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Search Results: 1 - 10 of 288 matches for " Berthold Bein "
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Vital organ blood flow during high-frequency ventilation
Patrick Meybohm, Jens Scholz, Berthold Bein
Critical Care , 2006, DOI: 10.1186/cc5075
Abstract: Firstly, the authors state that their study is limited due to the lack of more frequent blood flow measurements, as all parameters were measured only once thirty minutes after switching to a new mean airway pressure (Pmean). Indeed, changes in hemodynamic variables are most pronounced straight after increasing mean airway pressure [2]. It has been shown that cardiac output initially decreased substantially after an increase in positive end-expiratory pressure (PEEP), but that it adapted to the increased PEEP thereafter due to dynamic hemodynamic changes [3]. Consequently, compensatory mechanisms missed by insufficient data sampling could explain the only slightly decreased cardiac output and unchanged organ blood flow seen in the study by David and colleagues [1]. Therefore, it is of paramount importance to investigate parameters of individual organ perfusion more frequently, and obtain variables of tissue oxygenation and metabolism. Furthermore, brain tissue is extremely susceptible to ischemia, and even a few minutes of compromised cerebral perfusion affect the rate of cerebral oxygen metabolism and tissue integrity. To elucidate the impact of mechanical ventilation on brain tissue, the authors should have analyzed cerebral tissue biochemistry [4] or established biomarkers of cerebral ischemia, such as S-100β or neuron-specific enolase.Secondly, cardiac filling pressures have repeatedly been shown to only poorly reflect instantaneous cardiac preload. Right ventricular end-diastolic volume and global end-diastolic volume have been demonstrated to be clearly superior for this than cardiac filling pressures, particularly at high intrathoracic pressures in a model of acute lung injury [5], and would have provided more detailed information regarding interaction of recruitment manoeuvre, preload and organ perfusion.The authors declare that they have no competing interests.
Reliability of continuous cardiac output measurement during intra-abdominal hypertension relies on repeated calibrations: an experimental animal study
Matthias Gruenewald, Jochen Renner, Patrick Meybohm, Jan H?cker, Jens Scholz, Berthold Bein
Critical Care , 2008, DOI: 10.1186/cc7102
Abstract: Ten pigs were anaesthetised and instrumented for haemodynamic measurements. Cardiac output was obtained using CCO by pulse power analysis (PulseCO; LiDCO monitor), using CCO by pulse contour analysis (PCCO; PiCCO monitor) and using CCO by pulmonary artery catheter thermodilution (CCOPAC), and was compared with bolus transcardiopulmonary thermodilution CO (COTCP) at baseline, after fluid loading, at IAH and after an additional fluid loading at IAH. Whereas PulseCO was only calibrated at baseline, PCCO was calibrated at each experimental step.PulseCO and PCCO underestimated CO, as the overall bias ± standard deviation was 1.0 ± 1.5 l/min and 1.0 ± 1.1 l/min compared with COTCP. A clinically accepted agreement between all of the CCO methods and COTCP was observed only at baseline. Whereas IAH did not influence the CO, increased CO following fluid loading at IAH was only reflected by CCOPAC and COTCP, not by uncalibrated PulseCO and PCCO. After recalibration, PCCO was comparable with COTCP.The CO obtained by uncalibrated PulseCO and PCCO failed to agree with COTCP during IAH and fluid loading. In the critically ill patient, recalibration of continuous arterial waveform CO methods should be performed after fluid loading or before a major change in therapy is initiated.Monitoring cardiac output (CO) allows early detection of haemodynamic instability and may be used to guide intensive care, aiming to reduce morbidity and mortality in high-risk patients [1]. In the past decade, continuous cardiac output (CCO) was commonly obtained by pulmonary artery catheter (PAC) with integrated heating filaments. The risk–benefit ratio of right heart catheterisation simply for CO determination has been questioned due to associated complications and the availability of less invasive alternatives [2]. Various monitor devices have been recently introduced into clinical practise that use the arterial pressure waveform to calculate CO on a beat-to-beat basis, such as the LiDCO?plus system usi
