ACLS is a set of standardized, evidence-based procedures used by healthcare professionals to manage life-threatening emergencies, particularly cardiac arrest. Within these protocols, medications support high-quality chest compressions and electrical therapy. Lidocaine, an antiarrhythmic drug, helps stabilize dangerous heart rhythms. Its application is specifically targeted toward ventricular arrhythmias, which are disorganized electrical activities originating in the lower chambers of the heart.
Lidocaine’s Mechanism of Action in Cardiac Emergencies
Lidocaine is classified as a Class IB antiarrhythmic agent, acting primarily on the rapid sodium channels in cardiac cells. It blocks the influx of sodium ions into heart muscle cells during the rapid depolarization phase of the electrical cycle. This action slows electrical conduction and reduces the excitability of the ventricular tissue. By reducing the heart muscle’s ability to be prematurely stimulated, lidocaine helps interrupt the chaotic electrical loops that characterize dangerous arrhythmias.
Lidocaine preferentially binds to sodium channels in an inactivated state, which are more common in damaged or ischemic heart tissue. This selective action suppresses abnormal electrical impulses originating in injured areas of the heart. The overall effect stabilizes the cardiac cell membrane, reducing the likelihood of initiating or sustaining a life-threatening ventricular rhythm.
Use in Pulseless Ventricular Fibrillation and Tachycardia
Lidocaine’s primary use in ACLS is managing cardiac arrest caused by shock-refractory Ventricular Fibrillation (VF) or Pulseless Ventricular Tachycardia (pVT). These rhythms involve chaotic or rapid electrical activity resulting in no effective blood circulation. Lidocaine is administered after initial defibrillation attempts and the first dose of epinephrine fail to restore a normal rhythm. Current American Heart Association guidelines consider Lidocaine an acceptable antiarrhythmic alternative to Amiodarone for these shock-refractory rhythms.
The decision to administer Lidocaine occurs during the ongoing cycle of chest compressions and repeated defibrillation attempts. It is typically given after the third shock, following epinephrine administration, to increase the probability of successful defibrillation. The initial intravenous (IV) or intraosseous (IO) dose is 1 to 1.5 milligrams per kilogram (mg/kg). If VF or pVT persists, a second dose is often considered during a subsequent two-minute cycle of cardiopulmonary resuscitation (CPR).
Use in Stable Ventricular Tachycardia
Lidocaine also manages patients experiencing Ventricular Tachycardia (VT) who remain hemodynamically stable (i.e., the patient has a pulse and shows no immediate signs of collapse). This applies primarily to Monomorphic VT, where all electrical complexes on the electrocardiogram (EKG) appear identical. The goal is rhythm control, aiming to slow the heart rate and restore a normal sinus rhythm.
It is a treatment option when other initial measures have failed or are not appropriate, and the patient’s heart function is preserved. It may also be used for stable polymorphic VT, provided the patient does not have a prolonged QT interval. Unlike the cardiac arrest protocol, the patient is conscious and has a perfusing rhythm, allowing for controlled administration and monitoring.
Dosage, Administration, and Toxicity Monitoring
For cardiac arrest from pulseless VF/VT, the initial dose is a rapid IV or IO bolus of 1 to 1.5 mg/kg. If the arrhythmia continues, a second bolus of 0.5 to 0.75 mg/kg can be given every five to ten minutes, up to a maximum total dose of 3 mg/kg. Once a stable rhythm is achieved, a continuous maintenance infusion is started to keep the drug’s concentration steady in the bloodstream, usually dosed at 1 to 4 milligrams per minute.
Continuous EKG monitoring is required during and after administration to assess its effect. Monitoring for Lidocaine toxicity is equally important, as the drug is metabolized by the liver, increasing risk with high doses or liver dysfunction. Early signs of toxicity involve the central nervous system, including confusion, slurred speech, or a metallic taste in the mouth. Severe toxicity can progress to muscle twitching, seizures, and cardiovascular depression with low blood pressure and a slow heart rate.