Ketamine-induced QTc interval prolongation

نویسندگان

  • Tejinder S. Swaran Singh
  • Foad Elahi
  • Brian Cheney
چکیده

Sir, Ketamine is a noncompetitive antagonist of the N-methyl-D-aspartate (NMDA) receptor. It is widely used as a dissociative anesthetic and is also used as an adjunct in pain management, particularly in opioid-tolerant patients. It blocks calcium channels and depresses sodium channel function as well as having anticholinergic effects. It inhibits the re-uptake of the catecholamines and may have some nonanalgesic effects at mu and sigma opioid receptors. It is particularly useful as an anesthetic in patients with respiratory disease, as the increased catecholamines cause bronchodilation. Increased catecholamines also contribute to its stimulant effect on the cardiovascular system, where it is known to increase blood pressure and heart rate with higher doses. There have been very few reports of cardiac rhythm abnormalities related to ketamine in animal models and no human reports, specifically of ventricular arrhythmogenic effects. Drug-induced QT interval prolongation usually occurs via alterations of intracellular ion channel function. It's associated with either prolonged depolarization due to an increase in sodium influx via sodium channels or reduced repolarization by inhibition of outward potassium channels. Potassium and magnesium abnormalities alter potassium channel function, increasing the risk of arrhythmias like QT prolongation and Torsades de Pointes. This case will present a patient who experienced a prolonged QTc interval which was temporally associated with a sub-anesthetic infusion of ketamine, as well as discussion of available literature on potential cardiac effects of the medication. A 21-year-old male with a history of chronic intravenous (IV) BLOCKINheroin BLOCKINuse BLOCKINpresented BLOCKINfor BLOCKINa BLOCKINmitral BLOCKINvalve BLOCKINreplacement BLOCKINas well as aortic valve replacement. The patient had previously had his mitral valve replaced 6 months prior for valvular endocarditis. Two months following discharge from his first mitral BLOCKINvalve BLOCKINrepair, BLOCKINthe BLOCKINpatient BLOCKINbegan BLOCKINto BLOCKINuse BLOCKINIV BLOCKINheroin BLOCKINagain and subsequently developed both aortic and mitral valve endocarditis. He was admitted for repair of these valves, which was done with pericardial tissue bioprosthetic valves for both.

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عنوان ژورنال:

دوره 33  شماره 

صفحات  -

تاریخ انتشار 2017