CENTRAL SLEEP APNEA | SleepTech
Pathophysiology of Central Sleep Apnea
Central Sleep Apnea (CSA) syndromes are characterized by a lack of drive to breathe during sleep, resulting in insufficient or absent ventilation and compromised gas exchange. Unlike Obstructive Sleep Apnea (OSA), there is no respiratory effort during the central events.
The Role of PaCO2
The primary driver of ventilation is the arterial partial pressure of carbon dioxide (PaCO2). In many forms of CSA, such as primary central sleep apnea or high-altitude periodic breathing, the sleeping PaCO2 falls below the apneic threshold. When PaCO2 is below this critical level, central respiratory motor output ceases until PaCO2 rises back above the threshold.
Primary Phenotypes
- Primary Central Sleep Apnea: Idiopathic CSA, often characterized by high loop gain (chemoreceptor hypersensitivity).
- Cheyne-Stokes Respiration (CSR): A specific pattern of crescendo-decrescendo breathing separated by central apneas, highly prevalent in patients with congestive heart failure (CHF).
- Treatment-Emergent Central Sleep Apnea: Previously known as complex sleep apnea. Central apneas that appear during PAP titration for OSA without a backup rate.
- Narcotic-Induced CSA: Opioids depress the hypercapnic ventilatory response and can induce central apneas and ataxic breathing (Biot's respiration).
Polysomnographic Diagnostic Criteria (AASM)
To score a central apnea, the following criteria must be met:
- There is a drop in the peak signal excursion by ≥90% of pre-event baseline using an oronasal thermal sensor (or alternative sensor).
- The duration of the ≥90% drop is ≥10 seconds.
- Absent inspiratory effort is noted throughout the entire period of absent airflow.
Detailed diagnostic criteria and physiological markers required to confirm this condition via polysomnography or clinical evaluation. Reliance on objective data is paramount.
Diagnostic Protocols
Refer to ICSD-3 classifications and ensure rule-out of confounding comorbidities prior to finalizing diagnosis.