Circulation

At birth, the circulatory system changes from a fetal circulation pattern (which is in parallel), through a transitional circulation, to an adult circulation pattern (which is in series) (Figure 9-1).¹⁰ In the fetus, blood from the placenta travels through the umbilical vein and the ductus venosus to the inferior vena cava and the right side of the heart. The anatomic orientation of the inferior vena caval–right atrial junction favors the shunting (i.e., streaming) of this well-oxygenated blood through the foramen ovale to the left side of the heart. This well-oxygenated blood is pumped through the ascending aorta, where branches that perfuse the upper part of the body (e.g., heart, brain) exit proximal to the entrance of the ductus arteriosus.¹¹ Desaturated blood returns to the heart from the upper part of the body by means of the superior vena cava. The anatomic orientation of the superior vena caval–right atrial junction favors the streaming of blood into the right ventricle. Because fetal pulmonary vascular resistance is higher than systemic vascular resistance (SVR), approximately 90% of the right ventricular output passes through the ductus arteriosus and enters the aorta distal to the branches of the ascending aorta and aortic arch; therefore, less well-oxygenated blood perfuses the lower body, which consumes less oxygen than the heart and brain.

At the time of birth and during the resulting circulatory transition, the amount of blood that shunts through the foramen ovale and ductus arteriosus diminishes and the flow becomes bidirectional. Clamping the umbilical cord (or exposing the umbilical cord to room air) results in increased SVR. Meanwhile, expansion of the lungs and increased alveolar oxygen tension and pH result in decreased pulmonary vascular resistance and subsequently greater flow of pulmonary artery blood through the lungs.^12,13 Increased pulmonary artery blood flow results in improved oxygenation and higher left atrial pressure; the latter leads to a diminished shunt across the foramen ovale. Increased PaO₂ and SVR and decreased pulmonary vascular resistance result in a constriction of the ductus arteriosus.^14,15 Together, these changes in vascular resistance result in functional closure of the foramen ovale and the ductus arteriosus. This process does not occur instantaneously, and arterial oxygen saturation (SaO₂) remains higher in the right upper extremity (which is preductal) than in the left upper extremity and the lower extremities until blood flow through the ductus arteriosus is minimal.¹⁶ Differences in SaO₂ are usually minimal by 10 minutes and absent by 24 hours after birth. Provided that there is no interference with the normal drop in pulmonary vascular resistance, both the foramen ovale and the ductus arteriosus close functionally, and the infant develops an adult circulation (which is in series).

Persistent fetal circulation—more correctly called persistent pulmonary hypertension of the newborn—can occur when the pulmonary vascular resistance remains elevated at the time of birth. Factors that may contribute to this problem include hypoxia, acidosis, hypovolemia, and hypothermia.^13,17 Maternal use of nonsteroidal anti-inflammatory drugs may also cause premature constriction of the ductus arteriosus in the fetus and thus predispose to persistent pulmonary hypertension of the newborn.¹⁸

Respiration

Fetal breathing movements have been observed in utero as early as 11 weeks’ gestation. These movements increase with advancing gestational age but undergo a marked reduction within days of the onset of labor. They are stimulated by hypercapnia and maternal smoking and are inhibited by hypoxia and central nervous system (CNS) depressants (e.g., barbiturates). Under normal conditions, this fetal breathing activity results only in the movement of pulmonary dead space.¹⁹

The fetal lung contains a liquid composed of an ultrafiltrate of plasma, which is secreted by the lungs in utero²⁰; the volume of this lung liquid is approximately 30 mL/kg. Partial reabsorption of this liquid occurs during labor and delivery, and approximately two thirds is expelled from the lungs of the term neonate by the time of delivery.²¹ Small preterm infants and those requiring cesarean delivery may have a greater amount of residual lung liquid after delivery. These infants experience less chest compression at delivery than infants who are larger or delivered vaginally; this difference can lead to difficulty in the initiation and maintenance of a normal breathing pattern. Retained fetal lung liquid is the presumed cause of transient tachypnea of the newborn (TTN).²²

The first breath occurs approximately 9 seconds after delivery. Air enters the lungs as soon as the intrathoracic pressure begins to fall. This air movement during the first breath is important, because it establishes the neonate’s functional residual capacity (Figure 9-2).

Lung inflation is a major physiologic stimulus for the release of lung surfactant into the alveoli.²³ Surfactant, which is necessary for normal breathing, is present within the alveolar lining cells by 20 weeks’ gestation²⁴ and within the lumen of the airways by 28 to 32 weeks’ gestation. However, significant amounts of surfactant do not appear in terminal airways until 34 to 38 weeks’ gestation unless surfactant production has been stimulated by chronic stress or maternal corticosteroid administration.²⁵

Stress during labor and delivery can lead to gasping efforts by the fetus, which may result in the inhalation of amniotic fluid into the lungs.²⁶ This event can produce problems if the stress causes the fetus to pass meconium into the amniotic fluid before gasping.

Catecholamines

Transition to extrauterine life is associated with a catecholamine surge, which may be necessary for the process to be successful. In chronically catheterized sheep, catecholamine levels begin to rise a few hours before delivery and may be higher at the time of delivery than at any other time during life.²⁷ Catecholamines have an important role in the following areas: (1) the production and release of surfactant, (2) the mediation of preferential blood flow to vital organs during the period of stress that occurs during every delivery, and (3) thermoregulation of the neonate.

Thermal Regulation

Thermal stress challenges the neonate in the extrauterine environment. Neonates raise their metabolic rates and release norepinephrine in response to cold; this response facilitates the oxidation of brown fat, which contains numerous mitochondria. The oxidation results in nonshivering thermogenesis, the major mechanism for neonatal heat regulation.²⁸ This process may lead to significant oxygen consumption, especially if the neonate has not been dried off and kept in an appropriate thermoneutral environment, such as a radiant warmer. Thermal stress is an even greater problem in infants with low fat stores, such as preterm infants or infants who are small for gestational age. An alternative method to eliminate heat loss from evaporation is to provide an occlusive wrap rather than drying the infant. For infants born at less than 28 weeks’ gestation, the use of polythene wraps or bags is recommended to minimize heat loss.^29,30 The maintenance of a neutral thermal environment (i.e., 34° to 35° C) is recommended. However, in the neonate with a perinatal brain injury, mild hypothermia therapy through selective head or whole body cooling is initiated in the first 6 hours of life and may be neuroprotective in the setting of hypoxia-ischemia.^31,32 Hyperthermia may worsen neurologic outcomes and should be avoided.^2,33 Hypothermia therapy, via selective head cooling or whole body hypothermia, is continued for 72 hours after initiation. Consequently, if an infant is delivered at a center where hypothermia therapy is unavailable, passive cooling can be initiated by turning the radiant warmer off while awaiting infant transfer.

