View clinical trials related to Acute Circulatory Failure.
Filter by:Tissue perfusion has been identified as an early prognosis factor in patients admitted to intensive care. However, little is known about the effects of different hemodynamic interventions performed in clinical routine on peripheral tissue perfusion. The aim of this work is to study the kinetics of CRT and local skin blood flow following therapeutic intervention (fluid challenge, vasopressor or inotropic drug).
Capillary refill time (CRT) is a clinical sign for diagnosis of acute circulatory failure and response to treatment but is also associated with prognosis in patient with shock. CRT is clinically evaluated by physician with a high risk of inter and intra evaluator variations, depending, for example, on measurement site, pressure applicated or visual evaluation. The investigator hypothesizes that CRT measurement with second generation DICART prototype will be well correlated with clinical measurement.
Shock is a serious complication corresponding to acute circulatory failure resulting in multiorgan failure and death. In order to improve cellular oxygen utilization, several therapies can be used. To select one of them, the monitoring of cardiac output is helpful. However, there are several methods used in current practice in intensive care for evaluating hemodynamic. Currently, in patients with acute circulatory failure, no study has compared the concordance of therapeutic decision-making based on transpulmonary thermodilution or transthoracic echocardiography. The objective of the PICC-ECHO study is thus to assess the concordance of therapeutic decision-making by several experts, based on data from transpulmonary thermodilution or transthoracic echocardiography. Indeed, the investigators hypothesize that performing hemodynamic monitoring based on transpulmonary thermodilution or transthoracic echocardiography does not lead to the same therapeutic management in patients in shock.
Fluid administration is one of the main strategies for patients with acute circulatory failure. However, about half of the patients could not benefit from the fluid administration after the ICU admission. Thus predict the effect of fluid responsiveness is essential. There are sevral indices or tests can be used, such as pulse pressure variation (PPV), end-expiratory occulsion test (EEOT), passive leg raising (PLR), etc. Question of the prevalence of cases in which the different predictive indices of fluid responsiveness in intensive care unit (ICU) are not applicable.
Haemodynamic optimisation is a fundamental step and a daily issue in the management of intensive care patients with acute circulatory failure. Failure to optimise haemodynamics is recognised as a factor associated with morbidity and mortality. Although the first line of treatment is often vascular filling, many studies have found that excessive vascular filling alone is deleterious and leads to increased morbidity and mortality due to pulmonary and interstitial oedema. The use of catecholamines avoids this undue vascular filling. At present, the therapeutic strategy in acute circulatory failure is to perform a personalised "titrated" vascular filling after assessing the need for it. To do this, predictive criteria for the need to continue vascular filling in order to optimise cardiac output and tissue perfusion pressure, particularly by ultrasound, have been developed, notably by transesophageal approach. It also appeared to us that offering an alternative to the transesophageal approach would reduce invasiveness on the one hand, but would also offer an alternative when the transesophageal approach is contraindicated.
Acute circulatory failure (ACF) is a common cause of admission in intensive care unit (ICU). Echocardiography is a widespread tool nowadays for the initial assessment and the hemodynamic monitoring. An interesting data from this exam is the Left ventricular outflow tract (LVOT) velocity time integral (VTI), reflecting stroke volume, and therefore cardiac output. A new tool for automated recording has been developped on the VENUE GE echograph. This study aims at assessing this automated measurement of LVOT VTI compared with the classic manual method.
The outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been declared a public health emergency of international concern. Hospitalized COVID-19-positive patients requiring ICU care is increasing along with the course of epidemic. A large number of these patients developed acute respiratory distress syndrome (ARDS) according to current data. However, the related hemodynamic characteristic has so far been rarely described.
International guidelines recommend Methylene Blue (MB) as a second-line drug in the treatment of norepinephrine refractory vasoplegic shock (VS) after Cardiopulmonary Bypass CPB. Macrocirculatory effects of MB in this setting are now well established but microcirculatory effects of MB remain unknown. The purpose of this study is to assess the micro vascular effects of a single administration of methylene blue (1.5 mg/kg over 30 minutes) for norepinephrine-refractory VS post CPB. Microcirculatory effect will be monitored before and one hour after MB infusion through cutaneous refill time, video microscopy measurements of the sublingual microcirculation and tissue oxygen saturation combined with vascular occlusion test (VOT).
Sepsis is a common life-threatening inflammatory response to infection and is the leading cause of death in the intensive care unit. Septic patients exhibit a complex immunosuppressive response affecting both innate and adaptive components of immunity, with a possible link to nosocomial infections. However, the molecular and cellular mechanisms resulting in secondary immunosuppression remain poorly understood, but may involve the antigen-presenting cells (APC, including dendritic cells and monocytes/macrophages) that link innate and adaptive immunity. Furthermore, the increasing phenotypic and functional heterogeneity of APC subsets raise the question of their respective role in sepsis. We propose to address the pathophysiologal role of APC using systems biology approaches in human sepsis. The objective is to go from low- to high-resolution analysis of APC subset diversity and underlying molecular and functional features in sepsis. The global objective will be reached through: 1. Systematic description and phenotypic analysis of circulating APC subsets in sepsis 2. Association of APC subsets distribution, phenotype and function with severe sepsis physiopathology and relevant clinical outcomes (ICU-acquired infections and death) 3. High-resolution molecular profiling of circulating APC subsets using population level and single cell RNAseq. To this aim, the investigator designed a prospective interventional study in order to collect blood samples at significant time points in patients with sepsis or septic shock (the population of interest) and relevant control subjects, either critically ill patients with non-septic acute circulatory failure or age-matched healthy subjects. The study's intervention is limited to additional blood samples. The risks and constraints are related to additional blood samples (maximum 120mL), which will be performed either from an arterial catheter when present in ICU patients, or from a venous puncture for patients without arterial catheters and for healthy volunteers.
Fluid expansion is the first therapeutic option in patients presenting acute circulatory failure but the duration of its hemodynamic effects (persistency and time of maximal increase in cardiac output) is unknown. This study is seeking to describe in critically ill patients, the time course evolution of cardiac output over a 2-hours period after a fluid expansion. The objectives are: 1. to identify patterns of fluid responsiveness 2. to determine the time when the maximal increase in cardiac output occurs during and a after fluid expansion 3. to compare patients' characteristics between patterns Patients with acute circulatory failure will be recruited as soon as a fluid expansion will be decided by the physician in charge and the effects of fluid expansion on hemodynamic indices (cardiac output, arterial pressure) will be continuously recorded through a transpulmonary thermodilution device over a 2-hours period. No changes in ventilatory settings nor vasopressors or sedatives will be allowed during the study. Patients will be categorized into patterns according to the changes in cardiac output after fluid expansion and their characteristics will be compared.