Poole-Wilson P A
Cardiothoracic Institute, London, United Kingdom.
Am J Cardiol. 1988 Aug 11;62(5):4C-8C. doi: 10.1016/s0002-9149(88)80060-2.
The phrase "heart failure" encompasses many clinical entities. The therapeutic principles determining the treatment of these entities vary according to the etiology of congestive heart failure (CHF), the existing hemodynamics, and the mode of action of different drugs. In acute CHF due to myocardial ischemia, intracellular acidosis and the accumulation of phosphate may be the initial underlying causes of contractile failure while, minutes later, lack of high-energy compounds may be an important contributory factor. The cause of contractile failure in chronic syndromes is less well understood. There is evidence for the desensitization of beta receptors on the cell surface but the precise location of the defect is unclear. The receptors may be down-regulated but, in addition, abnormalities have been reported in several other parts of the contractile pathway including the contractile proteins and the sarcoplasmic reticulum. Deficiency of cyclic adenosine monophosphate has also been suggested as a mechanism of contractile failure. In both acute and chronic CHF, there is a redistribution of blood flow to the body organs. Of particular significance is the reduction of blood flow to the kidneys, and a reversal of this defect is one of the major therapeutic objectives. Positive inotropic drugs, vasodilators and drugs altering relaxation of the heart, have been evaluated in the treatment of CHF. Pure inotropic drugs can cause tachycardia, ischemia and "metabolic exhaustion" of the myocardium. The most advantageous profile for an "inotropic" drug in many patients with CHF would be a drug combining systemic vasodilatation, renal vasodilatation, increased relaxation of the myocardium only a mild positive inotropic effect and no chronotropic effect.
“心力衰竭”这一术语涵盖了许多临床病症。决定这些病症治疗方法的治疗原则会根据充血性心力衰竭（CHF）的病因、现有的血流动力学状况以及不同药物的作用方式而有所不同。在因心肌缺血导致的急性CHF中，细胞内酸中毒和磷酸盐蓄积可能是收缩功能衰竭的初始潜在原因，而数分钟后，高能化合物的缺乏可能是一个重要的促成因素。慢性综合征中收缩功能衰竭的病因尚不太清楚。有证据表明细胞表面的β受体存在脱敏现象，但缺陷的确切位置尚不清楚。受体可能下调，但此外，在收缩途径的其他几个部位也报告了异常情况，包括收缩蛋白和肌浆网。环磷酸腺苷缺乏也被认为是收缩功能衰竭的一种机制。在急性和慢性CHF中，都存在血流向身体各器官的重新分布。特别重要的是肾血流量的减少，而纠正这一缺陷是主要的治疗目标之一。正性肌力药物、血管扩张剂和改变心脏舒张的药物已被评估用于CHF的治疗。单纯的正性肌力药物可导致心动过速、心肌缺血和“代谢耗竭”。对于许多CHF患者来说，一种“正性肌力”药物最有利的特性应该是一种兼具全身血管扩张、肾血管扩张、增加心肌舒张但只有轻度正性肌力作用且无变时作用的药物。
