Rude R E
Adv Shock Res. 1983;10:35-49.
Cardiogenic shock is a relatively specific clinical syndrome characterized by decreased cardiac output, elevated left ventricular filling pressure, and arterial hypotension with vital organ hypoperfusion. It most commonly occurs as the consequence of extensive left ventricular damage due to myocardial infarction. The prognosis of patients with cardiogenic shock is very poor, because by definition there are no readily correctable metabolic, hemodynamic, humoral, or infectious problems whose treatment may lead to improved circulatory function. Pharmacologic support of the patient with cardiogenic shock plays a major role in clinical management. Diuretics, inotropic agents, and vasodilator drugs all have a place in the management of selected patients with low output states and cardiogenic shock following myocardial infarction. Diuretics such as furosemide may be used to relieve symptoms of pulmonary congestion, but are not effective in reversing hypotension or vital organ hypoperfusion; in advanced shock states with acute renal failure, they may be totally ineffective. The most commonly employed and effective inotropic agents are the sympathomimetic amines dopamine and dobutamine, which have complex effects on important variables in cardiogenic shock, including the heart's inotropic and chronotropic states, myocardial oxygen requirements, left ventricular filling pressure, and peripheral vascular tone. All inotropic agents have the capacity to intensify myocardial ischemia because they may increase myocardial oxygen requirements in the face of limited arterial blood flow; isoproterenol, epinephrine, and norepinephrine appear to be particularly troublesome in this regard. Vasodilator agents (phentolamine, nitroprusside, and nitroglycerin) have also been used to alter left ventricular loading conditions in patients otherwise supported by inotropic drugs, and may be particularly useful in the management of "mechanical" complications of infarction such as mitral regurgitation and interventricular septal rupture. The use of these drugs, just as that of inotropic agents, must be tailored to specific hemodynamic abnormalities documented in individual patients.
心源性休克是一种相对特殊的临床综合征，其特征为心输出量降低、左心室充盈压升高、动脉低血压以及重要器官灌注不足。它最常见于因心肌梗死导致广泛左心室损伤的后果。心源性休克患者的预后非常差，因为从定义上讲，不存在易于纠正的代谢、血流动力学、体液或感染性问题，其治疗可能导致循环功能改善。心源性休克患者的药物支持在临床管理中起着主要作用。利尿剂、正性肌力药物和血管扩张剂在治疗心肌梗死后低输出状态和心源性休克的特定患者中均有应用。呋塞米等利尿剂可用于缓解肺淤血症状，但对逆转低血压或重要器官灌注不足无效；在伴有急性肾衰竭的晚期休克状态下，它们可能完全无效。最常用且有效的正性肌力药物是拟交感胺类药物多巴胺和多巴酚丁胺，它们对心源性休克的重要变量具有复杂影响，包括心脏的正性肌力和变时状态、心肌需氧量、左心室充盈压以及外周血管张力。所有正性肌力药物都有加重心肌缺血的能力，因为在动脉血流有限的情况下它们可能增加心肌需氧量；在这方面，异丙肾上腺素、肾上腺素和去甲肾上腺素似乎尤其棘手。血管扩张剂（酚妥拉明、硝普钠和硝酸甘油）也已用于改变在其他方面接受正性肌力药物支持的患者的左心室负荷情况，并且在治疗梗死的“机械性”并发症如二尖瓣反流和室间隔破裂方面可能特别有用。这些药物的使用，就像正性肌力药物一样，必须根据个体患者记录的特定血流动力学异常情况进行调整。
