CO2, ERP, conversion, apnea, remission

Quick look:
Serum CO2 lengthens ERP, and slows conduction
This may be why apnea creates a risk for afib (slowed conduction after the apnea).
There may be an opportunity to use this to convert episodes without meds (I did this).
There may be an opportunity to put afib in remission (speculation) by training the serum CO2 chemoreceptor to accept a much higher steady state level of CO2.
There appears to be an afib risk period after doing certain kinds of intense breath hold training to reset the CO2 chemorecptor (like apnea).

There has been much written <[www.google.com] in our archives about ERP or effective refractory period.

“The period from the start of the QRS complex to the peak of the T wave is of particular interest when it comes to atrial fibrillation. During this period (the effective refractory period or ERP) myocyte depolarization cannot be triggered by stimulus originating from rogue atrial cells thus preventing afib from being initiated. However, atrial fibrillation can be triggered during the last half of the T wave (relative refractory period or RRP) making it highly desirable that the ERP is as long as possible and the RRP as short as possible. Several medications aim to exploit this fact by acting to extend the ERP so that the RRP (the vulnerable period) becomes as short as possible. This is particularly important in the case of the AV node as during the ERP the node cannot be stimulated and thus in essence filters out the erratic atrial impulses.”
<[www.afibbers.org]

In this sheep study <[www.ncbi.nlm.nih.gov] full <[scihubtw.tw] it was determined that elevated serum CO2 (from breathing a high CO2 gas) caused lengthened ERP as well as slowed conduction velocity. This is the same thing that flecainide does <[www.ncbi.nlm.nih.gov] . As well, changing electrolyte status can change ERP length.

In the sheep study, it was observed that during the high CO2 period (hypercapnia), the sheep could not be put into afib via an external stimuli. However after returning to normal CO2 levels, the sheep were at a >4x risk for afib (created by external stimulation) over baseline.



It was hypothesized in the paper that afib apena risk came after the apnea episode, not during it.

It appears that if serum CO2 could be kept high all the time, it could be protective (my hypothesis). Likewise, it appears possible that a high level of serum CO2 could lengthen ERP sufficiently to terminate an episode. Also that increased serum CO2 followed by a return to baseline CO2 levels would increase afib risk for a period of time.

I searched for and found this paper because I inadvertently (and later intentionally) tested the above.

The breathing center has sensors for serum CO2 (or serum pH) and also O2. The urge to breathe is usually controlled by CO2, not O2. The level at which this triggers can be changed with training. This training periodically presents the sensor with higher levels of CO2 and it will eventually adapt (free divers are an endpoint here). A reason to do this is because of the Bohr effect. Christian Bohr, in 1904, discovered that higher levels of CO2 will weaken the bond of O2 to hemoglobin <[en.wikipedia.org]. This allows more O2 to get into the cells. So paradoxically, the more CO2 (to a point) in the serum the more O2 to the cells (also noted as a right shift in the hemoglobin-oxygen disassociation curve <[en.wikipedia.org] ). Conversely, overbreathing or hyperventilation will reduce oxygen to the cells.

I’ve practiced nasal breathing for many years. I also tape my mouth shut at night (using either 1” 3M Micropore Paper Hypoallergenic Surgical Tape or “Snoreless Tape <[correctbreathing.com] ) so I will nasal breathe during sleep (helps prevent apnea). My control pause (CP) or BOLT score (breath holding time) is OK but nothing to write home about <[www.normalbreathing.com] . Hence I decided to practice strong breath holding during exercise as a way to adapt the CO2 sensor to higher levels.

Three or four weeks ago, I went to the park at lunch and was doing fairly strong breath holds while jogging. Some time after returning to my office, I went into afib. This is very unusual for me. I went home, took flecainide and after a while, converted. Then several weeks later I was jumping rope at lunch, again coupled with fairly strong breath holds. Again went into afib some time after stopping. I started doing pullups on a door molding and converted the episode. When I went home, I told my wife and she said, “then you obviously shouldn’t do breath holds.” I said that was the smart answer, but not the curious one. Later that evening, I found the sheep paper linked above and got the full copy. I noted that I experienced the same risk time that the sheep did, after a period of higher serum CO2.

