Cardiogenic shock complicating acute myocardial infarction - Expanding the paradigm
Cardiogenic shock complicating acute myocardial infarction - Expanding the paradigm
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DOI：
10.1161/01.cir.0000075927.67673.f2
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发表时间：
2003-06-24
期刊：
影响因子：
37.8
通讯作者：
Hochman, JS
中科院分区：
文献类型：
--
作者：
Hochman, JS
2998扩张型心肌病和轻度至中度慢性CHF的EF通常远低于此值，并且不会休克。12这些观察结果强调了心室扩张在维持慢性CHF的每搏输出量和外周血管和神经激素适应中的作用。然而，EF低于30 s在无CHF的无并发症近期MI患者中并不罕见。13在SHOCK登记研究和试验中，许多患者并未证实CO急性减少导致代偿性血管收缩的经典观点（Menon等14和Hochman等，未发表数据，2002）。SVR变化很大，但平均在1350 - 1400达因· s· cm 5时，尽管使用血管加压药，SVR仍没有升高。Cotter等15，16根据心脏功率对急性心力衰竭患者进行分类，并证明其在风险分层和治疗选择中的重要性。心功是心脏指数和平均动脉压的乘积，是慢性心力衰竭的一个有用的预后指标。17 SVR非常高且CO降低的急性心力衰竭患者具有高心功率指数，而大多数休克患者具有低心功率。在SHOCK试验和SHOCK登记研究中，心脏功率是与死亡率最密切相关的血流动力学变量。18 SHOCK登记研究中的一小部分患者根据全身灌注不足、低CO和心室充盈压升高，临床诊断为CS，无低血压。在这些患者中，血压通过SVR升高来维持。[14]尽管两组患者的LVEF（34%）、心脏指数（1.9 L/min/m2）和肺毛细血管楔压（25 mm Hg）相同，但他们的住院死亡率（尽管高达43%）低于经典扩张性休克患者的死亡率（66%）。血管收缩供应非生命器官的血管床的能力是对CO减少的重要代偿反应。血管扩张剂（内源性和外源性）干扰这种关键反应，这是维持脑和冠状动脉循环所需的。心脏功率在医学上也很重要，因为它反映了在面对高阻力时足以产生流量的心肌储备，尽管会减少。在随机SHOCK试验中，在许多确诊休克并发急性MI的患者中观察到临床上明显的全身炎症反应综合征，表现为发热、白色血细胞计数升高和低SVR。这些发现通常导致疑似脓毒症的二级临床诊断。然而，尽管使用血管加压药，但在休克发作时（疑似脓毒症前数天）记录到低SVR。19当40%的LV不可逆损伤时发生CS的经典概念与以下观察结果不一致：（1）接受早期血运重建的患者的存活率为50%，（2）血运重建后某些患者的EF改善的证据，11和
2998 dilated cardiomyopathy and mild to moderate chronic CHF often have EFs considerably lower than this and are not in shock. 12 These observations highlight the role of ventricular dilation to maintain stroke volume and peripheral vascular and neurohormonal adaptation in chronic CHF. However, an EF in the low 30s is not uncommon in uncomplicated patients with recent MI who do not have CHF. 13 The classic notion that acute reduction in CO leads to compensatory vasoconstriction was not confirmed in many patients in the SHOCK registry and trial (Menon et al14 and Hochman et al, unpublished data, 2002). SVR varied widely but on average was not elevated at 1350 to 1400 dyne· s· cm 5 despite vasopressor use. Cotter et al15, 16 categorized acute heart failure patients according to cardiac power and demonstrated its importance in risk stratification and selection of therapy. Cardiac power, the product of cardiac index and mean arterial pressure, is a useful prognostic indicator in chronic heart failure. 17 Acute heart failure patients with very high SVR and reduced CO have high cardiac power indices, in contrast to most shock patients, who have low cardiac power. In both the SHOCK trial and the SHOCK registry, cardiac power was the hemodynamic variable most strongly associated with mortality. 18 A small subset of patients in the SHOCK registry was clinically diagnosed with CS without hypotension, based on systemic hypoperfusion, low CO, and elevated ventricular filling pressures. In these patients, blood pressure was maintained by elevated SVR. 14 Their in-hospital mortality rate (although high at 43%) was lower than the rate of those patients with classic hypotensive shock (66%), despite the 2 groups having the same LVEF (34%), cardiac index (1.9 L/min per m2), and pulmonary capillary wedge pressure (25 mm Hg). The ability to vasoconstrict vascular beds that supply nonvital organs is an important compensatory response to a reduction in CO. Vasodilators (endogenous and exogenous) interfere with this critical response, which is needed to maintain flow to the cerebral and coronary circulations. Cardiac power is also prognostically important because it reflects myocardial reserve adequate to generate flow, albeit reduced, in the face of high resistance. A clinically overt systemic inflammatory response syndrome as evidenced by fever, elevated white blood cell count, and low SVR, was observed in many patients with confirmed shock complicating acute MI in the randomized SHOCK trial. These findings often led to a secondary clinical diagnosis of suspected sepsis. However, the low SVR despite vasopressors was documented at shock onset, days before sepsis was suspected. 19 The classic notion that CS develops when 40% of the LV is irreversibly damaged is inconsistent with the following observations:(1) survival of 50% of patients who undergo early revascularization,(2) evidence of improved EF in some patients following revascularization, 11 and