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Remember when SAG said using the setting the initial pressure higher than min. will keep the machine from going back down because that' what happened on the 418? Maybe he had IFL1 on on that one.

Any special reason you dropped the max, Bill?
O.

ozij wrote: Do you mean the PB420E will not trigger on any amplitude decrease hypopneas? I admit I've never had a chance to see that response (or lack of it) since my pressure zooms up immediately when IFL1 is on. And I suppose I have too few hypopnea+flow limitations to have maligned the machine the way I did - but I still can't get a grip on this.

Ozij, that's my take: that the 420e is going to avoid increasing pressure on hypopneas that do not show clear signs of obstruction. That's not to say that a hypopnea that unaccompanied by FL wave shape is guaranteed to be central. Some of those unchallenged hypopneas should be central and some should be obstructive---but they're too hard to differentiate without obstructive wavehape nuances.

ozij wrote:Does it make sense that this machines considers 30% of my breaths flow limited, goes nuts when allowed to respond to them, and yet considers all my hypopneas not flow limited?

You have to admit that's a very difficult presentation to temporally baseline---and FL differentiation is in part temporally based.

ozij wrote: In three years, my average number (total, not index) of hypopneas with flow limitation is 0.15, my average number of supposedly nice round amplitude decrease but not flow limited hypopneas is 2.67 (apnea /ca =2.65 apnea =2.57). 30% of my breaths flow limited, but only 5% of my hypopneas? That still doesn't make sense to me.

PB is using a five or six part weighted criteria to determine probability of a non-hypopneic flow-limited breath. And they are only using a subset of that in conjunction with amplitude reduction for their IFL2 or "flow limited hypopnea" criteria. That subset discards FL's own temporal amplitude reduction---but it factors in the wave shape criteria hinting at obstruction.

That subset can also account for a lower percentage of "flow limited hypopneas" compared to your higher percentage of "FL breaths". The amplitude-reduction weighted criteria for non-hypopneic FL can skew that percentage up in relation to other non-hypopneic breaths. WHen you compare percentages oh non-hypopneic FL with percentages of "flow limited hypopnea" you are comparing unique but overlapping criteria---which lends percentage-wise disparity to the comparison.

ozij wrote:By the way, those supposedly benign hypopneas disrupt my sleep, and decrease when I raise the minimum.

I'm not at all surprised to hear that Just because the 420e can't efficiently differentiate those hypopneas, and decides to leave them alone, doesn't mean they're not obstructive.

ozij wrote:As a person who had IFL1 on, did you ever have those nice round amplitude decreased hypopneas hanging about there?

My residual HI was usually pretty low. I'll have to have a peek at my old data. Better yet I'll get my 420e back into action now that my surgery is a done deal.
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Sorry but all those FL runs look like totally distressed sleep to me even in the absence of AHI.

I would disable BOTH IFL1 and IFL2 and see what happens, machine will still respond to Hypopnea and Apnea just not Flow Limitation.

If he was truly having that many FL runs I would suspect the Remstar to be scoring many more than it shows on the Encore Pro.

I see that distress as an intolerance to CPAP pressure.

(Bill I know you had IFL1 off, I was going by your graphs)

SWS & Ozij: Sorry, but I disagree with your understanding of IFL1 & IFL2 functions, here is what it says (cut-n-pasted from the manual):

· Using SilverLining with the GoodKnight® 420 Evolution device SilverLining with GK420E

Events for which the device automatically increases the pressure:
– Apneas (A),
– Acoustical Vibrations (AV),
– Flow Limitation (FL).


Flow Limitation Run (IFL1) and Flow Limitation combined with an amplitude decrease (IFL2) are the sole events for which you can choose to authorise an increase in pressure.

BOTH are on/off switches in how it responds to Flow Limitation in which you can change.

1=Stand Alone Flow Limitation
2=Flow Limitation+Hypopnea

Disabling IFL2 along with IFL1 means machine will no longer increase pressure in response to FL's either stand alone or associated with Hypopnea.

