The present study was designed to assess the efficacy of fentanyl combined with dilute lidocaine solution for intravenous regional anesthesia of the arm.In ten volunteers, the nondominant arm was exposed to three treatments: 100 mg lidocaine, 42 ml; 100 mg lidocaine plus 100 micrograms fentanyl, 42 ml; and 100 micrograms fentanyl, 42 ml. Each subject was tested on three occasions with three or more days between experiments. Sensory and motor function was tested to determine whether the neural effects of the particular treatments differed.When lidocaine and lidocaine plus fentanyl results were compared, no significant differences were found. However, anesthesia, analgesia, and loss of motor function generally were less complete and slower in onset with the fentanyl alone treatment. Two subjects became nauseated after tourniquet cuff deflation when lidocaine plus fentanyl was tested, as did one subject when fentanyl was tested.Results of this and other studies indicate there is no value in adding fentanyl to local anesthetics for intravenous regional anesthesia.
The trend in modern anesthesia is to "lighten up." This generally involves use of several drugs with selective and complementary actions. The pharmacokinetic properties of such drugs should allow rapid onset, rapid recovery, and rapid responses to changes in delivered doses. Peri-operative management issues also are inherent to use of modern drugs and techniques. For example, provisions must be in place for postoperative analgesia if rapid recovery is anticipated. Light anesthesia reduces morbidity and mortality, and reduces the drug, facility, and personnel costs associated with anesthesia. However, the requirements for anesthesia and the expertise of personnel administering anesthesia vary considerably. Many regulatory bodies and scientific journals require a description of how anesthesia adequacy and depth will be assessed, as well as extensive justification for the use of neuromuscular blocking agents. In environments where adequate experience and sophistication for the use of cutting edge drugs and methods are not available, older drugs and techniques may be adequate and preferable to protect animals from pain or distress.
Bupivacaine-induced cardiovascular collapse is a feared complication because of the difficulty in restoring stable circulation [1]. Early recognition is important so that the injection of bupivacaine can be discontinued. We used an animal model of near-cardiac arrest from bupivacaine infusion to identify the sequence of hemodynamic events that precedes bupivacaine-induced cardiovascular collapse. Twelve pigs (23-25 kg) were sedated with ketamine and anesthetized with halothane. Arterial blood pressure and cardiac output were measured. Bupivacaine (3.75 mg/mL) was administered at a rate of 5.73 mL/min (approximately 1 mg [middle dot] kg-1 [middle dot] min-1) through a central venous catheter until severe ventricular arrhythmia occurred. Blood pressure and heart rate were unchanged, but cardiac output decreased by 40% with increasing doses of bupivacaine. Calculated peripheral resistance increased by 54%. The QRS complex of the surface electrocardiogram widened, and the R-wave amplitude decreased 80%, together with the decrease in cardiac output. T-wave amplitude increased initially but returned toward baseline at the largest bupivacaine doses. The plasma concentration of bupivacaine after the infusion was 16 +/- 6.8 [micro sign]g/mL. Implications: The increase in vascular resistance that accompanies acute bupivacaine overdose maintains blood pressure but masks severe myocardial depression. (Anesth Analg 1999;88:1143-8)
