New Baseline PSG - What to expect?

OK, I recant this:

Are you talking about a new diagnostic PSG or a titration? If the former and you'll be sleeping without CPAP, I'm not sure why they would not see you at your baseline. I've never seen or read anything to suggest that there is some residual effect of previous CPAP use, but I could be wrong.

I now have read something to suggest that AHI level may remain decreased after 1 night without CPAP (Sahlman et al., 2007, "Evolution of Mild Obstructive Sleep Apnea after Different Treatments"). They cite these folks as the source of that info: Sforza & Lugaresi (1995), "Daytime Sleepiness and Nasal Continuous Positive Airway Pressure therapy in Obstructive Sleep Apnea Syndrome Patients: Effects of Chronic Treatment and 1-night therapy Withdrawal" AND Kribbs, et al. (1993), "Effects of one night without nasal CPAP treatment on sleep and sleepiness in patients with obstructive sleep apnea".

DreamDiver wrote:I'm not questioning the concept of central, obstructive or mixed apnea. My question is: why do they even have two columns for central and obstructive hypopneas in my sleep study if there is really only just plain 'hypopnea'. Why not just one column?

According to The Nuts and Bolts of Scoring Apneas and Hypopneas there are two types of hypopneas...

Central hypopneas are associated with reductions of purely in-phase thoracic and abdominal effort or movement signals, followed by an increase in chest and belly movements at the end. There is no evidence of phase shifting or paradoxical breathing, no airflow flattening, and no snoring throughout the entire central hypopnea.

Obstructive Hypopnea should be scored when there is evidence of even a slight degree of paradoxical breathing, including even slight phase shifting and/or snoring and/or airflow flattening in the airflow signal. This is particularly observable using a nasal pressure transducer, which is very readily capable of picking up the shoulders or flattenings in the airflow signal. A nasal pressure transducer detects the variations in negative airway pressures at the nares using a cannula inserted into the nose. A tube is connected to an air pressure transducer. Such systems have been shown to be much more sensitive in terms of detecting airflow flattening than thermistors or thermocouples. Also, nasal pressure transducers have been shown to detect far more hypopneas than either thermistors or thermocouples. Shoulders or flattening of slopes in the airflow signal are also an indication of upper airway obstruction, as is paradoxical breathing and/or snoring. However, it is possible for a hypopnea to be obstructive and still exhibit in-phase thoracic and abdominal movements (like a central hypopnea), as long as not enough negative airway pressure is created to cause paradoxical or even phase shifting of the thoracic and abdominal movement signals. In such cases there must be other evidence of upper airway obstruction such as airflow flattening or snoring in order to score an event as an obstructive hypopnea.

Don't know if that helps in any way?

Thanks
Dave

SleepingUgly wrote:OK, I recant this:

Are you talking about a new diagnostic PSG or a titration? If the former and you'll be sleeping without CPAP, I'm not sure why they would not see you at your baseline. I've never seen or read anything to suggest that there is some residual effect of previous CPAP use, but I could be wrong.

I now have read something to suggest that AHI level may remain decreased after 1 night without CPAP (Sahlman et al., 2007, "Evolution of Mild Obstructive Sleep Apnea after Different Treatments"). They cite these folks as the source of that info: Sforza & Lugaresi (1995), "Daytime Sleepiness and Nasal Continuous Positive Airway Pressure therapy in Obstructive Sleep Apnea Syndrome Patients: Effects of Chronic Treatment and 1-night therapy Withdrawal" AND Kribbs, et al. (1993), "Effects of one night without nasal CPAP treatment on sleep and sleepiness in patients with obstructive sleep apnea".

Thanks SleepingUgly.

