Is absence of snoring a good indicator of xPAP efficacy?

KLM wrote: As the previous post explains, the experiment you performed with your apap was invalid.

Sorry, How on can you justify such a statement. That comment from Mr Anonymous was his opinion & my response challenges his assumption about an AUTO having the ability to restart stopped breathing.

I fear that much of your posts also jump to wrong conclusions and thus make it very difficult to follow a consistent thread which started with your remark that an AUTO could detect and correct stopped breathing.

When questioned you deviated from the point with a long post about OSA when we all know that AUTO & CPAP are designed *prevent* obstructions. They do that by maintaining sufficient pressure to keep the users airway open, they don't have any mechanism that commands a user to breath, they *merely* allow the user to keep breathing.

BiLevels with T mode attempt to nudge the user back into breathing.

Cheers

DSM



DSM

_________________

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

KLM wrote:
A new PSG is paramount. If indeed you have Mixed Apnea to the degree that you require a bi-level machine with timed backup in order to continue breathing throughout the night, you should also schedule a complete neurological workup as soon as possible. This is serious business. Do not wait.

KLM,

Here is another example of you jumping to conclusions. There is *nowhere* I said that. But in fact as is highlighted in another part of one of your posts, this problem I was experiencing was happening winthin the 1st hour & last hour of sleep.

There is a big difference between centrals experinced throughout the night & in those periods of early & late sleep and I understand that.

But lets not yet again deviate from the point of how an AUTO can kick start breathing the way a BiLevel in T mode can. That was the initial point and you keep steering away from it.

DSM

dsm wrote:I fear that much of your posts also jump to wrong conclusions and thus make it very difficult to follow a consistent thread which started with your remark that an AUTO could detect and correct stopped breathing.

When questioned you deviated from the point

I will repeat, in the treatment of OSA, all modern apaps with flow sensors can detect and correct stopped breathing. The flow sensor indicates breathing has stopped; this is the detection. The pressure is increased until the airway is opened, the obstruction is cleared and breathing begins again; this is the correction.

Yes, autos can prevent stopped breathing caused by obstructions. They can also detect and correct stopped breathing caused by obstructions.

From the very definition of auto-adjusting CPAP:

An AutoPAP automatically varies the pressure to prevent and/or correct sleep disordered breathing events

What is ironic about this discussion, is that for years people understood how apaps could correct, but had a hard time understanding how they could prevent. Here we seem to be having the opposite problem.

KLM wrote:
<snip>

I will repeat, in the treatment of OSA, all modern apaps with flow sensors can detect and correct stopped breathing. The flow sensor indicates breathing has stopped; this is the detection. The pressure is increased until the airway is opened, the obstruction is cleared and breathing begins again; this is the correction.

We both agree that if the stopped breathing is due to a blockage that an AUTO can incrementally increase pressure to try to open the airway. That was never in dispute.

But you appear to be arguing that someone with stopped breathing not due to a blockage can also be started breathing again by an AUTO. My case all along is that this position is factually incorrect

Yes, autos can prevent stopped breathing caused by obstructions. They can also detect and correct stopped breathing caused by obstructions.

Yes we both already agreed to that.

From the very definition of auto-adjusting CPAP:

An AutoPAP automatically varies the pressure to prevent and/or correct sleep disordered breathing events

What is ironic about this discussion, is that for years people understood how apaps could correct, but had a hard time understanding how they could prevent. Here we seem to be having the opposite problem.

dsm wrote:But you appear to be arguing that someone with stopped breathing not due to a blockage can also be started breathing again by an AUTO.

No. I never said that. I'll borrow your phrase and say, here is an example of you jumping to conclusions. I clearly stated the auto was able to detect and correct stopped breathing in the case of OSA.

Yes you are right. I thought I had made it pretty clear I was talking about centrals but on re-reading the flow of posts I can see that it could be interpreted the way you did.

I did make the assumption that when I said 'slowing and stopping breathing' that I was describing classic central and that experienced xPAPers would understand that. If I had said stopped breathing due to a blockage or due to an obstructive aponea, I would have assumed the reader would take that as a OSA event.

So I conceed your point, there have been assumptions by both sides of the debate & that in the end we appear to be arguing the same case. I believe that most other posters understood that I was focussing on centrals.

I am still interested in your comments on BiLevels in T mode vs AUTOs.

Cheers

DSM

DSM,
Regarding central apneas experienced in those periods of early & late sleep, it is my understanding those are normal and do not require any special attention or treatment.

dsm wrote:Can you explain your understanding of the purpose of a BiLevel with T mode vs an AUTO for someone who has slowed & stopped breathing due to central rather than a blockage.

My understanding is that a bi-level's purpose is to function as a ventilator when used entirely in timed mode as prescribed for a Central Sleep Apnea patient who cannot rely on spontaneous (breath-triggered) breathing, or on a combination of spontaneous/timed backup breathing.

For an auto (in this case, specifically the Respironics auto), as I said previously, the apap's flow sensors will detect stopped breathing and respond by raising the pressure. If a correction is not detected, the pressure will drop. Then another series of additional attempts are made until it is determined this is a perceived central event, at which point the attempts stop.
The chain of events happens as follows:

In the interview with Respironics Product Managers: Jeff Maglin, Product Manager, CPAP, C-Flex and Humidification and Shawn Trautman, Product Manager, REMstar Auto and Encore Pro wrote: The REMstar Auto algorithm looks for apnea’s that are non-responsive to treatment which could indicate that these are central events. At any pressure 8 cm H2O or higher we will make three pressure increases in response to a sustained string of events. If there is no improvement after the third increase, indicated by the persistence of events, the pressure is dropped 2 cm and a constant pressure is held for several minutes. If there is snoring noted during this period of constant pressure, which would indicate obstruction, we will increase pressure and reset the non-responsive treatment, thus allowing for three more pressure increases. Apneas can potentially be treated up to the device's maximum pressure setting (20 cm H2O).

