Why doesn't APAP respond to apneas?

[-SWS]

attitude: alternates between being mischievous and making long-winded, often-misguided, attempts at being helpful.

I have a slight bifurcation problem, I guess.

Attributable to an underlying chaos susceptibility... And a great wit!

[StillAnotherGuest]

I was on 10 mg of Lexapro for both tests

OK, that's a far better explanation for the absence of REM in the Split Study and the severely-reduced REM in titration. Which now begs the question, "What is the effective pressure for REM?", since pressure looks to be up to 20/18 and 20 cmH2O flat at that point and there's still events. And now, it's probably safe to say, you have normal REM.

While the overall quantity of SWS in the Split Study should turn out to be normal (the 51 minutes in Pre-Treatment portion plus that block in Post-Treatment over a Total Sleep Time of 338.0 minutes), the Titration Study with 168.5 minutes would almost certainly qualify as a Rebound.

Which also begs questions, like "Rebound from what?", "Is that really SWS?" and "Is a lot of this artifact from disturbed sleep (the list of things you mentioned before, plus the added benefit of Lexapro destroying your architecture)?"

Is there a Position Graph somewhere? You've got that good block of stable everything at 0130 in Titration Study that would be important to know how/why that occurred.

SAG

[dsm]

Bev, absolutely no hard feelings between Doug and myself. He accepts me for the argumentative SOB that I can be at times, and that's the sign of an extraordinary friend. But now that I think about it... I accept his tendencies to debate points as well.

It took me months and threats to get a copy of my prescription and study. I really don't think they are going to give me any more info.

I certainly won't push the point. But if you think you may be inclined to at least try for that data, you could truthfully say that the manager of a sleep lab has kindly offered his assistance. I believe that we are all legally entitled to our medical records to solicit second or third opinions.

I would prefer to be using a lower pressure if I could get good therapy with it.

In that case you might want to start with that lower 9 or 10 EPAP and evaluate results. Then tweak up if you need to. If you decide to start with a higher 14 EPAP, then experimentally tweak down and evaluate data results as well as comfort. Metaphorically you can begin digging a tunnel from either end, and still yield the same end result.

Bev,

SWS & I respect each other too much to allow real conflict to get a hold here this is just banter - as you observed keeps us both on our toes
(maybe there are times when one or the other of us needs to bump up our CMs by a point or two )

Cheers Doug

PS I had gone looking for the part of your report that would have said titration = xx CMs but never found it and from other info I got from you just wasn't prepared to believe you needed an epap of 14. for example at my last titration in 2007 it was agreed with my sleep doc to be 13 CMs (CPAP mode) but I set epap to 10 & ipap 13 on the machine I had back then (PB330) and that worked well, The only reason I run my current machine 1 point higher for both ipap & epap is that the PB330 had a proximal sensing line & I almost always find (using a dial manometer) that machines without a proximal sensing line are 1 CM lower at the mask that what the LCD panels say the pressure is.

PPS Both SWS & I will let SAG trump us with his real world sleep lab experience - plus that he is an analytical thinker in too boot.

D

[Snoredog]

I was on 10 mg of Lexapro for both tests

OK, that's a far better explanation for the absence of REM in the Split Study and the severely-reduced REM in titration. Which now begs the question, "What is the effective pressure for REM?", since pressure looks to be up to 20/18 and 20 cmH2O flat at that point and there's still events. And now, it's probably safe to say, you have normal REM.

While the overall quantity of SWS in the Split Study should turn out to be normal (the 51 minutes in Pre-Treatment portion plus that block in Post-Treatment over a Total Sleep Time of 338.0 minutes), the Titration Study with 168.5 minutes would almost certainly qualify as a Rebound.

Which also begs questions, like "Rebound from what?", "Is that really SWS?" and "Is a lot of this artifact from disturbed sleep (the list of things you mentioned before, plus the added benefit of Lexapro destroying your architecture)?"

Is there a Position Graph somewhere? You've got that good block of stable everything at 0130 in Titration Study that would be important to know how/why that occurred.

SAG

SAG: the graphs you are looking for I think are on page 7 of this thread

Interesting, I thought she might be having a REM problem in the first few posts of this thread, what you indicate makes sense. I think Bev tried melatonin once (known to promote REM) and if not mistaken she dropped it after it left her with vivid dreams (not that those are even bad in my opinion, I think any kind of REM is good).

