Central Sleep Apnea (CSA) is defined by apnea caused by a loss of output from the central respiratory centres in the brainstem to the respiratory muscles. In CSA, the hypercapneic response is exaggerated --> ventilatory overshoot --> hyperventilation --> hypocapnea --> cessation of respiratory drive.

Risk Factors

• Primary CSA is uncommon.
• Secondary CSA is due to an underlying condition that destabilizes the ventilatory control system in the brainstem:
  • Heart failure (most common) which manifests as Cheyne-Stokes breathing
  • Atrial fibrillation with and without HF
  • Opioid analgesics
  • "Treatment-emergent CSA" is an entity which manifests as patients with OSA are treated with PAP (in about 10% of cases) --> many cases resolve as patients acclimate to regular PAP
  • Stroke, brainstem lesions
  • High-altitude period breathing (a form of Altitude Related Illness)

Diagnosis of CSA

On polysomnography, central apnea is identified by the absence of respiratory effort associated with loss of airflow for at least 10 seconds.

Note: the AHI is not validated as a predictor of important clinical outcomes in CSA as it has been in OSA.

Treatment of CSA

1. Treat underlying risk factors:
   1. Reduce opioids
   2. Optimize heart failure (shown to improve CSA and Cheyne-Stokes)
2. PAP for those with concomitant OSA, especially with "adaptive servo-ventilation" (ASV) that effectively suppresses CSA. However, a trial (Cowie et al NEJM 2015) showed an increased in mortality in patients with CSA and HFrEF treated with ASV --> avoid in HFrEF for now.
3. Supplemental oxygen for sleep-related hypoxia

References

1. MKSAP 19