Resmed vs. Respironics - Help

Snoredog wrote:But it seems reporting of CA's on PSG's seem to be subjective on the part of the PSG tech/scorer

I don't think so. Besides monitoring air flow, the full PSG study is using effort belts around upper and lower chest to see if the sleeper is struggling to breathe against an apnea, or is simply "not breathing" with no effort at all (a central apnea.)

Unless the belt has loosened and slipped, (which the sleep tech should notice easily enough during the monitoring) the scoring tech can certainly see whether the sleeper was, or was not, making an effort to breathe when airflow ceased or nearly ceased.

It's up to the scorer to identify any CAs (Central Apneas) correctly, and while there may be an element of art in expert scoring, there are definitely guidelines for identifying events that the scoring tech uses when going through the raw data, epoch by epoch. I think the scoring in sleep studies is quite objective and accurate for the most part.

Of course, a sleep study is a snapshot of one night in a strange environment, but if centrals have been happening at home to an undiagnosed person, I expect they are going to show up and be scored as such in the sleep study, too...in any decent sleep lab.

Sleep Review Magazine has an interesting article entitled "The Nuts and Bolts of Scoring Apneas and Hypopneas" (pub. Spring 2001):
http://www.sleepreviewmag.com/issues/ar ... -04_07.asp

Some of their comments go toward at least one or two points raised in this thread. In that article they discuss whether a combined apnea/hypopnea event should be thought of and scored as a new and separate event type. They also touch on CA scoring.

-SWS wrote:Bill, I offer a couple thoughts relative to some of your recent points:

NightHawkeye wrote: One point needs to be stated regarding complete blockage and the measurement of that blockage. As the blockage begins to severely restrict flow through the windpipe, the difference in pressures above and below the obstruction build quickly tending to force total occlusion.

Here we are speaking of passive characteristics contributing to the dynamics of airway collapse. Some researchers are also trying to understand what role neural input plays in addition to these passive airway characteristics (regarding airway patency or collapsibility).

My understanding is that the Starling Resister model is deemed by many researchers in the field to be the best physics model to describe those types of passive airway dynamics that you just mentioned above.

I think we'd agree, -SWS, that the Starling Resistor model is not applicable when the upper airway collapses. If it were, an increase in pressure at the upper end of the windpipe would simply re-expand and re-open the windpipe. (I think we've already firmly established that APAP's don't do that!) From what I've seen of the Starling Resistor model (admittedly a small sample) its use is more applicable to what we'd call flow limitations and hypopneas. A Google search showed it is a favorite model for APAP prediction algorithms.

Discussion of the Starling model would be both informative and entertaining though, so I'm game. Your call ...

-SWS wrote:However, a surprising finding (correct or incorrect) seems to be that the extreme vacuum pressures are more the survival response after the occlusion rather than the cause of the occlusion:

Kirkness, Krishnan, Patel, Schneider wrote: Rather, the markedly negative intraluminal pressures generated by the diaphragm during periods of upper airway obstruction were the consequence rather than the cause of upper airway occlusion.

An expanded quote from your reference is even more illuminating.

Kirkness, Krishnan, Patel, Schneider wrote:Initial efforts for modeling upper airway obstruction focused on the interplay between extraluminal pressures generated by the diaphragm that collapse the pharynx. It was originally postulated that upper airway patency was determined by the balance of pressures between the intraluminal and extraluminal space. As intraluminal 'suction' pressures overcame the dilating forces around the pharyngeal lumen, the theory held that the pharynx would progressively collapse and ultimately occlude during sleep.

In other words, pretty close to the situation DSM and I have been describing in various ways.

Kirkness, Krishnan, Patel, Schneider wrote:Later studies, however, have minimized the role of intraluminal suction pressures in the pathogenesis of upper airway obstruction by demonstrating that upper airway occlusion could occur spontaneously, even when intraluminal pressures were positive.

In other words obstruction can occur even when a CPAP is providing pressure. OK, I think we've all seen that. I'm not seeing anything new here yet, even though the authors seem to be surprised by it.

Kirkness, Krishnan, Patel, Schneider wrote:These observations resolved a major question regarding the role of negative intraluminal pressures in the pathogenesis of OSA, and confirmed that negative pressures were not required for airway occlusion to occur.

