APNEA -v- HYPOPNEA

[kurtr]

Thanks Chuck, SWS, and Snoredog for your comments.
I am on straight CPAP and feel much better when I wake up so I will keep on that path for a while then go back to auto and see how I feel and how the numbers look.
What was interesting to me is that my numbers on auto would have indicated that I was receiving good treatment yet I felt bad????
Also, I have tried many masks over the last two years and only can get throught the night on a Resmed full mask and I am now wondering about the "dead space" that you guys discussed.

Thanks,
Kurt

[-SWS]

Snoredog, very good find. However, a couple points or questions come to mind. First that corporate patent statement only cites an interpretive position or stance with respect to 8 cm of constant pressure. Unfortunately it says absolutely nothing about the effects of APAP's constantly varying pressures on rare individuals with either CSDB or a predominately hypercapnic respiratory drive. The other points that come to mind deal with the study and even its interpretation behind that corporate patent statement. Even though the statement speaks of constant pressure (and I believe the statement to be true, btw) I would still love to see precisely how the study was devised, executed, and exactly what the resulting data looked like. I would even love to know just how many statistically anomalous patients fell on the short side of probability's indicator stick during the experimental trial(s).

With that said I personally believe 8 cm of constant pressure can be problematic only in rare cases. I also think there may be an entirely different distribution curve regarding acceptable patient response to APAP's varying pressures (compared to CPAP). My position isn't a case of saying APAP is problematic. Far from it. In general terms I will recommend APAP over CPAP for benefits having to do with lower mean pressure, great efficacy data, easier acclimation for many. I am still an advocate of APAP. My position only says that there will always be patients falling on the short side of probability's stick, and when candidates for low probability occurence do arise it's not such a bad idea to scrutinize the details and postulate. If nothing more comes from that process than pure serendipity by way of a valid therapy change, then the exercise was, indeed, a fruitful one.

Chuck, I'm also starting to question whether your response had anything to do with pressure. And the difference in dead space between those two masks are thought to be absolutely negligible to the vast majority of patients with respect to CO2 retention---since slight-to-moderate amounts of CO2 variation are easily normalized in any stable respiratory system. I think only a rare CSDB respiratory drive (likely not the established CSDB case) might find a destabilizing hypocapnic trigger point (i.e. lacking adequate CO2) with respect to how marginally accelerated CO2 transition rates happen to be in the Swift compared to that of the Activa. Greater dead space can yield marginally retardant CO2 depletion in a mask. In unstable systems, transients, thresholds, and margins can become much more salient than in equivalent stable systems. I suppose the same can be true in even a marginally unstable respiratory sytem compared to the normal highly stable respiratory system. Thus I don't think the "normal case" CO2 assimilation model discussed and employed in that vast thread on TAS would necessarily be applicable in all cases of unstable, threshold-driven CSDB respiratory drives. Up for consideration is a hypercapnic respiratory drive that properly triggers with adequate CO2 levels during all adequate CO2 transitional rates, yet fails to properly trigger under comparatively hypocapnic albeit fleeting transitions. A destabilized CO2-based trigger if you may that is CO2-depletion "twitchy" because the respiratory drive itself is largely hypercapnic, inherently unstable, and thus destablizes (once again thus failing to trigger under fleeting CO2 transitions that are hypocapnic relative to the hypercapnic respiratory drive's CO2 trigger needs).

With that said, the question remains how rare is your response to APAP, pressure, CO2 depletion? Perhaps not so rare. Perhaps none of these issues are your driving factor regarding how you sleep, feel by day, and how high or low your AI and HI happen to fluctuate. The other outstanding question is why did you experience your best sleep the night you changed to 8 cm fixed pressure? And why were the ensuing nights of sleep also much better for you? How episodic on non-existent will your "bad" nights of sleep be in the future and what will the trigger events and relevant factors be? Mask? Pressure magnitude? Pressure fluctuation? Environmental changes? Dietary changes? Pharmaceutical changes? Stress? Known or unknown concomitant episodic disorders? Purely incidental fluctuations that are idiopathic?

In any event it will be great to see your data on a continued basis and hear your own conclusions relating to not only the data but how well you sleep by night and feel during the day. Yours is an interesting case, I am extremely glad you are willing to share your mystery with us! Please keep that data and your own thoughts rolling, Chuck.

