CPAPtalk.com

I'd try Nexium. Or, at least OTC Prilosec.

I'd give 'em at least a week to see if either helped the situation.

Snoredog,

What do you mean by train wreck? My ahi is a fair amount lower then before and it must be because i slept on my side (Thank you for that advice) Last night was even a bit better ahi at 6 something. I figure I might give it a few more nights to see what happens now before I change things again. I have been doing a bunch of changing and am afraid I could end up just chasing myself around. I can see where that could happen real easy!


ozij,

I did try 10 cm on straight cpap a while back and my ahi number went higher then on 11cm so going lower then that makes me wonder if it will work. But I am still learning and trying to get it right for sure, and 2 good nights in a row for me is still a good thing. I should post some of the first few weeks charts from when I used the nasal mask, want to see scary

Rested Gal,

I did try the Prilosec for 2 weeks when I was on the straight cpap. It didn't seem to change anything, I did like never having heartburn though. Maybe I need to give it a try again, I tried sleeping on my side these last 2 nights per Snoredogs suggestion and my ahi numbers are better, actually some of the best i have had since starting ( I had a 6 last night!)

Actually I am a side sleeper, but have been on my back since starting this, because I figured I would cause the mask to leak sleeping on my side. I spent all my time on my back during the sleep study too.


Thanks for all of you sticking with me on this, I really appreciate it!!!
Mark

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CPAPopedia Keywords Contained In This Post (Click For Definition): CPAP, AHI

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CPAPopedia Keywords Contained In This Post (Click For Definition): CPAP, AHI

I know you tried 10, and 11.

Some of us don't respond well when the pressure is too high, and it could be that 10 is too high for you most of the time.

With the pressure too high, some of us stop breathing - without having an obstruction. Respironics machines don't know why you stop breathing, they drive the pressure up some more - and some more. Eventually, for some breathing patterns, you may end up in a viscous cycle, with the machine raising its pressure to treat a non existent apnea, and inadvertently causing you to have even more. That was snoredog's point about non-responsive apneas and your pressure going higher and higher and higher. And I agree.

An AHI of 6 sounds much much better - take a break from making changes now, and let's see how it goes for about a week. What is the proportion of H to O your data?

O.

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CPAPopedia Keywords Contained In This Post (Click For Definition): respironics, AHI

MRH wrote:Snoredog,

What do you mean by train wreck? My ahi is a fair amount lower then before and it must be because i slept on my side (Thank you for that advice) Last night was even a bit better ahi at 6 something. I figure I might give it a few more nights to see what happens now before I change things again. I have been doing a bunch of changing and am afraid I could end up just chasing myself around. I can see where that could happen real easy!

Train wreck is based on the amount or frequency of the events seen on your EncorePro reports (lots of activity), it would be nice to see it settle down where fewer events were seen and that's how you know you have achieved ideal cpap therapy is when the number of events seen start dropping off. Increased pressure doesn't always eliminate those events.

Positional sleep aided in dropping your AHI dropping and requiring less pressure can be an indicator that the tongue was playing a major role in the obstruction causing your apnea. If you can stay sleeping on your side that is great, I had to resort to the same thing. I think Rooster has figured that one out also.

Personally, I don't think taking something for GERD is going to lessen the number of events seen, I was on prescription strength PrevAcid for a year and it didn't seem to help reduce mine any, but it got to where insurance (when I had it) didn't want to pay for it any longer, it was $225 per month for that stuff at one time. So now I just buy PepcidComplete at Costco and take one of those before bed when needed.

When you run those reports with the AHI=6, find out what is making up that score (apnea or hypopnea). Stay at it and do some fine tuning, you'll get that AHI down lower. You will still have some nights where things go nutso, but at least you know now what is causing it.

rested gal wrote:

Snoredog wrote:And I ain't buying any stubborn GERD theories here either.]

heheh

Well, I am.

Looks an awful lot like what was happening with loonlvr a long time ago:

Mar 10, 2005 subject: What is the REMStar Auto really doing? Derek, -SWS, Wader, and a very intelligent "Fascinated" Guest discuss loonlvr's posted charts. Extremely interesting 5 page topic.

Mar 18, 2005 subject: What's REMStar Auto Really Doing? - new thread Derek posts more of loonlvr's charts.

Nov 05, 2005 subject: SUCCESS AT LAST-GERD,420E, PRILOSEC AND BENADRYL -SWS's thoughts on loonlvr's massive clusters of events and loonlvr's followup post.

Ahh, the loonlvr story.

