What is Central Sleep Apnea?
Central sleep apnea (CSA) is a pattern of breathing caused by an increased sensitivity in the brainstem to changes in arterial blood carbon dioxide levels. CSA is common in cardiac patients, primarily patients with heart failure.
During sleep, respiration is regulated by the brain’s Respiratory Control Center (RCC) whose goal is to maintain a constant blood CO2.
To keep CO2 regulated, the RCC sends signals to the diaphragm via the phrenic nerves. These signals control the pattern of breathing.
In patients with increased sympathetic drive and overactive chemoreceptors, the RCC develops a respiratory arrhythmia that manifests as an oscillating pattern between hyperventilation and apnea called Central Sleep Apnea (CSA).
Heart Failure affects nearly 6 million people in the United States and over 23 million worldwide. Central Sleep Apnea occurs in approximately 1 in 3 heart failure patients and has been shown to be an independent predictor of mortality for this patient population.
CSA Speeds Progression of Heart Failure and Reduces Survival Rate
What is Sleep Disordered Breathing?
Sleep Disordered Breathing is a general category for irregular breathing patterns during sleep. The two main types are Obstructive Sleep Apnea, when the upper airway collapses during sleep, and Central Sleep Apnea, when increased sensitivity to arterial blood carbon dioxide levels disrupts breathing.
Both Obstructive Sleep Apnea (OSA) and Central Sleep Apnea (CSA) are recognized for their association with cardiovascular morbidity and mortality. Unlike CSA where breathing is interrupted by a temporary withdrawal of central respiratory drive, OSA is a temporary collapse of the upper airway during sleep. OSA also results in a disruption in airflow throughout the sleep cycle causing apneas (cessation of breathing) or hypopneas (shallow breathing). Symptoms, however, are different. OSA is often recognized by loud snoring and daytime sleepiness. CSA may present as fatigue, cardiac arrhythmias or worsening heart failure.
Ventilation patterns of obstructive and central sleep apnea. Periods of reduced (hypopnea) or absent (apnea) airflow are associated with oxygen desaturation.
Trends Cardiovasc Med 2008;18:240–247 n2008, Elsevier Inc.
How is Central Sleep Apnea Diagnosed?
Central Sleep Apnea diagnosis is based on a sleep study performed by a patient at home or overnight at a sleep center. During sleep, the number of apneic and hypopnic (abnormal decrease in depth and rate of respiration) events per hour are counted and reported as the Apnea Hypopnea Index (AHI), the most common measure of severity of sleep apnea. The study determines if a patient has Sleep Disordered Breathing and if their primary type of apnea is Central Sleep Apnea or Obstructive Sleep Apnea.
During a sleep study, external testing devices monitor the body’s oxygen, airflow, chest and abdominal movement during sleep.
At-home testing can be done with a pulse oximeter overnight. Results can indicate sleep apnea, but further diagnostic testing is needed to distinguish the type of apnea. Another at home option is utilizing Class III sleep testing devices which can distinguish Central Sleep Apnea from Obstructive Sleep Apnea. An observed overnight sleep study performed at a sleep center may offer further insight through EEG and leg movement monitoring.
During a sleep study, the severity of sleep-disordered breathing is defined by the Apnea Hypopnea Index, and the apneic and hypopnic events are further classified to determine the best course of treatment. Sleep testing metrics include:
- Apnea-Hypopnea Index (AHI)
Number of apneas and hypopneas per hour of sleep
Mild (5 – 14 events/hour), Moderate (AHI of 15 > to < 30 events/hour), and Severe (AHI ≥ 30 events/hour)
- Central apnea
≥10 second cessation of airflow, without effort
- Obstructive apnea
≥10 second cessation of airflow, while effort continues
30% reduction in airflow for 10 seconds with a 4% fall in oxygen saturation
Number of arousals per hour of sleep
- Oxygen Desaturation Index (ODI) 4%
Number of times oxygen saturation drops by 4% or more per hour
2007 AASM Guidelines