Questions on Aflex CAs and OAs

[don600]

Hi,
 
I’ve been using a Dreamstation 500 for about 10 months and have a few unanswered questions. I use Sleepyhead and a spreadsheet for data analysis. First, I’ll provide some context for the questions.
 
1. Pre-CPAP my sleep study showed AHI of 12.8 with SpO2 < 90% 0.5% of time, and <88% 0.1% of time.
 
2. With my CPAP Median hours of sleep = 6.7 Median events per night 23 Hypopnea, 5 CA, 2 OA.  Apneas are 77 percent Hypopnea, 17 percent CA, and 7 percent OA.
 
3. I’ve periodically used an oximeter and never seen any significant desaturations associated with any apnea or hypopnea events.
 
4. After many tweaks, motivated by insights gained from this forum, I have stabilized at pressure of 7.5-8.5 with Aflex off.
 
I have four questions:
 
1. For the last month I’ve completely turned off Aflex. This has had a profound effect on CAs, cutting them by 90-95%. Median CAs has dropped from 5 to 0.5 per night. Does this suggest that I am in the subset of patients whose CAs are therapy-induced, and that I should keep Aflex turned off?
 
2. One apparent consequence of turning off Aflex is a doubling of my 95% leak rate and a rise in “Time over leak redline”. What might be causing this, and should I worry about it?  
 
3. I’ve looked more closely at the nature of my OAs and find that 66 percent have durations less than 10 seconds. Furthermore, whenever I’ve used oximetry, I’ve never see any desaturations associated with any OAs. I’ve also frequently seen OAs reported when I was lying awake prior to getting out of bed, at times when I was experiencing no respiratory distress. Should I be trying to eliminate those last 2 OAs per night, of which only one is > 10 seconds long?
 
4. From the very beginning of my therapy Hypopneas have been over 75% of my events, and they are now at least 90%.  I never detect desaturations and don’t seem experience arousals associated with these Hypopneas. How hard should I be trying to reduce them? What would be a good approach to do so?
 
This forum has been a great source of quality information for me. I greatly appreciate the chance to access the knowledge of its participants.
 
Thanks

[Gideon]

Hi,
 
I’ve been using a Dreamstation 500 for about 10 months and have a few unanswered questions. I use Sleepyhead and a spreadsheet for data analysis. First, I’ll provide some context for the questions.
 
1. Pre-CPAP my sleep study showed AHI of 12.8 with SpO2 < 90% 0.5% of time, and <88% 0.1% of time.
 
2. With my CPAP Median hours of sleep = 6.7 Median events per night 23 Hypopnea, 5 CA, 2 OA.  Apneas are 77 percent Hypopnea, 17 percent CA, and 7 percent OA.
 
3. I’ve periodically used an oximeter and never seen any significant desaturations associated with any apnea or hypopnea events.
 
4. After many tweaks, motivated by insights gained from this forum, I have stabilized at pressure of 7.5-8.5 with Aflex off.
 
I have four questions:
 
1. For the last month I’ve completely turned off Aflex. This has had a profound effect on CAs, cutting them by 90-95%. Median CAs has dropped from 5 to 0.5 per night. Does this suggest that I am in the subset of patients whose CAs are therapy-induced, and that I should keep Aflex turned off?
 
2. One apparent consequence of turning off Aflex is a doubling of my 95% leak rate and a rise in “Time over leak redline”. What might be causing this, and should I worry about it?  
 
3. I’ve looked more closely at the nature of my OAs and find that 66 percent have durations less than 10 seconds. Furthermore, whenever I’ve used oximetry, I’ve never see any desaturations associated with any OAs. I’ve also frequently seen OAs reported when I was lying awake prior to getting out of bed, at times when I was experiencing no respiratory distress. Should I be trying to eliminate those last 2 OAs per night, of which only one is > 10 seconds long?
 
4. From the very beginning of my therapy Hypopneas have been over 75% of my events, and they are now at least 90%.  I never detect desaturations and don’t seem experience arousals associated with these Hypopneas. How hard should I be trying to reduce them? What would be a good approach to do so?
 
This forum has been a great source of quality information for me. I greatly appreciate the chance to access the knowledge of its participants.
 
Thanks

1. Keep Flex off.  Increased Pressure variance tends to increase Centrals
2. Did you reset the "redline" to a value appropriate for a PR device which is typically considerably more than ResMed (the default "redline")?
3. By definition, the duration of events must be >= 10 seconds.  That is not saying that you don't have events that are less than 10 seconds.  Eliminate ant events that occur when you are awake
4. With a lot of Hypopneas, you are likely to have plenty of Flow Limitations, and likely RERAs which are a series of Flow Limitations that in arousal.  For this discussion, you may assume that flow limitations are hypopneas that did not restrict enough to be classified as hypopneas.  The arousal is something that you would not be aware of and must be detected by a detailed examination of the flow rate.  They can be treated and ALL of these are best treated with increased Pressure Support or with your machine Flex.  See Number 1 above.  Ok, so you treat these with increased pressure.  The trouble with that is increased pressure also tends to increase central apneas.

