BILEVEL PAP Therapy Pearls: Clearing the First Hurdle

Very interesting information. I will need to mull it over sevearl times.

BarryKrakowMD wrote:If flow limitations were a normal variant, why are they causing sleepiness?

<o.k. merely me thinking out loud, doc>

Rhetorically: Despite FL as a good candidate-pathogen up for consideration, might a less obvious mechanism be responsible for that increased comfort/efficacy?

What if an extremely smooth, timely pattern of receptor stretch is actually the key mitigating mechanism at work (more so than any marginal blood-gas gains from elimination of FL) ? In this scenario we would consider the deceptive possibility that an optimal pressure-based pattern of vagal stimulation may actually exist. The ASV and Dr. Krakow's BiLevel titration protocols both aim for smooth flow curves. In this scenario we plausibly maintain that we are chasing that flow limitation pursuant increased comfort and efficacy. But perhaps we are unwittingly achieving that added comfort/efficacy via an optimal receptor stretch pattern instead. FL mitigation assumes a more incidental role in this hypothetical scenario. But it also unwittingly serves as our visual feedback mechanism as we achieve optimal stretch.

SWS, I'm not fully sure I understand the mechanism you are proposing, so I'll start by asking for more info, but I'll finish with a couple of thoughts they may be relevant to your point.

Do I believe that flow limitatoin could be the sign of something else, and that if you could treat the "something else" would we see the patient's sleepiness dissipate? As I understand it, that theory fits with cyclic alternating pattern (CAP), which alleges arousal variants destabilize the respiratory drive (or perhaps weaken the way airway dilator muscles operate) in ways that make the airway susceptible to SDB events. Somehow treat abnormal CAP arousals (I think it's Type A2 and A3), and then expect breathing to get better. But, what would it mean if you treat the UARS with bilevel or ASV, the airflow curve normalizes, and CAP arousals decrease?

Speaking of subtleties, remember that several researchers have shown the phenomenon of sustained flow limitation ending with a new normal breath, not an arousal, and they consider this to be an SDB event, treatable with PAP therapy, andr resulting in a decrease in symptoms among people who complain of pre-treatment sleepiness. I think this is Rapoport or Montserrat's works or both.

So, undoubtedly, the jury is out on the complex relationship of what causes what in this process, and the best guess is that our current perspective on arousal activity is very incomplete. Once we figure out how to measure say, change in heart rate, fluctuations in blood pressure, or some measure of sympathetic tone, my guess would be that PAP therapy titrations will jump a quantum leap forward.

Anyway, tell us more...

But, what would it mean if you treat the UARS with bilevel or ASV, the airflow curve normalizes, and CAP arousals decrease?

Sir, I'm thinking that it just might mean the roundedness of the flow curve may be at least as important as the area under the flow curve for these patients. That area under the flow curve represents gas volume exchanged. However, the roundedness of the flow curve also happens to indirectly reflect the smooth, kinetic neuromuscular activity you managed to achieve (presumably).

Please refer to this abstract: http://jap.physiology.org/cgi/content/a ... /101/2/609
I'm wondering if the physiologic mechanism you finally get around to treating/exercising with those rounded curves might be the stretch-related receptors themselves (described above). When you achieve those rounded curves by the time you get to titration's end-game, at that point is the smoothness of blood-gas exchange the final mitigating factor, or rather are you really achieving a final, smooth neuromuscular maintenance of airway (via stretch-related receptors)?

In my way of thinking rudimentary anxiety may have its evolutionary roots in reflexive physiology. Each offers a presumable measure of defensive survival value. If you don't find anxiety skewing sleep's autonomic control loop, then I suspect you may find the evolutionary origins of anxiety hiding there in wait--or both. I am admittedly wondering whether a propensity for certain types of neurologically-orchestrated defensive mechanisms tend to travel together in genetics as well.

P.S. I'm still doubtful the presence of flow limitations (irrespective of AH) are nearly as symptomatic/problematic in the affected general population (minus the SDB subset) as they are in the SDB population.

