congenital heart defects: PDA Flashcards

1
Q

most common defect associated with

A

maternal rubella syndrome

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2
Q

PDA are prominent in

A

females

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3
Q

abnormal transcription factors

A

TFAP2B-neural crest transcription factor

associated with Char syndrome and PDA

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4
Q

infants with high incidence

A

preterm

<28 weeks gestation

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5
Q

embryological from

A

VI pharyngeal arch artery

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6
Q

pathophysiology behind PDA

A

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

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7
Q

why does persistent DA remain open after a few weeks?

A
  • deficiency of endothelial and muscular layer of vessel, regulator proteins to direct fibrosis
  • or, another cardiac lesion needing this channel blood flow
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8
Q

what causes flow thru PDA?

A

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)

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9
Q

large PDA will?

A

increase LV pressure during diastole which will increase LA pressure and then pulmonary venous pressure

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10
Q

clinical presentation of PDA

A
  • normal at birth

- ALL INFANTS WITH PDA WITH SHOW INCREASED PERIPHERAL PULSE PALPATIONS

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11
Q

small PDA

A

at 2-6 weeks:
systolic murmur
maybe pulses may be present in an asymptomatic infant

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12
Q

large lesion PDA

A
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
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13
Q

small PDA will have a normal

A

CXR and ECG

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14
Q

CXR

A

increased pulmonary artery, aorta, pulmonary vascular markings,
-may have increased LV and LA if large

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15
Q

ECG

A

normal to LVH

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16
Q

Echo

A
  • normal LA and LV size with small shunt
  • large shunt gives increased LV and LA size (La:Ao root ratio increased)
  • visualized by suprasternal notch view
17
Q

PDA prognosis: small lesion

A

normal life span

-maybe CHF late in life, bacterial endocarditis, pulmonary or systemic embol

18
Q

PDA prognosis: large

A
  • risk for: CHF, bacterial endocarditis, pulmonary or systemic emboli
  • pulmonary HTN
  • eisenmonger’s syndrome
  • palpitations
  • ductal rupture
19
Q

treatment

A

closure of ALL lesions
-closure reverses cardiac failure: continuous murmur is gone leaving systolic flow murmur (turbulence in dilated pulmonary artery), LV size and function improves