Lidocaine is a local anaesthetic given by injection, spray or patch to numb skin, gums and mucosa in minor surgery and procedures. In controlled doses it is also used as a hospital antiarrhythmic.
Also known as: Xilocaína, Xylocaine
No documented drug–drug interactions for this medicine.
No documented food or drink interactions.
IV lidocaine (class Ib antiarrhythmic) is contraindicated in 2nd/3rd-degree AV block (conduction depression).
ECG before IV infusion; topical/infiltration use is unaffected.
Prontuário Terapêutico INFARMED, 3.1 (IV lidocaine — AV block).
Lidocaine is extensively hepatically metabolised — liver disease reduces clearance and raises CNS toxicity risk.
Reduce dose in hepatic impairment; monitor for CNS toxicity signs.
Prontuário Terapêutico INFARMED (lidocaine — hepatic metabolism, dose reduction).
Systemic lidocaine toxicity manifests with seizures — caution in epileptics.
Respect maximum dose (3 mg/kg without epinephrine); aspirate before injecting.
Prontuário/site monograph (lidocaine — maximum dose, CNS toxicity).
Lidocaine at local anaesthetic doses is considered safe in pregnancy; Annex 1 records "no malformations known; use if benefit outweighs risk" (3rd trimester, factor C). High IV doses (systemic toxicity) are associated with fetal CNS depression and arrhythmias — respect maximum doses.
Compatible in all trimesters for local/regional use; avoid toxic IV doses.
Present in milk in amounts too small to be harmful (Prontuário, Annex 2, l. 42834) — compatible with breastfeeding.
Prontuário Terapêutico INFARMED — Annex 1: "Lidocaine... use if benefit outweighs risk" (l. 40810); Annex 2: "Present in milk in amounts too small to be harmful" (l. 42834). EMC-UK (MHRA) — Lidocaine SmPC.
Clinical and educational support tool. The information does not replace a medical prescription or the opinion of a qualified healthcare professional.
Reference amide local anaesthetic, with reversible nerve block dependent on dose, concentration and tissue exposure time; with epinephrine, duration and safety margin increase.
Blocks voltage-gated sodium channels of the neuronal membrane (activated/inactivated state — use-dependent): interrupts action potential propagation in nociceptive fibres earlier in small (thin myelinated and C) than in large motor fibres. Epinephrine vasoconstricts the local bed, reducing absorption and plasma peak.
Local infiltration: absorption proportional to site vascularity (intercostal > caudal > epidural > subcutaneous); peak 30–45 min. Epinephrine reduces absorption rate by ~1/3. Oral bioavailability irrelevant (complete first pass).
N-dealkylation oxidation (CYP1A2 and CYP3A4) to monoethylglycinexylidide (MEGX) and glycinexylidide, renally excreted; high hepatic extraction (flow-dependent clearance). As an antiarrhythmic: efficacy reduced in heart failure (lower hepatic flow).
1.5–2 h (post-infusion); in systemic toxicity rapid distribution is followed by re-elevation (second phase). Neonates: 3–4 h.
Medicines from the same therapeutic group (ATC classification) or the same pharmacological class.
