Sleep Apnoea: Mechanism, Clinical Features, Investigation Management by NJE

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Sleep apnoea may be due to upper airways obstruction, described as obstructive sleep apnoea (OSA), or disturbances of control of breathing collectively termed central sleep apnoea (CSA). If severe, OSA causes significant daytime symptoms, especially sleepiness, impairs quality of life (QOL), reduces performance, and increases the risk of serious accidents and other cardiovascular and systemic diseases (e.g. hypertension, angina).

Obstructive sleep apnoea (OSA)/hypopnoea (OSAH)

OSA is defined as upper airways narrowing, provoked by sleep, causing sufficient sleep fragmentation to result in daytime symptoms, mainly sleepiness, and called OSAH syndrome. It is a common disorder, but prevalence depends on the thresholds used to define significant symptoms or abnormal sleep studies. However, 0.5–1% of men and 0.1–0.2% of women are candidates for treatment with nasal continuous positive airways pressure (CPAP) to splint open the upper airway during sleep. Prevalence increases with obesity and is determined by fat distribution, with causative truncal body and neck obesity more common in men.

Mechanism of Sleep Apnoea

Upper airways patency decreases during sleep due to loss of dilator muscle activity in the pharynx. This muscle relaxation is increased by neuromuscular diseases (e.g. stroke, dystrophies), age, and muscle relaxants (e.g. sedatives, alcohol). The pharyngeal airway is further narrowed by obesity, myxoedema, tonsillar enlargement, craniofacial factors (e.g. micrognathia), and specific syndromes (e.g. Marfan’s, acromegaly). In severe OSA, repetitive upper airways collapse (± hypoxaemia), and subsequent arousal, to reactivate pharyngeal dilator muscles, may occur every minute throughout the night. Recurrent arousal fragments sleep causes daytime sleepiness and is associated with increases in cardiovascular risk factors like hypertension.

Sleep Apnoea
Oximetry pattern in sleep apnea

Clinical features of Sleep Apnoea

These include unrefreshing sleep, excessive sleepiness, poor concentration, and nocturia. Risk of road traffic and work associated accidents is increased. Sleepiness can be difficult to assess due to concerns over driving, licensing, and employment. The Epworth scale scores the tendency to fall asleep; >10 is considered abnormally sleepy. Partners are often concerned by loud snoring, choking episodes, and apnoeic periods. Reduced libido, oesophageal reflux, and nocturnal sweating may also occur. Most patients are male and tend to have upper-body obesity (neck size >17 in) and a small or set-back mandible.

Investigation of Sleep Apnoea

This requires routine blood tests, including glucose, thyroid, and appropriate endocrine function tests and lipid profiles, as these patients have a high-risk cardiovascular profile. Overnight oximetry alone identifies most OSA cases, if its limitations are recognized, and allows onward referral for CPAP. In COPD or other patients with a low baseline SaO2, some caution is required when diagnosing OSA on the basis of oximetry alone. False negatives studies occur in younger, thinner patients, in whom it is the compensatory reflex increases in the inspiratory effort that arouse the patient, rather than hypoxaemia, which is less likely due to the larger oxygen stores in the lungs of less obese patients. Limited sleep studies, in which oximetry is combined with monitoring of snoring, chest/abdominal movement, heart rate, and oronasal airflow, are the routine investigation in most sleep units. Full polysomnography (PSG), including EEG, EMG, and eye movements is used to stage sleep electrophysiologically.

Management of Sleep Apnoea

Factors determining the need to treat include the impact of symptoms on quality of life (QOL), impact on livelihood (e.g. HGV driving), the presence of associated obesity or COPD, and motivation to undergo treatment. There is no evidence that hypertension, heart failure, or angina should influence the decision, but may reduce the threshold, to treat.

Simple therapeutic measures include weight loss and reduced consumption of alcohol in the evening. Patients should be encouraged to avoid sleeping supine. Some snorers with good dentition may benefit from mandibular advancement devices. In significant OSA, nasal CPAP can improve daytime symptoms and QOL dramatically. Tonsillectomy or mandibular surgery can be beneficial occasionally, but outcome from pharyngeal surgery is usually poor. Bariatric surgery (e.g. gastroplasty) may be considered in severe obesity. Patients with raised PaCO2 (± acidosis) may require a period of non-invasive positive pressure ventilation (NIPPV) prior to CPAP.

