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Mechanisms of Decreased Cardiac Function in Sepsis

  • Conference paper
Yearbook of Intensive Care and Emergency Medicine 1997

Part of the book series: Yearbook of Intensive Care and Emergency Medicine ((YEARBOOK,volume 1997))

Abstract

Sepsis is a very important medical problem occuring in approximately 1% of all hospitalized patients [1] with an incidence of approximately 1500 cases per million per year [2]. The key clinical features of sepsis are largely the result of release of inflammatory mediators so that the accompanying disturbances in organ system physiology are frequently termed the systemic inflammatory response syndrome (SIRS). These clinical signs include fever or hypothermia, tachycardia, and tachypnea as well as evidence of dysfunction of multiple organ systems [1]. Dysfunction of the cardiovascular system occurs in 40% of patients with sepsis [3, 4]. Mortality rate increases from 20 to 30% in sepsis without cardiovascular dysfunction [3, 5] to approximately 40-70% in septic shock [3, 6]. Cardiovascular dysfunction in sepsis occurs as part of the systemic inflammatory response. The cause of the systemic inflammatory response is complex and involves early exogenous chemical signals (typically bacterial cell wall products) which trigger expression of multiple endogenous signalling cytokines and mediators which, in turn, activate cells involved in the inflammatory response including leukocytes, endothelial cells and even parenchymal cells, which in turn release more signalling cytokines or effector molecules (e.g. lytic enzymes and oxygen free radicals).

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© 1997 Springer-Verlag Berlin Heidelberg

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Walley, K.R. (1997). Mechanisms of Decreased Cardiac Function in Sepsis. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 1997. Yearbook of Intensive Care and Emergency Medicine, vol 1997. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-13450-4_23

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  • DOI: https://doi.org/10.1007/978-3-662-13450-4_23

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-662-13452-8

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