Pharmacology

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   Lidocaine is a local anesthetic and a type Ib antiarrhythmic agent. It inhibits fast sodium channels and depresses automaticity within the His-Purkinje system and the ventricles but has a variable effect and may shorten the effective refractory period and action potential duration. Conduction within ischemic myocardial areas is depressed, abolishing reentrant circuits. Unlike quinidine and related drugs, lidocaine exerts a minimal effect on the automaticity of the sinoatrial node and on conduction through the AV node, and it does not decrease myocardial contractility or blood pressure in usual doses. It also has rapid “on-off” binding to sodium channels (to allow reactivation of the channel) and competes with other sodium channel blockers (that are slow to release and block the channel throughout the cardiac cycle). This may account for its antiarrhythmic effect with poisonings from other sodium channel blockers (type 1a antiarrhythmics, tricyclic antidepressants).

   
   
2. 
   

   The oral bioavailability of lidocaine is poor owing to extensive first-pass hepatic metabolism (although systemic poisoning is possible from ingestion). After intravenous administration of a single dose, the onset of action is within 60–90 seconds and the duration of effect is 10–20 minutes. The elimination half-life of lidocaine is approximately 1.5–2 hours; active metabolites have elimination half-lives of 2–10 hours. Lidocaine clearance declines with continuous infusions, which may be attributable to its metabolite monoethylglycinexylidide (MEGX). Drug accumulation may occur in patients with congestive heart failure or with liver or renal disease.

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