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Chuck where is your mask LEAK data?

Mask leak can play a critical role into how your numbers come out.


Also, if you are able to read data directly off the compact memory card importing it into the Excel for reports like that, that is great. All machines should be designed that way.

Actually, I haven't been recording leak simply because it is consistently below 0.06L/s with both the Swift and the Activa. I will start recording it if you think that it's useful, but I can't remember the time that it was above 0.06L/s.

C

APAP/Swift

AHI:2.8;AI=0.4;HI=2.4; Pressure (95%)=8.4.

And the plot thickens.........

Chuck

Indeed, the plot thickens! One very interesting observation is that this is also your lowest APAP/Swift 95% pressure score at only 8.4. Now, in the CO2 kinetics way of thinking we presume your fixed pressure threshold of central hypopnea induction may be somewhere between 8 cm and 9 cm (based on your drastic HI differences so far at those two fixed pressures with the Swift).

Now here we might postulate that your distribution of snore and flow limitation precursors last night did not evoke as much preemptive pressure response by the way of increases. So looking at the trend from a combinational CO2 depletion of kinetics view, that 95% pressure of only 8.4 sounds within reason regarding your low HI. However, analyzing simply "combination of APAP and Swift" tends to leave one a bit stumped. Perhaps this is a problem that is not best analyzed at the basic level of "which devices are in the equation and which devices are out of the equation"? Perhaps this is a problem best analyzed by questions like: 1) where's that pressure related threshold of CO2 induction this time? and 2) what combinational CO2 kinetics are at work here to make sense of that threshold's crossing?

I couldn't agree more! It was the 95% pressure of 8.4 that rang the bell for me.

C

Earlier in this thread we analyzed why the Harvard researchers essentially contraindicated APAP for the somewhat rare case of CSDB. We recognized that:

1) APAP-imposed pressure fluctuations might potentially contribute to the short-term homeostatic maladjustment of the CO2 trigger (by potentially making the sampled CO2 an even more transient target than in the case of no control factors or even fixed pressure control factors), and

2) Each APAP pressure increment in and of itself having a subtly adverse contributive effect to the overall depletive effects of CO2 kinetics (in an otherwise healthy pulmonary system having no other CO2-related complications that might factor into our overall CO2 considerations)

However, our hypothetical analysis of Chuck's APAP/Swift results last night bring out perhaps the most defining scenario for APAP's contraindication in the case of CSDB. Here are characteristics at play in this third and perhaps most prominent APAP/CSDB contraindication consideration:

1) Snores and flow limitations serving as prominent pressure-increasing triggers in any APAP,

2) Snores and flow limitations, in and of themselves, posing no adverse effects to the CSDB patient when and if they impose neither significant cortical arousals nor significant desaturation,

3) The APAP having justifiably increased pressure in preemptive response to snores and flow limitations (currently believed to be an algorithmically correct response for all patients without CO2-misadjusted respiratory drives)

4) That sustained, significantly heightened pressure (comprised of several or many APAP pressure increments) now imposing a significantly heightened adverse effect on the kinetics of CO2 depletion for the CSDB patient (compared to our earlier analysis of the comparatively subtle effects that any single APAP pressure increment would impose on CO2 depletion kinetics).

Under these circumstances that are hypothetically highlighted above, the CSDB respiratory drive is clearly better off with a lower fixed pressure that adequately addresses apneas and hypopneas than with a preemptively heightened pressure. Again, however, this is specifically and exclusively the hypothetical CSDB case of any APAP algorithm responding to inherently innocuous snore and flow limitation SDB signals (innocuous regarding cortical arousals, desaturation, and the onset of more severe obstructive events).

Deep in the realm of CSDB theoretical considerations once again...

