Reasons for so many RERAs?

Morbius wrote:

Machinehead wrote:I believe that RERAS are MORE disruptive than OSA. The problem with OSA people is that they usually maintain sleep. The defining characteristic of a RERA, is that there is always an arousal at the end of it. The majority of pts I see are Medicare, COPD. Its very Common to have an AHI of 5 and an RDI of 20-40. Its not a simple fix either. OSA, even at AHI's of 100+, pop the airway open, pt is fine. RERAS are much more difficult. You have to stabilize the airway, then open it a little. They usually require a much higher pressure. Just my opinion.

Well, I'm going to disagree with just about everything there. My generalizations are:

• OSA is more disruptive than UARS (low AHI/high RDI);
• OSA people do not maintain their sleep;
• COPD (moderate to severe anyway) have hypoventilation episodes and not UARS characteristics ("Overlappers");
• The fix for RERAs is not aggressive pressure attack ("The Krakow Kool-Aid"); and most importantly
• While the defining characteristic of a RERA is that there is always an arousal at the end of it, one wonders if scorers and reviewers are really checking to see if that is the case.

See http://jap.physiology.org/content/116/3/302 discussing the role of the arousal.

In the case of FL, are you seeing some benign flow limitation, an arousal somewhere near there, and going "AHA! There's a RERA!", try to hammer it to death with pressure, and then conclude that when the patient finally gets to consistent sleep (passes out, really) at 57 cmH2O that high pressure is the key?

Or have you found a poor sleeper with a little nose, and now made sleep even harder?

Morbius,

I'm intrigued (as usual) about what you've added to the whole RERA/Flow limitation conversation.

I know you've looked at my own data in the past and have had a lot of things to say about it. Much of why I no longer bother worrying about my flow limitations is that what you've said in the past about benign flow limitations seems to "fit" me. And it's clear from previous experiments that no matter where I set my max IPAP limit, the machine will go there and the flow limitation index doesn't decrease very much, but my own restlessness and aerophagia problems will increase a whole, whole lot with an increase in the nightly pressure levels. And feeling lousy in the daytime comes with increased restlessness and increased aerophagia.

In other words, when I'm actually sleeping with the machine in terms of sleep efficiency and I'm remembering a minimum number of very short wakes, I now feel better than I did pre-CPAP, regardless of what my machine says about my flow limitations and RERAs.

And when I'm NOT actually sleeping with the machine---i.e. the sleep efficiency drops below about 80-58% and/or I wake up remembering a lot of short wakes and/or I wake up and have serious trouble getting back to sleep in the middle of the night, I feel just as lousy as I did back before the First War on Insomnia. And that lousy feeling is regardless of what my machine says about the AHI, the FLI, and the RERAs.

So I'd like to know more about what you refer to as benign flow limitations: What causes them? Is there any way for a mere PAPer to sort out whether the flow limitations they see in their data are benign flow limitations (that don't need more pressure) or are a significant factor in why their sleep is still not good (and additional pressure might be useful)?

Also if an APAP or an Auto bilevel responds aggressively to flow limitations, can the increased pressure in response to benign flow limitations cause more problems than it fixes? If so, is limiting the upper pressure setting and ignoring the flow limitation data a reasonable response?

Morbius wrote:Well, I'm going to disagree with just about everything there. My generalizations are:
So if my generalizations are correct, what you really want to do is control arousal threshold, and not try to engineer breathing waveforms.

And the easiest way to do that, of course, is DRUGS!!

Morbius wrote:Oh look!

What a coincidence!

https://clinicaltrials.gov/ct2/show/NCT02264353

Any insight into why the researchers in that clinical trial are trying donepezil (Aricept), which is typically sold to treat Alzheimer's and dementia?

And do any of the current prescription sleep medications (Ambien, Lunesta, Sonata, etc.) do anything in help control the arousal threshold? And does suvorexant, which has just hit the US market under the name Belsomra, do anything to help control the arousal threshold?

Morbius wrote:

Machinehead wrote:I believe that RERAS are MORE disruptive than OSA. The problem with OSA people is that they usually maintain sleep. The defining characteristic of a RERA, is that there is always an arousal at the end of it. The majority of pts I see are Medicare, COPD. Its very Common to have an AHI of 5 and an RDI of 20-40. Its not a simple fix either. OSA, even at AHI's of 100+, pop the airway open, pt is fine. RERAS are much more difficult. You have to stabilize the airway, then open it a little. They usually require a much higher pressure. Just my opinion.

