Congestive heart failure

[Outlined -- congestive heart failure (CHF, or heart failure) is defined in the appropriate venous filling pressure, SHU heart and / or reduction dysfunction, Heart not emit enough blood to sustain human tissue needs of the clinical syndrome. Its essential character is inadequate cardiac output caused by congestive cardiac cycle (including systemic and / or pulmonary circulation). On the hemodynamic changes, the average atrial hypertension [left atrium to 1.6kPa (12mmHg) above, right atrium to 0.8kPa (mmHg) above], or congestive heart failure. The epidemiology of heart failure According to the Framingham area survey all heart failure mortality total of 25% two years, the two mild heart failure, the mortality rate for the 10% to 20%. serious heart failure in the two years up to 75% mortality. Its incidence is approximately 1%, and increased with age, the incidence of heart failure increased significantly, in the over 75 age population prevalence rate of 10%. ??Pathology (1) a cause. Basic reasons : from the perspective of pathophysiology can be summarized as the following : ?٠primary myocardial systolic and diastolic dysfunction; including cardiomyopathy (such as cardiomyopathy, myocarditis, myocardial infarction and myocardial fibrosis, poor prognosis), myocardial ischemia, Metabolism and poisoning (such as coronary heart disease and pulmonary heart disease, altitude sickness and shock, severe anemia and poisoning, etc.) myocardial contractility and lead to heart failure reduced. ?ڠventricular afterload (systolic pressure load) overweight : left ventricular overloading caused the common causes of hypertension, aortic stenosis, obstructive hypertrophic cardiomyopathy; After causing right ventricular overloading reason is pulmonary stenosis, various causes of pulmonary hypertension, both ventricular contraction resistance increased after heavier load where. ?۠ventricular preload (diastolic volume load) overweight : Left ventricular overloading common in the former mitral insufficiency, aortic insufficiency; Right before overloading common room in the pulmonary valve or tricuspid valve insufficiency, atrial septal defect. ?٠mechanical ventricular filling delay : If mitral or tricuspid stenosis, restrictive cardiomyopathy, constrictive pericarditis. Acute cardiac tamponade, etc.. ?ݠreduce ventricular diastolic compliance : common in myocardial ischemia, ventricular hypertrophy, heart aneurysm and heart amyloidosis, etc.. ?ޠhigh power cycle : Common in hyperthyroidism, severe anemia, beriberi heart disease and arteriovenous fistula. 2. Induced factors : heart failure in the majority of both incentives common : ?٠infections : respiratory tract infections accounted for the first, time for rheumatic fever. Children for the first rheumatic fever. Women with urinary tract infection is also common. ?ڠserious fast - or slow arrhythmia. ?۠excessive physical or emotional. ?ܠexcessive sodium intake. ?ݠlot of rapid intravenous infusion. ?ޠpregnancy and childbirth, anemia or hyperthyroidism deterioration. ?ߠmyocardial suppression of drug misuse : If beta blockers, quinidine, verapamil, such as digitalis. ?ࠥlectrolyte imbalance and acid-base balance : as hypokalemia or low calcium, magnesium and low acid poisoning. (2) the pathogenesis of heart failure in the hemodynamic changes are basically cardiac output reduction. Cardiac output depends upon several factors : 1. Diminished myocardial contractility : myocardial contractility and is unrelated to the load ventricular myocardial contractility itself, its weakening heart failure occurred the most common cause. Various heart diseases such as myocardial ischemia, myocardial infarction, myocarditis and cardiac diseases can cause damage myocardial ultrastructure and biochemical metabolic disorders, resulting in decreased myocardial contractility so reduced cardiac output. 2. Ventricular diastolic compliance obstacles : cardiac output, heart not only depend on the contractile function, also on the ventricular diastolic function and compliance. Ventricular diastolic compliance could hinder the reduction of ventricular filling (systolic function at this time able to maintain normal). thereby directly caused or exacerbated the development of heart failure. Common factors myocardial hypertrophy, left ventricular myocardial wall thickness and composition of the changes, such as hypertrophic cardiomyopathy, coronary heart disease and hypertension caused by concentric hypertrophy, aortic diastolic left ventricular obstacles, diastolic filling has slowed, filling and filling failure is increased resistance to the direct cause of heart failure. Other myocarditis cell infiltration, amyloidosis. edema and fibrosis could be reduced ventricular compliance (which increased stiffness). 3. Increased cardiac load before : it is end-diastolic intracardiac blood volume and the number of right ventricular Tension size. General with the left ventricular end-diastolic pressure as a former load indicator. Left ventricular end-diastolic pressure in 2.0~2.4kPa (15~18mmHg), cardiac blood reaches peak. According to the law Frank-Starling heart (myocardial contractility in the extent permitted, stroke volume by volume as decided upon reflection), and if in excess of the value of the ineffective law, the cardiac output but lower. 