During wakefulness, we have active airway dilator muscles to maintain upper airway patency, so even a patient with an anatomically compromised upper airway is able to breath normally when they are awake. During sleep, these dilator muscles relax and the excessive collapsing forces of the pharynx can compromise the patency of the upper airway. Snoring is an early marker of this collapse. If the upper airway collapses partially or fully, there is absence of airflow and the blood oxygen drops. The patient is still trying to breath against an occluded airway. To prevent asphyxia, airway occlusion is reversed by a brief awakening after 20 to 40 seconds. The patient is rarely aware of this arousal from sleep. In the most severe cases, patients experience these events every 30 seconds across the whole night, causing grossly fragmented sleep, recurrent sympathetic arousals and dips in oxygen levels.