A Question re: my AUTOPAP Trial

[Muffy]

Sorry, Muffy dear, but please indulge my sleepy brain here. You said earlier that time should improve things, but now you say it's getting worse. Confusion abounds.

You have to be specific as to which "it" you're referring to. While

simply allowing time for the body to equilibrate may solve a lot of the central problem.

at the beginning of the thread the poster

Your overall sleep architecture is awful (way too much wake), which is probably going to have to be dealt with separately-- however, a very important concept related to CompSAS is that sleep instability promotes breathing instability, so working on that aspect should pay good dividends.

But since you're

.. practicing solid sleep hygiene for awhile now. No naps, no matter how much I want one. Yawning all day, but not allowing myself to sleep. To bed at a reasonable hour, and getting up about 5-6 hours later, as usual (unfortunately). I've been walking every other day (briskly, for about 40 minutes, with the dog) and eating better than I ever have in my life (less meat, lots more fish, skinless chicken, lots of veggies, no junk, lots of protein, few carbs)

that's great, (except the 5-6 hours of sleep time, and I would not be surprised if you still had a few too many awakenings). As long as the lifestyle has changed (which is really how you have to think of it), then things should continue to improve.

but I'm not losing the weight. IDK what else to do.

Weight is determined by a scientific formula. Caloric Expenditure = Basal Metabolic Rate + Thermal Expenditure of Food + Exercise Expenditure. If caloric intake exceeds caloric expenditure, you gain weight. If caloric intake equals caloric expenditure you maintain weight. If caloric intake is less than caloric expenditure, you lose weight. If you burn 500 more calories a day than you take in, you'll lose about a pound a week (a deficit of about 3500 calories a week, which is a good goal).

I can call the lab again on Monday, I guess, to see if there's more from the titration report.

OK, just curious, it's still just an historical document.

BTW, that first study, as awful as it is, is just an historical document, too. Don't wave that one around to justify ASV because that's not you anymore. Other data suggests that you're not doing too badly:



I mean decreasing AHI from 107 to 6.7's not too shabby. If the remaining events are due largely to sleep instability, then ASV may not help all that much. As a tool to stabilize breathing, it takes a little time to "catch", so AHI 0.0 may be an unreachable goal.

That said, if your therapeutic pressure is going to be 14 cmH2O, then moving to an ASV approach, using much lower base pressures and a bilevel attack, could add a significant amount of overall comfort and contribute greatly to improving sleep quality.

I'll have to say, I certainly am curious about your most recent APAP trial. It seems like if it really was "fine", they would have handed it over and said "See, I told you so, now shaddup!" Ask 'em again, nicely, tell 'em then you'll go away, a War of Attrition doesn't do anybody any good. Most CompSAS patients have a tough time AHI-wise, so it's not a Capital Offense to flounder around a bit.

BTW, RG's analysis of the situation up there was "spot on". Either way they're stuck, and they know it. Let them know you know it, too. Nicely.

Don't forget the download.

And you should really try to get a data-capable machine. Have you ever looked into that?

Muffy

[-SWS]

Most CompSAS patients have a tough time AHI-wise, so it's not a Capital Offense to flounder around a bit.

True words... I don't think this message board ever had a CompSAS/CSDB patient who readily shoe-horned into both diagnosis and optimal treatment on the very first pass. So the anger and disappointment are understandable. However, I also think your doctor's office experienced a very typical human emotional reaction to your own very typical emotional human reaction. It's what we humans do, for better or worse...

But I definitely agree that your ever-changing complex SDB physiology should have presented a special diagnostic and treatment challenge to your doctors.

Speaking of ever-changing, SAG points out a pattern with some CompSAS/CSDB patients that you seem to fortunately fit: some degree of adaptation to that pressure treatment. That's an important part of the premise for that strategy of experimentally finding a best low fixed pressure to "sit on" for a while, as you measure residual AHI (think data capable machine ) and evaluate subjective sleep quality. As it turns out, ASV machines don't always perfectly solve sleep and breathing for all CompSAS/CSDB patients. True statement...