Kurt, wonderful! Be sure to give yourself plenty of time in collecting data with any one change before attempting to conclude about those changes. I peresonally think it is necessary to tentatively attribute or postulate along the way, but conclusions (if and when they can be reached) require methodical and prolonged experimentation. I am so glad your results are improved. See my comment above about the differences in mask dead space having a negligible effect in all but the very rarest cases of CO2 transitional thresholds.

[-SWS]

I am on straight CPAP and feel much better when I wake up... .What was interesting to me is that my numbers on auto would have indicated that I was receiving good treatment yet I felt bad????

Kurt, the placebo effect is a definite possibility. It is my mortal enemy when I run my own experiments. Other unforseen factors may be at play as well. However, in the extremely rare case of CSDB, anecdotes at this early stage just may indicate an overly symptomatic response to at least some CSDB sleep event components. The central components within CSDB just may be more debilitating or degrading than ordinary obstructive sleep events (my own guess). If there is any truth to this speculation, then an AHI comprised predominately of central CSDB components may yield more severe symptoms than the same AHI comprised either purely or predominately of ordinary obstructive SDB events.

If there's any truth to that far flung speculation, then an AHI at a higher pressure can feel worse than the same AHI at a lower pressure for any given CSDB patient---assuming central components are buried in that former AHI (because of pressure or CO2-related induction) and that there are either no or considerably fewer central components in that latter AHI.

Again, the ability to have identical AHI's at two given pressures presumably goes back to concurrent SDB etiologies at work with diametrically opposed pressure requirements. It can also be attributed to episodic fluctuation. However, when the trend becomes well defined over time, and distinctly parabolic on a pressure-versus-AHI graph, then the identical AHI scores at high and low pressures just may attribute to diametrically pressure opposed etiologies in my own mind (with a slight machine-induced CSDB effect quite possibly emerging as salient in the high-pressure score compared to the identical low-pressure AHI score in these admittedly rare cases).

I hope people do not misconstrue my own conjecture as any sort of scientific fact. My own speculation is not proven fact by any stretch of the imagination. Just one patient sharing his thoughts to others.

[Guest]

SWS wrote:

Snoredog, very good find. However, a couple points or questions come to mind. First that corporate patent statement only cites an interpretive position or stance with respect to 8 cm of constant pressure. Unfortunately it says absolutely nothing about the effects of APAP's constantly varying pressures on rare individuals with either CSDB or a predominately hypercapnic respiratory drive. The other points that come to mind deal with the study and even its interpretation behind that corporate patent statement. Even though the statement speaks of constant pressure (and I believe the statement to be true, btw) I would still love to see precisely how the study was devised, executed, and exactly what the resulting data looked like. I would even love to know just how many statistically anomalous patients fell on the short side of probability's indicator stick during the experimental trial(s).

that is true, we don't know much about the study behind that statement, but I am sure there are references to it in the original patent application for the examiner. But the statement itself is fairly common knowledge and it was only referencing what was already known. As mentioned, I had read a similar statement in one of Resmed's apap studies where they mention something similar. I believe they specified up to 70% of SDB events in that study. I may even have a copy of that study, will try and find it. If you go back to before the days of full PSG's and titration studies, they would just send you home with a cpap set at 10cm. My sleep doc is like 150yrs old (yes older than Keith Richards) and he is full of stories of the old days

But keep in mind when you make statements of fact in a patent application, they better be of such or the examiner will question it if their research does not find similar reference. This patent does have other statements as it relates to variable breathing and detection methods. The Remstars do have a variable breathing control circuit as described in (FIG.12) as part of their invention which also describes the logic behind its function.

In fact, I think the Remstar Auto actually does a better job at detecting and supporting variable breathing patterns than any other apap out there based upon my own experience with them.

I somewhat understand the theory behind CSDB in reference to variable pressures as a possible trigger for CSDB, but I also believe that some machines take special steps to avoid such triggers and that is not the case with every machine. If you compare how a apap titrates to a manual titration there is not a lot of difference. A good tech uses guidelines when changing pressure while observing the EEG channels as not to cause arousal. If they change pressure they may sit there for 5-15 minutes monitoring the same. The apap does the same, it is even spelled out in the Remstar patent.

