how to interpret Flow Limitation graphs

General Discussion on any topic relating to CPAP and/or Sleep Apnea.
-SWS
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Re: Response #1

Post by -SWS » Sat Mar 12, 2011 11:18 am

avi123 wrote: But how can we comply with our dumb CPAPs machines with any of those theories or should we let the Baby in the Avatars mature first?
If CPAP machines are Borg technology as I suspect, then resistance is futile. And it behooves us to comply.
avi123 wrote: We need to understand that those scholars who fill out thousands of pages in medical magazines get advancements and paid more by the noise that they are making with their publications. They also spread their hypotheses willy neely in the hope of fetching a Nobel award in the far future.
Well, in seriousness, I can't say I agree with how broad those group-based generalizations are... But I also think those motivational dynamics occur in the scientific community to some limited and unknown extent:

http://www.plosmedicine.org/article/inf ... ed.0050201

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1182327/
avi123 wrote: But how can we comply with our dumb CPAPs machines with any of those theories or should we let the Baby in the Avatars mature first?
I bet Nostradamus could have turned THAT into a real nice quatrain.

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avi123
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Location: NC

Re: how to interpret Flow Limitation graphs

Post by avi123 » Sat Mar 12, 2011 12:32 pm

jnk wrote:
idamtnboy wrote: . . . That's a new book, isn't it? . . .
Yep. Relatively speaking.
idamtnboy wrote: . . . So this author is saying the goal is no upper airway restrictions or disturbances at all. In other words the air passage should be clear and clean and slick as can be so air moves in and out with absolute freedom of movement, i.e., no OAs, no FLs, and a flow graph with uniform amplitude. I wonder, in light of the complexity of the human body and how it interacts with the environment it's in every day and night, how realistically needful or desirable this is. . . .
No one breathes perfectly. The goal is to find the lowest pressure at which one feels one's best, as I understand it.
idamtnboy wrote:
Also, relief of upper airway obstruction is associated with resolution of intermittent hypoxemia and hemodynamic swings that accompany obstructive events, with a consequent reduction in long-term cardiovascular morbidity and mortality.
What the heck do those terms mean?
Steady O2 leads to improved blood chemistry and better heart health.
idamtnboy wrote: . . . But, as has been said many times on this forum, too high a pressure can prompt centrals. . . .
An overhyped fear in the context of simple OSA, in my opinion. When you are home-titrating for better numbers, the centrals show up as apneas and are thus accounted for and factored into your pressure choice.
idamtnboy wrote: . . . My sleep doc's assistant said too high a pressure can also cause OAs. How does the author address the conflicting results that may result from the pressure that eliminates "all degrees of upper airway obstruction?" but prompts CAs and possibly OAs?
The words I quoted were an overview of the state of mainstream OSA treatment, as I read them.

The important thing to remember is that the significance of any given "degree of upper airway obstruction" differs from patient to patient. That is why titration is about the effect the breathing seems to have on the sleep of that particular patient, not just how the patient breathes in general in comparison to other patients or some theoretical ideal, from what I've read as a patient.

I guess too high of a pressure during a titration might sometimes cause a central that then allows the airway to close, I don't know, I ain't no tech--but the temporary nature of the unstable breathing that can cause those kinds of centrals in a plain-vanilla OSA patient would mean that those temporary centrals likely would not matter in the long run, once they go away. That's why, in my opinion, home-machine data over time allows for the sweet-spot to be hit: the lowest pressure with the least number of significant events.

But I'm still learning this stuff.

Slowly.

And I have a long way to go.
****************************************************
My thoughts:


jnk, it's interesting to read what all those authors are saying but there are specific Clinical Guidelines for Manual Titrarions for Patients with OSA by the Task Force of the American Academy of Sleep Medicine (standard practice for PSG). So who cares what those authors are saying?

Example as of 2008:



(1) All potential PAP titration candidates
should receive adequate PAP education, hands-on demonstration,
careful mask fitting, and acclimatization prior to titration.

(2) CPAP (IPAP and/or EPAP for patients on BPAP) should be increased until
the following obstructive respiratory events are eliminated (no specific
order) or the recommended maximum CPAP (IPAP for patients
on BPAP) is reached: apneas, hypopneas, respiratory effort-related
arousals (RERAs), and snoring.

