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Periodic breathing consisting of alternating hyperpnoea and hypopnoea (Fig. 1) was recognized in heart failure patients in the 19th century by John Cheyne and William Stokes. The clinical observation of Cheyne–Stokes respiration has been subsequently confirmed. Initially, attention was focused on the occurrence of oscillatory breathing during sleep and severity of heart failure, suggesting that the former had a potent role in causing further deterioration in cardiovascular function. Episodic apnoea during the night with concomitant hypoxaemia and arousal, characteristic features of Cheyne–Stokes respiration, resulted in patients complaining of dyspnoea and daytime somnolence and was associated with sympathetic overactivity and precipitation of ventricular arrhythmias. A recent study has shown that heart failure patients with oscillatory ventilation while sleeping have more ventricular arrhythmias than patients whose breathing is normal. The high rate of unpredictable sudden death in heart failure has stimulated the search for potential triggers of arrhythmias. This has resulted in interest in the pathophysiological meaning of the Cheyne–Stokes phenomenon during sleep.

european heart journal

Aetiology and pathophysiological implications of oscillatory ventilation at rest and during exercise in chronic heart failure. Do Cheyne and Stokes have an important message for modern-day patients with heart failure?