The minute ventilation is reduced compared to NREM sleep and wakefulness _[9], and the arterial Pco₂ rises by 2–5mmHg. Arousal in response to stimulation from mechanoreceptors in the lungs, airways and chest wall, cough receptors and chemoreceptors occurs at a higher threshold in REM sleep than in NREM sleep.

The ventilatory responses to hypercapnia and hypoxia are reduced to a greater extent in REM than in NREM sleep and the combination of a reduction in reflex responsiveness and irregular cerebral cortical activity leads to an erratic and unpredictable pattern of respiratory activity. This appears to be due to multiple semi-independently functioning respiratory pacemakers in the pontine reticular formation _[10].

Central apnoeas are more frequent and prolonged during REM sleep if other factors such as sleep deprivation, chronic hypercapnia, alkalosis, sedative drugs or alcohol are present. The respiratory frequency is not related to perceived physical activity during dreams, but is greater than in NREM sleep. The tidal volume and frequency both vary considerably in REM sleep. The intervals between respirations may be sufficiently prolonged to be classified as central sleep apnoeas according to the conventional criterion of a lack of airflow for 10s or more.

The intense supraspinal inhibition of motor activity in REM sleep contributes to the reduction in reflex responsiveness and is manifested by a reduction in tone in the postural muscles, including all the respiratory muscles except the posterior crico-arytenoid muscles which abduct the vocal cords and maintain glottic patency, the diaphragm and to a lesser extent the parasternal intercostal muscles. Respiration becomes virtually dependent on diaphragmatic function and, if this is impaired, ‘central’ sleep apnoeas and hypoventilation appear.

Selective sparing of diaphragm activity in REM sleep leads to abdominal expansion increasing relative to the rib cage expansion. Loss of activity in the other chest wall muscles alters the compliance of the chest wall so that the functional residual capacity falls.

This not only reflexly reduces the upper airway dimensions, but worsens ventilation and perfusion matching, reduces lung compliance and reduces the volume of the stores of oxygen in the lungs.

In REM sleep there is little tone in the upper airway dilator muscles and their reactivity to reflexes generated by negative pressure in the upper airway is reduced. The upper airway resistance rises, increasing the work of breathing, and may lead to closure of the airway and obstructive sleep apnoeas.

References