Myocardial Dysfunction and Shock after Cardiac Arrest.

Myocardial Dysfunction and Shock after Cardiac Arrest.
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DOI:
10.1155/2015/314796
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发表时间:
2015
影响因子:
--
通讯作者:
Dezfulian C
Dezfulian C
中科院分区:
生物学3区
文献类型:
--
作者:
Jentzer JC;Chonde MD;Dezfulian C

文献摘要

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静息后心肌功能障碍包括心脏骤停后低心输出量或心室收缩或舒张功能障碍的发展。据报道,心脏骤停后复苏的患者中有近三分之二的人左心室收缩功能受损。心脏骤停后需要血管加压药支持的低血压和休克同样常见。尽管需要血管加压药支持的休克与心脏骤停后的不良结局一致相关,但心肌功能障碍与结局之间的相关性尚不明确。心脏骤停后的心肌功能障碍和休克是由于先前存在的心脏病理加上复苏造成的多次叠加损伤而发生的。病理生理学涉及心血管缺血/再灌注损伤和心血管毒性,这些毒性来自过量水平的炎性细胞因子活化和儿茶酚胺等促成因素。类似的机制发生在心肺转流术后的心肌功能障碍、败血症和应激性心肌病中。心脏骤停复苏后的血流动力学稳定包括恢复前负荷、血管加压药支持动脉压,以及必要时的正性肌力支持,以逆转心肌功能障碍的影响并改善全身灌注。需要进一步的研究来确定休息后心肌功能障碍对心脏骤停结局的作用,并确定治疗策略。
Postarrest myocardial dysfunction includes the development of low cardiac output or ventricular systolic or diastolic dysfunction after cardiac arrest. Impaired left ventricular systolic function is reported in nearly two-thirds of patients resuscitated after cardiac arrest. Hypotension and shock requiring vasopressor support are similarly common after cardiac arrest. Whereas shock requiring vasopressor support is consistently associated with an adverse outcome after cardiac arrest, the association between myocardial dysfunction and outcomes is less clear. Myocardial dysfunction and shock after cardiac arrest develop as the result of preexisting cardiac pathology with multiple superimposed insults from resuscitation. The pathophysiology involves cardiovascular ischemia/reperfusion injury and cardiovascular toxicity from excessive levels of inflammatory cytokine activation and catecholamines, among other contributing factors. Similar mechanisms occur in myocardial dysfunction after cardiopulmonary bypass, in sepsis, and in stress-induced cardiomyopathy. Hemodynamic stabilization after resuscitation from cardiac arrest involves restoration of preload, vasopressors to support arterial pressure, and inotropic support if needed to reverse the effects of myocardial dysfunction and improve systemic perfusion. Further research is needed to define the role of postarrest myocardial dysfunction on cardiac arrest outcomes and identify therapeutic strategies.