Again, thanks.

"Cause vs Epiphenomenon"-I'm still wondering about those stretch receptors. I'm wondering whether "optimally patterned" stretch can have a mitigating effect--even when stretch-related receptors are presumably neither cause nor epiphenomenon.

Again I'm digging for parallels. I'm once again thinking of a mother, instinctively trying to sooth her crying infant. The child is crying for a reason unknown to the mother. Rocking has worked so often in the past, that the mother occasionally makes use of a small indoor swing. This time the mother places her crying infant in the swing. She repeatedly places her hand against the child's shoulder, gently swinging her child until the crying is eliminated.

Here the mother discerned neither the cause nor the epiphenomenon of the situation. She applied her mitigating technique to the infant's shoulder. While the infant's shoulder is certainly a physiologic mechanism, it most certainly was neither cause nor epiphenomenon.

However, anxiety was clearly involved here. So was maternal instinct. And maternal instinct is arguably a case of innate behavior very efficiently solving some extremely tough problems. Here the mother instinctively relies on a soothing rocking pattern to stabilize her infant's disturbed emotional state. The infant was crying and even happened to manifest highly disrupted breathing. The mother's rhythmic technique stabilized all that. And instinctive rocking is the same technique she uses to induce sleep in her child at bedtime.

Why do central apneas in CPAP-intolerant patients sometime resolve with BiLevel? Can rhythmic vagal input mitigate hypothetical anxiety-related central apneas (even when stretch receptors are presumably neither cause nor epiphenomenon)? Can yet other types of rhythmic or soothing neural input mitigate anxiety-related central apneas?

Does anybody have more ideas for Dr. Krakow? I admit that mine are far out there and pretty strange. So what's new?

-SWS wrote:Despite FL as a good candidate-pathogen up for consideration, might a less obvious mechanism be responsible for that increased comfort/efficacy?

Absolutely, -SWS. We really need to see all the data behind that result before we give aggressive bilevel titration any credit for that. That includes analysis of all parameters during sleep, is this really a comfort measure that applies only to Wake, and/or are a host of other factors (application of the traditional measures to gain compliance with pressure therapy that we must assume were applied simultaneously) really responsible for any increased efficacy.

If increased comfort/efficacy is a subjective assessment ("Boy, this feels great!") then this is a Wake comfort measure. If there is improvement in sleep efficiency after working with the patient for days, weeks, or even longer, then there are plenty of other factors (like simply "getting used to it").

-SWS wrote:What if an extremely smooth, timely pattern of receptor stretch is actually the key mitigating mechanism at work (more so than any marginal blood-gas gains from elimination of FL) ? In this scenario we would consider the deceptive possibility that an optimal pressure-based pattern of vagal stimulation may actually exist. The ASV and Dr. Krakow's BiLevel titration protocols both aim for smooth flow curves. In this scenario we plausibly maintain that we are chasing that flow limitation pursuant increased comfort and efficacy. But perhaps we are unwittingly achieving that added comfort/efficacy via an optimal receptor stretch pattern instead. FL mitigation assumes a more incidental role in this hypothetical scenario. But it also unwittingly serves as our visual feedback mechanism as we achieve optimal stretch.

Strong point. And the human body, using a negative-pressure ventilation system, would be the best at accomplishing that. A positive pressure system would be the worst. Fiddling with the inspiratory curve (adjusting rise time, etc.) would offer improvement, but that technology is rapidly become obsolete with the PAV-type of approach (supporting active respiratory effort).

-SWS wrote:The infant was crying and even happened to manifest highly disrupted breathing. The mother's rhythmic technique stabilized all that. And instinctive rocking is the same technique she uses to induce sleep in her child at bedtime.

That would be a Wake comfort measure.

-SWS wrote:I'm still doubtful the presence of flow limitations (irrespective of AH) are nearly as symptomatic/problematic in the affected general population (minus the SDB subset) as they are in the SDB population.