A week or so later, I’d had a very busy day and managed not to take my magnesium. Usually a trigger for me. The next noon, I went into afib during a phone call because of not taking the mag that day or the day before. I thought it was time for an experiment. I have an app on my phone (iPhisiometer iOS only or Camera HRV both IOS and Android) that, using the camera and light (Kardia device was at home), will show both pulse and pulse wave (which has a very different character in afib). I decided to turn on the app while I did very extended breath holds – exhale and then hold my breath out as long as possible. This converted me in one or two breath holds, which were in the 35 second range (I watched my pulse wave change as I did this). I should note, I’m sure my pCO2 was nowhere near what they gave the sheep. But it still worked. I was ecstatic as this was a nearly instant conversion, predicted by the data, with no medication!

EDIT - Liz recently reported she used this 3 times for successful conversions: <[www.afibbers.org]

So now the trick to test the remission theory is to significantly increase my serum CO2 permanently, but using more “gentle” techniques than strong breath holds.

The whole area of Buteyko Breathing is designed to do just this. There are also rebreathing devices, a mask, the Frolov and Samozdrav devices (available on eBay from Russia), Additionally, author John Douillard promoted using the glottis constriction on the outbreath during exercise (the outbreath part of ujjayi pranayama), never exercising harder than you could do while maintaining nasal breathing with glottis constriction. I’ve found I can do just about everything without causing a risk issue, except hard breath holds during exercise.

Summary for me:

1. strong breath holds during exercise created an afib risk period afterword for me as per the sheep paper.
2. a strong breath hold (or maybe two) was enough to convert me during an episode.
3. for the future, see if I can raise my steady state serum CO2 level to a point that it is protective

My benefits from these practices include a very large reduction in life long rhinitis, I no longer react to pollen or other allergens in the air, as well as the ability to almost never be out of breath. This includes skiing the steeps, off piste at 12,500’ (~3,800m) as well as HIIT Tabatas on a fan rower, breathing through my nose.

Serum CO2 devices and training references:

Frolov rebreathing device – can be purchased off eBay from Russia <[www.normalbreathing.com] I’ve made mine store more CO2 by cutting a 2L plastic bottle almost in half putting the Frolov device in it, putting the breathing tube out the top and taping the two halves back together. This device traps some of the CO2 from the end of your breath thereby increasing the CO2 in your next breath.

Samozdrav breathing device – also can be purchased on eBay from Russia. Same idea as the Frolov. <[www.normalbreathing.com]

Mask to wear at night, which will retain a bit of your exhaled CO2 <[humidiflyer.com]

PDF book about this training, sleep and apnea: < [www.snoring.ie]

First Five chapters of a training manual referencing a lot of the science behind this concept: <[www.normalbreathing.com]

Teacher Patrick McKeown has a number of books and several websites on breathing, including breathing for sport. Book, Oxygen Advantage <[www.amazon.com] His site and listing a lot of his podcasts: <[oxygenadvantage.com] and his YouTube channel <[www.youtube.com]


Teacher Dr Artour Rakhimov ‘s very extensive website: <[www.normalbreathing.com]



Edited 5 time(s). Last edit at 10/11/2020 04:44PM by GeorgeN.

I should also note that you can see apena in a tachogram - beat to beat heart rate vs time. There is a presentation on this using a tachogram from a Holter monitor. I noticed these apnea patterns in tachgrams in an overnight use of a recording (R to R) heart rate monitor. After taping my mouth at night and practicing the breathing exercises, my tachograms cleaned up nicely.

Here is a PPT on this: <[hrvlab.wustl.edu]



Edited 1 time(s). Last edit at 06/07/2018 06:45PM by GeorgeN.

