Ventricular Septal Defect
VSD is one of the most common congenital cardiac abnormalities; see earlier VSD discussion.
Atrial Septal Defect
An atrial septal defect has a loud S1 and a wide, fixed split S2; see earlier ASD discussion.
Patent Ductus Arteriosus
Within hours after birth, the increased oxygenation of blood and decreased circulation of prostaglandins through the ductus arteriosus mediate closure of the ductus. When
this does not occur, a patent ductus arteriosus (PDA) can persist, leaving a connection
between the left pulmonary artery and aortic arch. Because the left heart has higher pressures than right heart at birth, a left-to-right shunt develops, with blood flowing from the aorta into the pulmonary artery. It is most common in premature infants who are hypoxic. It does not result in early cyanosis, because there is no rightto- left shunting.
- Results in a continuous “machine-like” murmur because blood is flowing throughout
systole and diastole from aorta into pulmonary artery.
- Administration of prostaglandin inhibitors (eg, indomethacin, nonsteroidal antiinflammatory drugs [NSAIDs]) enhances closure of the PDA.
If these left-to-right shunts do not close, and high blood flow continues through the
pulmonary circulation, the pulmonary arterial system becomes hypertrophic and even
fibrotic, resulting in pulmonary hypertension. Increased right-sided pressure leads to
right ventricular hypertrophy. When the right-sided pressure becomes higher than leftsided pressure, the shunt reverses and becomes right-to-left. This shunt reversal is termed Eisenmenger syndrome and causes late cyanosis in early adulthood from shunting of deoxygenated blood into systemic circulation.