Administration of epidural analgesia during labor is associated with an increase in maternal and fetal temperature.³⁴ Concern has been expressed that the temperature elevation associated with intrapartum epidural analgesia might result in an increase in the frequency of neonatal sepsis evaluations.^34,35 However, a number of variables (e.g., preeclampsia/hypertension, gestational age, birth weight, meconium aspiration, respiratory distress at birth, hypothermia at birth, and group B beta-hemolytic streptococcal colonization of the maternal birth canal) have been observed to be strong predictors of the performance of neonatal sepsis evaluations, whereas maternal fever and epidural analgesia have not.³⁶ Confounding variables may influence the findings of these types of association studies; patients who choose either to receive or not receive epidural analgesia may be inherently different. The incidence of actual neonatal sepsis is not different in term infants whose mothers either did or did not receive epidural analgesia.

Apgar Score

Resuscitative efforts typically precede the performance of a thorough physical examination of the neonate. Because NRP instructions require simultaneous assessment and treatment, it is important that the neonatal assessment be both simple and sensitive. In 1953, Dr. Virginia Apgar, an anesthesiologist, described a simple method for neonatal assessment that could be performed while care was being delivered.⁴³ She suggested that this standardized and relatively objective scoring system would differentiate between infants who require resuscitation and those who need only routine care.⁴⁴

The Apgar score is based on five parameters that are assessed at 1 and 5 minutes after birth. Further scoring at 5- or 10-minute intervals may be done if initial scores are low. The parameters are heart rate, respiratory effort, muscle tone, reflex irritability, and color. A score of 0, 1, or 2 is assigned for each of these five entities (Table 9-1). A total score of 8 to 10 is normal; a score of 4 to 7 indicates moderate impairment; and a score of 0 to 3 signals the need for immediate resuscitation. Dr. Apgar emphasized that this system does not replace a complete physical examination and serial observations of the neonate for several hours after birth.⁴⁵

The Apgar score is widely used to assess neonates, although its value has been questioned. The scoring system may help predict mortality and neurologic morbidity in populations of infants, but Dr. Apgar cautioned against the use of the Apgar score to make these predictions in an individual infant. She noted that the risk for neonatal mortality was inversely proportional to the 1-minute score.⁴⁵ In addition, the 1-minute Apgar score was a better predictor of mortality within the first 2 days of life than within 2 to 28 days of life.

Several studies have challenged the notion that a low Apgar score signals perinatal asphyxia. In a prospective study of 1210 deliveries, Sykes et al.⁴⁶ noted a poor correlation between the Apgar score and the umbilical cord blood pH. Other studies, including those of low-birth-weight infants, have found that a low Apgar score is a poor predictor of neonatal acidosis, although a high score is reasonably specific for excluding the presence of severe acidosis.^47–53 By contrast, the fetal biophysical profile has a good correlation with the acid-base status of the fetus and the neonate (see Chapter 6).⁵⁴ The biophysical profile includes performance of a nonstress test and ultrasonographic assessment of fetal tone, fetal movement, fetal breathing movements, and amniotic fluid volume.⁵⁴

Additional studies have suggested that Apgar scores are poor predictors of long-term neurologic impairment.^55,56 The Apgar score is more likely to predict a poor neurologic outcome when the score remains 3 or less at 10, 15, and 20 minutes. However, when a child has cerebral palsy, low Apgar scores alone are not adequate evidence that perinatal hypoxia was responsible for the neurologic injury.

The ACOG Task Force on Neonatal Encephalopathy and Cerebral Palsy published criteria for defining an intrapartum event sufficient to cause cerebral palsy.⁵⁷ An Apgar score of 0 to 3 beyond 5 minutes of age is not included in the list of “essential criteria”; rather, it is one of five criteria that “collectively suggest an intrapartum timing (within close proximity to labor and delivery…) but are nonspecific to asphyxial insults.”^57–62

In a retrospective analysis of 151,891 singleton infants born at 26 weeks’ gestation or later between 1988 and 1998, Casey et al.⁶³ examined the relationship between Apgar scores and neonatal death rates during the first 28 days of life. The highest relative risk for neonatal death was observed in infants with an Apgar score of 3 or less at 5 minutes of age. The 5-minute Apgar score was a better predictor of neonatal death than the umbilical arterial blood pH. In term infants, the relative risk for neonatal death was eight times higher in infants with a 5-minute Apgar score of 3 or less than in those with an umbilical arterial blood pH of 7.0 or less.^63,64 In preterm infants, lower 5-minute Apgar scores were associated with younger gestational ages (i.e., mean score 6.6 ± 2.1 for infants born at 26 to 27 weeks’ and 8.7 ± 0.8 for infants born at 34 to 36 weeks’ gestation).^63,64 Similarly, earlier studies found that preterm infants were more likely than term infants to have low 1- and 5-minute Apgar scores, independent of neonatal oxygenation and acid-base status. Respiratory effort, muscle tone, and reflex irritability are the components of the score that are most influenced by gestational age.⁶⁵

The earlier the gestational age, the greater the likelihood of a low Apgar score, even in the presence of a normal umbilical cord blood pH. Preterm infants often require active resuscitation efforts immediately after delivery, and these manipulations may affect the components of the Apgar score. For example, pharyngeal and tracheal stimulation may cause a reflex bradycardia, which affects the heart rate score.⁴⁹ In addition, it is difficult to judge respiratory effort during suctioning or endotracheal intubation.

During cases of active neonatal resuscitation, the Apgar scores often are not assigned at the appropriate times; rather, these scores may be assigned retrospectively. In these situations, the individual must rely on recall of the infant’s condition at earlier times, introducing inaccuracy. Even if the scores are assigned at the appropriate times, there may be disagreement among the several individuals who are providing care for the infant. To avoid bias, Dr. Apgar recommended that someone not involved in the care of the mother assign the score.

