Pediatric Congestive Heart Failure

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The most likely causes of pediatric congestive heart failure depend on the age of the child. Congestive heart failure in the fetus, or hydrops, can be detected by performing fetal echocardiography. In this case, congestive heart failure may represent underlying anemia (eg, Rh sensitization, fetal-maternal transfusion), arrhythmias (usually supraventricular tachycardia), or myocardial dysfunction (myocarditis or cardiomyopathy). Curiously, structural heart disease is rarely a cause of congestive heart failure in the fetus, although it does occur. Atrioventricular valve regurgitation in the fetus is a particularly troubling sign with respect to the prognosis. (See Etiology.)

Neonates and infants younger than age 2 months are the most likely group to present with congestive heart failure related to structural heart disease. The systemic or pulmonary circulation may depend on the patency of the ductus arteriosus, especially in patients presenting in the first few days of life. In these patients, prompt cardiac evaluation is mandatory. Myocardial disease due to primary myopathic abnormalities or inborn errors of metabolism must be investigated. Respiratory illnesses, anemia, and known or suspected infection must be considered and appropriately managed. (See Etiology, Presentation, Workup, and Treatment.)

In older children, congestive heart failure may be caused by left-sided obstructive disease (valvar or subvalvar aortic stenosis or coarctation), myocardial dysfunction (myocarditis or cardiomyopathy), hypertension, renal failure, [1] or, more rarely, arrhythmias or myocardial ischemia. Illicit drugs such as inhaled cocaine and other stimulants are increasingly precipitating causes of congestive heart failure in adolescents; therefore, an increased suspicion of drug use is warranted in unexplained congestive heart failure. (See Etiology and Presentation.)

Although congestive heart failure in adolescents can be related to structural heart disease (including complications after surgical palliation or repair), it is usually associated with chronic arrhythmia or acquired heart disease, such as cardiomyopathy.

For patient education information, see the Heart Health Center, as well as Congestive Heart Failure.

Congestive heart failure occurs when the heart can no longer meet the metabolic demands of the body at normal physiologic venous pressures. Typically, the heart can respond to increased demands by means of 1 of the following:

Increasing the heart rate, which is controlled by neural and humoral input

Increasing the contractility of the ventricles, secondary to circulating catecholamines and autonomic input

Augmenting the preload, medicated by constriction of the venous capacitance vessels and the renal preservation of intravascular volume

As the demands on the heart outstrip the normal range of physiologic compensatory mechanisms, signs of congestive heart failure occur. These signs include tachycardia; venous congestion; high catecholamine levels; and, ultimately, insufficient cardiac output with poor perfusion and end-organ compromise. (See the image below.)

Diminished cardiac output is caused by a complex interaction of various factors. [2] Systolic dysfunction is characterized by diminished ventricular contractility that results in an impaired ability to increase the stroke volume to meet systemic demands. Factors such as anatomic stresses (eg, coarctation of the aorta) that contribute to an increased afterload (end-systolic wall stress), as well as neurohormonal factors that increase systemic vascular resistance, also lead to systolic dysfunction.

Diastolic dysfunction results from decreased ventricular compliance, necessitating an increase in venous pressure to maintain adequate ventricular filling. Causes of primary diastolic dysfunction include an anatomic obstruction that prevents ventricular filling (eg, pulmonary venous obstruction), a primary reduction in ventricular compliance (eg, cardiomyopathy, transplant rejection), external constraints (eg, pericardial effusion), and poor hemodynamics after the Fontan procedure (eg, elevated pulmonary vascular resistance).

In chronic heart failure, myocardial cells die from energy starvation, from cytotoxic mechanisms leading to necrosis, or from the acceleration of apoptosis or programmed cell death. Necrosis stimulates fibroblast proliferation, which results in the replacement of myocardial cells with collagen. The loss of myocytes leads to cardiac dilation and an increased afterload and wall tension, which results in further systolic dysfunction. In addition, the loss of mitochondrial mass leads to increased energy starvation.

