Fetal to Neonatal
Cardiovascular Changes In CHDs
Rush University
Rush Center for Congenital Heart Disease
Ra-id Abdulla, MD
Normal Fetal CV Physiology  

Changes in PVR at birth

       Drop in PVR (8 folds) at birth results from:

       Mechanical: expansion of lungs

       Vasodilation: increase O2 contents

       Liberation of PGE in expanded lungs


Volumes of flow (% of CVO)


Atrial Septal Formation

  • Septum primum initiates division of the common atrium

  • Fenestrations within the septum primum prevents complete separation of atria

  • Septum secundum forms a second layer, to the right of septum primum

  • Septum secundum is incomplete, resulting in foramen ovale

  • Incomplete growth of septum secundum leads to secundum ASD


Atrial Septal Defect

  • Changes in IVC and SVC flow may contribute to ASD formation:

    •  Lower SVC flow

    •  Higher IVC flow

  • Larger than normal flow across PFO:

    •  Larger LA flow, lower RA flow

    •  Larger LV flow, lower RV flow

    •  Larger Ao flow, lower MPA, PDA flow

    •  Higher O2 saturation difference between ascending and descending aorta

  •  Volume overload:

    • Fetal: left heart overload

    • Neonatal: right heart overload


Aortic Stenosis

  •  Increase LV afterload:

    • Decrease LV stroke volume

    • Increase LV, LA pressures

    • Reduce PFO right to left shunting

    • Further decrease in LV stroke

    • Increase LV mass through hyperplasia, not hypertrophy – decrease coronary arterial density

    • Reduction in LV cavity volume

  • More blood from ductus venosus to RV:

    • Reduction of ascending-descending O2 difference

    • Increase O2 content to pulmonary vasculature: abnormal arteriolar development

Hypoplastic Left Heart Syndrome

  • Mechanism: restriction of PFO:

    • Reduced LA, LV volume

    •  Reduced LV cavity

    • Higher flow from ductus venosus to right heart

    •  Greater flow across PDA

    •  Left to right shunting at the PFO

    •  Mono-phasic mitral inflow

    •  LV dysfunction

    •  Reversal flow in aortic arch

  •  Mitral hypoplasia is always less severe than LVOT obstruction

  •  Coarctation of aorta is present in 80% of patients


Coarctation of Aorta

  • Mechanism theories:

    •  Lasso of ductal tissue around aortic arch

    • Abnormal migration of left subclavian artery

  • Reduced flow in ascending aorta:

    •  AS

    • HLH

    • VSD

  • In Noonan: obstructed lymphatic flow leads to dilated thoracic duct

  • VSD: bidirectional shunt:

    •  Mostly left to right: decrease blood flow through isthmus and increases RV output oxygen content


Pulmonary Atresia

  • Reduced RA and RV flow

  •  Increase shunting (right to left) at PFO

  • RV either dilated due to TR, or hypoplastic

  • LV dilated

  • Same O2 content in ascending and descending aorta

  • Smaller PDA

  • Higher O2 content in pulmonary blood: reduced muscular formation of vasculature, increase PBF


Transposition of Great Arteries

  •  RV afterload is reduced as it faces placental circulation, therefore:

    •  Reduced PFO right to left shunting

    •  Increase RA, RV blood flow

  •  Increase flow through ascending aorta: dilation

  •  Increase flow through aortic isthmus

  •  Reduced flow in LA, LV, MPA, PDA

  •  Increase O2 content in blood flow to pulmonary arteries: reduced wall musculature and dilation: increase in PBF pre and postnatally

  •  Reverse ascending-descending aorta saturations


AV Canal Defect

  • Primum ASD allows right to left shunting of IVC blood to LV & aorta → decrease ascending-descending aorta O2 content difference

  •  LVOT narrowing by AVC defect provides resistance to outflow, if coupled with left AV valve regurgitation → drop in LV output → smaller aorta & isthmus


Ebstein Malformation

  • Most cases are mild to moderate: no significant consequences

  • Severe TR:

    • Elevated RA pressure:

    • Congested SVC & IVC → hydrops

    • Congested umbilical vein → placental edema

  • Dilated RV:

    • Poor RV output

    • LV compression  worsening → hydrops