M-Series really is detecting and misinterpreting Cheyne-Stokes breathing.

In my PSG for example, I have nearly ALL hypopnea's and a minimum desat of no less than 90%, and yet I'm still OSA. And I also am not 100% on CPAP, but I'm not sure how bad my central's are, they appear at 11cm and higher, so I'm stuck at 10.5cm.

AND

The hypopneas as someone described was correct. It is a partial blockage of the airflow. It blocks enough of the airway that it causes the O2 saturations to drop. You need a 4% drop on O2 to count it as a hypopnea. It used to be the same way for an obstructive, but now we don't need a desat in O2 to count it as obstructive as long as the flow is flat.

See, that's just it. In the titrations above, they show central and obstructive hypopneas as possibilities, but they're all in the obstructive category both times. I don't get how they can create two columns - obstructive and central - if there really is only one column somewhere between central and obstructive.

Well the difference between an obstructive apnea (and therefore also an obstructive hypopnea) vs. a central apnea is that they can measure respiratory effort on the obstructive apnea, whereas with a central there is no respiratory effort. So in fact they should have no confusion scoring those. I do not think that a central hypopnea exists.
I'm guessing that in the case of mixed apnea, there is initially respiratory effort, which is obstructed (hypopnea or apnea), and for some reason your brain stops the effort to breath, i.e. respiratory effort also stops, resulting in a central apnea. Technically those are called "Mixed apneas" because you have both types (central and obstructive) in ONE breathing episode, and you have NONE of those on your titration.

BUT what the mayo clinic reports as Complex apnea is (from what I understand) positive pressure induced Central's (which are what mine also tend to be but not nearly as severe as you). They are not mixed apneas, they are 100% central's: during breathing cessation they start and end as apnea's "with no respiratory effort" so simply the body ceases to give the trigger to breath at the higher pressures. The problem with this scenario is that too low a pressure doesn't stop the obstruction (resulting in many hypopneas) and a too high pressure stops the hypopneas but also causes the central's to appear.

So I'm just guessing here, but Cheyne-stokes respiration would most likely get logged as a hypopnea, not a central, since there IS respiratory effort present.

How your XPAP actually logs those, I have no idea.

Going back to the titration, you state

See, that's just it. In the titrations above, they show central and obstructive hypopneas as possibilities, but they're all in the obstructive category both times. I don't get how they can create two columns - obstructive and central - if there really is only one column somewhere between central and obstructive.

What are all in the obstructive category both times? You have Obstructive events for Apnea's as well as Hypopnea's, and Central events for Apnea's. It seems to fit with the Complex Apnea theory (NOT mixed apnea, except for the lone mixed event in 2008). Anything that starts out as an obstruction and then turns into a central should be marked as "Mixed" so anything else is just that: either an obstruction or a central.
Now I am really confused as to why you are confused, sorry DreamDriver.

The CPAP does not train the airway to stay open, so the second you fall asleep with out xpap, gravity takes over, and airway closes. Ive been on CPAP for just over a year now and the second I fall asleep without my mask, I snort, wake up, and head to bed with CPAP.

In my case, the training would be central, since gravity is not a factor. It makes sense that if all they check is whether there is breath and not airway patency via COS and/or FOT, there is truly no logic to the system. Under that method, anything over a certain number of seconds is going to look obstructive. I question the several 'obstructive' apneas they found in my case because there are only a couple and they're always over thirty seconds. I want to at least check for COS in the original flow and mask pressure graphs for those examples to discover whether they really are appropriately marked as obstructive. In other words, I question the original reading.

OK, that's a fair statement. I *think* but I'm not sure that they only way they can best detect respiratory effort (and therefore distinguish between centrals and obstructions) is with the abdominal sensor... though how some machines accurately detect central's without that, beats me. FOT/COS is probably less reliable than the abdominal measurement ... and some recent banter on that topic: viewtopic.php?f=1&t=47953&st=0&sk=t&sd= ... 30#p435772 (and page 10 too).

Part of the question is how his PSG looks for centrals while they are titrating him on a CPAP, I think, rather than how obstructives look without a CPAP. I say that because of other discussions DD and I have had.

Well that's where *I'm* confused again. Because how can a baseline PSG without xPAP help determine former? Maybe it goes back to DD's first comment that they since he's not the *doctor* they don't listen to him... etc...

...They've never found stage three or four sleep in any of my studies. My apneas are predominantly central - and apparently always have been. I don't look forward to the aftermath headache from a baseline study. I'm not convinced they'll find anything that says I should be on SV.

Well we've got a few different scenarios, I'm thinking:

Worst case scenario: PSG shows no events, nada, zip, zilch. Likelihood = zero. We know you've at least got something going on proven by the post-sleep hangovers (yeach).

Worse worst case scenario: PSG shows lots of obstructive events but no centrals. Outcome = You get put on CPAP/APAP and life goes back to the status quo (and the post-sleep hangovers continue). This is probably what will happen, right?

