APNEA -v- HYPOPNEA

[Snoredog]

abstracts from:

Recognition and Management of Complex Sleep-Disordered Breathing

Primarily Control Dysfunction (Central Disease)
Central apneas and severe periodic breathing including Cheyne-Stokes respiration are readily recognizable.[1,2] More subtle forms of periodic breathing are much more difficult to characterize, and in clinical practice 'central hypopneas' are not scored...

and...

Avoiding Pressure Toxicity
Patients with complex disease are sensitive to positive airway pressure, and usually flow limitation cannot be eliminated without worsening periodic breathing or inducing central apneas. An immediate worsening with bilevel ventilation may be seen, consistent with an effect of induced hypocapnia on the peripheral chemoreceptors. One approach is 'permissive flow limitation' - allowing some obstruction to persist and thus avoiding the worsening of control dysfunction.

and...

Minimizing Hypocapnia
The most critical component of any therapy for complex disease associated with CO2 dyscontrol is to minimize hypocapnia. Strategies include using the lowest pressure that allows reasonable control, avoiding modalities that destabilize (continuous and bilevel pressure may be less or more effective in individual patients; automatic continuous pressure machines should be avoided), the use of a nonvented mask, the use of enhanced expiratory rebreathing space, and controlled increases of CO2 concentrations in the inhaled air.[38]

Geoffrey S Gilmartin; Robert W Daly; Robert J Thomas

Curr Opin Pulm Med. 2005;11(6):485-493. ©2005 Lippincott Williams & Wilkins
Posted 10/27/2005

Strategies include using the lowest pressure that allows reasonable control, avoiding modalities that destabilize (continuous and bilevel pressure may be less or more effective in individual patients; automatic continuous pressure machines should be avoided)

Sorta explains why Chuck's numbers went down by lowering pressure by 1cm.

Chuck: Lastly, I would suggest reading the Remstar Auto patent dated Sept. 30, 2004 then tell me how it works, it is only about 50 pages long easy reading, pages 20 through about 24 explain the different control circuits and their priority. I would also look up the A10 algorithm and pay attention to the snore circuit on that one, I'd tell you where to look but my copy shows it hasn't been updated since 1956 .

Now my theory has been your machine's snore circuit takes control over the pressure increase circuit and the machine increases pressure without monitoring the apnea/hypoapnea circuit frequently enough to observe an increase in hypocapnia to release control of the snore circuit. The result is too much pressure from the snore circuit which causes your HI count to increase (central hypopnea). The Remstar enters a hold pattern and monitors either every 2.5 minutes or 5 minutes based upon the .5cm to 1.5cm ramp increase, then it uses timers to lock out the circuit if it was the last controlling circuit to increase pressure. It also looks for irregular breathing.

[GoofyUT]

Rough night, huh?

Don't worry. I get cranky too, so I understand........

Chuck

[Guest]

you have NO idea how either of these autopap machines function, it is why you are having so many problems with their use, now you are suggesting to others on what they should do and you don't even understand it yourself? I think you need to go back to your diametrically opposed planetary axis theory and review what happened.

But I'm not going to continually argue the point with you, personally I don't care what you do with your therapy. But I understand now why the RT guy threw the mask at you.

When you guys argue the point the rest of us learn. Don't stop now.

[-SWS]

Guest, when contrasting ideas are comfortably interleaved with respect for all participants involved, then the highest potential for learning exists. When contrasting ideas become squelched with anything other than logical albeit courteous discourse, then discovery of truths become potentially hindered.

I for one will be back in this thread with plenty of contrasting and supporting views as long as that discussion stays civil.

[inacpapfog]

What a great learning experience going on here! Thanks everyone for taking the time for such an in-depth discussion!

[GoofyUT]

Well folks, here's a twist!!!

We went to the Salt Lake Bees baseball game last night to celebrate the Fourth of July and watch the fireworks display afterwards. I had two beers while at the game, though none within the last two hours (Utah is a state with peculiar liquor laws, so most beer served in public is 3.2% beer).