Right, flow limitations can be a normal phenomenon. They are only a problem if they are a problem. If supply (airflow) is meeting demand (effort), then all you have is a flat waveform that bothers the tech more than it does the patient. If demand exceeds supply, as determined in the other channels, then the nature, extent and attack on FL can be made.

-SWS wrote:What if an extremely smooth, timely pattern of receptor stretch is actually the key mitigating mechanism at work

Aggressive bilevel would not be the way to attain that. As you implied above, a floating set of parameters like you see in ASV (the "smart inspiration" or PAV part, like the "ocean wave" of AdaptSV) would be far more efficient. In straight obstuctive disease, the ASV part is probably unnecessary, so one should look at VSet Auto and Malibu in ResMed, BiFlex/AFlex and BiPAP Auto in Respironics, etc.

The JAP article brings in highly relevant points about inspiration, -SWS. Now, if we add the recent findings of fellow poster and sometime sparring partner split_city from the Oktoberfest thread, we are reminded that there are multiple forces at work during expiration as well:

split_city wrote:Background: Our lab believes that increased pressure inside the abdomen, common in overweight/obese males, may contribute to OSA. How you ask? The increased abdominal pressure is likely to force the diphragm and airways upwards towards the head. This movement may reduce the tension or "tug" on the airway, thereby making the airway "floppier," thus more collapsible. There have been a series of studies in animals which have shown that if you reduce the tension on the airway, the airway becomes more collapsible. The reverse is seen if you stretch the airway.

Aim of study: Consequently, we thought to ourselves, what would happen to airway collapsibility if we simply increased pressure inside the abdomen? Would this make the airway floppier and more collapsible?

Study population: Obese (BMI 30-40) male OSA patients already established on CPAP.

Protocol: Allowed patients to go off to sleep on CPAP. Assessed airway collapsibility when there was no abdominal compression and when pressure inside the abdomen was increased via abdominal compression. Airway collapsibility measurements were taken only when subjects were in stage II sleep. Patients remained supine throughtout the study.

Results: 14 successful studies

Abdominal compression increased abdominal (stomach) pressure by ~50%

This led to an increase in airway collapsibility of about 0.6cmH2O (NOTE: Difference between an OSA patient and a non-OSA person is about 4-6cmH2O)

Abdominal volume decreased by ~1L, thoracic volume increased by ~0.5L i.e. abdomen went in while chest went out with abdominal compression. Net change in lung volume was ~0.5L.

Conclusion: This is the first study to show that abdominal compression increases airway collapsibility. These results may (partially) explain why more males have OSA compared to females.

So far, we have these considerations:

1. Inspiratory airway behavior.
2. Expiratory airway behavior.
3. The effect of sleep state (including Wake).
4. The effect of pressure therapy modality.
5. Choosing parameters to monitor effectiveness.

SAG

SAG wrote:So far, we have these considerations:

1. Inspiratory airway behavior.
2. Expiratory airway behavior.
3. The effect of sleep state (including Wake).
4. The effect of pressure therapy modality.
5. Choosing parameters to monitor effectiveness.

Absolutely no disrespect, sir... But that's what any subscriber to a biologically-mechanistic paradigm with a linear problem-solving approach might "have". I believe that type of paradigm and linear approach to be absolutely essential in science. However, it doesn't necessarily work well regarding exploration of a largely unknown behavioral/cognitive side of the autonomic sleep bridge. Rather, it politely says: "Everybody needs to get back on the biologically mechanistic side of the bridge and resume thinking inside the mechanistic box."


I also think many of your valid concerns go toward the important topic of exactly how medicine should be practiced, specifically with respect to CPAP therapy. I think your points are all tenable, SAG. Regarding Dr. Krakow's proposal that larger magnitudes of BiLevel PS be more routinely employed toward a very aggressive normalization of I and E: I also have my concerns about an FL "zero tolerance policy". Despite my concerns I will not press my views about possible epidemiological pitfalls because I very strongly feel that I have no proper place discussing policies related to the practice of medicine. I am a layman to your branch of science. Plain and simple.

