[Safety in anesthesia-from a "culture of blame" to a culture of safety].
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Biomedical subjects
Publications and source records attributed to G Hempelmann.
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Activation of the renin-angiotensin system during cardiopulmonary bypass (CPB) may be involved in early postoperative hypertension after coronary artery bypass grafting (CABG). As hypertensive episodes may be deleterious in the immediate postoperative period, we have assessed the effects of prophylactic treatment with the angiotensin-converting enzyme inhibitor quinaprilat in an open study. During steady state CPB, patients received quinaprilat 0.02 mg kg-1 (group A, n = 10), quinaprilat 0.04 mg kg-1 (group B, n = 10) or saline solution (group C, n = 10) as an i.v. bolus dose. Sodium nitroprusside (SNP) was given after operation when systolic arterial pressure was > 150 mm Hg. Requirements for SNP 1 h after arrival in the ICU were significantly less in groups A (two of 10) and B (two of 10) than in group C (eight of 10). Also, patients in group C had a greater systolic arterial pressure compared with groups A and B. There were no significant differences between groups in diastolic arterial pressure, heart rate, cardiac index or cardiac filling pressures. We conclude that quinaprilat can be used during CABG to reduce the incidence of postoperative hypertension. Further studies of the efficacy and safety of this technique are necessary.
UNLABELLED: Although dimenhydrinate has been used for treatment and prevention of postoperative nausea and vomiting (PONV) since the fifties, there have been few controlled studies about its efficacy. We performed a double-blinded study of 301 children aged 4 to 10 yr who underwent strabismus surgery. Preanesthetic medication with midazolam (0.5 mg/kg) as well as application of either dimenhydrinate suppositories or a placebo preparation was performed 30 min before the induction of anesthesia. Anesthesia was induced with thiopentone (5-10 mg/kg) and vecuronium (0.1 mg/kg) and maintained with halothane (1%-2%) in N(2)O/O(2) (65%/35%). The incidence of PONV, requirements for rescue dimenhydrinate, and time to recovery were recorded. The overall incidence of PONV was 60.1% in the placebo group and 30.7% in the dimenhydrinate group. In the dimenhydrinate group, children had to be observed in the recovery room significantly longer than those in the placebo group. Children having received dimenhydrinate were discharged from the recovery room with lower arousal scores. We conclude that the rectal administration of dimenhydrinate is effective for the prevention of PONV, although the sedative effect may require longer postoperative monitoring. IMPLICATIONS: We performed a double-blinded, randomized study to investigate the effects of prophylactic rectal dimenhydrinate application on postoperative nausea and vomiting in children undergoing strabismus surgery. In comparison with placebo, dimenhydrinate reduced the incidence of postoperative vomiting from 60.1% to 30.7%.
Tetrodotoxin (TTX)-sensitive Na(+) channels in the peripheral nervous system are the major targets for local anesthetics. In the peripheral nociceptive system, a Na(+) channel subtype resistant to TTX and with distinct electrophysiological properties seems to be of importance for impulse generation and conduction. A current through TTX-resistant Na(+) channels displays slower activation and inactivation kinetics and has an increased activation threshold compared with TTX-sensitive Na(+) currents and may have different pharmacological properties. We studied the effects of stereoisomers of piperidine local anesthetics on neuronal TTX-resistant Na(+) currents recorded with the whole-cell configuration of the patch clamp method in enzymatically dissociated dorsal root ganglion neurons of adult rats. Stereoisomers of mepivacaine, ropivacaine, and bupivacaine reversibly inhibited TTX-resistant Na(+) currents in a concentration and use-dependent manner. All drugs accelerated time course of inactivation. Half-maximal blocking concentrations were determined from concentration-inhibition relationships. Potencies for tonic and for use-dependent block increased with rising lipid solubilities of the drugs. Stereoselective action was not observed. We conclude that block of TTX-resistant Na(+) currents may lead to blockade of TTX-resistant action potentials in nociceptive fibers and consequently may be responsible for pain suppression during local anesthesia.
BACKGROUND: Among opioids, meperidine (pethidine) also shows local anesthetic activity when applied locally to peripheral nerve fibers and has been used for this effect in the clinical setting for regional anesthesia. This study investigated the blocking effects of meperidine on different ion channels in peripheral nerves. METHODS: Experiments were conducted using the outside-out configuration of the patch-clamp method applied to enzymatically prepared peripheral nerve fibers of Xenopus laevis. Half-maximal inhibiting concentrations were determined for Na+ channels and different K+ channels by nonlinear least-squares fitting of concentration-inhibition curves, assuming a one-to-one reaction. RESULTS: Externally applied meperidine reversibly blocked all investigated channels in a concentration-dependent manner, i.e., voltage-activated Na+ channel (half-maximal inhibiting concentration, 164 microM), delayed rectifier K+ channels (half-maximal inhibiting concentration, 194 microM), the calcium-activated K+ channel (half-maximal inhibiting concentration, 161 microM), and the voltage-independent flicker K+ channel (half-maximal inhibiting concentration, 139 microM). Maximal block in high concentrations of meperidine reached 83% for delayed rectifier K+ channels and 100% for all other channels. Meperidine blocks the Na+ channel in the same concentration range as the local anesthetic agent lidocaine (half-maximal inhibiting concentration, 172 microM) but did not compete for the same binding site as evaluated by competition experiments. Low concentrations of meperidine (1 nM to 1 microM) showed no effects on Na+ channels. The blockade of Na+ and delayed rectifier K+ channels could not be antagonized by the addition of naloxone. CONCLUSIONS: It is concluded that meperidine has a nonselective inhibitory action on Na+ and K+ channels of amphibian peripheral nerve. For tonic Na+ channel block, neither an opioid receptor nor the the local anesthetic agent binding site is the target site for meperidine block.