But if you think about it, CSDB or a form thereof and variable breathing were known and discussed going as far back as 1818-1854 area when Dr. J. Cheyne and Dr. W. Stokes did research on the topic for which the syndrome is named. It could also be why I have such a difficult time distinguishing the difference between CSR and CSDB. To me they appear one of the same as both can be influenced by changing CO2 levels as described in Cheyne-Stokes Respiration During Sleep in CHF (CHEST/111/12 FEBRUARY, 1997).

And I agree, like you, I'm also a big fan of apaps and use one myself, there was a reason behind me having at one time had more than 6 autopaps sitting my closet. I still have 2 or 3, I've sold several here recently at a pretty good loss from what I've actually paid for them, good for cpap.com, but not so good for my wallet, but for me it was all about finding the right machine for my own particular breathing pattern. For me, the Remstar remains the better machine for my particular breathing pattern, I do better on apap than cpap, better on AFLE than APAP. I found even a noticeable difference in the same machine going from firmware version 2.1 to 2.5 to 2.9.

My suggestion to Chuck is: not to draw too many conclusions from his findings so quickly, personally I think his machine is incapable of accurately responding to his particular breathing pattern automatically based upon my own experience with it (if it truly is CSDB). I've yet to read where they equipped that new machine with a more sensitive pneumotach sensor. If not equipped, it still has that old technology hall door effect sensor. I say that because of his ever moving 95% pressure, it simply doesn't vary by that much from night to night, if it is, something is wrong, like his breathing patterns are being totally misread. But that is just my opinion and people don't like to hear they possibly may have selected the wrong machine. But if it was me, I would do a careful manual titration above and below the found pressure of the other day to confirm it over several weeks plotting AI and HI carefully in a spreadsheet with corresponding pressures used so it is easy to see.

However, what will be missing from his data will be FL, snore and NR data. Like I said before, it is much easier to see this using a Remstar w/EncorePro report as it pretty much plots it all out for you. It also tracks and records information the other machine simply doesn't have. If he gets the Reslink option he will end up with actually more information, but then it will also change the way the machine currently responds as it now has the CO2 channel.

I think the most important thing out of this discussion is it makes a patient more aware of the syndrome should it exist and helps them spot it more readily especially if they have a recording machine. I think every patient should have a recording machine and get that information directly off the display. If they did, there would be a lot more people in compliance and better treated.

And I think it is also a good example that the first approach to a change is not always increase pressure.

[Snoredog]

Rats! that was me again!

[-SWS]

Snoredog, after composing a long post you may want to try: 1) highlighting and copying all text with your mouse, 2) hitting browser refresh, 3) if still "logged on" as shown at the top of your screen, then simply hit "submit" for your post and be done with your submission, 4) if not logged on, then re-log on, re-enter same thread as if making a brand new post, but use your mouse to instantly "paste" all your stored text, then 5) hit "submit" for your post now that you are logged on again.

Thanks as always for your well considered post above!

[roztom]

Great Discussion:

I regret being late to the party.

I had posted several months ago the issue you have been discussing n the data.

I have a similar situation as Chuck.

My AHI is 1.75 at 5-6 cm from 6-8 it jumps to AHI 5 at 9cm it drops to 2.0 at 10 cm it jumps jumps to 4.0. Just a 1cm change. At 11 it goes higher.

My snore goes up until 8cm but drops to 0 at 10cm but my AHI goes up at 10cm. Snore 0, AHI 4.0. COunter-intuitive.

I've self tested at 1cm increments 5-6, 6-7, etc to try to find my sweet spot.

5 seems to be my best pressure but it seems like an effort to breathe, otherwise 9 cm is the best for me. When I set the machine to APAP I range all over but my numbers follow the same track as when I set them in increments. MY AHI increased with the pressure with the exception as noted.

My sleep Doc disagrees with what my data is saying. He says the higher AHI at the higher numbers is the machine responding to HI & OA but I say what comes first the event or the pressure? The data indicates to me that the pressure is coming first and that is triggering the events.

This is a good discussion.

Thanks,

Tom

[-SWS]

SWS: MY OA goes up as my pressure goes up but my NR is zero. I've never had one. Also when I was titrated they ran the pressure up to 16 and I never had a Central.... ...MY OA are typically 12 seconds, no matter what pressure they are at.

