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Physiology of "treatment emergent" central sleep apnea
#31
RE: Physiology of "treatment emergent" central sleep apnea
This is definitely true and it's something that I have to remind myself of. I'm about to start ASV and I have to be careful not to magically expect to feel better, even if my AHI is close to zero. The effects of long-term untreated apnea alone can leave you feeling crappy, but even if your oxygen levels are only reduced a little, the disruption to your sleep alone is enough to cause you to feel exhausted. And so much gets screwed up if you're not resting completely, you're missing out on certain sleep stage time because of arousals, etc... So even beyond the harm of actual apneas and associated hypoxia, the waking itself can make you feel like garbage, even if that waking is only partial and momentary.
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#32
RE: Physiology of "treatment emergent" central sleep apnea
(01-09-2022, 05:27 PM)Gideon Wrote: Another trick we have is EERS http://www.apneaboard.com/wiki/index.php...ace_(EERS) to slightly increase CO2 concentrations

Also see this paper from one clinician/researcher who uses EERS (based on the chemoreflex theory) when people have trouble with ASV:

https://www.apneaboard.com/wiki/images/b...a-2014.pdf

In short, he sees a lot of patients whose respiratory numbers on ASV look just fine (since the machine is keeping them breathing), but who complain of poor sleep. His theory is essentially that the widely varying pressure of ASV disrupts their sleep, and that using a non-vented mask to increase CO2 concentration will stimulate the respiratory drive.
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#33
RE: Physiology of "treatment emergent" central sleep apnea
Hey a couple of dots that I've never connected before...

I have CMP panels run frequently because of a drug that I take for arthritis. One of the points in the standard test is blood CO2. And over the last decade, my CO2 has been creeping up to the top of normal, and even a bit above normal.

Does this have any relationship at all with apnea? Of course whenever I've been doing a blood test I've been up for hours, so I don't know if it could matter...
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#34
RE: Physiology of "treatment emergent" central sleep apnea
(01-10-2022, 03:28 PM)cathyf Wrote: One of the points in the standard test is blood CO2. And over the last decade, my CO2 has been creeping up to the top of normal, and even a bit above normal.

Does this have any relationship at all with apnea?

People with sleep apnea, or any kind of night-time hypoventilation, often develop high serum CO2/bicarb levels. If the measurement were made at night, my recollection is that there is often an acidosis (low pH) during the night because of the CO2 retention.

However, my recollection is that sleep apnea sufferers often have a paradoxical daytime alkalemia (high pH) because of all the bicarbonate retained by the kidneys to prop up the buffering system. So the CMP results do depend on when the measurement was made.

But... there are many (hundreds) of other reasons for CO2/bicarb to be high. You'd need to look at the pH, work out the anion gap from the other electrolytes, yadda, yadda, to have a clearer understanding of the situation.

Best wishes, DS
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#35
RE: Physiology of "treatment emergent" central sleep apnea
(01-10-2022, 03:28 PM)cathyf Wrote: Does this have any relationship at all with apnea? Of course whenever I've been doing a blood test I've been up for hours, so I don't know if it could matter...

I believe it can and a couple google results support that. For example.

https://www.reuters.com/article/us-sleep...7920071221
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#36
RE: Physiology of "treatment emergent" central sleep apnea
Yep. Hi! Fully compensated respiratory acidosis here from my sleep disordered breathing.

Right after waking up, pH is much lower (more acidic) but by the end of the day, it's much closer to the alkaline end of normal. Only to fall again overnight.

You need to get them to do a blood gas measurement to be sure. If your pH is within normal range, and you have high CO2 and High Bicarb - that's when you're in my shoes. The fact that my body has compensated by my kidneys keeping back extra bicarb is a sign that this is a chronic issue, not down to an acute illness etc.

But yes. Absolutely, untreated SDB can cause you to become hypercapnic and (eventually, when bad enough) acidotic.
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#37
RE: Physiology of "treatment emergent" central sleep apnea
Yeah, I think all of that really only applies to people with seriously abnormal results, while mine are just generally trending upward within the normal range. And also I would have to go back to all of my lab test printouts and check times as well as dates, and go back through my OSCAR data, too.

The mechanism where the pH follows a particular pattern from morning to night means that you would need to pay attention to whether the test was at the end of the day or the beginning of the day.

All of this is intriguing to me as someone whose data looks like I simply adapted pretty well to my sleep-disordered breathing, and then adding therapy on top makes for some interesting counterintuitive outcomes. Which is what we think "treatment emergent" is all about. By the time any of us start therapy our bodies have spent years -- decades even -- adapting gradually to a gradually progressing disease. Therapy which fixes what's broken requires the body to make new adaptations.

In the case of centrals which appear at treatment onset and then gradually recede over months, we think we are looking at someone who breathes "effectively enough" before therapy then after therapy it's "too effective" and the body needs to learn to trust the new environment and to turn down the master volume control to compensate.
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#38
RE: Physiology of "treatment emergent" central sleep apnea
Re: Timing of tests - yes, absolutely. In hospital in November, I was woken at 5 am every darn morning to have Deep Heat rubbed onto my earlobe to increase the blood flow before they took a blood gas reading. Then they would take another towards the end of the day and compare the two.

Would not recommend getting Deep Heat onto your eyes. 0/10.
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#39
RE: Physiology of "treatment emergent" central sleep apnea
I think it's useful to think about what it would look like if someone who spent years (decades?) with apnea then gets on CPAP, and has a nice soft landing of easy adjustments -- what would that look like?

This might be all bogus imaginings on my part, but here's what I see a lot of in my breathing:
   
https://www.dropbox.com/s/4ld9l591diwxl5...M.png?dl=0

That's a minute, 10 breaths, each about 6 seconds long. Each individual 6-second breath has the same character -- I do a breath's worth of inhale in 2 seconds, then a breath's worth of exhale in 2 seconds, and I've moved a whole six second breath's worth of air in 4 seconds. So what do I do?
   
https://www.dropbox.com/s/vdfv4tlwj13j5u...M.png?dl=0

I don't do anything.

I pause to kill the rest of the time, and then start the next inhale six seconds after the last one started.

Those little bumps are how the force of my heartbeat gets transferred into the air in my lungs, which you can only see when I'm not inhaling/exhaling.

My point is that if cpap allows you to do more breathing in less time, then when you are not having apnea, flow limits, etc., and breathing easily, then you need to do something with the extra time that you don't need.

If you waste that time unevenly, you will get into this hurry-up-and-wait cycle, where you get ahead, and then you stop, but you stop for too long, so then you start and hurry, and get ahead again, over and over.

When it's minor, it's periodic breathing. When it gets really uneven, you collect longer pauses, and if a pause gets more than 10 seconds, it gets scored as a central.

But the bottom line is that the extra breathing efficiency has to go somewhere or you hyperventilate. If it's gradual and regular, you don't see it at all, but if you get into a vicious cycle of hurry-up-and-wait where hyperventilation causes hypoventilation causes hyperventilation etc. then this is really disruptive to your sleep.

-- and we call it treatment-emergent.
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