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Lignocan (Lignocaine / Lidocaine)

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Classification

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Mechanism of Action

1. The drug (partly as uncharged base, partly as cation) penetrates the nerve sheath and axon membrane.
2. Binding to Na⁺ channel sites prevents the conformational changes needed for channel activation (opening).
3. Repetitive stimulation causes additional use-dependent (phasic) block — the more frequently a nerve fires, the more drug binds.
4. Clinical block duration is governed by slow diffusion of drug into/out of the whole nerve, not by fast channel binding/dissociation.

The uncharged base penetrates the membrane; the charged cation acts from the cytoplasmic surface as the dominant blocking form. — Miller's Anesthesia, 10e

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Pharmacological Effects

1. Local Anesthetic Effects

• Onset: Rapid (intermediate hydrophobicity → good membrane permeation)
• Duration: Shorter acting than bupivacaine/ropivacaine (approximately 1–2 hours for infiltration, up to 3–4 hours with epinephrine)
• Block sequence (sensitivity order): Small unmyelinated C fibers (pain, temperature) → small myelinated Aδ → large myelinated Aβ (motor, proprioception)
• Routes: Infiltration, nerve block, epidural, spinal, topical (2–10%), IV regional (Bier block), intravenous (antiarrhythmic)

2. Antiarrhythmic Effects (Class Ib)

• Reduces automaticity — suppresses spontaneous depolarization of ventricular pacemakers
• Suppresses ventricular ectopy
• Used for hemodynamically stable VT, refractory VF/pulseless VT (as second-line after amiodarone)
• Upon return of spontaneous circulation (ROSC) after VF: maintenance infusion 1–4 mg/min IV
• ⚠️ 2015 ACLS guidelines removed routine lidocaine from the cardiac arrest algorithm; a 2016 RCT found no survival benefit over placebo for out-of-hospital cardiac arrest — Tintinalli's Emergency Medicine

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Clinical Uses

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Toxicity

CNS Toxicity (dose-related, progressing order)

1. Numbness/tingling of tongue
2. Light-headedness
3. Tinnitus
4. Visual disturbances
5. Drowsiness (characteristic of lidocaine, unlike bupivacaine)
6. Muscle twitching
7. Convulsions / Seizures
8. Coma
9. Apnea

CNS stimulation occurs first (blockade of inhibitory synapses), followed by CNS depression from direct medullary suppression. — Roberts & Hedges' Clinical Procedures in Emergency Medicine

Cardiovascular Toxicity

• Moderate blood levels → mild ↑ in cardiac output, heart rate, BP (due to CNS stimulation)
• High levels → direct myocardial depression, hypotension, bradycardia, cardiac collapse
• Slows electrical conduction → reentry arrhythmias, ventricular dysrhythmias
• ⚠️ Lidocaine has a higher CC/CNS ratio than bupivacaine — meaning cardiovascular collapse requires much higher doses than seizures (relatively safer cardiovascular profile vs. bupivacaine)

Treatment of Systemic Toxicity (LAST)

• Airway management, benzodiazepines for seizures
• IV lipid emulsion (Intralipid) — reverses systemic local anesthetic toxicity

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Important Drug Interactions & Risk Factors for Toxicity

• Low α-acid glycoprotein (AAG) levels (neonates, liver disease) → ↑ free drug → ↑ toxicity risk
• Hepatic disease → reduced metabolism → ↑ plasma levels
• Mixtures of local anesthetics → additive toxicity
• CNS depressants → worsen apnea/cardiovascular depression
• Drugs inhibiting hepatic enzymes → ↑ lidocaine plasma concentration

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Dosage Summary

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Key Points to Remember

• Lignocaine is an amide — metabolized by the liver (not plasma cholinesterases)
• Allergic reactions are extremely rare (no p-aminobenzoic acid metabolite, unlike esters)
• Epinephrine prolongs duration and reduces systemic absorption (not used for digital/penile/ear blocks)
• Spinal lignocaine can cause transient neurologic symptoms (TNS) — radicular irritation
• Safer cardiovascular profile than bupivacaine (higher CC/CNS ratio)

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