POLL: Typical AHI for ResMed Users

jnk wrote:So if one brand continues to report assumed hypopneas during difficult-to-trend moments and another brand does not, is there any chance that one difference in the reporting approaches, if that is really true, could relate both to the differences in the hypopnea estimates and to the existence of the second brand's VB% category?

Jeff's post got me to wondering: what about a relationship between Variable Breathing and hypopneas, all on Respironics?
And it occurred to me that my separate data recording for three different masks might provide some level of control.
The numbers for each mask are different enough that the consistency of the ratio of VB % time to HI surprised me:



(If you do the numbers from this chart, the ratios will come out a bit differently. The ratios I present are from the original data nightly values, averaged.)
[Edit: and the table should read Fisher & Paykel 431 Full Face Mask]

I can't say that this has any meaning or significance. Could be coincidental. Surely is curious. Velbor

-SWS wrote:...Respironics is discarding hypopneas during the wake stage?...

Ah, er, ResMed counts as hypops certain categories of breathing that Respironics counts as VB because Respironics does not see a termination of 2 recovery breaths that are essential to Respironics' definition of a hypop...right? Or is my brain still too muddleheaded to grasp this clearly?

Velbor wrote:The numbers for each mask are different enough that the consistency of the ratio of VB % time to HI surprised me:
Could be coincidental. Surely is curious.

Very interesting to me as well, Velbor.

Intuitively, I wouldn't be surprised if hypopneas and amplitude variability tend to often correlate.

Muse-Inc wrote: Ah, er, ResMed counts as hypops certain categories of breathing that Respironics counts as VB because Respironics does not see a termination of 2 recovery breaths that are essential to Respironics' definition of a hypop...right? Or is my brain still too muddleheaded to grasp this clearly?

My understanding is that those large volume recovery breaths are reflexive survival characteristics often following apneas and hypopneas. So when you mentioned earlier in the thread that you think missing recovery breaths might be indicative of a hypoventilation event instead of a typical hypopnea, I think you may have been right with that assumption.

But I'm not sure the recovery breaths are actually required for hypopnea scoring by Respironics---or if they are simply probability/decision-weighting factors. The same with wave flattening. I'm not certain wave flattening is a Respironics hypopnea-scoring requirement either. Rather, I think wave flattening may simply be a means of differentiating obstructive hypopneas from central hypopneas instead of a scoring requirement.

Velbor, when I run the Respironics Auto Algorithm training simulation, this is the high-level definition Respironics gives for hypopneas (and apneas):

Respironics describing their Auto event detection wrote: Apneas and Hypopneas are determined by establishing a reference that is based on a moving flow signal window that is a few minutes in duration

So that's clearly different than the Respironics definition of "hypoventilation" that is compared against predicted awake supine volumes.

Respironics describing their auto event detection wrote: Apneas and Hypopneas are detected as a reduction in flow lasting for at least 10 seconds.

Apnea - 80% reduction in flow

Hypopnea - 40% reduction in flow

So, Velbor, I'm wondering how much of that hypopnea criteria in our summary chart are prerequisite, how much are decision-weighting factors, and how much are employed toward obstructive/central hypopnea differentiation versus overall hypopnea scoring.

Velbor wrote:

...
I can't say that this has any meaning or significance. Could be coincidental. Surely is curious.

Velbor, do you have the results of your sleep studies, specifically, the histograms showing sleep architecture?

If not those, then the "sleep variables" (TIB, TST, Sleep Efficiency, Sleep Stage%, Awakenings and Stage 1 Shifts) and spontaneous arousals?

Muffy

Velbor wrote:I can't say that this has any meaning or significance.

I would say it does not, because Muffpothesis says that VB is simply wiping out hypopneas that could have been scored by A10 (so it is the "unseen" hypopneas that would be significant) and those HI numbers, when extrapolated for the full night (let's say 8 hour periods) would be 6, 7 and 8 hypopneas, respectively, numbers so few that even they, too, could simply be artifact.

Muffy

Muffy wrote:

Velbor wrote:

Velbor, do you have the results of your sleep studies, specifically, the histograms showing sleep architecture? If not those, then the "sleep variables" (TIB, TST, Sleep Efficiency, Sleep Stage%, Awakenings and Stage 1 Shifts) and spontaneous arousals?

Only because you ask. The following are full-night study results. I have numerous other PSG reports, but they are either split-night (which I don't consider to be of particular value, especially in this regard) and/or involve dental appliance therapy.

