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Critical Care  2002 

Clinical review: Myocardial depression in sepsis and septic shock

DOI: 10.1186/cc1822

Keywords: contractility, cytokine, heart, myocardial depression, nitric oxide

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Sepsis and septic shock have been recognized as an increasingly serious clinical problem, accounting for substantial morbidity and mortality. The past four decades have seen the age-adjusted mortality of sepsis increase from 0.5 to 7 per 100,000 episodes despite major advances in the understanding of its pathophysiology [1]. The incidence of severe sepsis in the United States today is estimated at 750,000 cases per year, resulting in 215,000 deaths annually [2]. The majority of these sepsis patients die of refractory hypotension and of cardiovascular collapse.Sepsis has been defined as the systemic inflammatory response to infection [3]. An infectious stimulus (e.g. endo-toxin or another microbiologic element) induces the release of local and systemic inflammatory mediators, especially tumor necrosis factor alpha (TNF-α) and IL-1β, from monocytes/macrophages and other cells [4]. These cytokines stimulate polymorphonuclear leukocytes, macrophages and endothelial cells to release a number of downstream inflammatory mediators, including platelet activating factor and nitric oxide (NO), further amplifying the inflammatory response. Several anti-inflammatory mediators are also released as part of this amplification cascade; namely, IL-10, transforming growth factor beta and IL-1 receptor antagonist. The relative contribution of these cytokines will determine the severity of the septic episode. If the inflammatory reaction is particularly intense, homeostasis of the cardiovascular system will be disrupted, leading to septic shock. One of the manifestations of cardiovascular dysfunction in septic shock is myocardial depression.The present article reviews the clinical manifestations of cardiac dysfunction in sepsis, from the point of view of both the right and left ventricle, as well as cardiovascular prognostic factors in sepsis and septic shock. We will also review the potential pathophysiologic processes responsible for myocardial depression in sepsis, from the perspecti


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