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Physiology of "treatment emergent" central sleep apnea
#21
RE: Physiology of "treatment emergent" central sleep apnea
A good number of people won't. It very much seems to have a lot of variables, as to who develops them, how long for, if they improve over time or persist past the first few weeks.

The problem is that CPAP is still an invasive therapy. While it's one with minimal risks, it does carry risks and so obviously, asking people without sleep-disordered breathing to use it may carry some ethical issues. That said, we do it all the time in medicine when we test medications etc on healthy volunteers.

Honestly, if you aren't experiencing runaway centrals now, then you're much less likely to develop TECAs. At least from what I've seen, anyway, those who struggle to find that balance with treatment between managing obstructives and not triggering too many centrals have that issue often from the start of therapy, or after a change in pressure.

Really, if you're okay where you are, and you're not experiencing them, then I wouldn't worry too much about it right now. The ways to control it are basically the opposite of what you do to treat obstructives - so reduce pressure, avoid PS/EPR etc. For some people, just limiting the max pressure or dropping EPR lower or off fixes the issue. For some people, any amount of therapy results in TECAs, and they need to switch to something like ASV to control both their original OSA and the TECA.

Unfortunately, central apnea, in general, seems to be the underdog of apnea. So many people (including me) are told that their central/complex apnea doesn't need to be treated properly to control the central aspects and it's just not true.
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#22
RE: Physiology of "treatment emergent" central sleep apnea
(01-09-2022, 04:55 AM)desaturator Wrote: Sure; but I think what @FaceInTheCrowd is alluding to is a situation of hypocapnia, not hypercapnia.

What @FaceIntheCrowd is asking, I think, is why it matters whether we breath or not, if we are hypocapnic? If I'm not being stimulated to breath because my pCO2 is low, and I'm not actually desaturated, why should I care? I'll breath eventually, when my pCO2 increases to the level that stimulates me to breath.

Yes, that is what I was asking. I had to look up hypocapnia vs hypercapnia. I hadn’t ever realized that true CA’s were the brain not being able, or malfunctioning somewhat, to trigger a breath when the CO2 levels were high. How I missed that is another question, but I was focusing on treatment-emergent functionality as explained on this site exclusively.

‘ratchick’ Wrote:The point about centrals - real centrals, not sleep-wake junk or "just held my breath for 10 seconds after a big inhalation" centrals - is that the brain ISN'T recognising the need to breathe at the right time.

I wasn’t getting this distinction.

I find your additional comments something to consider for sure. ie are treatment-emergent CA’s an indication of something wrong or even possibly a sign of an existing situation that might become worse in the future. It’s a very technical and in-depth subject that I have a hard time understanding.
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#23
RE: Physiology of "treatment emergent" central sleep apnea
Here's one angle on treatment emergent Central Apnea.

First you have my definition of Central Apnea. A cession of breath that includes no effort to breathe and is at least 10 seconds. This CA is from a sensed too low CO2 to initiate a breath signal.

Next up is treatment emergent CA. This means that you have an increased level of CA, with the reason the CO2 level is lower is that PAP therapy has been introduced, which increases the CO2 flushing by more efficient than your normal rate.
Dave

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#24
RE: Physiology of "treatment emergent" central sleep apnea
(01-08-2022, 07:28 PM)FaceInTheCrowd Wrote: If it wasn’t for arousals or oxygen depletion would there be any issue with CA’s?

Yes it affects your nervous system, hormone levels and causes extra stress on the heart and other muscles. These effects aren't caused by the lack of breathing per say but by the recovery response (oh crap gotta breath recovery breaths). In short the nervous system has to send signals (via neurotransmitters, hormones etc) to take these recovery breaths and those signals are what the heart and other muscles use to take the larger, faster recovery breaths. As you can probably imagine it is easier and more efficient for our bodies to continuously take normal breaths compared to repetitive apnea and recovery breathing.

In a lot of these central apnea cases the issue isn't really the central apnea but the inability to regulate and stabilize the breathing afterward. The body holds the apnea too long then it takes too many deep breaths trying to compensate for it blowing out CO2 again causing another apnea over and over again. If the person's response was ideal it would have the apnea and then return to normal breathing immediately instead of getting stuck in this loop.

I don't know the exact mechanisms behind this but being a mechanical engineer I have a pretty good idea that it can be modelled as an underdamped harmonic oscillation and that the oscillation is due to the system controls (nervous system being the controller). To try and put into laymans terms our nervous system over years/decades has learned that if CO2 levels increase to x then our body needs to initiate y recovery breaths to lower CO2 levels to z which should stabilize breathing. Now the y recovery breaths are more effective than they used to be (because of PAP) so CO2 drops below z and initiates another apnea restarting the process. This is called an underdamped oscillation and the length of time it takes to return to normal depends on how good the controls are. Ideally a system is critically damped and it returns to normal without a single oscillation (returns to normal after single apnea/recovery breath). 

