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A Amann

Publications and source records attributed to A Amann.

34 records · Page 2Linked to original sources

Analysing ventricular fibrillation ECG-signals and predicting defibrillation success during cardiopulmonary resuscitation employing N(alpha)-histograms.

Mean fibrillation frequency may predict defibrillation success during cardiopulmonary resuscitation (CPR). N(alpha)-histogram analysis should be investigated as an alternative. After 4 min of cardiac arrest, and 3 versus 8 min of CPR, 25 pigs received either vasopressin or epinephrine (0.4, 0.4, and 0.8 U/kg vasopressin versus 45, 45, and 200 microg/kg epinephrine) every 5 min with defibrillation at 22 min. Before defibrillation, the N(alpha)-parameter histogramstart/histogramwidth and the mean fibrillation frequency in resuscitated versus non-resuscitated pigs were 2.9+/-0.4 versus 1.7+/-0.5 (P=0.0000005); and 9.5+/-1.7 versus 6.9+/-0.7 (P=0.0003). During the last minute prior to defibrillation, histogramstart/histogramwidth of > or =2.3 versus mean fibrillation frequency > or =8 Hz predicted successful defibrillation with subsequent return of a spontaneous circulation for more than 60 min with sensitivity, specificity, positive predictive value and negative predictive value of 94 versus 82%, 96 versus 89%, 98 versus 93% and 90 versus 74%, respectively. We conclude, that N(alpha)-analysis was superior to mean fibrillation frequency analysis during CPR in predicting defibrillation success, and distinction between vasopressin versus epinephrine effects.

Algorithms↗

Waveform analysis of biphasic external defibrillators.

BACKGROUND AND OBJECTIVE: All internal defibrillators and some external defibrillators use biphasic waveforms. The study analysed the discharged waveform pulses of two manual and two semi-automated biphasic external defibrillators. METHODS AND RESULTS: The defibrillators were discharged into resistive loads of 25, 50 and 100 Omega simulating the patient's transthoracic impedance. The tested biphasic defibrillators differed in initial current as well as initial voltage, varying from 10.9 to 73.3 A and from 482.8 to 2140.0 V, respectively. The energies of the manual defibrillators set at 100, 150 and 200 J deviated by up to +19.1 or -28.9% from the selected energy. Impedance-normalised delivered energy varied from 1.0 to 12.5 J/Omega. Delivered energy, shock duration and charge flow were examined with respect to the total pulse, its splitting into positive and negative phases and their impedance dependence. For three defibrillators pulse duration increased with the resistive load, whereas one defibrillator always required 9.9 ms. All tested defibrillators showed a higher charge flow in the positive phase. Defibrillator capacitance varied between approximately 200 and 100 mu F and internal resistance varied from 2.0 to 7.6 Omega. Defibrillator waveform tilt ranged from -13.1 to 61.4%. CONCLUSIONS: The tested defibrillators showed remarkable differences in their waveform design and their varying dependence on transthoracic impedance.

Calibration↗

Fibrillation power, an alternative method of ECG spectral analysis for prediction of countershock success in a porcine model of ventricular fibrillation.

BACKGROUND: Noninvasive prediction of defibrillation success after cardiac arrest and cardiopulmonary resuscitation (CPR) may help in determining the optimal time for a countershock, and thus increase the chance for survival. METHODS: In a porcine model (n=25) of prolonged cardiac arrest, advanced cardiac life support was provided by administration of two or three doses of either vasopressin or epinephrine after 3 or 8 min of basic life support. After 4 min of ventricular fibrillation and 18 min of life support, defibrillation was attempted. The denoised power spectral density of 10 s intervals of the ventricular fibrillation electrocardiogram (ECG) was estimated from averaged and smoothed Fourier transforms. We have eliminated the spectral contribution of artifacts from manual chest compressions and provide a definition for the contribution of ventricular fibrillation to the power spectral density. This contribution is quantified and termed "fibrillation power". RESULTS: We tested fibrillation power and two established methods in their discrimination of survivors (n=16) vs. non-survivors (n=9) in the last minute before the countershock. A fibrillation power > or =79 dB predicted successful defibrillation with sensitivity, specificity, positive predictive value and negative predictive value of 98%, 98%, 99% and 97% while a mean fibrillation frequency > or =7.7 Hz was predictive with 85%, 83%, 90% and 77% and a mean amplitude > or =0.49 mV was predictive with 95%, 90%, 94% and 91%. CONCLUSIONS: We suggest that fibrillation power is an alternative source of information on the status of a fibrillating heart and that it may match the established mean frequency and amplitude analysis of ECG in predicting successful countershock during CPR.

