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ANESTHETIC PHARMACOLOGY

Heart Rate Response to Intravenous Atropine During Propofol Anesthesia

Department of Anesthesia, Akita University School of Medicine, Akita, Japan

Address correspondence and reprint requests to Takashi Horiguchi, MD, Department of Anesthesia, Akita University School of Medicine, Hondo 1-1-1, Akita City, Akita 010-8543, Japan. Address e-mail to thorigu{at}doc.med.akita-u.ac.jp

We studied the dose-response relationships for atropine-induced heart rate (HR) changes in 61 patients during propofol anesthesia. The control group (n = 15) received no propofol. Group P-5 (n = 22) received IV propofol 1.25 mg/kg over 1 min followed by propofol at 5 mg · kg^-1 · h^-1. After tracheal intubation, anesthesia was maintained with propofol 5 mg · kg^-1 · h^-1 and 67% nitrous oxide in oxygen. Group P-10 (n = 24) received IV propofol 2.5 mg/kg over 1 min followed by propofol at 10 mg · kg^-1 · h^-1. The P-10 protocol was otherwise identical. All patients received incremental doses of IV atropine 5 µg/kg over 5 s at 2-min intervals until HR increased >20 bpm from baseline values. Heart rate response to atropine 10 µg/kg was attenuated in Groups P-5 (12 ± 7 bpm) and P-10 (9 ± 6 bpm) compared with the control group (28 ± 13 bpm, P<0.05). When atropine 20 µg/kg was administered, HR increased >20 bpm in all patients of the control group, but in only 43% and 13% of patients in Groups P-5 and P-10, respectively (P<0.05). These results indicate the decreased HR responsiveness to IV atropine in patients receiving propofol, which cannot be effectively overcome by a large dose of atropine, is possibly attributable to propofol-induced suppression of the sympathetic nervous system.

IMPLICATIONS: Heart rate response to IV atropine is attenuated during propofol anesthesia, and the decreased responsiveness to atropine cannot be effectively overcome by a large dose of atropine.

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