Esmolol pretreatment attenuates heart rate increase and parasympathetic inhibition during rapid increases in desflurane concentration: A preliminary randomized study

• Published in: Medicine (Baltimore) Vol. 96; no. 42; p. e8340
• Main Authors: Kao, Ming-Chang, Tzeng, I-Shiang, Chan, Hsiao-Lung
• Format: Journal Article
• Language: English
• Published: United States The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved 01.10.2017; Wolters Kluwer Health
• Subjects: Adult; Anesthetics, Inhalation - adverse effects; Clinical Trial/Experimental Study; Desflurane; Electrocardiography; Female; Heart Rate - drug effects; Humans; Isoflurane - adverse effects; Isoflurane - analogs & derivatives; Middle Aged; Parasympathetic Nervous System - drug effects; Propanolamines - pharmacology; Prospective Studies; Young Adult
• ISSN: 0025-7974; 1536-5964; 1536-5964
• DOI: 10.1097/MD.0000000000008340

Rapid increases in desflurane concentration can transiently increase the heart rate (HR). Esmolol possesses a high β1-adrenoceptor selectivity and a short duration of action. This preliminary study aimed at investigating the effects of esmolol on the HR and autonomic modulation during a desflurane-induced HR increase. American Society of Anesthesiologists physical status I female subjects, aged 20 to 50 years, who were undergoing minor breast surgery were randomly assigned to 2 groups. Rapid increases in desflurane concentration were commenced after induction of anesthesia. Each subject received either i.v. saline (control group) or esmolol 0.5 mg/kg (esmolol group) before desflurane inhalation. Using time-frequency spectral analysis of HR variability, the HR indices were studied at baseline, postinduction, posttreatment, as well as at minimal alveolar concentrations of desflurane reaching 1.0, 1.3, and 1.5. The low frequency (LF) power is influenced by both the sympathetic and parasympathetic activity, whereas the high frequency (HF) power reflects the parasympathetic activity. The LF/HF ratio is thought to reflect either sympathovagal balance or sympathetic modulation. Electrocardiograms for data analysis were obtained from 8 subjects in each group. Rapid increases in desflurane concentration after induction caused a HR increase. Both the corresponding LF and HF powers were low and the LF/HF ratio remained unchanged. This indicates that the desflurane-induced HR increase may be attributed to parasympathetic inhibition and may be independent of sympathetic activation. Esmolol pretreatment effectively attenuated desflurane-induced HR increase. Moreover, subjects receiving esmolol pretreatment had increased LF and HF powers, but did not have changes in their LF/HF ratios, as compared to those without esmolol. Esmolol pretreatment attenuates HR increase and parasympathetic inhibition during rapid increases in desflurane concentration.