420E Run Question ???

[ozij]

I've had both the Initial and Minimum below 7. The result was less aerophagia, but more events. I'm inclined to try this, Snoredog, because it might just help both aerophagia and the eustachian tube clogging I experience. Both are helped by lower pressures. I suspect it will raise the number of events though and to minimize that I'll need to raise the Initial pressure to 8.5 or so. Hmm ..., this is beginning to sound suspiciously like where I was just a couple of weeks ago ...

Bill
I'm having trouble keeping track on your setup / evnets / aerohpahgia /runs combination.

Could you create chart of that?

Thanks,
O.

[ozij]

Peggy,
Please keep on posting on this thread as well - question, thoughts, anything.

Peggy and Bill,
Can you check the relationship between the percentage of your flow limited breaths (not runs) (as reported nn the pressure tab pie chart?) and your aerophagia?

O.

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

[-SWS]

SO what happens to a Hypopnea at 40% reduction in flow as it progresses to 90% reduction in flow? Looks just like a apnea and the response is the same.

I'm fairly certain all hypopnea-related pressure increases occur only after the hyponea has transpired. A hypopnea only lasts as long as inspiration: typically 8 seconds or far less. That's a much shorter duration than the gradual static pressure increase that ensues following a hypopnea (if the 420e even elects to reactively raise pressure in response to that hypopnea).

By the time 90% reduction in flow occurs, then an apnea is detected and finally treated as such.

[Snoredog]

SO what happens to a Hypopnea at 40% reduction in flow as it progresses to 90% reduction in flow? Looks just like a apnea and the response is the same.

I'm fairly certain all hypopnea-related pressure increases occur only after the hyponea has transpired. A hypopnea only lasts as long as inspiration: typically 8 seconds or far less. That's a much shorter duration than the gradual static pressure increase that ensues following a hypopnea (if the 420e even elects to reactively raise pressure in response to that hypopnea).

By the time 90% reduction in flow occurs, then an apnea is detected and finally treated as such.

[Snoredog]

[quote="pjwalman"]SnoreDog, I'd respond except I don't have a clue how to do that to what you wrote. I sense the derision, of course, but I don't see constructive suggestions of what to do differently. I didn't say zero AHI -- I said zero apneas. Three days in a row of no plain-old apneas is a first for me -- pardon me for being excited about it. If I thought I was cured, why in the hell would I subject myself to your insults by asking my stupid questions so that I could better understand? I guess I'm supposed to go running off with my tail between my legs because I've exposed my stupidity in this thread. Sorry! Wasn't the first time, won't be the last, and brow-beating me won't get rid of me. I'll keep reading and trying to figure things out. Though maybe not in this thread as it looks like I stepped into something I should have kept my dainty little shoes out of.

Peggy

[ozij]

If a partially open LES can cause a PB documented flow limitation (or flow limitation run) because of diverting air flow to the stomach (and why not?), how does the following train of thought sound:


Weakened LES causes acid reflux. -->
--> Acid reflux reaches vocal cords causing some inflamation and swelling ->
--> Swollen vocal coards are not as flexible in moving out of the way of your airflow when you breathe. -->
--> Breath flow is not nice and round -->
--> PB registers flow limitation or flow limitation runs - those have nothing to do with sdb, but rather with the state of one's LES? -->

--> Losec while usually recommended to be taken in the morning may do a better job for cpap-ers if taken close to bed time -> reducing flow limitation and flow limitation runs if those are indeed caused by acid bathed vocal cords?


O.

[-SWS]

but doesn't a hypopnea have to last at least 10 seconds to be classified as a hypopnea?

It is my understanding that the machine looks for a 40% reduction in flow lasting 10 seconds or longer to classify a hypopnea and one 90% reduction in flow lasting 10 seconds or longer for an apnea.

Thanks for straightening that out, snoredog!

Don't mind Peggy's "feisty" approach, sir. She's just joining in the spirit of repartee, and I think her perseverance is just great. Speaking of high-spirited and persevering, that sure reminds me of one of my other favorite long-time posters who happens to be in this thread.
.

