BILEVEL PAP Therapy Pearls: Clearing the First Hurdle

[StillAnotherGuest]

But I will counter by saying that the APAP algorithm and PSG session perform completely different analytic methods on that flow channel. Out of algorithmic necessity, the APAP channel will derive multiple input signals that are not derived from the same flow channel during a PSG.

And toward the end of demonstrating precisely what/why/how an APAP misses what it does, human-eye analysis is unintentionally misleading IMO. The APAP does track multiple input signals. More importantly, the APAP necessarily works with temporal variables. The APAP algorithm does not at all have the time-domain micro-snippet limitations imposed by these demonstrations. And most importantly, any APAP algorithm is guaranteed to employ much more robust analytic methods than will ever be performed by a cursory inspection of human eyes.

Human eyes cannot perform algorithmic-equivalent exercises on PSG waveform analysis either---especially as depth-of-data analysis becomes increasingly important (such as in the domain of quantitative temporal analysis).

OK, y' lost me there, -SWS. It is my contention that the "human-eye" analysis of this waveform of Dr. Krakow



may be incorrect (as well as the circumstances of its acquistion). So does that mean we're in agreement?

As far as the APAP, it did what it's supposed to (impressively aggressively, at that). The human response would have been undoubtedly much slower (for whatever good or bad that would be).
SAG

[-SWS]

It is my contention that the "human-eye" analysis of this waveform of Dr. Krakow may be incorrect (as well as the circumstances of its acquistion). So does that mean we're in agreement?

Sorry, SAG. Yes, I agree this is one likely place to look for an erroneous theoretical sub-premise regarding the flow-curve response of CPAP-intolerant patients.

However, the question in my mind is just how often does Dr. Krakow encounter that expiratory nuance in CPAP-intolerant patients? If he's encountering it fairly frequently, and if he's achieving measurable gain in tolerance or efficacy by mitigating it, then it's a significant finding. Bear in mind, as Dr. O pointed out earlier, that Dr. Krakow may very well be seeing disporportionate numbers of CPAP-intolerant patients.

Speaking of clarifications, I have one of my own statements much earlier in this thread that I would like to fix up. Here's my erroneous statement:

By now most of us are aware that Dr. Krakow uses a more aggressive BiLevel titration protocol than industry standard. Regardless Dr. Krakow attributes increased efficacy to rather aggressively normalizing the expiratory flow curve.

The underlined part of that statement is truly in error. Dr. Krakow states that he aggressively normalizes both inspiratory and expiratory flow curves. There are undoubtedly significant numbers of clinicians who will not eliminate inspiratory flow limitations during titration. That alone distinguishes Dr. Krakow's titration protocol from many institutions. However, to aggressively normalize the expiratory flow curve probably distinguishes Dr. Krakow's methods from the vast majority of clinicians. And it would specifically be that two-fold objective (of normalizing both inspiratory and expiratory flow curves) that results in unusually heavy reliance on BiLevel modality.

If a patient simply seeks a traditional BiLevel titration because of what they have read in Dr. Krakow's threads, then I doubt they will see the same results as Dr. Krakow's patients (whatever those results may be). Replication of Dr. Krakow's technique would rely on both I and E flow curve normalization.

Regarding the reduction of central apneas when switching CPAP-intolerant patients to BiLevel (which I suspect may be avoidance of Herring Breuer "skew"). Indeed, Dr. Krakow's novel research has centered around the cognitive and psychological aspects of sleep. While Dr. Krakow's initial work is based heavily in the cognitive/psychological aspects of dreams, he now seems to be examining correlations he has undoubtedly encountered between cognitive/psychological issues (such as trauma) and sleep disordered breathing itself.

It's probably clear to everyone that cognitive/psychological issues can impact voluntary or daytime breathing. And it's probably clear that cognitive/psychological issues impact sleep as well. But I suspect it is not at all clear to most researchers what direct or indirect impact cognitive/psychological issues may have on autonomic breathing. The status-quo working assumption so far has been that autonomic breathing must be an immediate function of reactive cardiopulmonary biology--that cognitive/psychological issues have no direct or biasing impact on autonomic breathing during sleep.

That's an assumption that science is entirely obligated to challenge, in my opinion. And what a better researcher to challenge that assumption than a pioneer in the cognitive/psychological aspects of sleep.

[StillAnotherGuest]

Dr. Krakow states that he aggressively normalizes both inspiratory and expiratory flow curves. There are undoubtedly significant numbers of clinicians who will not titrate out inspiratory flow limitations. That alone distinguishes Dr. Krakow's BiLevel titration protocol from many institutions. However, to aggressively normalize the expiratory flow curve probably distinguishes Dr. Krakow's methods from the vast majority of clinicians.

