METHODS: S(+)-ketamine and xylazine-anesthetized rabbits were assigned to one of seven experimental groups: a control (vehicle only) group, a GGA group, a sevoflurane group, a GGA+sevoflurane group, a sodium 5-hydroxydecanoate (5HD) group, a GGA + 5HD group, and a heat stress group. All rabbits were subjected to 30 min of coronary artery occlusion followed by 3 h of reperfusion. Rabbits were pretreated with IV vehicle, GGA (10 mg/kg), or heat stress (42°C for 15 min) 24 h before coronary occlusion. Sevoflurane (0.5 minimum alveolar concentration) or 5HD (5 mg/kg) were administered before myocardial ischemia. Myocardial infarct size and the area at risk for ischemia were measured, and heat shock protein (Hsp) 70 levels in each experimental group were determined.

RESULTS: Compared with vehicle only, GGA significantly reduced the size of myocardial infarction in relation to the area at risk (39 ± 10% vs 59 ± 9%, P < 0.02). Sevoflurane enhanced the GGA-induced cardioprotection (23 ± 17%, P < 0.05 vs GGA). The cardioprotective effect of GGA was abolished by administration of 5HD (56 ± 15%, P < 0.01). GGA enhanced Hsp 70 expression compared with that in the control group (0.69 ± 0.15 vs 0.36 ± 0.05, P < 0.02). Administration of GGA with sevoflurane resulted in the same level of Hsp 70 expression as GGA (0.69 ± 0.16, P > 0.98).

CONCLUSIONS: GGA appears to reduce myocardial infarct size in association with increased Hsp 70 expression. Sevoflurane enhances the GGA-induced cardioprotective effect.

METHODS: Rabbits (n = 62) instrumented for hemodynamic measurement were subjected to a 30-min left anterior descending coronary artery occlusion and 3 h reperfusion, and received 0.9% saline (control) or three cycles of 70% helium–30% oxygen administered for 5 min interspersed with 5 min of an air–oxygen mixture before left anterior descending coronary artery occlusion in the absence or presence of pretreatment with the nonselective NOS inhibitor N-nitro-l-arginine methyl ester (L-NAME; 10 mg/kg), the selective inducible NOS inhibitor aminoguanidine hydrochloride (AG; 300 mg/kg), or selective neuronal NOS inhibitor 7-nitroindazole (7-NI; 50 mg/kg). In additional rabbits, the fluorescent probe 4,5-diaminofluroscein diacetate (DAF-2DA) and confocal laser microscopy were used to detect NO production in the absence or presence of helium with or without L-NAME pretreatment.

RESULTS: Helium reduced (P < 0.05) infarct size (24% ± 4% of the left ventricular area at risk; mean ± sd) compared with control (46% ± 3%). L-NAME, AG, and 7-NI did not alter myocardial infarct size when administered alone. L-NAME, but not 7-NI or AG, abolished helium-induced cardioprotection. Helium enhanced DAF-2DA fluorescence compared with control (26 ± 8 vs 15 ± 5 U, respectively). Pretreatment with L-NAME abolished these helium-induced increases in DAF-2DA fluorescence.

CONCLUSIONS: The results indicate that cardioprotection by helium is mediated by NO that is probably generated by endothelial NOS in vivo.

METHODS: Rabbits (n = 85) instrumented for hemodynamic measurement and subjected to a 30 min left anterior descending coronary artery (LAD) occlusion and 3 h reperfusion received 0.9% saline (control), or 1, 3, or 5 cycles of 70% helium-30% oxygen administered for 5 min interspersed with 5 min of an air-oxygen mixture (fraction of inspired oxygen concentration = 0.30) before LAD occlusion. Other rabbits received the GSK inhibitor SB 216763 (SB21; 0.2 or 0.6 mg/kg), the p53 inhibitor pifithrin- (PIF; 1.5 or 3.0 mg/kg), or SB21 (0.2 mg/kg) or PIF (1.5 mg/kg) plus helium (1 cycle) before LAD occlusion in the presence or absence of the mPTP opener atractyloside (5 mg/kg).