Central sleep apnoea

Central sleep apnoea (CSA) is much less common than OSA and is defined by short repetitive central apnoeas or more prolonged periods of hypoventilation. CSA is usually used to describe actual apnoeas and is termed Cheyne–Stokes breathing when there is regular symmetrical waxing and waning of ventilation, as in heart failure. Periodic breathing describes regular fluctuations in breathing (± apnoeas).

The causes of CSA include ‘lung failure, brain failure, and heart failure.

•  Failure of mechanical ability to ventilate, due to inspiratory muscle impairment in many neuromuscular diseases (e.g. motor neurone disease, muscular dystrophies or post-polio syndrome (in which recurrence of inspiratory muscle weakness occurs decades after the initial illness)) and obstructive (e.g. COPD) or restrictive (e.g. kyphoscoliosis) disorders, results in the use of accessory muscles to maintain ventilation. However, during non-REM sleep, recruitment of accessory muscles is attenuated, causing hypoventilation, and, during REM sleep, physiological paralysis of all postural muscles (i.e. REM atonia) results in isolated diaphragmatic breathing, with profound hypoventilation and apnoea.

•  Impaired ventilatory drive may be congenital or due to brainstem involvement in strokes, trauma, malignancy, or syringobulbia. These patients have no obvious respiratory or neuromuscular cause for hypoventilation. They maintain adequate daytime ventilation, as there is a non-metabolic ‘awake’ ventilatory drive equivalent to ~5 L/min. During non-REM sleep, the ‘awake’ drive is lost, and ventilation is dependent on blood gas stimulation (i.e. hypoxaemia, hypercapnia), although ‘awake-like’ drive may return during REM sleep.

•  Cheyne–Stokes breathing occurs in heart failure or at high altitude. In left heart failure, J receptor stimulation (i.e. due to raised left atrial pressure) and hypoxaemia increase ventilatory drive, causing respiratory alkalosis. At sleep onset, the PaCO2 threshold increases by 1 kPa and, with the loss of ‘awake’ ventilatory drive, causes hypoventilation and/or apnoea. Eventually, increasing PaCO2 (± hypoxia) causes arousal with associated hyperventilation and hypocapnia again, and the cycle repeats. Similarly, at high altitude, hypoxia causes respiratory stimulation with hypocapnia, and, at sleep onset, the loss of ‘awake’ ventilatory drive allows hypoventilation (± apnoeas).

Investigation

This includes simple spirometry to characterize respiratory muscle weakness and airways obstruction. Supine vital capacity may reveal diaphragmatic weakness masked during erect testing. Arterial blood gases detect respiratory failure. Sleep studies are required to confirm CSA:

•  Oximetry alone is variable and may show persistent oscillations (due to repeated arousals) or isolated REM sleep-related SaO2 dips (see Figure 5.47). In OSA, the fall in SaO2 is gradual, as oxygen stores are utilized, followed by a rapid recovery with the first deep breath after apnoea giving a ‘sawtoothed’ pattern. During Cheyne–Stokes breathing, the SaO2 oscillations are sinusoidal as the breathing pattern tends to wax and wane. However, it may mimic OSA if sudden arousals follow apnoea. In COPD, the findings are related to baseline SaO2, with dramatic dips occurring during REM sleep. The combination of hypoxic COPD and OSA can produce particularly dramatic oximetry traces and requires fuller sleep study evidence of OSA.

•  Limited respiratory sleep studies confirm SaO2 falls with hypoventilation but detects no evidence of obstruction or snoring.

•  Full PSG may be required in some cases and identifies the relationship to sleep stage.           Management depends on symptoms. Improved treatment of the underlying condition (e.g. heart failure, COPD) or raising inspired oxygen concentration (FiO2) in hypoxaemic patients may be helpful. If this fails to alleviate Cheyne–Stokes ventilation and sleep continues to be fragmented with associated daytime respiratory failure, consider trials of acetazolamide, benzodiazepines, or CPAP, although evidence of benefit is limited.

 In patients with hypercapnia, raising FiO2 may be detrimental. In these patients, overnight nasal or full face mask NIPPV may be beneficial. Likewise, in patients with sleep disturbance or respiratory failure due to slowly progressive neuromuscular disorders or chest wall restrictions (e.g. kyphoscoliosis), the response to NIPPV can be dramatic. However, increasing dependence on NIPPV, which is not designed to be life-sustaining, can raise difficult issues with progressive respiratory failure.

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