CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

SleepingUgly wrote:You seem more cheerful! You must be feeling better. What were the results of all your bloodwork?

Still waiting for those to emerge. Yes, I am getting better, especially according to my family. My kids are really enjoying having me more available, jokey and pat(i)ent. Let's see where this all ends for my energy levels, maybe: , but more likely ?

Just so you know, the Speedo over tights is not a good look for anyone, not even Batman.

SleepingUgly wrote:Just so you know, the Speedo over tights is not a good look for anyone, not even Batman.

Did you complete the sleep log?

http://users.adam.com.au/sixsome/ASV/04 ... 042710.JPG

Do you use an alarm clock to wake up? If so, do you use the "snooze" button?

Muffy

Muffy wrote:Did you complete the sleep log?

http://users.adam.com.au/sixsome/ASV/04 ... 042710.JPG

Do you use an alarm clock to wake up? If so, do you use the "snooze" button?

Hi Muffy, No I haven't been using an alarm clock but I will start using one. Thanks for the reminder to post the completed sleep diary. I will scan in tomorrow and post.

I properly read through that paper I found that you extracted the isopleth plot from. Based on this plot, I was wondering if my breathing instability could be simply explained by a higher UA resistance across the board (awake and asleep; flatter awake isopleth), thus causing continual cycling between aroused and sleep states as I keep hitting the arousal cutoff for PCO2 at my CR but without the need to reach such high ventilation rates on arousal? Reading that paper helped to further appreciate the importance of understanding my blood CO2 level, something you (and -SWS) have been trying to get me to understand for a while now...

blizzardboy wrote:

Muffy wrote:Do you use an alarm clock to wake up? If so, do you use the "snooze" button?

Hi Muffy, No I haven't been using an alarm clock but I will start using one.

Why would you want to do that?

Muffy

blizzardboy wrote:I properly read through that paper I found that you extracted the isopleth plot from. Based on this plot, I was wondering if my breathing instability could be simply explained by a higher UA resistance across the board (awake and asleep), thus causing continual cycling between aroused and sleep states as I keep hitting the arousal cutoff for PCO2 at my CR but without the need to reach such high ventilation rates on arousal?

I think you have a solution that is looking for a problem.

Muffy

Muffy wrote:

blizzardboy wrote:

Muffy wrote:Do you use an alarm clock to wake up? If so, do you use the "snooze" button?

Hi Muffy, No I haven't been using an alarm clock but I will start using one.

Why would you want to do that?

Oh, I read too much into your question then didn't I (just answer the question boy) - maybe a subconcious slip because I have long thought that I should be controlling the start point of my day, not leaving it open to the variations of sleep need.

Muffy wrote:I think you have a solution that is looking for a problem.

Not consistent with the data at hand, eh?

blizzardboy wrote:I properly read through that paper I found that you extracted the isopleth plot from. Based on this plot, I was wondering if my breathing instability could be simply explained by a higher UA resistance across the board (awake and asleep; flatter awake isopleth)

No. You would notice a change in your breathing when you're awake, the people in the paper were not on pressure support, you then change the testing conditions by going on a fancy machine that fixes all the problems of the universe, and it should do at least something to give you a good enough isopleth such that it can't find any appreciable events.

Let me get out my crayons...

Muffy

There's a couple of ifs here. If your VE is about 5 LPM and your pCO2 is about 50 mmHg, then you're at the intersection of the red and blue lines, have a fairly horrid isopleth, and all the incessant dial wingin' has done nothing (which, "IMHO", hasn't). The ASV (normal) isopleth represents all the people who say ASV is the Second Coming, and actually, objective data supports this (your DLs say you have virtually no events). So either the ASVers and your reports are a bunch of FLs or something else (or 2) is going on.

Muffy

Muffy wrote:going on a fancy machine that fixes all the problems of the universe, and it should do at least something to give you a good enough isopleth such that it can't find any appreciable events.

Let me get out my crayons...

OK, so ASV improves the patency of my airway to the point that the nature of my instability is not explained by the simple plot, so I

Muffy wrote:may have...an underlying metabolic disorder that causes CO2 retention...

Muffy wrote:There's a couple of ifs here. If your VE is about 5 LPM and your pCO2 is about 50 mmHg, then you're at the intersection of the red and blue lines, have a fairly horrid isopleth, and all the incessant dial wingin' has done nothing (which, "IMHO", hasn't). The ASV (normal) isopleth represents all the people who say ASV is the Second Coming, and actually, objective data supports this (your DLs say you have virtually no events). So either the ASVers and your reports are a bunch of FLs or something else (or 2) is going on.

I'd be interested to learn your take on the usefulness and limitations of ASV.

BB

Something like this may alleviate your worries ...

http://gheg.com/en/products/product/CAP ... index.html

http://www.weinmann.de/fileadmin/weinma ... N_0907.pdf

EXTRACT>>
The carbon dioxide content in the air expired by the patient
is determined with the help of capnometry. This noninvasive
method is used for the continuous monitoring of
ventilated patients, particulary in anesthetics, intensive care
and pre-hospital emergency medicine.
In the sleep lab the blood‘s CO2 content is one of the
measurements the physician uses to assess the quality of
respiration during sleep.
The sidestream capnograph CAPNOsleep transports the air
to be examined by means of a pump into the measurement
cell in the device. Therefore, is a slight delay of about one
to two seconds is seen between the standard respiratory
signals (flow, effort in thorax and abdomen) and the
CAPNOsleep capnogram.
<<


But these types of devices can prove to be expensive. Based on a quote I was given by Weinmann's Australian Agent for their SOMMNIOVent CR machine, this CO2 detector won't be cheap. I mentioned to you I had also approached a Shenzhen company but they were in the $600-$800 price bracket.

DSM

PS was thinking that with several cannula attachments, we could consider a shared purchase of such a device & loan it around (buy your own cannula) - pay say $75 into a pool & get to use it for a couple of weeks at a time to gather data & prove disprove points etc:. I'd be a starter.

Let's load another problem-seeking slug into the BB gun. Here are some ideas I mused as I tossed and turned from 0230-0430 last night.
1. Flight, fright and fight reflex is there to assist in protecting the end user
2. Blood PCO2 is central to the FFFR as is it rises with increased metabolic output, driving up ventilation in the process
3. My brain appears to be hypersensitive to external stimuli
4. Having had a stressful early childhood, maybe my FFFR triggers were programmed at a more sensitive level
5. My brain is now in a more heightened readiness for response (arousal PCO2<48mmHg)
6. The level at which my brain (CR; control centre) now alerts me to increased PCO2 is lower than average
7. My lungs (plant) and heart have normal response to increased PCO2 levels
8. My upper airway (UA) resistance is OK (normal isopleth) while under the influence of ASV
9. My sleep is disturbed due to my brain arousing me at too low PCO2
10. My brain tells my lungs to breathe rapidly on arousal but my lungs don't make a big effort as they are not alarmed by the current PCO2
11. So I exhibit rapid breathing with reduced tidal volume (negative correlation in ASV data)
12. My PCO2 drops and I re-commence sleep
13. The cycle of instability continues
14. My PCO2 is lower than normal, if anything, as indicated by the EtCO2 measurement from my titration PSG
15. My resp rate is lower because of my lower-than-average PCO2
16. Some other point that I just can't remember now...

So what do you think? Consistent with the data?