eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology
Heart Failure, Congestive
Updated: Mar 19, 2009
Introduction
Definition and compensatory mechanisms
Congestive heart failure (CHF) 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 one of the following:
- Increasing the heart rate, which is controlled by neural and humoral input
- Increasing the contractility of the ventricles, secondary to both 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.
Chest radiograph shows signs of congestive heart failure (CHF).
Contributory factors
Diminished cardiac output results from a complex interaction of various factors.1
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) and those resulting from 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 that 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.
Clinical Signs and Symptoms
Irrespective of the etiology, the first manifestation of congestive heart failure (CHF) is usually tachycardia. An obvious exception to this finding occurs in congestive heart failure due to a primary bradyarrhythmia or complete heart block. As the severity of congestive heart failure increases, signs of venous congestion usually ensue. Left-sided heart failure is generally associated with signs of pulmonary venous congestion, whereas right-sided heart failure is associated with signs of systemic venous congestion. Marked failure of either ventricle, however, can affect the function of the other, leading to systemic and pulmonary venous congestion. Later stages of congestive heart failure are characterized by signs and symptoms of low cardiac output. Generally, congestive heart failure with normal cardiac output is called compensated congestive heart failure, and congestive heart failure with inadequate cardiac output is considered decompensated.
Signs of congestive heart failure vary with the age of the child.2 Signs of pulmonary venous congestion in an infant generally include tachypnea, respiratory distress (retractions), grunting, and difficulty with feeding. Often, children with congestive heart failure have diaphoresis during feedings, which is possibly related to a catecholamine surge that occurs when they are challenged with eating while in respiratory distress.
Right-sided venous congestion is characterized by hepatosplenomegaly and, less frequently, edema or ascites. Jugular venous distention is not a reliable indicator of systemic venous congestion in infants because the jugular veins are difficult to observe. Also, the distance from the right atrium to the angle of the jaw may be no more than 8-10 cm, even when the individual is sitting upright. Uncompensated congestive heart failure in an infant primarily manifests as a failure to thrive. In severe cases, failure to thrive may be followed by signs of renal and hepatic failure.
In older children, left-sided venous congestion causes tachypnea, respiratory distress, and wheezing (cardiac asthma). Right-sided congestion may result in hepatosplenomegaly, jugular venous distention, edema, ascites, and/or pleural effusions. Uncompensated congestive heart failure in older children may have fatigue or lower-than-usual energy levels. Patients may complain of cool extremities, exercise intolerance, dizziness, or syncope.
Clinical findings may include hypotension, cool extremities with poor peripheral perfusion, a thready pulse, and decreased urine output. Chemical evidence of renal and liver dysfunction may be present, as well as a diminished level of consciousness. Children with uncompensated congestive heart failure, particularly older children, generally have a lower cardiac output than what most experienced clinicians would estimate on the basis of the clinical signs.
- Tachycardia
- Venous congestion
- Right-sided
- Hepatomegaly
- Ascites
- Pleural effusion
- Edema
- Jugular venous distension
- Left-sided
- Tachypnea
- Retractions
- Nasal flaring or grunting
- Rales
- Pulmonary edema
- Right-sided
- Low cardiac output
- Fatigue or low energy
- Pallor
- Sweating
- Cool extremities
- Poor growth
- Dizziness
- Altered consciousness
- Syncope
Differential Diagnoses and Causes of Congestive Heart Failure
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 (CHF) 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.
The most likely causes of 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.
Neonates and infants younger than 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.
In older children, congestive heart failure may be caused by left-sided obstructive disease (aortic stenosis or coarctation); myocardial dysfunction (myocarditis or cardiomyopathy); hypertension; renal failure; 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. 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.
Characteristic findings in children with heart failure include the following:- 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, patent ductus arteriosus, aortic or mitral valve regurgitation, complex cardiac lesions)
- Anemia
- Sepsis
- Pressure overload may be caused by the following:
- Structural heart disease (eg, aortic or pulmonary stenosis, aortic coarctation)
- Hypertension
- Systolic ventricular dysfunction or failure may be caused by the following:
- Myocarditis
- Dilated cardiomyopathy
- Malnutrition
- Ischemia
- Diastolic ventricular dysfunction or failure may be caused by the following:
- Hypertrophic cardiomyopathy
- Restrictive cardiomyopathy
- Pericardial or cardiac tamponade
Workup
Thorough history taking and physical examination, including an assessment of the upper-extremity and lower-extremity blood pressures, are crucial in the evaluation of an infant or child with congestive heart failure (CHF).
