BIPAP AUTO-SV SETTINGS HELP

Muffy wrote: CPAP creates the CompSAS scenario by changing the plant gain:

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

The above ventilatory control-feedback loop is always going, although not always oscillating out of control. I think just about everyone in sleep science agrees that CPAP adversely increases CO2-based plant gain in the case of CSDB/CompSAS patients. I agree with that as well and I'm not even in sleep science! And I also think that just about everyone in sleep science agrees that when loop gain is greater than one, that ventilatory instability (controller oscillations) will occur in response to system perturbations.

However, short of the occasional message board innuendo, I don't think anyone in science claims to understand all possible pathogenic factors adversely increasing plant or controller gain. Admittedly some of those pathogenic factors directly responsible for increasing either type of loop gain are well understood by contemporary medicine. Forgetting about any undiscovered control-system inputs affecting ventilatory loop gain for a minute, have you noticed there are researchers who acknowledge that the above highly-useful loop-gain respiratory model falls down---fails to model---under certain circumstances? It's just a model. Part of what makes it so applicable is its simplicity. And generally speaking, simplistic models often fail to correctly model under a variety of circumstances.

I think we both agree how genuinely useful that ventilatory loop gain model is. But we seem to disagree on the unknown realm of pathogenic factors that might alter plant gain and controller gain. Science very clearly does not claim to completely understand all gain-affecting inputs.

My theoretical premise: certain unexplored neural stimuli can alter loop gain itself---in at least some neurologically disordered breathing types.

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

Then we agree that Rapoport's near-perfect specificity was relevant to his equipment and COS processing. And I think we also agree that heightened sensitivity can outstrip that near-perfect specificity in this biomedical application. Not much COS advancement in the white papers in the last ten years regarding central apnea differentiation... And that's undoubtedly because sensor and signal-processing refinement yield greater sensitivity, which deteriorates specificity in this particular biomedical application.

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Crowpat, I'm still with you. And I still have a variety of parameter-based pressure experimentation to propose. Please let me continue looking through all your data details to date...

-SWS wrote:

Muffy wrote:The role of vocal cord closure...one certainly wouldn't be relaxed during VCD

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

Muffy wrote:The event I described would more appropriately be termed "reflex glottic closure".

More appropriately? Didn't you start off talking about VCD instead of something else? Because that more appropriate term "reflex glottic closure" doesn't show up often on the Internet while also discussing VCD:
http://www.google.com/search?q=VCD+%22r ... =firefox-a
-and-
http://scholar.google.com/scholar?q=VCD ... =en&tab=ws

Now that sneaky and less appropriate term "laryngospasm" just manages to wiggle its way right along side VCD descriptions:
http://www.google.com/search?q=VCD+lary ... =firefox-a
-and-
http://scholar.google.com/scholar?q=VCD ... =en&tab=ws

Muffy wrote: 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.

According to the medical literature, VCD is a largely unrecognized/undiagnosed disorder. Regardless, I'm not sure where you came up with all those "there must be these diurnal presentations" regarding largely unexplored nocturnal VCD symptomology.

I also disagree with your Powerball assessment, that through the magic of innuendo and metaphor, somehow manages to assign extreme numeric probability to largely unexplored nocturnal GERD-triggered VCD symptomology. So let's see... Take the Benydryl: no significant results---take the Prilosec: significant improvement. Conclusion: must have been the Benydryl. And the overarching conclusion about experimentation in general: people really need to quit finding solutions ( therapy "wingin'") when sleep medicine consistently leaves large numbers with suboptimal therapy. You're certainly welcome to ALL of those opinions. Can't say that I share them or even plan to argue about them... But I do sincerely appreciate your general expertise and fine upstanding character... and I highly doubt you leave your patients with suboptimal therapy.

Me? Just a brash, reckless cowboy... specifically the rodeo clown variety.

CROWPAT wrote: My BP stays very close to 120/80 whenever I check it at home or at a doctor's office. The highest ever recorded for me was 132/88.

Pat, those are nice, low numbers. In light of your Paroxysmal Supraventricular Tachycardia diagnosis, did the clinicians ever measure your blood pressure during or immediately after waking up while using ASV? A few patients become hypotensive in direct and immediate response to PAP therapy's increased interthoracic pressure:

Because of increased intrathoracic pressure, cardiac output may decrease resulting in hypotension, particularly in patients with atrial fibrillation

http://www.medscape.com/viewarticle/501709_7

Specifically, Pat, do YOU ever measure for hypotension immediately after waking up? If not, can I suggest that you do---but especially after those bad-feeling nights when your spontaneous breath rate drops below your comfortable threshold.

I have paroxymal supraventricular arrythmia, not tach.
Blood pressure is always in good range whether I measure it first thing in the morning or anytime during the day. THAT is something about my health that has always been good.

