APNEA -v- HYPOPNEA

kurtr wrote: So far I feel much better at fixed CPAP, so SWS your theory that a pressure induced central may make you feel worse than an obstructive one may be true even if just a theory.

Maybe it's not the central components after all. Maybe it's the inordinate amount of cortical arousals associated with CSDB that accounts for the overly symptomatic manifestations. Those surprisingly vast numbers of sleep arousals associated with CSDB have to be absolutely debilitating in and of themselves. If you're a marginal CSDB patient, decreasing your AHI from 5 to 1 may account for a significant clinical difference in how you feel based on a disporportionate reduction in sleep arousals. Yet for ordinary SDB patients that difference between an AHI of 1 and 5 is considered clinically insignificant.

At this point I think I've absolutely beat the CSDB topic to death. What I want to do now is simply let Chuck lead the discussion and analysis of his sleep mystery, and let every one else factor their opinions in. And, of course, let Kurt, Tom, Snoredog, et al lead their own personal sleep analyses as they see fit. Yup. -SWS has run out of bullets regarding this topic... He's shot his entire wad of cash.... He's sold his last cart of CSDB bananas for the day... You get the drift!

I'll definitely be reading this topic! It's much too interesting not to!

-SWS wrote:

GoofyUT wrote: It then reports the pressure that it operated at or LESS for 95% of the time for the session.

Just wanted to highlight this as the correct answer. Thanks for that much needed clarification.

Mmm...How can that be? Manual doesn't say it. Maybe you guys missed the part where it says it came straight out of the "Resmed Clinical Manual" but for reference it can be found on page 37 paragraph 2 entitled Pressure.

If that is correct, please explain to me how the pressure you spend 95% of the "session time" at becomes the correct pressure that addresses the majority of your SDB events?

Isn't that what your wanting to know? Any way you look at it, that pressure has to be the pressure that addresses the majority of your events (95th centile), not the avg. time spent at a pressure. What is the majority? 95th centile according to the manual.

And here's a new twist for your guys on the central hypopnea theory as it relates to Chuck's machine's A10 algorithm, again from the same Clinical manual (any typos of course would be mine because I cannot cut-n-paste it directly):

A hypopnea is defined as a 50 to 75% drop in ventilation. A hypopnea is scored if the 8-second moving average ventilation drops below 50%, but not below 25%, of the recent average for 15 consecutive
seconds. In order to avoid falsely responding to central hypopneas, the AutoSet algorithm does not respond to hypopneas but rather to the associated snore or flow limitation.

So if the machine knows about these central hypopnea triggers and does NOT even respond to ANY hypopnea to begin with (central or obstructive), then how can it be increasing as seen. My guess is it is NOT hypopnea causing the increase.

Now check out what happens if you trip the snore trigger:

Figure 3: Inspiratory flow/time curve affected by snore
The AutoSet algorithm assigns an arbitrary value between 0.0 and 2.0 to the average amplitude of the snoring detected for the past 5 breaths. A value of 1.0 is equivalent to approximately 75dBA measured 10cm from the nares. Treatment pressure increases by up to 0.2cm H2O per second (proportional to the severity of the snore) for snore above 0.2 snore units. When snore is less than 0.2 snore units, therapy is reduced towards the minimum pressure with a 20-minute time constant.

Personal experience: If you snore with that machine it will increase pressure and it won't stop until they stop or it blows the top of your head off whichever occurs first. If the mask you are using is making enough noise to confuse the machine you are snoring it can only get worse.

Thanks, snoredog, for the direct quotes from the ResMed manual. I can see now that even if I had had the manual, I'd still have had to ask the question.

Snoredog wrote:If that is correct, please explain to me how the pressure you spend 95% of the "session time" at becomes the correct pressure that addresses the majority of your SDB events?

I don't think GoofyUT said that was the pressure we spend 95% of our time at. I think he said 95% of the time is spent at that pressure or LESS pressures:

-SWS wrote:

GoofyUT wrote: It then reports the pressure that it operated at or LESS for 95% of the time for the session.

Just wanted to highlight this as the correct answer. Thanks for that much needed clarification.

Resmed wrote:"In order to avoid falsely responding to central hypopneas, the AutoSet algorithm does not respond to hypopneas but rather to the associated snore or flow limitation."

I was aware of the above Resmed statement regarding it's own A10 algorithm.