So I would recommend that you carefully analyze and digest the entire toolbox of possible CompSAS/CSDB treatment methods that SAG/Muffy is availing to you in this discussion. Often, several tandem treatment methods are necessary to optimally treat CompSAS/CSDB, which can be an incredible treatment challenge.

[BleepingBeauty]

BTW, that first study, as awful as it is, is just an historical document, too. Don't wave that one around to justify ASV because that's not you anymore. Other data suggests that you're not doing too badly:

<snip>

I mean decreasing AHI from 107 to 6.7's not too shabby.

Agreed. (But the STDD from 3/1 of that same trial period as the one you posted above lists my AHI at 24.7. Not so good.) Believe me, I know there's been improvement. I can actually function now, thanks to my therapy; how well I sleep and how well I function is still an issue. I told my ex-doctor that I love my machine, and I do, since it allows me to sleep. But I also know that I'm still not getting good quality sleep, and that's a big problem.

If the remaining events are due largely to sleep instability, then ASV may not help all that much. As a tool to stabilize breathing, it takes a little time to "catch", so AHI 0.0 may be an unreachable goal.

That's okay. I'd love it if everything was "perfect," but that's not reality, and I don't expect perfection from this treatment. I just want what every one of us wants - good quality sleep with an AHI under 5.0.

That said, if your therapeutic pressure is going to be 14 cmH2O, then moving to an ASV approach, using much lower base pressures and a bilevel attack, could add a significant amount of overall comfort and contribute greatly to improving sleep quality.

Well, considering where my diagnosis has been coming from, I have no idea if 14 cm is the right pressure for me. We'll see what the new doc has to say, about everything.

I'll have to say, I certainly am curious about your most recent APAP trial. It seems like if it really was "fine", they would have handed it over and said "See, I told you so, now shaddup!" Ask 'em again, nicely, tell 'em then you'll go away, a War of Attrition doesn't do anybody any good.

So am I. Can't help thinking there's something incriminating in there that they don't want me to see. But it's part of my medical record, and I'm entitled to a copy of it. This b.s. will only delay the inevitable, because I will get a copy of it eventually. But, whatever. I'm not going away quietly.

Most CompSAS patients have a tough time AHI-wise, so it's not a Capital Offense to flounder around a bit.

Well, two issues there. First, I don't recall my doctor ever mentioning CompSAS to me in the 16 months that I was his patient. Second, what's "a bit?" I've been at this for well over a year, and I'm still "floundering around."

BTW, RG's analysis of the situation up there was "spot on". Either way they're stuck, and they know it. Let them know you know it, too. Nicely.

Yes, RG is always spot on, and I'm grateful that she's here and has taken an interest in my situation. As to me letting them know that they're "stuck," well, I'm sure they've already gotten that message from my posts on this forum. (Are you enjoying the continuing "drama," "waytootransparent?")

As to letting them know "nicely?" Too late. Unfortunately for them, they've made it perfectly clear that they want to go down the animosity road with me, so I'll deal with that.

Don't forget the download.

The download? You think they're actually going to give me anything willingly?

And you should really try to get a data-capable machine. Have you ever looked into that?

Muffy

You a funny girl, Muffy.

[BleepingBeauty]

Most CompSAS patients have a tough time AHI-wise, so it's not a Capital Offense to flounder around a bit.

True words... I don't think this message board ever had a CompSAS/CSDB patient who readily shoe-horned into both diagnosis and optimal treatment on the very first pass. So the anger and disappointment is understandable. However, I also think your doctor's office experienced a very typical human emotional reaction to your own very typical emotional human reaction. It's what we humans do, for better or worse...

But I definitely agree that your ever-changing complex SDB physiology should have presented a special diagnostic and treatment challenge to your doctors.