No argument from me. This also doesn't disagree with anything I've stated. At least I don't think it does.

Kirkness, Krishnan, Patel, Schneider wrote:Rather, the markedly negative intraluminal pressures generated by the diaphragm during periods of upper airway obstruction were the consequence rather than the cause of upper airway occlusion.

We've come all the way back to your quotation, -SWS. I'm still not disagreeing with any of it. When the blockage does occur large vacuum pressures will build. Don't see that's much at odds with what I stated either.

-SWS wrote:Whether we believe the above statement or not, that document makes for an interesting read describing passive (non-neural) factors contributing to both snoring and airway collapse

I thank you for the references, -SWS (and I mean that seriously). I've actually learned a few things here tonight. None of it trumps basic physics yet though.

If anything, I have a much better appreciation for the communication divide here. It's pretty wide.

Regards,
Bill

SL3's machine settings screen is confusing in that the CPAP button is bold when you're setting up the parameters for APAP. French logic being what it is, the APAP button is faded out when you're setting it up- meaning "you can't go there because that's where you are". And there is nothing, big and bold on that screen to tell you you are in the APAP setting mode, except for the fact that the APAP button is faded out....

I'm referring to the first setup screen for APAP (after you press the APAP button, and it fades away), where you have 3 scales: Max pressure, Initial prressure, and Min. pressure. Initial pressure is the one I'm talking about.

NightHawkeye wrote: The CPAP setting is the initial setting your refer to.

Not sure what you mean by that, but on my machine my CPAP - setting is 20. True to form, the CPAP settings screen shows APAP in bold. What you set up after pressing the CPAP button has nothing to do with what you set up after pressing the APAP button.

NightHawkeye wrote:However, looking at the data I can see exactly what you are referring to. The charts clearly show the pressure bouncing between 4 cm and 6 cm frequently, sometimes staying down at 4 cm for a little while, but then also climbing up above 10 cm and plateauing up there for periods most often between 30 minutes and an hour

If your initial pressure=min, the charts are in tune with the interpertation that you told the machine to prefer 4 - so it always goes down there when it can - but it really can't stay there. I wonder what would happen if you set up the machine with min=6 max =12, and initial=8 or 9 or 10.

-SWS wrote: I wonder if anyone wouldn't mind taking a peek at SL3 to tell us what the online guide says (if anything at all) about "initial pressure". More importantly I'm wondering just what the 420e set up guide clearly (or vaguely) tells clinicians to do regarding "initial pressure".

That initial pressure wouldn't have been so much of a riddle to me if the manuals weren't so cryptic. There is an interesting hint - in the clincian's manual, describing the pressures:

Pmax is "Maximum pressure authorized"
Pmin is " Minimum pressure authorized"

And Pressure level (CPAP mode) or Initial pressure (APAP mode) is:
Pressure delivered at the end of ramp or at startup (in the absence of ramp).

SL3 basicall says nothing except for consistently distinguishing the three pressures, and talking of maximum and minimum permitted pressure (my empahsis).

However, the clincher is in what was submitted to the FDA and approved:, my emphasis added:
http://www.fda.gov/cdrh/pdf3/k031470.pdf

The GoodKnight 420 Evolution can operate in either Constant or Automatic mode. In Constant mode, the device delivers a constant positive airway pressure to the patient at a fixed level prescribed by the practitioner between 4 and 20 cmHrO. In Automatic mode (APAP mode), the practitioner sets a maximum and minimum pressure range above and below the prescribed reference pressure and between 4 and 20 cmHz0. The pressure is adjusted within this range according to the patient’s respiratory pattern and the type of respiratory events detected. Data concerning the type of events detected, their frequency and duration, etc. is stored in the device data memory and can be accessed by the practitioner through the use of the optional Silverlining'" software. Pressure delivery for
the GoodKnight 420 Evolution is regulated by a pressure sensor which monitors both ambient and output pressure and provides feedback to the control system.

Rooster - if you don't need exhalation relief, then you may be right about the 402E giving you better treatment.

O.

A very interesting article, indeed! Thanks for the link, -SWS!

