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Posted: **Thu Jun 29, 2006 11:58 am**

David-

I'm especially worried about this given my recent cardiac history. But, I'm also skeptical of another sleep study, the first of which was pitiful. What do you think about a few nights on RESLINK which'll correlate these hypops with sats as well as cardiac rates, to at least approximate any abrupt arousal or adrenergic events?

Chuck

Posted: **Thu Jun 29, 2006 12:59 pm**

-SWS wrote:
GoofyUT wrote:Well, I tried CPAP last night with the pressure set to 9.0 cmH2O and the EPR set to 3. My AHI went up to 7.8, but my AI stayed below 1. I'm still convinced that my S8 is scoring lots of artifactual wakeful hypops though. I was able to tolerate CPAP fine and it actually felt pretty comfortable.

I agree with the possibility of artifacts, Chuck. Especially if those increased hypopnea artifacts were primarily concentrated during that period of time just prior to sleep onset. In other words a higher HI concentrated only during preliminary wakefulness can skew an entire night's HI. And those artifact hypopneas could have been related to a higher floor pressure that was just uncomfortable enough (compared to your lower floor pressure) to cause anxiety-related breathing control before autonomic breathing is underway. This is a scenario where proper settling time can really help. However, this hypothetical scenario might be validated by normalizing your own data: experimentally discard the first hour of sleep and see how your HI fares during what should be primarily autonomic sleep.

You had mentioned that you don't sleep as well on xPAP as you had prior to xPAP therapy. The fact is that not only can SDB be highly complex, but so can sleep itself. And my understanding is that stepping through the complex possibilities of bad sleep can be even more complex than all the underlying contributing factors (more complex since the underlying possibilities far outweigh the underlying contributors). As an example, some concomitant non-SDB sleep disorders may only come to light once SDB is successfully treated. Some patients with untreated apnea never progress far enough into the deeper stages of sleep long enough to manifest their concomitant sleep disorders---until xPAP therapy effectively removes the very SDB that had been eclipsing their non-SDB sleep disorder symptoms.

Another possibility for poorer sleep on xPAP that comes to mind is my own observation and not published medical fact. I honestly feel that some people are more inclined toward sensory-based cortical arousals than others. After all, what physiological traits is science aware of that do not manifest with a fair degree of diversity across humanity? I'm personally not aware of any. However, my point is that I honestly think the mask interface itself and even positive pressure can cause an unacceptable level of cortical arousals in some patients. If so this might be one reason why someone might sleep more poorly on xPAP than prior to xPAP.

Another possibility for perceiving that you slept better prior to xPAP therapy might be your prior level of sleep debt related to sleep deprivation from untreated apnea. With heightened sleep deprivation and sleep debt comes a concept known as heightened "sleep pressure". You may very well now sleep with reduced "sleep pressure" because your apnea is now treated for the first time. With that reduced sleep pressure you might be waking up about as often as you would have had you never even suffered sleep apnea in the first place. I mentioned earlier that xPAP therapy can unmask additional non-SDB sleep disorders simply by allowing the deeper stages of sleep to occur. I also suspect xPAP therapy can similarly unmask additional sleep disorders simply by reducing sleep pressure and thereby increasing the likelihood for sensory-based cortical arousals.

Lastly, fixed pressure experiments alone are not enough to exonerate CSDB. Especially fixed pressure experiments that do not run the full course of achieving an adequate titration value. That is because some CSDB related breathing events are purely machine induced (and related to the CO2 respiratory trigger) while the other CSDB breathing events are primary. Those primary CSDB events (mostly obstructive SDB events) were the reason positive pressure had been deemed applicable in the first place. Now, with the application of positive pressure therapy, the CO2 respiratory trigger begins to generate machine-induced central events in a few patients. So here you have two sets of SDB events, simultaneously occurring, via two distinctly separate physiologic mechanisms. The unstable tight rope balancing act I referred to earlier: enough pressure to adequately address the primary obstructive components may also be enough pressure to induce the central components without adequate CO2 regulation; and a low enough pressure to stave off the machine induced central components may not be a high enough pressure to address those primary obstructive components. A theoretical tight rope balancing act in my own view.

