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  • Introduced 1948 & still the most widely used LA


LA Action:

  • As for cocaine but little euphoria/fever & more prompt, longer-lasting, more intense & more extensive anaesthesia than procaine;

VW class 1b anti-arrhythmic action:

  • rapidly blocks both activated & inactivated but not resting Na channels (cf quinidine which mainly blocks activated channels)
  • Thus, >50% of unblocked Na channels become blocked during each action potential in those cells with long plateaus & thus long periods of inactivation (ie. Purkinje fibers & ventricular cells).
  • During diastole, most of the Na channels in normally polarised cells rapidly become drug free & since it may shorten APD, diastole may be prolonged, thereby extending time for recovery resulting in little effect in normal cardiac cells.
  • In contrast, ischaemic depolarised cells where Na channels are inactivated remain largely blocked during diastole & more may become blocked.
  • Thus it suppresses electrical activity of the depolarised, arrythmogenic tissue.
  • It is NOT effective in arrythmias originating in normally polarised cells such as AF.
  • It exacerbates ventricular arrhythmias in < 10% of pts.
  • It ppts SA nodal standstill or worsens impaired conduction in 1% of pts with AMI.
  • It also may cause hypotension in high doses due to -ve inotropic activity.


  • IV 0.7-1.4mg/kg stat, rpt in 5min; less if CCF; max. 200-300mg/hr;
  • Infusion: 1-4mg/min → Rx [] of 1-5µg/ml in 7-10hrs but > double [] if shock/CCF!
  • Extensive 1st pass metabolism (only 3% of oral drug appears in plasma).
  • Eliminated by hepatic metabolism which may be impaired in CCF/shock but this may be offset by the decrease in Vd in CCF with minimal effect on half-life.
  • HOWEVER, liver disease decreases clearance & increases Vd with resultant increase in halflife of 3x or more which also means that steady state may require 24-36hrs rather than the usual 8-10hrs.
  • Likewise, drugs that reduce hepatic blood flow (B blockers, cimetidine) may increase its half-life & cause toxicity unless its infusion rate is reduced.
  • With infusions lasting > 24hrs, clearance falls & plasma concentrations rise!
  • Renal impairment has no significant effect on plasma levels.
  • Dealkylated in liver, metabolites excreted in urine;

adverse effects of lignocaine


  • plasma [] near 5µg/ml → paraesthesias, mild drowsiness/agitation;
  • higher [] > 9µg/ml → decr. hearing, disorientation, muscle twitching, convulsion;→ resp. arrest;


  • -ve inotropic esp. a problem if CCF;

drug interactions of lignocaine

  • beta-blockers may decr. hepatic blood flow if heart dis. → decr. hep. metabolism;
  • basic drugs displace linocaine from alpha2-globulin binding;
  • cimetidine → incr. plasma [];
  • can potentiate effects of suxamethonium;
lignocaine.txt · Last modified: 2009/03/17 02:24 by

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