I suppose that would depend on the lab protocol. If they were using the algorithm where EPAP is only added until apneas are addressed, one should be at lowest effective EPAP and the concept of Expiratory Intolerance becomes academic. You couldn't do anything about it even if it was there-- you couldn't go lower and shouldn't go higher. However, if they were using a protocol like run CPAP to 13 cmH2O and then go to IPAP increases then the concept might kick in. But that really isn't the way to do it, once the decision is made to change to bilevel one drops EPAP back to the pressure where apneas were successfully addressed.

But right, this approach to "Expiratory Intolerance" (dropping EPAP and increasing IPAP) during sleep defines CPAP failure and the necessity of Bilevel. The question then becomes what, if anything, untoward would happen if those waveforms are incorrectly identified, and there really wasn't a problem with CPAP tolerance. If the answer is "Nothing", then who cares. But some issues include (1) all CPAP machines, regardless of their breath-matching or exhalation relief capabilities are off the table because they can't create that kind of a PS gradient; (2) bilevel price is generally moderately to significantly higher; and (3) one must be more alert to CSBD, as noted by Morgenthaler et al with an incidence estimated at 15%. And since CSBD is sleep stage dependent, I'd be looking very closely at the whole pressure titration. Hopefully this would be identified in the lab beforehand. OK, not mortal wounds.

What people may not realize is that the patient Li'l Perky Nose above is the perfect patient to test this theory in that they have what appears to be upper airway obstruction refractory to any pressure approach. This was strongly suggested by their response to IFL1 on the PB420E over the years, where the APAP algorithm sent the pressure through the roof. So, at what point do you say that the inspiratory flow limitation is fixed and you bail?

Event analysis and attack in UARS was discussed years ago (Gad! Already?) in this classic post:

Below is a response I posted on TAS discussing UARS-specific hypopneas and apneas versus "classic" hypopneas and apneas that are most often attributed to typical OSA. The former airway closures are specifically believed to be associated with a lateral airway collapse from extreme negative pressure whereas the latter classic obstructions are most often attributed to a sagging palate. These are not the only two airway-obstruction or SDB etiologies by any stretch of the imagination! This particular discussion only compared the UARS airway failures versus the typical soft-palate sourced OSA airway failures, specifically focusing on the UARS case.

That discussion also touched on the 420e's IFL1 and IFL2 triggers in much the same way as we have discussed here in the past. I apologize in advance to those who do not like posts that are technically complex. My assumption is that there are at least a few members here who will find this UARS discussion either relevant or interesting.

Before posting the UARS part of that discussion, here's alink to the entire thread. The UARS portion of that discussion follows:

Mountainwoman, early PB 420e marketing literature touted IFL1 and IFL2 as being special functional parameters aimed at UARS. Yet IFL1 and IFL2 are merely on/off switches for the two algorithmic triggers dealing with: 1) flow limitation runs, and 2) hypopneas that are concomitant with flow limitation runs (respectively). Interestingly, the other "modern" AutoPAP models also trigger on flow limitations, they also aggresively trigger on concomitant hypopneas, and they tend to very cautiously treat (via proactive techniques) non-concomitant hypopneas for fear of pressure-inducing central apneas.

So what's the difference with the 420e design relative to UARS, then? My hunch is that the difference lies in how very aggressively the 420e will trigger on and elevate pressures when flow limitations are detected (via the IFL1 trigger). So aggressively, that more than a few 420e users have had to turn IFL1 off. There are actually two ways to turn IFL1 off: 1) within the environs of the Silver Lining 3 software, or 2) directly from the 420e's LCD control panel (by setting "FL" to 0 versus 1). There is no way to turn IFL2 off from the 420e's LCD control panel, however. In my way of thinking that probably implies that IFL1 must be turned off more often than IFL2. The 420e can be very pressure-aggressive relative to attempting to eliminate flow limitations which are believed to be associated with UARS.

Yet flow limitations can occur for an entire variety of reasons, many of which are not associated with UARS. Some UARS patients receive adequate elimination of their upper airway restrictions via air pressure, and yet others do not. When a UARS patient does happen to receive efficacious treatment from air pressure therapy, that implies the UARS patient's upper airway resistance was successfully eliminated via PAP's inflation of the elastic portions of the upper airway. Yet it is entirely possible that upper airway impedance can be high for rigid structural reasons entirely unrelated to soft tissue. In this latter UARS case, PAP inflation of the upper airway will not completely (if at all) alleviate UARS symptoms---assuming the UARS diagnosis adheres to the most common etiology attributed to UARS.

That most commonly accepted etiology of UARS entails exactly that which the acronym implies: Upper Airway Resistance Syndrome. Specifically this most commonly accepted UARS etiology entails extreme flow limitations that result from extremely high impedance in the upper airway---most often nasal impedance. The etiological distinction doesn't stop there, however. Because the upper airway is so severely flow-restricted, the diaphragm must create extreme negative pressure on inhalation in order to draw in an adequate volume of air necessary for normal respiration. When the diaphragm creates this excessive negative pressure, it can not only be measured all the way into the esophagus, but the UARS patient is typically pestered with negative-pressure-based cortical arousals throughout the night. The UARS specific etiology of sleep disordered breathing actually stops there for some patients. However, if the UARS sourced negative diaphragm pressures are of an extreme magnitude, then the airway itself can start to laterally collapse during inspiration, much as a paper straw collapses when you try to draw a very thick milk shake through it. If that lateral airway collapse is only partial, then a UARS-specific hypopnea tends to result. If that lateral airway collapse is a total collapse for adequate duration, then a UARS-specific apnea results. These UARS-specific hypopneas and apneas are quite different than the classic etiology of hypopneas and apneas that entail simple sagging of the soft palate.

