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Influence of lidocaine on human muscle sympathetic nerve activity during programmed electrical stimulation and
K A Ellenbogen1, M L Smith, L A Beightol
1Department of Medicine, Hunter Holmes McGuire Veterans Affairs Medical Center, Richmond, VA.
Abstract:
Lidocaine directly affects conduction and refractoriness of ventricular myocardium, and may also indirectly affect these electrophysiologic properties by inhibition of cardiac sympathetic nerve traffic. Both effects may play important roles in preventing ventricular arrhythmias in humans. To determine if lidocaine has a direct effect on sympathetic nerve activity, the effects of a 100 mg lidocaine bolus followed by a 2 mg/min infusion of lidocaine on muscle sympathetic nerve activity was assessed in seven patients during programmed ventricular stimulation with single extrastimuli (premature ventricular contractions [PVCs]) in sinus rhythm, and in seven patients during induced hemodynamically stable monomorphic ventricular tachycardia. During single extrastimuli, the mean (+/- SEM) area of PVC-associated bursts of sympathetic nerve activity was unaffected by lidocaine (1101 +/- 16 units pre-lidocaine versus 1075 +/- 19 units following lidocaine; p = 0.30). Likewise, the transient decrease in blood pressure with induced PVCs was similar before and after lidocaine infusion (p = 0.46). In seven patients with induced monomorphic ventricular tachycardia, tachycardia cycle length did not change after the lidocaine bolus (393 +/- 18 versus 399 +/- 17 msec; p = 0.34) but increased during lidocaine maintenance infusion (428 +/- 17 msec; p = 0.01). After induction of ventricular tachycardia, systolic pressure decreased from 150 +/- 6 to 117 +/- 9 mm Hg at 1 minute of tachycardia, to 109 +/- 6 mm Hg during the lidocaine bolus, and rebounded to 126 +/- 8 mm Hg during the lidocaine maintenance infusion (p = 0.04, bolus versus infusion).(ABSTRACT TRUNCATED AT 250 WORDS)
Insights
Lidocaine did not directly impact sympathetic nerve activity during premature ventricular contractions. However, lidocaine infusion prolonged ventricular tachycardia cycle length, suggesting an indirect antiarrhythmic effect.
Area of Science:
- Cardiology
- Neuroscience
Background:
- Lidocaine is known to affect cardiac electrophysiology and may influence sympathetic nerve activity.
- Both direct and indirect mechanisms are hypothesized to contribute to lidocaine's antiarrhythmic effects.
Purpose of the Study:
- To investigate whether lidocaine directly inhibits muscle sympathetic nerve activity.
- To assess the impact of lidocaine on electrophysiologic properties during ventricular arrhythmias.
Main Methods:
- Muscle sympathetic nerve activity was measured in patients undergoing programmed ventricular stimulation.
- Lidocaine was administered as a bolus followed by continuous infusion.
- Electrophysiologic parameters and blood pressure were monitored during premature ventricular contractions and induced ventricular tachycardia.
Main Results:
- Lidocaine did not alter sympathetic nerve activity bursts associated with premature ventricular contractions.
- The decrease in blood pressure during premature ventricular contractions was similar before and after lidocaine.
- Lidocaine bolus did not change ventricular tachycardia cycle length, but maintenance infusion significantly increased it.
- Systolic blood pressure showed a complex pattern during ventricular tachycardia with lidocaine administration.
Conclusions:
- Lidocaine's direct effect on sympathetic nerve activity appears minimal in the context of premature ventricular contractions.
- Lidocaine may exert antiarrhythmic effects during ventricular tachycardia through mechanisms that prolong the tachycardia cycle length, potentially independent of direct sympathetic inhibition.