Pediatric Congestive Heart Failure Medication

Updated: May 03, 2015
  • Author: Gary M Satou, MD, FASE; Chief Editor: Stuart Berger, MD  more...
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Medication

Medication Summary

The goals of pharmacotherapy include symptom relief, improved cardiac output, shortened hospital stay, fewer emergency department visits, and decreased mortality.

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Diuretics, Loop

Class Summary

Diuretics are reserved for congestive states.

Furosemide (Lasix)

Furosemide increases excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. The bioavailability of oral furosemide is 50%. If a switch is made from intravenous to oral administration, an equivalent oral dose should be used. Doses vary depending on the patient's clinical condition.

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Diuretics, Thiazide

Class Summary

Diuretics are reserved for congestive states.

Hydrochlorothiazide (Microzide)

Hydrochlorothiazide inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water, as well as potassium and hydrogen ions.

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Diuretics, Other

Class Summary

Diuretics are reserved for congestive states.

Metolazone (Zaroxolyn)

Metolazone is a quinazoline diuretic with properties similar to those of thiazide diuretics. It inhibits sodium resorption at the cortical diluting site and the proximal convoluted tubule.

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Aldosterone Antagonists, Selective

Class Summary

These agents are used for edema associated with congestive heart failure.

Spironolactone (Aldactone)

Spironolactone is used for the management of edema resulting from excessive aldosterone excretion. It competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions.

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Inotropic Agents

Class Summary

Long-term use of the phosphodiesterase inhibitor milrinone has deleterious effects on survival in patients with heart failure. Improvement of CHF symptoms occurs as the trade-off for this increase in mortality. Inotropic agents are reserved for patients who need hemodynamic-directed treatment during acute decompensation, those refractory to maximal standard therapy, as palliation for end-stage heart failure, or as a bridge to transplantation for appropriate candidates. Milrinone may have an advantage over beta-agonists in that it can be used for acute inotropic support during introduction of beta-blocker therapy.

Digoxin therapy for heart failure has no benefit on mortality rates. However, it does improve NYHA functional class, hemodynamics, symptoms, exercise capacity, and quality of life and reduces hospitalizations for heart failure. Patients with worse NYHA functional class and lower left ventricular ejection fraction benefit most from digoxin therapy.

Milrinone

Milrinone is a bi-pyridine positive inotrope and vasodilator with little chronotropic activity. It differs in mode of action from both digitalis glycosides and catecholamines. This agent is used for the short-term management of acute decompensated heart failure.

Digoxin (Lanoxin)

Digoxin is a cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. It acts directly on cardiac muscle, increasing myocardial systolic contractions. Indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

Dopamine

Dopamine is a naturally occurring endogenous catecholamine that stimulates beta1- and alpha1-adrenergic and dopaminergic receptors in a dose-dependent fashion. It stimulates release of norepinephrine.

In low doses (2-5 ug/kg/min), dopamine acts on dopaminergic receptors in renal and splanchnic vascular beds, causing vasodilatation in these beds. In midrange doses (5-15 ug/kg/min), it acts on beta-adrenergic receptors to increase heart rate and contractility. In high doses (15-20 ug/kg/min), it acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise blood pressure.

Dobutamine

Dobutamine is a sympathomimetic amine with stronger beta than alpha effects. It produces systemic vasodilation and increases the inotropic state. Vasopressors augment the coronary and cerebral blood flow during the low-flow state associated with shock.

Sympathomimetic amines with both alpha- and beta-adrenergic effects are indicated in cardiogenic shock. Dopamine and dobutamine are the drugs of choice to improve cardiac contractility, with dopamine the preferred agent in hypotensive patients. Higher dosages may cause an increase in heart rate, exacerbating myocardial ischemia.

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Alpha/Beta Adrenergic Agonists

Class Summary

These agents may be required for repletion of catecholamines and for the treatment of hypotension.

Epinephrine (Adrenalin)

Epinephrine is used for hypotension refractory to dopamine. Its alpha-agonist effects include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Its beta2-agonist effects include bronchodilation, chronotropic cardiac activity, and positive inotropic effects.

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Prostaglandins, Endocrine

Class Summary

An alprostadil (PGE1) infusion is indicated when ductal-dependent cardiac lesions are diagnosed or when they cannot be ruled out in a timely fashion. Absent femoral pulses or the inability to increase the systemic PaO2 to above 150 mm Hg with a fraction of inspired oxygen (FiO2) of 1 suggests a ductal-dependent lesion, and treatment with PGE1 is warranted.

PGE1 may theoretically aggravate the condition in some children with total anomalous pulmonary venous connection and obstruction or in children with other etiologies of congestive heart failure, such as sepsis. Whenever possible, echocardiography should be performed before PGE1 treatment is begun. On the other hand, when critical heart disease is present and echocardiography is not immediately available, prostaglandin infusion can be lifesaving.

Alprostadil IV (Prostin VR)

Alprostadil is identical to the naturally occurring PGE1 and possesses various pharmacologic effects, including vasodilation and inhibition of platelet aggregation. It is a first-line medication used as palliative therapy to temporarily maintain patency of the ductus arteriosus before surgery.

