Khavandi A, Walker P R
Department of Cardiology, Southmead Hospital, North Bristol NHS Trust, Bristol, UK.
Emerg Med J. 2007 May;24(5):e26. doi: 10.1136/emj.2006.044362.
A man presented with recurrent syncope, weakness and fatigue. His ECG showed marked QRS widening and he had gross hyponatraemia and hypokalaemia. His medications included bendroflumethiazide (long term) and flecainide (started 2 months previously). This presentation was consistent with flacainide cardiotoxicity exacerbated by electrolyte disturbance. The syncopal episodes probably represented life-threatening arrhythmias. The ECG and symptoms resolved completely once the electrolytes were corrected. Increased cardiotoxicity with hypokalaemia is documented, but not widely recognised. Hyponatraemia-induced flecainide cardiotoxicity has not been documented. The clinical effects of flecainide are due to use-dependent block of sodium channels. There are reports that support the use of hypertonic sodium salts to reverse flecainide toxicity via antagonism at the receptor. By this rationale, hyponatraemia would lead to Flecainide toxicity. Flecainide has been shown to reduce salt absorption in animal bowel. It is possible that in combination with bendroflumethiazide it acted synergistically to produce profound electrolyte disturbance. Flecainide cardiotoxicity has a significant mortality and can present non-specifically. Thus, early recognition is essential. This case demonstrates the importance of strict electrolyte control in patients who are on flecainide. We would discourage concomitant use of flecainide and bendroflumethiazide.
一名男性出现反复晕厥、乏力和疲劳症状。他的心电图显示QRS波明显增宽，且存在严重低钠血症和低钾血症。他的用药包括苄氟噻嗪（长期服用）和氟卡尼（2个月前开始服用）。这种表现符合因电解质紊乱而加重的氟卡尼心脏毒性。晕厥发作可能代表危及生命的心律失常。一旦电解质得到纠正，心电图和症状完全消失。低钾血症会增加心脏毒性，这已有文献记载，但尚未得到广泛认可。低钠血症诱发的氟卡尼心脏毒性尚无文献记载。氟卡尼的临床作用是通过对钠通道的使用依赖性阻滞实现的。有报告支持使用高渗钠盐通过在受体处的拮抗作用来逆转氟卡尼毒性。根据这一原理，低钠血症会导致氟卡尼毒性。氟卡尼已被证明可减少动物肠道对盐的吸收。有可能它与苄氟噻嗪联合使用产生协同作用，导致严重的电解质紊乱。氟卡尼心脏毒性具有显著的死亡率，且表现可能不具特异性。因此，早期识别至关重要。该病例表明在服用氟卡尼的患者中严格控制电解质的重要性。我们不建议同时使用氟卡尼和苄氟噻嗪。