Appropriate laboratory testing includes assessment of the following: oxygen saturation, CBC count and hemoglobin concentration, electrolyte levels, calcium level, BUN level, creatinine level, and renal and hepatic function. The CBC count can reveal signs of anemia or infection. Brain natriuretic peptide (BNP) or N -terminal prohormone BNP (NT-proBNP) levels are elevated as a result of ventricular dilation. Elevation of serum BNP level is particularly useful in distinguishing patients with congestive heart failure from those with a primary respiratory process. BNP levels of more than 100 pg/mL are associated with congestive heart failure in adults and children. Normal levels may be slightly higher in neonates.
The evaluation of serum electrolyte levels in the patient with congestive heart failure may demonstrate hyponatremia secondary to water retention. Elevated potassium levels may represent renal compromise or even tissue destruction due to low cardiac output. Significant tissue hypoxia increases serum lactate concentration and depletes the serum bicarbonate level. In more chronic congestive heart failure states, reduced renal blood flow may be expressed as increased BUN and creatinine levels.
In the presence of congestive heart failure, the cardiac silhouette is usually enlarged on the chest radiograph. As with BNP elevation, cardiac enlargement may help distinguish patients with congestive heart failure from those with respiratory disease. However, exceptions may include restrictive cardiomyopathy, venous obstruction (total anomalous pulmonary venous obstruction), and diastolic dysfunction due to high ventilator mean airway pressures displaying a normal cardiac size on chest radiographs. Increased pulmonary blood flow may be present, along with pulmonary edema or venous congestion.
A 12-lead ECG may reveal evidence of structural or coronary artery disease or a complete atrioventricular block or arrhythmia.
Echocardiography is indicated in any child with unexplained congestive heart failure to assess cardiac function and identify potential cardiovascular causes, particularly anatomic lesions. On the other hand, congestive heart failure itself is not an echocardiographic diagnosis; therefore, the underlying etiology is best identified by means of detailed history taking and physical examination, and often chest radiography. When oral sedation is performed for echocardiography, note that children with a low cardiac output can depend on endogenous catecholamine levels to maintain tissue perfusion. Sedation can cause withdrawal of the endogenous catecholamine drive, resulting in cardiac decompensation.
Pulse oximetry, and a hyperoxia test in newborns, may be useful. The systemic saturation on room air is a more reliable measure of oxygenation than observations alone, which are often misleading. The partial pressure of arterial oxygen (PaO2) when the patient is receiving 100% oxygen (hyperoxia test) may help in distinguishing intracardiac mixing malformations from pulmonary disease in the setting of hypoxia. Blood gas abnormalities may show respiratory alkalosis in mild forms of congestive heart failure or metabolic acidosis in patients with evidence of low cardiac output or ductal-dependent congenital heart disease.
General Treatment and Pharmaceutical Agents
The management of congestive heart failure (CHF) is difficult and sometimes dangerous without knowledge of the underlying cause. Consequently, the first priority is acquiring a good understanding of the etiology. The goals of medical therapy for congestive heart failure include reducing the preload, enhancing cardiac contractility, reducing the afterload, improving oxygen delivery, and enhancing nutrition. As previously emphasized, the causes of congestive heart failure vary, and they appear in different patients to variable degrees. Thus, the medical management of congestive heart failure in children should be tailored to the specific details of each case.
Preload reduction can be achieved with oral (PO) or intravenous (IV) diuretics (eg, furosemide, thiazides, metolazone). Venous dilators (eg, nitroglycerin) can be administered, but their use is rare in common practice. Contractility can be supported with intravenous agents (eg, dopamine) or mixed agents (eg, dobutamine, inamrinone, milrinone). Digoxin appears to have some benefit in congestive heart failure, but the exact mechanism is unclear. Afterload reduction is obtained PO by administration of ACE inhibitors or IV by administration of other agents such as hydralazine, nitroprusside, and alprostadil. Pharmaceutical agents used in the treatment of congestive heart failure are summarized below.