RESULTS: Helium reduced (P < 0.05) myocardial infarct size (35 ± 6 [n = 7], 25 ± 4 [n = 7], and 20 ± 3% [n = 6] of area at risk, 1, 3, and 5 cycles, respectively) compared with control (44 ± 6% [n = 7]). SB21 (0.6 [n = 7] but not 0.2 mg/kg [n = 6]) and PIF (3.0 [n = 6] but not 1.5 mg/kg [n = 7]) also reduced necrosis. SB21 (0.2 mg/kg) or 1.5 mg/kg PIF (1.5 mg/kg) plus helium (1 cycle; n = 6 per group) decreased infarct size to an equivalent degree as three cycles of helium alone, and this cardioprotection was blocked by atractyloside (n = 7 per group).

CONCLUSIONS: Inhibition of GSK or p53 lowers the threshold of helium-induced preconditioning via a mPTP-dependent mechanism in vivo.

METHODS: Male Fisher 344 rats were assigned from their respective age groups (young, 3–5 mo; old, 20–24 mo) to either receive 30 min of 1.0 minimum alveolar concentration isoflurane or to a control group. Rats were subjected to coronary artery occlusion for 30 min followed by 2 h of reperfusion. A fluorescent probe for superoxide anion production (dihydroethidium, 1 mg) was administered in the absence of the isoflurane or just before isoflurane exposure in four additional groups. Myocardial infarct size and superoxide anion production were assessed using triphenyltetrazolium staining and epifluorescence microscopy, respectively.

RESULTS: Isoflurane decreased myocardial infarct size of young rats (26.7% ± 3.0%) compared with young controls (50.9% ± 1.9%; P < 0.001), whereas isoflurane did not significantly affect myocardial infarct size of old rats (39.1% ± 0.9%) compared with old controls (46.5% ± 2.4%; P > 0.05). Isoflurane increased ROS levels in young rats (430.5 ± 95.9 arbitrary units [AU]) compared with young controls (162.7 ± 25.5 AU; P < 0.01). In contrast, no significant changes in ROS levels were observed in old animals (316.4 ± 56.3 AU isoflurane versus 233.8 ± 59.2 AU control).

CONCLUSIONS: Reduction in the cardioprotective effects of isoflurane and attenuation of isoflurane-stimulated ROS production were observed in the senescent myocardium in vivo.

METHODS: A prospective, double-blind, randomized study, evaluated 50 infants who underwent arterial switch operations for transposition of great arteries. Patients were randomized into a placebo group, 25 patients who received normal saline and a treatment group, 25 patients who received 20,000 KIU/kg of aprotinin after induction of anesthesia, followed by 20,000 KIU/kg of aprotinin added to pump prime. Postoperative blood loss through the thoracic chest tubes and blood product requirements (mL/kg/24 h) were measured for the first 24 h in the intensive care unit.

RESULTS: Postoperative blood loss in the first 24 h was significantly (P < 0.0001) higher in the placebo group (49.7 ± 11.9 mL/kg/24 h) as compared to the aprotinin group (37.1 ± 3.5 mL/kg/24 h). Requirements for fresh frozen plasma (mL/kg/24 h) and use of platelet concentrate transfusion (mL/kg/24 h) were significantly less in patients who received aprotinin (P < 0.0001), but did not reduce the proportion of patients transfused with blood products. The number of total donor exposures to all allogenic blood products was less in the aprotinin group [range (median) = 2–4 (3)] than the placebo group [range (median) = 7–14 (10)]. The re-exploration for excessive bleeding was significantly less with aprotinin group (16% vs 32%) (P = 0.01).

CONCLUSION: Our study concludes that aprotinin decreased the postoperative blood loss and requirement of transfusion of fresh frozen plasma and platelets (mL/kg/24 h) during the early postoperative period. Further, it reduced the number of donor exposures and re-exploration for excessive bleeding in the treatment population.

METHODS: Median nerve SEPs were recorded before premedication with midazolam 0.1 mg/kg IV, and at three separate times during anesthesia maintenance with sevoflurane 2% end-tidal concentration in air/oxygen (after 15 min of sevoflurane inhalation), supplemented with/without ketoprofen 1 mg/kg (after 25 min) and fentanyl 1 µg/kg (after 35 min).

RESULTS: Compared with baseline measurements, an increase both in N20 latency (P = 0.015) and in central conduction time (P = 0.001) was noted during anesthesia maintenance with sevoflurane. The administration of analgesics did not have an influence on the N20 latency or central conduction time. In children 5 to 8 yr of age, the mean cortical N20-P25 amplitude was decreased (P = 0.008). In addition, in older children, the N20-P25 amplitude decreased after the co-administration of ketoprofen and fentanyl compared with the values measured before the analgesics (P = 0.03). These decreases were not seen in the younger children.