PubMed wrote:Daytime sleepiness and nasal continuous positive airway pressure therapy in obstructive sleep apnea syndrome patients: effects of chronic treatment and 1-night therapy withdrawal.
Sforza E, Lugaresi E.
Sleep Center, University of Bologna, Italy.
Abstract
A multiple sleep latency test (MSLT) was performed in 30 patients with obstructive sleep apnea syndrome (OSAS) at the time of diagnosis and after 1 year of home therapy with nasal continuous positive airway pressure (nCPAP). The MSLT was administered after two consecutive polysomnographic studies, one with (CPAP) and one without nCPAP (NCPAP) at baseline and at follow-up. After a year of therapy, the MSLT significantly rose from 3.1 +/- 0.3 to 9.8 +/- 1.0 minutes (p = 0.001). The increase in mean sleep latency was significantly correlated with the decrease in the number of arousals during the night (r = -0.48, p = 0.009). On the basis of MSLT value at follow-up, patients were split into two subgroups: the normalized group, in which 15 patients had an MSLT > or = 10 minutes, and the unnormalized group, consisting of 15 patients with an MSLT < 10 minutes. Normalized patients differed for a higher apnea+hypopnea index (AHI) time at baseline, a greater improvement in nocturnal hypoxemia and a greater nCPAP use at follow-up. After 1 night of therapy withdrawal, MSLT fell dramatically to 5.3 +/- 0.6 minutes, even though the subjects said they did not feel sleepy. The changes in MSLT after the night of treatment suspension were not correlated with changes in body mass index (BMI), AHI or nocturnal hypoxemia, whereas they were correlated negatively with changes in AHI time (r = -0.53, p = 0.003) and with the decrease in the number of arousals (r = -0.47, p = 0.009).(ABSTRACT TRUNCATED AT 250 WORDS)

dave21 wrote:

DreamDiver wrote:I'm not questioning the concept of central, obstructive or mixed apnea. My question is: why do they even have two columns for central and obstructive hypopneas in my sleep study if there is really only just plain 'hypopnea'. Why not just one column?

According to The Nuts and Bolts of Scoring Apneas and Hypopneas there are two types of hypopneas...

Central hypopneas are associated with reductions of purely in-phase thoracic and abdominal effort or movement signals, followed by an increase in chest and belly movements at the end. There is no evidence of phase shifting or paradoxical breathing, no airflow flattening, and no snoring throughout the entire central hypopnea.

Obstructive Hypopnea should be scored when there is evidence of even a slight degree of paradoxical breathing, including even slight phase shifting and/or snoring and/or airflow flattening in the airflow signal. This is particularly observable using a nasal pressure transducer, which is very readily capable of picking up the shoulders or flattenings in the airflow signal. A nasal pressure transducer detects the variations in negative airway pressures at the nares using a cannula inserted into the nose. A tube is connected to an air pressure transducer. Such systems have been shown to be much more sensitive in terms of detecting airflow flattening than thermistors or thermocouples. Also, nasal pressure transducers have been shown to detect far more hypopneas than either thermistors or thermocouples. Shoulders or flattening of slopes in the airflow signal are also an indication of upper airway obstruction, as is paradoxical breathing and/or snoring. However, it is possible for a hypopnea to be obstructive and still exhibit in-phase thoracic and abdominal movements (like a central hypopnea), as long as not enough negative airway pressure is created to cause paradoxical or even phase shifting of the thoracic and abdominal movement signals. In such cases there must be other evidence of upper airway obstruction such as airflow flattening or snoring in order to score an event as an obstructive hypopnea.

Don't know if that helps in any way?

Thanks
Dave

I think I'm going to have to re-read it a few times. Right now, it might as well be Sanskrit. But thank you very much for finding this. I'll just read it until it sinks in.

I got the old sleep lab to resend me my baseline study. Apparently they marked everything as obstructive on the baseline, which makes me wonder about what echo said earlier where people who aren't on CPAP but need it suddenly start getting centrals when on CPAP, regardless of whether their baseline showed obstructive. Odd. I wonder what the new baseline will show. There was also a lot of bradycardia - which covers a lot of ground, I know.

