Harris P
Cardiothoracic Institute, University of London.
Br Heart J. 1987 Sep;58(3):190-203. doi: 10.1136/hrt.58.3.190.
A review of the history of our knowledge and understanding of the peripheral oedema of congestive cardiac failure points to the conclusion that an inability of the heart to maintain the arterial pressure is of central importance in this condition. Although the function of the circulation is to perfuse the tissues, the body monitors the adequacy of its perfusion, not not through metabolic messengers carried from the tissues in the blood stream, but by sensing the arterial pressure; and the mechanisms evoked act to maintain the arterial pressure. In the short term this is achieved by autonomic regulation of the heart and blood vessels; in the longer term the arterial pressure is maintained through an increase in the blood volume by a retention of salt and water by the kidney. To support the latter process, intrinsic renal mechanisms are successively magnified by the renin-angiotensin-aldosterone system and by the activities of the sympathetic system and vasopressin. The natriuretic influence mediated through volume receptors and the release of atrial peptide is overruled by the arterial baroreceptors, so that the body maintains the arterial pressure at the expense of an increase in blood volume. In these ways the syndrome of congestive cardiac failure may be regarded as one which arises when the heart becomes chronically unable to maintain an appropriate arterial pressure without support.
心脏无法维持动脉血压在这种情况下至关重要。尽管循环的功能是为组织供血,但身体监测其灌注是否充足,并非通过血液中从组织携带的代谢信使,而是通过感知动脉血压;并且引发的机制会维持动脉血压。短期内这通过心脏和血管的自主调节来实现;从长期来看,通过肾脏潴留盐和水使血容量增加来维持动脉血压。为支持后一过程,肾素 - 血管紧张素 - 醛固酮系统以及交感神经系统和血管加压素的活动会相继放大肾脏的内在机制。通过容量感受器介导的利钠作用和心房肽的释放被动脉压力感受器否决,因此身体以血容量增加为代价维持动脉血压。通过这些方式,充血性心力衰竭综合征可被视为一种当心脏长期无法在无支持的情况下维持适当动脉血压时出现的病症。