Lau I V
J Electrocardiol. 1985 Apr;18(2):151-6. doi: 10.1016/s0022-0736(85)80006-6.
Direct impact of the heart on the right ventricle induces transient ventricular tachycardia. Preconditioning the heart with a moderate dose of propranolol (0.4 mg/Kg, IV) did not affect impact-induced tachyarrhthmia although effective beta adrenergic blockage was evident. A high dose of propranolol (1.6 mg/Kg, IV) or a moderate dose of quinidine (3 mg/Kg, IV) prevented impact-induced ventricular tachycardia. High-dose propranolol and quinidine, an agent with no beta blockade properties, share similar local effects on the myocardial cell membrane which was sufficient to prevent the tachyarrhythmia. Pacing of the right ventricular free wall at the impact site resulted in an ECG similar to that observed following impact. Pacing of the subjacent septem, the other possible arrhythmogenic site affected by the impact, resulted in a large aberrant S wave (Lead II) different from the QRS complex during impact-induced tachyarrhythmia. Therefore, impact-induced ventricular tachycardia originates from the impact site by a direct ventricular mechanism.
心脏对右心室的直接撞击可诱发短暂性室性心动过速。用中等剂量的普萘洛尔（0.4毫克/千克，静脉注射）对心脏进行预处理，尽管明显存在有效的β肾上腺素能阻滞，但并未影响撞击诱发的心律失常。高剂量的普萘洛尔（1.6毫克/千克，静脉注射）或中等剂量的奎尼丁（3毫克/千克，静脉注射）可预防撞击诱发的室性心动过速。高剂量普萘洛尔和奎尼丁（一种无β阻滞特性的药物）对心肌细胞膜具有相似的局部作用，足以预防心律失常。在撞击部位对右心室游离壁进行起搏，可导致心电图与撞击后观察到的心电图相似。对受撞击影响的另一个可能的致心律失常部位——相邻的间隔进行起搏，可导致出现一个大的异常S波（II导联），与撞击诱发的心律失常期间的QRS波群不同。因此，撞击诱发的室性心动过速通过直接的心室机制起源于撞击部位。