So how many nights are you going to be off CPAP before you go to the sleep study, given the possibility that prior CPAP use affects AHI for at least a day (and who knows how much longer)? I will have to reread all that to figure out if there is a clue in there as to why it would last at all...

Are you scheduled for an MSLT? Did I recall correctly that you didn't want a narcolepsy diagnosis, but had had some SOREMS?

You learn something new everyday! I too will have to reread that. Thanks dave and sleepingugly.

DreamDiver wrote:I got the old sleep lab to resend me my baseline study. Apparently they marked everything as obstructive on the baseline, which makes me wonder about what echo said earlier where people who aren't on CPAP but need it suddenly start getting centrals when on CPAP, regardless of whether their baseline showed obstructive. Odd. I wonder what the new baseline will show. There was also a lot of bradycardia - which covers a lot of ground, I know.

Well for what it's worth (since a sample of ONE makes for great statistics ), after my titration study, the sleep doc said that she noticed positive pressure induced central's above 10cm. She said she then went back to my original PSG and noticed that there were indeed some centrals that she overlooked in the original PSG. But I'm guessing _not enough_ to rescore the PSG. I think they were mostly sleep-onset related.

Nevertheless while I still stand behind the original statement that it is very likely to have pressure induced centrals, there ARE people that DO have ONLY centrals, I think christinequilts comes to mind. It could very well be that all of your events are all centrals too, who I am to diagnose you!

So let's just have some hope that the new sleep lab knows what you're doing. I'm assuming you will give them copies of all your previous studies.
I would also prepare some summary reports from your current machine (maybe a one page word doc summarizing the last x month's AHI info as well as any home PulseOx info), and a clearly written list of observations/concerns/questions that you have, to put in their file as well.

And I would try to talk to the sleep doc who will be scoring your study, in advance of the new baseline PSG, so that he/she is aware of exactly what the issues are, so that they don't treat you like a new CPAP patient, and that they pay special attention to any potential centrals.

I'm sure I haven't said anything you haven't already thought of, but in case your sleep deprived state made you forget, that's the list of what I would do...

When's your appointment, I'm so excited for you

SleepingUgly wrote:So how many nights are you going to be off CPAP before you go to the sleep study, given the possibility that prior CPAP use affects AHI for at least a day (and who knows how much longer)? I will have to reread all that to figure out if there is a clue in there as to why it would last at all...

Are you scheduled for an MSLT? Did I recall correctly that you didn't want a narcolepsy diagnosis, but had had some SOREMS?

No MSLT. Not sure about SOREMs, but I know I start dreaming before I totally fall asleep.

echo wrote:I'm sure I haven't said anything you haven't already thought of, but in case your sleep deprived state made you forget, that's the list of what I would do...

When's your appointment, I'm so excited for you

Sunday evening. Thanks.

DreamDiver wrote:Not sure about SOREMs, but I know I start dreaming before I totally fall asleep.

So you have REMOS?

Good luck!

DreamDiver wrote:

-SWS wrote:DD, are you by any chance a sensitive sleeper---meaning that you wake easily to either sensory or psychological stimuli?

It has to be something out of the ordinary. If I hear a deer outside, or a pine cone fall on the roof, that 'scores' as normal background noise. I don't wake up. If I hear someone walking down the hall in the dark, I wake up immediately. Stealthy human movement is more apt to wake me than normal knocking around, opening or closing of doors, drawers, flushing of toilets, etc. Videos playing in the background - even more violent ones like 'Fifth Element' or 'Dark City' would put me to sleep as easily as 'Pride and Prejudice'. Kids yapping in the background is a comfortable white noise. Kids stopping yapping is not. Tip-toeing is not. I imagine I'm not outside the normal range there.

As to psychological stimuli... I am not sure. What would you mean? Illusory sensory stimuli produced by the mind? Like dreams?

