• Nozomi Toya, Shutaro Isokawa, Akiyoshi Suzuki, Norio Otani, and Shinichi Ishimatsu.
• Department of Emergency and Critical Care Medicine, St. Luke's International Hospital, 9-1 Akashi-cho, Chuo-ku, Tokyo 104-8560, Japan. Electronic address: tonozo@luke.or.jp.
• Am J Emerg Med. 2019 Nov 1; 37 (11): 2118.e1-2118.e3.

AbstractBidirectional ventricular tachycardia (BVT) is a tachyarrhythmia characterized by 180-degree beat-to-beat alteration in the QRS axis. BVT is traditionally known as an electrocardiography (ECG) finding pathognomonic of digitalis poisoning and a hallmark of catecholamine-induced ventricular tachycardia. Apart from digitalis poisoning, aconitine poisoning is the only reported cause of poisoning-related BVT, and no report of caffeine-poisoning-related BVT is as yet available. A-27-year-old woman was transported to hospital with cardiac arrest from ventricular fibrillation after taking a massive dose of a caffeine-containing supplement (corresponding to 6 g of caffeine) 6 h before presentation. Return of spontaneous circulation (ROSC) was achieved by defibrillation. She developed BVT after ROSC. Hemodialysis was performed to remove the causative drug from the blood, with subsequent resolution of BVT and hemodynamic stabilization. At presentation, she had a blood caffeine concentration of 232 μg/mL. A suggested mechanism of development of BVT is that increased intracellular calcium concentration causes delayed afterdepolarization, which induces alternate occurrence of triggered activities within different His-Purkinje fibers, and thereby produces characteristic ECG findings. Caffeine acts on the ryanodine receptor to promote calcium release from the sarcoplasmic reticulum, and thus can induce BVT via the same mechanism. Caffeine poisoning can be treated by dialysis. In cases of BVT induced by caffeine poisoning, hemodynamic stabilization can be achieved by emergency dialysis.Copyright © 2018. Published by Elsevier Inc.

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