Abnormal breathing in heart failure as originally described by Cheyne1 and subsequently by Stokes2 was observed in apparently awake patients as an agonal breathing pattern.

“. . . The only peculiarity in the last period of his illness was in the state of the respiration. For several days his breathing was irregular, then it would become perceptible, though very low, then by degrees it became heaving and quick, and then it would cease again: this revolution in the state of his breathing occupied about a minute, during which there were about 30 acts of respiration (Cheyne, 1818) . . .”

The patient described in this report was an obese, elderly, alcoholic who had suffered a substantial, and ultimately, fatal stroke. He probably had obstructive sleep apnoea prior to the stroke and developed central apnoea subsequently. In the literature subsequent to these reports periodic respiration associated with central apnoeas was believed to be a terminal consequence of end stage heart failure.3-5

More recently it has been recognised that central apnoeas occur commonly in heart failure, especially during sleep, being reported in 40–50% of patients, predominantly men, with stable, medically treated congestive heart failure.6 This sleep breathing abnormality leads to sleep fragmentation, alterations in sleep architecture—with relative increases in stage 1 and 2 sleep and reduction in REM sleep—and a clinical sleep disorder with symptoms of tiredness and sleepiness in some patients.7 The sleep disorder in central sleep apnoea is a consequence of the development of congestive heart failure. Although the pathophysiology is not completely understood, hyperventilation,8 increased chemoreceptor drive,9 and increased circulation time4 ,10 ,11 are all believed to be important factors promoting this sleep disorder.

Identification of obstructive sleep apnoea (OSA) in patients with primarily left ventricular (LV) dysfunction and …