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This post is to see if we can establish some accepted 'facts' re cpap therapy and how the therapy is applied


1) That originally the CPAP machine was designed to splint the airway open so as to prevent 'airway occlusions' from occurring. These occlusions primarily cause SpO2 desaturation and a range of other and further complications. Also that the original OSA cpap therapy approach of splinting the airway was to overcome occlusions brought on by the collapse of the airway due to lung pressure creating a vacuum that locks the airway shut at the neck and throat area and depending on the exact physiology of the sleeper.

2) That when the airway is occluded, the only way to clear it is for the sleeper's built in safety mechanism to kick in and arouse the sleeper who can changes position and/or exert additional muscular effort to clear their airway.

3) Splinting the airway is the titration approach to preventing basic occlusions - any higher pressure is used to reduce the effect of flow limitations in all their forms. Too high a pressure over the basic splinting pressure can induce central apnea in some people.

4) Apaps were introduced as a way to try and detect patterns of OSA events including both occlusions and flow-limitations and to adjust the therapy (pressure) to better reduce/eliminate events that occur above the original titration pressure. In effect they attempt to adjust for the changing environments of the sleeper (position, health, fitness, effects of medication/alcohol, etc:).

5) Central apneas are a complication that required considerable caution on the part of the apap designers as it is totally counter productive to increase pressure when a central apnea is in effect. Also Apaps must be careful not to induce centrals by raising the pressure too high when an OSA event pattern fails to return the sleeper to normal breathing.
Also the apap machine has limited evidence as to what is causing a cessation of airflow. One very helpful bit of evidence would be if the apap could be fed data indicating breathing effort vs actual airflow it is monitoring, but that added data input can usually only be obtained in sleep clinic studies). The best the apap has is snoring signals which are sound evidence of OSA events looming.

6) Also, increasing pressure in the presence of an airway occlusion will not clear that occlusion but is merely a reactive process triggered by the block in anticipation of preempting subsequent occlusions.

7) Bilevels go a step further than standard cpap therapy in that they can be set up with a timed mode that is used to apply therapy to irregular breathing and to try to restart breathing in the presence of a central. The centrals are dealt with by applying a cycling between two pressures (epap & ipap) in the expectation this will trigger the user to breathe again.


Now if any of these points are still in dispute then we are still well into the debate

#2 tidied up & clarified some points
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CPAPopedia Keywords Contained In This Post (Click For Definition): cpap machine, Titration, CPAP, APAP

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

dsm wrote:This post is to see if we can establish some accepted 'facts' re cpap therapy and how the therapy is applied


1) That originally the CPAP machine was designed to splint the airway open so as to prevent 'airway occlusions' from occurring. These occlusions primarily cause SpO2 desaturation and a range of other and further complications. Also that the original OSA cpap therapy approach of splinting the airway was to overcome occlusions brought on by the collapse of the airway due to lung pressure creating a vacuum that locks the airway shut at the neck and throat area and depending on the exact physiology of the sleeper.

2) That when the airway is occluded, the only way to clear it is for the sleeper's built in safety mechanism to kick in and arouse the sleeper who can changes position and/or exert additional muscular effort to clear their airway.

3) Splinting the airway is the titration approach to preventing basic occlusions - any higher pressure is used to reduce the effect of flow limitations in all their forms. Too high a pressure over the basic splinting pressure can induce central apnea in some people.

4) Apaps were introduced as a way to try and detect patterns of OSA events including both occlusions and flow-limitations and to adjust the therapy (pressure) to better reduce/eliminate events that occur above the original titration pressure. In effect they attempt to adjust for the changing environments of the sleeper (position, health, fitness, effects of medication/alcohol, etc:).

5) Central apneas are a complication that required considerable caution on the part of the apap designers as it is totally counter productive to increase pressure when a central apnea is in effect. Also the apap machine has limited evidence as to what is causing a cessation of airflow. One very helpful bit of evidence would be if the apap could be fed data indicating breathing effort vs actual airflow it is monitoring, but that added data input can usually only be obtained in sleep clinic studies). The best the apap has is snoring signals which are sound evidence of OSA events looming.