A comparison of transcranial Doppler with near infrared spectroscopy and indocyanine green during hemorrhagic shock: a prospective experimental study
Berthold Bein, Patrick Meybohm, Erol Cavus, Peter H Tonner, Markus Steinfath, Jens Scholz, Volker Doerges
Critical Care , 2005, DOI: 10.1186/cc3980
Abstract: After approval from the Animal Investigational Committee, 20 healthy pigs underwent a simulated penetrating liver trauma. Following hemodynamic decompensation, all animals received a hypertonic-isooncotic hydroxyethyl starch solution and either arginine vasopressin or norepinephrine, and bleeding was subsequently controlled. ICG passage through the brain was monitored by near infrared spectroscopy. BFI was calculated by dividing maximal ICG absorption change by rise time. Mean blood flow velocity (FVmean) of the right middle cerebral artery was recorded by TCD. FVmean and BFI were assessed at baseline (BL), at hemodynamic decompensation, and repeatedly after control of bleeding.At hemodynamic decompensation, cerebral perfusion pressure (CPP), FVmean and BFI dropped compared to BL (mean ± standard deviation; CPP 16 ± 5 mmHg versus 70 ± 16 mmHg; FVmean 4 ± 5 cm·s-1 versus 28 ± 9 cm·s-1; BFI 0.008 ± 0.004 versus 0.02 ± 0.006; p < 0.001). After pharmacological intervention and control of bleeding, FVmean and BFI increased close to baseline values (FVmean 23 ± 9 cm·s-1; BFI 0.02 ± 0.01), respectively. FVmean and BFI were significantly correlated (r = 0.62, p < 0.0001).FVmean and BFI both reflected the large variations in cerebral perfusion during hemorrhage and after resuscitation and were significantly correlated. BFI is a promising tool to monitor cerebral hemodynamics at the bedside.Reliable monitoring of cerebral oxygenation is an issue of paramount importance in anesthesia and critical care, since an impaired balance of oxygen demand and supply puts viable brain tissue at risk of ischemia [1]. Cerebral oxygenation is, among other influencing factors, highly dependent on cerebral blood flow (CBF). Despite its clinical relevance, a reliable and suitable method for measuring CBF rapidly, repeatedly and non-invasively at the bedside is currently still lacking. Perfusion magnetic resonance and computed tomographic imaging, though offering a very high spatial resolution,
Procalcitonin to guide duration of antibiotic therapy in intensive care patients: a randomized prospective controlled trial
Marcel Hochreiter, Thomas K?hler, Anna Schweiger, Fritz Keck, Berthold Bein, Tilman von Spiegel, Stefan Schroeder
Critical Care , 2009, DOI: 10.1186/cc7903
Abstract: All patients requiring antibiotic therapy based on confirmed or highly suspected bacterial infections and at least two concomitant systemic inflammatory response syndrome criteria were eligible. Patients were randomly assigned to either a PCT-guided (study group) or a standard (control group) antibiotic regimen. Antibiotic therapy in the PCT-guided group was discontinued, if clinical signs and symptoms of infection improved and PCT decreased to <1 ng/ml or the PCT value was >1 ng/ml, but had dropped to 25 to 35% of the initial value over three days. In the control group antibiotic treatment was applied as standard regimen over eight days.A total of 110 surgical intensive care patients receiving antibiotic therapy after confirmed or high-grade suspected infections were enrolled in this study. In 57 patients antibiotic therapy was guided by daily PCT and clinical assessment and adjusted accordingly. The control group comprised 53 patients with a standardized duration of antibiotic therapy over eight days. Demographic and clinical data were comparable in both groups. However, in the PCT group the duration of antibiotic therapy was significantly shorter than compared to controls (5.9 +/- 1.7 versus 7.9 +/- 0.5 days, P < 0.001) without negative effects on clinical outcome.Monitoring of PCT is a helpful tool for guiding antibiotic treatment in surgical intensive care patients. This may contribute to an optimized antibiotic regimen with beneficial effects on microbial resistance and costs in intensive care medicine.Results were previously published in German in Anaesthesist 2008; 57: 571–577 (PMID: 18463831).ISRCTN10288268Early differentiation between sepsis and systemic inflammatory response syndrome (SIRS) is of central importance for therapeutic decision-making. Although patients with SIRS will not require antibiotic therapy, immediate administration of antibiotics is essential for improved survival in patients with sepsis [1]. Despite apparently clear sepsis definition
Influence of Clonidine and Ketamine on m-RNA Expression in a Model of Opioid-Induced Hyperalgesia in Mice
