Gettes L S
Division of Cardiology, University of North Carolina, Chapel Hill 27599-7075.
Circulation. 1992 Jan;85(1 Suppl):I70-6.
It is well known that changes in serum potassium cause ventricular arrhythmias as a result of clearly documented changes in the electrophysiological characteristics of single fibers. Hypopotassemia induced by thiazide and loop diuretics may contribute to the incidence of sudden cardiac death in patients with hypertension and those with congestive heart failure. In addition, hypopotassemia appears to be an independent risk factor for lethal ventricular arrhythmias occurring in the setting of acute myocardial infarction and contributes significantly to arrhythmias associated with starvation and alcoholism. The increase in myocardial extracellular potassium that occurs in the ischemic zone after coronary occlusion is clearly a major factor in the genesis of lethal ventricular arrhythmias that occur in this setting. A decrease in serum magnesium is also believed to be arrhythmogenic, and magnesium depletion is thought to play a role in many of the arrhythmias associated with hypopotassemia. Moreover, the administration of magnesium salts may be effective in the management of life-threatening ventricular arrhythmias. However, definite evidence establishing a causal relation between ventricular arrhythmias and hypomagnesemia or intracellular magnesium depletion is lacking. Changes in intracellular calcium contribute to the arrhythmias associated with acute ischemia and with reperfusion and may be important in the genesis of ventricular tachycardia induced by exercise and by digitalis. Thus, electrolyte and metabolic abnormalities clearly underlie lethal ventricular arrhythmias in a wide variety of clinical situations and should be routinely considered as potential etiologic factors in patients with life-threatening ventricular arrhythmias, particularly those with hypertension and congestive heart failure who are receiving thiazide and loop diuretics.
众所周知，血清钾的变化会导致室性心律失常，这是由于单根纤维的电生理特性发生了明确记录的变化。噻嗪类和袢利尿剂引起的低钾血症可能会增加高血压患者和充血性心力衰竭患者心源性猝死的发生率。此外，低钾血症似乎是急性心肌梗死时发生致命性室性心律失常的独立危险因素，并且在与饥饿和酒精中毒相关的心律失常中起重要作用。冠状动脉闭塞后缺血区心肌细胞外钾的增加显然是该情况下发生致命性室性心律失常的主要因素。血清镁降低也被认为有致心律失常作用，镁缺乏被认为在许多与低钾血症相关的心律失常中起作用。此外，镁盐的给药可能对危及生命的室性心律失常的治疗有效。然而，缺乏确定室性心律失常与低镁血症或细胞内镁缺乏之间因果关系的确切证据。细胞内钙的变化导致与急性缺血和再灌注相关的心律失常，并且可能在运动和洋地黄诱导的室性心动过速的发生中起重要作用。因此，电解质和代谢异常显然是多种临床情况下致命性室性心律失常的基础，对于有危及生命的室性心律失常的患者，特别是那些正在接受噻嗪类和袢利尿剂治疗的高血压和充血性心力衰竭患者，应常规将其视为潜在的病因。