Bottom line, you treat obstructive events with increased pressure (EPAP, Pressure Support), You treat Central events with decreased pressure.  And yes they are in direct conflict with each other.  Treatment becomes a balancing act, mostly seeking comfort and viewing AHI.

[sheepless]

don600:

I'm not an expert so take with a grain of salt and look for confirmation.

regarding the part of Q#1 questioning whether you have treatment emergent or pressure induced ca. these are also known as complex apnea, often confused with mixed apnea which is the idiopathic type.

I don't think you can tell definitively with cpap whether ca is idiopathic or 'native' (my term) vs caused by cpap. apparently cpap can cause ca or simply aggravate existing ca. the conventional wisdom is that ca caused by the machine will subside after a couple weeks to a couple months. you have ca after 10 months.

one way to get some insight is to review the details of your sleep study to discover the breakdown of your untreated apnea. ca vs oa vs obstructive h vs central h. good chance your ca is native if you had more than a few during your sleep test. ((that won't stop them from diagnosing oa though. in 1987 I was diagnosed all central. in my latest 6 hour sleep test (40 pounds heavier) I had 198 ca and 204 oa, yet I was diagnosed obstructive and prescribed an apap, a machine that doesn't treat ca. makes no sense to me.))

if your machine collects data on an sd card, zoomed-in screenshots from Sleepyhead or OSCAR software might help determine if your h's are obstructive or central. I don't know how to tell the difference but others here might. knowing the extent to which your h is central might help you determine the extent to which you have mixed apnea.

posting data screenshots can also help determine if you're getting many RERA (arousals) and see the extent your breathing lapses for less than 10 seconds (and therefore aren't flagged). it's my opinion that a lot of under 10 second pauses will contribute to feeling poorly. unfortunately, it appears to me that the typical sleep docs / sleep centers pay little attention to RERA, flow limitations and even hypopnea, much less 'events' that are less than 10 seconds.

if after 10 months your overall ahi is 6.7, compared to 12.8 untreated, I'd say your present course is not working well. folks here may be able to help you drive your ahi below 5 but you may not want to do that if you want the system (insurers mostly) to support a move to a machine that treats ca. a strong indicator of mixed apnea and the need for a different machine is ahi's that vary a fair amount night to night. for example, my experience with apap produced daily ahi from about 3 to about 19 for a long term average of between 5 and 6 over 1.5 years.

the big question is how do you feel? I felt little relief after 1.5 years of apap so I sought an alternative (asv). you said your O2 levels are fine so if you feel fine too, why sweat the numbers? on the other hand, if you feel lousy, you might do better after guidance from the more-experienced members to reach optimal settings and/or you might consider discussing a different machine modality with your providers. you already know higher pressure increases your ca and you need relatively high(er) pressure to address oa & obstructive hypopnea and that these are at odds with the capabilities of your current machine.

again, I'm not an expert and I probably tend to project my own experience as a relatively happy convert to asv onto the situations of others with somewhat similar experiences. mull this over while we wait to see what else the more-experienced folks come up with.

[don600]

Hi,
 
I’ve been using a Dreamstation 500 for about 10 months and have a few unanswered questions. I use Sleepyhead and a spreadsheet for data analysis. First, I’ll provide some context for the questions.
 
1. Pre-CPAP my sleep study showed AHI of 12.8 with SpO2 < 90% 0.5% of time, and <88% 0.1% of time.
 
2. With my CPAP Median hours of sleep = 6.7 Median events per night 23 Hypopnea, 5 CA, 2 OA.  Apneas are 77 percent Hypopnea, 17 percent CA, and 7 percent OA.
 
3. I’ve periodically used an oximeter and never seen any significant desaturations associated with any apnea or hypopnea events.
 
4. After many tweaks, motivated by insights gained from this forum, I have stabilized at pressure of 7.5-8.5 with Aflex off.
 
I have four questions:
 
1. For the last month I’ve completely turned off Aflex. This has had a profound effect on CAs, cutting them by 90-95%. Median CAs has dropped from 5 to 0.5 per night. Does this suggest that I am in the subset of patients whose CAs are therapy-induced, and that I should keep Aflex turned off?
 
2. One apparent consequence of turning off Aflex is a doubling of my 95% leak rate and a rise in “Time over leak redline”. What might be causing this, and should I worry about it?  
 
