Lidocaine is a local anesthetic that also has Vaughan Williams classification type IB antiarrhythmic properties. It is indicated for ventricular fibrillation in patients who cannot undergo synchronized cardioversion and are hemodynamically stable who do not require electrical cardioversion. It can also be used for both monomorphic and polymorphic ventricular tachycardias. Lidocaine is considered an alternative to amiodarone as a second-line agent in patients with ventricular tachycardia or pulseless electrical activity who are resistant to electric cardioversion and intravenous epinephrine or vasopressin.1 The use of intravenous lidocaine has decreased with the elimination of lidocaine as the standard of practice for prophylaxis of asymptomatic premature ventricular contractions or nonsustained ventricular tachycardia after acute myocardial infarction.
Lidocaine serum concentrations decrease biexponentially, and intravenous lidocaine follows a two-compartment pharmacokinetic model (see Figure 9-1).2 After an intravenous loading dose, lidocaine distributes into cardiac tissue rapidly, with an alpha t½ of approximately 8 minutes (range 7–30 minutes), achieving maximum serum concentrations within an hour. The cardiac tissue is considered to be part of the central compartment for lidocaine with onset of effects quickly after a loading dose. The beta elimination phase is due to transfer of drug from the larger volume of distribution (Vdss) back into the central compartment (Vdc) with t½ of 87–108 minutes. Therefore, even if a maintenance infusion is started simultaneously to the loading dose, rapid redistribution can lead to subtherapeutic concentrations that may place the patient at risk for life-threatening arrhythmia.3 This rapid distribution phase justifies the repetition of a “loading dose,” generally 50 percent of the initial load, given at 5- to 20-minute intervals to maintain a therapeutic concentration.1,4,5,6
Most sources suggest therapeutic concentrations fall in the range of 1.5–5 mcg/mL.1,5,6,7 Unfortunately, lidocaine has a narrow therapeutic index and adverse effects are both dose- and concentration-related. As you approach the upper end of this range, adverse events such as paresthesias, dizziness, drowsiness, and euphoria may appear. If lidocaine concentrations rise above the therapeutic range into toxic concentrations, a host of adverse consequences may be seen, including general adverse events like confusion, dysarthria, muscular twitching or seizures, agitation, psychosis, and even coma.6,7 Cardiovascular adverse events include hypotension, atrioventricular blockade with concurrent hyperkalemia, and circulatory collapse.2,8,9,10,11 However, lidocaine-induced adverse drug events are often missed and attributed to the underlying disease pathology. Routine serum concentration monitoring is not recommended unless the clinician suspects an adverse drug event, the patient experiences recurrent ventricular arrhythmias, or the patient has disease states or conditions known to change the pharmacokinetics of lidocaine.12,13
METABOLISM AND ELIMINATIONA