bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Influence of the Obstetrician in the Relationship between Epidural Analgesia and Cesarean Section for Dystocia
Authors: Segal Scott , Blatman Robert , Doble Melissa , Datta Sanjay 
Published: November 2003

Background
The association between epidural analgesia for labor and the risk of cesarean section for dystocia remains controversial The authors hypothesized that if epidural analgesia were an important factor in determining cesarean section rates, then obstetricians with higher rates of utilization of epidural analgesia for labor would have higher rates of cesarean section for dystocia.

Methods
The frequency of use of epidural analgesia and frequency of occurrence of various patient risk factors for cesarean section were calculated for 110 obstetricians caring for > or = 50 low-risk parturients. These frequencies were compared by linear regression to obstetricians' rates of cesarean section for dystocia. Stepwise regression was used to attempt to predict obstetricians' cesarean rates from the incidence of various patient and provider risk factors.

Results
There was no relationship between frequency of epidural analgesia and rate of cesarean section for dystocia across practitioners (R2 = 0.019; P = 0.156). Weighting each obstetrician's data for the number of patients cared for during the study period did not change this result. Stepwise linear regression only modestly predicted obstetricians' cesarean section rates for dystocia, yielding a model containing 12 variables not including epidural analgesia (gestational age, induction of labor, maternal age, provider volume, nulliparity, and seven interactions; adjusted R2 = 0.312; P < 0.0001).

Conclusions
The frequency of use of epidural analgesia does not predict obstetricians' rates of cesarean section for dystocia. After accounting for a number of known patient risk factors, obstetrical practice style appears to be a major determinant of rates of cesarean section.
Optimal Propofol-Alfentanil Combinations for Supplementing Nitrous Oxide for Outpatient Surgery
Authors: Pavlin Janet D. , Arends Rosalin H. , Gunn Holly C. , Van Norman Gail , Koerschgen Meagan E. , Shen Danny D. 
Published: November 2003

Background
The combination of propofol and alfentanil with nitrous oxide provides balanced anesthesia with rapid recovery and minimal emetic side effects. The object of this study was to compare recovery parameters at varying proportions of propofol and alfentanil, and to determine the dosing rate and plasma concentration of propofol necessary to supplement nitrous oxide in the presence of varying concentrations of alfentanil

Methods
Forty-eight patients were anesthetized with nitrous oxide, targeted manual infusions of alfentanil (target plasma concentrations of 0, 50, 100, and 150 ng/ml), and propofol at rates that were varied up or down by 25% depending on the response (movement/no movement) of the preceding patient (at the same alfentanil target concentrations) to ulnar-nerve stimulation. The minimum concentrations of propofol and alfentanil required to prevent movement in 50% of patients (EC50) was determined by logistic regression. Speed of emergence and recovery of cognitive function, time to discharge, and incidence of side effects were compared for four different combinations of propofol and alfentanil with nitrous oxide.

Results
The EC50 for propofol alone with nitrous oxide was 6.1 microg/ml. AlfentaniL at concentrations of 41+/-17 (SD), 113+/-54, and 130+/-61 ng/mL reduced the EC50 of propofol to 3.3, 2.3, and 2.2 microg/ml, respectively, and decreased emergence time (eye opening) to 8.1, 4.9, and 3.4 min, compared with 24.3 min for propofol alone. Side effects did not differ between groups.

Conclusions
The authors conclude that there is a synergistic effect between propofol and alfentanil, and that combining alfentanil with propofol is associated with faster early recovery.
Oro- and Nasogastric Tube Passage in Intubated Patients
Authors: Ozer Steven , Benumof Jonathan L. 
Published: November 2003

Background
Insertion of a gastric tube (GT) in anesthetized, paralyzed, and intubated patients can be difficult The purpose of this study was to determine fiberoptically why GTs succeed or fail to enter the esophagus and, based on these findings, to determine a mechanism for converting failures into successes.

Methods
Sixty patients under general anesthesia and orotracheally intubated were studied. The larynx and hypopharynx of each patient were viewed via a fiberscope placed through the left naris. GTs were passed orally (OGT) and nasally (NGT) in all patients, and the pathway of passage or site of resistance was visualized. In cases of resistance, medially directed ipsilateral neck pressure was applied over the lateral thyrohyoid membrane (termed lateral neck pressure) to try to allow passage of the GT.