Animals↗

The beneficial effect of basic life support on ventricular fibrillation mean frequency and coronary perfusion pressure.

BACKGROUND AND OBJECTIVE: Chest compressions before initial defibrillation attempts have been shown to increase successful defibrillation. This animal study was designed to assess whether ventricular fibrillation mean frequency after 90 s of basic life support cardiopulmonary resuscitation (CPR) may be used as an indicator of coronary perfusion and mean arterial pressure during CPR. METHODS AND RESULTS: After 4 min of ventricular fibrillation cardiac arrest in a porcine model, CPR was performed manually for 3 min. Mean ventricular fibrillation frequency and amplitude, together with coronary perfusion and mean arterial pressure were measured before initiation of chest compressions, and after 90 s and 3 min of basic life support CPR. Increases in fibrillation mean frequency correlated with increases in coronary perfusion and mean arterial pressure after both 90 s (R=0.77, P<0.0001, n=30; R=0.75, P<0.0001, n=30, respectively) and 3 min (R=0.61, P<0.001, n=30; R=0.78, P<0.0001, n=30, respectively) of basic life support CPR. Increases in fibrillation mean amplitude correlated with increases in mean arterial pressure after both 90 s (R=0.46, P<0.01; n=30) and 3 min (R=0.42, P<0.05, n=30) of CPR. Correlation between fibrillation mean amplitude and coronary perfusion pressure was not significant both at 90 s and 3 min of CPR. CONCLUSIONS: In this porcine laboratory model, 90 s and 3 min of CPR improved ventricular fibrillation mean frequency, which correlated positively with coronary perfusion pressure, and mean arterial pressure.

Animals↗

Surfactant protein B labelled with [(99m)Tc(CO)3(H20)3](+) retains biological activity in vitro..

UNLABELLED: Labelling of the hydrophobic surfactant protein B (SP-B) under non-reducing conditions was achieved with [(99m)Tc(CO)(3)(H2O)(3)](+) prepared according to Alberto et al. (JACS, 1998). The binding of radioactivity was protein-specific, with an overall radiochemical yield of 50%. Gel electrophoresis and Westernblot analyses showed no structural changes of SP-B. Spreading properties and surface activity of (99m)Tc-labelled SP-B in an air/water interface coincided with those of unlabelled SP-B. (99m)Tc-SP-B seems to be a promising agent to observe surfactant spreading under clinical conditions. BACKGROUND: Therapeutic results for surfactant instillation in clinical trials are conflicting. The (99m)Tc-labelling of surfactant would allow to observe its spreading in the lung under clinical conditions. METHODS: [(99m)Tc(CO)(3)(H2O)(3)](+) was prepared as described by Alberto et al. (JACS, 1998). This carbonyl complex was used for the direct labelling of surfactant protein B (SP-B) under non-reductive conditions by direct incubation with SP-B at elevated temperature followed by extraction into CHCl(3)/MeOH. RESULTS: The hydrophobic protein SP-B was labelled with [(99m)Tc(CO)(3)(H2O)(3)](+). An overall radiochemical yield of about 50% was achieved. HPLC-analysis revealed a single radiolabelled species according to UV elution profile of SP-B, supported by paper and size exclusion chromatography. Gel electrophoresis confirmed that the dimer structure of SP-B was preserved. Spreading properties of (99m)Tc-labelled SP-B in an air/water interface coincided with those of unlabelled SP-B. Spreading of radioactivity observed in a glass trough of 26 cm x 27 cm with a gamma camera was completed during the first 7-9 sec after application of (99m)Tc-labelled SP-B. The corresponding decrease of surface tension to 45 mN/m at the peripheral surface tension sensors took 7 sec +/- 2 sec (MEAN +/- STD; n = 3). CONCLUSIONS: Direct and specific (99m)Tc-labelling of the hydrophobic surfactant protein B was achieved using the [(99m)Tc(CO)(3)(H2O)(3)](+) precursor. This procedure can easily be used to prepare specifically labelled surfactant mixtures with spreading properties that coincide with those of unlabelled surfactant.

