UARS, Flow Limit, and Flow Rate graphs

Sir NoddinOff wrote:

-SWS wrote:Anyway, to answer you question above, yes. If you need more static pressure during that part of the breathing phase, then it must be delivered with EPAP, since IPAP has not yet commenced. So reducing EPR is one way to present more airway stenting pressure during that part of the breathing phase.

I'm definitely going to be the first to take the plunge and try to get rid of my "squigglies", that is, by turning off my PR's EPR feature (my auto relief pressure, A-FLEX PR calls it, was set at 3). I've never had the slightest problem breathing without it before, so why not give it a try? Tho it should be noted to like minded people that my current pressure settings are 8/12, not very high thankfully.

Bear in mind Respironics' Flex design is different than Resmed's EPR. Flex is designed to return pressure to full CPAP/APAP before that part of the phase when the post-expiratory squigglies manifest. So disabling Flex won't deliver more stenting pressure at that precise moment. In other words, Flex returns to full CPAP/APAP pressure before exhalation is over, during each breath. Squigglies come along after that...

Resmed EPR is a slightly different animal, timing wise. Unlike Flex, Resmed EPR returns to full CPAP much later. EPR timing is more similar to traditional BiLevel than Flex timing. So the experiment makes a little more sense for Resmed EPR than Respironics Flex. You can always experiment with Flex anyway, just to see what happens. Some CPAP users fare better without Flex for a variety of reasons. And you might want to experiment with more CPAP/APAP-min pressure, since Flex delivers that CPAP/APAP pressure by the time post-expiratory squigglies appear. Good luck.

Interesting that you're looking to eliminate the pressure differential. Dr. Krakow recommends a higher differential pressure via BPAP per the info. found on this very site:
our-collective-cpap-wisdom/flow-limitat ... BiPAP.html

NotLazy, have you checked this:

http://doctorstevenpark.com/sleep-apnea ... e-syndrome

B/c you don't have OSA you might be lucky doing what Dr. Steven Park suggest.

blueh2o wrote:Interesting that you're looking to eliminate the pressure differential. Dr. Krakow recommends a higher differential pressure via BPAP per the info. found on this very site:
our-collective-cpap-wisdom/flow-limitat ... BiPAP.html

Krakow experiments with unusually high PS to address FL morphology at the top or peak of inspiration. That FL dynamic occurs well into inspiration and can be dealt with using IPAP. PS (the BiLevel differential) mechanically offloads resistance-based work of breathing (WOB). Researchers often model this flattening dynamic at the peak of inspiration using Starling Resistor---a collapsible tube model. In the case of UARS, this FL dynamic is the same collapse dynamic that occurs when you accidentally collapse a straw by drawing a thick milk shake: the collapsible tube is drawn in by suction pressure.

By contrast, when the collapse occurs while static pressure wanes toward the tail-end of expiration, then we clearly don't have the same collapse dynamic as above. There is no inspiratory draw yet. Therefore there is no Starling type suction just yet. Rather, when the collapse occurs at this earlier point---before inspiration gets going---then IPAP cannot be used to stent that collapse. Collapse that occurs before inspiration gets started tends to result from a more passive process of muscle relaxation---or failure to maintain the airway (e.g.. move the tongue out of the way to breathe). Based on the sheer timing of these collapse or occlusion types, EPAP or CPAP must be used since IPAP has not yet been triggered. Even Krakow must address collapse or occlusion during expiratory end-phase with EPAP. He will then titrate PS up from that reference point using heightened IPAP---that latter step to address FL that occurs during inspiratory peaks.

blueh2o wrote:Interesting that you're looking to eliminate the pressure differential. Dr. Krakow recommends a higher differential pressure via BPAP per the info. found on this very site:
our-collective-cpap-wisdom/flow-limitat ... BiPAP.html

Also interesting that Stanford apparently does not practice or subscribe to Krakow's experimental approach using such high PS. Nor does Stanford maintain that UARS and FL are one-in-the-same. Krakow equates the two and draws a zero-FL tolerance policy. I have yet to read of anyone else in sleep medicine doing that...

-SWS wrote:Also interesting that Stanford apparently does not practice or subscribe to Krakow's experimental approach using such high PS. Nor does Stanford maintain that UARS and FL are one-in-the-same. Krakow equates the two and draws a zero-FL tolerance policy. I have yet to read of anyone else in sleep medicine doing that...

FWIW, I do not subscribe to Krakow's zero-FL tolerance policy. The paper linked below is an interesting read, "Analysis of Inspiratory Flow Shapes in Patients with Partial Upper-Airway Obstruction During Sleep." In the study they found that 9 control subjects without sleep breathing disorders only showed the "normal" round shape of the inspiratory flow 48% of the time.

http://journal.publications.chestnet.or ... 956/37.pdf

It is a case of the fallacy of necessity. While it may be necessary for FL to exist to trigger arousals it need not exist 100% of the time. For example, if a baseball player can hit a home run every time at bat he will have a perfect 1000 batting average. However to have a perfect batting average he need not hit a home run every time. Krakows approach seems to be, "if I can hit a home run every time, I will have a perfect batting average." That, of course, is true, just very aggressive and unnecessary.