Speaking of ever-changing, SAG points out a pattern with some CompSAS/CSDB patients that you seem to fortunately fit: some degree of adaptation to that pressure treatment. That's an important part of the premise for that strategy of experimentally finding a best low fixed pressure to "sit on" for a while, as you measure residual AHI (think data capable machine ) and subjective sleep quality. As it turns out, ASV machines don't always perfectly solve sleep and breathing for all CompSAS/CSDB patients. True statement...

So I would recommend that you carefully analyze and digest the entire toolbox of possible CompSAS/CSDB treatment methods that SAG/Muffy is availing to you in this discussion. Often, several tandem treatment methods are necessary to optimally treat CompSAS/CSDB, which can be an incredible treatment challenge.

Well, I'm ready for the challenge. I'm tired of being tired, and I'm looking forward to working closely with my new doctor to figure out what will work for me. I don't care if it takes time. I just want (and need) to know that I'm on the road to getting there (which, obviously, has not been the case in the past).

Thank goodness this forum exists and people like you are willing to help someone like me. I'm going to continue to rely on all of you in the coming weeks and months, as I start down this new road. Many thanks.

[BleepingBeauty]

Well, I had the phone jack repaired today, and my fax machine is working again. I received the complete lab report from my 10/24/07 titration a little while ago.

Here's the page showing respiratory events, oximetry, etc.: http://s675.photobucket.com/albums/vv12 ... Graphs.jpg

(I tried to paste it here with the [img] code, but it didn't work.)

That page and two more are here: http://s675.photobucket.com/albums/vv12 ... %20Graphs/

[-SWS]

A far less "pressure aggressive" titration than the one only 20 days earlier. And at these lower titration pressures, you don't manifest CompSAS/CSDB anywhere nearly as picture-perfect as you did on the earlier BiLevel/CPAP titration:



That's a good sign... whether it's attributable to lower pressure, 20-days biological adaptation to CPAP, BiLevel avoidance (some people don't take well to that modality either) or some combination of the above.

[BleepingBeauty]

A far less "pressure aggressive" titration than the one only 20 days earlier. And at these lower titration pressures, you don't manifest CompSAS/CSDB anywhere nearly as picture-perfect as you did on the earlier BiLevel/CPAP titration:

<snip>

That's a good sign... whether it's attributable to lower pressure, 20-days biological adaptation to CPAP, BiLevel avoidance (some people don't take well to that modality either) or some combination of the above.

Thanks, -SWS. It appears this was a straight CPAP titration (it lists CPAP from 5-13 cmH2O) and concludes that "A CPAP of 9 cmH2O appeared to be optimal on her side, with minimal REM. A CPAP of 12 cmH2O appeared optimal in the supine position. The patient had persistent sleep/wake central events and an increased respiratory rate."

Whatever accounts for a better result with this study, it definitely wasn't 20 days of adaptation to CPAP, because I didn't get a machine until early November (about two weeks after this titration was done).

[-SWS]

Whatever accounts for a better result with this study, it definitely wasn't 20 days of adaptation to CPAP, because I didn't get a machine until early November (about two weeks after this titration was done).

Well, Bilevel Positive Airway Pressure Worsens Central Apneas During Sleep for some patients. And yet for other patients it's the exact opposite. Go figure. And as we already mentioned, your first titration was pressure-aggressive (not at all friendly to CompSAS/CSDB homeostasis problems) . But plain old night-to-night variation in your very apparent CompSAS/CSDB physiology is yet another possibility. Speaking of CompSAS/CSDB homeostasis problems:

"The patient had persistent sleep/wake central events and an increased respiratory rate."

That feature nicely fits with CompSAS/CSDB physiology because that transition from wake to sleep is where CNS sleep-related homeostasis first kicks in----for that transition to purely autonomic breathing during sleep. It very often doesn't kick in all that well for CompSAS/CSDB patients---who are "homeostasis challenged" so to speak.

