![]() ![]() ![]() She presented again to the ED and was found to be hypotensive, tachypneic, mildly encephalopathic, and bradycardic with a heart rate of 30–40 beat per minute (bpm). She also reported new visual disturbances with purple discoloration. The patient was briefly admitted for acute kidney injury, re-hydrated with intravenous fluids, and discharged home without change in medications.Ī few days later, the patient developed worsening fatigue and lightheadedness with several episodes of syncope. The patient’s creatinine was noted to be elevated at 2.09 compared to her baseline normal renal function. The patient had recently undergone a total right knee replacement for degenerative joint disease 4 weeks prior, and post-operatively the patient had developed these symptoms along with poor oral intake. A recent transthoracic echocardiogram had been performed a few months prior and had demonstrated a normal ejection fraction, concentric left ventricular hypertrophy, and biatrial enlargement. The patient’s medication list was notable for the use of flecainide 100 mg BID and metoprolol tartrate 50 mg BID. The patient presented for the first time to the Emergency Department (ED) complaining of nausea, lightheadedness, and generalized weakness. She also had sick sinus syndrome, with a dual-chamber pacemaker placed many years prior, COPD, and heart failure with preserved ejection fraction. The patient was a 91-year-old female with a history of paroxysmal atrial fibrillation maintained in normal sinus rhythm on flecainide for more than 3 years. We describe a case of flecainide toxicity secondary to acute kidney injury in the setting of dual-chamber pacing, resulting in ventricular capture latency and intermittent failure to capture. Although flecainide toxicity is described in the literature on acute kidney injury, there is a paucity of literature on the acute presentation of flecainide toxicity in the setting of a cardiac pacemaker. A mortality rate of 10–25% has been reported with class Ic antiarrhythmic agent toxicity. Flecainide has a narrow therapeutic window and a highly variable plasma half-life in the setting of renal dysfunction. Its primary action in atrial tissue is to prolong the effective refractory period (ERP), demonstrating use-dependence, resulting in a more pronounced effect as the heart rate increases. As a class Ic agent, its primary mechanism of action is blockade of fast sodium channels, resulting in a reduction in myocardial conduction velocity and a negative inotropic effect on the myocardium. Flecainide is a Vaughan-Williams class Ic antiarrhythmic agent used most commonly in the treatment of atrial fibrillation, atrial flutter, and supraventricular and ventricular arrhythmias in patients without known structural or ischemic cardiac disease.
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