CPAPtalk.com

Not cured. Going to do a treadmill stress test Monday, but that is just a once per 5 years test and I always do fine on it.

My conclusion is that it is either smoking or too many red blood cells - long name for the latter whose treatment is draining blood periodically. I don't particularly want to do that so I have not gone to a hematoligist about it.

Everyone vacated this thread all of a sudden. Guess they gave up on me too.

Pat

CROWPAT wrote:Everyone vacated this thread all of a sudden.

This thread needs more participation from Pat of all people. I was under the impression that we were waiting for a disposition from Muffy's suggested sleep/food diary. What became of that?


Toward the pressure experiments, here was my most recent comment:

-SWS wrote:

CROWPAT wrote:What do you think of me trying 10/10/20/Auto to try the 10 pressure but still let the machine go on up if it needs to?

Well, if banned gave the go-ahead then it must be perfectly safe.

Candidly, that's probably what I would have tried next in your situation as well, CROWPAT. Then, pending those results, I might have continued to drop everything by 1cmH2O per experimental increment. But I really wouldn't try it without a pulse oximeter to keep an eye on basic cardiopulmonary data---heart rate and SpO2 throughout each night.

Did you per chance catch the data significance of what Muffy and rested gal were getting at? If unknown or "silent" GERD were causing your sleep and breathing disturbances then:

1) your quality of sleep and sleep-related breathing might deteriorate as a result,
2) your spontaneous breathing rate might drop below your 99.8% following-day comfort threshold, and yet
3) you might not be able to fix that problem with pressure changes alone---despite observing a subtle deterioration pattern in your BiPAP autoSV data set

That last statement probably holds true as a generalization: certain data patterns or phenomena may never be addressable with pressure settings alone. Bear that in mind as you attempt to safely experiment with your doctor's permission. But please reconsider getting a recording oximeter...

But there are a variety of gradual pressure experiments that might be cautiously performed toward finding out if this observable symptom can be improved with optimized settings:

Crowpat wrote:The one thing I have noticed on the BiPapAutoSV is that when my "Breathing on my Own" number is 99.9% I feel better even if some of the other numbers are not as good as usual.

And my understanding is that you acquired a pulse oximeter to keep an eye on heart rate and SpO2 during your doctor-approved ASV pressure experiments.


Both Muffy's avenue of gastric investigation and the attempt to further optimize ASV pressure relate to the above observable symptom. We don't know yet if that key observable symptom can be improved with either gastric/diet alterations or ASV optimization---or something altogether different such as hematology. But essentially, the Pat thread needs Pat of all people, and I think that's why Banned asked.

Guess I overreacted when the thread seemed to die.
Pulse oximeter works fine. Posted data from one night at the usual link.
Seeing doctor 12 Jan and will bring oximetry data. Will ask him about silent GERD too.
Sleep diary sent to Muffy, but I messed up and did not include evening meal data. Could not see/feel any relationship between what I ate and how my sleep data was for the night or how I felt the next day.
I remain at 12/14-22 pending you suggesting a specific change to those settings.
Thank you, SWS, for returning to this effort.

CROWPAT wrote:Could not see/feel any relationship between what I ate and how my sleep data was for the night or how I felt the next day.

Probably a poor call.

Banned

CROWPAT wrote:Guess I overreacted when the thread seemed to die.
Pulse oximeter works fine. Posted data from one night at the usual link.
Seeing doctor 12 Jan and will bring oximetry data. Will ask him about silent GERD too.
Sleep diary sent to Muffy, but I messed up and did not include evening meal data. Could not see/feel any relationship between what I ate and how my sleep data was for the night or how I felt the next day.
I remain at 12/14-22 pending you suggesting a specific change to those settings.
Thank you, SWS, for returning to this effort.

I never actually left, Pat. I thought we were waiting for you to return here with information pending side-investigations. It's good Banned prompted.

Let me take the next day or two to re-familiarize myself with all the little details of your thread and sleep data, Pat.

