Clear Airway Apnea = Central Apnea?

[jnk]

Your sleep-related breathing, sleep patterns, and overall health have essentially been broken for quite some time now. And you have probably discovered, as many of us have, that fixing all of that can be more involved than simply putting on a CPAP mask at night.

Some people get lucky and discover that everything falls into place once they learn how to sleep comfortably with CPAP. Others discover that CPAP addresses only the first of those three underlined categories. Sometimes we have to work on circadian rhythm issues or sleep hygiene practices in general to get that second underlined category under control. And some of us end up having to address resulting or interrelated health problems such as thyroid disorders, diabetes, or even sleep-disturbing acid reflux disease for example.

Lastly, we are the sum total of all our energy-robbing health problems---whether they are related to apnea or not. As it turns out pain issues have probably robbed my own sleep and daytime energy even more than sleep apnea did over the years. All the CPAP tweaks in the world will never fix that problem. Nor will expertly ignoring that pain during the daytime fix the broken sleep that goes with that pain during the night. So, by all means, get your CPAP optimized and get your sleep hygiene fixed first. Then, if energy still seems a problem, look beyond SDB for possible explanations. Good luck!

Thank you for that post, -SWS. I think I need to hear that on a regular basis. I assume a lot of others do too. And you put it so perfectly that hopefully it will stick in my brain as the important reminder that it is. Posts like that keep me coming back to this forum again and again.

I am confused on the whole heart-oscillations-sensing thingy, though: Does the airway have to be 100% closed for an apnea to be considered obstructive? Likewise, can't an airway be mostly closed (even completely closed) during a central apnea? And if so, wouldn't sensing of heart oscillations all be a matter of sensitivity of the sensing--a matter of degree--depending on each patient's presentation? Or am I missing something very basic? And please don't hesitate to correct me directly if I am. I am not subtly trying to make any sort of point. I am genuinely confused. And I'm admitting it this time.

jeff

[rested gal]

-SWS and muffy are the best ones to answer the two questions you posed, Jeff, but for the fun of it, I'm gonna take a guess. Just a guess, mind...

Does the airway have to be 100% closed for an apnea to be considered obstructive?

I don't think it has to be 100% closed to be an OA.

Likewise, can't an airway be mostly closed (even completely closed) during a central apnea?

I'd say yes. I'm guessing a person could have both at same time.

And if so, wouldn't sensing of heart oscillations all be a matter of sensitivity of the sensing--a matter of degree--depending on each patient's presentation?

Makes sense (no pun intended) to me. Yep.

Again, my answers are just guesses. Dunno for a fact about any of them. Interesting questions, Jeff.

Thank you for that post, -SWS. I think I need to hear that on a regular basis.

I agree. Those words you quoted, Jeff... -SWS put it so well. Excellent!

[dsm]

MUFFY / SWS

Was that description of with 'airway closing', of a mixed apnea starting to occur (seemed so ?). I didn't catch the point as to if the airway was stented at the time (suspect not because it shouldn't be closing).

So if the machine can (could?) monitor the heartbeat oscillations continuously (they should always be there), and whilst monitoring airflow and detecting no flow, surely that becomes an evidence of obstruction when the cardiac oscillations also stop. Perhaps, when the machine sees a looming hypopnea and has a strong cardiac osc signal, it could raise EEpap (end expiration epap) by a small preset delta to ensure the airway remains stented so that following CA treatment can be initiated.

Interestingly, I see that the SOMMNOVent CR actually spreads Epap & Ipap apart equally when a CA is being observed (while its EEpap remains the same).

DSM

[Muffy]

Dr. Rapoport's team then goes on to speculate that a patent or open airway might be one of two possible factors in physiology conducive to placing those cardiogenic oscillations in the airflow signal:

Our data further lead us to speculate that transmission of cardiogenic oscillations to the airflow signal may be affected by relaxation of respiratory musculature, in addition to being influenced by patency of the airway. Thus, high muscle tone during respiratory efforts may alter coupling between the changes in volume due to cardiac contraction and volume changes in the airway.

If Dr. Rapoport's conjecture is true, then low muscle tone combined with a not-yet or not-completely closed airway plausibly lends this counterintuitive set of measurement circumstances:

cardiac oscillations in the FOT channel (while the airway is CLOSING?)

I maintain that the central apnea identification approach in the previously noted FOT example makes little to no sense.

In another look at the image, it is noted that the unstable FOT baseline actually begins during a period of active breathing:



I think it can be easily argued that none of that waveform could be clearly defined as cardiac oscillations, but if we accept that it is, then there is pre-event cardiac pulsation (blue), which is contrary to the concept that high muscle tone would mask COs. Now one could easily argue that airway closure component could have/should have dampened CO amplitude (unless one wants to argue the "piston" theory, but "piston" theory would allow COs to appear in purely obstructive apneas as well).

Regardless, I would think it impossible for computer-assisted scoring to differentiate pre-event pulsation from event pulsation to call it a central apnea in this case. As noted, I think it's slick, but do it again.