When I got home, it was late and I was concerned about the two beers relaxing the musculature surrounding my airway, which might increase my pressure requirements. So, I threw my S8 AutoSet BACK into Auto mode, and went to sleep, sure that my numbers would be horrible, but I wasn't much worrid about that.

I just woke up after a pretty good night's sleep! I feel pretty refreshed despite the short hours (have to get to work for an early meeting). But the strange part is my numbers!

AHI=0.9; AI=0; HI=0.9; Pressure (95%)=10.2

Now, I was pretty sure that my improvement recently was because I had returned to CPAP from APAP and was experencing fewer cortical arousals from the subtle sensory experiences associated with the pressure changes of auto-titration. And, maybe I was one of those folks who responded best to lower pressures, and degraded with pressure increases. But, last night's APAP experience argues against that!!!

Sorry for the twist folks! I felt an obligation to report this here to those who have been following this thread, since I didn't want to further what may be a misleading notion that APAP was BAD for me, particularly ResMed APAP. I used ResMed APAP last night under less than ideal circumstances and had my SECOND BEST NIGHT since starting xPAP! Go figure.

So, I don't believe any longer that whatever has been plaguing me is APAP/pressure related. My success last night couldn't have occured if this was a CSDB-related phenomenon that made me intolerant of pressure gradient or increases.

The other change that occured at the time that I started experiencing improvement was switching from my Swift to an Activa. I'm intending to switch back to my Swift to see if that causes a degradation, and I'll report back here the outcomes.

Chuck

_________________

CPAPopedia Keywords Contained In This Post (Click For Definition): resmed, activa, swift, CPAP, AHI, auto, APAP

[krousseau]

Why not continue the experiment for a couple more nights-then if the trend continues figure out what a little alcohol does for you that you can get some other way. Do you really want to change therapy based on a one night sample?

[-SWS]

Excellent find, Chuck! Very interesting, indeed. I too would just love to see extensive trial data with the Swift/Activa being your only delta in xPAP therapy.

Regarding your preliminary conclusion that a slight CSDB effect cannot possibly be involved. Perhaps that statement is true. However, here is a rhetorical question for your consideration: What are the known effects of alcohol on a marginally affected CSDB respiratory drive?

Alcohol is known to inhibit the normal respiratory drive that is thought to be well-balanced with respect to hypoxic/hypercapnic respiratory triggers (and perhaps even primarily driven by hypoxic respiratory triggers versus hypercapnic triggers). However, we might suspect the CSDB patient has a respiratory drive that is primarily hypercapnic. I'm not so sure a marginal CSDB respiratory drive can be ruled out just yet because you experienced the opposite effects of alcohol compared to ordinary patients with respiratory drives that are balanced with respect to hypoxic triggers.

Short of CSDB considerations there is a case for anxiety induced SDB events occuring during nightly intervening periods of wakefulness (including that initial sleep onset period)---and alcohol can presumably mitigate those anxiety induced SDB events as a relaxant.

Keep up the good work. We love hearing your results!

[Snoredog]

this proves as long as you drink a couple beers every night you will be fine

[GoofyUT]

I decided to return to APAP because it was my belief that my experience last night (good night's sleep, GREAT numbers) reflected that I was non-reactiveto either pressure changes or increases, and was therefore, a safe candidate for APAP, which I philosophically agree with the benefits of. The essence of my decision had to do with believing that I was non-reactive though, and I believe (and wonder) whether such a reactive -v- non-reactive distinction is reasonable.

Now, I'm still very intrigued with the prospect of a hypercapnic trigger based etiology. I wasn't trying to suggest anything otherwise. I am suggesting that I beleive that it may be more related to CO2 venting associated with the greater dead-space in the Activa versus the Swift.

Two things changed when I began noticing a marked improvement in my sleep: 1) I had just started a CPAP trial; and, 2) I switched from Swift to Activa.

