[Arrhythmia and syndrome of obstructive sleep apnea in adults]

Many nocturnal cardiac arrhythmias and conduction defects have been reported in the adult sleep apnoea syndrome. The most original is the great variability of the heart rate which is cyclical and related to the apnoeic episodes, and easily differentiated from simple respiratory sinus arrhythmia. It is characterised by an initial bradycardia followed by rebound tachycardia. The bradycardia is vagally dependent (inhibited by atropine) probably secondary to carotid chemoreceptor stimulation by the hypoxaemia. The tachycardia is mainly attributed to the cessation of vagal hypertonicity although catecholamine stimulation has been suggested. The origin of these changes is purely functional, regressing with treatment of apnoea (waking, tracheotomy), the maintenance of arterial oxygen concentrations with oxygen therapy and parasympathetic 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 overactivity is confirmed (suppression of vagotomy) with no organic pathology (diurnal absence, tracheotomy, normal electrophysiological testing) in favour of a relationship with apnoea. Though less common than conduction abnormalities, atrial arrhythmias (extrasystoles, flutter, fibrillation) are also possible complications of sleep apnoea. The absence of an organic substrate is indicated by their regression post-tracheotomy and the efficacy of atropine (again in favour of a vagally-induced mechanism). Finally, nocturnal ventricular hyper-excitabilty is sometimes observed, the probable mechanism being the association of severe hypoxaemias (SaO2 < 60%) and the increased sympathetic tone at the end of the apnoea.(ABSTRACT TRUNCATED AT 250 WORDS)