Better scenario: They decide to titrate you directly with an ASV or BiPAP or whatever is necessary for Complex Apnea (or whatever other flavor of apnea you might have).

You say

Unfortunately, I've been hoodwinked into believing I'll get a different result.

Is this the same sleep lab that did the last two titrations? WHY would the results be any different then? Have you looked up another lab that's more familiar with complicated apnea cases?

While I can understand having a GOOD baseline PSG would be useful, it sounds to me like your breathing patterns change drastically when on positive pressure, so you'd think they would want to look deeper into that. (Which is EXACTLY what you're saying too!)

Are you sure you had ONLY central's on your baseline PSG? It's quite possible that you have both obstructive hypopnea's as well as central's, explaining why

I have centrals only. That much is what the S9 is showing. When I titrate below 10.4, AHI rises. When I titrate above 10.4, again - AHI rises. So I know I should be on xPAP. However, they are all centrals, and I do have periodic breathing.

So are all the events below 10.4 ALSO centrals? Seems reasonable to think those are obstructive events. (But maybe I'm reading too much of my own situation into yours).

Can the s9 differentiate between obstructions and centrals??

IF indeed you have ONLY centrals, with or without xPAP, and you don't trust your initial baseline PSG, then yes it sounds like a new baseline PSG would be the way to go.

But if the problem is pressure induced central's, then I still have NO idea why a new baseline PSG would help.

Sorry to beat a dead horse, DD, just trying to understand better ...

[DreamDiver]

Well the difference between an obstructive apnea (and therefore also an obstructive hypopnea) vs. a central apnea is that they can measure respiratory effort on the obstructive apnea, whereas with a central there is no respiratory effort. So in fact they should have no confusion scoring those. I do not think that a central hypopnea exists.
I'm guessing that in the case of mixed apnea, there is initially respiratory effort, which is obstructed (hypopnea or apnea), and for some reason your brain stops the effort to breath, i.e. respiratory effort also stops, resulting in a central apnea. Technically those are called "Mixed apneas" because you have both types (central and obstructive) in ONE breathing episode, and you have NONE of those on your titration.

I'm not questioning the concept of central, obstructive or mixed apnea. My question is: why do they even have two columns for central and obstructive hypopneas in my sleep study if there is really only just plain 'hypopnea'. Why not just one column?

What are all in the obstructive category both times? You have Obstructive events for Apnea's as well as Hypopnea's, and Central events for Apnea's. It seems to fit with the Complex Apnea theory (NOT mixed apnea, except for the lone mixed event in 2008). Anything that starts out as an obstruction and then turns into a central should be marked as "Mixed" so anything else is just that: either an obstruction or a central.
Now I am really confused as to why you are confused, sorry DreamDriver.

No confusion here. I understand all of this. In general, I don't seem to have mixed apnea, according to the S9.

I *think* but I'm not sure that they only way they can best detect respiratory effort (and therefore distinguish between centrals and obstructions) is with the abdominal sensor... though how some machines accurately detect central's without that, beats me. FOT/COS is probably less reliable than the abdominal measurement ... and some recent banter on that topic: viewtopic.php?f=1&t=47953&st=0&sk=t&sd= ... 30#p435772 (and page 10 too).

I hear the argument that the sleep lab method using bands is more effective at measuring whether an apnea is obstructive than is FOT. I'm not sure what to think. On my last two studies, every apnea of a duration long enough to cause serious desaturation seems to be automatically labeled as obstructive. I think there is something screwy with the method. Either the sleep tech isn't fully aware of what constitutes a central apnea when grading visually, or the automatic grading algorithm they used is messed up.

Part of the question is how his PSG looks for centrals while they are titrating him on a CPAP, I think, rather than how obstructives look without a CPAP. I say that because of other discussions DD and I have had.

Well that's where *I'm* confused again. Because how can a baseline PSG without xPAP help determine former? Maybe it goes back to DD's first comment that they since he's not the *doctor* they don't listen to him... etc...

Precisely.

...Worst case scenario: PSG shows no events, nada, zip, zilch. Likelihood = zero. We know you've at least got something going on proven by the post-sleep hangovers (yeach).

Worse worst case scenario: PSG shows lots of obstructive events but no centrals. Outcome = You get put on CPAP/APAP and life goes back to the status quo (and the post-sleep hangovers continue). This is probably what will happen, right?

Better scenario: They decide to titrate you directly with an ASV or BiPAP or whatever is necessary for Complex Apnea (or whatever other flavor of apnea you might have).

BiPAP isn't going to cut it for complex apnea or central apnea. It's only because insurance companies insist a BiPAP trial that they go there.

Is this the same sleep lab that did the last two titrations? WHY would the results be any different then? Have you looked up another lab that's more familiar with complicated apnea cases?...
Are you sure you had ONLY central's on your baseline PSG?

The scenario where I continue to get more white matter lesions because the study system isn't 'set' to see what's actually going on in my particular situation. I don't fall into their neatly categorized pigeon holes. They'll tell me I no longer need CPAP. I can go home and stop using the mask because they only saw three apneas in four hours. They'll whisk me out the door to make room for the next number. That's probably the worst case.

