Division of Critical Care Medicine, Cincinnati Children's Hospital Medical Center, and Department of Pediatrics, College of Medicine, University of Cincinnati, Cincinnati, OH 45229, USA.
Int J Mol Sci. 2019 Jul 18;20(14):3523. doi: 10.3390/ijms20143523.
Myocardial dysfunction is common in septic shock and post-cardiac arrest but manifests differently in pediatric and adult patients. By conventional echocardiographic parameters, biventricular systolic dysfunction is more prevalent in children with septic shock, though strain imaging reveals that myocardial injury may be more common in adults than previously thought. In contrast, diastolic dysfunction in general and post-arrest myocardial systolic dysfunction appear to be more widespread in the adult population. A growing body of evidence suggests that mitochondrial dysfunction mediates myocardial depression in critical illness; alterations in mitochondrial electron transport system function, bioenergetic production, oxidative and nitrosative stress, uncoupling, mitochondrial permeability transition, fusion, fission, biogenesis, and autophagy all may play key pathophysiologic roles. In this review we summarize the epidemiologic and clinical phenotypes of myocardial dysfunction in septic shock and post-cardiac arrest and the multifaceted manifestations of mitochondrial injury in these disease processes. Since neonatal and pediatric-specific data for mitochondrial dysfunction remain sparse, conclusive age-dependent differences are not clear; instead, we highlight what evidence exists and identify gaps in knowledge to guide future research. Finally, since focal ischemic injury (with or without reperfusion) leading to myocardial infarction is predominantly an atherosclerotic disease of the elderly, this review focuses specifically on septic shock and global ischemia-reperfusion injury occurring after resuscitation from cardiac arrest.
心肌功能障碍在感染性休克和心搏骤停后很常见,但在儿科和成年患者中的表现不同。通过常规超声心动图参数,感染性休克儿童的双心室收缩功能障碍更为常见,尽管应变成像显示心肌损伤在成人中可能比以前认为的更为常见。相比之下,舒张功能障碍总体上和心搏骤停后心肌收缩功能障碍在成年人群中更为广泛。越来越多的证据表明,线粒体功能障碍介导危重病中的心肌抑制;线粒体电子传递系统功能、生物能产生、氧化和硝化应激、解偶联、线粒体通透性转换、融合、裂变、生物发生和自噬的改变都可能发挥关键的病理生理作用。在这篇综述中,我们总结了感染性休克和心搏骤停后心肌功能障碍的流行病学和临床表型,以及这些疾病过程中线粒体损伤的多方面表现。由于新生儿和儿科特有的线粒体功能障碍数据仍然很少,因此明确的年龄依赖性差异尚不清楚;相反,我们强调了现有的证据,并确定了知识空白,以指导未来的研究。最后,由于导致心肌梗死的局灶性缺血性损伤(有或无再灌注)主要是老年人的动脉粥样硬化性疾病,因此本综述专门关注感染性休克和心脏骤停后复苏时发生的全脑缺血再灌注损伤。