Pharmaceutical Agents used in the Treatment of Congestive Heart Failure
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Table
| Agent | Pediatric Dose | Comment |
Preload reduction | ||
| Furosemide | 1 mg/kg/dose PO or IV | May increase to qid |
| Hydrochlorothiazide | 2 mg/kg/d PO divided bid | May increase to qid |
| Metolazone | 0.2 mg/kg/dose PO | Used with loop diuretic, may increase to bid |
| Inotropic | ||
| Digoxin | Preterm infants: 0.005 mg/kg/d PO divided bid or 75% of this dose IV <10 y: 0.01 mg/kg/d PO divided bid or 75% of this dose IV>10 y: 0.005 mg/kg/d PO qd or 75% of this dose IV | ... |
| Dopamine | 5-28 mcg/kg/min IV | Gradually titrate upward to desired effect |
| Dobutamine | 5-28 mcg/kg/min IV | Gradually titrate upward to desired effect |
| Epinephrine | 0.01-0.03 mcg/kg/min IV | Not to exceed 0.1-0.3 mcg/kg/min |
| Milrinone | 0.5-1 mcg/kg/min IV | Typically used without loading dose, especially in unstable patients Load: 50 mcg/kg IV over 15 min |
| Afterload reduction | ||
| Captopril | 0.1-0.5 mg/kg/d PO divided q8h | ... |
| Enalapril | 0.1 mg/kg/d PO divided qd/bid, not to exceed 0.5 mg/kg/d | Adults: 2.5-5 mg/d PO qd-bid, not to exceed 40 mg/d |
| Lisinopril | Not established | Adults: 10 mg PO qd |
| Losartan | Not established | Adults: 25-100 mg/d PO qd or divided bid |
| Nitroprusside | 0.5-10 mcg/kg/min IV | May need to monitor cyanide level |
| Nitroglycerin | 0.1-0.5 mcg/kg/min IV | Vasodilator |
| Nesiritide | 0.01-0.03 mcg/kg/min IV | Initiate with 0.01 mcg/kg/min May cause dose-related hypotension |
| Alprostadil* | 0.03-0.1 mcg/kg/min IV | ... |
| Beta-blockade 3 | ||
| Carvedilol | 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 |
| Metoprolol | Not established | Adults: 25-100 mg PO qd |
| Agent | Pediatric Dose | Comment |
Preload reduction | ||
| Furosemide | 1 mg/kg/dose PO or IV | May increase to qid |
| Hydrochlorothiazide | 2 mg/kg/d PO divided bid | May increase to qid |
| Metolazone | 0.2 mg/kg/dose PO | Used with loop diuretic, may increase to bid |
| Inotropic | ||
| Digoxin | Preterm infants: 0.005 mg/kg/d PO divided bid or 75% of this dose IV <10 y: 0.01 mg/kg/d PO divided bid or 75% of this dose IV>10 y: 0.005 mg/kg/d PO qd or 75% of this dose IV | ... |
| Dopamine | 5-28 mcg/kg/min IV | Gradually titrate upward to desired effect |
| Dobutamine | 5-28 mcg/kg/min IV | Gradually titrate upward to desired effect |
| Epinephrine | 0.01-0.03 mcg/kg/min IV | Not to exceed 0.1-0.3 mcg/kg/min |
| Milrinone | 0.5-1 mcg/kg/min IV | Typically used without loading dose, especially in unstable patients Load: 50 mcg/kg IV over 15 min |
| Afterload reduction | ||
| Captopril | 0.1-0.5 mg/kg/d PO divided q8h | ... |
| Enalapril | 0.1 mg/kg/d PO divided qd/bid, not to exceed 0.5 mg/kg/d | Adults: 2.5-5 mg/d PO qd-bid, not to exceed 40 mg/d |
| Lisinopril | Not established | Adults: 10 mg PO qd |
| Losartan | Not established | Adults: 25-100 mg/d PO qd or divided bid |
| Nitroprusside | 0.5-10 mcg/kg/min IV | May need to monitor cyanide level |
| Nitroglycerin | 0.1-0.5 mcg/kg/min IV | Vasodilator |
| Nesiritide | 0.01-0.03 mcg/kg/min IV | Initiate with 0.01 mcg/kg/min May cause dose-related hypotension |
| Alprostadil* | 0.03-0.1 mcg/kg/min IV | ... |
| Beta-blockade 3 | ||
| Carvedilol | 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 |
| Metoprolol | Not established | Adults: 25-100 mg PO qd |
*Prostaglandin E1 (PGE-1).