OK, to review:

Muffy wrote:The Muffpothesis offers a possible explanation why some patients may have HI Respironics < HI ResMed, namely, potential events are excluded by VB in the Respironics algorithm that may otherwise appear as hypopneas in the ResMed algorithm:

-SWS wrote:The Muffpothesis states: 1) that the Respironics VB control layer is selectively discarding hypopneas during moments of wake, and 2) informally observed or projected HI discrepancies in cases of high VB% precisely support that conclusion.

Muffy wrote:an intractable (ResMed) HI would be strongly suggestive not of SBD, but disrupted sleep.

Because of the nature of the analysis, VB is most frequently associated with "troubled wake" (VB can appear in phasic REM, but in adults, you have to pretty phasic). Consequently, to support this concept, we need to demonstrate that in a given subject, the amount of wake during the sleep period needs to be at least as much as the VB%.

As noted, Velbor frequently recounts VB% in the high 20s and 30s. Although dated, his NPSGs show Sleep Efficiencies of 67.7%, 66.0% and 67.7%, for Wake of 32.3%, 34.0% and 32.3%, respectively. Sleep architecture histogram placed along the VB time plot could offer even more support to MP.

In summary:

Variable Breathing may be a reliable marker of poor sleep quality.

The exclusionary capability of the Variable Breathing Mode may make the Respironics algorithm more accurate in determining SDB events over the entire sleep period in that wake events may be ignored.

Intractable HI in ResMed A10 results may, in some patients, be a result of wake phenomena. In these cases, while an arbitrary "correction factor" may be applied, the first thing that should be examined is Sleep Efficiency.

Extraordinary high ResMed HI, however, should not be summarily dismissed under any circumstances.

Muffy

Muffy wrote: Because of the nature of the analysis, VB is most frequently associated with "troubled wake" (VB can appear in phasic REM, but in adults, you have to pretty phasic). Consequently, to support this concept, we need to demonstrate that in a given subject, the amount of wake during the sleep period needs to be at least as much as the VB%.

Well, it's possible to have a VB% of 40%, for instance, with half of that VB time comprised of troubled wake and half comprised of distressed REM/dreaming type breathing:

Most Respironics VB patents wrote:When a patient is awake, in REM sleep, or in distress, breathing tendsto be more erratic and the Auto-CPAP trending becomes unstable. It is, therefore, important to interrupt the auto-CPAP controller if the patient's breathing pattern becomes too variable. In essence, the variable breathing control layer keeps theAuto-CPAP control layer from being too erratic.

So it's possible to have wake as only a portion of VB time, with those Muffpothesis type scoring discards still happening.

But I agree with the underlying spirit of: 1) looking for one or more residual-hypopnea intensive patients, 2) noting their pattern of scored residual hypopneas while aseep, 3) noting whether hypopneic type reductions still manage to occur for that patient during wake, and 4) observing whether the Respironics algorithm discards those wake-moment hypopneas.

Unfortunately my hunch is that wakefulness tends to ameliorate obstructive SDB during wake. However, we also know some centrally-dysregulated patients will have homeostatic problems in breathing as they transition between wake and sleep states. So my hunch is that if it's sleep/wake transitional hypopneas being recorded, that perhaps the underlying hypopneic etiology has more to do with central homeostasis rather than obstruction.

Dunno about that last part, though, Muffy. Just thinking out loud as I attempt to sort of muddle through what factors might be involved...


Anyone interested in how Muffy's VB scoring hypothesis took roots may want to read this thread:
viewtopic.php?f=1&t=44022&st=0&sk=t&sd= ... 15#p394855

-SWS wrote: So my hunch is that if it's sleep/wake transitional hypopneas being recorded, that perhaps the underlying hypopneic etiology has more to do with central homeostasis rather than obstruction.

Dunno about that last part, though, Muffy. Just thinking out loud as I attempt to sort of muddle through what factors might be involved...


Anyone interested in how Muffy's VB scoring hypothesis took roots may want to read this thread:
viewtopic.php?f=1&t=44022&st=0&sk=t&sd= ... 15#p394855

My apologies for responding without having read the root -- and even most of the beginning parts of this thread -- however, that last part in -SWS's post reminded me that the ResMed algorithm is based on the assumption that all hypopneas are central in origin, and it does not attempt to treat them. (See that often quoted Berthon-Jones interview

Why doesn’t ResMed's AutoSet respond to hypopnoea?
When you are lying quietly awake, or when you first go to sleep, or when you are dreaming, you can have hypopneas (reductions in the depth of breathing) which are nothing to do with the state of the airway. For example if you sigh, which you do every few minutes, you usually have a hypopnea immediately afterwards. This can also happen if you have just rolled over and are getting settled, or if you are dreaming. And the annoying thing is that when you are on PAP, this tendency to have what are called central hypopneas - hypopneas that are nothing to do with the state of the airway - is increased. If you make an automatic CPAP device that responds to hypopneas, you will put the pressure up to the maximum while the patient is awake.
Do you think there is a misconception clinically that all hypopneas should be treated ?
For simple obstructive sleep apnea, central hypopneas should not be treated. They are not a disease. Everyone has them. And they don’t go away with CPAP.

