CDH is a severe birth defect, with a prevalence of 1:2000 to 1:3000 live births where a defect in the diaphragm results in, herniation of the abdominal contents into the chest with subsequent compression of the intrathoracic structures. Compression of the intrathoracic structures results in pulmonary and left ventricular (LV) hypoplasia and abnormal development of the pulmonary vasculature in utero. These abnormalities in the development of the heart and lungs in utero, result in persistent pulmonary hypertension of the newborn (PPHN) and respiratory insufficiency after birth. Respiratory insufficiency is managed with intubation and mechanical ventilation. In addition to managing respiratory insufficiency, intubation prevents entrainment of air into the intestines and further compression of the lungs and heart. As part of routine resuscitation in infants with CDH intubation is performed after the delivery personnel separates the baby from the placenta by cutting the umbilical cord. Resuscitation of infants with CDH also involves placement of a nasogastric tube (NG) into the stomach for removal of entrained air and secretions as well as placement of catheters in the umbilical artery and vein for administration of medications (vein) and continuous blood pressure monitoring and sampling of blood (artery). As part of routine practice at our institution, these initial steps of resuscitation are all performed in parallel such that while one team is intubating and initiating ventilation as well as placing the NG tube, another team is placing umbilical lines. This approach has allowed the investigators to obtain arterial blood gas samples in 20 infants with CDH at a median of 4 minutes of life (range 2-9 minutes). When compared to cord blood arterial samples, pCO2 increases by a median of 35mmHg (range 11-77mmHg) from a median cord ABG pCO2 of 55mmHg (range 28-78 mmHg) to 88mmHg (range 65-123 mmHg). In addition to these changes in pCO2 median base deficit changed from -2 ± 0.5350 in the arterial cord blood sample to -7.994 ± 0.8547 in the umbilical arterial blood sample. The resultant respiratory and metabolic acidosis decreased the pH from 7.289 ± 0.01946 in the arterial cord blood sample to 7.036 ± 0.02051 after birth. In addition to the above measures, as part of routine resuscitation, the investigators routinely obtain echocardiographic studies in the first hour of life, to guide pulmonary hypertension management. These studies demonstrate left ventricular (LV) dysfunction and right to left shunting at the ductus arteriosus about 50% of the time. The investigators speculate that the LV dysfunction and increased pulmonary vascular resistance are at least in part due to the acidemia described above. In addition, decreased preload to the LV from right to left shunting at the ductus arteriosus also likely contributes to LV dysfunction. Standard of care for infants with marked abnormalities in gas exchange and LV dysfunction is ECMO rescue early on in the delivery room.