Animals↗

Monitoring of immune activation using biochemical changes in a porcine model of cardiac arrest.

In animal models, immune activation is often difficult to assess because of the limited availability of specific assays to detect cytokine activities. In human monocytes/macrophages, interferon-gamma induces increased production of neopterin and an enhanced activity of indoleamine 2,3-dioxygenase, which degrades tryptophan via the kynurenine pathway. Therefore, monitoring of neopterin concentrations and of tryptophan degradation can serve to detect the extent of T helper cell 1-type immune activation during cellular immune response in humans. In a porcine model of cardiac arrest, we examined the potential use of neopterin measurements and determination of the tryptophan degradation rate as a means of estimating the extent of immune activation. Urinary neopterin concentrations were measured with high-performance liquid chromatography (HPLC) and radioimmunoassay (RIA) (BRAHMS Diagnostica, Berlin, Germany). Serum and plasma tryptophan and kynurenine concentrations were also determined using HPLC. Serum and urine neopterin concentrations were not detectable with HPLC in these specimens, whereas RIA gave weakly (presumably false) positive results. The mean serum tryptophan concentration was 39.0 +/- 6.2 micromol/l, and the mean kynurenine concentration was 0.85 +/- 0.33 micromol/l. The average kynurenine-per-tryptophan quotient in serum was 21.7 +/- 8.4 nmol/micromol, and that in plasma was 20.7 +/- 9.5 nmol/micromol (n = 7), which corresponds well to normal values in humans. This study provides preliminary data to support the monitoring of tryptophan degradation but not neopterin concentrations as a potential means of detecting immune activation in a porcine model. The kynurenine-per-tryptophan quotient may serve as a short-term measurement of immune activation and hence permit an estimate of the extent of immune activation.

Animals↗

Online monitoring of air quality at the postanesthetic care unit by proton-transfer-reaction mass spectrometry.

The subthreshold exposure to trace anesthetic gases is not associated with considerable risk of adverse health effects. Online control of ambient air exchange at the postoperative workplace may help in supervising air quality and lead to cost reduction. A proton-transfer-reaction mass spectrometer system was used for online monitoring of volatile organic compounds, especially anesthetic gases. The mean exposure to sevoflurane and isoflurane at the urological postanesthesia care unit (PACU) was 15.9 and 9.5 parts per billion, respectively. Sevoflurane and isoflurane concentrations at the urological PACU showed a patient turnover-dependent burden during our investigation period. Because modern PACUs have a high ventilation capacity, the 24-h occupational burden by anesthetic gases at the PACU is relatively low. Monitoring and controlling of ambient air by automatic built-in alarm systems would be useful for quality control of the postoperative workplace. Moreover, energy costs of ventilation systems could be reduced by coupling ventilation capacity to the effective exposure.

Air Pollutants, Occupational↗

The influence of atracurium, cisatracurium, and mivacurium on the proliferation of two human cell lines in vitro.

