USA Surgery Today

Persistent patency of the ductus arteriosus is a common problem in sick, premature infants and can lead to high-output cardiac failure due to aortic to pulmonary artery shunting. In the fetus, 69% of combined ventricular output is oxygenated blood that travels from the placenta to the fetal right atrium through the umbilical vein, ductus venosus, and inferior vena cava (Fig. 4-1:Calan). A portion of oxygen-rich blood that enters the right atrium from the inferior vena cava is shunted preferentially across the atrial septum through the foramen ovale to the left atrium. This oxygenated blood is pumped into the ascending aorta by the left ventricle and is thus more available to the coronary arteries and subclavian and carotid arteries than to the systemic circulation. Because only about 7% of fetal right ventricular output goes to the lungs, owing to supersystemic pulmonary vascular resistance during fetal life, the right ventricle performs about twice as much work as the left ventricle during fetal life. About 90% of right ventricular output flows to the systemic circulation through the ductus arteriosus. Fetal oxygen tension is usually 25 to 30 mm Hg.

The ductus arteriosus shunts blood flow from the pulmonary artery into the aorta. Within hours to days after delivery in full-term infants, as pulmonary vascular resistance falls and arterial oxygenation increases, the patent ductus arteriosus (PDA:Calan) closes by constriction of vascular smooth muscle in its wall, which shortens and narrows its lumen (9:Calan). Failure of the PDA to close after postnatal reduction in pulmonary vascular resistance results in left-to-right shunting from aorta to pulmonary artery, pulmonary hyperperfusion, high-output congestive heart failure, and a diastolic steal syndrome, which reduces perfusion to the splanchnic and renal vascular beds. Failure of closure with persistently supersystemic postnatal pulmonary vascular resistance results in right-to-left shunting from pulmonary artery to aorta and systemic hypoxia proportional to the magnitude of the pulmonic-aortic pressure gradient.

In the preterm infant, functional closure is often delayed. Clinical evidence of a hemodynamically significant PDA includes a systolic or continuous murmur, bounding pulses with widened pulse pressure, hyperdynamic precordium, tachypnea, tachycardia, hepatomegaly, and worsening respiratory failure. Confirmation of patency can be made by echocardiography.