Regarding scoring centrals, I've quoted a few parts, adding emphasis to a word or statement that particularly caught my eye:

"Individuals who have been scoring polysomnograms for many years may have occasionally seen central apneas, in which there is essentially no detectable effort in the abdominal or thoracic effort channels, but in which there is an apparent (but false) signal in the thermocouple or thermistor channel. In such circumstances, the apparent variations in the airflow tracing obviously must be deemed as artifact due to some sort of temperature fluctuations detected by the transducer."
(bold red emphasis mine)
---

"Central Apnea. Traditionally, a central apnea has been defined as a nearly complete (80% to 100%) reduction in both the thoracic and abdominal effort channels and, of course, the airflow signal, since logically there should be no airflow if there is no respiratory effort. There should be no paradoxical breathing before or after a purely central apnea. The abdominal and thoracic movement signals should be entirely in phase before and after a central apnea. However, there are some exceptions mentioned earlier, in which temperature variations produce artifacts, which mimic airflow.

Rather frequently, a false signal or ballistocardiogram artifact will appear in one or both of the effort channels. This can be identified as small to medium sized oscillations in the thoracic or abdominal movement channels. The cause of the ballistocardiogram is the force of the heart beat causing the chest to expand and contract slightly but at a rate exactly equal to the ongoing heart rate. Noting the almost perfect correlation between the oscillations in the effort channels and the ongoing electrocardiography (ECG) signal allows one to identify such ballistocardiogram artifact. The main point to recognize is that there is little or no movement in either the abdominal or thoracic movement channels for 10 seconds or longer. Again, such an event is considered by some to be clinically significant only if either an arousal of some sort and/or an oxygen desaturation follows it. Central apneas are often a significant cause of insomnia.6"
(bold red emphasis mine)
---

John Zimmerman, PhD, is laboratory director of Mountain Medical Sleep Disorders Center, Carson City, Nev. He is also a site visitor on the accreditation committee for the AASM.

There are a lot of other interesting things in the article.

As for the parts discussing centrals, I'd hope most credentialed (RPSGT) sleep technologists would be familiar with the two artifact scenarios mentioned by Zimmerman and would examine the data more closely at those ambiguous points -- to get the centrals scored correctly.

Just now noticed that article was from a 2001 issue. I wondered why not much was said about nasal pressure transducers in the paragraph where thermistors were talked about.

NightHawkeye wrote: Discussion of the Starling model would be both informative and entertaining though, so I'm game. Your call ...

I don't think there's any need to linger on the Starling Restor model, but I'll attempt to offer a few more interesting comments toward it's potential uselessness or usefulness (as anyone deems fit for any reason they see fit).

NightHawkeye wrote:

-SWS wrote:Bill, I offer a couple thoughts relative to some of your recent points:

NightHawkeye wrote: One point needs to be stated regarding complete blockage and the measurement of that blockage. As the blockage begins to severely restrict flow through the windpipe, the difference in pressures above and below the obstruction build quickly tending to force total occlusion.

Here we are speaking of passive characteristics contributing to the dynamics of airway collapse. Some researchers are also trying to understand what role neural input plays in addition to these passive airway characteristics (regarding airway patency or collapsibility).

My understanding is that the Starling Resister model is deemed by many researchers in the field to be the best physics model to describe those types of passive airway dynamics that you just mentioned above.

I think we'd agree, -SWS, that the Starling Resistor model is not applicable when the upper airway collapses.

Right. Starling Resistor model is but a model. And, of course, everyone in science knows the problem with models in general: all too often they don't model correctly for an entire variety of reasons. So the exact point on the continuum at which the Starling Resistor model may or may not break down is undoubtedly debated in this branch of science that employs it.

Regardless of the inevitable debates, researchers sure seem to employ the Starling Resistor model in an attempt to understand the various points on the SDB continuum describing airway closure. And on that continuum Starling Resistor model offers readers in this thread plenty of fascinating relevance to yet other topics we have been discussing.

NightHawkeye wrote: If it were, an increase in pressure at the upper end of the windpipe would simply re-expand and re-open the windpipe. (I think we've already firmly established that APAP's don't do that!)

I sure could be wrong here, Bill, but I think to simply establish that APAPs don't attempt to inflate occlusions wide open does not speak of technical feasibility considerations that might have accounted for that APAP strategy: how much pressure would have been required for successful timely inflation (most notably) as well as other disturbance-type issues in physiology, including homeostatic concerns.

