Pathophysiology
A common congenital defect caused by persistent fetal circulation that accounts for 5% to 10% of all congenital heart defects. When pulmonary circulation is established and systemic vascular resistance increases at birth, pressures in the aorta become greater than in the pulmonary arteries. Blood is then shunted from the aorta to the pulmonary arteries, increasing circulation to the pulmonary system.
Clinical Manifestations
Dyspnea; tachypnea; tachycardia; full, bounding pulses; widened pulse pressure; hypotension may be noted with cardiac output is low. May be asymptomatic. CHF, intercostal retractions, hepatomegaly, and poor growth when a large PDA exists. A continuous “machinery” murmur during systole and diastole, and a thrill in the pulmonic area. High risk for frequent respiratory infections and pneumonia.
Diagnostic Tests
The chest radiograph and ECG show left ventricular hypertrophy.
The PDA can be visualized, and left-to-right shunt can be measured on echo.
Clinical Therapy
Surgical ligation of PDA is the treatment of choice. Transcatheter closure by obstructive device is attempted in some older children.
IV Indomethacin often stimulates closure of the ductus arteriosus in premature infants, but cannot be used if CHF is present.
Prophylaxis for infective endocarditis is required until the PDA closes.
Prognosis
No long-term sequelae occur if treated before pulmonary vascular disease develops. If PDA is not treated, child’s life span is shortened because pulmonary artery hypertension and pulmonary vascular obstructive disease develop.