Thank you so much for that info, George. It also confirms what i sort of experienced after holding my breath during my ultrasound (it didn't convert me but i noticed a difference on the monitor and also a lower HR) . A junior doctor said that breathing does have a connection with afib. The chief doctor dismissed this quite sharply and said that breathing has nothing to do with afib.

Thanks for posting. This is very interesting.
Thanks to Dr Natale my afib has been gone for several years.
I do try to raise my co2 level before doing something that causes high stress.
It really helps to keep the adrenaline levels under control.

George,

This is very interesting.

Would you think converting by exercising shares the same mechanism as holding breath?

I converted by exercising for the last two espies, the first episode I ran really hard then converted after stopping for about 1 minute. The 2nd episode, I ran really hard again, but didn't convert, then after resting for a few minutes, I ran again but with a much gentle pace, then converted after about 1 minute. Per my experience, both time converted after I felt really short of breath while running. Could the fast heart rate by exercising didn't actually convert the episodes but the short of breath (low O2 / hight CO2) ?

George,

Fascinating info.

I'm currently 220lb (6' 4" & 48' chest, 36" waist) and slowly heading back to 205lb where I will be (as I was 20 years ago) at a BMI of 25. I appreciate I still have some way to go after that, but at least - unlike most of my peer group - I'm going the right rather than the wrong way!

In 2008 I was 260lb and experienced a lot of OSA as witnessed by my then partner who noted that I sometimes (presumably she only noticed the times she was awake - and she is a heavy sleeper) totally stopped breathing for a while making what she described as 'hitching' noises before - after 20 to 30 seconds I'd let out an almighty gasp and start breathing vigorously. When I met my current partner I still occasionally did this at which time I was 10-15lb heavier than I am now. It seems for me that anything significantly over 225lb will give me a propensity towards - at least noticeable-by-my-bedmate - OSA.

More than this, I on rare occasions experience sleep paralysis where I'm lying on my front with my head stuffed into the pillow and in my head I become totally aware that I can't breathe but for a most unpleasant 20 or 30 seconds (I think, but could be less) I cannot physically rouse myself awake to do something about it! In my head I start trying to rock myself from side to side, imagine myself falling out of bed, shouting out etc. but to no avail until I suddenly come to gasping for breath.

I'd always thought that it was the O2 deprivation during OSA that precipitated AF, but notwithstanding the chronic atrial stretch (from years of OSA) that does predispose towards AF, it would from your own typically thorough analysis appear that it isn't the CO2 saturation and O2 deprivation during OSA that's the problem but the subsequent reversal once one starts rapidly breathing again afterwards.

I also have life-long nasal polyp issues (that my current partner - a surgeon herself - says I should get sorted out) and had my adenoids out as a child. All that said, I do have AF on my mother's side.... or maybe it's a genetic large uvula and sinus issues that predispose to AF! Overall I wouldn't put my predisposition towards AF entirely (or even anywhere near 50%) down to OSA (most people with OSA don't get AF....or then again maybe they do later in life where they might otherwise have not?) but that said OSA certainly sets the scene for nocturnal AF with 98% of my episodes this last 19 years having occurred between 1 and 6 am.

Maybe I need to get a SPO2 device and see what's really going on whilst I'm asleep OSA-wise. Bot then again my current partner is a very light sleeper and I'm fairly sure she'd notice any breathing difficulties. She's certainly very quick to prod me with her foot on the relatively rare occasions I start snoring! (usually after a bit too much alcohol and/or a late meal - both of are becoming increasingly less frequent lapses in self-discipline).

Part of me says I should get to a BMI of 22.5 and see if that dramatically reduces my nocturnal AF burden, but after nearly 20 years of PAF and episodes increasing in frequency this last year I'm thinking that an ablation sooner or later is still definitely the right way to go where I'm concerned.

Thanks again George,

Mike



Edited 1 time(s). Last edit at 06/08/2018 04:51AM by mwcf.

