BiPAP ST User Needs Help with Centrals/Hypopneas

Mr Bill wrote:That is a very pertinent reference. Since I am at 4700 feet, that is an ~2 psi difference from that at sea level which is equivalent to about 55 inches or 139cm of water. Most therapy does not go over 30cm H2O. But induced centrals happen even over that range. On the other hand...
http://www.madsci.com/manu/gas_gas.htm

Chemical Control of Respiration

Special chemical receptors near the aorta and carotid arteries, called the aortic bodies and carotid bodies, are sensitive to an increase in carbon dioxide or acid concentration, or to a decrease in the pressure of oxygen (PaO2). When these receptors sense acidity or low oxygen, they stimulate the brain respiratory center to increase the speed and depth of breathing.
The area of the brain stem that controls respiration is directly responsive to increases in acid concentration in the cerebrospinal fluid, producing increased respirations. When acid buildup occurs, such as in diabetic ketoacidosis, strong stimulation of respiration results. The deep rapid breathing mixes alveolar air with increased amounts of low-CO2 air, leading to a decrease in the carbon dioxide in the blood as it passes by the alveolus. The reduction in CO2 raises the pH back towards normal.
When there is a rise in serum CO2, such as with the increased metabolism of exercise, ventilation is stimulated until the CO2 returns to normal levels.
Lack of oxygen also acts as a respiratory stimulant, although a weak one. In healthy individuals at normal altitudes, oxygen levels play no role in regulation of ventilation. As arterial oxygen pressure falls, there is not much stimulation of respiration until the level is below 60 mm Hg. Patients suffering from severe chronic bronchitis and emphysema may come to rely on the “hypoxic drive” to stimulate respirations, as they become habituated to high levels of carbon dioxide.

Emphasis added by me.
http://encyclopedia.thefreedictionary.c ... +breathing

Hyperventilating causes a drop in CO2 below normal levels, lowering blood and oxygen supply to vital organs due to CO2-induced vasoconstriction and suppressed Bohr effect. Voluntary hyperventilation can cause tissue oxygen levels to go to dangerously low levels leading to, for example, fainting due to brain hypoxia.

http://encyclopedia.thefreedictionary.com/Bohr+effect
I did not realize the Bohr Effect means that CO2 is needed in the blood for oxygen to be properly released to tissue! So, removing too much carbon dioxide from the lungs might induce lowering respiratory drive. So, if we over ventilate somebody, its like we are inducing hyperventilation, the body decides a pause in breathing is needed because CO2 levels in the blood are too low.

Maybe its that adding ~25 cm H2O pressure when you are at an elevation with 139 cm H2O less total pressure, is relatively more hyperventilating than doing so at sea level. Ach! I need to go to bed and sleep.

Thank you for the interesting response. It really got me thinking and I'll be thinking about it all day tomorrow in the environmental lab where I work.

For years, APAP manufacturers have been working with/around 10cm as a statistical barrier beyond which central apneas become progressively machine-induced in the SDB patient population.

Mr. Bill, although you're sleeping at a moderate 4700 ft, you might find white papers describing the pathophysiology and epidemiology of High Altitude Periodic Breathing (HAPB) interesting:
http://scholar.google.com/scholar?hl=en ... =&as_vis=0

And here's general discussion of HAPB on the web at-large:
http://www.google.com/search?hl=en&q=%2 ... a=N&tab=sw

Mr Bill wrote: Maybe its that adding ~25 cm H2O pressure when you are at an elevation with 139 cm H2O less total pressure, is relatively more hyperventilating than doing so at sea level.

I also happen to suspect a "threshold confluence" of: 1) moderate altitude, and 2) PAP machine pressure might contribute to CompSAS in some cases.

