Overview and Initial Management of Delivery Room Resuscitation

Fetus

In utero, the fetus depends on the placenta for gas exchange. Despite a Pa o ₂ of 20-30 mm Hg, the normal fetus carries on essential metabolism and is not hypoxic. The tissues receive adequate amounts of oxygen, and anaerobic metabolic pathways are not usually used. Adequate oxygen delivery is accomplished with an adaptive process primarily involving the architecture of the circulatory system, the characteristics of fetal hemoglobin, and the rate of perfusion of fetal organs.

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 travelling back to the placenta has a P o ₂ of 15-25 mm Hg. In humans, umbilical venous blood returning from the placenta to the fetus obtained by percutaneous umbilical vein sampling has a P o ₂ normally 20-40 mm Hg, but it may range up to 45 mm Hg. When the umbilical venous blood is mixed with venous return from the fetus, the resultant P o ₂ 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 fetal body flows into the right ventricle ( Fig. 31.1 ).

In the fetus, blood flow through the lungs is diminished because of the high resistance of the fetal pulmonary circuit, the open ductus arteriosus, and the lower resistance of the systemic and placental circuits. Nearly 90% of the right ventricular output crosses the ductus arteriosus and enters the aorta, bypassing the lungs. With little return from the pulmonary veins, oxygen in the umbilical venous blood crossing the foramen ovale into the left atrium is only slightly diluted. The most highly oxygenated blood perfuses the brain and heart through the carotid and coronary arteries before its oxygen concentration is decreased by blood entering the aorta through the ductus arteriosus.

Another adaptive mechanism keeping the fetal tissues oxygenated is the rate of perfusion. Fetal tissues are perfused with blood at a higher rate than in the adult. The increased delivery of blood compensates for the low oxygen saturation (Sp o ₂ ) in the fetus and the higher oxygen affinity of fetal hemoglobin. Finally, the fetus (except during labor) has less of an oxygen demand than the newborn. Because thermoregulation is unnecessary and respiratory effort is limited, two significant processes that consume oxygen in the newborn are either eliminated or markedly diminished in the fetus.

The P co ₂ of the fetus is slightly higher than adult levels. The normal umbilical venous P co ₂ is 35-45 mm Hg. Elimination of carbon dioxide from the fetus is enhanced by maternal hyperventilation and relative hypocarbia during pregnancy. Because of the lower P co ₂ of maternal blood, a gradient is created favoring the transfer of carbon dioxide across the placenta from fetal to maternal blood (Bohr effect).

The low fetal P o ₂ contributes to the flow characteristics of the fetal circulation by helping to keep the pulmonary vascular resistance (PVR) high. The ductus arteriosus remains patent because of fetal production of prostaglandins and a relatively low P o ₂ .

The fetus maintains metabolic homeostasis despite low oxygen tensions because of these adaptive and anatomic characteristics. However, any significant compromise of fetal gas exchange before labor (e.g., intrauterine growth restriction, placental abnormalities) or during the intrapartum period or lack of effective transition at birth quickly results in asphyxia, consisting of hypoxia, elevated P co ₂ , and metabolic acidosis.

Transition at Birth

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. With each contraction, uterine blood flow decreases, with a resulting decrease in placental perfusion and a temporary impairment of transplacental gas exchange resulting over time in a mild metabolic acidosis; 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 and may be exacerbated with an abnormal labor contraction pattern. Throughout a normal labor, the fetus undergoes a progressive but slow reduction in P o ₂ , some increase in P co ₂ , a decrease in pH, and the accumulation of a mild metabolic acidosis. 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 3-4 mmol/L. In the normal circumstance, these changes are not significant enough to depress the infant and prevent normal transition from intrauterine to postnatal existence.

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. 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 begin breathing. The American College of Obstetricians and Gynecologists (ACOG) now recommends delayed cord clamping for 30-60 seconds in vigorous term and preterm infants to increase blood volume, decrease need for inotropic support, and reduce several complications of prematurity. However, if the placental circulation is not intact (i.e., abruptio placenta) or the newborn needs immediate resuscitation, immediate cord clamping should be considered or care should be individualized.