In summary it is the extreme negative diaphragm pressures that are required in order to overcome the extreme upper airway impedances that cause both cortical arousals and obstructive airway events. A UARS patient might have: 1) UARS events only, 2) UARS events coupled with UARS-based lateral-airway-collapsing apneas and/or hypopneas, 3) UARS events coupled with classic soft palate apneas and/or hypopneas, 4) UARS events coupled with both types of apneas/hypopneas, 5) UARS events coupled with any sleep disordered breathing and/or other concomitant sleep disorder known to modern medicine. In addition we said that the UARS-based upper airway restrictions may be soft-tissue related and thus air pressure responsive, or perhaps related to hard or dense structure airway characteristics, and thus likely nowhere near as air pressure responsive as the soft-tissue case.

Add to that the fact that many MDs simply diagnose UARS if the patient's sleep events are exclusively/predominately flow limitations and/or hypopneas, and you likely have several failing airway etiologies attributed to UARS. When you put all the above UARS-related "ifs", "ands", as well as "buts" together, my very strong hunch is that the ability to achieve a total of four therapeutic combinations relative to IFL1 and IFL2 just may lend those diagnosed with UARS an edge in finding suitable/comfortable therapy. If a UARS patient happens to have air-pressure-unresponsive UARS events coupled with classic soft-palate-related apneas and/or hypopneas (which are generally very air pressure responsive) then that patient may fare better with IFL1 turned off and IFL2 turned on----or quite possibly with both IFL1 and IFL2 turned off. The conjecture being that there are very likely quite a few combinational sleep disordered breathing etiologies related to UARS, and the ability to experiment with IFL1 and IFL2 combinations is in and of itself an experimental advantage for UARS patients in general.

Further, a lot of this stuff really should be analyzed before you get to the sleep lab anyway. A visit to a good ENT guy will go a long way in helping to identify structure that could result in fixed flow limitation. There are also objective testing methods of assessing nasal airflow. And the analysis of flow volume loops in the PFT lab may be helpful in "looking" at areas that cannot be seen directly.

This assessment could result in something as simple as using some sort of oral interface (Hybrid/Liberty, Oracle or FFM) to bypass the fixed obstruction rather than trying to muscle through it.

I would also submit that a fixed or persnicky flow limitation may be far more efficiently addressed by flow rather than pressure, supporting inspiratory flow when needed (the concept of "Rise Time"). In the older techologies, all these parameters are fixed, so you still end up having to decide what set of parameters has the "most' benefit. It would be far more efficient to address this on an as-needed basis, in a Proportional Assist Ventilation (PAV) type of way. Of course, in someone with a tendency to CSDB, uncontrolled PAV would send 'em down the tubes at an exponential rate.

I've decided that this is like holding two mirrors together. Better run.

SAG

[ozij]

Bump, to have this on the first page again.

O.

[BarryKrakowMD]

I appreciate all the support and open-mindedness to our ideas, and I'm very appreciative of SAG's provocative attempts to raise our consciousness or insights on respiratory physiology. I just wish I could understand half of what SAG is trying to communicate, but I'm certain the fault lies in my own intellect.

Regardless, I still have trouble with what I understand to be SAG's points, because they either are exquisitely reductionistic or they are being communicated in reductionistic ways.

In contrast to this reductionism, the picture that keeps coming into my mind is Tiger Wood's golf swing, in particular the phase known as "change of direction," where you finish the backswing and then start the forward or downswing to strike the ball. It's the single most complex movement in the golf swing, and it literally sets top golfers (amateurs or pros) apart from everyone else. And, it's why a golfer can have a really weird looking swing, but still be an outstanding golfer if he or she has mastered the change of direction well and does so consistently.

Now if we take a reductionistic model to golf (e.g. Homer Kelley's The Golfing Machine wherein GOLF stands for Geometrically Oriented Linear Force), then we have one model of the golf swing that dramatically dissects all the nuances, angles and vectors of the swing such that if you could just repeat these positions, you'd have a perfect golf swing. It really is a great book, and many great golfers have learned much from it.

But, does it explain why Tiger Woods has mastered the "change of direction?" I don't think so, although I'd guess Woods has read the book or would understand everything in it if he ever read it.

