Hemodynamic Effects of Lidocaine in Patients with Heart Disease

Abstract

The intravenous administration of 50 mg of lidocaine as a single bolus to four patients with heart disease did not result in a significant change in cardiac output or left ventricular end-diastolic pressure (LVEDP). Two patients had moderate decrease in systemic arterial pressure which was not accompanied by symptoms, was of short duration, and did not require therapeutic intervention. Left ventricular function, as assessed by the relationship of changes in stroke volume index (SVI) and stroke work index (SWI) to changes in LVEDP, was not significantly affected nor was the maximum rate of rise of left ventricular pressure (dp/dt).

Vasodilatory Effects of Lidocaine on Epicardial Porcine Coronary Arteries

“…We have observed intravenous lidocaine (1.5-4.0 mg/ kg) to produce large increases in coronary blood flow in open-chest swine in our labo ratory [1]; others have observed similar ef fects in patients with recent myocardial in farction [2], Lidocaine has been shown to produce systemic arterial vasodilation in dogs [3] and man [4] over a wide dose range, and the coronary flow effects have been pos tulated to result from drug-induced systemic vasodilation, with secondary reflex tachy cardia and an associated increase in myo cardial oxygen consumption. Gould et al [2] questioned this observation, however, after measuring coronary blood flow by ru bidium clearance in men before and after lidocaine injection.…”

“…Some in vivo studies have demonstrated that lidocaine produces vasodilation, as indicated by an increase in peripheral arterial blood flow [3,11] and an increase in coronary arterial blood flow [1,2]. Other in vivo studies have indicated that lidocaine either produces va soconstriction [11,12] or no vascular effect at all [4,13]. Gould et al [2] demonstrated that lidocaine increased coronary blood flow as assessed by serial rubidium clearance measurements in men before and after lido caine injection.…”

Effect of lidocaine on the electrophysiological properties of ventricular muscle and Purkinje fibers

“…This assumption is not unreasonable when one considers the similarity of structure and of local anesthetic properties shared by these two drugs. Indeed, the strongest arguments made for the clinical use of lidocaine in the treatment of arrhythmias rather than procaine amide or quinidine usually have been related to either the pronounced differences in its mode and rate of metabolism (4)(5)(6)(7)(8) or to differences between the effects of lidocaine and these two drugs on blood pressure, cardiac output, and myocardial contractility (9)(10)(11)(12). Differences in electrophysiological properties or antiarrhythmic spectrum usually have been neglected in such discussions.…”

Relation between Plasma Lignocaine Levels and Induced Haemodynamic Changes

“…When given in a dose of about 1 mg./kg. intravenously as a single injection or as an infusion at a rate of 1-2 mg./minute there are no appreciable haemodynamic effects in patients (Binnion, 1968;Stannard et at., 1968;Schumacher et al, 1968) though doses of 200-400 mg. intravenously given to anaesthetized dogs (about [8][9][10][11][12][13][14][15][16] mg./kg.) produce a pronounced fall in myocardial contractile force and may even produce electromechanical dissociation of cardiac activity such that a normal E.C.G.…”