We tested the influence of atracurium and cisatracurium (final concentrations: 0, 0.96, 3.2, 9.6, 32, and 96 microM) on proliferation of human cells (hepatoma HepG2 cells and human umbilical vein endothelial cells) in vitro. In additional experiments, glutathione, N-acetylcysteine, or carboxyl esterase was added before the addition of either relaxant. The number of cells counted after 72 h of incubation was expressed as a percentage of the mean cell number in wells incubated without additives. Atracurium and cisatracurium progressively decreased cell proliferation in a concentration-dependent pattern. With human umbilical vein endothelial cells, atracurium or cisatracurium (3.2 microM) decreased the cell count to 67.7 % (SD, 14.8%) and 50% (SD, 8.6%), respectively. Cell proliferation was not inhibited by mivacurium. The results were similar to those with HepG2 cells. Glutathione, N-acetylcysteine, and carboxyl esterase partially reversed the effects of atracurium and cisatracurium. When incubated in a buffer with glutathione, atracurium decreased the number of glutathione-sulfhydryl groups. The findings that atracurium and cisatracurium inhibit proliferation of human cell lines in vitro, but that mivacurium does not, and that this effect is alleviated by glutathione and N-acetylcysteine, as well as by the carboxyl esterase, indicate that the inhibition may be caused by the reactive acrylate metabolites.

Acetylcysteine↗

The efficacy of epinephrine or vasopressin for resuscitation during epidural anesthesia.

Cardiopulmonary resuscitation (CPR) during epidural anesthesia is considered difficult because of diminished coronary perfusion pressure. The efficacy of epinephrine and vasopressin in this setting is unknown. Therefore, we designed this study to assess the effects of epinephrine versus vasopressin on coronary perfusion pressure in a porcine model with and without epidural anesthesia and subsequent cardiac arrest. Thirty minutes before induction of cardiac arrest, 16 pigs received epidural anesthesia with bupivacaine while another 12 pigs received only saline administration epidurally. After 1 min of untreated ventricular fibrillation, followed by 3 min of basic life-support CPR, Epidural Animals and Control Animals randomly received every 5 min either epinephrine (45, 45, and 200 microg/kg) or vasopressin (0.4, 0.4, and 0.8 U/kg). During basic life-support CPR, mean +/- SEM coronary perfusion pressure was significantly lower after epidural bupivacaine than after epidural saline (13 +/- 1 vs 24 +/- 2 mm Hg, P < 0.05). Ninety seconds after the first drug administration, epinephrine increased coronary perfusion pressure significantly less than vasopressin in control animals without epidural block (42 +/- 2 vs 57 +/- 5 mm Hg, P < 0.05), but comparably to vasopressin after epidural block (45 +/- 4 vs 48 +/- 6 mm Hg). Defibrillation was attempted after 18 min of CPR. After return of spontaneous circulation, bradycardia required treatment in animals receiving vasopressin, especially with epidural anesthesia. Systemic acidosis was increased in animals receiving epinephrine than vasopressin, regardless of presence or absence of epidural anesthesia. We conclude that vasopressin may be a more desirable vasopressor for resuscitation during epidural block because the response to a single dose is longer lasting, and acidosis after multiple doses is less severe compared with epinephrine.

Anesthesia, Epidural↗

Algorithms to analyze ventricular fibrillation signals.

Prediction of the success of defibrillation to avoid myocardial injury and performance feedback during CPR requires algorithms to analyze ventricular fibrillation signals. This report reviews investigations on different parameters of ventricular fibrillation electrocardiographic signals, including amplitude, frequency, bispectral analysis, amplitude spectrum area, wavelets, nonlinear dynamics, N(alpha) histograms, and combinations of several of these parameters. To date, no satisfactory methods have been found that cope with CPR artifacts and show adequate predictive power of successful defibrillation. The usual limitations of the studies are the small number of subjects, which precludes separation into training and test data. Because many investigations are animal studies of untreated short ventricular fibrillation, the results may be different for prolonged ventricular fibrillation in humans. The universality of threshold values has to be examined, and promising new parameters have to be monitored over longer time periods and analyzed for the effects of chest compressions, ventilation, and concomitant vasopressor therapy.

Algorithms↗

The effects of repeated doses of vasopressin or epinephrine on ventricular fibrillation in a porcine model of prolonged cardiopulmonary resuscitation.