[quote="-SWS"]Earlier in this thread we analyzed why the Harvard researchers essentially contraindicated APAP for the somewhat rare case of CSDB. We recognized that:

1) APAP-imposed pressure fluctuations might potentially contribute to the short-term homeostatic maladjustment of the CO2 trigger (by potentially making the sampled CO2 an even more transient target than in the case of no control factors or even fixed pressure control factors), and

2) Each APAP pressure increment in and of itself having a subtly adverse contributive effect to the overall depletive effects of CO2 kinetics (in an otherwise healthy pulmonary system having no other CO2-related complications that might factor into our overall CO2 considerations)

However, our hypothetical analysis of Chuck's APAP/Swift results last night bring out perhaps the most defining scenario for APAP's contraindication in the case of CSDB. Here are characteristics at play in this third and perhaps most prominent consideration for APAP contraindication in the somewhat rare case of CSDB:

1) Snores and flow limitations serving as prominent pressure-increasing triggers in any APAP,

2) Snores and flow limitations, in and of themselves, posing no adverse effects to the CSDB patient when and if they impose neither significant cortical arousals nor significant desaturation,

3) The APAP having justifiably increased pressure in preemptive response to snores and flow limitations (currently believed to be an algorithmically correct response for all patients without CO2-misadjusted respiratory drives)

4) That sustained, significantly heightened pressure (comprised of several or many APAP pressure increments) now imposing a significantly heightened adverse effect on the kinetics of CO2 depletion for the CSDB patient (compared to our earlier analysis of the comparatively subtle effects that any single APAP pressure increment would impose on CO2 depletion kinetics).

Under these circumstances that are hypothetically highlighted above, the CSDB respiratory drive is clearly better off with a lower fixed pressure that adequately addresses apneas and hypopneas than with a preemptively heightened pressure. Again, however, this is specifically and exclusively the hypothetical CSDB case of any APAP algorithm responding to inherently innocuous snore and flow limitation SDB signals (innocuous regarding cortical arousals, desaturation, and the onset of more severe obstructive events).

Deep in the realm of CSDB theoretical considerations once again...

That was me making a tweak then getting guested above.

Earlier I had wondered whether Herring Breur stretch receptors might possibly have any unexpected interplay with central apnea's chemoreceptors in the medulla oblongata. Specifically, I wondered about any kind of unexpected and dysregulating neurological trade off regarding signal priority between the stretch receptors and the central apnea CO2-related receptors. I'm admittedly getting ready to toss that idea in the discard pile.

However, regarding unexpected neurological interplay between chemoreceptor types by the way of dysregulating neurological prioritization... I got to wondering about GERD's role in apnea. The two or three GERD/apnea theories most often cited deal with: 1) GERD resulting in vocal chord dysfunction (GERD theoretically causing VCD apneas) and/or 2) a primary obstructive apnea results in a defensive albeit extreme thoracic respiratory effort, and that extreme effort inadvertently creates enough negative esophageal pressure to draw fluid up and past the LES (in this case an apnea thus theoretically causing GERD). A third theory that is commonly cited sometimes builds on that second theory above: reactive airway type SDB events occur in reaction to the caustic stomach acids (that may or may not have been brought on by theoretical etiologic scenario two). So what is/are the link(s) between apnea and GERD? Are there any other etiologic possibilities?

Can there be a dysfunctional and highly unexpected interplay between c-fiber afferents in the lungs brought on by either the immediate-term or perhaps even sustained degrading effects of acid reflux disease? Those c-fiber afferents are believed to be responsible for the coughing, choking, reactive suspension of inspiration, and a defensive neuromuscular airway closure (those last two being mentioned as concomitant and highly associative in the CSDB research currently being analyzed). To repeat, in that Harvard CSDB study they mentioned a surprisingly strong CSDB association with a neuromuscular defensive airway closure occurring simultaneously with CSDB central apneas (meaning a defensive airway obstruction occurring at the precise moment of the CSDB central apnea patient's lowest neurologically-driven respiratory effort, or "nadir"). Those c-fiber afferent chemoreceptors are specifically believed to be the ones responsible for our defensive coughing, choking, and reactive breath-holding in direct response to irritants such as smoke, chemicals, etc.