[-SWS]

If a partially open LES can cause a PB documented flow limitation (or flow limitation run) because of diverting air flow to the stomach (and why not?), how does the following train of thought sound:


Weakened LES causes acid reflux. -->
--> Acid reflux reaches vocal cords causing some inflamation and swelling ->
--> Swollen vocal coards are not as flexible in moving out of the way of your airflow when you breathe. -->
--> Breath flow is not nice and round -->
--> PB registers flow limitation or flow limitation runs - those have nothing to do with sdb, but rather with the state of one's LES? -->

--> Losec while usually recommended to be taken in the morning may do a better job for cpap-ers if taken close to bed time -> reducing flow limitation and flow limitation runs if those are indeed caused by acid bathed vocal cords?


O.

Spot on IMO! That was one of my candidate hypotheses for Bill. Swelling sure can occur. I know this first hand from my own acid-reflux related endoscopy in the distant past.

I also suspect in the midst of nightly GERD flareups that the LES can become swollen and physically distorted---to the point of temporarily having its functional closure impaired even more than usual. If so, this can probably become a veritable vicious cycle in physiology for some of us. As a side note I take my Nexium in the evening and sleep with my head elevated a good thirty degrees. As a result my LES closure seems pretty good now days.

There's another way that vocal chord exposure to acid reflux just just might cause genuine flow limitations in some patients: slight vocal chord closures. But that's merely a pet theory that I'd like to revisit once again in this thread.

However, the points you mentioned above are much more than theory, IMHO. They probably warrant some more consideration in this thread. Bill does think his aerophagia correlates with his excessive FL runs. And aerophagia and acid reflux disease can both entail poor LES closure. So I think it's not at all unreasonable to tie these three together in our discussions.

I was wondering what Peggy's situation happened to be regarding acid reflux, if any. We know she suffers aerophagia. Anyone else with excessive FL runs on the 420e suffer acid reflux or aerophagia?

[ozij]

but doesn't a hypopnea have to last at least 10 seconds to be classified as a hypopnea?

It is my understanding that the machine looks for a 40% reduction in flow lasting 10 seconds or longer to classify a hypopnea and one 90% reduction in flow lasting 10 seconds or longer for an apnea.

Thanks for straightening that out, snoredog!
CPAPopedia Keywords Contained In This Post (Click For Definition): Hypopnea

Whoa there!
If a normal breath is about 5 secs long, the thing identified on the PB as a hyponpnea can't be a one breath occurrence, can it, since during a hypopnea people breathe. Unlike a 10 sec breathing cessation which is an apnea. (And, in case you're wondering, my BPM is about 12-13).

The ten 40% reduction in flow lasting 10 seconds or longer to necessary to classify a hypopnea is therefore at least 2 breaths long under normal conditions....

Now, a hypopnea according to PB definitions is first and foremost an amplitude reduction that takes 10 secs. or longer. Which based on present math would be (don't stone me....) an "amplitude reduction run".


And what, pray is a two breaths long occurrence of flow limitations? That, if I am not much mistaken, is the minimum run needed to classify a "flow limitation run".

Anyone else with excessive FL runs on the 420e suffer acid reflux or aerophagia?

Its acid reflux for me -I take a minute (10mg) amount of generic Losec (doctor's orders). No aerophagia.

However, -SWS when you used the 420E you did not have the kind of flow limitations that drive the PB endlessly up....

O.

[pjwalman]

First my apologies to SnoreDog for being rude. Maybe it is just your way and you don't mean to, but I have had my feelings hurt more than once by how you speak to me, and I fired off immaturely in reaction to that. I'm sorry. I sometimes get lost in the technical explanations and don't see the concrete suggestions held within, and if I've been too dense to pick up your settings suggestions, I apologize. I will go back through and see if I can pick them out. Being tired and frustrated is no excuse for being rude, and again I apologize.

To O., I think I figured out what you are asking, percentage of flow reduction cycle on bad aerophagia days compared to normal. The percentages are all over the place. The first two days with the 420E where I had terrible aerophagia were 48% and 43%, IFL off. The two bad aerophagia days I had recently were 52% and 54%, IFL on. The first day after that when I had my first no apnea day, the flow limited cycle was 57%, IFL on. (I don't know if the IFL on or off matters, just thought I'd cover all bases just in case.) The next day was 54%. Both those days were with hardly any aerophagia at all. I hope that was what you wanted. If not, I'll be happy to go back and check again.

