BiPAP ST User Needs Help with Centrals/Hypopneas

[BrianinTN]

Per Pugsy's suggestion, I'm creating a new thread with some screenshots in the hopes some of you can offer advice on my centrals and hypopneas.

I've been using a new BiPAP S/T for a week with the settings of: IPAP 20, EPAP 20, Ti 1.0, 16 BPM, rise time 3. This comes on the heels of being prescribed a CPAP last summer with a pressure of 13. The old CPAP data and my latest sleep study showed a lot of central apneas while under CPAP therapy -- hence the BiPAP S/T prescription.

The BiPAP has eliminated the OSA events, but I still have a couple centrals per hour and, perhaps more alarmingly, a lot of hypopnea events. My mean and median AHI for the last week are both around 23.

As was the case with the CPAP, I'm absolutely exhausted the next day after using the unit. I realize this may be the "sleep debt" phenomenon at work, but given that I know my data doesn't look good, I'd like to read what others think.

I was surprised at the high pressures prescribed, given that I'm 31, mostly healthy (other than moderate hypertension), and not extremely overweight. I mention this only in case overtitration is a possible culprit for anything.

Images are posted in chronological order, starting with the summary report of indexes. Thanks in advance for any insights you all can provide.


AGGREGATE DATA



MARCH 12



MARCH 14



MARCH 15



MARCH 17


MARCH 18

[roster]

Bump

[-SWS]

I mention this only in case overtitration is a possible culprit for anything.

It's possible...

Above we see mainly residual central apneas and residual hypopneas. The hypopneas might be predominately obstructive, central, or some mix of the two. One overtitration scenario is that your obstructive component can be overtitrated with an EPAP that is too high. That, in turn, can induce some of the central events.

What was your mix of obstructive events versus central events during the diagnostic portion(s) of your sleep studies (without CPAP)?

[BrianinTN]

I mention this only in case overtitration is a possible culprit for anything.

It's possible...

Above we see mainly residual central apneas and residual hypopneas. The hypopneas might be predominately obstructive, central, or some mix of the two. One overtitration scenario is that your obstructive component can be overtitrated with an EPAP that is too high. That, in turn, can induce some of the central events.

What was your mix of obstructive events versus central events during the diagnostic portion(s) of your sleep studies (without CPAP)?

Right now, I don't know. I'm planning on asking my doctor for copies of those studies when I see him next, but I don't have physical copies. I do know that in the first one, I had 30+ OSA events per hour, and it was only after the second one (titration) that he said the central events were popping up.

FWIW, during my last week on CPAP at a pressure of 13, I had an AHI of 14.6, average CA index of 10.2, average OA index of 1.9, and average HI of 2.5, with 23% of the night in periodic breathing.

I also tried lowering my pressure last night to 17/13 on my BiPAP just to see what would happen. Results image below. I'm not sure why I've got all these gaps in reporting; I didn't take the mask off or discontinue use at any point during the night.

[-SWS]

I do know that in the first one, I had 30+ OSA events per hour, and it was only after the second one (titration) that he said the central events were popping up.

Based on that, it sounds as if your central component was treatment-emergent. When the central component crops up ONLY as a result of CPAP treatment, then CompSAS begins to look likely.

And in that case a Resmed Adapt SV or Respironics auto SV is often the best machine choice. Countering/correcting an over-aggressive titration is still worth investigating as one possible scenario IMO.

[BrianinTN]

That's certainly how the doctor described it to me months ago. He said that for some people, for some unknown reason, centrals begin to start popping up when they're under CPAP therapy. At the time, they sent me on my merry way with CPAP.

Months later, after I had been looking at my own data and realizing "this ain't right," I made a follow-up appointment to see him and showed him the waveforms and reports. They scheduled me for another (third) study, the result of which is the BiPAP S/T I'm using. The letter he sent me described it as being "very effective."

Having read a couple hundred threads on here in the past ten days or so, I agree that an ASV sounds like it would have been better. It's one of the first questions I'm going to ask him when I go back to see him. In the meantime, based on my data, any ideas for how I might tweak the various settings to make this work better for me? It's not just a data thing for me right now; I'm totally exhausted and not terribly dysfunctional during the day right now.

[-SWS]

You might want to review the three links I placed in this older post:
viewtopic.php?f=1&t=55279&st=0&sk=t&sd=a#p517465

[BrianinTN]

Thanks. That's good reading.

So, if y'all were me and you wanted to experiment between now and my doc's appointment next Monday, what would you do? I can think of a few options, but I figured the peanut gallery might help me narrow things down. They include:

* Taking the 17/13 I got last night (which seemed to have about the same number of OA, CA, and H events as the 20/16) and adjusting it further. If this, to what? Something like 17/8 maybe? 13/8, since the original CPAP at 13 dealt with the obstructive events too?
* Whip out the old trust Auto CPAP, put it on "Auto," and see what it spits out to get a new reference frame

Slightly complicating things is that I've been getting some reporting gaps, probably caused by leaks (see viewtopic/t61814/Gaps-in-Encore-Reports.html). I'll probably put the chin strap on over the F&P 432 mask tonight, rather than under, and see if that helps. I'm also headed to the DME to swap out a FitLife mask for something else that will be better for me as a natural side sleeper (probably a Quattro unless someone screams at me DON'T DO THAT on here in the next hour).

