CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

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-SWS
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Re: CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Post by -SWS » Thu May 20, 2010 10:54 pm

blizzardboy wrote:So last night (http://users.adam.com.au/sixsome/ASV/0510/051910/) I did an experiment comparing fixed CPAP@9.6 to ASV with EEP=9.4 and PS=4->9. Switching at 0330, when I awoke temporarily, there is quite a dramatic difference in my response to the two settings. I am particularly interested in the increase in baseline resp rate and reduction in resp variation following transfer to ASV. Please note that when I awoke this morning I had no joint pain. Having the ASV setup like that reminded my of when I used the Bipap ASV machine during my trial period, in that I could feel a more dramatic dump of air from my lungs when the machine dropped back to the EEP phase of the cycle. Also interesting to note that I first experienced joint pain when I went onto the S9 part of my trial period, which immediately followed my trial of the Bipap ASV.
It sure is starting to sound like the ASV is, overall, your better modality between those two. AHI certainly improves with ASV modality---despite tidal volumes showing more variation. More importantly, it seems that you report better daytime symptoms when using the ASV versus CPAP.
blizzardboy wrote:One thing that I hadn't thought to mention was that between the ages of 15 until 27 I suffered from chronic lungs infections (at least 2 per year). During this period I had regulary bouts of acute stomach pain and associated vomiting and nausea, once causing me to be hospitalised. I had a tests over this time but no-one ever found a cause. Finally, at the age of 27, during a work trip to Germany, I had a similar bout of stomach pain and vomiting but this time I got really sick. I crawled through the suburb I was living in a eventually located a doctor who proceeded to poke my appendix and nearly sent me through the roof. I was rushed to hospital and had an emergency appendectomy. Since that time (11 years) I haven't had one bout of stomach pain or a lung infection. I just wonder if 12 or so years of lung infections has taken its toll on my lungs some how? Maybe not on MVV, but on gas exchange efficiency?

Anyhow, let's see what comes of a comprehensive pulmonary function examination. I am now determined to make this happen!
Well, Muffy usually gives us good advice IMO. I would want the complete PFT as well if I were you.
blizzardboy wrote:So maybe the issues at play are (1) I need sufficient base pressure to keep my airway open and then (2) I need enough differential between IP and EP to ensure adequate ventilation of my lungs. Let's see what comes of it all.
Your outstanding slight flow limitations above 10cm might not even pose a significant sleep problem for you by the way of outstanding RERA's. And there's always the chance that attempting to address those flow limitations with higher pressures might create more machine-sourced problems or arousals than resolved. I suppose I would eventually get around to experimenting with higher pressures---since your doctor already approved that---to see if eliminating presumed flow limitations above 10cm enhanced daytime symptoms or slightly deteriorated daytime symptoms.

Note that flow limitations occur during inspiration. So they can be addressed with either base pressure (EEP) or IPAP. The current Resmed Adapt SV titration protocol prefers getting them with IPAP (thus increasing min PS as your doctor suggested). By contrast, the Respironics protocol starts with CPAP as base, and thus EPAP (EEP equivalent) increases are necessary to address those flow limitations by virtue of the CPAP base modality itself. Despite the Adapt SV suggested protocol preferring IPAP increases to address outstanding flow limitations, we can see in this excerpt that Dr. Brown's team chose to address them with EEP increases: viewtopic.php?f=1&t=51063&p=478152&hilit=brown#p478152

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Re: CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Post by blizzardboy » Thu May 20, 2010 11:09 pm

Picked up my PSG data from the sleep lab today. The sleep tech there is great. He spent nearly an hour going through my PSGs with me looking on and answered a whole swag of questions that I had. Here's some points that I recall:
  • My PLMs were "classic periodic" and in abundance!Whether or not I suffer from PLMD depends on the negative symptoms that arise from arousals caused by my PLMs i.e. EDS
  • My central apnoeas and central hypopnoeas are associated with arousals
  • Following arousal I go into a "textbook pattern" of hyperventilation/central apnoea/central hypopnoea/normalisation
  • I have OSA with both obstructive apnoeas and obstructive hypopnoeas
  • The tech was adamant that the 35bpm resp rate (RR) spikes reported by the Adapt SV on fixed CPAP were not real but pressure artifacts (e.g. heart rate pulsations) coming back up the hose during apnoeas and hypopnoeas, hence the apparent negative correlation between RR and TV seen in my fixed CPAP DLs
  • The tech was adamant that the large instability seen in my TV was not real but, again, a pressure artifact picked up by the ASV e.g. result of diaphragm movement associated with PLMs, saying that a severe OSA sufferer would not even show that frequency of TV swings
  • My respiration apparently looked OK during the ASV study, certainly not as bad as the ASV data would indicate
  • My issues are OSA and arousals, with uncertainty as to the extent of negative impact associated with PLMs
  • When I am asleep I sleep well, with good amounts of deep sleep and REM - just have to find the cause of my arousals
  • He didn't seem to be able to read too much into my EtCO2 results
  • He suggested that EEP=10 and PS=4->9 on ASV might be a good way to address my obstructive apnoeas (EEP=10) and obstructive hypopneas (PS=4->9) and to try to increase my TV
  • He also suggested that maybe a Bipap with fixed ventilation rate might be worth me trying given my tendancy to hypoventilate
  • He thought that the data produced by sleep machines is limited in its helpfulness and needs careful interpretation i.e. how much can you really conclude from a single channel of data (flow rate through tube)
  • He thought that ASV was being made out by some to be a panacea for SDB but still has its limitations
I can't think of anything else just now. I am looking forward to sitting down and having a look at my PSG data and video footage to see what my PLMs look like.

