I think you're right to regard it as not a big deal, or even a medium size deal, if pressure were wobbling a few tenths of a cm either way from the set pressure.me - woozle wrote:wonder if the difference is so slight not a big deal?
APNEA -v- HYPOPNEA
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rested gal
- Posts: 12881
- Joined: Thu Sep 09, 2004 10:14 pm
- Location: Tennessee
Re: Update
[quote="GoofyUT"]APAP/Activa
AHI=1.5;AI=0.0;HI=1.5;Pressure (95%)=10.2
This is my fifth straight day using APAP with a 95% pressure averaging 10.15, and my numbers, especially HYPOPNEAS have NOT demonstrated a degradation over my CPAP trial at 8cmH2O. I haven't calculated non-parametric statistics to see whether this is significant, and of course, the sample size is too small for parametrics.
And, I'm feeling better.
C
AHI=1.5;AI=0.0;HI=1.5;Pressure (95%)=10.2
This is my fifth straight day using APAP with a 95% pressure averaging 10.15, and my numbers, especially HYPOPNEAS have NOT demonstrated a degradation over my CPAP trial at 8cmH2O. I haven't calculated non-parametric statistics to see whether this is significant, and of course, the sample size is too small for parametrics.
And, I'm feeling better.
C
Re: Update
Snoredog wrote: it was probably your mask change, you went from a Swift to a Activa didn't you?
I'm sure Chuck will get around to quantitatively exploring the possible HI effects of those two masks. If it was the mask, I will say that he is then a candidate for a very marginal case of the CO2 depletion etiology regarding pressure induced hypopneas (pressure's CO2 kinetics within those masks). Extremely fleeting CO2 kinetics that previous analysis models have not adequately factored in relative to a very "transitionally twitchy" CO2-based respiratory trigger.
Extremely marginal CSDB manifestations if, indeed, this is the case.
Perhaps not enough CSDB effect to be clinically significant. Then again perhaps enough CSDB arousals at night to account for his awakenings. Very interesting.
Pressures
Snoredog wrote:From the Resmed Clinical Manual:rested gal wrote:A question that I've been meaning to ask for some time...now's as good as any.
A person is using the ResMed S8 Vantage or an S7 Spirit in auto mode. The next morning, when the person holds down the right and left buttons to get into the patient's menu and looks at the efficacy data from the night before, they get to see: Press (pressure), AHI, AI, HI and Leak.
The pressure number they see in the efficacy data...is that:
A. the 95th percentile pressure?
B. the mean (average) pressure?
C. the highest pressure the machine had to use during the night?
or... something else?
I've always assumed it was the 95th percentile pressure, but have never been absolutely sure.
Have used both those machines but didn't have either manual for them.I guess the key word is "calculated", because the pressure shown is not the pressure used for 95 percent of the time,The pressure transducer located in the unit measures treatment pressure; the average pressure is calculated and recorded each minute. The pressure reported in the Efficacy Data submenu (see Figure 9, The Clinical Menu Results series, on page 40) for a single session is the 95th centile pressure for mask-on time, excluding periods when the leak as exceeded hte 0.4L/s (24 L/min). For selected time intervals (lask week, last month, last 6 months or last year), the median of the daily 95th centril values is reported. Non-usage days are not included in calculations.
it is more likely the pressure found that eliminates 95 percent of the events seen.
The Remstars seem to have the same vague meaning, when you look at the reports it finds the lowest pressure resulting in the fewest number of events, that becomes your 90%.
Then when you look on the very last page of the report it shows the avg. pressure used for 90% of time?? So you go back to each daily report and SUM up all the minutes and calculate the percentages for each pressure from that, they don't even come close to being 90%. So I assume they also mean pressure that eliminates 90% of the events seen, which makes more sense than the percentage of time spent.
You want to know the pressure that addresses the most if not the worst events, just like a cpap titration.
