Pediatric Congestive Heart Failure Workup

Updated: Apr 23, 2019
  • Author: Gary M Satou, MD, FASE; Chief Editor: Stuart Berger, MD  more...
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Approach Considerations

Appropriate laboratory testing includes assessment of the following: oxygen saturation, complete blood count (CBC), hemoglobin concentration, electrolyte levels, calcium level, cardiac biomarkers, blood urea nitrogen (BUN) level, creatinine level, and renal [3] 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. Serial measurements of BNP levels in children with primary myocardial dysfunction and acute decompensated heart failure in which levels are persistently elevated and/or there is a lesser degree of decline in the first week of presentation are adverse prognostic factors. [6]

Cardiac troponin may be elevated in cases of myocarditis or after ischemic injury due to coronary anomaly or cardiomyopathy, as well as in noncardiac conditions in which cardiac perfusion may be compromised (sepsis).

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.

A 12-lead electrocardiogram (ECG) may reveal evidence of structural or coronary artery disease or a complete atrioventricular block or arrhythmia.

Pulse oximetry, as well as a hyperoxia test in newborns, may be useful. The systemic saturation on room air is a more reliable measure of oxygenation than are observations for cyanosis 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.


Radiography and Echocardiography

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 to 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. (See the image below.)

Chest radiograph shows signs of congestive heart f Chest radiograph shows signs of congestive heart failure (CHF).

Echocardiography is indicated in any child with unexplained congestive heart failure to assess cardiac function and identify potential cardiovascular causes, particularly anatomic lesions and cardiomyopathy. 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 by means of 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.