ASV users: the everything ASV thread.

[patrissimo]

While I haven't found any studies on CPAP vs. ASV for OSA-only (no centrals) patients..

Bear in mind ASV is off-label for OSA and UARS. I think that's why you haven't encountered CPAP vs. ASV studies for OSA. The adaptive part of ASV is what distinguishes ASV from CPAP. That adaptive part bolsters flow during central undershoot. By contrast CPAP stents the airway with static pressure to address obstruction. So ASV adaptively fluctuates PS to help ventilate during central undershoot, while also stenting with static pressure to address any incidental obstructive component.

...if we believe the scoring these three studies used to classify obstructive apneas, hypnopneas, and centrals, it seems quite telling that ASV decreases flow-limited events much better than CPAP.

I'm sorry, but I don't follow that line of reason. I have yet to see peer-reviewed literature that suggests ASV provides superior OSA treatment or superior UARS treatment. ASV is presently targeted for central-only patients or central patients also presenting obstruction.

I hesitate to disagree because I'm new and you are highly respected here, but if you buy my assumption above, those peer-reviewed studies all do demonstrate exactly that. To break it down:

Assumption 1: In those studies, they were correctly able to classify obstructive vs. central apneas.
Assumption 2: A machine which decreases obstructive apneas in people with complex apnea will also decrease it in people with plain-old OSA & UARS.
Data: In the studies I cited, ASV decreased AHI more than CPAP did (ignoring central apneas, which it also decreased more as well, of course). For example, as I said, in the Morgenthaler et al paper on the VPAP Adapt SV vs. Bilevel, "CPAP had a residual 6.2 AHI, primarily hypnopneas, while ASV had 0.8". Again, this is only counting *obstructive* apneas & hypnopneas, not centrals!

Now, you can disagree with either of these assumptions, but since I think they are both the simplest explanations (occam's razor), I think the burden would be on you to disprove them. It could be done - for example, if you showed me that OSA and mixed apnea are qualitatively different, such that the "obstructive" apneas in mixed apnea respond to a different type of pressure support, that would disprove Assumption 2.

But as I understand it, complex apnea consists of normal obstructive events (not alleviated by the pressure) combined with central apneas. Those central apneas may be different in character from other central apneas with other causes, but I don't know why the obstructive events would be different from those in people with regular OSA. If the ASV reduces obstructive events in people with complex sleep apnea better than CPAP, I would expect it to reduce obstructive events in people with OSA better than CPAP too.

Now, if Assumption 1 was wrong, or if the studies did not break down the apnea indices into obstructive vs. central, then of course you would be right. We wouldn't know if the decreased Total Apnea Index (apneas + hypnopneas + centrals) was due to merely reducing centrals (as an ASV is designed to do), or if the ASV was also decreasing obstructive events more than the CPAP does. But given that they do break it down, these studies do show that in a population with complex sleep apnea, ASV treats obstructive events better than CPAP, not just central. Doesn't prove that ASV would do the same in a plain OSA population, but it seems most likely.

[4betterO2]

There aren't any 'normal' ranges (besides ideally having no hypopneas, although that's hard to achieve)

OK hypopnea is easy to figure; Pressure Pulse I understand would be a very individual event, not a sort of "vitals signs" value.
But what about Minute Ventilation? does that mean how many breaths a patient takes per minute?
If so, wouldn't there be normal ranges for men and women without OSA or CSA or CA? If so, what is it?

[4betterO2]

now on the ASV has settled to 16-17, AHI's most days are 0

Where do you see the AHI on the ASV? in which menu?
Did you buy your machine on your own with just a prescription, and are choosing/setting all the non-Rx settings yourself, or are you under a DME?

[patrissimo]

...it seems quite telling that ASV decreases flow-limited events much better than CPAP.

Actually, I see no evidence to support that whatsoever.

By its very nature, even if it sees an event, ASV only attacks to the extent of 90% based on flow. Is this enough to do anything (or everything)? It seems to me that an obstructive-based algorithm would be far more capable of dealing with obstructive-based events.

Further, while ASV could theoretically attack an acute obstructive event (although if the baseline parameters are set up correctly, why would there be a heap of residual obstructive events)(and anyway, instead of being proactive, it would be reactive, with events continuing to occur) it would not address a baseline pattern of flow limitation because it would think that is (by definition) the baseline.

Then why is the residual AHI (for obstructive events only, not centrals) so much lower for ASV than CPAP in the studies I cited?

[4betterO2]

wouldn't it be a waste of money to use an ASV machine for plain OSA?
Complex sleep apnea
CompSA is a form of central sleep apnea specifically identified by the persistence or emergence of central apneas or hypopneas upon exposure to CPAP or an EO470 [Bi-level] device when obstructive events have disappeared. These patients have predominantly obstructive or mixed apenas during the diagnostic sleep study occurring at >= 5 times per hour. With use of a CPAP or EO470 [Bi-level], they show a pattern of apneas and hypopneas that meets the definition of CSA described above.[/i]

Your paragraph about Complex Sleep Apnea is the key, I'm expanding on this so you can see the possible scenarios and really see the need for a sleep study to see if you need an ASV.
More than that, I think that anyone changing from CPAP to BiPAP should get a BiPAP titration sleep study.

