Update on the Pathophysiology, Aetiology and Management of Central Sleep Apnoea

Central sleep apnoea (CSA) of the periodic breathing type occurs during the transition between wakefulness and stage 1 and 2 non-REM sleep. In adults at sea level, it occurs most commonly due to advanced heart failure (HF) or chronic opioid use and in ~5% of obstructive sleep apnoea patients initiating CPAP. The sudden development of CSA in a chronic CPAP user for obstructive sleep apnoea (OSA) may indicate the development of atrial fibrillation. Less commonly, idiopathic CSA occurs in which cardiac, neurological and endocrine causes should be excluded. Each cause of CSA has a characteristic appearance of apnoea, hyperpnoea and cycle length. Altitude induced CSA has recently been shown to reduce work of breathing whilst maintaining gas exchange, compared with regular breathing and thereby be considered adaptive rather than detrimental. The management of each type of CSA should be directed at the cause. Where there is residual CSA (e.g., post intensive treatment for HF), debate exists as to the next option. One argument is that CSA is adaptive (as seen with altitude) and therapeutic. An alternative argument is to treat the CSA directly with therapies such as respiratory stimulants (e.g., acetazolamide), positive airway pressure (e.g., adaptive servo-ventilation (ASV)), supplemental oxygen or phrenic nerve pacing. These four latter treatments remain speculative without strong foundations for recommending especially ASV in HF with reduced ejection fraction where increased mortality has been observed.