Based on my subjective experiences and discussions here, I was very intrigued with a hypercapnic-mediated etiology based on the sequellae of auto-titration. But, my experience last night (if my non-reactive hypothesis holds) tells me that it might not be related to auto-titration, but to some other CO2 respiration-mediated mechanism, like dead-space in the Activa. And that's why I'm going to try to hold APAP constant for a bit to confirm that I'm not repeating a degradation asociated with APAP, and then try switching masks back to the Swift, to see if it causes a degradation.

Two of you have focused on the role alcohol may have played. I'm going to discount this out of hand(and I hope not out of denial). I had two beers during the period of 6PM to Midnite. One at 6:15PM and the second at 8:30Pm. They were both 12 oz. beers of 3.2% strength. Having direcetd alcohol treatment services,I am confident that they were entirely metabolized and excreted well before I retired at Midnight. Other than these two beers, I have consumed no alcohol at all in months. I chose to use APAP last night out of the understanding that one of the uses of APAP is to compensate for use of alcohol by increasing pressure. But this was pretty much an intellectual exercise for me, not one that I thought was clinically indicated. However Krousseau, I am always looking for ways to have my needs met, and I'll look as you suggest as well.

I guess my main question is: Am I misleading myself by pursuing this reactive/non-reactive hypothesis with the prospect of CSDB based upon a hypercapnic trigger etiology?

Chuck

_________________

CPAPopedia Keywords Contained In This Post (Click For Definition): activa, swift, CPAP, auto, APAP

[-SWS]

I guess my main question is: Am I misleading myself by pursuing this reactive/non-reactive hypothesis with the prospect of CSDB based upon a hypercapnic trigger etiology?

Chuck, ultimately the results based on your trial and error will be the most important outcome in this experiment for you. Regarding the etiological theories and postulations at hand: we may never arrive at a definitive conclusion for lack of definitive means such as empirical data and adequately controlled experimentation.

This is a case of hypothetically exploring which highly improbable etiology or combination of etiologies may be you. To that end I hope others reading this thread do not attempt to generalize these discussions as if they were scientific fact. When considering less than optimal CPAP therapy, central apneas in general and a theoretical CSDB etiology in specific should be one of the very last considerations to make toward analyzing any suboptimal CPAP therapy.

Chuck. when/if we discard the possibility of a CO2-based etiology, there will be absolutely no apologies to make. Do we know of any worse enemy to the pursuit of truth in general and science in particular than biased expectations?

[-SWS]

Perhaps it's best to eliminate our frivilous discussions about etiological theories and simply concentrate on getting your AHI and awakenings down as well as increasing your overall sense of physical well being.

[-SWS]

A couple loose ends to tie up before this thread moves along or fades away:

Do pressure induced central apneas show up as HI's the next day on the menu?

Kurtr, the answer is that central apneas will show up "hidden" or buried in your AI on the standard S8. You won't be able to distinguish in that AI which are central apneas and which are obstructive apneas from either the scored events or the AI score itself. The same answer would hold true if they were central hypopneas, except these latter events would show up "hidden" or buried in your HI.

Here let me demonstrate with a picture.

Snoredog, thanks so much for posting that! The reason I wondered about the central apnea/hypopnea determination methods: a lack of definitive means to distinguish central events also implies a lack of definitive means to distinguish obstructive events. In this case any and all CSDB related or even incidental central events that happen to resolve or just plain disappear within the time frame of three pressure increments will not score as "NR". However, I do not think your events are hidden or fleeting central events.

In my own mind I haven't been able to establish a link between your highly atypical pressure-induced snore and Chuck's pressure-induced hypopneas. Rather I view these as two separate signal types likely entailing two separate physiologic mechanisms: 1) your snore is pressure induced acoustical noise in the same frequency and amplitude range the Remstar will score as snore, and 2) Chuck's pressure-induced hypopneas are machine-scored as amplitude reduction. In inanimate physics I can come up with several explanations for pressure induced snore (which I do not suspect to be palatial, btw). Conversely, in inanimate physics I cannot come up with an explanation whereby increased pressure intensifies an airway obstruction. I can, however, think of an as-of-yet-undiscovered sympathetic neuromuscular airway collapse in biophysics that might be in some conceivable way Herring Breuer or blood-gas-trigger related to increased xPAP pressure. That would be a theoretical case of increased xPAP pressure indirectly causing an obstructive apnea. That would certainly have to be a highly improbable theory since I personally thought it up.

