Transitioning Circulation The condition of the infant at birth is dependent, in part, on intrauterine wellbeing and growth Intrauterine growth retardation is the failure of the fetus or infant to achieve his or her predetermined genetic potential Typically, the preterm infant is less than the third centile for weight, length, and head circumference The consequences to the developing heart include cardiac hypertrophy, abnormal diastolic performance, and impaired vascular relaxation.11–13 Doppler interrogation of fetal and neonatal mitral valvar velocities revealed lower E wave amplitude compared with normal mature mitral E peaks.14,15 Impaired early left ventricular filling may relate to a diminished ability to relax and higher muscular stiffness The implications may include impaired myocardial performance, hypertension, and hypotension Poor glycemic control during pregnancy, particularly in the setting of maternal diabetes, is a known risk factor for structural heart disease and hypertrophic cardiomyopathy.16–18 In severe cases, where there is placental malfunction leading to retardation of growth, the same vascular and myocardial dysfunction may occur as described previously Physiology of the Postnatal Transition The preterm infant undergoes dramatic cardiorespiratory changes at birth, which coincide with improved lung compliance and termination of the placental circulation These critical adaptive changes: ▪ Include increased pulmonary blood flow, to approximately 20 times fetal levels ▪ Occur in part due to the exposure of the pulmonary vascular bed to higher alveolar concentrations of oxygen than the relatively hypoxic intrauterine environment Other metabolically active substances, such as metabolites of prostaglandin, bradykinins, or histamine, may play some role through inducing pulmonary vasodilation ▪ Include alteration in flow through fetal channels such as the arterial duct and oval foramen, which may last for many days The major change in flow through fetal channels is either a direct result of increased flow to the lungs or improved systemic arterial tensions of oxygen Increased left atrial pressure secondary to improved pulmonary venous return causes displacement of the flap of the oval foramen over the rims of the fossa, thus abolishing any rightto-left atrial flow The pattern of flow through the arterial duct is significantly altered as lung compliance improves and pulmonary vascular resistance decreases An increase in systemic vascular resistance also occurs once the compliant placenta is removed from the systemic circuit, and as a result of systemic vasoresponsiveness to increased tensions of oxygen This will also contribute to increased transductal flow The architecture of the arterial duct prior to term differs such that ductal tone is less responsive to oxygen, thus delaying closure and potentially contributing to excessive flow to the lungs and compromised systemic flow The administration of surfactant can alter transductal flow significantly through reduced pulmonary vascular resistance There is evidence of functional closure by 6 hours in some immature patients, although this is rare.19 Changes in transductal flow may have a major impact on endorgan perfusion; in particular, the relationship of augmented cardiac output on cerebral reperfusion hemodynamics and intraventricular hemorrhage is subject to recent investigation.20 ▪ Include improved left and right ventricular outputs to meet the metabolic needs of immature neonate with insufficient thermoregulatory mechanisms and increased work of breathing The transition from right to left ventricular dominance occurs over hours and is secondary to increased left atrial preload and left ventricular afterload In total, there is a threefold increase in left ventricular output, which is necessary