What if you have mostly hypnopeas and not apneas?

[Muse-Inc]

...http://circ.ahajournals.org/cgi/content/full/107/1/68

They showed a drop in blood pressure when effective CPAP was applied, but nada at subtherapeutic levels.

Thanks! This study of 1 says my BP of 215/110 at diagnosis following a lifetime of low BP took 18 mos of CPAP therapy using a dumb CPAP before I could stop taking Cozaar. I was fat, dumb, & happy in my ignorance as I was so much better off than I had been...but with data, it might been a lot faster than 18 months.

[larry63]

So like me,

Your diagnostic PSG was mostly hypopneas if I recall correctly.

But the S9 is reporting mostly apneas since the AI is 0.8 and the AHI is 1.1.

Interesting.

Of course, your CAI is greater than your OAI. My OAI was always essentially the same as my AI on the S9 and my AI was always essentially the same as my AHI. In other words, even though my diagostic sleep study showed that my main problem was hypopneas with arousal, the events the S9 was detecting were almost 100% classified as OA's. [And on bad nights, the S9 was detecting between 40% and 70% of the number of OA's that were scored during my diagnostic sleep study, but not detecting a single hypopnea.]

robysue

Sorry, I'm trying to wake up through a "get up at 6 am to drive 7 hours to mom's haze", but (or because!) I'm not sure what you're saying here.
I think you're wondering why the S9 is reporting more apneas vs. hypopneas. It kind of makes sense to me - when pressurized, wouldn't the hypnopneas be
the first to dissapear? (Just geussing from a layman's perspective).

Or (more likely - I'm really tired) am I missing your point?

[NotMuffy]

I vehemently disagree with the assertion that we should not care "how high the AHI goes as long as the bulk of it is from hypopneas," no matter what machine you use.

Me2.

Do you agree with the assertion that HI (on S7/S8) does not matter, or do you agree with me, that it might in fact matter?

I think you have to figure out the cause before you can conclude the significance.

For example, hypopneas with rounded waveforms could be a sign of poor sleep w/o evidence of of SDB. From an APAP's perspective, in that case, they wouldn't matter.

From the patient's perspective, maybe that would be something to look into.

Just not by dial wingin'.

Perhaps the real issue with the pre-S9 algorithm is that ResMed even chose to report "benign" hypopneas.

Well, in my case, those hypopneas that don't matter on my S7 machine happen when I am in REM (dreaming?), and are also accompanied by marked decreases in oxygen saturation level. Funny, that.

I think the oximetry needs to be closely examined before conclusions are made. Poor sleep might appear as artifact on oximetry.

Not every patient is the same. Not treating hypopneas while awake leads to not treating them during REM when they might actually matter.

Not necessarily. Phasic REM might look like significant SDB, when it is in fact, normal phenomenon.

To Fix or Not To Fix?

Poor algorithm.

I think it's pretty clever. Although I think the S9 FOT specificity sux.

At the very least they might try putting a configurable delay before treating hypopneas to avoid treating the awake ones.

They did. Their delay is "indefinite".

I don't snore, but I do have flow limitations.

Perhaps they are fixed (not "corrected" fixed, "unresponsive" fixed).

[larry63]

This is an interesting thread. We have several people here that think it doesn't matter how high the AHI goes, as measured by an S7 or S8 machine, as long as the AI is very low. I wonder if this is changing any minds on that view?

My concern all along has been that the S9 was seriously under reporting my hypopneas. And since its reported number for my apneas has consistently been only a little bit lower than my rather low number of apneas in my untreated diagnostic sleep study, the freak-out part of my brain has begun to become increasingly concerned about whether my true number of hypopneas with the S9 might also actually be much closer to the number of hypopneas in my baseline study. Because in 13 weeks of using the S9, I have not started feeling better; indeed I have continued to feel worse than before I started using the S9.

This is NOT meant to be a slam against the S9. Rather it is an indication of the current state of my sleep deprived, anxiety prone mind some 13 weeks into my specific therapy that has not been going particularly well with the S9 AutoSet. My medical team has been working with me to resolve my problems with CPAP/APAP, and I believe that my problems with the S9's therapy are more about how my body is put together (and not the S9) and how my body has been reacting to the S9's way of delivering therapy and are not actually any kind of an indication of a potential problem with the S9's quality. In any human-designed algorithm, there are design constraints and decisions: Those constraints and decisions will cause some instances of failure in outliers, and I am most likely an outlier. There is most likely something in my particular anatomical make-up and my tendancy to arousal and my apnea/hypopnea mixture that has caused my titrated settings on the S9 AutoSet to create more disruptions to my sleep patterns than expected. The sleep doctor recommended a bi-level titration a while back and I was able to switch to a PR BiPAP this week. It is very early in my BiPAP therapy, but already there are signs that the differences between bi-level therapy and S9's CPAP/APAP therapy modes are significant in my case. And if the positive trends continue to build as time goes by, it will not be because the PR BiPAP is somehow a "better" machine than the S9; rather it will be because the PR BiPAP will prove to be a more appropriate machine for my particular body to use than the rather remarkable S9 AutoSet turned out to be.