To say that APAPs elect not to inflate the airway does not say the airway ceases to behave as a Starling Resistor right up to the point of occlusion. IMO we don't need to stick with Starling Resistor modeling as any kind of requirement for your theory. It's just an interesting and relevant model for anyone reading this thread to note, utilize, or reject as they see fit.

NightHawkeye wrote:From what I've seen of the Starling Resistor model (admittedly a small sample) its use is more applicable to what we'd call flow limitations and hypopneas. A Google search showed it is a favorite model for APAP prediction algorithms.

Indeed! Toward that very interesting topic of establishing Pcrit, the Healthdyne model elected to induce Pcrit with a more disruptive pressure delta than the modernized algorithm does. I speculate that the more disruptive pressure delta probably even established a more accurate Pcrit, but perhaps at a price regarding sleep arousals. I would also speculate that if Pcrit is less disruptive in the modern algorithm, the designers have either devised more refined techniques to establish that Pcrit, or they relinquished Pcrit accuracy in favor of the higher-priority preemptive control layers (that also achieve preemptive pressures).

NightHawkeye wrote:

-SWS wrote:However, a surprising finding (correct or incorrect) seems to be that the extreme vacuum pressures are more the survival response after the occlusion rather than the cause of the occlusion:

Kirkness, Krishnan, Patel, Schneider wrote: Rather, the markedly negative intraluminal pressures generated by the diaphragm during periods of upper airway obstruction were the consequence rather than the cause of upper airway occlusion.

An expanded quote from your reference is even more illuminating.

Kirkness, Krishnan, Patel, Schneider wrote:Initial efforts for modeling upper airway obstruction focused on the interplay between extraluminal pressures generated by the diaphragm that collapse the pharynx. It was originally postulated that upper airway patency was determined by the balance of pressures between the intraluminal and extraluminal space. As intraluminal 'suction' pressures overcame the dilating forces around the pharyngeal lumen, the theory held that the pharynx would progressively collapse and ultimately occlude during sleep.

In other words, pretty close to the situation DSM and I have been describing in various ways.

Well, that's perhaps the communication barrier itself at work. At times it's difficult for me to understand where your descriptions converge with science and where they don't. But I think the whole point of discussion is to get to that understanding, unless the discussion becomes too cumbersome to serve that purpose.

NightHawkeye wrote:

Kirkness, Krishnan, Patel, Schneider wrote:Later studies, however, have minimized the role of intraluminal suction pressures in the pathogenesis of upper airway obstruction by demonstrating that upper airway occlusion could occur spontaneously, even when intraluminal pressures were positive.

In other words obstruction can occur even when a CPAP is providing pressure. OK, I think we've all seen that. I'm not seeing anything new here yet, even though the authors seem to be surprised by it.

The authors aren't surprised so much as they are filling us in on progressive scientific findings by their peers IMO. So the communication barrier truly is potentially everywhere, Bill. Fortunately it's not so much an ill-deed as much as it's a reality of diverse humanity---at least as far as I can tell.

NightHawkeye wrote:

Kirkness, Krishnan, Patel, Schneider wrote:These observations resolved a major question regarding the role of negative intraluminal pressures in the pathogenesis of OSA, and confirmed that negative pressures were not required for airway occlusion to occur.

No argument from me. This also doesn't disagree with anything I've stated. At least I don't think it does.

I don't know that anything in there disagrees with what you maintain. When you described an obstructive apnea, for instance, I thought you described it very well. It's just tough at least for me to predict what's going to work well for you and what will not.

NightHawkeye wrote:

-SWS wrote:Whether we believe the above statement or not, that document makes for an interesting read describing passive (non-neural) factors contributing to both snoring and airway collapse

I thank you for the references, -SWS (and I mean that seriously). I've actually learned a few things here tonight. None of it trumps basic physics yet though.

If anything, I have a much better appreciation for the communication divide here. It's pretty wide.

Maybe it is, Bill. I thought the Sterling Resistor model potentially held interest and relevance for an entire array of topics in this thread---and most importantly for those readers who had never been exposed to it.

