In quickly eyeballing this data from September 10, I would say many (but not all) of the OAs are likely post-arousal or sleep-wake-junk (SWJ) events---i.e. they likely occurred while you were not fully asleep and they may very well would not have been scored as an OA on an in-lab sleep test.
The overall pattern of the waveflow seems to indicate a pretty restless night with lots of arousals, and my guess is that many of those arousals were
spontaneous arousals rather than being related to breathing problems. I also think some of the clusters of OAs are occurring in what's often called "sleep-wake-junk" breathing around here: You're not fully asleep, your not fully awake, and you're bouncing back and forth between the two states. And so the breathing is a mess as much as anything because every time the brain tries to hand the control of the breathing off to the autonomic nervous system and slip beyond N1 sleep to N2 sleep, something causes the brain to re-arouse itself. And yes, sometimes what might be causing the re-arousal is the brain becoming overly aware that the transition to normal sleep breathing "got stuck" temporarily as the CO2 trigger for inhalation was reset to a higher CO2 concentration in the blood.
This data is from September 5. Again many, but not all, of the OAs appear to be scored after an arousal has already taken place. On this night, a quick perusal of the data seems to indicate that leaks may have been responsible for some (but not all) of your more obvious arousals. Now, the total length of these leaks is short enough where Mr. Green Smiley Face would have appeared on the machine's LCD and MyAir would have reported that your leaks were decently controlled. Nonetheless, the wave flow data indicates that you probably woke up multiple times to fiddle with the mask to fix a leak. Those arousals may have been so short that you didn't even remember them the next morning.
This data is from August 27. Again, many, but not all, of the OAs occur after what looks like arousal breathing. Again, there's some evidence that leaks may be triggering some of the arousals. In particular, between 2:55 and 3:40 leaks were an issue, as shown in the following screen shot:
I would guess that if EEG data were available for this stretch that it would show that you never really got back to sleep and that all of those CAs are wake breathing or normal sleep transition CAs where sound sleep was just not established. And if I had to guess, I would say that it's the leaking that is what was keeping you restless during this whole time frame.
As for the initial OA in that screen shot, here's the breathing just before that event:
There's a possible/probable arousal just before the OA is scored---the larger than usual inhalation. The shape of that particular apnea event is also something I've seen labeled elsewhere as being typical of what happens when someone (unconsciously) holds their breath while moving around in bed. It is possible that you aroused enough to move around in bed and that the new sleeping position is what triggered the leak which lead to the extended period of restlessness and multiple CAs being scored.
Now, there is also some evidence that your airway may have been at a slightly elevated risk of collapsing around 3-4 minutes
before that OA was scored---we can see that in the flow limitation graph. But whether those flow limitations led to restlessness or not is anybody's guess.
Now you also write:
Agreed that reducing arousals reduces AHI, but I do not agree with mechanism behind it. Arousals introduce airway instability in subsequent sleep. I didn't dig up all the details but following excerpt from
Confalonieri et al. might suffice:
it is believed that low AT contributes to the pathology of OSAS since the repeated awakenings determine destabilizing effects, such as (1) the absence of sufficient time for the respiratory drive to recruit the pharyngeal muscles and reopen the airways before arousal; (2) a reduced partial pressure of carbon dioxide, promoting dynamic ventilatory instability, which contributes to the perpetuation of the consequent respiratory events; and (3) a fragmentation of sleep, which does not allow the individual to achieve slow-wave sleep, i.e., to stabilize sleep [9, 12].
This is a fancy way of saying that once an arousal takes place, a person with (untreated?) OSA can have trouble transitioning back to sleep because the brain is overreacting to the normal pauses in breathing as the CO2 trigger is reset upwards in normal sleep breathing. That kind of thing is what we often call "sleep-wake-junk" breathing around here, or SWJ for short. And that's exactly what I'm seeing in some of your data: There is an initial arousal (that is not always tied to a respiratory event) and then you get stuck in a period of SWJ---your brain is having trouble ignoring the breathing glitches that are part of the normal transition to sleep breathing and each time one occurs, your brain re-arouses itself and you bounce from N1 to Wake if there were EEG data present.
