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This Month in Anesthesiology  |   December 2002
THIS MONTH IN ANESTHESIOLOGY
Article Information
This Month in Anesthesiology
This Month in Anesthesiology   |   December 2002
THIS MONTH IN ANESTHESIOLOGY
Anesthesiology 12 2002, Vol.97, 5A-7A. doi:
Anesthesiology 12 2002, Vol.97, 5A-7A. doi:
Propofol: The Relationship between Brain Concentrations, Electroencephalogram, Middle Cerebral Blood Flow Velocity, and Cerebral Oxygen Extraction during Induction of Anesthesia. Ludbrook et al  . (page 1363)
To measure the rate of propofol distribution to the brain, Ludbrook et al  . recruited seven adult volunteers scheduled to undergo elective orthopedic surgery. Following sedation with midazolam, each volunteer had catheters placed to enable blood sampling; one in the distal radial artery of the arm opposite the intravenous cannula, and one in the right internal jugular vein. After a 5 min baseline period following instrumentation, 1% propofol was administered via  continuous infusion at 110 mg/min for 5 min and then 10 mg/min for 20 min. Electroencephalography, electrocardiography, and blood flow velocity (Vmca) of the right middle cerebral artery were continuously measured throughout the infusion period. Blood pressure was measured every 3 min, and blood samples for later measurement of propofol concentrations were obtained from the arterial and jugular bulb catheters at regular intervals. The study took 35 min to complete, after which patients were intubated, their jugular bulb catheters removed, and surgery proceeded.
The net flux of propofol into the brain was calculated from the arteriojugular bulb concentration differences and estimations of cerebral blood flow (CBF), using the relative changes in Vmca, and assuming a baseline CBF of 55 ml · 100 g−1· min−1. The team applied effect compartmental modeling to the blood and brain concentration data to quantify the rate of equilibrium between blood and the brain.
Administration of propofol produced a significant decrease in subjects’ Vmcafrom baseline values (which ranged from 37–82 cm/s). Mean arterial pressure decreased significantly, but never fell below 60 mmHg. Phenylephrine support was required briefly during the study period for two of the participants. Rapid and significant decreases in bispectral index (BIS) values were noted after propofol infusion began, reaching their minimum mean values approximately 6.5–7.5 min into the infusion. There was a linear relationship between mean brain concentrations and mean BIS values throughout the study, with minimal hysteresis. Burst suppression was not evident until mean brain concentrations of greater than 5.5 mg/l were reached.
Global brain concentrations may not be reflective of propofol's anesthetic effects, as a result of the large CNS distribution volume and prolonged uptake into sites unrelated to sites of anesthetic action. As the BIS values were more closely related to brain concentrations, pharmacokinetic models incorporating this information might have utility when devising dose regimens to target the brain.
Does Transcutaneous Electrical Stimulation Relieve Postoperative Nausea and Vomiting? Coloma et al  . (page 1387)
Coloma et al  . designed a randomized, placebo (sham)-controlled study to evaluate the use of transcutaneous electrical P6 acupoint stimulation (acustimulation) as an alternative to ondansetron to treat postoperative nausea and vomiting (PONV). The ReliefBand® acustimulation device, (Woodside Biomedical, Inc., Carlsbad, CA) powered by batteries and worn as a watchband, is capable of delivering 10–35 mA, depending on the setting used. The circuitry was deactivated in the identical sham devices used in the experiment. To minimize bias, volunteers were told that they might or might not feel a tingling at their wrist from using the acustimulation device controls.
Out of 268 healthy volunteers undergoing laparoscopic surgery under general anesthesia, 90 developed PONV in the recovery unit. At that point, patients were randomized to receive one of three treatments: ondansetron (4 mg intravenously) and a sham acustimulation device; 2 ml intravenous saline and a working device; or a combination of 4 mg intravenous ondansetron and a working acustimulation unit. If the patients’ PONV persisted for more than 15 min after initiation of treatment, intravenous metoclopramide 10 mg was administered as a rescue antiemetic. Fentanyl, in 25 μg intravenous boluses, was used to manage postoperative pain. Patients were asked about PONV symptoms at 5–15 min intervals in the postanesthesia care unit (PACU), and at 30 min intervals thereafter until discharge. An emetic episode was defined as one or more vomiting or retching events occurring less than a minute apart. Nurses administering the treatment were blinded to group assignment, so the sham and active stimulus units were adjusted in an identical manner, and the devices started at the lowest setting. If symptoms persisted, settings were increased at 5-min intervals; rescue antiemetics were administered if symptoms persisted for 5 min beyond the highest setting. Patients were instructed to keep the devices on for the 72 h following discharge, except when bathing. Follow-up phone calls were made to all patients at 24 and 72 h to assess their satisfaction with the quality of their recovery from anesthesia and with the antiemetic treatment.
