Causes may include heart failure, kidney failure, narcotic poisoning, and raised intracranial pressure. The pathophysiology of<unk><unk><unk>  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. 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. 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 linearly 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<unk>  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 inspired tidal volume is no larger than the volume of the large airways such as the trachea. 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 the end-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. 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. When measured in patients with<unk> , 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.
Cheyne–Stokes respiration
Ataxic respiration
Auscultatory gap
Pursed-lip breathing
Autoinflation
Bronchial hyperresponsiveness
Dispokinesis
Bio-secure bubble