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.