SYSTEMIC EFFECTS OF INTRAVENOUSLY INFUSED COCAINE IN PIGS ANESTHETIZED WITH ISOFLURANE, HALOTHANE AND ENFLURANE

Sixteen male pigs were randomly assigned to 4 equal groups to investig ate the effects of volatile anesthetics (VA) on cocaine induced system ic toxicity. All pigs were anesthetized with sodium pentothal 30 mg/kg iv and 60 mg/kg im and after tracheal intubation for mechanical venti lation anesthesia was maintained with nitrous oxide [4 L/min (4L)] in oxygen [2 L/min (2L)]. Carotid and pulmonary artery catheters were pla ced for hemodynamic monitoring. No additional anesthetic was administe red in Group O (control group). Minimum Alveolar Concentration (MAC)-e quivalent concentrations of isoflurane (1.1%), halothane (0.7%), and e nflurane (1.7%), were added to the gas mixtures inhaled by pigs in gro ups I, H and E respectively. Cocaine hydrochloride (0.8 mg/kg/min) was administered iv to all pigs until cardiac arrest. After the start of cocaine infusion there was a significant decrease in cardiac output, m ean arterial pressure and heart rate in all groups of pigs as well as a significant increase in systemic and pulmonary vascular resistance, central venous and pulmonary capillary wedge pressure, and blood K+ le vels (p < 0.05). Convulsions (focal and general) present in Group O we re absent in groups I, H and E. Cardiac arrest (CA) occurred 2 to 3 ti mes faster in pigs receiving VA agents. In all groups studied the harb inger of serious cardiac decompensation was the development of complet e heart block (CHB). The time to CA after the onset of CHB was no diff erent between groups. It is proposed that the hastened onset of CA in animals receiving VA is caused by a rapid onset of CHB due to an addit ive effect of cocaine and VA agents in prolonging atrioventricular con duction.