Central Sleep Apnea

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.

Obstructive versus Central

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.

Prevalence

The prevalence of idiopathic central sleep apnea is unknown but thought to be rare. The prevalence of central sleep apnea is high in individuals with depressed cardiac ventricular ejection fraction. In individuals with an ejection fraction of less than 45%, the prevalence 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. Prevalence increases with age, and most patients are older than 60 years. Cheyne-Stokes breathing occurs in approximately 20% of individuals with acute stroke. Central sleep apnea comorbid with opioid use occurs in approximately 30% of individuals taking chronic opioids for nonmalignant pain and similarly in individuals receiving methadone maintenance therapy.

Criterion A

Evidence by polysomnography of 5 or more central apneas for each 1 hour of sleep.

Criterion B

The disorder is not better explained by another current sleep disorder.

Specifiers

Specifiers

Specify if:

  • Idiopathic central sleep apnea: Characterized by repeated episodes of apneas and hypopneas during sleep caused by variability in respiratory effort but without evidence of airway obstruction.
  • Cheyne-Stokes breathing: A pattern of periodic crescendo-decrescendo variation in tidal volume that results in central apneas and hypopneas at a frequency of at least five events per hour, accompanied by frequent arousal.
  • Central sleep apnea comorbid with opioid use: The pathogenesis of this subtype is attributed to the effects of opioids on the respiratory rhythm generators in the medulla as well as the differential effects on hypoxic versus hypercapnic respiratory drive.

Severity Specifier

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.

Apnea-Hypopnea Index (AHI)

Apnea-Hypopnea Index (AHI)

AHI (events/hours) Severity
0-5 Normal
5 - 15 Mild sleep apnea
15 - 30 Moderate sleep apnea
>30 Severe sleep apnea
Remember, 5 apneas within an hour are actually considered within normal range (apnea is > 10 seconds)

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.

Cheyene-Stokes Breathing

CSA in individuals with heart failure, stroke, or renal failure typically have a central sleep apnea breathing pattern called Cheyne-Stokes breathing, 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).

Medications
  • Alterations in neuromuscular control of breathing can occur in association with medications 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 disturbances and symptoms such as sleepiness, confusion, and depression.
  • Chronic use of long-acting opioid medications is often associated with impairment of respiratory control leading to central sleep apnea.

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.

Polysomnography

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.

  • Other breathing-related sleep disorders and sleep disorders
Key Questions on Patient History
  • Is it obstructive or central?
  • How severe it is?
  • Is it REM-related?
  • Is it positional?
    • Does your patient sleep on their back or sleep on their side?
  • Is it associated with desaturations?
  • Are there medical comorbidities?

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