In the meantime, I personally didn't think the silent GERD possibility was such a bad hypothesis. However, I don't think you can rely on a food diary or plan, or even lifestyle assessment, as a definitive means for either ruling silent GERD in or out. Years ago we had a poster named loonlvr, who episodically presented AHI spikes. He experienced those erratic AHI spikes while using either his RemStar Auto or his 420e APAP. The 420e APAP showed that many of those erratic events were central apneas and mixed apneas.

The long story short was that acid reflux medicine seemed to do a pretty good job at suppressing those previously uncontrollable and unpredictable AHI spikes. Our assumption at the time was that acid reflux disease was somehow to blame for those former wild and erratic AHI spikes. They essentially disappeared with OTC Prilosec acid reflux medication.

Regardless, something never felt quite right, to me, about that hard correlation between loonlvr's Prilosec treatment and resulting low AHI. For one thing, I never got to see if that pattern was sustained over the months and years. In retrospect I suspect that loonlvr might have suffered from CSDB/CompSAS. The 420e's central-apnea specificity of measurement is virtually 100%---meaning that when it measures a central apnea, that it really is a central apnea. My hunch is that acid reflux eruptions might have served as neural-stimuli for loonlvr's CSDB/CompSAS tendencies----exacerbating what might have otherwise been a much milder CSDB/CompSAS tendency.

I hope loonlvr comes back to the message boards some day to tell us what his long-term SDB outcome happened to be. Anyway, I believe acid reflux disease can sometimes exacerbate complex or central SDB problems as well as exacerbating much more common obstructive SDB.

CROWPAT wrote:... Everyone vacated this thread all of a sudden. Guess they gave up on me too. ...

Okay. I confess. I actually took vacation that did not include a computer or cell phone. Is that allowed? Don't tell anyone!

I've been monitoring. But I certainly don't have any bright ideas. I'm here to learn as much as anything. But we all definitely care and want to see you doing better than you are. So, hang in there!

-SWS wrote:The long story short was that acid reflux medicine seemed to do a pretty good job at suppressing those previously uncontrollable and unpredictable AHI spikes. Our assumption at the time was that acid reflux disease was somehow to blame for those former wild and erratic AHI spikes. They essentially disappeared with OTC Prilosec acid reflux medication.

Don't forget the Benadryl.

-SWS wrote:Regardless, something never felt quite right, to me, about that hard correlation between loonlvr's Prilosec treatment and resulting low AHI. For one thing, I never got to see if that pattern was sustained over the months and years. In retrospect I suspect that loonlvr might have suffered from CSDB/CompSAS. The 420e's central-apnea specificity of measurement is virtually 100%---meaning that when it measures a central apnea, that it really is a central apnea. My hunch is that acid reflux eruptions might have served as neural-stimuli for loonlvr's CSDB/CompSAS tendencies----exacerbating what might have otherwise been a much milder CSDB/CompSAS tendency.

Right. This point was presented in one of my favorite threads:

viewtopic.php?f=1&t=25751&st=0&sk=t&sd= ... r&start=30

in which a half dozen topics that continue to this day were touched on in Robin Williams fashion, including:

The appearance of cardiac pulsations in a waveform that could be misinterpreted as "expiratory breathing instability" and proposing a treatment plan for something that isn't there;

The role of vocal cord closure. Did you ever find yourself eating or drinking something, or even just sitting there quietly, and you go to take a breath and it seems like you're stuck in between breaths, can't inhale or exhale? And the sudden feeling of panic that sets in, like "OMIGOD I'M GONNA DIE RIGHT NOW!!!"? That's a vocal cord closure. On a GK420E download, it appears as the sudden end to a Session as the patient is clubbing their wife, husband, dog, goldfish whatever with the CPAP machine, trying desperately trying to communicate "CALL 911!!" but they forgot how to sign a "9";

Even if you subscribe to the "I'm so relaxed that my closed airway central apnea is able to transmit COs", one certainly wouldn't be relaxed during VCD;

Cardiac oscillations appearing in everything, including obstructive apneas (I forgot to go back and look for those in the RG study);