ResMed assumes it treats (prevents) osbtructive hypopneas by the way its algorithm responds to what it identifies as flow limitations. That fast response by the S8 seen in the bench test McCoy, Eiken and Diesem:

is a direct result of a planned ResMed escalation when encountering intractable flow limitations.

Here is the S8 responding to a series of intractable flow limitations -- the pressure gets even higher than in response to hypopneas -- and does so very quickly. OTO, the Respironics' response to those is much more careful.




The breathing pattern thrown at the machines can be seen here "Created Unequal" McCoy and Eiken 2006 - a previous version of the benchmarks, but the breathing patterns were not changed:



O.

-SWS wrote:

Muffy wrote: Because of the nature of the analysis, VB is most frequently associated with "troubled wake" (VB can appear in phasic REM, but in adults, you have to pretty phasic). Consequently, to support this concept, we need to demonstrate that in a given subject, the amount of wake during the sleep period needs to be at least as much as the VB%.

Well, it's possible to have a VB% of 40%, for instance, with half of that VB time comprised of troubled wake and half comprised of distressed REM/dreaming type breathing:

Most Respironics VB patents wrote:When a patient is awake, in REM sleep, or in distress, breathing tends to be more erratic and the Auto-CPAP trending becomes unstable. It is, therefore, important to interrupt the auto-CPAP controller if the patient's breathing pattern becomes too variable. In essence, the variable breathing control layer keeps theAuto-CPAP control layer from being too erratic.

So it's possible to have wake as only a portion of VB time, with those Muffpothesis type scoring discards still happening.

In re:

-SWS wrote:half of that VB time comprised of troubled wake and half comprised of distressed REM/dreaming type breathing

the Respironics patent states

The Patent wrote:awake, in REM sleep, or in distress

so the VB choices are:

Awake.
REM.
Distress.

And I would limit the "distressed" part, to "wake" so it would be "troubled wake". There is no "distressed REM". The two types of REM are tonic and phasic, and REM-related respiratory variation, if present, would be confined to phasic REM:

Phasic REM sleep events are intermittent (e.g., rapid eye movements and muscle twitches). Tonic REM sleep events are persistent (e.g., desynchronized [activated EEG] and striated [voluntary] muscle inhibition). As described below, these tonic versus phasic distinctions may be relevant to physiological changes that accompany sleep.

REM and NREM Sleep

In practice, you don't see so much REM-related respiratory variation in adults as to attribute ANY VB to that phenomenon. In other words, ALL VB should be considered to be troubled wake until proven otherwise.

If you're able to locate your VB like Velbor, then you might explain a VB block away as phasic REM if it occurs say, at the end of the night. And "IMO", I actually think the last block or two of VB in Velbor's case could be phasic REM:



and not necessarily because it coincidently occurs at the end of the night. If you review his REM onset in NPSG, by history he has had some severely delayed REM, which would increase the likelihood that REM, when it finally appears, would be phasic REM.

By-the-by, if you think "Oh boy, I gots to get me some of that phasic REM", don't, because tons of phasic REM usually means there's something else underfoot.

As an example of breathing in phasic REM:



Those "in the know" will recognize this as 100% (or whatever scale you use) REM density. Complete phasic REM. A one-in-a-I-don't-know-how-many occurrence.

But you can see breathing (in the CPAP Flow channel) as being highly erratic, including central apneas, hypopneas, desats and VB. Clearly, however, this is an area that needs to remain untouched by APAP algorithms.

Muffy

Just a general comment about high VB% correlating with repeated wakefulness throughout a sleep session or night. Let's accept that reasonable premise entirely unchallenged for the time being. And let's momentarily place all issues of manufacturer hypopnea-scoring discrepancies aside as well:

Theoretically, then, significant numbers of Respironics patients with high VB% scores might expect to see their high VB% scores reduced as they successfully work on problems with Sleep Hygiene.

The premise above is that if high VB% reflects wake-interspersed sleep architecture, then reducing that repeated wakefulness by improving Sleep Hygiene will probably also be reflected by reduced Respironics VB% scores----at least for a good number of Respironics patients previously presenting poor sleep architecture.

-SWS wrote:.... Theoretically, then, significant numbers of Respironics patients with high VB% scores might expect to see their high VB% scores reduced as they successfully work on problems with Sleep Hygiene.
The premise above is that if high VB% reflects wake-interspersed sleep architecture, then reducing that repeated wakefulness by improving Sleep Hygiene will probably also be reflected by reduced Respironics VB% scores----at least for a good number of Respironics patients previously presenting poor sleep architecture.