3. I’ve looked more closely at the nature of my OAs and find that 66 percent have durations less than 10 seconds. Furthermore, whenever I’ve used oximetry, I’ve never see any desaturations associated with any OAs. I’ve also frequently seen OAs reported when I was lying awake prior to getting out of bed, at times when I was experiencing no respiratory distress. Should I be trying to eliminate those last 2 OAs per night, of which only one is > 10 seconds long?
 
4. From the very beginning of my therapy Hypopneas have been over 75% of my events, and they are now at least 90%.  I never detect desaturations and don’t seem experience arousals associated with these Hypopneas. How hard should I be trying to reduce them? What would be a good approach to do so?
 
This forum has been a great source of quality information for me. I greatly appreciate the chance to access the knowledge of its participants.
 
Thanks

1. Keep Flex off.  Increased Pressure variance tends to increase Centrals
2. Did you reset the "redline" to a value appropriate for a PR device which is typically considerably more than ResMed (the default "redline")?
3. By definition, the duration of events must be >= 10 seconds.  That is not saying that you don't have events that are less than 10 seconds.  Eliminate ant events that occur when you are awake
4. With a lot of Hypopneas, you are likely to have plenty of Flow Limitations, and likely RERAs which are a series of Flow Limitations that in arousal.  For this discussion, you may assume that flow limitations are hypopneas that did not restrict enough to be classified as hypopneas.  The arousal is something that you would not be aware of and must be detected by a detailed examination of the flow rate.  They can be treated and ALL of these are best treated with increased Pressure Support or with your machine Flex.  See Number 1 above.  Ok, so you treat these with increased pressure.  The trouble with that is increased pressure also tends to increase central apneas.

Bottom line, you treat obstructive events with increased pressure (EPAP, Pressure Support), You treat Central events with decreased pressure.  And yes they are in direct conflict with each other.  Treatment becomes a balancing act, mostly seeking comfort and viewing AHI.

Thanks.

2. I didn't reset the redline value, and will sort out how to do that. I do track leak rate on a daily basis so I don't rely on the red line for any decisions.

3. I understand that for OA to be clinically significant it must be >=10 sec and result in a desaturation or arousal. The CPAP can't judge desats, and it probably takes an EEG to correctly assess an arousal. Therefore, it is had to say if flagged OAs are clinically significant. I am just judging their duration by the data that appears in Sleepyhead. Last night showed two OAs of duration 8 and 9 seconds. Perhaps Sleepyhead computes this incorrectly, but really wonder if such short OAs warrant attention.

Obstructive 2 events
#001: 01:19:53 (8)
#002: 02:56:23 (9)

4. I'm going to do a more careful analysis of the last 10 months of data. My impression is that most of my AHI improvement came from dropping pressure range from 5-15 to the current 7.5-8.5. I'm going to take a deeper look at all events under different settings to see if I can get some insight on this.

I appreciate your tips.

[don600]

don600:  

I'm not an expert so take with a grain of salt and look for confirmation.

regarding the part of Q#1 questioning whether you have treatment emergent or pressure induced ca.  these are also known as complex apnea, often confused with mixed apnea which is the idiopathic type.

I don't think you can tell definitively with cpap whether ca is idiopathic or 'native' (my term) vs caused by cpap.  apparently cpap can cause ca or simply aggravate existing ca.  the conventional wisdom is that ca caused by the machine will subside after a couple weeks to a couple months.  you have ca after 10 months.

one way to get some insight is to review the details of your sleep study to discover the breakdown of your untreated apnea.  ca vs oa vs obstructive h vs central h.  good chance your ca is native if you had more than a few during your sleep test.  ((that won't stop them from diagnosing oa though.  in 1987 I was diagnosed all central.  in my latest 6 hour sleep test (40 pounds heavier) I had 198 ca and 204 oa, yet I was diagnosed obstructive and prescribed an apap, a machine that doesn't treat ca.  makes no sense to me.))

if your machine collects data on an sd card, zoomed-in screenshots from Sleepyhead or OSCAR software might help determine if your h's are obstructive or central.  I don't know how to tell the difference but others here might. knowing the extent to which your h is central might help you determine the extent to which you have mixed apnea.

posting data screenshots can also help determine if you're getting many RERA (arousals) and see the extent your breathing lapses for less than 10 seconds (and therefore aren't flagged).  it's my opinion that a lot of under 10 second pauses will contribute to feeling poorly.  unfortunately, it appears to me that the typical sleep docs / sleep centers pay little attention to RERA, flow limitations and even hypopnea, much less 'events' that are less than 10 seconds.

if after 10 months your overall ahi is 6.7, compared to 12.8 untreated, I'd say your present course is not working well. folks here may be able to help you drive your ahi below 5 but you may not want to do that if you want the system (insurers mostly) to support a move to a machine that treats ca.  a strong indicator of mixed apnea and the need for a different machine is ahi's that vary a fair amount night to night.  for example, my experience with apap produced daily ahi from about 3 to about 19 for a long term average of between 5 and 6 over 1.5 years.  

