Background and objective: Desflurane has been shown to increase sympathetic activity and heart rate (HR) in a concentration-dependent manner. Nevertheless, desflurane, like all other volatile anaesthetics, increased HR in parallel to vagal inhibition in a previous study. Therefore, our hypothesis is that desflurane elicits tachycardia by vagal inhibition rather than by activation of the sympathetic nervous system.
Methods: Six dogs were studied awake and during desflurane anaesthesia (1 and 2 MAC) alone, after pre-treatment with propranolol (2 mg kg−1 followed by 1 mg kg−1 h−1), or after pre-treatment with atropine (0.1 mg kg−1 followed by 0.05 mg kg−1 h−1). The effects on HR and HR variability were compared by an analysis of variance (P < 0.05). HR variability was analysed in the frequency domain as power in the high-(0.15–0.5 Hz, vagal activity) and low-frequency range (0.04–0.15 Hz, sympathetic and vagal activity).
Results: HR increased during 2 MAC of desflurane from about 60 (awake) to 118 ± 2 beats min−1 (mean ± SEM) in controls and to 106 ± 3 beats min−1 in dogs pre-treated with propranolol. In contrast, pre-treatment with atropine increased HR from 64 ± 2 to 147 ± 5 beats min−1 (awake) and HR decreased to 120 ± 5 beats min−1 after adding desflurane. High-frequency power correlated inversely with HR (r2 = 0.95/0.93) during desflurane alone and in the presence of β-adrenoceptor blockade, with no significant difference between regression lines. There was no correlation between these variables during atropine/desflurane.
Conclusions: The increase in HR elicited by desflurane mainly results from vagal inhibition and not from sympathetic activation.