What happens by the way of dysregulated breathing when those c-fiber afferents are temporarily degraded by acid reflux? What happens by the way of dysregulated breathing when a certain percentage of those c-fiber afferents are permanently damaged by acid reflux? What exactly is the high-correlation role between SDB and GERD? Do CSDB patients have a higher incidence rate of either temporary or residual acid reflux c-fiber afferent damage? What exactly might that prominent role of GERD be with respect to both CSDB and non-complex SDB? And how many etiologically unique roles might GERD play with respect to SDB in general?

It will be very interesting to see the statistical correlation of acid reflux disease in the CSDB patient population compared to the remaining SDB patient population---especially in light of CSDB's highly characteristic yet counterproductive defensive airway closure that occurs during the respiratory nadir of a CSDB-related central apnea. More wondering than anything else....

All in all a pretty good discussion. Personally, I don't totally agree with all the findings of that Harvard study as it relates to apap use. I'm going to defend the little guy, the autopap.

Which autopaps contradict? did they test ALL of them in this research?

My feeling is Doctors already have so many bogus excuses in their back pocket to deny use of autopaps, they don't need any more. With the biggest one being the one they won't tell you, that being you don't need to go back and see them as often which impacts their revenue stream. If you are without insurance, it is the only machine to have in my opinion.

And it seems that CO2 mask retention rates play just as much as a role as fluctuating pressures from autopaps. True some autopaps increase pressure .2cm per second, very fast, some others only .5cm every 5-minutes. Some stop with that pressure, others do not.

They also lower that same pressure differently, again one drops it very fast as seen in the pressure sine wave graphs, while others stair-step the pressure back down in controlled decreases.

Contradictions may be the case in a "few" that have this CSDB (heck, I may even have it), but for the majority that machine allows us to sleep every night where cpap didn't.

Lack of understanding on how they actually work by doctors and DME's who set them up seems more of a problem in my opinion. You learn that quickly once you take control over your own therapy. Not all apaps are created equal. Some rely prominently on snore detection others on flow limitation, others yet something else.

Pick the wrong machine and it will only contribute to the effects of this CSDB (according to this review as I understand it).

But if what we are looking at here is not seen in a PSG or is intentionally ignored to begin with how in the world is a apap manufacturer supposed to develop a machine to address it?

We have thousands of sleep centers across the country performing thousands of PSG's every night on millions of patients. I think they should start in these sleep labs with this research FIRST to confirm it then trying the different modalities to confirm they also work.

Right now all we are going to see is Doctors printing out that Harvard study Journal Review and telling me why I cannot have an autopap.

My HI indices go UP with pressure. The also go UP if you lower any found pressure, sometimes I feel better just sleeping with NO machine at all. But 2 strokes tell me I have to continue using it, somehow, so I do.

Sometimes you cannot eliminate all the events seen, getting down to what is thought to be normal is about all you can expect in some cases. KNOWING what is happening in your own particular case can be critical to successful treatment. The autopap allows me to find that out much quicker for less money. I can look at a week or a months worth of data, I've had 3 titration studies, they never found anything different than what I already knew.

Sometimes you can have the best therapy in the world and still feel like crap the next day. I tell ya, I can sleep 12hrs, get up drink a cup of coffee and go back to sleep for another 12hrs no problem at all.

A good night sleep for me is going to sleep at midnight and waking up at 5AM ready to go with no alarm.

Many great points, Snoredog. The one point that I particularly resonate with was the point about machine setup being much more problematic than CSDB. To reiterate CSDB is presently thought to be a rare occurence in the SDB patient population.

So CSDB's APAP contraindication is really irrelevant to almost all of us. However, I don't think the APAP contraindication has to do with good-algorithm/bad-algorithm as much as it has to do with pressure change. And those pressure changes potentially being inherently counter-productive to any homeostatic maladjusting CO2 trigger that can't quite get a CO2-based inspiratory trigger target down pat. Fixed pressure does not impose the same CO2 kinetic transitions that varying pressure does, and is simply less adverse to homeostatic maladjustment based on expiratory end-phase "CO2 snap shots" or "CO2 data samples" if you may.