My time with this most-helpful-sleep-tech reinforced to me the quality of the advice that I have been getting from this forum. Thanks again for everyone's help to date. My goals for now are:
  • Get fit and eat well
  • Maintain sleep hygiene
  • Get PFT (comprehensive lung test)
  • Bit more tweaking of ASV settings
  • Trial weaning off fluoxetine
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-SWS
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Re: CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Post by -SWS » Thu May 20, 2010 11:20 pm

Great summary and treatment plan IMO.

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Re: CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Post by blizzardboy » Thu May 20, 2010 11:21 pm

-SWS wrote:Your outstanding slight flow limitations above 10cm might not even pose a significant sleep problem for you by the way of outstanding RERA's. And there's always the chance that attempting to address those flow limitations with higher pressures might create more machine-sourced problems or arousals than resolved. I suppose I would eventually get around to experimenting with higher pressures---since your doctor already approved that---to see if eliminating presumed flow limitations above 10cm enhanced daytime symptoms or slightly deteriorated daytime symptoms.
Hi -SWS, Good point. I have been aware of possible arousal increase resulting from increased pressures. My strategy has been to try to keep EEP as low as possible and then try to nudge up PS. Maybe it would be a good time for me to do a plot of AHI versus fixed CPAP pressure to help me choose a likely value for EEP_min. What do you reckon?
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Re: CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Post by Muffy » Fri May 21, 2010 3:24 am

What about that S9 file?

Keep in mind that the purpose of the Complete PFT was to try to explain that apparently elevated pCO2 based on an -HCO3 of 30. If your pCO2 is normal (based on -HCO3 of 27)(and this is an indirect calculation, the only way to truly determine pCO2 is by ABG) then the chances of significant findings on PFT are small.

OTOH, if those were truly "lung" infections (as opposed to upper airway stuff) I suppose a PFT can't hurt.

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Re: CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Post by Muffy » Fri May 21, 2010 4:52 am

blizzardboy wrote:
  • The tech was adamant that the 35bpm resp rate (RR) spikes reported by the Adapt SV on fixed CPAP were not real but pressure artifacts (e.g. heart rate pulsations) coming back up the hose during apnoeas and hypopnoeas, hence the apparent negative correlation between RR and TV seen in my fixed CPAP DLs
  • The tech was adamant that the large instability seen in my TV was not real but, again, a pressure artifact picked up by the ASV e.g. result of diaphragm movement associated with PLMs, saying that a severe OSA sufferer would not even show that frequency of TV swings
I severely doubt the effect of ballistocardiographical artifact as an explanation for the RR = 35. Among other reasons, the rate would have been 50. However, it's only one blip, probably due to some sleep/wake instability, and shouldn't be over-analyzed.

In re: VT swings generated by PLMs, if that's the case, then you really have to look closely at how many arousals the PLMs are generating. The succession of events is usually PLM > arousal > change breathing, and not PLM > generate a whole bunch of respiratory artifact > sleep through the whole thing.

However, that was, is, should be the area where microanalysis is warranted. In this example, the lovely volunteer is having tons of PLMs, "sleeping" through them (although the response to PLM #6 looks a little aggressive, we'll have to check EEG there), but if you look closely, is having some autonomic arousal (heart rate and respiratory depth pick up a little):

Image

viewtopic.php?f=1&t=25751&p=224585&hilit=plms#p224585

Continuing the but, however, although, etc., the PLM-induced respiratory disturbances will appear periodic vs. chaotic (chaos is implied in the ASV DL, but most of the values are trended and too coarse to draw any conclusions from)(maybe if the MF S9 DLs ever show up we'll have some better data to work with).

Anyway, when to treat PLMs has always been a subject of great debate, and unless you're having Teague-grade movements, not always clear-cut.

