View clinical trials related to Shock.
Filter by:the purpose of this study is to assess the effect of norepinephrine and fluid expansion on capillary refill time during septic shock.
Tracheal intubation, which is one of the most commonly performed procedures in the care of critically ill patients in intensive care unit, is associated with a high incidence of complications. Approximately 30% of emergent tracheal intubations in the ICU are associated with complications like hypotension, hypoxia, failed tracheal intubation, esophageal intubation, airway trauma, aspiration, cardiac arrest, and death. An observational study of tracheal intubation practices in critically ill patients across twenty-nine countries found cardiovascular instability to be the commonest among these adverse peri-tracheal intubation event. Tracheal intubation performed in a controlled, non-emergent setting, is associated with few complications. However in ICU, conditions like underlying shock, respiratory failure, metabolic acidosis, and other patho-physiological changes contribute to the increased peri-tracheal intubation complications. Post tracheal intubation hypotension frequently occurs within a few minutes following tracheal intubation. The additive effects of hypovolemia, the suppression of the endogenous activation of sympathetic response by the anesthetics drugs as well as the intrathoracic positive pressure due to mechanical ventilation are implicated in this cardiovascular collapse after tracheal intubation in critically ill patients. Post-tracheal intubation hypotension has been shown to be associated with higher in-hospital mortality and longer ICU and hospital length of stay. Hence patient optimization prior to tracheal intubation may be important to ensure hemodynamic stability to minimize further deterioration during tracheal intubation. Few techniques to optimize hemodynamics before tracheal intubation commonly involve the use of intravenous fluids and vasopressor medications; however, there are no standards of care guiding these practices. Jaber et al included pre tracheal intubation fluid loading (isotonic saline 500 ml or starch 250 ml) as a part of tracheal intubation care bundle management to show improved outcomes. However it was an observational study and also it was not possible to evaluate the contribution of the individual hemodynamic components of the bundle given the concurrent implementation of other interventions. And a recent study by Janz et al showed that pre loading with a 500-mL bolus of crystalloids before tracheal intubation did not identify any benefit. However this trial was stopped early for futility and moreover the volume of intravenous fluids that patients received before enrolment was not recorded. Few trials have used vasopressor bolus prior to tracheal intubation to avoid post tracheal intubation hypotension or use of prophylactic use of vasopressors in preventing post spinal hypotension. However currently, there are no randomized trials or evidence-based guidelines to support the choice between fluid loading or vasopressors for the tracheal intubation of critically ill adults. We would like to conduct a randomised controlled study comparing the effects of fluid bolus or low dose vasopressor given prior to tracheal intubation on post tracheal intubation hypotension among critically ill adults.
Sepsis is a life-threatening organ dysfunction caused by dysregulated host response. A Subset of sepsis is septic shock which has almost 4-6 times the mortality when compared to sepsis. Septic shock has underlying cellular and metabolic abnormalities in addition to circulatory dysfunction. The circulatory dysfunction in sepsis is in the form of severe vasodilatation with high cardiac index. Cirrhosis is a state of hyperdynamic circulation. The mortality of septic shock in these group of patients is still higher. At the onset of septic shock there is initially an increased secretion of Arginine vasopressin. However, this initial rise is short lasting, and the vasopressin levels come back to normal or low serum levels with continued hypotension. However, even normal levels are too low for the degree of hypotension in septic shock. This causes a relative deficiency of vasopressin in septic shock. The exact time when this fall happens is not known and it is likely to be variable. Vasopressin was therefore tried as an agent in septic shock. Terlipressin is a synthetic analogue of vasopressin. It has a greater selectivity for the V1 receptor. Terlipressin is also shown to be effective in septic shock in cirrhotics3. Other vasoactive agents are not preferred in cirrhotics - dopamine due to high risk of arrhythmias and dobutamine as baseline cardiac output of cirrhotics is high which further increases in sepsis and dobutamine would further add to it. However, it may be given in myocardial dysfunction. Noradrenaline is recommended as the first vasopressor to be started in general in septic shock population. No study has compared the effectiveness of vasopressin and Terlipressin when added to noradrenaline in patients with cirrhosis. Acute kidney injury is a very common complication of septic shock in cirrhotics.