Results
All 60 patients had both an OGT and NGT passed for a total of 120 attempts. The GT passed easily on the first attempt in 92 of 120 insertions (77%) (for OGT 51/60 = 85% and for NGT 41/60 = 68%, P < 0.05). In 92% of these first-pass successes, the GT entered the hypopharynx just lateral to the arytenoid cartilages. The GT met resistance and failed to pass in 28 of 120 insertions (23%) (for OGT 9/60 = 15% and for NGT 19/60 = 32%). The sites of impaction were the piriform sinuses (13/28 = 46%), arytenoid cartilages (7/28 = 25%), and trachea (6/28 = 21%), and two OGTs did not pass the oropharynx (2/28 = 70%). Lateral neck pressure was attempted 20 times (for the piriform sinus and arytenoid cartilage impactions) with 17 successes (85%) and three failures (15%). The average distance to passage of the OGT and NGT by the arytenoid cartilage was 13.2 and 16.2 cm, respectively.

Conclusion
GTs enter the hypopharynx just lateral to the arytenoid cartilages. Consequently, the most common sites of resistance at the laryngeal level are the arytenoid cartilages and piriform sinuses. Lateral neck pressure compresses the piriform sinuses and moves the arytenoid cartilages medially, relieving 85% of these GT impactions.
Fentanyl Pharmacokinetics in Hemorrhagic Shock
Authors: Egan Talmage D. , Kuramkote Suma , Gong Guoqing , Zhang Jie , McJames Scott W. , Bailey Peter L. 
Published: November 2003

Background
It is common clinical practice to administer reduced doses of opioid to patients suffering from hemorrhagic shock to minimize adverse hemodynamic consequences and to prevent prolonged opioid effect However, the scientific foundation supporting this practice is not well established. The aim of this study was to test the hypothesis that hemorrhagic shock alters both the distribution and clearance of opioids using fentanyl in a porcine isobaric hemorrhage model.

Methods
Eighteen pigs were randomized to shock or control groups. The animals in the shock group were subjected to hemorrhage using an isobaric method. Pigs in both groups received fentanyl (50 microg/kg) intravenously over 5 min. Frequent arterial blood samples were obtained for radioimmunoassay. Each animal's pharmacokinetic parameters were estimated by fitting a three-compartment model to the concentration versus time data Nonlinear mixed-effects population pharmacokinetic models examining the influence of mean arterial pressure and cardiac index were also constructed. Clinical simulations using the final population model were performed.

Results
The shock cohort reached substantially higher fentanyl concentrations. The shock group's central clearance and central- and second-compartment distribution volumes were significantly reduced. The most useful population model scaled all pharmacokinetic parameters to mean arterial pressure. The simulations illustrated that hemorrhagic shock results in higher fentanyl concentrations for any given dosage scheme.

Conclusion
The essential finding of the study is that fentanyl pharmacokinetics are substantially altered by hemorrhagic shock. The reduced opioid requirement commonly observed during hemorrhagic shock is at least partially attributable to pharmacokinetic mechanisms.
Effect of Isoflurane on In Situ Vascular Smooth Muscle Transmembrane Potential in Spontaneous Hypertension
Authors: Stekiel Thomas A. , Kokita Naohiro , Yamazaki Mitsuaki , Bosnjak Zeljko J. , Kampine John P. , Stekiel William J. 
Published: November 2003

Background
Administration of general anesthetics to patients with chronic hypertension often causes hemodynamic instability that has been attributed in part to a poorly understood increased loss of control of peripheral vascular smooth muscle tone. The purpose of the current study was to determine if such an increased loss occurs in the spontaneously hypertensive (SH) rat neurogenic model of chronic hypertension, as reflected by a greater volatile anesthetic-induced in situ vascular smooth muscle hyperpolarization compared with normotensive Wistar-Kyoto (WKY) rat controls.

Methods
Vascular smooth muscle transmembrane potentials (E(m)s) were measured in situ using glass microelectrodes in externalized small mesenteric resistance- and capacitance-regulating blood vessels in 10- to 12-week-old SH and WKY rats before, during and after administration of 1 minimum alveolar concentration levels (1.5%) of inhaled or 0.60 mM superfused isoflurane. Vascular smooth muscle E(m)s were also measured in vessels after local sympathetic denervation with superfused 6-hydroxydopamine.

