Lidocaine



Lidocaine has minimal effects on automaticity or conduction in vitro unless marked abnormal­ities are pre-existent. Lidocaine affects fast chan­nel-dependent tissues (atrial and ventricular muscle and His-Purkinje tissue) but usually not slow channel-dependent tissues (sinus and AVnodes). It appears to be particularly potent at al­tering electrophysiological parameters in is­chemic tissue. Lidocaine rarely causes clinically significant hemodynamic effects. It is used only parenterally because of extensive first-pass he­patic metabolism upon oral administration. Its metabolism is decreased in elderly patients and those with hepatic disease, heart failure, and shock. Maintenance doses should be reduced by one third to one half in patients with low cardiac output. Prolonged infusion of lidocaine can re­duce its clearance, and dosage may have to be de­creased after a day or so. Intramuscular admin­istration has been advocated for use by emergency medical technicians when caring for a patient with an acute myocardial infarction before reach­ing the hospital, but lidocaine is usually admin­istered intravenously. The ability to achieve rapid effective plasma concentrations and a fairly wide toxic-to-therapeutic ratio with a low incidence of hemodynamic complications makes lidocaine a very useful antiarrhythmic drug. It is effective against a variety of ventricular arrhythmias but is generally ineffective against supraventricular ar­rhythmias. The use of lidocaine prophylactically in patients with acute myocardial infarction is controversial (see Chapter 7). Lidocaine is usually the parenteral drug of first choice in patients with ventricular arrhythmias. Even though lidocaine may decrease ventricular response in some pa­tients with Wolff-Parkinson-White syndrome and atrial fibrillation, it usually has no effect or can even accelerate the ventricular response in pa­tients with rapid ventricular responses.