The periods of SWS also make sense in explaining why she sleeps for such long periods, some are over 10 hr sessions. That would indicate to me of the sleep she does get, it is not very good quality sleep. All that SWS sleep may also explain why she feels so fatigued during the day.

Maybe if she was experiencing 30-40 spontaneous arousals per hour I would think UARS, but I didn't see that on her PSG's, maybe I missed it but I didn't see any RERA score either. Some are inclined to suggest that I think from the daytime fatigue. If she does have muscle-skeletal pains that could contribute to those micro arousals.

Ideally, she needs to go into a lab with the SV with someone who knows what they are doing and titrate her correctly on the SV, if she has UARS that could be corrected. But it appears at this point her doctor has dinked her around so much he has exhausted her medical coverage for PSG's.

[-SWS]

OK, and what about you, -SWS who never needed IFL1 turned off: is that a baquet hall or a dancing hall on your chart?

Bookmark placed... I need to find my old data amidst an assortment of hard drives and computers.

That bookmark was placed in response to this post: viewtopic.php?f=1&t=35298&st=0&sk=t&sd= ... 75#p303444
Well, I'm starting to think I may have accidentally deleted my old data. But I believe the gist of my experience with those two machines went like this: 1) while using the 420e: some nights I experienced next to no scored FL and other nights there were significant but lightly scattered FL---never enough to cause pressure runaway or warrant turning IFL1 off, and 2) while using both tank generations of RemStar Auto: some nights I had pressure chairs and other nights I didn't----but I think the height or amplitude of my pressure chairs were of fairly low pressure amplitudes when they did occur.

One "apnea fried" memory disclaimer rightly issued, though.


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Snoredog, great points. I'll place another bookmark here...

That bookmark placed in response to this post: viewtopic.php?f=1&t=35298&st=0&sk=t&sd= ... 75#p303499
I think this big discussion eventually entertained additional points relevant to that bookmarked post. At this point, my own thoughts are probably summarized in response to this great rhetorical question and follow-up comment from Snoredog:

If they couldn't find her optimal pressure in the lab, what makes you think the Adapt SV will find it?

In response to that first question (and the comments leading up to it) I'm still thinking the PSG pressure data is ridden with problems that make it difficult to select an optimal pressure. Bev having spent only 13.5 minutes at 9 cm was only one of many concerns with using the data on that chart. By contrast Bev's 14 to 17 cm pressure range occurred after many nights of measurement by both Encore Pro and Bev. So that's the basis by which I give credibility to 14 cm. But you are correct: the ASV won't automatically find Bev's new optimum pressure for obstructions, but Bev can use Encore Pro along with trial and error in the same manner to ascertain what's best for her. Besides, she's got the peanut gallery warriors to help.

She is still going to need enough EPAP pressure to keep her obstructive events in check.

Agreed. Again, that's the basis for starting EPAP with her best prior home-based titration IMO. And that's the basis for Respironics recommending that a previous CPAP or fixed BiLevel titration will suffice as opposed to a dedicated but preferred autoSV titration. The AutoSV endeavors to automatically find Bev's best pressure, on a breath-by-breath basis, for outstanding central dysregulation. However, the obstructive component must be manually factored into that machine's IPAP min and especially EPAP settings. IMO the best counter point raised later on (by you) was that maybe some of those presumed obstructive events were actually central. So once again, therein lies the purpose of methodical trial-and-error with the aid of Encore Pro.


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I would like to see us discuss Inspiration Time and how that might change ones breathing to a particular scenario. Respironics keeps resorting to 1.2 seconds when it sees a problem, I wonder why they choose that value? With the range of that setting seems it could vary quite a bit.

Well, unfortunately I didn't turn up much by the way of Google. But two general characteristics of inspiration time have to do with either achieving a certain tidal volume, a certain I:E ratio, or both.

In certain cases of COPD, for instance, clinicians might try to achieve more expiratory time by influencing the I:E ratio. To accomplish that they need to factor BPM and IT together. BPM yields the total time spent in I + E. Of that total time spent in I + E, a set inspiratory time (IT) will drive the ratio of how much time is spent in each. The IT setting will specifically account for time spent in inspiration; and almost all of the remaining time will be allotted for expiration (there are also slight intervening pauses between respiratory phases only slightly contributing toward that total remaining respiratory time).