DISCUSSION: In children, anesthesia maintenance with 2% sevoflurane prolongs median SEP latencies in a manner that is similar to those reported for other volatile anesthetics. However, SEP monitoring can be done with sevoflurane inhalation, but the dosage should be adjusted due to interindividual variabilty. Co-administration of ketoprofen, and fentanyl did not affect the SEP latencies, but post hoc analysis suggested that older children had a decrease in cortical amplitudes.

METHODS: Sixty healthy unpremedicated children, aged 3–10 yr, were recruited. Subjects were randomized to receive target-controlled infusions of propofol, to achieve 1 of 3 plasma concentrations: 3, 4.5, and 6 µg/mL. A preoperative 12 lead ECG was performed and repeated 5 min after induction. Two investigators, blinded to group allocation and to the timing of the ECG traces, independently measured QTc and Tp-e within and between each group. Paired t-tests were used to compare QTc and Tp-e within groups. One-way analysis of variance was used for intergroup analysis. The primary outcome measure was a change of >25 ms in Tp-e both within and between groups.

RESULTS: ECG recordings were obtained in 51 children. There were no demographic or ECG differences at baseline, at which time QTc and Tp-e values were within normal limits. There were no differences in QTc or Tp-e after induction within or between the three different groups.

DISCUSSION: Propofol has no effect on myocardial repolarization in healthy children at clinically relevant doses. This suggests that propofol would be a rational choice for children with a preexisting repolarization abnormality.

METHODS: Fifty-two children were randomized to receive acupressure bead intervention either at the Extra-1 acupuncture point or at a sham point. A Bispectral Index (BIS) monitor was applied to all children before the onset of the intervention. Anxiety was assessed at baseline and before entrance to the operating room. Anesthetic techniques were standardized and maintained with IV propofol infusion titrated to keep BIS values of 40–60.

RESULTS: We found that after the intervention, children in the Extra-1 group experienced reduced anxiety whereas children in the sham group experienced increased anxiety (–9% [–3 to –15] vs 2% [–6 to 7.4], P = 0.012). In contrast, no significant changes in BIS values were observed in the preprocedural waiting period between groups (P = ns). We also found that total intraprocedural propofol requirements did not differ between the two study groups (214 ± 76 µg · kg^–1 · min^–1 vs 229 ± 95 µg · kg^–1 · min^–1, P = 0.52).

CONCLUSIONS: We conclude that acupressure bead intervention at Extra-1 acupoint reduces preprocedural anxiety in children undergoing endoscopic procedures. This intervention, however, has no impact on BIS values or intraprocedural propofol requirements.

METHODS: Patients undergoing gynecologic laparoscopic surgery were randomized to receive 30% oxygen with air (G0, n = 46), 50% N₂O with oxygen (G50, n = 46), or 70% N₂O with oxygen (G70, n = 45). A standardized general anesthetic was used with no PONV prophylaxis. Known risk factors for PONV were controlled. Metoclopramide was used as a rescue antiemetic. The incidence of nausea, vomiting, use of rescue antiemetic, and pain visual analog scale (VAS) score was measured at 2 and 24 h postoperatively.

RESULTS: Patient demographics were comparable, and there were no differences among groups regarding factors that may influence PONV. The incidence of PONV at 24 h was 33% (15 of 46) in the G0 group, 46% (21 of 46) in the G50 group, and 62% (28 of 45) in the G70 group (P = 0.018). Subgroup analysis revealed a difference between G0 versus G70 groups (P = 0.018), but no significant difference between G0 versus G50 groups and G50 versus G70 groups. The incidence of nausea showed a similar difference (G0 = 26%, G50 = 35%, and G70 = 56%; P = 0.012), but the incidence of vomiting was not different among the groups although there was a trend (G0 = 28%, G50 = 35%, and G70 = 42%; P = 0.377). The severity of nausea (measured by VAS 100 mm) was significantly increased with increasing N₂O concentration (G0 = 10.9, G50 = 12.7, and G70 = 20.5; P = 0.027). The highest VAS score during 24 h was used for the analysis. There was no difference in the use of a rescue antiemetic among groups. Pain VAS scores and opioids consumption were not different among groups (at 2 and 24 h after surgery).