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. 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. 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). The first breath of a spontaneously breathing term infant is generally characterized by short inspirations each followed by prolonged expiratory phases. Although the peak inspiratory pressure may be as high as −50 cm H ₂ O to −100 cm H ₂ O, the opening pressures are very low. That is, gas begins to enter the lungs at very low pressures, usually less than −5 cm H ₂ O pressure. Very high expiratory pressures are also generated; these pressures generally exceed the inspiratory pressure. This expiratory pressure, probably generated against a partially closed glottis, drives the liquid in the lung peripherally, increasing the FRC over the first several breaths with multiple inspiratory efforts. In a vigorous, spontaneously breathing, vaginally delivered infant, a significant FRC develops with the first several breaths. However, the depressed neonate may need assistance with establishing an FRC. A three-phase process proposed by Hooper et al. suggests that initial resuscitation of an apneic newly born baby should begin with a sustained inflation to aerate the lung followed by positive end expiratory pressure to maintain the FRC (see Chapter 32 ) ( Fig. 31.2 ). However, sustained inflations at birth are not recommended at this time by the Neonatal Resuscitation Program (NRP).

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 P co ₂ and an increase in pH and P o ₂ , also causing a decrease in PVR. The administration of oxygen is not necessary to produce this drop in PVR. In a study of lambs, Lakshminrusimha and colleagues showed that PVR decreased nearly as much (72%) in the first 30 minutes after birth with air resuscitation as with 100% oxygen. By 60-90 minutes after birth, the decrease in PVR in the air group had reached the same level as the 100% oxygen group. Fig. 31.3 illustrates the relationships between pH, P o ₂ , and PVR. Clearance of lung fluid, establishment of FRC, and a decrease in PVR with an increase in pulmonary blood flow facilitate postnatal ventilation and oxygenation.

With the onset of ventilation, the fetal circulatory system assumes the adult pattern. Coincident with clamping of the cord, the low-resistance placenta is removed from the systemic circuit, and systemic blood pressure increases. This increase in systemic pressure, coupled with the decrease in PVR and in pulmonary artery pressure, decreases the right-to-left shunt through the ductus arteriosus. The increase in Pa o ₂ further stimulates functional closure of the ductus arteriosus. With ductal shunting diminished, pulmonary artery blood flow increases, resulting in increased pulmonary venous return to the left atrium and increased pressure in the left atrium. When the left atrial pressure exceeds right atrial pressure, the foramen ovale functionally closes.

An uncomplicated transition from fetal to newborn status is characterized by loss of fetal lung fluid, secretion of surfactant, establishment of FRC, decrease in PVR, increased systemic pressure after removal of the low-resistance placenta from the systemic circuit, functional closure of two shunts (ductus arteriosus and foramen ovale), and increase in pulmonary artery blood flow. In most circumstances, the mild metabolic acidosis associated with labor is insufficient to interfere with this process. Regardless of the mode of birth, the transition may be significantly altered by various antepartum or intrapartum events, resulting in cardiorespiratory depression, asphyxia, or both. Infants who are very premature are especially vulnerable to these untoward events.

Causes of Depression and Asphyxia

A newborn may be compromised because of problems initiated in utero with the mother, the placenta, or the fetus itself ( Box 31.1 ). 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.

Maternal causes of fetal compromise may be related to decreased uterine blood flow, which decreases the amount of oxygen transported to the placenta. Diminished uterine blood flow may result from maternal hypotension (such as hypovolemia, allergic reaction, or as a result of drugs used to treat hypertension), regional anesthesia, eclampsia, or abnormal uterine contractions. Problems with the placenta, such as chronic structural abnormalities, infarcts, premature separation, edema, or inflammatory changes may impair gas exchange. The fetus also may be compromised because of fetal problems related to cord compression, such as nuchal cord, prolapse, or a breech presentation with cord compression by the aftercoming head, or by intrinsic fetal problems such as anemia or congenital abnormalities. In some cases, inflation of the lung occurs normally, but there may be a deficiency in oxygen-carrying capacity, as in severe hypovolemia from acute hemorrhage or fetal-maternal transfusion, or there may be inadequate cardiac output from numerous causes. A neonate may not have adequate ventilation after delivery because of many problems, including asphyxia, drug-induced central nervous system (CNS) depression, CNS anomalies or injury, spinal cord injury, mechanical obstruction of the airways, congenital facial or airway deformities, immaturity, pneumonia, or congenital anomalies.

Finally, there are some circumstances in which the infant may initiate breathing only to diminish markedly or stop breathing soon after birth. Examples include extreme prematurity with inadequate ventilatory support after birth, drug-induced depression in which the stimuli surrounding birth initially overcome the depression, congenital diaphragmatic hernia (CDH), and spontaneous pneumothorax.

