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 investigate the effects of volatile anesthetics (VA) on cocaine induced systemic toxicity. All pigs were anesthetized with sodium pentothal 30 mg/kg iv and 60 mg/kg im and after tracheal intubation for mechanical ventilation anesthesia was maintained with nitrous oxide [4 L/min (4L)] in oxygen [2 L/min (2L)]. Carotid and pulmonary artery catheters were placed for hemodynamic monitoring. No additional anesthetic was administered in Group O (control group). Minimum Alveolar Concentration (MAC)-equivalent concentrations of isoflurane (1.1%), halothane (0.7%), and enflurane (1.7%), were added to the gas mixtures inhaled by pigs in groups 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, mean 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⁺ levels (p < 0.05). Convulsions (focal and general) present in Group O were absent in groups I, H and E. Cardiac arrest (CA) occurred 2 to 3 times faster in pigs receiving VA agents. In all groups studied the harbinger of serious cardiac decompensation was the development of complete heart block (CHB). The time to CA after the onset of CHB was no different 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 additive effect of cocaine and VA agents in prolonging atrioventricular conduction.