Results
Local sympathetic denervation caused a significant hyperpolarization of arterial and venous vascular smooth muscle in SH but not WKY rats. Hyperpolarization induced by either inhaled or superfused isoflurane was significantly greater in innervated than in denervated arterial and venous vascular smooth muscle, particularly in SH rats. In addition, for innervated (but not denervated) arterial and venous vascular smooth muscle, hyperpolarization induced by inhaled (but not superfused) isoflurane was significantly greater in SH than in WKY rats.

Conclusions
In the neurogenic SH rat model of human hypertension, a primary mechanism underlying elevated isoflurane-induced vascular smooth muscle hyperpolarization (and reduced vascular smooth muscle tone) in both resistance- and capacitance-regulating blood vessels is a central neural inhibition of excitatory sympathetic input. Peripheral neural and nonneurally mediated hyperpolarization by isoflurane is similar in SH and WKY rat vascular smooth muscles.
Confirmation of Caudal Needle Placement Using Nerve Stimulation
Authors: Tsui Ban C. H. , Tarkkila Pekka , Gupta Sunil , Kearney Ramona 
Published: November 2003

Background
The study was designed to examine a new method of confirming proper caudal needle placement using nerve stimulation.

Methods
Thirty-two pediatric patients were studied. A 22-gauge insulated needle was inserted into the caudal canal via the sacral notch until a "pop" was felt. The needle placement was classified as correct or incorrect depending upon the presence or absence of anal sphincter contraction (S2-S4) to electrical simulation (1 to 10 mA).

Results
Three patients were excluded, two because they inadvertently received neuromuscular blockers and one because the patient's anatomy precluded any attempt at a caudal block. The sensitivity and specificity of the test were both 100% in predicting clinical outcomes of the caudal block. Six patients had a negative stimulation test after the first attempt to place the needle. Four of these went on to receive a second attempt of needle insertion after a subcutaneous bulge or resistance to local anesthetic injection were observed. Following needle reinsertion, positive stimulation tests were elicited. These patients received the local anesthetic injection with ease and had good analgesia postoperatively. No attempt was made to reinsert the needle in the remaining two patients with a negative stimulation test, as they did not show subcutaneous bulge or resistance upon injection. These patients had poor analgesia postoperatively. The positive predictive value of the test was greater than the presence of a "pop" alone (P < 0.05) but not significantly different (P = 0.492) over the presence of "pop" and easy injection.

Conclusion
This test may be used as a teaching and adjuvant tool in performing caudal block.
Length-dependent Regulation of Left Ventricular Function in Coronary Surgery Patients
Authors: De Hert Stefan G. , Gillebert Thierry C. , Ten Broecke Pieter W. , Moulijn Adriaan C. 
Published: November 2003

Background
Load-dependent impairment of left ventricular (LV) function was observed after leg elevation in a subgroup of coronary surgery patients. The present study investigated underlying mechanisms by comparing hemodynamic effects of an increase in LV systolic pressures with leg elevation to effects of a similar increase in systolic pressures with phenylephrine.

Methods
The study was performed in patients undergoing elective coronary surgery prior to cardiopulmonary bypass. High-fidelity LV pressure tracings (n = 25) and conductance LV volume data (n = 10) were obtained consecutively during leg elevation and after phenylephrine administration (5 microg/kg).

Results
Leg elevation resulted in a homogeneous increase in end-diastolic volume. The change in stroke volume (SV), stroke work (SW) and dP/dtmax was variable, with an increase in some patients but no change or a decrease in other patients. For a matched increase in systolic pressures, phenylephrine increased SW and dP/dtmax in all patients with no change in SV. Load dependence of relaxation (slope R of the tau-end-systolic pressure relation) was inversely related for changes in SV, SW, and dP/dtmax with leg elevation but not with phenylephrine.

