bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Cardiac Anesthesia Risk Evaluation Score
Authors: Dupuis Jean-Yves , Wang Feng , Nathan Howard , Lam Miu , Grimes Scott , Bourke Michael 
Published: November 2003

Background
The Cardiac Anesthesia Risk Evaluation (CARE) score is a simple risk classification for cardiac surgical patients. It is based on clinical judgment and three clinical variables: comorbid conditions categorized as controlled or uncontrolled, surgical complexity, and urgency of the procedure. This study compared the CARE score with the Parsonnet, Tuman, and Tu multifactorial risk indexes for prediction of mortality and morbidity after cardiac surgery.

Methods
In this prospective study, 3,548 cardiac surgical patients from one institution were risk stratified by two investigators using the CARE score and the three tested multifactorial risk indexes. All patients were also given a CARE score by their attending cardiac anesthesiologist. The first 2,000 patients served as a reference group to determine discrimination of each classification with receiver operating characteristic curves. The following 1,548 patients were used to evaluate calibration using the Pearson chi-square goodness-of-fit test.

Results
The areas under the receiver operating characteristic curves for mortality and morbidity were 0.801 and 0.721, respectively, with the CARE score rating by the investigators; 0.786 and 0.710, respectively, with the CARE score rating by the attending anesthesiologists (n = 8); 0.808 and 0.726, respectively, with the Parsonnet index; 0.782 and 0.697, respectively, with the Tuman index; 0.770 and 0.724 with the Tu index, respectively. All risk models had acceptable calibration in predicting mortality and morbidity, except for the Parsonnet classification, which failed calibration for morbidity (P = 0.026).

Conclusions
The CARE score performs as well as multifactorial risk indexes for outcome prediction in cardiac surgery. Cardiac anesthesiologists can integrate this score in their practice and predict patient outcome with acceptable accuracy.
Cardiovascular Effects of Sevoflurane, Isoflurane, Halothane, and Fentanyl–Midazolam in Children with Congenital Heart Disease
Authors: Rivenes Shannon M. , Lewin Mark B. , Stayer Stephen A. , Bent Sabrina T. , Schoenig Heather M. , McKenzie E. Dean , Fraser Charles D. , Andropoulos Dean B. 
Published: November 2003

Background
The cardiovascular effects of halogenated anesthetic agents in children with normal hearts have been studied, but data in children with cardiac disease are limited. This study compared the effects of halothane, isoflurane, sevoflurane, and fentanyl-midazolam on systemic and pulmonary hemodynamics and myocardial contractility in patients with congenital heart disease.

Methods
Fifty-four patients younger than age 14 scheduled to undergo congenital heart surgery were randomized to receive halothane, sevoflurane, isoflurane, or fentanyl-midazolam. Cardiovascular and echocardiographic data were recorded at baseline and at randomly ordered 1 and 1.5 minimum alveolar concentrations, or predicted equivalent fentanyl-midazolam plasma concentrations. The shortening fraction and ejection fraction (using the modified Simpson rule) were calculated. Cardiac index was assessed by the velocity-time integral method.

Results
Halothane caused a significant decrease in mean arterial pressure, ejection fraction, and cardiac index, preserving only heart rate at baseline levels. Fentanyl-midazolam in combination caused a significant decrease in cardiac index secondary to a decrease in heart rate; contractility was maintained. Sevoflurane maintained cardiac index and heart rate and had less profound hypotensive and negative inotropic effects than halothane. Isoflurane preserved both cardiac index and ejection fraction, had less suppression of mean arterial pressure than halothane, and increased heart rate.

Conclusions
Isoflurane and sevoflurane preserved cardiac index, and isoflurane and fentanyl-midazolam preserved myocardial contractility at baseline levels in this group of patients with congenital heart disease. Halothane depressed cardiac index and myocardial contractility.
Anticoagulation during Cardiopulmonary Bypass in Patients with Heparin-induced Thrombocytopenia Type II and Renal Impairment Using Heparin and the Platelet Glycoprotein IIb–IIIa Antagonist Tirofiban
Authors: Koster Andreas , Kukucka Marian , Bach Friedhelm , Meyer Oliver , Fischer Thomas , Mertzlufft Fritz , Loebe Matthias , Hetzer Roland , Kuppe Hermann 
Published: November 2003

Background
Patients with heparin-induced thrombocytopenia type II require an alternative to standard heparin anticoagulation. However, in patients with renal impairment, anticoagulation during cardiopulmonary bypass with agents such as danaparoid sodium or r-hirudin are associated with hemorrhage. Anticoagulation with unfractionated heparins combined with prostacyclin, a potent platelet aggregation inhibitor, is associated with severe hypotension. The authors investigated a new concept using unfractionated heparins after platelet inhibition with the short-acting platelet glycoprotein IIb-IIIa antagonist tirofiban.