I am not an expert in this, but is seems to me this is pretty basic, that if one holds there breath during Exercise, creating an Acute Oxygen deprivation, that the Atria will stretch out. This can contribute greatly to having an AFIB episode.

The connection between elevated Serum CO2 levels and the effect that the Drug Flecainide is interesting.

Great post George,

So the next time I go into Afib I take a deep breath or 2 and hold for 30 seconds or as long as I can.

I must try it.

Quote
colindo
Great post George,

So the next time I go into Afib I take a deep breath or 2 and hold for 30 seconds or as long as I can.

I must try it.

NO!!!!

If you want to try this for conversion (also don't suggest this for those who aren't basically healthy), next time you go into afib, take a small breath in, a small breath out (repeating one or more times) then hold your breath out on the exhale. Hold for as long as possible. Repeat if needed.. What you are trying to do is accumulate CO2. Deep should mean using the diaphragm, but I'm guessing in your context means a large breath. We don't want to do this as it gets rid of more CO2. The whole purpose is to accumulate CO2..

George

Thanks, George for offering this very informative report.

Jackie

Quote
The Anti-Fib
I am not an expert in this, but is seems to me this is pretty basic, that if one holds there breath during Exercise, creating an Acute Oxygen deprivation, that the Atria will stretch out. This can contribute greatly to having an AFIB episode.

Though I wasn't wearing an SpO2 meter, I doubt if I was creating significant O2 depravation. Though it certainly can be done, in my case the exercise was actually very light. Just enough to increase CO2 production. Because I live at some altitude (5,500'), my SpO2 is normally a little anyway (94-96%). If I dropped it much below 90, I'd be surprised. I'm pretty sure the effect was the "rebound effect" after hypercapnia.

Quote
mwcf
George,

Fascinating info.

I'm currently 220lb (6' 4" & 48' chest, 36" waist) and slowly heading back to 205lb where I will be (as I was 20 years ago) at a BMI of 25. I appreciate I still have some way to go after that, but at least - unlike most of my peer group - I'm going the right rather than the wrong way!

In 2008 I was 260lb and experienced a lot of OSA as witnessed by my then partner who noted that I sometimes (presumably she only noticed the times she was awake - and she is a heavy sleeper) totally stopped breathing for a while making what she described as 'hitching' noises before - after 20 to 30 seconds I'd let out an almighty gasp and start breathing vigorously. When I met my current partner I still occasionally did this at which time I was 10-15lb heavier than I am now. It seems for me that anything significantly over 225lb will give me a propensity towards - at least noticeable-by-my-bedmate - OSA.

More than this, I on rare occasions experience sleep paralysis where I'm lying on my front with my head stuffed into the pillow and in my head I become totally aware that I can't breathe but for a most unpleasant 20 or 30 seconds (I think, but could be less) I cannot physically rouse myself awake to do something about it! In my head I start trying to rock myself from side to side, imagine myself falling out of bed, shouting out etc. but to no avail until I suddenly come to gasping for breath.

I'd always thought that it was the O2 deprivation during OSA that precipitated AF, but notwithstanding the chronic atrial stretch (from years of OSA) that does predispose towards AF, it would from your own typically thorough analysis appear that it isn't the CO2 saturation and O2 deprivation during OSA that's the problem but the subsequent reversal once one starts rapidly breathing again afterwards.

I also have life-long nasal polyp issues (that my current partner - a surgeon herself - says I should get sorted out) and had my adenoids out as a child. All that said, I do have AF on my mother's side.... or maybe it's a genetic large uvula and sinus issues that predispose to AF! Overall I wouldn't put my predisposition towards AF entirely (or even anywhere near 50%) down to OSA (most people with OSA don't get AF....or then again maybe they do later in life where they might otherwise have not?) but that said OSA certainly sets the scene for nocturnal AF with 98% of my episodes this last 19 years having occurred between 1 and 6 am.

