Lidocaine (also known as lignocaine) is a commonly used amide-type local anesthetic and a Class 1B antiarrhythmic drug . It acts primarily by blocking voltage-gated sodium channels , thereby preventing the initiation and conduction of nerve impulses and abnormal cardiac electrical activity.
Chemical Structure and Classification
Lidocaine belongs to the amide group of local anesthetics, which is characterized by the presence of an amide bond (–CONH–) . This bond features:
- A nitrogen-hydrogen (–NH–) group connected to a carbonyl group (C=O) .
- The aromatic ring in lidocaine is substituted with two methyl groups in the ortho positions , enhancing its lipophilicity.
- The amide nitrogen is linked to a diethylamino side chain , contributing to its anesthetic and antiarrhythmic properties
High-Yield
- Ester anesthetics (e.g., procaine , cocaine ) have one "i" in their names.
- Amide anesthetics (e.g., lidocaine , bupivacaine ) have two or more "i"s .
Indications
Lidocaine is widely used for both local anesthesia and management of ventricular arrhythmias . Key indications include:
- Acute ventricular tachycardia , especially post-myocardial infarction.
- Ventricular arrhythmias related to digoxin toxicity.
- Open-heart surgery as an antiarrhythmic agent.
- Local anesthesia for:
- Infiltration and nerve block
- Epidural and spinal anesthesia
- Ocular procedures (eyelid or globe surgeries)
- Minor surgical or dental procedures
- Topical anesthesia (gel, spray, or aerosol) for mucosal surfaces (e.g., larynx, bronchi, urethra)
Mechanism of Action
Lidocaine acts by:
- Blocking open and inactivated voltage-gated sodium channels , preventing sodium influx into neurons or cardiac cells.
- This inhibits depolarization , thereby halting nerve signal propagation or ectopic pacemaker activity.
- Lidocaine has rapid association and dissociation kinetics , making it more effective in ischemic or depolarized cardiac tissue .
- In nerves: it prevents pain signal transmission .
- In the heart: it suppresses abnormal ventricular activity without significantly affecting atrial conduction.
Pharmacokinetics and Pharmacodynamics
- Onset : Rapid
- Duration : Intermediate (1–2 hours)
- Route : Poor oral bioavailability → IV or parenteral administration is preferred
- Metabolism : Hepatic (via CYP450 enzymes, primarily oxidative N-dealkylation )
- Clearance : Hepatic blood flow-dependent
- Half-life : ~2 hours in healthy individuals
- Therapeutic range : 1.5–5.0 mcg/mL
- Toxic levels : >5 mcg/mL
Reduced clearance is seen in heart failure or liver disease , increasing the risk of toxicity.
Dosing and Administration
- For arrhythmias: IV bolus followed by continuous infusion.
- For minor surgery: 1% plain lidocaine
- For dental procedures: 2% lidocaine with epinephrine
Dose adjustments are necessary in:
- Congestive heart failure
- Liver impairment
Side Effects
Central Nervous System (CNS):
- Drowsiness
- Nausea, vomiting
- Paresthesia
- Twitching
- Seizures (focal → generalized)
Cardiovascular System:
- Bradycardia
- Hypotension
- Negative inotropy
- Cardiac arrest or asystole (at toxic doses)
Lidocaine is considered less cardiotoxic compared to other antiarrhythmic drugs.
Toxicity
Toxicity occurs when plasma levels exceed 5 mcg/mL .
Mnemonic: SAMS
- S : Slurred speech
- A : Altered CNS
- M : Muscle twitching
- S : Seizures
Drug Interactions
- Negative inotropic agents (e.g., beta-blockers, calcium channel blockers) may reduce hepatic blood flow , increasing lidocaine plasma levels and predisposing to toxicity.
- Enzyme inducers/inhibitors may also affect metabolism.