6) Also, increasing pressure in the presence of an airway occlusion will not clear that occlusion but is merely a reactive process triggered by the block in anticipation of preempting subsequent occlusions.

7) Bilevels go a step further than standard cpap therapy in that they can be set up with a timed mode that is used to apply therapy to irregular breathing and to try to restart breathing in the presence of a central. The centrals are dealt with by applying a cycling between to pressures (epap & ipap) in the expectation this will trigger the user to breathe again


Now if any of these points are still in dispute then we are still well into the debate

#2 tidied up & clarified some points
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I have no problem with what you've written, Doug, except #2.

I think what you described in #2 is the way an obstructive apnea is most often resolved -- through enough arousal on the part of the sleeper (even the xpap-using sleeper) to open the airway enough to breathe in at least a little air again.

My problem with your #2 is the word "only." I don't think an arousal or change in position is necessarily the only way an obstructive apnea might be cleared by a person using xpap. "x" standing for any type of cpap machine...cpap, autopap, bilevel.

I don't think it is necessarily always that simple when you consider that there are a lot more dynamics involved in the anatomy of the mouth, tongue, throat and airway. Soft tissue, muscles, tendons, nerves, etc.

Where the REMstar Auto is involved, I think its entirely possible that some -- (some, not all, not even the majority -- some obstructive apneas in some people, may very well be "opened" at least somewhat -- (somewhat, not fully) by the first rise in pressure the machine uses when it goes into the NRAH routine.

But I can imagine that ("that" being...opening somewhat) happening only IF the minimum pressure is already set high enough to be where it takes very little additional pressure to move some soft tissue aside, breeching the full closure, and allowing the sleeper to get at least a little air through. The "effort" on the part of the obstructed airway sleeper might then open things even a bit more. Dunno.

In all the discussion about what autopap designers might have been thinking, I also wonder about this... the designers probably expected their autopaps to be used for the most part (not exclusively, but mostly) for temporary auto-titration purposes. If so, they probably also expected the autopaps to be left set at 4 - 20 in most (not all..."most") cases.

Interesting ... this "sleep" and "cpap treatment" stuff.

My edit: Apparently when I quoted your post, it was before one of your edits. Not sure what you changed before I saw it...there was only one edit at the time I quoted you. At any rate, your point #2 that I was looking at seems to be the same as it was.

Toward earnestly exploring this theory, I'm perfectly willing to assume that Doug's second statement is true. I'm not sure this theory is hindered or helped by discerning that fact either way, but I could be wrong. If that second point is germane to the theory then let's work that point. If it's not germane to developing the theory, then I propose not sidetracking the theory by splitting hairs.

Also, I always tend to think of partial occlusions versus full occlusions (whether right or wrong regarding semantics). I tend to think that way because it is my understanding that you can score plenty of residual obstructive apneas with the airway just slightly open. Is that statement off base?

Also, earlier Bill said the term he had in mind for this situation is "obstructive apnea". Toward building this theory, does anyone think it's useful to come up with more distinguishing terms? Is it at all useful to attempt to devise distinguishing terms such as "untreated apnea", "residual apnea", "persistent apnea", "extremely persistent apnea"? Or is that type of distinction merely a waste of time for the way you envision this theory progressing?

Let us build and question as we go along to see just how far we can support this theory. I would strongly prefer to have Bill and Doug lead this theory, with both of them knowing that I am not here to arbitrarily tear that theory down.

-SWS wrote:Also, I always tend to think of partial occlusions versus full occlusions (whether right or wrong regarding semantics). I tend to think that way because it is my understanding that you can score plenty of residual obstructive apneas with the airway just slightly open. Is that statement off base?

That's my understanding, too. And not only pertaining to our machines' scoring. As far as I know, it doesn't have to be a total 100% cessation of airflow in a PSG sleep study either, to score as an obstructive apnea.

-SWS wrote:I would strongly prefer to have Bill and Doug lead this theory, with both of them knowing that I am not here to arbitrarily tear that theory down.

