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Cheyne-Stokes respiration

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<span style="color:#FF0000">This article '''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 [[stubapnea]]. You can help the '''Apnea Board Wiki''' by expanding it The pattern repeats, with additional information and sectionseach cycle usually taking 30 seconds to 2 minutes. For help on the proper way to edit It is an oscillation of ventilation between apnea and hyperpnea with a wiki pagecrescendo-diminuendo pattern, go to the [[Apnea Board Editor Guide]]and is associated with changing blood plasma 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, and is also seen in newborns with immature respiratory systems and in visitors new to high altitudes. ==Scoring==Cheyne-Stokes Breathing Rule for Adults [Recommended] (Consensus) Score a respiratory event as Cheyne-Stokes respirationbreathing if both of the following are met: # There are episodes of at least 3 consecutive central apneas and/or central hypopneas separated by a crescendo and decrescendo change in breathing amplitude with a cycle length of at least 40 seconds (typically 45 to 90 seconds).# There are 5 or more central apneas and/or central hypopneas per hour associated with the crescendo/decrescendo breathing pattern recorded over a minimum of 2 hours of monitoring. Note: The duration of CSB (absolute or as a percentage of total sleep time) or the number of CSB events should be presented in the study report. <small>''[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3459210/ Rules for Scoring Respiratory Events in Sleep: Update of the 2007 AASM Manual]'' is </small>==History==The condition was named after John Cheyne and William Stokes, the physicians who first described it in the pattern 19th century. ==Pathophysiology==The pathophysiology of Cheyne–Stokes breathing with gradual increase can be summarized as apnea leading to increased CO<sub>2</sub> which causes excessive compensatory hyperventilation, in turn causing decreased CO<sub>2</sub> which causes apnea, restarting the cycle. In heart failure, the mechanism of the oscillation is unstable feedback in depth 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 sometimes carbon dioxide (CO<sub>2</sub>). At the steady state, the rate of production of CO<sub>2</sub> equals the net rate at which it is exhaled from the body, which (assuming no CO<sub>2</sub> in rate the ambient air) is the product of the alveolar ventilation and the end-tidal CO<sub>2</sub> concentration. Because of this interrelationship, the set of possible steady states forms a hyperbola: Alveolar ventilation = body CO<sub>2</sub> production/end-tidal CO<sub>2</sub> 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 CO<sub>2</sub> production to be exactly compensated for by exhalation of CO<sub>2</sub>. Meanwhile, there is another curve, shown in the figure for simplicity as a maximumstraight line from bottom left to top right, followed which is the body's ventilatory response to different levels of CO<sub>2</sub>. 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 CO<sub>2</sub> concentration which is sensed by the respiratory control system so that there is a decrease resulting subsequent small compensatory rise in ventilation (B) above its steady state level (S) that helps restore CO<sub>2</sub> back to its Steady state (chemistry) value. In general, transient or persistent disturbances in ventilation, CO<sub>2</sub> or oxygen levels can be counteracted by the respiratory control system in this way. [[File:Spiraling-stable.png]] However, in some pathological states, the feedback is more powerful than is necessary to simply return the system towards its Steady state (chemistry). 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. [[File:Spiraling-unstable.png]] The cycle of enlargement of disturbances reaches a limit when successive disturbances are no longer larger, which occurs when physiological responses no longer increase Linear regression 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 CO<sub>2</sub> is not, however, at apnea. It occurs when ventilation is so small that air being breathed in never reaches the alveolar space, because the inspired tidal volume is no larger than the volume of the large airways such as the Vertebrate trachea. Consequently, at the nadir of periodic breathing, Ventilation (physiology) of the alveolar space]]may be effectively zero; the cycles ordinarily easily observable counterpart of this is failure at that time point of the Capnography 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 30 seconds hyperventilation, prolonged circulation time, and reduced blood gas buffering capacity. They are physiologically interlinked in that (for any given patient) circulation time decreases as cardiac output increases. Likewise, for any given total body CO<sub>2</sub> production rate, alveolar ventilation is inversely proportional to end-tidal CO<sub>2</sub> concentration (since their mutual product must equal total body CO<sub>2</sub> 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 CO<sub>2 minutes </sub> will fall. Because ventilation and CO<sub>2</sub> 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 durationthe literature. However, other variables, such as chemoreflex sensitivity can only be measured by specific experiment, with 5–30 seconds and therefore abnormalities in them will not be found in routine clinical data. ==Associated conditions==This abnormal pattern of apnea; [[breathing]], in which breathing is absent for a period and then rapid for a period, can be seen in patients with bilateral deep cerebral hemispheric lesionsheart failure,strokes, hyponatremia, traumatic brain injury and brain tumors. In some instances, with it can occur in otherwise healthy people during [[sleep]] at high altitudes. It can occur in all forms of toxic metabolic encephalopathy. It is a symptom of carbon monoxide poisoning, along with Syncope (medicine) or coma. This type of respiration is also often seen after morphine administration. Hospice care sometimes document the presence of Cheyne–Stokes breathing as a patient nears death, andreport that patients able to speak after such episodes do not report any distress associated with the breathing, characteristicallyalthough it is sometimes disturbing to the family. ==Related patterns==Cheyne–Stokes respirations are not the same as Biot's respirations ("cluster breathing"), in coma which groups of breaths tend to be similar in size. They differ from affection of Kussmaul breathing respirations in that the nervous centers Kussmaul pattern is one of respirationconsistent very deep breathing at a normal or increased rate.   [[Category:Medical terms]][[Category:Conditions]][[Category:Symptoms]]
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