4. Increased load heart : ventricular ejection means encountered by the impedance, including wall tension and vascular resistance. According to Laplace's law, tension and heart wall indoor pressure and heart cavity was directly proportional to the radius, and wall thickness was inversely proportional. Left ventricular ejection impedance, in the absence of aortic stenosis, aortic depends on compliance, peripheral vascular resistance, blood viscosity and arterial blood volume, but peripheral vascular resistance is most important. Generally only used to value arterial pressure after left ventricular load. After the load and stroke volume were negatively correlated. If the left ventricle after lasting load increased, often leads to compensatory left ventricular hypertrophy expansion, which would ultimately reduce cardiac contractility. cardiac output also decreased. 5. HR : The impact of cardiac output to stroke volume and the product of heart rate. In a certain range, stroke volume constant circumstances, the heart rate will speed up the increase in cardiac output, heart rate too fast, ventricular filling inadequate cardiac output is reduced. If the heart rate is too slow, stroke volume tends to limit a further relaxation period would not raise the stroke volume, cardiac output also declined. 6. Cardiac structural integrity owed : such as acute myocardial infarction ventricular septal perforation, rheumatic heart disease caused heart valve damage and other structural abnormalities can be reduced cardiac output. 7. Cardiac systolic and diastolic dysfunction : cardiac contractile function of ministries high degree of coordination, is the heart of the integration, for the maintenance of normal heart pump function is important. It's a major imbalance sick rational myocardial hypertrophy, myocardial contractile and the loss of myocardial cells linked to abnormal structure. If myocardial ischemia or infarction, ventricular wall motion disorders, stroke volume lower, thereby reducing cardiac output. These factors, in cardiac contractility, heart rate before and after loading and the role is most important. (3) pathophysiology of heart failure, cardiac output decrease, leading to arterial insufficiency; Meanwhile, due to reduced cardiac output, ventricular end-diastolic pressure increased significantly, upon reflection volume reduction can lead to pulmonary circulation and / or systemic venous stasis. Heart failure occurred in the course of development, in the beginning stages of cardiac reserve mobilization can make up for reduced cardiac output; If decompensated heart failure, will appear in the clinical signs of heart failure. The main compensatory mechanisms : 1. Neurohormonal mechanisms : cardiac output is reduced after the first compensatory mechanisms. Adrenaline can include heart and adrenal medulla neurons increased catecholamine release enhancing myocardial contractility, accelerated heart rate and help to increase contraction of intravenous fluid upon reflection; and through activation of renin-angiotensin system (RAS), vasoconstriction, reducing water and sodium excretion, to increase blood volume and the former load. Recent studies have demonstrated the heart of RAS can lead to coronary contraction induced myocardial ischemia, promote cardiac sympathetic catecholamine release tips to increase cardiac contractility and cardiac thickening; Vascular and the RAS, Sympathetic tips through the release of norepinephrine, vascular smooth muscle contraction. In recent years, for many of ANP, atrial natriuretic peptide called atrial natriuretic peptide (ANP) or atrial natriuretic factor (ANF). It is one of the main atrium from the synthesis, storage and secretion of a powerful diuretic, the role of sodium peptides. Early in heart failure, with the increased pressure on the atrium and atrial was distraction, atrial compensatory enhanced secretion of ANF, ANF result, the blood concentration increased, reaching confrontation and offset heart failure vasoconstrictor system Po Na cause excessive water, sodium retention and the overloading of the heart before and after, this is the time of heart failure from other compensatory response. If sustained and severe heart failure, atrial ANF exhaustible resulting plasma ANF may be reduced. The mechanism was mainly caused by reflex tachycardia, artery and vein shrinkage and water and sodium retention, to compensate guarantee cardiac output. But excessive and long reaction, anti-increasing heart load before and after further aggravating cardiac dysfunction. 2. Enlarged heart : heart failure through this mechanism former load, stroke volume increased, and induced ventricular enlargement. myocardial fibers were distraction. Frank-Starling according to the law of ventricular muscle fibers longer extension, myocardial contraction forces also increased, stroke volume increased. According to the electron microscope, cardiac sarcomere length 2.0~2.2 μ m, the strongest myocardial contractility and stroke volume increased; But ventricular further expansion of its length "2.2 μ m, stroke volume is reduced. 3. Hypertrophic cardiomyopathy : it is a slow and effective compensatory mechanisms to reduce tension and wall myocardial contractility. After those long overloading caused ventricular concentric hypertrophy, overloading long ago there were the same compensatory myocardial hypertrophy, But often happens after heart enlargement, known as the eccentric hypertrophy. But long-term cardiac load increased, compensatory hypertrophy cardiomyopathy ultimately unsustainable where myocardial injury and a decrease in cardiac contractility, Cardiac Function on the further deterioration. 4. Enhance the surrounding tissue oxygen : This is a compensatory can improve cardiac output units the oxygen capacity The result is arteriovenous oxygen content difference increased. In short, these compensatory ability to have certain limits, but these limits are exceeded decompensated heart. will appear on the clinical symptoms of heart failure.