I'd like to offer the following discussion points:

1. You can't tell anything about the existence or extent of GERD with PAP Software.

2. The use of benadryl in any capacity to affect sleep these days is darn near negligent. With a half life of about 9 hours (actually, who knows what it is in a given individual), if you take it at bedtime, or later, you could very well be driving to work in a grog.

3. If you do get into an accident, and the Officer says, "Here, we want you to pee into this container", reread #2. On second thought, forget it.

4. Any airway involvement that was severe enough to respond to benadryl would have a myriad of other symptoms, it certainly wouldn't be "silent".

5. The behavior of the 420E (identifying mostly central apneas), if anything, suggests there that isn't obstructive involvement.

SAG

StillAnotherGuest wrote:5. The behavior of the 420E (identifying mostly central apneas), if anything, suggests there that isn't obstructive involvement

How's that again? There are very few central apneas on this "before " report - almost all the ones on the "Apenea/CA" line have an obstructive one on the line above - which means they do have obstructive involvement.

-SWS in his letter to Rested Gal thought it might be the pressure changes, or, among others, vocal cord spasms.

Laura, I thought of another possibility to throw into
the mix after I sent you that email. Namely, vocal chord
spasms. Researchers believe that at least some apneas
and hypopneas may not involve the upper dilator muscles---
but rather are a function of the vocal chords themselves
experiencing spasms. Those who subscribe to this school
of thought attribute these vocal chord spasms to repeated
or ongoing exposure to stomach acid (among other possible
causes or physiological triggers such as stress).

Looking at Mike's (somewhat atypical) "strings" or
clusters of SDB events I can't help but wonder if this
vocal-chord-based etiology doesn't fit his particular
pattern of events:

1) isolated episodes, as are typical of spasms in general.

2) unrelated to sleep stage, unlike typical upper airway
dilator muscle apneas. (Mike can have one-to-two hour
episodes, which outlast several sleep stages.)

3) long strings of mixed events are sometimes shown on
Mike's SL3 reports---meaning sometimes his airway is
open enough to convey cardiac oscillations (as an
inefficient acoustical waveguide) and yet other times
there are no cardiac oscillations present (sometimes
there are even interspersed snores).

I was struck by a strange and interesting thing when comparing these
before and after data:

The range for before is a minimum of 10, max 14, and most of the time, the machine is at 11 (or 10.5). I can't see the range markings for after, but the machine starts out at 12, and never goes below that. Which makes me wonder what the setting was on this "after prilosec" thing, and whether raising the bottom pressure didn't help too. You can see this graph is using a different setting (no. 3) whereas the before graph is using setting no. 4.

RG, did you only get the jpegs, or do you by any chance still have the original data files?

O.

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CPAPopedia Keywords Contained In This Post (Click For Definition): 420E

StillAnotherGuest wrote:Ahh, the loonlvr story.

Yeah, the good old loonlvr story.

StillAnotherGuest wrote:I'd like to offer the following discussion points:

1. You can't tell anything about the existence or extent of GERD with PAP Software.

I agree, the software can't tell us that. But I think when pressure (and more pressure and more pressure) doesn't control events, that might sometimes be a clue to look a little more closely at the possibility of GERD interfering with how a cpap does its job...the job being to push aside soft tissue while we breathe.

StillAnotherGuest wrote:2. The use of benadryl in any capacity to affect sleep these days is darn near negligent. With a half life of about 9 hours (actually, who knows what it is in a given individual), if you take it at bedtime, or later, you could very well be driving to work in a grog.

3. If you do get into an accident, and the Officer says, "Here, we want you to pee into this container", reread #2. On second thought, forget it.

Yes, let's do forget about benadryl for a sec, and concentrate on Prilosec.

StillAnotherGuest wrote:4. Any airway involvement that was severe enough to respond to benadryl would have a myriad of other symptoms, it certainly wouldn't be "silent".

Hey, I'm forgetting about benadryl. Remember?

Back to the Prilosec, which is what I think really did the trick for loonlvr.

When the loonlvr mystery was unfolding, -SWS speculated that IF a person's esophagus was getting nightly acid baths from GERD, it could lead to irritated, inflamed tissue. Swollen tissue. Rigid tissue. Hard tissue that's more difficult for cpap air to push aside.

Treat the acid reflux problem. The swollen tissue returns (one hopes) to normal. CPAP air can do its thing.

Just one small piece in the treatment puzzle, as I see it. Might not be the answer for every pressure run-up situation, but is worth checking into, imho.

