Key points

  • During normal sleep tidal volume is reduced, with maximal reduction in ventilation occurring during rapid eye movement sleep when breathing also becomes irregular.

  • Reduction in the speed and strength of pharyngeal muscle reflexes causes increased airways resistance, leading to snoring in many normal individuals.

  • Sleep-disordered breathing describes a continuum of abnormalities ranging from occasional snoring to frequent periods of airway obstruction and hypoxia during sleep.

Normal sleep

Sleep is classified on the basis of the electroencephalogram (EEG) and electro-oculogram (EOG) into rapid eye movement (REM) and non-REM (stages N1–N4) sleep.

Stage N1 is dozing, from which arousal easily takes place. The EEG is low voltage, and the frequency is mixed but predominantly fast. This progresses to stage N2 in which the background EEG is similar to stage N1 but with episodic sleep spindles (frequency 12–14 Hz) and K complexes (large biphasic waves of characteristic appearance). Slow, large-amplitude (delta) waves start to appear in stage N2, but become more dominant in stage N3 in which spindles are less conspicuous and K complexes become difficult to distinguish. In stage N4, which is often referred to as deep sleep, the EEG is mainly high voltage (more than 75 μV) and more than 50% slow (delta) frequency.

REM sleep has quite different characteristics. The EEG pattern is the same as in stage N1, but the EOG shows frequent rapid eye movements that are easily distinguished from the rolling eye movements of non-REM sleep. Skeletal muscle tone generally decreases, and dreaming occurs during REM sleep.

The stage of sleep changes frequently during the night, and the pattern varies between different individuals and on different nights for the same individual ( Fig. 14.1 ). Sleep is entered in stage N1 and usually progresses through stage N2 to N3 and sometimes into stage N4. Episodes of REM sleep alternate with non-REM sleep throughout the night. On average there are four or five episodes of REM sleep per night, with a tendency for the duration of the episodes to increase towards morning. Conversely, stages N3 and N4 predominate in the early part of the night.

• Fig. 14.1, Patterns of sleep on three consecutive nights in a 20-year-old fit man. The thick horizontal bars indicate rapid eye movement (REM) sleep.

Respiratory changes

Ventilation

Tidal volume decreases with deepening levels of non-REM sleep and is minimal in REM sleep, when it is about 25% less than in the awake state. Respiratory frequency is generally unchanged, although breathing is normally irregular during REM sleep. Minute volume is progressively reduced in parallel with the tidal volume. These changes in ventilation are brought about by the same neurochemical changes that cause sleep. Increased activity of gamma aminobutyric acid (GABA)-secreting neurones during sleep has a direct depressant effect on the respiratory centre (see Fig. 4.4 ), and activation of cholinergic neurones is thought to be responsible for the respiratory patterns seen during non-REM sleep.

Arterial P co 2 is usually slightly elevated by about 0.4 kPa (3 mmHg). In the young healthy adult, arterial P o 2 decreases by about the same amount as the P co 2 is increased, therefore the oxygen saturation remains reasonably normal. The rib cage contribution to breathing (page 63) is close to the normal awake supine position value of 29% during REM sleep, but increases during non-REM stages.

Chemosensitivity

In humans, the slopes of the hypercapnic and hypoxic ventilatory responses are markedly reduced during sleep. In both cases, the slope is reduced by approximately one-third during non-REM sleep, and even further reduced during REM sleep, but fortunately the responses are never abolished completely.

Effect of age

Compared with young subjects, the elderly have more variable ventilatory patterns when awake, which seems to result in more episodes of breathing instability and apnoea when asleep. Elderly subjects also have significant oscillations in upper airway resistance during sleep (see later), which may contribute to the observed variations in ventilation. Thus as age advances, episodes of transient hypoxaemia occur in subjects who are otherwise healthy, with saturations commonly falling to as low as 75% during sleep. Such changes must be regarded as a normal part of the ageing process.

Pharyngeal airway resistance

Air flow through the sharp bends of the upper airway is normally laminar, but is believed to be very close to becoming turbulent even in normal subjects. Pharyngeal muscles may play a crucial role in maintaining the optimum shape of the airway to maintain laminar flow, and the speed at which these control mechanisms can respond to changes in pharyngeal pressure (page 59) may be critical. Any condition that attenuates or delays these reflexes even slightly, such as sleep or alcohol ingestion, will then have a major effect on air flow in the pharynx, causing breakdown of the normally laminar flow.

The nasal airway is normally used during sleep, and upper airway resistance is consistently increased, especially during inspiration and in REM sleep. The main sites of increase are across the soft palate and in the hypopharynx. Changes in pharyngeal muscle activity with sleep are complex. Muscles with predominantly tonic activity, such as the tensor palati, show a progressive decrease in activity with deepening non-REM sleep, reaching only 20% to 30% of awake activity in stage N4 sleep. This loss of tonic activity correlates with increased upper airway resistance. Unlike in the awake state, the tensor palati also fails to respond to an inspiratory resistive load. The activity of muscles with predominantly phasic inspiratory activity (e.g., geniohyoid and genioglossus) is influenced little by non-REM sleep. In spite of maintained phasic activity during non-REM sleep, tonic activity of geniohyoid is reduced, whereas that of genioglossus is well-preserved and responds appropriately to resistive loading. It thus appears that the major effect is upon the tonic activity of nasopharyngeal muscles, and the increase in hypopharyngeal resistance seems to be because of secondary downstream collapse.

The ventilatory response to increased airway resistance is important in normal sleep because of the increased pharyngeal resistance and is generally well preserved. There are substantial and rapid increases in both diaphragmatic and genioglossal inspiratory activity following nasal occlusion in normal sleeping adults.

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here