IF they didn't want you at times disabling that ability they would have never made it a changeable switch, they would have hard coded it.

Now in Bill's graphs, IF IFL1 was unchecked I would have expected to see the pressure instead of blocks to be more Up take care of the event and then back down again in sharp peaks and valleys, but in Bill's case we are NOT seeing that, so what is causing the pressure to remain high, in some periods the pressure seems to stop at the 10 cm maximum and hang there for some time.

I don't see his pressure going up and down too rapidly, I see the opposite which seems to contribute to the runs.

What is strange IF IFL2 was involved I would expect to see more activity on Hypopnea +FL on his reports, just not that many events logged.

Snoredog wrote: I would disable BOTH IFL1 and IFL2 and see what happens, machine will still respond to Hypopnea and Apnea just not Flow Limitation.

Well, that's a different take than I have of IFL2. And maybe it's a correct take! It seems to go along with ozij's interpretation as well.

Does anyone have data showing pressure increases to solitary hypopneas with IFL1 and IFL2 both turned off?

I had both off for a while, back in 2005. No response at all to hypopneas.

-SWS, I need a translation of this:

You have to admit that's a very difficult presentation to temporally baseline---and FL differentiation is in part temporally based.

I don't understand it.

(Guess I have to start setting up a picture account somewhere...)
O.

-SWS wrote:

Snoredog wrote: I would disable BOTH IFL1 and IFL2 and see what happens, machine will still respond to Hypopnea and Apnea just not Flow Limitation.

Well, that's a different take than I have of IFL2. And maybe it's a correct take! It seems to go along with ozij's interpretation as well.

Does anyone have data showing pressure increases to solitary hypopneas with IFL1 and IFL2 both turned off?

ozij wrote:I had both off for a while, back in 2005. No response at all to hypopneas.

-SWS, I need a translation of this:

You have to admit that's a very difficult presentation to temporally baseline---and FL differentiation is in part temporally based.

I don't understand it.

(Guess I have to start setting up a picture account somewhere...)
O.

The Bold part is the part I disagree with, not saying it didn't happen in your experiment, just that it doesn't say that any where in the documentation to support that. In the past (back when that machine came out) even sleep labs were not paying all that much attention to FL's.

I have 4 PSG's and not a single one show a FL listed anywhere.

ozij wrote: -SWS, I need a translation of this:

You have to admit that's a very difficult presentation to temporally baseline---and FL differentiation is in part temporally based.

Sorry, ozij. Part of FL differentiation entails comparing against previous breaths. Anyone running 30% FL cycles will present a waveform that is significantly more variable than usual.

In general heightened variability can make for a dicey process of establishing both running baselines and comparisons.

Snoredog, cardiac oscillations cannot be efficiently used for any hypopnea differentiation, because the airway is always part way open. Cardiac oscillations will be present during: 1) most central apneas, 2) most central hypopneas, 3) most obstructive hypopneas. However, they won't be acoustically present during full-closure obstructive apneas.

Distressed Sleep: Why do I picture a motel right next to all-night road construction with a sign up that says: "Distressed Sleep--Half Price!!!" They do it with distressed books and furniture, so why not sleep?

-SWS wrote:Part of FL differentiation entails comparing against previous breaths.

Thank, -SWS. If I understand you correctly, that's what Respironics does, too - and they get very different results (no only for Bill).


By the way, I have *.pat file I saved from when I had sleep clinic's trial machine. All patients were run with both IFL's off. Could be a coincidence, could be lack of knowledge - but it makes me wonder...

IFL1, as quoted by snoredog, controls response to flow limitation runs.