Specific Treatments
Acute congestive heart failure in the neonate or infant
Acute presentation of the ill newborn or infant with congestive heart failure (CHF) warrants immediate concern regarding potential sepsis or ductal-dependent congenital heart disease. The evaluation and treatment of these patients are often best performed in the neonatal or pediatric intensive care unit.
The initial management involves the usual assessment of the patient's airway, breathing, and circulation (ABCs); achieving intravenous access; laboratory testing (see Workup) including a blood culture; and empiric antibiotic therapy. Management of low cardiac output can be initiated by using a dopamine infusion at 5-10 mcg/kg/min, acidosis can be corrected with the administration of fluid and/or bicarbonate. Calcium should be administered when hypocalcemia is documented. Because ductal-dependent structural heart disease is a common cause of congestive heart failure in early infancy, echocardiography should be considered early in the evaluation if a diagnosis is not immediately forthcoming.
Anatomic lesions that may appear early and that should be considered include coarctation or interruption of the aortic arch, total anomalous pulmonary venous return, hypoplastic left heart syndrome (or variants including severe mitral valve stenosis and/or aortic valve stenosis or atresia), truncus arteriosus, pulmonary atresia, and transposition of the great arteries. Conditions to consider in young infants with a more protracted congestive heart failure course include those producing significant left-to-right shunts, including large ventricular septal defects, aortopulmonary shunts, and an arteriovenous malformations.
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 arterial 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.
Nonstructural cardiac problems that occur during this stage include tachyarrhythmias (usually supraventricular tachyarrhythmia [SVT]) and complete heart block. Prompt pharmacologic or electrical cardioversion is warranted in any patient with a tachyarrhythmia who presents with congestive heart failure. Primary cardiomyopathy or myopathic disease secondary to inborn errors of metabolism should be considered in the absence of structural cardiac disease or arrhythmia when cardiac dysfunction is present.
Acute congestive heart failure in the older child
In older children with acute congestive heart failure, admission to the ICU for diuresis with intravenous (IV) furosemide and IV dopamine (5-10 mcg/kg/min) or milrinone (0.3-1.0 mcg/kg/min) infusion are appropriate until stabilization is achieved. Older children may require the placement of a central venous or pulmonary artery catheter to monitor venous pressure and cardiac output during stabilization.
Nitrates (nitroprusside, nitroglycerin) or nesiritide may be useful in patients with elevated pulmonary capillary wedge pressure and pulmonary congestion due to their venous dilating effects. Nesiritide carries the additional theoretical benefits of reversing deleterious neurohumoral responses and increasing natriuresis. Small studies have been conducted to measure hemodynamic effects of nesiritide in children with dilated cardiomyopthy.4,5 However, nesiritide has demonstrated no mortality advantage compared with nitroglycerin for acute decompensated heart failure in a large adult trial.6Chronic or stable congestive heart failure
If the underlying cause of the congestive heart failure cannot be immediately corrected in a patient who is hemodynamically stable, outpatient management can be initiated by using several agents. Afterload reduction using an ACE inhibitor is indicated in the presence of left ventricular (LV) dysfunction regardless of symptoms. In mild forms of congestive heart failure, low-dose furosemide (1 mg/kg/dose PO bid) may be initiated with addition of another agent for inotropic effect (digoxin) or afterload reduction (ACE inhibitor).7 The dose of digoxin (0.008-0.010 mg/kg/d PO divided bid, maximum 0.125-0.250 mg PO qd) is almost never increased, either for effect or according to digoxin levels, which are notoriously unreliable. However, the dose may be decreased in the presence of signs of toxicity. The suspicion of digoxin toxicity should increase if an infant is uninterested in feedings, gags, or vomits frequently. These symptoms are typically due to an overdose or renal failure.For more severe congestive heart failure, diuretic therapy with oral (PO) furosemide may be increased to 2 mg/kg/dose PO tid or a second agent, such as hydrochlorothiazide or metolazone, can be added. To be most effective, hydrochlorothiazide and metolazone are best administered simultaneously with furosemide to achieve their synergistic effect.
