View clinical trials related to Shock.
Filter by:In shock patients, fluid resuscitation, infusion of vasopressors and transfusion are guided on hemodynamic macrovascular parameters. Analysis of sublingual microcirculation in shock patients is predictive of mortality and organ dysfunction. To optimize the quality of the resuscitation in shock patients, it could be useful to have an assessment of sublingual microcirculation in addition to the macrovascular parameters usually assessed by the nurses. But, this requires to have a monitor of sublingual microcirculation easy to use and to analyze at the bedside. The primary outcome of the present study is to test the ability of visual analysis of sublingual microcirculation by nurses to predict needs for fluid challenge, vasopressors or transfusion in patients in shock. After ICU admission and study inclusion, the nurses in charge of the patient will perform a set of measurements of macrocirculatory and microcirculatory parameters every 4 h during the first three days after ICU admission and before and after every hemodynamic therapeutic intervention, such as fluid challenge, transfusion of red blood cells or change in catecholamine rate. The secondary outcomes are to test 1/ to test the ability of visual analysis of sublingual microcirculation to predict organ dysfunction (SOFA score), and 2/ to evaluate the relationship between hemodynamic macrovascular and microvascular parameters. Intensive care patients in shock who need sedation, mechanical ventilation and invasive hemodynamic monitoring (Pulse Contour Cardiac Output (PiCCO 2 device)) will be included. In addition, patients will be included only when patients will obviously stay more than 24 hours in the ICU.
SHIPSS is a multi-institutional, prospective, controlled, randomized, double-blinded interventional trial that will examine the potential benefits and risks of adjunctive hydrocortisone prescribed for children with fluid and vasoactive-inotropic refractory septic shock. It is hypothesized that adjunctive hydrocortisone will significantly reduce the incidence of new and progressive organ dysfunction (primary outcome) and proportion of children with poor outcomes, defined as death or severely impaired health-related quality of life (HRQL) (secondary outcome), as assessed at 28 days following study enrollment (randomization).
This is a randomized, double blind, single center trial to study of the effects of Ivabradine vs. Placebo on patients hospitalized for Stage D heart failure (HF)/ and cardiogenic shock (CS) who will require continuous infusion of Dobutamine and have developed sinus tachycardia (ST) (heart rate >100 beats/min). The aim of the study will be to assess the potential of Ivabradine to slow ST and improve hemodynamics in patients with stage D HF/CS on Dobutamine treatment.
To collect retrospective clinical outcomes related to acute decompensated heart failure cardiogenic shock, acute myocardial infarction cardiogenic shock and compare current versus historical survival rates. To collect Inova Heart and Vascular Institute (IHVI) site specific outcomes before and after initiation of the Cardiogenic Shock team on January 1, 2017. To collect outcomes related to implementation of mechanical circulatory support versus no circulatory intervention and type of intervention (extracorporeal membrane oxygenation (ECMO) versus intracorporeal axial-flow (Impella). • Assess survival at three time points.
Consecutive patients with ACLF (Acute on Chronic Liver Failure) and septic shock with AKI (Acute Kidney Injury) who give written informed consent will be included in this prospective trial at ILBS. At baseline s, endotoxin levels, NT-Pro BNP, , urine N-GAL will be done for all patients. A 10 ml serum sample will be stored for doing a cytokine profile. Septic shock will be defined by the presence of two or more diagnostic criteria for the systemic inflammatory response syndrome, proven or suspected infection with hypotension non-responsive to adequate fluid resuscitation assessed by no evidence of stroke volume variation on flow track and need of a vasopressor to achieve a target mean arterial pressure (MAP) of ≥ 65 mm Hg. A record of CVP, IVC diameter and B-lines on ultrasound lung would also be done. Patients with age less than 18 years, severe known cardiopulmonary disease (structural or valvular heart disease, coronary artery disease, COPD) pregnancy, chronic kidney disease, patients already meeting emergency criteria for immediate hemodialysis at the time of randomization as specified in the late group, patients transferred from other hospitals who have already been on hemodialysis before their arrival in the intensive care unit, extremely moribund patients with an expected life expectancy of less than 24 hours, failure to give informed consent from family members.
