Effects of too much pressure

[ozij]

These latter hypothetical patients, whose symptoms seem to be largely transitional, just may avoid some transitional homeostatic maladjustment by wearing their masks twenty minutes or so before allowing themselves to fall asleep (I cannot find the medical study where I read that advice).

You do mean wearing their masks with the machine running, don't you? My somewhat literal, visual mind had me viewing an upsetting mask only picture for a few seconds there....

(Glad to see you posting, -SWS).

O.

[-SWS]

There is a reason they call it NR vs central, they can't tell the difference. Those series of Hypopnea before the NR can just as easily be central hypopnea, and since they didn't respond to 3 pressure increases, the circuit paused (straight line of constant pressure), when monitoring resumed after 30 seconds pause it seen they were still there (did not respond) so it dropped pressure.

I already agreed with you before you even wrote it, Snoredog.

However, the NR category unfortunately does not perfectly document central apneas. Respironics has traditionally employed that NR category to document apneas that were not responsive to three pressure increments above 8 cm.

Just call me clairvoyant!

[-SWS]

You do mean wearing their masks with the machine running, don't you? My somewhat literal, visual mind had me viewing an upsetting mask only picture for a few seconds there....

(Glad to see you posting, -SWS).

O.

Glad you clarified that one, O! Yes, the study I read (and now can't seem to find) suggested wearing the mask with the machine running. That advice, of course would not apply to the vast majority of us---only those very rare birds who seem to experience a transitional homeostatic maladjustment when pressure is first applied.

Good to see you posting!

[cwsanfor]

Cswanfor, did you per chance eat or drink anything during that therapy break lasting nearly an hour? Or even within an hour or two of your initial bed time that evening?

I am traveling, and had to respond using a PDA. The last Guest was me, and I neglected to answer -SWS's question.

I would typically have a swallow or two of water or juice when I awake that long. I do not typically eat during the night, or near bed time. Because I didn't have reason to note any of that at the time, I have no specific record in my notes, so I might possibly have engaged in some unusual behavior that night. I'll note such in the future.

It is possible that I took off the mask, laid down "for just a minute", a bad habit I am breaking, and so put the mask back on and started the machine after being asleep and not under pressure, for some brief period of time. I can't say for sure. What did not happen, I think, is a long breathing cessation, so I'll hold off on ordering an ST. But that's a good point to consider and rule out.

[Snoredog]

Cswanfor, did you per chance eat or drink anything during that therapy break lasting nearly an hour? Or even within an hour or two of your initial bed time that evening?

I am traveling, and had to respond using a PDA. The last Guest was me, and I neglected to answer -SWS's question.

I would typically have a swallow or two of water or juice when I awake that long. I do not typically eat during the night, or near bed time. Because I didn't have reason to note any of that at the time, I have no specific record in my notes, so I might possibly have engaged in some unusual behavior that night. I'll note such in the future.

It is possible that I took off the mask, laid down "for just a minute", a bad habit I am breaking, and so put the mask back on and started the machine after being asleep and not under pressure, for some brief period of time. I can't say for sure. What did not happen, I think, is a long breathing cessation, so I'll hold off on ordereing an ST. But that's a good point to consider and rule out.

Don't count out makin whoopee during that break, that would account for the rapid breathing when you returned!

[StillAnotherGuest]

The best answer is always get PSG, cause you can't match up sleep staging, oximetry, etc. to properly identify the events. But since that don't sell newspapers...

I suppose you could also make a case for sleep-onset centrals. If you look at your sleep study:



you'll see that there's quite a few centrals after each of the first 3 periods of wake.

However...

1. Sleep-onset centrals (if that's what they truly are) are generally harmless;

2. One NR won't make the world stop, and anyway,

I have not before or since seen the odd pattern of hypopneas and final NRA like here.

so any changes go in the "cut off off your face to spite your..." whatever.

