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Clinical Trial
. 2005 Jan;94(1):74-9.
doi: 10.1093/bja/aeh293. Epub 2004 Oct 14.

Haemodynamic effects of remifentanil in children with and without intravenous atropine. An echocardiographic study

Affiliations
Free PMC article
Clinical Trial

Haemodynamic effects of remifentanil in children with and without intravenous atropine. An echocardiographic study

C Chanavaz et al. Br J Anaesth. 2005 Jan.
Free PMC article

Abstract

Background: Remifentanil is known to cause bradycardia and hypotension. We aimed to characterize the haemodynamic profile of remifentanil during sevoflurane anaesthesia in children with or without atropine.

Methods: Forty children who required elective surgery received inhalational induction of anaesthesia using 8% sevoflurane. They were allocated randomly to receive either atropine, 20 microg kg(-1) (atropine group) or Ringer's lactate (control group) after 10 min of steady-state 1 MAC sevoflurane anaesthesia (baseline). Three minutes later (T0), all children received remifentanil 1 microg kg(-1) injected over a 60 s period, followed by an infusion of 0.25 microg kg(-1) min(-1) for 10 min then 0.5 microg kg(-1) min(-1) for 10 min. Haemodynamic variables and echocardiographic data were determined at baseline, T0, T5, T10, T15 and T20 min.

Results: Remifentanil caused a significant decrease in heart rate compared with the T0 value, which was greater at T20 than T10 in the two groups: however, the values at T10 and T20 were not significantly different from baseline in the atropine group. In comparison with T0, there was a significant fall in blood pressure in the two groups. Remifentanil caused a significant decrease in the cardiac index with or without atropine. Remifentanil did not cause variation in stroke volume (SV). In both groups, a significant increase in systemic vascular resistance occurred after administration of remifentanil. Contractility decreased significantly in the two groups, but this decrease remained moderate (between -2 and +2 sd).

Conclusion: Remifentanil produced a fall in blood pressure and cardiac index, mainly as a result of a fall in heart rate. Although atropine was able to reduce the fall in heart rate, it did not completely prevent the reduction in cardiac index.

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Figures

Fig. 1
Fig. 1
Heart rate (beats min−1) values under remifentanil compared with 1 MAC sevoflurane steady-state values (baseline). T0=time after injection of atropine (AT) or Ringer (RL); time (min) 5 and 10 under remifentanil at 0.25 μg kg−1 min−1; time 15 and 20 under remifentanil at 0.5 μg kg−1 min−1. Vs baseline, *P<0.05; vs T0, P<0.05; vs T10, $P<0.05. Open circles correspond to minimum and maximum values.
Fig. 2
Fig. 2
Cardiac index values under remifentanil compared with 1 MAC sevoflurane steady-state values (baseline). T0=time after injection of atropine (AT) or Ringer (RL); time (min) 5 and 10 under remifentanil at 0.25 μg kg−1 min−1; time 15 and 20 under remifentanil at 0.5 μg kg−1 min−1. Vs baseline, *P<0.05; vs T0, P<0.05; vs T10, $P<0.05. Open circles correspond to minimum and maximum values.
Fig. 3
Fig. 3
Contractility values (stress–velocity index, SVI) under remifentanil compared with 1 MAC sevoflurane steady-state values (baseline). T0=time after injection of atropine (AT) or Ringer (RL); time (min) 5 and 10 under remifentanil at 0.25 μg kg−1 min−1; time 15 and 20 under remifentanil at 0.5 μg kg−1 min−1. Vs baseline, *P<0.05; vs T0, P<0.05; vs T10, $P<0.05. Open circles correspond to minimum and maximum values.

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