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Higher pressures = much higher hypopnea/events. Why?
#1
Higher pressures = much higher hypopnea/events. Why?
Background: I have long and complex case and I've yet to find any relief, despite using an ASV, having 100% compliance, and history of very low AHI. However, for someone like me, AHI or similiar are absolutely meaningless metrics, as I have near constant arousals of a variety of flavors, movement and respiratory related but also idiopathic (as confirmed by every sleep study I've ever done). 

So with my symptoms never lessening, I have continued to try and find solutions (including much outside of sleep). But I can say confidently after a lot, that interrupted sleep is clearly the primary cause of my EDS and hypersomnia. 

So after my latest ASV titration, my sleep doc prescribed higher (MUCH higher) EPAP pressures: 13-15. Though it did not eliminate the arousals that test night, I (sort of) had less when pressures stayed high. Before this I was formerly on min 4-6 EPAP open to anything higher, and throughout the night I'd average 5-7 EPAP. So according to the machine (two of them), I did NOT need higher pressures (even though I experience subclinical events anyhow). Aerophagia and leaks have proved difficult to overcome as I adjust to these higher pressures, but I'm finally starting to manage.

Here is my confusion: Why would my monitored events (mostly hypopnea, and tons of UF2) multiply like 5x with higher pressures? Why would I have more apparent airway restriction? Is this something that's understood at all? And how is it that I can have virtually no monitored events on open/low pressures, without proper treatment? It would be an easy call to say "because I don't need these higher pressures" except that 1-There are days when I have felt better on them, even with some mask leaks, and 2-Disrupted sleep is monitored on lower pressures, and I consistently feel awful on them, thus why I am desperately tweaking and trying and searching for solutions. 

Thanks in advance for any thoughts or insights, I would appreciate it.
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#2
RE: Higher pressures = much higher hypopnea/events. Why?
lostie42,

I think you've got a question that is best answered by a professional. There are a lot of things that we as patients are not knowledgeable enough to really speculate on. But if your machine reported AHI is running significantly higher since the pressure change, that warrants a call to the doctor who prescribed the pressure change. Have him/her take a stab at explaining it.

My two cents as a reasonably well read patient:

Are the hypopneas actually obstructive or are they perhaps central in nature? There are times when too much pressure can create breathing instability and it is possible under certain circumstances that the breathing instability manifests itself as an increase in central events---both central apneas and central hypopneas. But you're already using an ASV, and you'd think that the ASV algorithm would kick in if the events are actually central hypopneas.
Questions about SleepyHead?  
See my Guide to SleepyHead
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#3
RE: Higher pressures = much higher hypopnea/events. Why?
agree with ask doctor, your results are the opposite that would be expected. goes against standard titration, where you increase epap for OA/H events.
What are the PS numbers?
is 13 your min epap and 15 your max?

It would help if you put up a sleepyhead chart, link at the top of the page
mask fit http://www.apneaboard.com/wiki/index.php...ask_Primer
For auto-cpap, from machine data or software. You can set the min pressure 1 or 2cm below 95%. Or clinicians commonly use the maximum or 95% pressure for fixed pressure CPAP, this can also be used for min pressure.
https://aasm.org/resources/practiceparam...rating.pdf
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#4
RE: Higher pressures = much higher hypopnea/events. Why?
I was told by my doc that if the pressure was too high, you would, essentially, over-ventilate, and not have enough carbon dioxide to trigger normal breathing. Elevated levels of CO2 trigger breathing (as well as decreased levels of O2).
                                                                                                                          
Note: I'm an epidemiologist, not a medical provider. 
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