Central sleep apnea (CSA) is characterised by repeated episodes of airflow reduction or interruption due to short decreases or pauses in central ventilatory drive during sleep (Randerath et al., 2017). While it has lower prevalence in the general population than obstructive sleep apnea (OSA), it is overrepresented in specific subpopulations including patients with heart failure, a history of stroke, those receiving opioid medications or continuous positive airway pressure (CPAP) therapy.
Visit different sections of the Sleep Apnea Learning Zone to find out about the incidence of CSA, its pathophysiology, symptoms and diagnosis and current treatment options.
Central sleep apnea epidemiology
In the general population, the prevalence of CSA is less than 1% (Bixler et al., 1998), but it has been reported in 2–37% of patients with heart failure and in 3–72% of patients who have had a stroke (Randerath et al., 2017).
Treatment-emergent central sleep apnea (TE-CSA) can also be observed in patients treated with opioids and in patients treated with continuous positive airway pressure (CPAP) (Baillieul et al., 2019).
Central sleep apnea pathophysiology
Patients with central sleep apnea (CSA) have a disorder of the mechanisms that control breathing. As opposed to OSA, CSA is characterised by repetitive cessation of ventilation during sleep resulting from lack of ventilatory drive to breathe. Normally, ventilation is tightly regulated to ensure levels of arterial oxygen (PaO2) and carbon dioxide (PaCO2) are maintained within narrow ranges.
This is achieved by feedback loops that involve peripheral and central chemoreceptors, intrapulmonary vagal receptors, the respiratory control centres in the brainstem and the respiratory muscles (figure 16).
Central sleep apnea symptoms and diagnosis
Central sleep apnea symptoms
Current central sleep apnea treatment options
Central sleep apnea disease awareness references
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