During acute congestive heart failure, the sympathetic nervous system and renin-angiotensin system act to maintain blood flow and pressure to the vital organs. Increased neurohormonal activity results in increased myocardial contractility, selective peripheral vasoconstriction, salt and fluid retention, and blood pressure maintenance. As a chronic state of failure ensues, these same mechanisms cause adverse effects.

The myocardial oxygen demand, which exceeds the supply, increases because of an increase in the heart rate, in contractility, and in wall stress. Alterations in calcium homeostasis and changes in contractile proteins occur, resulting in a hypertrophic response of the myocytes. Neurohormonal factors may lead to direct cardiotoxicity and necrosis.

Many classes of disorders can result in increased cardiac demand or impaired cardiac function. Cardiac causes include arrhythmias (tachycardia or bradycardia), structural heart disease, and myocardial dysfunction (systolic or diastolic).

Noncardiac causes of congestive heart failure include processes that increase the preload (volume overload), increase the afterload (hypertension), reduce the oxygen-carrying capacity of the blood (anemia), or increase demand (sepsis). For example, renal failure can result in congestive heart failure due to fluid retention and anemia. Renal failure may also occur following heart transplantation as a result of long-term immunosuppression. [3]

Cardiac rhythm disorders may be caused by the following:

Complete heart block

Supraventricular tachycardia

Ventricular tachycardia

Sinus node dysfunction

Volume overload may be caused by the following:

Structural heart disease (eg, ventricular septal defect, [4] patent ductus arteriosus, aortic or mitral valve regurgitation, complex cardiac lesions)



Pressure overload may be caused by the following:

Structural heart disease (eg, aortic or pulmonary stenosis, aortic coarctation)


Systolic ventricular dysfunction or failure may be caused by the following:


Dilated cardiomyopathy



Diastolic ventricular dysfunction or failure may be caused by the following:

Hypertrophic cardiomyopathy

Restrictive cardiomyopathy


Cardiac tamponade (pericardial effusion)

Rajagopal SK, Yarlagadda VV, Thiagarajan RR, Singh TP, Givertz MM, Almond CS. Pediatric heart failure and worsening renal function: Association with outcomes after heart transplantation. J Heart Lung Transplant. 2011 Oct 18. [Medline].

Talner N. Heart failure. Heart Disease in Infants, Children, and Adolescents. 1995:1746-73:

Hoskote A, Burch M. Peri-operative kidney injury and long-term chronic kidney disease following orthotopic heart transplantation in children. Pediatr Nephrol. 2015 Jun. 30(6):905-18. [Medline].

Kaza AK, Colan SD, Jaggers J, Lu M, Atz AM, Sleeper LA, et al. Surgical interventions for atrioventricular septal defect subtypes: the pediatric heart network experience. Ann Thorac Surg. 2011 Oct. 92(4):1468-75. [Medline].

Erickson LC. Medical issues for the cardiac patient. Critical Care of Infants and Children. 1996:259-62:

Medar SS, Hsu DT, Ushay HM, Lamour JM, Cohen HW, Killinger JS. Serial measurement of amino-terminal pro-B-type natriuretic peptide predicts adverse cardiovascular outcome in children with primary myocardial dysfunction and acute decompensated heart failure. Pediatr Crit Care Med. 2015 Apr 8. [Medline].

Frobel AK, Hulpke-Wette M, Schmidt KG, Läer S. Beta-blockers for congestive heart failure in children. Cochrane Database Syst Rev. 2009 Jan 21. CD007037. [Medline].

Behera SK, Zuccaro JC, Wetzel GT, Alejos JC. Nesiritide improves hemodynamics in children with dilated cardiomyopathy: a pilot study. Pediatr Cardiol. 2009 Jan. 30(1):26-34. [Medline].

Jefferies JL, Price JF, Denfield SW, Chang AC, Dreyer WJ, McMahon CJ, et al. Safety and efficacy of nesiritide in pediatric heart failure. J Card Fail. 2007 Sep. 13(7):541-8. [Medline].

