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[脓毒症中的心肌功能障碍——定义与发病机制]

[Myocardial dysfunction in sepsis--definition and pathogenetic mechanisms].

作者信息

Muriová K, Maláska J, Otevrel F, Slezák M, Kratochvíl M, Sevík P

机构信息

Klinika anesteziologie, resuscitace a intenzivnl medicíny Lékarské fakulty MU a FN Brno.

出版信息

Vnitr Lek. 2010 Mar;56(3):220-5.

Abstract

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 ofventricles, 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 ofSMD as a temporary protective compensatory mechanism could be advantageous for of an individual patient. A large body ofevidence about mechanisms ofSMD was described; endothelial dysfunction with consequent microcirculatory and mitochondrial dysfunction and role of circulating factors are considered to be the most important.

摘要

脓毒症被认为是入住重症监护病房患者发病和死亡的主要原因。它被定义为机体对感染的全身性炎症反应。在重症脓毒症患者的研究中,心肌功能障碍的发生率高达三分之二的患者。心脏功能障碍表现为一个连续过程,从孤立的轻度舒张功能障碍到严重的舒张和收缩功能联合衰竭,在某些患者中甚至类似心源性休克。脓毒性心肌功能障碍(SMD)的典型特征是射血分数(EF)降低伴心室扩张,例如舒张末期容积(EDV)增加。幸存者在7至10天内心肌功能障碍的可逆性是SMD的另一个典型表现。因此,可以推测,这种类型的SMD作为一种暂时的保护性代偿机制的发展可能对个体患者有利。关于SMD机制的大量证据已被描述;内皮功能障碍以及随之而来的微循环和线粒体功能障碍以及循环因子的作用被认为是最重要的。

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