Methods
Ten patients with heparin-induced thrombocytopenia type II and renal impairment were enrolled in the investigation. All had heparin-induced thrombocytopenia type II antibodies present as proved by the heparin-induced platelet aggregation assay, the heparin-platelet factor 4 enzyme-linked immunosorbent assay, or both. In all patients, preoperative anticoagulation to an activated partial thromboplastin time of 40-60 s was performed with r-hirudin. Anticoagulation during cardiopulmonary bypass was achieved with a bolus of 400 IU/kg unfractionated heparins after a bolus of tirofiban 10 microg/kg followed by an infusion of tirofiban at a rate of 0.15 microg x kg(-1) x min(-1) until 1 h before conclusion of cardiopulmonary bypass. Additional unfractionated heparins were only administered if activated clotting time decreased below 480 s. Coagulation was monitored by a abciximab-modified TEG and the adenosine diphosphate-stimulated (20 microm) platelet aggregometry. D-dimer concentrations, as a marker of venous thromboembolism, were measured before and 12, 24, and 48 h after surgery. Postoperative antithrombotic therapy was started immediately with r-hirudin to anticoagulation to an activated partial thromboplastin time of 40-60 s.

Results
The postoperative blood loss ranged from 110 to 520 ml. No patient needed reexploration. In no patient was there clinical evidence of thrombosis or embolism in the postoperative period or of a critical increase of the D-dimer concentrations, suggesting venous thromboembolism. Transfusion of platelets was necessary in only two patients.

Conclusions
The protocol is easy to perform and no increased postoperative bleeding and no thromboembolic complications occurred. The combination of unfractionated heparins and tirofiban may be an alternative to other anticoagulation strategies in patients with heparin-induced thrombocytopenia.
Epidural Anesthesia Retards Intestinal Acidosis and Reduces Portal Vein Endotoxin Concentrations during Progressive Hypoxia in Rabbits
Authors: Ai Kimiaki , Kotake Yoshifumi , Satoh Tomoyuki , Serita Ryohei , Takeda Junzo , Morisaki Hiroshi 
Published: November 2003

Background
Because it is postulated that gut is important via bacterial translocation in the development of the systemic inflammatory response and multiple organ dysfunction, the preservation of gut integrity is a therapeutic goal for physicians who care for critically ill patients. The aim of the current study was to evaluate whether epidural anesthesia prevented gut injury and subsequent translocation of endotoxin during acute progressive hypoxia in rabbits.

Methods
After the placement of an epidural catheter, 18 male rabbits, anesthetized with buprenorphine-midazolam, were allocated randomly to two groups: 0.5% lidocaine (group E) and saline (group C) groups. The solutions (0.4 ml/kg) were injected epidurally, followed by continuous infusion (0.1 ml x kg(-1) x h(-1)) during the study period. Portal blood flow, portal endotoxin concentrations, and intramucosal pH (pHi) of the ileum were measured at baseline and during two stages of progressive hypoxia (fraction of inspired oxygen [Fio2] = 0.15 and 0.10).

Results
In both study groups, the portal blood flow was preserved to a similar extent during acute hypoxia. However, pHi was reduced to a lesser extent in group E (7.33 +/- 0.12 versus 7.22 +/- 0.12 at an Fio2 of 0.15 and 7.13 +/- 0.15 versus 7.03 +/- 0.12 at an Fio2 of 0.10; mean +/- SD, P < 0.01), concurrently with lower portal endotoxin concentrations (P < 0.05) compared with group C.

Conclusions
The current study showed that epidural anesthesia slowed the progression of intestinal ischemia during acute hypoxia, subsequently preventing translocation of endotoxin through the gut mucosa.
Suppression of Potassium Conductance by Droperidol Has Influence on Excitability of Spinal Sensory Neurons
Authors: Olschewski Andrea , Hempelmann Gunter , Vogel Werner , Safronov Boris V. 
Published: November 2003

Background
During spinal and epidural anesthesia with opioids, droperidol is added to prevent nausea and vomiting. The mechanisms of its action on spinal sensory neurons are not well understood. It was previously shown that droperidol selectively blocks a fast component of the Na+ current. The authors studied the action of droperidol on voltage-gated K+ channels and its effect on membrane excitability in spinal dorsal horn neurons of the rat.

