Central Sleep Apnea

Excerpt

Central sleep apnea (CSA) is characterized by transient diminution or cessation of the respiratory rhythm generator located within the pontomedullary region of the brain. In general, CSA represents an array of sleep-disordered breathing (SDB) conditions due to the brief absence of ventilatory output during sleep. CSA manifests as a cyclical phenomenon/pattern during sleep; periods of apnea or hypopnea alternating with hyperpnea. Although there is a lack of effort during central events, it has been found that the upper airway narrows or nearly collapses during these events. Upper airway narrowing consistently occurs at the retropalatal level during induced hypocapnic central apnea (video 1) and induced central hypopnea.

Though the prevalence of CSA is lower than OSA, both conditions often coexist, and patients can exhibit features of both states. The International Classification of Sleep Disorders – Third Edition (ICSD-3) has divided CSA syndromes into several categories based on distinct clinical and polysomnographic features;

1. Primary CSA

2. CSA with Cheyne-Stokes Breathing (CSB)

3. CSA due to a medical disorder without CSB

4. CSA due to a periodic high-altitude breathing

5. CSA due to a medication or substance

6. Treatment-emergent CSA

Both hypoventilation and hyperventilation can result in central apneas, and each one acts through a distinct pathophysiological pathway. Thus, the degree of alveolar ventilation often serves as a basis for an alternate classification of CSA. Patients with heart failure are often hypocapnic during wakefulness and have an increased propensity to develop hyperventilation related CSA; however, hypoventilation related CSA commonly occur in neuromuscular diseases (amyotrophic lateral sclerosis, brainstem stroke), overuse of medications with side effects of central nervous system depression (opioids), cervical spinal cord injury and structural abnormalities affecting pulmonary dynamics (kyphoscoliosis).