Conclusions
The different effects of leg elevation and phenylephrine suggest that the observed decrease in SV, SW, and dP/dtmax with leg elevation in some patients could not be attributed to an impaired contractile response to increased systolic LV pressures. Instead, load-dependent impairment of LV function after leg elevation appeared related to a deficient length-dependent regulation of myocardial function.
Comparative Pharmacodynamic Modeling of the Electroencephalography-slowing Effect of Isoflurane, Sevoflurane, and Desflurane
Authors: Rehberg Benno , Bouillon Thomas , Zinserling Jorg , Hoeft Andreas 
Published: November 2003

Background
The most common measure to compare potencies of volatile anesthetics is minimum alveolar concentration (MAC), although this value describes only a single point on a quantal concentration-response curve and most likely reflects more the effects on the spinal cord rather than on the brain. To obtain more complete concentration-response curves for the cerebral effects of isoflurane, sevoflurane, and desflurane, the authors used the spectral edge frequency at the 95th percentile of the power spectrum (SEF95) as a measure of cerebral effect.

Methods
Thirty-nine patients were randomized to isoflurane, sevoflurane, or desflurane groups. After induction with propofol, intubation, and a waiting period, end-tidal anesthetic concentrations were randomly varied between 0.6 and 1.3 MAC, and the EEG was recorded continuously. Population pharmacodynamic modeling was performed using the software package NONMEM.

Results
The population mean EC50 values of the final model for SEF95 suppression were 0.66+/-0.08 (+/- SE of estimate) vol% for isoflurane, 1.18+/-0.10 vol% for sevoflurane, and 3.48+/-0.66 vol% for desflurane. The slopes of the concentration-response curves were not significantly different; the common value was lambda = 0.86+/-0.06. The Ke0 value was significantly higher for desflurane (0.61+/-0.11 min(-1)), whereas separate values for isoflurane and sevoflurane yielded no better fit than the common value of 0.29+/-0.04 min(-1). When concentration data were converted into fractions of the respective MAC values, no significant difference of the C50 values for the three anesthetic agents was found.

Conclusions
This study demonstrated that (1) the concentration-response curves for spectral edge frequency slowing have the same slope, and (2) the ratio C50(SEF95)/MAC is the same for all three anesthetic agents. The authors conclude that MAC and MAC multiples, for the three volatile anesthetics studied, are valid representations of the concentration-response curve for anesthetic suppression of SEF95.
The Role of Tumor Necrosis Factor-α in the Pathogenesis of Aspiration Pneumonitis in Rats
Authors: Davidson Bruce A. , Knight Paul R. , Helinski Jadwiga D. , Nader Nader D. , Shanley Thomas P. , Johnson Kent J. 
Published: November 2003

Background
Aspiration pneumonitis is characterized by proteinaceous pulmonary edema and acute infiltration of neutrophils into the alveolar space. This study examined the role of the proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), on the pathogenesis of the injury produced by the different components that may be present in the aspirate, acid, or gastric particles.

Methods
Rats were injured by intratracheal instillation of a vehicle containing acid or gastric particles. TNF-alpha concentration of bronchoalveolar lavage fluid was determined using a bioassay. upregulation of lung TNF-alpha mRNA was also measured. The effect of intratracheal anti-rat TNF-alpha treatment was assessed by lung protein permeability, blood gases, and lung myeloperoxidase activity.

Results
Injury vehicle alone and acid injury resulted in a small TNF-alpha peak 1-2 h after injury in the lavage fluid. Both particulate and acidic particulate groups produced a much more robust TNF-alpha signal that reached a plateau at 2-4 h after injury and declined at 8 h. Upregulation of TNF-alpha mRNA was only detected in the particulate-containing groups. Acidic particulate exposure yielded a synergistic increase in protein permeability and decrease in blood oxygenation. Anti-TNF-alpha treatment reduced protein permeability and myeloperoxidase activity and increased blood oxygenation in the groups exposed to only acid. Such treatment had no effect on either of the particulate containing injuries.