Although there is some appeal to the use of objective measurements (i.e., SaO_2, heart rate) rather than subjective observations, it should not be inferred that the subjective components of the Apgar score (e.g., muscle tone) are less important. There are some practical limitations that may make objective measurements difficult to obtain (e.g., movement artifact with pulse oximetry).¹⁶ However, newer-generation pulse oximeters provide more accurate estimations of SaO₂ (see later discussion).⁶⁶

In summary, the usefulness of the Apgar score is still being debated more than 50 years after its inception.^63,64 The Apgar scoring system is used throughout the world, but its limitations must be kept in mind. Low Apgar scores alone do not provide sufficient evidence of perinatal asphyxia; rather, Apgar scores can be low for a variety of reasons. Preterm delivery, congenital anomalies, neuromuscular diseases, antenatal drug exposure, manipulation at delivery, and subjectivity and error may influence the Apgar score.

Umbilical Cord Blood Gas and pH Analysis

Umbilical cord blood gas and pH measurements reflect the fetal condition immediately before delivery and can be obtained routinely after delivery or measured only in cases of neonatal depression. These measurements may be a more objective indication of a neonate’s condition than the Apgar score. However, there is a delay between obtaining the samples and completing the analysis; during this interval, decisions must be made on the basis of clinical assessment. The ACOG⁶⁷ has recommended that cord blood gas measurements be obtained in circumstances of cesarean delivery for fetal compromise, low 5-minute Apgar score, severe growth restriction, abnormal FHR tracing, maternal thyroid disease, intrapartum fever, and/or multiple gestations.

The fetus produces carbonic acid (from oxidative metabolism) and lactic and beta-hydroxybutyric acids (primarily from anaerobic metabolism). Carbonic acid, which is often called respiratory acid, is cleared rapidly by the placenta as carbon dioxide when placental blood flow is normal. However, metabolic clearance of lactic and beta-hydroxybutyric acids requires hours; thus, these acids are called metabolic or fixed acids. In the fetus, metabolic acidemia is more ominous than respiratory acidemia because the former reflects a significant amount of anaerobic metabolism.

The measured components of umbilical cord blood gas analysis are pH, PCO₂, PO₂, and HCO₃⁻. Bicarbonate (HCO₃⁻) is a major buffer in fetal blood. The measure of change in the buffering capacity of umbilical cord blood is reflected in the delta base, which is also known as the base excess or deficit; this value can be calculated from the pH, PCO₂, and HCO₃⁻. Ideally, blood samples from both the umbilical artery and vein are collected. Umbilical artery blood gas measurements represent the fetal condition, whereas umbilical vein measurements reflect the maternal condition and uteroplacental gas exchange. Unfortunately, it may be difficult to obtain blood from the umbilical artery, especially when it is small, as it is in very low-birth-weight (VLBW) infants. Caution should be used in the interpretation of an isolated umbilical venous blood pH measurement, which can be normal despite the presence of arterial acidemia.

Proper blood sampling and handling are necessary. The measurements should be accurate, provided that (1) the umbilical cord is double clamped immediately after delivery^68–70; (2) the samples are drawn, within 15 minutes of delivery,⁷¹ into a syringe containing the proper amount of heparin⁷²; and (3) the samples are analyzed within 30 to 60 minutes.^71,73 The PO₂ measurement is more accurate if residual air bubbles are removed from the syringe.

Historically, a normal umbilical cord blood pH measurement was believed to be 7.2 or higher.⁷⁴ However, investigators have challenged the validity of this number, given its lack of distinction between umbilical arterial and venous blood despite clear differences in their normal measurements.⁷⁵ One study noted that the median umbilical arterial blood pH in vigorous infants (those with 5-minute Apgar scores of 7 or higher) was 7.26, with a measurement of 7.10 representing the 2.5^th percentile.⁷⁶ Published studies suggest that the lower limit of normal umbilical arterial blood pH measurements may range from 7.02 to 7.18 (Table 9-2).^46,77–86 A number of factors may also influence the umbilical arterial blood pH measurement. A fetus subjected to the stress of labor has lower pH measurements than one born by cesarean delivery without labor.⁸³ Offspring of nulliparous women tend to have a lower pH than offspring of parous women, a difference that is likely related to a difference in the duration of labor.⁸⁷

Some studies have suggested that preterm infants have a higher incidence of acidemia; however, later studies have observed that term and preterm infants have similar umbilical cord blood gas and pH measurements.^78,79,87 Preterm infants often receive low Apgar scores despite the presence of normal umbilical cord blood gas and pH measurements; therefore, the assessment of umbilical cord blood may be especially helpful in the evaluation of preterm neonates.

Physicians should use strict definitions when interpreting umbilical cord blood gas and pH measurements. Terms such as birth asphyxia should be avoided in most cases.⁵⁷ Acidemia refers to an increase in the hydrogen ion concentration in the blood. Acidosis occurs when there is an increased hydrogen ion concentration in tissue. Asphyxia is a clinical situation that involves hypoxia (i.e., a decreased level of oxygen in tissue), damaging acidemia, and metabolic acidosis.

When acidemia is present, the type—respiratory, metabolic, or mixed—must be identified (Table 9-3). Metabolic acidemia is more likely to be associated with acidosis than respiratory acidemia and is clinically more significant. Similarly, mixed acidemia with a high PCO₂, an extremely low HCO₃⁻, and a high base deficit is more ominous than a mixed acidemia with a high PCO₂ but only a slightly reduced HCO₃⁻ and a low base deficit. Mixed or metabolic acidemia (but not respiratory acidemia) is associated with an increased incidence of neonatal complications and death.⁸⁷ In their study of 3506 term neonates, Goldaber et al.⁸⁸ noted that an umbilical arterial blood pH measurement less than 7.00 was associated with a significantly higher incidence of neonatal death. All neonatal seizures in their study occurred in infants with an umbilical arterial blood pH less than 7.05. By contrast, a short-term outcome study failed to show a good correlation between arterial blood pH and the subsequent health of an infant.⁵³ In the previously discussed large study reported by Casey et al.,⁶³ an umbilical arterial blood pH of 7.0 or less was a poorer predictor of the relative risk for neonatal death during the first 28 days of life than a 5-minute Apgar score of 3 or less. However, 6264 infants were excluded from their study because umbilical arterial blood gas measurements could not be obtained, and these infants had a higher incidence of neonatal death than those for whom blood gas measurements were available (4.5 per 1000 versus 1.2 per 1000, respectively). In a separate review of 51,519 term deliveries, Yeh et al.⁸⁹ found an increased risk for adverse outcomes in infants with a pH less than 7.10, with the lowest risk in infants with a pH between 7.26 and 7.30; however, 75% of infants with neurologic morbidity had a normal pH. Thus, it is important to remember that neonates may suffer multiorgan system damage, including neurologic injury, even in the absence of low pH and Apgar scores.

