Publications by authors named "M Flick"

Most postoperative deaths occur on general wards, often linked to complications associated with untreated changes in vital signs. Monitoring in these units is typically intermittent checks each shift or maximally every 4-6 h, which misses prolonged periods of subtle changes in physiology that can herald a critical downstream event. Continuous monitoring of vital signs is therefore intuitively necessary for patient safety.

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Background: Intraoperative hypotension is associated with acute kidney injury (AKI). Clinicians thus frequently use vasopressors, such as norepinephrine, to maintain blood pressure. However, vasopressors themselves might promote AKI.

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Cardiac output can be estimated non-invasively by electrical cardiometry with the ICON® monitor (Osypka Medical GmbH, Berlin, Germany). Conflicting results have been reported regarding the cardiac output measurement performance of electrical cardiometry. In this prospective method comparison study, we compared cardiac output measured using electrical cardiometry (EC-CO; test method) with cardiac output measured using intermittent pulmonary artery thermodilution (PATD-CO; reference method) in patients after coronary artery bypass graft (CABG) surgery.

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Study Objective: We hypothesize that personalized perioperative blood pressure management maintaining intraoperative mean arterial pressure (MAP) above the preoperative mean nighttime MAP reduces perfusion-related organ injury compared to maintaining intraoperative MAP above 65 mmHg in patients having major non-cardiac surgery. Before testing this hypothesis in a large-scale trial, we performed this bicentric pilot trial to determine a) if performing preoperative automated nighttime blood pressure monitoring to calculate personalized intraoperative MAP targets is feasible; b) in what proportion of patients the preoperative mean nighttime MAP clinically meaningfully differs from a MAP of 65 mmHg; and c) if maintaining intraoperative MAP above the preoperative mean nighttime MAP is feasible in patients having major non-cardiac surgery.

Design: Bicentric pilot randomized trial.

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Impaired secretion of an essential blood coagulation factor fibrinogen leads to hepatic fibrinogen storage disease (HFSD), characterized by the presence of fibrinogen-positive inclusion bodies and hypofibrinogenemia. However, the molecular mechanisms underlying the biogenesis of fibrinogen in the endoplasmic reticulum (ER) remain unexplored. Here we uncover a key role of SEL1L-HRD1 complex of ER-associated degradation (ERAD) in the formation of aberrant inclusion bodies, and the biogenesis of nascent fibrinogen protein complex in hepatocytes.

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