Resmed vs. Respironics - Help

[Snoredog]

So in the Chest bench test WHICH machine did they test?

The Autoset II Plus, Snoredog. that much is clear.

I get the impression that the Autoset II Plus is a quite different machine from either the Autoset Spirit or Autoset Vantage. Apparently, it is a lab machine which includes provisions for oximetry and thoracic measurements.

Regards,
Bill

No it sounds more like they tested them both, only the Autoset II produced the 5hz FOT. Oximetry comes from adding the optional Reslink module which can be added to either machine.

That bench test doesn't sound like a very level playing field was adhered to. Once again every time we see one of these so called "bench tests" it is biased towards Resmed seems they are allowed to bring in equipment not available in the US and add modules like the Reslink. As expected I bet they also came out on top in that comparison (and I haven't read the study). Last time we seen one of these it was found later they had actually funded the study.

[NightHawkeye]

Well, does anybody know exactly what the Autoset II Plus is? Whatever it is, apparently it's been around for a good part of the last decade as one of the references I found for it was dated 2002.

Regards,
Bill

[Snoredog]

Well, does anybody know exactly what the Autoset II Plus is? Whatever it is, apparently it's been around for a good part of the last decade as one of the references I found for it was dated 2002.

Regards,
Bill

Think it is only available outside the US and/or in Australia Bill.

Note: This abstract was also linked to the above bench test:

http://www.chestjournal.org/cgi/content/full/130/2/312

and it is only fair to point out:

Dr. Brown has received grant support from the ResMed Foundation and ResMed, Inc.

[rested gal]

I am getting a little confused with what you are saying and the graph Bill put up. Is EPAP pressure lower during early expiration and then rises towards the end of expiration? I see a downwards deflection followed by a rise towards the EPAP line.

The graph Bill put up was describing how a comfort feature called "Bi-Flex" works. Bi-Flex is a trademark name for a comfort feature included only in Respironics bi-level machines.

You are absolutely right, split -- after bi-flex does its "comfort thing" (dropping pressure a tad more at the beginning of the lower EPAP) bi-flex allows the regular EPAP to come back in BEFORE exhalation is finished...that rise towards the EPAP line you mentioned. Same way that C-flex in a Respironics cpap machine allows the regular cpap pressure to come back in BEFORE exhalation is finished.

A plain bi-level machine that does not have bi-flex would simply switch from IPAP to the "regular" EPAP, without giving that extra bit of drop at the beginning of EPAP.

If EPAP is set (as it should be) during a bilevel PSG titration in a sleep lab, EPAP will be set at enough pressure to keep the airway from collapsing completely with an obstructive apnea.

As I understand it, that's ALL that EPAP really has to do...prevent full obstructive apneas from happening.

If EPAP does THAT -- prevents full collapse of the airway -- then the person can START to inhale again. Starting to inhale triggers IPAP (higher pressure) to make the airway patent (open) for breathing in.

"Bi-Flex" (which doesn't mean "bi-level") is simply a feature Respironics uses to smooth the transitions between the two bi-level pressures (IPAP and EPAP.)

Bi-flex can be used at three degrees of "smoothing", or can be turned off.

A traditional bi-level setting for a rise time (time it takes for the machine to move up to delivering the FULL IPAP pressure when a person starts to breathe in again) can be used instead of the bi-flex feature.

One or the other (bi-flex or a rise time) can be used in a Respironics bi-level machine and in the BiPAP Auto (not talking about the BiPAP Auto SV.) Can't use both (bi-flex and a rise time) at the same time. It's either/or. Or, both can be turned off, in which case the BiPAP would operate like a plain bi-level machine using its default "rise time."

As far as what "Bi-Flex" does at the BEGINNING of EPAP (when a person STARTS to exhale) that icing on the cake extra bit of drop Bi-Flex gives to the start of exhaling is exactly like what C-flex does. Both Bi-Flex and C-Flex let the "regular" pressure come back in before exhalation is completely finished. That way the pressure needed to keep the airway open to allow an inhalation to get started is ALREADY in place.

The "regular" pressure needed to allow a person to START to inhale again is:

In a CPAP machine - the prescribed cpap pressure.

In a Bi-level machine - an EPAP set high enough to prevent obstructive apneas from the get go. That is not necessarily as high a pressure as the pressure that results from a CPAP titration.

The CPAP titration has to find a pressure which will prevent more than just obstructive apneas. The CPAP pressure needs to prevent partial closures too. The single CPAP pressure has to prevent everything from the partial collapses to the full collapse.

A bi-level (like the BiPAP) machine's EPAP has to be effective ONLY in preventing full obstructive apneas during and after exhalation. Events (flow limitations, hypopneas, and residual snores) that need MORE pressure than what it takes to prevent full collapse (obstructive apnea) are then handled by the higher IPAP.

I think of EPAP (the lower pressure) as keeping the airway "open enough" to ALLOW a person to START to draw in the next breath.

I think of IPAP (the higher pressure) as then taking care of keeping the airway "completely open" -- preventing all the partial closures, so that a person can inhale fully.