4. We're not talking huge pressure gradients here. While the sequence looks impressive, we've gone from like 16.5/14 to 18.5/16. Once. And most importantly;

5. You can't lose sight of the fact that your supine REM makes your OSA exponentially worse, and there's no evidence to show what pressure you really need to control it. If you were on your back following BR break and/or in REM, then a rapid pressure increase would need to be summoned up. So there's just as much of a chance that that whole sequence of events represented normal AutoBiPAP response (except why did it label all them things hypopneas? That messed up the algorithm somewhat. Apneas would have run the EPAP up first, and the whole response might have been entirely different).

So anyway, if it was NREM, then you might make the case of central stuff. If it was REM, then you have to consider that the pressure was insufficient rather than excessive.

Course it could have been CPAP elves.
SAG

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

[StillAnotherGuest]

Now if you wanna talk about pressure-induced central apneas with an APAP, get a load of this:

This is a known CSBD on an 420E AutoPAP at 4-20cmH2O. Both IFLs are turned on, not that I think that would have changed things a lot, perhaps the event-reporting, not the end result. Anyway, it don't take long for the pressure to go through the roof:


It's Miller, errr, AdaptSV time!
SAG

[cwsanfor]

Don't count out makin whoopee during that break, that would account for the rapid breathing when you returned!

I'd have remembered that, trust me.

[Snoredog]

SAG wrote:

I suppose you could also make a case for sleep-onset centrals. If you look at your sleep study:

I guess that would explain why patients manifesting CSDB characteristics possibly do better when Settling or AutoRamp is available and used? Would they not avoid those sleep-onset centrals?

[rested gal]

Now if you wanna talk about pressure-induced central apneas with an APAP, get a load of this:

This is a known CSBD on an 420E AutoPAP at 4-20cmH2O. Both IFLs are turned on, not that I think that would have changed things a lot, perhaps the event-reporting, not the end result. Anyway, it don't take long for the pressure to go through the roof:


It's Miller, errr, AdaptSV time!
SAG

Might not have changed things a lot, but I'd sure like to have seen that same CSBD'er on the 420E with IFL1 turned off for a few nights. Just outta curiosity.

[Snoredog]

Now if you wanna talk about pressure-induced central apneas with an APAP, get a load of this:

This is a known CSBD on an 420E AutoPAP at 4-20cmH2O. Both IFLs are turned on, not that I think that would have changed things a lot, perhaps the event-reporting, not the end result. Anyway, it don't take long for the pressure to go through the roof:


It's Miller, errr, AdaptSV time!
SAG

Might not have changed things a lot, but I'd sure like to have seen that same CSBD'er on the 420E with IFL1 turned off for a few nights. Just outta curiosity.

I think SAG's chart was to demonstrate pressure induced centrals.

If you observe the Indicators at the top of the chart and compare to the pressure changes below, there are NO events corresponding to the pressure changes, not even vibratory snore. You will note the first 2 CA's right before hour 49h, these are a result of the pressure.

The question I'd have is: WHY did the 420E increase pressure from about 11cm to 17 or 18cm when there were no events logged to warrant those increases?

it's too small to be a door stop

[rested gal]

Well, my point was that with IFL1 turned off, the pressure might not have taken off up into the stratosphere in the first place. The 420E auto can read some people's breathing wrong with IFL1 on.

I've got garden variety mild OSA, not Complex Sleep Disordered Breathing, but I got the same kind of pressure line shooting right up to the top EVERY session when I first began using the 420E with IFL1 On. Turning IFL1 off settled it right down. As SAG said, that person presumably has CSDB, so turning off IFL1 might not matter a bit. Would just be interesting to see.

[StillAnotherGuest]

Well, my point was that with IFL1 turned off, the pressure might not have taken off up into the stratosphere in the first place. The 420E auto can read some people's breathing wrong with IFL1 on.

I've got garden variety mild OSA, not Complex Sleep Disordered Breathing, but I got the same kind of pressure line shooting right up to the top EVERY session when I first began using the 420E with IFL1 On. Turning IFL1 off settled it right down. As SAG said, that person presumably has CSDB, so turning off IFL1 might not matter a bit. Would just be interesting to see.

