Myocardial dysfunction in sepsis – definition and pathogenetic mechanisms

Czech version

Authors: K. Muriová; J. Maláska; F. Otevřel; M. Slezák; M. Kratochvíl; P. Ševčík
Authors‘ workplace: Klinika anesteziologie, resuscitace a intenzivní medicíny Lékařské fakulty MU a FN Brno, pracoviště Bohunice, přednosta prof. MU Dr. Pavel Ševčík, CSc.
Published in: Vnitř Lék 2010; 56(3): 220-225
Category: Reviews

Overview

Sepsis is considered to be the major cause of morbidity and mortality of patients hospitalised in intensive care. It’s defined as a systemic inflammatory response of organism to infection. Incidence of myocardial dysfunction in studies with severe sepsis patients is up to two thirds of patients. Cardiac dysfunction shows a continuum from isolated and mild diastolic dysfunction to combined severe diastolic and systolic failure of both ventricles mimicking even cardiogenic shock in some patients. Typical features of septic myocardial dysfunction (SMD) are decrease in ejection fraction (EF) with dilatation of ventricles, e. g. increase in end‑diastolic volume (EDV). Reversibility of myocardial dysfunction during a period from 7 to 10 days in survivors is other typical manifestation of SMD. Hence, one can speculate that development of such a type of SMD as a temporary protective compensatory mechanism could be advantageous for of an individual patient. A large body of evidence about mechanisms of SMD was described; endothelial dysfunction with consequent microcirculatory and mitochondrial dysfunction and role of circulating factors are considered to be the most important.

Key words:
sepsis – myocardial dysfunction – endothelium – cytokines – NO – mitochondria – troponin – BNP

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