People are dying every day in Darfur simply for who they are!!! PLEASE HELP THEM!
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Re: Pressures
Just wanted to highlight this as the correct answer. Thanks for that much needed clarification.GoofyUT wrote: It then reports the pressure that it operated at or LESS for 95% of the time for the session.
Re: Update
[quote="Snoredog"][quote="GoofyUT"]APAP/Activa
AHI=1.5;AI=0.0;HI=1.5;Pressure (95%)=10.2
This is my fifth straight day using APAP with a 95% pressure averaging 10.15, and my numbers, especially HYPOPNEAS have NOT demonstrated a degradation over my CPAP trial at 8cmH2O. I haven't calculated non-parametric statistics to see whether this is significant, and of course, the sample size is too small for parametrics.
And, I'm feeling better.
C
AHI=1.5;AI=0.0;HI=1.5;Pressure (95%)=10.2
This is my fifth straight day using APAP with a 95% pressure averaging 10.15, and my numbers, especially HYPOPNEAS have NOT demonstrated a degradation over my CPAP trial at 8cmH2O. I haven't calculated non-parametric statistics to see whether this is significant, and of course, the sample size is too small for parametrics.
And, I'm feeling better.
C
People are dying every day in Darfur simply for who they are!!! PLEASE HELP THEM!
http://www.savedarfur.org
_______________________________
http://www.savedarfur.org
_______________________________
Re: Update
GoofyUT wrote:... either by pressure transients or amplitude.
But that still puts you back in the theoretical CSDB domain of transient CO2 depletion kinetics differing both marginally and yet crucially between those two masks. Even in the mask case you're talking highly unconventional analysis of the transient CO2 kinetics of depletion. Again toward a theoretically marginal CSDB effect.
Relevant multifactorial inputs would still need to be isolated and adequately tested. Relevant multifactorial inputs would be all factors that can presumably alter the transitory kinetics of CO2 depletion, Chuck.
In other words, if you discover that a mask's dead space and exhaust vent combination serves as either an adequate mediator or trigger, then you must isolate, analyze, and test all factors that also impact the highly transient kinetics of CO2 depletion.
If you discover the mask is a CO2 mediator or trigger, then what other factors in the overall therapeutic equation also contribute or serve as CO2 mediators or triggers? It is highly theoretical that such fleeting and subtle CO2 kinetics of either the (properly vented) mask and/or machine should even cause this. Either way it's great to be exploring this!
Last edited by -SWS on Sat Jul 08, 2006 2:20 pm, edited 1 time in total.
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rested gal
- Posts: 12881
- Joined: Thu Sep 09, 2004 10:14 pm
- Location: Tennessee
Chuck, there may be some other way to do that, but what I'd do is take a screen shot of the Excel chart. Make it be a jpg and put it up on a website.
Then, while writing a post, click the Img button. Paste or type the complete URL to the picture, including the ".jpg" at the end, and click the Img button again to enclose the URL.
Then, while writing a post, click the Img button. Paste or type the complete URL to the picture, including the ".jpg" at the end, and click the Img button again to enclose the URL.
Re: Update
In other words here's a hypothetical CO2 multifactorial pattern that may shape up in your CO2 depletion test runs:
1) Swift with APAP: increased HI
2) Activa with APAP: normal HI
3) Swift with CPAP: normal HI
4) Activa with CPAP: normal HI
If hypothetical scenario one above is the only scenario that entails an increased HI, then you might assume the combinational transitory effects of CO2 kinetics are at play. And, of course, to simply test with"APAP" (instead of quantified pressure variation itself) then pressure-related CO2 depletion kinetics have been analytically short changed in the equation of understanding what's happening. Yet most definitely not short changed in understanding a therapeutic combination that works for you.