This agent is beneficial in infants with congenital defects that restrict pulmonary or systemic blood flow and in patients who depend on a patent ductus arteriosus for adequate oxygenation and lower body perfusion. It produces vasodilation and increases cardiac output.

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ACE Inhibitors

Class Summary

Use of ACE inhibitors (in the absence of contraindications to ACE inhibition) is the current criterion standard in the treatment of left ventricular dysfunction. ACE inhibitors have been shown to decrease mortality rates in both symptomatic and asymptomatic patients with left ventricular dysfunction and to reduce re-admissions caused by heart failure. The absolute benefits are greater in patients with severe heart failure.

The dosage necessary for maximal benefit is debatable. However, authorities have generally accepted that maximizing ACE inhibitor therapy is important and should be accomplished in conjunction with other necessary therapies.

Enalapril (Vasotec)

Enalapril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. This agent helps control blood pressure and proteinuria. It decreases the pulmonary-to-systemic flow ratio in the catheterization laboratory and increases systemic blood flow in patients with relatively low pulmonary vascular resistance.

Enalapril has a favorable clinical effect when administered over a long period. It helps prevent potassium loss in distal tubules. Because the body conserves potassium, less oral potassium supplementation is needed.

Lisinopril (Prinivil, Zestril)

Lisinopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Captopril

Captopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, and reduces aldosterone secretion.

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Angiotensin II Receptor Blockers (ARBs)

Class Summary

Angiotensin receptor blockers are as effective as ACE inhibitors in the treatment of heart failure. Their adverse-effect profile is similar to that of ACE inhibitors with regard to renal insufficiency or hyperkalemia, but they do not cause potentiation of bradykinin and therefore do not cause cough.

Losartan (Cozaar)

Losartan is an ARB that blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. It may induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors, it does not affect the response to bradykinin, and it is less likely to be associated with cough and angioedema. It is used for patients unable to tolerate ACE inhibitors.

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Vasodilators

Class Summary

Preload reduction with vasodilators is thought to be helpful in acute decompensated heart failure by reducing congestions and minimizing cardiac oxygen demand. Afterload reduction is also thought to be helpful in some patients with acute decompensated heart failure by decreasing myocardial oxygen demand and improving forward flow.

Sublingual nitroglycerin spray, topical ointment, and IV nitroglycerin have been advocated in the treatment of pulmonary edema secondary to CHF. Morphine also has significant vasodilatory effects and can be useful.

Nitroglycerin (Nitro-Bid, Nitro-Dur, Minitran)

Nitroglycerin causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate (cGMP) production, resulting in a decrease in blood pressure.

Nitroprusside (Nitropress)

Nitroprusside produces vasodilation and increases inotropic activity of the heart. At higher dosages, it may exacerbate myocardial ischemia by increasing heart rate.

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Beta-Adrenergic Blockers

Class Summary

General guidelines for initiating beta-blocker therapy include treating all patients with left ventricular dysfunction except those who are acutely decompensated. Therapy should be initiated at low dosages, which should be increased gradually over several weeks. Patients' conditions may deteriorate over the short term, but they generally improve in the long term with continued therapy.

Carvedilol, bisoprolol, and metoprolol CR/XL are the only agents currently approved by the US Food and Drug Administration (FDA) for use in persons with heart failure. Carvedilol acts in 3 ways: as a beta-blocker, an alpha-blocker, and an antioxidant and may be more beneficial than metoprolol in heart failure. [19]

Carvedilol (Coreg, Coreg CR)

Carvedilol blocks beta1-, alpha-, and beta2-adrenergic receptor sites, decreasing adrenergic-mediated myocyte damage.

Metoprolol (Lopressor, Toprol XL)

Metoprolol is a selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During intravenous administration of metoprolol, carefully monitor the patient's blood pressure, heart rate, and electrocardiogram.

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Cardiovascular, Others

Class Summary

Human B-type natriuretic peptide (BNP) is a new class of drug in the treatment of heart failure. It is produced through recombinant DNA technology and has the same amino acid sequence as naturally occurring human BNP.

Nesiritide (Natrecor)

Nesiritide is a recombinant DNA form of human BNP that dilates veins and arteries. Human BNP binds to the particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells. Binding to receptor causes increase in cGMP, which serves as second messenger to dilate veins and arteries. This, in turn, leads to smooth muscle relaxation and vasodilation. Venous and arterial dilation results in decreased preload and afterload and reductions in pulmonary capillary wedge pressure. Human BNP is indicated for temporary use in patients with acutely decompensated CHF.

Human BNP has additional beneficial effects for heart failure patients. Neurohormonal effects on the rennin-angiotensin-aldosterone system (RAAS) result in reductions in plasma norepinephrine and a trend toward a decrease in aldosterone levels. Renal effects include diuresis and natriuresis with at least preservation, if not an increase, in renal blood flow and glomerular filtration rate.

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