Response to Asphyxia

The goal with any depressed or asphyxiated infant, whether the process is initiated in the fetal or the neonatal period, is to reverse the ongoing events as soon as possible and avoid death or permanent injury. An understanding of the response of the fetus or neonate to asphyxia forms the basis of the resuscitative process.

Intrapartum asphyxia can be divided into two major types: acute near-total asphyxia and partial prolonged asphyxia. Acute near-total asphyxia has an abrupt onset, usually lasts 5-30 minutes, and causes complete or near-complete cessation of blood flow to the fetus. Etiologies include maternal cardiac arrest, uterine rupture, complete placental abruption, and severe cord compression. Partial prolonged asphyxia occurs more slowly over one to many hours and usually results from various causes of uteroplacental insufficiency. When a fetus or neonate is subjected to partial prolonged asphyxia, the classic “diving” reflex occurs; this is simply an attempt either to accentuate or restore a fetal type of circulation. Hypoxia and acidosis, regardless of their duration, increase vasoconstriction of the pulmonary vasculature (see Fig. 31.3 ). The increase in PVR results in a decline in pulmonary blood flow, decreasing left atrial return, which lowers left atrial pressure. The decline in left atrial pressure increases right-to-left shunting across the foramen ovale. In the fetus, this shunting directs the most highly oxygenated blood coming from the placenta to the left side of the heart. In a neonate with no placenta, this shunting merely bypasses the lungs, perpetuating a vicious cycle of hypoxia, more acidosis, and more shunting. In acute near-total asphyxia, there may not be time for the diving reflex to have a physiologic effect; in contrast to partial prolonged asphyxia, there may not be significant multisystem organ damage from shunting of blood away from the kidneys, liver, bones, and other organs not essential to the immediate preservation of life.

In the fetus and the neonate, the increase in noncerebral peripheral resistance during prolonged asphyxia results in a redistribution of blood flow, with increased flow to the head, heart, and adrenal glands, and decreased flow to organs not vital to immediate survival. Although the oxygen content of the blood is low, during the early stages of asphyxia the amount of oxygen brought to the head and heart is maximized by the maintenance of cardiac output and the increased flow to these organs. The increased peripheral resistance sustains blood pressure early in asphyxia. The blood pressure remains at reasonable levels as long as the myocardium is able to maintain cardiac output. As the asphyxia progresses and hypoxia and acidosis worsen, the myocardium fails, and cardiac output and blood pressure decrease.

Hypoxic cardiomyopathy is the intermediary step to significant brain and other organ damage in partial prolonged asphyxia. The asphyxiated newborn will usually be born with little muscle tone, apnea, and a low heart rate. However, most healthy babies are born with a heart rate less than 100 beats/min, and the clinician should use other signs of significant acidosis (i.e., hypotonia, apnea) to determine which baby needs immediate resuscitation. The resuscitation algorithm of children and adults emphasizes interventions to promote the return of spontaneous circulation and does not apply in newborns; the provision of adequate ventilation is the mainstay of neonatal resuscitation with the goals to reverse the bradycardia and restore adequate circulation. Superimposed on these circulatory and hemodynamic changes is a characteristic change in respiratory pattern. Initially, there are gasping respirations (which may occur in utero). With continuing asphyxia, respirations cease in what is known as primary apnea. If the asphyxia is not corrected, the infant again begins to gasp irregularly, and the respirations cease (secondary apnea) unless effective positive pressure ventilation (PPV) and successful resuscitation occur ( Fig. 31.4 ).

Primary apnea usually responds to the cessation of the asphyxiating insult and stimulation. Secondary apnea is usually accompanied by severe metabolic acidemia and requires much more vigorous resuscitation for the newborn to recover. The longer the asphyxia has gone on, the longer it takes for the onset of spontaneous ventilation to occur after PPV is started ( Fig. 31.5 ). Asphyxia may begin before birth, and the infant may pass through any or all of these stages of the asphyxial cascade in utero. It may be difficult to determine at birth how far the asphyxial episode has progressed. With any depressed infant, it is essential to assume that the infant is in secondary apnea, and resuscitation should be initiated without delay. The goal of resuscitation, although not always attainable, is to initiate interventions in a timely and effective manner so that the insults of hypoxia, ischemia, and acidosis are reversed before they cause permanent injury ( Box 31.2 ).