And here's a great altitude-comparison graph previously posted by one of our sleep professionals, StillAnotherGuest/Muffy/NotMuffy/deltadave:


viewtopic.php?f=1&t=41034&p=360468&hilit=hapb#p360468

So far this experiment hasn't of modifying pressures has raised more questions for me than answers. Check out the images for the previous two nights of experimentation. The first is from Sunday night, where I lowered my pressures from the prescribed 20/16 down to 17/13; the second is last night, where I used the conservative 14/10. Both have been as bad as my previously prescribed pressures as far as the hypopneas go; the very low pressure seemed to allow a lot more centrals to pop up (CA 7.4). All of these pressures have dealt just fine with obstructive events.


MARCH 21 (actually, night of March 20)



MARCH 22


So, um, given the understandable IANAD preface, where do I go from here? It seems that the hypopneas are popping up at a pretty broad range of pressures -- so perhaps the problem is somewhere else? For reference, on my CPAP at a pressure of 13, it wasn't recording very many hypopneas at all, so that suggests to me that the perhaps the pressure itself isn't the culprit.

So, turning to BiPAP S/T specific settings then: since you should put the BPM setting 2-3 below the patient's resting BPM, it's calibrated correctly at 16. Any chance the Ti (inspiration time, right?) of 1.0 is too small? I don't see many other settings to poke and prod on the BiPAP, aside from turning off "T" mode, which definitely wouldn't help with my centrals.

Thank you all again.

BrianinTN wrote: All of these pressures have dealt just fine with obstructive events.

We can't know whether those hypopneas are central, obstructive, or both types. The bad news is that CompSAS can be a challenge for a skilled technician to properly titrate in a lab with full PSG instrumentation. Unfortunately there aren't many useful conclusions amateurs on a message board can or should draw given your data----other than your complex SDB is a challenge to treat.

At this point your doctor might want to order another PSG titration with your current BiPAP machine---possibly adding supplemental O2 on an experimental basis. Or your doctor might prefer moving on to an ASV trial. If your doctor has not yet trained with or embraced ASV, then you can expect him/her to either continue working with BiPAP S/T or to say "that's the best we can do". In the latter case, you should get another doctor willing to explore additional treatment avenues.


Here's a graph previously posted by JohnBFisher comparing CompSAS treatment efficacy of ASV vs other treatment methods:

http://chestjournal.chestpubs.org/conte ... /1839.full

Given your BiPAP S/T results, guess which one of those treatment modalities I would want to try next?

BrianinTN wrote: I'm totally worried about the insurance side of this. I've already had a CPAP and a BiPAP S/T paid for by them, at 100%, in the past year. I know the DME won't take the BiPAP back, either. So while it seems like I should have been put on an ASV from the very beginning, and that fact that I haven't is by no fault of my own, I worry about someone at Blue Cross deciding they're tired of taking care of me as a patient.

Don't worry about that. If ASV works while the other treatment modalities do not work, then insurance should cover it. Here are some useful documents I just searched:

http://www.resmed.com/us/documents/1013 ... et_rad.pdf
http://bipapautosvadvanced.respironics. ... lHints.pdf
http://www.resmed.com/us/documents/LMN_ ... riodic.pdf


In case you haven't seen these links yet:
http://bipapautosvadvanced.respironics.com/
http://www.resmed.com/us/products/vpap_ ... c=patients

Thanks. Yep, I'd been reading up on the ASV and had even stumbled across that Respironics factsheet you linked about requirements for reimbursement. My DME seems to stock the Respironics equipment rather than ResMed, so I think that's what I'd end up getting. I showed the DME my data on Monday, after we got past the obligatory, "How do you have access to [Encore]?", she too all but agreed that it looks like I'm headed down the ASV route.

What puzzles me is that when I had seen my doc last, he mentioned both the BiPAP and ASV as options, but in his letter to me, he said the BiPAP was "extremely effective" in treating me. Surely these hypopneas showed up in my sleep study? It's perplexing.

I guess I'll go back up in pressure tonight. Why can't anything ever be simple?

BrianinTN wrote: What puzzles me is that when I had seen my doc last, he mentioned both the BiPAP and ASV as options, but in his letter to me, he said the BiPAP was "extremely effective" in treating me.