I'm sorry for not replying sooner, DreamDiver. Regarding the psychological stimuli: I think sometimes people wake up in response to their disconcerting dreams. I also think they can wake up during stage one, which is nearly lucid, in response to disconcerting ruminations. I don't know if lucid thoughts or ruminations can even occur during stage two, however.

I suspect your tendency to be more easily aroused by sensory stimuli based on certain situational contexts might not be uncommon. It sounds like adaptive sleep behavior entailing what Darwinians or sociobiologists might view as "genetic survival value".

-SWS wrote:... I'm sorry for not replying sooner, DreamDiver. Regarding the psychological stimuli: I think sometimes people wake up in response to their disconcerting dreams. I also think they can wake up during stage one, which is nearly lucid, in response to disconcerting ruminations. I don't know if lucid thoughts or ruminations can even occur during stage two, however.

I suspect your tendency to be more easily aroused by sensory stimuli based on certain situational contexts might not be uncommon. It sounds like adaptive sleep behavior entailing what Darwinians or sociobiologists might view as "genetic survival value".

Agreed.

Sometimes, I get the impression in a dream state that someone has tossed water on my face, or that I'm falling. It feels very real. Sometimes I'll hear a really weird noise that is impossible to describe. An example noise from last night was the sound of a small stone bouncing and echoing down a very long curving metal tube, but the sound had an adaptive flanginess to it that started natural but ended as very synthetic. It was very loud. My wife didn't wake up at all, so that confirmed my suspicion that it was a dream. I suspect my body does these little tricks to wake me up when 02 gets dangerously low, since my normal systems aren't doing it for me. Sometimes it's a very bad dream. Sometimes it's a location joke. Sometimes it feels like a very large dinosaur stomped me - that's the worst because my whole body feels like it's been crushed.

So last night, I tried without a mask. Almost two hours in, the alarm went off. It was set by default to 84% SPO2. It wouldn't stop beeping. I decided not to continue without a mask. It felt very bad. This was the first time that I felt my heartbeat in my kidneys. The tinitus was louder than ever, along with the wooshing noise of blood pumping. So this morning, I checked the graph. I don't think I'll be trying that again until the sleep study. I don't think they'll allow me to continue the full night. I suspect it will likely end as a split study with titration, if only to keep things from getting dangerous. Most of the time off the mask, I was at 87%. I spent the rest of the night on the mask, trying to fall asleep. That really cannot be good.

Here's last night with oximetry:

Plenty of ventilatory instability during sleep onset... That's for sure. Some clinicians would prefer to at least endeavor addressing that sleep-onset related ventilatory instability pharmaceutically---especially if ASV either fails to address it or exacerbates it. Others might endeavor to work on more rapid/stable sleep onset by increasing sleep-onset pressure via better sleep hygiene or improved circadian rhythm methods in some cases. And in some cases that residual problem limited to sleep-onset is the best treatment a patient might find...

And that Sans mask segment of desaturation demonstrates a clear need for PAP.

DreamDiver, what happened with the PSG? Did they do it without CPAP the whole night? MSLT?

-SWS wrote:...Some clinicians would prefer to at least endeavor addressing that sleep-onset related ventilatory instability pharmaceutically---especially if ASV either fails to address it or exacerbates it. Others might endeavor to work on more rapid/stable sleep onset by increasing sleep-onset pressure via better sleep hygiene or improved circadian rhythm methods in some cases. And in some cases that residual problem limited to sleep-onset is the best treatment a patient might find...

And that Sans mask segment of desaturation demonstrates a clear need for PAP.

I hope they don't try pharmaceuticals. I don't do well with most of these. Nasonex has been the first surprise pharmaceutical to ever really work for me without noticeable side effects. Thank goodness I don't need it anymore while I'm on CPAP, though.

Yeah - sleep hygiene. I scored 55 on that site muffy provided. However, I've noticed that I seem to do better during sleep onset if I spend at least 20 minutes doing something like watching part of a dvd. Something about the defocusing of my thoughts from body sensory input seems to make a difference.

