Effects of Nitrous Oxide and Remifentanil on Cardiovascular Response to Endotracheal Intubation during Desflurane Anesthesia.
- Author:
Jeen Wook HONG
1
;
Kyung Yeon YOO
;
Cheol Won JEONG
;
Seok Jai KIM
;
Sung Tae CHUNG
;
Hong Beom BAE
Author Information
1. Department of Anesthesiology and Pain Medicine, Chonnam National University Medical School, Gwangju, Korea. kyyoo@chonnam.ac.kr
- Publication Type:Original Article ; Randomized Controlled Trial
- Keywords:
desflurane;
hemodynamic response;
nitrous oxide;
remifentanil
- MeSH:
Anesthesia;
Arterial Pressure;
Heart Rate;
Hemodynamics;
Humans;
Hypertension;
Inhalation;
Intubation;
Intubation, Intratracheal;
Isoflurane;
Nitrous Oxide;
Norepinephrine;
Piperidines;
Plasma;
Tachycardia;
Thiopental;
Vecuronium Bromide
- From:Anesthesia and Pain Medicine
2008;3(1):27-32
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Desflurane is known to causes hypertension and tachycardia when its inspired concentration is rapidly increased. We determined whether nitrous oxide (N2O) or remifentanil alters cardiovascular responses to intubation and/or inhalation of high concentrations of desflurane during induction of anesthesia. METHODS: Sixty patients were assigned randomly into three groups (n = 20 each). Anesthesia was induced with thiopental 5 mg/kg followed by saline (control and N2O groups) or remifentanil 1microg/kg (remifentanil group). Tracheal intubation was facilitated with intravenous vecuronium 0.12 mg/kg and 12% desflurane was given soon after the intubation. In addition, 75% N2O was given beginning 3 min before the intubation in the N2O group. Systolic arterial pressure (SAP), heart rate (HR), and plasma catecholamine concentrations were determined. RESULTS: The intubation resulted in an immediate increase and an additional second increase of SAP and HR at 3 to 5 min after intubation in all groups. SAP but not HR in the N2O group and both SAP and HR in the remifentanil group at first and second peak responses were lower than in the control group. Norepinephrine increased at 1 min after intubation and increased further at 5 min in the control and N2O groups but only increased at 5 min in the remifentanil group. CONCLUSIONS: A biphasic pressor and tachycardiac response in response to intubation and desflurane were noted. Although N2O did not affect tachycardiac response, it suppressed the pressor responses and augmented norepinephrine release. However, remifentanil significantly attenuated hemodynamic and catecholamine responses to endotracheal intubation and desflurane.
