Abstract Introduction Dexmedetomidine (Precedex) is widely used in intensive care units for sedation and is generally considered hemodynamically stable. It is a selective α2-adrenergic agonist that produces sedation and analgesia by inhibiting central norepinephrine release and reducing sympathetic outflow. Although some studies suggest it may attenuate QTc prolongation, data in critically ill patients remain limited. Recent reports, however, describe QTc prolongation and malignant ventricular arrhythmias associated with its use. We present a fatal case of torsades de pointes possibly related to dexmedetomidine. Case Description A 63-year-old man with end-stage renal disease on hemodialysis, heart failure with preserved ejection fraction, moderate-to-severe aortic stenosis, and mitral regurgitation was admitted with fever. He was found to have necrosis of the left toe with plans for surgical amputation. During hemodialysis, after receiving one unit of packed red blood cells, he developed acute pulmonary edema with pink frothy sputum, likely due to rapid fluid shifts, requiring emergent intubation. Chest radiograph showed new bilateral opacities, and systolic blood pressure exceeded 190 mm Hg, consistent with hypertensive emergency. A nicardipine infusion led to rapid improvement. ECG showed sinus tachycardia with QTc 484 ms. Dexmedetomidine was started for agitation prior to extubation. He was extubated to BiPAP and remained stable, but ECG revealed QTc 510 ms. Later that evening, telemetry captured torsades de pointes with transient unresponsiveness that resolved spontaneously. Vital signs were otherwise stable. He received 2 g of intravenous magnesium. Laboratory results showed magnesium 2.0 mg/dL, potassium 3.7 mmol/L, and phosphorus 1.8 mg/dL. Repeat ECG demonstrated QTc 681 ms. The patient was DNR status. Recurrent torsades progressed to ventricular fibrillation, and he was pronounced dead. Discussion Prior studies have shown inconsistent effects of dexmedetomidine on cardiac repolarization. Some ICU and perioperative data suggest mild QTc prolongation and increased repolarization heterogeneity, while others report little change or even attenuation under specific anesthetic conditions. These differences likely reflect variations in autonomic tone and comorbidities rather than a electrophysiologic effect. The drug’s bradycardic and sympatholytic properties may indirectly increase susceptibility to QT-related arrhythmia in vulnerable patients. In this case, dialysis-associated electrolyte shifts and dexmedetomidine exposure created a substrate for torsades de pointes. The timing of infusion, progressive QTc prolongation, and subsequent arrhythmia supports a contributory role. While dexmedetomidine remains a valuable sedative, clinicians should be alert to this risk, particularly in patients with baseline QT prolongation or kidney disease and maintain continuous ECG monitoring with prompt electrolyte correction. This abstract is funded by: NONE
Pulipaka et al. (Fri,) studied this question.