Chemical Factors.

The activation of chemoreceptors in the carotid arteries and aorta results from the relative state of hypoxia associated with labor. With each labor contraction there is a temporary decrease in uterine blood flow and transplacental gas exchange, resulting in transient fetal hypoxia and hypercarbia. Although the fetus is able to recover between contractions, there appears to be a cumulative effect that results in progressive decline in Po₂, increased Pco₂, and lowered blood pH. Decreased levels of oxygen and increased levels of carbon dioxide seem to have a cumulative effect that is involved in initiating neonatal breathing by stimulating the respiratory center in the medulla. Another chemical factor may also play a role; it is thought that, as a result of clamping the cord, there is a drop in levels of a prostaglandin that can inhibit respirations.

Mechanical Factors.

Respirations in the newborn can be stimulated by changes in intrathoracic pressure resulting from compression of the chest during vaginal birth. As the infant passes through the birth canal, the chest is compressed. With birth this pressure on the chest is released, and the negative intrathoracic pressure helps draw air into the lungs. Crying increases the distribution of air in the lungs and promotes expansion of the alveoli. The positive pressure created by crying helps to keep the alveoli open.

Thermal Factors.

With birth the newborn enters the extrauterine environment, in which the temperature is significantly lower. The profound change in environmental temperature stimulates receptors in the skin, resulting in stimulation of the respiratory center in the medulla.

Sensory Factors.

Sensory stimulation occurs in a variety of ways with birth. Some of these include handling the infant by the physician or midwife, suctioning the mouth and nose, and drying by the nurses. Pain associated with birth can also be a factor. The lights, sounds, and smells of the new environment can also be involved in stimulation of the respiratory center.

At term the lungs hold approximately 20 mL of fluid per kilogram. Air must be substituted for the fluid that filled the fetal respiratory tract. Traditionally it had been thought that the thoracic squeeze occurring during normal vaginal birth resulted in significant clearance of lung fluid. However, it appears that this event plays a minor role. In the days preceding labor there is reduced production of fetal lung fluid and concomitant decreased alveolar fluid volume. Shortly before the onset of labor there is a catecholamine surge that seems to promote fluid clearance from the lungs, which continues during labor (Goldsmith, 2011). The movement of lung fluid from the air spaces occurs through active transport into the interstitium, with drainage occurring through the pulmonary circulation and lymphatic system. Retention of lung fluid can interfere with the infant’s ability to maintain adequate oxygenation, especially if other factors (e.g., meconium aspiration, congenital diaphragmatic hernia, esophageal atresia with fistula, choanal atresia, congenital cardiac defect, immature alveoli) that compromise respirations are present. Infants born by cesarean in which labor did not occur before birth can experience some lung fluid retention, although it typically clears without deleterious effects on the infant. These infants are also more likely to develop transient tachypnea of the newborn (TTNB) caused by the lower levels of catecholamines (Abu-Shaweesh, 2011).

The alveoli of the term infant’s lungs are lined with surfactant, a protein manufactured in type II cells of the lungs. Lung expansion depends largely on chest wall contraction and adequate secretion of surfactant. Surfactant lowers surface tension, therefore reducing the pressure required to keep the alveoli open with inspiration, and prevents total alveolar collapse on exhalation, thereby maintaining alveolar stability. The decreased surface tension results in increased lung compliance, helping to establish the functional residual capacity of the lungs. With absent or decreased surfactant, more pressure must be generated for inspiration, which can soon tire or exhaust preterm or sick term infants.

Breathing movements that began in utero as intermittent become continuous after birth, although the mechanism for this is not well understood. Once respirations are established, breaths are shallow and irregular, ranging from 30 to 60 breaths/min, with periods of breathing that include pauses in respirations lasting less than 20 seconds. These episodes of periodic breathing occur most often during the active (rapid eye movement [REM]) sleep cycle and decrease in frequency and duration with age. Apneic periods longer than 20 seconds indicate a pathologic process and should be evaluated.

In most newborn infants auscultation of the chest reveals loud, clear breath sounds that seem very near because little chest tissue intervenes. Breath sounds should be clear and equal bilaterally. The ribs of the infant articulate with the spine at a horizontal rather than a downward slope; consequently the rib cage cannot expand with inspiration as readily as that of an adult. Because neonatal respiratory function is largely a matter of diaphragmatic contraction, abdominal breathing is characteristic of newborns. The newborn infant’s chest and abdomen rise simultaneously with inspiration. Characteristics of the respiratory system of the neonate and the effects of these characteristics on respiratory function are listed in Table 22-1.