In guidelines norepinephrine is the first line vasopressor recommended in case of septic shock. Use of vasopressin is recommended when norepinephrine fails to maintain a mean arterial pressure above 65mmHg or in salvage. Several studies failed to show a superiority of vasopressin over norepinephrine but none evaluated the effect of an early association on organ failure. Terlipressin is a pro-drug of vasopressin which has the same vasoconstrictor effect. We hypothesize that the early association of terlipressin and norepinephrine during septic shock reduces organ failure. This bi centric, double-blinded, randomised, controlled versus placebo study includes 40 patients. Randomisation will be stratified between centers (two university affiliated intensive care units of Assistance-Publique-Hôpitaux de Marseille, Marseille, France). All patients with septic shock needing more than 0,5µg/kg/min of norepinephrine to reach PAM objectives are randomised, after hemodynamic evaluation and optimisation, to receive continuous infusions of terlipressin (0,01mg/kg/min) or placebo (physiologic serum). The 2 groups receive steroid therapy (continuous intravenous hydrocortisone perfusion) at this time. Clinicians are blinded of perfusion used. Use of terlipressin remains possible in salvage when patients need more of 1µg/kg/min of norepinephrine on physician's decision. Patients with acute ischemic or septic heart failure are excluded of the study. Primary objective is sepsis related Sequential Organ Failure Assessment (SOFA) score difference between the groups at day 3. Secondary objectives are mortality at day 28, lactates clearance in the first 48hours, renal function (evaluates with AKIN criteria) and use of renal replacement therapy.
International, observational registry to investigate the outcome in patients with cardiogenic shock. The primary aim of this study is to investigate the clinical outcome of patients in cardiogenic shock.
The classic physiopathology of cardiogenic shock is explained by a systolic ventricular failure, responsible for a decrease in cardiac output associated with high systemic vascular resistances (SVR). This theory is currently challenged in light of the data collected in the SHOCK study, which assessed outcome of early revascularization versus initial medical stabilization, in cardiogenic shock following myocardial infarction.13 A sub-study highlighted depressed SVR in the population with ischemic cardiogenic shock, related to a systemic inflammatory response syndrome.14 Furthermore, mean FEVG was 30% in the SHOCK trial,13 with a similar distribution with post myocardial infarction heart failure patients without signs of shock.15-19 Thus, alteration of myocardial contractility can be only moderate in cardiogenic shock and isn't the only cause responsible for the hemodynamic instability.20 Recent studies suggest the important roles of the peripheral vascular system and neurohormonal system in the genesis and prolongation of cardiogenic shock.12 Vasodilation caused by nitrous oxide synthase activation27 explains the absence of compensating vasoconstriction observed during the SHOCK trial13, and leads to decreased systemic and coronary perfusion, thus increasing myocardial ischemia and initial ventricular dysfunction. 28,29 Cotter et al. conducted an interesting study of hemodynamic evaluation of various cardiac conditions where they observed a significant variability in the peripheral vascular status, with systemic vascular resistances collapsed in certain patients (similar to those observed in septic shock) and rather close to normal or very high resistances in other patients.21 However these data were obtained from a selected group of patients without differentiating the etiology of cardiogenic shock. Finally, the majority of available studies were limited to cardiogenic shock whose etiology was myocardial infarction. Therapeutic management of cardiogenic shock is based in first intention on an inotropic support by Dobutamine.11,23 However, better outcomes on contractility and microcirculatory state have been observed with the use of a vasopressor support by Norepinephrine, suggesting the importance of SVR decreasing in genesis of cardiogenic shock.14,24 Recent reviews showed very few data on inotropic treatment and association with vasopressor support,22 hence the low level of recommendations in current guidelines.11,23 So far it is crucial to accurately characterize hemodynamic status and in particular the systemic vascular resistance for patients with cardiogenic shock. Important variabilities in hemodynamic profiles observed in Cooter's trial could explain the difficulty in defining an optimal therapeutic strategy. the investigators hypothesize that the hemodynamic profile, particularly SVR, of patients with cardiogenic shock is different depending on their etiology. Ischemic cardiogenic shock should be characterized by lower SVR, in relation to a major role of systemic inflammatory response syndrome. On the contrary, non-ischemic cardiogenic shock could be associated with normal or elevated SVR, and thus could explain the variability in distribution of SVR.
Comparison of volumetric measurements obtained by three dimensional echocardiography with measurements obtained by thermodilution using a pulmonary artery catheter in the intensive care unit.
Hemorrhagic shock is a pathologic state in which intravascular volume and oxygen delivery are impaired. During circulatory failure associated with hypovolemia and low cardiac output, redistribution of blood flow caused by increased vasoconstriction results in decreased perfusion of the skin. Skin temperature and capillary refill time has been advocated as a measure of peripheral perfusion.