If it was off track I apologize. If it was inadequate for your purposes, then I apologize as well. But since I admit that I am communication-barrier prone, Bill, I will happily sit back and watch your theory unfold. I'm not sure my attempts at facilitating serves the theory at hand. I still find reading of the unfolding of this theory enjoyable.

And I will gladly partake in all the other great topics that are going on in this thread. But long live the theory! Unfold it as you may! .

[quote="-SWS"]Superb discovery and text emphasis by ozij regarding the 420e!

I don't currently have Silver Lining installed on any of my computers. I wonder if anyone wouldn't mind taking a peek at SL3 to tell us what the online guide says (if anything at all) about "initial pressure". More importantly I'm wondering just what the 420e set up guide clearly (or vaguely) tells clinicians to do regarding "initial pressure".

The great discussion continues!

ozij wrote:A-pnea comes frorm Greek. The "a" "denotes" "without", or "not"; the "pnea" is breathing (or breath).

See also:
http://en.wikipedia.org/wiki/Apnea

http://www.nlm.nih.gov/medlineplus/ency ... 003069.htm

Breathing that slows down or stops from any cause is called apnea. Apnea can come once in a while and be temporary. This can occur with obstructive sleep apnea, for example. Prolonged apnea means a person has stopped breathing. This is also called respiratory arrest when the heart is still active. Prolonged apnea accompanied by lack of any cardiac activity and a patient who is not responsive is called cardiac arrest.

My emphasis.

Apnea is also not total cessation of breathing when scored during a PSG.

O.

I knew it was one of those foreign words

you mean it is not from Brazil or Venezuela or one of those other latin countries?

And, should you so want, the minimal ramp pressure can be even lower than the minimal therapy pressure.

So we have Initial - where the machine goes when you turn it on and when the ramp is finished - should be the preferred pressure after your PSG

Ramp - start as low as you want, and you can make it lower than the minimum

Minimum - which should be lower than the preferred pressure

Maximum - which should be higher than the preferred presssure.

4 different pressures to set.

O.

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

ozij wrote:I was reading Rapoport's paper on Caridac Oscillations, and Rapoports patents, and I think I've finally discovered why the "initial pressure" is there, and it's by no means idiocy, on the contrary -it's brilliant.

I think it depends on how fast is fast. What this patent tell me is that if you set Initial Pressure for a low pressure requirement state (let's say SWS or stable Stage 2 and lateral position) and the patient turns supine and/or enters REM and has high pressure requirements, since response will by defintion be (relatively) slower, one might as least theoretically wonder if this thing is reacting quickly enough to achieve sleep stability.

And without knowing exactly what's in the algorithms (Is what's in these patents actually in the machines?) there's often little chance of matching patients up with the "best" algorithm.

SAG

snoredog wrote:When you first tun on the machine, it goes to Initial pressure, and in the example above to 8.0, if you hit the center Ramp button it drops down to the Minimum pressure set of 6.5, it then stays there until Ramp timer expires.

I thought you guys knew this

Thanks!! Yea, that's the part I think we all knew and understood perfectly well. I haven't looked at the 420e clinician manual for a couple years and have no clue where mine is.

What I couldn't remember is if any of the manuals explicitly used that word "prescription" as Rapoport did in his patent description. But it sounds as if PB elected to scoot around the word "prescription". I would think that word should be a very helpful "bell ringing" word for clinicians setting that machine up.

So if PB elected not to use the very clear term "prescription" was it because they implicitly disagreed about prescription being necessary as an initial pressure? I'm wondering if they thought the term somehow made for ineffective marketing (eg. "the machine somehow sounds less automatic to the public if a doctor's prescription is an input requirement")? Or perhaps PB felt there were yet additional intitial-pressure settings that yielded different benefits. For instance, if someone has no homeostatic problems regarding pressure transition, then it might be advantageous for them to receive a more aggressive pressure strategy even above their prescription (assuming a patient with plenty of night-to-night variability for instance).

That was the basis of my wondering whether that word "prescription" showed up anywhere besides the patent description. Thanks for checking! .

Greetings, -SWS. I'll take a moment to thank you for your considered response. It's the continued discussion, even when the going gets rough, that allows amazing insights to spring from this board. Individually, we're all about as dumb as a box of rocks. And, yep, I lump myself in that same category as well.

