Why doesn't APAP respond to apneas?

OutaSync wrote:Thanks, guys, I'll do all of the above. There will be no "weaning" of the Lyrica. I just won't take another one. I was only on for two days and I felt terrible both days. I don't have time to adjust to it. I have to drive and work every day and can't afford to be a basket case all weekend, either.

Thanks, SAG, for taking the time to review my data. I know you are a busy guy, so that meant a lot to me.

Bev

Bev,

Sorry to hear that last night was not good. Nothing more I can add at this time but am here willing you through this.

Cheers

DSM

Well SAG may be right about this thread potentially turning into the "The Mother Of The Mother Of All Threads" (TMOTMOAT).

There's still plenty of interesting discussion to go IMO. Here's one interesting part of this thread that we haven't even discussed yet. I personally don't have time to discuss it right now .. but want to highlight it for a little more interesting around-the-fire conversation later.

StillAnotherGuest wrote: Zolpidem (Ambien) may be very helpful in some cases of SDB by promoting stable sleep, which in turn promotes stable airway.

Recently, it has been suggested that zolpidem may also have a direct effect on increasing genioglossus activity:

Systemic vs. Central Administration of Common Hypnotics Reveals Opposing Effects on Genioglossus Muscle Activity in Rats Volume: 31 (3) p. 355-365; Eileen Park, MSc; Magdy Younes, MD; Hattie Liu, MSc; Xia Liu, PhD; Richard L Horner, PhD

Lorazepam and zolpidem have an inhibitory effect on GG activity via local effects at the HMN (hypoglossal motor nucleus). Following systemic administration, however, this inhibitory effect can be outweighed both by a delay in arousal (allowing greater CO2-mediated respiratory stimulation in sleep) and excitatory influences on baseline GG activity via mechanisms operating outside the HMN.

I did just now suggest to Bev in a PM that IMO daytime BiLevel desensitization techniques may be her only chance of ever being able to comfortably fall asleep while attempting to use either BiLevel or SV modalities. But CBT type desensitization to BiLevel pressure fluctuations conceivably helps only with the wake/stage-1 transition---and it still leaves compatibility with her disruption-oriented autonomic physiology as one big "servo-ventilation unknown" IMO.

My opinion:

-her main complaint is Excessive Daytime Fatigue

Factors that can influence daytime fatigue:
Medications for pain: She has taken medication(s) for muscle-skeletal pain in the past and recently suspect in disturbing her sleep architecture (lack of Rem on PSG). Results from these PSG's may be skewed by these pain medications themselves. So past PSG's are inconclusive. Same medications are suspect in contributing to daytime fatigue (her major complaint), doesn't matter if it is Lexapro or Lyrica, last two days on Lyrica seems to confirm that finding (nearly going thru red light),

Medications:

for Insomnia: Takes Ambien daily for sleep, results inconclusive if it improves her sleep any, adverse side effects can included daytime fatigue.

for Insomnia: Also takes Melatonin: purpose is to reduce insomnia, a higher dose to encourage REM sleep, adverse side effect can be daytime fatigue if dose too high, trial and error to find correct personal dose.

for Muscle-Skeletal pain: Has taken Lexapro in the past, chemical known to delay prohibit REM sleep. Recent trial on Lyrica
adversely produced greater daytime fatigue.

Has severe desats at certain pressures as seen on PSG results.

Hope was use of SV would improve sleep quality and reduce daytime fatigue. SV experiment shows she does not tolerate pressure support from bilevel. Similar PSG results show she did not find or tolerate fixed Bilevel at 4cm Pressure Support.

At this point she does NOT feel any better when AHI is at 2 or below. AHI is more than acceptable with no improvement to daytime fatigue seen. Use of CPAP pressure on SV only seems to encourage the insomnia and greater need for Ambien and other sleep aids. Higher pressure is preferred based upon skewed results seen on past PSG's due to dangerous desaturations seen at lower pressure (most likely long duration of central apnea seen).

Since a reduced AHI doesn't improve daytime fatigue, I would work on elimination of items KNOWN to contribute to daytime fatigue, from my own experience with it, I would start with elimination of Ambien.

What factors contribute to insomnia where Ambien is needed?
Use of the xpap machine? High pressure? Mask discomfort?

Suggestions:

-short of a double-odd buck shot of trying some fixed radical bilevel pressure like 17/9 (6 cm pressure support, not attempted so far) with a fixed backup set to protocol on SV to ensure that any Central dysregulation is eliminated (and eliminating any dangerous desats), if this is done, target alarms should be enabled, use of recording pulse oximeter to confirm result. I would only attempt this on a weekend where you don't have to work the next day.

