The present study compared the effects of anesthesia induction with sevoflurane and propofol on hemodynamics, P-wave dispersion (Pwd), QT interval and corrected QT (QTc) interval. A total of 72 adult patients were included in this prospective study. All patients had control electrocardiograms (ECGs) before anesthesia induction. Anesthesia was induced with sevoflurane inhalation or intravenous propofol. Electrocardiography for all patients was performed during the 1(st) and 3(rd) minutes of induction, 3 minutes after administration of muscle relaxant, and at 5 minutes and 10 minutes after intubation. Pwd and QT intervals were measured on all ECGs. QTc intervals were determined using the Bazett formula. There was no significant difference in Pwd and QT and QTc intervals on control ECGs. In the sevoflurane group, except for control ECGs, Pwd and QTc interval on all ECGs were significantly longer than those in the propofol group (p < 0.05). We conclude that propofol should be used for anesthesia induction in patients with a predisposition to preoperative arrhythmias, and in those whose Pwd and QTc durations are prolonged on preoperative ECGs.
The aim of this study was to compare the effects of fentanyl or dexmedetomidine when used in combination with propofol and lidocaine for tracheal intubation without using muscle relaxants. Sixty patients with American Society of Anesthesiologists stage I risk were randomized to receive 1 mg/kg dexmedetomidine (Group D, n = 30) or 2 mg/kg fentanyl (Group F, n = 30), both in combination with 1.5 mg/kg lidocaine and 3 mg/kg propofol. The requirement for intubation was determined based on mask ventilation capability, jaw motility, position of the vocal cords and the patient's response to intubation and inflation of the endotracheal tube cuff. Systolic arterial pressure, mean arterial pressure, heart rate and peripheral oxygen saturation values were also recorded. Rate pressure products were calculated. Jaw relaxation, position of the vocal cords and patient's response to intubation and inflation of the endotracheal tube cuff were significantly better in Group D than in Group F (p < 0.05). The intubation conditions were significantly more satisfactory in Group D than in Group F (p = 0.01). Heart rate was significantly lower in Group D than in Group F after the administration of the study drugs and intubation (p < 0.05). Mean arterial pressure was significantly lower in Group F than in Group D after propofol injection and at 3 and 5 minutes after intubation (p < 0.05). After intubation, the rate pressure product values were significantly lower in Group D than in Group F (p < 0.05). We conclude that endotracheal intubation was better with the dexmedetomidine-lidocaine-propofol combination than with the fentanyl-lidocaine-propofol combination. However, side effects such as bradycardia should be considered when using dexmedetomidine.
Wound infiltration with combined levobupivacaine and tramadol resulted in elimination of postoperative analgesic demand and reduction in the incidence of side effects. We conclude that infiltration of the wound site with combined levobupivacaine and tramadol provides significantly better analgesia compared with levobupivacaine or tramadol alone.
Ischemia reperfusion injury causes the release of free oxygen radicals. Free oxygen radicals initiate the production of toxic metabolites, such as malondialdehyde (MDA), through the lipid peroxidation of cellular membranes. Following lipid peroxidation, the antioxidant enzyme system is activated against reactive oxygen species (ROS) and attempts to protect cells from oxidative damage. There is a balance between the scavenging capacity of antioxidant enzymes and ROS. Because of this balance, the total antioxidant capacity (TAC) measurement is a sensitive indicator of the overall protective effects of the antioxidants. Alpha(2) receptor agonists are effective in preventing hemodynamic reactions during extremity surgeries by preventing the release of catecholamines secondary to tourniquet application. They have also been shown to possess preventive effects in various ischemia-reperfusion injury models. In our study, we examined the effects of dexmedetomidine on tourniquet-induced ischemia-reperfusion injury in lower extremity surgeries performed under general anesthesia. The effects of dexmedetomidine were measured with serum MDA and TAC levels. We studied 60 adult American Society of Anesthesiologists (ASA) physical status I or II patients undergoing one-sided lower extremity surgery with tourniquet. The patients were randomly divided into two groups. Group D was administered a dexmedetomidine infusion at a rate of 0.1μg/kg/minute(-1) for 10 minutes prior to induction and then at 0.7μg/kg/hour(-1) until 10 minutes before the end of the operation. The control group (Group C) received a saline infusion of the same amount and for the same period of time. General anesthesia was induced with thiopental, fentanyl, and rocuronium and maintained with nitrous oxide and sevoflurane in both groups. Venous blood samples were obtained before the administration of the study drugs (basal) at 1 minute before tourniquet release and at 5 and 20 minutes after tourniquet release (ATR). In both groups, MDA levels decreased at 5 and 20 minutes ATR when compared with the basal values (p<0.05). TAC levels decreased at 1 and 5 minutes ATR and then returned to basal values at 20 minutes ATR (p<0.05). In reference to the prevention of lipid peroxidation in tourniquet-induced ischemia-reperfusion injury, the results from the two groups in our study showed that dexmedetomidine did not have an additional protective role during routine general anesthesia.
The aim of this study was to evaluate the effect of education on the knowledge, attitude and behavior of anesthesiology staff and residents towards low-flow anesthesia. The staff and residents in the Department of Anesthesia and Reanimation, Zonguldak Karaelmas University were given theoretical and practical training in delivering low-flow anesthesia. To evaluate their attitudes and behaviors toward low-flow anesthesia, we collected data during the 6 months before training, during the first 3 months after training, and at 4-6 months after training. Anesthesia follow-up records, operation time, volatile anesthetic agent used, and the amount (in liters) of fresh gas low mid-anesthesia were recorded in all three stages. A total of 3,158 patients received general anesthesia and inhalation anesthesia was used in 3,115 of these patients. Our study group consisted of 2,752 patients who had no absolute or relative contraindications to low-flow anesthesia. While the mean fresh gas flow was 4.00 +/- 0.00 L/min before training, this level dropped to 2.98 L/min in the first 3 months after training, and to 3.26 L/min in the following 3 months. The mean fresh gas flow was significantly lower at the two post-training assessments than before training (p < 0.05). In conclusion, low-flow anesthesia may be used more frequently if educational seminars are provided to anesthetists. The use of low-flow anesthesia may increase further by allocating more time to this technique in anesthesia training programs provided at regular intervals.
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