[split_city]

RG, as usual, you offered a different way of describing this than I've been using. Thank you for that. It completes the picture very nicely (at least how I think about it).

As I understand it, in a bilevel titration EPAP is set to prevent obstructive apneas, which can be eliminated at a lower pressure than the higher pressure required to eliminate hypopneas, flow limitations, and residual snores.
...
If the airway can be kept even partially open (by EPAP) during exhalation, at the end, and during the pause after exhalation is finished...then it is open "enough" to allow the person to start the next inhalation. And that's when the higher IPAP kicks in. Voila' -- a patent airway for full inhalation.

Voila indeed! The lower pressure used during expiration is insufficient to keep the airway open during inspiration. If pressure is not raised sufficiently as inspiration begins, then at some point collapse finally occurs.

This is the very shift I was getting at. Rather than collapse occurring during expiration, it would be shifted in time to inspiration. As the flow begins to increase during inspiration, at some point the airway finally collapses.

Hmm, I think it might be a bit more complicated than that. Even though the pressure during expiration is relatively "low," and if continued into inspiration, it is still well above the collapsing pressure of the airway. The airway collapses at about 2-3cmH20 in severe OSA patients. I assume that EPAP is well above this number, meaning that the airway would still fail to collapse during inspiration. You would likely have flow limitation/hypopneas but not apneas. CPAP/EPAP pressure would need to be close to this closing pressure for there to be a shift from an expiratory collapse to an inspiratory collapse.

For example, consider how an individual's apnea may progress. DSM has already commented about how his needs have changed over time. In the beginning phase of apnea perhaps, generally, airway collapse occurs during inhalation and only a slight pressure increase is needed to correct that.

This is probably a bit more complex then meets the eye. Unless the original pressure was close to closing pressure, I would predict there would be little change in the number of obstructive events following a small increase in pressure. I would have thought that small changes in pressure would primarily impact upon hypopneas. DSM's initial EPAP would likely be way above closing pressure, thus obstructions should not occur. It would be interesting to see what happened around the time of these residual obstructions, particularly if pressure was maintained at therapeutic levels.

As an individual's apnea gets worse over time then more pressure might be needed which would correspond with collapse occurring toward the end of the expiration phase. (Now, I'm not saying that apnea progresses like this in everyone. However, we know from what has been posted on this forum that pressure needs do change, often considerably, over time. Usually, not always, required pressure increases over time.)

Age certainly affects closing pressure.

Again, I would be interested to hear of the changes in apneas with small changes in pressure.

There certainly could be times during the night where closing pressure is much higher than 2-3cmH2O. A lot of factors determine the closing pressure such as activity of airway dilator muscle activity, posture, blood gases and lung volume.

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

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

[split_city]

RG: Thanks so much for that in depth post. You have certainly helped me understand how some of these machines work.

The problem with being physiological orientated is that I don't get much of a chance to look at the clinical side. It's threads like this which help me incorporate both sides

[-SWS]

Well, does anybody know exactly what the Autoset II Plus is? Whatever it is, apparently it's been around for a good part of the last decade as one of the references I found for it was dated 2002.

Regards,
Bill

Think it is only available outside the US and/or in Australia Bill.

I have long suspected that each CPAP company maintains a "secret weapon" in their respiratory arsenal---a secret weapon reserved only for virulent cases of SDB and, of course, press junkets.

So this must be Resmed's secret weapon. Eureka!

And what a tough balancing act this must be, to allow for medical press junkets while still managing to keep the corporate "secret weapon"... well, top secret!! How very clever!


.

[NightHawkeye]

The airway collapses at about 2-3cmH20 in severe OSA patients. I assume that EPAP is well above this number, meaning that the airway would still fail to collapse during inspiration.

Allow me to question this, split_city. Are you saying that complete obstructions simply don't occur when CPAP pressures are much above 2 cm to 3 cm?

[split_city]

The airway collapses at about 2-3cmH20 in severe OSA patients. I assume that EPAP is well above this number, meaning that the airway would still fail to collapse during inspiration.

Allow me to question this, split_city. Are you saying that complete obstructions simply don't occur when CPAP pressures are much above 2 cm to 3 cm?

No, not at all. However, the general consensus from several studies is that closing pressure is <5cmH20 in even the most severe OSA patients. Furthermore, this is generally classified as the passive collapsing pressure i.e. under no influence of dilator muscle activity. This pressure is lower i.e. closer to atmospheric pressure when dilator muscles are active.

There are certainly times where the airway collapses above this pressure. But the number of events would be much lower.

It can also go the other way. There are times in which a lower closing pressure or even -ve pressure for that matter is required to collapse the airway. For example, I had this patient who generally had a closing pressure of about 3cmH20. However, there was a couple of instances where his airway remained patent even when mask pressure reached -6cmH20. This was despite the fact that the patient was in the same sleep stage and he remained in the same posture.

[NightHawkeye]

... However, the general consensus from several studies is that closing pressure is <5cmH20 in even the most severe OSA patients. Furthermore, this is generally classified as the passive collapsing pressure i.e. under no influence of dilator muscle activity. This pressure is lower i.e. closer to atmospheric pressure when dilator muscles are active.