That statement says four very important things in my view: 1) Resmed acknowledges that central hypopneas occur in general, 2) unfortunately the machine has absolutely no way of differentiating central hyponeas from obstructive hypopneas, 3) it is potentially counter-productive to increase pressure in direct response to central hypopneas, and therefore 4) the machine will not trigger on any hypopneas whatsoever, to be on the safe side; rather the machine will rely on preempting obstructive hypopneas by triggering on snore and flow limitation.

As a side note the A10 algorithm will trigger on apneas, but only up to 10 cm. Again it will rely on preemptively triggering only on snore and flow limitations above 10 cm.

A10 Triggers below 10 cm: snore, flow limitation, apneas
A10 Triggers above 10 cm: snore, flow limitation

Apnea is the only "direct response" trigger while snore and flow limitation are both "preemptive" triggers in the A10 algorithm. All because of valid concern regarding the induction of central hypopneas and central apneas. That central hypopneas exist is not theoretical. That their etiology can be attributed to a mild hypocapnic CSDB effect is highly theoretical. Either way central versus obstructive hypopnea differentiation is extremely difficult in the PSG sleep study and absolutely impossible with the measurement and scoring technology inside any APAP algorithm or model. Not just Resmed.

And it is very interesting (and wise in my opinion) that Resmed will cautiously steer away from triggering on hypopneas at even pressures below 10 cm or 8 cm. However, you'll note that hypopneic pressure induction concern is irrespective of the old 8 cm and 10 cm school of thought. Rather it goes toward recognition of a gradual gradation of pressure induced central effects.

Thanks for the Resmed quote, Snoredog!

SWS
You sure make things understandable for the technically challenged, like me!
Thanks for taking the time!

APAP/SWIFT

AHI=5.4;AI=0.3;HI=5.1;Pressure (95%)=10.2

I had a GREAT and restful night's sleep after a poor one the night before that left me feeling achey after going to the gym and then later as I walked around the Salt Lake Jazz festival last evening.

INTERESTING huh?

Chuck

So, Chuck, are you saying that jazz soothed the savage beast or just bored you so badly you slept soundly?

Glad you're back to feeling well and energetic again. You should know by now, one bad night does not a relapse make. We all have those "wonderful" nights where we ask ourselves, "What the ****happened???"

Hope you enjoyed the Jazz Fest.

GoofyUT wrote:APAP/SWIFT

AHI=5.4;AI=0.3;HI=5.1;Pressure (95%)=10.2

I had a GREAT and restful night's sleep after a poor one the night before that left me feeling achey after going to the gym and then later as I walked around the Salt Lake Jazz festival last evening.

INTERESTING huh?

LOL! Okay, Chuck. Since you injected a little sarcasm, I'll inject my interpretation a bit more. Here you reintroduced Swift to APAP and received an elevated HI.

Now... reintroduce Swift to 8 cm fixed pressure and watch your HI go down yet again. Good-mask/bad-mask theory does not at all account for that. The presumed to be bad mask is still in the equation is it not? Good-mask, bad-mask theory does not at all account for your increased HI when you elevate your floor pressure, either But combinational kinetics of CO2 depletion accounts for all the above HI occurences.

Is this not a clear pattern to anyone else but me?

Morning Lori!

The jazz was good and bad. Patty Austin sang Ella with the Salt Lake JAzz Orchestra, which was WONDERFUL!! Then, an a-cappela group called the Groove Society from Denver sang and made my ears bleed!!! Average White Band is performing tonight, and I can't wait!

Here's the interesting thing though: I went back to the Swift last evening. I did it mostly for experimental reasons, but also to let my nose heal from the Activa which, while very comfortable, had eroded a sore on the bridge of my nose (but that I didn't feeL). As you may remember, I was getting GREAT numbers with the Activa.

Well, I slept very well last night with the Swift, woke up feeling refreshed, but my AHI had shot up over 5 for the first time in 12 days, mostly from hypops which also shot up over 5. Just from switching to the Swift. GOOD sleep, BAD numbers. Go figure.

Chuck

-SWS wrote:

GoofyUT wrote:APAP/SWIFT

AHI=5.4;AI=0.3;HI=5.1;Pressure (95%)=10.2

I had a GREAT and restful night's sleep after a poor one the night before that left me feeling achey after going to the gym and then later as I walked around the Salt Lake Jazz festival last evening.

