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Flecainide/indapamide QRS widening and hyponatraemia led to worsening of the conduction abnormalities: case report

A 74-year-old woman experienced QRS widening and hyponatraemia during treatment with flecainide and indapamide. Also, she developed hyponatraemia during treatment with indapamide, which led to worsening of the conduction abnormalities [routes and frequencies not stated]. The woman, who had acute renal failure and mild cognitive impairment, presented to the emergency department due to repetitive falls. She reported extreme fatigue with nausea. She was observed to be pale with prolonged capillary refill time on clinical examination. Bilateral pulmonary crackles and irregular heart sounds were noted on auscultation, and this indicated cardiogenic shock. A surface ECG revealed an irregular, broad QRS complex rhythm, which was most compatible with a very wide right bundle branch block and left anterior fascicular block, and this accounted for the left axis deviation. Fractional excretion of sodium was noted to be 0.6%, which suggested renal hypoperfusion. She had been receiving indapamide 0.625mg along with levothyroxine sodium [levothyroxine], rosuvastatin [rosuvastatine], perindopril and pantoprazole. In the recent past, she had started receiving flecainide 150mg along with apixaban and bisoprolol for paroxysmal atrial fibrillation. Also, she had been receiving bumetanide for peripheral oedema. Based on the clinical and lab examination, drug toxicity (flecainide intoxication) was considered to be the most probable cause of the QRS widening. Based on drug panel, which was negative for tricyclic antidepressants, the diagnosis of flecainide accumulation due to acute renal failure was made. Additionally, she developed hyponatraemia secondary to indapamide (thiazide diuretic), which worsened the conduction abnormalities. The woman was treated with sodium bicarbonate, which was titrated for pH 7.5. A spectacular change in QRS duration was noted following the initial infusion of sodium bicarbonate. During the first hours, she developed several episodes of non-sustained ventricular tachycardia, followed by immediate and spontaneous recuperation. In the following days, the QRS normalised, and she was discharged in good clinical condition. The acute renal failure had caused accumulation of flecainide, and this led to the typical ECG appearance of flecainide intoxication with extreme QRS broadening and potentially lethal conduction disturbances, which were worsened by hyponatraemia [durations of treatments to reactions onsets not stated]. Wilgenhof A, et al. An irregular, extremely broad QRS complex rhythm. American Journal of Emergency Medicine 37: 1989.e1-1989.e3, No. 10, Oct 2019. Available from: 803444765 URL: http://doi.org/10.1016/j.ajem.2019.158356

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Reactions 11 Jan 2020 No. 1786