Mehra MR. Optimizing outcomes in the patient with acute decompensated heart failure. Am Heart J. 2006 Mar. 151(3):571-9. [Medline].

Konstam MA, Neaton JD, Poole-Wilson PA, Pitt B, Segal R, Sharma D, et al. Comparison of losartan and captopril on heart failure-related outcomes and symptoms from the losartan heart failure survival study (ELITE II). Am Heart J. 2005 Jul. 150(1):123-31. [Medline].

Rosenthal D, Chrisant MR, Edens E, Mahony L, Canter C, Colan S, et al. International Society for Heart and Lung Transplantation: Practice guidelines for management of heart failure in children. J Heart Lung Transplant. 2004 Dec. 23(12):1313-33. [Medline].

Cvelich RG, Roberts SC, Brown JN. Phosphodiesterase type 5 inhibitors as adjunctive therapy in the management of systolic heart failure. Ann Pharmacother. 2011 Dec. 45(12):1551-8. [Medline].

Pitt B, Zannad F, Remme WJ, Cody R, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med. 1999 Sep 2. 341(10):709-17. [Medline].

Pitt B, Remme W, Zannad F, et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med. 2003 Apr 3. 348(14):1309-21. [Medline].

Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, Perez A, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med. 1999 Sep 2. 341(10):709-17. [Medline].

Packer M, Colucci WS, Sackner-Bernstein JD, Liang CS, Goldscher DA, Freeman I, et al. Double-blind, placebo-controlled study of the effects of carvedilol in patients with moderate to severe heart failure. The PRECISE Trial. Prospective Randomized Evaluation of Carvedilol on Symptoms and Exercise. Circulation. 1996 Dec 1. 94(11):2793-9. [Medline].

Blume ED, Canter CE, Spicer R, Gauvreau K, Colan S, Jenkins KJ. Prospective single-arm protocol of carvedilol in children with ventricular dysfunction. Pediatr Cardiol. 2006 May-Jun. 27(3):336-42. [Medline].

Shaddy RE, Boucek MM, Hsu DT, Boucek RJ, Canter CE, Mahony L, et al. Carvedilol for children and adolescents with heart failure: a randomized controlled trial. JAMA. 2007 Sep 12. 298(10):1171-9. [Medline].

McAlister FA, Ezekowitz J, Hooton N, Vandermeer B, Spooner C, Dryden DM, et al. Cardiac resynchronization therapy for patients with left ventricular systolic dysfunction: a systematic review. JAMA. 2007 Jun 13. 297(22):2502-14. [Medline].

Janousek J, Gebauer RA. Cardiac resynchronization therapy in pediatric and congenital heart disease. Pacing Clin Electrophysiol. 2008 Feb. 31 Suppl 1:S21-3. [Medline].

van der Hulst AE, Delgado V, Blom NA, et al. Cardiac resynchronization therapy in paediatric and congenital heart disease patients. Eur Heart J. 2011 Sep. 32(18):2236-46. [Medline].

Beiras-Fernandez A, Deutsch MA, Kainzinger S, Kaczmarek I, Sodian R, Ueberfuhr P, et al. Extracorporeal membrane oxygenation in 108 patients with low cardiac output – a single-center experience. Int J Artif Organs. 2011 Apr. 34(4):365-73. [Medline].

US Food and Drug Administration (FDA). FDA approves mechanical cardiac assist device for children with heart failure. December 11, 2011. US Food and Drug Administration. Available at Accessed: December 16, 2011.

[Guideline] Lindenfeld J, Albert NM, Boehmer JP, et al. HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail. 2010 Jun. 16(6):e1-194. [Medline].