I believe that Woods has worked on his "change of direction" in every conceivable way, using many analytic and technical insights, but I would be quite stunned if he also didn't use a lot more of his brain than the average golfer might know how to use to perfect a swing. Of course, I'm referring to more right brain elements: sensations, feelings, emotions, imagery, and perhaps above all, some sort of intuitive understanding of golf mechanics that might approach ineffable perceptions.

But, you can throw all this out the window once you get on the golf course, because no one can repeat the "perfect swing" for even 18 holes, let alone in a tournament. The golfer must rely on other elements beside reductionistic mechanics. He must use those other elements of intelligence to solve immediate problems when mechanics begin to fail or when they generate a greater margin of error that radically raises the risks for misdirected golf shots.

When you watch Woods, you see a tremendously emotional yet focused person, but when you listen to Woods, most of the time, he sounds like a diplomat, a politician and a wise man all rolled up into one personality.

My point is that I believe that Woods calls upon many elements of both his mind and body to play golf at the level he has attained, and his success with the change of direction is explained more by mind-body principles than by mechanics alone. One might say that he "knows" the change of direction and can therefore repeat it with the least amount of variance to get the job done.

Long analogy, sorry. The change of direction in golf is similar to the change of direction in breathing, although in the latter we have 2 different opportunities for the transition: I to E or E to I.

I remain convinced that these transitional stages of respiration, particularly the E to I phase, are incredibly dynamic and complex, and even if a reductionistic model purports to explain them, I've seen too much in my work in medicine to believe that a perfected model has been developed. Again, to reiterate for SAG's sake, I'm sure the current model has good to great validity, but that doesn't mean it's a complete model.

My hunch is that to complete the model, psychophysiological variables, such as the role of anxiety on breathing or the way anxiety influences how a person holds or positions his or her neck, are needed to understand why so many people don't receive an outstanding response to CPAP or why bilevel might produce a better response in some of these patients.

My experience also tells me why the comment about ENT is generally untrue, unless we're talking about some superstar ENT surgeon who has developed techniques that are as yet unpublished. The ENT track record in predicting changes in RDI (apneas + hypopneas + flow limitations) following surgery are abysmal. In fact, ENT predictions on baseline diagnostic RDIs are frequently inaccurate as well. We can all agree I think that part of the problem lies in the absurd way in which SDB events are measured. Nonetheless, a purported ENT model, let's say using a "collapsible tube" analogy is highly flawed when it comes to predicting SDB events with precision, because the airway is so much more complex and dynamic.

I'm sure I haven't rested my case, but my sleep techs tell me I can go to sleep now.

Rest Wishes

[roster]

............ I would be quite stunned if he also didn't use a lot more of his brain than the average golfer might know how to use to perfect a swing. Of course, I'm referring to more right brain elements: sensations, feelings, emotions, imagery, and perhaps above all, some sort of intuitive understanding of golf mechanics that might approach ineffable perceptions.

.............RDI

I learned this fact as an eleven-year old playing baseball. The previous year there was a coach who painstakingly taught us the mechanics of swinging the bat. I was still a poor hitter at the end of the season.

The next season a new coach took me aside and basically said, "Forget everything you have been taught about mechanics. Start going to all the high school games and watch very closely how the players in the top of the batting order swing the bat. Think about their swings when you come up to the plate."

I made the starting lineup and was moved to third in the batting order before the end of that season. Imagery.

[StillAnotherGuest]

My experience also tells me why the comment about ENT is generally untrue, unless we're talking about some superstar ENT surgeon who has developed techniques that are as yet unpublished. The ENT track record in predicting changes in RDI (apneas + hypopneas + flow limitations) following surgery are abysmal. In fact, ENT predictions on baseline diagnostic RDIs are frequently inaccurate as well. We can all agree I think that part of the problem lies in the absurd way in which SDB events are measured. Nonetheless, a purported ENT model, let's say using a "collapsible tube" analogy is highly flawed when it comes to predicting SDB events with precision, because the airway is so much more complex and dynamic.

I showed this comment to one of the ENT surgeons, whom we affectionally call "Luca" (because of the strong resemblance to the character Luca Brasi in "The Godfather") and he seemed to take exception to it. He became quite agitated, his singular giant eyebrow became furrowed and his eyes narrowed as he said, "Meet Krakow. Eat Krakow". Don't worry, tho, we hit him with the tranquilizer gun, and I'm sure he'll be fine when he wakes up.

Let us not dismiss these thoughts:

A visit to a good ENT guy will go a long way in helping to identify structure that could result in fixed flow limitation. There are also objective testing methods of assessing nasal airflow. And the analysis of flow volume loops in the PFT lab may be helpful in "looking" at areas that cannot be seen directly.

with this generalization:

My experience also tells me why the comment about ENT is generally untrue, unless we're talking about some superstar ENT surgeon who has developed techniques that are as yet unpublished. The ENT track record in predicting changes in RDI (apneas + hypopneas + flow limitations) following surgery are abysmal. In fact, ENT predictions on baseline diagnostic RDIs are frequently inaccurate as well. We can all agree I think that part of the problem lies in the absurd way in which SDB events are measured. Nonetheless, a purported ENT model, let's say using a "collapsible tube" analogy is highly flawed when it comes to predicting SDB events with precision, because the airway is so much more complex and dynamic.

