CARDIAC-ARRHYTHMIAS IN THE ADULT SHEEP AP NEA SYNDROME

Many nocturnal cardiac arrhythmias and conduction defects have been re ported in the adult sleep apnoea syndrome. The most original is the gr eat variability of the heart rate which is cyclical and related to the apnoeic episodes, and easily differentiated from simple respiratory s inus arrhythmia. It is characterised by an initial bradycardia followe d by rebound tachycardia. The bradycardia is vagally dependant (inhibi ted by atropine) probably secondary to carotid chemoreceptor stimulati on by the hypoxaemia. The tachycardia is mainly attributed to the cess ation of vagal hypertonicity although catecholamine stimulation has be en suggested. The origin of these changes is purely functional, regres sing with treatment of apnoea (waking, tracheotomy), the maintenance o f arterial oxygen concentrations with oxygen therapy and parasympathet ic blockade (atropine). The intensity of the phenomenon is related to the degree of arterial desaturation, which is itself related to basal arterial saturation (SaO2) and the duration of the apnoeas. Prolonged systole due to paroxysmal sino-atrial or atrioventricular block may be observed at night in these patients. The influence of vagal overactiv ity is confirmed (suppression of vagotomy) with no organic pathology ( diurnal absence, tracheotomy, normal electrophysilogical testing) in f avour of a relationship with apnoea. Though less common than conductio n abnormalities, atrial arrhythmias (extrasystoles, flutter, fibrillat ion) are also possible complications of sleep apnoea. The absence of a n organic substrate is indicated by their regression post-tracheotomy and the efficacy of atropine (again in favour of a vagally-induced mec hanism). Finally, noctumal ventricular hyper-excitability is sometimes observed, the probable mechanism being the association of severe hypo xaemias (SaO2 < 60 %) and the increased sympathetic tone at the end of the apnoea. This poses the problem of possible underlying ischaemic h eart disease with acute myocardial ischaemia caused by the fall in SaO 2 which, in association with catecholamine release, could induce extra systoles, episodes of ventricular tachycardia or even fibrillation. Al l these noctumal abnormalities may be recorded by Holter ECG and shoul d enable a firm diagnosis of the sleep apnoea syndrome.