Pediatric Dose


Preload Reduction


1 mg/kg/dose PO or IV

May increase to qid


2 mg/kg/d PO divided bid

May increase to qid


0.2 mg/kg/dose PO

Used with loop diuretic, may increase to bid



Preterm infants: 0.005 mg/kg/d PO divided bid or 75% of this dose IV; age 10 y: 0.005 mg/kg/d PO qd or 75% of this dose IV


5-10 mcg/kg/min IV (usual dosage; maximal dosage may be up to 28 mcg/kg/min)

Gradually titrate upward to desired effect


5-10 mcg/kg/min IV

Gradually titrate upward to desired effect


0.01-0.03 mcg/kg/min IV

Not to exceed 0.1-0.3 mcg/kg/min


0.3-1 mcg/kg/min IV

Typically used without loading dose, especially in unstable patients

Load: 50 mcg/kg IV over 15 min

Afterload Reduction


0.1-0.5 mg/kg/d PO divided q8h


0.1 mg/kg/d PO divided qd/bid, not to exceed 0.5 mg/kg/d

Adults: 2.5-5 mg/day PO qd/bid initially; titrate slowly at 1- to 2-wk intervals; target dose is 10-20 mg PO bid; not to exceed 40 mg/day


Not established

Adults: Usual dosage is 10mg PO qd (range, 2.5-10 mg)


Initial dose for hypertension is 0.1 mg/kg/day PO; dosage for treatment of CHF is not established in children

Adults: 25-100 mg/d PO qd or divided bid


0.5-10 mcg/kg/min IV

May need to monitor cyanide level


0.1-0.5 mcg/kg/min IV



0.01-0.03 mcg/kg/min IV

Initiate with 0.01 mcg/kg/min

May cause dose-related hypotension


0.03-0.1 mcg/kg/min IV

Beta-Blockade  [7]


Limited data suggest a therapeutic dosage range of 0.2-0.4 mg/kg/dose PO bid; initiate with lower dose and gradually increase dose q2-3wk to therapeutic range

Adults: 12.5-25 mg PO bid

Initiate with 3.125 mg PO bid


Not established

Adults: 25-100 mg PO qd

Selective Aldosterone Antagonists


1-3.3 mg/kg/day PO in single or divided doses

Adults: 12.5-50 mg PO qd; reduce dose to 25 mg qod if hyperkalemia occurs


Not established

25-50 mg PO qd

*Prostaglandin E1 (PGE1).

Gary M Satou, MD, FASE Director, Pediatric Echocardiography, Co-Director, Fetal Cardiology Program, Mattel Children’s Hospital; Associate Clinical Professor, Department of Pediatrics, University of California, Los Angeles, David Geffen School of Medicine

Gary M Satou, MD, FASE is a member of the following medical societies: American Academy of Pediatrics, Society of Pediatric Echocardiography, American College of Cardiology, American Heart Association, American Society of Echocardiography

Disclosure: Nothing to disclose.

Nancy J Halnon, MD Assistant Professor, Division of Pediatric Cardiology (Heart Transplantation and Pediatric Cardiology), Mattel Children’s Hospital, University of California, Los Angeles, David Geffen School of Medicine

Nancy J Halnon, MD is a member of the following medical societies: American Academy of Pediatrics, American Heart Association, American Society of Transplantation, Society for Pediatric Research

Disclosure: Nothing to disclose.

Stuart Berger, MD Executive Director of The Heart Center, Interim Division Chief of Pediatric Cardiology, Lurie Childrens Hospital; Professor, Department of Pediatrics, Northwestern University, The Feinberg School of Medicine

Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Lars C Erickson, MD, MPH Associate Professor of Pediatrics, University of Massachusetts Medical School; Consulting Staff, Department of Pediatrics, Division of Pediatric Cardiology, University of Massachusetts Medical Center

Lars C Erickson, MD, MPH is a member of the following medical societies: American Heart Assocation and Sigma Xi

Disclosure: Nothing to disclose.

Ira H Gessner, MD Professor Emeritus, Pediatric Cardiology

Ira H Gessner, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Gilbert Z Herzberg, MD Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center

Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Ameeta Martin, MD Clinical Associate Professor, Department of Pediatric Cardiology, University of Nebraska College of Medicine

Ameeta Martin, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Pediatric Congestive Heart Failure

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