Well, I'm going to disagree with just about everything there. My generalizations are:

• OSA is more disruptive than UARS (low AHI/high RDI);
• OSA people do not maintain their sleep;
• COPD (moderate to severe anyway) have hypoventilation episodes and not UARS characteristics ("Overlappers");
• The fix for RERAs is not aggressive pressure attack ("The Krakow Kool-Aid"); and most importantly
• While the defining characteristic of a RERA is that there is always an arousal at the end of it, one wonders if scorers and reviewers are really checking to see if that is the case.

See http://jap.physiology.org/content/116/3/302 discussing the role of the arousal.

In the case of FL, are you seeing some benign flow limitation, an arousal somewhere near there, and going "AHA! There's a RERA!", try to hammer it to death with pressure, and then conclude that when the patient finally gets to consistent sleep (passes out, really) at 57 cmH2O that high pressure is the key?

Or have you found a poor sleeper with a little nose, and now made sleep even harder?

I believe machinehead meant OSA patients are generally not very sensitive to airway resistance.

robysue wrote:So I'd like to know more about what you refer to as benign flow limitations: What causes them?

Well, one must ask if FLs are really all that bad-- or maybe they are the norm:

Nose breathing imposes approximately 50 percent more resistance to the air stream in normal individuals than does mouth breathing, resulting in 10-20 percent more 02 uptake (Cottle, 1972; Rohrer, 1915). Resistance during inhalation is regulated by the turbinates in wide noses and by other structures in narrow 50 PAT A. BARELLI noses. There must be adequate nasal resistance to breathing to maintain elasticity of the lungs (Cottle, 1980). Breathing through the mouth when the nose is obstructed usually imposes too little resistance and can lead to micro-areas of poor ventilation in the lungs (atelectasis). Alternatively, many years of breathing against excessive resistance, as with nasal obstruction, may also cause microareas of poor ventilation (emphysema).

Ogura confirmed that a nasopulmonary nervous system exists by which breathing through a constantly blocked nose can alter pulmonary function in a reflex manner (Cottle, 1981; Ogura et al., 1964). He also found that in nasal obstruction the hemilateral lung complied to this increased resistance (Ogura and Harvey, 1971; Ogura et al., 1964).

Maybe nasal breathing is better than CPAP:

...obstructive (but not central) apnoeas and hypopnoeas were profoundly more frequent when breathing orally (apnoea-hypopnoea index 43+/-6) than nasally (1.5+/-0.5). Upper airway resistance during sleep and the propensity to obstructive sleep apnoea are significantly lower while breathing nasally rather than orally. This mechanical advantage may explain the preponderance of nasal breathing during sleep in normal subjects.

http://www.ncbi.nlm.nih.gov/pubmed/14621092

robysue wrote:So I'd like to know more about what you refer to as benign flow limitations: What causes them?

When Guillenminau invented UARS, he was looking at a "narrow posterior airway space". This is an area that is responsive to CPAP (although interestingly, he didn't seem to be a big CPAP fan back in the day).

But does nasal FL create a problem?

Although participants in all AHI categories that indicated the presence of sleep-disordered breathing, including snoring with AHI less than 5, had lower airflow than those without sleep-disordered breathing, there appeared to be no difference between simple snorers and those with a high AHI. Similarly, linear regression analysis of AHI and airflow as a continuous variable showed no significant association between AHI and airflow.

https://www.ocf.berkeley.edu/~dshuster/ ... g_1997.pdf

There is no criteria to treat FLs, only



But now we have an FL graph in software, so it must be important, indeed the Devil Incarnate.

Except they aren't hammering FLs



http://journal.publications.chestnet.or ... ID=1079416

What they are really hammering is tick marks on a graph...

Morbius wrote: There is no criteria to treat FLs, only
...

But now we have an FL graph in software, so it must be important, indeed the Devil Incarnate.

Except they aren't hammering FLs

....

What they are really hammering is tick marks on a graph...

Questions:

1) Can nasal flow limitations and flow limitations caused by narrow posterior airway space be distinguished from each other by looking at the shape of the flow rate curve? (I'm talking about flow limitations that do NOT meet the criteria for scoring a RERA because there's no arousal.)