And we had that very thought in mind, as well as putting some sort of limit on the 420E should that therapy be allowed to continue. However, when PSG showed


then condoning any kind of APAP pretty much went out the window. Nice mixed apneas again, BTW.

If the opportunity does come up, tho, I'd be curious myself. I'd also be curious, RG, to see what your response would look like with IFL1 on and taking Mirapex.
SAG

[rested gal]

I'd also be curious, RG, to see what your response would look like with IFL1 on and taking Mirapex.
SAG

Well, when I hit Medicare age three years hence, I might just try that. I kinda' like that "cpap" is doing a good job for me so far. Feel great and not on a single prescription med. But hey, if I ever run across some samples, I'll lab rat with enthusiasm.

Actually, what probably would let me turn IFL1 on would be snorting saline rinses and stopping smoking. And maybe roto-rootering the sinuses, checking the turbinates, and such. But ENT'ish things'll have to wait for 2009.

[StillAnotherGuest]

SAG wrote:

I suppose you could also make a case for sleep-onset centrals. If you look at your sleep study:

I guess that would explain why patients manifesting CSDB characteristics possibly do better when Settling or AutoRamp is available and used? Would they not avoid those sleep-onset centrals?

I'm not sure what it is we're trying to fix here, or the mechanism with which we're trying to fix it with, given the number of variables. The list includes such things like are we dealing with hypocapnia or hypercapnia, CPAP or BiPAP, controlled OSA or not, and CPAP tolerance.

Sleep-onset centrals are a normal phenomenon. Why even bother with them. And interestingly, they are a hypercapnic event, as opposed to CSBD, which is a hypocapnic phenomenon. We might add that uncontrolled OSA could contribute to hypercapnia, further distancing us from the hypocapnia of CSBD or CSR/CHF.

CPAP generally does not create pressure-induced events, at least not in the way you might think. BiLevel, by it's nature, can increase minute ventilation, and that can be the trigger for central events. In anybody.

Once the hypocapnic central can of worms is opened, then a cascade of centrals comes out. The phenomenon perpetuates itself at an index of about 40-60 hour. Sporadic centrals, however, should not automatically be classified as pressure-induced. If high pressure creates an arousal, and there's a post-arousal central, that's not a pressure-induced central. That's a post-arousal central.

So if we're trying to fix post-arousal centrals with CPAP desensitization, then maybe ramp, etc. will help. If you're trying to correct sleep-onset centrals, I don't think you can do it with CPAP, and if you tried to do it with BiPAP, you'd run the risk of exchanging hypercapnia-induced centrals for those that are hypocapnia-induced. If you're trying to fix CSBD or CSR/CHF with aggressive pre-sleep pressure support (as in non-ASV), that's pretty much doomed.

If the sleep-onset centrals are post-arousal, and due to an inability to achieve sustained sleep, then some form of CPAP desensitization may be helpful.

Perhaps the greater question is, how many centrals should be of concern (as in, "what is it we're trying to fix, before we decide how to fix it?") It's not 1, or 4. If they're not post-arousal, I would say CA Index of >5 is of concern, cause that's where the CompSAS definition seems to headed for. I'm not sure if you should blanket-treat at CAI of 5 (as in enhanced CO2 or ASV), but hey, you gotta start somewhere. If you've got a post-arousal CAI of >5, then you have to fix the arousal problem, not the CAI problem.

The phenomena of pressure-induced central apneas is tossed around far too freely. The vast majority of people do not get centrals because of ultra-therapeutic CPAP levels. BiLevel, Pressure Support (PSV) and Proportional Assist (PAV) Ventilation are another matter. You need some mechanism to drive the pCO2 below the sleeping apneic threshold, and plain old CPAP rarely is able to do that. OK, if you wanna argue that CPAP increases base lung volume (Functional Residual Capacity)(FRC), and since that increases gas exchange, some people can generate centrals that way, fine. But it's not as many as you might think.
SAG