In many cases the nervous system will eventually learn that it is more effective and only needs say y-1 recovery breaths to more efficiently damp this system. In some cases it doesn't seem to do so (or not within a time frame we consider acceptable) and we deem that it needs external help to do so (ASV etc). In essence ASV works as a secondary controller modifying our breathing and helping regulate it faster than our on board controller (nervous system). I am rusty on terms but if I remember right this could be considered a driven harmonic oscillation.

Hopefully that makes some sense. If interested in trying to understand the terms etc there are probably some good youtube videos on underdamped harmonic oscillation and controls systems that a guy could find that might help understand it.
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#25
RE: Physiology of "treatment emergent" central sleep apnea
Another trick we have is EERS http://www.apneaboard.com/wiki/index.php...ace_(EERS) to slightly increase CO2 concentrations
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#26
RE: Physiology of "treatment emergent" central sleep apnea
(01-09-2022, 05:09 PM)Geer1 Wrote: Hopefully that makes some sense.

Yes, very much! I agree that the stress created by the brain and nervous system trying to control a vital function that keeps going out of wack would be very destructive to your overall system.

(01-09-2022, 05:09 PM)Geer1 Wrote: If interested in trying to understand the terms etc there are probably some good youtube videos on underdamped harmonic oscillation and controls systems that a guy could find that might help understand it.

Actually, the memories of working on digital systems to emulate PID controllers gives me terrible flashbacks and worse dreams than too many centrals. Wink
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#27
RE: Physiology of "treatment emergent" central sleep apnea
Very interesting discussion here. I particularly appreciate Ratchick's input around hypercapnia and associated risks.

What seems clear is that there are multiple factors that may lead to CA events, and this is encapsulated in Figure 1 of the paper Gideon referenced. The 'ventilatory control instability (high loop gain)' mode is what Geer1 is referencing and pressure support / EPR seems much more likely to produce instability compared to no pressure support. Without pressure support C/APAP is just splinting the airway open and one breathes (more or less) naturally, whereas with pressure support the machine detects the start of a breath and increases pressure to push more air in to your lungs. This will increase your minute ventilation (MV) which may wash out CO2 and lead to hypocapnia. A breathing pattern that waxes and wanes gradually is more likely due to excess PS compared to a pattern that has a deep breath followed by a pausing in breathing, which is more likely due to an arousal of some sort.

IMO, CA is an indication of an issue, but it requires deeper analysis to determine the cause and there's no simple/single answer. Use of ASV may stop the reporting of events but not address the root cause.
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#28
RE: Physiology of "treatment emergent" central sleep apnea
(01-09-2022, 05:39 PM)FaceInTheCrowd Wrote: Yes, very much! I agree that the stress created by the brain and nervous system trying to control a vital function that keeps going out of wack would be very destructive to your overall system.

The big question I have is how much effect this has on symptoms compared to say oxygen levels. A lot of people focus on the oxygen side of apnea and think it is the cause of symptoms but I have a feeling the effort and changes in hormones etc has just as much if not more of an effect. Case in point UARS patients who usually have no oxygen issues.

(01-09-2022, 11:46 PM)kappa Wrote: IMO, CA is an indication of an issue, but it requires deeper analysis to determine the cause and there's no simple/single answer. Use of ASV may stop the reporting of events but not address the root cause.

100%. PAP whether basic CPAP or ASV is a treatment of symptoms not cause. Always best to treat the cause if possible but for most with apnea related issues that isn't easily done.
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#29
RE: Physiology of "treatment emergent" central sleep apnea
(01-10-2022, 12:14 AM)Geer1 Wrote: The big question I have is how much effect this has on symptoms compared to say oxygen levels. A lot of people focus on the oxygen side of apnea and think it is the cause of symptoms but I have a feeling the effort and changes in hormones etc has just as much if not more of an effect. Case in point UARS patients who usually have no oxygen issues.

Yep, another way of saying this is that when the medical profession says the name of our disease in their heads it comes out as "(sleep) APNEA" when it's really "SLEEP (apnea)" The way it was described to me it's that every time I stop breathing my body stages a mini panic attack to jolt me back into breathing, and so I then spend the night marinating in stress hormones. For most of us, it's not the oxygen deprivation that's killing us, it's all the violent things our bodies do all night to wake us up before the oxygen deprivation gets to the point where it would kill us.

I have a theory that this is inherent in medicine itself. A patient who is not breathing means "call a code!" and people come running, and they bring something called a "crash cart" and the doctors who get the patient breathing again are triumphant heroes. Sleep deprivation is entirely different! A resident who has been awake for 60 hours straight is called "bragging rights" and proves how tough and capable and that the resident is a true doctor. In medicine, "not breathing" is very bad, while "not sleeping" is heroic.
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#30
RE: Physiology of "treatment emergent" central sleep apnea
(01-10-2022, 12:51 AM)cathyf Wrote: For most of us, it's not the oxygen deprivation that's killing us, it's all the violent things our bodies do all night to wake us up before the oxygen deprivation gets to the point where it would kill us.

Fair point; but I guess oxygen saturation is easy to measure, while the insidious effect of constant sleep interruption is not. I generally feel relieved if my overnight oxygen saturation has been "good", and worried if it has been "bad", but I have no way of knowing how significant these variations are.

BW, DS
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