Maybe I need to get a SPO2 device and see what's really going on whilst I'm asleep OSA-wise. Bot then again my current partner is a very light sleeper and I'm fairly sure she'd notice any breathing difficulties. She's certainly very quick to prod me with her foot on the relatively rare occasions I start snoring! (usually after a bit too much alcohol and/or a late meal - both of are becoming increasingly less frequent lapses in self-discipline).

Part of me says I should get to a BMI of 22.5 and see if that dramatically reduces my nocturnal AF burden, but after nearly 20 years of PAF and episodes increasing in frequency this last year I'm thinking that an ablation sooner or later is still definitely the right way to go where I'm concerned.

Mike

Mike,

I'd suggest you watch Patrick McKeown's presentation to the North American Association of Facial Orthotropics <[www.youtube.com]

With what you describe, I'm guessing your return to breathing may have been triggered by very low SpO2. People with a history of apena can develop a tolerance to CO2 and therefore have fairly high CP/BOLT scores (see my first post above). One of the reasons for airway collapse in OSA is excessive breathing volume - kind of like sucking hard on a paper straw, causing it to collapse. Hence the idea is to train yourself to breath very lightly when you are awake so that this will tend to carry over when you are asleep. Part of the reason for the paper tape on the mouth at night is to limit breathing volume. You can over breathe through your nose (I do), but usually much less than through the mouth, hence apnea is less likely. When breathing is light, the upper airway is less likely to get inflamed.

My overbreathing at night has diminished. When I have been overbreathing through the nose, one of my nostrils may be somewhat blocked when I wake up. A few minutes of just normal, but very light nose breathing (thereby increasing serum CO2) opens up both my nostrils now.

When I observe those around me, very many are obviously overbreathing. The sicker people are, the more they overbreathe, at least that is my perception.

George

George, If I'm understanding well, your technique was basically, inhaling then exhaling and then hold for as long as possible, correct?

Quote
GeorgeN
Quick look:
Serum CO2 lengthens ERP, and slows conduction
This may be why apnea creates a risk for afib (slowed conduction after the apnea).
There may be an opportunity to use this to convert episodes without meds (I did this).
There may be an opportunity to put afib in remission (speculation) by training the serum CO2 chemoreceptor to accept a much higher steady state level of CO2.
There appears to be an afib risk period after doing certain kinds of intense breath hold training to reset the CO2 chemorecptor (like apnea).

There has been much written 4x risk for afib (created by external stimulation) over baseline.

[scontent-ort2-1.xx.fbcdn.net]

It was hypothesized in the paper that afib apena risk came after the apnea episode, not during it.

It appears that if serum CO2 could be kept high all the time, it could be protective (my hypothesis). Likewise, it appears possible that a high level of serum CO2 could lengthen ERP sufficiently to terminate an episode. Also that increased serum CO2 followed by a return to baseline CO2 levels would increase afib risk for a period of time.

I searched for and found this paper because I inadvertently (and later intentionally) tested the above.

The breathing center has sensors for serum CO2 (or serum pH) and also O2. The urge to breathe is usually controlled by CO2, not O2. The level at which this triggers can be changed with training. This training periodically presents the sensor with higher levels of CO2 and it will eventually adapt (free divers are an endpoint here). A reason to do this is because of the Bohr effect. Christian Bohr, in 1904, discovered that higher levels of CO2 will weaken the bond of O2 to hemoglobin <[en.wikipedia.org]. This allows more O2 to get into the cells. So paradoxically, the more CO2 (to a point) in the serum the more O2 to the cells (also noted as a right shift in the hemoglobin-oxygen disassociation curve <[en.wikipedia.org] ). Conversely, overbreathing or hyperventilation will reduce oxygen to the cells.

I’ve practiced nasal breathing for many years. I also tape my mouth shut at night (using either 1” 3M Micropore Paper Hypoallergenic Surgical Tape or “Snoreless Tape <[correctbreathing.com] ) so I will nasal breathe during sleep (helps prevent apnea). My control pause (CP) or BOLT score (breath holding time) is OK but nothing to write home about <[www.normalbreathing.com] . Hence I decided to practice strong breath holding during exercise as a way to adapt the CO2 sensor to higher levels.

