Circulatory adaptation at birth
Oxygenated
placental blood (PaO2 75kPa) returns to the foetus via the umbilical vein. Blood bypasses the
liver via the ductus venosus and flows into the inferior vena cava, and then
the right atrium. This blood is then channeled to the left atrium and so to the
left ventricle (via the foramen ovale). Oxygenated
blood is then pumped to the cerebral and coronary vessels. The right ventricle
mostly receives deoxygenated blood
from the superior vena cava. About 15% is pumped to the lungs and the rest is
diverted, via the ductus arteriosus, to the descending aorta so that it can go
to the placenta via the umbilical arteries.
At birth, oxygen inhalation leads
to pulmonary arterial vasodilatation, lead-ing to ‘fall’ arterial resistance
and ‘rise’pulmonary blood flow. At the same time systemic vascular resistance
‘rise’due to loss of the low resistance placental circulation. The ductus
arteriosus constricts as PaO2 i. The foramen ovale closes as
pulmonary venous return to left atrium ‘rise’and right atrial pres-sure d.
Although initially rapid, these changes consolidate over 2–3wks.
Failure of pulmonary vascular
resistance to fall after birth causes decreased pulmonary blood flow; incidence
1/1000–1500 live births.
Causes
Rarely primary/idiopathic due to
disease of pulmonary vasculature.
More commonly, it is a secondary
complication of severe illness.
•
Hypoxia
disproportionate to any difficulty with CO2 elimination.
•
Discrepancy
between pre- and post-ductal arterial oxygen saturations >10%.
•
Mild
breathlessness (as PaCO2, not PaO2, is the main
physiological determinant of respiratory rate), acidosis, hypotension.
•
Loud
single second heart sound.
Echocardiography shows ‘rise’pulmonary
arterial pressure, large right to left shunt at the level of the foramen ovale
and ductus arteriosus.
•
Treat
cause; minimal handling.
•
Optimize
BP, pH (aim high-normal), Hb, U&E, blood glucose.
•
Ventilate
(aim for high PaO2 and normal PaCO2). HFOV may be
helpful.
•
Inhaled
nitric oxide (results in selective pulmonary vasodilatation): dose 20ppm for
6hr initially and monitor for toxic levels of NO2 and
methaemoglobin.
•
ECMO,
if severe.
10–30% mortality. Risk of
neurodevelopmental impairment in survivors.
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