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Background: Conflicting results have been reported on the effect of anxiety on the propofol dose required for inducing loss of consciousness (LOC). The hemodynamic effects of anxiety, increased heart rate (HR), and cardiac output may account for these discrepancies. We therefore designed this study to address, first, the effect of perioperative HR on propofol dose required for LOC and, second, the effect of perioperative anxiety on HR., Methods: Forty-five ASA physical status I-II female patients undergoing gynecological surgery were studied. Anxiety was assessed in the operating room with the State-Trait Anxiety Inventory (STAI)-state Spielberger scale (situational anxiety). After HR recording, anesthesia was induced with a 200-mL/h 1% propofol infusion with the Base Primea pump (Fresenius-Vial, Brezins, France) until LOC. The propofol dose was recorded at the time of LOC. Relationships between STAI-state and HR versus propofol dose at LOC were tested with the Spearman test with a P value of 0.01., Results: A significant relationship was observed between HR and propofol dose at LOC (rho = 0.487, P = 0.0012) but not between STAI-state and propofol dose (rho = 0.330, P = 0.0306). However, a significant relationship was observed between STAI-state and HR (rho = 0.462 and P = 0.0054)., Conclusion: Increased perioperative HR is associated with increased propofol dose required for LOC. Perioperative anxiety accounts for increased HR.

Background: Pregnancy is associated with decreased hypnotic requirement, allegedly related to progesterone. However, the effects of pregnancy and progesterone on propofol requirement have not been thoroughly investigated. We conducted this study to determine whether propofol dose and predicted effect-site concentration for loss of consciousness (LOC) during induction of anesthesia, and eye opening during emergence from anesthesia, are decreased during early pregnancy. We also investigated whether blood progesterone was correlated with propofol dose and effect-site concentration for LOC., Methods: We studied 57 ASA I-II women patients undergoing elective termination of pregnancy and 55 control patients undergoing transvaginal oocyte puncture for in vitro fertilization. Anesthesia was induced by administration of a 1% propofol infusion at 200 mL/min. Propofol dose and calculated effect-site concentration (Schnider model) were recorded at the time of LOC during induction. We also calculated effect-site concentration at the time of eye opening upon emergence from anesthesia. Blood progesterone was measured after surgery., Results: Mean (+/-1 SD) propofol dose at LOC was significantly reduced in the pregnant patients compared with the nonpregnant control patients (108.57 +/- 20.04 vs 117.59 +/- 17.98 mg, respectively; P = 0.014). Similarly, the calculated propofol effect-site concentration at LOC was significantly lower in the pregnant patients than the nonpregnant control patients (4.59 +/- 0.72 vs 5.01 +/- 0.64 microg/mL, respectively; P = 0.0014). There was no difference in the calculated effect-site concentration on eye opening upon emergence. No significant relationship was observed between blood progesterone and propofol dose or calculated propofol effect-site concentration at LOC., Conclusion: Propofol dose and predicted propofol effect-site concentration at LOC are decreased during early pregnancy. Progesterone does not explain this result.

Background: Chronic alcoholic patients are frequently presented for anesthesia and surgery. These patients require higher doses of propofol than control patients for induction of anesthesia, but whether this is because of changes in pharmacokinetics or pharmacodynamics is not known. This study was designed to investigate the influence of chronic ethanol intake on propofol pharmacokinetics., Methods: Fifteen chronic alcoholic and 15 control patients, receiving propofol by target-controlled infusion for otolaryngologic surgery, were studied. Blood propofol concentrations were measured at regular intervals during and after the propofol infusion. Nonlinear mixed-effects population models (NONMEM) examining the influence of alcoholism were constructed. The influence of recovery on propofol pharmacokinetic parameters was also addressed., Results: The total amount of propofol and the predicted and measured concentrations during all phases of anesthesia did not differ between the two groups. The fact that the measured concentrations at the time of opening eyes were similar further confirmed that the potency of propofol was not modified by the alcoholic status of the patients. Chronic alcoholism was associated with only mild changes in propofol pharmacokinetics (increase in rapid intercompartmental clearance and greater interindividual variability in the central volume of distribution). The rebound in concentration frequently observed during the recovery phase could be related to decreased propofol peripheral volumes of distribution despite an increase in elimination clearance., Conclusions: Chronic alcoholism induces only mild changes in the pharmacokinetics of propofol. Conversely, propofol pharmacokinetics are markedly different during anesthesia and surgery or after opening eyes in the recovery period.