sure and oxygen desaturation, and elevated sy mpathetic nervous system activity that can
promote progression of heart failure. The clinic al significance of Cheyne-Stokes breathing
in the setting of stroke is no t known, but Cheyne-Stokes breathing may be a transient find-
ing that resolves with time after acute stro ke. Central sleep apnea comorbid with opioid
use has been documented with chro nic use (i.e., several months). 
Risk and Prognostic Factors
Genetic and physiological. Cheyne-Stokes breathing is freq uently present in individu-
als with heart failure. The coexistence of atrial fibrillation further increases risk, as do older
age and male gender. Cheyne-Stokes breathing is also seen in association with acute stroke
and possibly renal failure. The underlying ventila tory instability in the setting of heart fail-
ure has been attributed to increased ventilatory chemos ensitivity and hyperventilation
due to pulmonary vascular congestion and ci rculatory delay. Central sleep apnea is seen
in individuals taking long-acting opioids.
Diagnostic Markers
Physical findings seen in individuals with a Cheyne-Stokes breathing pattern relate to its
risk factors. Findings consiste nt with heart failure, such as jugular venous distension, S3
heart sound, lung crackles, and lower extremity edema, may be present. Polysomnogra-
phy is used to characterize the breathing characteristics of  each breathing-related sleep
disorder subtype. Central sl eep apneas are recorded when periods of breathing cessation
for longer than 10 seconds occur. Cheyne-Sto kes breathing is characterized by a pattern of
periodic crescendo-decrescend o variation in tidal volume that results in central apneas
and hypopneas occurring at a frequency of at least five events per hour that are accompa-