To determine if you need an ASV machine, a sleep study is absolutely needed, both to determine the presence of CNS events, and for the titration of the machine (sometime both are done in 1 night, usually 2) .
Ironically, the titration study when using BiPAP sometimes unveils a CNS problem that may not have been showing before. While CPAP is actually in a way, treating undiagnosed CNS events by the fact of applying continuous pressure, and thus might hide their presence, in some patients it can actually cause these events. In that case, if the patient switches to BiPAP during the study, where IPAP pressure comes only as a response to the patient-triggered breaths, the CNS events now show up.

WORD OF CAUTION:
Here I quote this admission from Respironics:
"Complex sleep apnea is a condition that occurs when a patient is identified as having OSA, but with the application of Continuous Positive Airway Pressure (CPAP) to eliminate the OSA, the patient develops Central Sleep Apnea. The cause of complex sleep apnea is not known at this time."

When this side-effect of CPAP therapy happens, ASV is not only a better treatment for the original OSA, it becomes in effect, the only advisable treatment at this time.

So to answer your question, you would have to get a sleep study using non-CPAP mode, only BiPAP, to find out. Then if you do not have CNS events, you do not need an ASV.
Sorry for being wordy, (I don't have time to trim right now); I'm writing this because I'm under the impression that a lot of PAP users are buying their own machines, and upgrading possibly off CPAP to BiPAP without a sleep study, just with a prescription. So they might not know about this possible, hidden CNS-causing side-effect of CPAP, and they might decide on their own to change from CPAP to a BiPAP machine and not know that they now have CNS events, and instead of a BiPAP, need an ASV.

P.S If you want to save money, you could just look at the data/report from a BiPAP machine if you can borrow one from a reputable institution for a home study. Then if the CNS are there you could decide to get a hospital-based sleep study, to get the ASV covered by insurance.

[-SWS]

Patrissimo, I certainly welcome your opinions----including healthy disagreement based on parsimony. However, the studies you cited didn't differentiate central hypopneas from obstructive hypopneas. So when we read this:

CPAP had a residual 6.2 AHI, primarily hypnopneas, while ASV had 0.8.

...we can't assume the central patients' residual hypopneas on CPAP are obstructive hypopneas rather than central hypopneas.

Additionally, I think your parsimony reasonably assumes that obstructive apneas are obstructive apneas are.... well, obstructive apneas. However, in pathogenesis there are a few types of obstructive apneas. This pathogenesis document describes some of the neural inputs that account for patency as well as dysregulation of the upper airway:
http://ajrccm.atsjournals.org/content/172/11/1363.full

Essentially, all of those neural inputs are dependencies for airway patency. And failure in any one of those dependencies can account for upper airway obstruction. Rhetorically: what DOESN'T fail in physiology across the populace---Occam's razor be damned? You'll notice in the pathogenesis document I linked that changes in lung volume can influence airway patency. Often machine-triggering a patient's failing inspiratory drive, with a backup rate, and proportionally ventilating the lungs with ASV is sufficient to avert a central apnea and improve airway patency via normalizing lung volume. When that happens with ASV, then the central pathophysiology is compensated with the backup rate and the obstructive pathophysiology is compensated with proportional/adaptive IPAP.

That above improvement in airway patency has to do with ventilating via ASV's adaptive PS. That treatment for obstruction is very different than dilating the upper airway with CPAP or EPAP to alleviate crowding at the base of the tongue. So in this example the two types of obstructive apneas are very different, and thus the two treatments are different as well. When we see ASV correcting obstructive apneas across the central, mixed, and complex patient populations, we cannot assume those corrections will travel with identical efficacy to the obstructive population.

[Taringa542]

now on the ASV has settled to 16-17, AHI's most days are 0

Where do you see the AHI on the ASV? in which menu?
Did you buy your machine on your own with just a prescription, and are choosing/setting all the non-Rx settings yourself, or are you under a DME?

Look at my location! No DME's here, no prescription needed to buy in the US

[patrissimo]

Patrissimo, I certainly welcome your opinions----including healthy disagreement based on parsimony. However, the studies you cited didn't differentiate central hypopneas from obstructive hypopneas. So when we read this:

CPAP had a residual 6.2 AHI, primarily hypnopneas, while ASV had 0.8.

...we can't assume the central patients' residual hypopneas on CPAP are obstructive hypopneas rather than central hypopneas.

Well, the data is starting to get scanty, but from Table 2 of the opioid study:

Code: Select all

Variables	Baseline	CPAP	APSSV	p
Obstructive apnea index, n/hr	6 ± 7	1 ± 2	0 ± 0	0.01

so that's a p=0.01 difference between ASV and CPAP on obstructive apneas, ignoring hypnopneas. And from Morgenthaler, the same statistic:

Code: Select all

Obstructive 
 Apnea Index 0.4±0.9 0±0.2 -0.3±0.7 0.044

so p = 0.04.