Henning Ohnesorge, Zhiying Feng, Karina Zitta, Markus Steinfath, Martin Albrecht, Berthold Bein
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0079567
Abstract: Background We investigated the influence of morphine and ketamine or clonidine in mice on the expression of genes that may mediate pronociceptive opioid effects. Material and Methods C57BL/6 mice received morphine injections thrice daily using increasing doses (5-20mg?kg-1) for 3 days (sub-acute, n=6) or 14 days (chronic, n=6) and additionally either s-ketamine (5mg?kg-1, n=6) or clonidine (0.1mg?kg-1, n=6). Tail flick test and the assessment of the mechanical withdrawal threshold of the hindpaw was performed during and 4 days after cessation of opioid treatment. Upon completion of the behavioural testing the mRNA-concentration of the NMDA receptor (NMDAR1) and β-arrestin 2 (Arrb2) were measured by PCR. Results Chronic opioid treatment resulted in a delay of the tail flick latency with a rapid on- and offset. Simultaneously the mice developed a static mechanical hyperalgesia with a delayed onset that that outlasted the morphine treatment. Sub-acute morphine administration resulted in a decrease of NMDAR1 and Arrb2 whereas during longer opioid treatment the expression NMDAR1 and Arrb2 mRNA increased again to baseline values. Coadministration of s-ketamine or clonidine resulted in a reversal of the mechanical hyperalgesia and inhibited the normalization of NMDAR1 mRNA expression but had no effect on the expression of Arrb2 mRNA. Conclusion In the model of chronic morphine therapy the antinociceptive effects of morphine are represented by the thermal analgesia while the proniceptive effects are represented by the mechanical hyperalgesia. The results indicate that the regulation of the expression of NMDAR1 and Arrb2 may be associated to the development of OIH in mice. Perspective The results indicate that co-administration of clonidine or ketamine may influence the underlying mechanisms of OIH.
Mild hypothermia alone or in combination with anesthetic post-conditioning reduces expression of inflammatory cytokines in the cerebral cortex of pigs after cardiopulmonary resuscitation
Patrick Meybohm, Matthias Gruenewald, Kai D Zacharowski, Martin Albrecht, Ralph Lucius, Nikola F?sel, Johannes Hensler, Karina Zitta, Berthold Bein
Critical Care , 2010, DOI: 10.1186/cc8879
Abstract: Thirty pigs (28 to 34 kg) were subjected to cardiac arrest following temporary coronary artery occlusion. After seven minutes of ventricular fibrillation and two minutes of basic life support, advanced cardiac life support was started according to the current American Heart Association guidelines. Return of spontaneous circulation was achieved in 21 animals who were randomized to either normothermia at 38°C, hypothermia at 33°C or hypothermia at 33°C combined with sevoflurane (each group: n = 7) for 24 hours. The effects of hypothermia and the combination of hypothermia with sevoflurane on cerebral inflammatory response after cardiopulmonary resuscitation were studied using tissue samples from the cerebral cortex of pigs euthanized after 24 hours and employing quantitative RT-PCR and ELISA techniques.Global cerebral ischemia following resuscitation resulted in significant upregulation of cerebral tissue inflammatory cytokine mRNA expression (mean ± SD; interleukin (IL)-1β 8.7 ± 4.0, IL-6 4.3 ± 2.6, IL-10 2.5 ± 1.6, tumor necrosis factor (TNF)α 2.8 ± 1.8, intercellular adhesion molecule-1 (ICAM-1) 4.0 ± 1.9-fold compared with sham control) and IL-1β protein concentration (1.9 ± 0.6-fold compared with sham control). Hypothermia was associated with a significant (P < 0.05 versus normothermia) reduction in cerebral inflammatory cytokine mRNA expression (IL-1β 1.7 ± 1.0, IL-6 2.2 ± 1.1, IL-10 0.8 ± 0.4, TNFα 1.1 ± 0.6, ICAM-1 1.9 ± 0.7-fold compared with sham control). These results were also confirmed for IL-1β on protein level. Experimental settings employing hypothermia in combination with sevoflurane showed that the volatile anesthetic did not confer additional anti-inflammatory effects compared with hypothermia alone.Mild therapeutic hypothermia resulted in decreased expression of typical cerebral inflammatory mediators after cardiopulmonary resuscitation. This may confer, at least in part, neuroprotection following global cerebral ischemia and resuscitation.Althoug
Effect of norepinephrine dosage and calibration frequency on accuracy of pulse contour-derived cardiac output
