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.

PATHOPHYSIOLOGY

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 flow to the lungs. The postnatal circulation is now that of a low-resistance pulmonary circuit and high-resistance systemic circuit, and the lungs assume the responsibility of gas exchange and oxygenation.²

Asphyxia is defined as failure of gas exchange leading to a combination of hypoxemia, hypercapnia, and metabolic acidemia. If adequate ventilation and pulmonary perfusion are not rapidly established, a progressive cycle of worsening hypoxemia, hypercapnia, and metabolic acidemia ensues. Initially, blood flow to the brain and heart is preserved, whereas blood flow to the intestines, kidneys, muscles, and skin is sacrificed. However, maintenance of blood flow, even to vital organs, cannot be sustained endlessly. Ultimately, ongoing ischemia, hypoxia, and acidosis result in myocardial dysfunction and impaired cardiac output. Inadequate blood flow, perfusion, and tissue oxygenation result in brain injury, multiorgan injury, and even death.

Clinical signs and symptoms of disrupted fetal-to-neonatal transition include cyanosis, bradycardia, hypotension, decreased peripheral perfusion, depressed respiratory drive, and poor muscle tone. Apgar scoring is an objective method of quantifying the infant’s status and to convey information about response to resuscitation, depicted in Table 123-1. The newborn is assessed at 1 and 5 minutes, and if the 5-minute score remains less than 7, additional scores should be assigned every 5 minutes for up to 20 minutes.¹ Because resuscitation must be initiated before a 1-minute score is assigned, Apgar scores should not be used to determine need for resuscitation or to guide steps of resuscitation. However, changes in Apgar scores at sequential time points after birth can reflect how well the infant is responding to resuscitation.

Multiple maternal, placental, mechanical, and fetal problems may occur at any point in the process of pregnancy, labor, or delivery and can jeopardize a smooth fetus-to-newborn transition. The fetoplacental circulation can be compromised for a variety of reasons, all of which may cause deceleration of the fetal heart rate and result in hypoxia and ischemia. In the case of maternal hypotension, the maternal side of the placenta is inadequately perfused. In placental abruption, gas exchange between the fetus and mother is impaired. Blood flow from the placenta or through the umbilical cord (or both) may be compromised, such as with cord compression. A fetus with intrauterine growth restriction may be intolerant of even brief and intermittent interruptions of umbilical blood flow during contractions.

Insufficient respiratory effort as a result of respiratory distress syndrome, maternal narcotic administration, or anesthesia will hamper lung expansion and replacement of fetal lung fluid with air. Other disturbances to normal tissue function can also lead to fluid retention. Foreign material such as meconium or blood may obstruct the neonate’s airway and prevent adequate lung inflation. The end result of any of these situations is inadequate alveolar oxygenation, which in turn sets the stage for the development of persistent pulmonary hypertension of the newborn (PPHN). In this condition, which is also known as persistent fetal circulation, the pulmonary arterioles remain constricted, thereby preventing adequate blood flow to the lungs and resulting in hypoxia and acidosis. Hypoxia and acidosis mediate sustained constriction of the pulmonary arterioles, and a vicious cycle ensues as progressively deoxygenated blood circulates. Transitional physiology does not occur normally, and unoxygenated blood is shunted away from the high-pressure lung circuit. Systemic organ dysfunction and, more importantly, long-term neurologic compromise may result. Other causes of PPHN include problems that cause systemic hypotension, such as excessive blood loss or hypoxia-induced cardiac dysfunction.

OPTIMIZING DELIVERY ROOM RESUSCITATION

Anticipation, adequate preparation, accurate evaluation, and prompt initiation of support are critical for successful neonatal resuscitation. Well-trained personnel must be immediately available in any setting in which an infant might be delivered. Every birth should be attended by at least one person whose primary responsibility is the newly born infant and who is able to initiate resuscitation if needed. Resuscitation equipment should be readily available for each and every birth and lists exist to help this preparation.¹ Personnel attending deliveries should be familiar with the organization of the equipment so that resuscitation can be promptly initiated and support provided. Equipment should be checked at regular intervals and immediately before any delivery. Expiration dates of medications should be monitored regularly.¹

Significant maternal medical history, gestational age, prenatal complications, medications, illicit drug use, and prenatal laboratory values should be recorded. Risk factors for sepsis, including group B streptococcus carrier status, length of rupture of membranes, maternal fever, evidence of chorioamnionitis, and use of intrapartum antibiotics, should be assessed. Specific indicators of fetal condition such as heart rate monitoring, lung maturity, and antenatal ultrasound findings should be communicated. Many conditions exist that place newly born infants at risk for disrupted transition.¹ If a high-risk delivery is anticipated in which significant resuscitative intervention may be necessary, a prenatal consultation by the pediatric team should be performed if time permits, and additional skilled personnel should be present at delivery.¹