Heart failure has been the inability of the circulatory system adequately organs and tissues and blood oxygen sufficient to sustain human life. The heart failure on the pumping function of one or both testing. Etiology Chronic heart failure develops in a variety of diseases where the drought heart and violated its pumping function. The pumping of diverse functions : 1. The defeat muscles heart miocardialnaya deficiency : a) primary (myocarditis, ZUC cardiomyopathy); B) secondary (ateroskleroticeski and postinfarknetary cardiosclerosis, hypothetical or Ray, the defeat to heart disease diffuse connective tissue, toxico-allergicaki defeat occurred). 2. Gemodinamical overload cardiac muscles : a) pressure (stenozy Mitral, trejstvorchatogo valves, the mouth of rivers and pulmonary artery hypertension small or large circulation); B) the amount of (lack of heart valves that vnutriserdechnykh shunts); C) combined (complex congenital heart disease, the combination of pathological processes leading to the port pressure and volume). 3. Violation diastolic ventricular filling (slipchivi pericardit, restrictive cardiomyopathy, a heart accumulation-amiloidoz, hemochromatosis, glikogenoz). AA main trigger chronic heart failure (HSN) is the reduction of contractile ability to attack and, as a consequence, the fall release of a heart. This in turn has led to a deterioration in the blood and tissues, and the inclusion of a number of compensating mechanisms, one of which is giperaguation simpatiko-adrainalovo System (SAS). Kateholamin, mostly noradrenalin are narrowing arteriol venul and that adds to the return of venous blood to the heart, increasing diastolic filling suspect turned left and alignment to standards reduced heart release. But NAC policy, as originally compensatory, in the future becoming one of the factors contributing to the progression of pathological changes in the cardiovascular system, and signs of worsening heart failure. Arteriol patients, in particular kidney, it is activation renin-angiotenzinovo system (RRA) and giperproduktia vazopressonego powerful factors - angiotenzina II. In addition to strengthening the angiotenzina II in plasma, activated local tissue RRA, in particular miocarde, making his progressive atrophy. Angiotenzin II also promotes increased education concentration, which in turn increases the reabsorbqiyu sodium increases the plasma osmolarity of blood and, ultimately, contributes to the activation of antidiuretic hormone (ADU) - worth.
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