Cheyne-Stokes Respiration | Why Does Breathing Sometimes Follow a Rhythmic Waxing and Waning Pattern?

Cheyne-Stokes respiration is a distinct and abnormal pattern of breathing. It is characterized by a cyclical sequence that begins with progressively deeper and faster breathing, a phase known as crescendo or hyperpnea. This peak is followed by a gradual decrease in both depth and rate of breathing, a phase called decrescendo. The cycle culminates in a temporary cessation of breathing, which is defined as apnea. After this pause, the entire cycle repeats. This pattern is not random; it is a highly regular rhythm of waxing and waning ventilation, typically with a cycle length of 45 to 90 seconds. The underlying cause of this oscillation is a delay in the feedback loop between the lungs and the brain's respiratory control center. Specifically, the brain's sensors that detect carbon dioxide (CO2) levels in the blood, called chemoreceptors, are slow to respond to changes. When breathing stops (apnea), CO2 builds up. The brain eventually detects this high CO2 level and triggers a period of rapid, deep breathing to expel it. However, due to the delayed feedback, the brain continues this rapid breathing even after CO2 levels have normalized, causing them to drop too low. When the brain finally senses the low CO2, it signals breathing to stop, thus restarting the cycle.

This breathing pattern is a clinical sign that indicates instability in the body's respiratory control system. It is most commonly associated with two major types of medical conditions: congestive heart failure and neurological diseases, such as stroke or brain injury. In heart failure, the heart's reduced pumping efficiency slows down blood circulation. This increased "circulation time" means it takes longer for blood carrying updated CO2 information from the lungs to reach the respiratory centers in the brainstem. This delay is the primary driver of the overcorrection cycle of hyperpnea and apnea. In the context of neurological damage, the respiratory centers in the brainstem may themselves be impaired, reducing their sensitivity to CO2 changes and leading to the same unstable, oscillating pattern of breathing.

Cheyne-Stokes respiration is considered a serious medical sign because it points to significant underlying systemic instability, most often advanced heart failure or neurological compromise. The recurrent periods of apnea lead to intermittent hypoxia (low blood oxygen levels), which places considerable stress on the cardiovascular system. Over time, this can worsen the underlying heart failure, increase the risk of cardiac arrhythmias, and is associated with a poorer prognosis. It is a marker that the body's automatic control systems are failing to maintain a stable internal environment.

Cheyne-Stokes respiration is a form of central sleep apnea, meaning the brain fails to send the signal to breathe. This differentiates it from the more common obstructive sleep apnea (OSA), where the airway is physically blocked despite efforts to breathe. Diagnosis is formally made through an overnight sleep study, or polysomnography. This test records brain waves, heart rate, blood oxygen levels, and breathing patterns. The distinct crescendo-decrescendo pattern of airflow, coupled with the absence of respiratory effort during the apneic pauses, confirms Cheyne-Stokes respiration and distinguishes it from OSA.

In patients with advanced congestive heart failure, the heart muscle is weak and cannot pump blood effectively. This leads to a longer circulation time—the time it takes for blood to travel from the lungs back to the brain. When a patient with heart failure has a brief apnea, blood CO2 levels rise. This high-CO2 blood eventually reaches the brain, which triggers a strong stimulus to breathe rapidly. However, because of the slow circulation, by the time this rapid breathing has lowered the CO2 in the lungs, the "old" high-CO2 blood is still arriving at the brain, sustaining the hyperventilation. This drives CO2 levels excessively low. When this low-CO2 blood finally reaches the brain, the stimulus to breathe is eliminated, causing another apnea. This creates a self-perpetuating cycle of over- and under-breathing directly tied to poor cardiac output.