In Morrell et al, airflow was measured by a Hans Rudolph pneumotachometer in an absolutely sealed system. Give Rapopport that thing (which costs about 3 times as much as a CPAP machine) and see what he comes up with.

I'd also like to see Morrell measuring obstructive apneas in REM (there goes your muscle tone)(her study was limited to NREM centrals) and see what she comes up with.

Muffy

[Muffy]

Some recent comments here have made me aware that some readers may take some of my comments literally instead of the spirit in that they were originally intended, and that, in turn, might cause confusion and/or misunderstanding. If I have caused that, I most sincerely apologize. My only intent was that I had hoped my exaggerated opinion(s) would help to spur additional debate, and, eventually, a greater overall understanding and appreciation of the concepts involved.

I hope you aren't referring to me, being the newbie making fun of the technotalk.

Of course not! That was simply another example of "quirky humor" and sarcastic retort to

With high priests & mystical rituals and religious mumbo-jumbo - some of which can be used to awe the masses.

Muffy

[-SWS]

I am confused on the whole heart-oscillations-sensing thingy, though: Does the airway have to be 100% closed for an apnea to be considered obstructive? Likewise, can't an airway be mostly closed (even completely closed) during a central apnea? And if so, wouldn't sensing of heart oscillations all be a matter of sensitivity of the sensing--a matter of degree--depending on each patient's presentation? Or am I missing something very basic? And please don't hesitate to correct me directly if I am. I am not subtly trying to make any sort of point. I am genuinely confused. And I'm admitting it this time.

Well, IMHO, it's a genuinely confusing topic---in its entirety. But yes, an obstructive apnea very often does not entail a completely closed airway; and yet sometimes it does. And you also correctly stated that while a central apnea is usually an open-airway apnea, the airway can sometimes be closed during a central apnea.

The underlying distinction between obstructive events/disease and central events/disease differentiates with PSG-measurable respiratory effort. Hmmm... But that still doesn't answer the somewhat puzzling question about WHY cardiogenic oscillations don't show up in the airflow signal during any of those obstructive apnea scenarios above. Does it? Those cardiogenic oscillations show up during normal breathing and they show up during about 60% of all central apneas. But the airflow signal never presents those acoustic heartbeat pulsations during the above obstructive apnea scenarios. Unfortunately I don't have the answer to that very interesting flow-signal-component puzzle.

And if so, wouldn't sensing of heart oscillations all be a matter of sensitivity of the sensing--a matter of degree--depending on each patient's presentation?

Makes sense (no pun intended) to me. Yep.

Yep. Here's that epidemiological breakdown highlighted by Muffy formerly posting as SAG: viewtopic.php?f=1&t=25751&st=0&sk=t&sd= ... 60#p223956

Interestingly, I see that the SOMMNOVent CR actually spreads Epap & Ipap apart equally when a CA is being observed (while its EEpap remains the same).

Well, it needs to leave EEpap where it is since that's needed for somewhat common expiratory-end-phase apneas. So here the EEpap is designated for the obstructive-apnea component, but the IPAP and remainder of EPAP can widen to address central-apnea and especially PB-based ventilatory flow targets with that wider PS.

I think it can be easily argued that none of that waveform could be clearly defined as cardiac oscillations

Signal artifact is always a possibility IMO as well...

but if we accept that it is, then there is pre-event cardiac pulsation (blue), which is contrary to the concept that high muscle tone would mask COs

I'm not so sure that it would be contrary. That wouldn't be genuinely "high" muscle tone. It would be the same (eupnic breathing) "normal" muscle tone that also presents rather easily signal-processed COS during eupnic expiration. Now I might have this very wrong, but think Dr. Rapoport et al were referring to that much denser "dammit I can't breath" survival-based muscle tone characteristic of obstructive apnea/disease---much more so than central.

With high priests & mystical rituals and religious mumbo-jumbo - some of which can be used to awe the masses.

Muffy

You know, people on this message board can make fun of that accolade all they want. But the proudest day of my life was when ozij awarded me that purple robe:
viewtopic.php?f=1&t=29927&p=257978&#p257978. Man how I love that purple robe!

[ozij]

Muffy wrote:
With high priests & mystical rituals and religious mumbo-jumbo - some of which can be used to awe the masses.
MuffyYou know, people on this message board can make fun of that accolade all they want. But the proudest day of my life was when ozij awarded me that purple robe:
viewtopic.php?f=1&t=29927&p=257978&#p257978. Man how I love that purple robe!

Robe to be found on the next page of that dialogue.... all those religious war... The War of Roses.... The War of Hoses....

O.

[dsm]

On religions,
There are some where the participants are taught to recite content without question and not to argue but there are a very few where the participants are taught to debate all teachings and to be prepared to argue opposite points of view. And as long as we aren't asked to debate how many angels can dance on the head of a pin, I'll sign up for the latter religion and be a dutiful supplicant of the cpap therapy god. In the latter religions the wisemen (vs prophets) emerge due to the respect they earn. So with SWS & perhaps a purple robe may be we have a good start for a wiseman



DSM

[Muffy]

And if so, wouldn't sensing of heart oscillations all be a matter of sensitivity of the sensing--a matter of degree--depending on each patient's presentation?