The mechanisms involved for machine-induced CSDB central SDB components are not yet fully understood. Because these CSDB patients tend not to fare well with APAP's ever changing pressures, we can only speculate at this point about some of the possibilities. To what extent does an APAP's positive pressure slope or rate of change exacerbate CSDB? To what extent does pressure's amplitude or magnitude alone trigger CSDB manifestations in some patients? How many patients manifest only slight xPAP-induced CSDB breathing patterns with neither significant cortical arousals nor accompanying desats? Patients falling in this latter category, if any, would certainly be those for whom xPAP therapy introduces a beneficial trade off: trading a slight albeit inconsequential CSDB effect for much worse obstructive sleep disordered breathing obstructions. And so the speculation goes on...

Posted: **Thu Jun 29, 2006 1:16 pm**

Actually, I tolerated my PSG-titrated 10 cm easily and I used EPR last night just out of curiosity. I will try titrating to 8 without EPR and see what happens.

Chuck

Posted: **Thu Jun 29, 2006 1:22 pm**

Interesting. Everyone seems so different. 8 cm for me (which is my minimum) seems like barely enough to even qualify as air coming through the tube. But I get used to it once my breathing stablizes. It sounds like others find 9 too much. It's all very interesting to me.

I have a question for guest though. (LOL!) You mentioned the Remstar report vs. the Resmed report. Are you referring to what the software shows you? Not what the little window on the machine tells you? I'm assuming so. Because I've never seen any of that for either machine. I did see something in the form of a print out on my 1 month check-up recently. I kept that print out. It showed my entire sleep study including time where they put me on a BI-PAP during a certain period where oxygen levels were starting to drop. But the doc says I don't need the bi-level based on those results.

I feel like having an APAP instead of a CPAP, if only because I have BOTH options available at any time. But this whole business about trying to figure out minimum and maximum pressure is for the birds! Hehe. It's not the easiest short-term task, is what I really mean. No instant gratification to be found here.

Posted: **Thu Jun 29, 2006 1:46 pm**

GoofyUT wrote:What do you think about a few nights on RESLINK which'll correlate these hypops with sats as well as cardiac rates

I'm not a sleep tech or doctor so I just couldn't say. The sats information would be very useful and interesting. Heart rate would only report very dramatic arousals. I would think a non split night study would give better data by giving you a much longer adjustment period and giving them a chance to get a better look but what do I know?

If I had your history I would be concerned and would want real answers which I think you are seeking but I certainly wouldn't just blow it off regardless of how frustrated I was (not that I think you will but I sense you have a low tolerance level for frustration which I recognize and relate to).

I wish I knew more myself but I don't think my responses are as complicated as yours. I do wonder about CSDB, UARS, additional non-SDB sleep disorders, etc, because I just don't feel that much better but it certainly could be because of other health issues. It is pretty complex to figure out.

David

Posted: **Thu Jun 29, 2006 3:25 pm**

Guest wrote:SWS: What percentage of OSA patients actually fall under this CSDB category? ...Seems to me, ever since that 7,000 post and single study was completed (if it was one) they like to throw a lot of patients under it and there is really no scientific fact they should even be there.

If that's who I think it is, it's very good to see you, bud! There is no patient-population or epidemiology type empirical data yet for CSDB that I am personally aware of. I don't think that type of data is even possible yet at this very early stage of this particular disorder's research cycle. I will admit that I've read some very poorly designed medical studies in my time. That 2.75 bed Vancouver study comes to mind, as does a comparative APAP study that was performed with an "open looped" simulator (even a "closed loop" simulation study is highly suspect, pending detailed scrutiny of the designed "closed loop" response itself). However, I happen to think this Harvard study is very adequately designed for precisely what it attempts to convey: that there are some patients who manifest a complex SDB condition and that the condition itself is linked, in one way or another, to the CO2 respiratory trigger itself----presumably in patients with primarily hypercapnic respiratory drives. The researchers in that Harvard study really do not and cannot attempt to establish CSDB prevalence at this early stage in research, other than to put the word out that they encountered CSDB in surprisingly significant numbers.

Guest wrote:But the risk of centrals remains low if your pressure is 12cm or less. Granted I've seen with pressures under 10cm, 1cm too much pressure can trigger additional hypos...

Resmed and Puritan Bennet both implicitly cap that statistical risk at 10 cm within their own algorithmic safeguard or default settings. There will be some patients outside those statistical margins, for whom less static pressure at various positive pressure slopes will trigger central SDB events. It seems that static pressure amplitude as well as pressure's positive rate of change may factor in a combinational way. To that end, not only do the APAP algorithms all statistically cap their risk by capping a pressure limit to their apnea/hypopnea response, but some APAP algorithms also allow the pressure increments themselves to be adjusted. A patient who experienced pressure induced SDB events might thus fare better with smaller pressure increment settings if they are, indeed, positive pressure slope sensitive.