A correction if I may:

-SWS really shoulda wrote:I would strongly prefer to have Bill and Doug lead this theory, with both of them knowing that I am here to support the building of that theory.

There's a big difference between those two statements and it is really that second statement I am after.

It would be extremely helpful, at least to me, if a theory statement were available. However, if that's not the way you would like to build or progress with your ideas, then please don't work that way on my account. If you get to the point where your preference is to build a theory statement, then it helps me know if the theory relates to apnea only, or if the theory still relates to both apnea and CPAP. But again, if you don't work best with a theory statement up front, then I suggest postponing that part as you freely build ideas. Whatever structure or lack of structure seems best.

dsm wrote:This post is to see if we can establish some accepted 'facts' re cpap therapy and how the therapy is applied

rested gal wrote:I have no problem with what you've written, Doug, except #2.

-SWS wrote:Let us build and question as we go along to see just how far we can support this theory.

This is a welcome and entirely surprising development. Thank you for taking the initiative, Doug. It looks good at first glance to me, although I'd like to review it in more detail later, and encourage all attempts at clarification.

Regards,
Bill

[quote="Wulfman"]xyz,

You only see those events (NR & FL and a few different charts/reports) from a machine that's capable of being set to Auto mode and when it IS set to Auto mode.

Den

Points 2 & 6 are somewhat related.

RG has raised #2 as the point to debate (and I agree it is one area where we don't have clarity yet).

SWS has pointed out that occlusions can be considered full and partial. This poses the qustion when is a block not a block ? (when it is a partial block ?).

Harking back to a point I keep raising is the issue of vacuum induced occlusions & me hammering the question of what is an occlusion if it is not vacuum induced ? - as said before a central is not an occlusion & neither is a flow-limitation/hypopnea.

I accept SWS's point that a partial occlusion can be said to exist but where is the dividing line between a partial occlusion and a severe hypopnea ?.

The heart of this question is does the designer of an Auto CPAP machine believe he can clear someone's full occlusion by raising pressure or is his real goal to use the current 1st & 2nd occlusion pair (put hypops aside for a min just here) as the 'trigger' to raise pressure to address future (iminent) OSA events (be they full or partial occlusions).

The point I believe I can make here is that not even an SV machine can clear a full occlusion - they are primarily designed so that the titration EEP or epap, will address full occlusions while the varying PS (pressure support - PSmin & PS max) are used as a device to shift the sleepers breathing rate & minute ventilation *but* the gap between EEP & epap and the lower PS setting (PSmin) add extra splinting on the inhale cycle but exhale drops to that titration pressure that is the primary mechanism for splinting the airway open as much as it can be.

RG & I have discussed the issue of OSA events that occur on exhale vs on or during inhale & we probably haven't explored the idea to its fullest extent as I strongly suspect there are two groups of OSA patients, those who aren't subject to exhale occlusions & those that readily are.

I am very happy to explore the two aspects raised above as while I have some thoughts on them, I don't have clear answers.

DSM

rested gal wrote:
<snip>
My problem with your #2 is the word "only." I don't think an arousal or change in position is necessarily the only way an obstructive apnea might be cleared by a person using xpap. "x" standing for any type of cpap machine...cpap, autopap, bilevel.

I don't think it is necessarily always that simple when you consider that there are a lot more dynamics involved in the anatomy of the mouth, tongue, throat and airway. Soft tissue, muscles, tendons, nerves, etc.

<snip>

RG

Fair comment - this point brings us back to the dynamics of the block.

If the lungs are creating a vacuum & that is pulling the throat / back of tongue in to form a plug, then I am not sure I can see that adding any pressure above the block will do any more than reinforce the block, unless the pressure applied is so much greater than the vacuum that it can breech the block by forcing a path around the obstructing material (remeber the vacuum is still trying to suck the blocking material into the airway).