To -SWS, definitely a history of acid reflux for me. I've been a Tums popper for several years. A couple years back, I started noticing the acid coming up at times in the night, tried elevating my head, stopped having wine or other suspicious possible contributors at night. Then I started getting this "bubble" sometimes when I would eat. Very painful, could only be alleviated by basically throwing up the bubble and whatever food was sitting on top of it. I quit drinking pop, and I started taking Prilosec OTC every morning at my doctor's suggestion. And up until starting CPAP, that "bubble" problem was gone. Now, on bad aerophagia days, I am back to having to burp to dislodge that bubble to the point of throwing up. So I think that probably means I have a damaged LES, but my doctor never suggested seeing anybody about it, and I didn't make the connection until I started reading in this forum.

I hope I covered the questions. To all, I apologize if I am a PITA. I work at home, all by myself, and maybe I have lost some of my social skills because of that.

Peggy

[ozij]

Yes, that was what I was asking. The IFL1 on off is relevant in the sense that somehow IFL1=off lowers that percentage for many of us.
I have no idea why - tend to think it might be part of the algorithm problem.
O.

[-SWS]

Anyone else with excessive FL runs on the 420e suffer acid reflux or aerophagia?

Its acid reflux for me -I take a minute (10mg) amount of generic Losec (doctor's orders). No aerophagia.

However, -SWS when you used the 420E you did not have the kind of flow limitations that drive the PB endlessly up....

By the time I started using a 420e I supposedly had my acid reflux well controlled. Aerophagia was not much of a problem for me by then as well. My aerophagia by then occurred only occasionally. And when it did it was extremely mild IIRC.

As soon as I get back on my 420e (post swelling from TN-related oral surgery) I might have to eat a late-night pepperoni pizza and sleep horizontal just to see what my 420e FL runs might do!

Whoa there!
If a normal breath is about 5 secs long, the thing identified on the PB as a hyponpnea can't be a one breath occurrence, can it, since during a hypopnea people breathe. Unlike a 10 sec breathing cessation which is an apnea. (And, in case you're wondering, my BPM is about 12-13).

The ten 40% reduction in flow lasting 10 seconds or longer to necessary to classify a hypopnea is therefore at least 2 breaths long under normal conditions....

Now, a hypopnea according to PB definitions is first and foremost an amplitude reduction that takes 10 secs. or longer. Which based on present math would be (don't stone me....) an "amplitude reduction run".

Yes, I agree. And I think that's what snoredog nicely pointed out as well. A single hypopneic breath is insufficient to score a hypopnea. If it only lasts one breath, then it is not a hypopnea. A hypopnea will be comprised of several hypopneic breaths in all but highly rare instances (if that rarity exists at all).

And what, pray is a two breaths long occurrence of flow limitations? That, if I am not much mistaken, is the minimum run needed to classify a "flow limitation run".

Well, I think the 420e may be scoring FL runs and H events as if they were separate occurrences with separate scoring criteria. I think lesser amplitude reductions (not meeting H amplitude-reduction criteria) are probably what the 420e includes among its FL scoring criteria (clinics never double-score H as FL, but they do differentiate obstructive H from central H---see my next post).

I also suspect that when the amplitude reduction is of large enough magnitude, that it is scored exclusively as a hypopnea on the 420e. But that may not be the case. I would love to hear more thoughts and analysis on this.

Then I started getting this "bubble" sometimes when I would eat. Very painful, could only be alleviated by basically throwing up the bubble and whatever food was sitting on top of it.

I know that "bubble" very well, Peggy. That "bubble" prompted an ER visit by me many years ago. Guess what? It wasn't the air "bubble" that I believed. Rather, it was food repeatedly getting stuck in a very swollen and "beat up" esophagus. It sure felt like some pesky air bubble caught in my throat, though.