The whole game has changed in three years. Now we have RERA's. Besides REM, there are now only three stages of sleep instead of 4. Then there's FOT, etc. I have no earthly idea of what this new sleep lab is capable or incapable. I can't have any expectations. The facility is only a couple years old anyway.

It's quite possible that you have both obstructive hypopnea's as well as central's

Again - why is there even a column for central hypopneas and obstructive hypopneas if the distinction does not exist? The same reason that all my 'hypops' were labeled obstructive leads me to question every apnea labeled as obstructive in all my previous sleep studies from that lab.

So are all the events below 10.4 ALSO centrals? Seems reasonable to think those are obstructive events. (But maybe I'm reading too much of my own situation into yours).

I self titrated from 8 up to 11.5. The sweet spot with the fewest apneas was 10.4. All apneas except 4 total in the last month are marked by the S9 as central. One of those four was intentional, at the end of one mask event as a test. I just recently had one labeled as 'Unknown'.

Can the s9 differentiate between obstructions and centrals??

Yes.

Enhanced AutoSet™ Algorithm
The S9’s Enhanced AutoSet algorithm now differentiates between obstructive and central sleep apneas and responds appropriately. You can enjoy peace of mind because you'll know you’re always receiving optimal therapy at the lowest necessary pressure.

IF indeed you have ONLY centrals, with or without xPAP, and you don't trust your initial baseline PSG, then yes it sounds like a new baseline PSG would be the way to go.

But if the problem is pressure induced central's, then I still have NO idea why a new baseline PSG would help.

I suspect I've had centrals since childhood. Obstructive apnea is what they're looking for, though, so that's how I was labeled. I even asked the doctor about it at the 2008 titration. The response was 'Oh, well a few centrals are no big deal.' Except there was only one OA. The rest were central. He just wanted to get me out the door because I was asking too many questions. I had gone over the fifteen-minute limit slated per patient.

Looks like we're both beating a dead horse...

[echo]

It's quite possible that you have both obstructive hypopnea's as well as central's

Again - why is there even a column for central hypopneas and obstructive hypopneas if the distinction does not exist? The same reason that all my 'hypops' were labeled obstructive leads me to question every apnea labeled as obstructive in all my previous sleep studies from that lab.

OK, now I get it. I have no idea. I don't know if there is such a thing as a central hypopnea, and if there is, whether they might have scored them incorrectly.

Looks like we're both beating a dead horse...

I'm all out of words of wisdom. Maybe you need to find a good sleep clinic with a neurologist rather than a pulmonologist?

Well in any case, I hope the baseline PSG finds _something_ and that they do a decent followup! Sending you lots of good wishes....

[-SWS]

It's quite possible that you have both obstructive hypopnea's as well as central's

Again - why is there even a column for central hypopneas and obstructive hypopneas if the distinction does not exist? The same reason that all my 'hypops' were labeled obstructive leads me to question every apnea labeled as obstructive in all my previous sleep studies from that lab.

OK, now I get it. I have no idea. I don't know if there is such a thing as a central hypopnea, and if there is, whether they might have scored them incorrectly.

Central hypopneas really do exist and are thought by many researchers and practitioners to be part-and-parcel to CompSAS/CSDB in some patients. Not all researchers and practitioners share that opinion, though.

My understanding is that PSG differentiation of central apneas versus obstructive entails a fairly high sensitivity and specificity of measurement. However, IMHO PSG differentiation of central hypopneas versus obstructive should theoretically not entail the same high measurement sensitivity/specificity that PSG differentiation of apneas afford.

Again - why is there even a column for central hypopneas and obstructive hypopneas if the distinction does not exist?

Well, the distinction exists in the machine's data set----which says nothing about accuracy regarding measurement sensitivity or specificity. But I also doubt that all your PSG hypopneas were obstructive---based on my belief that complacent PSG scoring often occurs because the hypopnea-differentiation methodology is lacking. I personally happen to have far less doubt about the PSG differentiation of your apneas, however.

DD, are you by any chance a sensitive sleeper---meaning that you wake easily to either sensory or psychological stimuli?

[DreamDiver]

DD, are you by any chance a sensitive sleeper---meaning that you wake easily to either sensory or psychological stimuli?

It has to be something out of the ordinary. If I hear a deer outside, or a pine cone fall on the roof, that 'scores' as normal background noise. I don't wake up. If I hear someone walking down the hall in the dark, I wake up immediately. Stealthy human movement is more apt to wake me than normal knocking around, opening or closing of doors, drawers, flushing of toilets, etc. Videos playing in the background - even more violent ones like 'Fifth Element' or 'Dark City' would put me to sleep as easily as 'Pride and Prejudice'. Kids yapping in the background is a comfortable white noise. Kids stopping yapping is not. Tip-toeing is not. I imagine I'm not outside the normal range there.

As to psychological stimuli... I am not sure. What would you mean? Illusory sensory stimuli produced by the mind? Like dreams?