Again, that's the underlying reason why rapidly-changing static pressures of APAP modality are thought to exacerbate CompSAS/CSDB worse than other modalities: homeostasis or adjustment problems related to central breathing itself are problematic. Sometimes that creates central dysregulation, sometimes that creates bistable/unstable Cyclic Alternating Pattern issues, but very often it creates both sets of problems.

Either of those CompSAS/CSDB resultant problems in sleep-related neurology is potentially disruptive to maintenance of sleep and also that of wake or daytime energy.

[BleepingBeauty]

Well, Bilevel Positive Airway Pressure Worsens Central Apneas During Sleep for some patients. And yet for other patients it's the exact opposite. Go figure. And as we already mentioned, your first titration was pressure-aggressive (not at all friendly to CompSAS/CSDB homeostasis problems) . But plain old night-to-night variation in your very apparent CompSAS/CSDB physiology is yet another possibility. Speaking of CompSAS/CSDB homeostasis problems:

"The patient had persistent sleep/wake central events and an increased respiratory rate."

That feature nicely fits with CompSAS/CSDB physiology because that transition from wake to sleep is where CNS sleep-related homeostasis first kicks in----for that transition to purely autonomic breathing during sleep. It very often doesn't kick in all that well for CompSAS/CSDB patients---who are "homeostasis challenged" so to speak. Again, that's the underlying reason why rapidly-changing static pressures of APAP modality are thought to exacerbate CompSAS/CSDB worse than other modalities: homeostasis or adjustment problems related to central breathing itself are problematic. Sometimes that creates central dysregulation, sometimes that creates bistable/unstable Cyclic Alternating Pattern issues, but very often it creates both sets of problems.

Either of those CompSAS/CSDB resultant problems in sleep-related neurology is potentially disruptive to maintenance of sleep and also wake or daytime energy.

Thanks, -SWS. It's starting to make a lot more sense to me now. (Sorry if it's somewhat redundant for you and SAG to try to educate me on what I'm dealing with here. There's a lot of terminology I'm unfamiliar with, and my continued sleepiness makes it more of a struggle to grasp it all. But I sure do appreciate the effort you're both making.)

Can't wait to see the new doc and get this new show on the road...

[Muffy]

Whoa, better post something before all the good comments are taken!

Interestingly, you've got some good response there at 7.0 cmH2O (there goes that number again).

This study has some very revealing information. There seems to be some good thought process in this titration, and not just running a staircase.

Look at the vast improvement in oxygenation at low level CPAP vs the ambient study. Given that horrible oximetry on baseline, I think one would have been very leery about unmonitored prolonged low PAP levels (like that extended period on 7.0 cmH2O in the last APAP trial), but this is encouraging. However...

This area needs closer scrutiny:



That salvo of events (with the well-defined desaturations) may be due to one of two things (or a combination of both), namely sleep-onset breathing instability and/or position change (to supine).

Jumping ahead, would a decrease to low level PAP once sleep is stabilized be worth investigating? I think that's not only worth a shot, but may enjoy a good likelihood of success (as an aside, this may have been the thought process at about 0400 where a decrease in PAP was done during a flurry of desaturating centrals, then hypopneas appeared). If you look at the supine respiratory events, they're either central apneas or "only" hypopneas. It would also be interesting to throw those hypopneic events under the microscope to see if they had a "central flavor" to them as well, or if they were truly obstructive in nature, with evidence of flow limitation (assuming a pressure transducer was in use).

It may be that the position component is not particularly strong. If this is so, then this lends more support to pushing low level PAP.

Muffy

[Muffy]

Defining the 0400 area a little more clearly:



it would seem quite possible that the abrupt change of central apneas to hypopneas represented a continuation of central phenomenon vs the appearance of obstructive component.

Muffy

[BleepingBeauty]

Whoa, better post something before all the good comments are taken!

Interestingly, you've got some good response there at 7.0 cmH2O (there goes that number again).

This study has some very revealing information. There seems to be some good thought process in this titration, and not just running a staircase.

