Korean J Anesthesiol.  2003 Apr;44(4):521-526. 10.4097/kjae.2003.44.4.521.

Effects of Nitrous Oxide on Cardiovascular Response to Laryngoscopy and Endotracheal intubation

• Jeong ST
• Park HC
• Choi JI
• Jeong SW
• Kim HS
• Yoo KY

• KMID: 1860815
• DOI: http://doi.org/10.4097/kjae.2003.44.4.521

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.

Keyword

Anesthetic, nitrous oxide; catecholamines; hypertension; tachycardia

MeSH Terms

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
Catecholamines
Epinephrine
Nitrous Oxide
Norepinephrine
Oxygen
Thiopental
Vecuronium Bromide