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Questions

  

B.6. What are the causes of heart failure (HF) in this infant? How would you assess this infant in your preoperative evaluation for signs of HF?

Answer:

The causes of HF in this infant can be divided into five major areas:

HF occurs either in response to an excessive volume or pressure load or as a consequence of myocardial muscle impairment. Volume overload is due to factors causing a large increase in cardiac output (eg, large VSD or ductus arteriosus). In these circumstances, there must be a sufficiently large left-to-right shunt to cause severe strain on the heart. In the normal newborn, these lesions do not usually produce HF until 1 to 2 months of age because it takes longer than usual for the pulmonary vascular resistance to fall. Elevated pulmonary vascular resistance protects the left ventricle from the stress of overcirculation. This is not true in premature neonates who do not manifest the same degree of pulmonary arteriolar constriction; therefore, they are susceptible to large left-to-right shunts early and show HF more readily.

Regurgitant valvular lesions can also lead to HF. In complex CHD (ie, TA or tricuspid atresia with transposition), the additional stress of hypoxemia or univentricular overload can herald the early onset of HF. Large arteriovenous malformations can also occur intracranially and cause HF. Excessive pressure loads are seen in obstruction to cardiac output from aortic stenosis, aortic coarctation, and aortic interruption.

In the immediate newborn period, right-sided HF is seen with greater frequency because of severe pulmonary hypertension. Pulmonary hypertension has many causes including intrinsic lung parenchymal insufficiency or pathology (ie, diaphragmatic hernia, meconium aspiration, or hyaline membrane disease), chronic hypoxemia, hypervolemia, and polycythemia.

Primary myocardial failure is unusual and rare in the newborn. If it occurs, it is likely due to endocardial fibroelastosis and anomalous coronary circulation. Nonetheless, the myocardium in the infant is susceptible to depression from metabolic derangements such as hypoglycemia, hypocalcemia, hypoxemia, and hypercarbia. Also, severe anemia with the associated decreases in systemic and myocardial oxygen supply forces an increase in myocardial work that can lead to HF.

Infants are different from adults in their manifestations of HF. Signs of cardiac dilation can be absent because of decreased systemic venous return from the elevated intrathoracic pressure as a consequence of coexisting lung disease in premature infants. Although immature, the carotid baroreceptors still initiate an increase in sympathetic outflow in response to reduced perfusion. The increased α-adrenergic stimulation impairs blood flow to the systemic arteriolar beds, resulting in cold, underperfused extremities and diminished splanchnic perfusion. Fatigue, loss of appetite, and failure to thrive quickly follow. Tachycardia from β-adrenergic receptor stimulation occurs. Generalized sweating results from sympathetic cholinergic fiber stimulation. Extracellular water increases because of decreased renal excretion of sodium due to a decreased glomerular filtration rate; however, peripheral pitting edema is much less common in infants compared to older children and adults. The venous system in infants is extremely distensible, so much so that elevated right atrial pressures might not show jugular venous engorgement. The most prominent manifestation of HF in the infant is tachypnea. Because pulmonary venous pressure is elevated from left ventricular failure, the lung compliance decreases because of the augmented interstitial fluid. Breathing becomes rapid and shallow, further increasing oxygen requirements, which leads to a cyclic dependency to maintain both tachycardia and tachypnea. It is common to see subcostal retractions due to the increase in respiratory effort in infants with HF.

Infants have a greater lymphatic drainage capacity compared to adults and can clear interstitial fluid more readily. Therefore, rales are less often appreciated in infants with HF, as opposed to adults with HF. The bronchial mucosa can become swollen because of engorgement of the bronchial venous system, resulting in narrowing of the airway lumen. This can produce an audible wheeze that is often seen in infantile HF. Lastly, hepatomegaly is a cardinal sign of right ventricular failure in infants.

References