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).

Figure 106-1 Circulation in placenta.

Figure 106-2 Prenatal and postnatal circulation.

Transition to Neonatal Circulation

This system changes dramatically when the infant is born. Because of the stress of labor and delivery, the baby experiences a catecholamine surge at birth. Catecholamines regulate fluid resorption in the lungs, surfactant release into the alveoli, temperature, glucose mobilization, and blood flow to the brain and vital organs. When the umbilical cord is clamped, the placenta is removed from the circulation, causing a large increase in systemic vascular resistance. When the infant takes his or her first breath, the pulmonary vascular resistance decreases precipitously, causing blood to travel through the right atrium to the right ventricle and then the lungs rather than through the foramen ovale to the left atrium. The lower pulmonary pressures also result in less blood flow across the ductus arteriosus and more flow from the pulmonary artery to the lungs. The ductus venosus, ductus arteriosus, and umbilical vessels eventually constrict, leaving the infant with a fully intact neonatal circulatory system (see Figure 106-2). The initial breaths taken by the infant also must inflate the lungs and effect a change in vascular pressures so lung water is absorbed into the pulmonary arterial system and cleared from the lung.

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

Neonatal Resuscitation Guidelines

The NRP was introduced in 1987; its goal is to ensure that a health care professional trained in providing care to newborns just after delivery is present at every birth in the United States. To accomplish this goal, the NRP has compiled an algorithm standardizing neonatal resuscitation techniques, which was last revised in 2005 (Figure 106-3).

Figure 106-3 Overview of neonatal resuscitation.

The first step in neonatal resuscitation is the initial evaluation of the infant, beginning with assessment of four parameters: the infant’s gestational age, the presence or absence of breathing, respiratory effort or crying, and muscle tone. See below for a discussion of meconium and the resuscitation of premature infants.

If an infant is not breathing or has poor muscle tone, the first steps in resuscitation are to provide warmth, clear the airway, position the infant so that the airway is open, and dry and stimulate the baby.

After 30 seconds, the baby’s respiratory rate, heart rate, and color should be reevaluated. If the baby is apneic or the heart rate is less than 100 beats/min, positive-pressure ventilation should be initiated at a rate of 40 to 60 breaths/min. If the baby is breathing and has a heart rate greater than 100 beats/min but is cyanotic, supplemental oxygen should be provided. If the baby remains cyanotic despite this intervention, positive-pressure ventilation must commence. Positive-pressure ventilation should be administered via a bag and mask; endotracheal intubation can also be considered at this point to facilitate ventilation. Effective ventilation is the most important step in neonatal resuscitation; the baby will not be able to generate adequate cardiac output if the lungs are not adequately inflated. High inflating pressures (25-40 cm H₂O) may be necessary initially because the lungs remain filled with fluid, but with expansion, pressures must be decreased to only that which adequately moves the chest wall.

Thirty seconds later, if the heart rate remains less than 60 beats/min with effective positive-pressure ventilation, chest compressions should be initiated with the two-thumb technique. The chest should be compressed to one-third to one-half the anteroposterior diameter of the chest at a ratio of three compressions to one breath given (Figure 106-4). Chest compressions continue until the heart rate rises above 60 beats/min. If, after 30 seconds, the heart rate does not rise, then epinephrine should be administered. Epinephrine can be administered through the endotracheal tube or intravenously (often via the umbilical vein); the intravenous route is preferred because the endotracheal route yields lower serum concentrations. The dose is 0.01 to 0.03 mg/kg of epinephrine diluted to a 1 : 10,000 concentration. Thirty seconds later, the heart rate should be assessed again; if the heart rate remains less then 60 beats/min, epinephrine can be repeated every 3 to 5 minutes until the heart rate increases.

Figure 106-4 Bag and mask ventilation and chest compressions.

The Apgar scores are also assessed during this time; the infant is given a score at 1 and 5 minutes of life but should continue to be scored every 5 minutes until a score of 7 is achieved (Table 106-2).

Volume expansion is indicated if the baby still does not respond to resuscitative efforts and appears pale with delayed capillary refill or weak pulses. Hypovolemic shock can result from an acute hemorrhage from a placental abruption or placenta previa or blood loss from the umbilical cord (Figure 106-5). Isotonic, crystalloid solutions, including normal saline and lactated Ringer’s solution, are best for acutely treating hypovolemia. O-negative, Rh-negative packed red blood cells can also be given if there is evidence of fetal anemia or severe fetal blood loss. Volume expansion should be accomplished with small volumes, 10 mL/kg at a time, to decrease the risk of intraventricular hemorrhage.

