View clinical trials related to Shock.
Filter by:Fluid responsive is defined as increasing in Cardiac output or Stroke volume by 10-15% after fluid challenge. Left ventricular diastolic dysfunction is associated with lower left ventricular end-diastolic volume (LVEDV) resulting in a less cardiac output increment after fluid challenge. However, Left ventricular diastolic function indicated by the Mitral E/e' ratio from transthoracic echocardiography, was rarely studied for fluid responsiveness evaluation.
This study is a prospective, stepped-wedge implementation trial to test the effects of implementing a Clinical Decision Support (CDS) tool for prediction of septic shock in four Emergency Departments within a pediatric healthcare network. The primary outcome will be the proportion of sepsis patients who receive guideline-concordant septic shock care after implementation of the CDS, and the secondary outcome will be time-to-antibiotic after sepsis recognition.
The purpose of this research study is to evaluate whether timely and aggressive temporary Mechanical Circulatory Support (tMCS) through the Impella 5.5® in patients with acute decompensated heart failure complicated by cardiogenic shock (ADHF-CS) has the potential to reduce the HF-CS related clinical events compared to the current standard of care.
Septic shock is associated with a high mortality risk. Fluid overload occurs when fluids are administered to fluid unresponsive patients, but also when inappropriate resuscitation goals are pursued. Alongside, evidence confirms that abnormal peripheral perfusion after resuscitation is associated with increased morbidity and mortality. Targeted resuscitation associates with lower mortality, less organ dysfunction, and less intensity of treatment. Over-resuscitation may contribute to a worse outcome. Many patients remain hypovolemic after initial resuscitation. Others present very low diastolic arterial pressures (DAP) reflecting profound vasoplegia and may benefit from early norepinephrine (NE) instead of fluids. Administering fluids in this setting could increase the risk of fluid overload. In addition, relevant myocardial dysfunction is present in a significant number of patients. Pulse pressure (PP) and DAP evaluation may help clinicians to individualize initial management sparing unnecessary fluid loading. Objective: To test if a CRT-targeted resuscitation based on clinical hemodynamic phenotyping can improve a hierarchical clinical outcome - mortality, time to cessation of vital support, and length of hospital stay, all within 28 days - in septic shock patients as compared to usual care. A2 is a multicenter randomized controlled trial (RCT) comparing a CRT-targeted, hemodynamics-based resuscitation strategy with usual care in patients with early septic shock during a 6 h intervention period. A sample size of 1500 patients was calculated to detect a 6% absolute reduction in mortality in the CRT group, and the win-ratio method will be used to test the superiority in the hierarchical outcomes mentioned above. The combination of a CRT-targeted strategy with a clinical hemodynamic phenotyping may aid to personalize initial resuscitation with potential additional fluid-sparing effects. To categorize patients at baseline according to PP may conduct patients with low PP (<40mmHg) to fluid responsiveness (FR) assessment and eventually fluid boluses, while patients with normal PP will be treated according to DAP, adjusting NE when to avoid further fluids loading in patients who normalize CRT. Fluid resuscitation will be focused on FR+ hypoperfused patients to prevent harmful fluid administration in FR- patients.
Initial fluid resuscitation remains the first treatment step for most children experiencing circulatory failure and/or systemic hypotension. Only one-half of these patients respond to fluid administration by a significant increase in cardiac output. A positive fluid balance is a poor prognostic factor that increases mortality. There are few markers validated in children to assess volume reactivity by dynamic ultrasound parameters mainly based on heart-lung interaction. In this work, the investigators propose to investigate whether dynamic parameters validated in adults, such as the superior vena caval collapsibility and the variability of cardiac output during an end-expiratory and end-inspiratory occlusion, are also reliable indicators of volume responsiveness in sedated children under controlled-mode ventilation.
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.
Septic shock is a common reason for admission to intensive care units and severe infections are responsible for 6 million deaths a year worldwide. Fluid management appears to be a major issue in resuscitation and particularly in septic shock, where generalised oedema is almost systematic and is a major factor in poor prognosis during sepsis. The formation of oedema corresponds to an imbalance, according to Frank-Starling's law of the heart, between the vascular compartment and the interstitial compartment, which is composed of the interstitial liquid and an extracellular matrix. This extracellular matrix consists essentially of a network of collagen and fibroblast fibres. Even though all of the plasma in the body transits through the interstitium in 24 hours and desite its major importance in the microenvironment and intercellular communication, the interstitial compartment has not been fully described. In oncology, interstitial tissue seems to contribute to tumour growth through changes in matrix composition and pressure in the interstitium. This pressure actively contributes to the regulation of transcapillary filtration, and thus to the oedema and hypovolemia observed during sepsis. In usual conditions, the fibroblasts exert a tension on the collagen fibres of the matrix via integrin Beta-1 (ITGB1). This tension is released under the action of pro-inflammatory mediators, resulting in negative pressure which potentiates the formation of oedema. It has been shown in an endotoxemia model that there is a thousandfold higher concentration of ITGB1 in the interstitium compared to the vascular compartment, suggesting a local secretion of this cytokine. The alteration of the extracellular matrix could also play a role in the perpetuation of oedema during septic shock. Considered as an organ in its own right, interstitial tissue is far from playing a passive role between the vascular compartment and the cells. The hypothesis is that interstitial fluid analysis could improve our understanding of the physiopathology of sepsis, in particular on the alteration of the mechanisms of fluid movement regulation, which remains very poorly understood while being closely associated with prognosis in patients with sepsis.
