• J E de La Coussaye, J J Eledjam, J Brugada, and A Sassine.
• Département d'Anesthésie-Réanimation, CHU Nîmes.
• Cah Anesthesiol. 1993 Jan 1;41(6):589-98.

AbstractThe intravascular administration and the high blood resorption of local anesthetic agents are known to induce neurotoxic accidents. However, the use of potent local anesthetic drugs such as bupivacaine is responsible for serious cardiotoxic accidents with a mortality of about 50%. Indeed, bupivacaine induces both electrophysiologic and haemodynamic disturbances with the occurrence of conduction blocks, arrhythmias and cardiovascular collapse. Moreover, cardiotoxicity is worsened by: bupivacaine-induced sympathetic activation which facilitates tachycardia and arrhythmias, metabolic abnormalities such as hypoxia, acidosis, hyperkaliemia and hypothermia, pregnancy, diazepam pretreatment, and the antiarrhythmic drugs. In case of cardiac arrest, CPR must be made. In the other cases, the first treatment is to oxygenate, to intubate the trachea and to ventilate the lungs, and then to stop convulsions. Specific cardiac resuscitation remains controversial because it is based principally on experimental results. We demonstrated that the combination of clonidine and dobutamine is efficient to reverse both haemodynamic and electrophysiologic impairments induced by a large dose of bupivacaine in anesthetized dogs. Whatever the efficiency of specific resuscitation, it must be emphasized that prevention of toxic accident must always include: the best choice of local anesthetic drug (e.g.: lidocaine+alpha-2 agonist vs bupivacaine), test dose, aspiration and slow administration. Finally, the monitoring of regional anaesthesia must be similar to that in use for general anaesthesia and drugs and devices for resuscitation must be ready.

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