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Physiology of "treatment emergent" central sleep apnea
#11
RE: Physiology of "treatment emergent" central sleep apnea
EPR is the same as pressure support, both provide ventilation (PS is literaly how ventilators work) and higher ventilation evacuates more CO2 decreasing respiratory drive.

EPR/PS are the main settings that drive treatment emergent centrals but in some cases I think just the pressure effects keeping airway open allow spontaneous ventilation to increase enough to start creating central effects.

Many patients have years/decades of their bodies adapting to worse and worse ventilation and then pretty much overnight PAP reverses the problem and body has to start adapting to better ventilation. Body adapting is a slow process which is why treatment emergent centrals often subside or at least lessen months into treatment.

So in short CO2 drives respiration and better ventilation lowers CO2. PAP pressure alone or combined with pressure support can improve ventilation to the point your body doesn't think it needs to breath as much therefor causing treatment emergent central apnea.
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#12
RE: Physiology of "treatment emergent" central sleep apnea
If it wasn’t for arousals or oxygen depletion would there be any issue with CA’s?
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#13
RE: Physiology of "treatment emergent" central sleep apnea
You mean other than not breathing?
Apnea will always be an issue for just that reason.

We do mitigate it by attempting to minimize it by minimizing desats and arousals but that threshold varies by individual.

Is an AHI of 100 acceptable? No significant desats or arousals, is it acceptable? Not in my book.
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#14
RE: Physiology of "treatment emergent" central sleep apnea
Not breathing for a bit can be somewhat hazardous to your health regardless whether it's an Obstructive or Central.
Dave

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#15
RE: Physiology of "treatment emergent" central sleep apnea
(01-08-2022, 08:30 PM)Gideon Wrote: You mean other than not breathing?
Apnea will always be an issue for just that reason.

No, I mean if your brain measures the carbon dioxide levels and decides you don’t need to breathe yet then what’s the problem with not breathing?

If it wakes you up continually or if you don’t have enough oxygen I can see the problem though.
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#16
RE: Physiology of "treatment emergent" central sleep apnea
I hate posting this in a main thread, but "Textarea cache" can be used as an add-on to Firefox and Chrome browsers to store responses as they are typed. If you accidentally delete or forget to hit post, the text and code is saved. I used to lose complex answers that I can now recover.
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INFORMATION ON APNEA BOARD FORUMS OR ON APNEABOARD.COM SHOULD NOT BE CONSIDERED AS MEDICAL ADVICE. ALWAYS SEEK THE ADVICE OF A PHYSICIAN BEFORE SEEKING TREATMENT FOR MEDICAL CONDITIONS, INCLUDING SLEEP APNEA. INFORMATION POSTED ON THE APNEA BOARD WEB SITE AND FORUMS ARE PERSONAL OPINION ONLY AND NOT NECESSARILY A STATEMENT OF FACT.
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#17
RE: Physiology of "treatment emergent" central sleep apnea
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. It means carbon dioxide builds up in your system, further dampening the breathing response because your body gets used to having higher than normal carbon dioxide. Even if the centrals are SHORT and you're not significantly desaturating, yes, it's bad for you. Hypercapnia long term leads to respiratory acidosis. If you're lucky, like me, your metabolic system and kidneys gradually compensate for that respiratory acidosis by increasing the bicarbonate in your blood to counter the shift in pH - because carbon dioxide makes your blood more acidic. This, when you reach certain thresholds, is called fully compensated respiratory acidosis... or in other words, fully compensated type 2 respiratory failure.

