Camera shows highly disturbed sleep but numbers are "good"

[geauxdbl]

Update: numbers have stayed consistently good, mostly less than 1, but the "how I feel" index has taken a nosedive.  I've been feeling a level of tired during the daytime that I haven't seen in a long time.  Have been getting angrier, more anxious, and more depressed.  I tried switching mattresses with no effect.  

Sleeprider, I tried your suggestion of setting trigger to high but changed it back after a night.  I don't recall exactly why, but as best I can remember I didn't like the feel as much.

In my tired haze yesterday I found this article:
Arousal from sleep: implications for obstructive sleep apnea pathogenesis and treatment
https://www.physiology.org/doi/full/10.1...00649.2013

It's long, but the part that stuck with me was the following:

Arousals often follow, rather than precede, upper airway opening in OSA patients (113). In many such examples, there is a loud “snort” 0.5 to 1.0 s before the onset of the cortical arousal. Thus pharyngeal vibration or the loud noise associated with airway opening might be the source of, or at least contribute to, arousal in some patients

Last night I finally set my camera back up.  Taped my mouth under my FFM, and took some melatonin.  Since my camera marks instances of motion on its timeline, it's really easy to find arousals that don't correspond with events in OSCAR. 

What I see the most of is what that article describes: a snort, or a sharp inhale, then an arousal.  Sometimes it happens after a decrease in flow rate, sometimes not.  But the pattern is remarkably consistent.  Even the one OA event that was tagged as actually mislabeled, as it was just me holding my breath as I rolled over after snorting.  Sometimes it will happen and I'll stay asleep.  But the majority of the time, it wakes me up.  

Now that I'm more aware of this pattern, I find myself noticing when it happens during the day.  I'll be sitting at my desk and then snort, stretch, and yawn.  The couple instances of nighttime leg movement that I can find fit this pattern as well: the leg movement happens right before the snort, but I think that's just my body signaling more aggressively that it needs to breathe better.  I don't think it's PLM.

What I think this means is that I'm still periodically not getting enough air, and my tightly wound body is overreacting to very minor reductions in flow by opening up the muscles in my airway.  That process has the side effect of waking me up.  A lot.  This aligns nicely with the results of my two PSGs in 2015.

Another interesting thing happened last night: I intentionally held my breath at the start of the night to give myself an event to sync the time of the camera to, and my Aircurve responded by increasing the pressure by 1 point.  That increase was enough to produce a 4 minute string of CA events as I went to sleep and send my heart rate up to 117.  After everything settled back down it was between 72 and 53 the rest of the night.

Any ideas?  At this point I'm considering increasing pressure support, or looking for time release melatonin in the hopes that it will help me sleep through the events.

Note: I have set UF1 to a 20% flow restriction for 4 seconds so it will more aggressively flag events.

[Sleeprider]

Therapy looks very good in all respects and does not explain your sense of anxiety, restlessness or fatigue. Your time of therapy use appears adequate. I just am not getting a clue on how to advise on this, but will suggest that the problems may be external to your therapy.

[geauxdbl]

Right? I'm confused too. I can tell you that my hunch is that if the problems are external to my therapy, they're internal to my nose. I learned this year that I have a moderately deviated septum. Pressure Support has been a godsend.

Correlation is not necessarily causation, so all I can do at this point is keep tinkering.

[Sleeprider]

If you are open to some experimentation, direct nasal pressure can often provide very different results for someone with a deviated septum. I have first hand knowledge. If you can avoid mouth breathing, then the Resmed Airfit P10 may be a revelation. If nasal pillows are not an option, then a hybrid full face which directs flow to the nostrils and covers the mouth may be worth a try. These masks fit under the nose rather than across the bridge, and air is directly applied. Philips Dreamwear Full Face, Amara View and Mirage Liberty are examples. I'm sure there are review threads in the review forum.

[geauxdbl]

That makes sense - I've tried several pillows masks without much success, as they irritate my nose and wake me up, but each time I've felt like I was getting waaaaay more air at the same pressure settings.  It seems like it only takes a small amount of movement to cross the line from great airflow to pinched airflow.

I also have a very large head, size 7 7/8 hat, and headgear is frequently a problem.  If the chinstrap I ordered ever arrives I'll give nasal masks another shot.