One point (or question) here, if I might - Is the data from _any_ xPAP machine very useful? For example, if we were to some how hook up with a sleep specialist, whould he or she actually use the data from xPAP machine? All the xPAP machine can measure is flow and pressure, right? It have no way of knowing (unlike Santa Claus!) if you're sleeping or awake, for one.

[HoseCrusher]

That is a very interesting study.

I find this statement interesting:

"...apart from the AHI and Epworth sleepiness scale scores, only mean SaO2 was significantly higher on therapeutic than on subtherapeutic nCPAP. This finding further emphasizes the role of hypoxia in the evolution of daytime arterial hypertension and the importance of preventing hypoxia to achieve optimal treatment of arterial hypertension in OSA patients."

I may not be at my "therapeutic" pressure because my oxygen saturation level has not "significantly" increased while being on xPAP.

They go on to state:

"Unexpectedly, nCPAP at a pressure of 3 or 4 cm H2O reduced mean AHI by around 50%, improved sleep structure, and reduced desaturation. nCPAP at the pressure applied is therefore not a placebo but a suboptimal form of treatment, because even the low treatment pressure used here may be sufficient to at least partly reverse upper airway obstruction in many patients. However, the reduction in AHI in the control group would have acted against our hypothesis that nCPAP lowers blood pressure. Despite the reduction in AHI in the subtherapeutic treatment group by around 50%, there was no reduction in blood pressure in this group. The unexpected result that suboptimal nCPAP has a substantial effect on AHI but no effect on blood pressure emphasizes the importance of optimal treatment to reduce cardiovascular sequelae."

This would indicate that while having a low AHI is a sign that the obstructions have been removed, a more important indication of therapeutic use of xPAP would be higher oxygen saturation during sleep and lower blood pressure during sleep and while awake.

I also found it interesting that a pressure of 4 reduced AHI by around 50%.

[LoQ]

Do you agree with the assertion that HI (on S7/S8) does not matter, or do you agree with me, that it might in fact matter?

I think you have to figure out the cause before you can conclude the significance.

That is why I used the word might. They might matter; I didn't say all of them matter. But to say that it doesn't matter how high the AHI goes as long as the bulk is from hypopneas leads inevitably to the conclusion that HI doesn't matter. It is syntatically equivalent, and people who say it isn't are play imaginary word games.

Perhaps the real issue with the pre-S9 algorithm is that ResMed even chose to report "benign" hypopneas.

Well, it seems to me like that is not the problem, because ResMed freely admitted it. The real problem is that some here are discounting genuine problematic hypopneas because the are considering apneas to be the only problem, their view being bolstered by an incomplete understanding of ResMed's pre-S9 algorithm.

Well, in my case, those hypopneas that don't matter on my S7 machine happen when I am in REM (dreaming?), and are also accompanied by marked decreases in oxygen saturation level. Funny, that.

I think the oximetry needs to be closely examined before conclusions are made. Poor sleep might appear as artifact on oximetry.

I absolutely agree with this. I don't know if sleep labs' oximeters are subject to this problem, but if not, then I definitely have REM desaturations. Some home oximeters also graph movement, and even when you take those "desats" out of the picture, I still have desats during REM.

Not every patient is the same. Not treating hypopneas while awake leads to not treating them during REM when they might actually matter.

Not necessarily. Phasic REM might look like significant SDB, when it is in fact, normal phenomenon.

I said, again, they might matter. Until you say they NEVER matter, you are not disagreeing with me.

To Fix or Not To Fix?

Poor algorithm.

I think it's pretty clever. Although I think the S9 FOT specificity sux.

What is FOT? It doesn't seem to be in the abbreviations.

At the very least they might try putting a configurable delay before treating hypopneas to avoid treating the awake ones.

They did. Their delay is "indefinite".

I suggested a configurable delay. Is this indefinite delay configurable? Heh.

I don't snore, but I do have flow limitations.

Perhaps they are fixed (not "corrected" fixed, "unresponsive" fixed).

Well, we will never know if they are unresponsive or not. I don't have an auto that shows the flow data.


Thank you for your interesting comments, as always, NotMuffy.

[SleepingUgly]

I don't snore, but I do have flow limitations.

Perhaps they are fixed (not "corrected" fixed, "unresponsive" fixed).

What is an unresponsive/fixed flow limitation?

Also, another question, is 4cm of pressure a therapeutic pressure or is it tantamount to NO pressure? If the latter, shouldn't the number of hypopneas per hour in 4cm of pressure at least remotely correlate with what was seen on NPSG?

[Muse-Inc]

...What is FOT?