(3) The recommended minimum starting PAP should be 4 cm H2O for pediatric and adult patients, and
the recommended minimum starting IPAP and EPAP should be 8 cm
H2O and 4 cm H2O, respectively, for pediatric and adult patients on
BPAP.

(4) The recommended maximum CPAP should be 15 cm H2O
(or recommended maximum IPAP of 20 cm H2O if on BPAP) for patients
<12 years, and 20 cm H2O (or recommended maximum IPAP of
30 cm H2O if on BPAP) for patients ≥12 years.

(5) The recommendedminimum IPAP-EPAP differential is 4 cm H2O and the recommended
maximum IPAP-EPAP differential is 10 cm H2O

(6) CPAP (IPAP and/orEPAP for patients on BPAP depending on the type of event) should be
increased by at least 1 cm H2O with an interval no shorter than 5 min,
with the goal of eliminating obstructive respiratory events.

(7) CPAP (IPAP and EPAP for patients on BPAP) should be increased from any
CPAP (or IPAP) level if at least 1 obstructive apnea is observed for
patients <12 years, or if at least 2 obstructive apneas are observed for
patients ≥12 years.

(8) CPAP (IPAP for patients on BPAP) should be
increased from any CPAP (or IPAP) level if at least 1 hypopnea is observed
for patients <12 years, or if at least 3 hypopneas are observed
for patients ≥12 years.

(9) CPAP (IPAP for patients on BPAP) should
be increased from any CPAP (or IPAP) level if at least 3 RERAs are
observed for patients <12 years, or if at least 5 RERAs are observed
for patients ≥12 years.

(10) CPAP (IPAP for patients on BPAP) may
be increased from any CPAP (or IPAP) level if at least 1 min of loud or
unambiguous snoring is observed for patients <12 years, or if at least
3 min of loud or unambiguous snoring are observed for patients ≥12
years.

(11) The titration algorithm for split-night CPAP or BPAP titration
studies should be identical to that of full-night CPAP or BPAP titration
studies, respectively.

(12) If the patient is uncomfortable or intolerant
of high pressures on CPAP, the patient may be tried on BPAP. If there
are continued obstructive respiratory events at 15 cm H2O of CPAP
during the titration study, the patient may be switched to BPAP.

(13)
The pressure of CPAP or BPAP selected for patient use following the
titration study should reflect control of the patient’s obstructive respiration
by a low (preferably <5 per hour) respiratory disturbance index
(RDI) at the selected pressure, a minimum sea level SpO2 above 90%
at the pressure, and with a leak within acceptable parameters at the
pressure.

(14) An optimal titration reduces RDI <5 for at least a 15-
min duration and should include supine REM sleep at the selected
pressure that is not continually interrupted by spontaneous arousals
or awakenings.

(15) A good titration reduces RDI ≤10 or by 50% if the
baseline RDI <15 and should include supine REM sleep that is not
continually interrupted by spontaneous arousals or awakenings at the
selected pressure.

(16) An adequate titration does not reduce the RDI
≤10 but reduces the RDI by 75% from baseline (especially in severe
OSA patients), or one in which the titration grading criteria for optimal
or good are met with the exception that supine REM sleep did not occur
at the selected pressure.

(17) An unacceptable titration is one that
does not meet any one of the above grades.

(18) A repeat PAP titration
study should be considered if the initial titration does not achieve a
grade of optimal or good and, if it is a split-night PSG study, it fails to
meet AASM criteria (i.e., titration duration should be >3 hr).



So jnk, the language that you posted above (some from authors) such as:

In other words the air passage should be clear and clean and slick as can be so air moves in and out with absolute freedom of movement, i.e., no OAs, no FLs, and a flow graph with uniform amplitude.

The goal is to find the lowest pressure at which one feels one's best, as I understand it.

That's why, in my opinion, home-machine data over time allows for the sweet-spot to be hit: the lowest pressure with the least number of significant events.