2) If the machine can't distinguish between nasal flow limitations and flow limitations caused by narrow posterior airway space, are the Auto machines too aggressive when it comes to increasing the pressure due to flow limitations when there's nothing else going on in the breathing? And is that a good enough reason to cap the max pressure setting at level that fixes the obvious OSA stuff even if there are still a lot of flow limitations being scored by the machine?

Morbius wrote:Oh look!

What a coincidence!

https://clinicaltrials.gov/ct2/show/NCT02264353

Interesting. Makes me wonder if the improvement (but not delay in progression) that some Alzheimer's patients show is due to improved sleep (less arousals).

robysue wrote:1) Can nasal flow limitations and flow limitations caused by narrow posterior airway space be distinguished from each other by looking at the shape of the flow rate curve? (I'm talking about flow limitations that do NOT meet the criteria for scoring a RERA because there's no arousal.)

Absolutely not (I mean, theoretically one would think as largely fixed obstruction they would be a little class 7-y, but I wouldn't be having my turbinates drilled out based on that), and it would seem that assessing/correcting nasal airflow is Dartboard Medicine:

http://www.hindawi.com/journals/ijoto/2014/717419/

robysue wrote:2) If the machine can't distinguish between nasal flow limitations and flow limitations caused by narrow posterior airway space, are the Auto machines too aggressive when it comes to increasing the pressure due to flow limitations when there's nothing else going on in the breathing? And is that a good enough reason to cap the max pressure setting at level that fixes the obvious OSA stuff even if there are still a lot of flow limitations being scored by the machine?

That's where you need to do breath-by-breath assessment of the D/L to try to get a good grip on what's happening rather than dial wingin' and hoping for the best ("Well, turn it up/down/sideways and see how you feel.")

All,

Having just got back and read this post and some of the attached articles, I had a question. Hope no one minds me bringing it back.

http://journal.publications.chestnet.or ... ID=1079416

In the CHEST study, Type 1 normal flow shapes and the flow limited shapes are normalized. Thus, we get the normal Type 1 as the standard upside down smile. However, in Figure 4. we see an example of each study group's flow rate in a 1 minute sample. To me, Type 1 looks like the description of Type 6 on the actual flow rate display. I assume this is the normalization. If this is the case, does anyone have an example or link to what Type 6 actually looks like on the actual flow rate display. My untrained eye doesn't see much difference when comparing the normal group's 1 minute sample to the group sample which should be showing Type 6. In other words, what does "a peak during late phase preceded by a plateau" actually look like if not similar to Type 1?

I like anything that helps me learn about what I'm actually seeing on the flow rate and really appreciate your thoughts and expertise.

Best,

Mike

Morbius wrote:

Machinehead wrote:I believe that RERAS are MORE disruptive than OSA. The problem with OSA people is that they usually maintain sleep. The defining characteristic of a RERA, is that there is always an arousal at the end of it. The majority of pts I see are Medicare, COPD. Its very Common to have an AHI of 5 and an RDI of 20-40. Its not a simple fix either. OSA, even at AHI's of 100+, pop the airway open, pt is fine. RERAS are much more difficult. You have to stabilize the airway, then open it a little. They usually require a much higher pressure. Just my opinion.

Well, I'm going to disagree with just about everything there. My generalizations are:

• OSA is more disruptive than UARS (low AHI/high RDI);
• OSA people do not maintain their sleep;
• COPD (moderate to severe anyway) have hypoventilation episodes and not UARS characteristics ("Overlappers");
• The fix for RERAs is not aggressive pressure attack ("The Krakow Kool-Aid"); and most importantly
• While the defining characteristic of a RERA is that there is always an arousal at the end of it, one wonders if scorers and reviewers are really checking to see if that is the case.

See http://jap.physiology.org/content/116/3/302 discussing the role of the arousal.

In the case of FL, are you seeing some benign flow limitation, an arousal somewhere near there, and going "AHA! There's a RERA!", try to hammer it to death with pressure, and then conclude that when the patient finally gets to consistent sleep (passes out, really) at 57 cmH2O that high pressure is the key?

Or have you found a poor sleeper with a little nose, and now made sleep even harder?

I appreciate your comments. As a long time UARS sufferer I have yet to find an optimal treatment. Are you suggesting that pap therapy is not the best treatment option and perhaps drugs that increase the arousal threshold are?