Certainly far weaker than the strength of the evidence for reduction of central apneas, but also far stronger than the claim you and some others seem to be making that there is no evidence ASVs are better for purely obstructive events.

[mollete]

Mollete, you need a project. How about taking Patrissimo on?

I don't think so. At this point I'm not sure if he's interested in looking right or being right.

Besides, I'm busy playing with my PAV right now.

If RobySue has left the forum, I think this guy is going to take her place among the "top 3 smartest people on this board".

Oh really? Then who are the other 2 [Stands back to watch the fur fly] ?

Sadly, I've never been your Blizzard Boy.

Now that I think about it, neither have I.

[mollete]

Certainly far weaker than the strength of the evidence for reduction of central apneas, but also far stronger than the claim you and some others seem to be making that there is no evidence ASVs are better for purely obstructive events.

I guess I am an "others".

In re: the opioid study, going from OAI 1.0 to 0.0 in a group of 5 patients is not even worth tal...

[mollete]

...what is the Pressure Pulse measurement, in this context?

"One or more test pulses delivered by the device during an apnea to determine if the event is a clear airway apnea or an obstructed airway apnea."

By "clear airway apnea" do you mean a CNS event?
Does these test pulses apply to the PR (Respironics) ASV machine, or only to the ResMed?
I saw those terms in SleepyHead, but I did not think that the PR ASV machine sent those pulses?
I thought the PR ASV machine determines central apnea events by the length of time a patient waits before triggering a breath?

Pressure Pulse technology is the PR method of detecting open airway events. ResMed uses Forced Oscillation Technology.

PR ASV Technology does not send in Pressure Pulses (cause by that time it needs to send in a breath, so the PP would get buried). Rather, it looks for response to the Pressure Support in its decision to put the event in the central or obstructive bucket.

[mollete]

There aren't any 'normal' ranges (besides ideally having no hypopneas, although that's hard to achieve)

OK hypopnea is easy to figure; Pressure Pulse I understand would be a very individual event, not a sort of "vitals signs" value.
But what about Minute Ventilation? does that mean how many breaths a patient takes per minute?
If so, wouldn't there be normal ranges for men and women without OSA or CSA or CA? If so, what is it?

Minute Ventilation is total amount of air moved per minute, or

Minute Ventilation = Tidal Volume X Respiratory Rate

In a spontaneously breathing patient with a normal respiratory rate (12), normal Minute Ventilation is calculated using using a Tidal Volume of 5 ml/kg body weight.

[mollete]

But as I understand it, complex apnea consists of normal obstructive events (not alleviated by the pressure) combined with central apneas.

Negative. CompSAS is characterized by the emergence of central events when the obstructive events are treated. Obstructive events are responsive and would be resolved (however, the cost of 100% resolution would be running the CAI through the roof).

[SleepingUgly]

Mollete, you need a project. How about taking Patrissimo on?

I don't think so. At this point I'm not sure if he's interested in looking right or being right.

I think he's interested in being cured. As proof, he's already dismantled his face.

Herein lies the problem: You have an obvious preference for "projects" who are very bright (although you've at times made exceptions and settled for average mortals). It's not that easy to find someone really bright who is not going to do some thinking about things for themselves, but any questioning in an effort to understand things themselves you may perceive as a "challenge" (and not the kind you like). And, on top of that, they need to be very emotionally stable.

Besides, I'm busy playing with my PAV right now.

In public?!

If RobySue has left the forum, I think this guy is going to take her place among the "top 3 smartest people on this board".

Oh really? Then who are the other 2 [Stands back to watch the fur fly] ?

I don't know. You're the one who told RobySue that she's one of the top 3 smartest people on the board:

viewtopic.php?f=1&t=62755&p=587402&hili ... ue#p587402

I think you're one of the 3 smartest guys (and/or guyettes) here

[-SWS]

Code: Select all

Obstructive 
 Apnea Index 0.4±0.9 0±0.2 -0.3±0.7 0.044

so p = 0.04.

Certainly far weaker than the strength of the evidence for reduction of central apneas, but also far stronger than the claim you and some others seem to be making that there is no evidence ASVs are better for purely obstructive events.

Of course you're welcome to interpret that data as you see fit. In my view, interpreting how well ASV treats obstruction in a centrally-dysregulated population says nothing of how well or poorly ASV might treat the OSA population. What are the pathogenic differences in those two populations with respect to cause and mitigation?

Well, the data is starting to get scanty, but...

Your following analysis assumes that obstructive apneas in a central population are of the same pathogenesis and treatment requirement as OSA. Ignoring that there are multiple pathogenic types of airway obstruction---with some types responding better to volumetric treatments while others respond better to static pressure---seems more specious than parsimonious to me.

All argumentation aside, good luck with your quest to treat your residual EDS. I see nothing wrong in trying ASV.