Methods
Using a combination of the patch-clamp technique and the "entire soma isolation" method, the action of droperidol on fast-inactivating A-type and delayed-rectifier K+ channels was investigated. Current-clamp recordings from intact sensory neurons in spinal cord slices were performed to study the functional meaning of K+ channel block for neuronal excitability.

Results
Droperidol blocked delayed-rectifier K+ currents in isolated somata of dorsal horn neurons with a half-maximum inhibiting concentration of 20.6 microm. The A-type K+ current was insensitive to up to 100 microm droperidol. At droperidol concentrations insufficient for suppression of an action potential, the block of delayed-rectifier K+ channels led to an increase in action potential duration and, as a consequence, to lowering of the discharge frequency in the neuron.

Conclusions
Droperidol blocks delayed-rectifier K+ channels in a concentration range close to that for suppression of Na+ channels. The block of delayed-rectifier K+ channels by droperidol enhances the suppression of activity in spinal sensory neurons at drug concentrations insufficient for complete conduction block.
Effects of Xenon on Cerebral Blood Flow and Cerebral Glucose Utilization in Rats
Authors: Frietsch Thomas , Bogdanski Ralph , Blobner Manfred , Werner Christian , Kuschinsky Wolfgang , Waschke Klaus F. 
Published: November 2003

Background
The effects of xenon inhalation on mean and local cerebral blood flow (CBF) and mean and local cerebral glucose utilization (CGU) were investigated using iodo-[14C]antipyrine and [14C]deoxyglucose autoradiography.

Methods
Rats were randomly assigned to the following groups: conscious controls (n = 12); 30% (n = 12) or 70% xenon (n = 12) for 45 min for the measurement of local CBF and CGU; or 70% xenon for 2 min (n = 6) or 5 min (n = 6) for the measurement of local CBF only.

Results
Compared with conscious controls, steady state inhalation of 30 or 70% xenon did not result in changes of either local or mean CBF. However, mean CBF increased by 48 and 37% after 2 and 5 min of 70% xenon short inhalation, which was entirely caused by an increased local CBF in cortical brain regions. Mean CGU determined during steady state 30 or 70% xenon inhalation remained unchanged, although local CGU decreased in 7 (30% xenon) and 18 (70% xenon) of the 40 examined brain regions. The correlation between CBF and CGU in 40 local brain structures was maintained during steady state inhalation of both 30 and 70% xenon inhalation, although at an increased slope at 70% xenon.

Conclusion
Effects of 70% xenon inhalation on CBF in rats are time-dependent. During steady state xenon inhalation (45 min), mean values of CBF and CGU do not differ from control values, and the relation of regional CBF to CGU is maintained, although reset at a higher level.
Absence of Direct Antioxidant Effects from Volatile Anesthetics in Primary Mixed Neuronal–Glial Cultures
Authors: Kudo Masaya , Aono Mitsuo , Lee Yoonki , Massey Gary , Pearlstein Robert D. , Warner David S. 
Published: November 2003

Background
Volatile anesthetics decrease ischemic brain injury. Mechanisms for this protection remain under investigation. The authors hypothesized that volatile anesthetics serve as antioxidants in a neuronal-glial cell culture system.

Methods
Primary cortical neuronal-glial cultures were prepared from fetal rat brain. Cultures were exposed to iron, H2O2, or xanthine-xanthine oxidase for 30 min in serum-free media containing dissolved isoflurane (0-3.2 mm), sevoflurane (0-3.6 mm), halothane (0-4.1 mm), n-hexanol, or known antioxidants. Cell damage was assessed by release of lactate dehydrogenase (LDH) and trypan blue exclusion 24 h later. Lipid peroxidation was measured by the production of thiobarbituric acid-reactive substances in a cell-free lipid system. Iron and calcium uptake and mitochondrial depolarization were measured after exposure to iron in the presence or absence of isoflurane.

Results
Deferoxamine reduced LDH release caused by H2O2 or xanthine-xanthine oxidase, but the volatile anesthetics had no effect. Iron-induced LDH release was prevented by the volatile anesthetics (maximum effect for halothane = 1.2 mm, isoflurane = 1.2 mm, and sevoflurane = 2.1 mm aqueous phase). When corrected for lipid solubility, the three volatile anesthetics were equipotent against iron-induced LDH release. In the cell-free system, there was no effect of the anesthetics on thiobarbituric acid-reactive substance formation in contrast to Trolox, which provided complete inhibition. Isoflurane (1.2 mm) reduced mean iron uptake by 46% and inhibited mitochondrial depolarization but had no effect on calcium uptake.

