Seminars in respiratory and critical care medicine
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Cardiogenic shock has long been a difficult problem for clinicians. The most common cause is left ventricular pump failure after myocardial infarction, but other important causes include mechanical complications of infarction, right ventricular dysfunction, prolonged cardiopulmonary bypass, valvular disease, and cardiomyopathy. Cardiogenic shock is the leading cause of in-hospital death after myocardial infarction. ⋯ Improved understanding of the pathophysiology of cardiogenic shock has led to renewed emphasis on the notion that stunned or hibernating myocardium may recover function with hemodynamic support and restoration of flow. This concept has underscored the importance of expeditious initiation of supportive measures to maintain blood pressure and cardiac output, including both medications and intraaortic balloon counterpulsation. Finally, the theory that coronary revascularization would be beneficial by reversing the vicious cycle in which ischemia causes myocardial dysfunction, which in turn worsens ischemia, which had been supported by an extensive body of observational and registry studies, has now been strongly buttressed by the results of two randomized, controlled trials, both of which show improved mortality with early revascularization for cardiogenic shock in the setting of acute infarction.
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Shock is a broad category of injury to the human body caused by a variety of insults. Fluid resuscitation is the cornerstone of initial therapy for nearly all forms of shock. This article reviews the basic physiology determining body fluid composition, the goals of fluid resuscitation in shock, the types of fluids available for use, and clinical evidence for use of specific fluids based on etiology of the insult.
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Semin Respir Crit Care Med · Dec 2004
Corticosteroid therapy in patients with severe sepsis and septic shock.
Corticosteroids have been considered for decades for the treatment of severe sepsis and septic shock, based on their pivotal role in the stress response and their hemodynamic and antiinflammatory effects. Whereas short-term therapy with high doses of corticosteroids (up to 42 g hydrocortisone equivalent for 1-2 days) has been ineffective or potentially harmful, prolonged therapy with lower doses (200-300 mg hydrocortisone for 5-7 days or longer) in septic shock has recently revealed beneficial effects in several randomized, controlled trials. Assuming relative adrenal insufficiency (RAI) and peripheral cortisol resistance, treatment with low-dose hydrocortisone improved shock reversal, reduced inflammation, and improved outcome. ⋯ In addition the role of fludrocortisone is uncertain. Nevertheless, based on current data, low-dose hydrocortisone therapy should definitely be considered in vasopressor-dependent septic shock. This review will address some critical points.
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Vasopressin is a hormone that is essential for both osmotic and cardiovascular homeostasis. A deficiency of vasopressin exists in some shock states and replacement of physiological levels of vasopressin can restore vascular tone. ⋯ We then highlight the areas of uncertainty in using vasopressin for septic shock and summarize the reasons for clinical equipoise. We close by suggesting that further randomized controlled trials of vasopressin in septic shock are required before vasopressin is used routinely for management of septic shock.
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Intensive monitoring is a crucial component of the management of shock. However, there is little consensus about optimal strategies for monitoring. ⋯ In addition, there is evolving evidence that targeting and monitoring certain physiological goals may be most important early in the course of shock. In this chapter, we examine many of the available monitoring techniques and the evidence supporting their use.