Alternately, IT can be used to help with central dysregulation since IT directly helps regulate the amount of inspired O2---while indirectly regulating the rate of expired CO2 (via expiratory time implicitly defaulted or remaining by employing the IT and BPM parameters). A shorter IT or inspiratory time period amounts to less O2 volume inspired, which can supposedly help with periodic breathing. Again, if IT is employed toward I:E ratio-adjustment (by also utilizing the BPM parameter), a clinician can even influence CO2 expiration rates via the time allotted for the expiratory phase relative to inspired volume. However, that's not the same as directly influencing CO2 retention via additional appropriate methods.

So when the autoSV titration guide says "Set Fixed Rate to a minimum of 10 BPM... Start I time: 1.2 seconds" we can at least see how those 10 BPM and 1.2 second IT parameters play against each other ratio-wise: here the I:E ratio would be 1.2 sec to 4.8 sec (which can be numerically reduced to an I:E ratio of 1:4). However, that "minimum of 10 BPM" recommendation tells us that the starting ratio might favor a somewhat smaller E number. Regardless, if we compare that against a default setting of 1:1 or say an acceptable spontaneous 1:2 ratio, we can see that Respironcics implies that central apneas can be countered, at least in part, with comparatively shorter inspiratory volumes and times.

However, also bear in mind that the AutoSV's BPM setting is only a backup setting, and that faster spontaneous breathing rates by the patient will diminish time spent in E while still holding the above 1.2 second inspiratory time constant. Recall that BPM is typically set at the patient's spontaneous rate minus 2. Here setting BPM rate much closer to a machine-affected or influenced spontaneous rate can allow the clinician to additionally impose tighter control over time spent in E. Allowing for BPM as a non-salient backup rate (as opposed to either tightly enforced or purely timed mode scenarios), the above spontaneous I:E ratios can thus be more accurately estimated during periods that are free of central dysregulation by also including that BPM offset of 2 into the above ratio calculations. Easier yet: just calculate that I:E scenario of a non-salient backup rate using the patient's measured spontaneous BPM, rather than employing machine backup rate along with spontaneous offset.

[-SWS]

Well, the above is pretty much a "numerical exploration" of how the inspiratory time (IT) parameter can interact with BPM to affect an I:E ratio. It's also an acknowledgment that in general, shorter IT volumes and times can help, at least in part, to counter certain types of central dysregulation. But the above still doesn't answer Snoredog's solid rhetorical question of why an IT of 1.2 seconds keeps cropping up again and again in literature.

Respironics keeps resorting to 1.2 seconds when it sees a problem, I wonder why they choose that value? With the range of that setting seems it could vary quite a bit.

Snoredog, while I'm pretty confident that the "numerical explorations" I have above are fairly sound, the remaining part of what I have to say about that IT setting of 1.2 seconds is just an educated guess. I think the significance of that 1.2 second suggestion may be driven by two factors: 1) significantly decreasing inspiratory time is often a viable method of countering central dysregulation, and 2) going below 1.2 seconds simply doesn't allow enough time for proper airway inflation or ventilation.

Recall that in the case of central dysregulation, BiLevel is ventilating the airway (for CSA, PBR, etc.) rather than stenting an obstruction (for OSA). As inspiratory pressure (IPAP) is applied to that human airway, the pressure gradient of airway inflation occurs gradually rather than instantly. Think of the gradual (rather than instant) pressure-related process of blowing up an air mattress. Or better yet, think of one of those party favors that somewhat gradually unfurls as you blow through it.

I'm thus guessing that the human airway typically receives inadequate inflationary time when IT is allowed to go below 1.2 seconds. In summary, I think that Respironics recommendation just may boil down to: "Decreasing inspiration time to cope with central dysregulation, but decreasing to no less than 1.2 seconds since adequate inflationary time is still necessary". Just my best guess, though.

[dsm]

SWS,

Surely a factor that has to be considered along with this Insp 1.2 (& thus Inh to exh ratio) is the risetime as I imagine the INSP time combined with the risetime and an individual's typical pattern of how they breathe (the ratio), will all combine to vary the results achieved (tidal flow).

Just thinking out loud

DSm

[-SWS]

Absolutely agree, Doug. The shorter the IT time period employed to counter central dysregulation, the shorter the rise time needs to be as well. That's why Respironics has rise time suggested at only 2 or 3 as opposed to say 4 or 5.

As a side note, shorter rise times also account for less neuromuscular work of breathing (WOB) for the patient. That tends to be a consideration in neuromuscular disorders, COPD, etc. Shorter rise times are also theorized in sleep medicine to give vagal afferent receptors a more efficient CNS related patterning effect for certain etiologies as well.