There are a number of different anatomical structures that contribute to airway patency, some of which may be treated with pressure approach, some of which may not (fixed obstructions). If your measuring methodology is composed of nasal pressure transducer during diagnostic testing, the effect of nasal airway narrowing (if present) will be included in the waveform. If you're using nasal interface during pressure titration, nasal narrowing now becomes a significant contributor to that waveform. And you're not going to change that waveform, that patency a heckuva lot by increasing or decreasing pressure. Further, the contributions of these "upper" upper airway structures can be assessed by a good ENT guy, or in your own garage using rhinomanometry. Once identified, a different treatment approach should be considered. It may be as simple as using a ResMed Mirage Quattro FFM and Breathe Right Nasal Strips, or perhaps surgical intervention may help.

Regardless, I still have trouble with what I understand to be SAG's points, because they either are exquisitely reductionistic or they are being communicated in reductionistic ways.

I must go head-to-head with this assessment, and resort to the "I-know-you-are-but-what-am-I?" debating strategy.

I respectfully submit that basing treatment approach on this singular event



is "reductionalistic". It not only fails to take into account the numerous previously mentioned forces, but is highly susceptible to artifact. And again, looking at those other channels will be able to give us a much better idea of the contribution of these other factors.
SAG

[BarryKrakowMD]

The dictionary.com definition of reductionism:
1. the theory that every complex phenomenon, esp. in biology or psychology, can be explained by analyzing the simplest, most basic physical mechanisms that are in operation during the phenomenon. (italics added)

Stating that something is “reductionistic” is not meant to be perjorative; it’s just meant to convey that the paradigm might be incomplete; whereas a reductionistic “purist” might argue that reductionism is very complete by definition.

I’m not a reductionist, because I don’t find it helpful in solving PAP therapy titration problems, but I admit there are many things I don’t know and many things to be discovered that might demonstrate that mechanistic theories are more valuable. For example in seeing some of the remarkable results of ASV, it’s easy to imagine that science has produced an effective device for a condition (CSA), for which previous treatments were clearly inadequate. Hooray for reductionism!

My single sensor graphic is minimalist not reductionistic. I have clearly stated that the expiratory intolerance (the bumps) might be caused by all sorts of physical mechanisms, but maybe they are also caused by an anxious patient struggling to deal with pressurized air coming in while breathing out. This anxiety component along with assorted physical factors suggests a mind-body process, not a reductionistic (physical only) problem. Moreover, the “bumps” on expiration go away with bilevel or reducing CPAP, which leads me to believe that the patient’s anxiety is lessened when exhalation is up against a lesser intensity of pressurized air.

Regarding ENT claims, I’m tempted to leave at, “Bring it on!,” but I would be remiss if I didn’t at least ask whether or not the views expressed take into account the following real-world experiences that should arguably lead many sleep patients away from ENT physicians as first-line sleep medicine providers:

1. The astonishing data on UPPP, how often it doesn’t work, how it actually worsens the condition in some people, how it may subsequently worsen the future capacity of an SDB patient to use PAP therapy, and how many ENT surgeons still recommend and use this procedure with impunity.
2. The fact that several power-brokers in the ENT community are pushing for portable monitoring for the expressed purpose of cutting out (no pun intended) the sleep medical community from interacting with patients who unquestionably need their services. How so? By recommending to CMS (Medicare) a simplistic model of using home oximetry (a technique that has never failed to disappoint in research comprising 20 or 30 years) to diagnose SDB, and the encouraging these patients to proceed to surgery without every trying PAP therapy. Presumably, you have read the disturbing commentaries coming out of the ENT community when they announce to their colleagues, “the sleep medicine market is ours for the taking.”
3. The fact that ENTs across the USA continue to treat snoring as if there were no chance that it’s really SDB and making that erroneous judgment without any testing whatsoever.
4. The fact that ENTs are woefully ignorant of the concepts behind UARS (flow limitation) and continue to conduct research only with AHI metrics or conduct surgery based on AHI metrics pre and post, and then proceed to make invalid claims that a patient has been “cured” because they dropped their AHI below 10 or 5 without making the slightest attempt to know what the RDI is or whether the patient might still be suffering from flagrant UARS.
5. The fact that a fair number of ENT surgeons continue to make castigating remarks about PAP therapy in a self-serving attempt to discourage patients from using it, despite it being gold standard therapy, yet encouraging patients to undergo a variety of surgical procedures, almost none of which ever lead to a genuine cure of SDB if one uses the scientific standard of the American Academy of Sleep Medicine known as the RDI (apneas + hypopneas + UARS).
6. The continuing fact that sleep medicine doctors all across the USA and elsewhere are constantly having to clean up the mess caused by ENT surgeons who promised the moon and stars to their patients and then unload them at the sleep medical center, when the patient’s sleepiness, nocturia, and concentration problems (to name a few) haven’t gotten the least bit better and sometimes have gotten worse.

