persistant ductus arteriosus

7. Within the first few hours after birth Decreased circulating PGE2 &PGI2 levels due to elimination of placental source & increased metabolism in lung Abrupt increased arterial PaO2 Medial smooth muscle fibers in the ductus contract The inner muscle wall of the ductus arteriosus develops profound ischemic hypoxia Formation of vascular endothelial growth factor, transforming growth factor beta and other inflammatory mediators and growth factors Transform the ductus arteriosus into a non-contractile ligament How ductus close after birth Inhibite ductal smooth muscle voltage dependant K channel Influx of Ca

9. Failure of closure of DA IN PRETERM NEONATE PATENT DUCTUS ARTERIOSUS Poor PG metabolism by immature lung High sensitivity to prostaglandin (premature ductus) Reduced Ca sensitivity to O2 in ductal musculature

12. Structural Defects and Cardiac Circulation with PDA Where does the blood shunt to? Is the shunted blood oxygenated or deoxygenated? What happens to the blood flow in the aorta?

15. Oxygenated blood passes from the aorta to the pulmonary artery Pulmonary Overcirculation Left heart volume overload Increased left atrial and left ventricular end-diastolic pressures The left ventricle compensates by increasing stroke volume Hypertrophy Effect of shunting

16. Effect of long standing Left-to-right shunting Progressive morphological changes in the pulmonary vasculature Arteriolar medial hypertrophy, intimal proliferation and fibrosis Obliteration of pulmonary arterioles and capillaries Progressive increase in pulmonary vascular resistance Pulmonary vascular resistance exceeds systemic vascular resistance Shunting reverses & becomes right-to-left [ Eisenmenger’s Syndrome ]

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