CROWPAT wrote:I have paroxymal supraventricular arrythmia, not tach.

I realize you have paroxymal supraventricular arrythmia and not tach . Your heart rate flirts with the opposite of tach: bradycardia. So my next question is just how often do you bottom out that oximeter heart-rate chart which is low-end capped at 50 BPM?

(on edit: I just realized I have the wrong link above... now I know why you said that about tach )

CROWPAT wrote:Blood pressure is always in good range whether I measure it first thing in the morning or...

Well, I think the idea here is to see if CPAP's interthoracic pressure impedes venous return. So if you're already sitting at a desk or kitchen table while investigating CPAP's immediate pressure-based hypotensive effects, then CPAP's interthoracic pressure is no longer there.

I think the idea is to check for impeded and hypotensive venous return while still in bed and CPAP is still applying its interthoracic pressure. It's admittedly just a cautious check...

-SWS wrote:Forgetting about any undiscovered control-system inputs affecting ventilatory loop gain for a minute, have you noticed there are researchers who acknowledge that the above highly-useful loop-gain respiratory model falls down---fails to model---under certain circumstances?

In CompSAS? Like what?

Muffy

-SWS wrote:

CROWPAT wrote:I have paroxymal supraventricular arrythmia, not tach.

I realize you have paroxymal supraventricular arrythmia and not tach . Your heart rate flirts with the opposite of tach: bradycardia. So my next question is just how often do you bottom out that oximeter heart-rate chart which is low-end capped at 50 BPM?

What supraventricular arrythmia could you have that is not a tachycardia?

Muffy

Muffy wrote:What supraventricular arrythmia could you have that is not a tachycardia?

Thanks for straightening that out.

Hmmmph! As if I know anything about medicine. ...Ask me something about Yahtzee or rock gardening instead...

Pat, what exactly did your doctor say about how your paroxymal supraventricular arrythmia presented during the diagnostic workup? If you per chance ask your doctor for details during an upcoming visit, can I suggest asking your doctor's opinion about your heart rate bottoming out at that 50 BPM lower-limit on your oximeter graph?

Muffy wrote:

-SWS wrote:Forgetting about any undiscovered control-system inputs affecting ventilatory loop gain for a minute, have you noticed there are researchers who acknowledge that the above highly-useful loop-gain respiratory model falls down---fails to model---under certain circumstances?

In CompSAS? Like what?

That sleep science is anywhere close to a consensus regarding the pathophysiology of CSDB/CompSAS? That something in biology in known to pin loop-gain as an immutable constant rather than researchers observing what appears to be both longitudinally wandering and at times short-term disordered loop gain? That any respectable researcher should conclude science has a handle on all pathogenic factors affecting disordered ventilatory loop-gain?

...And you're asking ME precisely what medical researchers have yet to discover as they grapple with disordered loop-gain that clearly wanders? I'm honored!

Albert Einstein wrote:If we knew what we were doing, it wouldn't be called research, would it?

-SWS wrote:...Ask me something about ...rock gardening instead...

OK.

Do you start your rocks from seed or get those little 6-packs from the quarry?

Do rocks need a lot of water in the summer?

Are your rocks perennials? It seems like rocks would be pretty cold-weather hardy.

Muffy

-SWS wrote:That sleep science is anywhere close to a consensus regarding the pathophysiology of CSDB/CompSAS?

Well, "IMHO", I think the Good Ship CompSAS has sailed, hit the iceberg, sank and has been made into a movie already.

Another article, this one out this month in American Journal of Respiratory and Critical Care Medicine Vol 181. pp. 189-193, (2010):

http://ajrccm.atsjournals.org/cgi/conte ... /181/2/189

that says "Yeah there's instability, PAP changes things, sit tight for a month and you'll be fine."

Muffy

Muffy wrote:

-SWS wrote:...Ask me something about ...rock gardening instead...

OK.

Do you start your rocks from seed or get those little 6-packs from the quarry?

Do rocks need a lot of water in the summer?

Are your rocks perennials? It seems like rocks would be pretty cold-weather hardy.

Muffy

Well, the missus and I have only been at this hobby for three short years...

So far here's what we learned about rock gardening: 1) it clearly takes more than three growing seasons to even sprout those suckers, and 2) Dixie cups get all yellow and ugly sitting on the window ledge year after year. ...so best to pick much nicer containers next time.

Since we both have a sweet tooth, we anticipate that very first rock-candy harvest will be WELL worth the wait. Thank you for asking!

Muffy wrote:

-SWS wrote:That sleep science is anywhere close to a consensus regarding the pathophysiology of CSDB/CompSAS?

Well, "IMHO", I think the Good Ship CompSAS has sailed, hit the iceberg, sank and has been made into a movie already.