1) Swift with APAP: increased HI
2) Activa with APAP: normal HI
3) Swift with CPAP: normal HI
4) Activa with CPAP: normal HI
If hypothetical scenario one above is the only scenario that entails an increased HI, then you might assume the combinational transitory effects of CO2 kinetics are at play. And, of course, to simply test with"APAP" (instead of quantified pressure variation itself) then pressure-related CO2 depletion kinetics have been analytically short changed in the equation of understanding what's happening. Yet most definitely not short changed in understanding a therapeutic combination that works for you.
Last edited by -SWS on Sat Jul 08, 2006 2:42 pm, edited 1 time in total.
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Guest
I have never been able to use a swift. It was when I was first starting to try and use a swift at a higher pressure (going 8 to 10) that I first asked my doctor about centrals because when I would fall asleep ( say 10 minutes into it) my eyes would pop open and I would be awake. It did not "feel" like my obstructive wake ups. I attributed it to the higher pressure being shot straight into my nose at the time not CO2, but I think from my experience that some of us are sensitive to different masks and it obviously makes a huge difference in the therapy. I use a Resmed ff mask and nose breath through it! And I don't like a ff mask! If I go to a Respironics nasal that I have again I wake up early on into sleep so it has something to do with the space and venting.....
I guess some of us have to buy 10 masks and basically be our own sleep technician to get it right. At some point now that I am doing well at straight CPAP at 9 I will pull some of the masks out of the dead mask pile and try them again (now that I can see the results the next day!).
This brings up another question for me. Of the 40-50% of people who are prescribed a CPAP but are non-compliant, how many have a weird problem like this that is never addressed so they just don't use it?
Kurt
I guess some of us have to buy 10 masks and basically be our own sleep technician to get it right. At some point now that I am doing well at straight CPAP at 9 I will pull some of the masks out of the dead mask pile and try them again (now that I can see the results the next day!).
This brings up another question for me. Of the 40-50% of people who are prescribed a CPAP but are non-compliant, how many have a weird problem like this that is never addressed so they just don't use it?
Kurt
I POSTED THIS ON THE WRONG THREAD- MUST BE DAYTIME CENTRALS
(RG: Remember this discussion from a few months ago? tb)
I believe my incremental stepping of the pressure 5-6,6-7, 7-8, 8-9, 9-10, 10-11 accomplished determining if the pressure raises were event triggered or the pressure increases were causing the events.
Clearly the pressure was causing the events. The algorithm was raising pressure based on snore or??? and then an event would be recorded, at the higher pressure. I questioned if the event was the cause of the pressure rise in APAP or the event was recorded because of the pressure raise.
The data clearly indicates less recorded events at 9cm. My AHI was 1.4 over 5 days at 9-10 CM at 10-11 AHI 1.8 at 6-7 cm AHI 5.0+ ,7-8 cm 6.0+,
SO in APAP 6-11 my AHI would follow the same range, my AHI would vary with the pressure.
TO reiterate: In APAP I got the same AHI across the pressure range (According to MyEncore AHI/Pressure) as I did when I set the APAP to 1 CM increments.
In APAP with the range opened up when the machine would respond to triggers the pressure it was transversing was causing the events. When the machine spent time at 7-8 while in APAP mode my AHI would be bad. I would read the time at pressure in EncorePro and see the AHI jump at the various pressures. When I locked the pressure down to one cm increments I had almost the identical AHI at those specific pressures. At 9-10, I had a minimum of events whether it passed thru there in APAP or fixed at 9-10cm.
Ergo: The pressures were inducing the events.
The question of what type of events is open to discussion. We can't determine that based on the data collection ability of the Auto, but it is clear that pressure is the issue. Whether these are some form of Central, I don't know - probably or Nervous System destabilization as SWS suggests - the net is the same. The pressure is inducing the response.
What is a bit counterintuitive is that it seems to happen at lower pressure, stop or drops to a minimum at 9-10 cm and then increases again. IT is strange that it is prevalent at a lower pressure as well as a higher pressure. Centrals tend to be higher pressure events, not lower.
