Bradycardia and hypotension were the first major signs of toxicity from a 250 mg bupivacaine axillary brachial plexus block experienced by a patient with chronic renal failure, who had an anion gap acidosis and hyperkalemia. Without these metabolic abnormalities, this patient received four similar blocks: three were without incident and one was complicated by seizure. Acidosis and/or hyperkalemia in man appears to increase the myocardial susceptibility to bupivacaine toxicity into the range of arterial concentrations of the drug normally produced by plexus blocks, even in the absence of drug‐induced cerebral toxicity, seizures and hypoxi
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