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  • Title: [Synopsis of endocrine and hemodynamic changes in heart failure].
    Author: Wedler B.
    Journal: Z Kardiol; 1991; 80 Suppl 8():53-6. PubMed ID: 1796635.
    Abstract:
    In contradiction earlier viewpoints, cardiac failure cannot be defined as a purely hemodynamic problem nor as only a cardiac problem. On the other hand decreased cardiac output (Co), increased filling pressure, increased wallstress and myocardial O2-consumption (MVO2) are the cause of many humoral counterregulations. Therefore, it is not always certain if the observed alterations are the causes or consequences of cardiac failure. The systemic counter-regulations will be modulated by desensitized cardiopulmonary mechanoreceptors, followed by decreased inhibition of central vasomotoric stimuli and endothelial and endocardial function, by altered signal transmission, as well as by altered gene expression within the myocytes. Depending on the degree of insufficiency, it may be attempted, by increase of the preload and of the contractility, to restore the hemodynamic basic situation. Such an attempt is based upon increased activity of the sympathetic nervous system, stimulation of the renin-angiotensin-aldosterone-system (RAAS) or the increased level of ADH. The reduced contractility and response of the myocytes, caused by the downregulation of beta 1-receptors and Gs-proteins, as well as by the upregulation of Gi-proteins, and the increased afterload with increased MVO2 and decreased CO all lead to a vicious circle. There are only some mechanisms that are directed against these regulations. The decreased response of the myocardium to endogenous catecholamines, the stimulation of ANP-secretion, as well of the prostaglandin-secretion are among the favorable regulations. They cause increase of natri- and diuresis, improved renal perfusion, vasodilatation, and inhibition of the RAAS and ADH-secretion with reduction of true thirst and craving for salt.(ABSTRACT TRUNCATED AT 250 WORDS)
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