Waxman M B, Wald R W
Circulation. 1977 Sep;56(3):385-91. doi: 10.1161/01.cir.56.3.385.
Out of 12 patients in whom phenylephrine terminated ventricular tachycardia, four were selected for detailed studies of its mechanism of action. Pretreatment with edrophonium (15-20 mg, i.v.) decreased, while atropine (2.4 mg, i.v.) increased by at least a factor of two, the dose of phenylephrine required to break ventricular tachycardia. Carotid sinus massage following pretreatment with edrophonium in unusually high (15-20 mg, i.v.) doses broke ventricular tachycardia in all four patients. The evidence presented supports the assumption that a vagal mechanism caused both instances of termination. These findings significantly alter our interpretation of vagal interventions in the bedside clinical diagnosis of wide QRS complex tachycardias.
在12例使用去氧肾上腺素终止室性心动过速的患者中，选取了4例对其作用机制进行详细研究。静脉注射依酚氯铵（15 - 20毫克）进行预处理后，使终止室性心动过速所需的去氧肾上腺素剂量减少，而静脉注射阿托品（2.4毫克）则使其至少增加两倍。在使用异常高剂量（静脉注射15 - 20毫克）的依酚氯铵预处理后进行颈动脉窦按摩，4例患者的室性心动过速均被终止。所提供的证据支持这样一种假设，即迷走神经机制导致了这两种终止情况。这些发现显著改变了我们对床边临床诊断宽QRS波群心动过速时迷走神经干预的解读。
