The transition from fetus to neonate represents a series of rapid and dramatic physiologic changes during which the placenta is replaced by the lungs as the primary organ of gas exchange. Although this transition goes smoothly most of the time, in approximately 10% of births the active intervention of a skilled individual or team is necessary to ensure that the newborn receives the appropriate assistance to assume independent existence as quickly as possible.18,19 The need for full resuscitation, including chest compressions and/or medication administration is relatively rare, occurring in approximately 1 to 2 per 1000 live births.31 For these severely depressed newborns and for extremely premature infants, to avoid or minimize injury, the process of resuscitation during the first hour of life requires excellent communication, cognitive knowledge, skilled technical providers, and behaviors that are integral to a collaborative team effort. Although certain episodes of fetal asphyxia cannot be prevented, there are many circumstances in which, in the immediate neonatal period, a prompt and skilled resuscitation may prevent death or ameliorate lifelong adverse sequelae. Newborns who require medication and/or chest compression in the first few minutes after birth usually have significant fetal acidemia or inadequate ventilation after birth, or both.31 Because the need for significant intervention cannot always be predicted, the American Heart Association (AHA)/American Academy of Pediatrics (AAP) Textbook on Neonatal Resuscitation and the Guidelines for Perinatal Care have advised: “At least one person skilled in initiating neonatal resuscitation should be present at every delivery. An additional person capable of performing a complete resuscitation should be immediately available.”4,19 The Guidelines also suggest that “the identification and resuscitation of a distressed neonate requires an organized plan of action” and that hospitals should assure the competency and periodic credentialing of individuals who perform these tasks.4 In the past two decades, neonatal resuscitation has been the subject of extensive research and review. The evidence evaluation process of the International Liaison Committee on Resuscitation (ILCOR) provides perhaps the most evidence-based guidelines in all of medicine.47 Although many elements of a resuscitation sequence have been agreed upon, debate and discussion regarding certain aspects of the process continue.44 Moreover, the ILCOR guidelines are a Consensus of Science and Treatment Recommendations (CoSTaR) document, and each national resuscitation council may modify the treatment recommendations based on its members’ own deliberations of the science and what is deemed appropriate for its country. Thus, despite one international scientific document, there are often significant differences among the recommendations for performing neonatal resuscitation in various countries.33 Research continues to search for answers to many difficult questions. The US guidelines published by the AAP and the AHA19 are essentially derived from the ILCOR CoSTaR.47 These recommendations represent the best distillation of the available science at the time of their publication as viewed by the Neonatal Resuscitation Program Steering Committee of the AAP and should serve as the foundation for any resuscitation program or algorithm in the United States. This chapter presents the current guidelines for neonatal resuscitation and reviews the evolving science in this area to provide an appreciation of common and controversial questions and a basis for understanding conflicting views. The placenta has the lowest resistance in the circulatory system of the fetus and preferentially receives blood from the systemic circulation. Approximately 40% of the total cardiac output of the fetus flows through the placenta. Blood in the umbilical artery leaving the fetus en route back to the placenta has a Po2 of 15 to 25 mm Hg.24 In humans, umbilical venous blood returning from the placenta to the fetus obtained by percutaneous umbilical vein sampling has a Po2 normally 20 to 40 mm Hg, but it may range up to 45 mm Hg.28 When the umbilical venous blood is mixed with venous return from the fetus, the resultant Po2 is lower. Although the arterial oxygen tension of the fetus is low compared with postnatal values, the high affinity of fetal hemoglobin for oxygen shifts the oxyhemoglobin curve to the left, resulting in only mildly diminished oxygen content of the blood. Several adaptive and anatomic mechanisms help keep fetal tissue well perfused and oxygenated despite low oxygen tension. When the umbilical vein enters the abdomen of the fetus, the stream splits, with slightly more than half of the blood flowing through the ductus venosus into the inferior vena cava. The remaining blood perfuses portions of the liver. The umbilical venous return entering the inferior vena cava tends to stream and does not completely mix with less oxygenated blood entering the inferior vena cava from below. In the right atrium, the crista dividens splits the inferior vena cava stream so that oxygenated blood from the umbilical vein flows through the foramen ovale into the left side of the heart. The less oxygenated blood returning from the body flows into the right ventricle (Figure 32-1). The circumstances and process of delivery contribute to the condition of the infant at birth. A cesarean section done before the onset of labor has a different