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Management of heart failure is multidimensional and requires a stepwise approach. A pediatric cardiologist should be involved early on in the child's care. In the emergency department setting, the goal is to recognize the child in acute CHF and begin management, remembering always the ABCs. Current therapy for acute heart failure focuses on improving myocardial performance with inotropic agents, adjustments to afterload and preload, and on correcting the underlying cause. When the cause is known, correctable tasks must be undertaken. Examples include interventional techniques for obstructive lesions, exchange transfusion for profound anemia, β-blocker for thyroid storm, or pericardiocentesis for cardiac tamponade. When the cause is unknown, empiric therapy is initiated based on the need to control rate, decrease preload, and improve afterload and/or contractility (Fig. 40-4 and Table 40-5).
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Pharmacologic therapy is directed at the specific cause of CHF when dealing with known cardiac disease. Treatment involves the use of diuretics, digoxin, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARB), aldosterone antagonists, and β-blockers.14–16 (See Tables 40-6A 40-6B for specific drug classes and dosing guidelines.)
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Fluid overload is initially treated with diuretics to reduce increased work of breathing, peripheral edema, and ascites.17,18 Digoxin has a positive inotropic effect, negative chronotropic effect, and a vagotonic effect. Years ago, digoxin was the drug of choice in the management of children in heart failure. It is no longer the first-line agent and reserved for patients with ventricular dysfunction with symptoms consistent with Class III heart failure.15
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Afterload reduction is obtained by ACE inhibitors. They are vasodilators, but they affect neurohormonal mechanisms. In the setting of low output with increased systemic resistance, such as in hypertensive cardiomyopathy, afterload reduction with ACE inhibitors may be helpful. Captopril and enalapril are used most frequently. Contraindications include patients with renal insufficiency and those with right-to-left shunts. In right-to-left shunt, the systemic circulation may improve at the expense of the pulmonary circulation.19
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Contractility can be supported with intravenous agents (dopamine) or mixed agents (dobutamine, milrinone). Milrinone, a phosphodiesterase inhibitor has gained popularity in many institutions as a first-line agent. Milrinone is shown to increase cardiac muscle contractility, vascular smooth muscle relaxation, and cardiac output without increasing myocardial oxygen consumption or ventricular afterload. Dobutamine has fallen out of favor because of increased mortality in adult heart failure patients.20,21
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β-blockers may have a role in chronic CHF. They “upregulate” cell wall receptors, increasing contractility.5,6,22 The decision to begin long-term agents, digoxin, ACE inhibitors, or β-blockers is best made in consultation with a pediatric cardiologist or intensivist. An algorithmic approach to CHF is presented in Figures 40-4 and 40-5.
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The child in moderate-to-severe CHF will require the intensive care unit or transfer to a tertiary care facility. Intubation may be necessary to improve oxygenation and provide positive end-expiratory pressure (PEEP), useful in pulmonary edema. Inotropic support includes milrinone to increase cardiac muscle contractility, vascular smooth muscle relaxation, and cardiac output without increasing myocardial oxygen consumption or ventricular afterload, dopamine to increase contractility and blood pressure, and epinephrine to improve blood pressure.14–16
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In severe cases, such as myocarditis with cardiogenic shock, the weakened myocardium ineffectively pumps against increased afterload. Vasodilators such as sodium nitroprusside may be helpful. It has venodilator and arteriolar dilator effects and is easily titratable.14–16