[geauxdbl]

And for a better understanding of why I'm concerned about arousals, here's what my old sleep doctor (who I will call The Good One) found in 2015:

BASELINE DATA: 
Sleep Scoring Data  
Lights were turned off at 10:42 PM and lights were turned on at 
5:38 AM. Treatment total recording time was 416.5 minutes and 
total sleep time was 132.5 minutes. Sleep onset latency was 18.5 
minutes. Sleep efficiency was 31.8%.  
 
Sleep was very fragmented with long blocks of wake throughout the 
night. Although he fell asleep in 18 minutes, he immediately 
woke up and was awake for a prolonged period of time. He had 
similar prolonged awakenings all night with many position changes 
and appeared very restless.  
 
The patient spent 252.0 (65.5%) minutes in wake, 56.0 (42.3%) 
minutes in stage N1, 40.5 (30.6%) minutes in stage N2, 36.0 
(27.2%) minutes in stage N3, and 0.0 (0.0%) minutes in stage REM. 
A total of 62 spontaneous arousals were noted with an index of 
28.08 per hour. 
 
Respiratory Events 
This study demonstrates mild sleep apnea but the severity of OSA 
may be inaccurate given the significant sleep fragmentation and 
short sleep time on this study. OSA appeared worse in the supine 
position but only 17 minutes of sleep time was seen in the supine 
position. No REM sleep was seen. Moderate snoring was noted.  
Obstructive hypopneas were quite subtle and associated with 
minimal oxygen desaturation. 
 
This study documented 1 obstructive apneas, 0 central apneas, 0 
mixed apneas, 50 obstructive hypopneas, and 0 central hypopneas 
over the 132.5 minutes of recorded sleep for a combined total of 
51 apneas and hypopneas with an apnea hypopnea index (AHI) of 
23.09 per hour. The supine AHI is 60.00, while the non-supine AHI 
is 17.66. The total number of RERAs was 15 with a combined RDI of 
29.89 per hour. The AHI4% is 3.17. 
 
A total of 11 desaturations were noted with an oxygen 
desaturation index (ODI) of 1.6. The patient's mean oxygen 
saturation was 94%. The lowest recorded SpO2 saturation was 85%. 
The patient spent 1 minutes with an SpO2 at or below 88%, which 
was 0.2% of the total sleep time.  
 
Cardiac Events 
The mean heart rate during sleep was 59 beats per minute. The 
highest heart rate recorded during sleep was 85 beats per minute. 
The highest heart rate recorded during sleep or wake was 94. The 
lowest heart rate recorded during sleep was 48. The ECG showed 
normal sinus rhythm. 
 
Movement Events 
A total number of 4 periodic limb movements were noted during 
sleep, 1 associated with arousals, yielding a periodic limb 
movement index of 1.81 per hour and a periodic limb movement 
associated with arousal index of 0.45. 
 
************************************************************** 
 
DIAGNOSES: 
#Obstructive sleep apnea (327.21) 
 
IMPRESSIONS:  
#Mild OSA with minimal oxygen desaturation and moderate snoring 
noted on this sleep study; however the accuracy of OSA severity 
is compromised by the very fragmented sleep and short total sleep 
time.  
 
Given this patient's strong clinical history suggestive of OSA, 
it may be reasonable to puruse a trial of therapy and follow 
clinical response. Treatment options include a trial of PAP 
therapy, a trial of oral appliance therapy, or surgical 
interventions. Weight loss may also be beneficial.  
Alternatively, a repeat sleep study with the use of a sedative to 
facilitate sleep in the lab could be considered. 

That was at 15 pounds lighter than my current weight.  I then lost 50 pounds and tried it again, this time after taking an Ambien.  

BASELINE DATA: 
Sleep Scoring Data  
Lights were turned off at 11:38 PM and lights were turned on at 
5:49 AM. Treatment total recording time was 371.0 minutes and 
total sleep time was 216.5 minutes. Sleep onset latency was 24.0 
minutes and REM latency was 154.5 minutes. Sleep efficiency was 
58.4%. 
 
Despite using zolpidem on the night of this study, the patient 
had significant sleep fragmentation with frequent long blocks of 
wake. 
 