-substitute prescribed pain medications for simple aspirin regiment for 10 days or more. Any effects from prescription pain medications may have a residual effect for 10 or more days and up to or as long as 20 days. So it may be the latter before you can conclude that the pain meds are no longer a contributing factor towards sleep disturbance or daytime fatigue. Aspirin regiments are known to address chronic pain with No known adverse side effects to sleep (may cause stomach irritation and contribute to bleeding, so that should be considered).

-lack of REM seen on PSG's suggest that more REM may be needed to improve quality of sleep. Ambien use doesn't appear to improve this any, Ambien suspect in a contributing factor in daytime fatigue. Melatonin has few side effects and can help with insomnia and promote REM sleep at a higher dose. A higher dose up to 6mg may allow you to substitute the higher dose for Ambien. Some experimentation may be needed to rule out it contributing to daytime fatigue. May take 10 to 20 days to ween off Ambien use and recognize any change. Use of TylenolPM is not so bad, it addresses pain and insomnia at the same time.

-Suggest use of a Pulse Oximeter to monitor desaturations. If you can reasonably arrange it, I would try a 420e or Sandman Auto for a week or two with specific settings to avoid any response to CA. I do NOT recommend purchase of these machines until you have a chance to use them for a week (from own experience purchasing more than a dozen machines chasing the same thing). If you could borrow/rent one from a local DME that would be ideal. You may be able to use one of these machines at 9 cm pressure, avoid dangerous desaturations and machine will better ignore any response to centrals seen. You would also have a better picture from their reports if you are able to obtain those. If you can get by with a much lower pressure, your aerophagia should improve, insomnia should improve, leaks less hassle and you may even sleep better as a result of the lower pressure. Sometimes we have more apnea when we relax further and are sleeping better.

-Improve daytime fatigue: I would add to the above a B-50 or Super B Complex vitamin supplement daily to promote daytime energy.

Right now I'm experimenting with 100% Cayenne to control GERD and its effects. It is known to kill H-Pylori bacteria, only on it 2 days so far (come on ice cream) but it seems to be helping a lot. ($8 at GNC for 100 capsules, contents: 500mg ground up red chili peppers).

You forgot to mention that she:
1. Does not Breath Properly (e.g. gas, and why she can't tolerate bilevel therapy)
2. Breathes Light (Low VT)

Mitigated by:
1. Breathing/Body awareness class. Perhaps some basic Yoga training.
2. I could send her the AVAPs for a home trial on S/T AVAPS at a Tidal Volume not to exceed 400 ml. May help mitigate any CO2 concerns in the process.

Banned

Regarding the headaches. SAG kind of wondered if those might have been hypercapnic headaches from too much CO2 retention.

They seemed to occur primarily on BiLevel/SV. And Bev found BiLevel/SV modality to be extremely uncomfortable, even disconcerting. If that disconcerting response caused her to "breath stack" that might be one possible reason for CO2 headaches. Breath stacking entails not breathing out all the way before taking that next breath in. It happens to some patients who are very uncomfortable on BiLevel. But that means CO2 retention can occur because those patients aren't breathing out all the way---they're repeatedly retaining pockets of air that should be exhaled. So quite possibly that could explain the headaches. If so, SAG's suspicions would have been right on the money.

Banned, I don't think AVAPS is going to help right now, since BiLevel itself seems so intolerable to Bev. I think that's a defensive upper airway reflex that quite a few people seem to have.

-SWS wrote: Banned, I don't think AVAPS is going to help right now, since BiLevel itself seems so intolerable to Bev. I think that's a defensive upper airway reflex that quite a few people seem to have.

Then why not truck on down to a local dive shop and take some basic SCUBA lessons? Or get in a pool with a swim mask and snorkel. I'm actually serious. People can learn to breathe. Or we can say they are not capable of breathing properly and we can keep beating our heads against a wall. Just brainstorming, here.

Banned

-sws wrote:Also, here's the place I would consider arranging a sleep study if I were in this particular situation of apparently suffering deteriorated sleep with excessive unresolved RDI (and having shown central emergence on my BiLevel titration):
http://www.bidmc.org/CentersandDepartme ... Staff.aspx

That's Harvard medical school's teaching hospital. And the team members above that I might try to arrange my sleep study with would be any of these authors:
http://www.ncbi.nlm.nih.gov/pubmed/16217173

And while you're up there, run down the street to B&W's.

In this month's issue of JCSM, they take the position

Complex Sleep Apnea: It Isn’t Really a Disease, Journal of Clinical Sleep Medicine, Vol. 4 (5), p. 406-408, Atul Malhotra, M.D.; Suzie Bertisch, M.D., M.P.H.; Andrew Wellman, M.D.

and note how in complex disease, specifically, central disturbance created by pressure therapy, that the relief of obstructive events followed by a period of acclimatization may change the arousal threshold and then the central events will resolve spontaneously. This process may take days to weeks.

