Brain fog, lack of energy -- why did dropping my EPR make such a difference?

[Albigensian]

Can you help me to understand why decreasing EPR has changed my life?    
 
I can’t figure out why increased expiratory pressure has dramatically decreased my lassitude, brain fog, and general exhaustion.    I need to understand it because, once I do, I might be able to make even more improvements in my quality of life.

I hope that this post and its threat will help others struggling with the problems that I had.

THE OUTCOME OF ADJUSTING EPR:  About a month ago,  I dropped EPR from 3 to 1; minimum pressure was kept at 5.   I then had a dramatic decrease in AHI, which has dropped to below 1 from around 4 or 5 and up to 9 or 10.  The decrease in AHI is mostly due to a dramatic decrease in clusters of clear airway events.  (I append OSCAR data from 8/17 with EPR of 3 and from 8/18 when EPR was decreased to 1.)   

I am much less foggy, less in a stupor, less cognitively challenged.   I feel more like myself prior to beginning therapy:  alert, focused, capable of moving from intention to action.

 A big change in how well I feel -- but, why?

CLEAR AIRWAY EVENTS – TRYING TO FIGURE OUT WHAT THEY WERE:    because I did not do an in-lab sleep test, I didn’t get detailed results that would tell me the ratio of obstructive to central apnea.     As I learned by reading (thanks to all), my machine doesn’t know if my “open airway” events are central apnea or something else.   All it knows is that I wasn’t breathing and then, when it gave me a pop of air, it didn’t hit an obstruction.    (I think that’s correct.)   When I learned that open airway events were associated with the dreaded central apneas, I read and worried about that for a while.   

But reading a lot of posts on Apneaboard gradually moved me to experiment with EPR.   One of the last ones that I read was:   “Leak rate super low, Low AHI ..waking up with brain fog?” as posted on 8/10/21.    That thread was full of AHA moments for me.   Sheepless writes, “without epr, inhale pressure = exhale pressure. epap (exhale) is what keeps the airway open against obstruction. with epr, epap is inhale pressure - epr. if you need a min of 8 to treat obstructives, you only get 5 at epr 3, which is easier to exhale against but isn't sufficient to do the job of keeping your airway open.”   And cathyf wrote a blistering analysis of the way that the engineers have designed the EPR option.  Sarcastic Dave, whose analyses I’d read in other “why I am still having brain fog if my AHI is good” posts, also chimed in.   So, I made the change. 

But, I will confess, I still can’t visualize what the change did.  All I know is that it worked.    Based on what I’ve read, it has something to do with keeping my airway open.   But, why?  Can someone give me the For Dummies version?  

SO, I am turning to the community of experts with the hope that you will:

•  Offer your ideas about why changing the pressure against which I expire – oh, that sounds so wrong! – made such a difference.     Why would changing the expiratory pressure decrease these clusters of clear airway events?   And why would these clear airway events have been causing this array of problems – brain fog, lassitude, enervation, cognitive challenge, stupor.
  
• Offer your ideas about what was causing the bursts of Clear Airway events that were a primary problem before the change in EPR.     If I wasn’t breathing (and OSCAR says that I wasn’t), what was causing me not to breathe?
  
• Offer your ideas about the relationship (if any) between Clear Airway events and “lip flutter.”   I thought that they were related but, as my clear airway events have largely vanished, lip flutter still remains and still disturbs my sleep.   (Read the section below on lip flutter, if you can stand more details   )
  
  

BACKGROUND INFORMATION: 68 years old, female, healthy and fit.  Not overweight.    Under treatment for nothing but lifelong allergies.   No prescription drugs except for Montelukast and nasal sprays.    Good sleep hygiene, regular exercise (treadmill, weights, yoga).    I drink alcohol (hello, single malt!) but always moderately and always with periods of abstinence to avoid physical dependence.    Lifelong sleep problems:  insomnia, early morning awakening (beginning in mid-life), broken sleep.   On and off with sleep medication during midlife, always careful to never take it more than two days in a row (to avoid physical dependence).     Over the past decade, worsening sleep problems—struggling to fall asleep, waking up a lot, nocturia, unable to get back to sleep after awakening – that I had chalked up to aging.   

