Motté G
Arch Mal Coeur Vaiss. 1984 Apr;77 Spec No:17-22.
Although experimental hypokalaemia leads to a wide range of arrhythmias and conduction defects, the only significant clinical result of potassium depletion (with or without hypokalaemia) is observed at ventricular level: ventricular extrasystoles, typical forms of ventricular tachycardia or, more commonly, the form suggesting torsades de pointe . The mechanism of these ventricular arrhythmias is obscure and may involve either reentry phenomena favored by the heterogenicity of the refractory periods at the Purkinje-ventricular junction or automaticity related to the increase in the slope of diastolic depolarisation or with the appearance of early post-potentials in series. Although arrhythmias are rare in isolated hypokalaemia and a healthy heart, they are common and serious if hypokalaemia complicates organic cardiac disease, especially when associated with another factor of cellular desynchronisation such as bradycardia or myocardial impregnation by certain antiarrhythmic drugs. The increased toxicity of digitalis in hypokalaemia is a well known example. Treatment is based essentially on compensating the potassium depletion, bearing in mind the risks of massive supplements administered too rapidly, and on the administration of potassium-sparing drugs (spironolactone and others). Rapid cardiac pacing is often useful in preventing recurrence of torsades de pointe while waiting for adequate potassium repletion.
尽管实验性低钾血症会导致多种心律失常和传导缺陷,但钾缺乏(无论有无低钾血症)唯一显著的临床后果出现在心室层面:室性期前收缩、典型的室性心动过速形式,或者更常见的是尖端扭转型室速形式。这些室性心律失常的机制尚不清楚,可能涉及浦肯野纤维-心室交界处不应期异质性所促进的折返现象,或者与舒张期去极化斜率增加或相继出现早期后电位相关的自律性。尽管在孤立性低钾血症和健康心脏中,心律失常很少见,但如果低钾血症使器质性心脏病复杂化,尤其是与另一个细胞不同步因素(如心动过缓或某些抗心律失常药物导致的心肌浸润)相关时,心律失常就很常见且严重。低钾血症时洋地黄毒性增加就是一个众所周知的例子。治疗主要基于补充钾缺乏,同时要牢记快速大量补充钾的风险,以及使用保钾药物(螺内酯等)。在等待充分补钾的过程中,快速心脏起搏通常有助于预防尖端扭转型室速的复发。