Sevoflurane anesthesia decreases cardiac vagal activity and heart rate variability
Anesthesiology Department, University of Illinois at Chicago, 1740 W Taylor, Suite 3200, Chicago, IL 60612, USA.Clinical Autonomic Research (Impact Factor: 1.49). 01/2008; 17(6):370-4. DOI: 10.1007/s10286-007-0437-9
We evaluated cardiac vagal activity during sevoflurane anesthesia in neurosurgical patients. Heart rate variability was determined by power spectral analysis and entropy with the patient awake and during sevoflurane anesthesia. High frequency power (0.15-0.50 Hz) and heart rate entropy decreased during sevoflurane and these effects were significantly correlated (r = 0.71 +/- 0.12, P < 0.05). The results confirm that cardiac vagal activity was the primary determinant of heart rate variability, which was attenuated by sevoflurane.
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- "It has also been postulated that sevoflurane depresses the sympathetic activity without altering the parasympathetic response. Paisansathan demonstrated that sevoflurane anesthesia decreased cardiac vagal activity and heart rate variability. "
ABSTRACT: Drug combinations can be used for optimum obtundation of the hemodynamic response to tracheal intubation. The objective of this trial was to compare the hemodynamic response to laryngoscopy and tracheal intubation after administration of 2 μg/kg fentanyl bolus or a placebo with 2% end tidal sevoflurane at induction of anesthesia. A total of 70 surgical patients of either gender, age 18-45 years were selected for this double blind, randomized, placebo controlled trial, with 35 in each group. All patients received a standardized induction with thiopentone, atracurium, and an end tidal concentration of 1 minimum alveolar concentration (MAC) sevoflurane. Heart rate and noninvasive blood pressure were compared to the baseline post induction and for seven minutes post intubation. Some adverse events were noted. The maximum heart rate response was significantly less in the sevoflurane fentanyl group (15% vs. 22%). Significant difference between groups was observed in the systolic blood pressure at six minutes post intubation. Hemodynamic adverse events recorded were similar. Addition of 2 μg fentanyl bolus to 1 MAC sevoflurane anesthesia at induction attenuated the hemodynamic response to a maximum of 15% above baseline values.
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ABSTRACT: The effects of anesthetics on ischemia-induced ventricular arrhythmias remain poorly studied. This study investigated the effects of propofol and sevoflurane on the survival rate and morbidity as a result of ventricular arrhythmias, and defined a possible mechanism for the arrhythmogenic properties of anesthetics during acute myocardial ischemia. Under anesthesia with intraperitoneal sodium pentobarbital, Sprague-Dawley rats underwent 30 min of left anterior descending coronary artery ligation. The rats were divided into a low-dose propofol (Prop-LD) group (39 mg X kg(-1) X hr(-1), n = 18), a high-dose propofol group (78 mg x kg(-1) x hr(-1), n = 18), a sevoflurane group (2.5%, n = 18) and a control group (n = 18). The survival rate and morbidity as a result of ventricular arrhythmias were determined, and the amount of phosphorylated connexin 43 protein was measured 30 min after coronary artery ligation. The survival rate was 83% (15 of 18), 94% (17 of 18), 89% (16 of 18), and 67% (12 of 18, P = 0.038 vs. Prop-LD) in the control, Prop-LD, high-dose propofol, and sevoflurane groups, respectively. Sustained ventricular tachycardia was observed in 83% (15 of 18), 39% (7 of 18, P = 0.011 vs. control), 50% (9 of 18, P = 0.039 vs. control) and 94% (17 of 18, P < 0.01 vs. Prop-LD) in the control, Prop-LD, high-dose propofol, and sevoflurane groups, respectively. Immunoblotting showed a marked reduction in the amount of phosphorylated connexin 43 in the control and sevoflurane groups, as compared with the Prop-LD and high-dose propofol groups (P < 0.05). The authors' results suggest that propofol preserves connexin 43 phosphorylation during acute myocardial ischemia, as compared with sevoflurane, and this might protect the heart from serious ventricular arrhythmias during acute coronary occlusion.
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