Supplemental Reading

Eger EI. Uptake and distribution. In Miller RD (ed.). Anesthesia (5th ed.). Philadelphia: Churchill Livingstone, 2000.

Evers AS and Crowder CM. General Anesthetics. In JG Hardman and LE Limbird (eds.). Goodman and Gilman's the Pharmacological Basis of Therapeutics (10th ed.). New York: McGraw Hill, 2001.

Koblin DD. Mechanism of Action. In Miller RD (ed.). Anesthesia (5th ed.). Philadelphia: Churchill Livingstone, 2000.

Reves JG, Glass PSA, and Lubarsky DA. Non-barbiturate Intravenous Anesthetics. In Miller RD (ed.). Anesthesia (5th ed.). Philadelphia: Churchill Livingstone, 2000.

|^Case Study Bradycardia and p-Blockers

A 77-year-old man is admitted to the hospital for a coronary artery bypass. He has been treated with a p-blocker (Tenormin 100 mg per day), which he took every morning. He is induced with propofol 1 mg/kg, fentanyl 5 ^g/kg and vecuronium 8 mg for muscle relaxation. After 3 minutes a decreasing heart rate becomes a worry for the anesthesiologist. The heart rate continues to fall until it reaches 38 BPM. At this point the patient's blood pressure is 80/60 and the anesthesiologist gives atropine 0.4 mg and ephedrine 10 mg. This treatment results in a stable patient. What effects were most likely produced by the anesthesia procedure? Could this have been avoided?

Answer: This feature of bradycardia is typical of patients who take p-blockers, which should be continued so they result ultimately in better anesthetic management. The drugs given could have been modified (i.e., etomidate instead of propofol, which does not raise or may cause a slower heart rate). The potent opioids in the fentanyl family all cause vagal transmitted bradycardia. The muscle relaxant vecuronium (norcuron) has no effect on heart rate and could have been replaced by pancuronium, which has a vagolytic effect and will counter bradycardia in the usual induction bolus doses.

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