Hering-Breuer reflex, CO2 levels, and apnea

[Miss Emerita]

After reading a fascinating post by dataq1 in gfox's thread, I looked up more information about the phenomenon he was pointing to. The basic idea is that some pauses between breaths are caused by inputs to pulmonary sensors and then mediated by the vagal nerve. This is different from a pause that is caused by depletion of CO2 in the bloodstream.

The vagal-mediated pauses are called the Hering-Breuer reflex, and they can occur immediately after a deep sigh or inhalation. Pulmonary sensors respond to the pulmonary inflation, and through a complicated but quick neural pathway, they lengthen exhalation or pause breathing. This helps to prevent over-inflation of the lungs. This kind of pause can occur so soon after a deep breath that the CO2 explanation doesn't work for them, since it takes a little time for the CO2 reduction to result in a pause in breathing.

More information here:

https://www.sciencedirect.com/topics/ag ... uer-reflex

and here:

https://www.annualreviews.org/doi/full/ ... 522-094142

My next question would be how we know how long it generally takes before the depletion of CO2 in the bloodstream causes a longer-than-normal pause in breathing. I'm wondering whether the usual timing in the special case of Cheyne-Stokes breathing might point toward an answer.

Finally, I wonder whether in many cases there is really no way to tell which route produced the longer-than-normal pause between breaths.

[lazarus]

I believe that the various mechanisms do be complicated, that they can interact at various speeds and distances and intensities, and that individual sensitivities and biological variations occur among individuals in various sleep states/stages, body positions, and environments that have effects in many, many interactive ways.

They all broadly fall under "central" phenomena, though, and thus there may be no easy way to speak of them more broadly than as "centrals" "caused" by the nervous system/brain (and CO2 does seem to be the primary driver overall), just to differentiate them from the more mechanical aspects of the airway in sleep breathing.

And even that differentiation has many technical gray areas, since there is substantial overlap, in that central sensitivities have physical manifestations in the airway and vice versa.

But working theories in applied science always have to draw arbitrary lines for practical applications, so wording can get fuzzy and nebulous for the workaday definitions used in reports from mechanical devices and used by practitioners.

And there are always difficulties when you have researchers, practitioners, technicians, manufacturers, and the public all in the same room, since they all tend to pretend that the words they use always have the same meaning, definitions, and connotations for all of them in all the different trade unions.

So in forums, I tend to be a follower of Mediocrates, whose disciples follow the doctrine of, "Meh, good enough."

Said another way, there can be a fine line between "oversimplified" and "overly complicated."

Very interesting and educational stuff, though. Many thanks!



And for the record, . . .

. . . I think you do absolutely amazing work here!

[Miss Emerita]

"Mediocrates" -- too funny!

Yeah, I agree about what ultimately matters for us in practical terms, and it would be counterproductive to try to convey a lot of complexities to people who are just trying to understand their charts. And I feel certain you're right about the enormous variation from one person to another of how all these mechanisms interact under a variety of circumstances.

I just got kind of excited to learn about a whole new mechanism that causes pauses. Pausal Causal Mechanisms??

[Rubicon]

Well this part in that reference baffles me:

So there are types where we have an arousal, by the way, arousal after event is a normal
physiology. It's if it's an expected physiological response. Now, is it contributing to the
subsequent central apnea? If I see a period of hyperventilation. And again, you need you need
some time of this hyperventilation. Think of we're decreasing the arterial CO2, that low CO2 has
to travel all the way to the medulla. It's not going to get all the way to the medulla in five breaths.
It needs somewhere between 2 to 3 minutes to get there. So if I see that pattern, which is what
you see in Cheyne-Stokes respiration, then the arousal is contributing.

CSR cycle time is generally ~45 seconds so I don't know where he's getting 2 or 3 minutes.

And this

So if I see that pattern, which is what you see in Cheyne-Stokes respiration, then the arousal is contributing.

is just a bunch of words slung together.

But what do I know-- I'm just a sometime cycling fisherman on permanent vacation.

[lazarus]

The loop gain thing and the other forms of waxing and waning and destabilized breathing can involve sensors throughout the body and in various parts of the brain, some of which sensors discern things like muscle activity and some of which can not only sense blood chemistry and communicate blood chemistry but sometimes react to it almost immediately. Maybe not all that dissimilar to discussions about the so-called "gut brain" and digestive chemistry.

I believe sometimes the brain research dudes don't always differentiate well between the communication from the nerves to the brain and discussing the changes in the blood that would actually be sensed in the brain itself once changes in blood chemistry reach there, in the blood itself, meandering along the circulatory system.

The problem is when two mechanisms of sensing-and-reacting get out of sync with one another or have dulled function or have overreactive functions. The resulting pattern in breathing does not have to match the frequency of the sensory parts of the mechanism, the frequency of the reacting part of the mechanism, or the speed of the nature of the communication between them. Dysregulated breathing is dysregulated breathing and may or may not find a stasis or larger pattern of waxing and waning.

And one simple mechanical glitch in breathing OR SLEEP can set the whole thing off when there are chemistry and/or nerve issues just waiting for an excuse to go off the rails.

But I'm just a bad guitarist who enjoys singing off key.

And I'm wandering waaay too far out of my lane.

Besides, if Oppie's life history taught us nothing else, it's that trying to have one foot in the theoretical and one foot in the practical only results in getting fired by both sides, getting blacklisted, losing your clearance, and risking the destruction of the planet. Which contrary to the thinking of some, would not really be a happy ending.

[dataq1]

Here is an (apparent example):

Note that the several minutes prior to the "deep inspiration" does not appear to be hyperventilation but does appear to be regular "asleep breathing"

So, is this Clear Airway a result of CO2 blow-off (from the deep inspiration at 03:52:45) - Does not appear so, particularly if it takes 2-3 minutes for the arterial blood to react and be reflected by the brain respiratory centers.

I have (somewhere) other examples, but this is what I was able to find right away.

I still maintain that Dr B (in the AASM interview) was suggesting that some Clear Airway Apneas can be ascribed to vagal activity, and not to hypo CO2 (because of latency or lag)