In this before-after monocenter study, the authors teste the hypothesis that the implementation of a dedicated shock team could improve the outcome of patients with refractory cardiogenic shock assisted by mechanical circulatory support.
Venovenous extracorporeal membrane oxygenation (VV-ECMO) is a supportive therapy, indicated in case of severe, possibly reversible pulmonary failure, refractory to conventional therapies. Despite advances, morbidity and mortality remain high. Severe neurological complications can occur during ECMO, but their exact etiology is not well understood. It is hypothesized that fast correction of severe hypercapnia, a common indication for venovenous ECMO, may be detrimental for the brain. The supposed mechanism is that fast correction of hypercapnia may result in massive cerebral vasoconstriction and impaired cerebral blood flow (CBF). In this prospective, observational study the aim is to quantify change in CBF during routine initial correction of severe hypercapnia during VV-ECMO. Furthermore, the investigators will record any other hemodynamic changes during VV-ECMO. The hypothesis is that a larger decline in PaCO2 will result in a larger decline of CBF.
Mitral regurgitation may be seen in the setting of cardiogenic shock. Transcatheter edge-to-edge repair (TEER) has been shown to improve outcomes in patients with chronic heart failure. Observational studies suggest improvements in clinical outcomes in patients with mitral regurgitation in the setting of cardiogenic shock; however, there remains a lack of randomized clinical data to support the use of TEER in cardiogenic shock. This study will be a multicenter, open-label, randomized-controlled trial with two study arms: medical therapy and TEER. Patients admitted to the Cardiac Intensive Care Unit (CICU), Cardiac Surgery Intensive Care Unit (CSICU) or Intensive Care Units (ICU) at participating centers will be recruited. The study aims to answer the question: "Does TEER in patients with SCAI stage C or D cardiogenic with concomitant moderate or greater mitral regurgitation improve outcomes as compared to medical therapy?" The study hypothesis is that TEER will lead to an overall improvement in the composite outcome as compared to the medical therapy arm.
Septic shock is a life-threatening condition with mortality rate of up to -40%. Septic shock is catheterized by altered microcirculation that leads to tissue hypoperfusion and ultimately multi-organ dysfunction. Hence, maintenance of adequate tissue perfusion is the mainstay of resuscitation of patients with septic shock. Serum lactate is still considered the gold standard for evaluation of tissue perfusion. Thus, according to the latest definition, elevated serum lactate, as an indicator of tissue hypo-perfusion, is required for diagnosis of septic shock. However, lactate level change in response to resuscitation is slow even in survivors. Capillary refill time (CRT) is a simple method for assessing peripheral perfusion. Monitoring CRT was found to be a good tool for guiding resuscitation and delayed CRT showed good ability in predicting mortality in patients with septic shock. To the best of our knowledge, there is no previous report assessing the reliability of an index that include both serum lactate and CRT (lactate/CRT index) in predicting mortality in patients with septic shock. We hypothesize that the lactate/CRT index would have good accuracy in predicting mortality in patient with septic shock.
Methods:Ten patients were enrolled in the study. Adipose derived-MSCs infusions were given (1x 106/ kg, on 1st, 3rd, 5th, 7th and 9th days of therapy) together with Standard therapy. Before the MSCs applications, blood samples were collected for cytokine assessment (TNF-α, IFN-γ, IL-2, IL-4, IL-6, IL-10). The clinical and laboratory improvements were recorded and compared with control groups selected retrospectively.
The study aims to determine whether the infusion of DEX in septic shock can reduce in-hospital mortality, norepinephrine infusion, need and duration for mechanical ventilation, and acute kidney injury without significant adverse events.
Resuscitation of critically ill patients has changed since the advent of goal directed therapy. Today, practitioners providing fluid resuscitation are attentive of the danger associated with volume depletion while being aware of the morbidity of volume overload. Fluid resuscitation must be rapid, precise, and individually tailored to each patient based on reliable data obtained by various means inside ICU setting. There is no non-invasive method that can reliably and accurately identify fluid responsiveness. As such, in patients with undifferentiated shock, treatment often involves empiric fluid administration, in the hopes that volume expansion will increase preload, which will then serve to increase cardiac output (CO). However, for patients on the flat portion of the Starling curve, aggressive fluid administration results in no appreciable increase in CO and may be detrimental to hemodynamically unstable patients.