The content exists and concentration leads to the progressive delay in the body of sodium and water, increasing mass circulating blood increased venous pressure (which is also associated with constrikciei venul). There has been a further increase in venous return blood to the heart, resulting in the left Expansion has turned. Angiotenzin II and aldosteron, acting in Local miocarde resulted in a change in the structure of the affected heart (left chamber), the so-called remodelirovaniu. In miocarde a further loss miocardiotitov and develops fibrosis, which further reduces the pumping function of the heart. Reduced heart release (more precisely, the fraction of the release) leads to an increase in residual systolic volume and the growth of the end-diastolic pressure in the cavity of the left heart chamber. Expansion is further reinforced. This phenomenon began, according to the Franka-starlinga to exacerbate contractile function and myocardial heart equalization release. But as the progression of dilatation of the Franka-starlinga stop working, and the increasing pressure vchelejath divisions krovenosny bed-pressure pulmonary circulation (hypertension develops pulmonary circulation type of "passive" pulmonary hypertension). Among нейрогормональных violations in ХСН The increase in the blood-gli вазоконстрикторного powerful factor секретируемого эндотелием. Along with vazopressoriani factors increases the predserdnyi natriyureticski peptide (PNP), secretiruemogo heart blood in a way which relates to increased voltage predserdy wall, the increased pressure of filling the heart chambers. TNG expands arteries and promotes excretion of salt and water. However, HSN severity of the effect vazodilatatonego hampered by the effects vazokonstrictornogo angiotenzina II and the rest, and potentially beneficial impact on TNG kidney function decreases. Thus, in the pathogenesis of HSN emit cardialny and ekstrakardialny (neirogormonalny) mechanisms. The trigger factor is cardialny mechanism, reducing the contractile heart (sistolical deficiency), or the filling of the heart during diastola (diastolical insufficiency). Classification Currently, the classification of circulatory failure proposed ND Strazhesko. According to the scheme, providing three stages. Phase I : Primary : hidden circulatory insufficiency, reflected the emergence of breath, heartbeat and fatigue only with physical activity. Rest these phenomena disappear. Gemodinamika alone is not disrupted. Phase II : A period : signs of circulatory failure alone expressed moderately tolerant of physical activity is reduced. There are violations of hemodynamics in a large or a small range of diseases, the severity of moderate; Between B : expressed signs of heart failure at rest, heavy gemodinamicakie violations in a large, and in terms of small blood. Phase III-final : distrofica step with the views expressed violations hemodynamics and metabolic disorders and irreversible changes in the structure of organs and tissues. There is also HSN classification proposed by the New York Heart Association (NYHA). According to this classification, providing four functional class based on the physical efficiency patients. Class I is not limiting physical activity (with heart disease). Class II-heart disease is a limitation of physical activity. Class III-heart disease is a significant limitation of physical activity. IV class is the minimum physical activity causing discomfort. The beauty of this job is that it allows for the possibility of moving the patient from a higher class in lower, but it does not take into account the state of internal organs and the severity of the circulatory system in a large range of diseases.
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