My concern with the above suggestion is that it seems to imply that disturbed sleep architecture, as reflected by high levels of Variable Breathing, is sometimes or often associated with issues of sleep hygiene. To some degree, that may well be so. But it may also be the case for some individuals (as I believe it to be in my own situation) that disturbed sleep architecture may be a distinct primary rather than a secondary disorder, and that it is not, with current behavioral, pharmacologic and technologic resources, directly and completely treatable. I would further posit that such "primary sleep architecture disorders" may be associated with (though not necessarily causally, in either direction) sleep apnea. I arrive at these conclusions more empirically than theoretically - they fit my own data and experience.

I suspect that this issue may be a contributing factor to the frequent postings regarding ongoing tiredness or sleepiness despite "technically successful" xPAP therapy of OSA. I think it important to remember that xPAP (properly used, compliantly used, and in the absence of some very specific problems) is highly successful in treating OSA, but it is not a cure for all sleep disorders, some of which may be associated with OSA.

Besides, I don't really care for the particular survey tool referenced! Love the discussion. Velbor

Velbor wrote: . . . I don't really care for the particular survey tool referenced! . . .

Really? Don't tell -SWS, but I liked it so much I stole it and posted it on another forum as if I had found it myself!

Velbor wrote: My concern with the above suggestion is that it seems to imply that disturbed sleep architecture, as reflected by high levels of Variable Breathing, is sometimes or often associated with issues of sleep hygiene.

I'm admittedly surprised to hear that. But I'm also curious how one might support the antithesis of the central implication I have underlined in red text above?

Or stating my own view another way: "Disturbed sleep architecture is" most definitely "sometimes or often associated with issues of sleep hygiene." Excessive wakefulness and good sleep architecture are mutually exclusive. And poor sleep hygiene is known to adversely impact sleep architecture---sometimes inducing wakefulness.

And since the Muffpothesis states that high VB% is primarily associated with wakefulness, then reducing that same associated wakefulness would theoretically reduce the VB% numbers in a significant percentage of those patients. That statement (let alone contrived by this sorry SOB with recurring pain-related sleep architecture problems ) does not insinuate that poor sleep architecture is caused exclusively by poor sleep hygiene---at least not that I can tell as I reexamine the logic.

So where does the statement or position fall down then?

Velbor wrote:Besides, I don't really care for the particular survey tool referenced!

Well, I'll have to admit that rather journalistic-sounding survey I linked to is intended as neither a scientific tool nor comprehensive treatise on the subject matter. But to me it seemed a rather nice and brief introduction to the concept of Sleep Hygiene for many of our "sleep challenged" newcomers, who have undoubtedly never heard of the concept.

Awe... you're just picking on me because I'm still hoping to hear more about those Respironics summary definitions from my query a mere twelve posts up. And thank you for that summary chart, BTW! For instance, I'm wondering if the Respironics hypopnea definition(s) were compiled from various patent descriptions, clinician set-up manuals, training guides, marketing literature, etc.

There seems to be a certain amount of discrepancy among the hypopnea definitions contained in the various Respironics text media. And those discrepancies, in turn, impede at least some of the highly detailed technical analyses in this and other threads.

-SWS wrote: So where exactly is the above logic failing? :?:

No failure of logic. Just a sense of incompleteness. And defensiveness on my part, with overreaction to a non-existent "accusation" that I might be "unhygenic". Since my own data was being used as an example for discussion, I would much prefer that my own "excessive wakefulness" not be attributed to any presumed violation of the standard "sleep hygiene" rules (which, again being defensive, I would insist that I follow rigorously - being a rigorous - read obsessive - sort of person by nature).

By the way, I regularly cycle through a careful regimen of Ambien or Klonopin, not to get to sleep, but with the goal of lowering my threshold for waking through the night. Codeine works best, but it's not something a "hygenic" person would want to take regularly!

-SWS wrote: I'm still hoping to hear more about those Respironics summary definitions from my query a mere twelve posts up. :lol: And thank you for that, BTW! :D For instance, I'm wondering if the Respironics hypopnea definition(s) were compiled from various patent descriptions, clinician set-up manuals, training or marketing literature, etc. There seems to be a certain amount of discrepancy among the hypopnea definitions contained in the various Respironics text media.

Sorry, didn't realize that this was a puzzlement. The source of information for my now infamous chart, the source for all of the Respironics and ResMed definitions (the PB data was contributed by ozij) is direct quotation from manufacturer clinical manuals. Here is an image of the Respironics defintion page from the M-Series Auto manual:



Thanks!! Velbor