StillAnotherGuest wrote:5. The behavior of the 420E (identifying mostly central apneas), if anything, suggests there that isn't obstructive involvement.

Lost me there...?

ozij wrote:RG, did you only get the jpegs, or do you by any chance still have the original data files?

O.

loonlvr sent me the Silverlining .pat file. But that's long gone in a computer crash I had a year or so ago.

-SWS might still have it. I'll ask him.

OK, let's blow this up:



I think 420E here is seeing wide open airway, so all that acute airway closure is extremely unlikely. The events that are proposed (complete bathing of the esophagus and upper airway in gastric acid) disappear completely without a trace in minutes? No residual effect (sore throat, chronic cough)? "Vocal cord closure" without any evidence of residual stridor? There's "Silent GERD" and then there's "Houdini".

rested gal wrote:When the loonlvr mystery was unfolding, -SWS speculated that IF a person's esophagus was getting nightly acid baths from GERD, it could lead to irritated, inflamed tissue. Swollen tissue. Rigid tissue. Hard tissue that's more difficult for cpap air to push aside.

SAG would speculate that if that's what was occurring, loonlvr's sleep efficiency would be about 25%.

rested gal wrote:Yes, let's do forget about benadryl for a sec, and concentrate on Prilosec.

Actually, I think Benadryl made a critical contribution here, just not in the way you think.

rested gal wrote:Back to the Prilosec, which is what I think really did the trick for loonlvr.

I think you can make a good case for that. But I don't think that what you think about what -SWS thinks about loonlvr is what I think you should be thinking. Ya think?

SAG

StillAnotherGuest wrote:

rested gal wrote:Back to the Prilosec, which is what I think really did the trick for loonlvr.

I think you can make a good case for that. But I don't think that what you think about what -SWS thinks about loonlvr is what I think you should be thinking. Ya think?

SAG

I think I still think what I was thinking thanks to -SWS's thinking.

I'm about all thunk-out now.

StillAnotherGuest in his catchy post title wrote:Didn't You Think Peeing in the Cup Was Funny?

Yep...I'm still chuckling.

Ok, back to raking. Hey o., you got any trees out there?

SAG

Yes, we got trees... why?

And why do you think that airway is wide open? I mean, how do you explain those apnea (non c/a) above the apnea non c/a marks?

And, what is it you think we should think?

O.

ozij wrote:Yes, we got trees... why?

Cause if you weren't busy raking, you could help me.

ozij wrote:And why do you think that airway is wide open? I mean, how do you explain those apnea (non c/a) above the apnea non c/a marks?

As I understand the concurrent ticks concept in SL3, it is not a "mixed apnea", rather, it is a "mixed acquisition of cardiac oscillation signals". The only way you could call it a mixed apnea is if SL3 was 100% accurate in identifying central apneas, which it's not. It's only 100% accurate (in a small study) in saying that the centrals it does find are centrals.

But let's say they were mixed (and BTW, real mixed are very rare, I think in this case, the cardiac oscillations were simply lost). But a mixed will start out central, which is my point, at the beginning of these events, the airway is open, so that can't be a "Vocal Cord Closure". Further, in true mixed apneas, it is more likely that there is obstruction throughout the event anyway. Obstruction only becomes apparent when effort begins.

ozij wrote:And, what is it you think we should think?

I think you should think about what the role of the benadryl is here.

SAG

Ah, but our trees don't drop their leaves for winter the way yours do...

StillAnotherGuest wrote:As I understand the concurrent ticks concept in SL3, it is not a "mixed apnea", rather, it is a "mixed acquisition of cardiac oscillation signals". The only way you could call it a mixed apnea is if SL3 was 100% accurate in identifying central apneas, which it's not. It's only 100% accurate (in a small study) in saying that the centrals it does find are centrals

So, a "double tick apnea" is one which is central, but part of the time the machine is loosing the heartbeat and that's why it's adding the top tick?

I don't know enough about benadryl to have any idea what it's role may have been... And I've probabley "out-thunk" myself for today... (it almost bedtime around here...).

O.

StillAnotherGuest wrote:It's only 100% accurate (in a small study) in saying that the centrals it does find are centrals.

I've kept forgetting (for two years now!) to ask about something:

If the 420E is 100% accurate that when it says it saw a central, it really was a central, how come there was this:


click here for larger picture of same 420E graph

Along with this on the PSG report during the same session that night:


Of course I think the PSG was right. So...the 420E was reporting centrals that weren't really happening during that one session. Wonder why? When I got home and pulled the you-know-what sensor tube out and fed it back through, no more "centrals" showed up. A mystery.