Conclusions
Volatile anesthetics reduced cell death induced by oxidative stress only in the context of iron challenge. The likely reason for protection against iron toxicity is inhibition of iron uptake and therefore indirect reduction of subsequent intracellular oxidative stress caused by this challenge. These data argue against a primary antioxidant effect of volatile anesthetics.
Influence of Hemorrhagic Shock on Remifentanil
Authors: Johnson Ken B. , Kern Steven E. , Hamber Elizabeth A. , McJames Scott W. , Kohnstamm Katelijne M. , Egan Talmage D. 
Published: November 2003

Background
Hemorrhagic shock is known to alter significantly the pharmacokinetics of fentanyl, an opioid that requires delivery to the liver for metabolism. The authors hypothesized that the pharmacokinetics and pharmacodynamics of remifentanil, an esterase metabolized opioid that does not require delivery to a metabolic organ, would be altered less by hemorrhagic shock that those of fentanyl.

Methods
Sixteen pigs were assigned randomly to control and shock groups. The shock group was bled using an isobaric hemorrhage model. Remifentanil 10 microg x kg(-1) x min(-1) was infused for 10 min to both groups. Arterial samples were collected for remifentanil concentration assay. Pharmacokinetic parameters were estimated using a three-compartment model. The electroencephalogram spectral edge was used as a measure of drug effect. The pharmacodynamics were characterized using a sigmoid inhibitory maximal effect model.

Results
Remifentanil blood levels were higher in the shocked group. The central clearance was slower and the central compartment was smaller in shocked animals. No difference between groups was observed in the magnitude or time course of the remifentanil-induced decrease in spectral edge.

Conclusions
Hemorrhagic shock altered the pharmacokinetics of remifentanil, suggesting that less remifentanil would be required to maintain a target plasma concentration. However, because of its rapid metabolism, the impact of hemorrhagic shock on the concentration decline of remifentanil after termination of the infusion was minimal. Hemorrhagic shock did not alter the pharmacodynamics of remifentanil.
The Effect of Hypothermia on Isoflurane MAC in Children
Authors: Liu Mingzheng , Hu Xiaoqin , Liu Jin 
Published: November 2003

Background
Hypothermia has been shown to decrease the requirement for inhaled anesthetics in animals, but information in humans is limited.

Methods
Thirty-three unpremedicated children with congenital left-to-right shunt heart diseases undergoing open heart surgeries were assigned to one of three groups, with nasopharyngeal temperatures at the time of skin incision of 37, 34, or 31 degrees C. Anesthesia was induced and maintained with isoflurane in oxygen. End-tidal isoflurane concentration and nasopharyngeal temperature were kept at stable levels for at least 15 min before the skin incision. Isoflurane minimum alveolar concentration was determined by using the Dixon up-and-down approach.

Results
Isoflurane minimum alveolar concentration values were 1.69 +/- 0.14%, 1.47 +/- 0.10%, and 1.22 +/- 0.15% (mean +/- SD) at 37, 34, and 31 degrees C, respectively.

Conclusions
Hypothermia decreases the isoflurane requirement in children by 5.1 degrees C.
Reduced Need for Vasopressors in Patients Receiving Aprotinin during Orthotopic Liver Transplantation
Authors: Quintus Molenaar I. , Begliomini Bruno , Martinelli Gerardo , Putter Hein , Terpstra Onno T. , Porte Robert J. 
Published: November 2003

Background
Graft reperfusion in orthotopic liver transplantation is often associated with significant hemodynamic changes, including decreased systemic vascular resistance and arterial blood pressure. Vasopressive drugs are often required to maintain adequate perfusion pressure during the early postreperfusion period. The exact mechanism of this postreperfusion syndrome is unknown, but release of bradykinin, a potent vasodilatator, via the kallikrein system may play a role. Aprotinin is a broad-spectrum inhibitor of serine proteases such as kallikrein and therefore may ameliorate the postreperfusion syndrome and reduce the need for vasopressors.

Methods
In a randomized, double-blind study, the authors compared hemodynamic variables (systemic vascular resistance, cardiac index, arterial blood pressure, mean pulmonary artery pressure, central venous pressure) and the requirement of epinephrine during transplantation in 67 patients who received either high-dose aprotinin (2 x 10(6) kallikrein inhibitor units [KIU] at induction, continuous infusion of 1 x 10(6) KIU/h, 1 x 10(6) KIU before reperfusion; n = 24), regular-dose aprotinin (2 x 10(6) KIU at induction, continuous infusion of 0.5 x 10(6) KIU/h; n = 21), or placebo (n = 22).

