CO. washout During intrauterine life the fetus does not breathe. The .fetus does not require .functioning lung to oxygenate its blood. The fetus receives oxygenated blood from the mother through the umbilical vein. The lungs remains collapsed during the fetal life and the pulmonary circulation is a high pressure circuit. So, the fetal blood does not pass through the lungs. Instead, it requires a duct that can bypass the lung and can carry the blood straight way to systemic circulation i.e., Aoa. This function is carried out by ductus aeriosus. During intrauterine life only 10% of the cardiac output passes through the lungs the remaining 90% is shunted through the ductus aeriosus to the Aoa and the systemic circulation. After bih, the umbilical vein is cut off The blood must now pass through the lungs for oxygenation.Soon, after bih fetus stas breathing, the lung is filled with air and it expands. The pulmonary vasculature changes from high pressure circuit to low pressure circuit.Now, the fetal blood must pass through the lungs to facilitate proper gas exchange. In order to make this possible, the ductus aeriosus undergoes constriction, and functional closure occur soon after bih in term neonates. Eighty percent of the ductus aeriosus in term infants close by 48 hours and nearly 100% by 96 hours. Oxygen and endothelins are very strong vasoconstrictors and pro- staglandins E2 and 12 are strong vasodilator of the ductus aeriosus. During fetal life, the 02 concentration is Low and PGE2 and PGI2 level in high. This keeps the ductus aeriosus patent. Soon after bih there is sudden elevation in circulating oxygen tension and fall in prostaglandin levels. This results in strong vasoconstriction and functional closure of the ductus aeriosus soon after the delivery. The functional closure is followed by anatomic closure in the next 1-3 months.But in ceain infants the ductus aeriosus does not close after the bih it remains open and is called patent ductus aeriosus. Since after bih the systemic circulation has higher pressure than the pulmonary circulation the blood flows from Aoa to the pulmonary aery through the patent ductus aeriosus. Hemodynamic consequences of the PDA Shunting of blood from the systemic circulation to the pulmonary circulation results in congestive cardiac failure, which manifests clinically "with wide pulse pressure" and "bounding pulses". Overloading of the pulmonary vasculature leads to pulmonary edema/hemorrhage which predisposes the neonate to "chronic lung" disease (CO2 retention may occur). Blood flow to the kidney and gastrointestinal tract is compromised due to shunting of blood front systemic circulation, predisposing to acute renal failure (ARE) and "necrotizing enterocolitis (NEC) and metabolic acidosis". Hypoperfusion followed by reperfusion increases the risk of "Intraventricular hemorrhage" (1VH). Clinical features :- Hyperdynamic circulation A wide pulse pressure (> 25 mm Hg), prominent precordial pulsations and "bounding pulses"Q. An ejection systolic murmurQ heard best at the 2nd left parasternal area. Metabolic acidosis not attributable to hypoperfusion and sepsis. Deteriorating respiratory status on day 3-4 after a period of relative stability. Increasing ventilator requirements and recurrent apneas. Unexplained CO2 retention, fluctuating F102 requirements.