Delay in waveform transmission:



The COs in the flow channel appear to have a definite pattern in the abdominal channel, yet appear almost random in the flow channel, which is the one we really need. That one needs to be put under the microscope. I mean, since this is measuring flow generated by an xPAP machine, could the machine by affected by COs and "stuttering"?;

Since waveform transmission can be delayed depending on the technology, can those measurements of "intrinsic PEEP" be misinterpreted (hence the importance of the synchronization of signals during "biocals"):

Use Benadryl at your own risk. It can give you "The Grog" for hours;

And finally, how Gabby playing the didgeridoo should be considered in every discussion:



Damn.

brb.

Muffy

Muffy wrote:This point was presented in one of my favorite threads:

Nicely done. In retrospect, loonlvr's mix of sleep events seems to have an overall pattern similar to the CSDB/CompSAS charts that have since become available. More below why I personally won't rule out a VCD theory just yet. But suffice to say that I currently STRONGLY favor the theory that loonlvr was a CSDB/CompSAS case. I still strongly favor the idea that GERD was likely loonlvr's exacerbating/precipitating SDB factor.

However, if loonlvr really was a CSDB/CompSAS patient... and if GERD really did trigger those SDB flareups... then a slight analytical paradigm shift might be in order: Is CPAP one of several possible stimuli capable of inducing that CSDB/CompSAS pattern of disruption. If other stimuli can induce that pattern of disruption, then is CPAP absolutely prerequisite in all cases? Or are there presently unknown cases in which neural stimuli other than CPAP are sufficient for that CSDB/CompSAS pattern of central disruption. Doubtful IMO, but potentially significant for CompSAS/CSDB research if cases can be found...

Muffy wrote:The role of vocal cord closure. Did you ever find yourself eating or drinking something, or even just sitting there quietly, and you go to take a breath and it seems like you're stuck in between breaths, can't inhale or exhale? And the sudden feeling of panic that sets in, like "OMIGOD I'M GONNA DIE RIGHT NOW!!!"? That's a vocal cord closure. On a GK420E download, it appears as the sudden end to a Session as the patient is clubbing their wife, husband, dog, goldfish whatever with the CPAP machine, trying desperately trying to communicate "CALL 911!!" but they forgot how to sign a "9";

Even if you subscribe to the "I'm so relaxed that my closed airway central apnea is able to transmit COs", one certainly wouldn't be relaxed during VCD;

You just described a laryngospasm---which can be an extreme symptom of VCD. Kind of like a sneeze: it's not the same as a cold. But a sneeze can be a symptom of a cold. And yet you can sneeze without having a cold. Anyway, the person who has a laryngospasm or two without the other symptoms is probably not a person with VCD. And while laryngospasms are a symptom of VCD, most VCD larynx presentations are not those extreme spasms you just described. Many VCD patients never quite experience those extreme laryngospasms you just described. That's what makes VCD so difficult to differentiate from asthma.

VCD patients can supposedly have vocal chord apneas as well. I suppose the question is whether VCD patients might also reflexively withhold inspiratory effort with the neural stimuli of acid eruptions presented at the vocal chords. If so, are those flow-signal occurrences presented to the 420e as central apneas with cardiac oscillations? How about when the vocal chords are open, but central effort is still reflexively withheld in response to that same neural stimuli presented at the vocal chords?

While GERD is well-documented as a VCD trigger in medical literature, I don't think VCD's GERD-based sleep response is choreographed in the annals of medical literature just yet. So plenty of room to wonder IMHO---albeit with no definitive medical answer.

Muffy wrote:Cardiac oscillations appearing in everything...

Yes... even in that luxurious consumer case of COS acquisition and signal processing by Volvo. But the context (or specific implementation) of signal acquisition & mathematical/algorithmic processing are REALLY what matters with respect to Rapoport's high specificity. The Volvo example is irrelevant because of such high sensitivity. And the Volvo method is not at all how the 420e acquires or signal-processes its cardiac oscillation signal (COS) sitting in the flow stream.