Matthias Gruenewald, Patrick Meybohm, Jochen Renner, Ole Broch, Amke Caliebe, Norbert Weiler, Markus Steinfath, Jens Scholz, Berthold Bein
Critical Care , 2011, DOI: 10.1186/cc9967
Abstract: This prospective, observational study was performed with a sample of 73 patients (mean age, 63 ± 13 years) requiring invasive hemodynamic monitoring on a non-cardiac surgery intensive care unit. PCCO was recorded immediately before calibration by COTCP. Bland-Altman analysis was performed on data subsets comparing agreement between PCCO and COTCP according to NE dosage and the time interval between calibrations up to 24 hours. Further, central artery stiffness was calculated on the basis of the pulse pressure to stroke volume relationship.A total of 330 data pairs were analyzed. For all data pairs, the mean COTCP (±SD) was 8.2 ± 2.0 L/min. PCCO had a mean bias of 0.16 L/min with limits of agreement of -2.81 to 3.15 L/min (percentage error, 38%) when compared to COTCP. Whereas the bias between PCCO and COTCP was not significantly different between NE dosage categories or categories of time elapsed between calibrations, interchangeability (percentage error <30%) between methods was present only in the high NE dosage subgroup (≥0.1 μg/kg/min), as the percentage errors were 40%, 47% and 28% in the no NE, NE < 0.1 and NE ≥ 0.1 μg/kg/min subgroups, respectively. PCCO was not interchangeable with COTCP in subgroups of different calibration intervals. The high NE dosage group showed significantly increased central artery stiffness.This study shows that NE dosage, but not the time interval between calibrations, has an impact on the agreement between PCCO and COTCP. Only in the measurements with high NE dosage (representing the minority of measurements) was PCCO interchangeable with COTCP.Cardiac output (CO) monitoring in high-risk patients has gained increasing interest because early detection of hemodynamic instability can reduce morbidity in these patients [1-3]. Investigators in several studies evaluating goal-directed protocols have reported improved outcomes due to immediate treatment to prevent or resolve organ ischemia [4,5]. The PiCCOplus system (Pulsion Medical Syst
Uncalibrated pulse power analysis fails to reliably measure cardiac output in patients undergoing coronary artery bypass surgery
Ole Broch, Jochen Renner, Jan H?cker, Matthias Gruenewald, Patrick Meybohm, Jan Sch?ttler, Markus Steinfath, Berthold Bein
Critical Care , 2011, DOI: 10.1186/cc10065
Abstract: Forty-two patients scheduled for elective coronary surgery were studied after induction of anaesthesia, before and after CPB respectively. Each patient was monitored with the pulse contour cardiac output (PiCCO) system, a central venous line and the recently introduced LiDCO monitoring system. Haemodynamic variables included measurement of CI derived by transpulmonary thermodilution (CITPTD) or CI derived by pulse power analysis (CIPP), before and after calibration (CIPPnon-cal., CIPPcal.). Percentage changes of CI (ΔCITPTD, ΔCIPPnon-cal./PPcal.) were calculated to analyse directional changes.Before CPB there was no significant correlation between CIPPnon-cal. and CITPTD (r2 = 0.04, P = 0.08) with a percentage error (PE) of 86%. Higher mean arterial pressure (MAP) values were significantly correlated with higher CIPPnon-cal. (r2 = 0.26, P < 0.0001). After CPB, CIPPcal. revealed a significant correlation compared with CITPTD (r2 = 0.77, P < 0.0001) with PE of 28%. Changes in CIPPcal. (ΔCIPPcal.) showed a correlation with changes in CITPTD (ΔCITPTD) only after CPB (r2 = 0.52, P = 0.005).Uncalibrated pulse power analysis was significantly influenced by MAP and was not able to reliably measure CI compared with TPTD. Calibration improved accuracy, but pulse power analysis was still not consistently interchangeable with TPTD. Only calibrated pulse power analysis was able to reliably track haemodynamic changes and trends.Measuring left ventricular stroke volume and cardiac index (CI) have gained increasing impact regarding perioperative monitoring of critically ill patients either in the operating theatre or on the intensive care unit. Goal-directed perioperative optimization of left ventricular stroke volume and CI have a positive impact on the morbidity and the length of stay on the intensive care unit [1-4]. Measurement of CI with the pulmonary artery catheter (PAC) is still widely used and often considered as a kind of "gold standard" in different clinical settings [5,
Effects of interventional lung assist on haemodynamics and gas exchange in cardiopulmonary resuscitation: a prospective experimental study on animals with acute respiratory distress syndrome