As a layperson, I was very impressed with the lab and the tech who monitored me that night. It's nice to have confirmation that she knew what she was doing, so thanks for that.

Look at the vast improvement in oxygenation at low level CPAP vs the ambient study. Given that horrible oximetry on baseline, I think one would have been very leery about unmonitored prolonged low PAP levels (like that extended period on 7.0 cmH2O in the last APAP trial), but this is encouraging. However...

This area needs closer scrutiny:

<snip>

That salvo of events (with the well-defined desaturations) may be due to one of two things (or a combination of both), namely sleep-onset breathing instability and/or position change (to supine).

Jumping ahead, would a decrease to low level PAP once sleep is stabilized be worth investigating? I think that's not only worth a shot, but may enjoy a good likelihood of success (as an aside, this may have been the thought process at about 0400 where a decrease in PAP was done during a flurry of desaturating centrals, then hypopneas appeared).

Should I lower my current pressure of 14 a bit to see if I sleep better? I'm not asking you to dispense medical advice (and I promise no lawsuits!), but you obviously know much more about this than I do, and I certainly am NOT sleeping as well as I should (or want to) be. Feel free to PM me if you don't want to answer that here. Of if you'd rather not answer it at all, that's perfectly understandable and acceptable, and I'll respect that. Just wondering if I can feel better sooner without doing any harm.

If you look at the supine respiratory events, they're either central apneas or "only" hypopneas. It would also be interesting to throw those hypopneic events under the microscope to see if they had a "central flavor" to them as well, or if they were truly obstructive in nature, with evidence of flow limitation (assuming a pressure transducer was in use).

Is there any way to tell whether a pressure transducer was used, from the paperwork generated? Under "Description of Procedure," it says, "The following variables were monitored: EEG, EOG, chin EMG. Right and left EMG, ECG, airflow, chest movement, abdominal movement, snoring by tracheal microphone, and pulse oximetry."

Under the "Summary" written by the tech, it says, "The patient had DBE's with and without arousals and/or desaturation. The patient had a sinus rhythm." I don't know what any of that means, but I'm sure it means something to you.

It may be that the position component is not particularly strong. If this is so, then this lends more support to pushing low level PAP.

Muffy

I remember asking the RT at the DME about positional therapy (i.e., staying off my back), and he said that it wouldn't matter what position I slept in once I was on the machine. Is that true? And if so, why would any doctor recommend positional therapy, ever? (Or is this more likely just another example of a DME saying anything off the top of his/her head?)

TIA

P.S. BTW, I'm really glad you asked me if there was more to the reports that I had copies of, as I never knew any of this additional info existed. Now, I'll have a more complete record to hand to my new doctor.

[-SWS]

Interestingly, you've got some good response there at 7.0 cmH2O (there goes that number again).

Should I lower my current pressure of 14 a bit to see if I sleep better?

And you should really try to get a data-capable machine. Have you ever looked into that?

that strategy of experimentally finding a best low fixed pressure to "sit on" for a while, as you measure residual AHI (think data capable machine )

Look at the vast improvement in oxygenation at low level CPAP vs the ambient study.... but this is encouraging.

Well, BB, if you were going to experimentally "sit" at 7 cm or any other low pressure, the way to safely do it would be with a data capable PAP machine and recording pulse oximeter during a trial-run nap or two for starters. Of course, the best way would be under the supervision of a savvy sleep doc.