The SilverLining Manual on page 33 of Revsion D wrote:RUNs:
A RUN is an indicator of a respiratory period with flow limitation, defined as follows: a RUN is detected after two respiratory cycles with flow limitation or ten intermediate respiratory cycles that end after two successive respiratory cycles without flow limitation

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A RUN and a flow limitation are not the same. Maybe some of us have too many RUNS - and that's why we have to disable IFL1. Edit: We have a pie chart of the flow limited, normal and intermediate cycles on the pressure screen..

OK, here's both IFLs off:, Min and Intial = 4.0, Max=7.5 Max for command on Apnea =7.5
Note the non-response to the hyponea+FL that seems to have snuck in:



And this is with IFL1 on and IFL2 off Min=6.0 Initial =7.0 Maximum pressure for command on Apnea =8.0. Max=9.0





To make things even more confusing: I have reports (with IFL2 on) where you don't see the ticks on theHypopnea + FL line, you see 4 hypopnea ticks, and the number in the report is 2 Hypopneas + FL and 2 regular.

O.

The edit was a correction of hasty statement referring to flow limitation traking....
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CPAPopedia Keywords Contained In This Post (Click For Definition): respironics, Hypopnea

ozij wrote:

-SWS wrote:Part of FL differentiation entails comparing against previous breaths.

Thank, -SWS. If I understand you correctly, that's what Respironics does, too - and they get very different results (no only for Bill).

Respironics and PB both carry a running baseline for comparison. They are very similar there. However, they both score flow limitations with their own unique criteria, with each criteria set being patent protected. Each proprietary criteria set undoubtedly yields different results for at least some patient or waveform presentations that diverge from commonality (with any salient criteria-subset that happens to meet either company's mathematical criteria, but not both companies).

ozij wrote:IFL1, as quoted by snoredog, controls response to flow limitation runs.

The SilverLining Manual on page 33 of Revsion D wrote:RUNs:
A RUN is an indicator of a respiratory period with flow limitation, defined as follows: a RUN is detected after two respiratory cycles with flow limitation or ten intermediate respiratory cycles that end after two successive respiratory cycles without flow limitation

.

A RUN and a flow limitation are not the same. [/quote] Right when we compare FL with FL runs, we are not comparing apples with oranges. Rather, we are comparing the quantitative scoring of single apples (FL) with multiple apples (FL runs). PB is looking at some very specific waveform characteristics to declare "FL". And they are looking at additional quantitative criteria to declare "FL runs".

In any event, baseline and comparison variability is a function of what you happen to be looking for, calculating, and ultimately scoring as the end result. If you score 30% FL runs with PB, then you are inherently "highly variable" relative to what PB (not Respironics) happens to be mathematically differentiating.

Anyway, when PB tells us that they are combining "amplitude reduction" ("hypopnea") with "flow limited" wave shape for IFL2, then they tell us that this single hypopneic breath must have wave shape that is "flow limited" or obstructive to meet the IFL2 criteria. By the way, has anyone ever seen "flow limitation" in the sleep industry ever referring to a central event? I personally haven't. It almost always, or exclusively, refers to obstruction. If it's central in etiology, that minimized flow is referred to as "central hypoventilation" of varying amplitudes.

More head-scratching chit-chat next about what might be going on in those graphs.... my wife is calling me to go out to breakfast.

-SWS wrote:Bill, is your 420e set to increase pressure with 0.5 cm increments or 1.0 cm increments instead? You might want to experimentally set your pressure increments to 0.5 cm if your machine is not already set that way.

Also, consider setting your initial pressure equal to your minimum pressure (yup---"hobble" the 420e's pressure attack pattern). If your excessive flow runs diminish after those two experiments, then this thread is going to get extremely interesting.

OK. Here is the data from last night with Initial Pressure = Min Pressure = 8 cm.



Not sure I can tell much from this chart as last night exhibited a bit of an abnormal pattern. I tend to have the most events later in the night, whereas last night showed little happening for the last couple of hours.

Here's some data taken a few weeks ago though when Initial Pressure = 8 cm, Min Pressure = 5.5 cm, which may be a little more illuminating.



