Chronic heart failure

Etiopathologic etiology and pathogenesis affect cardiac output decision of the five factors : ① heart of the former load after load ②, ③ myocardial contractility, ④ heart rate, myocardial contractility ⑤ coordination. These factors were single or multiple changes may affect cardiac function, or even heart failure. 1, the basic cause (1) ventricular diastolic overload before returning excess fluid, If aortic or mitral regurgitation, ventricular septal defect, PDA etc, make left ventricular diastolic overloaded, resulting in left ventricular failure; congenital atrial septal defect can right ventricular diastolic overloaded, leading to right heart failure. Anemia, hyperthyroidism high cardiac output disease, upon reflection increased output and increased left, The right ventricle diastolic load, which led to the whole-hearted failure. (2) after overloading such as high blood pressure, aortic stenosis or left ventricular outflow tract obstruction. make left ventricular systolic heavier load can lead to left ventricular failure. Pulmonary hypertension, right ventricular outflow tract obstruction, right ventricular systolic heavier load can lead to right heart failure. (3) myocardial contractility in common weakened as a result of coronary atherosclerosis caused by ischemia or myocardial necrosis. various causes of myocarditis (viral, immunologic, toxic, bacterial), unexplained cardiac disease, severe anemia and heart disease hyperthyroid heart disease, myocardial contractility can be significantly weakened, lead to heart failure. (4) ventricular systolic uncoordinated myocardial ischemia suffered serious local myocardial contractility unable or uncoordinated contraction. If aneurysm. (5) reduced ventricular compliance as ventricular hypertrophy, hypertrophic cardiomyopathy, ventricular compliance markedly reduced, can affect the ventricular diastolic heart function and influence. 2, inducing factor (1) of viral infection on the flu and lung infection-induced heart failure is the common incentive, In addition to direct infection of myocardial damage, fever enable faster heart rate also increased cardiac load. (2) the heavy manual work or emotional. (3) arrhythmia particularly rapid arrhythmia, such as paroxysmal tachycardia, atrial fibrillation. all can increase the heart load, reduce cardiac output, which led to heart failure. (4) pregnancy maternity increase blood volume in women during pregnancy, childbirth due to contraction of the uterus, upon reflection markedly increased blood volume, coupled with the forced labor, the heart is heavier load. (5) infusion (or excessive or excessive blood transfusion) or liquid sodium excessive importation, sudden increase in blood volume, overloading induced heart failure. (6) severe anemia or bleeding myocardial ischemia, heart rate faster, increasing heart load. Pathogenesis and pathophysiology of heart failure in the development process can be divided into cardiac decompensation and decompensated. A cardiac function decompensated heart of a large reserve force, when the sick in the heart load increase cardiac output decrease, Heart through the following channels for compensatory and cardiac output increased even close to normal, the cardiac function of the decompensated stage. Compensatory starting role ways : (1) cardiac sympathetic nerve dysfunction excited at the beginning, cardiac output reduction blood pressure dropped to stimulate the body aortic and carotid sinus baroreceptor. Meanwhile ventricular end-diastolic pressure and blood volume increase atrial stimulation, venous pressure sensors, both can lead to reflex sympathetic excited that the myocardial contractility strengthen, rapid heart rate, cardiac output increase. (2) ventricular end-diastolic volume increased due to sympathetic excitement through increased catecholamine release, the body tissues and organs within the vessels, including vascular resistance and capacitance vessels have different degrees of contraction so that blood volume redistribution to ensure that the heart, brain and other vital organs supply. Vasoconstriction capacity so that blood volume decrease venous hypertension, the increase in blood volume upon reflection. In addition, a renin angiotensin-aldosterone system activity, strengthening the kidney on sodium and water absorption, cell and the extracellular fluid increased blood volume, upon reflection volume increased even more. Frank - Starling law, that is not ventricular diastolic volume in scope, can enhance cardiac contractility, thereby increasing cardiac output. (3) cardiac hypertrophy lasting capacity load heavier load or pressure, can myocardial hypertrophy, myocardial contraction of a muscle functional unit increase in the number of sections, thus enhancing myocardial contractility. Through the above compensatory function, cardiac output, but they can also adapt to the human body in the middle degree of manual metabolism, bleeding occurred without symptoms, known as decompensated heart function. 2, heart function decompensated heart when change has been increasing, cardiac dysfunction than its compensatory function, appeared decompensated heart function, its main pathophysiological changes are : (a) speed up the heart rate, cardiac output to reduce heart failure early compensatory accelerated heart rate, While helping to increase cardiac output to reach or come close to the normal level, however, the heart rate also increased myocardial oxygen consumption. and coronary blood supply and ventricular filling time, so stroke volume decreased cardiac output but lower. (2) water, sodium pool wandering cardiac output, the reduction caused by the redistribution of blood, renal blood flow reduction. Renal blood flow decreased glomerular filtration rate can reduce or increase renin secretion. further role in the liver of angiotensinogen, angiotensin I-formation. Angiotensin after lung and renal circle, converting enzyme in the role, the formation of tension-2, The latter will have to make systemic and renal artery spasm small increase renal ischemia, has also prompted more adrenocortical secretion of aldosterone and enable increased sodium retention, plasma osmolality increased to stimulate the hypothalamic supraoptic nucleus near the osmotic pressure sensors, Reflex to make posterior lobe of the pituitary gland secretion of antidiuretic hormone increase, which would cause sodium and water retention, increased blood volume. venous and capillary pressure and congestive increased. (3) ventricular end-diastolic pressure increased heart failure, decreased myocardial contractility and cardiac output decrease, ventricular cavity residual blood volume increased ventricular end-diastolic pressure increased venous obstruction. caused venous stasis and venous pressure, however, When the capillary hydrostatic pressure higher than plasma osmolality and organizational pressure, capillary fluid extravasation, edema.