-SWS wrote:

blueh2o wrote:Interesting that you're looking to eliminate the pressure differential. Dr. Krakow recommends a higher differential pressure via BPAP per the info. found on this very site:
our-collective-cpap-wisdom/flow-limitat ... BiPAP.html

Krakow experiments with unusually high PS to address FL morphology at the top or peak of inspiration. That FL dynamic occurs well into inspiration and can be dealt with using IPAP. PS (the BiLevel differential) mechanically offloads resistance-based work of breathing (WOB). Researchers often model this flattening dynamic at the peak of inspiration using Starling Resistor---a collapsible tube model. In the case of UARS, this FL dynamic is the same collapse dynamic that occurs when you accidentally collapse a straw by drawing a thick milk shake: the collapsible tube is drawn in by suction pressure.

By contrast, when the collapse occurs while static pressure wanes toward the tail-end of expiration, then we clearly don't have the same collapse dynamic as above. There is no inspiratory draw yet. Therefore there is no Starling type suction just yet. Rather, when the collapse occurs at this earlier point---before inspiration gets going---then IPAP cannot be used to stent that collapse. Collapse that occurs before inspiration gets started tends to result from a more passive process of muscle relaxation---or failure to maintain the airway (e.g.. move the tongue out of the way to breathe). Based on the sheer timing of these collapse or occlusion types, EPAP or CPAP must be used since IPAP has not yet been triggered. Even Krakow must address collapse or occlusion during expiratory end-phase with EPAP. He will then titrate PS up from that reference point using heightened IPAP---that latter step to address FL that occurs during inspiratory peaks.

blueh2o wrote:Interesting that you're looking to eliminate the pressure differential. Dr. Krakow recommends a higher differential pressure via BPAP per the info. found on this very site:
our-collective-cpap-wisdom/flow-limitat ... BiPAP.html

Also interesting that Stanford apparently does not practice or subscribe to Krakow's experimental approach using such high PS. Nor does Stanford maintain that UARS and FL are one-in-the-same. Krakow equates the two and draws a zero-FL tolerance policy. I have yet to read of anyone else in sleep medicine doing that...

SWS,

First of all, thank you for some very informative posts. They are of great interest to me since I feel I have an UARS component in addition to sleep apnea.

I do have a different take on what Krakow is doing. Just because no one else in sleep medicine is doing what he is doing doesn't mean it isn't legitimate. I say that by the way with no knowledge like you have as to whether he is correct or not.

A great example is Barry Marshall, who was ridiculed by doctors for years for claiming that ulcers were due to helicobacter pylori and not stress only to finally prove he was correct.

http://www.achievement.org/autodoc/page/mar1pro-1

Again, thank you for some great topics.

49er

PS- I also thank NotLazyJustTired for starting this thread.

Sir NoddinOff wrote: Now I have to go back and look at my flow lines more critically, maybe even experiment further turning off A-Flex.

As I wrote above I turned off my PR's A-Flex feature in the clinician's menu, mostly as a test trying to eliminate some of the 'squigglies' on inhale. This morning, after a not so great night, I looked at my flow line during my the periods where I was totally asleep and can't really see any improvement on the inhalation side like I'd hoped. SWS did caution that it might not work with PRs, but could possibly work with ResMeds algorithm. I'll probably try a few more nights of A-Flex off - it didn't seem too uncomfortable.

Sir NoddinOff wrote:As I wrote above I turned off my PR's A-Flex feature in the clinician's menu, mostly as a test trying to eliminate some of the 'squigglies' on inhale. This morning, after a not so great night, I looked at my flow line during my the periods where I was totally asleep and can't really see any improvement on the inhalation side like I'd hoped. SWS did caution that it might not work with PRs, but could possibly work with ResMeds algorithm. I'll probably try a few more nights of A-Flex off - it didn't seem too uncomfortable.

I turned AFlex off once...as an experiment. It was a total disaster experiment.
viewtopic.php?f=1&t=67883&p=631376&hili ... mb#p631376
But remember I had been using AFlex for a couple of years so my body had become real accustomed to its comfort.
SWS is right...the reduction in Flex options can't be compared to EPR reductions in the S9. It simply doesn't work the same way. It's really hard to describe (and I have used EPR in cpap mode on my machine to try to get a grasp on how it feels) but it has more to do with the timing of the respiration than it does with the actual amount of reduction during exhale.
I found that AFlex at 3 made me feel like the machine was wanting me to breathe too fast...almost like hyper ventilating fast.
The setting of 1 seemed to be a bit slow but the setting of 2 on AFlex matched my own respiration pattern and timing perfectly.
I know the reduction in pressure wasn't all that different but the timing made it feel much more natural.

The amount of reduction offered by the Flex settings simply is not going to come close to the amount that EPR offers and since it is flow based anyway...even a setting of AFlex 2 is going to vary in reduction amount offered between 2 different people using the same setting because they breathe differently.

OK, so I have a really boneheaded question about these flow rate graphs.

is there a standard scale at which the graph should be set? Because I can sure flatten out the curves if I zoom in on a shorter segment of time in the graph. If I back out the zoom the graph looks pretty spiky.