However, this layman has extreme gratitude for the intellectual efforts and professional struggles of Dr. Krakow, SAG, split_city, ProfessorSleep, BrianRT, et al.

I suppose one caveat of message board discussions is the highly unstructured nature of the venue regarding not only objectives in general, but also prioritization of topics. Dr. Krakow's threads bring an entire array of topics to the table regarding medical theory, research, and practice. My interests as a layman lie primarily in the theoretical inquiry that cognitive/psychological issues may have an unknown impact on autonomic breathing during sleep--perhaps in a biasing or directly skewing manner.

I also suspect the evolutionary cradle of rudimentary anxiety may reside very close to reflexive physiology in autonomic anatomy. However, I will not press my own curiosity any longer, as I fear my subconscious may have assumed the role of Ahab, with apnea's origins looming somewhere on the horizon as my nemesis whale.

P.S. Split_city, well done!!!

-SWS wrote:Rather, it politely says: "Everybody needs to get back on the biologically mechanistic side of the bridge and resume thinking inside the mechanistic box."

I dunno there, -SWS. First, I have to swear off graphics, now I have to climb outside of my box (actually, it's a "loop")? Seems like all this "bold thinking" is getting pretty restrictive to me! What's next, having to post in a white shirt and "sincere" tie?

OK, seriously, since not a lot of people (really, none that I know of) utilize aggressive PS bilevel to attack sub-clinical FL, trying to figure out all the things that may occur requires a bit of conjecture. So SAG offers these "out of the box" thoughts:

Fixed, large-gradient pressure support can have an overall destabilizing effect as it cannot adjust to sleep-stage specific conditions (which sleep-stage do you titrate to? If it's REM, then light NREM is going to get one heck of a PS barrage).

Pressure-based therapy should impinge as little as possible on existing pharyngeal muscle dilation activity such as timing with inspiration, duration of stimulation and degree of activation.

IPAP may suppress desirable pharnygeal muscle activity by inhibition via stretch receptor mechanism, creation of a relatively hypocapneic state, and negating perhaps the most powerful of PMD stimuli, that of localized negative pressure (the "why some FL may be good FL" concept).
Aggressive PS gradient then becomes an inevitable foregone conclusion. It is the end result of pharyngeal dilator muscle activity suppression.

-SWS wrote:Despite my concerns I will not press my views about possible epidemiological pitfalls because I very strongly feel that I have no proper place discussing policies related to the practice of medicine. I am a layman to your branch of science. Plain and simple.

Me too, -SWS. Frankly, I disagree with the cliche "The only way a CPAP machine can hurt you is if it falls on your head." Arbitrarily wingin' the dials around will automatically get at least 15% of patients into trouble.

But I would also submit that if "out-the-box", "new paradigm" or whatever cliche de jour proposed therapy can't get by cross-examination by a couple of hackers like us, then what chance does it have in peer-review?

Coming up next: If raising IPAP is bad, why lowering EPAP is worse.

SAG

The bi-level breathing info was very helpful and informative
I am new to cpap breathing, just started two days ago. I have a Remstar M series Auto A-flex (pressure range 6-12). It was set on A-Flex the first night and liked it except it felt as if it cut off intake pressure after 3 seconds forcing me to drag air in to finish my intake breath. I thought it had a sensor to detect my change from inhale to exhale and automatically adjust. When I first start to sleep I breath in long and slow, between 3 to 10 seconds intake and was frustrated by the machine’s pattern. I called my RT the next morning, she said that the pressure remains constant, it just “feels” that way, I could learn to adjust to it. She suggested switching to the C-Flex feature. I did so, this was better with regard to the intake breath but I liked the sense the A-flex gave on the exhale. Is there a way to fine tune this Remstar’s A-Flex mode to accommodate a longer intake breath?

