I think a fairly definitive assessment of UARS can and should be made through physical exam and PSG, and in the end, there shouldn't be too many questions left on the table for any given UARS patient. BTW, "upper airway" refers to anything north of the vocal cords, so all the structures involved in apnea and hypopnea also participate in UARS. If there is a fixed "upper" upper airway obstruction, this should easily be identified by any good ENT guy, and then the surgical approach opens up (or maybe FF alternatives).
UARS is not that hard to identify in even the most basic of sleep labs. Increasing effort seen in the thoraco-abdominal belts, flattening in the sum channel, concomitant snoring, flow limitation in the pressure transducer (even if the sleep laboratory is not using pressure transducers in the diagnostic, they're
definitely using them in intervention), and the use of suprasternal notch pressure transducers are all diagnostic aids in identifying UARS. As an aside, if the PB IFL1 is seeing a flow limitation, then you can rest assured that the sleep lab is seeing it as well.
Is there really such a thing as an unresponsive flow limitation? If such a "fixed" obstruction exists (and in re: prevalence, we're talking about a subset of a subset), we have to consider what it is actually unresponsive to. Saying it's exclusively pressure ignores the equally dynamic force in "pressure" therapy, which is flow. Pressure gradient seen because of fixed obstruction can be largely, if not completely, overcome by flow. Just because an obstruction is not affected mechanically by pressure does not mean it is not affected whatsoever.
If you meet diagnostic criteria for UARS (like AHI <5, RERAI >10), then we would expect
some sort of improvement during titration. Or alternatively, UARS that is unresponsive to pressure therapy probably isn't UARS, or at the very least, there are significant other issues underfoot. If during titration, the underlying sleep architecture continues to be a train wreck (delayed sleep latency, increased WASO, WAFA, Stage 1, arousals and awakenings) then there is more searching to do.
jenny wrote:...i think i see a titration study in my future - though i think i'll need to be heavily sedated for it.
Let's say, for arguments sake, you then get a normal sleep architecture during the titration. How would you account for that? Was it the pressure or the medication? Unless you plan on duplicating that medication regime every night, you've added a whole new variable. What if the OSA/UARS is minimal to non-existent? You know, CPAP titration unto itself can be a good diagnostic tool for UARS (i.e., it disappears with pressure therapy). I believe in your case, PSG is going to provide a lot more insight that just a titration number.
So OK, let's say there is truly a fixed resistance component in a specific case of UARS. A different strategy may be considered, for instance, utilizing a somewhat more aggressive flow-based approach (basically a pressure-support methodology) to overcome the work of breathing associated with the resistive forces. Ideally, this would take the form of some form of Proportional Assist Ventilation, but might also be accomplished through the use of bilevel support (and consider tailoring inspiratory waveforms by adjusting rise time when available), or in a rudimentary form, through the use of EPR.
One must view this strategy in the light of a very important concept. When looking at UARS under ambient conditions, the body is breathing in a "negative pressure" mode. Diaphragm drops down, negative force in the airway is generated and breath is drawn in. Unfortunately, this negative force can serve to collapse unstable airways. As positive pressure is applied, particularly bilevel, increasing positive pressure is applied during inspiration, and breathing is done in a "positive pressure" fashion. While distendable structures may be mechanically dilated, another effect is the relief of some of the Work of Breathing that would have normally be needed to overcome the forces of resistance. And relief from the negative pressure swings.
SAG