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充血性心力衰竭的病理生理学

Pathophysiology of congestive heart failure.

作者信息

Parmley W W

出版信息

Am J Cardiol. 1985 Jan 11;55(2):9A-14A. doi: 10.1016/0002-9149(85)90790-8.

Abstract

Over the past several years, additional information has been accumulated on the pathophysiology of congestive heart failure. The primary cardiac defect is a decrease in intrinsic contractility of the myocardium, usually brought on by prolonged pressure or volume overload. Several associated biochemical changes have been described, although no precise cause-and-effect relation has been determined. A number of neurohumoral changes occur, which increase systemic vascular resistance. This increased resistance contributes further to a decrease in cardiac output. In fact, many such "compensatory mechanisms" that are initially beneficial may overshoot and produce deleterious hemodynamic effects. Therapeutic interventions such as diuretics, inotropic drugs and vasodilators are frequently helpful by correcting compensatory mechanisms that overshoot.

摘要

在过去几年中,关于充血性心力衰竭的病理生理学已积累了更多信息。主要的心脏缺陷是心肌内在收缩力下降,通常由长期压力或容量超负荷引起。虽然尚未确定确切的因果关系,但已描述了一些相关的生化变化。发生了许多神经体液变化,这些变化会增加全身血管阻力。这种增加的阻力进一步导致心输出量减少。事实上,许多最初有益的此类“代偿机制”可能会过度反应并产生有害的血流动力学效应。利尿剂、强心药物和血管扩张剂等治疗干预措施通常有助于纠正过度反应的代偿机制。

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