No abstract

Introduction: Flecainide is a class IC anti-arrhythmic used to treat atrial fibrillation. Toxicity can cause bradycardia, QRS prolongation, and ventricular tachyarrhythmia (VT) due to blockade of sodium channels. Although most metabolism occurs through the liver, up to 30% excretion is renal but not dialyzable. The case here represents two arrhythmogenic challenges associated with flecainide treated with alkalization and lipid emulsion. Case: A 75-year-old woman with atrial fibrillation initially presented with syncope and hematemesis. Initial ECG showed junctional bradycardia with narrow escape in HR 30s. Labs notable for creatinine 2.55 (nl <1.2 mg/dl) and potassium 4.8 (3.5-5.0 mmol/L). pH was 7.28 with bicarbonate 18 (22-31 mmol/L). She was treated with glucagon and atropine for suspected B-blocker toxicity but quickly went into shock. Rhythm then changed to a wide complex tachycardia (Fig) with wide QRS 280ms, VT rates in 100s. Due to development of this slow VT, flecainide toxicity was highly suspected, and a bicarbonate drip was started to maintain pH>7.50 in addition to intralipid infusion. In the span of 12 hours, she was able to wean off her vasopressor support. On hospital day 3, she started metoprolol and remained in sinus bradycardia at the time of discharge. Discussion: This case represented acute renal failure secondary to flecainide toxicity and gastrointestinal bleed. Toxicity led to QRS widening and slow VT, which diminished contractility. Serum alkalization and sodium load works to displace flecainide from its channel receptor; intralipid sequesters lipophilic toxin in a “lipid sink” mechanism. In extreme cases, ECMO and overdrive pacing are used. Conclusions: Early recognition of flecainide-related arrhythmias is key. The subsequent approach to flecainide toxicity includes reducing absorption (charcoal, lipid emulsion), antagonizing drug effect (alkalization), and proving hemodynamic support (phenylephrine, vasopressin).