Cheyne–Stokes respiration

Cheyne–Stokes respiration is an abnormal pattern of breathing characterized by progressively deeper, and sometimes faster, breathing followed by a gradual decrease that results in a temporary stop in breathing called an apnea. The pattern repeats, with each cycle usually taking 30 seconds to 2 minutes. It is an oscillation of ventilation between apnea and hyperpnea with a crescendo-diminuendo pattern, and is associated with changing serum partial pressures of oxygen and carbon dioxide. Cheyne–Stokes respiration is an abnormal pattern of breathing characterized by progressively deeper, and sometimes faster, breathing followed by a gradual decrease that results in a temporary stop in breathing called an apnea. The pattern repeats, with each cycle usually taking 30 seconds to 2 minutes. It is an oscillation of ventilation between apnea and hyperpnea with a crescendo-diminuendo pattern, and is associated with changing serum partial pressures of oxygen and carbon dioxide. Cheyne–Stokes respiration and periodic breathing are the two regions on a spectrum of severity of oscillatory tidal volume. The distinction lies in what is observed at the trough of ventilation: Cheyne–Stokes respiration involves apnea (since apnea is a prominent feature in their original description) while periodic breathing involves hypopnea (abnormally small but not absent breaths). These phenomena can occur during wakefulness or during sleep, where they are called the central sleep apnea syndrome (CSAS). It may be caused by damage to respiratory centers, or by physiological abnormalities in congestive heart failure, and is also seen in newborns with immature respiratory systems and in visitors new to high altitudes. One example is the breathing pattern in Joubert syndrome and related disorders. Causes may include cardiac failure, renal failure, narcotic poisoning, and raised intracranial pressure. The pathophysiology of Cheyne–Stokes breathing can be summarized as apnea leading to increased CO2 which causes excessive compensatory hyperventilation, in turn causing decreased CO2 which causes apnea, restarting the cycle. In heart failure, the mechanism of the oscillation is unstable feedback in the respiratory control system. In normal respiratory control, negative feedback allows a steady level of alveolar gas concentrations to be maintained, and therefore stable tissue levels of oxygen and carbon dioxide (CO2). At the steady state, the rate of production of CO2 equals the net rate at which it is exhaled from the body, which (assuming no CO2 in the ambient air) is the product of the alveolar ventilation and the end-tidal CO2 concentration. Because of this interrelationship, the set of possible steady states forms a hyperbola: Alveolar ventilation = body CO2 production/end-tidal CO2 fraction. In the figure below, this relationship is the curve falling from the top left to the bottom right. Only positions along this curve permit the body's CO2 production to be exactly compensated for by exhalation of CO2. Meanwhile, there is another curve, shown in the figure for simplicity as a straight line from bottom left to top right, which is the body's ventilatory response to different levels of CO2. Where the curves cross is the potential steady state (S). Through respiratory control reflexes, any small transient fall in ventilation (A) leads to a corresponding small rise (A') in alveolar CO2 concentration which is sensed by the respiratory control system so that there is a subsequent small compensatory rise in ventilation (B) above its steady state level (S) that helps restore CO2 back to its steady state value. In general, transient or persistent disturbances in ventilation, CO2 or oxygen levels can be counteracted by the respiratory control system in this way.