Pulmonary Hypertension Christina T. Sheridan, MD Pediatric
cardiologist October 16, 2014
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Disclosures I have no financial disclosures.
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Neonatal Pulmonary HTN Incidence ~2/1000 term births Three main
types Lung parenchymal diseases Idiopathic: normal parenchyma, but
remodeled vasculature Hypoplastic vasculature Symptoms: tachypnea,
increase O2 requirement or vent settings, differential O2 sats in
upper and lower limbs
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Normal transition PVR falls rapidly immediately after birth due
to Mechanical stretch of lung as pulmonary blood flow increases 10x
Decreasing CO2 tension Increasing O2 tension Increase in local
production of vasodilators (NO- cGMP pathway)
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Differential pre-post ductal sats To arms To legs
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Etiologies Lung parenchymal diseases Infection MEC aspiration
Respiratory distress syndrome Idiopathic Premature closure of the
PDA due to maternal use of NSAIDS or maternal use of SSRIs Can
cause RV failure and hydrops in utero Hypoplastic vasculature
Diaphragmatic hernia, chest masses, etc
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Work-up CXR Head US : rule out intraventricular bleed Lab work:
Infection? Polycythemia? Echocardiogram: Rule out structural
defects Assess pulmonary veins Assess direction of PDA and PFO
shunts Quantify degree of PAp via septal curvature and tricuspid
regurgitation (TR) jet
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Quantifying degree of TR PISA refers to the degree of color
bleed of a regurgitant jet. The vena contracta is the narrowest
width of the TR jet where the max velocity is measured by Doppler
Image source: www.echobasics.de
Definitions Normal PVR (pulmonary vascular resistance) is 1-3
Woods units after about 2 months of age Normal SVR (systemic
vascular resistance) is 15-30 Woods units Normal RVsp