What Is Central Sleep Apnea?

Central vs obstructive sleep apnea

An apnea is a stop in airflow of at least 10 seconds. What happens to breathing effort during that stop decides the type.

In a review in the Journal of the American College of Cardiology, Javaheri and colleagues describe obstructive sleep apnea as complete closure of the upper airway while the inspiratory muscles of the chest keep working. Central sleep apnea is different: the brainstem's breathing rhythm generator briefly stops sending the signal to breathe, usually because carbon dioxide in the blood has fallen below the apneic threshold, the level below which breathing pauses (Javaheri et al., JACC, 2017).

The AASM's 2012 scoring update kept classification by respiratory effort: obstructive, central, and mixed apneas are told apart by whether effort is present (Berry et al., Journal of Clinical Sleep Medicine, 2012). Hypopneas, partial drops in airflow, can also be scored as central or obstructive, though that step is optional. The same paper describes a central hypopnea as one where flow falls mainly because effort falls, without the flattened inspiratory flow shape or the chest-abdomen paradox typical of an obstructive event.

Both kinds of events count toward the apnea-hypopnea index (AHI). A sleep report usually splits the count so a clinician can see how much of the total is central.

Cheyne-Stokes breathing

Cheyne-Stokes breathing is a CSA pattern in which breathing waxes and wanes, with central apneas or hypopneas at the low point of each cycle. The AASM adult scoring rule needs both of these (Berry et al., 2012):

• At least 3 consecutive central apneas or central hypopneas separated by a crescendo-decrescendo change in breathing amplitude, with a cycle length of at least 40 seconds (typically 45 to 90 seconds).

• At least 5 central apneas or hypopneas per hour with that pattern, over at least 2 hours of monitoring.

In heart failure the oxygen dip lags behind the apnea, because blood takes longer to circulate from the lungs to the sensor. Javaheri and colleagues note this delay in their polysomnography example.

Why central apneas happen

Javaheri and colleagues describe the mechanism this way. During sleep, breathing depends heavily on carbon dioxide. A sigh or brief arousal can make a person breathe more than needed. The overshoot lowers arterial CO2, and a fall of about 1 to 4 mm Hg can be enough to cross the apneic threshold. Breathing then pauses until CO2 builds back up. Loop gain describes how strongly the breathing control system reacts to a disturbance. When it is high, each overshoot is followed by an undershoot, and the cycle repeats.

The same review calls CSA rare in the general population but common in people with heart failure, stroke, and atrial fibrillation. It names heart failure and opioid use as the two most common causes in adults.

The 2017 AASM guideline on diagnostic testing for OSA lists the conditions that raise the risk of non-obstructive sleep-disordered breathing such as CSA: significant cardiopulmonary disease, possible respiratory muscle weakness from neuromuscular conditions, history of stroke, and chronic opiate use (Kapur et al., Journal of Clinical Sleep Medicine, 2017).

Why a home sleep apnea test can miss CSA

A home sleep apnea test is built to answer one question: does this adult have obstructive sleep apnea? The 2017 guideline recommends it only for uncomplicated patients, and it defines uncomplicated partly as having none of the CSA risk conditions above. For people with those conditions, its Recommendation 4 is polysomnography rather than a home test. It also recommends polysomnography when a home test is negative, inconclusive, or technically inadequate. The home sleep apnea test vs polysomnography guide covers that choice.

Telling central from obstructive events depends on measuring effort well. The 2012 scoring update quotes the 2007 manual: hypopneas should not be classified as obstructive, central, or mixed without a quantitative measure of effort, such as esophageal manometry, calibrated inductance belts, or diaphragm or intercostal EMG. It also notes that calibrated belts do not always track true effort and that esophageal manometry is rarely used. That is a high bar even in a lab.

What wearables can and cannot see

A watch or ring with PPG records pulse rate, pulse amplitude, and, with red and infrared light, blood oxygen. Cyclical oxygen dips and pulse changes can show that breathing is being disrupted at night. Neither signal measures airflow or breathing effort directly, and effort is what separates a central event from an obstructive one. Most published wearable apnea work targets OSA; the PPG sleep apnea detection guide notes that consumer algorithms are generally not trained to tell central events apart.

How PPG models build an AHI-like estimate is covered in wearable AHI estimation, and published results sit on the sleep apnea AHI leaderboard. For oximetry alone, see overnight oximetry vs a sleep study and normal SpO2 while sleeping. Sensor Bio keeps a review of wearable sleep apnea studies. The sleep apnea condition page covers PPG detection more broadly.

This page explains what central sleep apnea is. It is not a diagnosis and not treatment advice. Central sleep apnea is identified on a sleep study and interpreted by a sleep clinician.