CPAPtalk.com

I think one discussion point here that creates a pile of confusion in my mind relates to using the terms "Expiratory Flow Limitation" (EFL) and "Expiratory Intolerance" seemingly interchangeably. I would view these as entirely different entities that would require different tools to quanitify (are they there, and are we using the right data channel to identify them), qualify (do they, in fact, create a problem) and treat (and an equally important concept here is whether treating one entity in one set of criteria results in overall improvement of sleep architecture). Bilevel 25/12 is a bear, and I would also argue that if a patient had a tendency for central apnea you'd be more apt to start that cascade using that modality rather than expecting to see it from "expiratory intolerance". I would also also submit that if central apnea may be/is a concern, I'd be tracking that using some sort of CO2 monitoring device, (on sale this week at Circuit City during their "Red Tag" sale).

Back to the previously submitted waveform:



I would question if this is EFL. The first segment is rounded, which is where I would look first for signs of EFL; the phenomenon occurs during periods of zero to near-zero flow, so is it really a flow-anything; the person is now in SWS, which is a more airway-stabilizing sleep state, so it is paradoxical that there is stable airway in light NREM sleep and then it disappears in deep SWS; and in re: exipratory intolerance, if the patient is in SWS, any intolerance would only be exhibited by the sleep technician. And one really needs to look at all the other data channels to properly interpret this. Those "bumps" are occurring at 60 cycles per minute, and if that patient's HR is 60/minute I'd really be thinking "hey, what the heck am I really doing here".

Closer analysis of the other effort channels will greatly assist in the interpretation. In peeling back the onion to micro-analyze waveform, admittedly it's difficult to isolate cause and effect. Not only are there multiple forces contributing to the waveform, but most of them will in turn be affected by another pile of factors (sleep state, anatomy, position, machine, machine mode, acquisition settings).

Again, same patient, PB420E, respiratory cycle filtered out of Patient Flow and Abdomen, moving from normal breathing to obstructive apnea (no flow):



The cardiac oscillation has now disappeared from the Patient Flow channel, so this is an opportunity to view the contribution of the machine pressure fluctuations as it reacts to changes in flow and/or patient anatomy. As you can see, they are significant.

SAG

Meanwhile, we need to back up a little (like to a 2-minute view as oppsoed to the 30-second windows we've been looking at so far) to get a better handle on what's happening here. Even with only 5 out of 16 channels, this is a veritable treasure trove of information:



Get started on this, right now I gotta run. Really.

SAG

Absolutely, Expiratory Intolerance is different than Expiratory Flow Limitation. I don't think I said otherwise, but sorry if I'm causing that confusion.

An FLE event whether on inspiration or expiration should mean the airway experiences resistance. Using the standard collapsible cyclinder/tube analogy, with UARS we expect to either see a slight narrowing of the tube diameter or if this is not visible, then dynamically, we expect there to be measurable resistance likely caused by some change in the tension in the airway dilator muscles, which prevents air from passing through the tube as smoothly as in a normal breathe. Again, you can develop this problem on inspiration or expiration.

Expiratory intolerance suggests the the wall of the tube is fluttering or wobbly or doing something dynamically that appears to indicate (in our experience) that the patient is fighting the incoming pressurized airflow while trying to breathe out. Expiratory intolerance has been called expiratory instability by our group in the past, but after having done a more careful reading of older literature, I realized that the term "instability" has been used by many pulmonologists to describe the collapsibility of the airway, that is, an unstable airway is one that is prone to SDB events, etcs.

Any flow limitation event requires higher pressure, higher CPAP, IPAP, or EPAP, because you are trying to splint the airway open. but on expiration as CPAP pressure goes higher, it causes the wobbly airway, indicating the high pressure is making the airway intolerant to the process. In my clinical experience, although I concur that many variables influence the process, the single most constant variable that predicts this problem is anxiety in general or just a report of initial discomfort from the patient when using CPAP while awake during the initial desensization prior to the start of the titration. By the way,patients report the cessation of this discomfort when switched to bilevel, again while awake. Then, of course, during the titration and the night of sleep, you can still see the intolerance crop up from time to time on expiration, which is a cue to the sleep tech to drop CPAP pressure, switch to bilevel, or if on bilevel, drop EPAP.

Now, an incredibly key aspect of this phenomenon is whether or not you think the patient is going to adapt to the sensation of pressurized airflow during that first titration or whether it will take several weeks or months to do so, or will the patient always suffer too much anxiety to ever be able to use PAP therapy effectively. Thus, it is not at all uncommon to see a patient return for a full night bilevel titration a month or two later, and both IPAP and EPAP can be raised (as individually indicated to normalize the inspiratory or expiratory flow curve) to new pressures, and the patient reports having slept better that very morning compared to all their sleep experiences in the prior month of PAP use. Which really means that they had diminished their intolerance problem and were ready to test out higher pressures. In my opinion, this finding technically means that they needed higher pressure at the first titration, but it would have been impossible to have them use such pressure due to intolerance.