Tom, when you say that your OA is typically 12 seconds, no matter what pressure they are at, this tells me the resolution of that apnea just may be pretty darn pressure independent. And if those 12 second apneas are pressure independent, then what might be resolving them if not pressure?

Here's a rhetorical question: What would a 12 second central apnea register as in Encore Pro software? The answer is that unfortunately it would register the same as any 12 second obstructive apnea. It would not show up as an NR event because it disappears before the amount of time three pressure increments would take. That's right. In Encore Pro software a 12 second central apnea is indistinguishable from a 12 second obstructive apnea. And if your 12 second apneas are resolving in a pressure-independent manner, it sure sounds to me like a marginally destabilized respiratory drive taking about 12 seconds to stabilize emergent CSDB-induced apneas. Again, very rare and likely of little or no consequence to you. Thus the manufacturer of your APAP would not consider your response to in any way be problematic. Neither would I.

Why no machine-induced centrals in the PSG then? If they titrated nice and slow exactly as they should have, then this effect is avoided in many patients. When they titrate upward, very quickly, they know that they will see pressure-related emergent central apneas in some rare cases. you are a rare bird, Tom. But in my opinion you are a good candidate for someone who manifests just a slight machine-induced CSDB effect.

More on the challenges of measuring/attributing central hypopneas and central flow limitations later. More later on the theoretical machine-induced CSDB effect hiding rather cleverly in the details of measurement when that CSDB effect is marginal-to-moderate...

[Ric]

5 seems to be my best pressure but it seems like an effort to breathe, otherwise 9 cm is the best for me. When I set the machine to APAP I range all over but my numbers follow the same track as when I set them in increments. MY AHI increased with the pressure with the exception as noted.

My sleep Doc disagrees with what my data is saying. He says the higher AHI at the higher numbers is the machine responding to HI & OA but I say what comes first the event or the pressure? The data indicates to me that the pressure is coming first and that is triggering the events.

Tom,

I am puzzled as to how you think the pressure arrives first, then the HI/OA event. The pressure only goes up in response to a detected "event". If the pressure goes to 10, say, (assuming you are operating in APAP mode) and is successful, and it takes 12 seconds to clear the event, then lingers there for several minutes "just to be sure", there will be an OI recorded at that pressure. That doesn't mean the pressure is "bad". The pressure of 10 should not be punished for being at the scene of the crime. There is nothing (that I know of) in the data to suggest it is the other way around. What I usually see in the MyEncore detailed report is a tick mark indicating an event detection, then a rise in pressure, followed by a lingering "at pressure". That seems like exactly what you would hope it would do. That represents APAP at it's finest.

[-SWS]

I believe the sequence of events that just may support Tom's suspicions necessitates that we separate the "event" types to see precisely how they are sequenced. Specifically, the pressure might increase to either snore or flow limitation, the suspected pressure-induced apnea/hypopnea would then occur, and it would be hard to distinguish from equivalent obstructive events (short of a pressure-versus-AHI trend analysis tool that might be indicative of pressure-opposed etiologies). In this admittedly highly theoretical machine-induced CSDB scenario the fleeting central apnea will very likely be riding the tail end of a pressure-invoking sequence of one or more lesser obstructive events. In other words a seqeunce of one or more lesser SDB events occur, APAP pressure consequently increases, the marginal CSDB respiratory drive becomes mildly destabilized in response to the pressure increase, a fleeting central apnea then occurs, and Tom's respiratory drive takes approximately 12 seconds to restabilize before his respiration is neurologically resumed (Tom's 12 second apnea cases only). That fleeting 12 second central apnea is completely undistinguishable as central to Encore Pro because of its short duration. As far as Encore Pro is concerned it was resolved in 12 seconds and is thus not "NR". It is therefore assumed to be obstructive and relegated to the OA category. The next morning Tom reads his pre-interpreted data and notes his mis-categorized 12 second "obstructive" apnea(s) on the charts, not realizing they were really central.

Tom, can you tell us exactly what the sequence for your four recorded "event" types (s, fl, a, h) happen to be when these 12 second apneas occur? Also, can you tell us how your flow limitation index trends happen to manifest with respect to pressure? Thanks.

This, of course, is all admittedly highly questionable conjecture on my part at this point.

[GoofyUT]

APAP/Activa

AHI=2.6;AI=0.0;HI=2.6;Pressure(95%)=10.2.

