| Cheyne–Stokes respiration | |
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| Graph showing Cheyne–Stokes respiration (bottom) and other pathological breathing patterns | |
| Pronunciation | |
Cheyne–Stokes respiration is an abnormal pattern ofbreathing characterized by progressively deeper, and sometimes faster, breathing followed by a gradual decrease that results in a temporary stop in breathing called anapnea. The pattern repeats, with each cycle usually taking 30 seconds to 2 minutes.[1] It is an oscillation of ventilation between apnea andhyperpnea with acrescendo-diminuendo pattern, and is associated with changingserumpartial pressures ofoxygen andcarbon dioxide.[2]
Cheyne–Stokes respiration andperiodic 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 involveshypopnea (abnormally small but not absent breaths).
These phenomena can occur during wakefulness or during sleep, where they are called thecentral sleep apnea syndrome (CSAS).[3]
It may be caused by damage torespiratory centers,[4] or by physiological abnormalities incongestive heart failure.[5] It is also seen in newborns with immature respiratory systems, in visitors new to high altitudes, and in severely ill patients approaching end-of-life.[6]
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Causes may includeheart failure,kidney failure, narcotic poisoning,intracranial pressure, andhypoperfusion of the brain (particularly of the respiratory center). 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 ahyperbola:
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 itssteady 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.
However, in some pathological states, the feedback is more powerful than is necessary to simply return the system towards itssteady state. Instead, ventilation overshoots and can generate an opposite disturbance to the original disturbance. If this secondary disturbance is larger than the original, the next response will be even larger, and so on, until very large oscillations have developed, as shown in the figure below.
The cycle of enlargement of disturbances reaches a limit when successive disturbances are no longer larger, which occurs when physiological responses no longer increaselinearly in relation to the size of the stimulus. The most obvious example of this is when ventilation falls to zero: it cannot be any lower. Thus Cheyne–Stokes respiration can be maintained over periods of many minutes or hours with a repetitive pattern of apneas and hyperpneas.
The end of the linear decrease in ventilation in response to falls in CO2 is not, however, at apnea. It occurs when ventilation is so small that air being breathed in never reaches the alveolar space, because the inspiredtidal volume is no larger than the volume of the large airways such as thetrachea. Consequently, at the nadir of periodic breathing,ventilation of the alveolar space may be effectively zero; the easily observable counterpart of this is failure at that time point of theend-tidal gas concentrations to resemble realistic alveolar concentrations.
Many potential contributory factors have been identified by clinical observation, but unfortunately they are all interlinked and co-vary extensively. Widely accepted risk factors are hyperventilation, prolonged circulation time, and reduced blood gas buffering capacity.[7][8]
They are physiologically interlinked in that (for any given patient) circulation time decreases as cardiac output increases. Likewise, for any given total body CO2 production rate, alveolar ventilation is inversely proportional to end-tidal CO2 concentration (since their mutual product must equal total body CO2 production rate). Chemoreflex sensitivity is closely linked to the position of the steady state, because if chemoreflex sensitivity increases (other things being equal) the steady-state ventilation will rise and the steady-state CO2 will fall. Because ventilation and CO2 are easy to observe, and because they are commonly measured clinical variables which do not require any particular experiment to be conducted in order to observe them, abnormalities in these variables are more likely to be reported in the literature. However, other variables, such as chemoreflex sensitivity can only be measured by specific experiment, and therefore abnormalities in them will not be found in routine clinical data.[9] When measured in patients with Cheyne–Stokes respiration, hypercapnic ventilatory responsiveness may be elevated by 100% or more. When not measured, its consequences—such as a low mean PaCO2 and elevated mean ventilation—may sometimes appear to be the most prominent feature.[10]
This abnormalpattern ofbreathing, in which breathing is absent for a period and then rapid for a period, can be seen inpatients withheart failure,[11][12]strokes,hyponatremia,traumatic brain injuries, andbrain tumors. In some instances, it can occur in otherwise healthy people duringsleep at high altitudes. It can occur in all forms oftoxic metabolic encephalopathy.[13] It is a symptom ofcarbon monoxide poisoning, along withsyncope orcoma. This type of respiration is different from respiratory depression, often seen aftermorphine administration.[14]
Cheyne-Stokes is one of several abnormal breathing patterns potentially seen inJoubert syndrome and related disorders.
Hospices sometimes document the presence of Cheyne–Stokes breathing as a patient nears death, and report that patients able to speak after such episodes do not report any distress associated with the breathing, although it is sometimes disturbing to the family.[15]
Cheyne–Stokes respirations are not the same asBiot's respirations ("cluster breathing"), in which groups of breaths tend to be similar in size.
They differ fromKussmaul respirations in that the Kussmaul pattern is one of consistent very deep breathing at a normal or increased rate.
The condition was named afterJohn Cheyne andWilliam Stokes, the physicians who first described it in the 19th century.[16][17]
The term became widely known and used in the Soviet Union after thedeath of Joseph Stalin in 1953, because the Soviet press announced that the ailing Stalin had Cheyne–Stokes respiration.[18]
