Sleep apnoea (or sleep-disordered breathing) is common, with a vast potential for improvement in quality of life. It is caused by obstruction of the upper airways (obstructive sleep apnoea), and more rarely central sleep apnoea (CSA), where the central control of ventilation is disturbed. It can lead to significan sleep deprivation and fragmentation and thus daytime hypersomnolence (sleepiness), with consequent decreased quality of life, mental and physical performance, and increased risk of accidents and cardiovascular disease, such as hypertension. Sleep-disordered breathing is diagnosed using polysomnography (Fig. 44a), which records the electroencephalography (EEG) for sleep patterns, movements of abdomen and thorax to assess breathing, oronasal f ow and oximetry for O2 saturation. Normal sleep (Fig. 44a) consists of rapid eye movement (REM, ̴25%) and non-rapid eye movement (NREM) sleep. REM sleep is characterized by an awakepattern EEG, voluntary muscle atonia and dreaming. Ventilatory drive is normally diminished in REM sleep, causing a slight fall in Pao2 and a rise in Paco2. Sleep apnoea is associated with multiple periods of hypoxaemia and partial awakenings (Fig. 44b and c).
Obstructive sleep apnoea
Obstructive sleep apnoea (OSA) is characterized by absence of airflow with continued respiratory effort (Fig. 44b). About 90% of patients with sleep apnoea have OSA. OSA is far more common in males than females, and is associated with alcohol consumption, increasing age, obesity, increased neck circumference, hypertension and hypothyroidism. Obstruction typically occurs in the upper airway and pharynx, and is related to the normal decrease in upper airway muscle tone that occurs in REM sleep coupled with narrowing of the pharyngeal airways due to obesity or enlarged tonsils. Neuromuscular disease (e.g. stroke) and muscle relaxants (e.g. alcohol and sedatives) may further reduce upper airway muscle tone. These factors, in conjunction with individual anatomy and posture, result in airway obstruction during inspiration, when airway pressure is reduced (Fig. 44d).
Apnoea resolves with arousal and restoration of muscle tone. Al-though hundreds or thousands of episodes of apnoea and arousal may occur each night in severe cases, patients are often unaware of them; sleep partners commonly report loud snoring, snorting or apnoea. Patients commonly report unrefreshing sleep and nocturia, develop daytime hypersomnolence and gain weight, and may show pedal oedema, nasal congestion, enlarged tongue, shallow palate, enlarged uvula or retrognathia. Most patients have normal arterial blood gases and haemoglobin. In chronic obstructive pulmonary disease (COPD), nocturnal hypoxia can be severe even with mild OSA, as gas exchange is already compromised.
Polysomnography reveals repeated episodes of OSA or hypopnoea (reduced airfl w with oxygen desaturation or arousal), which terminate with arousal (Fig. 44b). These episodes are quantifie by the apnoea plus hypopnoea index (AHI, episodes/hour). Normal sleep has an AHI of less than 10. Severe OSA usually has an AHI of more than 40. A minority of patients with very severe OSA may develop obesity hypoventilation syndrome (Pickwick syndrome). Obstructive episodes can cause pulmonary hypertension (Chapter 27) from hypoxic pulmonary vasoconstriction. Systemic blood pressure increases during ap- noea, possibly due to sympathetic stimulation, and left ventricle (LV) afterload increases during obstructive apnoeas due to the marked fall in pleural pressure. There is a strong association between OSA and systemic hypertension, although the cause is unknown.
Therapy requires relief of obstruction. Moderate weight loss ( ≥10%) often results in substantial improvements, as does limiting evening consumption of alcohol. When OSA is significant nasal continuous positive airway pressure (CPAP, Chapter 42) is the most commonly prescribed therapy, but 50% of patients do not comply in the long term. Some patients respond to oral appliances or removal of tonsils, though uvulopalatopharyngoplasty (surgery) is rarely beneficial O2 alone may decrease or eliminate hypoxia, but not the obstruction or arousals.
Central sleep apnoea
CSA is characterized by cessation of airfl w during sleep without evidence of respiratory effort, and is due to a loss or inhibition of central respiratory drive (Fig. 44c). Patients with CSA may be subdivided into those with daytime hypercapnia or normocapnia. CSA with day-time hypercapnia is usually due to central alveolar hypoventilation, neuromuscular disease or restrictive chest wall disease (e.g. kyphoscoliosis). Central alveolar hypoventilation may be congenital or due to brainstem disease and strokes (see also Ondine's curse; Chapter 12). Neuromuscular causes include muscular dystrophy, phrenic nerve dys- function, myositis (muscle inflammation and myasthenia gravis. Inspiratory muscle impairment in restrictive or obstructive (e.g. COPD) respiratory disease can lead to increased use of accessory muscles during ventilation, but voluntary muscle atonia during REM sleep can therefore lead to profound hypoxaemia.
Cheyne-Stokes respiration is an abnormal pattern of breathing characterized by gradual waxing and waning of the depth of breathing, leading to periods of hypoventilation and desaturation (Fig. 44d). It is commonly experienced in patients with heart failure and at altitude. The underlying causes are not fully understood, but may include dysregulation of feedback from the chemoreceptors (Chapter 11). Under these conditions hypoxaemia can lead to hyperventilation and thus hypocapnia and alkalosis. On sleeping, ventilatory drive may be depressed, leading to hypercapnia or apnoea and hypoxaemia, which causes arousal and hyperventilation again, and the sequence repeats throughout the sleeping period.
Therapy for CSA depends on symptoms. Patients with a CNS cause for hypoventilation ('won't breathe') may benefi from a respiratory stimulant. Patients with weakness or chest wall disease ('can't breathe') benefi from assisted mechanical ventilation, specificall non-invasive intermittent positive pressure ventilation (NIPPV, Chapter 42). Cheyne-Stokes respiration can be improved by treatment of the dition (heart failure) or raising the inspired O2.