It seems clear enough here that the machine is responding to the runs and adjusting pressure up to 8 cm whenever it senses Flow Limitation. This seems to be the same pattern of runs as seen earlier. This roughly corresponds with how the Respironics algorithm increased and decreased pressure for me, too. Other events occasionally drive pressure higher. The 420E algorithm also often goes up to the 10 cm Central-line-of-demarcation, but occasionally blows right past that as well.

Not sure what other conclusions can be drawn from the above charts.

-SWS wrote:I'm thinking about your aerophagia and your occasional frank central events... I'm also going back to your very first post about those mysterious cardiac episodes...

Yeah, I still have some of those. Thankfully, not as many as before. The edema I got while using BiPAP pretty much cinched the connection in my own mind. I'm really inclined to think in terms of my problems being PFO related. A cardiologist tested for that several years ago (pre-CPAP) and that test was negative, but that test was also static. My stress tests have always been good though. Ever since reading the study a year or so ago indicating that many/most apnea patients suffer from PFO's which greatly aggravate their condition, I keep thinking that the pattern the researchers observed fits my circumstances pretty well. Not sure what to do with that info though. Obviously, getting another test just like the last one probably won't help any. .

-SWS wrote:I'm specifically wondering whether your FL runs are slight albeit defensive airway closures. And if they are physiologically-defensive closures (as opposed to allergy congestion) are they defensive in response to the 420e's pressure changes?

... or, maybe the 420E's algorithm just can't discriminate waveshapes very well. After all, Respironics didn't indicate FL's for me. Then again, my runs seem to be "worse" than anyone else here observes ...

-SWS wrote:That was why I was wondering about an experiment in which you severely restrict your 420e's pressure swings. Like you, I'm wondering whether those FL runs might be aggravated by the 420e's pressure swings.

Thought I already had ... 8 cm - 10.5 cm is a pretty narrow range.

-SWS wrote:And I'm still wondering whether your somewhat unique etiology makes you a good candidate for excessive cyclic alternating pattern (CAP). Also wondering about an alternate or even complementary possibility of a very slight CompSA/CSDB tendency. Please forgive my wondering out loud, Bill. I honestly don't mean to be rude.

Not considered rude at all, -SWS. My hope in posting was to explore the possibilities. I know for certain that I don't have this stuff under control ... Since the 420E is quite definite about a "slight" amount of CA, there is obviously some of that. Again, the cardiac connection ..., but as I understand things, that's a chicken/egg connection.

Any help to pin things down a little is greatly appreciated.


Regards,
Bill

Enjyoy you Sunday breakfast!

Just a reminder for all of us for the contiunued discsussion:

IFL1 is a switch controling response to flow limitation runs
IFL2 is a switch controling response to "flow Limitation combined with an amplitude decrease" - supposedly a bona fide obstructive hypopnea.

And a hypopnea is according the Silverlining manual "a decrease in the amplitude of breathing" and according to the 420E clincian's manual:
"A hypopnea event occurs when there is a period of at least 10 seconds where hypopneic breathing occurs. Hypopneic breathing is considered to be a reduction in breathing peak airflow by at least 40% when compared to the average of the preceding eight breaths, but not enough reduction to be considered an apnea. A hypopnea event is terminated when the patient delivers 2 consecutive non-hypopneic breaths."

I don't score 30% FL runs with PB. I usually score 25% to 30% flow limited cycles (thats data from the pressure screen).

Which makes my base rate comparison relevant.
O.

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CPAPopedia Keywords Contained In This Post (Click For Definition): 420E, Hypopnea

I've come to the conclusion you do better with NO pressure at all Bill, got any doors that won't stay open?

Well, call me confused! I still don't understand exactly what a flow-limitation "run" is. I understand that it's measured over a much longer time period than a single flow-limitation, but a "run" seems to be declared independently of flow-limitation, per se, and the "runs" can be declared in the absence of flow limitation, or so it seems.

