Central Sleep Apnea Mechanisms and Treatment

Pathophysiology

During sleep, especially light sleep, breathing becomes primarily dependent on chemical control, making it vulnerable to instability with high loop gain, which promotes breathing instabilities by creating an overly sensitive response to small changes in blood gases, leading to oscillatory breathing patterns 1
High loop gain causes an exaggerated ventilatory response to small disturbances in blood gases, creating a cycle of hyperventilation followed by apnea, manifesting as periodic breathing patterns, including Cheyne-Stokes respiration in heart failure patients 2

High loop gain can be detected through polysomnography showing central apneas without respiratory effort, and cycle length assessment during polysomnography can help distinguish between different forms of central sleep apnea 1

The American Academy of Sleep Medicine suggests that suppressing central sleep apnea/Cheyne-Stokes breathing may be detrimental in heart failure patients as it may be a compensatory mechanism, and optimizing guideline-based heart failure therapy should be the primary approach for heart failure-associated central sleep apnea rather than directly targeting the breathing pattern 2, 4
Volume-assured pressure support with a backup rate can help prevent central apneas induced by fixed pressure support ventilation 5
Opioids can induce or worsen central sleep apnea by depressing respiratory drive and causing upper airway relaxation, according to the British Journal of Pharmacology 6