Maybe this is the oscillations SWS refers to. There is no way to tell, and even if we knew, what could we change in the therapy?
I seem to demonstrate that pressure can be a culprit for some as well as a solution. For me anything outside of my "sweet spot" generates events - pressure does not seem to clear them and many pressure ranges seem to create them, other than my sweet spot.
As SWS said, I may be a rare bird but it is important to be conscious that APAP and variable pressure therapy may be counter productive for treatment of certain individuals.
When some on this board can't figure out their APAP, my experience may be worth recalling.
Best,
Tom
(RG: Remember this discussion from a few months ago? tb)
I believe my incremental stepping of the pressure 5-6,6-7, 7-8, 8-9, 9-10, 10-11 accomplished determining if the pressure raises were event triggered or the pressure increases were causing the events.
Clearly the pressure was causing the events. The algorithm was raising pressure based on snore or??? and then an event would be recorded, at the higher pressure. I questioned if the event was the cause of the pressure rise in APAP or the event was recorded because of the pressure raise.
The data clearly indicates less recorded events at 9cm. My AHI was 1.4 over 5 days at 9-10 CM at 10-11 AHI 1.8 at 6-7 cm AHI 5.0+ ,7-8 cm 6.0+,
SO in APAP 6-11 my AHI would follow the same range, my AHI would vary with the pressure.
TO reiterate: In APAP I got the same AHI across the pressure range (According to MyEncore AHI/Pressure) as I did when I set the APAP to 1 CM increments.
In APAP with the range opened up when the machine would respond to triggers the pressure it was transversing was causing the events. When the machine spent time at 7-8 while in APAP mode my AHI would be bad. I would read the time at pressure in EncorePro and see the AHI jump at the various pressures. When I locked the pressure down to one cm increments I had almost the identical AHI at those specific pressures. At 9-10, I had a minimum of events whether it passed thru there in APAP or fixed at 9-10cm.
Ergo: The pressures were inducing the events.
The question of what type of events is open to discussion. We can't determine that based on the data collection ability of the Auto, but it is clear that pressure is the issue. Whether these are some form of Central, I don't know - probably or Nervous System destabilization as SWS suggests - the net is the same. The pressure is inducing the response.
What is a bit counterintuitive is that it seems to happen at lower pressure, stop or drops to a minimum at 9-10 cm and then increases again. IT is strange that it is prevalent at a lower pressure as well as a higher pressure. Centrals tend to be higher pressure events, not lower.
Maybe this is the oscillations SWS refers to. There is no way to tell, and even if we knew, what could we change in the therapy?
I seem to demonstrate that pressure can be a culprit for some as well as a solution. For me anything outside of my "sweet spot" generates events - pressure does not seem to clear them and many pressure ranges seem to create them, other than my sweet spot.
As SWS said, I may be a rare bird but it is important to be conscious that APAP and variable pressure therapy may be counter productive for treatment of certain individuals.
When some on this board can't figure out their APAP, my experience may be worth recalling.
Best,
Tom
"Nothing To It, But To Do It"
Un-treated REM AHI: 71.7
Almost All Hypopneas
OXY Desat: 83.9%
Trying To Get It Right
Un-treated REM AHI: 71.7
Almost All Hypopneas
OXY Desat: 83.9%
Trying To Get It Right
Amazing!!!!!
Steve-
I was having PRECISELY the same thought as you, this morning!!!! Wouldn't it be neat to run some multivariate anaylses of my data set when I accumulate enough observations to aupport it! Like a factor analysis, or maybe a multiple discriminant to try to distinquish between nights rated as good -v- bad, using a multi-factorial anaylsis. Now, how would we go about ordinalizing masks. Bias rates? Dead-space volumes?
FASCINATING!!!!!
