Lazarus A, Py A, Guérin F, Valty J, Le Heuzey J Y
Service de cardiologie, hôpital Cochin, Paris.
Arch Mal Coeur Vaiss. 1993 Dec;86(12):1753-9.
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)
成人睡眠呼吸暂停综合征中已报告了许多夜间心律失常和传导缺陷。最典型的是心率的巨大变异性，这种变异性呈周期性且与呼吸暂停发作相关，很容易与单纯的呼吸性窦性心律失常区分开来。其特征是起初心动过缓，随后出现反弹性心动过速。心动过缓依赖迷走神经（可被阿托品抑制），可能继发于低氧血症对颈动脉化学感受器的刺激。心动过速主要归因于迷走神经张力亢进的停止，尽管也有人提出存在儿茶酚胺刺激。这些变化的起源纯粹是功能性的，随着呼吸暂停的治疗（清醒、气管切开术）、氧疗维持动脉血氧浓度以及副交感神经阻滞（阿托品）而消退。该现象的强度与动脉血氧饱和度降低的程度有关，而动脉血氧饱和度降低程度本身又与基础动脉血氧饱和度（SaO2）和呼吸暂停持续时间有关。这些患者夜间可能会出现因阵发性窦房或房室传导阻滞导致的收缩期延长。迷走神经活动过度的影响得到了证实（迷走神经切断术的抑制作用），且不存在器质性病变（白天未出现、气管切开术、电生理测试正常），这支持了与呼吸暂停的关系。虽然比传导异常少见，但房性心律失常（早搏、扑动、颤动）也是睡眠呼吸暂停的可能并发症。气管切开术后心律失常的消退以及阿托品的疗效（同样支持迷走神经诱发机制）表明不存在器质性基础。最后，有时会观察到夜间心室过度兴奋，其可能机制是严重低氧血症（SaO2 < 60%）与呼吸暂停末期交感神经张力增加共同作用的结果。（摘要截选至250字）