CONCLUSIONS: N₂O increases the incidence of postoperative nausea after gynecologic laparoscopic surgery. This preliminary finding indicates that N₂O may increase PONV in a dose-dependent fashion. A study with a sample size of >400 patients in each group would be necessary to demonstrate a statistically significant difference among each of these three groups. We do not recommend using a high concentration of N₂O in this clinical setting.

METHODS: Ninety patients presenting for transurethral resection of bladder tumor or prostate were assigned to one of three groups by double blind randomization to receive intrathecal 1.5 mL of hyperbaric 0.5% bupivacaine, plus 0.6 mL of one of three solutions: saline (Group I, n = 30, control), 1% lidocaine (Group II, n = 30), and 2% lidocaine (Group III, n = 30). Peak sensory block level, time to peak sensory block, times to two-segment, L1, and S2 regressions from peak sensory block, motor blocks at peak sensory block, L1, and S2 regressions, and postanesthesia care unit stay time (PACU time) were measured.

RESULTS: Times to peak sensory block were similar in all three groups. Times to two-segment, L1, and S2 regressions from peak sensory block, and PACU time were significantly reduced in Group II compared to Group I. Times to L1, S2 regressions, and PACU times in Group III were significantly prolonged.

CONCLUSIONS: We conclude that lidocaine (6 mg) mixed to spinal bupivacaine (7.5 mg) can shorten the duration of bupivacaine spinal anesthesia, therefore provide more rapid recovery from the spinal anesthesia compared to the same dose of bupivacaine (7.5 mg) alone.

In particular, it is hypothesized that 1) the beneficial trait that was selected for in one-celled organisms was the coordinated response of ion channels to compounds that were present in the environment, which influenced the conformational equilibrium of ion channels; 2) this coordinated response prevented the deleterious consequences of entry of positive charges into the cell, thereby increasing the fitness of the organism; and 3) these compounds (which may have included organic anions, cations, and zwitterions as well as uncharged compounds) mimicked inhaled anesthetics in that they were interfacially active, and modulated ion channel function by altering bilayer properties coupled to channel function.

The proposed hypothesis is consistent with known properties of inhaled anesthetics. In addition, it leads to testable experimental predictions of nonvolatile compounds having anesthetic-like modulatory effects on ion channels and in animals, including endogenous compounds that may modulate ion channel function in health and disease. The latter included metabolites that are increased in some types of end-stage organ failure, and genetic metabolic diseases. Several of these predictions have been tested and proved to be correct.

METHODS: The effect of seven surfactants with different head group charges (anionic, cationic, zwitterionic, and uncharged) and tail lengths (8 carbons and 12 carbons) on homomeric wild type 1 and mutant ₁ (S267I) glycine receptors, wild type ₁β_22s and mutant ₁(S270I)β_22s GABA_A receptors, and wild type NR1/NR2A and mutant NR1(F639A)/NR2A NMDA receptors was studied. Receptors were expressed in Xenopus laevis oocytes and studied using two-electrode voltage clamping.

RESULTS: All seven surfactants, isoflurane, and ethanol enhanced GABA_A receptor function. Six of seven surfactants, isoflurane, and ethanol enhanced glycine receptor function. Six of seven surfactants, isoflurane, and ethanol inhibited NMDA receptor function. For the mutant receptors, five of seven surfactants increased currents through GABA_A receptors, whereas six of seven surfactants increased currents through glycine receptors. Six of seven surfactants decreased currents through the NMDA receptor. In contrast to isoflurane and ethanol, surfactants as a group did not diminish modulation of mutant compared to wild type receptors.

CONCLUSION: These findings identify another large class of compounds (surfactants) that modulate the function of GABA_A, glycine, and NMDA receptors in a manner that is qualitatively similar to inhaled anesthetics. We cannot reject the hypothesis that interfacial activity is a sufficient condition for anesthetic-like modulation of these receptors. Mutations that diminish the modulatory effect of isoflurane and ethanol did not diminish the modulatory effect of the surfactants.

METHODS: We measured the change in isoflurane MAC caused by intrathecal infusion of various concentrations of veratridine into the lumbothoracic subarachnoid space of rats. We compared these result with those obtained from intracerebroventricular infusion.