According to the ACOG Task Force, an umbilical arterial blood pH less than 7.0 and a base deficit greater than or equal to 12 mmol/L at delivery are considered one part of the definition of an acute intrapartum hypoxic event sufficient to cause cerebral palsy.⁵⁷ The base deficit and bicarbonate (the metabolic component) values are the most significant factors associated with morbidity in neonates with an umbilical arterial blood pH less than 7.0. Ten percent of infants with an umbilical arterial base deficit of 12 to 16 mmol/L have moderate to severe complications, which increases to 40% when the deficit is greater than 16 mmol/L.⁶⁷

Abnormal FHR patterns and umbilical cord blood gas measurements are not consistently correlated with poor neonatal outcomes.³⁷ In a longitudinal study that evaluated outcomes at 6.5 years of age, Hafstrom et al.⁹⁰ found that infants with an umbilical arterial blood pH less than 7.05 but a normal examination at birth had outcomes that did not differ from those for matched infants with a normal umbilical arterial blood pH.

As Dr. Apgar emphasized in 1962, the most important components of neonatal assessment are a careful physical examination and continued observation for several hours.⁴⁵ Additional information can be gained from the antenatal history, Apgar scores, and umbilical cord blood gas and pH measurements, provided that clinicians are aware of the proper methods of interpretation as well as the limitations of these methods of assessment.

Respiration and Circulation

There are some similarities between the initial assessment of the neonate and the initial assessment of an adult who requires resuscitation. In both situations, the physician should give immediate attention to the ABCs of resuscitation (i.e., airway, breathing, circulation).

The normal neonatal respiratory rate is between 30 and 60 breaths per minute. Breathing should begin by 30 seconds and be regular by 90 seconds of age. Failure of the neonate to breathe by 90 seconds of age represents either primary or secondary apnea, based on the neonatal rhesus monkey asphyxia model.⁹¹ In this model, gasping motions were observed for approximately 1 minute immediately after delivery; this was followed by a 1-minute period of apnea (primary apnea), then 5 minutes of gasping motions, and a final period of apnea (secondary or “terminal” apnea). During primary apnea, but not secondary apnea, tactile stimulation of the newborn monkey initiated breathing efforts. In addition, although heart rate was low with both periods of apnea, a reduction in blood pressure was observed only during secondary apnea. With the onset of secondary apnea (approximately 8 minutes after birth), the pH was 6.8 and the PaO₂ and PaCO₂ measurements were less than 2 and 150 mm Hg, respectively.

This experimental model illustrates two important points. First, distinguishing primary from secondary apnea is not possible unless blood pressure and/or blood gases and pH are measured. Second, by the time secondary apnea has begun, blood gas measurements have deteriorated significantly. Therefore, during evaluation of the apneic neonate, aggressive resuscitation must be initiated promptly if tactile stimulation does not result in the initiation of spontaneous breathing.

Assessment of the adequacy of respiratory function requires comprehensive observation for signs of neonatal respiratory distress. These signs include cyanosis, grunting, flaring of the nares, retracting chest motions, and unequal breath sounds. The adequacy of respiratory function can also be assessed by the estimation of SaO₂. The reliability of pulse oximetry for the assessment of neonatal SaO₂ was questioned initially because of concerns about the accuracy of spectrophotometric assessments of fetal hemoglobin and the difficult signal detection caused by the rapidity of the neonate’s heart rate.^92,93 The newer generation of pulse oximetry monitors, which employ signal extraction and averaging techniques, are able to provide more reliable measurements, especially in the presence of poor perfusion, patient movement, and ambient light artifacts.^66,94

Pulse oximetry provides accurate estimates of SaO₂ during periods of stability but may overestimate values during rapid desaturation.⁹⁵ In addition, the SaO₂ (SpO₂) measurements may fluctuate in the delivery room as a result of the ongoing transition from the fetal to the neonatal circulation, and it may take more than 10 minutes to achieve a preductal SaO₂ greater than 95% in a healthy term infant. Overall, the newer-generation pulse oximeters reliably provide continuous noninvasive SaO₂ measurements and are useful for neonatal monitoring.^96–98

The pulse oximeter sensor should be applied to the neonate’s right upper extremity, which receives preductal blood flow (see earlier discussion); because CNS blood flow is also preductal, right upper extremity SaO₂ measurements provide a more accurate assessment of CNS oxygenation.¹⁶ Sensor placement can be difficult on skin that is wet and covered with vernix caseosa; therefore, it may be easier to place the sensor over the right radial artery, especially in preterm infants.⁹⁴

Neonatal arterial blood sampling is technically difficult and thus rarely obtained in the delivery room. Cannulation of the umbilical artery is useful in infants who will require frequent blood sampling. This procedure often requires the use of microinstruments (especially in preterm and VLBW infants) and the ability to monitor the infant when obscured from view by surgical drapes; therefore, this procedure is usually performed in the neonatal intensive care unit (NICU).

The normal neonatal heart rate may be greater than 160 beats per minute (bpm) in the very early preterm neonate, but it should be within the range of 120 to 160 bpm by 28 weeks’ gestational age. The heart rate can be determined in several ways. The clinician can lightly grasp the base of the umbilical cord and feel the arterial pulsations. (This method cannot be used in situations in which the pulsations become difficult to feel, such as in an infant with a low cardiac output.) Alternatively, the clinician can listen to the apical heartbeat. When either of these two methods is used, the evaluator should tap a hand with each heartbeat so that other members of the resuscitation team are aware of the rate. By contrast, the use of a pulse oximeter provides an audible heart rate, the additional benefit of SaO₂ monitoring, and the ability to eliminate the need for an additional team member.

Measurement of arterial blood pressure is not a priority during the initial assessment and resuscitation of the neonate.² However, observation for signs of abnormal circulatory function is considered essential. These signs include cyanosis, pallor, mottled coloring, prolonged capillary refill time, and weakness or absence of pulses in the extremities. One of the causes of abnormal circulatory function is hypovolemia, which should be anticipated in cases of bleeding from the umbilical cord or the fetal side of the placenta or whenever a neonate does not respond appropriately to resuscitation. The hypovolemic neonate may exhibit not only signs of abnormal circulatory function but also tachycardia and tachypnea. (Neonatal hypovolemia usually does not accompany placental abruption, which may cause maternal bleeding or other conditions associated with fetal asphyxia.)

