SEPSIS AND SEPTIC SHOCK: PATHOPHYSIOLOGICAL AND CARDIOVASCULAR BACKGROUND AS BASIS FOR THERAPY
SEPSIS AND SEPTIC SHOCK: PATHOPHYSIOLOGICAL AND CARDIOVASCULAR BACKGROUND AS BASIS FOR THERAPY
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DOI：
10.1179/acb.2010.070
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发表时间：
2010-09-01
影响因子：
1.6
通讯作者：
Poelaert, J.
中科院分区：
文献类型：
--
作者：
De Kock, I.;Van Daele, C.;Poelaert, J.
脓毒症和脓毒性休克是重症监护病房的常见原因。尽管有先进的治疗方法，发病率和死亡率仍然高得令人无法接受。目的回顾最常见的脓毒症和脓毒性休克的潜在机制，并讨论脓毒症引起的心血管功能障碍。本文简要讨论了脓毒症引起的心肌抑制的治疗策略。脓毒症和感染性休克的发生是多因素的。两个主要的机制有助于血流动力学崩溃。外在和内在机制诱导了一个复杂的级联反应，导致促炎和抗炎介质的释放。当宿主对感染最初的适当反应被放大，然后失调，导致血流动力学和循环改变时，败血症就发生了。促炎介质肿瘤坏死因子α、白细胞介素-1 β和一氧化氮在脓毒症相关性低血压、休克和心肌细胞收缩性抑制中发挥重要作用。脓毒性心功能障碍可以通过多种机制来解释：循环容量的改变，β -肾上腺素能受体的下调，受体后信号通路的抑制，肌浆网钙释放减少，机电耦合受损，肌纤维水平钙敏感性降低。线粒体紊乱似乎在组织损伤和脓毒症相关的多器官功能衰竭中具有重要意义。没有一致的方案治疗败血症和感染性休克。指导方针包括早期目标导向治疗、源头控制和血流动力学支持措施。结论需要进一步的研究来区分这些不同机制的重要性，我们建议进一步的研究工作应该集中在线粒体相关的生物能关闭的恢复上，因为线粒体可能在理解细胞凋亡和保护措施中发挥关键作用。了解脓毒症和感染性休克的病理生理学将不可避免地导致更准确的治疗这些仍然经常致命的综合征。
Introduction Sepsis and septic shock are common causes for admission to intensive care units. The morbidity and mortality remain unacceptably high despite the advanced treatments.Objectives To review the most commonly reported underlying mechanisms of sepsis and septic shock, besides discussion of sepsis-induced cardiovascular dysfunction.Therapeutic strategies for sepsis-induced myocardial depression are briefly discussed.Data synthesis The development of sepsis and septic shock is multifactorial. Two major mechanisms contribute to the haemodynamic collapse. The extrinsic and intrinsic mechanisms induce a complex cascade which results in the release of pro- and anti-inflammatory mediators. Sepsis develops when the initial, appropriate host response to an infection becomes amplified and then dysregulated Leading to haemodynamic and circulatory changes. The pro-inflammatory mediators tumour necrosis factor alpha, interleukin-1 beta and nitric oxide play a significant role in sepsis-related hypotension, shock and depression of cardiomyocyte contractility. Septic cardiac dysfunction can be explained by various mechanisms: changes in circulating volume, down-regulation of beta-adrenergic receptors, depressed post-receptor signalling pathways, reduced calcium release from the sarcoplasmic reticulum and impaired electromechanical coupling and reduced calcium sensibility at the myofibrillar level. Mitochondrial derangement seems to be of great importance in tissue injury and sepsis-associated multi organ failure.There is no consistent protocol for treating sepsis and septic shock. Guidelines include early goal-directed therapy, source control and haemodynamic supportive measures.Conclusion Further studies are needed to distinguish the importance of these various mechanisms: We-recommend that further investigational work should focus on the recovery of the mitochondria-related bio-energetic shut down as the mitochondria could play a key role in the understanding of apoptosis and protective measures. Understanding the pathophysiology of sepsis and septic shock will inevitably lead to a more accurate treatment of these still too often fatal syndromes.