Prompted by a recent submission asking why BiPAP is effective, I thought I'd reflect a little on why spontaneous bi-level CPAP
(BiPAP S, henceforth BiPAP) is effective, and in my opinion essential for treatment of UARS. (And why Wikipedia is wrong
in parts) I am not a doctor, but I've read a lot of medical publications and I've dedicated a lot of shower thoughts to reflecting on my own experiences in light of these publications.
What distinguishes the typical UARS patient from the typical OSA patient? Both can have the same anatomical features that manifest as complete (apnea) or severe (hypopnea) obstruction in the typical OSA patient but "only" lead to airway restriction in the typical UARS patient. The UARS patient seems to be more sensitive
, such that restriction leads to a physical (without conscious awareness) arousal such as a RERA which is concluded by a temporary reversal of the restriction. A RERA is a Respiratory Effort Related Arousal or rather an arousal caused by increasing breathing effort. It seems that the typical OSA patient, lacking this sensitivity, allows the same scenario to escalate to apnea or hypopnea of 10 seconds or more before the body is aroused. The arousals are a form of stress and cause sleep fragmentation and diminished sleep quality in general.
In my view the typical UARS patient can have a number of different problems: sensitivity to breathing effort while awake, sensitivity to breathing effort while asleep combined with anatomy prone to restriction leading to RERAs, and finally I conjecture, anatomical factors that aren't very susceptible to stenting using static pressure.
What does a CPAP do? Only one thing, maintaining a fixed, constant pressure throughout the airway. This prevents airway collapse because the pressure exerts an outward force that compensates for the inward force of gravity. 1 cmH2O is equal to 1 gram per square centimeter. However, this increases breathing effort due to the fact that expiration (exhalation) is normally a passive act. The chest and diaphragm have a certain amount of internal spring force that requires a physical effort to expand the spring to achieve inspiration, but allows expiration to be achieved by simply relaxing all muscles. This is why we "blow out our last breath" when we die, since in death initially all muscles relax. The constant pressure of CPAP changes that, because the static pressure is opposed to the spring tension of the chest. Fully relaxed, the volume of the chest is higher than it would be without CPAP. To compensate and achieve the normal tidal volume we'd either have to make an effort to inspire deeper so that the maximum volume during inspiration minus the volume at rest after expiration equals the desired tidal volume, or an effort is made to exhale forcefully against the static pressure exerted by CPAP so that the chest volume at the end of expiration equals that when no CPAP is applied. In both cases, an additional effort needs to be made which increases total Work of Breathing (WOB).
Needless to say, the typical UARS patient being sensitive to increased breathing effort typically experiences a strong reaction to the resistance imposed by CPAP as described in the previous paragraph. Anxiety attacks ensue etc, as was my personal experience when I tried plain CPAP three years ago. Furthermore, if the UARS patient for some reason does fall asleep on CPAP, and the pressure is adjusted to stabilize the airway, typically what is gained by stabilizing (opening up) the airway is immediately lost by the increased resistance imposed by CPAP. Now, the patient doesn't suffer from RERAs because of obstructive airway resistance, but by the resistance imposed by CPAP. Barry Krakow MD calls this "Expiratory Pressure Intolerance."
Furthermore, I conjecture, the nature of the anatomical factors that lead to obstruction in UARS patients may differ subtly from those of OSA patients in that they are less susceptible to stenting using static pressure. What this means in practice is that with respect to raising the static pressure to open up the airway, a point of "diminishing returns" or a kind of ceiling is reached, such that when a pressure is reached where total collapse (apnea) or severe restriction (hypopnea) is resolved, the airway still presents resistance sufficient to trigger RERAs while increased pressure does not enlarge the aperture
. Clear examples of these factors would be nasal valve collapse (if nasal pillows aren't or nasal cradle isn't used) or nighttime nasal congestion. I do believe that other factors in the upper airway can play a similar role, such as the position of the head in relation to the chest and bending of the neck.
The result is that static pressure is both unsuitable and inadequate for the typical UARS patient. Something more is needed. Enter Pressure Support. Pressure Support is the unique feature of bi-level CPAP (BiPAP) resulting from alternation between two pressure settings in specific synchronization with the user's breath. The lower pressure EPAP is applied when the user isn't actively inhaling, and the higher pressure IPAP is applied exactly while the user is actively inhaling
. EPAP works like the constant pressure in plain CPAP in that it allows us to stabilize the airway, while Pressure Support, resulting from the gap or difference between EPAP and IPAP (always a positive number since IPAP > EPAP) decreases work of breathing
at the same time. On the face of it Pressure Support is like power steering for breathing. Like power steering turning weak and stringy arms "virtually" into big burly trucker arms, Pressure Support turns a small breathing aperture (perhaps the end result of airway stabilization with static pressure reaching the "ceiling") virtually into an sufficiently large aperture for easy breathing. By decreasing breathing effort across the board, the threshold for RERAs to occur is raised, ideally until RERAs are eliminated entirely. Pressure Support is versatile, low amounts (up to ~5 cmH2O) increase comfort, low to medium amounts raise the threshold for RERAs, while higher amounts (~20 cmH2O) can be used to achieve air exchange with no active effort on the part of the user
. Indeed, this is how Positive Pressure Ventilation (PPV) works.