Three or four weeks ago, I went to the park at lunch and was doing fairly strong breath holds while jogging. Some time after returning to my office, I went into afib. This is very unusual for me. I went home, took flecainide and after a while, converted. Then several weeks later I was jumping rope at lunch, again coupled with fairly strong breath holds. Again went into afib some time after stopping. I started doing pullups on a door molding and converted the episode. When I went home, I told my wife and she said, “then you obviously shouldn’t do breath holds.” I said that was the smart answer, but not the curious one. Later that evening, I found the sheep paper linked above and got the full copy. I noted that I experienced the same risk time that the sheep did, after a period of higher serum CO2.

A week or so later, I’d had a very busy day and managed not to take my magnesium. Usually a trigger for me. The next noon, I went into afib during a phone call because of not taking the mag that day or the day before. I thought it was time for an experiment. I have an app on my phone (iPhisiometer iOS only or Camera HRV both IOS and Android) that, using the camera and light (Kardia device was at home), will show both pulse and pulse wave (which has a very different character in afib). I decided to turn on the app while I did very extended breath holds – exhale and then hold my breath out as long as possible. This converted me in one or two breath holds, which were in the 35 second range (I watched my pulse wave change as I did this). I should note, I’m sure my pCO2 was nowhere near what they gave the sheep. But it still worked. I was ecstatic as this was a nearly instant conversion, predicted by the data, with no medication!

EDIT - Liz recently reported she used this 3 times for successful conversions: <[www.afibbers.org]

So now the trick to test the remission theory is to significantly increase my serum CO2 permanently, but using more “gentle” techniques than strong breath holds.

The whole area of Buteyko Breathing is designed to do just this. There are also rebreathing devices, a mask, the Frolov and Samozdrav devices (available on eBay from Russia), Additionally, author John Douillard promoted using the glottis constriction on the outbreath during exercise (the outbreath part of ujjayi pranayama), never exercising harder than you could do while maintaining nasal breathing with glottis constriction. I’ve found I can do just about everything without causing a risk issue, except hard breath holds during exercise.

Summary for me:

1. strong breath holds during exercise created an afib risk period afterword for me as per the sheep paper.
2. a strong breath hold (or maybe two) was enough to convert me during an episode.
3. for the future, see if I can raise my steady state serum CO2 level to a point that it is protective

My benefits from these practices include a very large reduction in life long rhinitis, I no longer react to pollen or other allergens in the air, as well as the ability to almost never be out of breath. This includes skiing the steeps, off piste at 12,500’ (~3,800m) as well as HIIT Tabatas on a fan rower, breathing through my nose.

Serum CO2 devices and training references:

Frolov rebreathing device – can be purchased off eBay from Russia <[www.normalbreathing.com] I’ve made mine store more CO2 by cutting a 2L plastic bottle almost in half putting the Frolov device in it, putting the breathing tube out the top and taping the two halves back together. This device traps some of the CO2 from the end of your breath thereby increasing the CO2 in your next breath.

Samozdrav breathing device – also can be purchased on eBay from Russia. Same idea as the Frolov. <[www.normalbreathing.com]

Mask to wear at night, which will retain a bit of your exhaled CO2 <[humidiflyer.com]

PDF book about this training, sleep and apnea: < [www.snoring.ie]

First Five chapters of a training manual referencing a lot of the science behind this concept: <[www.normalbreathing.com]

Teacher Patrick McKeown has a number of books and several websites on breathing, including breathing for sport. Book, Oxygen Advantage <[www.amazon.com] His site and listing a lot of his podcasts: <[oxygenadvantage.com] and his YouTube channel <[www.youtube.com]


Teacher Dr Artour Rakhimov ‘s very extensive website: <[www.normalbreathing.com]