And throwing up or expelling the stuck food was the only way that I could ever get rid of that persistent air "bubble" as well. Except the night even that method didn't work on what I also thought was a trapped air "bubble". Lobster tail was hopelessly caught in my esophagus that night. That was when the upper GI specialist in the ER gave me the news that I had a humdinger case of silent acid reflux disease.

Peggy, if you're still getting that "bubble" then you have a serious health problem requiring a visit to an upper GI specialist IMHO. I don't think you're going to ever get your FL runs in order or even achieve restorative sleep until you get your GERD and now damaged esophagus properly taken care of.

I doubt you can fix this problem with optimal patterns of positive air pressure alone.

[ozij]

As soon as I get back on my 420e (post swelling from TN-related oral surgery) I might have to eat a late-night pepperoni pizza and sleep horizontal just to see what my 420e FL runs might do!

The things you will do in the service of science!!! Intrigued as I am, I will not be considered responsible for that experiment!


O.

[pjwalman]

-SWS, thank you for explaining that "bubble". Guess it is time to get my head out of the sand and get to an upper GI doctor then. I see my sleep doctor on June 10th, and hopefully he can refer me to one. Can a sleep doctor/pulmonologist refer to an upper GI specialist? I had already decided to terminate the relationship with my primary care physician because of a few times she's dropped the ball, and the fact that she didn't pick up on the seriousness of the "bubble" pretty much cements the thought that I'd better get a new primary physician soon, especially if the sleep doc can't refer.

Not looking forward to what I'm imagining an upper GI specialist will want to do to investigate -- ugh! -- but neither do I want to end up wasting a perfectly good lobster tail in the ER!

Peggy

P.S. So just out of curiosity, the reason the "bubble" came back when I started CPAP is probably because the pressurized air is beating up the esophagus a little bit more each night? Or it has made the acid return? Or it is just coincidental and the Prilosec OTC just can't do its work anymore efficiently because of the level of damage I've now reached?

Sheesh! Turned 50 and totally fell apart -- obviously there was a good reason I was dreading that milestone.

[-SWS]

Can a sleep doctor/pulmonologist refer to an upper GI specialist? I had already decided to terminate the relationship with my primary care physician because of a few times she's dropped the ball, and the fact that she didn't pick up on the seriousness of the "bubble" pretty much cements the thought that I'd better get a new primary physician soon, especially if the sleep doc can't refer.

I think any doctor can give a referral. Your insurance coverage may require referrals through a primary-care physician, however.

Regarding physicians dropping the ball. Sometimes they do. However, I personally think the field of medicine is just too vast and too complex for any one human mind---even that of a GP.

None of the doctors in the ER room could figure out my "bubble" either. They threw every test known to a man's pocket book at me and were still stumped. Finally they called the upper GI specialist who was on call to see if he had any clue what might be going on. His immediate answer at 3AM was: "I know exactly what's wrong with your patient and I'll be right in for the procedure."

So just out of curiosity, the reason the "bubble" came back when I started CPAP is probably because the pressurized air is beating up the esophagus a little bit more each night? Or it has made the acid return? Or it is just coincidental and the Prilosec OTC just can't do its work anymore efficiently because of the level of damage I've now reached?

I don't know for sure, Peggy. I'm just a layman. But fluid dynamics clearly work in both directions of the LES on an alternating basis throughout the night for people like us. And the LES undoubtedly has variable closure pressure throughout the night, not constant closure pressure. So it's entirely possible to fill the stomach with pressurized CPAP air, kind of like intermittently blowing up a balloon part way.

That gradual filling of the stomach with pressurized air probably happens intermittently with momentary lapses in the LES closure pressure, I would think. And when the pressure just beneath the LES exceeds LES musculature closure pressure, then reverse flow of air and often stomach acid will occur. I would also think typical momentary neuromuscular contraction of the stomach is even sufficient to overcome poor LES closure in a reverse-flow scenario.

Good luck with your upper GI endoscopic exam. It's not at all a big deal. But they need to assess damage and devise an appropriate treatment plan.


P.S. I personally wouldn't be surprised if your central apneas were physiologically-defensive responses to vocal-chord stimuli of repeated acid reflux eruptions.