WHAT PROMPTED ME TO GET A SLEEP STUDY?   My allergist was the one who recommended the sleep study.  During annual check-ins over the course of two years,  I had complained of early morning headaches that lasted for hours and of being tired during the day and sometimes feeling unable to breathe out (expiration) during the night.   I was also being forced to sleep on my side at some point during the night (something that’s physically hard on me because of joint issues) and had a vague sense that my body was demanding this “so that I could breathe.”    I was blaming all of this on allergies but he didn’t think I was right.

SLEEP STUDY RESULTS:   My sleep study (appended) showed an AHI of 26, with the OAI score of 18.   It was at at-home study (COVID, hello).    I was put on Resmed Airsense for Her, the version that has two algorithms in it.   I got a cursory visit from a DME who didn’t do much or know much.    However, I adapted rapidly to wearing the nasal pillows and using the machine.   I had very little leakage.   I wore the device for 8 or more hours.  No problem.

STARTING TREATMENT:    I adapted rapidly and was delighted with initial results.   I could feel the difference that therapy made.  I was sleeping through the night after years of constant awakening and struggling to get to sleep and stay asleep.   For the first few months, slept A LOT and was groggy almost all of the time.   But I was SO happy to be sleeping!  I was groggy but good natured.    And all of the advice said, “it can take six months to get used to therapy.  Be patient.”   My AHI was good – generally, about 5 and only occasionally up to 8 or 10.

PROBLEMS REMAINING/EMERGING AFTER SIX MONTHS OF TREATMENT:   After six months of treatment (with EPR set to 3), it was clear that something was not right:    my dominant state was lassitude; my brain was foggy; I felt as if I was in a stupor; my usually-sharp brain was slow and dull; I was more likely to stare into space than to get things done.    Even with my lifetime of sleep problems, I had been sharp, on task, clear-headed, active.  (True, some of that was through jacked-up levels of cortisol.)    The contrast between pre-treatment and post-treatment was dramatic:  yes, I was sleeping – but I was also dull-witted and drained.   I could pull myself together for short periods of time and interact/act “normally” but, afterwards, I was drained.

WHAT DID THE SLEEP DOCS SAY?  Surprise!  Sleep docs (two of them) didn't find the problem.  The first one told me that therapy for sleep apnea was not about improving my quality of life; it was about extending my life.    The next one listened to me more carefully.  He dropped my maximum pressure from 16 to 12.  That made no difference in how I felt.   He had a guess about why I felt so drained and foggy:   some people had "residual sleep issues" that couldn’t be fully controlled by machine therapy.  So, he gave me  prescription for Armodafinil.   I tried it and it just made me feel like I was on speed when I finally stepped up to the full prescribed dose:   a nasty feeling of agitation and buzzing consciousness, nothing close to normal wakefulness.  

So, the sleep doc sent me back to my primary care physician to look for the underlying cause of whatever was going on.  I began the rounds of non-sleep docs, looking for a non-sleep-related/non-treatment-related reason for my life-changing brain fog and lassitude:     a broad range of blood tests from my primary care physicians produced no clues, so I moved on to ENT’s (“no, there is no hidden sinus infection or issue – we’ve checked everything”),  cardiologists (“doesn’t really seem like a heart problem, but we’ll run some tests”), rheumatologists and neurologists and endocrinologists.    The final stop was going to be a psychiatrist, as some on-line research showed me that Welbutrin was sometime used for treatment-emergent problems like brain fog.

But, then, this tiny change in EPR seems to have shifted everything.

WHAT DID OSCAR SHOW BEFORE I DECREASED THE EPR?  Prior to decreasing the EPR, I had generally good AHI’s, typically a bit less than five but sometimes spiking up to 8 or so.    Not bad, by any typical (sleep doc) measure.

Until my most recent adjustment (dropping EPR to 1), OSCAR showed clusters of clear airway events that coincided with periods of wakefulness during the night or that forced me into awakening.   These often came near the end of the night but sometimes hit in the middle.  When they hit in the middle of the night, I wound up needing to roll over on to my side to struggle back to sleep.   This was a problem because, even if I got to sleep, joint pain would wake me up in about an hour.

