LIDOCAINE INCREASES THE VENTRICULAR-FIBRILLATION THRESHOLD DURING BUPIVACAINE-INDUCED CARDIOTOXICITY IN PIGS

Ventricular fibrillation (VF) is a cause of death in bupivacaine-induc ed cardiovascular toxicity. We have examined the therapeutic effects o f lidocaine on the threshold for bupivacaine-induced VF in in situ bea ting swine hearts. Twenty-four animals were allocated to one of three groups: 0.25% bupivacaine, 1% lidocaine or 0.25% bupivacaine with 1% l idocaine were infused into the left anterior descending coronary arter y in increasing doses of 0, 1, 2, 4, 8 and 16 ml h(-1) for 15 min, res pectively. ECG and haemodynamic variables were monitored continuously during infusion. Regional myocardial function in the area supplied by the left anterior descending coronary artery was assessed using the so nomicrometry technique. VF did not occur in the lidocaine group. VF de veloped at higher infusion rates in animals given bupivacaine with lid ocaine (in one animal at an infusion rate of 8 ml h(-1) and in seven a t 16 ml h(-1)) compared with animals given bupivacaine alone (in one a t an infusion rate of 4 and in seven at 8 ml h(-1)). Although regional myocardial function decreased with increases in the infusion rate in each group, the depressant effects of the bupivacaine solution (medial inhibitory infusion rate of systolic shortening: IR50 = 2.43 (0.43) m l h(-1)) were significantly greater than those of the lidocaine soluti on (IR50 = 5.83 (0.87) ml h(-1)), but did not differ from those of the bupivacaine with lidocaine solution (IR50 = 3.54 (0.56) ml h(-1)). Th is study indicates that a combination of lidocaine and bupivacaine inc reased the threshold for bupivacaine-induced VF without further depres sing myocardial contractility.