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Effects of Procainamide and Lidocaine on Defibrillation Energy Requirements in Patients Receiving Implantable Cardioverter Defibrillator Devices
Author(s) -
ECHT DEBRA S.,
GREMILLION STEVEN T.,
LEE JOHN T.,
RODEN DAN M.,
MURRAY KATHERINE T.,
BORGANELLI MARK,
CRAWFORD DIANE M.,
STEWART JAMES R.,
HAMMON JOHN W.
Publication year - 1994
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.1994.tb01198.x
Subject(s) - procainamide , lidocaine , defibrillation , defibrillation threshold , medicine , anesthesia , sodium channel blocker , ventricular fibrillation , cardioversion , implantable cardioverter defibrillator , cardiology , sodium channel , sodium , chemistry , atrial fibrillation , organic chemistry
Effects of Procainamide and Lidocaine on Defibrillation. intntduction: In acute canine studies, lidocaine. but not prucainamidc, increases defibrillation energy requirements. We evaluated the effects of lidocaine or procainamide on defihrillation energy requirements in 27 patients undergoing intraoperative testing fur implantable cardioverter dcfibrillator device placement. Methods and Results: Patients were tested off antiarrhythmic drugs and again following either lidocaine (200 to 250 mg loading and 3 mg/min maintenance infusions) or procainamide (1 gm loading and 3 to 4 mg/min maintenance infusions). The defibrillation testing protocol consisted of initial testing at 15 J, followed by higher or lower energies to determine the lowest energy producing three consecutive successful defibrillations. Overall, the mean defibrillation energy increased from 14 ± 5 J to 18 ± 7 J during lidocaine (plasma concentration 5.1 ± 1.6 μ/mL; P < 0.02) but were similar at baseline (12 ± 5 J) and during procainamide infusion (13 ± 6 J) (plasma concentration: procainamide 10.7 ± 7.2 μ/rnl.; N‐acetyl procainamide 1.0 ± 0.4 μ/niL). A positive linear correlation was found between lidocaine plasma concentration and percent change in defibrillation energy (lidocaine: r = 0.61; P = 0.01). Procainamide raised the defibrillation energy in three patients, two with supra therapeutic plasma concentrations. The increase in defibrillation energy equaled or exceeded 25 J in four patients after lidocaine and in one patient after procainamide. Conclusion: The data suggest that at high plasma concentrations, lidocaine and procainamide adversely affect defibrillation energy requirements consistent with an adverse, concentration‐dependent effect of sodium channel blockade on defibrillation energy requirements in patients.