OSCAR also showed OA events but these tended to be scattered throughout the night and didn’t tend to cluster. 

Because the Clear Airway events tended to cluster at the end of my sleep period and often woke me up and cut my sleep short, I struggled to understand them and what could be done about them.    I knew that many people would dismiss them as SWJ (“sleep/wake junk”) but I became convinced that they could be causing problems for me.


LIP FLUTTER -- MAJOR CHALLENGE THAT I (KIND OF) SOLVED DURING THE FIRST NINE MONTH:   At first, I thought that lip flutter was disturbing my sleep and causing my brain fog, lassitude, etc.   I also thought it might be related to the Open Airway events.  So, here is a brief overview of my experience with it.

About six months into treatment, I realized that I was being awakened by lip flutter (i.e., air being forced out of my mouth because it had nowhere to go).    I actually recorded the sounds that I made while sleeping and identified clusters of these events.   I couldn’t synch those records with OSCAR’s records of my open airway events, but they seemed connected.    (For newcomers:   “lip flutter” is not the same as mouth breathing.  It is when the machine is trying to send air into your trachea but something blocks or slows the air flow and so the air has nowhere to go but into your mouth.    It is often released with a pop-pop-pop sound and the weird feeling of a ball of air rolling around in your mouth as it searches for an exit point.)    I read posts about this problem and  guided to a solution:  wearing a cloth band (a headband, like a girl would use to keep her hair back) over my mouth.    This doesn’t solve the problem but it does do away with the pop-pop-pop sound that was waking me up.    I think I’ve mostly gotten used to the sensation of a ball of air rolling around in my mouth.   Air forced into my mouth is still sometimes a problem near the end of my sleep cycle.  If I am not fully asleep, the ball of air and the now-mostly-silent pops can keep me from falling back to sleep.

As I said, I mention this because I originally thought that lip flutter was related to the Clear Airway events.   Does anyone out there have any insights?   I still seem to have some lip flutter but, as I have been sleeping through it, I don’t know if it’s decreased.   I guess I should record myself again and see what I hear, but I thought I’d put the issue out there for expert/experienced commentators.

CONCLUSIONS AND QUESTIONS:    To summarize, I understood half of what I read on Apneaboard in a zillion different posts about “low AHI but I still feel terrible” or “clear airway events” but I somehow stumbled my way into understanding enough to get me to drop my EPR from 3 to 1.   This made an incredible difference in how I felt and almost completely wiped out the clusters of Open Airway events that used to be clumped in the hour or two before my alarm was supposed to go off.

Why did the change in EPR make the clusters of Open Airway events mostly disappear?    Given that the change in EPR made them disappear, does that tell us what was causing the Open Airway events?  If so, can someone please explain it to me?    I’m delighted at the change but know that, if I don’t understand it, I won’t be able to deal with any similar issues on a another machine (in the future) or make any further progress on pushing back against brain fog, lassitude, and the other drains on consciousness.

I should probably keep experimenting.   Raise minimum pressure?   Keep minimum pressure the same but eliminate EPR?    Your thoughtful input is requested.

Thanks to all who take the time to read this and offer ideas/suggestions/questions/comments.

[Gideon]

EPR and Central Apnea
There are many causes of Central Apnea, The most common one here is Treatment-Emergent Central Apnea. This is a CO2 induced central apnea. First know that CO2 levels At a "normal" level is what triggers our breathing. It is NOT the need for oxygen, though that triggers other changes. Deep breathing increases the flushing of CO2 from our system, as CO2 concentrations decrease our depth of breath or v\olume decreases until it drops below your apneic threshold and you cease breathing. When you are not breathing your CO2 levels increase and once above your apneic threshold you gradually resume breathing. Then the cycle repeats.
Higher EPR/Pressure support (PS) and even just using a CPAP/APAP/BiLevel can cause this though without EPR/PS it is unusual.

[Albigensian]

Thanks!    So, somehow, I started breathing very slowly and deeply and then my CO2 levels drop so much that they don't trigger the next breath.  Is that correct?