-SWS wrote:Well, that's perhaps the communication barrier itself at work. At times it's difficult for me to understand where your descriptions converge with science and where they don't.

Tar and feather me, why don't ya.

Lawyers supposedly just throw the book at their opponents when they run out of arguments. Well, at least we've moved past the laughter and ridicule stage of this discussion. (I think.)

The frustration we both have expressed (please correct me if I've mis-stated that), I believe, is that the discussion has reached the limit of what researchers have documented about the modeling of obstructive apnea. I fall back on basic physics hoping to garner an explanation, while you fall back on the models ...

Both have well known shortcomings. In other words, it appears neither of us has any more useful arguments to employ.

Regards,
Bill

StillAnotherGuest wrote: I think it depends on how fast is fast. What this patent tell me is that if you set Initial Pressure for a low pressure requirement state (let's say SWS or stable Stage 2 and lateral position) and the patient turns supine and/or enters REM and has high pressure requirements, since response will by defintion be (relatively) slower, one might as least theoretically wonder if this thing is reacting quickly enough to achieve sleep stability.

Especially when people have been setting it up regularly with the initial to equal the minimum, instead of setting up the initial to equal the Rx (or anything else higher than the minimum). By setting up an initial pressure > minimum , you move from the minimum to the initial faster than you would if initial=minimum. And since you're getting a faster response on all pre-emptive indicators as well...

And without knowing exactly what's in the algorithms (Is what's in these patents actually in the machines?) there's often little chance of matching patients up with the "best" algorithm.

SAG

No argument about that. But do look at the FDA quote - PB is pretty clear there about how the auto mode is expected to be used in this machine.

-SWS: I was wondering who wrote the original manual, and in what language... found the SL3 manual in French - but nothing new in it.


O.

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

On the contrary Bill. Please let me explain.

The perceived cumbersome part of our conversation right now goes on my part. I'm having some trigeminal neuralgia pain just "nipping" away throughout much of my discussions (hopeful surgery in early May! Woohoo!). I'm fairly certain that TN pain is making both me and my analytic approach downright insufferable for some people (sorry!!!).

When I work theories all by myself, I at least attempt to build just as many competing theories as I can. Then I very comfortably proceed to analytically kick the living daylights out of just as much as I possibly can---both as I go along and when I reach some tentatively conclusive endpoints.. So I'll analytically flip and flop with myself just like a carp---only much quicker than my bud, Snoredog, could ever humorously document for my own benefit of laughter.

But I'm very comfortable when I approach problems in my preferred manner this way. It's when I attempt to employ that approach with others where I get in trouble because of my lacking social acumen. Not yours, my friend. So the reason I wanted to step out of only that part of the discussion is because I think I may be hindering it. And I don't want it hindered.

Everyone agrees that at least after occlusion everything that you and Doug say is happening. Ozij even succinctly points out that before administering CPR we need to literally pull the tongue up and out of the way.

I think what you guys are saying (despite my poor attempts at searching for any possible refinements along the way) is that once that occlusion occurs, it can render CPAP momentarily useless. I'm inclined to agree on that point.

So here are only a few points I was hoping people might have gotten around to at least speculating about:

1) Might this be a rare or prevalent problem regarding excessive residual AI (since residual AI varies widely across the population)?

2) Might this hypothetical problem in relation to CPAP be associated with certain craniofacial characteristics?

3) Might this hypothetical problem be alleviated with a supplemental dental device? etc., etc., etc.

I can't force anyone to further explore this issue. But I was hoping for a rest as I quite enjoyably watched others explore the issue. Bill, don't you dare think I'm scooting around you. Very specifically it's your contrasting views that I appreciate most. Why the hell would -SWS want to have conversations with clones of -SWS? Makes no darn sense to me I tell you!

Kudos to what you guys do with topics and how you do it! Me thinks you'd never guess I'm such a big fan!

ozij wrote: -SWS: I was wondering who wrote the original manual, and in what language... found the SL3 manual in French - but nothing new in it.

Ooooh... That's a very good possibility IMO!

I never even thought about the possibility of an altogether important single-word point having been lost in the shuffle of cultural or language translation!