This may be due to our clinical practice of pretreatment with a nondepolarizing muscle relaxant. In one of our patients who developed bradycardia, the remifentanil infusion and other agents used for induction of anesthesia were administered in the same intravenous line. This particular patient may have received an inadvertent overdose of remifentanil.
It is generally accepted that the cause of opioid-induced bradycardia is vagally mediated. Bilateral vagotomy has been shown to abolish this effect. Therefore, it takes the pump 24 s to deliver a bolus to a kg patient, 28 s for a kg patient, and so on. This is faster than the recommended rate of 30—60 s for a bolus dose. The presence of beta-adrenergic or calcium-channel blockade is another predisposing factor.
Although 3 of 6 patients who had bradycardia were on beta-blockers, so were 13 of 24 who did not receive a remifentanil bolus and did not develop bradycardia. None of our patients were on a combination of beta- and calcium channel blocking agents. However, we could detect no correlation between the various muscle relaxants we used to facilitate tracheal intubation and the occurrence of bradycardia Table 1. Two of 6 patients who had bradycardia and 6 of 24 who had no bradycardia also received 1.
Bradycardia has been reported in dogs given 5 mg of intrathecal morphine, [ 7 ] and in humans after epidural or intrathecal administration of sufentanil. We do not believe that the intrathecal morphine contributed to the bradycardia. The most likely mechanisms for opioid-induced hypotension are a centrally mediated decrease in sympathetic tone and vagally induced bradycardia.
Because remifentanil has a rapid onset of action, this seems to be the most likely explanation for the hypotension accompanying the bradycardia. Table 1. Sign In or Create an Account. Advanced Search.
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Download other formats More. Related articles. Korean Journal of Anesthesiology ;27 10 Severe bradycardia has been associated with a number of medications used for induction of anesthesia. Fentanyl and other potent opioids are well known for their central vagotonic effect, particularly when given rapidly in high doses.
Propofol administration has also been associated with bradycardia, and may even exert a central vagotonic or sympatholytic ef- fect, or both. The anesthetic induction with propofol fentanyl may be followed by severe bradycardia in patients who have not received atropine.
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