The Effect of Doxapram Hydrochloride on the Ventilation Responses during General Anesthesia with Volatile Agent by Laryngeal Mask Airway.
10.4097/kjae.2004.46.6.684
- Author:
Heon Chang PARK
1
;
Won Jong JIN
;
Geong Duck PARK
;
Seong Wook JEONG
;
Myung Ha YOON
;
Kyung Yeon YOO
;
Sang Hyun KWAK
Author Information
1. Department of Anesthesiology, Chonnam National University Medical School, Gwangju, Korea.
- Publication Type:Original Article ; Randomized Controlled Trial
- Keywords:
doxapram hydrochloride;
respiratory depression;
sevoflurane
- MeSH:
Adult;
Anesthesia;
Anesthesia, General*;
Anesthetics, Inhalation;
Carbon Dioxide;
Doxapram*;
Humans;
Laryngeal Masks*;
Respiratory Insufficiency;
Respiratory Rate;
Tidal Volume;
Ventilation*
- From:Korean Journal of Anesthesiology
2004;46(6):684-689
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Inhalation anesthetics are known to depress ventilatory response to hypercapnea. Doxapram hydrochloride is an analeptic drug, which acts as a respiratory stimulant via peripheral and central chemoreceptors. Although the postoperarive infusion of doxapram hydrochloride is known to attenuate the impairment of respiratory function, no report is available on respiratory response to this drug when applied during anesthesia. Therefore, the present study aimed to evaluate the effect of doxapram hydrochloride on respiratory function during anesthesia. METHODS: Sixty adult patients undergoing operation under spontaneous ventilation via laryngeal mask airway (LMA) were randomly categorized into 3 groups: A control group, which received 5% dextrous infusion, and two groups in which patients were infused with doxapram hydrochloride (0.5 or 2 mg/kg/hr) starting 15 min after commencement operation. Anesthesia was maintained with 1 MAC sevoflurane - 4 L N2O - 2 L O2 under spontaneous ventilation via LMA. Tidal volume (VT), respiratory rate (RR), and arterial carbon dioxide tension (PaCO2) were measured just before and 15 min after the induction of anesthesia, 15 min after the start of operation and 15, 30, 45, and 60 min after the start of doxapram hydrochloride infusion. RESULTS: Measured values of RR and PaCO2 were significantly elevated during anesthesia venous those measured just before the induction of anesthesia in all groups. VT was significantly reduced during anesthesia venous just before the induction of anesthesia in all groups. All percent changes of VT, RR and PaCO2 were similar all any measurement times, and showed no significant changes after the infusion of doxapram hydrochloride in all groups. CONCLUSIONS: Intraoperative doxapram hydrochloride treatment did not produce any significant respiratory response improvement during 1 MAC sevoflurane anesthesia.