Makes sense (no pun intended) to me. Yep.

Yep. Here's that epidemiological breakdown highlighted by Muffy formerly posting as SAG: viewtopic.php?f=1&t=25751&st=0&sk=t&sd= ... 60#p223956

As an aside, during his lectures at conference, Rappopart always starts his lectures out by saying

Is SAG here today? I'm going to KHFA for not spelling my name right once during these last 5 years!!

Muffy

[split_city]

Does the airway have to be 100% closed for an apnea to be considered obstructive?

Kind of OT, but I would like to add to this. The below figure is from another thread. This patient demonstrates small bursts of expiratory flow without inspiratory flow i.e. continues to lose lung volume. I would be interested to hear how common this type of apnea is seen in other labs? Of note, flow was measured using a pneumotach which has increased sensitivity.

[Muffy]

Signal artifact is always a possibility IMO as well...

Well then that whole area is artifact and should not have been scored as a central apnea based on COs. If we are to look at respiratory event #3 in the FOT example, all scorers have called this a hypopnea. This is probably a central hypopnea, but I am baffled why the FOT algorithm would call it a hypopnea because it should have been called an apnea as it is using the pressure waveform for waveform identification, which is flat.

Anyway, what is clear there is (1) increasing Rrs says there is obstruction occurring (pretty soon (like maybe now) we'll have to differentiate open-airway centrals from closed airway centrals)(say, isn't this where we came in?) and (2) COs are much more clearly defined:



so I would have thought the FOT algorithm would have called this one central apnea but let the second event pass as obstructive. Don't forget, the FOT algorithm can't use RIP belts.

but if we accept that it is, then there is pre-event cardiac pulsation (blue), which is contrary to the concept that high muscle tone would mask COs

I'm not so sure that it would be contrary. That wouldn't be genuinely "high" muscle tone. It would be the same (eupnic breathing) "normal" muscle tone that also presents rather easily signal-processed COS during eupnic expiration. Now I might have this very wrong, but think Dr. Rapoport et al were referring to that much denser "dammit I can't breath" survival-based muscle tone characteristic of obstructive apnea/disease---much more so than central.

Since the breathing in that area is recovering from a respiratory event, I would think it would be high(er) muscle tone relative to baseline and fit into his "e.g. at arousal" category as evidenced by that increase in EMG in EMG1.

Unfortunately I don't have the answer to that very interesting flow-signal-component puzzle.

Looking at the huge number of closed airway centrals that have been "dis"closed in this discussion, either the pressure pulsation methodology of Respironics is going to have a sensitivity problem of staggering proportions or they are hoping that if patients are on some kind of pressure support that the incidence of closed airway centrals will be less. Kinda like A10 philosophy (all respiratory events over 10 cmH2O must be central vs all centrals over x cmH2O are open airway).

All these references are practically anectdotal in nature. The algorithm kids need to show data on a large scale demonstrating specificity AND sensitivity or into the TF Bucket it goes.

This might sound like a very picky, technical question..

OK, just a couple more points and we'll get to the technical part...

Muffy

[Muffy]

LOL! Did you see how Mary Morrell made her way into this thread, too?

Muffy

[ozij]

Muffy, -SWS I'm having trouble following this thread - could either of you post a glossary of all those short cuts you're using?
And what is "ballistocardiography" in words that a non-physicist can understand?

Thanks,
O.

[Muffy]

Muffy, -SWS I'm having trouble following this thread - could either of you post a glossary of all those short cuts you're using?
And what is "ballistocardiography" in words that a non-physicist can understand?

Thanks,
O.

Why, ballistocardiography is everywhere, even in your own back seat!

viewtopic/p437118/viewtopic.php?f=1&t=2 ... hy#p246205

As also suggested by S_C, and trying to look at the Morrell study in context, if you use a sensitive-enough device and amplify the ever-living daylights out of it, you can see COs 5 feet away.

Give all these kids the same equipment and THEN do the studies.

Muffy

[jnk]

So if what differentiates a central from an obstructive is effort and not so much the state of the airway, why are all these manufacturers (two, soon to be three, anyway) claiming that their machines' guess about the condition of the airway is so useful for differentiating centrals from obstructives in trending data? Is it purposeful ignorance for marketing purposes? Why are the manufacturers of home machines trying to sell a technology to the docs and the public that doesn't have years of continuous use at all the sleep centers to perfect it? I say that the day my sleep center doesn't need belts to differentiate centrals is the day I'll believe my home machine knows the difference without belts, and not a day before.

And wouldn't it be cheaper to have effort belts (with a wireless link that runs on an AAA battery) included with every auto than to keep trying to deduce effort from a single channel for trending? Seems to me more is known about how bellies and chests move in the general population than how airways move, and the belly and chest are a lot easier to get to. If manufacturers really want to differentiate, it wouldn't be that hard.