nearenough - Therapy Thread

[Gideon]

Try EPR=2, full time (IMHO never use ramp only). Then EPR=1

Choose the one that feels best.

This will be a trade off between obstructive and central events.

[nearenough]

First, thanks to everyone who initially helped me acclimate to therapy.  I’m adjusting well, but I still have questions about interpreting data and managing treatment.


I think I’ve generally picked up an understanding of the variables that affect the various kinds of apnea events.  In my case (at least during this adjustment period) the data shows EPR is one of the factors causing CA events.  I understand the rationale that EPR can cause CO2 wash out leading to CA events for some people.  A few threads also highlight the physical stress OA and H events can cause compared to CA events.  I know I’m generalizing, but suffice it to say I think I understand the big picture, and I’m narrowing in on what settings will deliver the most ideal sleep with the most consistency.


That said, I’m ready for you all to take me to school on the periodic breathing.  Every night, without exception, I have a very distinct pattern that surrounds my apnea event clusters.  They’re similar to the infamous crescendo/decrescendo pattern.  Often the pattern lasts for 20 or 30 minutes.  Not all of the patterns result in a flagged apnea; many do.


I’d like to know your opinions on what causes the pattern, how common it is, why it happens consistently, etc.  I understand how EPR can cause the phenomenon, but what the other factors?  What are the risks, if any?  Is it worth changing machine settings, or is it a waste of time.  School me - I’m eager to understand how it all works. 


In full disclosure, I understand my heart to be in good condition.  However I was diagnosed with PVCs in 2018, right when I started having sleep trouble.  There is ample evidence that PVC onset can be caused by sleep apnea.  Since starting APAP therapy, PVC frequency has diminished significantly.  Still, I don’t know which came first; apnea or an arrhythmia. I’ve had 2 doctors (1 cardiologist) run tests and assert they’re benign.  I want to make sure we’re conjecturing with all the  information; I’ve read enough to know these things can be related.


So, here’s a couple attachments to start the lesson.  Consider school in session.

   

   

   

[Sleeprider]

I assume you know this is a feedback look resulting from a delay in your respiratory drive response to decreases and increases in CO2. You seem to trigger the periodic breathing with some brief hyperventilation which decreases CO2, diminishing respiratory drive, leading to the hypoventilation phase. This alternately results in hyper and hypoventilation, and eventually dampens out to normal breathing. Sometimes you have strong recovery breathing, and other times respiration seems to smoothly transition from hypoventilation to hyperventilation. I suspect you are not aware of it happening, and that it is minimally disruptive to sleep. At any time you are near your apneic threshold, so small disturbances in breathing volume may trigger periodic breathing. Fortunately they self-resolve fairly quickly. These do not appear to be triggered by obstructive events. it might be interesting to chart your tidal volume and respiration rate through this periodic breathing. I suspect we could identify a tidal volume that initiates the cycle. I don't think there is any therapy setting changes I would suggest here, other than to limit the minimum and maximum pressure to keep CPAP pressure more constant. You are already using no EPR which would likely exacerbate the periodic breathing or initiate CA events.

If you want to go to school on the apneic threshold and the chemical feedback loop that causes periodic breathing, you can start with this from our wiki http://www.apneaboard.com/wiki/index.php...y_Clusters, or for a whole lot more detail and scholarly discussion try this https://physoc.onlinelibrary.wiley.com/d...004.028985

[nearenough]

Thanks for the feedback.  I'm reading through both links today.

Funny I posted this yesterday.  Last night I had the worst numbers I've had since starting therapy.  Gideon mentioned that ResMed can be aggressive with how it flags CSRs, possibly causing false positives.  I guess my follow-up question is whether it's worth targeting some of the hypopneas since my pattern seems to be a mix of CAs and H events.  It seems like I don't want to wash out and cause excessive CAs, but I wonder if dealing with hypopneas would help stabilize the chemical spiral.  What are your thoughts?

Here's last night, for example.  I threw tidal volume in if that helps.
   

   

[nearenough]

I don't think there is any therapy setting changes I would suggest here, other than to limit the minimum and maximum pressure to keep CPAP pressure more constant. 

http://www.apneaboard.com/wiki/index.php...y_Clusters

I read the post on the wiki - very informative.  When it says, "This [events] can be ignored unless it is a common occurrence or happens fairly often or for longer periods of time."

What would constitute as common or fairly often?  Should I be concerned if I see the same pattern every night.

[Sleeprider]

Even with all the periodic breathing, your AHI does not qualify under most plans for a therapeutic option like ASV. With CPAP we are treating obstructive sleep apnea and obstructive flow restrictions that can respond to increased pressure to stent the airway. Your residual issues with periodic breathing do not fit into this category. Beyond AHI, we want to ensure you have good respiratory function and gas exchange to maintain a healthy oxygen saturation, and we want to minimize respiratory related sleep disruption that results in fatigue and other symptoms that affect your life. I'm not hearing that this is a problem for you, but consider the question asked.

A couple more questions. Have you tried EPR? What was the result? Do you find this pattern is disruptive to your sleep, or is it just something you're aware of due to looking at Oscar charts? Have you ever slept with an oximeter to measure if this pattern affects your oxygen saturation?

