Pathophysiology and treatment of Cheyne-Stokes respiration
- Alfred Sleep Disorders and Ventilatory Failure Service, Department of Respiratory Medicine, Alfred Hospital, Commercial Road, Prahran 3181, Victoria, Australia
- Dr M T Naughton.
Cheyne-Stokes respiration is a disorder characterised by recurrent central apnoeas during sleep alternating with a crescendo-decrescendo pattern of tidal volume.1 2 It is often observed in patients with congestive heart failure, usually during stages 1 and 2 non-REM sleep when ventilation is under chemical-metabolic control.2 Patients with Cheyne-Stokes respiration usually present with the symptoms of orthopnoea, paroxysmal nocturnal dyspnoea, excessive daytime sleepiness and witnessed apnoeas in the setting of congestive heart failure.1 3 Excessive weight and snoring may be absent. Approximately 50% of patients with symptomatic congestive heart failure have sleep apnoea, mainly of the Cheyne-Stokes respiration variety.4-6 As congestive heart failure occurs in 1% of the adult population and doubles in prevalence for each decade beyond 60 years,7 Cheyne-Stokes respiration is common but often left unrecognised.
Adverse effects
Based upon small case series, patients with congestive heart failure and Cheyne-Stokes respiration have a significantly greater mortality,8 9 particularly if present during wakefulness,10 than those without Cheyne-Stokes respiration. Although Cheyne-Stokes respiration is likely to arise as a result of congestive heart failure, once present it is likely to have adverse effects upon cardiac function akin to a vicious cycle. Following an initial cardiac insult there is a compensatory increase in sympathetic activity11 12 which in susceptible patients causes hyperventilation,13 destabilises respiratory control, and leads to Cheyne-Stokes respiration. Once Cheyne-Stokes respiration is established, apnoea related hypoxaemia causes cardiac diastolic dysfunction.14 Hypoxaemia and arousals lead to further increases in sympathetic activity15 which contribute to potentially fatal arrhythmias16-18 and further cardiotoxicity.19
Hyperventilation and resultant increased work of the respiratory muscles probably play a part in the symptom of paroxysmal nocturnal dyspnoea1 and place an increased demand upon the already reduced cardiac output.20
Finally, patients with congestive heart failure and Cheyne-Stokes …
