This work was supported by a Grant-in-Aid from the American Heart Association Southeast Affiliate. Dr. Sims was supported by The American College of Clinical Pharmacy/Merck and Company Cardiovascular Fel-lowship.
Lidocaine Increases the Proarrhythmic Effects of Monophasic but not Biphasic Shocks
Article first published online: 13 AUG 2003
© Futura Publishing Company, Inc. 2001
Journal of Cardiovascular Electrophysiology
Volume 12, Issue 12, pages 1363–1368, December 2001
How to Cite
SIMS, J. J., MILLER, A. W. and UJHELYI, M. R. (2001), Lidocaine Increases the Proarrhythmic Effects of Monophasic but not Biphasic Shocks. Journal of Cardiovascular Electrophysiology, 12: 1363–1368. doi: 10.1046/j.1540-8167.2001.01363.x
This work was presented in part at the 20th Annual Scientific Sessions of the North American Society of Pacing and Electrophysiology, Toronto, Ontario, Canada, May 1999.
- Issue published online: 13 AUG 2003
- Article first published online: 13 AUG 2003
- Manuscript received 29 June 2001; Accepted for publication 28 September 2001.
- Cited By
- biphasic waveform;
- monophasic waveform;
- ventricular fibrillation;
- vulnerable period
Lidocaine and Shock Proarrhythmia. Introduction: Lidocaine increases monophasic shock defibrillation energy requirement (DER) values but does not alter biphasic shock DER values. However, the mechanism of this drug/shock waveform interaction is unknown. It may be that lidocaine increases the proarrhythmic actions of monophasic shocks but not biphasic shocks. Thus, lidocaine may increase monophasic shock DER values by increasing myocardial vulnerability to shock-induced ventricular fibrillation.
Methods and Results: Area of myocardial vulnerability (AOV), defined by a two-dimensional grid according to shock strength (y-axis) and shock coupling interval (x-axis), was assessed for biphasic shocks (n = 11) and monophasic shocks (n = 13) in intact swine hearts. Shocks were randomly delivered during right ventricular pacing at 10 shock strengths (50 to 500 V) and five coupling intervals (160 to 240 msec). AOV was defined as the number of points within the test grid that induced ventricular fibrillation. AOV, upper limit of vulnerability (ULV), and DER values were determined at baseline and during systemic infusion of lidocaine (10 mg/kg/hour). Lidocaine increased AOV, ULV, and DER values by 35%, 23%, and 36%, respectively, for monophasic shocks. However, lidocaine did not alter AOV, ULV, or DER values for biphasic shocks.
Conclusion: Lidocaine increases the AOV to monophasic shocks, which is directly related to changes in ULV and DER values. This implies that lidocaine increases the proarrhythmic activity of monophasic shocks but not biphasic shocks. This may explain why lidocaine increases monophasic shock DER values.