Feld G K, Nademanee K, Singh B N, Kirsten E
Department of Research and Medicine, Wadsworth VA Medical Center, Los Angeles, CA.
J Clin Pharmacol. 1987 Jan;27(1):52-9. doi: 10.1177/009127008702700108.
The hemodynamic and electrophysiologic effect of a combined intravenous infusion of lidocaine (100 mg bolus followed by 2 mg/min infusion) and propafenone (1 or 2 mg/kg) in patients with a history of ventricular arrhythmia was studied. Lidocaine infusion alone significantly increased the mean pulmonary artery (+28%) and pulmonary capillary wedge (+17%) pressure, with no effect on cardiac index. Lidocaine alone produced no consistent change in any measured electrophysiologic parameter, except slight QTc shortening (-2%, P less than .05). Propafenone alone, particularly at the higher dose (2 mg/kg), produced significant increases in mean blood pressure (+14%), right atrial pressure (+78%), pulmonary artery pressure (+50%), pulmonary capillary wedge pressure (+65%), systemic vascular resistance (+29%), and pulmonary vascular resistance (+61%) and a decrease in cardiac index (-12%). Significant prolongation of PR (+9%), AH (+29%), and HV (+23%) intervals, atrial functional refractory period (+12%), ventricular effective (+7%) and functional (+6%) refractory period, and Wenckebach cycle length (+13%) also occurred after the administration of propafenone alone. Only the effects on atrioventricular (AV) node were observed at the lower dose of propafenone (1 mg/kg). Combined infusion of lidocaine with propafenone produced a mild, statistically insignificant additional negative inotropic effect but reversed the prolongation in atrial and ventricular refractoriness produced by propafenone alone. Thus, the data show that lidocaine attenuates certain electrophysiologic effects of propafenone, which might alter its antiarrhythmic efficacy, while producing mild additive negative inotropic effects that may be of hemodynamic significance.
研究了利多卡因（100mg 推注后以 2mg/min 输注）和普罗帕酮（1 或 2mg/kg）联合静脉输注对有室性心律失常病史患者的血流动力学和电生理效应。单独输注利多卡因可显著增加平均肺动脉压（+28%）和肺毛细血管楔压（+17%），对心脏指数无影响。单独使用利多卡因除使 QTc 轻度缩短（-2%，P<0.05）外，对任何测量的电生理参数均无一致的改变。单独使用普罗帕酮，特别是高剂量（2mg/kg）时，可使平均血压（+14%）、右心房压（+78%）、肺动脉压（+50%）、肺毛细血管楔压（+65%）、体循环血管阻力（+29%）和肺血管阻力（+61%）显著增加，心脏指数降低（-12%）。单独给予普罗帕酮后，PR 间期（+9%）、AH 间期（+29%）和 HV 间期（+23%）、心房功能不应期（+12%）、心室有效不应期（+7%）和功能不应期（+6%）以及文氏周期长度（+13%）也显著延长。在普罗帕酮低剂量（1mg/kg）时仅观察到对房室（AV）结的影响。利多卡因与普罗帕酮联合输注产生轻度、无统计学意义的附加负性肌力作用，但可逆转普罗帕酮单独引起的心房和心室不应期延长。因此，数据表明利多卡因可减弱普罗帕酮的某些电生理效应，这可能改变其抗心律失常疗效，同时产生可能具有血流动力学意义的轻度附加负性肌力作用。