So if this is true, then it stands to reason that the balance can be upset immediately by arbitrary dial wingin' with an inability to determine what's appropriate by using short-term observations ("let's try this today, let's try that tomorrow").

So I calls up B&W, and they say

B&W: Brigham and Women's Hospital, how can we help you?

SAG: Hi, this is SAG. Is Atul there?

B&W: One moment, please, I'll connect you.

SAG: Cool.

B&W: Department of Sleep Medicine, how can we help you?

SAG: Atul home?

B&W: One moment, please, I'll check.

SAG: Cool.

B&W: This is Dr. Malhotra, how may I help you?

SAG: Hey, Tulmeister, wazzup?

B&W: SAG you old &#@*&%!!!

SAG: Old? Who you calling "old" you $#*%^#*!!!

B&W: You, you old &#@*&%!!!

SAG: Oh yeah, well come down here, we'll do a 10K and then we'll see who's an old &#@*&% you old &#@*&%!!!!!!

B&W: OK, so what do you want besides complaining about how the Mets collapsed again?

SAG: Well, what do you think about this dial wingin' case?

B&W: The AHI on CPAP 14.0 cmH2O is 1.4.

SAG: Good point. I wish I had thought of that.

B&W: OK, I gotta split.

SAG: Right, thanks. Say hi to the family.

B&W: Back atcha.

Interesting article. I think the human mind---including that of researchers---tries very hard to consolidate vast interrelated bodies of information into patterns and quite often single conclusions when several conclusions are really required. I think the article cited above may be one such case.

Rhetorically: how might the B&W conclusion fit the opposite documented cases of complex sleep apnea onset after months or years of PAP use? It doesn't.

I honestly suspect there are a variety of pathophysiologic ways in disordered physiology to yield those complex disordered sleep-breathing patterns. I would even be so bold as to venture a guess that physiologically defensive breathers---the ones with perhaps nothing more than a defensive upper airway reaction to pressure stimuli (especially variations)----are going to longitudinally express different complex disease cycle characteristics than patients who have developed an inherently fixed neurochemical loop/gain issue.

That first proposed complex pheno subtype might be pathogenically based in defensive autonomic reflexology (regarding initial PAP maladaptation) while that second proposed pheno subtype might be based in a more fixed receptor-signal mistranslation somewhere else in dysfunctional neurochemistry. If so, we can probably expect much better long-term efficacy from traditional PAP by that former proposed subpopulation (after long-term adaptation) than the latter. Additionally, I'm guessing that former proposed subpopulation are the ones having the greatest difficulty with the wake/stage-1 transition on adaptive/auto servo ventilation---whereas the latter subpopulation may initially be much better suited for adaptive/auto servo ventilation pressure variations. That latter proposed complex SDB pheno subtype might also receive comparatively greater long-term or sustained benefits by respiratory-controller-oscillation correction via adaptive/auto servo ventilation as well.

Truth is I don't think there's a more challenging branch of science out there.

StillAnotherGuest wrote:In this month's issue of JCSM, they take the position

Complex Sleep Apnea: It Isn’t Really a Disease, Journal of Clinical Sleep Medicine, Vol. 4 (5), p. 406-408, Atul Malhotra, M.D.; Suzie Bertisch, M.D., M.P.H.; Andrew Wellman, M.D.

and note how in complex disease, specifically, central disturbance created by pressure therapy, that the relief of obstructive events followed by a period of acclimatization may change the arousal threshold and then the central events will resolve spontaneously. This process may take days to weeks.

So if this is true, then it stands to reason that the balance can be upset immediately by arbitrary dial wingin' with an inability to determine what's appropriate by using short-term observations ("let's try this today, let's try that tomorrow").

OK sorry to interrupt your scientific discussion with an anecdote, but I think they are totally onto something.
When I was titrated, I was getting CA's all over the place. Recently when I increased my pressure a notch I started getting them again. After a few days they settled down. Even though the sleep doc told me (after the titration) that I was prone to CA's above 9 or 10cm, I can now use 12cm and get the same number of central's as I have at 7cm (in the range of 0-4 per night). So WHO has a problem with CA's??? My only explanation is the above - at first the body thinks the additional pressure is a threat, and at some point the body adapts. (they put it slightly more scientifically in the article )

Here's the full article: http://www.aasmnet.org/JCSM/Articles/040502.pdf

Thanks for the link SAG. I'm learning so much from you guys

BTW was the possibility of GERD already addressed in this thread?

We know that Bev has GERD.

