Definition
Heart failure is a condition in which the heart as a pump patofisiologik unable to meet the need for blood to tissue metabolism. Important traits of this definition is the first definition of failure is relative to metabolic body kebtuhan, both aimed at the suppression of the sense failed overall cardiac pump function. The term failing myocardium is aimed specifically at the function of the myocardium; failing myocardium generally lead to heart failure, but the mechanism sirkulai kompensatorik can delay or even prevent progression to heart failure in the functioning of the pump.
The term failed circulation is more common than heart failure. Failed circulation shows the inability of the cardiovascular system to perform with adequate tissue perfusion. This definition includes Segal abnormalities of circulation resulting in inadequate tissue perfusion, including changes in blood volume, vascular tone and heart. Heart failure is someone kongetif situation where there is a dam circulation due to heart failure and kompenstoriknya mechanism. Congestive heart failure need to be distinguished from the more general term. Failed circulation, which just means excess bebabn circulation due to increased blood volume in heart failure or causes beyond the heart, such as excessive transfusion or anuria.
Etiology
Heart failure is the most frequent complication of all types of disease or acquired heart failure. Physiological mechanisms that lead to heart failure include conditions that increase the initial load, the load end or reduce myocardial contractility. Circumstances that increase the initial load include: aortic regurgitation and ventricular septal defect. And the final load situation where there is elevated in aortic stenosis and systemic hypertension. Myocardial contractility may decrease the imfark infarction and cardiomyopathy.
Factors that can trigger fktor progression of heart failure through a sudden penekanana circulation can be: arrhythmias, systemic infections, and infections of the lungs and pulmonary embolism. Pennganan effective against heart failure requires not only the recognition and handling of the mechanisms underlying physiological and penykit, but also the factors that trigger heart failure.
Pathophysiology
Abnormalities of intrinsic myocardial contractility in heart failure due to typical ischemic heart disease, impairs the ability of effective ventricular emptying. Left ventricular contractility decreased sekuncup reduce bulk and improve ventricular residual volume.
Pressure rteri lungs can be increased in response to a chronic increase in pulmonary venous pressure. Pulmonary hypertension increased resistance to right ventricular ejection. A series of bleak events that occurred in the left heart, will also occur in the right heart, which eventually will terjdi systemic congestion and edema.
The development of systemic congestion or edema of the lungs and can be exacerbated by functional regurgitation and valve-valve trikuspidalis or mitralis turns. Functional regurgitation can be caused by dilatation of the valve annulus atrioventrikularis or changes in the orientation of the papillary muscles and kordatendinae that occurs secondary to dilation space.
In response to heart failure, there are three primary meknisme visible; increased sympathetic adrenergic activity, increasing the initial load due to activation of complement system renin-angiotensin-aldosterone system and ventricular hypertrophy. All three of these responses reflect an attempt to maintain cardiac curh. Meknisme-meknisme may be sufficient to mempertahnkan cardiac output at normal or near-normal levels in heart failure early, in the resting state. But kerj pad ventricular abnormalities and decreased cardiac output typically looks at the state of berktivitas. Heart failure with less berlanjutny then compensation will be more effective now.
Handling
Heart failure ditngani with common measures to reduce the workload of the heart and selective manipulation of the three major determinants of myocardial function, both in abundance alone or a combination of: the initial load, contractility and load akhir.Penanganan usually begins when symptoms arise during the move pad usual. Treatment regimen progressively increased in abundance until it reaches the desired clinical response. Acute exacerbation of congestive heart failure or progress to severe heart failure could be a reason to be hospitalized or receive more aggressive treatment. ; 0
Strict restriction of physical activity is the act of beginning a simpler but very precise in pennganan heart failure. But it should be noted jngn to impose unnecessary lrngan yng to avoid musculoskeletal weakness. Now has dikethui that skeletal muscle weakness may increase intolerance to exercise. Bed rest and limited activity can also cause flebotrombosis. Giving antikoagulansia pad may be required strict activity restrictions to control symptoms. :>
Diagnostic Examination
1. ECG: atrial or ventricular hypertrophy, axis deviation, ischemia san damage pattern may be seen. Dysrhythmias eg takhikardi, atrial fibrillation. The increase in segment ST / T persistent 6 weeks or more after imfark aneurime ventricular infarction showed.
2. Sonogram: May indicate an enlarged chamber dimensions, changes in the function / structure of the valve or are decreased ventricular contractility.
3. Skan heart: Actions injection fraction and wall motion estimate.
4. Cardiac catheterization: Pressure bnormal an indication and help differentiate right-sided heart failure verus the left side, and stenosi valves or insufficiency, also assess the potential kororner arteries. Contrast agent is injected into the ventricle showed bnormal size and ejection fraction / kontrktilitas change.