Neurologic Status

The initial neonatal neurologic assessment requires only simple observation. The neonate should demonstrate evidence of vigorous activity, including crying and active flexion of the extremities. Signs of possible neurologic abnormalities include apnea, seizures, hypotonia, and unresponsiveness. Neonates should be assessed for physical signs of hypoxic-ischemic encephalopathy (Table 9-4). The stages of hypoxic-ischemic encephalopathy are associated with different outcomes: stage I, good; stage II, moderate; and stage III, poor.⁹⁹ Although detailed neurologic assessment is performed after the neonate is transferred to the NICU, assessment of tone, baseline heart rate, respirations, and reflex activity is part of both the Apgar scoring system and the assessment for hypoxic-ischemic encephalopathy and is made initially in the delivery room.

Gestational Age

When assessing a very small neonate whose gestational age appears to be lower than that of viability, the evaluator must consider whether it is appropriate to initiate and maintain resuscitation efforts. The neonatal gestational age is often assessed with the use of the scoring systems described initially by Dubowitz et al.¹⁰⁰ and subsequently modified by Ballard et al.¹⁰¹ The Dubowitz system makes use of an external score based on physical characteristics, described previously by Farr et al.,^102,103 and a neurologic score. The Ballard system uses simplified scoring criteria to assess gestational age. Ballard et al.¹⁰¹ eliminated certain physical criteria such as edema and skin color because of the unreliability of these criteria in some clinical conditions. In addition, they abbreviated the neurologic criteria on the basis of observations by Amiel-Tison.¹⁰⁴

The Dubowitz and Ballard scores are most accurate when used to estimate gestational age at 30 to 42 hours, rather than during the first several minutes, after birth. These scoring systems are also less accurate in very small preterm infants. In one study of 100 preterm infants with birth weights less than 1500 g, agreement among antenatal measures of gestational age (e.g., last menstrual period, ultrasonography determination) and postnatal measures (e.g., Dubowitz and Ballard scores) was poor.¹⁰⁵ Both scoring systems overestimated gestational age in this subset of VLBW infants. Ballard et al.¹⁰⁶ refined their scoring system to provide a more accurate estimate of gestational age in preterm infants (Figure 9-3). The new Ballard score assesses physical criteria, such as eyelid fusion, breast tissue, lanugo hair, and genitalia, and neurologic criteria, such as wrist “square window.” (The square window assessment is performed by flexing the infant’s wrist on the forearm and noting the angle between the hypothenar eminence and the ventral aspect of the forearm.) Although the new Ballard score may be more accurate than the older score for the assessment of preterm infants, inconsistencies occur with all of these methods. Of particular interest is the observation that fetuses of different racial origin appear to mature at different rates (i.e., black fetuses mature faster than white fetuses).¹⁰⁷

Another commonly used criterion for the estimation of gestational age is birth weight. Normal values for birth weight are published and readily available.¹⁰⁸ Although birth weight may help physicians estimate the gestational age of an otherwise healthy preterm infant, physicians cannot rely on birth weight to provide an accurate estimate of gestational age in an infant who suffered from intrauterine growth restriction or who is large for gestational age.

Because of the potential for inaccurate gestational age estimation in the delivery room, it is best not to use these scoring systems to guide decisions regarding the initiation or continuation of neonatal resuscitation immediately after delivery. In most circumstances, the neonate’s response to resuscitative efforts is the best indicator as to whether further intervention is warranted.

Meconium Aspiration

There has been significant interest in the management of the neonate whose airway has been exposed to meconium-containing amniotic fluid. Meconium is present in the intestinal tract of the fetus after approximately 31 weeks’ gestation. Meconium-stained amniotic fluid is present in 10% to 15% of all pregnancies; the incidence is higher in post-term pregnancies. Intrapartum passage of meconium may be associated with fetal stress and hypoxia.^158,159

Meconium aspiration syndrome (MAS) is defined as respiratory distress in a neonate whose airway was exposed to meconium and whose chest radiographic study exhibits characteristic findings, including pulmonary consolidation and atelectasis.¹⁶⁰ Treatment of MAS often involves the use of positive-pressure ventilation and is associated with a 5% to 20% incidence of pneumothorax from pulmonary air leaks.¹⁶¹ In one study of 176,790 infants born between 1973 and 1987, the annual death rate from MAS was as high as 6 per 10,000 live infants.¹⁶² Extracorporeal membrane oxygenation (ECMO) and inhaled nitric oxide have been used for the treatment of pulmonary hypertension associated with MAS and have been observed to reduce mortality rates.^163–165

Neonatologists have attempted to determine whether peripartum suctioning of the neonate’s airway reduces the risk for developing MAS. Gregory et al.¹⁶² published the original study of 80 meconium-exposed neonates who were born either vaginally or by cesarean delivery. All infants underwent tracheal intubation and suctioning after delivery. In 34 infants, no meconium was observed below the vocal cords; none of these infants demonstrated MAS. Meconium was noted below the cords in the remaining 46 infants, and MAS developed in a total of 16 (35%) of these infants. These investigators concluded that “all infants born through thick, particulate, or ‘pea soup’ meconium should have the trachea aspirated immediately after birth.”¹⁶² Subsequent studies documented similar findings for all infants born through meconium-stained fluid,¹⁶⁶ with a suggestion that earlier suctioning could decrease the incidence of MAS.¹⁶⁷ However, additional investigators documented that airway suctioning at birth does not prevent MAS and its associated mortality^168,169; these studies indicated that MAS was primarily a result of intrauterine events such as asphyxia or sepsis. Hypoxia induces pathologic changes in the pulmonary vasculature, which results in pulmonary hypertension and respiratory distress after birth. The pulmonary damage is independent of meconium aspiration; therefore, it is not prevented by the suctioning of meconium.

