Cardiac arrest bupivacaine

Amide-type agents include articaine, lidocaine, bupivacaine, prilocaine, mepivacain and ropiva-caine. These are metabolized in the liver by microsomal enzymes with amidase activity. The amide group is preferred for parenteral and local use. If by accident rapidly administered intravascularly these agents, especially bupivacaine but also lidocaine, can produce serious and potentially lethal adverse effects including convulsions and cardiac arrest. They can more easily accumulate after multiple administrations. Intravenous lidocaine is sometimes used for regional anesthesia, for infiltration procedures, for the induction of nerve blockade and for epidural anesthesia. However, it is also used as an antiarrhythmic. Bupivacaine is a long-acting local anesthetic used for peripheral nerve blocks and epidural anesthesia. 

Intravenous. A double cuff is applied to the arm, inflated above arterial pressure after elevating the limb to drain the venous system, and the veins filled with local anaesthetic, e.g. 0.5-1% lidocaine without adrenaline (epinephrine). The arm is anaesthetised in 6-8 min, and the effect lasts for up to 40 min if the cuff remains inflated. The cuff must not be deflated for at least 20 minutes. The technique is useful in providing anaesthesia for the treatment of injuries speedily and conveniently, and many patients can leave hospital soon after the procedure. The technique must be meticulously conducted, for if the full dose of local anaesthetic is accidentally suddenly released into the general circulation severe toxicity and even cardiac arrest may result. Bupivacaine is no longer used for intravenous regional anaesthesia as cardiac arrest caused by it is particularly resistant to treatment. Patients should be fasted and someone skilled in resuscitation must be present. 

Although adrenaline is a first-line drug for pediatric advanced life support, there are emerging concerns that it impairs resuscitation with intravenous lipid emulsion in rats above a dose threshold of lOmicro-grams/kg [66 ]. In bupivacaine-induced cardiac arrest in rabbits adrenaline seemed to be necessary for return of spontaneous circulation, but was also associated with declining hemodynamic variables when the animals were resuscitated with intravenous lipid emulsion [67 ]. Some benefit to cardiac conduction may be achieved by hjqjer-tonic saline co-administration with lipid emulsion, as shown in rabbits [68 ]. 

Cordell CL, Schubkegel T, Light TR, Ahmad F. Lipid infusion rescue for bupivacaine-induced cardiac arrest after axillary block. J Hand Surg Am 2010 35 144-6. 

Harvey M, Cave G, Prince G, Lahner D. Epinephrine injection in lipid-based resuscitation from bupivacaine-induced cardiac arrest transient circulatory return in rabbits. Anesth Analg 2010 111 791-6. 

Rosenblatt MA, Abel M, Fischer GW, et al. Successful use of a 20% lipid emulsion to resuscitate a patient after a presumed bupivacaine-related cardiac arrest. Anesthesiology 2006 105 217-218. 

A 17-year-old patient had seizures directly after receiving 20 ml of bupivacaine 0.5% over 2-3 minutes for femoral nerve blockade aspiration tests every 5 ml were negative. He was bag-ventilated and given 3 mg of midazolam intravenously, followed by Intralipid 20% 1-2 minutes later he went into cardiac arrest with ventricular fibrillation. He was successfully resuscitated. 

Cardiovascular Insulin effectively reverses bupivacaine-induced circulatory collapse in dogs. In a randomised controlled animal study, cardiac arrest elicited by an IV bolus of bupivacaine was treated with administration of either insulin (2U/kg) or the same volume of saline [30. The primary outcome was successful resuscitation (MPs60mmHg). All insulin-treated dogs were successfully resuscitated within 15min, whereas none of the control dogs were resuscitated. 

The earliest signs of CNS toxicity are circumoral and tongue numbness, tinnitus, tremor, and dizziness. These appear at plasma lidocaine (lignocaine) concentrations of about 5 pg-mL-1. The value for prilocaine is similar to lidocaine but bupivacaine toxicity appears at about half those of lidocaine. Further progression is evidenced by drowsiness, visual disturbances, or muscle twitching (plasma lidocaine of 5-10 pg-mL-1). Over 10 p-mL-1 grand mal convulsions, coma and respiratory arrest are likely. Serious CNS toxicity is indicative of imminent and potentially fatal cardiac toxicity since lidocaine is associated with direct cardiac depression at plasma concentrations in excess of 20 pg-mL-1. 

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