Guazzi M D, Agostoni P, Perego B, Lauri G, Salvioni A, Giraldi F, Matturri M, Guazzi M, Marenzi G
Istituto di Cardiologia dell'Università degli Studi, Milan, Italy.
Br Heart J. 1994 Dec;72(6):534-9. doi: 10.1136/hrt.72.6.534.
Hypovolaemia stimulates the sympathoadrenal and renin systems and water retention. It has been proposed that in congestive heart failure reduction of cardiac output and any associated decrease in blood pressure cause underfilling of the arterial compartment, which promotes and perpetuates neurohumoral activation and the retention of fluid. This study examined whether an intravascular volume deficit accounts for patterns that largely exceed the limits of a homoeostatic response, which are sometimes seen in advanced congestive heart failure.
In 22 patients with congestive heart failure and water retention the body fluid mass was reduced by ultrafiltration and the neurohumoral reaction was monitored. A Diafilter, which was part of an external venous circuit was regulated to produce 500 ml/hour of ultrafiltrate (mean (SD) 3122 (1199) ml) until right atrial pressure was reduced to 50% of baseline. Haemodynamic variables, plasma renin activity, noradrenaline, and aldosterone were measured before and within 48 hours of ultrafiltration. After ultrafiltration, which produced a 20% reduction of plasma volume and a moderate decrease in cardiac output and blood pressure (consistent with a diminished degree of filling of the arterial compartment), there was an obvious decrease in noradrenaline, plasma renin activity, and aldosterone. In the next 48 hours plasma volume, cardiac output, and blood pressure recovered; the neurohumoral axis was depressed; and there was a striking enhancement of water and sodium excretion with resolution of the peripheral oedema and organ congestion. The neurohumoral changes and haemodynamic changes were not related. There were significant correlations between the neurohumoral changes and increase in urinary output and sodium excretion.
In advanced congestive heart failure arterial underfilling was not the main mechanism for activating the neurohumoral axis and retaining fluid. Because a decrease in circulating hormones was associated with reabsorption of extravascular fluid it is likely that hypoperfusion and/or congestion of organs, such as the kidney and lung, reduce the clearance of circulating noradrenaline and help to keep plasma concentrations of renin and aldosterone raised. A positive feedback loop between fluid retention and plasma hormone concentrations may be responsible for progression of congestive heart failure.
血容量不足会刺激交感肾上腺系统和肾素系统，并导致水潴留。有人提出，在充血性心力衰竭中，心输出量的降低以及任何相关的血压下降会导致动脉腔充盈不足，从而促进并维持神经体液激活和液体潴留。本研究探讨了血管内容量不足是否能解释在晚期充血性心力衰竭中有时会出现的、大大超出稳态反应限度的情况。
对22例充血性心力衰竭伴水潴留患者，通过超滤减少体液量，并监测神经体液反应。调节作为外部静脉回路一部分的透析滤过器，使其产生每小时500毫升的超滤液（平均（标准差）3122（1199）毫升），直至右心房压力降至基线的50%。在超滤前及超滤后48小时内测量血流动力学变量、血浆肾素活性、去甲肾上腺素和醛固酮。超滤后，血浆量减少20%，心输出量和血压适度下降（与动脉腔充盈程度降低一致），去甲肾上腺素、血浆肾素活性和醛固酮明显降低。在接下来的48小时内，血浆量、心输出量和血压恢复；神经体液轴受到抑制；水和钠排泄显著增加，外周水肿和器官充血消退。神经体液变化与血流动力学变化无关。神经体液变化与尿量和钠排泄增加之间存在显著相关性。
在晚期充血性心力衰竭中，动脉充盈不足不是激活神经体液轴和潴留液体的主要机制。由于循环激素的减少与血管外液的重吸收有关，很可能是肾脏和肺等器官的灌注不足和/或充血降低了循环去甲肾上腺素的清除率，并有助于维持血浆肾素和醛固酮浓度升高。液体潴留与血浆激素浓度之间的正反馈回路可能是充血性心力衰竭进展的原因。
