Pathophysiology of hyperkalemia presenting as brugada pattern on electrocardiogram (ECG)

Objective: Unknown ethiology Background: Brugada phenocopies (BrP) are clinical and electrocardiographic (ECG) entities elicited by reversible medical conditions speculated to have pathogenesis rooted in ion current imbalances or conduction delays within the myocardial wall. During an inciting pathologic condition, it produces ECG patterns identical to those of con-genitally-acquired Brugada syndrome and subsequently returns to normal ECG patterns upon resolution of the medical condition. This case report describes a 26-year-old man presenting to the Emergency Department (ED) for suspected heroin overdose with a rare ECG consistent with BrP secondary to acute hyperkalemia. Case Report: A 26-year-old man with a history of substance abuse and a seizure disorder presented to the ED for acute encephalopathy secondary to a heroin overdose complicated by severe rhabdomyolysis and acute renal fail-ure. Laboratory investigations showed acute hyperkalemia (potassium of 7.2 mmol/L) in addition to an elevated creatine kinase, severe transaminitis, and elevated creatinine. His ECG on admission revealed Brugada-like changes in leads V1-V2, with subsequent resolution upon bicarbonate administration and normalization of po-tassium. After initial stabilization, the patient was admitted to the Intensive Care Unit (ICU). His rhabdomyol-ysis and acute kidney injury improved after copious rehydration. He was found to have community-acquired pneumonia, with a negative infectious disease workup, that improved with antibiotics. Upon resolution of his hypoxemic respiratory failure and improvement in mentation, he was discharged from the hospital. Conclusions: Our case report adds to the growing literature on BrP and highlights the importance of recognizing its charac-teristic ECG pattern as a unique presentation of a common electrolyte derangement.