Central sleep apnoea and heart failure (Part I).
Central sleep apnoea (CSA) in congestive heart failure is sleep state dependent and occurs typically in stages I and II of non-REM sleep. The pre-requisites are hypocapnia and some prolongation of the circulation time. It is not certain whether abnormalities in after-discharge activity in the brainstem are also important. The presence of CSA in patients with left ventricular dysfunction is a poor prognostic sign and associated with a higher mortality in that group compared to age, sex and ejection fraction matched patients with congestive cardiac failure alone. It is reasonable to speculate that the CSA causes an increase in sympathetic nervous system activity which would maintain afterload at a high level or tend to increase it with time. The application of a high afterload to an impaired left ventricle leads over time to a further reduction in ejection fraction. From other studies, particularly ACE inhibitor studies, it is known that ejection fraction and prognosis are almost linearly related. It could therefore be said that once CSA has developed it may lead to a vicious circle of increasing afterload and further reduction in ejection fraction, causing worsening CSA and further increases in afterload. A number of treatments have been shown to be of benefit: supplemental nocturnal oxygen therapy, acetazolamide and nasal CPAP therapy have all been shown to reduce CSA. In addition nasal continuous positive airways pressure (CPAP) has been shown by two groups in Canada to also improve ejection fraction. The beneficial effects on ejection fraction in particular, persist after the treatment has been withdrawn, which suggests either remodelling of the left ventricular musculature or a resetting of the baseline sympathetic nervous system activity. The impressive increase in ejection fraction due to three months nasal CPAP therapy in one study (an average 35% increase) is both dramatic and exciting for the future. It is reasonable to expect improvement in prognosis for patients with CCF whose ejection fraction rises with CPAP treatment. Finally, only a limited number of studies have been published. Unfortunately the impressive results from Canada have not yet been reproduced in other centres around the world.
Burgess
K R
KR
Department of Critical Care, Manly Hospital, New South Wales, Australia.
D000818:Animals; D005260:Female; D006333:Heart Failure / Q000150:complications / Q000175:diagnosis / Q000401:mortality / Q000503:physiopathology*; D006801:Humans; D008297:Male; D011379:Prognosis; D015656:Respiratory Mechanics / Q000502:physiology*; D012307:Risk Factors; D012891:Sleep Apnea Syndromes / Q000175:diagnosis / Q000209:etiology / Q000401:mortality / Q000503:physiopathology*; D015996:Survival Rate; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000401:mortality / Q000503:physiopathology*