ArticleFrontiers in medicine2026
Case Report: Amiodarone-triggered refractory ventricular fibrillation storm in septic cardiomyopathy with pre-existing QT prolongation: termination using lidocaine and anisodamine.
Article in Frontiers in medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Septic cardiomyopathy (SCM) is a reversible acute cardiac dysfunction caused by sepsis. The use of QT-prolonging agents such as moxifloxacin and amiodarone may induce life-threatening arrhythmias, including torsades de pointes (TdP) and ventricular fibrillation (VF), both associated with high morbidity and mortality, posing significant challenges in clinical management. Case presentation: We report the case of an 89-year-old male who developed septic cardiomyopathy secondary to enterogenic septic shock, presenting with marked corrected QT (QTc) prolongation and impaired cardiac function. Following intravenous administration of moxifloxacin and amiodarone, QTc interval further prolonged, leading to frequent premature ventricular contractions that progressed to refractory TdP and VF. Despite conventional treatment, including electrolyte correction, defibrillation, and cardiopulmonary resuscitation, the arrhythmias remained uncontrollable. Intravenous maintenance therapy with lidocaine combined with anisodamine was initiated, resulting in gradual resolution of arrhythmias. No further TdP or VF episodes occurred. After 2 weeks, left ventricular function returned to baseline, and the patient was discharged in stable condition. A 9-month follow-up revealed near-complete recovery of cardiac function. Conclusion: Moxifloxacin and amiodarone may trigger refractory TdP and VF in patients with septic cardiomyopathy. Intravenous lidocaine combined with anisodamine may be a potential therapeutic option for terminating these refractory arrhythmias.
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