Results
Baseline characteristics were similar for all three groups. Erythrocyte transfusion requirement was significantly higher in the placebo group compared with both aprotinin-treated groups. No major differences in hemodynamic variables were found between the three groups. The total amount of epinephrine (median, range) used during transplantation, however, was significantly lower in patients who received aprotinin (high dose, 20, 0-170 microg; regular dose, 30, 0-140 microg), compared with patients who received placebo (70, 0-2,970 microg; P = 0.0017). This difference was largely attributable to differences in the early postreperfusion period.

Conclusions
Prophylactic use of aprotinin ameliorates the postreperfusion syndrome in orthotopic liver transplantation, as reflected by a significant reduction in vasopressor requirements.
Analgesic Effect of Low-dose Intrathecal Morphine after Spinal Fusion in Children
Authors: Gall Olivier , Aubineau Jean-Vincent , Bernière Josée , Desjeux Luc , Murat Isabelle 
Published: November 2003

Background
This study was designed to assess the postoperative analgesic effect of low-dose intrathecal morphine after scoliosis surgery in children.

Methods
Thirty children, 9-19 yr of age, scheduled for spinal fusion, were randomly allocated into three groups to receive a single dose of 0 (saline injection), 2, or 5 microg/kg intrathecal morphine. After surgery, a patient-controlled analgesia device (PCA) provided free access to additional intravenous morphine. Children were monitored for 24 h in the postanesthesia care unit.

Results
The three groups were similar for age, weight, duration of surgery, and time to extubation. The time to first PCA demand was dose-dependently delayed by intrathecal morphine. The first 24 h of PCA morphine consumption was 49 +/- 17, 19 +/- 10, and 12 +/- 12 mg (mean +/- SD) in the saline, 2 microg/kg morphine, and 5 microg/kg morphine groups, respectively. Pain scores at rest were significantly lower over the whole study period after 2 and 5 microg/kg intrathecal morphine than after saline, but there was no difference between intrathecal doses. Pain scores while coughing and the incidence of side effects were similar in the three groups.

Conclusions
These data demonstrate that low-dose intrathecal morphine supplemented by PCA morphine provides better analgesia than PCA morphine alone after spinal fusion in children. The doses of 2 and 5 microg/kg seem to have similar effectiveness and side-effect profiles, whereas a reduction of intraoperative bleeding was observed in patients who received 5 microg/kg but not 2 microg/kg intrathecal morphine.
Mathematical Modeling of Carbon Monoxide Exposures from Anesthetic Breakdown
Authors: Woehlck Harvey J. , Mei David , Dunning Marshall B. , Ruiz Franklin 
Published: November 2003

Background
Carbon monoxide (CO) is produced by reaction of isoflurane, enflurane, and desflurane in desiccated carbon dioxide absorbents. The inspiratory CO concentration depends on the dryness and identity of the absorbent and anesthetic. The adaptation of existing mathematical models to a rebreathing circuit allows identification of patient factors that predispose to more severe exposures, as identified by carboxyhemoglobin concentration.

Methods
From our companion study, the authors used quantitative in vitro CO production data for 60 min at 7.5% desflurane or 1.5% isoflurane at 1 l/min fresh gas flow. The carboxyhemoglobin concentration was calculated by iteratively solving the Coburn Forster Kane equation modified for a rebreathing system that incorporates the removal of CO by patient absorption. Demonstrating good fit of predicted carboxyhemoglobin concentrations to published data from animal and human exposures validated the model. Carboxyhemoglobin concentrations were predicted for exposures of various severity, patients of different sizes, hematocrit, and fraction of inspired oxygen.

Results
The calculated carboxyhemoglobin concentrations closely predicted the experimental results of other investigators, thereby validating the model. These equations indicate the severity of CO poisoning is inversely related to the hemoglobin quantity of a subject. Fraction of inspired oxygen had the greatest effect in patients of small size with low hematocrit values, where equilibrium and not the rate of uptake determined carboxyhemoglobin concentrations.

Conclusion
This model predicts that patients with low hemoglobin quantities will have more severe CO exposures based on the attainment of a higher carboxyhemoglobin concentration. This includes patients of small size (pediatric population) and patients with anemia.