延长心脏动作电位复极期可以终止心律失常。早在1918年用奎尼丁作为抗心律失常药物用来控制心房纤颤,作用机制是通过增加心肌不应期,使 QT 间期延长。Lewis 和Drury 提出奎尼丁的作用主要是延长心肌有效不应期(ERP)。临床上有效浓度可抑制心脏动作电位上升速率,不是延长心脏复极期,传导速度明显缓慢,然而仅终末部份复极稍延长,动作电位的平台期很少受影响。延长心 Prolong cardiac action potential repolarization can terminate arrhythmia. As early as 1918 with quinidine as anti-arrhythmic drugs used to control atrial fibrillation, the mechanism is through the increase of myocardial refractory period, the QT interval prolongation. Lewis and Drury proposed the role of quinidine is to extend the effective myocardial refractory period (ERP). Clinically effective concentrations can inhibit the rate of rise of cardiac action potential, not to extend the heart repolarization period, the conduction velocity was slow, but only some of the terminal part of the repolarization slightly extended, the action potential of the platform is rarely affected. Extend the heart