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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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