The ENTs in Albuquerque are terrific. We talk routinely about select cases. They order sleep studies on all patients pre and post operatively. They regularly encourage patients to use PAP therapy, to return for retitration studies, and to use surgery either as a last resort or as a specific technique to improve tolerance to PAP therapy (septoplasty, turbinoplasty, T & A, sinus surgeries). These relationships developed, because we worked diligently to communicate with the ENT groups in town and to express our vision of the multi-disciplinary model of sleep medicine. Nearly all our local ENTs with whom we work have embraced many components of a sleep medicine specialty model, and thus our collaborations serve the best interests of the patients.

I have also consulted with other surgeons across this country who share similar high standards and goals in their operations with sleep patients. But, unfortunately, there is nothing that I or most my colleagues are aware to suggest that the majority of ENT surgeons follow these basic principles or have the desire or time to educate themselves to attain the necessary background in managing sleep breathing patients.

ENT surgeons have an incredibly valuable role to play in sleep medicine. In our practice, we refer more than one-third of our patients for ENT evaluations and regularly encourage our patients to undergo "tolerance-improving" surgeries. It’s more than unfortunate that a substantial number of these physicians have not pushed themselves to the next level of care.

A final pearl from my book (p.296): "But when you go down the surgical pathway, you simply want to ask your surgeon one question: 'What were the average postoperative changes in the RDI** in the last 25 patients for whom you performed this surgical intervention?'” If the surgeon cannot answer the question, try to find one who can.

**not the AHI, the RDI.

P.S. A previous question was raised about oral appliances combined with PAP therapy. They have promise; I used to use that combo myself before going on bilevel. My biggest concern is that by increasing the vertical dimension (by slightly separating the upper and lower teeth from each other), they can actually decrease the size of the airway in some patients, and they may increase mouth breathing or mouth leaking in others. Again, RDI assessment at retitration studies is invaluable in sorting out whether combo therapy works.

[StillAnotherGuest]

What people may not realize is that the patient Li'l Perky Nose above is the perfect patient to test this theory in that they have what appears to be upper airway obstruction refractory to any pressure approach. This was strongly suggested by their response to IFL1 on the PB420E over the years, where the APAP algorithm sent the pressure through the roof. So, at what point do you say that the inspiratory flow limitation is fixed and you bail?

Further, a lot of this stuff really should be analyzed before you get to the sleep lab anyway. A visit to a good ENT guy will go a long way in helping to identify structure that could result in fixed flow limitation. There are also objective testing methods of assessing nasal airflow.

This assessment could result in something as simple as using some sort of oral interface (Hybrid/Liberty, Oracle or FFM) to bypass the fixed obstruction rather than trying to muscle through it.

There are a number of different anatomical structures that contribute to airway patency, some of which may be treated with pressure approach, some of which may not (fixed obstructions). If your measuring methodology is composed of nasal pressure transducer during diagnostic testing, the effect of nasal airway narrowing (if present) will be included in the waveform. If you're using nasal interface during pressure titration, nasal narrowing now becomes a significant contributor to that waveform. And you're not going to change that waveform, that patency a heckuva lot by increasing or decreasing pressure. Further, the contributions of these "upper" upper airway structures can be assessed by a good ENT guy, or in your own garage using rhinomanometry. Once identified, a different treatment approach should be considered. It may be as simple as using a ResMed Mirage Quattro FFM and Breathe Right Nasal Strips, or perhaps surgical intervention may help.

Acoustic rhinometry predicts tolerance of nasal continuous positive airway pressure: A pilot study
Morris, Luc G.; Setlur, Jennifer; Burschtin, Omar E.; Steward, David L.; Jacobs, Joseph B.; Lee, Kelvin C.
American Journal of Rhinology, Volume 20, Number 2, March-April 2006 , pp. 133-137(5). (Abstract)

Background: Nasal continuous positive airway pressure ( nCPAP) is usually the first-line intervention for obstructive sleep apnea, but up to 50% of patients are unable to tolerate therapy because of discomfort—usually nasal complaints. No factors have been definitively correlated with nCPAP tolerance, although nasal cross-sectional area has been correlated with the level of CPAP pressure, and nasal surgery improves nCPAP compliance. This study examined the relationship between nasal cross-sectional area and nCPAP tolerance.

Methods: We performed acoustic rhinometry on 34 obstructive sleep apnea patients at the time of the initial sleep study. Patients titrated to nCPAP were interviewed 18 months after starting therapy to determine CPAP tolerance. Demographic, polysomnographic, and nasal cross-sectional area data were compared between CPAP-tolerant and -intolerant patients.