Does expiratory intolerance precede central apneas? Absolutely. It is one of the most common findings in a sleep lab. It may be more generally perceived as pressure that is too high, because all sleep techs report the finding of "pressure was raised, central apneas developed, so pressures was dropped." But, if you consider the distinctive feelings of inspiration and expiration, it is certainly easier to adapt to a feeling of high air pressure coming in when you breathe in than it is to adapt to high pressure when you breathe out, so the more common antecedent to a central apnea would be predicted to be during expiration. Are some of these centrals related to loop gain and changes in CO2? While the answer is probably yes in some cases, this type of central might also be primarily mechanical forces at work: you don't like the feeling of pressurized air, so you "check" your breathing (as you might when sticking your head out the window of a rapidly moving vehicle).

Last, for now, many pulmonologists are quick to state that patients are "passive" to the experience of PAP therapy while asleep, that is, they believe the patient does not experience emotional responses to it. I strongly disagree and always counter with our common experiences in REM sleep, namely dreaming and the enormous emotional responses we have to our dreams. I remain convinced, at this point, that anxious patients tend to bring their anxiety with them into the sleep state, and expiratory intolerance manifests when a threshold of discomfort is crossed between level of pressurized air and level of comfort in breathing out against that pressurized air. Remarkably, I encounter at least 25% of our patients who "think" they are not anxious, but who really suffer significant anxiety, yet because their TFI System (thoughts, feelings, images) is so out of balance, they do not know how to recognize or measure anxiety (see posts on the topic "Dr. Krakow's book" regarding emotional processing or hey, buy the book Sound Sleep, Sound Mind at http://www.sleeptreatment.com.

P.S. I find 120 sec epochs much less clarifying that 30 second epochs, especially if you are trying to spot the subtle bumpiness of intolerance.

P.S.S. Don't think it's cardiac oscillations linked to intolerance, but I will try to find another epoch in coming weeks to verify and demonstrate.

BarryKrakowMD wrote:Does expiratory intolerance precede central apneas? Absolutely.

Actually, if forced to explain the cause of central apneas in this scenario in 10 words or less, I would say that central apneas occur when the pCO2 drops below the apnea threshold.

BarryKrakowMD wrote:It may be more generally perceived as pressure that is too high, because all sleep techs report the finding of "pressure was raised, central apneas developed, so pressures was dropped." But, if you consider the distinctive feelings of inspiration and expiration, it is certainly easier to adapt to a feeling of high air pressure coming in when you breathe in than it is to adapt to high pressure when you breathe out, so the more common antecedent to a central apnea would be predicted to be during expiration.

I always thought that a better way to look at this was

Stimulus > Arousal > Hyperventilation > pCO2 Decrease Past Apnea Threshold > Central Apnea.

BarryKrakowMD wrote:Are some of these centrals related to loop gain and changes in CO2?

Right, the CSDB thing.

BarryKrakowMD wrote:While the answer is probably yes in some cases, this type of central might also be primarily mechanical forces at work: you don't like the feeling of pressurized air, so you "check" your breathing (as you might when sticking your head out the window of a rapidly moving vehicle).

Hah?

BarryKrakowMD wrote:P.S. I find 120 sec epochs much less clarifying that 30 second epochs, especially if you are trying to spot the subtle bumpiness of intolerance.

Right, this example is to demonstrate a couple of other phenomena, including a way to assess flow limitation with a much greater degree of reliability and accuracy. While dissecting waveforms is fun, it takes too long to account for all the variables, and we kinda beat up on that enough.

SAG

BarryKrakowMD wrote:Absolutely, Expiratory Intolerance is different than Expiratory Flow Limitation. I don't think I said otherwise, but sorry if I'm causing that confusion.

BarryKrakowMD wrote:Expiratory intolerance suggests the the wall of the tube is fluttering or wobbly or doing something dynamically that appears to indicate (in our experience) that the patient is fighting the incoming pressurized airflow while trying to breathe out. Expiratory intolerance has been called expiratory instability by our group in the past, but after having done a more careful reading of older literature, I realized that the term "instability" has been used by many pulmonologists to describe the collapsibility of the airway, that is, an unstable airway is one that is prone to SDB events, etcs.

My confusion remains in 2 areas. First, if Expiratory Intolerance is Expiratory Instability resulting in Increased Collapsibility of the Airway that is Prone to SDB Events (of which Expiratory Flow Limitation can be one), then we're right back where we started from, and the algorithm would be more pressure (CPAP in unilevel or EPAP in bilevel), and not less.

