Journal of The Association of Physicians of India ■ Vol. 63 ■ September 2015 74 Transient Trifascicular Block in Severe Hyperkalemia Navnit Agarwal 1 , Anurag Singh 2 , Ripudaman Gaba 2 , Pankaj Jaiswal 2 , Mandavi Agarwal 2 , Ranjeet Shukla 2 Case RepoRts Introduction H yperkalemia is a life-threatening electrolyte abnormality requiring urgent management. 1 Serum potassium levels greater than 5.5 mmol/l is considered hyperkalemia. Hyperkalemia is often asymptomatic until plasma potassium concentration is above 6.5-7 mmol/L when it results in fatal arrhythmias, hence its called silent killer. Hyperkalemia is associated with significant disturbances in cardiac conduction, ranging from QT interval shortening, to PR interval lengthening and QRS widening. 2 Reversible fascicular blocks, as well as bundle branch blocks or intraventricular conduction delay can be seen. Moreover, hyperkalemia is known to cause potentially lethal dysrhythmias including ventricular tachycardia, ventricular fibrillation, idioventricular rhythms, and asystole. 1-5 Case Report A 65 year old female was brought to Emergency Eepartment of MLB Government Medical College, Jhansi, with complaints of retrosternal chest pain, diaphoresis and syncopal attacks. Patient was a known case of diabetes mellitus and systemic hypertension. Right nephrectomy had been performed 24 years back. Patient was not on any treatment at the time of presentation. Patient’s blood pressure was 166/92 mm of Hg and pulse rate 30/min. Patient was given injection atropine and was immediately transferred to Coronary Care Unit. On examination in Coronary Care Unit patient’s blood pressure was 160/90 mm of Hg, pulse rate 72/ minute, cardiac auscultation revealed no finding and all other systems were within normal limit. Patient’s initial electrocardiogram showed heart rate of 78/min, PR interval of 255 millisec, QRS duration of 146 millisec and mean QRS axis to be 266° . ECG was interpreted as trifascicular block i.e. right bundle branch block (RBBB), left anterior fascicular block (LAFB) and first degree atrioventricular (AV) block. Patient’s Random Blood sugar was 350 mg%. Patient experienced two episodes of Stokes Adams attack following which isoprenaline drip was started. General management of acute coronary syndrome was also started. ABG showed metabolic acidosis with compensatory respiratory alkalosis and hyperkalemia (pH 7.349, bicarbonate 10.6 mmol/L, pCO 2 19.2 mm of Hg, S. Na+ 131 mmol/L and S. K+ 7.2 mmol/L). Complete blood count showed TLC of 15200/mm 3 , hemoglobin of 6.2 g%, DLC P 90 L 7 E 3 and hematocrit of 20.5%. Serum creatinine was 4 mg% and blood urea 96.6 mg%. Anti-hyperkalemic measures (calcium gluconate, insulin, kayexalate, and albuterol nebulization) were urgently commenced and then patient underwent hemodialysis. Three units of blood were transfused. On second day her hyperkalemia and acidosis recovered (S. K + 4.2 mmol/L, pH 7.5, pCO 2 36.6 mm of Hg, HCO 3 28.9 mmol/L). Her ECG on second day showed heart rate 85/min, PR interval of 137 millisec, QRS duration of 102 millisec with mean QRS axis -53°. ECG was interpreted as LAFB. Thus RBBB and first degree AV block reversed after correction of hyperkalemia. To rule out coronary artery disease (CAD) CPK-MB and Troponin-I were done. CPK-MB was 1.2 IU/L and Troponin-I was 0.1 ng/ml (CPK-MB was normal and Troponin-I only slightly raised but in renal failure threshold is raised and upto 0.15 ng/ml is considered to be normal). 2-D echo was normal with LVEF 66%. She was discharged on day 5 of admission. Discussion This case demonstrates an atypical presentation of hyperkalemia-induced trifascicular block that resolved to LAFB with lowering of the serum potassium levels. Although electrophysiologic studies at the AV node and His-Purkinje system would be needed to confirm our theory that hyperkalemia induced the ECG pattern of trifascicular block in this patient, the absence of any other explanation, such as medication overdose, myopericarditis, rheumatic fever, or acute myocardial ischemia, suggests that hyperkalemia was the underlying etiology. The resolution of trifascicular block to LAFB with aggressive treatment of hyperkalemia also suggests that this electrolyte disturbance produced the higher-grade AV block. Abstract Hyperkalemia is a commonly encountered electrolyte abnormality that can significantly alter normal cardiac conduction. Potentially lethal dysrhythmias associated with hyperkalemia include complete heart block and Mobitz Type II second-degree AV block. We report a case of trifascicular block, due to hyperkalemia. The patient’s symptoms and electrocardiogram (ECG) evidence of trifascicular block resolved with lowering of serum potassium levels, with subsequent ECG showing left anterior hemiblock. This paper highlights an infrequently reported dysrhythmia associated with hyperkalemia that emergency physicians should be familiar with. 1 Professor, 2 Resident, Department of Medicine, MLB Medical College, Jhansi, Uttar Pradesh Received: 27.04.2011; Accepted: 20.08.2014