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Isoflurane Anesthesia Does Not Add to the Bronchodilating Effect of a beta (2-Adrenergic) Agonist After Tracheal Intubation

Rick Sai‐Chuen Wu, King‐Chuen Wu, Teresa Kit-Man Wong, Ying‐Huang Tsai, Robin Ka-Shun Cheng, P P Tan, Michael J. Bishop

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Abstract

This double-blind study investigates whether isoflurane/N2O anesthesia adds to the bronchodilating effect of the beta 2-adrenergic agonist, fenoterol, after an endotracheal tube (ETT)-induced increase in airway resistance. Forty-five patients with ASA physical status I-II were randomly assigned to two groups: fenoterol-treated patients (n = 23) were given three metered-dose inhaler puffs (600 micrograms) of fenoterol 10 min before induction of anesthesia and placebo-treated patients (n = 22) received three puffs of an aerosol containing no medication. Anesthesia was induced with thiopental and vecuronium intravenously. Respiratory system resistance (Rrs) was measured using a CP-100 pulmonary function monitor 5 min after endotracheal intubation. Inhalation anesthesia was then begun using 50% N2O in O2 with end-tidal 1.3% isoflurane. Rrs measurements were repeated at 5, 15, and 30 min after the initiation of inhalation anesthesia. Postintubation Rrs was significantly lower in the fenoterol-treated patients than in the placebo-treated patients. Rrs declined by a mean of 17.1% after 30 min of inhalation anesthesia in the placebo-treated patients but declined by only 1.4% in the fenoterol-treated patients (P < 0.05 for fenoterol provides protection versus placebo). Our results confirm that fenoterol provides protection against ETT-induced increase of airway resistance. However, isoflurane, while a potent bronchodilator, does not add to the effect of fenoterol.

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What this paper is about

This double-blind study investigates whether isoflurane/N2O anesthesia adds to the bronchodilating effect of the beta 2-adrenergic agonist, fenoterol, after an endotracheal tube (ETT)-induced increase in airway resistance. Forty-five patients with ASA physical status I-II were randomly assigned to two groups: fenoterol-treated patients (n = 23) were given three metered-dose inhaler puffs (600 micrograms) of fenoterol 10 min before induction of anesthesia and placebo-treated patients (n = 22) received three puffs of an aerosol containing no medication. Anesthesia was induced with thiopental and vecuronium intravenously. Respiratory system resistance (Rrs) was measured using a CP-100 pulmonary function monitor 5 min after endotracheal intubation. Inhalation anesthesia was then begun using 50% N2O in O2 with end-tidal 1.3% isoflurane. Rrs measurements were repeated at 5, 15, and 30 min after the initiation of inhalation anesthesia. Postintubation Rrs was significantly lower in the fenoterol-treated patients than in the placebo-treated patients. Rrs declined by a mean of 17.1% after 30 min of inhalation anesthesia in the placebo-treated patients but declined by only 1.4% in the fenoterol-treated patients (P < 0.05 for fenoterol provides protection versus placebo). Our results confirm that fenoterol provides protection against ETT-induced increase of airway resistance. However, isoflurane, while a potent bronchodilator, does not add to the effect of fenoterol.

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Available abstract

This double-blind study investigates whether isoflurane/N2O anesthesia adds to the bronchodilating effect of the beta 2-adrenergic agonist, fenoterol, after an endotracheal tube (ETT)-induced increase in airway resistance. Forty-five patients with ASA physical status I-II were randomly assigned to two groups: fenoterol-treated patients (n = 23) were given three metered-dose inhaler puffs (600 micrograms) of fenoterol 10 min before induction of anesthesia and placebo-treated patients (n = 22) received three puffs of an aerosol containing no medication. Anesthesia was induced with thiopental and vecuronium intravenously. Respiratory system resistance (Rrs) was measured using a CP-100 pulmonary function monitor 5 min after endotracheal intubation. Inhalation anesthesia was then begun using 50% N2O in O2 with end-tidal 1.3% isoflurane. Rrs measurements were repeated at 5, 15, and 30 min after the initiation of inhalation anesthesia. Postintubation Rrs was significantly lower in the fenoterol-treated patients than in the placebo-treated patients. Rrs declined by a mean of 17.1% after 30 min of inhalation anesthesia in the placebo-treated patients but declined by only 1.4% in the fenoterol-treated patients (P < 0.05 for fenoterol provides protection versus placebo). Our results confirm that fenoterol provides protection against ETT-induced increase of airway resistance. However, isoflurane, while a potent bronchodilator, does not add to the effect of fenoterol.

Key concepts: Fenoterol, Medicine, Anesthesia, Bronchodilator, Isoflurane, Placebo, Inhalation, Tracheal intubation

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