What is a central hypopnea?

Guest, the various definitions of hypopnea deal with the concepts of airflow reduction, duration, and desaturation. At this point the definition does not in any way attempt to describe the physiologic mechanism that causes that air flow reduction. However, when the terms "obstructive hypopnea" and "central hypopnea" are used, the etiology itself begins to enter the definition. In the case of "obstructive hypopnea" the airflow reduction is purely related to partial anatomical airway obstruction. In the case of "central hypopnea" that airflow reduction is purely related to the respiratory drive itself. A "mixed hypopnea" might thus entail reduced airflow for both obstructive and central reasons.

I did my first test last night and went straight CPAP at a pressure of 9. I slept very well and woke feeling rested for the first time since I started APAP a month ago.
My numbers were down significantly; AI down from a 1.0 ave to a 0.2 and HI down from a 3.0 ave to a 1.2. Even thought they were low originally I was waking up feeling terrible which was my main issue.
I will stay at 9 for a while then try a lower pressure and see how that feels.
Questions:
1. Does this mean the auto mode was causing centrals?
2. Before I had a Respironics and tried the cflex and it made me feel terrible also, was it creating the same thing?
3. Are we the exception to the rule, people feeling worse on auto?

Thanks for the info on this forum. I would not have figured this out....

Kurt

Kurt, there is no way to know whether you were experiencing APAP induced centrals. It is a possibility. However, there are likely several possibilities. The bottom line is that if you feel better on CPAP, then CPAP is the best choice for you. Give yourself plenty of time to validate that conclusion, however. Congratulations on what may be a good therapeutic breakthrough for you. At a personal level the end results are really more important than our speculation.

So, I don't believe any longer that whatever has been plaguing me is APAP/pressure related. My success last night couldn't have occured if this was a CSDB-related phenomenon that made me intolerant of pressure gradient or increases.

I mentioned this in a PM, Chuck, but I'll mention it here for the benefit of others. Perhaps more than a single night trial is in order. Perhaps hypercapnic homeostasis/stabilization/destabilization does not necessarily occur instantaneously, or even in a single night after exposure/de-exposure to relevant or degrading factors. Stabilization seemed to occur quickly abandoning APAP in favor of CPAP experimentation. However, destabilization going from CPAP to APAP just may take more than a single night. I would suggest using APAP for an extended period, then reevaluating. If you eventually come back around to higher HI scores and increased awakenings, then you will know that APAP's destabilizing effects on your respiratory drive are gradual rather than a single-night phenomenon.

Loose ends tied. Speculations done. .

[Snoredog]

It appears according to Respironics US Auto patent, Sept. 30, 2004, that 8cm pressure may have some special meaning according to paragraph [0280], page 22 of said patent:

Retyped:

[0280] In a preferred embodiment, the pressure threshold is set
at 8cm, which has been determined from analysis of clinical
data to be a pressure level that provide a moderate degree of pressure
support for most patients, but is not too high as to cause unduly
high pressures to be delivered should the patient be experiencing
a central apnea/hypopnea. It is to be understood that this threshold
can have other values and can be adjustable depending on the char-
acteristics of the patient's history.

It says clinical data shows 8cm pressure to be a level providing moderate degree of pressure support for most patients but not too high as to cause unduly high pressures to be delivered should the patient be experiencing a central apnea/hypopnea.

This is not the first time I have read about something like this, believe something similar was once stated in one of Resmed's autopap studies going back several years ago.

SWS: I don't know if it was that Iron Lung Simulator study or not, but it could have been

[GoofyUT]

APAP: AHI=1.3;AI=0.3;HI=1.0;Pressure=10.2

C