-SWS wrote:I'm specifically wondering whether your FL runs are slight albeit defensive airway closures. And if they are physiologically-defensive closures (as opposed to allergy congestion) are they defensive in response to the 420e's pressure changes?

That was why I was wondering about an experiment in which you severely restrict your 420e's pressure swings. Like you, I'm wondering whether those FL runs might be aggravated by the 420e's pressure swings.

How does 8.5 - 9.5 cm sound? That's almost CPAP, but if it helps answer your question, -SWS, I'll do that.

-SWS wrote:And I'm still wondering whether your somewhat unique etiology makes you a good candidate for excessive cyclic alternating pattern (CAP).

It took a little while, but I found an article which related CAP with PAP:
http://www.journalsleep.org/ViewAbstrac ... ionid=3226

Journal Sleep wrote:The Cyclic Alternating Pattern (CAP) is a well described morphological feature of NREM sleep, characterized by phasic amplitude and frequency cycling of the EEG with specific periodic characteristics.1 Periods of NREM sleep without CAP are labeled non-CAP. CAP itself consists of activating “A” phases alternating with baseline “B” phases devoid of the above phasic activity. A1 CAP is dominated by slower waves and considered to reflect in part sleep promoting processes, while A2/A3 CAP have various proportions of alpha/beta frequencies that are markers of sleep disruption and transitions. The literature generally supports the assertion that an increase in CAP rate (as a percentage of NREM sleep) is seen with many sleep disrupting influences, such as sleep apnea in adults, restless legs, chronic fatigue, circadian phase mismatch, fibromyalgia and inflammatory arthritis, epilepsy, auditory stimuli, depression, and primary insomnia.2 Conversely, CAP rate is reduced (and thus non-CAP increased) during recovery sleep following sleep deprivation3 or positive airway pressure titration,4 and by sedative hypnotics (benzodiazepine and non-benzodiazepine GABA receptor modulators).

I'd never heard of CAP before this thread, but the article indicates that CAP is expected to be eliminated during effective PAP therapy. Also, I believe my own sleep disturbances generally correlate with REM sleep because of the times I've been awakened from dreams starved for air.

-SWS wrote:Also wondering about an alternate or even complementary possibility of a very slight CompSA/CSDB tendency.

After trying to think this through for the past couple of days, let me toss out an alternate possibility which might correlate, at least a little, with this, -SWS. My pulse rate tends significantly toward the "slow" side and has for many years. The cardiologists I've seen have generally taken this as an indication of cardiac health. I'm not so sure. My pulse oximeter certainly alarmed much more frequently for pulse rate below 40 bpm than it did for oxygen saturation below 88%. I experienced only a few instances when saturation dropped to 88%, but many alarms for pulse rate below 40. In fact, I eventually changed the alarm threshold to 35 bpm to keep from being constantly awakened.

In regard to hypoventilation, I should have observed desaturations independent of apneas if that were significant, wouldn't I? I didn't.

Apparently, the 420E is measuring something, so how many possibilities are there? Our small sample reveals that one other here (ozij) sees something similar in her own data. She's also shown that a large number of folks must turn off IFL1 to keep the "runs" from adversely affecting therapy. While I'm not sure that totally rules out CSDB, or cardiac issues, as dominant contributors to the effect, it sure seems to me that nasal congestion seems the far more likely possibility for being the dominant contributor.

That, of course, points me toward an ENT, something I've considered for a while anyway. Might even be interesting.

Regards,
Bill

ozij wrote:How about a lower humidifier temp, now that the ambient air is (presumably) not as dried up by winter heating?

Actually, I believe the humidifier was empty the first night I provided data for, although last night it was running in pass-over mode which is the way I mostly have it operating these days.

Ozij, thanks for providing all the explanations and especially for providing the charts. The explanations have been immensely helpful and it is quite reassuring to see some similarities in the data.

Regards,
Bill