Conclusions
TNF-alpha is differentially manifested according to the components that make up the aspirate but the levels of TNF-alpha expression do not correlate with the severity of the resultant injury. However, the reduction in acid-induced lung injury by anti-TNF-alpha treatment indicates that TNF-alpha plays a role in the pathogenesis of aspiration pneumonitis.
Thermoregulatory Thresholds for Vasoconstriction in Patients Anesthetized with Various 1-Minimum Alveolar Concentration Combinations of Xenon, Nitrous Oxide, and Isoflurane
Authors: Goto Takahisa , Matsukawa Takashi , Sessler Daniel I. , Uezono Shoichi , Ishiguro Yoshiki , Ozaki Makoto , Morita Shigeho 
Published: November 2003

Background
Nitrous oxide limits intraoperative hypothermia because the vasoconstriction threshold with nitrous oxide is higher than with equi-minimum alveolar concentrations of sevoflurane or isoflurane, presumably because of its stimulating actions on the sympathetic nervous system. Xenon, in contrast, does not cause sympathetic activation. Therefore, the authors tested the hypothesis that the vasoconstriction threshold during xenon-isoflurane anesthesia is less than during nitrous oxide-isoflurane anesthesia or isoflurane alone.

Methods
Fifteen patients each were randomly assigned to one of three 1-minimum alveolar concentration anesthetic regimens: (1) xenon, 43% (0.6 minimum alveolar concentration) and isoflurane, 0.5% (0.4 minimum alveolar concentration); (2) nitrous oxide, 63% (0.6 minimum alveolar concentration) and isoflurane 0.5%; or (3) isoflurane, 1.2%. Ambient temperature was maintained near 23 degrees C and the patients were not actively warmed. Thermoregulatory vasoconstriction was evaluated using forearm-minus-fingertip skin temperature gradients. A gradient exceeding 0 degrees C indicated significant vasoconstriction. The core-temperature threshold that would have been observed if skin had been maintained at 33 degrees C was calculated from mean skin and distal esophageal temperatures at the time of vasoconstriction.

Results
The patients' demographic variables, preinduction core temperatures, ambient operating room temperatures, and fluid balance were comparable among the three groups. Heart rates were significantly less during xenon anesthesia than with nitrous oxide. The calculated vasoconstriction threshold was lowest with xenon (34.6+/-0.8 degrees C, mean +/- SD), intermediate with isoflurane alone (35.1+/-0.6 degrees C), and highest with nitrous oxide (35.7+/-0.6 degrees C). Each of the thresholds differed significantly.

Conclusions
Xenon inhibits thermoregulatory control more than isoflurane, whereas nitrous oxide is the least effective in this respect.
Additive Contribution of Nitrous Oxide to Sevoflurane Minimum Alveolar Concentration for Tracheal Intubation in Children
Authors: Swan Hilton D. , Crawford Mark W. , Pua Hwee Ling , Stephens Derek , Lerman Jerrold 
Published: November 2003

Background
To study the interaction between nitrous oxide and sevoflurane during trachea intubation, the authors determined the minimum alveolar concentration of sevoflurane for tracheal intubation (MAC(TI)) with and without nitrous oxide in children.

Methods
Seventy-two children aged 1-7 yr were assigned randomly to receive one of three end-tidal concentrations of nitrous oxide and one of four end-tidal concentrations of sevoflurane: 0% nitrous oxide with 2.0, 2.5, 3.0, or 3.5% sevoflurane: 33% nitrous oxide with 1.5, 2.0, 2.5, or 3.0% sevoflurane; or 66% nitrous oxide with 1.0, 1.5, 2.0, or 2.5% sevoflurane. After steady state end-tidal anesthetic concentrations were maintained for at least 10 min, laryngoscopy and intubation were attempted using a straight-blade laryngoscope and an uncuffed tracheal tube. The interaction between nitrous oxide and sevoflurane was investigated using logistic regression analysis of the responses to intubation.

Results
Logistic regression curves of the probability of no movement in response to intubation in the presence of sevoflurane and 0, 33, and 66% nitrous oxide were parallel. The interaction coefficient between nitrous oxide and sevoflurane did not differ significantly from zero (P = 0.89) and was removed from the logistic model. The MAC(TI) (+/- SE) of sevoflurane was 2.66+/-0.16%, and the concentration of sevoflurane required to prevent movement in 95% of children was 3.54+/-0.25%. Thirty-three percent and 66% nitrous oxide decreased the MAC(TI) of sevoflurane by 18% and 40% (P<0.001), respectively.

Conclusions
We conclude that nitrous oxide and sevoflurane suppress the responses to tracheal intubation in a linear and additive fashion in children.