PATH - Congenital Heart Diseases - L-to-R Shunts Flashcards
LEFT-TO-RIGHT SHuNTS
Late cyanosis (2° to Eisenmenger syndrome)—“blue kids.”
Frequency: VSD > ASD > PDA.
Right-to-Left shunts: eaRLy cyanosis.
Left-to-Right shunts: “LateR” cyanosis
Ventricular septal defect
Most common congenital cardiac defect.
Asymptomatic at birth, may manifest weeks later or remain asymptomatic throughout life.
O2 saturation INC in RV and pulmonary artery
Most self resolve; larger lesions may lead to LV overload and HF.
Atrial septal defect
Defect in intertribal septum
loud S1; wide, fixed split S2.
Ostium secundum defects
most common
O2 saturation in RA, RV, and pulmonary artery.
Symptoms range from none to HF.
Distinct from patent foramen ovale in that septa are
missing tissue rather than unfused
Patent ductus arteriosus
In fetal period, shunt is right to left (normal).
In neonatal period shunt becomes left to right–>progressive RVH and/or LVH and HF
Associated with a continuous, “machine-like” murmur
“Endomethacin” (indomethacin) ends patency of PDA; PGE keeps ductus Going
Uncorrected PDA can eventually result in late cyanosis in the lower extremities (differential cyanosis)
Eisenmenger syndrome
Uncorrected left-to-right shunt (VSD, ASD,PDA)–>INC pulmonary blood flow–>pathologic remodeling of vasculature–>pulmonary
arterial hypertension–>RVH occurs to compensate–>shunt becomes right to left
Causes late cyanosis, clubbing, and polycythemia
Coarctation of the aorta
Aortic narrowing near insertion of ductus arteriosus (“juxtaductal”)
Hypertension in upper extremities and weak, delayed pulse in lower extremities (brachial-femoral delay)
Associated with bicuspid aortic
valve, other heart defects, and Turner syndrome.
With age, intercostal arteries enlarge due to collateral circulation; arteries erode ribs–> notched appearance on CXR
Complications include HF, risk of cerebral hemorrhage (berry aneurysms), aortic rupture, and possible endocarditis.