Günther Zick, Dirk Sch?dler, Gunnar Elke, Sven Pulletz, Berthold Bein, Jens Scholz, Inéz Frerichs, Norbert Weiler
Critical Care , 2009, DOI: 10.1186/cc7716
Abstract: The study was designed to be prospective and experimental. The experiments were performed on 12 anaesthetised and mechanically ventilated pigs (weighing 41 to 58 kg). One femoral artery and one femoral vein were cannulated and connected to an ILA. ARDS was induced by repeated bronchoalveolar lavage. An indwelling pacemaker was used to initiate ventricular fibrillation and chest compressions were immediately started and continued for 30 minutes. In six animals, the ILA was kept open and in the other six it was clamped.Systolic and mean arterial pressures did not differ significantly between the groups. With the ILA open mean ± standard deviation systolic blood pressures were 89 ± 26 mmHg at 5 minutes, 71 ± 28 mmHg at 10 minutes, 63 ± 33 mmHg at 20 minutes and 83 ± 23 mmHg at 30 minutes. The clamped ILA system resulted in systolic pressures of 77 ± 30 mmHg, 90 ± 23 mmHg, 72 ± 11 mmHg and 72 ± 22 mmHg, respectively. In the group with the ILA system open, arterial partial pressure of CO2 was significantly lower after 10, 20 and 30 minutes of CPR and arterial partial pressure of oxygen was higher 20 minutes after the onset of CPR (191 ± 140 mmHg versus 57 ± 14 mmHg). End-tidal partial pressure of CO2 decreased from 46 ± 23 Torr (ILA open) and 37 ± 9 Torr (ILA clamped) before intervention to 8 ± 5 Torr and 8 ± 10 Torr, respectively, in both groups after 30 minutes of CPR.Our results indicate that in an animal model of ARDS, blood pressures were not impaired by keeping the ILA system open during CPR compared with the immediate clamping of the ILA with the onset of CPR. The effect of ILA on gas exchange implied a beneficial effect.Interventional Lung Assist (ILA) describes a technique, which uses a pumpless arteriovenous extracorporeal membrane oxygenator to facilitate carbon dioxide (CO2) removal. Its ability to remove CO2 has been well demonstrated [1-6]. The aim of the extracorporeal CO2 elimination by the ILA system is to decrease the minute ventilation and the peak ins
Postoperative cognitive deficit after cardiopulmonary bypass with preserved cerebral oxygenation: a prospective observational pilot study
Axel Fudickar, S?nke Peters, Claudia Stapelfeldt, G?tz Serocki, J?rn Leiendecker, Patrick Meybohm, Markus Steinfath, Berthold Bein
BMC Anesthesiology , 2011, DOI: 10.1186/1471-2253-11-7
Abstract: cSO2 was measured by near infrared spectroscopy in 35 patients during cardiopulmonary bypass. cSO2 was kept above 80% of baseline and above 55% during anesthesia including cardiopulmonary bypass. POCD was tested by trail making test, digit symbol substitution test, Ray's auditorial verbal learning test, digit span test and verbal fluency test the day before and 5 days after surgery. POCD was defined as a decline in test performance that exceeded - 20% from baseline in two tests or more. Correlation of POCD with lowest cSO2 and cSO2 - threshold were determined explorative.POCD was observed in 43% of patients. Lowest cSO2 during cardiopulmonary bypass was significantly correlated with POCD (p = 0.015, r2 = 0.44, without Bonferroni correction). A threshold of 65% for cSO2 was able to predict POCD with a sensitivity of 86.7% and a specificity of 65.0% (p = 0.03, without Bonferroni correction).Despite a relevant decrease of cerebral oxygen saturation was avoided in our pilot study during cardiopulmonary bypass, incidence of POCD was comparable to that reported in patients without monitoring. A higher threshold for cSO2 may be needed to reduce the incidence of POCD.Neurologic deficits after cardiac surgery are common complications with clinical manifestations ranging from stroke to subtle neurocognitive deficits [1].Postoperative cognitive deficit (POCD) is a frequent complication of cardiac surgery with and without cardiopulmonary bypass (CPB) [2]. In a study by Newman and colleagues a significant cognitive decline, defined as a 20% reduction from baseline, occurred in 53% of patients at discharge, 36% at 6 weeks, 24% at 6 months, and 42% at 5 years [3]. Other authors report an incidence ranging from 8% to 40% [4].Cognitive impairment is associated with lower general health after cardiac surgery with important implications for the care of patients undergoing cardiac surgery [5]. A retrospective examination of the influence of multimodal neuromonitoring on the incidence o
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