Résumé
Local anesthetic drugs can induce potentially severe toxic accidents following accidental intravascular injection or significant tissue resorption. The severity of the accident depends on the potency of the local anesthetic used and the rapidity of the increase in its plasma level. Lidocaine is a moderately potent local anesthetic. The main manifestations of its toxic accident are neurologic signs, with convulsions and no, or slight, cardiac effects on the intact heart. In contrast, bupivacaine is a potent local anesthetic which is widely used in regional anesthesia. However, when toxic accidents occur with bupivacaine, there is an important risk of lethality which is mainly due to its cardiovascular manifestations with both potent depression of myocardial contractility and major electrophysiological disturbances such as cardiac blocks and/or ventricular arrhythmias. In an editorial in 1979, Albright [1] reported six deaths following accidental intravascular injection of bupivacaine. These deaths ware due to cardiovascular collapse associated with extreme bradycar-dia or ventricular arrhythmias. In contrast to lidocaine, bupivacaine-induced cardiac manifestations occurred simultaneously with the neurotoxic signs. In addition, Albright also drew attention upon the great difficulty in resuscitating these patients. In a study conducted for the FDA, this author reported that almost 50% of the accidents resulted in death of the patients or the parturients in spite of well conducted cardiopulmonary resuscitation [2]. Thus, the aim of this chapter is to describe present knowledge of the mechanisms of bupivacaine cardiotoxicity and of the treatment of this toxic event.