INTERESTING huh?

LOL! Okay, Chuck. Since you injected a little sarcasm, I'll inject my interpretation a bit more. Here you reintroduced Swift to APAP and received an elevated HI.

Now... reintroduce Swift to 8 cm fixed pressure and watch your HI go down yet again. Good-mask/bad-mask theory does not at all account for that. The presumed to be bad mask is still in the equation is it not? Good-mask, bad-mask theory does not at all account for your increased HI when you elevate your floor pressure, either But combinational kinetics of CO2 depletion accounts for all the above HI occurences.

Is this not a clear pattern to anyone else but me?

Chuck, the Swift will deplete your CO2 more quickly than the Activa. CO2 depletion is what all your HI trends have been about from the very get go: depleting your CO2 too quickly results in an elevated HI. Perform that Swift with 8 cm fixed pressure experiment again and your HI will go back down despite the suspected bad mask still being in the equation. It goes down because your hypocapnic CO2 trigger doesn't necessarily react to any one therapeutic factor in particular, it simply reacts to a hastened rate of CO2 depletion, despite what happened to have (single handedly or combinationally) caused that crucial rate of CO2 depletion.

Here are all the factors in your experiments that have affected the rate of CO2 depletion in your trials:

1) increased floor pressure (accelerates CO2 depletion)
2) APAP's varying pressures (accelerates CO2 depletion)
2) lowered to 8 cm fixed pressure (decelerates CO2 depletion)
3) Swift-to-Activa (decelerates your CO2 depletion)

For you, my new marginally-afflicted CSDB friend, the transient sum total of all kinetics regarding CO2 depletion either cross your hypocapnic trigger threshold or they do not. And you can effect that hypocapnic threshold crossing with a variety of factors that influence CO2 depletion. Not just the mask.

We really must analyze the big picture here. .

Steve-

I absolutely agree with you regarding your analysis of the basic etiology of my marginal-CSDB destabilizations, and I admire and respect your amazing analytical skills!!! I strongly agree that my case appears to be CO2-hypocapnic trigger mediated (I use the term mediated in the medical sense to mean the mechanism that appears to be responsible for a phenomenon.)

What I remain confused about though, is the role of APAP pressure variations. I held that constant in switching masks, and loe and behold, the Swift with its greater C02 venting increased hypops independentof APAP related pressure variations which remained constant between the Swift and the Activa.

So, this says to me that CO2 venting is the critical factor here, not the "irritability" that may be brougtht about by APAP pressure variations.

I intend to go back to a CPAP trial at 8cmH2O after a week of collecting more observations to confirm last night's data. And, I'll bet you dollars to donuts that you're right! When I return to CPAP at 8cm with the Swift, my numbers will go back down. But, I believe that this is caused by a reduction in CO2 venting associated with the lower pressure because of factors that have to do with fluid dynamics, that as I've said, I know NOTHING about.

Now, here's the really fascinating question regarding the clincial implications of all of this: Does this indicate that the Swift is better suited for low pressure CPAP usage for those with the same hypocapnic trigger brittleness and resultant marginal CSDB response, whereas the Activa is better suited for those with higher pressures or those choosing to use APAP???? I still don't buy in to the notion that APAP is contrad-indicated given my success with an APAP/Activa trial. It just might be though, that APAP/Swift is contra-indicated.

What do you think????

Chuck

This "Swift vs other mask" CO2 depletion rate fact is quite interesting! Sure makes sense considering the differences in pressure and mask air chamber sizes! Very interesting !
SWS
Could there also be a "Swift vs other mask" pressure need equation? Does the Swift always inflate a person's general pressure need as compared to other masks?
Let me explain....I have used Swift as my main interface for over a year, switching at times for a 2-5 day stint on the Aura, Activa or UMFF. (HI's have always been my major issue as AI is only .1 or 0.) I feel fine during the day when I use the Swift and because my AHI's have always been below 3, I've been satisfied. I recently bought the Hybrid, seeking to get away from a chin strap and mouthtape. Now, granted I've only used the Hybrid 2 nights, but the drop in pressure and rise in leak rate surprises me! 7.0 and 7.1 pressure as opposed to 10.0 being my average pressure need with Swift. Leaks with Hybrid .35 and .34 as opposed to .05 and less with Swift.

