C99. Torsade de pointes in coronavirus disease 2019 patient: hypopotassemia, cardiac injury, and drug-induced arrhythmia

Abstract

Abstract Background Coronavirus disease 2019 (COVID-19) is a viral disease with wide spectrum of clinical manifestation. Malignant arrhythmia had been reported, however the exact mechanism remains unclear. We present a case of Torsade de Pointes (TdP) in COVID-19 patient. Case Description A 28 years old female, post caesarean section, confirmed COVID-19, was consulted to cardiology department due to acute lung oedema and premature ventricular complex (PVC) bigeminy. Oxygen saturation dropped to 78% with non-rebreathing mask, so she was intubated. She got furosemide and amiodarone drip. Later on, she developed pulseless ventricular tachycardia, TdP. Defibrillation 200 J was done and MgSO4 2 gram intravenous bolus was delivered. The rhythm converted to normal sinus rhythm, with prolonged QT Interval (503 ms). Potassium level was 2.7, hs-troponin I level was 510.6, and IL-6 level was 33.95. Echocardiogram showed global normokinetic with EF 64% on dobutamin. Amiodarone was stopped. She got MgSO4 drip and potassium chloride drip. Discussion Cardiac involvement in COVID-19 are common. Possible mechanisms are systemic inflammation and cytokine storm, as shown by increased IL-6. Cardiac injury, marked by increased hs-troponin I, causes abnormal conduction and prolonged repolarization due to interstitial edema and cardiac fibrosis, with abnormal Ca2+ handling and down regulation of K+ channels. These, together with QT-prolonging effect of amiodarone and hypokalemia, hypoxia, or neurohormonal stress, can induce TdP. Early treatment, ECG monitoring, and correcting electrolyte imbalance are very crucial in COVID-19. Once lethal arrhythmia ensues, proper anti-arrhythmia administration and withdrawal of contributing medications can prevent mortality.