Second, the area that is described as having Expiratory Intolerance or Expiratory Instability



is occurring at end- or even post-expiration (this phenomenon continues after 3 seconds (in that software, I believe "dotted" lines are 1-second increments)). I would submit that at that point, flow is so slow it can't generate a "flutter", and that if flow is continuing after 2 seconds, then there could well be another underlying medical issue (time your exhalation at home during quiet breathing, and if you're still exhaling after "Two Mississippi", you need a PFT).

SAG

Wonderful, wonderful discussion. Thank you so much!

I can see that the use of the term Expiratory Instability is now causing more confusion. As I said, we used it to equate it to Intolerance, but older literature uses it to equate it with collapsibility. So, let's remove Instability to avoid confusion.

Intolerance in the graph is occurring at the point that looks like there is no or little flow, but it is my understanding from discussing this point with pulmonologists that this area is called, "end-expiration."

Whatever we call it, this is the finding we keep seeing in patients who don't seem to tolerate CPAP, thus the word intolerance, and it is relieved by a lower pressure, e.g. switching to EPAP, but if the pressure were lowered too much then you would see a potential for EFL to develop and the EPAP pressure would need to be raised to normalize the airflow curve.

Again, too high a pressure induces intolerance and too low a pressure leads to flow limitation (the likely subtlest form of collapsibility).

Loop gain advocates certainly make their case for changes in apnea threshold and fluctuations in CO2, but there's a funny wrinkle in this theory that I've always wondered about and in asking a few pulmonologists I have not gotten a clear answer. So, I'll provide the scenario to you and see what you think:

The theory of loop gain says that after apnea termination, you breathe too hard and hyperventilate off too much CO2, which then lowers CO2 to the point that respiratory drive should diminish since you don't need to blow off as much CO2. As a result, a central apnea can arise from this drop in respiratory drive. Now, in either the literature or the conventional wisdom, probably both, bilevel allegedly eases ventilation by virtue of its lower EPAP, and therefore it is easier to blow off more CO2.

Now if I've stated the above properly, when someone suffers pressure intolerance due to CPAP, then switching to bilewel should actually increase the risk of central apneas because it would lead to further CO2 reductions, but what we in fact see repeatedly, is that if you switch someone from CPAP to bilevel, they will often eliminate the centrals. That is why the central apneas triggered by CPAP could be solely or mostly due to pressure intolerance, not a CO2 effect. That's just my opinion. As you may know it's expensive and difficult to accurately monitor CO2 while someone is using PAP therapy.

Clearly, there are a group of patients where the loop gain problem is the primary factor, and bilevel either wouldn't work or arguably might make it worse. These patients often respond or so the research shows to ASV devices (adapto-servo-ventilation).

BarryKrakowMD wrote:Loop gain advocates certainly make their case for changes in apnea threshold and fluctuations in CO2, but there's a funny wrinkle in this theory that I've always wondered about and in asking a few pulmonologists I have not gotten a clear answer. So, I'll provide the scenario to you and see what you think:

The theory of loop gain says that after apnea termination, you breathe too hard and hyperventilate off too much CO2, which then lowers CO2 to the point that respiratory drive should diminish since you don't need to blow off as much CO2. As a result, a central apnea can arise from this drop in respiratory drive. Now, in either the literature or the conventional wisdom, probably both, bilevel allegedly eases ventilation by virtue of its lower EPAP, and therefore it is easier to blow off more CO2.

Now if I've stated the above properly, when someone suffers pressure intolerance due to CPAP, then switching to bilewel should actually increase the risk of central apneas because it would lead to further CO2 reductions, but what we in fact see repeatedly, is that if you switch someone from CPAP to bilevel, they will often eliminate the centrals. That is why the central apneas triggered by CPAP could be solely or mostly due to pressure intolerance, not a CO2 effect. That's just my opinion. As you may know it's expensive and difficult to accurately monitor CO2 while someone is using PAP therapy.

Clearly, there are a group of patients where the loop gain problem is the primary factor, and bilevel either wouldn't work or arguably might make it worse. These patients often respond or so the research shows to ASV devices (adapto-servo-ventilation).

In depends if you're having sporadic centrals that are caused by arousal, in which centrals are the expected response to arousal and are self-limiting, and attention needs to be given to the cause of the arousal, not the central; or, if the centrals are of the self-perpetuating type, and central begets central. Them is a problem.

Loop gain needs a couple of components in breakthru quantities. The CSBD group probably all have in common an increased chemoresponsiveness (it's not the "breathe too hard after apnea termination", it's the "breathe WAY too hard after termination".

Graphically, the increased chemoresponsiveness group shifts the vector to the left in Feedback Gain, such that a given change in pCO2 will elicit a stronger ventilatory response.