I'm not sure if hygiene is all of the answer. I'm in a lot of fibromyalgia-like pain most of the night. (Well - most of the day too, but I can usually find something to do that will take my attention away from pain.) That wakes me up as much as anything, along with headaches. I end up having to move all night long in order to reduce pain. Just the pressure of the bed sheets and blankets at night is enough to cause pain on my toes. I keep my legs elevated to keep the pressure of my heels pressing into the bed from causing pain enough to wake me up too. I have to turn over continuously or something is bound to go numb or become painful. I've gotten to the point where my arms don't go numb anymore, but that means not sleeping on my sides and elevating them so the elbows aren't touching the flat of the bed. I guess centrals are only a part of what's going on.

SleepingUgly wrote:DreamDiver, what happened with the PSG? Did they do it without CPAP the whole night? MSLT?

No MSLT. I went the whole night. Not as bad as I expected, but I slept hardly at all.
The tech did not discuss anything with me, except to say the oximetry fell into the high 80's a number of times. Wouldn't talk about centrals. That's okay.
The lab is right next to a major highway - eighteen wheelers all night long.
The heating/cooling system made sounds that my brain interpreted as a stealthy opening of a door - a perfect wake-que for me.
Either that or the sleep tech was having to stealthily open and close doors all night long.

I dozed off at least four times, probably more, but spent most of the time trying to relax enough to get to sleep. I kicked off the leg sensors once. They had to be resnapped. I used a papcap to approximate what for me would be a 'normal' night's sleep. I think the sleep tech liked the papcap, if for nothing other than it stabilized the sensors on the head.

There were more wires than my last sleep study. Fourteen for the head alone - I could be wrong, I think that's what the tech said.
No capnography. They're not equipped to do it. ACH!

I slept for four hours this morning after I got home, then another two hours this afternoon.

The sleep study results should be in my doctor's office just before my next visit in two weeks. They're supposed to discuss the sleep study results with me before the visit to the doctor.

I just got a call from the sleep lab:
Only slept for about half the time being recorded in spurts – apparently typical for baseline PSG with people already on CPAP.
AHI - 17
AHI on back 17.8
AHI off back 10.7
AHI in REM - 30
12 minutes in REM (Very little, apparently)
SpO2 down to 84% a number of times
7 minutes Delta – that’s a first. I don’t usually have any delta in a sleep study.
At 87-89% SpO2 during 47% of actual time in sleep.
Very little limb movement.
No centrals – all obstructive, just like my baseline study in 2007 prior to titration.
So I guess this could mean CompSAS for me.
I go in for the new titration next Sunday.
I'm going to pick up the report with condensed graphs at the same time.

I want to get a CD of the data they compiled.
They're using XLTek software to score the data.
I know there's the free EDF Browser, and I suspect XLTek is using the .edf format.
Is that correct?
Is there anything specific I should ask for when asking for a data CD?

by DreamDiver on Tue Apr 13, 2010 3:43 pm

DreamDiver wrote: I have centrals only. That much is what the S9 is showing.

by DreamDiver on Tue Apr 20, 2010 9:33 am

DreamDiver wrote:I just got a call from the sleep lab:
No centrals – all obstructive, just like my baseline study in 2007 prior to titration.

I'm curious as to what this indicates about the "new and improved" S9.

Thoughts/comments/suggestions

carbonman wrote:by DreamDiver on Tue Apr 13, 2010 3:43 pm

DreamDiver wrote: I have centrals only. That much is what the S9 is showing.

by DreamDiver on Tue Apr 20, 2010 9:33 am

DreamDiver wrote:I just got a call from the sleep lab:
No centrals – all obstructive, just like my baseline study in 2007 prior to titration.

I'm curious as to what this indicates about the "new and improved" S9.

Thoughts/comments/suggestions

Well if he's getting pressure-induced centrals (Complex Apnea) then it means it works. Only way to know for sure is the titration they will do next week.