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Physiology of "treatment emergent" central sleep apnea - desaturator - 01-07-2022
Hi folks
I'm aware that the notion of "treatment emergent" central apnea comes up on this forum all the time, but my searching hasn't really turned up an explanation that I understand. If this is already explained elsewhere, please accept my apologies.
That some people develop or increase central apneas after starting CPAP treatment seems to be well-documented. What doesn't seem to be well-documented is why. What particularly intrigues me is the notion that expiratory pressure relief can contribute to the development of central apneas.
Does anybody have a detailed explanation for this in terms of respiratory physiology? Is there actual research evidence linking EPR and central apneas? I have to say that I couldn't find anything in the medical literature.
Best wishes, DS
RE: Physiology of "treatment emergent" central sleep apnea - Gideon - 01-07-2022
How is this
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7725531/
RE: Physiology of "treatment emergent" central sleep apnea - quiescence at last - 01-07-2022
Yay. Gideon. Plus, op is conflating EPR worse for partially controlling real central apnea with the causes of treatment emergent CA counts.
Hope the article helps.
QAL
RE: Physiology of "treatment emergent" central sleep apnea - quiescence at last - 01-07-2022
(01-07-2022, 05:49 PM)quiescence at last Wrote: Yay. Gideon. Plus, op is conflating EPR worse for partially controlling real central apnea with the causes of treatment emergent CA counts.
Hope the article helps.
QAL
When I read the article, I also did not see the things I had hoped would be much clearer. For one, the article seemed to lump central apnea that exists and continues to plague those with OSA under pressurized airway treatment, with the artifact CA counts that appear during early pressurized airway treatment which gradually fades to small or no CA counts.
I think of "REAL" central apnea is the retardation or complete signal disconnect between the signal (PaCO2 has risen above a threshold) and the receptor in the central nervous system that triggers a breath (energizing abdominal muscles to draw a vacuum in the lungs for inhale.) All other reactions that seem to stop breathing for the "proscribed" and arbitrary 10 seconds without obstructions is only called CA because of a convention instead of a physiological event.
Hope that helps a bit.
Combined with the article, we can see that the parts of central apnea that are physiological are being studied and tentatively explained.
You, who have CA counts because there is an unobstructed pause meeting those conventions, but is not caused by the too high PaCO2, should find means of discounting them. The only concern you should consider is if you find you are desaturating too far. Oximeters are useful for that.
QAL
RE: Physiology of "treatment emergent" central sleep apnea - desaturator - 01-08-2022
Thank you for posting the link. I typed a long, over-complicate response earlier, but it's disappeared. I don't know whether there's some sort of gremlin, or I just didn't click the right button.
In shorter terms:
To conclude that EPR is related to TECSA, either we have to understand the pathophysiology of TECSA reasonably well, or there needs to be well-conducted studies that show the link. The linked article proposes some tentative ideas about the pathophysiology of TECSA, but none are conclusive, and none (so far as I can see) allow for a link with EPR. And, although I've looked high and low for studies that tested the link between EPR and TECSA, I was not able to find any.
Some I'm curious about how this link came to be so widely accepted, when there's so little evidence for it.
Best wishes, DS
RE: Physiology of "treatment emergent" central sleep apnea - Gideon - 01-08-2022
Now look at what pressure support does for your breathing and how that compares to your breathing without it.
And don't look for EPR because that is officially only a comfort feature
RE: Physiology of "treatment emergent" central sleep apnea - OpalRose - 01-08-2022
(01-08-2022, 09:59 AM)desaturator Wrote: Thank you for posting the link. I typed a long, over-complicate response earlier, but it's disappeared. I don't know whether there's some sort of gremlin, or I just didn't click the right button.
I can guarantee there's no gremlin.
After previewing a post, you must hit "Post Reply", or it all disappears.
RE: Physiology of "treatment emergent" central sleep apnea - quiescence at last - 01-08-2022
most of my best work is randomly deleted, often in a time-out situation. i try to remember to copy periodically my typing to notepad (or some other text program). that, i often forget too when I am really blithering about something.
QAL
RE: Physiology of "treatment emergent" central sleep apnea - Crimson Nape - 01-08-2022
Try using "Save as Draft", then go back and edit the file until you're ready to publish it. You will find the saved drafts in, UserCP/Miscellaneous/Save Drafts.
RE: Physiology of "treatment emergent" central sleep apnea - Dormeo - 01-08-2022
Try googling central apnea bilevel. There are some articles attesting to an association, though no really confident accounts of the underlying mechanism.
I have had the idea it works this way: with pressure support, we get a boost as we inhale, which supports our breathing in more oxygen. This results in an decrease in the proportion of CO2, which in turn reduces the drive to breathe. But this may be way too simplistic.
I will say it accords with a related phenomenon: brief arousal breathing -- with deeper breaths than usual -- followed by a CA. Again, we are in effect washing out CO2, it seems.
Why this happens in some people and not others probably has a lot to do with their apneic thresholds, the muscles in their chests, and other individualized factors.