1994Journal of Cardiovascular ElectrophysiologyRequires access

Effects of Procainamide and Lidocaine on Defibrillation Energy Requirements in Patients Receiving Implantable Cardioverter Defibrillator Devices

Debra S. Echt, STEVEN T. GREMILLION, John Tayu Lee, Dan M. Roden, Katherine T. Murray, Mark Borganelli, Diane M. Crawford, James R. Stewart, John W. Hammon

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Abstract

INTRODUCTION: In acute canine studies, lidocaine, but not procainamide, increases defibrillation energy requirements. We evaluated the effects of lidocaine or procainamide on defibrillation energy requirements in 27 patients undergoing intraoperative testing for implantable cardioverter defibrillator 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 micrograms/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 micrograms/mL; N-acetyl procainamide 1.0 +/- 0.4 micrograms/mL). 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 supratherapeutic 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.

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INTRODUCTION: In acute canine studies, lidocaine, but not procainamide, increases defibrillation energy requirements. We evaluated the effects of lidocaine or procainamide on defibrillation energy requirements in 27 patients undergoing intraoperative testing for implantable cardioverter defibrillator 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 micrograms/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 micrograms/mL; N-acetyl procainamide 1.0 +/- 0.4 micrograms/mL). 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 supratherapeutic 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.

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Available abstract

INTRODUCTION: In acute canine studies, lidocaine, but not procainamide, increases defibrillation energy requirements. We evaluated the effects of lidocaine or procainamide on defibrillation energy requirements in 27 patients undergoing intraoperative testing for implantable cardioverter defibrillator 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 micrograms/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 micrograms/mL; N-acetyl procainamide 1.0 +/- 0.4 micrograms/mL). 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 supratherapeutic 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.

Key concepts: Procainamide, Lidocaine, Defibrillation, Defibrillation threshold, Medicine, Anesthesia, Sodium channel blocker, Ventricular fibrillation

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