Is that what the flow rate is showing in this screenshot that shows details from some of the clear airway events prior to decreasing the EPR?

And this is just something that (inexplicably) happens to some (presumably small) subset of APAP users?    I guess that this would create "treatment emergent apnea" or something like that, but Armodafinil was sure not the first solution to try.

Can you try to explain why decreasing the EPR made such a difference?    Does it somehow just keep me from breathing too slowly and deeply and dropping my CO2 level?    Maybe it forces me to breath out with such strength that I can't drift into this (bizarre and rather unsettling) pattern of long/slow breath?

This is all ... so .... strange.

[staceyburke]

I see no reason for lessening Your EPR made any difference in your therapy.  It looks like you had more centrals and that is not due to lowering your EPR

First how the setting work -

Min pressure is the inhale pressure
EPR is exhale pressure relief - It is subtracted from the min pressure to get the exhale pressure
Max pressure is the highest the machine will go when it detects obstructions. (O, H, FL)

Types of Apnea
Central - cannot be controlled with the machine you have - you need a much more expensive machine.  But you very well may have treatment emerge central apnea.  I say that because you did not have many in your sleep study.  So I’m sure that they will go away as your body gets use to the therapy.

Obstructive Apnea is the largest apnea (see my signature for percentage of blockage) and they must last for at least 10 seconds to be recorded.

Hypopnea Apnea - Just like obstructive but less percentage of blockage and also must be 10 sec

Flow Limits - They are also obstructive but they are the smallest percent of blockage and are not timed.  You had a large amount of these (look at the 2nd graph of flow limits).

We use EPR to help with Hypopnea and Flow Limits.

The problem you have is that the min is too low.  All pap machines have the lowest setting possible of 4cm.  And that setting is used for children - same machine is used.

Your settings are Min 5, Max 12 and EPR 3 - EPR is doing little (only 1) because the min you have set is almost as low as the machine can go.  So what we need to do is raise the min and keep the EPR at 3 to help with the H events and flow limits.  Flow limits are small but for most people they interfere with sleep by not allowing you to get into deep sleep and sometimes waking you up.  Also the machine reacts to the flow limits by raising the pressure (max) to stop them from becoming larger events (H and O).

So the EPR is important and I think it is a reason you are not sleeping well.

Try the following settings for tonight and post tomorrow.

Min 7
EPR 3
Max 12

I think you will breathe easier and sleep better tonight.

[Albigensian]

Thanks for looking at this, Stacey!

Maybe I did not explain my results clearly.

The number and clustering of "clear airway" events dropped a LOT after I decreased EPR to 1. I felt a lot better after I decreased EPR to 1.

The 8/18 OSCAR screenshot shows what happened after I dropped the EPR to 1. The other screenshot shows what my results were like when the EPR was set to three. (On both dates, minimum pressure was set to five.)

I can definitely experiment with a higher minimum pressure and raising the EPR, but I wanted to be sure that you understood that decreasing the EPR had cleared up the problem of brain fog, lassitude, etc.

I know that EPR and minimum pressure interact with one another. Currently, minimum is 4 and EPR is 1. If I change minimum to 7 and EPR to 3, the gap between them remains the same. Was that part of your logic in suggesting this?

I will post about my results with the 7/3 setup.

Thanks so much. I am trying to learn as much as I can, so I have to keep asking for clarification.

[Rich66]

As for the lip fluttering (I call them mouth farts), you can try a Full Face Mask -- or some people, including me are taping their mouth shut. I found 2 inch cloth tape on Amazon works pretty good without being too difficult to remove. But, it is "air permeable", so some air still exits the mouth. There are others options of tape and other discussions on here you could research. Another tape is Somnifix, also available on Amazon. I found the Somnifix is too small and weak to do me any good. BUT it is not "air permeable" to speak of. Lately, I've been using both of them -- I put on the Somnifix and then a layer of the cloth tape. And it is working pretty good for me. I have not had luck with a Full Face Mask Also, searches on YouTube can be productive.

[SevereApnea]

Hi Albigensian (love that name)

This can get very complicated. I understand you wanting to grapple with the underlying reasons, hoping to give some pointers in the right direction.

