Cheyne-Stokes Respiration (CSR) describes an unusual pattern of breathing characterized by cycles of gradually increasing and decreasing respiratory depth, followed by a temporary pause in breathing. While not a disease itself, CSR is a physical manifestation of severe underlying health issues, most often affecting the heart or brain. This pattern signals a profound instability in the body’s system for regulating respiration, reflecting a breakdown in communication between the lungs, circulation, and the brain’s control centers.
The Defining Pattern of Cheyne-Stokes Respiration
The Cheyne-Stokes pattern is a distinct, predictable oscillation of ventilation, typically completing a full cycle in 30 seconds to two minutes. The cycle begins with central apnea, a period of absent breathing where respiratory muscles receive no signal from the brain. This is followed by the crescendo phase, where breaths start shallowly and progressively increase in both rate and depth.
This period of deep, rapid breathing, known as hyperpnea, causes a significant amount of carbon dioxide to be exhaled. Following the peak, the pattern enters the decrescendo phase, where breaths gradually become shallower and slower. The respiratory effort continues to diminish until it leads back to temporary cessation, restarting the cycle with central apnea.
The Underlying Physiological Breakdown
Cheyne-Stokes Respiration stems from an unstable and oversensitive respiratory control system driven by the body’s response to carbon dioxide (\(\text{CO}_2\)) levels. In healthy individuals, the brain’s respiratory centers constantly monitor blood \(\text{CO}_2\) and quickly adjust breathing to maintain stable levels. The problem in CSR is a prolonged circulation time, which introduces a delay in the feedback loop between the lungs and the brain’s chemical sensors, or chemoreceptors.
When breathing stops during the apnea phase, \(\text{CO}_2\) levels in the blood begin to rise. Due to the delayed circulation, this rise takes longer than normal to reach the brain’s chemoreceptors. When the signal finally arrives, the brain overcorrects for the high \(\text{CO}_2\) by initiating an exaggerated period of hyperventilation (the crescendo phase).
This excessive breathing rapidly lowers the \(\text{CO}_2\) level, driving it down past the apneic threshold—the minimum level required to stimulate breathing. The slow circulation time again delays the signal that \(\text{CO}_2\) is too low from reaching the brain. By the time the brain registers the low \(\text{CO}_2\), the respiratory drive is suppressed, resulting in the decrescendo and subsequent apnea. This instability is characterized by a high “loop gain,” meaning small changes in blood gas levels result in large, oscillating swings in ventilation.
Primary Medical Conditions Linked to Cheyne-Stokes Respiration
The underlying causes of Cheyne-Stokes Respiration are conditions that impair the circulatory system or directly damage the central nervous system’s respiratory centers. Congestive Heart Failure (CHF) is the most frequent associated condition, occurring in an estimated 30% to 50% of people with moderate to severe heart failure. A weakened heart muscle in CHF leads to low cardiac output and a prolonged circulation time.
This slow movement of blood provides the physiological delay that destabilizes the respiratory feedback loop. Pulmonary congestion, which often accompanies heart failure, also increases the sensitivity of peripheral chemoreceptors to \(\text{CO}_2\), contributing to over-breathing. The presence of CSR in a person with CHF generally indicates a more severe stage of the illness.
Damage to the central nervous system, particularly the brainstem, is another major cause of CSR. Conditions like stroke, traumatic brain injuries, and brain tumors can directly affect the sensitivity of the respiratory centers. When these centers are injured, their ability to maintain a steady breathing pattern is compromised, leading to irregular and fluctuating cycles.
Severe kidney failure can also contribute to the development of this breathing pattern. Renal failure leads to metabolic imbalances and the accumulation of toxins, which affect the central nervous system and influence the respiratory drive. These changes in blood chemistry destabilize the \(\text{CO}_2\) buffering system, making the respiratory center prone to overcorrection.
A similar, temporary pattern, known as high-altitude periodic breathing, can occur in healthy individuals at very high altitudes. The low oxygen environment (hypoxia) stimulates the respiratory drive and causes hyperventilation. This initial over-breathing reduces the blood \(\text{CO}_2\), which then triggers the central apnea.