Now, let us reflect on RERAs and "Auto BiPAP." A RERA is primarily a matter of breathing effort exceeding a threshold of individual sensitivity. This means that it manifests subjectively, and can only be detected from outside the body in an indirect fashion such as Pes (esophageal negative pressure) reversal or directly by detecting EEG arousals. A plain CPAP or BiPAP lacks both data channels, and is therefore unable to detect RERAs. Some CPAP makes/models pretend they do, but this is a fantasy. I've seen more shooting stars in the night sky than I've seen RERAs detected in OSCAR in the past 3 years of my using a PR BiPAP Auto 761P (in constant mode) even when my pressure (support) was clearly inadequate. Moreover, even if xPAP devices were perfectly capable of detecting RERAs I believe that while the typical OSA patient can get by with "failure driven" Auto CPAP -- apneas/hypopneas/snoring need to occur for the pressure to increase -- in the typical UARS patient RERAs are best prevented completely. Consequently, I believe Auto BiPAP has no value for UARS, while ASV (auto/adaptive servo ventilation) may have some value.
How to self-titrate BiPAP S for UARS? In my view it's relatively straightforward. Initially a "middle of the road" EPAP is chosen, say 6 cmH2O. Then Pressure Support is chosen to set the user at ease while using the BiPAP, say 3 cmH2O or even higher. Monitor with OSCAR, and increase settings on a week-by-week basis, 1 cmH2O per week essentially. If obstructive apneas/hypopneas occur, or snoring, raise EPAP (keeping PS constant). Note that false positives can occur, I tend to get one or two "obstructive apneas" when I'm rolling over, apparently I clench my vocal cords. A good indication whether the EPAP is adequate is when the airway feels "pinned" while awake, supine, and relaxed. If the airway feels like it's "flopping up and down" while EPAP and IPAP alternate, I'd say EPAP needs to be raised. Then, raise Pressure Support until UARS symptoms are relieved, including: drooling in the mask, jaw thrusting (waking up with and extended jaw), daytime dizzy spells (if applicable) etc. If large amounts of Clear Airway apneas occur, then back off pressure support (for a while) and hope for TECSA (treatment emergent central apnea) to dissipate.
I often ask myself whether my current pressure of 14 over 9 is adequate. (I have not yet done any sleep studies while using BiPAP, since the sleep studies I have had so far haven't even been able to diagnose my condition) I conject that it's possible for my body's need for pressure support to vary during sleep, analogously to the need for static pressure varying in a typical OSA patient. I get too much CAs if my PS exceeds 5 cmH2O. But what if that happens while my restriction is low (low need for PS) while at other times my restriction is high (high need for PS)? That would mean that I'd need 6 cmH2O or more at times, but at other times it would be excessive (causing TECSA). I think ASV can be useful in this scenario. ASV is unique in that it adjusts PS dynamically on a breath by breath basis
. It could be titrated similarly to BiPAP S, with a static EPAP but a minimum PS that is equal to the adequate/not excessive baseline (5 cmH2O in my case) and a maximum PS that allows for an increase when the ASV needs to combat increased airway resistance.
Thanks for reading all of this, I welcome your thoughts and comments.
PS. I hope I've explained it all well enough for you all to understand why the following statement in Wikipedia is nonsensical:
Recent studies have shown that more advanced PAP devices, such as Bilevel PAP and Adaptive Servo Ventilation, are more effective for treating UARS as they provide better pressure support on exhale, mimicking normal breathing and making higher pressures more tolerable.
Basically, I'm trying to figure out whether I'm experiencing one right now.
To start: my psych put me on Lamictal starting a little over a month ago, and we've now titrated up to 100mg per day, which I've been at for the past week or so.
I've definitely been more functional since I started lamictal. Five weeks into the school semester, I'm doing much better than I did during my first two years of college. But that hasn't been uniform--over those weeks, I self-harmed on 3 different occasions, albeit to a much lesser extent than I used to, and yesterday I actually threw away the utility blade that I used to cut (though I've done this in the past and ended up buying new ones when things got bad). But I've been getting my work done and doing relatively well. And I've been planning for the future, which, given my suicidal tendencies in the past, is something very new for me.
But this past week has been...weird. I've been really stressed, anxious, and agitated. But I've also been really active in ways that I haven't been since my last hypomanic episode. The only thing that's missing is the associated feelings of euphoria.
For example, I've decided to double major. The last time something like that happened was when I decided to switch my first major (from math to stats), which was an impulse decision when I was hypomanic. Also, I'm usually pretty controlled when it comes to working on side projects that aren't for my academic work, but in this past week, I've decided to start a new literary journal, reboot an undergraduate academic journal that I'm EIC of but haven't put much work into, and started a programming project. I've also started applying to summer internships, which is usually something that I end up pushing off until late in the semester.
And my thoughts have been a little all over the place. When I'm with my girlfriend, I've recently been getting pretty agitated and angry over really small things, but when I'm not around her I'm super lovey-dovey. I've also taken onto myself a lot of community responsibilities that I had initially delegated to other people and been very on top of those. But at the same time I've been very forceful about them, and very anxious about them turning out well.
So yeah, like I said, I feel like I have the energy of hypomania without the good feelings. Is this what a mixed episode is like? Or is this just what I'm like at my baseline? Things feel kind of topsy-turvy. But a part of me doubts that it's a mixed episode just because I'm on lamictal.