Forced Air Oscillation. It is the mechanism used in the S9 to determine if the airway is open (clear)or closed (obstructed). When you drop the time scale low enough (in the detailed graphs), you can see these small increases in air pressure that the machine uses to evaluate the state of the person's airway during an identified apnea. Respironics used a similar mechanism tho the pressure is much larger...some can detect it while awake.

[LoQ]

...What is FOT?

Forced Air Oscillation.

Hmmm, wouldn't that be FAO, then, and not FOT?

[robysue]

...What is FOT?

Forced Air Oscillation. It is the mechanism used in the S9 to determine if the airway is open (clear)or closed (obstructed). When you drop the time scale low enough (in the detailed graphs), you can see these small increases in air pressure that the machine uses to evaluate the state of the person's airway during an identified apnea. Respironics used a similar mechanism tho the pressure is much larger...some can detect it while awake.

I've used both the S9 AutoSet and and a PR S1 BiPAP. I can detect these oscillations on both machines if I hold my breath for more than 10 seconds when I'm awake. On the S9 they seem to kick in by around 6 or 7 seconds. Haven't quite figured out how quick they kick in on the PR S1 yet.

[ozij]

...What is FOT?

Forced Air Oscillation. It is the mechanism used in the S9 to determine if the airway is open (clear)or closed (obstructed). When you drop the time scale low enough (in the detailed graphs), you can see these small increases in air pressure that the machine uses to evaluate the state of the person's airway during an identified apnea. Respironics used a similar mechanism tho the pressure is much larger...some can detect it while awake.

Muse-Inc is right.


http://www.resmed.com/us/assets/documen ... er_eng.pdf

Enhanced AutoSet
with CSA detectionThe S9 AutoSet uses the forced
oscillation technique (FOT) to determine
the state of the airway during an apnea.
When an apnea is detected, small
oscillations are added to the pressure
to measure airway patency. The CSA
algorithm uses the resulting flow and
pressure to measure airway patency
and differentiate central and obstructive
events.

[rested gal]

What is an unresponsive/fixed flow limitation?

I may be guessing wrong, but I'd say he means someone whose breathing is almost always slightly flow limited. That person's normal way of breathing, so to speak. Part and parcel of that person. Slightly flow limited breathing is the way I "normally" breathe. With no ill effects that I've noticed. So far.

CPAP prevents my "fixed" flow limited way of breathing while awake from deteriorating during sleep into worse flow limitations. I wouldn't want to try to find the kind of high pressure it would probably take to "round out" and "normalize" what for me, seems to be a benign, fixed flow limited way of breathing. The fixed flow limited way I breathe is close enough to normal to keep me feeling fine. So far.

[NotMuffy]

At the very least they might try putting a configurable delay before treating hypopneas to avoid treating the awake ones.

They did. Their delay is "indefinite".

I suggested a configurable delay. Is this indefinite delay configurable? Heh.

Oh, you mean you want to configure it.

What exactly would you configure? Event identification? Choice of event to attack? Time delay? (Although I can't imagine how that would work, or even why you want to do that in the first place)?

Keep in mind that we're not talking about all hypopneas, only what ResMed has decided are "benign" hypopneas, because

AutoSet devices respond to obstructive hypopnea events when they are associated with flow limitation or snoring. Hypopneas that are central in origin (related to your central nervous system, not physical obstruction) should not be treated with increased pressure.

http://www.resmed.com/us/service_and_su ... c=patients

and returning to my original point:

Well, "IMHO", I think you have to specifically define hypopnea; identify the type that one has on diagnostic NPSG; and then decide if a ResMed algorithm is the way one chooses to go in the treatment of their SDB.

because it's starting to sound like you want a central (ASV) algorithm instead of a flow limitation algorithm.

[Muse-Inc]

...What is FOT?

Forced Air Oscillation.

Hmmm, wouldn't that be FAO, then, and not FOT?

My bad...Forced Oscillation Technique is what I think the acronym is... tho IMHO "FAO" perfectly describes it as I understand it (that a buck might buy ya a cuppa joe @ the local diner)

[LoQ]

Keep in mind that we're not talking about all hypopneas, only what ResMed has decided are "benign" hypopneas

ResMed assumes that any hypopnea not associated with flow limitation or snoring is central. I have no way of knowing if that is true or not, but whatever, their algorithm doesn't respond to those "benign" hypopneas.

because it's starting to sound like you want a central (ASV) algorithm instead of a flow limitation algorithm.

Now you're talking. Actually, I don't know what I want. But I know that I have flow limitations that are not being identified, and I doubt that auto responds to them. I also know that I have a tendency to develop central events with treatment. I really would like to have bilevel because it feels so swell, but I threw a bunch of centrals when they tried that.

Well, what I want is for a machine to fix my breathing when I sleep so that I feel great during the day. Is that too much to ask? The current Rx from the doctor doesn't work; neither did the first one. They clearly don't know how to fix it for me. So I'm left to wander around, coping with a fair amount of ignorance, hoping that I can stumble upon the solution.