RESULTS: As predicted, intrathecal infusion of veratridine increased MAC. The greatest infused concentration (25 µM) also produced neuronal injury in the hindlimbs of two rats and decreased the peak effect on MAC. A concentration of 1.6 µM produced the largest (21%) increase in MAC. Intraventricular infusion of 1.6 and 6.4 µM veratridine did not alter MAC. Rats given 25 µM died.

CONCLUSIONS: Intrathecal administration of veratradine increases MAC of isoflurane, a finding consistent with a role for sodium channels as potential mediators of the immobility produced by inhaled anesthetics.

METHODS: In rats prepared with chronic indwelling intrathecal catheters, we infused solutions deficient in K⁺ and with an excess of K⁺ into the lumbar space and measured MAC for isoflurane 24 h before, during, and 24 h after infusion. Rats similarly prepared were tested for the effect of altered osmolarity on MAC (accomplished by infusion of mannitol) and for the penetration of Na⁺ into the cord.

RESULTS: MAC of isoflurane never significantly increased with increasing concentrations of K⁺ infused intrathecally. At infused concentrations exceeding 12 times the normal concentration of KCl, i.e., 29 mEq/L, rats moved spontaneously at isoflurane concentrations just below, and sometimes at MAC, but the average MAC in these rats did not exceed their control MAC. At the largest infused concentration (58.1 mEq/L), MAC significantly decreased and did not subsequently return to normal (i.e., such large concentrations produced injury). Infusions of lower concentrations of K⁺ had no effect on MAC. Infusion of osmotically equivalent solutions of mannitol did not affect MAC. Na⁺ infused intrathecally measurably penetrated the spinal cord.

CONCLUSIONS: The results do not support a mediation or modulation of MAC by K⁺ channels.

METHODS: We conducted our study using a murine lumbar spinal cord slice model. We evoked norepinephrine release with nicotine in the presence and absence of isoflurane. To identify the type of nicotinic receptor involved, we studied the effect of receptor and subtype-specific ligands and genetically engineered mice, which lacked the gene expression for the nicotinic β2 subunit. The amount of [³H]-norepinephrine released was measured under the different conditions.

RESULTS: Nicotine-facilitated norepinephrine release was significantly and maximally inhibited by isoflurane at concentrations that enhance pain sensitivity in vivo (0.38%). Facilitation of norepinephrine release was mimicked by the 7 selective agonist choline and inhibited in the presence of -bungarotoxin, an 7-nicotinic selective antagonist. Facilitation of norepinephrine release was not different in animals lacking β2 subunits compared with matched controls.

CONCLUSIONS: Nicotinic facilitation of norepinephrine release in the spinal cord is inhibited by isoflurane at low clinically relevant concentrations. Because the net effect of noradrenergic tone in the spinal cord is inhibitory, the removal of this mechanism might be responsible for the enhanced pain sensitivity seen at these concentrations of isoflurane.

METHODS: A new miniaturized esophageal pulse oximeter has been developed. Five patients (one child and four neonates) were studied.

RESULTS: Spo₂ values were obtained in the esophagus of all patients. A Bland and Altman plot of the difference between Spo₂ values from the esophageal pulse oximeter and a commercial toe pulse oximeter against their mean showed that the bias and the limits of agreement between the two pulse oximeters were +0.3% and +1.7% to –1.0%, respectively.

CONCLUSIONS: This study suggests that the esophagus can be used as an alternative site for monitoring blood oxygen saturation in children and neonates.

METHODS: Two microdialysis probes with attached microtubing for trigger injection were inserted into the lateral vastus muscle of eight previously diagnosed MHS patients (representing three genetic variants Gly2434Arg, Thr2206Met, and Arg614Cys), seven MHN patients, and seven control individuals. After equilibration and lactate baseline recording, a single bolus of 200 µL caffeine 80 mM and a suspension of 200 µL halothane 4%V/V in soy bean oil (triggers) were injected locally. Lactate was measured spectrophotometrically. Data are presented as medians and interquartile ranges.

RESULTS: Although baseline lactate values were similar in the investigated groups before trigger injection, caffeine increased local lactate in MHS patients significantly more (2.0 [1.8–2.6] mM) than in MHN (0.8 [0.6–1.1] mM) or in control individuals (0.8 [0.6–0.8 mM]). Similarly, halothane lead to a significant lactate increase in MHS compared to MHN and control individuals (8.6 [3.7–8.9] mM vs 0.9 [0.5–1.1] mM and 1.7 [0.9–2.3] mM, respectively). However, a relevant increase of lactate was observed in one MHN and in two control individuals. Systemic hemodynamic and metabolic variables did not differ between the investigated groups.

