Lidocaine (IV)

Class IB sodium-channel blocker for ventricular arrhythmias — fast on/off kinetics, best on ischemic and scar-related VT. An alternative to amiodarone in shock-refractory VF/pVT.

Indication

Ventricular tachycardia and VF — particularly ischemic; rescue for VT during procedures and in arrest

Typical dose

1–1.5 mg/kg IV bolus, repeat 0.5–0.75 mg/kg q5–10 min (max ~3 mg/kg), then 1–4 mg/min infusion

Why we use it

Lidocaine is the classic class IB antiarrhythmic for ventricular rhythms. In the EP lab and on the code cart it is reached for in ischemic VT/VF, as a rescue when VT recurs during a procedure, and as the amiodarone alternative in shock-refractory VF/pulseless VT. It has essentially no role in atrial arrhythmias.

Mechanism

Lidocaine blocks the fast sodium channel with rapid on-off kinetics and a preference for inactivated/depolarized channels. That makes it selective for ischemic, depolarized, or scar tissue — exactly where reentrant VT lives — while sparing normal, well-polarized myocardium. It shortens the action potential duration and does not prolong the QT.

Dose and route

Bolus: 1–1.5 mg/kg IV. For breakthrough VT, repeat 0.5–0.75 mg/kg every 5–10 minutes, up to a total of ~3 mg/kg.
Infusion: 1–4 mg/min after load (lower end for HF/hepatic dysfunction/elderly).
Arrest dosing (VF/pVT): 1–1.5 mg/kg IV/IO, may repeat 0.5–0.75 mg/kg.

Onset and clearance

Onset within minutes of a bolus; short duration, so an infusion is needed to sustain effect.
Hepatic clearance, highly dependent on hepatic blood flow. In low-output states, HF, hepatic disease, and the elderly, clearance falls and levels accumulate — reduce the infusion and watch for toxicity.

Monitoring and toxicity

Lidocaine toxicity is dose- and level-related and presents neurologically before cardiac:

Early/CNS: perioral numbness, lightheadedness, tinnitus, slurred speech, tremor, confusion.
Severe: seizures, then respiratory depression.
Cardiac (high levels): myocardial depression, bradycardia, hypotension, conduction block.

Monitor mental status and the rhythm; consider levels with prolonged infusions or in patients at risk of accumulation. Stop or reduce the infusion at the first CNS signs.

Cautions

Reduce dose in heart failure, hepatic impairment, shock, and the elderly.
Caution with high-grade conduction disease without backup pacing.
Additive CNS/cardiac effects with other antiarrhythmics and CNS depressants.

Common pitfalls

Reaching for lidocaine in an atrial arrhythmia — it does not work there.
Running a standard infusion in a low-output or hepatic patient and causing toxicity.
Missing early CNS signs (numbness, tinnitus) that precede a seizure.
Forgetting that it is second-line to amiodarone in most VF/pVT algorithms unless the arrest is clearly ischemic or amiodarone has failed.