Figure 106-5 Placental abruption and previa.

Consideration of anatomic or structural abnormalities affecting the airway is necessary if the baby remains depressed after these interventions. The presence of pneumothorax, congenital diaphragmatic hernia (CDH), congenital heart disease, and airway malformations would require adjusted therapies to resuscitate the infant.

Resuscitation of Premature Infants

Premature infants, particularly extremely premature infants (weight <1000 g) require special attention during resuscitation. The same algorithm is followed, with some additions to account for their specific needs. Premature infants are more likely to develop respiratory distress than term infants. As a result, assisted ventilation must be provided effectively but gently. Endotracheal intubation is usually necessary for surfactant administration. Premature infants are much more fragile than term infants; therefore, they must be gently handled to avoid inducing injury or intraventricular hemorrhage. Because premature infants have a much larger relative surface area and less well-developed skin, careful attention must be paid to drying the infant immediately and keeping the infant warm, usually via a radiant warmer bed.

Ventilation of preterm infants also warrants particular consideration. Prevention of lung overinflation is crucial; hyperexpansion of the lungs can lead to interstitial emphysema and pneumothorax. In addition, rapid fluctuations in blood carbon dioxide levels can predispose infants to developing intraventricular hemorrhage and periventricular leukomalacia. Hyperoxia should also be avoided; oxygen toxicity can increase the risk of retinopathy of prematurity, necrotizing enterocolitis, and bronchopulmonary dysplasia. Moreover, preterm infants are likely to have respiratory distress syndrome; surfactant therapy can help mitigate that risk.

Umbilical vessel catheterization is often beneficial during the resuscitation of premature infants. Arterial access allows for monitoring of blood gas values and central blood pressures. Central venous access via the umbilical vein allows for administration of fluids, drugs, and blood as needed during the resuscitation.

Special Circumstances

Meconium passage occurs during approximately 11% of deliveries; 2% of infants have aspiration syndrome as a result. Meconium obstructs the large airways and induces inflammation of the small airways, and the sequelae of meconium aspiration syndrome can range from mild initial tachypnea to development of pulmonary hypertension. To thwart this outcome, direct suctioning of the trachea is recommended if meconium is present at a delivery and the infant has decreased respiratory effort, heart rate, and tone. Tracheal suctioning is not recommended for vigorous infants born through meconium.

Infants born with CDH have small, underdeveloped lungs caused by compression by the herniated intestines and abdominal organs. As a result, CDHs typically present with immediate marked respiratory distress, a scaphoid abdomen, and the presence of bowel sounds in the chest. After a CDH is recognized, the duration of positive-pressure ventilation via bag and mask should be limited to avoid gaseous distension of the stomach and intestines and further constriction of the lungs. To this end, endotracheal intubation should occur rapidly, and an orogastric tube should be placed to decompress the gastrointestinal tract.

Several other malformations require different additional techniques for delivery room resuscitation. Infants with Pierre Robin sequence should be placed prone if possible so that the tongue can fall forward and clear the airway; a jaw thrust can also be performed until a more stable airway can be established, usually via the nasopharynx. Neonates with myelomeningocele should be placed in the decubitus position, and the defect must be covered with sterile plastic to prevent infection, desiccation, and trauma. Omphalocele or gastroschisis is initially treated in a similar way; infants born with either of these malformations should be placed in a sterile plastic bag up to the chest to cover the abdominal defect and prevent trauma and insensible water loss.

Postresuscitation Care

Infants who are stressed enough to require resuscitation at birth also require close monitoring after birth for signs and symptoms of further complications. These infants are at higher risk of developing pulmonary hypertension, systemic infections, hypotension, seizures, hypoglycemia, acute tubular necrosis of the kidney, necrotizing enterocolitis, electrolyte abnormalities, and difficulties with feeding because of ischemia and depression at birth. As a result, after an infant is resuscitated, the focus of care shifts to include several other parameters, including temperature regulation to achieve normothermia, assessments of blood glucose and electrolytes, and close monitoring of vital signs in anticipation of further complications that may occur.