Central sleep apnea (CSA) is a serious sleep-related breathing disorder characterized by repeated pauses in breathing during sleep (apneas). Unlike Obstructive Sleep Apnea (OSA), which involves a physical blockage, CSA is rooted in a neurological issue. It occurs because the brain temporarily fails to send the necessary signal to the muscles that control breathing, meaning the body makes no effort to inhale. CSA is often a complication of other underlying health issues but is manageable with specific, targeted therapies.
Defining Central Sleep Apnea and Its Causes
Central sleep apnea is fundamentally a problem with the respiratory control center in the brainstem, which regulates the automatic function of breathing. When the brainstem does not respond correctly to changes in carbon dioxide levels, the signal to the diaphragm and chest muscles is diminished or absent. This results in a period of no airflow and no respiratory effort, a distinct feature observed during diagnostic testing.
A number of health conditions and external factors can destabilize the brain’s ventilatory control system, leading to CSA. Congestive heart failure (CHF) is a major cause, often resulting in Cheyne-Stokes breathing, where respiration waxes and wanes cyclically. Neurological events like a stroke or brain tumors can directly damage the brainstem, impairing signal transmission.
End-stage kidney disease and exposure to high altitudes can also trigger CSA. High altitude causes hyperventilation, which drops carbon dioxide levels below the apneic threshold, initiating periodic breathing. Opioid pain medications are a significant cause of CSA, as these drugs depress the brain’s respiratory centers. In some cases, CSA occurs without any apparent cause, termed primary or idiopathic CSA.
Confirming the Diagnosis
The definitive method for diagnosing central sleep apnea is a formal overnight sleep study, known as polysomnography (PSG). The PSG monitors physiological signals, including brain activity, heart rate, blood oxygen levels, respiratory effort, and airflow. Monitoring respiratory effort is the key differentiator between CSA and OSA.
During a central apneic event, the PSG records a cessation of airflow for ten seconds or longer without detectable movement in the chest or abdomen, indicating an absence of breathing effort. This contrasts sharply with OSA, where airflow stops despite persistent movements of the chest and diaphragm. Severity is quantified using the Apnea-Hypopnea Index (AHI), which counts the total number of apneas and hypopneas per hour of sleep.
Treatment Through Managing Underlying Health Issues
The most effective approach to correcting central sleep apnea involves addressing the underlying medical condition destabilizing the respiratory control system. Since many CSA cases are secondary to other illnesses, a multidisciplinary approach involving specialists like cardiologists or neurologists is essential. Optimizing the treatment of congestive heart failure (CHF) is particularly important, as this can significantly reduce the severity of Cheyne-Stokes breathing.
Medical management of CHF, including diuretics and other heart medications, lessens pulmonary congestion and improves circulatory efficiency. These improvements stabilize blood gas concentrations, reducing the ventilatory instability that triggers central apneas.
For individuals with CSA linked to chronic opioid use, careful medical supervision is required to reduce or discontinue the medication. This process must be managed by a healthcare team to mitigate withdrawal symptoms and restore the brain’s natural respiratory drive.
If CSA results from kidney failure, optimizing nocturnal dialysis can improve the body’s fluid and chemical balance, often improving sleep breathing patterns. CSA caused by high-altitude exposure resolves by descending to a lower altitude. Treating the root cause often diminishes central apneas, sometimes eliminating the need for complex breathing support devices.
Direct Respiratory and Pharmacological Interventions
When managing the underlying condition is insufficient or when the CSA is primary (idiopathic), direct interventions stabilize nocturnal breathing. The gold standard device therapy for complex or idiopathic CSA is Adaptive Servo-Ventilation (ASV). ASV devices are more sophisticated than standard Continuous Positive Airway Pressure (CPAP) machines, using advanced algorithms to monitor the patient’s breathing pattern continuously.
The ASV device learns the user’s normal breathing rate and volume. When it detects a central apnea or a significant drop in breathing, it delivers a pressure-supported breath. This response helps normalize the erratic breathing cycle characteristic of CSA. ASV is generally not recommended for patients with symptomatic heart failure and a severely reduced left ventricular ejection fraction (EF ≤ 45%) due to potential adverse outcomes.
While CPAP and BiPAP (Bilevel Positive Airway Pressure) are primary treatments for OSA, their role in pure CSA is limited. BiPAP is sometimes used for CSA associated with chronic hypoventilation, providing a backup rate to ensure a minimum number of breaths per minute. Supplemental oxygen can be prescribed to ensure adequate oxygen saturation during apneic events, though it does not fix the underlying instability.
Pharmacological Options
Pharmacological options, such as acetazolamide, act as respiratory stimulants by altering the blood’s chemical balance, effectively lowering the threshold at which the brain signals a breath. These medications are typically considered secondary treatments, reserved for cases where positive airway pressure devices are not tolerated or are ineffective.