Effects of Nitrous Oxide on Cardiovascular Response to Laryngoscopy and Endotracheal intubation.
10.4097/kjae.2003.44.4.521
- Author:
Sung Tae JEONG
1
;
Heon Chang PARK
;
Jung il CHOI
;
Seong Wook JEONG
;
Hak Song KIM
;
Kyung Yeon YOO
Author Information
1. Department of Anesthesiology, Chonnam National University Medical School, Gwangju, Korea.
- Publication Type:Original Article ; Randomized Controlled Trial
- Keywords:
Anesthetic, nitrous oxide;
catecholamines;
hypertension;
tachycardia
- MeSH:
Anesthesia;
Anesthesia, General;
Arrhythmias, Cardiac;
Arterial Pressure;
Bradycardia;
Catecholamines;
Epinephrine;
Ethics Committees, Research;
Heart Rate;
Humans;
Hypertension;
Incidence;
Intubation;
Intubation, Intratracheal*;
Laryngoscopy*;
Nitrous Oxide*;
Norepinephrine;
Oxygen;
Plasma;
Tachycardia;
Thiopental;
Vecuronium Bromide
- From:Korean Journal of Anesthesiology
2003;44(4):521-526
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGORUND: Endotracheal intubation in patients undergoing general anesthesia often causes hypertension and tachycardia. Nitrous oxide (N2O), which is frequently used during the induction of anesthesia, is known to augment sympathetic nervous activity in humans. The aim of the present study was to investigate whether N2O affects cardiovascular response to intubation. METHODS: After iRB approval, 100 ASA i patients (aged 35 60 yr) were assigned randomly to receive one of four concentrations (0, 25, 50 or 75%; n = 25 for each) of N2O in oxygen throughout the study period, beginning 3 min before intubation. Anesthesia was induced with iV thiopental (5-7mg/kg) and tracheal intubation was faciliated with iV vecuronium (0.12 mg/kg), while patients were ventilated with the designated concentrations of N2O in oxygen. After intubation, all patients received 2% sevoflurane and N2O in oxygen via a semiclosed anesthesia circuit. Systolic arterial pressure (SAP), heart rate (HR) and rhythm were recorded before and after intubation at intervals for up to 5 min. Plasma concentrations of catecholamines were measured before and 3 min after induction, and 1 and 5 min after intubation. RESULTS: The intubation caused significant increases in SAP and HR in all groups (P<0.05). increasing concentrations of N2O gradually attenuated the pressor response to intubation, without affecting the tachycardiac response. No significant differences were observed between the groups in plasma concentrations of either norepinephrine or epinephrine:norepinephrine concentration increased significantly 1 min after intubation in all N2O-treated groups, while it remained unchanged in the control group. in contrast, the epinephrine concentration remained unaltered in all N2O-treated groups, but increased significantly in the control group. incidence of tachycardia, bradycardia, and arrhythmia was not different among the groups. CONCLUSiONS: These results indicate that N2O suppresses the pressor but not the tachycardiac response associated with endotracheal intubation, while it enhances the increases in plasma norepinephrine concentrations.