DISCUSSION: Metabolic monitoring of IM lactate after local caffeine and halothane injection may allow less invasive testing to detect MH susceptibility, without systemic side effects.

METHODS: Patients classified as a grade 4 Cormack and Lehane on direct laryngoscopic view, and who required more than two attempts for successful endotracheal intubation, were referred to the study by consultant anesthesiologists at four hospitals. Apnea-hypopnea index (AHI) data and postoperative events were collected. Patients with AHI >5/h were considered positive for OSA. Clinical and PSG variables were compared using t-tests and ² test.

RESULTS: Over a 20-mo period, 84 patients with a difficult intubation were referred into the study. Thirty-three patients agreed to participate. Sixty-six percent (22 of 33) had OSA (AHI >5/h). Of the 22 OSA patients, 10 patients (64%) had mild OSA (AHI 5–15), 6 (18%) had moderate OSA (AHI >15/h), and 6 (18%) had severe OSA (AHI >30/h). Of the 33 patients, 11 patients (33%) were recommended for continuous positive airway pressure treatment. Between the OSA group and the non-OSA group, there were significant differences in gender, neck size, and the quality of sleep, but there were no significant differences in age and body mass index.

CONCLUSIONS: Sixty-six percent of patients with unexpected difficult intubation who consented to undergo a sleep study were diagnosed with OSA by PSG. Patients with difficult intubation are at high risk for OSA and should be screened for signs and symptoms of sleep apnea. Screening for OSA should be considered by referral to a sleep clinic for PSG.

METHODS: This was a prospective, multicenter, observational study in three Dutch intensive care units over a 5-mo period. MV data were collected during steady-state after arrival in the intensive care unit.

RESULTS: Data were collected for 346 consecutive patients after cardiothoracic surgery: 262 patients weaned with ASV, and 84 patients weaned with pressure-controlled/pressure-support MV. With ASV the mean (± sd) Vt expressed per kilogram actual body weight was 7.1 ± 1.6 mL. Expressed per kilogram ideal body weight (IBW), Vt was 8.3 ± 1.5 mL. In patients with a correctly set body weight (SBW) (i.e., the IBW), Vt was 8.1 ± 1.4 mL/kg. With pressure-controlled/pressure-support-MV Vt was 7.3 ± 1.4 mL/kg IBW (P < 0.001 vs ASV). Multivariate logistic regression analysis showed Vt with ASV to be dependent on only two parameters: respiratory rate and the correctness of SBW.

CONCLUSIONS: Vt with ASV seems to be dependent on two parameters: respiratory rate and the correctness of SBW. The first factor is not clinically important because respiratory rate is automatically chosen by the microprocessor. The second factor is clinically important because it is the only factor that can be influenced by the operator. Our data show the importance of setting the correct weight with ASV. With ASV, Vt are >8 mL/kg IBW in a substantial number of patients. Randomized clinical trials should be performed to compare ASV with other ventilation modes.

METHODS: Using a crossover design, postoperative cardiac surgery patients (n = 20) received three different suctioning methods in randomized order: closed suctioning during pressure-controlled ventilation, closed suctioning during volume-controlled ventilation, and open suctioning. FRC was measured before and 20 min after the intervention.

RESULTS AND CONCLUSIONS: FRC is reduced in postcardiac surgery patients after suctioning, regardless of which method is used. Certain patients may have very pronounced changes of FRC. Routine FRC measurements could complement respiratory monitoring to optimize respiratory therapy.

METHODS: Ninety-six parturients undergoing elective cesarean delivery were randomly assigned to receive intrathecal bupivacaine-sufentanil (BS group), bupivacaine-sufentanil-clonidine 75 µg (BSC group), or bupivacaine-clonidine 150 µg (BC group). The primary outcome was the extent and the incidence of periincisional punctate mechanical hyperalgesia as assessed by response to application of a von Frey filament at 24 and 48 h after cesarean delivery. Postoperative morphine requirements and pain scores, as well as residual pain at 1, 3, and 6 mo, were also assessed.

