Cheyne-Stokes respiration

Cheyne-Stokes respiration

ICD-10	R06.3
ICD-9	786.04
MeSH	D002639

Cheyne-Stokes respiration (pronounced /ˈtʃeɪnˈstoʊks/) is an abnormal pattern of breathing characterized by breathing becoming shallower until it stops for a while and then breathing starts again and rapidly crescendos to a peak before decaying away again. The pattern repeats, with one cycle typically lasting about 1 minute. It is an oscillation of ventilation between apnea and hyperpnea with a crescendo-decrescendo 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 we observe happening at the trough of ventilation: if there is apnea, we describe it as Cheyne-Stokes respiration (since apnea is a prominent feature in their original description); if there is only hypopnea (abnormally small but not absent breaths) then we call it periodic breathing. Physiologically and mathematically, the phenomena are less different than they appear, because breaths that are smaller than the anatomical dead space do not actually ventilate the lung and so - from the point of view of an alveolus - the nadir of periodic breathing may be indistinguishable from apnoea.

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 chronic heart failure, and is also seen 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

In heart failure, the mechanism of the oscillation is instability of respiratory control. Many potential contributory factors have been identified by clinical observation, but unfortunately they are all interlinked and covary extensively. Widely accepted risk factors are hyperventilation, prolonged circulation time, and reduced blood gas buffering capacity. But hypercapnic ventilatory responsiveness which unlike the other contributors may be elevated by 100% or more in Cheyne-Stokes respiration, is rarely measured in routine clinical practice, and therefore its consequences - such as a low mean PaCO2 and elevated mean ventilation - may sometimes appear to be the most prominent feature. .

Circulatory delay may determine the length of the apnea-hyperpnea cycle although it is rarely sufficiently prolonged itself to be a major driving factor for instability.

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 ("cluster breathing"), 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

bg:Чейн-Стоксово дишане sv:Cheyne-Stokes andning