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Electrophysiologic and Electrocardiographic Pharmacodynamics of Cocaine
Author(s) -
Tisdale James E.,
Ducharme Murray P.,
Shimoyama Hisashi,
Webb Charles R.,
Sabbah Hani N.,
Edwards David J.
Publication year - 1996
Publication title -
pharmacotherapy: the journal of human pharmacology and drug therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.227
H-Index - 109
eISSN - 1875-9114
pISSN - 0277-0008
DOI - 10.1002/j.1875-9114.1996.tb02975.x
Subject(s) - qt interval , pharmacodynamics , qrs complex , anesthesia , heart rate , medicine , placebo , effective refractory period , blood pressure , electrocardiography , ventricular fibrillation , cardiology , discontinuation , refractory period , pharmacokinetics , alternative medicine , pathology
To determine and describe relationships between plasma cocaine concentrations and electrophysiologic and electrocardiographic effects, 10 anesthetized dogs with normal intact hearts received a continuous 3‐hour infusion of cocaine 0.11 mg/kg/minute (total dose 20 mg/kg). Data were collected as part of a randomized, blinded, placebo‐controlled study investigating the effects of cocaine on ventricular fibrillation threshold. Every 30 minutes during infusion of cocaine or placebo and for 3 hours after discontinuation of the infusion, heart rate and mean arterial pressure were determined, effective refractory period (ERP) was measured, and QRS duration and PR, QT c , and JT c intervals were recorded. At the time of each 30‐minute measurement, arterial blood was obtained to determine plasma cocaine concentrations. Hysteresis curves were observed for cocaine‐induced increases in ERP and PR interval. The effects of cocaine on QRS duration and QT c and JT c intervals were not well described by tested models. Pharmacodynamic modeling techniques may be used to describe relationships between plasma cocaine concentrations and specific cardiovascular effects of cocaine. Further study is required to determine applicability of this model for prediction of cocaine's cardiovascular effects in humans.