Ketamine is a dissociative anesthetic with N-methyl-d-aspartate and glutamate receptor antagonist properties. It has been the most popular agent to facilitate emergency department procedures for three decades. Considered a safe and effective option for procedural sedation, ketamine has rapid onset, short effective sedation time, and a low risk profile. Ketamine's sympathomimetic effects could theoretically induce stress-related cardiac dysfunction, including cardiomyopathy. A review of the literature demonstrates one prior report of stress (Takotsubo) cardiomyopathy after ketamine sedation.

In this case report, we present a case of Takotsubo cardiomyopathy after ketamine sedation for distal radius fracture reduction. The patient presented hemodynamically normal with an unremarkable cardiac ultrasound and progressed to hypoxia from bilateral pulmonary edema, eventually requiring intubation. Inpatient evaluation revealed elevated high sensitivity troponin, non-obstructive coronary arteries on catheterization, and echocardiogram findings of Takotsubo cardiomyopathy. She received operative fixation of her radius fracture by orthopedics and was discharged home on hospital day 9. She had an unremarkable follow up with cardiology but had no echocardiogram to determine full resolution.

Although ketamine has robust evidence of safety and efficacy, physicians should be aware of the potential complications of its sympathomimetic effects, from hypertension and tachycardia to overt Takotsubo cardiomyopathy.