RESULTS: The BC group had a significantly reduced area of periincisional hyperalgesia at 48 h (median, 25th–75th percentiles): 1.0 (1.0 – 3.3) cm² vs 9.5 (5.0–14.0) cm² in the BS group vs 5.0 (2.5–12.3) cm² in the BSC group (P = 0.02 with the BS group). The incidence of hyperalgesia at 48 h was also lower in the BC group: 16% vs 41% in the BS group vs 34% in the BSC group (P = 0.03 with BS group). Postoperative morphine consumption, pain scores, and incidence and intensity of residual pain did not differ among groups.

CONCLUSIONS: Intrathecal clonidine 150 µg combined with bupivacaine had a postoperative antihyperalgesic effect expressed as a significant reduction in the extent and incidence of periincisional punctate mechanical hyperalgesia at 48 h after elective cesarean delivery compared with intrathecal bupivacaine-sufentanil and intrathecal clonidine 75 µg-bupivacaine-sufentanil.

METHODS: We compiled room location error rates from prior analyses of ORIMS data. Data from 24 consecutive 4-wk periods (45,459 cases) were analyzed from one hospital where both ORIMS and AIMS data were available. The actual location of cases was inferred from the physical location of the workstation recording the majority of pulse oximetry saturations. These were compared to the listed location in the AIMS and the final corrected location in the ORIMS. The scheduled and final ORIMS locations were compared to determine how often location changes were updated before the start of anesthesia. The location of cases was inferred in near real-time by using the identifier of the AIMS workstation transmitting pulse oximetry saturated electrocardiogram heart rate, and end-tidal CO₂ partial pressures.

RESULTS: Location error rates ranged from 0% to 7.5% at 42 hospitals. The error rate at the studied hospital was just 0.4%, showing that the hospital was suitable for investigation. The 0.4% error rate was based on cases listed as overlapping in the same OR, and thus under-estimated the actual error rate in the ORIMS (1.0%). With education, there was a decrease in the moved cases in the ORIMS whose location was not changed before the start of anesthesia (9.3%–2.0%, P < 10^–5). Despite the significant improvement (P < 10^–5) in the error rate between the AIMS listed and actual locations, the residual AIMS real-time error rate was 4.1% of cases. Use of vital sign data reduced errors to <0.1%.

CONCLUSIONS: Education can only modestly improve the accuracy of OR locations in ORIMS and AIMS data. The actual location can be inferred, either in near real-time or afterwards, from the AIMS workstation transmitting vital sign data. This addresses the fundamental problem of cases having more than one location during the course of anesthetic care (e.g., holding area, block room, OR, and postanesthesia care unit), which cannot be determined from scheduled ORIMS or listed AIMS locations.

METHODS: We studied the information-giving practices of anesthesiologists and nurse practitioners during preoperative teaching by examining transcripts from 26 tape recorded preoperative evaluation appointments. We developed a novel coding system to measure: 1) quantity of information, 2) frequency of medical terminology, 3) number of patient questions, and 4) number of memory reinforcements used during the consultation. Results are reported as mean ± sd.

RESULTS: Anesthesiologists and nurse practitioners vastly exceeded patients’ short-term memory capacity. Nurse practitioners gave significantly more information to patients than did physicians (112 ± 37 vs 49 ± 25 items per interview, P < 0.01). This higher level of information-giving was not influenced by the question-asking behaviors of the patients. Nurse practitioners and physicians used similar numbers of medical terms (4.0 ± 2.4 vs 3.7 ± 2.8 explained terms per interview), and memory-supporting reinforcements (2.3 ± 3.0 vs 1.4 ± 2.0 reinforcements per interview).

DISCUSSION: Given the known limits of short-term memory, clinicians would be well advised to carefully consider their patterns of information-giving and their use of memory-reinforcing strategies for critical information.

METHODS: Twenty patients undergoing elective surgery were studied. The airway was divided into three segments: upper incisor to vocal cords (UI-VC), vocal cords to sternal notch (VC-SN), and sternal notch to the carina (SN-CA). After general anesthesia and tracheal tube placement, the circuit was connected and the lungs ventilated. A bronchoscope was inserted through a ported elbow adapter until the tip just contacted carina. A marker tape was placed on the bronchoscope immediately above the adapter port. As the bronchoscope was withdrawn to the sternal notch (by transillumination), vocal cords and upper incisor (endoscopic visualization), three corresponding markers were placed along the bronchoscope. The three segments of the airway were obtained by measuring the distances between the four markers. Measurements were taken with the patient’s neck in f