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 while periodic breathing involves hypopnea.
These phenomena can occur during wakefulness or during sleep, where they are called the
central sleep apnea syndrome.
It may be caused by damage to respiratory centers, or by physiological abnormalities
in chronic heart failure, and is also seen in newborns with immature respiratory systems
and in visitors new to high altitudes.
History The condition was named after John Cheyne
and William Stokes, the physicians who first described it in the 19th century.
Pathophysiology 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.
At the steady state, the rate of production of CO2 equals the net rate at which it is
exhaled from the body, which 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.
Through respiratory control reflexes, any small transient fall in ventilation leads
to a corresponding small rise in alveolar CO2 concentration which is sensed by the respiratory
control system so that there is a subsequent small compensatory rise in ventilation above
its steady state level 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.
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.
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 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 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 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.
Chemoreflex sensitivity is closely linked to the position of the steady state, because
if chemoreflex sensitivity increases 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 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.
Associated conditions This abnormal pattern of breathing, in which
breathing is absent for a period and then rapid for a period, can be seen in patients
with heart failure, strokes, traumatic brain injuries and brain tumors.
In some instances, 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 or coma.
This type of respiration is also often seen after morphine administration.
Hospice personnel 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..
Related patterns Cheyne–Stokes respirations are not the same
as Biot's respirations, in which groups of breaths tend to be similar in size.
They differ from Kussmaul respirations in that the Kussmaul pattern is one of consistent
very deep breathing at a normal or increased rate.
References