View clinical trials related to Shock.
Filter by:The study contains the result from a comparison of diagnostic outcomes about lung collapse by using lung ultrasonography as a new diagnostic test compares to fiberoptic bronchoscopy as the standard test.
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.
Haemodynamic insufficiency after birth is seen commonly in babies born prematurely and is associated with adverse outcomes. In current clinical practice, a combination of blood pressure and clinical signs is used to guide therapy. However, blood pressure is a poor surrogate of systemic and organ (brain) blood flow distribution during transitional circulation. This state is characterised by increased peripheral vascular resistance and increased afterload causing myocardial depression and impaired blood flow distribution in spite of 'normal' blood pressure. Echocardiography-Doppler (Echo-D) measurement of superior vena cava (SVC) flow has been proposed as a more clinically relevant marker of circulatory impairment shortly after birth than systemic hypotension. When there is low SVC flow, several small-scale clinical trials have suggested dobutamine as the optimal therapeutic option. However the associations between SVC flow and short- and long- term outcomes are not strong enough to allow SVC flow alone to be the basis for the inclusion of patients into a confirmatory trial to demonstrate the efficacy and safety of dobutamine. NeoCirc-001 - The primary objective is to answer some important questions required for the design of a subsequent placebo-controlled trial (NeoCirc-003), which will evaluate the effectiveness of a new neonatal formulation of dobutamine to treat haemodynamic insufficiency in the first 72 hours after birth in babies born at less than 33 weeks' gestation. Observational data will be collected from this population with a view to determining the degree to which diagnostic measures influence treatment decisions. The primary outcome is death or worst cranial ultrasound (CUS) appearance at or before 36 weeks' gestation. NeoCirc-001A - The primary objective is to estimate the elimination half-life, and consequently the time to steady-state of dobutamine in extremely premature neonates. NeoCirc-001B - The primary objective is to construct a population pharmacokinetic pharmacodynamic model that will be validated using samples collected during the confirmatory trial (NeoCirc-003).
The study measures the plasma and bronchoalveolar lavage fluid concentrations of linezolid in septic shock patients comparing with non-septic shock patients to confirm the impact of septic shock on PK/PD of linezolid.
The study measures the plasma concentrations of imipenem in septic shock patients and non-septic shock patients and observes hypoalbuminemia and the impact of the severity of critical illness on Vd
This study aims to investigate the effect of angiotensin II on microcirculation and peripheral perfusion in patients with septic shock.
Less than ten years after their intial description, the comprehension of Innate Lymphoid Cells (ILCs) biology is rapidly improving. They can be classified into four subgroups (ILCs 1, 2, 3 and NK cells) on the basis of their cytokine production and transcription factor expression. They seem to be players in infectious diseases in animals but their role in human anti-bacterial defense remains unknown. In this prospective work, the investigators will compare ILCs phenotyping in ICU patients managed for a septic shock, comparing them to ICU patients without any infectious disease on their inclusion. The investigators will also make a large immune mapping in all patients, to place ILCs in the global immune depressed state observed in septic patients.
This project aims to determine the feasibility of conducting a randomized controlled trial investigating point of care ultrasound guided resuscitation compared with usual care in the management of shock at the Critical Care Trauma Centre (CCTC) in London Health Science Centre (LHSC).
The current study plants to create a patient registry of patients who present to the emergency department with signs and symptoms of shock and evaluate the ability of a multi-step cardiopulmonary ultrasound protocol to determine the need for fluid therapy.
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.