Now one reasonable explanation for why your brain might have trouble ignoring those normal breathing glitches is that when your OSA was still
untreated, the brain needed to become hyperaware of
all breathing glitches because the vast majority of them were
real obstructive events---in other words, your brain trained itself to react to
any breathing glitch, even those that normally occur when we're in the process of establishing genuine N2 sleep. Now that the xPAP machine is preventing the vast majority of those
real obstructive events from happening, the brain is still reacting to the temporary unstable breathing following a
spontaneous arousal by getting "stuck" in SWJ, which can then perpetuate the unstable breathing which perpetuates the SWJ/arousals which perpetuates the unstable breathing and so on and so forth. And before you know it, you get a whole string of events scored in ragged SWJ breathing. But because we don't have the EEG data we have no idea how many of those events would have been scored (because they appear in an epoch where the EEG says N1 sleep) or how many of those events would not have been scored (because they appear in an epoch where the EEG data says Wake).
But the effect on
subjective sleep quality really doesn't matter on trying to sort out how many of the events are "false positives" and how many are "real". The effect on the
subjective sleep quality is pretty simple: If the SWJ resolves itself in less than a minute, it doesn't really affect how you feel the next morning. But if the SWJ goes on for 30-40 minutes? Yeah, you're going feel the sleep was less than good when you wake up in the morning. The problem is the extended time in SWJ: If only the spontaneous arousal had not happened in the first place, you wouldn't have had the extended SWJ. Or if only the brain was able to ignore the first glitch or two when going back to sleep after the spontaneous arousal, the extended period of SWJ would not have happened.
So
reducing the SWJ breathing by decreasing the number of spontaneous arousals as well as the brain's response to spontaneous arousals is likely to reduce the number of events scored by the machine simply by reducing the number of SWJ "events"---events that may very well not be "real" in the sense of occurring when the missing EEG data would say for sure that you were asleep when the event happened.
Ambien helps reduce the number of your spontaneous arousals as well as makes it less likely for you to get trapped in a SWJ mess after an arousal does occur. And that goes a long way towards explaining why you can see a reduction in your treated AHI when you take Ambien.
My events are almost all expiratory apneas. Since I have many lucid dreams, I am somotimes aware of them from within dreams - either it is just palate that flipped and cut off the airflow, or it is catathrenia (somewhat conscious forced exhale through closed epiglottis maybe). Catathrenia is very loud (groaning) and for a long time it was considered to be parasomnia. It feels like it is self soothing in nature and feels like a tic (bordering between voluntary and involuntary).
This would explain why your sleep transition events are typically scored as OAs---when you are in that "self soothing" stage and that "tic" that borders between voluntary and involuntary happens and your epiglottiis closes while you are trapped in SWJ breathing, the FOT algorithm is going to say OA not CA, even though the breathing glitch is happening when EEG data could well indicate that your brain is in Wake rather than N1/N2 sleep.
Unfortunatelly, ambien is somewhat habit forming and crosstalks with other GABA agonists/antagonists. It is good to be aware of it and take it from time to time, but it is not long term solution.
I basically agree with what you are saying: Ambien can be a very good short term tool for some people when they are learning how to sleep with the machine. The choice of whether to continue to take Ambien on a nightly basis long term is something that needs careful consideration and should only be done in consultation with a doctor and with full cognizance of the potential problems.
For what it was worth, I was on long term usage of Ambien for about a 1.5 year period while waiting on Belsomra to become available. Because I had some significant problems with daytime grogginess while on Ambien, my sleep doc prescribed the minimum dosage pill available and had me cutting them in half. That made the residual daytime grogginess tolerable while still helping to keep my sleep onset insomnia under control, stabilize my bedtime, and reduce the number of spontaneous arousals so that I felt like I was getting some decent sleep at night.
When Belsomra finally hit the market, my then sleep doc convinced my insurance company that it was medically necessary for me. And the Belsomra worked miracles for me, and I took it for several years. During the 2020 COVID pandemic, my script for Belsomra ran out and I was unable to get in to see a doctor who could prescribe it and send a note to my insurance company to justify it as "medically necessary". I was pleasantly surprised that when I ran out of Belsomra, my insomnia did not return, and when things finally opened back up and I was able to see a sleep doc, I didn't see any reason to ask for a new Belsomra script. Yeah, I have a few more spontaneous arousals than I had on the Belsomra, and it's much harder for me to enforce a stable bedtime. But overall, I was able to quit the Belsomra cold turkey (because of the pandemic) without having my sleep significantly deteriorate.
Joined as robysue on 9/18/10. Forgot my password & the email I used was on a machine that has long since died & gone to computer heaven.
Correct number of posts is 7250 as robysue + what I have as robysue1
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