ADMINISTRATION ROUTES:
IV, IO
ALTERNATIVE NAMES:
Lidocaine, Xylocaine, Lignospan
ICU INDICATIONS:
- Ventricular arrhythmias
Note: this monograph is for intravenous lignocaine administration for ventricular arrhythmias only. It does not cover subcutaneous, topical or neuraxial use for local anaesthesia.
PRESENTATION AND ADMINISTRATION:
IV / IO:
Do NOT give any lignocaine preparation also containing adrenaline intravenously
Lignocaine is available in vials containing 1% (10 mg/mL) & 2% (20 mg/mL) solutions.
- Lignocaine 1% solution is available as either 50 mg in 5mL or 200 mg in 20 mL
- Lignocaine 2% solution is available as either 100 mg in 5 mL or 400 mg in 20 mL
Compatible with the following IV fluids: Normal saline, 5% dextrose, sodium chloride with glucose and Hartmann's. Solutions prepared in these diluents are stable for up to 48 hours.
Store at room temperature. Do not refrigerate. Use immediately once opened. Discard any residue.
Lignocaine is incompatible when mixed with amphotericin or glyceryl trinitrate (GTN)
For maintenance infusion, use plain lignocaine 2% ampoules (100 mg/5 mL or 400 mg/20 mL)
- Withdraw 20 mL from 100 mL 5% glucose
- Add lignocaine 400 mg (20 ml of 2%) to the remaining 80 mL of fluid to give total volume of 100 mL
- Final concentration is 4 mg/mL lignocaine solution
DOSAGE:
During CPR for refractory ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT):
1 - 1.5 mg/kg IV or IO (maximum 100 mg)
Administer undiluted as slow push over 1 - 2 mins
For refractory VF:
Additional 0.5 - 0.75 mg/kg slow push
Repeat after 5 - 10 mins to maximum 3 doses or total dose 3 mg/kg
For perfusing ventricular arrhythmias (stable VT, ventricular ectopy causing haemodynamic compromise, wide-complex tachycardia):
0.5 - 1.5 mg/kg IV or IO (maximum 100 mg)
Administer undiluted as slow push over 1-2 mins
If no response:
Additional 0.5 - 0.75 mg/kg every 5 - 10 mins, to maximum total dose 3 mg/kg, then commence maintenance infusion.
Maintenance infusion:
- 4 mg/min (60 mL/hr) for first 30 mins
- 3 mg/min (45 mL/hr) for next 60 mins
- 2 mg/min (30 mL/hr) for a further 5 hours then review
An extended infusion beyond this period may sometimes be required, however total duration should not normally exceed 24 hours due to the increasing risk of lignocaine toxicity. If infusion is still required beyond this period, reduce the rate to 1 mg/min (15 mL/hr). Change the infusion bag every 24 hours.
If ventricular arrhythmias recur during infusion:
Additional bolus of 0.5 mg/kg and increase infusion rate by 1 mg/min (15 mL/hr).
DOSAGE IN RENAL, HEPATIC OR HEART FAILURE:
Lignocaine metabolites are really excreted. Lignocaine is not cleared by haemodialysis. Single dosing does not require dose reduction in renal impairment. If repeated doses are used or a maintenance infusion is commenced, protein binding and clearance are altered with an increased risk of lignocaine toxicity (see WARNINGS).
Lignocaine metabolism is dependent on hepatic blood flow so repeat or continuous doses should be reduced by 50% in hepatic impairment.
For patients with known left ventricular ejection fraction of <30%, start infusion at 2 mg/min (30 mL/hr) for 12 hours then reduce rate to 1 mg/min (15 mL/hr).
Increase vigilance for lignocaine toxicity and reduce or stop any infusion if suspected.
DOSAGE IN PAEDIATRICS:
IV for ventricular arrhythmias:
Loading dose of 1 mg/kg followed by maintenance infusion of 20 - 50 mcg/kg/min
Do not exceed 20 mcg/kg/min in children with shock, hepatic disease or congestive heart failure. Not recommended for use in neonates or those less than six months of age.