KLM wrote:DSM,
Regarding central apneas experienced in those periods of early & late sleep, it is my understanding those are normal and do not require any special attention or treatment.

<snip>

An assumption being made here - the point about stopping breathing in early or late sleep is if these 'centrals' cause noticable desats. In that case they do need addressing.

Cheers

DSM

Not an assumption, really, as it is based in fact.

An excerpt from the previous quote by:
Kathe Henke, Ph.D.,A.B.S.M.,
Sleep Disorders Center of Virginia,
Richmond,Virginia

Most of the time these central apneas—not to be confused with central sleep apnea—are normal physiologic events.

I think the greater assumption being made here, is that of presuming you have Mixed Apnea. Now we've come full circle. I asked this previously, but you did not answer. In the absence of even a single central apnea event during your PSG, wouldn't it be logical to assume the stopped breathing your wife observes is caused by obstructive apnea, not central apnea? I don't understand your assumption that, in your case, this is the result of CSA or Mixed Apnea and not the result of your clinically diagnosed OSA.

It is possible your self-diagnosis of Mixed Apnea may have missed the mark. As was explained, the experiment you performed with your apap was invalid unless the "settling period" criteria had been met. There are previous posts on this subject if you'd like to research it. Also, relying on your wife's observations as evidence of central apnea is invalid, since it is not always humanly possible to visually differentiate between stopped breathing which results from obstructive apnea vs. central apnea. In addition, your assertion the apap data was inaccurate because it did not corroborate your hypothesis of central or mixed apnea is problematic because, in fact, all verifiable evidence points to the likelihood it is your hypothesis which may be inaccurate. It reminds me of the old saying: if it looks like a duck, walks like a duck and quacks like a duck; it's a duck.

I do hope you've scheduled a PSG and will publish the findings. We'll be waiting with bated breath.

KLM,

I might have been willing to discuss further with you privately. But I see you are not registered and I cant PM you.

Also I have no idea who you are or what you do - are you a sleep specialist ? - are you in the employ of an xpap manufacturer ?

Also who is this 'we are waiting with baited breath' ??? that beggars more questions.

If you were a proven sleep specialist I *might* be willing to explain a lot more about what was occuring with the observations of my wife and the studies that I conducted, but you appear to know more about her observations than she does (IMHO, your characteristic jumping to conclusions) and, at the moment I don't have any real confidence in the clarity of communication with you.

With PM we could have avoided some of the ambiguity.

And you want me to go into greater detail to please you ?,

Thanks but no thanks who ever you are.

Cheers

DSM

It's fine

KLM,

Getting back to our BiLevel machines topic you wrote ...

KLM: "My understanding is that a bi-level's purpose is to function as a ventilator when used entirely in timed mode as prescribed for a Central Sleep Apnea patient who cannot rely on spontaneous (breath-triggered) breathing, or on a combination of spontaneous/timed backup breathing."

This again is interesting because I don't know of any brand of home BiLevel machine that can operate in T mode only. That is the domain of hospital ventilators. The home BiLevel machines with T mode AFAIK all only activate T mode in combination with S mode.

Am happy to learn on this matter as it will add to my knowledge on the subject.
Question: "Which home BiLevels allow the user to set them exclusively into T mode ?"

Cheers & thanks

DSM

Oh, and one other question re AUTOs responding to flow cessation. When the machine you mentioned detects zero flow (such as in the test I suggested you try), how fast does this AUTO, from the time of detection, increase the pressure ? is this within seconds of the detection, do you have any links covering this that actually mention the speed with which the AUTO responds ? - it really is an interesting aspect of what AUTOs can do and do do.

Cheers again
DSM

_________________

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

I posted this to the wrong thread. Hmmm... I must be sleep deprived.

Here's a model of bilevel ventilator that at least a few members of this message board happen to own:
http://www.newsrx.com/newsletters/Medic ... 327QW.html

The respiratory profession has considered bilevel machines to be "noninvasive ventilators" for years. Why? Because the pressure difference between IPAP and EPAP yields support to the respiratory drive for many patients. This is referred to as pressure support ventilation or simply PSV. And, of course, that is not to mention when bilevel ventilation is used with a timed backup rate. To the best of my knowledge the medical and scientific communities don't know precisely why an IPAP/EPAP differential lends the respiratory drive support. Likely Herring Breur stretch receptors throughout the respiratory tract come into play as the IPAP/EPAP stretch receptors are literally massaged by bilevel's IPAP/EPAP pressure differential. However, that is just a guess work on my part.

The fact that APAP machines directly trigger in direct response to apneas is very well documented in manufacturer literature including patent descriptions.

Regarding whether APAP machines respond to complete obstructions (complete cessation of flow). The manufacturers and patent descriptions are all under the impression that they do. All modern APAPs by design trigger on snore, flow limitation, and apneas. Each model triggers on snore and flow limitation in an attempt to prevent apneas. Each model also triggers on apneas in an attempt to clear the apnea via static inflation of the respiratory tract itself. However, an APAP machine will not trigger on apneas under certain circumstances. Those circumstances include but are not limited to: 1) settling period is in effect, 2) a breathing normalization software controller is in effect, and 3) central apnea probability criteria has been met. The Remstar Auto infers this latter probability via three failed pressure increment attempts. The Resmed Spirit addresses central apnea probability by simply limiting pressure to all apneas at 10 cm. The 420e infers central apnea probability via open airway cardiac oscillation coupled with a provider-controlled command-on-apnea pressure limit.

This has been a very interesting and thought provoking discussion for many here. Thanks to all parties involved for a very good read!

Very informative post, Guest. Thank you.