Results: Between 13 tolerant and 12 intolerant patients, there were no significant differences in age, gender, body mass index, CPAP level, respiratory disturbance index, or subjective nasal obstruction. Cross-sectional area at the inferior turbinate differed significantly between the two groups (p = 0.03). This remained significant after multivariate analysis for possibly confounding variables. A cross-sectional area cutoff of 0.6 cm2 at the head of the inferior turbinate carried a sensitivity of 75% and specificity of 77% for CPAP intolerance in this patient group.

Conclusion: Nasal airway obstruction correlated with CPAP tolerance, supporting an important role for the nose in CPAP, and providing a physiological basis for improved CPAP compliance after nasal surgery. Objective nasal evaluation, but not the subjective report of nasal obstruction, may be helpful in the management of these patients.

Not to mention the nasal symptomology that may develop with the application of pressure therapy, which should be reversible.

I have clearly stated that the expiratory intolerance (the bumps) might be caused by all sorts of physical mechanisms, but maybe they are also caused by an anxious patient struggling to deal with pressurized air coming in while breathing out.

Anxious? In Stage 3 sleep? I'm going to scream right past "highly unlikely" and go straight to "absolutely impossible".

Go Eli.

SAG

[ozij]

Anxious? In Stage 3 sleep? I'm going to scream right past "highly unlikely" and go straight to "absolutely impossible".

Why? A person (person) in stage 3 is not comatose or dead, her or his brain responds to various stimuli, anxiety is not necessarily a cortical reaction - why in the world assume they can't be anxious? The unconscious is just that - something that happens in the body/brain/mind complex that is a person, that this person is not necessary conscious of. The mere fact that a person is not conscious of something does not mean it doesn't exist.

O.

[Guest]

HI Dr.Krakow,

Good explanation of in the senarios of how tiger woods play on the golf field. External's dynamic changes and that received to the golf player of how the player processed and followed up by decision of what to be executed for the swings. I believed this reductionism is just one way of solving problems....in the golf player's mind besides STRATERGY for the execution of the swing is just execution technically. In contrast, breathing from the natural human body is executed totally different way conciously or unconsiciusly. I wondered how the reaction will be if one use the mind to control the breathing instead of let the brain take full or half of the control function. Is the brain executing the breathing in the strategic manner or it is just yet another in built fucntion that capable to switch in between changes? Simplicity, Complexity or Reductionism, the breathing is as amusing as how correlate between body, mind , soul and physiologically...left alone in the senarios of OSA etc. Any comment?

Mckooi

[-SWS]

I suppose that would depend on the lab protocol. If they were using the algorithm where EPAP is only added until apneas are addressed, one should be at lowest effective EPAP and the concept of Expiratory Intolerance becomes academic. You couldn't do anything about it even if it was there-- you couldn't go lower and shouldn't go higher. However, if they were using a protocol like run CPAP to 13 cmH2O and then go to IPAP increases then the concept might kick in. But that really isn't the way to do it, once the decision is made to change to bilevel one drops EPAP back to the pressure where apneas were successfully addressed.

But right, this approach to "Expiratory Intolerance" (dropping EPAP and increasing IPAP) during sleep...

I don't think significant numbers of clinicians today frequently and readily accept such large PS values toward achieving rounded I and E curves as described below:

Using a zero tolerance attitude about flow limitation, Dom titrated me to 18/14 (which we both thought insane since I’d been using APAP of 8 to 12 and rarely 10 to 14), and I titrated Dominic to 20 over whatever. It was around 4 am, and the assigned sleep tech kept saying, “are you sure that’s flow limitation?” My response, “I’m not sure, but it’s not rounded, so keep increasing until it rounds,” which it did at IPAP of 20.

From that point forward I started using bilevel at pressures around 14/10 and fairly rapidly worked my way up to 18/10…”and loving it!” to quote the immortal secret agent Maxwell Smart. Now, I'm at 21/12.5.

That final PS value of 8.5 is an aggressive BiLevel spread by most standards. Here are yet more characterizing details, consolidated merely for for the sake of convenience:

Should you be able to produce the same results with CFLEX, APAP, etc? Presumably so, except for one “large” difference. You cannot generate the same gradient or gap between IPAP and EPAP with any of the other devices. And, in our clinical and research experience, we are using gaps of 4 to 12 cm of water in our patients. My personal bilevel settings are 21/12.5 for a gap of 8.5.

In our prescriptions for bilevel, I would venture that the average gap is in the 5 to 6 range with tremendous variation, including some with a gap of only 2 or 3. Those with a lower gap requirement would likely do as well on FLEX or APAP, but to repeat, the large majority of our patients have a gap of 4 or greater.

If Dr. Krakow's methods represent a deviation from current standard practices (and I think they do), then it seems entirely logical that other practitioners would/should want to question the details. Very understandable.

I'm not a practitioner, but I have a question for Dr. Krakow. My question regards Dr. Krakow's repeated verbal equation between the phrase "flow limitations" and the acronym representing the syndrome referred to as UARS. Dr. Krakow, do you consciously intend to equate "flow limitations" and "UARS" as implied equivalents?