I will say that in my own mind, regulation of CO2 to alleviate the central component in CSDB does not necessarily pin the causal or failing physiologic mechanism to the hypercapnic respiratory trigger itself. Rather I personally reserve the possibility that the Herring Breur reflex itself might actually be the mechanism that dysregulates breathing under abnormal pressure---and that the hypercapnic respiratory trigger might merely be an overriding albeit separate physiologic mechanism that very adequately regulates this disorder in some patients. That is certainly not speculation to take to the bank, however. .

Posted: **Thu Jun 29, 2006 4:29 pm**

Chuck, what's a boy to do when sleep science is still in its infancy and is unfortunately ill-equipped to diagnose largely undocumented and unexplored sleep disorders? What's a patient to do when modern medicine seems overly challenged to diagnose various concomitant disorders (that can be separately well documented yet largely unrecognized when they just so happen to occur in moderately challenging combinations)? In my opinion sleep medicine's underdeveloped state represents a quandary for many of us here. Perhaps the answer to your question regarding what a boy is to do under these circumstances is simply: One does what one can with whatever means one has at their disposal.

I would not be so presumptuous as to give anyone here medical advice. But I can tell you what I would personally consider if i were in your shoes. I would consider taking the clues and other means at your disposal, and using them to flush out certain patterns that might help your doctor in his diagnosis. Very specifically I would be interested in devising some method of better exploring: 1) those sleep onset hypopneas that occurred before you had your settling time properly set (they may not be purely artifacts---see below), 2) exploring a normalized HI trend relative to your APAP floor (discarding sleep onset data), 3) a highly methodical and thus prolonged fixed-pressure titration, and 4) correlating or separating your awakenings with SDB events. I'll give you my own thoughts or rationale regarding each of these three items.

1) Sleep Onset "Artifact" Hypopneas: You had mentioned that you are convinced your sleep onset hypopneas were artifacts when settling time was turned off. That goes along with my own suspicions in a previous discussion we had in another thread altogether. I agree that breathing artifacts just prior to sleep and autonomic breathing are a likely possibility. However, CSDB can even factor in here as well. Consider that a twitchy hypercapnic respiratory trigger is not necessarily dependent on autonomic breathing. If your settling time was turned off, and your APAP was increasing pressure during that period (for any reason---even in response to some SDB artifacts) you cannot be positive that some or many of those sleep onset hypopneas did not occur because of the very APAP pressure increases themselves. A Resmed rep in an interview on TAS employed the phrase "runaway central apneas" when describing what the A10 algorithm was trying to avoid by the way of pressure induction. It is theoretically possible that just prior to sleep onset, that you may have reached a gradually escalating state of machine induced hypopneas. Artifacts are very possible during that early stage, but so would the CSDB effect, at least for those who are so inclined.

2) Exploring a normalized HI trend relative to your APAP floor (discarding sleep-onset data): this is a key clue that I would personally want to capitalize on. Simply put: if apneas are obstructive, increased pressure inflates the airway to a greater diameter (including at the obstruction point) and diminishes apneas; conversely greater pressures that increase apnea/hypopnea rates tend to do so because those events are central and machine induced---not obstructive. I would be very inclined to very methodically capitalize on this clue even more than the others: does increasing your floor pressure increase HI or decrease HI? I personally wouldn't attribute anything to artifacts without further data-based exploration. If I discovered that my HI did increase after an increased floor pressure, then I would strongly consider at least a slight CSDB effect is at play here.

3) A highly methodical and thus prolonged fixed-pressure titration: Especially if you do suspect any degree of machine-induced CSDB may be involved. If it were, your fixed pressure titration could very well be a matter of finding your own personal "optimal" pressure that strikes a happy medium between primary obstructive events and CO2 respiratory-trigger driven central events. A poster by the name of Jerry69 performed the best long-term fixed pressure titration I have seen to date. I would recommend searching his posts and using his long-term fixed titration experiments as a model (especially if further investigation reveals that increased floor pressure does show an increase in HI).

4) Correlating or separating your awakenings with SDB events: I would be very interested in trying to correlate the times of my awakenings with the clusters of events on my overnight sleep reports. If I saw no correlation here, I would be tempted to focus my analysis on factors other than SDB.

No matter how you decide to go about it, I wish you the very best luck in solving your own personal sleep enigma, Chuck!