Murphy et al.¹⁷⁰ examined the lungs of 11 neonates who had MAS and died within 4 days of birth. Ten of these neonates also had a diagnosis of persistent pulmonary hypertension, and all had evidence of excessive muscularization of the intra-acinar arteries, which is an abnormal finding in the fetus or neonate.^171,172 Meyrick and Reid¹⁷³ demonstrated that chronic hypoxia (i.e., at least 4 weeks’ duration), but not acute hypoxia, results in pulmonary vascular muscularization in an animal model. Murphy et al.¹⁷⁰ concluded that the pathologic findings in the 1- to 4-day-old human lung could not be explained by the postdelivery effects of meconium aspiration; a more likely origin was the intrauterine maldevelopment of the pulmonary vasculature. They suggested a potential link between greater intestinal motility, passage of meconium, and precocious muscularization of the intra-acinar arteries.

A prospective study designed to assess the efficacy of routine tracheal suctioning of meconium to prevent MAS indicated little or no benefit to this practice.¹⁷⁴ Among the infants who underwent tracheal suctioning, four experienced MAS and two had laryngeal stridor. By contrast, none of the infants who did not undergo suctioning had complications, suggesting that vigorous neonates who have begun breathing before transfer to the resuscitation table may derive little or no benefit from tracheal suctioning and, in fact, may suffer some harm.

A subsequent review of studies published between 1980 and 1999 found that most cases of severe MAS were not causally related to meconium aspiration but rather resulted from intrauterine stress.¹⁷⁵ The authors concluded that severe MAS is a misnomer because, in most cases, much more than meconium aspiration has contributed to the lung damage. The implication is that when severe MAS occurs, inadequate suctioning at delivery or during resuscitation should not be considered the cause; therefore, other causes of intrauterine lung damage should be investigated.

Amnioinfusion—the instillation of saline into the amniotic cavity—has been used successfully for reduction of cord compression in the presence of oligohydramnios during labor. It has also been proposed as a potential treatment to reduce the incidence of MAS in infants born to women with thick meconium staining of the amniotic fluid. Potential benefits include (1) the reduction of cord compression, thus alleviating fetal compromise and acidemia that contribute to MAS, and (2) the dilution or washing out of the meconium in the amniotic fluid. A large multicenter randomized trial found no difference in rates of MAS or other neonatal disorders with the use of amnioinfusion.^176,177 Thus, the routine practice of amnioinfusion for meconium-stained fluid alone is not recommended.¹⁷⁸

Current guidelines do not recommend routine intrapartum oropharyngeal and nasopharyngeal suctioning before delivery of the infant’s head,^2,179 given that a large multicenter randomized trial showed no benefit to this practice in term-gestation infants.¹⁸⁰ After stabilization of the infant, meconium may be gently cleared from the mouth and nose by means of a bulb syringe or a large suction catheter (e.g., 12F to 14F).

Preterm Infant

The preterm neonate, especially the VLBW infant, is at higher risk for problems with multiple organ systems simply because of immaturity. During resuscitation, the physician should give special attention to the effect of prematurity on the lungs and the brain. Before the addition of surfactant and high-frequency ventilation to the therapeutic armamentarium of the neonatologist, pulmonary hyaline membrane disease (also known as neonatal respiratory distress syndrome) was the overwhelming obstacle to the attempted salvage of the very preterm infant.

Between 1970 and 2005, the proportion of infants weighing less than 1500 g at delivery rose from 1.17% to 1.5%; in 2009, the proportion stabilized at 1.45%.¹⁸¹ The survival rate of these 500- to 1500-g infants has increased to approximately 85%.¹⁸¹ Of these, 5% to 10% have what is characterized as cerebral palsy and 25% to 50% exhibit behavioral and cognitive deficits that lead to important school problems (see Chapter 10).^182,183 These VLBW infants constitute a tiny proportion of the birth population, but they are at the highest risk for development of cerebral palsy; infants weighing less than 1500 g at birth account for 25% of cases of this disorder.⁵⁸

Markers for brain injury affecting preterm infants are germinal matrix intraventricular hemorrhage (IVH) and periventricular leukomalacia. The brain injury may occur either as a consequence of the IVH and its sequelae or as an associated finding. The incidence of germinal matrix IVH in preterm infants declined from 35% to 50% in the late 1970s and early 1980s to approximately 15% in the mid 1990s.¹⁸⁴ Despite the decreased incidence of germinal matrix IVH, which is directly related to prematurity,¹⁸³ the overall burden of disability has sharply increased in recent years due to the proportion of very preterm infants who are surviving.¹⁸⁴ Periventricular leukomalacia, which is the classic neuropathology associated with hypoxic-ischemic cerebral white matter injury in the preterm infant, commonly accompanies IVH.¹⁸⁵

The fragility of the immature subependymal germinal matrix predisposes the preterm infant to the development of IVH. The hemorrhage originates from the endothelial cell–lined vessels that course through the germinal matrix in free communication with the venous circulation (i.e., the capillary–venule junction). The mechanism of damage to these endothelial cells and to the integrity of these capillaries has been investigated in animal models¹⁸⁶ and in human neonates by means of Doppler velocimetry.¹⁸⁷

Volpe,^188,189 who has reviewed the theories of the pathogenesis of germinal matrix IVH, has concluded that the pathogenesis is multifactorial; different combinations of factors are relevant in different patients. The three major categories in the pathogenesis of IVH are intra­vascular, vascular, and extravascular. Intravascular factors include fluctuating cerebral blood flow (CBF), which can result from respiratory disturbances in the ventilated preterm infant with neonatal respiratory distress syndrome^187,190; increases in CBF^186,191; increases in cerebral venous pressure¹⁹²; decreases in CBF followed by reperfusion; and platelet and coagulation disturbances.¹⁹³ Vascular factors include the tenuousness of the capillary integrity of the germinal matrix and the vulnerability of the matrix capillaries to hypoxic-ischemic injury.¹⁹⁴ Extravascular factors include deficient vascular support, excessive fibrinolytic activity, and a possible postnatal decrease in extravascular tissue pressure.¹⁹⁵

Of special interest in the discussion of antepartum and intrapartum care and neonatal resuscitation are the possible interventions that may prevent or lessen the severity of IVH. The best way to prevent germinal matrix IVH is to prevent preterm birth. Infection and inflammation are the most common identified causes of preterm birth at the lowest relevant gestational age.¹⁹⁶ Antenatal treatment of infections has not been proved to prevent preterm labor or premature rupture of membranes⁵⁸; however, prevention of infection, if possible, may be an important way to reduce the risk for IVH. Another intervention that lowers the incidence of IVH is the transportation of the preterm mother while the fetus is still in utero to a center that specializes in the care of high-risk neonates.¹