Magnification of biomedical COS would be a case in which extremely heightened sensitivity actually detracts from near-perfect CA specificity. Sufficiently heightened COS sensitivity would detract from CA specificity simply because COS would then be detectable under all breathing circumstances---and hence the COS would no longer be that same highly-specific CA signal. Similarly, incidental COS sitting in various proprietary PSG instrumentation channels can entail varying degrees of signal acquisition and processing relevance. High-powered imaging by geosynchronous satellites are similarly "capability irrelevant" to the reliable and unreliable image signals acquired and processed by a hand-held camcorder, for instance.

CROWPAT

goodluck

DSM

-SWS wrote:Is CPAP one of several possible stimuli capable of inducing that CSDB/CompSAS pattern of disruption. If other stimuli can induce that pattern of disruption, then is CPAP absolutely prerequisite in all cases? Or are there presently unknown cases in which neural stimuli other than CPAP are sufficient for that CSDB/CompSAS pattern of central disruption.

CPAP creates the CompSAS scenario by changing the plant gain:



Then, any ventilatory disturbance (including, for example, an arousal-producing PLM) starts The Loop.

-SWS wrote:You just described a laryngospasm---which can be an extreme symptom of VCD. Kind of like a sneeze: it's not the same as a cold. But a sneeze can be a symptom of a cold. And yet you can sneeze without having a cold. Anyway, the person who has a laryngospasm or two without the other symptoms is probably not a person with VCD. And while laryngospasms are a symptom of VCD, most VCD larynx presentations are not those extreme spasms you just described. Many VCD patients never quite experience those extreme laryngospasms you just described. That's what makes VCD so difficult to differentiate from asthma.

"IMHO", loonlvr should have been buying Lotto tickets instead of "drug wingin'" (part of the "Yahoo Sisterhood of x-Wingin'"), cause they would have stood a much greater likelihood of hittin' Powerball than for the syllogistic chain of events that you describe happening.

The event I described would more appropriately be termed "reflex glottic closure". But in order for your theory to work, both the VCD and GERD (or really, a reflux event) would have to be silent. As suggested in the last part of your comment ("That's what makes VCD so difficult to differentiate from asthma"), reflux significant enough to generate the issues you propose would certainly have more symptomology, including going to wake instead of arousal during the night, chronic cough, sore throat, etc.

In my view, the more likely scenario would be that the Benadryl generated sleep stability which in turn created breathing stability.

However, the long acting properties of Benadryl make it a drug that should be used with great caution. (Hey, I can't stop anybody from using it. It's OTC, and besides, I ain't the Drug Police.)

Muffy wrote:Then, any ventilatory disturbance starts The Loop.

OK, fine, I suppose a reflex glottic closure could do it, too.

Muffy

-SWS wrote:You just described a laryngospasm---which can be an extreme symptom of VCD.

I did have the opportunity to observe a laryngospastic event that required emergency tracheostomy once.

It was very exciting!

Muffy

Muffy wrote:It was very exciting!

Although maybe I should qualify that from a "point of view" point of view.

That wasn't the exact terminology the patient used.

Muffy

-SWS wrote:Magnification of biomedical COS would be a case in which extremely heightened sensitivity actually detracts from near-perfect CA specificity. Sufficiently heightened COS sensitivity would detract from CA specificity simply because COS would then be detectable under all breathing circumstances---and hence the COS would no longer be that same highly-specific CA signal. Similarly, incidental COS sitting in various proprietary PSG instrumentation channels can entail varying degrees of signal acquisition and processing relevance. High-powered imaging by geosynchronous satellites are similarly "capability irrelevant" to the reliable and unreliable image signals acquired and processed by a hand-held camcorder, for instance.

My point 'zactly! Mary was using an $800 pneumotach.

Muffy

Muffy wrote:OK, fine, I suppose a reflex glottic closure could do it, too.

As long as it didn't cause Wake.

Muffy

BTW, there's a dozen muffins this AM cause I'm on the road again and need to prefill my contract quota.

Muffy