Normal Sleep and Respiration

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Many neurophysiologic changes occur during sleep. Normal sleep has complex architecture, with several stages of non-REM sleep alternating with periods of REM sleep. Each sleep stage is defined by characteristic electrophysiologic patterns. Normal sleep begins with a progression from light (stage 1) through deep (stages 3 and 4) non-REM sleep, which is also called slow wave sleep due to the slow (low frequency), highly synchronized electrical activity recorded over the brain cortex by surface electroencephalography (EEG). REM sleep follows the non-REM sleep period, and this cycle is repeated several times a night. Except for the diaphragm, there is generalized skeletal muscle atonia in REM sleep. However, the REM sleep EEG resembles the EEG of wakefulness. Rapid eye movements on the electrooculogram (EOG) and skeletal muscle atonia on chin electromyography (EMG) recordings help identify REM sleep. REM sleep is also known as dream or paradoxical sleep because the brain cortex is active but the somatic musculature is inactive.

Important changes in respiration occur during sleep. Ventilation declines and arterial carbon dioxide increases, despite a lower metabolic rate during sleep. Although respiratory drive may decline during sleep, the sleep-related fall in alveolar ventilation may be better explained by sleep-related changes in upper airway mechanics. For instance, with sleep onset, partial pharyngeal collapse causes an increase in inspiratory resistance. Hypoventilation results if this added resistive “load” is not compensated for by increased respiratory effort.

It is not fully understood why the human pharynx partially collapses during normal sleep. In humans, the pharynx is unsupported by rigid structures and depends on muscle forces to maintain patency. Muscle groups that influence pharyngeal patency include the geniohyoid, genioglossus, and tensor veli palatini muscles, controlling the hyoid, tongue, and palate regions, respectively. These muscles are activated slightly before and in synchrony with the diaphragm, presumably to prepare the collapsible pharynx for the inspiratory fall in intraluminal pressure generated by diaphragm contraction. In contrast to the diaphragm, however, most upper airway muscles are less active during sleep, which may render the pharynx more collapsible. Sleep-associated changes in the relative timing and force of upper airway versus thoracic muscle activation could account for the increase in upper airway resistance.

Ventilation during sleep is also more dependent on autonomic carotid and brain stem chemoreceptor control systems because of the loss of awake behavioral input. Because cortical influences are diminished, compensatory responses to perturbations such as partial pharyngeal collapse are slower during sleep than during wakefulness.

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