Various antenatal pharmacologic interventions have been evaluated for the prevention of IVH. Clinical trials of antenatal maternal administration of phenobarbital^197,198 and vitamin K^199,200 have yielded conflicting results, and their routine use is not currently recommended.⁵⁸

Corticosteroids are currently the most beneficial antenatal pharmacologic intervention for the prevention of IVH. This effect was first noticed when obstetricians began giving betamethasone and dexamethasone to pregnant women to help accelerate fetal lung maturity. The mechanism behind this protection is thought to be improved neonatal cardiovascular stability, which results in less hypotension and less need for blood pressure treatment in these infants.²⁰¹ Antenatal betamethasone administration leads to lower placental vascular resistance and higher placental blood flow.²⁰² This improvement in placental blood flow may decrease impairment of the preterm infant’s cerebral autoregulation. In addition, corticosteroids may stimulate the maturation of the germinal matrix. There is consensus regarding the efficacy of a single course of corticosteroids in patients at risk for preterm delivery, but the risks and benefits of multiple courses of corticosteroids for women who remain undelivered 7 days after the initial dose are still controversial. Obstetricians must balance the possible benefits of these agents against their potentially deleterious effects on neuronal and organ growth (see Chapter 34).

Multiple studies have demonstrated a lower incidence of cerebral palsy in infants of mothers given magnesium sulfate for the treatment of preeclampsia or for tocolysis^203,204; subsequent studies have observed a similar benefit when magnesium has been given specifically for fetal neuroprotection.^205–207 An ACOG committee opinion²⁰⁸ now recommends the administration of magnesium sulfate to mothers in preterm labor. Maternal magnesium sulfate administration does not result in a decreased incidence of IVH, although the incidence of high-grade (grade III or IV) lesions may be reduced.²⁰⁹ Although some investigators have suggested that antenatal exposure to magnesium sulfate results in a higher risk for adverse neonatal outcomes,²¹⁰ others have observed no association between umbilical cord blood magnesium concentration and the need for delivery room resuscitation when magnesium was administered for neuroprotection in anticipation of a preterm birth.²¹¹

Postnatal interventions that may prevent IVH include the avoidance of overly rapid infusion of volume expanders or hypertonic solutions such as sodium bicarbonate.^143,212 The establishment of adequate ventilation is the most beneficial immediate intervention that helps preserve cerebrovascular autoregulation in the preterm infant. The prevention of hypoxemia and hypercarbia is essential, because they are both linked to pressure-passive cerebral circulation, which in turn leads to the development of IVH.²¹²

Among infants who exhibit fluctuating CBF velocity, Pearlman et al.²¹³ found that treatment with pancuronium bromide, which corrects this fluctuation, reduced both the incidence and severity of IVH.²¹³ Other clinical trials have evaluated the efficacy of other pharmacologic agents for the correction of fluctuating hemodynamic disturbances. Studies of meperidine²¹⁴ and fentanyl²¹⁵ have shown some benefit, but the side effects and need for prolonged ventilation associated with these agents must be weighed against any potential benefits.

If the use of antepartum and intrapartum pharmacologic prophylaxis against IVH becomes part of preterm delivery management, the practice of obstetric anesthesia for preterm patients will be directly affected. For example, the conventional wisdom is that preterm infants are more sensitive than term infants to the effects of maternally administered agents such as analgesics²¹⁶ and that this effect is inherently deleterious. However, if this effect is found to protect the preterm infant brain from factors that may lead to IVH (e.g., hemodynamic instability), perhaps obstetric anesthesia providers will no longer attempt to avoid the placental transfer of pharmacologic agents but will deliberately administer these agents to the mother with the intent that they reach the fetus.

Congenital Anomalies

Occasionally, neonatal resuscitation is complicated by congenital anomalies of the airway or diaphragm. These anomalies may manifest as respiratory distress, which resolves only when appropriate resuscitation techniques are used. For example, neonates are obligatory nose breathers. The diagnosis and management of choanal stenosis and atresia include placement of an oral airway or endotracheal tube until a definitive surgical procedure can be performed.

Other congenital anomalies that cause upper airway obstruction include (1) micrognathia, as in Pierre Robin sequence; (2) macroglossia, as in Beckwith-Wiedemann syndrome or glycogen storage disease type II; (3) laryngeal webs; (4) laryngeal atresia; (5) stenosis or paralysis at the level of the vocal cords; (6) subglottic stenosis; (7) subglottic webs; (8) tracheal agenesis; and (9) tracheal rings. Obstruction also can occur as a result of tumors such as subglottic hemangiomas. The presence of a cleft palate may lead to difficulty with manual ventilation. In an infant with micrognathia or macroglossia, airway patency may be maintained if the neonate is kept in the prone position, which reduces posterior movement of the tongue into the pharynx. If macroglossia is extreme, use of an oral airway or a small nasogastric or orogastric suction catheter may be necessary to prevent complete obstruction of the pharynx by the tongue.

When respiratory distress and difficulty with bag-and-mask ventilation are encountered, laryngoscopy should be performed. The cause of the obstruction may be evident if it is supraglottic in location. Some supraglottic entities (e.g., laryngeal webs) may be treated successfully by passing an endotracheal tube through the obstruction and into the trachea. Subglottic lesions may require tracheostomy. The help of an otolaryngologist may be invaluable during resuscitation of a neonate with congenital airway obstruction. If there is antepartum evidence of such a condition (e.g., laryngeal stenosis), it is best to have an otolaryngologist present at the time of delivery.²¹⁷ If obstruction is discovered after delivery, the resuscitator should not hesitate to call for surgical assistance.

Fetal neck masses such as cervical teratoma and lymphangioma can lead to extrinsic airway compression. The resulting distortion of the airway can result in airway obstruction, and it may be difficult—if not impossible—to secure an airway in a timely fashion at delivery. These masses often are diagnosed before delivery because of the associated occurrence of polyhydramnios resulting from esophageal compression. In these rare cases, a multidisciplinary team should be assembled before delivery to assist in securing the airway. Leichty et al.²¹⁸ described a way of providing the time necessary to secure an airway, known as the ex utero intrapartum treatment (EXIT) procedure (see Chapter 7). An EXIT procedure delivers the fetal head and shoulders, but keeps the lower torso and umbilical cord intact within the uterus, thereby maintaining placental perfusion and oxygenation. The fetus can be given additional agents intramuscularly (fentanyl, vecuronium, and atropine) to provide fetal analgesia and to prevent movement and breathing. The FHR and SaO₂ are monitored continuously via a pulse oximeter probe attached to the fetal hand. The pediatric surgeon can then perform direct laryngoscopy, rigid bronchoscopy, or tracheostomy if necessary. After establishment of the airway, the delivery of the infant is completed.