Patients receiving the combination treatment (ondansetron and the active unit) had higher complete response rates and fewer emetic events than those receiving acustimulation alone. Interestingly, more patients in the group receiving acustimulation alone reported a regular sleep pattern 24 h after surgery. With respect to patient satisfaction and quality of recovery scores, there were no significant differences between groups. The results suggest that ondansetron enhanced the efficacy of acustimulation in treating PONV.
Four Scenarios of Critical Anesthetic Events Tested using Mannequin Simulation. Schwid et al  . (page 1434)
Schwid et al  . enlisted 99 anesthesia residents from 10 institutions to take part in a study assessing their management of four critical anesthesia scenarios using mannequin- based simulators. Two evaluators at each institution independently viewed videotapes of residents’ management techniques during the scenarios and scored their performances. A third evaluator from an outside institution reviewed the videotapes, and a fourth evaluator viewed the tapes to determine the frequency and types of management errors. Statistical analysis was performed for construct and criterion-related validity, internal consistency, interrater reliability, and intersimulator reliability.
Residents’ levels of training ranged from clinical base year (n = 7); to first year of clinical anesthesia training (n = 52); to second clinical year (n = 25); and third year of anesthesia training (n = 15). All of the residents were familiar with and had trained with the mannequin-based simulators used, and none of the residents was tested on the simulator on the day post-call. All participants were instructed to manage the patient as they would in the operating room, and to verbalize all observations, possible problems, and treatments administered.
The simulated scenarios included esophageal intubation; anaphylactic reaction to administration of antibiotic and muscle relaxant; bronchospasm in a patient with chronic obstructive pulmonary disease (COPD); and myocardial ischemia. All of the participants diagnosed and treated the esophageal intubation adequately, although clinical base year residents took longer to reestablish ventilation than did their peers with more training.
In the anaphylaxis reaction scenario, 34% of the residents did not make the correct diagnosis. Management errors included failure to check the patient's simulated pulse (to verify what they thought was a faulty blood pressure monitor), and misinterpretation of sinus tachy-cardia as supraventricular tachycardia. Ten residents administered esmolol, labetalol, or adenosine to slow the heart rate despite presence of severe hypotension.
Some residents never arrived at the correct diagnosis for the bronchospasm scenario, and 50% did not consider a mechanical cause (such as an endotracheal tube kink, incorrect positioning, or mucus plug) for increased difficulty ventilating. During management of the myocardial ischemia episode, 22% omitted pressors, 45% omitted β1 blockers to slow the heart rate, and 31% omitted administration of nitroglycerin. Of those who did give nitroglycerin, many made dosing errors.
Residents’ long and short form scores improved from CA-1 to CA-2 level of training, but that improvement leveled out and did not increase from CA-2 to CA-3 yr. The progression of scores with level of training and the subjects’ rating of the scenarios as realistic both support the construct-related validity of this method. Excellent interrelater reliability was noted, with the third independent evaluator showing ratings nearly identical to those of the two institutional evaluators. The study authors believe that, with further improvements in realism and scenario design, anesthesia simulators show promise as valid and reliable methods to evaluate anesthesia residents.
Acute Opioid-induced Hyperalgesia Reversed by Ketorolac in Rats Kang et al  . (page 1641)
Kang et al  . used three types of nociceptive tests (one thermal and two mechanical) to establish baseline paw withdrawal thresholds in rats. To test whether intrathecal ketorolac would reverse the hypersensitivity to pain following acute opioid exposure, the researchers first induced hyperalgesia by injecting a total dose of 320 μg/kg of fentanyl, injected in four equal doses at 15-min intervals. Another group of animals received saline injections. Animals were again tested for paw withdrawal to mechanical and heat stimuli at 1, 2, and 4 days after fentanyl or saline injections. These preliminary experiments demonstrated a maximal hypersensitivity to mechanical testing 1 day after fentanyl exposure.
Animals were randomized to receive 5, 15, or 50 μg of intrathecal ketorolac 1 day after fentanyl-induced hyperalgesia by an investigator blinded to the dose of ketorolac. Testing was performed before and at 30 min intervals after injection. The rats were then killed and their spinal cords (L4 to L6) extracted for subsequent immunocytochemical analysis. At the lowest dose of 5 μg, intrathecal ketorolac did not affect withdrawal threshold to von Frey filament testing. The 15 and 50 μg doses, however, increased withdrawal thresholds for 30–60 min after injection. Results of COX-1 and COX-2 immunoreactivity assays revealed that acute fentanyl exposure was not associated with an increase in COX-1 or COX-2 expressing elements in the spinal cord. But the hypersensitivity induced by fentanyl was blocked in a dose-dependent manner by intrathecal injection of the COX-1 preferring inhibitor, ketorolac.