[-SWS]

Regarding patient-population statistics, 10 cm EPAP or lower might be a good pressure to explore. A 10 cm EPAP just might be enough to address most of your obstructive component without inducing too many central events.

I'd give the doctor a call and ask about comparing 14cm/10cm, 15cm/10cm, and 16cm/10cm nights. The idea is to get most of your obstructive component addressed by EPAP. Then use the higher IPAP to address both obstructive and central hyopneas. Your backup rate, in tandem with an optimal IPAP/EPAP combination, will ideally address those comparatively few residual central apneas...

[-SWS]

reporting gaps, probably caused by leaks (see viewtopic/t61814/Gaps-in-Encore-Reports.html).

My own theoretical view is that leaks can conceivably cause loop-gain havoc with a CompSAS patient's disordered respiratory drive:
viewtopic.php?f=1&t=55279&st=0&sk=t&sd= ... 30#p518839

I suspect leaks just might introduce breathing perturbations which can result is respiratory-controller oscillations for CompSAS patients. So I'd work hard to get the leak line just as flat as possible if I had CompSAS. I'm not a health professional of any kind. So take my theoretical view of leaks-as-perturbations vs CompSAS with a grain of salt.

[BrianinTN]

I like the doc okay, but I don't think I'm going to hear anything between now and my appointment next Monday -- so for tonight I'll try with the 16/10 as you suggested and see how it goes.

My leak line was actually rather flat with the F&P 432 *without* the chin strap, despite it waking me up with leaks all the time. Maybe I'm just getting more leaks with the chin strap, but they are of the type that they aren't perturbing me? Either way, I've got a new Quattro which I guess I'll try tonight as well.

Fingers crossed. Thanks for the tips!

[-SWS]

Bear in mind that central apneas caused by CPAP are "iatrogenic" versus central apneas that are primary or "non-iatrogenic". An EPAP too high can machine-induce iatrogenic central apneas. But a PS value that is too wide can ALSO machine-induce iatrogenic central apneas. PS ("Pressure Support") is the difference between IPAP and EPAP. Here we can see that JIMCHI introduced a significantly greater iatrogenic effect on his respiratory drive when going from PS of 5 to 6:
viewtopic.php?f=1&t=60687&p=573999&hili ... ic#p573999

If that were a spontaneous BiLevel instead of an ST model, many/most of his additional "missing breaths" would have likely finalized as untreated and machine-scored central apneas.

Anyway, the 14cm/10cm end of that range is probably the more conservative end to start experimenting. I think it's important to get your doctor's okay before running any of those experimental pressures. Good luck.

[Mr Bill]

SW, I met a sleep doctor tonight and tried to explain the understanding I had evolved (after reading some here and elsewhere) with respect to central apneas (CA) as a stand alone phenomenon versus CA's induced by therapy. I asked him if people were on some sort of bell curve as to how well they delt with the CO2 signal in their lungs, heart, and brain. I was wondering if some people just have CA and it gets worse under therapy or if some people are fine but then develop CA under therapy because the CO2 they would normally accumulate in their lungs or around their face is purged more quickly by therapy and thus they develop CA because now the CO2 is not at a level that makes their system kick in the breathing. (I am terrible at writing out things). He was interested that during the initial phase of my sleep study most of my apneas were central. But they also got worse with therapy pressure during the titration phase of the sleep study.

He expressed that his own theory was that many CA patients would probably be fine at sea level but that at altitude people tend to have more CA problems. That makes it sound like a partial pressure with respect to dissolved gasses sort of problem. If it were only that, why would this tendency run in families? Is there some gene that codes for sensitivity of the respiratory system to CO2 buildup?

I felt bad annoying the man with my particulars. I felt like a young grad student annoying the great professor with my thesis data. But I have to ask the question, because I want to know.

[-SWS]

He expressed that his own theory was that many CA patients would probably be fine at sea level but that at altitude people tend to have more CA problems. That makes it sound like a partial pressure with respect to dissolved gasses sort of problem.

Here's one relevant excerpt:

The AHI decreased with descent to lower elevations, with the reduction being primarily secondary to fewer hypopneas and central apneas. This finding suggests that the increased oxygen content in the air at lower elevation is the more important of the three atmospheric factors affecting respiratory events with elevation change, within the altitude range studied.

http://chestjournal.chestpubs.org/conte ... /1744.full

If it were only that, why would this tendency run in families? Is there some gene that codes for sensitivity of the respiratory system to CO2 buildup?

Perhaps the chemoreceptor sensitivity itself is what's inheritable. Perhaps it's even polygenic, meaning several genes and interrelated traits are involved.

But I have to ask the question, because I want to know.

[Mr Bill]

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.