Cheyne stokes and periodic breathing, what can you tell me?

[vsheline]

My pattern of falling to sleep is characterized by a decreasing flow from about 90 ml/sec to 30 ml/sec and corresponding tidal volumes until I settle into more or less regular breathing. Then for no apparent reason, I start periodic breathing with about 7 breaths between minimum points nodes with the flow in fully developed periods from near 0 ml/sec to roughly 40 ml/sec. This will be followed by scored RERA's, then scored hypopneas and then scored CA's where after expiration, there is a cessation of breathing for a period of time. In between the major CA events there may be more periodic breathing. These clusters last about 45 minutes when they occur.

Hi Walt.

I think CSR observed during a diagnostic sleep study (PSG) without CPAP treatment is true CSR.

I think the CSR-like breathing pattern which some of us get with CPAP treatment (CPAP-induced CSR-like breathing pattern) is not necessarily "true" CSR, meaning only that it does not exist except when we are on CPAP and does not necessarily indicate the beginning of heart failure or any of the other major conditions associated with CSR when not induced by CPAP treatment.

I think some of us have fairly low heart rate or other conditions which, when combined with "CO2 washout" from CPAP therapy, can create PB or CSR-like breathing patterns, without us having any of the worrisome health conditions which can cause CSR breathing pattern when not induced by CPAP therapy.

[wolson]

I think some of us have fairly low heart rate or other conditions which, when combined with "CO2 washout" from CPAP therapy, can create PB or CSR-like breathing patterns, without us having any of the worrisome health conditions which can cause CSR breathing pattern when not induced by CPAP therapy.

Thank you for your answer.

That is consistent with one theory I have read regarding the causes of central apnea. Apparently, we have an "apnea threshold (AT)" for carbon dioxide in our blood that triggers us to take a breath during involuntary breathing such as during sleeping. The theory is that during central apnea, we go into a hypocapnea state (that is, a decreased blood oxygen state) which is lower than the AT thereby suppressing the need to take a breath.

Whereas CO2 seems to control the breathing rate, I have not yet found a theory that determines what the magnitude of intake is controlled by. During these periodic periods of breathing without CA's, my breathing rate seems more or less constant but the magnitudes of the breaths are changing. In otherwords, what controls our oxygen demand? I am still researching this.

Walt

[vsheline]

The theory is that during central apnea, we go into a hypocapnea state (that is, a decreased blood oxygen state) which is lower than the AT thereby suppressing the need to take a breath.

Hypocapnia means decreased blood carbon dioxide, not decreased blood Oxygen.

Whereas CO2 seems to control the breathing rate, I have not yet found a theory that determines what the magnitude of intake is controlled by.

I think it is the short term breathing *volume* (by which I mean a short term average of the Tidal Volume, averaged across a few breaths), not the breath *rate* which is regulated by blood CO2.

In other words, I think it is a closed-loop system where the amount of ventilation is regulated to maintain a consistent amount of CO2 in the blood.

During these periodic periods of breathing without CA's, my breathing rate seems more or less constant but the magnitudes of the breaths are changing. In otherwords, what controls our oxygen demand?

I think the Tidal Volume is being regulated by the varying concentration of CO2 in the blood which is reaching the brain center which controls the urge to breathe more deeply. There is a lag in the time we breathe more deeply until the decrease in CO2 reaches the brain, because the blood from the lungs first travels back to the heart and then travels to the brain. I think it is this lag in the feedback loop which most commonly causes Periodic Breathing or CSR-like pattern in CPAP users.

I think there are other mechanisms leading to PB and CSR, too, which I don't know much about, such as PB and CSR when the blood CO2 concentration is elevated, when perhaps the PB or CSR is caused by drugs or Traumatic Brain Injury or neural or lung or heart diseases/conditions.

Take care,
--- Vaughn

[wolson]

The theory is that during central apnea, we go into a hypocapnea state (that is, a decreased blood oxygen state) which is lower than the AT thereby suppressing the need to take a breath.

Hypocapnia means decreased blood carbon dioxide, not decreased blood Oxygen.

Thank you for correcting my inadvertant mistake... it should have read decreased CO2. My ability to proofread what I write is very suspect. I apologize if I confused anybody.

Controls Systems Engineers often see these types of responses where the gain in the control loop is raised too high. I wonder if anyone has performed an constructed a Root Locus or a Bode plot from lung test data ... it would answer several questions here and could probably be associated with/to lung physiology.

This is an interesting discussion for me in more than one way!

Walt

[vsheline]

Controls Systems Engineers often see these types of responses where the gain in the control loop is raised too high.

I have a tendency toward PB. In my case perhaps the gain is normal (don't know) but I have bradycardia and slow blood circulation, which I think adds delay in the feedback loop.

I haven't looked into it but I would guess various researchers have developed various models of our breathing regulation system. It would be interesting to see a control systems analysis.

[wolson]

Well found out I have COPD (mild) and they gave me an inhaler and day one I was sleeping great! and have been ever since.

All this really means is periodic breathing may not be that big of a deal. Doctor said that unless I was having 30-40 centrals an hour that it was not a big deal, for me he was right. As for CSR, I would suggest that you be very happy that you do not have CSR and get on with discovering the culprit that is keeping you from sleeping well. Is your COPD well treated? COPD and Sleep Apnea evidently interact with each other a lot.
.

About a year ago, I was having bronchitis and my doctor prescribed Symbicort for it. The bronchitis resolved and I quit taking the Symbicort. About a half year ago, my doctor asked me how the Symbicort did and if I was still using it. Of course I wasn't and nothing was said more about it. But I still have a Symbicort inhaler.

Symbicort is a prescribed COPD drug. So after reading your experience, I started the Symbicort again and the results were dramatic: my AHI was cut in half and much of the periodic breathing that I saw was gone. My CA' went from over 30 a night to 6 last night.

Looks like I should be using the Symbicort: something to bring up with my doctor!

Walt

[PoolQ]

Well that's sure good news! Congrats!

[richb]

...

Hi kameeleun,

I think your Flow pattern is predominantly obstructive. The slow variations which kinda look like Periodic Breathing may instead just be you in shallow sleep struggling (and succeeding) to breathe while your airway is nearly collapsed, sleeping but not restfully.

I suggest gradually raising the pressure, by 1 cm H2O per week for several weeks, while keeping an eye on your weekly AHI that it remains less than 5. If the pressure seems uncomfortably high, I suggest using EPR.

I suspect that by the time the pressure is gradually increased to 10 with EPR of 3, that you'll be feeling better and your Flow waveform will be more consistent.


Or, if your weekly average AHI starts increasing close to 5 because the CA events are increasing, try to reduce the EPR, because for some of us using EPR can increase the number of CAs we get.

If you can get used to higher pressures, increasing the pressure should eventually eliminate the obstructive breathing, unless you have UARS and need a bilevel CPAP machine, which is probably not needed.

Take care,
--- Vaughn

Hi kameeleun,

I have to agree that Vaughn has a good approach on this one. A pressure of 6 is not quite theraputic for Obstructive apnea. Gradually increasing the pressure and adding some EPR might just regulate your breathing pattern. It is very difficult to score the difference between types of hypopneas during a PSG. Higher pressures will tell if what you are experiencing is the result of obstructive or central problems. Keep us informed.

Rich