Chuck
I was having PRECISELY the same thought as you, this morning!!!! Wouldn't it be neat to run some multivariate anaylses of my data set when I accumulate enough observations to aupport it! Like a factor analysis, or maybe a multiple discriminant to try to distinquish between nights rated as good -v- bad, using a multi-factorial anaylsis. Now, how would we go about ordinalizing masks. Bias rates? Dead-space volumes?
FASCINATING!!!!!
Chuck
People are dying every day in Darfur simply for who they are!!! PLEASE HELP THEM!
http://www.savedarfur.org
_______________________________
http://www.savedarfur.org
_______________________________
Re: Update
[quote="-SWS"]In other words here's a hypothetical CO2 multifactorial pattern that may shape up in your CO2 depletion test runs:
1) Swift with APAP: increased HI
2) Activa with APAP: normal HI
3) Swift with CPAP: normal HI
4) Activa with CPAP: normal HI
If hypothetical scenario one above is the only scenario that entails an increased HI, then you might assume the combinational transitory effects of CO2 kinetics are at play. And, of course, to simply test with"APAP" (instead of quantified pressure variation itself) then pressure-related CO2 depletion kinetics have been analytically short changed in the equation of understanding what's happening. Yet most definitely not short changed in understanding a therapeutic combination that works for you.
1) Swift with APAP: increased HI
2) Activa with APAP: normal HI
3) Swift with CPAP: normal HI
4) Activa with CPAP: normal HI
If hypothetical scenario one above is the only scenario that entails an increased HI, then you might assume the combinational transitory effects of CO2 kinetics are at play. And, of course, to simply test with"APAP" (instead of quantified pressure variation itself) then pressure-related CO2 depletion kinetics have been analytically short changed in the equation of understanding what's happening. Yet most definitely not short changed in understanding a therapeutic combination that works for you.
People are dying every day in Darfur simply for who they are!!! PLEASE HELP THEM!
http://www.savedarfur.org
_______________________________
http://www.savedarfur.org
_______________________________
No need to apologize, Chuck. This is a great collaborative melding of the minds as far as I'm concerned. However, I would propose a new analytical problem solving paradigm here. When we look at this problem as if CO2 depletion is being "mediated" I honestly think we have a flawed view of the biophysics and CO2 kinetics involved. There really is no "mediation" of any kind going on here other than pressure mediating non-CSDB obstructive events at times throughout the night. There is no mediation of CO2 involved. Rather, this is presumably a case of CO2's instantaneous magnitude or perhaps CO2's mathematical rate of descent staying either on: 1) the "safe side" of depletion kinetics or 2) the "hypocapnic side" of depletion kinetics. And if CO2 depletion kinetics are presumed to be involved here, then all CO2 depletion kinetics must necessarily add to the overall transient equation. Not just the mask.
Thus regarding analytical paradigms, when we grapple to analyze any single depleting CO2 kinetics factors such as mask, pressure variation, etc., then we risk analyzing which single tree is bad versus recognizing the problem is with the entire canopy of the CO2 forest.
When we analyze the problem as if it were CO2-depletion related, highly transient, and multifactorial, then your record lows at 8 cm fixed pressure begin to make a great deal of sense versus standing out as a big mystery. Let me give an example of analyzing all depleting CO2 kinetic factors combinationally:
Assumption: Chuck's respiratory drive is mildly affected by CO2's depletion. When transitory breathing and pressure kinetics deplete Chuck's CO2 too rapidly, then his hypocapnic threshold is reached and his respiratory drive becomes ever so slightly destabilized. Under any highly transient CO2-depleting circumstances that happen to cross Chuck's hypocapnic trigger threshold, he begins to manifest slightly more hypopneas (as might be the case with a very mildly CSDB inclined patient).
Factor 1: Chuck increases his APAP floor pressure and notes an elevated HI.
Observation 1: A higher floor pressure results in increased CO2 washout in any given mask. These are less favorable CO2 depletion kinetics for Chuck.