But that strategy of using a lower pressure to avoid inducing CompSAS/CSDB problems at higher pressures is a treatment strategy called "permissive flow limitation":

Avoiding Pressure Toxicity

Patients with complex disease are sensitive to positive airway pressure, and usually flow limitation cannot be eliminated without worsening periodic breathing or inducing central apneas. An immediate worsening with bilevel ventilation may be seen, consistent with an effect of induced hypocapnia on the peripheral chemoreceptors. One approach is 'permissive flow limitation' - allowing some obstruction to persist and thus avoiding the worsening of control dysfunction.

http://www.medscape.com/viewarticle/515202_8

The idea behind that CompSAS/CSDB treatment method is to allow a few more obstructive events through, if treating those higher-pressure obstructions just so happens to create more problems (central dysregulation and/or CAP)----than not addressing those obstructions requiring higher pressures. That treatment strategy essentially strives to find a happy balance. However, that happy balance is not always close to any kind of treatment ideal. Still, your 7 cm data may be worth closely investigating as SAG/Muffy points out...

And again, that may have been the intended point for the 7cm split-study setting on the APAP. Then again...

__________________________________________________________________________________________________________


Once again that same quoted paragraph from above---but this time with an emphasis on the BiLevel part of that statement:

Avoiding Pressure Toxicity

Patients with complex disease are sensitive to positive airway pressure, and usually flow limitation cannot be eliminated without worsening periodic breathing or inducing central apneas. An immediate worsening with bilevel ventilation may be seen, consistent with an effect of induced hypocapnia on the peripheral chemoreceptors.One approach is 'permissive flow limitation' - allowing some obstruction to persist and thus avoiding the worsening of control dysfunction.

http://www.medscape.com/viewarticle/515202_8

I'm thinking the Respironics autoSV might actually make for a better trial for you than the Resmed adaptSV equivalent. I say that because the Respironics autoSV model allows you to run SV modality with either BiLevel as the base pressure or with CPAP as your base pressure. The Resmed model, on the other hand, runs SV treatment with a BiLevel base pressure only. That BiLevel base pressure may not be your best SV treatment choice----if your central breathing just so happens to destabilize more easily with BiLevel than CPAP.

[BleepingBeauty]

Well, BB, if you were going to experimentally "sit" at 7 cm or any other low pressure, the way to safely do it would be with a data capable machine and recording pulse oximeter during a trial-run nap or two for starters. Of course, the best way would be under the supervision of a savvy sleep doc.

He shoots, he scores. Yeah, I knew that. I just want to feel better asap... *muttering* (But, after all this time of feeling crappy, another couple of weeks won't kill me.)

But that strategy of using a lower pressure to avoid inducing CompSAS/CSDB problems at higher pressures is a treatment strategy called "permissive flow limitation":

Avoiding Pressure Toxicity

Patients with complex disease are sensitive to positive airway pressure, and usually flow limitation cannot be eliminated without worsening periodic breathing or inducing central apneas. An immediate worsening with bilevel ventilation may be seen, consistent with an effect of induced hypocapnia on the peripheral chemoreceptors. One approach is 'permissive flow limitation' - allowing some obstruction to persist and thus avoiding the worsening of control dysfunction.

http://www.medscape.com/viewarticle/515202_8

The idea behind that CompSAS/CSDB treatment method is to allow a few more obstructive events through, if treating those higher-pressure obstructions just so happens to create more problems (central dysregulation and/or CAP)----than those obstructions that would have required the higher pressures. That treatment strategy essentially strives to find a happy balance. However, that happy balance is not always close to any kind of treatment ideal. Still, your 7 cm data may be worth closely investigating as SAG/Muffy points out...

And again, that may have been the intended point for the 7cm split-study setting on the APAP. Then again...

I wish I could give them the benefit of the doubt. But it pains me to realize that I've wasted well over a year on this journey, under their direction, and I just can't cut them any more slack. Every fiber of my being says the split-night setting for my recent apap trial was NOT intentional. If it had been, then the Clinical Director surely would have said something about it on the phone when I called to ask if the results had been mailed to me yet. She's been reading this thread, so she already knew what I thought had happened with the settings; if it really had been intended as a split-night, she would've defended that decision and reamed me a new one for questioning her "treatment plan."