This is what I have now from years of untreated central apnea, even when my oxygen levels are better with supplemental oxygen and CPAP improving my ventilation (while waiting for my Drs to get their butts in gear and give ASV). I had a relatively great night Friday. My AHI was 6, and I spent less than 20 minutes under 90%, with an average of 94%. I'm still in respiratory failure though and will continue to be until I actually breathe properly all night. It's possible to look at my blood gas results from morning to evening and you can see how my pH shifts more towards the upper end of normal (so more alkaline, less acidic) as I manage to get rid of some of that excess CO2 while awake, but as soon as I'm asleep again, even when my oxygen levels look okay and they aren't waking me, I'm STILL building up CO2. And all it takes now is one cold, one bout of flu, one infection to make it impossible for my body to keep compensating for the levels of CO2 in my blood, and I will end up incredibly sick in hospital and praying I don't end up on invasive ventilation.

Tl; Dr - hypercapnia can be a problem even if hypoxia and arousals aren't, and long-term hypercapnia is potentially life-threatening.
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#18
RE: Physiology of "treatment emergent" central sleep apnea
(01-09-2022, 04:10 AM)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. It means carbon dioxide builds up in your system, further dampening the breathing response because your body gets used to having higher than normal carbon dioxide.

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.

I think (please correct me if I'm wrong) what you're referring to is a situation in which a person has been hypercapnic for a long time, because of respiratory insufficiency. In that case, people lose the ability to respond to pCO2 as an indicator of reduced gas exchange. Unsatisfactory though it is, this isn't, I think, a treatment emergent phenomenon -- it's a continued manifestation of the underlying disease.

So: if there is no reason to think that your respiratory responses are defective, and you're having CA's, but are not desaturating, does it even matter? I suppose it matters if they wake you up all the time; and I guess everybody that starts CPAP will have some measure of respiratory derangement right from the start.

Best wishes, DS

PS. You have a better night than me, oxygen-wise; I spent nearly two hours < 90%, even though my AHI was < 1. Oh, well.
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#19
RE: Physiology of "treatment emergent" central sleep apnea
Ha trust me, last night fixed that, I was right back to AHI 18 and 3 hours <90 despite CPAP and O2. It didn't last, I'm afraid. I'm sorry you had such a cruddy night too though.

The point is that treatment-emergent centrals happen BECAUSE you're relatively hypercapnia to start with, in many cases. Because the increased ventilation increases the amount of CO2 that you lose to a "normal" level, that means you stop breathing. As a result, you build up more CO2 in your bloodstream because you're breathing less, and that then pushes your brain's recognition higher.

And that can happen, even if you start off WITHOUT the hypercapnia, if you start off at normal range, if you keep having more than a certain amount of apneas, eventually you're going to start to shift that balance, build up the CO2 in your blood and then you end up with the problems of respiratory acidosis.

My centrals either weren't always this bad, or my body compensated better ten years ago. Hell, even TWO years ago, my overall sats were better than now, even at night. But my body just got to a point where it couldn't keep compensating and my apnea and sats suddenly became dramatically worse. Sure, it's possible that something else could have triggered that change, but there's nothing obvious that it would be, no new or worsening conditions that could cause that, no medication changes, nothing. This is why my doctors believe that my respiratory failure is purely a result of long-term untreated centrals when I started out with normal blood gases.

Now sure, if we're talking just a handful, way less than the 5/hour limit, then that's going to be something that your body probably compensates for just fine, especially if you're otherwise well. But when we start talking about silent central apnea, with no big desats, then yes, that can still potentially trigger problems, either cardiac, or with retaining too much CO2.
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#20
RE: Physiology of "treatment emergent" central sleep apnea
(01-09-2022, 05:27 AM)Ratchick Wrote: The point is that treatment-emergent centrals happen BECAUSE you're relatively hypercapnia to start with, in many cases. 
This is something that could, in theory, be tested. Perhaps it already has been, but I couldn't find anything. You'd "just" have to give CPAP treatment for, say, three months to a group of people who had no respiratory or sleep problems to start with, and see if they developed CAs as well.
Problem is, I can't imagine anybody being crazy enough to volunteer for such a study.
As you can probably guess, I'm interested in this subject because I don't have any CAs, and don't want to do anything that will cause them, if I can help it.
Best wishes, DS
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