Tentative Conclusion 1: Chuck has presumably accelerated his CO2 washout rate just enough to experience a very mild hypocapnic reaction resulting in CSDB-related central hypopneas.
Factor 2: Chuck switches from APAP to 9 cm fixed pressure and notices no noticeable improvement in a single night trial; Chuck then switches to 8 cm fixed pressure and experiences record low HI indices.
Observation 2: The 9 cm fixed pressure eliminated the APAP pressure variations (APAP pressure variations in themselves are known to influence CO2 kinetics unfavorably in hypocapnic CSDB patients). Additionally the drop to 8 cm fixed pressure marginally lowered the CO2 washout rate in Chuck's mask.
Tentative Conclusion 2: The CO2 depletion kinetics of 8 cm pressure are clearly better than the CO2 depletion kinetics of varying APAP (especially varying APAP with higher floor pressures). The CO2 depletion kinetics at 9 cm fixed pressure were clearly not advantageous enough to avoid crossing Chuck's unique hypocapnic trigger threshold of mild respiratory destabilization. The CO2 depletion kinetics of 8 cm fixed pressure (even with the Swift mask) were favorable enough to keep Chuck from experiencing noticeable hypocapnic respiratory destabilization.
Factor 3: Chuck switches to APAP but with an Activa mask and notes continued HI success.
Observation 3: Back to APAP-influenced CO2 depletion kinetics, but this time with the Activa mask which has better CO2 retention characteristics than the Swift.
Tentative Conclusion 3: The combined CO2 depletion kinetics of APAP and Activa once again keep Chuck on the safe side of his hypocapnic trigger threshold of mild respiratory destabilization.
If you're going to factor the mask in as being a likely culprit, then you must attribute exactly why that might be. And if you tentatively attribute it to a twitchy CO2 respiratory trigger, then you implicitly pin the phenomenon on the masks CO2 depletion kinetics. And if you tentatively pin the phenomenon on CO2 depletion kinetics, then you must add up the entire equation of CO2 depletion kinetics. It's a combinational thing. It's like trying to figure out why your great aunt gained 50 pounds last year. It doesn't make any sense to pin her weight gain on any one food item she eats in a given day. Rather you must count all her calories to come out of the analysis with the correct answer to the problem.
Absolutely no apologies are necessary if you disagree with my analysis, Chuck. Honest! It's just that we have to factor in those record low HI's at 8 cm while using your Swift mask some how. Multifactorial or combinational CO2 kinetics is the only way that I can make everything neatly fit. .
Thus regarding analytical paradigms, when we grapple to analyze any single depleting CO2 kinetics factors such as mask, pressure variation, etc., then we risk analyzing which single tree is bad versus recognizing the problem is with the entire canopy of the CO2 forest.
When we analyze the problem as if it were CO2-depletion related, highly transient, and multifactorial, then your record lows at 8 cm fixed pressure begin to make a great deal of sense versus standing out as a big mystery. Let me give an example of analyzing all depleting CO2 kinetic factors combinationally:
Assumption: Chuck's respiratory drive is mildly affected by CO2's depletion. When transitory breathing and pressure kinetics deplete Chuck's CO2 too rapidly, then his hypocapnic threshold is reached and his respiratory drive becomes ever so slightly destabilized. Under any highly transient CO2-depleting circumstances that happen to cross Chuck's hypocapnic trigger threshold, he begins to manifest slightly more hypopneas (as might be the case with a very mildly CSDB inclined patient).
Factor 1: Chuck increases his APAP floor pressure and notes an elevated HI.
Observation 1: A higher floor pressure results in increased CO2 washout in any given mask. These are less favorable CO2 depletion kinetics for Chuck.
Tentative Conclusion 1: Chuck has presumably accelerated his CO2 washout rate just enough to experience a very mild hypocapnic reaction resulting in CSDB-related central hypopneas.
