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Background This study assessed the effect of a single bolus administration of lidocaine on the prevention of tourniquet-induced hypertension (TIH) and compared the effect of lidocaine to that of ketamine in patients undergoing general anesthesia. Methods This randomized, controlled, double-blind study included 75 patients who underwent lower limb surgery using a tourniquet. The patients were administered lidocaine (1.5 mg/kg, n = 25), ketamine (0.2 mg/kg, n = 25) or placebo (n = 25). The study drugs were administered intravenously 10 min before tourniquet inflation. Systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were measured before tourniquet inflation, after tourniquet inflation for 60 min at 10 min intervals, and immediately after tourniquet deflation. The incidence of TIH, defined as an increase of 30% or more in SBP or DBP during tourniquet inflation, was also recorded. Results SBP, DBP, and HR increased significantly over time in the control group compared to those in the lidocaine and ketamine groups for 60 min after tourniquet inflation (P < 0.001, P < 0.001, and P = 0.007, respectively). The incidence of TIH was significantly lower in the lidocaine (n = 4, 16%) and ketamine (n = 3, 12%) group than in the control group (n = 14, 56%) (P = 0.001). Conclusion Single-bolus lidocaine effectively attenuated blood pressure increase due to tourniquet inflation, with an effect comparable to that of bolus ketamine.

BackgroundInhalation anesthetics are an important factor for postoperative hepatic and renal dysfunction. In this regard, TIVA can reduce the risk of hepatic and renal dysfunction inherited to inhalation anesthetics. The present study was conducted to determine whether hepatic and renal functions differ after anesthesia with sevoflurane and propofol.MethodsTwo hundred patients, ASA physical status class I, II, scheduled for an elective thyroidectomy were randomly divided into two groups. Anesthesia was maintained with sevoflurane 1-2% and remifentanil in the sevoflurane group (Group S) and propofol 2-5 ug/ml and remifentanil 2-5 ng/ml at the effect site, using a target controlled infusion (TCI) pump in the TIVA group (Group T) to maintain BIS of 40-60. To evaluate the hepatic and renal function, aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN) and creatinine were tested at preoperation (baseline), postoperative 1 day and 3 days.ResultsAST was increased at postoperative 1 day and 3 days, compared with that of the preoperation in Group S, and postoperative 1 day in Group T, but the values were within its normal limit. ALT was not changed after anesthesia in both groups. BUN was increased at postoperative 1 day, compared with that of the preoperation in Group S, but the value was within its normal limit. Creatinine was not changed after anesthesia in both groups.ConclusionsThe changes of hepatic and renal function after inhalation anesthesia with sevoflurane and TIVA with propofol and remifentanil for thyroidectomy were clinically insignificant, and there was no difference between the two methods.

Background: Sedation by dexmedetomidine, like natural sleep, often causes bradycardia. We explored the nature of heart rate (HR) changes as they occur during natural sleep versus those occurring during dexmedetomidine sedation. Methods: The present study included 30 patients who were scheduled to undergo elective surgery with spinal anesthesia. To assess HR and sedation, a pulse oximeter and bispectral index (BIS) monitor were attached to the patient in the ward and the operating room. After measuring HR and BIS at baseline, as the patients slept and once their BIS was below 70, HR and BIS were measured at 5-minute intervals during sleep. Baseline HR and BIS were also recorded before spinal anesthesia measured at 5-minute intervals after dexmedetomidine injection. Results: During natural sleep, HR changes ranged from 2 to 19 beats/min (13.4 ± 4.4 beats/min), while in dexmedetomidine sedation, HR ranged from 9 to 40 beats/min (25.4 ± 8.5 beats/min). Decrease in HR was significantly correlated between natural sleep and dexmedetomidine sedation (R2 = 0.41, P < 0.001). The lowest HR was reached in 66 min during natural sleep (59 beats/min) and in 13 min with dexmedetomidine sedation (55 beats/min). The time to reach minimum HR was significantly different (P < 0.001), but there was no difference in the lowest HR obtained (P = 0.09). Conclusions: There was a correlation between the change in HR during natural sleep and dexmedetomidine sedation. The bradycardia that occurs when using dexmedetomidine may be a normal physiologic change, that can be monitored rather than corrected. [ABSTRACT FROM AUTHOR]