C

[-SWS]

Snoredog, you talked about the possibility of obstructive events being possible in response to pressure increases. In the very words of the CSDB researchers who authored the Harvard study:

"Associations include native cephalometric abnormalities, acquired soft tissue abnormalities such as enlarged tonsils, obesity, effects of androgenic hormones, dysfunctional protective upper airway reflexes, upper airway neuropathy/myopathy, and increased airway length. (bold emphasis mine)

"The mathematics of unstable CO2 oscillations may have underestimated the destabilizing effect of the upper airway. The upper airway is in effect doing exactly the opposite of what is ideal to counteract instability - the airway is widely patent when the system is maximally eliminating CO2 and closed when respiratory effort is at its nadir." (bold emphasis mine)

So yes, it does seem that as CSDB respiratory effort reaches its nadir in response to dysregulating depletion of CO2 that the airway may contract or collapse as a purely neurological response. This particular neuromuscular reaction is what the CSDB researchers termed as a "dysfunctional protective upper airway reflex".

More interesting statements from the authors of that study: "These oscillations in CO2 may manifest as either frank central apneas if the threshold is crossed or perhaps as central hypopneas as the apnea threshold is approached." (bold emphasis mine)

There is the theoretical CSDB associated central hypopneas we have been referring to all along in wondering about Chuck's increased HI and now Tom's pressure-related hypopnea trends. However, I mentioned earlier that CSDB just may be rather cleverly hiding in the details of measurement. Certainly in the Encore Pro example I cited above. But much more importantly:

"Qualitative scoring of this type of disease is limited by imprecision of terms such as 'mixed apnea,' and accurate scoring of central hypopneas is impractical in routine clinical practice." (bold emphasis mine)

"More subtle forms of periodic breathing are much more difficult to characterize, and in clinical practice 'central hypopneas' are not scored." (bold emphasis mine)

In other words, current PSG instrumentation, measurement, and scoring techniques fall short in the extremely difficult task of differentiating a central hypopnea from an obstructive hypopnea. And as that frank central apnea threshold is approached, if the neurologically associated flow reduction does not quite meet the scoring criteria for hypopnea, then we presumably have our suspected CSDB associated central flow limitations rather cleverly hiding on the sleep charts as well (my own conjecture). Of course, the differentiation challenges of measuring and scoring theoretical central flow limitations may be even greater than those of central hypopneas.

[Snoredog]

SWS:

I agree, and I'm pretty much all but convinced these ARE central hypopnea and the machine IS confusing and "scoring" them as obstructive in the reports.

If they have a difficult time in a PSG scoring them correctly, then a machine is not going to be any better at it. We have always known that too much pressure can trigger pressure induced central apnea and reason I have always advocated setting a high pressure limit on any autopap used especially when you got over 10cm pressure.

But I didn't realize central hypopnea were so prevalent at lower pressures below 10cm. In fact all my years on these boards I've never seen it really discussed before as being an item of concern. I see now they are central hypopnea being scored by these machines as obstructive. If they are central hypopnea and you have hundreds per night, that is a lot of time without oxygen, could also explain why I feel so lousy.

It also makes sense as to WHY when the pressure is lowered they decrease in count. You have seen from my sample report these events increase with pressure, this I have known for several years but never quite nailed down the cause.

I did see a few Centrals and Mixed scored on my original PSG and several thereafter but they were never were a count to be concerned with according to the PSG tech and my sleep doc. I always looked for that "dip" in the reports and if I used my RemstarPro I set it to that pressure. I used a 30-min ramp with it. I like the Pro because it was the only machine I had that had C-Flex feature which I really like.

I would use my Remstar Auto to check pressure every now an then or to pull a report but I would always go back to the Pro which had no reporting feature. Now that I have a new Remstar Auto with C-Flex I don't have to go back to the Pro and can still get the reports. I have been using it in the AFLE mode, (one night in CFLE) and it seems to work fine, I actually feel better with it.

I guess you could say the reports can be good or bad for the patient, but for me it was good as it helped identify a pattern trend that they also didn't pick up on in the 4 different PSG's I had (last 3 where titration).

Now that I know what it is I can avoid it. It also explains why the other autopaps I had tried didn't come close in working for me either.

