Mechanism of Lignocaine (Lidocaine) in Reducing Heart Rate
Lignocaine reduces heart rate primarily by blocking voltage- and pH-dependent sodium channels in cardiac tissue, which decreases automaticity of ectopic pacemakers and suppresses abnormal rhythms, rather than by directly slowing the sinus node. 1
Primary Mechanism of Action
Lignocaine binds preferentially to inactivated sodium channels, which decreases the action potential duration and increases the refractory period in ventricular tissue. 1 This selective binding is particularly effective in ischemic or abnormal cardiac tissue where channels remain in the inactivated state longer. 1
The drug blocks both transient and persistent sodium currents, though at therapeutic concentrations it has greater effect on the persistent sodium current that is resistant to inactivation. 2 This persistent sodium current blockade may be responsible for much of its antiarrhythmic action. 2
Effects on Different Cardiac Pacemakers
Lignocaine has differential effects on various cardiac pacemaker sites:
The drug has minimal direct effect on the sinus node, causing only modest slowing of sinus rhythm (approximately -5% at 1 mg/kg IV). 3
Lignocaine markedly suppresses idioventricular and ectopic ventricular pacemakers (reducing rate by -16.7% to -67% depending on dose and conditions), which is far more pronounced than its effect on the sinus node. 3
The drug prolongs ventricular standstill during vagal stimulation by +25-53%, indicating it enhances suppression of escape rhythms. 3
Lignocaine shifts the threshold potential to less negative values and decreases the diastolic depolarization slope (-23.6%), which slows spontaneous automaticity in Purkinje fibers and other ectopic foci. 3
Clinical Context: Rate Reduction in Arrhythmias
The perceived "heart rate reduction" with lignocaine is not due to direct sinus node suppression, but rather:
Termination or slowing of ventricular tachyarrhythmias through interruption of re-entrant circuits, especially in ischemic tissue. 1
Suppression of abnormal automaticity in ectopic ventricular pacemakers that may be driving rapid rhythms. 3
Abolition of digitalis-induced tachycardias, including bidirectional tachycardia and atrial tachycardia with block. 4
Important Clinical Caveats
Lignocaine's rate-reducing effects are enhanced by beta-blockade, as propranolol exaggerates the suppression of idioventricular rhythms when combined with lignocaine. 3 This interaction should be considered when both drugs are used together.
The drug depresses myocardial contractility (reducing contractile force by approximately -48% at therapeutic concentrations), which can contribute to circulatory depression, particularly in patients with poor cardiac output. 5, 3
Lignocaine is indicated for ventricular arrhythmias, not for primary rate control of supraventricular rhythms. 5 The American Heart Association guidelines specify that lignocaine decreases automaticity and suppresses ventricular arrhythmias, but it is not as effective as amiodarone for improving outcomes in cardiac arrest. 5