Alterations in neuromuscular control of breathing can occur in association with med- ications or substances used in individuals with mental health conditions, which can cause or exacerbate impairments of respiratory rhythm and ventilation. Individuals taking these medications have a sleep-related breathing disorder that could contribute to sleep distur- bances and symptoms such as sleepiness, confusion, and depression. Specifically, chronic use of long—acting opioid medications is often associated with impairment of respiratory con- trol leading to central sleep apnea.
Individuals with central sleep apnea hypopneas can manifest with sleepiness or insomnia.
There can be complaints of sleep fragmentation, including awakening with dyspnea.
Some individuals are asymptomatic. Obstructive sleep apnea hypopnea can coexist with
Cheyne—Stokes breathing, and thus snoring and abruptly terminating apneas may be ob- served during sleep.
The prevalence of idiopathic central sleep apnea is unknown but thought to be rare. The prevalence of Cheyne-Stokes breathing is high in individuals with depressed cardiac ven- tricular ejection fraction. In individuals with an ejection fraction of less than 45%, the prev- alence has been reported to be 20% or higher. The male-to-female ratio for prevalence is even more highly skewed toward males than for obstructive sleep apnea hypopnea. Prev- alence increases with age, and most patients are older than 60 years. Cheyne-Stokes breath- ing occurs in approximately 20% of individuals with acute stroke. Central sleep apnea comorbid with opioid use occurs in approximately 30% of individuals taking chronic opi- nance therapy.
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 pres- sure 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. Central sleep apnea comorbid with opioid use has been documented with chronic use (i.e., several months).
Genetic and physiological. Cheyne-Stokes breathing is frequently present in individu- als with heart failure. The coexistence of atrial fibrillation further increases risk, as do older age and male gender. Cheyne—Stokes breathing is also seen in association with acute stroke and possibly renal failure. The underlying ventilatory instability in the setting of heart fail- ure has been attributed to increased ventilatory chemosensitivity and hyperventilation due to pulmonary vascular congestion and circulatory delay. Central sleep apnea is seen in individuals taking long-acting opioids.
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. Polysomnogra- phy 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 and hypopneas occurring at a frequency of at least five events per hour that are accompa- nied 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.
Functional Consequences of Central Sleep Apnea