Afterload reduction is indicated in patients who have large left-to-right shunts at the ventricular or arterial level (ventricular septal defect or patent ductus arteriosus), left-sided regurgitant lesions (aortic insufficiency or mitral regurgitation), or poor systolic function (myocarditis or dilated cardiomyopathy). ACE inhibitors are the medications of choice. Alternatively, an angiotensin receptor blocker (ARB), such as losartan, may be used in patients in whom ACE side effects (particularly cough) may be unacceptable.8
For patients taking more than 1 mg/kg of PO furosemide bid without ACE inhibitors, spironolactone should be added for its potassium-sparing effect and theoretical beneficial effects on cardiac remodeling. Adult studies have suggested it prolongs survival in chronic heart failure.9 Alternatively, serum potassium levels may be monitored, and appropriate supplementation should be provided. Supplemental potassium chloride may be required when high doses of diuretics are used, but most children are extremely averse to the taste of most preparations. Because ACE inhibitors cause potassium retention, spironolactone and supplemental potassium should be avoided except in the presence of documented hypokalemia in patients taking these medications.
Hyponatremia often accompanies congestive heart failure and is caused by water retention in response to vasopressin (antidiuretic hormone) produced as a result of renin-angiotensin activation but may be exacerbated by use of diuretics and salt wasting by the kidney. Sodium supplementation is almost never indicated in infants or children with congestive heart failure except in emergency situations. Severe hyponatremia is generally best managed by reducing the dose of diuretics or by restricting fluid intake, although the latter has little use in small children. In any child taking more than 2 mg/kg/d of furosemide, electrolyte levels should be checked every few months or so, as in any child taking furosemide in conjunction with other diuretics or ACE inhibitors.
Experience with beta-blocker therapy in pediatric patients has increased. The selective beta1-blocker metoprolol and the nonselective beta1-blocker and beta2-blocker carvedilol, used primarily in adults, have generally shown encouraging results in select patients with cardiomyopathy and mild or moderate chronic congestive heart failure. Adults using these beta blockers (carvedilol) have demonstrated an increased stroke volume and stroke work index during exercise, along with a decreased heart rate and left ventricular (LV) chamber size.10
In addition, carvedilol has been shown to decrease pulmonary artery mean and wedge pressures, decrease cardiac norepinephrine levels, and increase peripheral vasodilation by means of alpha1-blockade. For these reasons, in part, use of carvedilol has increased in recent years, particularly in cardiomyopathies. However, a double-blind randomized trial (carvedilol vs placebo) in pediatric patients with mild-to-moderate congestive heart failure failed to demonstrate a benefit in reduction of symptoms or mortality. The power of the study was affected by an unexpectedly high rate of improvement among all patients, including those who received placebo.11 Thus, the exact indications and benefits of carvedilol therapy in children with heart failure remain somewhat unclear.3
Often overlooked in the management of chronic congestive heart failure is the role of the oxygen-carrying capacity of the blood. Anemia aggravates congestive heart failure by increasing the demands for cardiac output, and often, careful attention to iron stores or the administration of red cell transfusions results in a significant improvement.
Nutrition is crucial in the management of chronic congestive heart failure. Particularly during infancy, congestive heart failure increases the metabolic demands while making feeding itself more difficult. Enhanced caloric content feedings and, in some cases, nasogastric or gastrostomy feedings may be necessary to maintain the patient's growth.
