congenital heart defects: PDA Flashcards
most common defect associated with
maternal rubella syndrome
PDA are prominent in
females
abnormal transcription factors
TFAP2B-neural crest transcription factor
associated with Char syndrome and PDA
infants with high incidence
preterm
<28 weeks gestation
embryological from
VI pharyngeal arch artery
pathophysiology behind PDA
ductus arteriosus constricts in response to increased pO2 and decreased PGE2 in arterial blood shortly after birth
-not closed-> blood shunted from aorta thru ductus into pulmonary artery
why does persistent DA remain open after a few weeks?
- deficiency of endothelial and muscular layer of vessel, regulator proteins to direct fibrosis
- or, another cardiac lesion needing this channel blood flow
what causes flow thru PDA?
decreasing pulmonary VR and lower diastolic pressures in pulmonary artery causes flow through the PDA
-initially in systole (systolic murmur) then in both systole and diastole (continuous)
large PDA will?
increase LV pressure during diastole which will increase LA pressure and then pulmonary venous pressure
clinical presentation of PDA
- normal at birth
- ALL INFANTS WITH PDA WITH SHOW INCREASED PERIPHERAL PULSE PALPATIONS
small PDA
at 2-6 weeks:
systolic murmur
maybe pulses may be present in an asymptomatic infant
large lesion PDA
at 2-6 weeks: -signs of CHF -LV thrust -continuous murmur (diastolic) at ULSB, radiates to back -liver enlarged -peripheral pulse bounding diastolic rumble at apex
small PDA will have a normal
CXR and ECG
CXR
increased pulmonary artery, aorta, pulmonary vascular markings,
-may have increased LV and LA if large
ECG
normal to LVH