This study evaluated ventricular fibrillation mean frequency and amplitude to predict defibrillation success in a porcine cardiopulmonary resuscitation (CPR) model using repeated administration of vasopressin or epinephrine. After 4 min of cardiac arrest and 3 min of CPR, 10 pigs were randomly assigned to receive either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 units/kg, respectively, n = 5) or epinephrine (early epinephrine: 45, 45, and 200 microg/kg, respectively, n = 5). Another 11 animals were randomly allocated after 4 min of cardiac arrest and 8 min of CPR to receive every 5 min either vasopressin (late vasopressin: 0.4 and 0. 8 units/kg, respectively, n = 5) or epinephrine (late epinephrine: 45 and 200 microg/kg, n = 6). Ventricular fibrillation mean frequency and amplitude on defibrillation were significantly higher in the vasopressin groups than in the epinephrine groups, respectively. In vasopressin versus epinephrine animals, mean frequency immediately before defibrillation was 9.6 +/- 1.5 Hz vs 7. 0 +/- 0.7 Hz (P < 0.001), mean amplitude was 0.65 +/- 0.26 mV vs 0. 21 +/- 0.14 mV (P < 0.001, and coronary perfusion pressure was 27 +/- 9 mm Hg vs 8 +/- 4 mm Hg (P < 0.00001), respectively. In contrast to no epinephrine animals, all vasopressin animals were successfully defibrillated and survived 1 h (P < 0.05). Mean fibrillation frequency and amplitude predicted successful defibrillation and may serve as noninvasive markers to monitor continuing CPR efforts. Furthermore, vasopressin was superior to epinephrine in maintaining these variables above a threshold necessary for successful defibrillation.

Animals↗

Waveforms of external defibrillators: analysis and energy contribution.

BACKGROUND AND OBJECTIVE: Defibrillation is the most important therapy for terminating ventricular fibrillation in cardiac arrest patients. In addition to performing defibrillation at the earliest possible time, appropriate pulse energy and optimal waveform seem to be crucial for success. Emergency medical service personnel use different defibrillators and rely on their similarity of energy content. This study examined the true pulse energy content and waveform of 17 commonly used defibrillators. METHODS AND RESULTS: Defibrillation energies were selected to be 30, 200 or 360 J and defibrillators were discharged into test resistors, simulating transthoracic impedances of 25, 50 or 100 Ohms. Pulse energy deviated by up to +23% or -29% from the selected energy. Pulse energy within the initial 8 ms ranged from 90 to 30% of total pulse energy. Fourteen defibrillators utilising damped sinusoidal waveforms produced a monophasic pulse when discharged into resistances of 50 Ohms and 100 Ohms. CONCLUSIONS: Defibrillators used at the same energy settings do not necessarily produce the same defibrillation pulse energy. All but one defibrillator actually use monophasic waveforms, leaving the potential advantage of biphasic waveforms unused. Energy accuracy of defibrillators needs to be improved, and biphasic waveforms should be used more.

Calibration↗

Intropin (dopamine hydrochloride) intravenous admixture compatibility, Part 3: stability with miscellaneous additives.

The compatibility of dopamine hydrochloride (Intropin) with various additives in 5% Dextrose Injection, USP, was studied. Dopamine hydrochloride stability for 24 hours in the admixture was established by colorimetric and thin-layer chromatographic procedures. Dopamine hydrochloride solutions are generally stable at an acidic pH and all admixtures produced a slightly acidic solution. Additives tested and found stable for 24 hours in the presence of Intropin included heparin sodium, lidocaine hydrochloride, neutral cephalothin sodium, oxacillin sodium and gentamicin sulfate. The chemical stability of methylprednisolone sodium succinate and hydrocortisone sodium succinate was not established. Potassium chloride, calcium chloride and calcium gluceptate may be assumed to be stable in the presence of Intropin. Above pH 5.0, the calcium gluceptate-Intropin admixture exhibited a color change indicating physical incompatibility. The pH and physical compatibility of all admixtures were established. In order to avoid a fixed combination of potent drugs, it is recommended that a "piggyback" administration set or administration into a second injection site be employed when another drug is to be administered with Intropin.

Dopamine↗