The Importance of Carbon Dioxide for Sleep-Disordered Breathing

Key Points

• Sleep-disordered breathing is common, even among healthy individuals

• The normal inputs to and reflexes of the respiratory system are dampened during sleep

• Added carbon dioxide (CO2) might be the best treatment for sleep-disordered breathing

The Breathing Diabetic Summary

Sleep-disordered breathing is common, even among healthy individuals. As we have discussed before, breathing during sleep is shallow and irregular. Not exactly what we would expect. But, the word “disordered” could be a misconception. It is only disordered relative to wakefulness. It might be completely normal for sleep.

I digress. This paper examines the mechanisms behind sleep-disordered breathing at large, and for more serious issues such as central sleep apnea.

Our normal breathing system does not work correctly during sleep. For example, while awake, our bodies do amazing things to make sure blood gases stay within a specific range and that the breathing muscles do as little work as possible.

During sleep, however, we commonly experience respiratory acidosis. Additionally, the upper airways often get narrower because the breathing muscles are not recruited in the same way they are while awake. Thus, both chemical and mechanical breathing deficiencies occur during sleep.

There are several reasons for these deficiencies.

To begin with, sleep reduces input to the breathing muscles. This reduction causes the airways to narrow (these muscles act to keep them open) and increases breathing resistance.

Sleep also reduces chemoreflexes, meaning that your body is less sensitive to high CO2 and low O2. This can cause respiratory acidosis or blood gas imbalance.

On the more severe side, many patients with central apnea syndrome have chronic hypocapnia (low CO2), which might predispose them to apnea. For example, if you are chronically low on CO2, your body might try to compensate for this during sleep. It might compensate by reducing breathing or even stopping it. (That’s my speculation, not the paper’s.)

So, what does all of this mean for you? Interestingly, this “Sleep and Breathing State-of-the-Art Review” concludes that CO2 might be the best treatment for SDB. Added CO2 will stimulate the respiratory muscles and therefore prevent narrowing of the upper airways. Additionally, CO2 is a smooth muscle dilator, which will help increase blood flow to the muscles.

There are two simple ways we can “add” our own CO2 tonight. First, you can tape your mouth while sleeping. This will reduce breathing volume and increase CO2. Paradoxically, nose breathing also reduces upper airway resistance during sleep, while it increases breathing resistance during the day.

Second, we can practice light breathing during the day, and before sleep, to increase our tolerance to CO2. By doing this consistently, we can reset our baseline CO2 back to normal values and improve our breathing during sleep. 

Abstract

We present a view of the neuromechanical regulation of breathing and causes of breathing instability during sleep. First, we would expect transient increases in upper airway resistance to be a major cause of transient hypopnea. This occurs in sleep because a hypotonic upper airway is more susceptible to narrowing and because the immediate excitatory increase in respiratory motor output in response to increased loads is absent in non-REM sleep. Secondly, sleep predisposes to an increased occurrence of ventilatory "overshoots", in part because abruptly changing sleep states cause transient changes in upper airway resistance and in the gain of the respiratory controller. Following these ventilatory overshoots, breathing stability will be maintained if excitatory short-term potentiation is the prevailing influence. On the other hand, apnea and hypopnea will occur if inhibitory mechanisms dominate following the ventilatory overshoot. These inhibitory mechanisms include: a) hypocapnia-if transient, will inhibit carotid chemoreceptors and cause hypopnea, but if prolonged will inhibit medullary chemoreceptors and cause apnea; b) a  persistent inhibitory effect from lung stretch; c) baroreceptor stimulation, from a transient rise in systemic blood pressure immediately following termination of apnea or hypopnea may partially suppress the accompanying hyperpnea; d) depression of central respiratory motor output via prolonged brain hypoxia. Once apneas are initiated, reinitiation of inspiration is delayed even though excitatory stimuli have risen well above their apneic thresholds, and these prolonged apneas are commonly accompanied by tonic EMG activation of expiratory muscles of the chest wall and upper airway.

Journal Reference:

Dempsey JA, Smith CA, Harms CA, Chow C, Saupe KW.  Sleep-Induced Breathing Instability.  Sleep.  1996;19(3):236-47.

