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Search Results: 1 - 10 of 9826 matches for " Patrick Meybohm "
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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.
Aprotinin May Increase Mortality in Low and Intermediate Risk but Not in High Risk Cardiac Surgical Patients Compared to Tranexamic Acid and ε-Aminocaproic Acid – A Meta-Analysis of Randomised and Observational Trials of over 30.000 Patients
Patrick Meybohm, Eva Herrmann, Julia Nierhoff, Kai Zacharowski
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0058009
Abstract: Background To compare the effect of aprotinin with the effect of lysine analogues (tranexamic acid and ε-aminocaproic acid) on early mortality in three subgroups of patients: low, intermediate and high risk of cardiac surgery. Methods and Findings We performed a meta-analysis of randomised controlled trials and observational with the following data sources: Medline, Cochrane Library, and reference lists of identified articles. The primary outcome measure was early (in-hospital/30-day) mortality. The secondary outcome measures were any transfusion of packed red blood cells within 24 hours after surgery, any re-operation for bleeding or massive bleeding, and acute renal dysfunction or failure within the selected cited publications, respectively. Out of 328 search results, 31 studies (15 trials and 16 observational studies) included 33,501 patients. Early mortality was significantly increased after aprotinin vs. lysine analogues with a pooled risk ratio (95% CI) of 1.58 (1.13–2.21), p<0.001 in the low (n = 14,297) and in the intermediate risk subgroup (1.42 (1.09–1.84), p<0.001; n = 14,427), respectively. Contrarily, in the subgroup of high risk patients (n = 4,777), the risk for mortality did not differ significantly between aprotinin and lysine analogues (1.03 (0.67–1.58), p = 0.90). Conclusion Aprotinin may be associated with an increased risk of mortality in low and intermediate risk cardiac surgery, but presumably may has no effect on early mortality in a subgroup of high risk cardiac surgery compared to lysine analogues. Thus, decisions to re-license aprotinin in lower risk patients should critically be debated. In contrast, aprotinin might probably be beneficial in high risk cardiac surgery as it reduces risk of transfusion and bleeding complications.
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,
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,
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
Methylene Blue Modulates Transendothelial Migration of Peripheral Blood Cells
Isabella Werner, Fengwei Guo, Nicolai V. Bogert, Ulrich A. Stock, Patrick Meybohm, Anton Moritz, Andres Beiras-Fernandez
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0082214
Abstract: Vasoplegia is a severe complication after cardiac surgery. Within the last years the administration of nitric oxide synthase inhibitor methylene blue (MB) became a new therapeutic strategy. Our aim was to investigate the role of MB on transendothelial migration of circulating blood cells, the potential role of cyclic cGMP, eNOS and iNOS in this process, and the influence of MB on endothelial cell apoptosis. Human vascular endothelial cells (HuMEC-1) were treated for 30 minutes or 2 hours with different concentrations of MB. Inflammation was mimicked by LPS stimulation prior and after MB. Transmigration of PBMCs and T-Lymphocytes through the treated endothelial cells was investigated. The influence of MB upon the different subsets of PBMCs (Granulocytes, T- and B-Lymphocytes, and Monocytes) was assessed after transmigration by means of flow-cytometry. The effect of MB on cell apoptosis was evaluated using Annexin-V and Propidium Iodide stainings. Analyses of the expression of cyclic cGMP, eNOS and iNOS were performed by means of RT-PCR and Western Blot. Results were analyzed using unpaired Students T-test. Analysis of endothelial cell apoptosis by MB indicated a dose-dependent increase of apoptotic cells. We observed time- and dose-dependent effects of MB on transendothelial migration of PBMCs. The prophylactic administration of MB led to an increase of transendothelial migration of PBMCs but not Jurkat cells. Furthermore, HuMEC-1 secretion of cGMP correlated with iNOS expression after MB administration but not with eNOS expression. Expression of these molecules was reduced after MB administration at protein level. This study clearly reveals that endothelial response to MB is dose- and especially time-dependent. MB shows different effects on circulating blood cell-subtypes, and modifies the release patterns of eNOS, iNOS, and cGMP. The transendothelial migration is modulated after treatment with MB. Furthermore, MB provokes apoptosis of endothelial cells in a dose/time-dependent manner.
Dynamic and Volumetric Variables Reliably Predict Fluid Responsiveness in a Porcine Model with Pleural Effusion
Ole Broch, Matthias Gruenewald, Jochen Renner, Patrick Meybohm, Jan Sch?ttler, Katharina He?, Markus Steinfath, Berthold Bein
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056267
Abstract: Background The ability of stroke volume variation (SVV), pulse pressure variation (PPV) and global end-diastolic volume (GEDV) for prediction of fluid responsiveness in presence of pleural effusion is unknown. The aim of the present study was to challenge the ability of SVV, PPV and GEDV to predict fluid responsiveness in a porcine model with pleural effusions. Methods Pigs were studied at baseline and after fluid loading with 8 ml kg?1 6% hydroxyethyl starch. After withdrawal of 8 ml kg?1 blood and induction of pleural effusion up to 50 ml kg?1 on either side, measurements at baseline and after fluid loading were repeated. Cardiac output, stroke volume, central venous pressure (CVP) and pulmonary occlusion pressure (PAOP) were obtained by pulmonary thermodilution, whereas GEDV was determined by transpulmonary thermodilution. SVV and PPV were monitored continuously by pulse contour analysis. Results Pleural effusion was associated with significant changes in lung compliance, peak airway pressure and stroke volume in both responders and non-responders. At baseline, SVV, PPV and GEDV reliably predicted fluid responsiveness (area under the curve 0.85 (p<0.001), 0.88 (p<0.001), 0.77 (p = 0.007). After induction of pleural effusion the ability of SVV, PPV and GEDV to predict fluid responsiveness was well preserved and also PAOP was predictive. Threshold values for SVV and PPV increased in presence of pleural effusion. Conclusions In this porcine model, bilateral pleural effusion did not affect the ability of SVV, PPV and GEDV to predict fluid responsiveness.
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