I say "her" treatment plan because she claims the trial was done without the doctor's prescription and as a favor to me. (Don't do me any favors, lady!) And since this telephone conversation took place almost a week after she'd dismissed me as a patient, there was nothing stopping her from telling me off. Instead, she was defensive, uttered the most ridiculous reasons re: why I wouldn't be getting a copy of that medical record, and hung up on me. So it's pretty clear to me.

Once again that same quoted paragraph from above---but this time with an emphasis on the BiLevel part of that statement:

Avoiding Pressure Toxicity

Patients with complex disease are sensitive to positive airway pressure, and usually flow limitation cannot be eliminated without worsening periodic breathing or inducing central apneas. An immediate worsening with bilevel ventilation may be seen, consistent with an effect of induced hypocapnia on the peripheral chemoreceptors.One approach is 'permissive flow limitation' - allowing some obstruction to persist and thus avoiding the worsening of control dysfunction.

http://www.medscape.com/viewarticle/515202_8

I'm thinking the Respironics autoSV might actually make for a better trial for you than the Resmed adaptSV equivalent. I say that because the Respironics autoSV model allows you to run SV modality with either BiLevel as the base pressure or with CPAP as your base pressure. The Resmed model, on the other hand, runs SV treatment with a BiLevel base pressure only. That BiLevel base pressure may not be your best SV treatment choice----if your central breathing just so happens to destabilize more easily with BiLevel than CPAP.

I'm still taking notes from both you and SAG and will compare them to what the new doc has to say. As usual, my thanks.

[Muffy]

I'm still taking notes from both you and SAG...

It's "Muffy"! Do you think SAG would be dressed up like this?

It's nice to have confirmation that she knew what she was doing, so thanks for that.

On the other hand, that first study might have been a tad too aggressive, continuing to raise pressures in the face of unresponsive events. On the other, other hand, the pressure charge was done during REM, which, if you were a "textbook" CompSAS, should have been relatively event-free. Back to the first hand, when NREM made it's initial appearance in earnest, you were already on a fairly high pressure, so in retrospect, centrals were a foregone conclusion (that's a great expression! A retrospective foregone conclusion! I thought only Nostradamus could do that!). Of course, this second-hand information is largely academic, given the behavior of your SDB, I think getting the total picture during a split study was going to be a tough chore regardless. Trying to pack in REM vs NREM, stable NREM vs unstable NREM, lateral vs supine, CPAP vs BiPAP, putting all those combinations together and on top of that, trying to allow time for equilibration to occur was a pretty full agenda.

Of if you'd rather not answer it at all, that's perfectly understandable and acceptable, and I'll respect that.

Thank you. I do not concur with the saying "The only way a CPAP machine can hurt you is have it fall on your head." Let's say you guess wrong, events are added and/or the new "plan" results in an even worse sleep efficiency. Driving home in the afternoon (it probably wouldn't happen in the morning) you drift off to sleep on I-5. Or in one of those quiet little parks in Phoenix. Where a new Mom is pushing the twins in a stroller. If you were following the advice of a physician, he would be culpable. If you were following the advice of some guy on the internet dressed up in a flowery chiffon jumper, I think you'd have a problem at the trial.

Is there any way to tell whether a pressure transducer was used, from the paperwork generated?

Not unless they specifically say it, or the actual study is reviewed.

Under the "Summary" written by the tech, it says, "The patient had DBE's with and without arousals and/or desaturation. The patient had a sinus rhythm." I don't know what any of that means, but I'm sure it means something to you.

You're correct.

I remember asking the RT at the DME about positional therapy (i.e., staying off my back), and he said that it wouldn't matter what position I slept in once I was on the machine. Is that true?

It would if the selected pressure addressed all of the various above-noted combinations and permutations without generating additional issues.

And if so, why would any doctor recommend positional therapy, ever?

In purely obstructive disease (which occurs at least 85% of the time, but Muffy thinks the incidence of problem-generating CompSAS is inflated if one lists it at 15%) it's a heckuva lot easier to define, you pretty much just have to look at position vs sleep stage.

Muffy