My hunch is that because this homeostatic maladjusting CO2 respiratory trigger is new sleep science territory, the researchers have decided to error on the side of contraindication caution. From the experiments Chuck has been running, however, I really don't get the impression his depletive CO2 threshold is highly erratic. However, when his SDB APAP-triggering precursor events become somewhat erratic, then so do his APAP efficacy results become somewhat erratic based on varying pressure's effects on CO2 kinetics.

This is definitely not a Harvard adventure in APAP bashing in my own view. Nor is it a case of -SWS APAP bashing either, since I'm still the same APAP advocate I have been ever since I discovered that I slept better with APAP. It's a rare SDB case with rare considerations that should be driven by science instead of political or marketing forces. Keep the great ideas rolling.

SWS wrote:

This is definitely not a Harvard adventure in APAP bashing in my own view. Nor is it a case of -SWS APAP bashing either, since I'm still the same APAP advocate I have been ever since I discovered that I slept better with APAP. It's a rare SDB case with rare considerations that should be driven by science instead of political or marketing forces. Keep the great ideas rolling.

Ah I know that man, I was just rambling

Now I wonder what kind of role the leaking mask would have to play into all this info, your buzzzzzin along on your ideal straight cpap machine with your ideal CSDB avoidance pressure, no ramp and suddenly....

you develop a mask leak...

ah oh the pressure drops... machine revs up that motor to 10,000RPM to compensate... you snort, scratch your nose the leak stops suddenly... mmm.....

what I found is: I really have to limit my autopap on the Max. pressure side. There is no upper range for me, no +/-2cm, I have to set my Max. pressure to that "sweet" spot pressure found from the reports. Then I can do what I want with the lower pressure of 6.5cm and numbers consistently will be lower than if I left it some room for a pressure increase. If I loosen up and increase that Max. pressure, my HI's immediately jump up. For me it seems that pressure above the sweet spot is what triggers all those extra HI's.

And that would be my suggestion to Chuck to try,

if the 8.4cm pressure is his ideal sweet spot pressure he needs to set the max. pressure on his Vantage to that value and he can do what he wants with the bottom pressure.

Now I can easily tolerate 9cm cpap and don't really need to use a lower Min. pressure but I found over time I get consistently lower numbers by leaving the bottom pressure set at 6.0cm or 6.5cm than I do at higher up close to 9cm Max. pressure. The change in pressure doesn't seem to bother me.

Last night using 6.5 as my Min. in AFLE mode and a Max at 9cm, I had the lowest AHI ever. I had 1 OA and 2 HI, probably felt better than I have in months. When I woke up this morning it was blowing at 7.5cm not even close to my titrated pressure.

APAP/Swift

AHI=3.1;AI=0.0;HI=3.1;Pressure (95%)=8.6.

Slept well last night with virtually NO awakenings and feel very refreshed this AM.

I intend to switch to a CPAP trial when my week of APAP/Swift ends in two days. At that time, I'll publish another graph displaying the results of the APAP/Swift trial. I'll then continue for one week with a CPAP (8cmH2O)/Swift trial and then publish a graph displaying the results of that week. And then, I'll let this thread die a quiet death. Its provoked amazing thought and discussion and I hope has proven to be useful to some in terms of their knowledge and understanding of this wonderful, wacky world of sleep disordered breathing.

Chuck

APAP/Swift

AHI=2.6;AI=0.1;HI=2.5;Pressure (95%)=10.6.

Slept well. Feel tired on awakening, but its the end of the week and I've been working hard.

C

-SWS wrote: From the experiments Chuck has been running, however, I really don't get the impression his depletive CO2 threshold is highly erratic.