CLINICAL PHARMACOLOGY:
Lignocaine is a tertiary amine that suppresses action potentials in excitable tissues by blocking voltage-gated sodium channels. It is a class 1B antiarrhythmic agent. In cardiac myocytes, it slows the rise of the cardiac action potential during phase 0, thereby increasing the effective threshold potential and so reducing the automaticity of conduction tissue. It has a mild negative inotropic effect and weak neuromuscular blocking activity. Lignocaine has a rapid onset of action with a half-life of 90 - 120 mins. However, for the first 30 minutes of an infusion, the plasma half-life is less than 10 minutes due to rapid distribution into tissues. The half-life may be prolonged in liver or cardiac failure as previously described. Lignocaine is mostly hepatically cleared, with two active metabolites cleared renally that can cause central nervous system toxicity.
CONTRAINDICATIONS:
- Known hypersensitivity to lignocaine or other amide local anaesthetics
- Heart block or conduction abnormality without a functioning pacemaker. This includes second or third degree heart block, severe sinoatrial of intraventricular block, and Wolff-Parkinson-White or Adam-Stokes syndrome
- Co-administration with other sodium channel blocking antiarrhythmic drugs (e.g. flecainide)
WARNINGS:
Monitoring:
Continuous ECG monitoring is mandatory during lignocaine administration, with a baseline 12-lead ECG obtained prior to commencing any infusion. Resuscitation equipment must be available and easily accessible. Monitoring for any signs or symptoms of toxicity should be frequent - see toxicity paragraph below.
Local anaesthetic toxicity:
Effects are predominantly seen within the central nervous followed by the cardiovascular system as toxicity progresses.
Central nervous system signs of lignocaine toxicity may be biphasic with an initial excitation phase followed by a depression phase. The former includes blurred vision, tinnitus, restlessness, tongue or lip numbness, vertigo, slurred speech, visual or auditory hallucinations shivering, muscle twitching, or seizures. The latter includes decreased level of consciousness or apnoeas. In awake patients, specific symptoms should be enquire about frequently with patients encouraged to report any abnormality early. In sedated or anaesthetised patients, toxicity may only become apparent when cardiovascular signs appear.
Cardiovascular signs may initially be tachycardia and hypertension, followed by sinus bradycardia, hypotension (which may be profound), conduction defects on ECG (prolonged PR & QRS duration), ventricular arrhythmias, or cardiac arrest.
If any signs or symptoms appear, the lignocaine infusion should be stopped and medical staff notified. Mild agitation, restlessness or seizures may be managed with midazolam boluses.
If the patient deteriorates to the point they require resuscitation, CPR (if appropriate) should be prolonged. Additional actions should include hyperventilation and/or bicarbonate administration to reduce acidosis, and administration of lipid emulsion (20% intralipid). Intralipid should be administered as soon as possible as 1 mL/kg bolus every 3 minutes followed by an infusion of 0.25 mL/kg/min until haemodynamics are restored.
PRECAUTIONS:
General: See WARNINGS
Laboratory Tests: No additional laboratory tests are required
Laboratory Test Interactions: None known
Pregnancy: Lignocaine has been frequently administered to pregnant women without evidence of increased incidence of malformations. Lignocaine readily crosses the placental barrier and metabolism has been demonstrated by a term fetus. Fetal or neonatal bradycardia or tachycardia have been shown, as have neonatal hypotonia or respiratory depression.
Nursing Mothers: Lignocaine may enter breast milk but is general considered to have minimal effects on a neonate
IMPORTANT DRUG INTERACTIONS FOR THE ICU:
Drugs that lower the seizure threshold such as tramadol or selective serotonin reuptake inhibitors (SSRIs) can increase the risk of CNS toxicity.
Cimetidine and propranolol alter lignocaine metabolism by affecting hepatic blood flow, requiring a dose reduction of lignocaine.
Co-administration with clarithromycin or voriconazole may increase lignocaine concentration, contributing to toxicity.
Lignocaine should be used with caution if co-administering other local anaesthetics. The safe total dose of local anaesthetics are additive, inclusive of all routes of administration.
Mexiletine is an oral analogue of lignocaine and should not be administered in conjunction with IV lignocaine.
Suxamethonium action may be prolonged in the presence of high-dose lignocaine
Lacosamide my increase lignocaine toxicity with a prolonged PR interval, bradycardia, or ventricular tachyarrhythmias
ADVERSE REACTIONS:
Nervous System: See 'local anaesthetic toxicity' under WARNINGS above
Cardiovascular System: See 'local anaesthetic toxicity' under WARNINGS above
Digestive: Nausea, vomiting
Haematological: Methaemoglobinaemia