Factor 2: Chuck switches from APAP to 9 cm fixed pressure and notices no noticeable improvement in a single night trial; Chuck then switches to 8 cm fixed pressure and experiences record low HI indices.
Observation 2: The 9 cm fixed pressure eliminated the APAP pressure variations (APAP pressure variations in themselves are known to influence CO2 kinetics unfavorably in hypocapnic CSDB patients). Additionally the drop to 8 cm fixed pressure marginally lowered the CO2 washout rate in Chuck's mask.
Tentative Conclusion 2: The CO2 depletion kinetics of 8 cm pressure are clearly better than the CO2 depletion kinetics of varying APAP (especially varying APAP with higher floor pressures). The CO2 depletion kinetics at 9 cm fixed pressure were clearly not advantageous enough to avoid crossing Chuck's unique hypocapnic trigger threshold of mild respiratory destabilization. The CO2 depletion kinetics of 8 cm fixed pressure (even with the Swift mask) were favorable enough to keep Chuck from experiencing noticeable hypocapnic respiratory destabilization.
Factor 3: Chuck switches to APAP but with an Activa mask and notes continued HI success.
Observation 3: Back to APAP-influenced CO2 depletion kinetics, but this time with the Activa mask which has better CO2 retention characteristics than the Swift.
Tentative Conclusion 3: The combined CO2 depletion kinetics of APAP and Activa once again keep Chuck on the safe side of his hypocapnic trigger threshold of mild respiratory destabilization.
If you're going to factor the mask in as being a likely culprit, then you must attribute exactly why that might be. And if you tentatively attribute it to a twitchy CO2 respiratory trigger, then you implicitly pin the phenomenon on the masks CO2 depletion kinetics. And if you tentatively pin the phenomenon on CO2 depletion kinetics, then you must add up the entire equation of CO2 depletion kinetics. It's a combinational thing. It's like trying to figure out why your great aunt gained 50 pounds last year. It doesn't make any sense to pin her weight gain on any one food item she eats in a given day. Rather you must count all her calories to come out of the analysis with the correct answer to the problem.
Absolutely no apologies are necessary if you disagree with my analysis, Chuck. Honest! It's just that we have to factor in those record low HI's at 8 cm while using your Swift mask some how. Multifactorial or combinational CO2 kinetics is the only way that I can make everything neatly fit. .
Tom, did you ever run your Remstar Auto at fixed pressure? Or was yours only a case of narrowing your APAP pressure range down to 1 cm windows?
Not to be a purist but pressure magnitude experiments that are diluted by 1 cm pressure fluctuations still contain 1 cm pressure fluctuations. And the pressure transients themselves of APAP machines are known to influence CO2 depletion kinetics unfavorably in CSDB patients. Even with a very wide APAP range, no single APAP pressure fluctuation is ever really greater than 1 cm. And those always 1 cm or lower APAP pressure fluctuations are presumably the ones that impact CO2 depletion kinetics unfavorably for some CSDB patients. Very marginally transitory, yes, but amazingly crucial, none the less, in the case of CSDB.
Regardless, if you ran your experiments again at purely fixed pressure to eliminate transient pressure's effects on CO2 depletion kinetics, you just might achieve the same results yet again. Who really knows?
Not to be a purist but pressure magnitude experiments that are diluted by 1 cm pressure fluctuations still contain 1 cm pressure fluctuations. And the pressure transients themselves of APAP machines are known to influence CO2 depletion kinetics unfavorably in CSDB patients. Even with a very wide APAP range, no single APAP pressure fluctuation is ever really greater than 1 cm. And those always 1 cm or lower APAP pressure fluctuations are presumably the ones that impact CO2 depletion kinetics unfavorably for some CSDB patients. Very marginally transitory, yes, but amazingly crucial, none the less, in the case of CSDB.
Regardless, if you ran your experiments again at purely fixed pressure to eliminate transient pressure's effects on CO2 depletion kinetics, you just might achieve the same results yet again. Who really knows?