If what you're saying is true for the vast majority of apneas in all patients, then what possible benefit could be provided from FOT (or FOM for ResMed) when pressures are considerably higher than that? The benefit to FOT is to determine whether the airway is "open" or "closed" in order to distinguish between OSA and CSA.

I can easily believe what you're saying is true during the exhalation phase of respiration, but how true is it during inspiration?

Regards,
Bill

[split_city]

... However, the general consensus from several studies is that closing pressure is <5cmH20 in even the most severe OSA patients. Furthermore, this is generally classified as the passive collapsing pressure i.e. under no influence of dilator muscle activity. This pressure is lower i.e. closer to atmospheric pressure when dilator muscles are active.

If what you're saying is true for the vast majority of apneas in all patients, then what possible benefit could be provided from FOT (or FOM for ResMed) when pressures are considerably higher than that? The benefit to FOT is to determine whether the airway is "open" or "closed" in order to distinguish between OSA and CSA.

I can easily believe what you're saying is true during the exhalation phase of respiration, but how true is it during inspiration?

Regards,
Bill

FOT would likely be useful during suboptimal therapy. But I would predict that once pressure was well above closing pressure, FOT would become redundant as the airway *should* remain patent for most of the time. Nonetheless, FOT would still be useful for distinguishing between residual events.

But here is an alternative for distinguishing obstructive events from central events:

Distinguishing Central Sleep Apnea from Obstructive Sleep Apnea with Esophageal Diaphragm EMG, [Publication Page: A579]

J. Tang, M.B., C. Jolley, M.D., H.D. Wu, M.B., Z.H. Qiu, M.B., J. Steier, M.D., J. Moxham, M.D., M.I. Polkey, DR., Y.M. Luo, DR., N.S. Zhong, M.D., Guangzhou, Guangdong, China, London, England

It is clinically and scientifically important to distinguish central sleep apnea from obstructive sleep apnea because different types of apneas require different treatment. Diagnosis of the type of apnea requires recording respiratory effort during overnight polysomnography. Chest-abdominal wall motion is usually taken as a measure of respiratory effort for clinical diagnostic purposes. However, respiratory effort can often not be reliably assessed by this method because chest-abdominal wall motion can be influenced by lung volume and body position, leading to an overestimation of the frequency of central apneas. We hypothesised that more central apneas would be diagnosed by quantifying changes in chest-abdominal wall motion than would be diagnosed using diaphragm electromyogram (EMGdi). Nine patients with central apnea were studied. An esophageal catheter with ten metal coils was used to continually record EMGdi during full overnight polysomnography. All subjects tolerated the electrode catheter and achieved a sleep time of (meanSD) 407+/-108 minutes. Significantly more central apneas were diagnosed by chest-abdominal wall motion (11+/-6/hour) than were diagnosed using EMGdi (7+/-5/hour)(P<0.01). We conclude that the frequency of central apneas may be overestimated if the diagnosis is dependent on observations of chest-abdominal wall motion. Recording EMGdi using an esophageal electrode is a useful alternative method for the accurate diagnosis of central sleep apnea.

I'm sure you would be all happy to have a nasal catheter inserted

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CPAPopedia Keywords Contained In This Post (Click For Definition): resmed, CSA

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CPAPopedia Keywords Contained In This Post (Click For Definition): resmed, CSA

[NightHawkeye]

FOT would likely be useful during suboptimal therapy. But I would predict that once pressure was well above closing pressure, FOT would become redundant as the airway *should* remain patent for most of the time. Nonetheless, FOT would still be useful for distinguishing residual events.

And yet, it is at higher pressures where FOT is employed to determine whether the airway is "open" or "closed", specifically to distinguish between OSA and CSA in order to limit exposure to even higher pressures if the airway is already "open" (meaning CSA).

[rested gal]

Distinguishing Central Sleep Apnea from Obstructive Sleep Apnea with Esophageal Diaphragm EMG, [Publication Page: A579]

It may not matter, but wonder what they were using to measure the patients' airflow in the PSG hookups during that study? Thermistor? Pressure transducer? Both?

I'm sure you would be all happy to have a nasal catheter inserted

heheh, yeahhhhh, riiiiight.

Bet there are a few people you'd like to use that on!!

A post in 2004 on a board many sleep techs frequent:

One of the techs asked:
Several years ago it seemed like esophageal pressure monitoring (Pes) was becoming a standard in polysomnography. I haven't heard much about it lately. Are many centers/labs still using Pes or is this invasive procedure fading out?


Among the replies by other techs was this:
In the center I ran there was a physician who wanted to do this. He did not know, could not tell me, what the normal values would be so, he decided he would wer one and be monitored all night to establish a baseline. He showed the technologist how to place the catheter, on me. Then the technologist nervously placed it on him. He had it in for about 15 seconds, tossed his cookies then exclaimed he would never put a patient through that.

[dsm]

RG

Loved that last sentance in the last para

DSM

[rested gal]

RG

Loved that last sentance in the last para

DSM

LOL!! I did, too.