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Heart failure is a complex condition with many potential causes, but with the end result that the heart is unable to meet the metabolic demands of the body (including growth in children). Many believe that there must also be a component of systemic or pulmonary congestion. However, some patients with heart failure may have no significant congestion at rest, but only develop congestion with exertion or other forms of increased oxygen demand. Heart failure is generally precipitated by an insult to the cardiovascular system, either acquired or congenital. In adults, the most common insult is ischemic coronary artery disease with resultant left ventricular dysfunction. In children, heart failure is rarely ischemic, and the causes are quite varied and age dependent; refer to Chapters 483 and 484 for specific lesions associated with heart failure in children of different ages. Although infants with large left-to-right shunts and pulmonary overcirculation are commonly referred to as being in heart failure, their ventricular performance is usually normal, and their “heart failure” is usually a manifestation of pulmonary overcirculation with or without elevated ventricular filling pressures. They may have decreased systemic blood flow as well. Severe left-sided obstructive lesions (eg, hypoplastic left heart syndrome) often present with heart failure in the newborn period because the left ventricle cannot adequately eject blood to the systemic circulation. Both of these groups of lesions are generally managed by surgery or transcatheter intervention, but symptomatic therapy is often needed prior to surgical correction

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Once the body has sensed a low cardiac output, a complex neurohormonal cascade is activated that includes the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (Fig. 497-1). This adaptive process causes fluid retention and stimulates release of vasopressive neurohormones such as norepinephrine in order to maintain or increase circulating blood volume and blood pressure. However, this cascade soon becomes maladaptive because it increases preload and afterload in an already overstressed system. Cellular responses are also initiated. For example, the augmentation of beta-adrenergic activity increases intracellular calcium which in turn increases myocardial inotropy and chronotropy. These adaptive mechanisms also soon become maladaptive, as prolonged beta-adrenergic stimulation of the heart leads to apoptosis and fibrosis.

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Figure 497-1.
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Schematic representation of heart failure syndrome. Regardless of the etiology, the pathogenesis of heart failure has similar mechanisms. A decrease in cardiac output results in decreased end organ perfusion and activation of a neurohormonal cascade. Stimulation of endogenous catecholamines and activation of renin angiotensin aldosterone system causes increasing heart rate, preload and afterload. These compensatory mechanisms increase myocardial oxygen consumption and eventually lead to reverse remodeling, ventricular dilatation, increased propensity for arrhythmias, and decreased coronary reserve.

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The American Heart Association and the American College of Cardiology have divided heart failure into 4 stages: stage A: at risk for heart failure; stage B: structural heart disease without signs or symptoms; stage C: structural heart disease ...

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