Well, that's certainly a qualitative rather than quantitative assessment of how well your doctor treated you with that BiPAP S/T. And not to sound disrespectful to any doctor, but who wants or trusts anyone's professional self-assessment---let alone a qualitative assessment--- when it comes to OUR own health?

BrianinTN wrote: Surely these hypopneas showed up in my sleep study? It's perplexing.

They might have titrated your BiPAP S/T to a point where the hypopneas did not show up for an hour or two---perhaps near the end of your sleep study. So an "extremely effective" treatment conclusion could have been a premature and incorrect assessment given CompSAS long-term variability. Also bear in mind that PSG hypopnea scoring is generally more accurate than home PAP machine scoring. So a healthy dose of skepticism about the BiPAP S/T's reported HI is warranted as well. But given the way you feel during the day, you should pursue your symptoms and even machine-scored AHI with your doctor...

Or line up a second-opinion doctor. And if you do, be sure to ask all kinds of questions about how many CompSAS patients they successfully treat and what their CompSAS treatment methods happen to be. Also ask them how they define successful CompSAS treatment, if you decide to go that second-opinion route.

Sleep centers in TN:
http://www.sleepcenters.org/Centers.aspx?state=TN

BrianinTN wrote: Surely these hypopneas showed up in my sleep study? It's perplexing.

first-person yokel in the peanut gallery wrote: Also bear in mind that PSG hypopnea scoring is generally more accurate than home PAP machine scoring. So a healthy dose of skepticism about the BiPAP S/T's reported HI is warranted as well.

The machine-scored hypopneas might actually be repeated sleep/wake artifacts. And if they are, then treating the more primary issue---sleep maintenance---makes more sense than treating the hypopneic breathing patterns.

Ventilation is Unstable During Drowsiness Before Sleep Onset
-and-
viewtopic.php?f=1&t=20405&p=178465&#p178465

One surprising but potentially-effective experiment your sleep doc might offer is a pharmaceutical sleep aid. In that CompSAS scenario, stabilizing disordered sleep can sometimes stabilize resulting disordered ventilation. In any event, good luck forging ahead with your sleep doctor(s).

I had seen you link that article in another thread, I believe. Unfortunately, I already take Ambien or Lunesta, depending upon the night in question. Usually Ambien of late, since it's hard to *get* to sleep with the new setup.

Looking at my data, the hypopneas that the machine is identifying are somewhat inconsistent; sometimes they're more clustered than others. So your theory about my getting an hour or two of seemingly "good" sleep certainly seems plausible. They kicked me out of that lab at 6:30 a.m., so there wasn't a ton of observation time. (And frankly, the whole study is pretty uncomfortable for me given that my natural inclination is to go to sleep around 3-4 a.m. my time, but they insist in having me in bed by 11 p.m.)

The doc I have came highly recommended from my PCP, and while I've tried searching online to find other patient reviews of him, I haven't had any luck. So far he has seemed both nice and knowledgeable, and while he's in pulmonology group at one of the top hospitals here, he's also the only guy in his group explicitly listed as a specialist in sleep disorders. I'll definitely report back on how my appointment next week goes though.

-SWS wrote:We can't know whether those hypopneas are central, obstructive, or both types.

Sorry to back things up 3 steps, but I was thinking about this in the shower. (Hopefully no one from the "Perverts Only" thread is reading this right now. ) Don't we? A sample day of CPAP data from the end of January is below. If regular CPAP eliminated most OAs and left very few hypopneas with a bunch of CAs, doesn't that suggest that the hypopneas I'm seeing now on the BiPAP S/T are central rather than obstructive in nature?



(FWIW, this was a pretty "bad day." I had other days on CPAP that were much better, e.g., an AHI of 3.1 and an AHI of 6.9. Data would fly all over the place. I know we expect AHI to vary, and as you pointed out, maybe the machines aren't doing a very good job of properly flagging and identifying events.)

BrianinTN wrote: If regular CPAP eliminated most OAs and left very few hypopneass with a bunch of CAs, doesn't that suggest that the hypopneas I'm seeing now on the BiPAP S/T are central rather than obstructive in nature?