As this new Hybrid users have been reporting over the last several days, I've read the following;
birdiebaby says,
The vent flow on these masks is much higher than the ResMed masks are.
Maybe my Spirit is interpreting this higher air discharge as a leak?
oldgearhead says,
I believe the Hybrid holds the record for CO2 flush holes. At almost 50 L/Min at 10 cm/H2O
Again, it would seem that the Hybrid certainly discharges more volume of air than any other mask does?
maskjkie says,
...the upward force that the chin strap applies, the upper airway actually narrows and the resistance to flow increases. So a higher pressure is needed...
Perhaps this is the sole reason for my lower pressure need ?
Am I thinking right on these issues?

GoofyUT wrote: What I remain confused about though, is the role of APAP pressure variations. I held that constant in switching masks, and loe and behold, the Swift with its greater C02 venting increased hypops independentof APAP related pressure variations which remained constant between the Swift and the Activa.

So, this says to me that CO2 venting is the critical factor here, not the "irritability" that may be brougtht about by APAP pressure variations.

This is such a highly complex, multifactorial problem, Chuck. Not only are the CO2 kinetics themselves highly complex and multifactorial, but so is the homeostatic and highly transient role of the hypocapnic CO2 respiratory trigger itself.

Go back and take a peek at the Harvard medical study. You will see that very specifically there is a short-term homeostatic maladjustment of the CO2 trigger itself regarding even slight xPAP-imposed pressure fluctuations. Here are characterizing factors involved relative to APAP's degrading influence on the CSDB respiratory drive:

1) Homeostatic short-term maladjustment of the hypocapnic trigger itself,
2) Thus a dysregulated highly fluctuating hypocapnic trigger at that,
3) xPAP pressure variations very specifically being the machine-driven feedback forces at play influencing the fluctuating homeostatic maladjustments that account for this highly twitchy CO2-based respiratory trigger, and
4) Each APAP imposed pressure increase in and of itself also having a subtly negative yet contributive influence on the sum total of CO2 depletion kinetics

CO2 depletion kinetics are to blame for when that hypocapnic threshold is crossed (regardless of whether mask, machine, hose contributed to those CO2 kinetics). However xPAP imposed pressure fluctuations in and of themselves are to blame for the fluctuating and maladjusted homeostatic trigger itself (with a prerequisite that the CO2 trigger be inherently unstable and thus so inclined to pressure-fluctuation maladjustment in the first place). So in the case of APAP, pressure increases and pressure decreases both contribute toward short-term homeostatic maladjustment. However, only APAP's pressure increases (not decreases) happen to adversely contribute to CO2 depletion kinetics in an admittedly very subtle way.

When contraindicating APAP for the CSDB respiratory drive, APAP's CO2 depletion kinetics would only be secondary, to APAP's adverse impact on short-term homeostatic adjustment of the CO2 trigger itself. Extremely complex CO2 kinetic physics are occuring in the mask, and extremely complex biophysics/biochemistry are occuring with regard to the homeostatic CO2 respiratory trigger itself. A very twitchy biofeedback loop, indeed. Throw away the old CO2 kinetics and CO2 biophysics/biochemical considerations and out with the new. That's why the math in the TAS monster thread didn't add up for the CSDB case. These consideration can only be termed "micro transient" in my mind.

The two highly multifactorial forces at play here: 1) CO2 depletion kinetics, and 2) homeostatic maladjustment. All multifactorial contributers will yield a hypocapnic threshold itself and whether that threshold has been crossed toward increasing gradations of respiratory destabilization. Pressure and CO2 will influence the homeostatic setting of that hypocapnic threshold. CO2's accumulative transient total (based on kinetics) will influence whether that hypocapnic threshold is crossed.


This problem is so bogged down with multifactorial contributors that it's no wonder science hadn't discovered it until recently. To make the discovery of CSDB even more elusive, everything about CSDB has been hiding in the details of measurement all along. As far as I am concerned, Chuck, you are the first confirmed case of marginal CSDB. Congratulations.

Inacpapfog, all masks facilitate CO2 depletion at what would be an acceptable rate for most of us. The Swift will facilitate CO2 depletion at a rate that is acceptable for the vast majority of patients as well.

Regarding which masks to try. At this point it is a matter of trial and error for all of us. And yes, I believe that mask and chin straps that cause the mandible to recede can most definitely increase the occurence and even severity of obstructive events in patients who are so inclined.

Thanks for your kind words!