Central Sleep Apnea (CSA) is a sleep disorder characterized by episodes of apnea (cessation of breathing) during sleep because the brain does not cue the body to continue breathing. Cheyne-Stokes breathing is a subtype of CSA, seen in patients with severe cardiac, neurologic, or renal impairment.
Central sleep apnea (CSA) is different from obstructive sleep apnea (OSA), because in since in CSA, breathing stops because there is no drive to breathe. On the other hand, in OSA, there is always a drive to breath, but that drive is impeded by airway collapse.
Evidence by polysomnography of 5 or more central apneas for each 1 hour of sleep.
The disorder is not better explained by another current sleep disorder.
| AHI (events/hours) | Severity |
|---|---|
| 0-5 | Normal |
| 5 - 15 | Mild sleep apnea |
| 15 - 30 | Moderate sleep apnea |
| >30 | Severe sleep apnea |
Specify if:
Severity of central sleep apnea is graded according to the frequency of the breathing disturbances as well as the extent of associated oxygen desaturation and sleep frag mentation that occur as a consequence of repetitive respiratory disturbances.
In its primary form, CSA is the result of instability of the breathing control system as the individual transitions from wakefulness to sleep. There is increased gain of the ventilatory control system, also referred to as high loop gain, which leads to instability in ventilation and PaCO2 levels. This instability is termed periodic breathing and can be recognized by hyperventilation alternating with hypoventilation. Individuals typically have pCO2 levels while awake that are slightly hypocapneic or normocapneic. Central sleep apnea may also manifest during initiation of treatment of obstructive sleep apnea hypopnea or may occur in association with obstructive sleep apnea hypopnea syndrome (termed complex sleep apnea).
The onset of Cheyne-Stokes breathing appears tied to the development of heart failure. The Cheyne-Stokes breathing pattern is associated with oscillations in heart rate, blood pressure and oxygen desaturation, and elevated sympathetic nervous system activity that can promote progression of heart failure. The clinical significance of Cheyne-Stokes breathing in the setting of stroke is not known, but Cheyne-Stokes breathing may be a transient find ing that resolves with time after acute stroke. The coexistence of atrial fibrillation further increases risk, as do older age and male gender.
CSA in individuals with heart failure, stroke, or renal failure typically have a central sleep apnea breathing pattern called Cheyne-Stokes breathing (oscillations between apnea and hyperpnea). This is characterized by periodic crescendo-decrescendo variation in tidal volume that results in central apneas and hypopneas (least 5 events per hour that are accompanied by frequent arousals).
Physical findings seen in individuals with a Cheyne-Stokes breathing pattern relate to its risk factors. Findings consistent with heart failure, such as jugular venous distension, S3 heart sound, lung crackles, and lower extremity edema, may be present.
Polysonmography is used to characterize the breathing characteristics of each breathing-related sleep disorder subtype. Central sleep apneas are recorded when periods of breathing cessation for longer than 10 seconds occur. Cheyne-Stokes breathing is characterized by a pattern of periodic crescendo-decrescendo variation in tidal volume that results in central apneas and hypopneas occurring at a frequency of at least five events per hour that are accompanied by frequent arousals. The cycle length of Cheyne-Stokes breathing (or time from end of one central apnea to the end of the next apnea) is about 60 seconds.