[dsm]

Absolutely agree, Doug. The shorter the IT time period employed to counter central dysregulation, the shorter the rise time needs to be as well. That's why Respironics has rise time suggested at only 2 or 3 as opposed to say 4 or 5.

As a side note, shorter rise times also account for less neuromuscular work of breathing (WOB) for the patient. That tends to be a consideration in neuromuscular disorders, COPD, etc. Shorter rise times are also theorized in sleep medicine to give vagal afferent receptors a more efficient CNS related patterning effect for certain etiologies as well.

Steve, it has seemed to me for a long while now that risetime is far more important that we have given it credit for in the past - esp when issues of central dysregulation are part of a patients problems. For someone with no centrals, risetime can almost be seen as a comfort adjustment providing no desats are occurring & they feel the therapy is working. It seems to me that anyone who has a timed bilevel, needed to treat centrals, really should not be playing with risetime without expert RT advice assuming it is available and forthcoming. Even then, taking the setting out to 6 seems questionable.

DSM

[-SWS]

For someone with no centrals, risetime can almost be seen as a comfort adjustment providing no desats are occurring & they feel the therapy is working. It seems to me that anyone who has a timed bilevel, needed to treat centrals, really should not be playing with risetime without expert RT advice assuming it is available and forthcoming.

Again I absolutely agree with you, Doug.

That's why the Respironics FAQ procedures suggest it would be suitable to employ Auto along with previous known CPAP or BiLevel values (that latter to address the obstructive component). Those manual titration procedures on the titration page really aren't intended for home experimentation.

But the Respironics FAQ clearly says the Auto setting along with followup smart card reviews is, indeed, an acceptable way to go. I think on that basis Bev is good to trial her AutoSV.

[dsm]

Steve, (and SAG if you would like to comment)

One other query I am sure you can clarify for me is just what is it (which actual aspect) that gets a central sufferer breathing again.

By this I am meaning,
1) Is it the gap between epap-ipap that plays the primary role
2) Is it the risetime and gap that play an equal role
3) Is it the cycling pattern of epap-to-ipap-etc: that plays the primary role

My instinctive 'guess' is that it is 1) for most centrals people & 2 for some others & 3 rarely for a lesser number of centrals people.

Do you know of any links to docs discussing this ?

Tks

DSM

[-SWS]

Here's the formula I would use, based on the FAQ:

EPAP=P cm (or best CPAP/single pressure)
IPAP min=(P+3) cm
IPAP max=(P+10) cm
Backup Rate=Auto

where P above is a single pressure that adequately addresses Bev's obstructions. So with Bev's 14 to 17 APAP range, I noticed that she had an acceptable AI and and acceptable HI at 14. If Bev wants to start with that she can just plug that 14 cm into the above as her P value.

However, the one thing that dsm, Snoredog, and I agree on is that we think Bev can probably get by with a lower range. She still needs a P value high enough to address obstructive apneas and obstructive hypopneas. However, if that 14 pressure was dropped three points, Bev still might have all her apneas addressed, but with some outstanding hypopneas. In that case, there's an excellent chance IMO that Bev's P value toward the above settings can be dropped 3 cm below 14. That would entail an 11 cm EPAP presumably addressing apneas and some hypopneas, with 14 cm IPAP min addressing remaining hypopneas---then IPAP max to fluctuate higher, on an as-needed basis, to address central dysregulation.

So plugging into the above equation, that 11 cm presumed obstructive-addressing pressure would yield these initial settings:

EPAP= 11 cm (addressing obstructive apneas and some hypopneas)
IPAP min= 14 cm (addressing hypopneas)
IPAP max= 21 cm (addressing any central dysregulation on an as-needed basis)
Backup Rate=Auto

If IPAP max frequently hits 21, then she can extend that value
If too many outstanding A or H, then Bev might presume some unaddressed obstruction, and thus experimentally raise the above pressures

Thoughts about these initial first-night settings? They presume that some outstanding hypopnea can be addressed with IPAP min of 14.

[-SWS]

Steve, (and SAG if you would like to comment)

One other query I am sure you can clarify for me is just what is it (which actual aspect) that gets a central sufferer breathing again.

By this I am meaning,
1) Is it the gap between epap-ipap that plays the primary role
2) Is it the risetime and gap that play an equal role
3) Is it the cycling pattern of epap-to-ipap-etc: that plays the primary role

My instinctive 'guess' is that it is 1) for most centrals people & 2 for some others & 3 rarely for a lesser number of centrals people.