[quote="sombu"]The bi-level breathing info was very helpful and informative
I am new to cpap breathing, just started two days ago. I have a Remstar M series Auto A-flex (pressure range 6-12). It was set on A-Flex the first night and liked it except it felt as if it cut off intake pressure after 3 seconds forcing me to drag air in to finish my intake breath. I thought it had a sensor to detect my change from inhale to exhale and automatically adjust. When I first start to sleep I breath in long and slow, between 3 to 10 seconds intake and was frustrated by the machine’s pattern. I called my RT the next morning, she said that the pressure remains constant, it just “feels” that way, I could learn to adjust to it. She suggested switching to the C-Flex feature. I did so, this was better with regard to the intake breath but I liked the sense the A-flex gave on the exhale. Is there a way to fine tune this Remstar’s A-Flex mode to accommodate a longer intake breath?

Hello everyone, I'm new to the site and cpap in general. I was prescribed a Malibu bipap, and have been trying to use a rental for the last few nights. I haven't been ables to sleep for longer than an hour or so with it, and actually have a hard time falling asleep because of the breath timing. Full face mask. I think my pressures are 7 and 10.

I think the main issue is the timing of breaths, or the transition between inhaling and exhaling. Before I'm asleep, if I take a deep breath and exhale the machine ups the pressure before I'm done exhaling. It leads to a choking sensation, and my body fights against inhaling. I notice this is the same feeling when I'm woken up by the machine. It seems as if the machine also wants me to breath quicker, or the trigger for breathing transitions is too sensitive, aka making me try to breath when I just slow my exhale, but am not ready for another breath.

What can be adjusted? I called my DME provider, and I'm scheduled to go back in sometime. They were thinking of using auto mode.

Hi folks.

WOW !

That's all I can say after just reading this entire set of posts. Have been busy these past few months & missed most recent discussions but this caught my eye during a rare return peep (BiLevels are a topic dear to my heart). Dr Krakow's comments resonate so closely to my experience with BiLevels.

What great input from so many thinking minds. But, 1st I want to thank Dr Barry Krakow for this thread and in particular your wonderful way with words - for myself, I really connect with the way you describe things and the comments you have made in regard to certain types of BiLevels - at a later time I'll explore some of the issues with Auto BiLevels and the challenges posed to their designers.

Re use of charts & graphs etc: in this thread. I will add that they have always been an interesting input, but am in support of the views of those who in this thread, have leaned towards describing things verbally, much in the way Dr K has. To SAG, I add that there really is value to the bulk of us plebs to the way Barry K is dealing with this topic. Taking it into very scientific realms no matter how accurate the issues, looses too many of us along the way.
To SWS, you really should be in the diplomatic core - while Barry is showing a wonderful talent for describing the BiLevel experience verbally from his highly qualified perspective, you are again showing your kindness and diplomatic skills in regard to some of the responses - thanks.

Ozij, enjoyed your comments - as always very insightful & measured.

To the other contributors - great input to an excellent thread.


Thanks

DSM

#2 - corrected Dr K's surname spelling
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CPAPopedia Keywords Contained In This Post (Click For Definition): auto

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

This is a question for Dr Krackow in regard to BiLevel settings for ipap & epap.

In some documentation I have read (in particular the PB330 clinical manual). It mentions that having a gap of around 8 CMS between ipap & epap is not unreasonable. In fact when I 1st set up the PB330 I chose 8/15 as the settings.

At the time I felt I was getting great therapy. for 8 months prior I had been on cpap then apap but in both cases dropped them because after an initial gain they seemed to no longer be delivering adequate therapy.

After about 6 or so months I managed to obtain a VPAP III S plus had a recording Pulse Oximeter so started collecting the nights data. The VPAP III S was set up as close to the settings of the PB330 as I could set them. To my great surprise the data showed AHI results in the 40-60 range. After some feedback from a cpaptalk past regular - I changed the gap to 4 CMS and dropped the ipap to 14 thus had the machine set for 10/14. At this point the AHI scores droppe to around AHI of 1.0 up to about 3.0. But liking the quietness of the PB330 I went back to it set with these new settings.

Just before reverting to the PB330 I did a number of experiments recording the data from straight CPAP and from BiLevel incl SpO2 numbers. In the end I dropped the ipap by one more CMS (to 10/13). And had 12 months of great therapy.

