Heart failure is a clinical syndrome caused by the inability of the heart to pump sufficient blood to meet the metabolic needs of the body.
Heart Failure can result from any disorder that reduces ventricular filling (diastolic
dysfunction) and/or myocardial contractility (systolic dysfunction).
Pathophysiology
1. Causes of systolic dysfunction (decreased contractility) are reduction in muscle mass (e.g., myocardial infarction [MI]), dilated cardiomyopathies, and ventricular hypertrophy. Ventricular hypertrophy can be caused by pressure overload (e.g., systemic or pulmonary hypertension, aortic or pulmonic valve stenosis) or volume overload (e.g., valvular regurgitation, shunts, high-output states).
2. Causes of diastolic dysfunction (restriction in ventricular filling) are increased ventricular stiffness, ventricular hypertrophy, infiltrative myocardial diseases, myocardial ischemia and infarction, mitral or tricuspid valve stenosis, and pericardial disease (e.g., pericarditis, pericardial tamponade).
3. The leading causes of Heart Failure are coronary artery disease and hypertension.
4. As cardiac function decreases after myocardial injury, the heart relies on the following compensatory mechanisms: (1) tachycardia and increased contractility through sympathetic nervous system activation; (2) the Frank-Starling mechanism, whereby increased preload increases stroke volume; (3) vasoconstriction; and (4) ventricular hypertrophy and remodeling. Although these compensatory mechanisms initially maintain cardiac function, they are responsible for the symptoms of Heart Failure and contribute to disease progression.
5. The neurohormonal model of Heart Failure recognizes that an initiating event (e.g., acute MI) leads to decreased cardiac output but that the Heart Failure state then becomes a systemic disease whose progression is mediated largely by neurohormones and autocrine/paracrine factors. These substances include angiotensin II, norepinephrine, aldosterone, natriuretic peptides, arginine vasopressin, proinflammatory cytokines (e.g., tumor necrosis factor ?, interleukin-6 and interleukin-1 ?), and endothelin-1.
6. Common precipitating factors that may cause a previously compensated patient to decompensate include noncompliance with diet or drug therapy,coronary ischemia, inappropriate medication use, cardiac events (e.g., MI, atrial fibrillation), pulmonary infections, and anemia.
7. Drugs may precipitate or exacerbate Heart Failure because of their negative inotropic, cardiotoxic, or sodium- and water-retaining properties.
Treatment of Chronic Heart Failure
The first stride in managing chronic heart oversight is to determine the etiology or precipitating factors. scheme of underlying disorders (e.g., anemia, hyperthyroidism) may obviate the need for treating Heart Failure.
Nonpharmacologic interventions receive cardiac rehabilitation further superintendence of fluid intake (utmost 2 L/day from all sources) and dietary sodium (approximately 2 to 3 g of sodium per day).
Stage A:
The weight is on identifying and modifying risk factors to stop development of structural spotlight disease besides subsequent Heart Failure. Strategies admit ovenlike casualty also control of hypertension, diabetes mellitus, again dyslipidemia according to current treatment guidelines. Angiotensin-converting enzyme (ACE) inhibitors (or angiotensin receptor blockers [ARBs]) should be strongly definitive in that antihypertensive therapy in patients with confused vascular risk factors.
Stage B:
In these patients with structural heart indisposition but no symptoms, treatment is targeted at minimizing supplementary injury again preventing or slowing the remodeling process. In addition to chart measures outlined for modus operandi A, patients ditch a previous MI should receive both ACE inhibitors (or ARBs in patients intolerant of sans pareil inhibitors) and ?- blockers regardless of the ejection cut. Patients with low ejection fractions (less than 40%) should also receive both agents, regardless of whether they credit had an MI.
Stage C:
Most patients with structural heart disease again previous or current Heart omission symptoms should receive the treatments for Stages A and B because well over initiation and titration of a diuretic (if clinical evidence of liquor retention), ACE inhibitor, and ?-blocker (if not already receiving a ?- blocker thanks to previous MI, alone ventricular [LV] dysfunction, or contrasting indication). If diuresis is initiated and symptoms improve once the patient is euvolemic, long-term monitoring can begin. If symptoms do not improve, an aldosterone receptor antagonist, ARB (in ACE inhibitorintolerant patients), digoxin, and/or hydralazine/isosorbide dinitrate (ISDN) may be applicable in carefully selected patients. Other general measures take moderate sodium restriction, standard weight measurement, immunization lambaste influenza and pneumococcus, modest physical activity, again avoidance of medications that can exacerbate Heart Failure.
Stage D:
Patients eclipse symptoms at stick to despite maximal medical therapy should mean considered due to specialized therapies, including mechanical circulatory support, identical intravenous kosher inotropic therapy, cardiac transplantation, or hospice onus. Treatment of Chronic Heart Failure
Treatment of Chronic Heart Failure
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