Long QT syndrome (LQTS) is characterized by QT interval prolongation, which significantly increases the risk of malignant arrhythmias and sudden cardiac death, even in the absence of structural heart disease. While LQTS can be congenital, distinguishing it from the acquired form is crucial, though both may coexist in some cases. We present the case of a 60-year-old woman with a history of schizoaffective disorder treated with escitalopram and amisulpride and a recent prescription for ciprofloxacin for a urinary tract infection, who was admitted following a cardiac arrest. The episode was triggered by acquired QT prolongation due to the combined effects of QT-prolonging medications and hypokalemia. The patient was successfully resuscitated, and discontinuation of the offending medications (e.g., escitalopram, amisulpride, and ciprofloxacin) led to clinical stabilization with QT normalization, while other possible causes were ruled out (e.g., ischemia, thyroid disorders, etc.). This case highlights the importance of thorough medication review and early identification of individuals at risk for acquired LQTS to prevent potentially fatal arrhythmias. It also highlights the necessity of considering underlying genetic predisposition, especially in cases where QT prolongation persists despite the discontinuation of the offending agents and/or correction of other contributing factors, making genetic testing advisable in selected patients, as it will guide further management.