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Pathophysiology and treatment of Cheyne-Stokes respiration
  1. M T Naughton
  1. Alfred Sleep Disorders and Ventilatory Failure Service, Department of Respiratory Medicine, Alfred Hospital, Commercial Road, Prahran 3181, Victoria, Australia
  1. Dr M T Naughton.

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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 …

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