Breathing becomes shallower and lighter when falling asleep

Key Points

• CO2 increases significantly prior to or simultaneously with sleep onset

• Breathing becomes shallower with sleep onset

• Breathing rate does not change with sleep onset

The Breathing Diabetic Summary

We have reviewed several studies on sleep and breathing (here, here, and here).  However, we have not looked at how breathing changes as we fall asleep.  This study sheds light on central nervous system changes occurring during sleep onset.

Four women and 8 men that had no history of respiratory or sleep disorders were studied. They were instructed to relax in a reclined bed in the dark and go to sleep for ~1 hour.  Five of the subjects also were asked to relax in the bed, but stay awake for 45 minutes for control measurements.

(This is a very small sample size, so let’s remember that as we go through the results.)

Measurements of alveolar CO2 and chest and abdominal breathing motions were taken to reflect central nervous system changes during sleep onset.  Breathing rate also was measured.  The subjects went through 3 separate sessions to acclimate to the laboratory setting.

During all three sessions, when the participants fell asleep, their CO2 rose significantly and their breathing became shallower.  The significant increase in CO2 was not associated with a change in breathing rate.  This implies that breathing became not only shallower, but also lighter.

In every case, CO2 rose and breathing became shallower either prior to or simultaneously with falling asleep.  And because breathing rate did not change, the rise in CO2 indicates that the subjects were breathing less.

The close correlation between CO2, shallow breathing, and sleep onset indicates that breathing patterns might be a reliable indicator of drowsiness in a person.

Abstract

This study provides a systematic examination of factors that may contribute to respiratory changes associated with sleep onset. The electroencephalogram, alveolar CO2 tension, patterns of abdominal and thoracic respiratory movements, and respiratory rate were measured in three sessions each on 12 normal subjects as they fell asleep, and also on 5 of them as they lay awake. Nonintrusive respiration measurement devices were used. Resting awake CO2 tension was found to increase significantly across sessions. In addition, CO2 tension was significantly higher during stages 1 and 2 of sleep than during wakefulness on days 2 and 3. There was also a shift from relatively greater abdominal expansion toward relatively greater thoracic expansion with sleep onset. None of these changes occurred when subjects remained awake during a session. We conclude that changes in respiration with sleep onset cannot be accounted for solely by changes due to habituation, merely lying quietly, or the effects of the measuring devices. Rather, they appear to be caused by a central interaction between centers controlling the level of wakefulness and those controlling respiration.

Journal Reference:

Naifeh KH, Kamiya J.  The nature of respiratory changes associated with sleep onset.  Sleep.  1981;4(1):49-59.

Your breathing is shallow and irregular for 1/3 of your life

Key Points

• Breathing volume decreases between 6% and 16% during sleep

• Breathing is shallow and irregular during sleep

• We experience relative hypoxia and hypercapnia during sleep

The Breathing Diabetic Summary

To understand sleep-related breathing disorders, we first have to understand normal breathing during sleep.  That was the goal of this study.

Experiments were conducted with 19 subjects (8 males, 11 females) that had no history of sleep complaints.  Additionally, they were all nocturnal sleepers.  The researchers studied them between 10 PM and 7 AM.  They studied one subject on 3 nights, 9 subjects on 2 nights, and 9 subjects on 1 night.

Baseline measurements were obtained while the patients were lying in bed either before falling asleep or after waking up (using EEG-confirmed wakefulness).  Theses recordings were subsequently averaged to produce the “awake” value. 

For measurements of breathing during different sleep stages, the subjects had to stay in that sleep stage continuously for at least 2 minutes.  Additionally, there could not be any detectable leaks within the breathing mask they were wearing.

Comparison of the awake versus sleeping parameters revealed that breathing volume reduced significantly during sleep.  For non-REM sleep, breathing volume decreased between 6% and 8%.  During REM sleep, ventilation reduced by ~16%.  Interestingly, the breathing rates of these subjects were slightly faster during sleep than while awake, suggesting that breathing becomes shallower during sleep.

