Sleep disordered breathing

Significant physiologic changes in breathing take place during normal sleep related to alterations in respiratory drive and musculature.

Set point of ventilation is different in wakefulness and sleep. pCO2 is higher and ventilation is lower in sleep. Sleep onset in normal subjects is not immediate, but oscillates between arousal, stage I and II sleep before steady NREM sleep is obtained. So falling asleep results in decreased ventilation and a higher pCO2, above the wakefulness set point. On wakefulness, this constitutes an error signal which provokes hyperventilation until the wakefulness set point is reached. When the subject falls asleep, ventilation decreases and pCO2 rises, resulting in hypoventilation or even apnea. These oscillations continue until steady state sleep is obtained. The medulla oblongata controls our respiration.

Breathing is remarkably regular, both in amplitude and frequency in steady NREM sleep. Steady NREM sleep has the lowest indices of variability of all sleep stages. Minute ventilation decreases by 13% in steady stage II sleep and by 15% in steady slow wave sleep (Stage III and Stage IV sleep). Mean inspiratory flow is decreased but inspiratory duration and respiratory cycle duration are unchanged, resulting in an overall decreased tidal volume.

In a study of 19 healthy adults, the minute ventilation in NREM sleep was 7.18 ± 0.39(SEM) liters/minute compared to 7.66 ± 0.34 liters/minute when awake.

Rib cage contribution to ventilation increases during NREM sleep, mostly by lateral movement, and is detected by an increase in EMG amplitude during breathing. Diaphragm activity is little increased or unchanged and abdominal muscle activity is slightly increased during these sleep stages.

Airway resistance increases by about 230% during NREM sleep. Elastic and flow resistive properties of the lung do not change during NREM sleep. The increase in resistance comes primarily from the upper airway in the retroepiglottic region. Tonic activity of the pharyngeal dilator muscles of the upper airway decreases during the NREM sleep, contributing to the increased resistance, which is reflected in increased esophageal pressure swings during sleep. The other ventilatory muscles compensate for the increased resistance, and so the airflow decreases much less than the increase in resistance.

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