Anesth Analg 2006;103:1606-1608
© 2006 International Anesthesia Research Society
doi: 10.1213/01.ane.0000246428.17118.4b
LETTER TO THE EDITOR
Editor-in-Chief Steven L. Shafer
Does Atropine Reduce the Risk of Propofol-Induced Cardiovascular Depression?
Norihito Kitagawa, MD,
Mitsuhiro Katoku, MD,
Takanori Kasahara, MD,
Toshiyuki Tsuruta, MD,
Mayuko Oda, MD, and
Tadahide Totoki, MD
Department of Anesthesiology; 04923004{at}edu.cc.saga-u.ac.jp (Kitagawa)
Department of Orthopedic Surgery; Tsuruta Orthopedic Clinic; Ushizu (Katoku, Kasahara, Tsuruta)
Department of Anesthesiology; Saga Memorial Hospital; Takagise (Oda)
Saga Medical School Hospital; Saga Medical School; Nabeshima; Saga, Japan (Totoki)
To the Editor:
Propofol-induced bradycardia is common, and in some instances life-threatening (1–3). Administration of atropine with propofol may block parasympathetic activation, preventing bradycardia (4). We investigated whether atropine could prevent propofol-induced cardiovascular depression during and after induction of anesthesia.
After obtaining institutional ethical committee approval and written informed patient consent, we randomly assigned 160 ASA physical status I or II patients without arrhythmic or ischemic heart disease to two groups (n = 80 each) to receive either atropine or saline. We monitored all patients using electrocardiography, pulse oximetry, end-tidal carbon dioxide, and noninvasive arterial blood pressure beat-to-beat using tonometric methods (BP-608 Evolution monitor; Colin Medical Technology, Komaki, Japan) (5). Anesthesia was induced with 2–3 mg/kg propofol and 0.3 mg/kg pentazocine given over 30 s, followed by either 0.01 mg/kg of atropine diluted with physiological saline (Group A) or physiological saline only (controls) over 15 s (unblinded). We inserted a laryngeal mask airway (LMA) and maintained anesthesia with 2 L/min each of oxygen and nitrous oxide, adding sevoflurane under spontaneous breathing without muscular relaxants. If necessary, we assisted ventilation to maintain Spo2  96% and end-tidal expiratory carbon dioxide tension  50 mm Hg. We recorded arterial blood pressure and heart rate before induction and at 1, 5, 10, and 15 min after LMA insertion. Surgery began after the 15-min measurement. Bradycardia (heart rate <50 bpm) was treated with 0.01 mg/kg of atropine. Hypotension (systolic blood pressure <75 mm Hg) was treated with 4 mg of ephedrine. We compared patient characteristics and hemodynamics using an unpaired t-test, and the use of rescue drug using Mann–Whitney test. A P < 0.05 was considered statistically significant.
Patient characteristics, including induction dose of propofol, were similar in both groups. Hemodynamics results are shown in Figure 1. After induction, the heart rate decreased in the control group and increased in Group A, with a significant difference at every time point after induction. Arterial blood pressure decreased after induction in both groups. Arterial blood pressure was significantly higher in Group A at 5, 10, and 15 min after induction. Use of additional atropine or ephedrine medication is shown in Table 1. Significantly fewer Group A patients needed treatment for bradycardia or hypotension than control patients.
Although direct inhibition of myocardium or atrio-ventricular conduction by propofol has also been suggested as a cause of the bradyarrhythmia (6), relative activation of the parasympathetic nerve system including varoreflex resetting or attenuation of varoreflex regulation is generally considered responsible (4). Administration of vagolytics would thus be reasonable for preventing propofol-induced bradycardia and some investigators have recommended this strategy (1,2). On the other hand, Horiguchi and Nishikawa (4) suggested that even large doses of atropine (0.03 mg/kg) cannot prevent vagotonic activation caused by propofol. However, they used propofol for both inducing and maintaining anesthesia, differing from the present method of using sevoflurane for anesthesia maintenance after anesthesia induction with propofol. In conclusion, our results suggest that 0.01 mg/kg of atropine can adequately prevent cardiovascular depression associated with propofol, unless propofol is used for maintaining anesthesia.
REFERENCES
- Baraka A. Severe bradycardia following propofol-suxamethonium sequence. Br J Anaesth 1988;61:482–3.[Abstract/Free Full Text]
- Egan TD, Brock UJG. Asystole after anesthesia induction with a fentanyl, propofol, and succinylcholine sequence. Anesth Analg 1991;73:818–20.[Free Full Text]
- Freysz M, Timourt Q, Betrix L, Faucon G. Propofol and bradycardia. Can J Anaesth 1991;38:137–8.[Web of Science][Medline]
- Horiguchi T, Nishikawa T. Heart rate response to intravenous atropine during propofol anesthesia. Anesth Analg 2002;95:389–92.[Abstract/Free Full Text]
- Kemmotsu O, Ueda M, Otsuka H, et al. Blood pressure measurement by arterial tonometry in controlled hypotension. Anesth Analg 1991;73:54–8.[Abstract/Free Full Text]
- Alphin RS, Martens JR, Dennis DM. Frequency-dependent effects of propofol on atrioventricular nodal conduction in guinea pig isolated heart. Mechanism and potential antidysrhythmic properties. Anesthesiology 1995;83:382–94.[Web of Science][Medline]
|