Do you know of any links to docs discussing this ?

Tks

DSM

I personally think they all play a key role. However, current Respironics BiPAP AutoSV viewgraphs attribute timed backup as treating central apneas (that means backup rate along with either fixed or dynamic PS). With traditional BiLevel that fixed PS was thought to mitigate central apneas by both ventilating (primarily a gas-exchange benefit) and stimulating (primarily a neurological timing benefit). That still happens with BiPAP AutoSV.

Those viewgraphs also attribute dynamically fluctuating PS as fixing periodic breathing---specifically offsetting PB's overshooting and undershooting (which can, in turn also cause central apneas, by the way). That overshoot/undershoot compensation never happened with traditional BiLevel that employed fixed PS.

[dsm]

SWS,

Re those suggested settings - agree they represent a great start. I would point out that the PS (SV) and the way the Peak Flow targeting work, will eliminate any hypopneas short of any caused by very unusual events (meal or drink just prior to sleep etc: )

I would still lean towards starting at 10 myself as I believe it is easier to analyze the machine data whilst titrating upward epap pressures than it is going downward with the epap setting. I say this based on the universal approach in the labs of titrating upward. Bev's weight & build seem to point to her not having such a big need for a higher epap. Bev did mention that she kept adjusting her pressure up seeking some improvement & thus implied it was her own experimenting that took her machine to 14 CMs.

Just to revisit the PS mechanism

> machine uses a 4 min window to track peak flow
> halfway through each breathing cycle it decides if at the current rate of flow the sleeper will meet the target
> if the target is not going to be met, immediately (within the same breath, bump PS by approx 3 CMs (that is my guesstimate of how much it bumps)
> repeat that every breath & adjust PS again up or down, needed to maintain the target peak flow

My machine will regularly go to 20 CMs or close between 7-12 times a night & my data almost always shows 0 HI & a tiny number of AI scores.

The other remarkable aspect of the SV is that I can have a big leak (over 100) all night & I will never know & my AI HI data will be as good as any other night. This is a consistent finding over the months. Whereas, any leak with the Vpap Adapt SV causes it to trigger arousals & skew the data. It is an accepted given that the Vpap Adapt SV is leak intolerant. I know the Vpap Adapt SV is a very 'tight' machine suited to anyone with serious irregular breathing & can be a better choice in such cases, but I am more than glad the Bipap SV isn't so aggressive in tracking breathing and is that the most leak tolerant machine I have ever come across.
My point here is that, other machines than the Vpap SV (Cpaps, Autos & Bilevels), can also be leak intolerant to varying degrees & thus the Bipap SV in particular is the most unique xPAP device I have come across in being able to take massive leaks in its stride (using that magic PS) whilst delivering the same high level of therapy. That is just one magnificent feature this particular machine's approach introduced.

One other comment, on the rare occasions I have woken (turned over etc: ) & the machine & I got out of synch, I just take one deep mouth breath and the PS *immediately* relaxes & reverts to std settings of epap-ipapMin. It is like I can use one mouth breath to send a message to the machine to re-synch with me rather than having that irritating feeling I have to re-synch to it. This signaling effect doesn't always happen if I try to send the signal with a deep nose breath - I do get a lot of nasal constriction. Often when I try this same trick with my nose, it causes PS to rise. It seems the machine knows my breathing is laboured through my nose (rate of flow is too low vs my mouth breathing rate of flow). But, always, one good mouth breath (I am using a F/F mask) and the machine says I (dsm) am back to normal & it (BipapSV) goes to normal settings too.

DSM

[-SWS]

Bev can start with whatever EPAP setting satisfactorily happened to address all her obstructive apneas in the past. That's really what the Respironics FAQ suggests in a nutshell. Respironics and Resmed both want obstruction out of the way with fixed pressure to allow IPAP peak (going as high as IPAP max) to work on peak flow variations related to central respiratory drive.

So whatever that pressure value is, she can plug it in as follows IMO:

EPAP=P cm (or best CPAP/single pressure)
IPAP min=(P+3) cm
IPAP max=(P+10) cm
Backup Rate=Auto

Maybe her best obstructive-addressing P is 9 or 10, or 14. If Bev has a firm idea, that's the pressure value she should start with as P. If Bev doesn't have a firm idea, it's not going to kill her to experimentally start with any of those P values IMO.