The management of a patient with shock is based on improving tissue oxygenation through hemodynamic optimization. Lactate is a marker of tissue hypoperfusion commonly used in the ICU. In principle, hyperlactatemia can be caused by either increased tissue production (tissue hypoperfusion: type A), decreased lactate uptake (type B), or a combination of both mechanisms. It is important to correctly determine the cause(s) of hyperlactatemia, as this determines the treatment (expanders, inotrope, vasopressor, blood derivative transfusion), and the patient's morbidity and mortality. A classic example of this concept is volume expanders, which are frequently used to correct hyperlactatemia secondary to tissue hypoperfusion, but are associated with mortality if used excessively (fluid overload). In clinical practice, it is difficult to differentiate the exact causes of hyperlactatemia (type A and type B). From work carried out over the last 20 years in septic shock and then in other states of shock and in the operating theatre, it has been shown that the arteriovenous CO2 gradient (pCO2gap) measured from arterial and venous blood gases is a marker of tissue hypoperfusion with better predictive ability than the usual markers (clinical examination, SVO2....). Furthermore, when we relate pCO2gap to the arteriovenous O2 difference (pCO2gap /C(a-v)O2), this ratio allows us to distinguish with greater accuracy between states of acute circulatory failure associated with anaerobiosis (tissue hypoperfusion, type A) and those related to the underlying disease. Also, several studies have demonstrated a strong ability of the pCO2gap and the pCO2gap/CavO2 ratio to predict the severity of shock, mortality of the shock patient, hyperlactatemia, and correction of hyperlactatemia with hemodynamic treatment. As a result, many authors have proposed algorithms for the management of shock patients based on the measurement of these CO2-derived indexes. The hypothesis of this study is that the use of an algorithm based on CO2gap and the CO2gap/CavO2 ratio is superior in terms of correction of hyperlactatemia to usual practice based on clinical and macro-hemodynamics.
Norepinephrine is recommended as first-line vasopressor in critically ill patients, regardless of shock etiology. Its advantages over dopamine and/or epinephrine have been demonstrated, especially by reducing tachycardia events. The current guidelines recommend a mean arterial pressure of at least 65 mmHg that in the resuscitation from sepsis-induced hypoperfusion. Some study reported that delay in initiation of vasopressor therapy was associated with an increase mortality risk in patient with septic shock .The recent experts' opinion suggest that " vasopressors should be started early, before (complete) completion of fluid ressuscitation ". In the event of refractory septic shock, high-dose vasopressors may be used. The precise maximal dose of norepinephrine associated with mortality excess has been poorly studied. High doses have been defined by a cutoff value ranging from 0.5 μg/kg/min to 2 μg/kg/min and recently by 1 μg/kg/min for mortality at 90% and by 0,75 μg/kg/min for mortality at 60%. Furthermore, an increasing vasopressor dosing intensity during the first 24 hours after shock septic was associated with increased mortality depending of fluid administration. If a threshold value of norepinephrine score can be obtained, it could indicate the association with another vasopressor such as vasopressin or surrogates. The primary aim of the present study aimed to confirm if a given norepinephrine dose is associated with mortality. The secondary aims were the link between mortality and norepinephrine duration, cumulative dose in order to build a score that predicts a futility of increasing norepinephrine dose.
Prospective monocentric study designed firstly to estimate the proportion of patients who tolerated the continuation of the COVID-19 2nd injection (absence of anaphylactic manifestations). secondly, to know the proportion of definite anaphylactic reactions in cases of suspected anaphylaxis after the first administration of a COVID-19 vaccine the very complete allergological explorations with both the clinical side, skin tests and biological tests will allow us to highlight the responsibility or not of the components of the vaccine,in particular of the excipients (PEG2000, PS80 and tromethamine) in anaphylactic reactions to COVID-19 vaccines A biological collection will be set up during this clinical study in order to study the immunological mechanisms; the effector cells and the signalling pathways involved in these reactions.