Gowda Ramesh M, Fox John T, Khan Ijaz A
Division of Cardiology, Beth Israel Medical Center, New York, New York, USA.
Int J Cardiol. 2008 Jan 24;123(3):221-8. doi: 10.1016/j.ijcard.2006.03.099. Epub 2007 Nov 26.
Cardiogenic shock is a state of tissue hypoperfusion induced by heart failure after correction of preload. There are no clear numerical cutoffs to define of the hemodynamic parameters of cardiogenic shock but it is usually characterized by low blood pressure (systolic blood pressure <90 mmHg or a drop in mean blood pressure >30 mmHg, both with a heart rate >60 bpm) with low urine output (<0.5 ml/kg/h), with or without evidence of organ congestion. Acute myocardial infarction is the most common cause. Mortality is high but intra-aortic balloon counterpulsation and early coronary interventions have improved the outcome. Activation of inflammatory response resulting in expression of inducible nitric oxide synthase, activation of inflammatory cytokines, and activation of complement system appear to play an important role in the pathogenesis and outcome of cardiogenic shock. Nitric oxide synthase inhibitors and C5 complement inhibitors are being investigated as potentially useful agents for the treatment of cardiogenic shock. Historical perspective, epidemiology, etiology, pathophysiology, risk predictors, and management of cardiogenic shock are described in this review.
心源性休克是一种在纠正前负荷后由心力衰竭引起的组织灌注不足状态。目前尚无明确的数值界限来定义心源性休克的血流动力学参数,但其通常表现为低血压(收缩压<90 mmHg或平均血压下降>30 mmHg,心率均>60次/分钟)伴少尿(<0.5 ml/kg/h),伴有或不伴有器官淤血证据。急性心肌梗死是最常见的病因。死亡率很高,但主动脉内球囊反搏和早期冠状动脉介入治疗改善了预后。炎症反应的激活导致诱导型一氧化氮合酶的表达、炎性细胞因子的激活以及补体系统的激活,似乎在心源性休克的发病机制和预后中起重要作用。一氧化氮合酶抑制剂和C5补体抑制剂正在作为治疗心源性休克的潜在有用药物进行研究。本文综述了心源性休克的历史背景、流行病学、病因、病理生理学、风险预测因素及管理。