Posted: **Thu Jun 29, 2006 4:41 pm**

-SWS for PRESIDENT

(at least of these messages boards).

What a nice man you are to go out of your way to such an extreme to help another member here.

I just thought it needed to be said...

Posted: **Thu Jun 29, 2006 4:45 pm**

Thanks, Lori. Perhaps the most apolitical member of this message board as president. Wouldn't that be a disaster?

Posted: **Thu Jun 29, 2006 6:14 pm**

Well, you forever have my vote for President (though I wouldn't wish that on you), and my deepest gratitude as well.

Chuck

Posted: **Thu Jun 29, 2006 7:35 pm**

SWS wrote:

If that's who I think it is, it's very good to see you, bud! There is no patient-population or epidemiology type empirical data yet for CSDB that I am personally aware of. I don't think that type of data is even possible yet at this very early stage of this particular disorder's research cycle. I will admit that I've read some very poorly designed medical studies in my time. That 2.75 bed Vancouver study comes to mind, Mr. Green

Ah c'mon SWS did you REALLY have to bring up that 2-bed Mom & Pop sleep study on C-Flex! ...

Geeze do I really write that bad where you can pick it out that easy? Hey it was nice reading your stuff again too man, I hope you can stay for a while your a great asset to this sleep stuff and many of these people don't know what they have been missing. Hang around will ya.

Chuck's case seems very similar to mine, as you recall I had tried the snore killer... the Spirit, the PB420e, the Devilbiss and Remstars all trying to get around it with not much success.

Most people associate higher pressures with fewer events and in an ideal world that may be the case. During a titration study they increase pressure until the events stabilize, blows a central or wakes you and they then are done.

But for some of us... as pressure increases some events actually get much worse such as snores and even hypoapneas. Below is an example from my brand new Remstar Auto w/cflex report I got just yesterday (gloat). I was using it in AFLE mode set to 6.5 to 20cm pressure range with a C-Flex setting of 2. I just wanted to see what it would do, so I left the high ceiling at 20cm. I've been using the regular Remstar auto or pro machine for past 4 or 5 years.

Now here is WHY I say it is easier to SEE on a Remstar report than it is on a Resmed autopap machine.

If you look at the attached table below, you will see the pressure used across the top (try to ignore the 90% highlight for time being and try and determine how it actually got there).

Start with the Snore line, notice how the snores increase as the pressure increases? Snores increase from the start and continue UP, this is not good if you use the snore killer machine a Resmed Spirit... because what does it do when it sees snores?

Well it increases pressure for as long as the event exists... does it stop at say the A10 limit? LOL, it won't respond to apnea...better wear a chin strap

Next look at Hypoapnea line on the left then watch what the numbers do as you move to the right as pressure increases, notice that it dips down to 6.1 at 9cm and then INCREASES at 10cm? (really easy to see in Derek's reports) Hypoapnea AND snores BOTH go UP as pressure increases. Note: I only had 2 apneas for the whole night, I don't even worry about those.

Now for me using the Spirit in BOTH of these conditions the machine would continue to increase pressure in what I can only guess was an effort to eliminate these snores and hypoapneas er flow limitations.

But as you can see as the number of events INCREASE WITH PRESSURE. sorta shoots that higher pressure fewer events theory in the foot.

Fortunately the Remstar algorithm doesn't function the same as the Resmed and other autopaps and has a limit and will back off if Informational pressures (pressure tests above 90%) show the number of events increase with pressure and whola the 90% pressure lands where the lowest HI's are seen. The PB420e responded very similarly to the Spirit (lots of pressure), as you recall it was brand new at the time I got it and not much was known about the 1FL and 2FL settings at the time. But I had tried them both and it didn't seem to help then it died.

Based upon the Resmed autopap machine and the way it responds to events, it may be the wrong machine for some patients if the particular event patterns you have trigger the machine into higher pressures (in my case snores seemed to be that trigger).

There are ways with the Resmed I found to get around it, like using Settling feature and limiting the high pressure ceiling to your 90% pressure or simply use it in the cpap mode. Note: on the Remstars, the 90% pressure is the pressure that clears 90% of the events seen. That is easy to see on the table report below.

As for how one feels? I think CFS would be nice to have, it can't be any worse. I actually feel better if I DON'T use cpap at all, but after several weeks it catches up to me big time, and due to history of stageIII hypertension and strokes, I continue use it and keep exploring for options. Then all I have to do is pull out my original diagnostic PSG and see those 72 events per hour and 38 second apnea and SAO2 at 67% to see I still need to use it.