There is much online (too much) that helps us understand the effects of PAP therapy (Non Invasive Positive Pressure)
For one of the better ones look for
positive pressure ventilation in the cardiac intensive care unit Alviar
Too much information but enough to hint at the complexity of this.

I can only offer two possible reasons why you felt better with a lower EPR.

1. For some folks the Clear Airways events are sleep disruptive. Less of these means less disruption, deeper sleep.

2.You have already been told your Min Pressure was too low.

With Pressures of Min=5 Max=12 EPR=3 you are starting the night with a Minimum EPAP of 4. (5-3 = 2 but the machine defaults to minimum of 4)

With Pressures of Min=1  Max=12 and EPR=1 you still only starting the night with a Minimum EPAP of 4. Too low for most.

Now it gets interesting. Let's look at your machine readings of what happened during the night.
Look at EPAP for example. These are Results Achieved by the your therapy, not the same as pressures you set to start off with.

17 Aug 2021 with EPR=3 you achieved Med EPAP of only 5.86, but with good 95% Flow Limitation (anything under 0.1 is acceptable for most.)

But on 18 Aug with EPR=1 you achieved Med EPAP of 8.52. Why? because EPR=1 did not treat the FL as well.
So the machine upped the pressure for you in an attempt for it to try and reduce your FL.
It did not succeed in that. Your 95% FL were higher at 0.17.

But it did give you a Median EPAP of 2.66 cm H20 more than with EPR=3.
And it increased your 95% EPAP by 3.02 cm H20.

We know that higher PEEP or EPAP can be used to increase blood oxygenation.
That might be one reason.

This suggests to me that your initial starting pressures are too low for you.

Also have a look at what your changes do to your other results: tidal volume, minute ventilation, etc.

We can't measure C02 so don't how this effects our brain fog.

Most NB is to keep a diary of what changes you made and how that made you feel.

With OSCAR we can do this daily or weekly!

The Sleep Labs only get one bite at the cherry for the one night you are there.

For what it is worth, if you are interested in numbers, here are some correlation data from my therapy this year so far: EPR and EPAP show similar trends to your two charts.

A lot of this CPAP is paradoxical and difficult to understand. 

[attachment=35857]

[Albigensian]

Thanks!  BTW, I called them "mouth farts," too, when I posted about them.    The headband-over-the-mouth seems to help me.   Tape was difficult, as the skin near my mouth is thin.

I am considering a full face mask but have read conflicting reports about their usefulness in dealing with this problem.   If I could have my mouth slightly open inside the FFM, then the air would escape easily and without building up pressure to force its way out.  That would be ideal.   But I am not clear on whether this would be possible.    I will continue to explore the idea, though, as I'm sure the air's search for an exit does disturb my sleep.

[Albigensian]

        Thanks, Stacey.

I did as you suggested and raised minimum to seven with EPR set at three.   Alas, I had a poor night of sleep.   Inexplicably, I had lots of obstructive apneas and my sleep was broken and shallow.

I notice that my flow limit went to .35 and that there was a messy set of issues during the hours before my alarm went off.   I was struggling into and out of sleep during that period after awakening earlier; I briefly took off my mask to have an indicator of when I woke up, so you can see when that period of unrest began (about 7:30).

During the period in which the flow limit indicators turned messy, I developed a small but sharp headache.    Interesting.   I do not understand flow limit and must read about it.

I will leave the setting as is (unless I am advised otherwise) and see what happens tonight.

Do you see anything in my OSCAR chart that is worth considering as a clue about what is going wrong and what I should be doing differently?

Thanks to you and to all who comment.

---

Stacey, I tried to reply directly to you but the post went to the bottom of the stack.  Please read down to see the results of last night's experiment.  Thanks!

[SleepyHenry]

Severe Apnea;
If I am reading you chart correctly:
     EPR has a negative (moderate ) correlation with Flow Limitation...Therefore as the EPR increases the Flow limitation decreases?
Streching the data: EPR explains about 45% of the variation in Flow Limitation "in you"....Wonder what it is in other members of the Forum?
How many nights did you use to collect these resuts?