Buerke M, Lemm H, Dietz S, Werdan K
University Clinic of Internal Medicine III, Martin Luther University Halle-Wittenberg, Ernst-Grube-Str. 40, 06120, Halle/Saale, Germany.
Herz. 2011 Mar;36(2):73-83. doi: 10.1007/s00059-011-3434-7.
Cardiogenic shock is characterized by inadequate tissue perfusion due to cardiac dysfunction, and it is often caused by acute myocardial infarction. The mortality rate in patients with cardiogenic shock is still very high (i.e., 50-60%). The pathophysiology of cardiogenic shock involves a vicious spiral circle: ischemia causes myocardial dysfunction, which in turn aggravates myocardial ischemia. Myocardial stunning and/or hibernating myocardium can enhance myocardial dysfunction, thus, worsening the cardiogenic shock. Low perfusion pressures with global ischemia leads to multiorgan dysfunction. Ischemia and reperfusion can result in systemic inflammation or within the first few days sepsis due to the translocation of bacteria or bacterial toxins from the intestines, which can result in increased mortality. The key to an optimal treatment of cardiogenic shock patients is a structured approach: (1) rapid diagnosis and prompt initiation of therapy to increase blood pressure and augment cardiac output with subsequently improved perfusion. (2) Rapid coronary revascularization is of critical importance. Using this approach, mortality can be reduced. In many hospitals, initial stabilization is achieved by intraaortic balloon counterpulsation (IABP). However, evidence for improved survival from randomized studies on the use of IABP in combination with PCI is lacking. (3) In order to achieve adequate perfusion, dobutamine and sometimes in combination with norepinephrine might be necessary. Recent studies have shown that the calcium sensitizer levosimendan in cardiogenic shock can be a useful addition to medical therapy. In this overview, epidemiology, pathophysiology, and guideline-oriented treatment strategies for cardiogenic shock are presented.
心源性休克的特征是由于心脏功能障碍导致组织灌注不足，通常由急性心肌梗死引起。心源性休克患者的死亡率仍然很高（即50%-60%）。心源性休克的病理生理学涉及一个恶性循环：缺血导致心肌功能障碍，进而加重心肌缺血。心肌顿抑和/或冬眠心肌可加重心肌功能障碍，从而使心源性休克恶化。全身缺血导致的低灌注压力会导致多器官功能障碍。缺血和再灌注可导致全身炎症反应，或在最初几天因肠道细菌或细菌毒素移位而引发脓毒症，这可能导致死亡率增加。优化治疗心源性休克患者的关键是采用结构化方法：（1）快速诊断并迅速开始治疗，以提高血压、增加心输出量，进而改善灌注。（2）快速进行冠状动脉血运重建至关重要。采用这种方法可降低死亡率。在许多医院，通过主动脉内球囊反搏（IABP）实现初始稳定。然而，关于IABP联合PCI使用的随机研究缺乏改善生存的证据。（3）为了实现充分灌注，可能需要使用多巴酚丁胺，有时还需联合去甲肾上腺素。最近的研究表明，钙增敏剂左西孟旦可作为心源性休克药物治疗的有益补充。本综述介绍了心源性休克的流行病学、病理生理学和以指南为导向的治疗策略。