Another article, this one out this month in American Journal of Respiratory and Critical Care Medicine Vol 181. pp. 189-193, (2010):

http://ajrccm.atsjournals.org/cgi/conte ... /181/2/189

that says "Yeah there's instability, PAP changes things, sit tight for a month and you'll be fine."

Muffy

All of the recent CSDB/CompSAS adaptation studies have been extremely interesting IMHO... and promising for a good number of patients! However, I honestly don't think that CSDB/CompSAS researchers are even close to closing up shop with comments like: "Dang! You mean all we had to do was put our patients on CPAP for 30 days? How did we ever manage to miss that?"

So my CSDB/CompSAS views apparently differ a little: I think abandoning that CSDB/CompSAS research ship would be tantamount to abandoning a significant number of patients who either: 1) didn't completely adapt to CPAP, or even 2) eventually acquired disordered loop-gain problems much later in the treatment cycle. Instead I would offer that the CSDB/CompSAS research ship hasn't quite left the dock yet based on these thoughts and observations:

1) Disordered plant gain in the above study is proven longitudinally variable rather than fixed,

2) Purely obstructive patients, in which the central component becomes emergent only after the introduction of CPAP, might prove more adaptable to CPAP than other CSDB/CompSAS patients,

3) Mixed and central patients, in which the central component becomes more severe after the introduction of CPAP, might longitudinally prove more susceptible to a variety of pathogenic factors adversely affecting loop gain,

4) Purely obstructive patients, in which the central component becomes emergent only after the introduction of CPAP, still have an unknown long-term prognosis regarding any distant-future progression of disordered loop-gain,

5) More extensive longitudinal studies might actually reveal that supposedly "adapted" CSDB/CompSAS patients periodically present disordered loop-gain flareups,

6) More extensive longitudinal studies might reveal that supposedly "adapted" CSDB/CompSAS patients are the ones much more inclined to never feel adequately rested while using CPAP

7) More extensive research might reveal even better diagnostic and treatment benchmarks for these patients than contemporary sleep-science methodology can offer.

SWS- Will talk with my cardiologist about low heart rate at night when I see him about my stress test results. The initial diagnosis of Paroxymal supraventricular arrythmia was that it was benign. He said it would not kill me, was mostly an irritant, and that we would treat it with tambacor. The alternatives to drugs were invasive and I did not want to go that route for something that was not serious. I learned to live with it and not worry about it.
Could not see family doctor about silent GERD as he had a family emergency - rescheduled for early February.
AHI remains 3 or below almost all nights, but feel the same during the day. Have carefully tried to correlate what I eat at night with AHI and how I feel, but have not observed any correlation.

-SWS wrote:I honestly don't think that CSDB/CompSAS researchers are even close to closing up shop

Me neither, but I believe the focus is less on "Let's get out the Techno-Flash" and more on "Let's figure out what we're doing first."

-SWS wrote:"Dang! You mean all we had to do was put our patients on CPAP for 30 days? How did we ever manage to miss that?"

We didn't.

-SWS wrote:I think abandoning that CSDB/CompSAS research ship...

They aren't.

-SWS wrote:1) Disordered plant gain in the above study is proven longitudinally variable rather than fixed,

How does that raise the HMS CompSAS?

-SWS wrote:2) Purely obstructive patients, in which the central component becomes emergent only after the introduction of CPAP, might prove more adaptable to CPAP than other CSDB/CompSAS patients,

3) Mixed and central patients, in which the central component becomes more severe after the introduction of CPAP, might longitudinally prove more susceptible to a variety of pathogenic factors adversely affecting loop gain,

4) Purely obstructive patients, in which the central component becomes emergent only after the introduction of CPAP, still have an unknown long-term prognosis regarding any distant-future progression of disordered loop-gain,

These points are somewhat confusing to me since any definition of CompSAS requires treatment-emergent central component. And while people can study whatever they want

http://www.resmed.com/us/patients_and_f ... c=patients

I would look very carefully at initial therapeutic approach and/or F/U on stable therapy at 1 to 3 months.

That said, there will be some CompSAS patients that need ASV sooner rather than later, but "IMHO" it's a pretty tiny number.

-SWS wrote:5) More extensive longitudinal studies might actually reveal that supposedly "adapted" CSDB/CompSAS patients periodically present disordered loop-gain flareups,

The anectdotal studies are already there. Search "dial wingin'".

-SWS wrote:6) More extensive longitudinal studies might reveal that supposedly "adapted" CSDB/CompSAS patients are the ones much more inclined to never feel adequately rested while using CPAP

7) More extensive research might reveal even better diagnostic and treatment benchmarks for these patients than contemporary sleep-science methodology can offer.

Perhaps.

Muffy

BTW, keep in mind that the key component of The Loop in CompSAS is this one:



Without increased PcrCO2, that increase in Plant Gain back there would result in one (1) CSA.

Muffy