physiologic effect on the process of transition than the standard labor process. Delivery of a multiple gestation and anesthesia administered to the mother may also be significant contributing factors. The labor process causes mild hypoxia and acidosis to some extent. With each contraction, uterine blood flow decreases, with a resulting decrease in placental perfusion and a temporary impairment of transplacental gas exchange; this is accompanied by transient hypoxia and hypercapnia. The intermittent nature of normal labor permits the fetus to “recover” between each contraction; however, the effect is cumulative. Throughout a normal labor, the fetus undergoes a progressive but slow reduction in Po2, some increase in Pco2, a decrease in pH, and the accumulation of a base deficit (Table 32-1).9 The normal fetus enters labor with a base excess of −2 mmol/L; with uncomplicated progression of labor to vaginal delivery, the base excess will be reduced by an additional 3 to 4 mmol/L.9,35 In the normal circumstance, these changes are not significant enough to depress the infant and prevent normal transition from intrauterine to postnatal existence. TABLE 32-1 Fetal Scalp Blood Values during Labor* Data from Boylan PC, et al. Fetal acid-base balance. In: Creasy RK, et al, eds. Maternal-fetal medicine. Philadelphia: Saunders; 1989. With birth, the neonate must establish the lungs as the site of gas exchange; the circulation, which in the fetus shunted blood away from the lungs, must now fully perfuse the pulmonary vasculature. Postnatal breathing is on a continuum with in utero breathing movements that are well established but intermittent in the term fetus.30 Clamping of the cord at birth stimulates peripheral and central chemoreceptors, and in conjunction with tactile and thermal stimulation, results in an increased systemic blood pressure. This combination of events is usually enough stimulation for a noncompromised infant to pursue breathing vigorously. However, it should be noted that when feasible, cord clamping should be delayed 30 to 60 seconds in preterm infants to increase blood volume, decrease need for inotropic support, and reduce several complications of prematurity.32 The clearance of lung fluid after birth is the result of multiple processes and only minimally caused by the “thoracic squeeze” during passage through the birth canal. A few days before a normal term vaginal delivery, the fetal production of lung fluid slows, and alveolar fluid volume decreases.7 The process of labor is a powerful stimulus for the clearance of lung fluid, and that transfer of fluid from the air spaces is predominantly a process of active transport into the interstitium and drainage through the pulmonary circulation, with some fluid exiting through lymphatic drainage.17 Although started before labor and influenced by the increasing levels of endogenous catecholamines, the process accelerates immediately after birth. The first few breaths must facilitate clearance of fluid from the lungs and establish a functional residual capacity (FRC) (see Chapter 33).41,42,46 The first breath of a spontaneously breathing infant has some unique characteristics. Although the peak inspiratory pressure is usually between −20 cm H2O and −40 cm H2O, the opening pressures are very low. That is, gas begins to enter the lungs at very low pressures, usually less than −5 cm H2O pressure. Very high expiratory pressures are also generated; these pressures generally exceed the inspiratory pressure. This expiratory pressure, probably generated against a closed glottis, aids in clearing lung fluid and leads to a more even distribution of air throughout the lung. In a vigorous, spontaneously breathing, vaginally delivered infant, a significant FRC develops at the end of the first breath (Figure 32-2).26 Expansion of the lungs is a stimulus for surfactant release, which reduces alveolar surface tension, increases compliance, and helps maintain a stable FRC. Simultaneously the act of ventilation alone reduces PVR. Ventilation leads to a decrease in Pco2 and an increase in pH and Po2, also causing a decrease in PVR.10 The administration of oxygen is not necessary to produce this drop in PVR. In a study of lambs, Lakshminrusimha and colleagues20 showed that PVR decreased nearly as much (72%) in the first 30 minutes after birth with air resuscitation as with 100% oxygen. By 60 to 90 minutes after birth, the decrease in PVR in the air group had reached the same level as the 100% oxygen group. Figure 32-3 illustrates the relationships between pH, Po2, and PVR.36 Clearance of lung fluid, establishment of FRC, and a decrease in PVR with an increase in pulmonary blood flow facilitate postnatal ventilation and oxygenation. A newborn may be compromised because of problems initiated in utero with the mother, the placenta, or the fetus itself (Box 32-1). A process initiated in utero may extend into the neonatal period, preventing a normal transition. An asphyxial process also may be neonatal in origin; that is, the infant seems well until required to breathe on his or her own.
Overview and Initial Management of Delivery Room Resuscitation
Fetus
Transition at Birth
Early First Stage
Late First Stage
Second Stage
pH
7.33 ± 0.03
7.32 ± 0.02
7.29 ± 0.04
Pco2 (mm Hg)
44 ± 4.05
42 ± 5.1
46.3 ± 4.2
Po2 (mm Hg)
21.8 ± 2.6
21.3 ± 2.1
16.5 ± 1.4
Bicarbonate (mmol/L)
20.1 ± 1.2
19.1 ± 2.1
17 ± 2
Base deficit (mmol/L)
3.9 ± 1
4.1 ± 2.5
6.4 ± 1.8
Causes of Depression and Asphyxia