The EXIT procedure has been considered an option for fetuses with a number of congenital anomalies.^219,220 A common indication for the EXIT procedure is an intrinsic airway obstruction. Intrinsic airway obstruction of the larynx or upper trachea (e.g., laryngeal web, subglottic cyst, tracheal atresia) can lead to retention of bronchial secretions and subsequent pulmonary distention; this constellation of findings is often classified as congenital high airway obstruction syndrome (CHAOS).²¹⁹ Use of the EXIT procedure resulted in the first long-term survival of a child with this syndrome.²²¹

The EXIT procedure also may be useful in conditions such as severe congenital heart disease, in which the need for emergency ECMO at birth is anticipated. The EXIT procedure allows for the placement of arterial and venous cannulas before umbilical cord clamping, thereby avoiding an unstable period between the termination of placental perfusion and the institution of ECMO. ²¹⁹ Other possible indications for the EXIT procedure include the resection of congenital cystic adenomatoid malformations and as a first step in separation procedures for conjoined twins with cardiovascular involvement.

Noah et al.²²² compared the short-term maternal outcomes of 34 patients who underwent the EXIT procedure between 1994 and 1999 with those in a control group who underwent nonemergency primary cesarean delivery. The EXIT procedure group had a higher estimated blood loss, but there was no difference in the postoperative hematocrit or duration of hospital stay. The EXIT procedure group also had a higher rate of superficial wound infection (15% versus 2%), but the incidence of endometritis was not different. A review of fetal and maternal outcomes after performance of an EXIT procedure in 12 infants with a giant neck mass found that 11 infants survived and 10 had normal development. All of the six mothers who desired future pregnancies subsequently had uncomplicated deliveries.²²³

Anesthetic considerations for the mother during an EXIT procedure include those relevant to general anesthesia for the mother undergoing cesarean delivery or other surgical procedures during pregnancy (see Chapters 7, 17, and 26). Several volatile halogenated agents have been used for the EXIT procedure, including isoflurane, desflurane, and sevoflurane.²¹⁹ The anesthetic management for an EXIT procedure differs from that for a routine cesarean delivery in the following ways: (1) general anesthesia is used much more often than neuraxial anesthesia, (2) a greater depth of anesthesia is achieved and maintained, (3) maximum uterine relaxation is desirable, (4) warm fluid is occasionally instilled into the uterus, and (5) a second anesthesiologist provides care for the fetus.²²⁰

George et al.²²⁴ described an alternative approach for the EXIT procedure with the use of combined spinal-epidural anesthesia (1.5 mL of bupivacaine 0.75%, fentanyl 15 µg, and morphine 0.15 mg, administered intrathecally, followed by placement of a multiorifice epidural catheter). Supplemental oxygen was provided through a face mask at 6 L/min. Immediately before uterine incision, the patients were given intravenous nitroglycerin 50 to 100 µg, followed by an infusion of nitroglycerin (0.5 to 1.5 µg/kg/min), allowing adequate uterine relaxation for partial delivery of the infant’s head. Maternal hypotension occurred in two of the three women and required vasopressor administration. After the infant’s airway was secured and the infant’s delivery was completed, the nitroglycerin was discontinued at the time of umbilical cord clamping.

Esophageal atresia and tracheoesophageal fistula occur in 1 of every 3000 births.²²⁵ There are many variations of these anomalies, the most common being esophageal atresia with a distal tracheoesophageal fistula (80% to 90% of cases). Neonates with a tracheoesophageal fistula are at increased risk for the pulmonary aspiration of gastric contents through the fistula into the lung. When the presence of a tracheoesophageal fistula is not known antepartum, it should be suspected if bubbling secretions are observed during spontaneous or bag-and-mask ventilation. Once a tracheoesophageal fistula is suspected, bag-and-mask ventilation should be discontinued, because its use may contribute to overdistention of the gastrointestinal tract with air, possibly leading to difficulty in ventilation from impingement of the enlarged stomach on the diaphragm. A suction catheter should be placed in the esophageal pouch to facilitate the removal of oral secretions. If mechanical ventilation is necessary, an endotracheal tube should be inserted with the tip distal to the entrance of the fistula. This positioning can be accomplished by performing an intentional right mainstem bronchial intubation followed by slowly withdrawing the tube until breath sounds are auscultated on the left; a lack of breath sounds over the stomach should then be confirmed. Percutaneous gastrostomy placement may be necessary during resuscitation to facilitate decompression of the gastrointestinal tract.

Congenital diaphragmatic hernia (CDH) occurs in approximately 1 in 3000 live births.²²⁶ The mortality rate from CDH is 30% to 60%. In 80% to 90% of cases the CDH occurs on the left side and is the result of herniation of the gut through the posterolateral defect of Bochdalek. During formation of the lung, herniation of the gut into the thoracic cavity results in hypoplasia of the lung tissue and pulmonary vasculature. This hypoplasia may be unilateral, but often it is bilateral because of the shift in mediastinal structures to the other side. CDH should be suspected when a neonate has respiratory difficulty and a scaphoid abdomen; this abnormal abdominal shape results from the presence of abdominal contents in the thorax.

During resuscitation of the neonate with CDH, bag-and-mask ventilation is contraindicated because it allows further distention of the gut, which would further impinge on the lung. Tracheal intubation is recommended, followed by the placement of a nasogastric or orogastric tube to ensure decompression of the gastrointestinal tract. Ventilation should consist of low-positive-pressure breaths to decrease the risk for causing a pneumothorax on the side contralateral to the CDH. If a pneumothorax does occur, it must be evacuated promptly. In the neonate, evacuation is accomplished initially by placement of a 22-gauge needle into the second intercostal space in the midclavicular line and aspiration of air with an attached stopcock and syringe. Severe pulmonary hypertension often accompanies CDH. Maintenance of euthermia, normoxia, and adequate systemic blood pressure promotes pulmonary artery blood flow.

Whenever congenital anomalies of the respiratory tract are noted, the presence of other anomalies should be suspected. It is important to evaluate the neonate promptly for cardiac malformations, especially if appropriate resuscitative efforts are not successful. Echocardiography is used to evaluate cardiac structures and function.