Great question... But unfortunately there's STILL not enough information to deductively reason central hypopneas vs obstructive hypopneas:

1) your obstructive and central components can each be highly variable, and
2) obstructive apneas that are under-addressed with insufficient pressure can easily convert to residual obstructive hypopneas

That latter point is why it takes more CPAP pressure during NPSG titration to clear obstructive hypopneas than apneas. It's also why BiLevel titration protocol calls for obstructive apneas to be cleared with lower EPAP, but for hypopneas to be addressed with higher IPAP...

I put my machine back on the prescribed pressure (20/16) last night, although I raised the Ti from 1.0 to 1.3. That did make it more comfortable to go to sleep, and my numbers were fairly middle of the road (AHI of 17.. The trend I've spotted of of hypopneas appearing more common later in my sleep cycle continued.

Anyway, I'm exhausted as usual today. Is it the case that higher pressures simply kick your butt more so that I perhaps *should* be more tired (e.g., from lots of nighttime respiratory work)? I definitely wasn't as tired the two nights when I was experimenting with lowering the pressure.

P.S. Just heard back from my doc's nurse. Apparently the Ti setting isn't part of the prescription at all. Is there any reason to, say, increase the Ti a little more tonight? Lower the rise time at the same time (it's at the max of "3" now)? I told her I'm experimenting between now and my appointment on Monday so we have plenty of data to discuss. I imagine I'm nibbling at the edges of irrelevant stuff here, but hey, I'm happy to continue to be the guinea pig here. I'm not doing anything else at night.

On a lark, I tried 20/13 last night. Results below. Thoughts? I see the doc tomorrow, so I may just leave it like this for another night.

the leak line on that one was much better... FWIW... I'd keep that setting and let it settle in for awhile, it might get a little better over the next few days.

Well, you originally had mainly residual hypopneas. Standard BiLevel titration protocol calls for IPAP increases to address hypopneas. And three things seemed to happen as a result:

1) Your respiratory drive now fails to produce a spontaneous breath two-thirds of the time because of that IPAP increase, yet
2) The machine's backup rate now initiates all those missing (and formerly spontaneous) breaths, and
3) The higher machine Pressure Support (PS) now mechanically ventilates a greater portion of your Work of Breathing (WOB) to ameliorate those hypopneas

How do you subjectively FEEL after: a) lowering your AHI, b) eliminating most of your spontaneous respiratory drive, while c) mechanically eliminating much of your own Work of Breathing (WOB) ? Also, please let us know whether your sleep doctor views that as a desirable improvement or unnecessary risk. Good luck with this.

I was pretty open with his nurse earlier this past week about what I was doing, and she didn't voice any concerns. My DME had already seen the data and called her (the nurse), so I think everyone's clear that the prescribed therapy hasn't been working. I'll pick his brain of course tomorrow, but based on what I've been reading on these forums and elsewhere online, I haven't found anything suggesting there's a medical risk to playing with pressures -- other than getting sub-optimal therapy, which I was obviously getting anyway.

Subjectively: I still don't feel great. I still woke up a fair amount during the night and didn't make it a full night with the mask (slept another couple hours after flipping the machine off). Maybe I simply still need time to acclimate. And maybe this is just a "good" night of data on something where the variance has seemed quite high. I guess with more data, we'll know soon enough.

BrianinTN wrote:I haven't found anything suggesting there's a medical risk to playing with pressures -- other than getting sub-optimal therapy, which I was obviously getting anyway.

I would ask the doctor if there are any known long-term risks to mechanically eliminating two-thirds of your spontaneous respiratory drive.

If a different treatment modality reduced your AHI WITHOUT disabling your spontaneous respiratory drive that way, then the alternative modality would clearly be preferable. BiLevel with supplemental O2 would be one alternate treatment modality for comparison. ASV would be yet another. Either of those treatment modalities might not impose such a severe iatrogenic effect on your spontaneous drive...

Then again, your autonomic breathing might eventually acclimate to that 7cm PS value, allowing your spontaneous drive to better tolerate those settings. Again good luck.