[nearenough]

I've tried EPR, yes.  Gideon had me do 3 days with and 3 days without to see what happened.  The data showed EPR may cause an increase CAs, possibly due to CO2 wash out (not helped by the fact that I'm in Denver @ 5600 feet, so lower partial pressure).  I don't find the pattern disruptive, at least so far as I'm aware; just seeing the patterns and events in Oscar data. I have had a few occasions where I have excessive daytime fatigue, even to the point of taking a mid-day nap which I have never done in the last 20 years.

I plan on picking up a good oximeter this week.  I've used my Apple watch previously, but the measurements do not seem accurate, particularly compared to my baseline diagnostic numbers.  My diagnosis oximetry was:

• 22 desaturations
  
• Time <= 8*%: 3 minutes, 1%
  
• Oximetry baseline: 96%
  
• Lowest desaturation: 87%
  
• CA Index: 5.0, 11%
  

Here's a couple examples of EPR data

Min Pressure = 7
EPR = 1cm
   

Min Pressure = 7
EPR = 3cm
   

[Sleeprider]

Interesting that the EPR trial appears to result in an insignificant change in events, especially with the setting at 3. Your pressure stabilized and all flow limit was treated. I see some periodic breathing, but it actually appears to be less than more current charts with no EPR and the CA event rate is very low. This looks far better than your chart from August 15. It may be worth repeating this long enough to get a more meaningful range of data. Most respiratory statistics are about equal, but your inspiration/expiration time ratios are much better with EPR. Based on this, I'm not convinced fixed pressure without EPR is the best solution. It's a little counter-intuitive that you can have a central apnea related periodic breathing issue, that is improved with some pressure support, but that's where I'm at on this. If this turns out to be confirmed in further trials with EPR, I suspect that it is because clearing up the flow limitation, avoids the initiation of a periodic breathing cycle by preventing flow limitation, which in turn prevents the initiating hyperventilation or recovery breathing.

[nearenough]

That's an incredibly compelling hypothesis.  August 15th represents the words numbers I've seen aside from my first night of treatment.  If you're at all interested, you can view a few previous night attachments at the post linked below.  There you'll find the 3 days without EPR followed by 3 days with EPR set to 3cmH2O.  I also posted a couple days of EPR=1 for comparison.  I have no issue doing some experimentation if I can get closer to an 'ideal' therapy. 

I also have a SPO2 monitor that will arrive this afternoon, so I'll start tracking those measurements in tandem.

What's a good target range for insp/exp values?   I'll take any suggestion on a good trial setup if there's an EPR you think makes sense to start with.

Previous Post EPR/Non-EPR data

[Sleeprider]

In your other thread, there was a lot of good advise, and I don't know that we will greatly expand on that here. What I notice is a consistent tendency for inspiration time to be longer than expiration time when EPR is not in use, but a normal I:E ratio is consistently present with the use of EPR. This also affect the volatility of the pressure changes with the machine, and what appears to be a small reduction in periodic breathing. Focusing on comfort and sleep quality would go a long way towards helping you to make a decision on how to proceed with your therapy. You don't have a therapeutically significant CA or PB problem.

Something that would be really interesting for you to try is to get a script for Acetazolamide (Diamox). You could request it to reduce symptoms of traveling to, or staying at high elevations in Colorado. This is completely appropriate as you certainly travel into the mountains, and I bet you have a relatively high CA event rate when you do. I have a feeling it may help you even at your current elevation and may even completely eliminate periodic breathing. Let's consider school in session:

Acetazolamide is the most effective pharmacologic intervention to prevent AMS. It is a non-antibiotic sulfonamide that was developed as the world’s first oral diuretic agent and used for hypertension therapy in the1950s, before it was replaced by the much more effective thiazide agents. Its mechanism of action is to block carbonic anhydrase, and in the small dosage used to enhance altitude acclimatization, its primary action is in the kidney, where it interferes with the reabsorption of bicarbonate, resulting in a bicarbonate diuresis and metabolic acidosis. The kidneys normally compensate for the respiratory alkalosis of high-altitude-induced hyperventilationquot over 3–7 days, producing a compensatory metabolic acidosis that gradually increases ventilation and raises oxygenation as the pH returns toward normal, a process known as ventilatory acclimatization. Instead of taking 3–7 days, acetazolamide achieves the same effect in <1 day. Thus, acetazolamide mimics the natural process of acclimatization, but more rapidly. The great benefit of acetazolamide is that it shifts all travellers towards being better at ventilatory acclimatization.

https://academic.oup.com/jtm/article/27/...ogin=false

Respiratory drive function on CO2 which causes a small reduction in the blood pH (carbonic acid), which is detected in the carpal bodies. If carbon dioxide builds up, the blood becomes more acidic increasing the need to breathe faster or deeper to restore balance. Similarly, if you hyperventilate, lower CO2, the blood becomes more alkaline which can result in diminished drive to breathe or even central apnea. https://pubmed.ncbi.nlm.nih.gov/29494021/

Going back to the quoted paragraph above, Acetazolamide increases blood acidity and increases respiratory drive, offsetting the effects of altitude. So my suggestion to try this therapy, while somewhat experimental for your circumstances, is valid due to your exposure and sensitivity to altitude, and may actually be important when you travel to higher altitude.