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

Nitrous oxide (N(2)O) is a frequently used adjunct to propofol anesthesia. Although N(2)O 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 N(2)O 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.Thirty ASA I-II patients (aged 30-66 yr) were randomly assigned to receive propofol with oxygen-enriched air (FIO(2) = 0.3; air group) or propofol with 70% N(2)O (N(2)O group). Following intubation, a computerized target-controlled infusion technique was used to administer propofol from 0 micro g x mL(-1) (baseline) to 5 micro g x mL(-1) in 1 micro g x mL(-1) increments.Mean arterial pressure (MAP) decreased more in the N(2)O group than in the air group only at 5 micro g x 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.Propofol causes dose-dependent decreases in ABF and MAP; however, 70% N(2)O produces minimal hemodynamic and Doppler-derived variable changes under target-controlled propofol infusion at therapeutic concentrations.