The patient spent 130.0 (37.5%) minutes in wake, 51.5 (23.8%) 
minutes in stage N1, 71.0 (32.8%) minutes in stage N2, 77.0 
(35.6%) minutes in stage N3, and 17.0 (7.9%) minutes in stage 
REM. A total of 77 spontaneous arousals were noted with an index 
of 21.34 per hour. 
 
Respiratory Events 
This study demonstrates very mild obstructive sleep apnea with no 
significant oxygen desaturation. Soft to moderate snoring was 
heard. OSA is significantly improved over prior study. The 
patient slept in the supine position for only 30 minutes. 
 
This study documented 0 obstructive apneas, 0 central apneas, 0 
mixed apneas, 27 obstructive hypopneas, and 0 central hypopneas 
over the 216.5 minutes of recorded sleep for a combined total of 
27 apneas and hypopneas with an apnea hypopnea index (AHI) of 
7.48 per hour. The supine AHI is 10.00, while the non-supine AHI 
is 7.08. The total number of RERAs was 12 with a combined RDI of 
10.81 per hour. The AHI4% is 0.28. 
 
A total of 3 desaturations were noted with an oxygen desaturation 
index (ODI) of 0.5. The patient's mean oxygen saturation was 95%. 
The lowest recorded SpO2 saturation was 90%.  
 
Cardiac Events 
The mean heart rate during sleep was 53 beats per minute. The 
highest heart rate recorded during sleep was 96 beats per minute. 
The highest heart rate recorded during sleep or wake was 97. The 
lowest heart rate recorded during sleep was 43. The ECG showed 
normal sinus rhythm with ST elevation. Patient said he has benign 
fast repolarization typically seen in athletic males. 
 
Movement Events 
A total number of 8 periodic limb movements were noted during 
sleep, 2 associated with arousals, yielding a periodic limb 
movement index of 2.22 per hour and a periodic limb movement 
associated with arousal index of 0.55. 
 
************************************************************** 
 
DIAGNOSES 
#Obstructive sleep apnea (G47.33) 
 
IMPRESSIONS:  
#Very mild OSA which is significantly improved since prior study. 
There has been considerable interval weight loss. 

I bailed on therapy in late 2015 after losing all that weight.  I have since gained all the weight back.  Will see this doctor again in March.

[geauxdbl]

Update: still can't find a pillows mask that I can tolerate for more than 2 hours.  Have returned to the F&P Vitera.

Home with a sick child today so I have some time to kill, and I scrolled all the way back in OSCAR to 2015 when I was first diagnosed.  There were only 3 months of therapy, and it was interesting to see all the mistakes, but by the end the pattern is the same: AHI in the zeros and the OA events are in fact preceded by a sharp inhale breath, they're not periods of stopped breathing with a recovery breath afterwards.  That was me at one of my healthiest weights.

I found this today:
http://www.sleepreviewmag.com/2019/12/co...d-devices/

The biggest question about PAP modes revolves around how patients breathe out against incoming air. And, the answer may surprise many sleep professionals, because they probably haven’t given it that much attention, otherwise they would have ceased using CPAP as we did back in 2005. What we learned is that patients either self-report the discomfort of trying to breathe out against CPAP…what we call subjective expiratory pressure intolerance or EPI. Or, in the sleep lab we observe irregularities on the expiratory limb of the airflow curve (objective EPI). Once you take note of these poor responders, you switch the patient to bilevel modes, and you will often see improvement straightaway. We have found during the past 10 years that either ABPAP or ASV are the most effective in resolving this issue.

Last, keep in mind we’ve only mentioned expiration. The second part of this equation, once you prevent or eradicate EPI, is to then raise inspiratory pressures to more effective levels to eliminate the flow limitation. Because ABPAP and ASV devices have special proprietary algorithms to solve these problems, we found we could fine-tune the settings by overriding these algorithms in the sleep lab environment.

If you appreciate this approach to care, then you need to develop a great deal of sensitivity when you attempt to start PAP therapy on a PTSD or other anxiety patient. If you force CPAP on such a patient, they will not only reject it, but they will engage in classic avoidance behavior and drop out of care for months or years or longer. In my view, we have unintentionally traumatized the patient with CPAP, causing them both short-term and long-term harm. Regrettably, this model of care approaches a medical malpractice scenario, because the provider offered the patient no other PAP modes at the get-go to rescue the patient from experiencing the phenomenon of “drowning in air.”

