Why would pressure increase while I'm sitting up awake?

[quote="jrgood27"]Well I'm not sure I can see a definitive answer - not that I would understand it anyway. The flow dynamics stuff is a little too close to physics for me, lol.

I did double check that I'm set to APAP and not CPAP. So that's all set. My settling time was off - so now when I'm sitting with it in the evenings I will leave it on.

I'm a bit concerned because my SDB is on the unusual side - all hypopneas, no desats, not much flow obstruction and a zillion arousals. And it seems like there's some murkiness in the whole APAP treating hypopnea arena.

I can't for the life of me fall asleep with my machine. Well, I fall asleep and wake up every 1 to 10 minutes with a strange little startle or gasp. I'll keep this up for 1 to 3 hours depending how sleep deprived I am before I give up for the night. This is with sleep meds.

But I digress...

This is all really interesting though thanks for all the food for thought. Jenny

neversleeps wrote:

GoofyUT wrote:But if the algorithm ignores hypops, why does it titrate when I'm awake, experiencing what are presumably "central hypopneas?" And why is it detecting hypops so aggressively if its ignoring them?

Chuck

Chuck, that is an excellent question for which I do not have an excellent answer. I don't even have a mediocre answer. My only thought is to suggest searching
-SWS's posts to shed some light on the subject. I just don't know.

the events seen while awake are more likely snores than centrals. the machine can trigger on snores that are inaudible but can also be loud snoring.

jrgood27 wrote:Well I'm not sure I can see a definitive answer - not that I would understand it anyway. The flow dynamics stuff is a little too close to physics for me, lol.

I did double check that I'm set to APAP and not CPAP. So that's all set. My settling time was off - so now when I'm sitting with it in the evenings I will leave it on.

I'm a bit concerned because my SDB is on the unusual side - all hypopneas, no desats, not much flow obstruction and a zillion arousals. And it seems like there's some murkiness in the whole APAP treating hypopnea arena.

I can't for the life of me fall asleep with my machine. Well, I fall asleep and wake up every 1 to 10 minutes with a strange little startle or gasp. I'll keep this up for 1 to 3 hours depending how sleep deprived I am before I give up for the night. This is with sleep meds.

Guest has some really good advice for you two posts above. As you probably surmised your machine was increasing the pressure while you were wide awake and sitting up because: 1) you had the settling period turned off (as you already figured out), 2) we often manifest flow limitations and hypopneas while we are awake---especially when we are relaxed, and 3) your machine thought you were asleep (for lack of either a settling period or accurate wakefulness detection) and tried to treat those flow limited and/or hypopneic breathing patterns of yours. As a side note wakefulness detection is most difficult at the beginning of any sleep session when any autoPAP is first baselining respiratory parameters. Wakefulness detection fortunately gets much more accurate after that baselining period has occurred. So settling period allows the patient a chance to comfortably fall asleep, but also allows the autoPAP a chance to wait until sleep has occurred to finish the task of baselining.

I would suggest turning your settling period to the maximum allowable setting if it's not there already. Then limit your wide-awake practice sessions to that amount of time. Turn your machine off, then back on for several consecutive practice sessions if necessary. Consider initially leaving that maximum settling time in place for your nightly sleep sessions as well. That will be a time for you to get settled in, and fall asleep without the autoPAP hiking pressure in response to your preliminary sleep events just prior to sleep onset. Once you are used to sleeping with the autoPAP, then reduce the settling period to the amount of time that it typically takes you to fall asleep.

Also, if your starting pressure seems uncomfortably low or high for you, consider changing that pressure as well to make it easier to fall asleep.

Anonymous wrote:

neversleeps wrote:

GoofyUT wrote:But if the algorithm ignores hypops, why does it titrate when I'm awake, experiencing what are presumably "central hypopneas?" And why is it detecting hypops so aggressively if its ignoring them?

Chuck

Chuck, that is an excellent question for which I do not have an excellent answer. I don't even have a mediocre answer. My only thought is to suggest searching
-SWS's posts to shed some light on the subject. I just don't know.

the events seen while awake are more likely snores than centrals. the machine can trigger on snores that are inaudible but can also be loud snoring.

My guess is that it's more likely detecting wakeful hypopneas as hypopneas---perhaps a few flow limitations as well. Some autopap models will not trigger on any hypopneas whatsoever, but will simply try to prevent them by triggering on snores and flow limitations as likely precursor events to hypopneas. Other autopap models will perform the above steps, but will additionally trigger on hypopneas that specifically show high probability of being obstructive versus central (that probability being based on characteristic wave shape in addition to amplitude assessment). All autoPAP algorithms are preoccupied with avoiding the pressure induction of central events (yup, that fact is leading up to a future CSDB discussion from me). When an autopap uses flow wave shape to detect a high-probability occurence of an obstructive versus central hypopnea, it probably does so with high specificity yet mediocre sensitivity at best (my own personal assesment, not published fact). That is likely why some autopap models elect to prevent hypopneas and not even trigger on them.

