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14 Anti-arrhythmicsinduction) while cimetidine will increase quinidine levels (hepatic enzyme inhi-
bition). The effects of depolarizing and non-depolarizing muscle relaxants are
increased.Kinetics
Quinidine is well absorbed from the gut and has an oral bioavailability of about
75%. It is highly protein bound (about 90%) and is metabolized by the liver to active
metabolites, which are excreted mainly in the urine. The elimination half-life is 5–9
hours.Ventricular tachyarrhythmias
Lidocaine
Lidocaine is a class Ib anti-arrhythmic agent.Presentation
The 1% or 2% solutions (10–20 mg.ml−^1 )arethe preparations used in this setting.Uses
Lidocaine is used to treat sustained ventricular tachyarrhythmias especially when
associated with ischaemia (where inactivated Na+channels predominate) or re-
entry pathways. An initial intravenous bolus of 1 mg.kg−^1 is followed by an intra-
venous infusion of 1–3 mg.min−^1 for an adult. This infusion rate should be slowed
where hepatic blood flow is reduced as hepatic metabolism will also be reduced.Mechanism of action
Lidocaine reduces the rate of rise of phase 0 of the action potential by blocking
inactivated Na+channels and raising the threshold potential. The duration of the
action potential and the refractory period are decreased as the repolarization phase
3isshortened.Side effects
Cardiac – cardiovascular toxicity becomes apparent as plasma levels exceed
10 μg.ml−^1 and are manifest as AV block and unresponsive hypotension due to
myocardial depression. Some of the cardiac effects may be due to central medullary
depression.
Non-cardiac – these become apparent only when the plasma levels exceed
4 μg.ml−^1 .Initially central nervous system toxicity is manifest as circumoral tin-
gling, dizziness and parasthesia. This progresses to confusion, coma and seizures
as plasma levels rise above 5μg.ml−^1.