That was my experience in 2015, to a T.  High levels of anxiety.  At a pressure of 4, felt like I was suffocating.  At 9-10, ability to exhale crushed by the pressure.  Quietly bailed on treatment and put the machine in my attic.  For years.  (Avoidant behavior).  Had a pretty serious blow-up with a new GP and a new sleep specialist last year in regards to me starting treatment back up again. 

I'm adding a screenshot that I skipped the other day with the Minute Vent visible:
[attachment=19476]

Let me ask 2 off the wall questions: 

1) Do I have UARS?

2) My Minute Vent chart shows a lot of variation.  Dispensing with the insurance requirements for a moment, would an AirCurve 10 ASV respond differently to my variations in breathing patterns and keep me asleep longer?

[Geer1]

Since my first post I have done my own sort of sleep study. I used my cpap machine, recording oximeter and webcam. To sync everything I start the night off by holding my breath while removing the oximeter from my finger in view of the camera. I could then sync the oximeter data to my CPAP by adjusting oximeter start time in OSCAR so that the paused breath lines up with loss of signal from the oximeter. I figured out what time I removed oximeter in the video and compare that to OSCAR data so I know what video time correlates to the OSCAR data, that gets everything within a couple seconds and can fine tune it by finding a couple of these instances. I then could easily calculate times of events I was seeing in OSCAR and watch them in the video. 

My blips like this are not what I would consider the issue with my sleep. They almost seem like the equivalent of a yawn, for some reason I go to take a big breath(whole rib cage etc will expand) and because hooked up to CPAP it fills up fast. Sometimes this is followed by a central apnea (usually some form of reduced breathing) and sometimes by arousal but not always. Your examples seem similar and like mine do not indicate flow limitations or worsening flow limitations prior to the event so its hard to believe they are being caused by restricted breathing.

I don't think you need ASV, I just don't see how it would really help avoid these situations as your breathing prior to the event isn't showing signs of struggling. ASV works off of minute vent, it tries to maintain 90% of previous minute vent but yours doesn't seem to drop that much (more that it seems to increase at times which is probably related to arousal breathing) and you don't have obviously flow limited breaths that it would react to. 

Your Vauto is already a good machine if this is UARS like symptoms as PS is what fights the arousals in UARS, it does this by increasing ventilation which helps avoid arousals caused by increasing CO2 levels. You could try increasing PS (try 5 for a bit) to see if that helps. I would also consider lowering EPAP as your graphs don't really indicate obstructive apneas being a problem. The lower you can set EPAP the lower your IPAP will be which will make the pressure effects smaller making it easier to sleep. The machine will increase pressure if you are having obstructive events so I would consider dropping EPAP all the way down to 4 and then increasing back to 5 or 6 if you need to. I see you made a comment about struggling at 4 cm pressure before, I am curious if that was with a different machine (APAP or CPAP)? With those machines you would struggle at 4 cm pressure because you would be getting no pressure support, with your Vauto the pressure support stays the same and just gets added to EPAP so it being set at 4 cm shouldn't cause the same issues.

I am not sure if over ventilation (too high a PS) can cause an issue but I would just try adjusting it until you feel you are getting the best results and seeing what appears to be the fewest arousals.

[geauxdbl]

struggling at 4 cm pressure before

That was back in the early days of the Autoset.  Switching to Bilevel was a revelation.

I'll try increasing pressure support again as my next step.

[Geer1]

struggling at 4 cm pressure before

That was back in the early days of the Autoset.  Switching to Bilevel was a revelation.

I'll try increasing pressure support again as my next step.

That is what I was guessing. Any particular reason you have EPAP at 6.8?

Titration protocol is to start EPAP and PS at 4, increase EPAP if obstructive apneas are occurring. Once obstructive apneas are resolved increase PS/IPAP to deal with hypopneas, flow limitations and RERAs. Some good info in the titration guide, might be worth a read.

https://www.resmed.com/us/dam/documents/...er_eng.pdf