GoofyUT wrote:
AHI=3.1;AI=0.0;HI=3.1;Pressure (95%)=8.6
AHI=2.6;AI=0.1;HI=2.5;Pressure (95%)=10.6

But then again Chuck's CO2 threshold may be a bit more erratic than we thought, or he may not have any CO2 depletive thresholds related to very mild CSDB after all (although I more than secretly suspect he really does based on various highly-correlative HI rises and drops that neatly follow most of his experimental deltas in pressure therapy so far. ). However, the S8 95% pressure score in and of itself does not really paint any sort of picture regarding CO2 kinetic transitions due to APAP pressure variability itself. Fixed pressure experiments actually make it easier to see CSDB patterns by removing kinetic transitions and variability that are directly related to pressure's transitions and variability. While we are waiting for Chuck's data to gradually roll in, I thought some of the folks reading this thread would like to see the actual CSDB charts that we have been discussing.

We have been talking about central events, but the letter "C" in CSDB refers to the "complex" aspect of this SDB phenotype. And part of that complex aspect means obstructive apneas as shown below:


Note the thermistor, nasal pressure, chest effort, and abdominal effort channels way up top. Each high and low oscillation corresponds to inspiration and expiration. When the thermistor and nasal pressure channels flatten out, you are seeing an apnea. The fact that the data channel labelled "chest effort" still shows respiratory effort results in these CSDB apneas getting scored as obstructive and not central.

What I find most interesting about these obstructive CSDB apneas is the fact that they occur in short approximately 25-second cyclic bursts, almost like clock work. They are of short enough duration that they do not even cause significant desaturation. And that oscillating highly cyclic nature of the obstructive apneas themselves hint very strongly at neurology dysregulating the airway for lack of properly maintaining one or more chemoreceptor signal channels. Not all obstructive apneas have to happen because the upper airway dilator muscles simply "relaxed" as you fell asleep. Gets you to wondering how most of those upper airway dilator apneas really happen. Doesn't it?

Here's the highly cyclic pattern occurring on the topmost PSG chart above: one breath, two breaths, three breaths, apnea... one breath, two breaths, three breaths, apnea... and so on, in a highly "monotonous" manner as the researchers put it. Here's the text excerpt from that CSDB research study describing the two PSG charts you see above:

"Polysomnographic recognition of complex sleep-disordered breathing in 90-second epochs. Above, polysomnogram showing the typical features of complex disease not associated with classic periodic breathing, Cheyne-Stokes respiration, or central apneas. The cycles of respiratory abnormality are short (~25 seconds) and are obstructive. Oxygen desaturations are relatively mild, perhaps in part because the events are short. The same subject during rapid eye movement (REM) sleep shows the other characteristic feature of this form of disease: minimal abnormality during REM sleep. This patient had immediate induction of central apneas during non-REM sleep by even low levels of positive airway pressure, easy control of disease in REM sleep, and required added dead space for adequate control. CO2 while the patient was awake was 38 mm Hg, and End-tidal decreased to 36 mm Hg at sleep onset. Dead space of 150 ml kept the end-tidal CO2 between 39 and 42 mm Hg."

I will post a similar PSG chart from that same Harvard study showing cyclic central events next. Then a little discussion about chemoreceptor roles in a closed loop biologic system such as the human respiratory drive itself. We'll work through the CO2-based feedback loop of the peripheral chemoreceptors in the medulla oblongata before exploring the role of c-fiber afferents in the lungs a bit more.

Saturday, 7/15

APAP/Swift

AHI=5.0;AI=0.2;HI=4.8;Pressure (95%)=9.6

Sunday, 7/16

APAP/Swift

AHI=2.8;AI=0.0;HI=2.8;Pressure (95%)=9.4

I intend to start the CPAP trial tonight, for a week and will report the data.

I tried to post a graph displaying the results of the APAP trial, as I did before on this thread. However, when I tried to upload to Photobucket, it returned an error message saying that TIFF files were unacceptable. Now, with the chart I previously posted (with Lori's help), I used exactly the same procedure; I captured a screenshot of the chart using "Grab", a MacOS program. I then uploaded the image to Photobucket and then pasted the IMG tag into my cpaptalk.com post. No problems whatsoever. And, that image was identified as a TIFF. This time, same image, same TIFF, but Photobucket wouldn't take it. Any suggestions? The chart is very worthwhile to view.

Chuck