The success of medical therapy of congestive heart failure in infants and small children is judged according to the child's growth. The failure to gain weight in the setting of marked congestive heart failure signifies that the current regimen is not sufficient. A failure to thrive is an indication for increased medical management or, when the option is available, surgical repair of structural heart disease.
Patient education
For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education article Congestive Heart Failure.
Device-Based Therapies
Cardiac resynchronization therapy (CRT) has emerged as a useful therapy in the treatment of chronic congestive heart failure (CHF). CRT involves the use of biventricular pacemakers to improve ventricular function by electrically adjusting the timing of right and left ventricular contraction to optimize wall motion and increase filling time. In addition to increasing stroke volume, CRT may allow for reverse remodeling to delay disease progression. Clinical trials in adults with moderate-to-severe heart failure have demonstrated beneficial effects of CRT use, including reduction of symptoms, increased exercise capacity, and decreased morbidity and mortality.12
In pediatric practice resynchronization therapy has been limited; initial studies describe results for this modality instituted in children with chronic heart failure who required pacemakers for treatment of rhythm disorders. Use of this therapy is more difficult to institute in children, whose small size requires use of surgically placed epicardial rather than percutaneously placed pacemakers. As more registry and retrospective data have accumulated, use of this therapy has increased, and indications based on echocardiographic and ECG parameters continue to be refined.13
Mechanical support may be used in the treatment of acute heart failure (ie, myocarditis or postcardiotomy syndrome) or in chronic heart failure to bridge to recovery or heart transplant. The choice of support therapy depends on the expected duration of use. Extracorporeal membrane oxygenation (ECMO) therapy may be quickly initiated in unstable patients. Generally, its duration of use is limited to days to weeks because complications related to infection or anticoagulation. ECMO is used to provide acute temporary support as a bridge to recovery or transplantation.
Ventricular assist devices (eg, Berlin Heart or Thoratec VAD) may be used to provide long-term ventricular support. Currently, none are approved for permanent therapy in pediatric patients and should only be used as a bridge to transplantation in appropriate candidates.7
Multimedia
 | Media file 1: Chest radiograph shows signs of congestive heart failure (CHF). |
Keywords
congestive heart failure, CHF, congestive heart disease, CHD, heart failure, cardiac failure, cardiac insufficiency, congestive heart failure, myocardial insufficiency, mechanical inadequacy of the heart, left-sided heart failure, right-sided heart failure, compensated heart failure, compensated CHF, decompensated heart failure, decompensated CHF, tachycardia, venous congestion, end-organ compromise, coarctation of the aorta, pulmonary venous obstruction, cardiomyopathy, pericardial effusion, bradyarrhythmia, heart block, respiratory distress, hepatosplenomegaly, ascites, failure to thrive, treatment, diagnosis, renal failure, hepatic failure, syncope, hypertension, hydrops fetalis, patent ductus arteriosus, sinus node dysfunction, dilated cardiomyopathy, malnutrition, ischemia, hypertrophic cardiomyopathy, restrictive cardiomyopathy, cardiac tamponade
The authors and editors of eMedicine gratefully acknowledge the contributions of previous coauthors Gilbert Herzberg, MD, and Lars C Erickson, MD, MPH, to the original writing and development of this article.
More on Heart Failure, Congestive |
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References
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Further Reading
Keywords
congestive heart failure, CHF, congestive heart disease, CHD, heart failure, cardiac failure, cardiac insufficiency, congestive heart failure, myocardial insufficiency, mechanical inadequacy of the heart, left-sided heart failure, right-sided heart failure, compensated heart failure, compensated CHF, decompensated heart failure, decompensated CHF, tachycardia, venous congestion, end-organ compromise, coarctation of the aorta, pulmonary venous obstruction, cardiomyopathy, pericardial effusion, bradyarrhythmia, heart block, respiratory distress, hepatosplenomegaly, ascites, failure to thrive, treatment, diagnosis, renal failure, hepatic failure, syncope, hypertension, hydrops fetalis, patent ductus arteriosus, sinus node dysfunction, dilated cardiomyopathy, malnutrition, ischemia, hypertrophic cardiomyopathy, restrictive cardiomyopathy, cardiac tamponade