the big question is how do you feel?  I felt little relief after 1.5 years of apap so I sought an alternative (asv).  you said your O2 levels are fine so if you feel fine too, why sweat the numbers?  on the other hand, if you feel lousy, you might do better after guidance from the more-experienced members to reach optimal settings and/or you might consider discussing a different machine modality with your providers.  you already know higher pressure increases your ca and you need relatively high(er) pressure to address oa & obstructive hypopnea and that these are at odds with the capabilities of your current machine.

again, I'm not an expert and I probably tend to project my own experience as a relatively happy convert to asv onto the situations of others with somewhat similar experiences.  mull this over while we wait to see what else the more-experienced folks come up with.

Thanks. The main condition that caused me to get a sleep study was snoring and the CPAP solved that problem. I wasn't having a significant problem with daytime sleepiness and, if anything, I probably feel somewhat less well-rested using the CPAP than without it. Of course, this could be, at heart, a Dreamstation issue, but I want to use the Dreamstation as well as I can, before I blame the machine.

Unfortunately my in-home sleep study did not code the different apneas, it just gave me an overall AHI, RDI for REM and Non-REM sleep.  I think my initial post was unclear.  The "6.7" was average sleep hours so with 30 events per night my AHI averaged 4.5 over the full period and these days is typically between 3 and 4.

That said, as you point out, the problem may not be the way I am using my machine, but that I may have the wrong machine. I ultimately may have to deal with that. Initial use of the CPAP cut my AHI from sleep study 12.8 to 6.5, about a 50 percent reduction. My tweaks over the last 10 month have cut it to an average of 3.3, which is another 50 percent improvement. Eliminating ALL CA and OAs would only get me in the range of 2.6 to 3, so substantial improvement at this point has to come from the hypopneas. For me, because higher pressures seem to elevate my hypopneas, I suspect that this is a sign of CPAP induced hypocapnia that slightly lowers my respiratory drive and create a reduction in flow. I need to do more work on this. My best path forward seems to be better analysis of my existing data, and some careful experiments focused on reducing hypopneas. 

Thanks for your guidance.

[sheepless]

you were clear; I misread it in haste. and not guidance so much as information and then mostly just personal experience.

my provider seemed reluctant to give me more than a one page summary of my in-home study, maybe even surprised I wanted more. it took 3 requests, obtaining a little more each time. still don't know if I got it all but think I got everything I wanted. you should be able to get more detailed results too.

someone may correct me but it's my understanding that pressure helps resolve obstructive hypopnea, and in your case pressure makes hypopnea worse, suggesting to me that they may be central in origin.

clarification / correction: above I said "these are also known as complex apnea, often confused with mixed apnea which is the idiopathic type". actually, mixed apnea includes idiopathic and apnea stemming from an underlying cause / condition / disease. I use the term 'native' to mean existing independent of cpap.

still, it's worth noting generally, that while complex apnea and mixed apnea are frequently used interchangeably, there is a difference in their meaning.

it sounds like you're pretty tuned in and able to manage well, while I'm reaching a bit, so I'll follow along but leave it to you and the more-experienced members.

[don600]

Hi,

Just wanted to update this thread with what I've learned in the past few months. When I posted in April my monthly average AHI was 3.5. In the month of July, thanks to additional  adjustments, it was 1.7.

The key  for me was shifting my Dreamstation from APAP mode to CPAP.  I used a fixed pressure equal to my 95%  APAP pressure, which reduced my Hypopneas by 75%.  Ironically, when I first started therapy APAP appeared technically superior with its adaptive pressure adjustment and the pressure relief of Aflex. I assumed it was intriinsically better than fixed pressure. By paying attention to this forum and my Sleepyhead data, I decided to try downgrading my Dreamstation to straight CPAP. In my particular case, it worked surprisingly well, which suggests that my CA and H events really were therapy-induced. (I saw on my charts the CAs and Hs were typically briefly preceded by a rise in Minute Ventilation which appears to have been sufficient to reduce respiratory drive.)

So far, my main takeaways have been:

1. OSA is a system problem with the patient and machine interacting. It's great to start with a likely solution, but very important to actively pursue better optimization.

2. I incorrectly assumed that APAP's advanced technology was the best solution for me.  Because of this assumption and acceptable therapy results, I didn't consider fixed pressure until 11 months into my therapy. I could have tried this much earlier.

3. Because I was responding to therapy, my pulmonologist was not aggressive in providing useful tips for adjusting my prescription. I doubt if the problem is one of lack of intelligence or knowledge. I think the real cause is that I have far more time and motivation to pore over my own data, than a physician with hundreds of patients. This made a difference.

Thanks to everyone for making this forum such a great resource.