BACKGROUND: Dorsal horn neurons of the spinal cord participate in neuronal pain transmission. During spinal and epidural anesthesia, dorsal horn neurons are exposed to local anesthetics and opioids. Droperidol is usually given with opioids to avoid nausea and vomiting. A recently developed method of "entire soma isolation" has made it possible to study directly the action of droperidol on different components of Na+ current in dorsal horn neurons. METHODS: Using a combination of the whole-cell patch-clamp recording from spinal cord slices and the entire soma isolation method, we studied the direct action of droperidol on two types of Na+ currents in dorsal horn neurons of young rats. RESULTS: The tetrodotoxin-sensitive Na+ current in isolated somata consisted of a fast inactivating (tauF, 0.5-2 ms; 80-90% of the total amplitude) and a slow inactivating (tauS, 6-20 ms; 10-20% of the total amplitude) component. Droperidol, at concentrations relevant for spinal and epidural anesthesia, selectively and reversibly suppressed the fast component with a half-maximum inhibiting concentration (IC50) of 8.3 microm. The slow inactivating component was much less sensitive to droperidol; the estimated IC50 value was 809 microm. CONCLUSIONS: Droperidol selectively blocks fast Na+ channels, the fast and slow components of the Na+ current in dorsal horn neurons are carried through pharmacologically distinct types of Na+ channels, and the effects of droperidol differ from those of local anesthetics and tetrodotoxin, which equipotently suppress both components. Droperidol may be suggested as a pharmacologic tool for separation of different types of inactivating tetrodotoxin-sensitive Na+ channel.
BACKGROUND: The transcription factor NF-kappaB plays a pivotal role in gene expression of inflammatory mediators such as cytokines or adhesion molecules. NF-kappaB-mediated transcriptional activation of these genes is inhibited by nitric oxide (NO) in a variety of cells, including monocytes. Morphine mediates NO release in a naloxone antagonizable manner in monocytes and neutrophils. METHODS: The influence of morphine on NF-kappaB activation was investigated in a whole-blood flow cytometric assay. A specific antibody against the p65 subunit of NF-kappaB was used and detected by fluoresceine-isothiocyanate-labeled anti-immunoglobulin G. Nuclei were stained with propidium iodide. Leukocyte subpopulations were evaluated by gating on neutrophils and monocytes. The median fluorescence channel was determined. Different morphine concentrations (50 nm, 50 microm, 1 mm) and incubation intervals (10-150 min) were used. RESULTS: Morphine inhibits lipopolysaccharide-induced NF-kappaB nuclear binding in human blood neutrophils and monocytes in a time-, concentration-, and naloxone-sensitive-dependent manner. Similar effects were achieved with the NO donor S-nitroso-N-acetyl-pencillamine and the antioxidant N-acetyl-cysteine. The NO synthase inhibitors Nomega-nitro-l-arginine-methyl-esther and Nomega-nitro-l-arginine completely abolished the morphine-induced attenuation of NF-kappaB nuclear binding, demonstrating that the inhibitory action is mediated by NO release. CONCLUSION: Morphine causes immunosuppression, at least in part, via the NO-stimulated depression of NF-kappaB nuclear binding.
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The aim of this project was to develop a cost-effective, standard-based and scalable clinical information system for use in Intensive Care Units (ICUs). The development started in 1998 at the University Giessen, Germany. Since its introduction as the basic documentation system at the ICU ward of the Department of Anesthesiology and Intensive Care Medicine in January 1999, all relevant clinical data of 1723 patients have been recorded. The implementation of the system in two further ICUs is scheduled for the year 2000. The following article describes some of the principal design goals of the system, including the medical vision that drove its interface design, and focuses on the technological underpinnings of the overall system architecture.
In this study, an Anesthesia Information Management System (AIMS) is used for the comparison of manually recorded adverse events with automatically detected events from anesthesiological procedures. In 1998, data from all anesthesia procedures, including the data set for quality assurance defined by the German Society of Anesthesiology and Intensive Care Medicine (DGAI), were recorded online with the documentation software NarkoData 4 (IMESO GmbH, Hüttenberg, Germany) followed by storage into a relational database (Oracle Corporation). The occurrence of manually recorded adverse events, as defined by the DGAI, is compared with automatically detected events. Automated detection was done with SQL-statements. The following adverse events were selected: hypotension, hypertension, bradycardia, tachycardia and hypovolemia. Data obtained from 16,019 electronic anesthesia records show that in 911 patients (5.7%), one of the selected adverse events was documented manually whereas in 2,996 patients (18.7%) a adverse event was detected automatically. The incidence of automatically detected events is obviously higher compared to manually recorded events. With the help of an AIMS, automatic detection proved significant deficiencies in the manual documentation of adverse events.
Main requirements for an Anesthesia Information Management System (AIMS) are the supply of additional information for the anesthesiologist at his workstation and complete documentation of the anesthetic procedure. With the implementation of an AIMS (NarkoData) and effective user support, the quality of documentation and the information flow at the anesthesia workstation could be increased. Today, more than 20,000 anesthesia procedures are annually recorded with the AIMS at 112 decentralized workstations. The network for data entry and the presentation and evaluation of data, statistics and results directly available at the clinical workstation was made operational.
The described procedure allows quantitative, highly precise and reproducible analysis of free amino acid concentrations in single polymorphonuclear leucocytes (PMLs). This method is superior to previously described procedures with regard to sample size, PML separation, sample preparation and stability, as well as the chosen fluorescence high-performance liquid chromatography procedure, and can satisfy the high demands for ultra-sensitive and comprehensive amino acid analysis, especially for the continuous surveillance of severe diseases and organ dysfunction.