I snore (hence name snoredog), the snore triggers a pressure response form the machine, that pressure increase triggers more central hypopnea and the cycle goes on and on as seen in my reports.

If you remember going back a few years when we were on TAS and Nuggy (now known as Titrator) was there with his 418 I had gotten the Spirit and came back after the first night complaining it was blowing 16cm! My pressure has never gone over 10cm in all those PSG's. If you recall afterward we engaged in the snore killer posts. We thought then killing snores was the thing to do, but man it isn't, for some of us it can make things go really south in a hurry

I tried every way possible to use that machine after all I paid over a thousand bucks for it, only way it really worked for me was in cpap mode, in autoset mode pressure was all over the place, I must have changed the floor pressure on that thing a thousand times. If I didn't set a high limit it would blow the top of your head off.

But if I was going to use straight cpap might as well use the RemstarPro and take advantage of C-Flex feature which I believe results in a better night's sleep for me. If your SDB is like mine, a Resmed Autopap simply isn't going to work due to how it responds to snore. If a Vantage functions the same as a Spirit (which I believe it does), it isn't going to work either.

As mentioned the Remstar Auto has that limiting control circuit where it will pause in event detection and if no improvement seen from previous pressure increases it backs off pressure, this probably the only reason I have been able to use that machine in autopap mode. You can clearly see that in the posted report.

I didn't have the 420e long enough to really play fully with the 1FL and 2FL settings to know if it would have danced around this issue. First few nights on it and it did the same as the Spirit and would just blow. When they blow to a point where they wake you up, that is not good.

I also made a mask change last night. For the past 2+ years I have been using the UMFF as my main mask. This last one I got sounds like a bull frog croaking when you breathe in/out. It looked identical to my old one. With the use of this new Auto the past week, I noticed on my daily reports my snore counts were going through the roof. My snores are not loud or even audible with cpap, so WHY is EncorePro showing a snore count SI of 280!

So last night I pulled out the old Activa mask as leaks with the UMFF have been of concern. I didn't even bother taping my mouth, I figured I'd wing it, I pulled a report this morning, my pressure remained the same at 9cm, leaks were WAY down all night in the 25-30L/m range compared to 50-75+, snore count dropped from avg. 80 to 18.

Everything was down:

NR:0.0
FL: 0.8 (new for me, old machines never scored this before).
OA: 0.3
HI=2.0 (13 for the whole night)
SI=7.3 (overall for night, 18 at 9cm pressure, a drop from 80 overall)
AHI=2.3 overall for night

As for CO2 having an impact on my HI count? I know the Activa doesn't have as good as washout characteristics as the UMFF, the Activa has always felt more "stuffy" indicating higher CO2 concentrations compared to the UMFF when I switch. I have always switched to the UMII which had similar washout characteristics as that of the UMFF. But last night I was trying to STOP leaks and wanted to keep my mustache.

I ordered a Hybrid mask the other, when it gets here hopefully it will be better. If you have one of those Bull-Frog sounding UMFF masks, you might want to look at your snore index, I suspect not only does these machines confuse central hypopnea for obstructive hypopnea it can confuse that bull-frog breathing mask noise for snores. It is the only thing I can think of at this time.

This recent Resmed price gouging could not have come at a better time for me, I'm finding the more I divorce myself of Resmed equipment the better off I'll be.

[-SWS]

The interesting thing about hypopnea discussions throughout the years is that for many of us the assumption was that they were probably obstructive hypopneas in all but the rare cases. However, when I see that PSG sleep studies and all APAPs do not differentiate obstructive from central hypopneas, a scenario comes to mind: I tell someone that my sleep event distribution is almost exclusively hypopneic. They are rare and savvy enough to ask me if mine are primarily obstructive or central. The only correct answer I can come up with is, "At this point in sleep science we have no friggin' idea exactly what's going on."

Regarding the neuromuscular airway collapse the Harvard researchers point out. The collapse occurs simultaneously with a central apnea. In other words no respiratory effort occurring as the airway is closed. The dilemma of how to define or term "mixed apnea" thus emerges. Who knew this simultaneous obstructive and central single SDB event was occurring? Most of mainstream sleep science likely did not. To many of them, the term "mixed apnea" meant a fair mix of discrete central and obstructive SDB event types occurring throughout the night, and/or a single migrational event that transforms from being obstructive to central, or the other way around. Yes, sleep science is still in its infancy regarding having any clue whatsoever about how many underlying etiologies are involved in SDB.