As SWS has continually reminded us, the throat & airway are elastic & if we accept there is this vacuum below the block & it is greater than the pressure above the block then a greater suction will always win and pull more of the blocking material into any attempted expansion created by the small increase in pressure. On the other had, why try, let this one pass naturally & try to catch the next one. In the broadest sense once an occlusion has taken place the damage is done as far as that one occlusion is concerned, I suspect that trying to clear an individual occlusion will do more harm than good but this is still just my opinion & not backed up with any published data.

But on one plane, perhaps for some people the added pressure is greater than the lung vacuum & I guess you will be right to believe that pressure can clear an occlusion. But I have to admit I don't know enough about the pressures involved to know if one pressure (vacuum vs CMS) has any hope at overcoming the other.

DSM

rested gal wrote: <snip>
In all the discussion about what autopap designers might have been thinking, I also wonder about this... the designers probably expected their autopaps to be used for the most part (not exclusively, but mostly) for temporary auto-titration purposes. If so, they probably also expected the autopaps to be left set at 4 - 20 in most (not all..."most") cases.

Interesting ... this "sleep" and "cpap treatment" stuff.

<snip>

RG
Quite a while back I did find a Respironics patent that stated the intent of the invention was to introduce improved therapy by adjusting the pressure to adapt to changing conditions. There was not any mention in that patent of just using the machine for lab or home titrations.

I am certain I posted a link to the patent but would have to go digging back over 6+ months to locate the post.

I am sure the others who recently posted from patents can look at the statement of intent at the start of the patent to see what the goal is said to be. I think it will be that the device is to provide improved therapy.

DSM

Excellent summary by DSM.

An apnea, accoring to Respironics is an 80% reduction in flow (or worse). So clearly, not all breathing events defined - and identified - as apneas by Respironics (ditto for other comapnies) are full obstructions.

When a person is unconcious (and I mean unconcious, not "asleep") the fist thing you have to do is make sure they are not choked by swallowing their tongue - you roll them to their side, pull their tounge, and even pin it to their cheek with a safety pin to make sure it doesn't slip back in.
So yes, as far as physics goes, the tongue can create a total - and life endagering blockage.

You, know, Respironics' statement

When the device encounters a non-responsive apnea or hypopnea, it will decrease pressure by 2 cmH2O and hold the pressure for 15 minutes

is actually quite misleading, and I agree with snoredog: they are changing a bug into a feature. There have be 8 pressure induced events occuring in a row, before Respironic's has a "whoa there" response. No wonder auotomode, or at least Respironics' automode is no good for some people. Makes you wonder how Liam would have done on a PB...

I'd like to add something to Doug's point no. 6:
When you read the companies' reasons for creating APAPs, I think they honestly believed their pattern detection algorithms would enable event preemption that would let a person spend more time at a lower than prescribed fixed pressure.

A further comment about algorithms:
PB's algorithm, as I've recently discovered, is based on the assumption that once you have prescribed pressure, you add this information to the machine's auto mode, and give the machine leeway to go up and down. Fruthermore, on PB the prescribed pressure is not what you're supposed to set up as the minimum pressure. The Rxed pressure is to be set up as the initial pressure, and then a lower nubmer (Respironics' Pcrit) is set up as the minimum. The machine will go down from the initial (Rxed, 90% pressure) only after spending some time there.

It would be very interesting to find out how using a PB like that effects people's sleep quality and results.

It seems very good for me - but I've also made humidification changes recently, so I don't know for sure yet which has effected my results.

Biil, what is your PB set up at present?

I have learned a lot a on this thread Thanks everyone!
O.

Edit: I started composing this before DSM's two recent posts... the "improved therapy" aim is in both the patents, and PR blurbs.
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CPAPopedia Keywords Contained In This Post (Click For Definition): respironics, Liam, Hypopnea, auto

-SWS wrote:Toward earnestly exploring this theory, I'm perfectly willing to assume that Doug's second statement is true. I'm not sure this theory is hindered or helped by discerning that fact either way, but I could be wrong. If that second point is germane to the theory then let's work that point. If it's not germane to developing the theory, then I propose not sidetracking the theory by splitting hairs.

Also, I always tend to think of partial occlusions versus full occlusions (whether right or wrong regarding semantics). I tend to think that way because it is my understanding that you can score plenty of residual obstructive apneas with the airway just slightly open. Is that statement off base?

