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Nitrous oxide produces minimal hemodynamic changes in patients receiving a propofol-based anesthetic: an esophageal Doppler ultrasound study

[Le protoxyde d’azote produit des changements hémodynamiques minimes chez des patients qui reçoivent une anesthésie à base de propofol : une étude de l’effet Doppler sophagien]

Toshiya Shiga, MD PhD^*, Zen’ichiro Wajima, MD PhD^*, Tetsuo Inoue, MD PhD^* and Ryo Ogawa, MD PhD

^* From the Department of Anesthesia, Chiba Hokusoh Hospital, Nippon Medical School, Chiba;
and the Department of Anesthesiology, Nippon Medical School Hospital, Tokyo, Japan.

Present corresponding address: Dr. Toshiya Shiga, Department of Anesthesia, Nippon Medical School Chiba Hokusoh Hospital, Kamagari 1715, Inba, Chiba 270-1694, Japan. Phone: 81-476-99-1843; Fax: 81-476-99-1931; E-mail: Shigat{at}aol.com

Purpose: Nitrous oxide (N₂O) is a frequently used adjunct to propofol anesthesia. Although N₂O reduces the requirement of propofol for induction and maintenance, the effects of both drugs on overall hemodynamics remain controversial. We tested the hypothesis that the addition of N₂O to therapeutic doses of propofol alters hemodynamics and Doppler-derived variables evaluated with the esophageal Doppler monitor in a randomized, double-blinded, placebo-controlled design.

Methods: Thirty ASA I-II patients (aged 30–66 yr) were randomly assigned to receive propofol with oxygen-enriched air (FIO₂ = 0.3; air group) or propofol with 70% N₂O (N₂O group). Following intubation, a computerized target-controlled infusion technique was used to administer propofol from 0 µg•mL^-1 (baseline) to 5 µg•mL^-1 in 1 µg•mL^-1 increments.

Results: Mean arterial pressure (MAP) decreased more in the N₂O group than in the air group only at 5 µg•mL^-1. Aortic blood flow (ABF) showed a similar dose-dependent decrease in both groups. Peak aortic flow acceleration, as a myocardial contractility index, decreased significantly and similarly in both groups in a dose-dependent manner whereas peak velocity of ABF, as another measure of myocardial contractility, remained unchanged. Heart rate-corrected left ventricular ejection time, as a measure of preload, remained constant in both groups at any target plasma concentration.

Conclusion: Propofol causes dose-dependent decreases in ABF and MAP; however, 70% N₂O produces minimal hemodynamic and Doppler-derived variable changes under target-controlled propofol infusion at therapeutic concentrations.