Abstract Introduction Bupropion overdose is associated with adverse cardiovascular events, including wide-complex arrhythmias and cardiogenic shock, particularly in patients with a prolonged QTc interval. Traditional therapies for other atypical antidepressants such as sodium bicarbonate have shown limited efficacy in bupropion toxicity. While veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is increasingly recognized as a rescue therapy for drug-induced cardiac collapse, there is no clear role for transitioning to veno-venous ECMO (VV-ECMO). We present a case that highlights a transition from VA-ECMO to VV-ECMO in a patient who had persistent respiratory failure due to pulmonary injury despite improvement in his cardiogenic shock. Description A 28-year-old man presented after intentional ingestion of approximately 20 tablets of bupropion, 7-8 tablets of clonazepam, alcohol, cocaine, and other unidentified substances. He was initially intubated for worsening lethargy and decreased airway protection. Continuous monitoring revealed progressive QRS widening and a maximum QTc interval of 552 ms. He subsequently developed multiple seizures followed by a pulseless electrical activity (PEA) arrest. Post-arrest echocardiogram revealed an ejection fraction (EF) of 10%, prompting VA-ECMO cannulation for presumed bupropion-induced toxic cardiomyopathy. After three days, his cardiogenic shock had improved, but severe hypoxemia persisted, thought to be due to a combination of lung injury due to bupropion overdose, pulmonary edema, and pneumonia. ECMO support was thus transitioned to VV-ECMO. The patient continued to improve and was eventually decannulated off ECMO. A tracheostomy was placed due to the need for prolonged ventilation. Two weeks later, he completed red cap trials and was successfully decannulated. EF normalized to 75%, and he was discharged with outpatient psychiatric follow-up. Discussion This report contributes to the growing evidence supporting ECMO as a life-saving therapy in severe cardiogenic shock secondary to bupropion toxicity. It serves as a bridge to metabolism of the drug and recovery of the cardiac myocytes. The VA-to-VV ECMO transition is rarely described in previous cases and it not only highlights the evolving cardiopulmonary needs of this group of patients, but also optimizes outcomes for patients with pulmonary injury as a complication of bupropion overdose. Progression through PMV and decannulation stages also reflects both neurologic and respiratory recovery through the coordinated care of the ICU, speech therapy, and caregiver support. Ultimately, this report emphasizes the value of multidisciplinary critical care in achieving full physiologic recovery after bupropion arrest. This abstract is funded by: None
Veeramachineni et al. (Fri,) studied this question.