Also, earlier Bill said the term he had in mind for this situation is "obstructive apnea". Toward building this theory, does anyone think it's useful to come up with more distinguishing terms? Is it at all useful to attempt to devise distinguishing terms such as "untreated apnea", "residual apnea", "persistent apnea", "extremely persistent apnea"? Or is that type of distinction merely a waste of time for the way you envision this theory progressing?

Let us build and question as we go along to see just how far we can support this theory. I would strongly prefer to have Bill and Doug lead this theory, with both of them knowing that I am not here to arbitrarily tear that theory down.

Don't quiet understand your meaning here, but since you placed a ? at the end, it is my understanding that apnea (that latin word) means complete cessation of breath, we know the machine (thinks like you do) and uses criteria of partial occlusion and/or short of cessation to determine the event (if that was the jist of your statement meaning i.e. machine may use 80% reduction in flow to flag it an apnea).

But how can you have a "residual" apnea?

I would see and call that inadequate therapy, but I would agree and call a Hypopnea or FL or even snore a "residual event" with those falling in line with your thinking on partial occlusion.

When I look at someone's report, I first look at the worst offender of oxygen levels that being apnea, if they exist not high enough pressure used, if they persist and/or don't go away I highly suspect they are central in origin,

then I suggest they pull out their PSG and look for CA's or MA's denoted on that report. But it seems reporting of CA's on PSG's seem to be subjective on the part of the PSG tech/scorer because many times they have NO CA's denoted on the first PSG but when the patient mentions them they suddenly appear on their 2nd or 3rd PSG (especially if the patient has mentioned those to the tech prior to the study, its akin to the tech saying he/she mentioned centrals, I better pay better attention and score those if seen).

Once the apnea has been addressed with adequate pressure, I look at those "residual" events such as snore, hypopnea and FL and continue with pressure until they dissipate. It seems to me if AI is higher than 1.5 on these autopaps you haven't gone far enough in addressing them, you have to get below AI=1.0 before those "residual" events begin to fall (my experience anyway).

Only curve in that as mentioned is if I suspect the machine is not correctly scoring those events and confusing them for something else as in the case of that NRAH.

My thought process is the machine is LESS accurate in differentiating those residual events like hypopnea and Fl, snore is easy to spot even by the machine. If a machine cannot score a snore accurately you might as well toss it out the window.

But exactly what do you mean by residual apnea?

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.

SWS has raised the issue of just how many OSA events are full vs partial & it is a very good point.

The more I think about the issue of occlusions being cleared by pressure, the more it seems to me it would be very very helpful to have input from someone like SAG who may be able to give us some meaningful stats on the actual number of full occlusions someone exhibits in his lab who is being evaluated for OSA and clearly has OSA (say 40+ AHI).

If the % of full occlusions is tiny then the debate may be bigger than the importance of it. But, if SAG's data were to show that full occlusions are a significant % of an evaluation study, then the debate has legs.

DSM

#2 I guess it would then be good to know what % of occlusions are full vs partial once a PSG study is complete & a titration pressure is set.

I believe I have full occlusions quite often when I sleep on my back (my wife certainly seems to think so ). Also when we have done a bit of partying involving above average food & drink, am sure the full occlusion % goes up. Nightly data when I can get it (PB330 doesn't provide it - my travel S8 Vantage does) tends to show higher AIs when I party & also when I lower the CMS setting esp if I drop it below the magical 10 CMS.

As a habit I will often bump up CMS (ipap & epap) by 1 CMS point for both, if we had a particularly indulgent dinner party (we Aussies are a great partying community - love our wine/beer & enjoy our food )

DSM

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

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

ozij wrote:........ the fist thing you have to do is make sure they are not choked by swallowing their tongue - you roll them to their side, pull their tounge, and even pin it to their cheek with a safety pin to make sure it doesn't slip back in.
........

Idea! That is one I haven't tried yet! Seems so simple. Tonight is Saturday night - can sleep in tomorrow. So maybe give it a try?