Anyone aware of bradypnea (slow breathing rate) or CO2 issue?

ryan31337

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Hi all,

Has anyone had treatment for respiratory issues in relation to their ME/CFS? I'm aware Breakspear clinic have prescribed O2/CO2 therapy to some patients, curious if any here could share their experience?

I've had some awareness of breathing issues over the years, stuff like: excessive yawning & sighing, 'forgetting' to breathe and gasping (both awake & asleep) and odd habits like holding breath and exhaling slowly & forcefully without realising - much to the annoyance of others! A recent positive tilt table test really gave me a clear indication of shortness of breath during pre-syncope too, I had a really dramatic desire to breathe excessively deeply, something I have experienced from time to time previously without associating. I don't think any of this is particularly unusual in ME/OI circles.

However, yesterday I had a CPET and the physiologist couldn't believe that I wasn't actively slowing my breathing, apparently I was doing ~6 breaths per minute during the low intensity phase, which was considerably less than her whilst she was just standing there. I'm generally comfortable breathing 4x times a minute at rest, if I meditate this will drop to 3x or lower. Apparently <12x is Bradypnea...who knew :woot:

I assumed this would just be related directly to dysautonomia in some unhelpful way, but having seen the list of potential causes for bradypnea like hypertension, electrolyte imbalance, hypothyroidism etc. perhaps there's more to be done. Its quite fascinating seeing the implications of low CO2 as well, vasoconstriction, hypoperfusion etc...
 
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I've had episodes of inexplicable yawning attacks, air hunger, and pretty consistent bradypnea without forceful exhalation. My breathing tends to especially slow down when I'm laid out with PEM, yet despite not breathing notably deeply, never seems to leave me gasping for air. I wouldn't be surprised if I only do breath 6-8 times per minute on average.

In my case, I also have a heart rate in the 40s most of the time.

Bradypnea, and more likely the autonomics factors that precipitate it, are also associated with central sleep apnea. You describe central sleep apnea in your 2nd paragraph.
 

leokitten

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Hi @ryan31337 yes definitely yes! I just posted on this symptom as I’ve had it since getting ME. My breathing rate is significantly slower than normal and compared to what it used to be. I breathe a lot slower than my spouse and didn’t used to. I don’t have any breathing issues though aside from the ME causing me breathing rate to slow down.
 

pattismith

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My resting respiratory rate is 6-7 breaths per minute. Far slower than the adult normal of 12-20.
Hello @leokitten

did you investigate your bradypnea issue?

I realised I have bradypnea after I checked my blood gas (I have moderate hypercapnia = high CO2 and my blood bicarbonates are at the higher limit).

My breathing rate is less than 12 (8 to 10 at rest), but it's normal when I take methylphenidate.

Bradypnea and hypoventilation can happen with hypothalamic or brainstem dysfunction, but myopathy can also weaken the respiratory muscles and cause it. In these cases, hypoventilation/hypercapnia lead to a chronic respiratory acidosis with a compensatory increase of bicarbonate by kidneys.

A decrease ability of kidneys to excrete bicarbonate can also be involved , or a compensatory attempt to correct some intracellular acidity. In these two cases, The bradypnea is a compensatory effect for a chronic metabolic alkalosis.

I think for those with breathing anomalies, it's important to investigate all the possible causes and to find it before any event may break the frail compensated pH equilibrium we have.

Up to now, I didn't find any doctor interested in my blood result, but i just recently realised my low breath rate, maybe I will have more chance to get a doc looking into it?

Most of the time docs only get interested when you are in a very bad shape with an acute acidosis or alkalosis, and I wish to avoid it at all cost!

@ryan31337 did you investigate more on this issue? Did you check if you have a kind of breathing abnomaly like these ones:

Cheyne Stokes Breathing and Other Abnormal Respiration (healthline.com)
..
 
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pattismith

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Interesting to note that in this study (children with central apnea), they didn't find correlation with brainstem anomaly at MRI.

I remember Jen Brea (who was suffering with brainstem compression because of craniocervical instability) was explaining she could experience central apnea when her head was turned in some way.
I wonder if they looked for craniocervical instability?

@JenB


Robert C. Stowe, MD
,
Monica Miranda-Schaeubinger, MD, MSPH
,
Savvas Andronikou, MBBCh, PhD
,
Ignacio E. Tapia, MD, MS

Published Online:July 1, 2021https://doi.org/10.5664/jcsm.9210



Abstract

STUDY OBJECTIVES:

Evaluation of elevated central apnea-hypopnea index (CAHI) or prolonged central apneas in pediatric patients typically includes neuroimaging with a focus on brainstem pathology.
There is little evidence guiding thresholds of polysomnographic variables that accurately predict abnormal neuroimaging.
We sought to evaluate whether additional polysomnographic variables may help predict brainstem pathology.

METHODS:

A 10-year retrospective review of patients ages 1–18 years who received a brain magnetic resonance imaging (MRI) for an indication of central sleep apnea diagnosed via polysomnography was performed. Demographics, medical history, polysomnogram variables, and MRI results were compared.

RESULTS:

This study included 65 patients (69.2% male). The median age was 5.8 years (interquartile range, 3.0–8.3). Most patients had negative (normal or nonsignificant) MRIs (n = 45, 69.2%); 20 (30.8%) had abnormal MRIs. Of the patients with abnormal MRIs, 13 (20.0%) had abnormalities unrelated to the brainstem. Seven patients (10.8%) were found to have brainstem pathology and had a median CAHI of 10.8 events/h (interquartile range, 6.5–21.9), and three of seven (42.9%) had hypoventilation and were more likely to have developmental delay, abnormal neurological examinations, and reflux. Other patients (n = 58) had a median CAHI of 5.6 events/h (interquartile range, 3.1–9.1), and seven (12.1%) had hypoventilation. Area under the curve and receiver operating characteristic curves showed a CAHI ≥ 9.5 events/h and ≥ 6.4% of total sleep time with end-tidal CO2 ≥ 50 mm Hg predicted abnormal brainstem imaging. Prolonged central apneas did not predict abnormal brainstem imaging.

CONCLUSIONS:

Most patients with central sleep apnea do not have MRIs implicating structurally abnormal brainstems.

Utilizing a cutoff of CAHI of ≥ 9.5 events/h, ≥ 6.4% total sleep time with end-tidal CO2 ≥ 50 mm Hg and/or frank hypoventilation, and additional clinical history may optimize MRI utilization in patients with central sleep apnea.