Thanks so much for your rich and informative posts Guest and SWS. They both were enormously helpful.

As an aside, the "lightbulb" finally went on over my head yesterday as I realized that my S8 was titrating when I was awake, because it thought that I was asleep and was therefore, doing its job of attempting to pre-empt SDB events by increasing pressure.

Now, I'd always had "Settling" set to off on the advice of my DME who had initially set it that way stating "This way, the machine can begin hunting for the pressure that you need from the very beginning." So, last night I turned "Settling" on with a settling period of 30 minutes.

Well, I SLEPT GREAT last night, and this morning, I checked my stats for last night, and for the first time, I crossed the AHI=5=Normal barrier for the FIRST TIME! My AHI was 4.2, with an AI of 0.2!

So once again, thanks so much and once again, my hat's off to the folks of the CPAPtalk community for the wealth of knowledge that you share with one another!

Chuck[/i]

So glad you achieved better results last night, Chuck!

GoofyUT wrote:...I realized that my S8 was titrating when I was awake, because it thought that I was asleep and was therefore, doing its job of attempting to pre-empt SDB events by increasing pressure.

That pretty much sums it up nicely. Regarding the detection of wakeful hypopneas. Perhaps only some but not all are genuine wakeful hypopneas. And even those genuine wakeful hypopneas are not necessarily worrisome. A wakeful hypopnea would fit the autoPAP definition of hypopnea largely as a measurement of amplitude reduction of your own baselined flow of breath. However, that amplitude reduction is only with respect to your breathing having been baselined while you were wide awake. That's when breathing tends to be more irregular and consequently baselining tends to be less than optimal (we sometimes tend to subconsciously restrict or otherwise modify our own breathing parameters under voluntary muscle control while we are awake). And if that wakeful albeit highly irregular breathing can amount to less than optimal autoPAP baselining, then it can certainly result in erroneous amplitude reduction (a.k.a. "hypopnea") calculations. An autoPAP optimally baselines our respiratory parameters while autonomic breathing occurs, versus voluntary breathing.

Bottom line is that straight CPAP is great for wide awake practice sessions but AutoPAP needs to have the settling time in effect for wide awake practice sessions or even prolonged sleep onset.

SWS-

Thanks again so much for your illuminating and thoughtful post(s).

You raise an interesting point (one of many) that I've been curious about. What ResMed and Respironics write about their algorithms, and the comments about them that appear in most of the literature that I've reviewied, talk little about baselining. I was always curious about that, and I wondered how the algorithm developed a model for flow shape and amplitude waveforms. Since I didn't see much about baselining,I figured that the waveform was fairly standard between individuals, much like normal sinus rhythm, and so the algorithm contained a "normal" waveform model (though that didn't make alot of sense to me).

From what you say, it appears that the algorithms develop a "normal" autonomic waveform for the individual, and then use that waveform for measuring degradations in shape and amplitude. Am I correct in drawing this conclusion? If you're correct, then I can see how a waveform distorted by our "voluntary" efforts during wakefulness would distort the model that the algorithm uses to judge degradations during the night.

Again,many thanks!!

Chuck

Bump

GoofyUT wrote:...Since I didn't see much about baselining,I figured that the waveform was fairly standard between individuals, much like normal sinus rhythm, and so the algorithm contained a "normal" waveform model (though that didn't make alot of sense to me).

From what you say, it appears that the algorithms develop a "normal" autonomic waveform for the individual, and then use that waveform for measuring degradations in shape and amplitude. Am I correct in drawing this conclusion?

Yes, Chuck. I believe you are correct. The autoPAP necessarily baselines against each patient. Respiratory parameters such as peak and tidal volumes, peak flow shape, BPM, even rate-of-change for each inspiratory flow curve (based on respiratory effort), etc. would all be highly variable and quite diverse across any population.

One person's maximum inspiratory amplitude is yet another person's significantly diminished inspiratory flow. This baselining challenge alone is why apnea detection tends to yield better sensitivity and specificity than hypopnea detection: in that former case, any apnea's "zero airflow" is universal from one patient to another, very easy to measure, and just as easy to score; in that latter case, hypopnea detection is a matter of measuring but a degree of diminished air flow against a baselined amplitude that can be challenging to algorithmically pin down in some patients.