Central sleep apnea (CSA) is characterized by a lack of drive to breathe during sleep, resulting in insufficient or absent ventilation and compromised gas exchange. In contrast to obstructive sleep apnea (OSA), in which ongoing respiratory efforts are observed, central apnea is defined by a lack of respiratory effort during cessations of airflow. However, as will be discussed, considerable overlap exists in the pathogenesis and pathophysiology of obstructive and central apnea, making this distinction somewhat difficult at times. CSA, like OSA, is associated with important complications, including frequent nighttime awakenings, excessive daytime sleepiness, and increased risk of adverse cardiovascular outcomes.1,2
There are several manifestations of CSA. These include high altitude-induced periodic breathing, idiopathic CSA (ICSA), narcotic-induced central apnea, obesity hypoventilation syndrome (OHS), and Cheyne-Stokes breathing (CSB). While the precise precipitating mechanisms involved in the various types of CSA may vary considerably, unstable ventilatory drive during sleep is a principal underlying feature.
The prevalence of CSA varies greatly between the various forms of CSA. Most healthy individuals will have periodic breathing on high-altitude ascent, provided the magnitude of the ascent is sufficient to cause substantial alveolar hypoxia.3
Given the global increase in obesity, the prevalence of OHS is likely on the rise.4
ICSA is relatively uncommon and may constitute < 5% of patients referred to a sleep clinic.5
Conversely, within certain clinical populations the presence of CSA may be extremely high. For example, a recent, prospective prevalence study6
of patients with heart failure and left ventricular ejection fraction < 45% revealed that 37% of patients had CSA. Interestingly, OSA is not uncommon in this population at 12%.6
Indeed, instances whereby central respiratory events lead to obstructive respiratory events in patients with vulnerable pharyngeal anatomy, and vice versa
, are observed in the majority of sleep apnea patients.7
The overlap between CSA and OSA suggests that common mechanistic traits are likely involved. Typically, CSA is considered to be the primary diagnosis when ≥ 50% of apneas are scored as central in origin (ie
, > 10 s cessation of breathing in the absence of respiratory effort); however, such thresholds are clearly arbitrary.