Echo, if you tentatively/hypothetically place yourself in the B&W adaptation-oriented population, then you also seem to fit in with some of those patients in yet other ways: experiencing improved AHI, yet with unresolved daytime symptoms. Would love to know what's happening with outstanding RDI/RERA and even Cyclic Alternating Pattern (CAP) with you guys.

IMO sleep science still has a far way to go understanding complex SDB patients who eventually achieve adequate AHI on PAP and yet still manifest unacceptable daytime symptoms. Are we the least bit surprised that the Respironics researchers claim Complex SDB is not a disease and really requires sticking with PAP? I agree adaptation issues need to be properly factored. But let's not over-attribute short-term PAP maladaptation as a complex SDB universalism...

I still think Bev has been overtitrated both in the lab and at home and if that is the case she will never stabilize. If it was me, I'd:

1. Get a decent Pulse Oximeter like the one James Skinner has or one of those wrist types with reports so
she can determine if her oxygen level is truly dropping to dangerous levels.

2. Set the machine on CPAP at 8 cm pressure and ignore the reported AHI unless the pulse oximeter says otherwise.

The machines she has used to date cannot differentiate the difference between a obstructive apnea and a central one. She probably
has a sweet spot below 10 cm totally missed by reading of the software.

IF she had monitored her reports using James Skinners Pressure vs AHI report it should confirm if I'm right or not. With the Minimum pressure currently set so high it can be totally masking her sweet spot if there was one. My opinion is she went over the bell curve on that report and is in one of the spots on the other side. Think Jerry did the same thing once.

That issue of why people on cpap an still feel daytime sleppyness is a very interesting one. Has anyone noticed the sheer number of people starting or posting to threads on this theme. "Why do I still feel so tired after going on cpap". I put myself into that category big time prior to going on bilevel & SV.

I had intended starting a poll on this issue but didn't complete it because I want to rethink the questions. But will do one possibly next week.

The intent of the poll is to 1st ask people what they think the reason is, then to try to explore patterns among those who report the problem.

DSM

And interesting longitudinal study currently underway trying to assess CPAP's efficacy:
https://apples.stanford.edu/

Note that they are focusing not simply on AHI, but a host of other symptomatic/quality-of-life and comorbidity type issues with/despite compliant CPAP use.

-SWS wrote:Echo, if you tentatively/hypothetically place yourself in the B&W adaptation-oriented population, then you also seem to fit in with some of those patients in yet other ways: experiencing improved AHI, yet with unresolved daytime symptoms. Would love to know what's happening with outstanding RDI/RERA and even Cyclic Alternating Pattern (CAP) with you guys.

IMO sleep science still has a far way to go understanding complex SDB patients who eventually achieve adequate AHI on PAP and yet still manifest unacceptable daytime symptoms. Are we the least bit surprised that the Respironics researchers claim Complex SDB is not a disease and really requires sticking with PAP? I agree adaptation issues need to be properly factored. But let's not over-attribute short-term PAP maladaptation as a complex SDB universalism...

I'm not sure I understand the extent of CAP, and I'm not even sure if I fit into that category - but I do know that I seem to be very sensitive to all sleep related changes. For example my sleep is worse if I sleep in a new place (lasts a few nights) or even a new pillow, if there's too much light in the bedroom or noise pollution (e.g. urban setting), but maybe that's normal.
What I find more interesting, at least in my case (and not to hijack this thread sorry!) is the link between my OSA, my insomnia, and my (lack of) circadian rhythm. I can easily adjust my sleep/wake times with no problem , i am not at all a creature of habit. Or rather, I can easily delay sleep for hours on end with no problem. I get insomnia if the therapy isn't working - as the day goes on I just get more awake, and I do my best work at night (not anymore though, with therapy I've become a morning person ). Is THAT correlation normal?

I personally think that the biggest failing of sleep doctors is not necessarily the inability to understand complex SDB patients (who may be smaller in number), but the failing to identify all the factors that may contribute to a person's individual sleep disorder - as shown for example by the sheer number of people who figure out that GERD is a problem, not from their doctor, but from this forum. Second to that, I do think that this field is still maturing and that there is way more they don't understand, than that they do understand, about complex SDB. I think a part of that problem is due to the fact that all doctors are so specialized - either pulmonologists, or neurologists, but neither have a good overview or understanding of how it all ties in together. At the university hospital clinic I go to, there are no neurologists in the sleep clinic (only pulmonologists) - yet these people are all interpreting our EEGs. Am I missing something?

dsm - if you do write up a poll, i think you should do two polls, or somehow distinguish between : people that have already sorted out their problems (and their solutions), and people that are still trying to sort out their therapy (and for how long?)