In the past "flow limitation" as a phrase most often (albeit not exclusively) referred to (lower-magnitude) characteristic upper-airway impedances, which in turn were equated specifically with only the first three letters in the UARS acronym: the UAR subset if you may. Doctor Krakow, I'm not splitting hairs when I pose this question. I'm trying to understand if your wording intends to impart the strong implication that I suspect it may: that the presence of flow limitation itself has a near-absolute correlation with problematic symptoms.

I suspect that is exactly what you mean to convey (but sir, please correct me if I am wrong). If that's what you mean to convey, will you also comment on : 1) the expected prevalence of "flow limitation" itself in the general population, 2) "symptomatic presentations" of flow limitations in the general population (both including and subtracting the SDB-population subset from that assessment), and 3) the problem of "flow-limitation-associated disorder" in the general population as a potentially large-scale health problem? Thank you, sir.

And again, thank you to all the posters in this thread for what I think is an absolutely wonderful discussion!!



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[Rachael]

I wanted to ask this earlier: what do you mean (any of you) by "feeling anxious" in sleep?

There is the conscious realization that the tightness in your chest and agitated movements and shallow breathing are because you are worried about xyz. But often I have anxiety that is unrelated to thoughts or feelings, but seems to arise out of physiological factors. My heart pounds or my blood pressure goes up, I feel that tingly adrenaline feeling. There is no doubt at all in my mind that that happens while I am asleep, I used to wake up that way 5 or 6 times a night.

So, do we feel, or consciously notice, or emote anxiety while asleep? Who knows? Do we have the physiologic symptoms associated with anxiety? I think we do. Isn't that why sleep apnea messes us up so bad?

[BarryKrakowMD]

FL vs UARS

In some of my earlier posts, I raised the question about what is normal sleep, and I offered the hypothesis that a normal sleeper might have little or no daytime sleepiness. Recently, we started looking at patients who claim they are normal sleepers, and in the first 3 individuals we tested all of them had significant flow limitations and flow limitation events (with arousals). They also had sustained flow limitations. Would I expect to see this in a normal? No. In hindsight, we probably lowered our guidelines just enough to let these people into the protocol.

One patient reported excellent sleep quality, yet he said he could doze off occasionally during the afternoon. Another said she slept great all through the night, but she started off the day with one cup of coffee. A third reported minimal sleep symptoms but was on a medication that might confound the results.

In sum, we looked at 3 people who said they were normal sleepers and they came close to meeting our standards, but not close enough. Still, they had flow limitations, and my bet is that if treated, they would see a reduction in sleepiness, caffeine use or perhaps some other improvement in function.

My point is that flow limitations probably do not equate to UARS but they come close, meaning that if you look hard and long for people who think they are normal sleepers, I think you will discover that many of them are not.

So, someone has to make the determination as to what constitutes a normal amount of daytime sleepiness, and I vote for zero tolerance, not because I think it's a feasible goal to reach, but I think it's a logical goal to guide us because of the following scenario: a series of patients with sleepiness who show ridiculously subtle flow limitations responding dramatically to PAP therapy to the point of virtually eliminating their sleepiness.

If flow limitations were a normal variant, why are they causing sleepiness? Could it be that normal would mean no sleepiness, or is it abnormal to experience no sleepiness? My sense is that we do not know what constitutes normal sleep or normal daytime sleepiness.

So, pragmatically, it's generally useful to equate flow limitation with UARS, but I concur that technically, there may be patients who suffer flow limitations for other reasons for which PAP therapy may not be the answer. Although I don't know what causes this problem, I think it is important to note that some of these cases show flow limitation ending not in an EEG arousal but in a new normal breath. I suspect these FLEs are clinically relevant.

Anxiety

I'm confused as to why there is any argument about feeling emotions during sleep. We do it all the time in REM during dreaming. And, the major consensus on dream interpretation research for last few decades is "to follow the emotions." Ask patients to describe their feelings as best they can remember feeling during the dream, and those emotions are the secret to unlock the dream's message. The book I wrote with Joseph Neidhardt in 1992, Turning Nightmares into Dreams (now out of print, but available on most internet booksellers) discusses this theory in depth.

More recent dream research shows we dream in all stages of sleep including delta, and unquestionably we have various forms of mentation in all stages of sleep. I think the data are there to support the view, then, that we have active imagery and feeling systems throughout the night in all stages of sleep. Surely, we all know about the intense emotions of sleep terrors emerging from delta sleep.

I can't prove that patients respond anxiously to masks and pressurized airflow while asleep, but that's my working theory, and it may or may not surprise you, but more than 90% of our patients (with PAP adjustment problems) immediately resonate with this concept, find it plausible, and wish to pursue its resolution through whatever psychophysiological treatments we have to offer.

[-SWS]

I think the Doctor's line of inquiry and answers are tenable. I also suspect that FL, irrespective of AH, may represent a large-scale, small-severity problem in the general population.

Thank you for those answers, Doctor.