Snoredog wrote:But can we positively conclude that Prilosec was what eliminated the central apnea? There is a huge difference between those. If so you may have come up with a cure for central apnea that Scientists have been struggling with for years.
Actually, it wasn't the few centrals that showed up on Carla's Encore Pro data that I was looking at. There were so few of those that I didn't even consider them to be significant.Snoredog wrote:I am still interested in learning how the acid reflux triggers these central events (that is a huge discovery in my opinion), what receptors is it may be influencing, that would be an interesting read.
What struck me was how bad the Obstructive apneas and hypopneas were on so many of the nights, and then.... suddenly such a good night. With nothing changed in the pressure settings or mode of operation of the machine.
Just reminded me of loonlvr's problem, and what -SWS suggested might be causing it.
Unless a person has had pure, or almost pure Central Apnea turn up on their PSG sleep study, I just don't go looking for "centrals" or start suspecting that obstructives reported on the software data are really centrals that have cleared up on their own before the REMstar's three pressure nudges and enough time has gone by to mark them as NR's (possible centrals.)
Some events could get marked in Encore Pro as "obstructive" when they were actually short centrals. But subscribing to Occam's Razor as I do, I figure most, if not all, of the events that get marked as Obstructive really are....obstructives. Following that perhaps too simple line of thought, then I wonder (because of what -SWS discussed about loonlvr):
"Why so many obstructives with autopap running the pressure up more and more? Why is more pressure not working...not splinting the airway open? Could there be something else going on that has nothing to do with OSA per se....something that's made the tissues in the airway more rigid? Too rigid for Positive Air Pressure to push aside?"
That's all. No discovery about something causing centrals or curing centrals. Centrals didn't enter my mind (no pun intended! LOL!!) at all when looking at Carla's data. I was looking at the stuff marked as obstructives, and accepting those as obstructives.
Nor was I looking at, or trying to analyze, what events were happening at each pressure or what her AHI was at each pressure. Once I saw that good night she had, -SWS's work with loonlvr came to mind. I figured that if acid reflux was an underlying issue for her on the bad nights, it would be like chasing one's tail to try to draw any cause/effect conclusions about how pressure affected AHI on any of her data.
Adjusting pressure either way -- whether more or less pressure -- wasn't going to be useful, I didn't think, until GERD was looked into first. I thought she might need an acid adjustment first, so to speak, before worrying about pressure adjustments which might not even be needed at all. That good night looked pretty darn good.
As a side note, for quite some time I've been wondering.... wonder how many PSG titrations land a GERD sufferer up on a rather high pressure on a night when acid reflux happens to be acting up badly?