My main interest on this is that I became convinced based on the data gathered, that a gap of greater than 4 was problematic, less than 2 seemed pointless. 2 itself seemed minimalist & of debatable value but 3 seemed optimal. Although I was my own guinea pig, I am sure the results would be more typical than not with others. So the experiments led me to believe that a gap greater than 4 should only be set by a specialist & probably only if the patient has some breathing complications and gaps under 3 seemed of questionable use.

So conclusions reached included that BiLevel was always at its best if I kept the gap at 3 and occasionally went to 4 but even a setting of 4 seemed to result in less harmonious sleep. Currently I have the machine set to 11/14 as I needed to increase the CMS due to a recent decline in therapy quality brought on by a minor weight gain - the change from 10/13 to 11/14 seems to have made a dramatic improvement back to the best of a few months back. In fact have been able to resume daily exercise & in 2 weeks dropped from the increased 92.5 kg back to 90kg today.

What I am interested to hear from you is if you have observed any issues related to patients on ipap/epap gaps greater than 3 or 4. Do you have any thoughts on these gap settings.

Also I began to doubt the goodness of a BiLevel that changes the gap dynamically during the night (which is what the Bipap Auto does). I have one of these machines but stopped using it for 2 reasons. 1) I cant set & hold the ipap/epap gap the way I would like it (as explained above) and 2) the machine has a habit for me, of dropping out of ipap into epap too early & I can do nothing to stop it (it has very few settings to work with). I see you are trialling the Malibu which I gather does allow the ipap/epap gap to be held - any data from its use will be interesting.

Thanks

DSM

dsm wrote:Re use of charts & graphs etc: in this thread. I will add that they have always been an interesting input, but am in support of the views of those who in this thread, have leaned towards describing things verbally, much in the way Dr K has. To SAG, I add that there really is value to the bulk of us plebs to the way Barry K is dealing with this topic. Taking it into very scientific realms no matter how accurate the issues, looses too many of us along the way.

OK then, I must apologize! I guess I take the expression "Stay loose" too literally! I thought that was a good thing!

If the concept that Dr. Krakow proposes (bilevel titration with potentially wide PS gradient, lowering EPAP and raising IPAP based on zero flow limitation tolerance) has merit, then it should absolutely become a consideration of the Titration Algorithm. This should also include "Admission Criteria" defining who may or may not benefit, for even in your own case, you are clearly a "non-qualifier".

However, eventually some objective data will need to be presented before the medical community moves en masse to adopt this new protocol, even if that objective data is subjective data ("I feel better"), as long as it's double-blind. Physiologically, I find little justification, in fact the scientific evidence seems to contradict this concept pretty much across the board. As a scientist, I would think that Dr. Krakow would welcome robust debate challenging his theory. Clearly, I cannot get through a single sentence without using at least one comma.

Coming up next: The Autonomic Response: Heart Rate Variability vs. Pulse Transit Time

SAG

SAG wrote:Clearly, I cannot get through a single sentence without using at least one comma.

Don't downplay the importance of commas for one minute, sir. I remember glancing at a medical curriculum once. In that catalog I saw an entire course centered around "Commatose Patients". Clearly commas are somehow extremely important to the practice of modern medicine. My vote is that you continue using commas (with or without judicious use of a white buttoned-down dress shirt and one nicely accented necktie).

Dsm, it's good to see you! See you guys in a few unknown units of time. I'm getting ready to head off to warmer latitudes. This weather is nuts.

Seriously, though, thanks for the educational and entirely stimulating thread. Special thanks to Dr. Krakow!

P.S. Any functionally "flat" system control model lacks spatially-related dimensions of cardiopulmonary interaction (not space-time dimensions, rather functional degrees of physiologic interrelatedness/indirection regarding pathophysiology). Additionally many low-level contributing physiologic details are clearly unknown to modern medicine--and thus remiss in presently employed control system models. That any researcher might want to step outside any given model in an attempt to discern what might be missing from that or other contemporary control system models makes perfect sense to me.