Neonatal Resuscitation

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106 Neonatal Resuscitation

Resuscitation of newborns has been documented as far in the past as the 16th century BC, at which time descriptions were recorded of newborns that were likely to survive versus those who were not. The development of assisted ventilation, endotracheal intubation, and oxygen delivery can be traced through the writings of physicians and midwives dating back to the 1600s. In current times, approximately 10% of neonates require some assistance with initiating respiration at birth, and 1% of neonates have need of more aggressive interventions. Neonatal resuscitation has been standardized by the Neonatal Resuscitation Program (NRP), but recognizing the reasoning behind this algorithm requires an understanding of the transition between fetal and neonatal circulation.

Etiology and Pathogenesis

Fetal Circulation

In fetuses, the placenta performs the primary gas exchange function rather than the lungs, and several circulatory adaptations exist to facilitate flow of oxygenated blood through the body and placenta. Deoxygenated blood from the body of the fetus flows to the placenta via the umbilical artery and becomes oxygenated through gas exchange with maternal blood. The oxygenated blood then flows back to the fetus via the umbilical vein (Figure 106-1). The umbilical vein deposits the blood to the inferior vena cava via the ductus venosus, which subsequently delivers it to the right atrium of the heart. In the right atrium, the blood partially mixes with blood from the superior vena cava, and the majority of it streams across the foramen ovale to the left atrium because of the high pulmonary vascular resistance. From the left atrium, blood flows through the left ventricle to the aorta, thereby delivering the most oxygenated blood to the brain via the carotid arteries. The remaining blood in the right atrium, largely from the superior vena cava, flows into the right ventricle and then into the pulmonary artery. A small amount of blood perfuses the lungs and then travels to the left atrium via the pulmonary veins. Most of the blood, however, is diverted across the ductus arteriosus to the descending aorta, where it joins the blood from the left ventricle. From the aorta, the blood is distributed via branches off the aorta and ultimately reaches the umbilical artery and the low pressure placenta again (Figure 106-2).

Asphyxia

Fetuses are relatively hypoxemic compared with neonates; fetal partial pressures of arterial oxygen are between 20 and 25 mm Hg. Therefore, fetuses are particularly vulnerable to asphyxia. However, several adaptations exist to protect fetuses. Fetal hemoglobin has a higher affinity for oxygen than adult hemoglobin, and fetal tissues are more efficient at extracting oxygen than adult tissues. In addition, the “diving reflex” allows for blood flow to be distributed preferentially to the brain, adrenal glands, and heart and away from the lungs, gut, liver, spleen, kidney, and extremities to decrease oxygen consumption in the event of asphyxia.

In some cases, the fetal reserve is not enough to protect the infant from difficulties with transition. Neonatal asphyxia can result from multiple factors, both maternal and fetal (Table 106-1), and may begin in utero. The initial response to asphyxia is a brief period of rapid breathing followed by “primary apnea.” During primary apnea, stimulation such as drying or slapping the feet will restart breathing. If the apnea is prolonged, the infant loses muscle tone and becomes cyanotic and then bradycardic. After a few gasping respirations, the neonate enters “secondary apnea.” At this point, ventilatory support must be provided for the newborn to survive. In this situation, an infant requires resuscitative efforts to aid in the transition to extrauterine life.

Table 106-1 Conditions Predisposing to Neonatal Asphyxia

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Maternal  
Uterus Uterine malformations, hypertonus, rupture
Infection Chorioamnionitis
Blood Anemia, hemoglobinopathy
Vascular Diabetes, hypertension, preeclampsia, hypotension