Key result
Baseline heart rate was the only independent predictor of bradycardia induced by a 1 μg/kg bolus of remifentanil (OR 0.877; 95% CI 0.796-0.966), with no relation to baseline autonomic tone.
Why the study?
Does a bolus dose of remifentanil cause bradycardia and hypotension related to baseline autonomic tone in adults?
Observational (n=70)
Does a bolus dose of remifentanil cause bradycardia and hypotension related to baseline autonomic tone in adults?
Baseline heart rate, rather than baseline autonomic tone, is the only independent predictor of remifentanil-induced bradycardia in healthy adults.
Baseline heart rate may warrant caution before remifentanil boluses; leaves open autonomic tone's role pending prospective validation.
Remifentanil stimulates the parasympathetic nervous system, and patients with increased parasympathetic tone may be at greater risk of bradycardia after its administration. We aimed to establish if adult patients with increased baseline parasympathetic tone were at higher risk of bradycardia and hypotension when given a bolus dose of remifentanil. Seventy adults (age 20-60 years and ASA physical status 1 or 2) were given remifentanil 1 μg.kg(-1) . A Holter ECG monitor was used to assess heart rate changes. Heart rate variability in the frequency domain during the 5 min after remifentanil administration was analysed. Multivariate analysis demonstrated that baseline heart rate was the only independent predictor of remifentanil-induced bradycardia [odds ratio (95% CI) 0.877 (0.796-0.966)]. The vagotonic action of remifentanil does not appear to be related to baseline autonomic tone in adult patients.
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Wujtewicz et al. (2016) reported an observational. Baseline heart rate (prior to remifentanil bolus) was evaluated on Remifentanil-induced bradycardia (OR 0.877, 95% CI 0.796-0.966). Baseline heart rate was the only independent predictor of bradycardia induced by a 1 μg/kg bolus of remifentanil (OR 0.877; 95% CI 0.796-0.966), with no relation to baseline autonomic tone.
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