Muffy
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Re: CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Post by blizzardboy » Fri May 21, 2010 6:36 am

Muffy wrote:What about that S9 file?
Aah, yes the S9 DLs. I must confess that I have neglected to do my homework. Emailing right now...done.
Muffy wrote:Keep in mind that the purpose of the Complete PFT was to try to explain that apparently elevated pCO2 based on an -HCO3 of 30. If your pCO2 is normal (based on -HCO3 of 27) then the chances of significant findings on PFT are small...
OTOH, if those were truly "lung" infections (as opposed to upper airway stuff) I suppose a PFT can't hurt.
When in the grip of a bout, I used to saturate my sheets with sweat when I slept at night and painfully cough up green gunk from my lungs. Definitely not upper airway. Cheers,
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Re: CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Post by blizzardboy » Fri May 21, 2010 6:41 am

Muffy wrote:Anyway, when to treat PLMs has always been a subject of great debate, and unless you're having Teague-grade movements, not always clear-cut.
I just viewed my infrared movies from both my diagnostic and titration and my leg movements are not violent but fairly rhythmic, like I am pointing/curling my toes. I have my EDF viewer setup and can view all the PSG channels fine. Cheers,
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Re: CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Post by SleepingUgly » Fri May 21, 2010 8:03 am

blizzardboy wrote:
Muffy wrote:Anyway, when to treat PLMs has always been a subject of great debate, and unless you're having Teague-grade movements, not always clear-cut.
I just viewed my infrared movies from both my diagnostic and titration and my leg movements are not violent but fairly rhythmic, like I am pointing/curling my toes. I have my EDF viewer setup and can view all the PSG channels fine. Cheers,
What EDF viewer are you using? Is it available online?
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Re: CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Post by blizzardboy » Fri May 21, 2010 4:30 pm

Rebecca R wrote:
Muffy wrote:
blizzardboy wrote:I'll at least ask for a copy of the raw data just in case someone wants to review my PSGs in the future.
There is a movement to standardize PSGs to a common format (*.edf)(then all you need is an *.edf reader)...
Muffy is the *.edf format you refer to this: http://www.edfplus.info/downloads/downl ... #downloads???
Hi SU, Here you go. Cheers
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Re: CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Post by blizzardboy » Fri May 21, 2010 6:58 pm

Here are my diagnostic and ASV PSGs in hour blocks: http://users.adam.com.au/sixsome/PSG/, PLMs occur at a rate of around 2/min and are quite regular. Does this:Image indicate that my arousal from REM to n-REM (and subsequent unstable breathing) is driven by something first picked up in the EMG 1-2 channel (possibly related to my slowing RR; maybe the left leg PLM but that is a only a tiny one compared to the PLMs earlier in the night)? There doesn't seem to be any evidence of oscillation between slow (e.g. 10-12bpm) and rapid (e.g. 30-35bpm) RR in the diagnostic. Cheers,
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Re: CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Post by Muffy » Sat May 22, 2010 5:01 am

Muffy wrote:However, that was, is, should be the area where microanalysis is warranted. In this example, the lovely volunteer is having tons of PLMs, "sleeping" through them (although the response to PLM #6 looks a little aggressive, we'll have to check EEG there), but if you look closely, is having some autonomic arousal (heart rate and respiratory depth pick up a little)
"Sleeping" can be continuous, broken up by arousals (disturbances from 3 to 15 seconds) or fragmented by awakenings (disturbances > 30 seconds)(at which point, it's not "sleeping" any more, it's "Wake").

In the example above, all the PLMs result in arousals, yet Stage 2 was maintained (barely, a couple of those Epochs could easily be scored Stage 1, all I gotta say is Thank God for spindles) albeit a very unstable Stage 2.

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Re: CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Post by Muffy » Sat May 22, 2010 5:10 am

blizzardboy wrote:Here are my diagnostic and ASV PSGs in hour blocks: http://users.adam.com.au/sixsome/PSG/, PLMs occur at a rate of around 2/min and are quite regular.
Can you upload the file? Frankly, those one hour blocks mean as much to me as they probably mean to you right now (way too coarse for anything), and since it's ("IMHO") sleep that's the issue, it's the EEG channels that need to be processed and analyzed.

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Re: CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Post by blizzardboy » Sat May 22, 2010 6:03 am

Muffy wrote:Can you upload the file? Frankly, those one hour blocks mean as much to me as they probably mean to you right now (way too coarse for anything), and since it's ("IMHO") sleep that's the issue, it's the EEG channels that need to be processed and analyzed.
Hi Muffy, I wondered what use the data would be in the resolution I supplied! Oh well, got the ball rolling. The EDF file is 124MB in size so I won't be able to load them onto my website due to space limitation. Maybe there is way that I can extract channels to reduce file size, or I will see if a file hosting site will take a file of such size. Cheers,
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