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REGIONAL ANESTHESIA

Lipid Emulsion Improves Recovery from Bupivacaine-Induced Cardiac Arrest, but Not from Ropivacaine- or Mepivacaine-Induced Cardiac Arrest

York A. Zausig, MD, DEAA^*, Wolfgang Zink, MD, DEAA^*, Meike Keil, MS, Barbara Sinner, MD, DEAA^*, Juergen Barwing, MD, DEAA, Christoph H. R. Wiese, MD^*, and Bernhard M. Graf, MD, MSc^*

From the *Department of Anaesthesiology, University of Regensburg, Regensburg; and Department of Anaesthesiology, Emergency and Intensive Care Medicine, University of Goettingen, Goettingen, Germany.

Address correspondence and reprint requests to York A. Zausig, MD, DEAA, University of Regensburg, Department of Anaesthesiology, Franz-Josef-Strauss-Allee 11, 93053 Regensburg, Germany. Address e-mail to york.zausig{at}klinik.uni-regensburg.de.

BACKGROUND: Cardiac toxicity significantly correlates with the lipophilicity of local anesthetics (LAs). Recently, the infusion of lipid emulsions has been shown to be a promising approach to treat LA-induced cardiac arrest. As the postulated mechanism of action, the so-called "lipid sink" effect may depend on the lipophilicity of LAs. In this study, we investigated whether lipid effects differ with regard to the administered LAs.

METHODS: In the isolated rat heart, cardiac arrest was induced by administration of equipotent doses of bupivacaine, ropivacaine, and mepivacaine, respectively, followed by cardiac perfusion with or without lipid emulsion (0.25 mL · kg^–1 · min^–1). Subsequently, the times from the start of perfusion to return of first heart activity and to recovery of heart rate and rate-pressure product (to 90% of baseline values) were assessed.

RESULTS: In all groups, lipid infusion had no effects on the time to the return of any cardiac activity. However, recovery times of heart rate and rate-pressure product (to 90% of baseline values) were significantly shorter with the administration of lipids in bupivacaine-induced cardiac toxicity, but not in ropivacaine- or mepivacaine-induced cardiac toxicity.

CONCLUSIONS: These data show that the effects of lipid infusion on LA-induced cardiac arrest are strongly dependent on the administered LAs itself. We conclude that lipophilicity of LAs has a marked impact on the efficacy of lipid infusions to treat cardiac arrest induced by these drugs.