Add in bilevel (respresented by PAV (Proportional Assist Ventilation)) and you compound this with another left shift in Controller Gain:



Add in a circulatory delay so you pile response on top of response and now you got a BIG problem.

So, in these patients, if

BarryKrakowMD wrote:bilevel allegedly eases ventilation by virtue of its lower EPAP, and therefore it is easier to blow off more CO2.

you will really make them FUBAR.

Monitoring CO2 is not that expensive, especially if reserved for only those that need it.

Thanks to Dr. Younes.

SAG

As I've said before, I'm not a respiratory physiologist, nor could I play one on TV, but as I comb through your responses, I did not find an answer to my question, unless you misunderstood the question I'm driving at:

Given the paradox of bilevel and CO2, why does bilevel reduce central apneas in so many patients that develop them while using CPAP?

As much as I love images, I would appreciate a response that doesn't rely on graphics but rather might be spelled out in words so most of us (or maybe it's just me) will follow.

Thanks for your efforts.

BarryKrakowMD wrote:Given the paradox of bilevel and CO2, why does bilevel reduce central apneas in so many patients that develop them while using CPAP?

LOL! That would be like me asking you, "There's this patient that can't sleep. What do you think the problem is?"

Seriously, there's even more layers of the onion in addressing CA (and I don't mean, "Omigod! There's ONE central apnea, it's the APOCALYPSE!!!") than there were in waveform analysis, but the concepts of the Loop are fairly universal, and can be applied in pretty much any form of central apnea, whether its long-cycle, short-cycle or even isolated ("There's another one!! Quick!! Buy a thousand rolls of toilet paper!").

If you have a specific or representative case you'd like to present, post some epochs and history and I'm sure we'll get a robust discussion going.

SAG

Hedging, are we?

Okay, how about if I ask the negative of the paradoxical question, given that you seem to have a either a bias or some other insight into why bilevel would not help to reduce centrals in a patient who started having centrals while on CPAP. Here goes:

Why wouldn't or shouldn't bilevel therapy reduce central apneas in this specific type of case in which CPAP appears to trigger centrals?

In other words, in terms of science, the fact that I've seen hundreds of cases of this phenomenon does not prove that bilevel does indeed reduce centrals in these particular patients, but I've put forward a theory as to why it might be pivotal in correcting centrals. Help us out here and put forward your theory as to why bilevel should not help these patients.

Fair enough?

BarryKrakowMD wrote:P.S.S. Don't think it's cardiac oscillations linked to intolerance, but I will try to find another epoch in coming weeks to verify and demonstrate.

BarryKrakowMD wrote:Hedging, are we?

Yes, apparently.

SAG will consider your request. However, he really needs to see the material he has previously requested to get a better understanding of the skill level he is dealing with. This will aid him in determining the content of his explanations.

SAG

Dr. Krakow wrote:Given the paradox of bilevel and CO2, why does bilevel reduce central apneas in so many patients that develop them while using CPAP?

I personally don't think the loop gain theory explains intolerance-related central apneas (yet it explains certain other central apneas very well).

Right about now I'm favoring the theory that central respiration has a "memory-like" affect, and that rhythmic reinforcement sourced by BiLevel (pressure-based vagal stimulation) is what does the trick in these cases. That rhythmic reinforcement may even be comforting in a primal sort of way--like a mother rocking a child--quite possibly alleviating CPAP-related discomfort/anxiety in some cases.

-SWS wrote:

Dr. Krakow wrote:Given the paradox of bilevel and CO2, why does bilevel reduce central apneas in so many patients that develop them while using CPAP?

I personally don't think the loop gain theory explains intolerance-related central apneas (yet it explains certain other central apneas very well).

Right about now I'm favoring the theory that central respiration has a "memory-like" affect, and that rhythmic reinforcement sourced by BiLevel (pressure-based vagal stimulation) is what does the trick in these cases. That rhythmic reinforcement may even be comforting in a primal sort of way--like a mother rocking a child--quite possibly alleviating CPAP-related discomfort/anxiety in some cases.

-SWS wrote:I personally don't think the loop gain theory explains intolerance-related central apneas (yet it explains certain other central apneas very well).

What?! Blaspheme! Of course it does! Utilizing the upper Loop Graphic, an Arousal will create a Ventilatory Disturbance which will increase Minute Ventilation in Plant Gain, such that the pCO2 will drop below the Apnea Threshold (represented by the lower curve dropping below the horizontal line) and apnea ensues. However, it is not allowed to perpetuate as short-term potentiation of respiration provides a dampening effect against ensuing overshoot.

I have a great graphic to help illustrate this, but "apparently" some people are offended by "graphics", which strikes me as quite ironic, since these same people appear to be so interested in "imagery".

SAG