vv Journal of Cardiovascular Medicine and Cardiology ISSN: 2455-2976 DOI CC By 033 Citation: Eng M, Wung W, Srivatsa UN, Singh GD (2017) “C” Trouble: Class IC Anti-arrhythmic Toxicity. J Cardiovasc Med Cardiol 4(2): 033-037. DOI: http://doi.org/10.17352/2455-2976.000047 Medical Group Case Report “C” Trouble: Class IC Anti-arrhythmic Toxicity Maia Eng # , William Wung # , Uma N Srivatsa # and Gagan D Singh* # 1 Division of Cardiovascular Medicine, University of California (Davis) Medical Center, Sacramento, CA, USA #Contributed equally Dates: Received: 09 June, 2017; Accepted: 29 June, 2017; Published: 30 June, 2017 *Corresponding author: Gagan D Singh, Assistant Professor, Division of Cardiovascular Medicine, Uni- versity of California Davis Medical Center, 4860 Y Street, Suite 2820, Sacramento CA 95817, USA, E-mail: https://www.peertechz.com Introduction The most common cardiac arrhythmia encountered in clinical practice is atrial fibrillation (AFib). AFib has significant effects on long-term mortality and stroke, and contributes greatly to overall healthcare costs, affects quality of life and the functional status of many patients [1]. The incidence and prevalence of AFib continues to rise with age, when co- morbidities that affect rhythm management frequently co- exist [1]. Due to improved quality of life, rhythm control is a common treatment strategy [2,3]. This is accomplished with the use of antiarrhythmic agents across the Singh-Vaughn- Williams classification [4]. In patients with structurally normal hearts, Class IC agents such as flecainide and propafenone are commonly prescribed for maintenance of sinus rhythm as the first line therapy [5]. Despite their prevalent use, the relative toxicities of these agents are infrequent, and therefore seldom emphasized in the most recent guidelines and reviews [4]. The lack of survival benefit from rhythm management strategy utilizing antiarrhythmic drugs have been suggested to be due to adverse effects from these agents [6]. The mechanism of action is on the cellular action potential and can be pro- arrhythmic due to the lack of specificity on the atrial tissue. It is critical that clinicians be able to recognize the causes, signs and symptoms of toxicity from these antiarrhythmic agents. We present two cases of drug toxicities in different clinical settings, the pathophysiology, and the overall management approach. Case 1 A 75-year-old female with a history of paroxysmal AFib, heart failure with preserved ejection fraction, idiopathic pulmonary fibrosis, and hypertension is admitted with fevers, chills, productive cough, worsening dyspnea, anorexia, lightheadedness, nausea and vomiting. Approximately one year prior, the patient had recurrent bouts of debilitating palpitations. A 24hour continuous Holter monitor confirmed the diagnosis of paroxysmal AFib. A transthoracic echocardiogram showed a structurally normal heart, and a pharmacologic stress test did not demonstrate reversible ischemia. Shortly thereafter the patient was started on flecainide 50mg orally twice a day and metoprolol succinate 25mg orally once a day; this intervention lessened the frequency of her symptoms. One month later, her flecainide was titrated up to 100mg orally twice a day resulting in complete abatement of her palpitations with follow-up electrocardiograms demonstrating stable QRS intervals (Figure 1). On this admission, the patient’s vitals were notable for an elevated temperature of 39 degrees Celsius, blood pressure of 145/56 mm Hg, heart rate of 98 beats per minute and a peripheral oxygen saturation of 98% on supplemental oxygen (60% FiO2). She was in mild respiratory distress, tachypneic, and diaphoretic. Her respiratory exam was notable for inspiratory rales and expiratory rhonchi bilaterally. The remainder of her physical exam was unremarkable. Laboratory data was notable for a leukocytosis of 18.4 L/mm3 (ref 4.5-11 K/ mm3) with left shift and bandemia (95% neutrophils, and 20% bands), serum potassium of 4.9 mEq/L (ref 3.5-5.0 mEq/L) and serum creatinine of 3.4 mg/dL (ref 0.4-1.3 mg/dL). A chest Figure 1: Baseline electrocardiogram in patient after starting flecainide demonstrating normal QRS interval.