What Is Cheyne-Stokes Respiration?

Whether in sleep or exercise, your brain regulates breathing, no thinking required.

Usually without your awareness, your brain regulates respiration, maintaining an even breathing pattern at rest. With exercise, respiration rate accelerates, as your brain, responding to chemical signals in the blood, adjusts respiration to answer the body's heightened need for oxygen and release of carbon dioxide. Brain damage or the slowing of blood to the brain can impair the brain's control of respiration, causing abnormal breathing patterns, which may include Cheyne-Stokes respiration.

Definition

Cheyne-Stokes respiration is a breathing pattern named after the British physicians John Cheyne and William Stokes. In the early nineteenth century, they identified and wrote about the pattern. Cheyne-Stokes respiration consists of a period of cessation in breathing (apnea) lasting 10 to 60 seconds, followed by gradually increasing depth and frequency of respirations, according to "Taber's Cyclopedic Medical Dictionary."

Cause

In their book "Understanding Pathophysiology," Sue Huether and Kathryn McCance state that Cheyne-Stokes respiration can result from any condition that slows the blood to the brainstem. Such conditions include dysfunction or depression of the cerebral hemispheres, as in coma; basal ganglia disease; and congestive heart failure, observes "Taber's Cyclopedic Medical Dictionary." Slowing blood flow to the brainstem can produce Cheyne-Stokes respiration because it is mainly the brainstem that controls breathing.

Brain and Respiration

Breathing depends as much on the brain as on the lungs.

Breathing reflects the rhythmic contraction and relaxation of the diaphragm muscle and intercostal muscles. These muscles depend on nerve impulses transmitted mainly from a part of the brainstem called the medulla oblongata. The nerve impulses from the medulla that produce Cheyne-Stokes respiration are triggered by nerve signals from receptor cells high in the neck and inside the medulla itself.

Carbon Dioxide

Chemoreceptors in the neck and brain monitor hydrogen-ion concentration in body fluids.

Known as chemoreceptors because they respond to chemical changes in the blood, these receptor cells detect changes in hydrogen ion (H+) concentration. During the apnea phase of Cheyne-Stokes respiration, the concentration of carbon dioxide in arterial blood goes up. This raises the H+ concentration which, detected by chemoreceptors, triggers nerve impulses to respiratory neurons inside the medulla. These neurons then fire impulses to the respiratory muscles (diaphragm and intercostals). The respiratory muscles contract, accounting for the rapid breathing phase in Cheyne-Stokes respiration. Rapid breathing speeds up the rate at which blood releases excess carbon dioxide in the lungs, thus lowering H+ concentration and slowing respiration down again.

Prognosis

Cheyne-Stokes respiration often indicates a grave prognosis. This is largely because it often results from severe brain injuries. Normal breathing depends on the forebrain. Damage to the forebrain shifts respiration control to the brainstem. As consciousness decreases due to brain injury, the brainstem increasingly regulates breathing. Reflecting not oxygen levels but only changes in the blood's carbon dioxide concentration, the resultant breathing pattern goes from apnea to accelerated, rapid breathing, followed by deceleration, and a return to apnea---the pattern Cheyne and Stokes identified two centuries ago.

References

• "Human Physiology"; Arthur Vander, James Sherman, and Dorothy Luciano; 2001
• "Taber's Cyclopedic Medical Dictionary"; Donald Venes, M.D.; 2001
• "Understanding Pathophysiology"; Sue E. Huether and Kathryn L. McCance; 2000