Because the participants were breathing less, they became significantly more hypoxic (low O2) and hypercapnic (high CO2) while asleep compared to while awake.

The researchers used this information, along with assumptions regarding lung dead space and dead space due to the breathing mask, to estimate the change in gas exchange occurring in the lungs.  These calculations revealed a reduction in gas exchange between 19% and 39% during sleep, helping explain why the participants experienced hypoxia and hypercapnia.

Lastly, during non-REM sleep, breathing rates were somewhat regular (although a few patients still showed irregular rates during non-REM).  In REM sleep, all participants exhibited shallow and irregular breathing patterns. 

Overall, these results show that breathing volume is reduced during all stages of sleep. The greatest reductions occur during REM sleep, which is also when breathing rate is the most irregular and unstable. The reduction in breathing leads to relative hypoxia and hypercapnia. Interestingly, these breathing patterns are normal and are part of the natural physiological changes our bodies makes during sleep.

Abstract

Respiratory volumes and timing have been measured in 19 healthy adults during wakefulness and sleep. Minute ventilation was significantly less (p less than 0.05) in all stages of sleep than when the subject was awake (7.66 +/- 0.34(SEM) 1/min), the level in rapid-eye-movement (REM) sleep (6.46 +/- 0.29 1/min) being significantly lower than in non-REM sleep (7.18 +/- 0.39 1/min). The breathing pattern during all stages of sleep was significantly more rapid and shallow than during wakefulness, tidal volume in REM sleep being reduced to 73% of the level during wakefulness. Mean inspiratory flow rate (VT/Ti), an index of inspiratory drive, was significantly lower in REM sleep than during wakefulness or non-REM sleep. Thus ventilation falls during sleep, the greatest reduction occurring during REM sleep, when there is a parallel reduction in inspiratory drive. Similar changes in ventilation may contribute to the REM-associated hypoxaemia observed in normal subjects and in patients with chronic obstructive pulmonary disease.

Journal Reference:

Douglas NJ, White DP, Pickett CK, Weil JV, Zwillich CW.  Respiration during sleep in normal man.  Thorax.  1982;37(11):840-844.

Our somewhat unusual breathing patterns during sleep

Key Points

• Breathing volume is reduced by as much as 16% during sleep

• Breathing rate is variable during sleep, especially in REM

• Hypoxic and hypercapnic responses are reduced by as much as 66% during sleep

The Breathing Diabetic Summary

We spend approximately 1/3 of our life sleeping.  And although sleep science is still relatively new, it’s undeniable that sleep is a key component of achieving optimal health.  Which begs the question, if sleep is so restorative, what is happening to our breath during this time?

Published in 1984, this review study found that breathing is significantly reduced during all stages of sleep.  This reduction can be as great as 16%.

Somewhat surprisingly, our breathing rate is extremely variable during sleep.  I expected that our breathing would become rhythmic and deep.  However, research shows that the opposite is true.  We breathe shallower and our breathing rate remains the same, or even increases slightly.

Additionally, it differs for different stages of sleep.  During non rapid eye movement sleep (non-REM), our breathing volume reduces and we sometimes achieve a steady rhythm.  In REM sleep, however, our breathing volume reduces even more, but our rate becomes more sporadic.

We also experience relative hypoxia (low O2) and hypercapnia (high CO2).  In fact, our tolerance to CO2 increases dramatically.  One study suggested that during non-REM, CO2 tolerance increases by ~33%.  During REM sleep, it increases by about 66%.  That’s fairly remarkable.

So, to summarize, here is what happens to breathing during sleep:

• Breathing volume reduces

• Breathing rate is variable

• Hypoxic and hypercapnic responses are reduced

The processes occurring during sleep clearly serve a purpose in restoring health.  If we interrupt these processes, we will not harness the full power of sleeping.

Therefore, if you are breathing with an open mouth during sleep, you are probably breathing too much and not supporting restorative sleep.Luckily, it’s an easy fix.Simply taping your mouth at night is the first step toward achieving optimal breathing volumes during sleep.

Journal Reference:

Douglas NJ.  Control of Breathing during Sleep.  Clin Sci (Lond).  1984;67(5):465-471.