What is the effect of lidocaine on heart rate in patients with arrhythmias?

Lidocaine's Effect on Heart Rate in Arrhythmias

Lidocaine does not have a clinically significant negative chronotropic (heart rate-slowing) effect in most patients with arrhythmias; however, it can paradoxically increase ventricular rate in atrial flutter and atrial fibrillation, and may cause bradycardia or asystole as a toxic effect, particularly in patients with acute myocardial infarction. 1

Primary Cardiac Effects

Lidocaine is primarily a sodium channel blocker (Class Ib antiarrhythmic) that does NOT work through rate control mechanisms. 1, 2 Unlike beta-blockers, calcium channel blockers, or digoxin, lidocaine does not slow AV nodal conduction or reduce heart rate as its therapeutic mechanism. 1

Key Electrophysiologic Actions:

• Blocks voltage- and pH-dependent sodium channels, primarily in ventricular tissue 2
• Decreases action potential duration and increases refractory period in ventricular myocardium 2
• Does NOT significantly affect AV nodal conduction or sinus node automaticity at therapeutic doses 1

Paradoxical Rate Increases in Supraventricular Arrhythmias

Critical Warning: Lidocaine can dangerously INCREASE ventricular rate in patients with atrial flutter or atrial fibrillation. 3

Atrial Flutter:

• Ventricular rate increased significantly (21-47 beats/minute) in 3 of 18 patients (17%) with atrial flutter after lidocaine administration 3
• The atrial flutter rate itself decreased in 94% of patients (mean 27 beats/minute decrease), but improved AV conduction paradoxically increased ventricular response 3

Atrial Fibrillation:

• Mean ventricular rate increased by 6 beats/minute after rapid lidocaine injection in atrial fibrillation patients 3
• 9% of atrial fibrillation patients experienced ventricular rate increases >20 beats/minute, with 6% having potentially serious clinical events 3
• This effect is particularly pronounced in patients also receiving quinidine 3

Mechanism of Paradoxical Tachycardia:

The rate increase occurs because lidocaine may improve AV nodal conduction while slowing the atrial rate, allowing more atrial impulses to conduct to the ventricles. 3

Contraindication in Specific Arrhythmias

The ACC/AHA explicitly contraindicates lidocaine (along with other AV nodal blocking agents) in Wolff-Parkinson-White syndrome with atrial fibrillation, as it can facilitate antegrade conduction along the accessory pathway, resulting in acceleration of ventricular rate, hypotension, or ventricular fibrillation. 1

Negative Chronotropic Effects as Toxicity

Bradycardia and asystole represent TOXIC effects of lidocaine, not therapeutic actions. 1

Bradycardia/Asystole Risk:

• Increased incidence of asystole with lidocaine use in acute MI may obscure the favorable influence of ventricular arrhythmia suppression 1
• Deaths from asystole and electromechanical dissociation offset the reduction in ventricular fibrillation deaths, explaining why lidocaine does not reduce overall mortality despite reducing VF 1
• Bradycardia and sinus arrest are recognized cardiovascular toxic effects requiring monitoring 4, 5, 6

Monitoring Requirements:

• Watch for cardiovascular effects including bradycardia, sinus arrest, and hypotension 4, 5
• Careful monitoring is essential in patients with severe shock or heart block 6

Negative Inotropic Effects (Not Chronotropic)

Lidocaine DOES have significant negative inotropic (contractility-reducing) effects, which should not be confused with chronotropic effects. 7

• Lidocaine produces significant prolongation of pre-ejection period (PEP) and PEP/LVET ratio, indicating reduced contractility 7
• This negative inotropic effect is more profound in patients with acute myocardial infarction 7
• The effect persists for at least 2 hours after bolus injection when followed by maintenance infusion 7
• Lidocaine depresses myocardial contractility, requiring careful monitoring especially in hemodynamically compromised patients 4

Clinical Implications

When Lidocaine is Appropriate:

• Ventricular tachycardia and ventricular fibrillation in acute MI setting 1
• Frequent (>6/min), closely coupled (R on T), multiform, or runs of ≥3 ventricular premature beats 1, 8
• VF resistant to defibrillation 1

When to Avoid Lidocaine:

• Atrial fibrillation or atrial flutter where rate control is the goal 1, 3
• WPW syndrome with atrial fibrillation (absolute contraindication) 1
• Patients requiring negative chronotropic effects—use beta-blockers, calcium channel blockers, or digoxin instead 1

Common Pitfalls

• Do not use lidocaine expecting heart rate reduction—it is NOT a rate-control agent 1
• Be prepared for paradoxical ventricular rate acceleration in atrial flutter/fibrillation 3
• Recognize that bradycardia with lidocaine represents toxicity, not therapeutic effect 4, 5
• Distinguish between negative inotropic effects (common and expected) and negative chronotropic effects (uncommon and usually toxic) 7