Observations on intravenous administration of lignocaine in patients with myocardial infarction.

Abstract

suMMARY Lignocaine was administered intravenously to 36 patients with acute myocardial infarction.A bolus of 100 mg followed by an infusion of 2 mg/minute failed to maintain plasma levels above 2 ,g/ml. A bolus of 100 mg followed by 4 mg/minute also failed to maintain satisfactory plasma concentrations during the first hour of therapy.A bolus of 75 mg was combined with an infusion of 10 mg/minute for 20 minutes followed by 1.5 mg/ minute. Satisfactory plasma concentrations during the first hour were observed in 94 per cent of the estimations. No important adverse side effects occurred during the infusion of 10 mg/minute.Lignocaine has been found to be relatively ineffective in controlling ventricular arrhythmias occurring immediately after the onset of acute myocardial infarction (Geddes et al., 1972). This may be related in some cases to the presence of sympathetic overactivity in the acute phase of myocardial infarction since the drug has been shown to be more effective when the heart rate is within the normal range (Pantridge et al., 1974). However, failure to achieve adequate plasma concentrations may be an important reason for therapeutic ineffectiveness. It has been said that plasma concentrations of lignocaine of 2 to 5 ,ug/ml are usually effective (Koch-Weser, 1972). In this study, the plasma concentrations of lignocaine obtained with conventional doses of the drug have been investigated.We have used a theoretical approach to design a regimen that might give therapeutic plasma concentrations, particularly throughout the first hour of therapy. Patients and methodsThirty-six patients were studied (Table 1). All received lignocaine because of ventricular arrhythmias complicating acute myocardial infarction. Six had self-terminating ventricular tachycardia. The remainder had ventricular extrasystoles (frequent, consecutive, or R on T). The drug was given to-all patients within 48 hours of the onset of symptoms Received for publication 9 January 1978 of infarction (median 10 hours). Twenty-six (72%) of the patients had clinical or radiographic evidence of left ventricular failure when treatment was started. None had pulmonary oedema or cardiogenic shock.The 36 patients were divided into 4 groups. Group 1 (10 patients) received an initial 100 mg injection of lignocaine over 30 seconds. This was followed immediately by a continuous infusion of the drug at a rate of 2 mg/minute. Groups 2 and 3 (each containing 10 patients) also received an initial 100 mg injection but this was followed by a 4 mg/ minute infusion for 20 and 45 minutes, respectively. The rate of infusion was then reduced to 2 mg/ minute. Group 4 (6 patients) received an initial 75 mg injection of lignocaine given over 30 seconds followed by a 10 mg/minute infusion for 20 minutes. The infusion rate was then reduced to 1-5 mg/ minute. The regimen in Group 4 was devised using the method of Wagner (1974). Wagner suggested that a drug might be given intravenously using 2 different infusion rates-an initial rapid rate (Q1) and a later slower rate (Q2). ...

Is there an ideal antiarrhythmic drug? A review — with particular reference to class I antiarrhythmic agents

“…Mexiletine is effective in treating ventricular arrhythmias (Campbell et al, 1973;Talbot et al, 1973). It has, however, some cardiac adverse effects (Table III); for example, Cocco and colleagues (1980) reported that it induced atypical ventricular arrhythmia not associated with QTc prolongation.…”