IS IRELEVANT IN LIGHT OF CITY HALL INSTRUCTIONS

_________________
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Additional Comments:  S9 Autoset machine; Ruby chinstrap under the mask straps; ResScan 5.6
Last edited by avi123 on Sat Mar 12, 2011 2:07 pm, edited 1 time in total.
see my recent set-up and Statistics:
http://i.imgur.com/TewT8G9.png
see my recent ResScan treatment results:
http://i.imgur.com/3oia0EY.png
http://i.imgur.com/QEjvlVY.png

jnk
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Re: how to interpret Flow Limitation graphs

Post by jnk » Sat Mar 12, 2011 1:07 pm

So jnk, the language that you posted above (some from authors) such as:

In other words the air passage should be clear and clean and slick as can be so air moves in and out with absolute freedom of movement, i.e., no OAs, no FLs, and a flow graph with uniform amplitude.
I did not write or post those words. Another poster in this thread did.
In my opinion, home-machine data over time allows for the sweet-spot to be hit: the lowest pressure with the least number of significant events.
In the context of a plain-vanilla patient tweaking his own pressure for personal comfort, low numbers, and successful treatment, I consider that statement a truism and stand by it, in or out of context.

Please, though, be assured that I deeply treasure all personal estimates of the relevance of my posts. Thank you.

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Mr Bill
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Re: how to interpret Flow Limitation graphs

Post by Mr Bill » Sat Mar 19, 2011 5:14 pm

NotMuffy wrote:
The vast majority of people do not get centrals because of ultra-therapeutic CPAP levels.
This incidence would be the number of patients with CompSAS tendency, which, although is generally considered to be 15%, I believe that's a very aggressive number. They threw tons of people in there with low CAIs, current definition of CompSAS being CAI > 5. But when they show examples of CompSAS, they show these huge runs of chain centrals of like 50 in a row.

The argument:

Yes!

No!
...if you wanna argue that CPAP increases base lung volume (Functional Residual Capacity)(FRC), and since that increases gas exchange, some people can generate centrals that way, fine. But it's not as many as you might think...
Especially when one considers that (1) there is a relationship between low FRC and the incidence of SBD; and (2) increasing FRC will undoubtedly improve obstructive SDB (see all of split_city's work).
I had to Wikipedia FRC and PEEP to understand that picture. During my sleep study I apparently did have more centrals as CPAP pressure was increased.
Mr Bill wrote:
posting.php?mode=quote&f=1&p=568572
During this first study, there was an observation period of 4.5 hours during which I actually only got 75 minutes of no REM sleep (24% sleep efficiency). I was having a respiratory disturbance index of 76 events per hour and apnea/hyponea index of 67.7 events per hour. 59 of the 84 events during actual sleep were central events and persisted between 7cm (51 CA/hr) and 10cm (68 CA/hr) of CPAP. Lowest oxygen saturation during that first study was 81%.The next sleep study was scheduled for 11/12/10, so I had a couple months to survive till then. This was a low point for me. I was super tired and not at all sure there was any hope. Now, I have no idea if my little wrist pulse oximeter was accurate and I did not wear it that night. But at home I was seeing desaturation down to less than 60%...
...So the next sleep study with the ASV was 11/12/10. This time, I show the tech my pulse oximeter data and he opines that it looks like REM specific sleep apnea which is typically obstructive rather than central. Its a trying night, he felt we had to try titrating oxygen first. This was because I brought along a sleep study from my mother (done in that lab a year before) which showed that she also had central apneas and that an oxygen cannula was sufficient to fix her problem. He said we had to spend the first part of the night trying oxygen. I get all wired again and this time I brought a camera so I could get a picture of at least the wiring job. I was praying at that point that a simple oxygen cannula would be all I needed. But after a couple hours the tech comes back in and tells me there is no setting that does not make it worse.
I have found it most comfortable to sleep on my back (once I realized I could trust this ASV) because I seem to be able to breath with the least effort that way. Sleeping on my side wakes me because the effort to breath drops away as I fall asleep and anything I can do to reduce breathing effort lets me get past that waking/sleeping threshold. On my side, I feel my diaphragm move or not move and it wakes me when I stop breathing just as I nod off. I am guessing that my low Min EPAP is to keep from inducing centrals and let the ASV take care of those that show up. Anyway, I am becoming of the opinion that central sleep apnea can be induced by too much air lowering CO2 and reducing respiratory drive but its probably on a continuum with straight up CSA.
EPAP min=6, EPAP max=15, PS min=3, PS max=12, Max Pressure=30, Backup Rate=8 bpm, Flex=0, Rise Time=1,
90% EPAP=7.0, Avg PS=4.0, Avg bpm 18.3, Avg Min vent 9.2 Lpm, Avg CA/OA/H/AHI = 0.1/0.1/2.1/2.3 ... updated 02/17/12