In order for a normal transition from fetal to newborn physiology to occur, a complicated and well-orchestrated sequence of physiologic changes must transpire. While the majority of newborns transition from fetal to postnatal circulation without significant difficulty, it is estimated that 10% require some degree of resuscitation in the delivery room and about 1% require significant resuscitation.1 Birth asphyxia accounts for approximately 23% of the 4 million neonatal deaths per year.1 Delays in establishing effective cardiorespiratory function may increase the risk for hypoxic-ischemic cerebral injury, pulmonary hypertension, and systemic organ dysfunction. Some of these injuries may be preventable with prompt resuscitation. However, some of these outcomes are related to events or exposures that precede the birth process, such as prenatal injuries, abnormal development, and insults to the intrauterine environment.
The adaptation from intrauterine life to extrauterine life starts during the process of labor.2 Labor not only increases oxygen consumption in the transitioning fetus but also causes brief periods of asphyxia during contractions as umbilical venous blood flow is briefly interrupted. The fetus tolerates this interruption in blood flow because fetal tissue beds have greater resistance to acidosis than adult tissue beds do. The fetus responds to bradycardia with the “diving reflex” whereby blood preferentially flows to the brain, heart, and adrenal glands. Finally, the fetus is capable of switching to anaerobic sugar production, provided that liver glycogen stores are adequate.
During labor and delivery, catecholamine levels surge and increase lung fluid resorption, release of surfactant, and stimulation of gluconeogenesis. This surge also helps direct blood flow to vital organs such as the heart and brain. With clamping of the umbilical cord, the low-resistance placental circuit is removed from the newborn’s circulation. Systemic blood pressure increases, and transition to the postnatal circulation begins.2
As a newly born infant takes the first few breaths, negative intrathoracic pressure is generated, which helps the lungs expand and become filled with air. Alveolar oxygenation increases as air replaces the fetal lung fluid. The negative intrathoracic pressure, however, is countered by lung compliance, lung fluid viscosity, and surface tension forces. Because these factors need to be overcome to establish adequate alveolar expansion, the infant must take deep enough breaths to create the large transpulmonary pressure initially required after birth. Surfactant, a phospholipid-protein complex that is produced by type II pneumocytes and is deposited along the alveolar surfaces, also helps counteract alveolar surface tension and promote alveolar stability. As a result of the increasing effect of surfactant, less transpulmonary pressure is needed for subsequent breaths, and functional residual capacity is soon established. Pulmonary blood flow increases as the lungs expand, and pulmonary vascular resistance declines under the influence of oxygen-mediated relaxation of the pulmonary arterioles. This increase in pulmonary blood flow in turn allows the patent foramen ovale and the patent ductus arteriosus to functionally close, thereby allowing further blood ...