Effects of lidocaine on impulse formation and conduction defects in man

Abstract

The acute electrophysiologic effects of a bolus injection of 100 mg. of lidocaine were investigated in 39 patients with impulse formation and conduction defects by means of His-bundle recording and were correlated with plasma lidocaine levels. The effects of therapeutic plasma levels on conduction intervals and refractory periods were subsequently studied during sinus rhythm and atrial pacing. The sinus-node function was studied by measurement of the sino-atrial recovery time. Seventeen patients had conduction defects in or distal to the His bundle, six exclusively proximal to the His bundle, and nine at both levels. Nine patients had pre-existent sinus-node malfunction. Ten out of 39 patients suffered from acute myocardial infarction. Two patients were studied twice because of changed A-V conduction. Intravenous injection of 100 mg. of lidocaine within 20 seconds produced peak arterial plasma levels (mean 26.6 mug per milliliter) 60 seconds after the beginning of the injection. Seven out of 26 patients showed transient progression of their pre-existent infra-His conduction impairment, coincident with peak plasma levels, apparently due to drug toxicity. Even at therapeutic plasma levels, five out of 26 patients showed decremental intraventricular conduction during atrial pacing when compared to control tracings. His-Purkinje refractoriness was not shortened in these patients and increased in two. Lidocaine had no effect on ventricular automaticity in three patients with complete heart block. Lidocaine had no consistent effects on sinus rate, SART, atrial refractoriness, or A-V nodal conduction as measured by pooled AH intervals and the Wenckebach point, and on A-V nodal refractoriness. It is concluded that lidocaine is safe in patients with high degrees of A-V nodal block and in patients with impulse formation disturbances. However, patients with intraventricular conduction defects are prone to deterioration of their conduction disturbance due to drug toxicity. The drug should be given to such patients preferably if monitoring and pacemaker facilities are available and by the intramuscular route to avoid peak plasma levels.