The Remstar Auto that arrived yesterday was my 6th autopap, think I still have 3 others. The best machine for me so far has been a Remstar Pro w/Cflex set to 9cm, but the one I have doesn't record any sleep data at all so I purchased the new Auto w/cflex, I need the record ability and like C-Flex price wasn't all that different.

Chuck: I suspect you may have a similar condition where events increase as pressure increases, if so it would explain WHAT may be happening in your case, "you want to land in that camel hump low". Reason I suggest rolling back the pressure by 1cm to 8cm and see what happens. This is exactly what was found with Jerry and his RemstarPro2. It may put you at the bottom of the proverbial camels hump. And as SWS mentioned increasing your LOW or floor pressure can sometimes get you over that same hump by eliminating those first flow limitations and hypoapnea.

Posted: **Thu Jun 29, 2006 7:58 pm**

Well, once again, thanks for the very thoughtful post. I certainly believe, based on clinical response, that higher pressures evoke more events for me. And, I found as well that my ResMed was responding to that increase in events by increasing pressure which aggravated the occurence of events. Whether this is caused by cortical arousals or by a CO2-mediated etiology I don't know. But I do believe that I'm one of those folks that have a degradation with increased pressure.

Needless to say, I'm curious as to whether I'm ill-suited for the ResMed algorithm. But, given the prospect that changes in pressure may adversely effect the O2/CO2 mechanisms, I'm skeptical that a testing algorithm such as Respironics would be especially wise with the possibility of CSDB.

So, I'm gonna try to fiddle with CPAP titration, going to 8cm tonight without EPR, and try to reach that magic nadir in the pressure-response curve.

Thanks again for all the time and effort that all of you have devoted. I sincerely hope that others who have been following this amazing discussion have benefitetd as much from it as I have.

Chuck

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CPAPopedia Keywords Contained In This Post (Click For Definition): respironics, resmed, Titration, CPAP

Posted: **Thu Jun 29, 2006 8:24 pm**

GoofyUT wrote: Thanks again for all the time and effort that all of you have devoted. I sincerely hope that others who have been following this amazing discussion have benefitetd as much from it as I have.

Chuck

Yes, I have. I think I have a similar response but I haven't looked at my data for 5 days now. My original titration was 8, my initial look at APAP (nasty old used Remstar sans C-Flex) data said 9. With my wonderful new Remstar Auto with C-Flex I set my range to 7-12, C-Flex = 2. I wanted to get a good look over time. When I first set up on the new APAP at the Drs 6-16 my 90% kept climbing day by 10.3, 10.9, 12.5, 12.9 and I was feeling like crap. My events were nothing at 6cm but neither was time. They went up at 7, and 8, went to almost zilch at 9 and then started going back up at above 9. I expect my 6-7 day experiment to show me the same thing (best a straight 9) but if it doesn't I'll report back. I feel better at 7-12 than I did at 8 but I'll bet not as good as I'll feel at 9. If it does the machine gets set at straight 9 and fuggitaboubit unless I change interfaces.

So, thanks a bunch, at least I don't feel like the lone stranger.

David

Posted: **Fri Jun 30, 2006 3:45 am**

Well, its 3:30 in the morning, I've been up since two, after retiring at 10. I tried a CPAP trial at 8 cm. My "numbers" when I awoke at 2:00 showed a dramatic improvement. My HI was around 2.4-as low as it has EVER been. AI was 0.2 for an AHI of about 2.6. And, I actually feel pretty good! But, its 3:30 in the morning and I'm watching a re-run of Leno.

Ho hum.............

Chuck

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CPAPopedia Keywords Contained In This Post (Click For Definition): CPAP, AHI

Posted: **Fri Jun 30, 2006 8:29 am**

Well, its now 8:30 and I just woke up. I FEEL GREAT! My AHI was 2.4, AI was 0.4 and most importantly, my HI was 2.0, my lowest ever! Usage total was 8.9 hrs. I tried a CPAP trial at 8.0 cmH2O/no EPR/30 min ramp.

Now, I'm loathe to proclaim miracles after one night, but I feel really refreshed despite my couple of hour wakeful interval. And, I'm pretty sure that I actually dreamt!. All in all, a GOOD night's sleep.

Regardless of whether this is a fluke or not, BRAVO SWS et. al.!!!! You have my DEEPEST THANKS!!!!

Chuck
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