Resuscitation from bupivacaine-induced cardiovascular toxicity during partial inferior vena cava occlusion.
The hemodynamic effects and ability to resuscitate animals experiencing bupivacaine cardiovascular toxicity after partial inferior vena cava occlusion were investigated in anesthetized dogs (n = 12). Partial occlusion of the inferior vena cava resulted in a 12% decrease in mean arterial pressure, a 62% decrease in cardiac output, a 66% decrease in stroke volume, and a 135% increase in systemic vascular resistance. Bupivacaine, 20 mg/kg intravenously, resulted in cardiovascular collapse in all animals. The resuscitation time for animals without partial caval occlusion was 2.1 +/- 0.5 min, whereas that for animals with partial caval occlusion was 22.2 +/- 6.9 min (P less than 0.05). Significantly increased amounts of epinephrine and NaHCO3 were required to resuscitate the animals with caval occlusion. We conclude that partial inferior vena cava occlusion can significantly alter the ability to resuscitate animals experiencing bupivacaine cardiovascular toxicity.[1]References
- Resuscitation from bupivacaine-induced cardiovascular toxicity during partial inferior vena cava occlusion. Kasten, G.W., Martin, S.T. Anesth. Analg. (1986) [Pubmed]
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