Drowsy Dancer wrote:is there a standard scale at which the graph should be set? Because I can sure flatten out the curves if I zoom in on a shorter segment of time in the graph. If I back out the zoom the graph looks pretty spiky.

I try to use the scale that Encore offers in the wave form graphs. As you have found out we can play with the scale and get some funny looking and hard to interpret results. I figure (just my WAG) that waveform offers a certain scale for a reason.
Much harder to do with S9 data though...they don't get a special waveform graph to compare to.

avi123 wrote:NotLazy, have you checked this:

http://doctorstevenpark.com/sleep-apnea ... e-syndrome

B/c you don't have OSA you might be lucky doing what Dr. Steven Park suggest.

Thanks for the pointer. Yes, I've read that and his book as well. I am considering the MAD and even surgery if it will help. However, as I believe I have a component of mild OSA, I am pursuing PAP treatment as a first step. I suspect I have a moderate case of non-allergic rhinitis which may be where the UARS originates, so I am thinking surgery may be in my future. I haven't as yet seen an ENT. Baby steps . . .

Drowsy Dancer wrote:OK, so I have a really boneheaded question about these flow rate graphs.

is there a standard scale at which the graph should be set? Because I can sure flatten out the curves if I zoom in on a shorter segment of time in the graph. If I back out the zoom the graph looks pretty spiky.

You raise a good point. I try to compare my flow rate graphs at different pressures while keeping the scale the same and showing about a dozen breaths at a time. That way I am comparing apples with apples. Using this methodology I can see how my Flow Limitation is improved at higher pressures and that is what prompted this whole discussion.

Please don't get too obsessed over this. As I have posted earlier, even "normal sleep breathers" have some amount of flow limitation. It really only matters for individuals who a) did not score an AHI over 5 in their sleep study, or b) have reduced their AHI to below 5 with PAP treatment, and c) they continue to experience daytime fatigue. Only then can we begun to discuss whether this residual fatigue is related to arousals that stem from flow limitation or some other cause. Not everyone exhibits this syndrome.

In my particular situation I believe that my sleep architecture gets all junked up because of arousals from flow limitation (and perhaps mild OSA events), so that is why I am becoming a bit obsessive about at least understanding it better.

NotLazyJustTired wrote:

-SWS wrote:Also interesting that Stanford apparently does not practice or subscribe to Krakow's experimental approach using such high PS. Nor does Stanford maintain that UARS and FL are one-in-the-same. Krakow equates the two and draws a zero-FL tolerance policy. I have yet to read of anyone else in sleep medicine doing that...

FWIW, I do not subscribe to Krakow's zero-FL tolerance policy. The paper linked below is an interesting read, "Analysis of Inspiratory Flow Shapes in Patients with Partial Upper-Airway Obstruction During Sleep." In the study they found that 9 control subjects without sleep breathing disorders only showed the "normal" round shape of the inspiratory flow 48% of the time.

http://journal.publications.chestnet.or ... 956/37.pdf

It is a case of the fallacy of necessity. While it may be necessary for FL to exist to trigger arousals it need not exist 100% of the time. For example, if a baseball player can hit a home run every time at bat he will have a perfect 1000 batting average. However to have a perfect batting average he need not hit a home run every time. Krakows approach seems to be, "if I can hit a home run every time, I will have a perfect batting average." That, of course, is true, just very aggressive and unnecessary.

Your obsession is to our benefit. This discussion has opened my eyes to a whole other arena to attempt to understand.
I also do not agree with all of what Krakow espouses. His focus on the "psychanalytics" such as what he terms "anxiety" and in his book "end-of-day closure" I think can be off-putting to someone like myself. I can't even finish his book because of that focus (not to mention all of the acronyms). I think Park describes this psychological phenomena better as "constant low grade stress" due to sleep deprivation. I feel like the sleep deprivation feeds on itself becoming the vicious cycle that they mention. This may be reflected in our breathing patterns?

LOL, thanks, I am glad to be helping. I shared with my wife yesterday what I had learned here and she stated that I am learning way more about my condition and treatment from the internet and this forum than I ever have from the Drs. I mean no disrespect to medical professionals, but she is right! It is really a time priority thing. Truth is, we have more time to research and learn than Drs. have time to spend with us and educate. At any rate, I will be a much more informed patient for my next appointment!

Of course, yesterday after reading your post I immediately went home to SleepyHead and starting studying my flow shapes. Regarding "Analysis of the Flow Shapes", I find it interesting that my shapes somewhat mirror those of the women (I'm OK with my masculinity) with my shapes being primarily composed of Class 6, secondarily of Class 2, and thirdly of Class 7. The authors assume that the women's flow shape has some correlation with postmenopausal levels of progesterone. I would argue and say this subset of women are most likely to be diagnosed with UARS and thus the similarities to my flow shapes.
Having said all that, it also occurs to me that you need to have some experience studying flow shapes to be able to come to any sort of reasonable conclusions and it appears this is a relatively new part of sleep medicine science. So, you can throw everything I just said out the door because I have no idea what I'm talking about.