The only APAP that indirectly measures central apneas with at least fair accuracy is the 420e. It measures central apneas with virtually a 100% specificity, meaning when it spots a central apnea that it really is a central apnea. However, the 420e also measures central apneas in general with a rather poor 62% sensitivity, meaning that 38% of all central apneas go undetected. It occurs to me that the CSDB central apneas simultaneously manifesting with a closed airway are probably to account for much of the 420e's mediocre cental apnea sensitivity. The 420e relies on cardiac oscillations conveyed through an open airway to determine whether a central apnea has occurred. That means the 420e will miss every single CSDB central apnea that manifests with a simultaneously closed airway. There's a sensitivity of measurement killer right there.

Not so sure I agree with your assessment of the Resmed algorithm compared to the other manufacturers. It's just that I personally haven't been able to analyze all the factors to a great enough level or depth to positively arrive at that same conclusion in my own mind. I am of the opinion, however, that overt or frank CSDB patients should avoid any and all APAP machines regardless of brand, unless they plan to run them at fixed pressure. Marginal cases of CSDB are perhaps debatable at this point.

I wonder just how many marginal-to-moderate CSDB cases there are out there. Significant numbers for sure. But just how rare or common remains to be proven.

[roztom]

I am copying this from the "Pressures All Over the Place " THread because it belongs here:

Well I've run my range from 5-14 and here's what happened, using MyEncore to see AHI vs Pressure. At 5 my AHI was under 2.0 then it went up to 4.5 as pressure increased until pressure got to 9 cm then AHI dropped to 2.0 and then at 10cm it started to climb sharply up to 4 at 11 hits AHI 5.

Here's the rub this happens in APAP mode - of course I'm thinking the machine is responding to events right? Logic says yes.

I then try an experiment locking the APAP in 1 CM ranges. 5-6, 6-7, 7-8, 8-9, etc and give it 5 nights each. What do you think the results would be?

They are the SAME as when the APAP was set for 5 -14. The AHI/Pressure curve is the same !!! You could almost overlay the 2 graphs.

It demonstrates to me that the events are pressure related not that the pressure is event related. I know this is a very debatable issue. MY Doc doesn't see it this way. The data is saying that the pressure is causing the events otherwise they would be happening at all pressures - why does AHI fall off the table at 9-10ish?

We assume pressure is prophylactic: IT should splint and prevent events. Logic says the higher the pressure the better the splint. Less OA. SO logic says higher pressure with higher OA= Centrals.. that was my rationale - the Doc disagrees.

The good news is 12 second OSA's is not a big deal. Inquiring minds though would really like to know what's going on. This may be an anomaly.

The flags are printed at the higher pressures not the other way around. Logic says OA would start at lower pressures and the machine would raise pressure to clear them. The data shows the flags at the higher pressures. When the pressure is locked and it can't rise - there are almost no flags (at my sweet spots 5 and/or 9cm) Pressures in between or above 9cm have event flags - otherwise they don't happen or register.

For me it probably means setting my machine to CPAP 9 or 10. Last night at 10-11 cm, I spent 90% at 10 with an AHI of .04. AMazing to me. Snore zero.

So where do I set it?

TO answer SWS question FL stays at 1 most of the time. At 9cm & above HI goes to almost zero, At 10 Snore goes to zero (Typically around 6.0)

OA goes UP from 6-8 but dips below 1 at nine, which is when HI dips and then at 10 HI stays low and OA starts climbing sharply. I suspect Centrals - Doc says NO. ??

It seems according to the data, so far either CPAP 9 or APAP 9-10 or 9-10.5. This is not what I expected from an APAP but it looks to me that a fixed pressure is more conducive for my therapy.

I originally got the APAP so I could stay at Lower pressure until higher was needed to clear the events. Instead my AHI went up from where I was with CPAP at 9cm. I never expected it to work that way. My numbers jumped from under 2.0 at CPAP 9cm for 30 days - a decent sample size, to all over the board up to 9 AHI. I had expected the APAP to allow lower pressures and still respond if needed, the data seems to show that the APAP is causing the events, not preventing them.

I never expected it to work this way but the data seems to support it.

Thanks,

Tom

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