Heart Rate and Sounds

The heart rate for a term newborn ranges from 120 to 160 beats/min, with brief fluctuations above and below these values usually noted during sleeping and waking states (Blackburn, 2013). The range of the heart rate in the term infant is about 85 to 100 beats/min during deep sleep and can increase to 180 beats/min or higher when the infant cries. A heart rate that is either high (more than 160 beats/min) or low (fewer than 100 beats/min) should be reevaluated within 30 minutes to 1 hour or when the activity of the infant changes. Immediately after birth the heart rate can be palpated by grasping the base of the umbilical cord.

The apical impulse (point of maximal impulse [PMI]) in the newborn is at the fourth intercostal space and to the left of the midclavicular line. The PMI is often visible and easily palpable because of the thin chest wall; this is also called precordial activity.

Apical pulse rates should be determined for all infants. Auscultation should be for a full minute, preferably when the infant is asleep. An irregular heart rate in newborns is not uncommon in the first few hours of life. After this time an irregular heart rate not attributed to changes in activity or respiratory pattern should be evaluated. Heart sounds during the neonatal period are of higher pitch, shorter duration, and greater intensity than during adult life. The first sound (S₁) is typically louder and duller than the second sound (S₂), which is sharp. The third and fourth heart sounds are not auscultated in newborns. Most heart murmurs heard during the neonatal period have no pathologic significance, and more than half of the murmurs disappear by 6 months. However, the presence of a murmur and accompanying signs such as poor feeding, apnea, cyanosis, or pallor are considered abnormal and should be investigated. There can be significant cardiac defects without symptoms in the early newborn period. This reinforces the importance of ongoing assessment (Sadowski, 2010).

Blood Pressure

Values for newborn BP vary with gestational age and weight. The term newborn infant’s average systolic BP is 60 to 80 mm Hg, and average diastolic BP is 40 to 50 mm Hg. The mean arterial pressure (MAP) should be equivalent to the weeks of gestation. For example, an infant born at 40 weeks of gestation should have a MAP of at least 40. The BP increases by the second day of life, with minor variations noted during the first month of life. A drop in systolic BP (about 15 mm Hg) in the first hour of life is common. Crying and movement usually cause increases in the systolic BP. The measurement of BP is best accomplished with an oscillometric device while the infant is at rest. A correctly sized cuff must be used for accurate measurement of an infant’s BP.

Policies on routine assessment of neonatal BP vary. In many agencies, unless a specific indication exists, BP is not measured in the newborn on a routine basis except as a baseline. In some institutions nurses obtain four extremity BPs in the presence of any cardiovascular symptoms such as tachycardia, murmur, abnormal pulses, poor perfusion, or abnormal precordial activity. If the systolic pressure is more than 10 mm Hg higher in the upper extremities than in the lower extremities, further diagnostic testing may be needed (Kenney, Hoover, Williams, et al., 2011).

Blood Volume

Blood volume in the term newborn ranges from 80 to 100 mL/kg of body weight. Immediately after birth the total blood volume averages 300 mL, but this volume can increase by as much as 100 mL, depending on the length of time to cord clamping and cutting. The infant born prematurely has a relatively greater blood volume than the term newborn. This occurs because the preterm infant has a proportionately greater plasma volume, not a greater red blood cell (RBC) mass.

Early or delayed clamping of the umbilical cord changes the circulatory dynamics of the newborn. Delayed clamping expands the blood volume from the so-called placental transfusion of blood to the newborn. Delayed cord clamping (≥2 minutes after birth) has been reported to be beneficial in improving hematocrit and iron status and decreasing anemia; such benefits can last up to 6 months (Andersson, Hellström-Westas, Andersson, et al., 2011; Arca, Botet, Palacio, et al., 2010). Polycythemia that occurs with delayed clamping is usually not harmful, although there can be an increased risk of jaundice that requires phototherapy.

Signs of Cardiovascular Problems

Close monitoring of the infant’s vital signs is important for early detection of impending problems. Persistent tachycardia (more than 160 beats/min) can be associated with anemia, hypovolemia, hyperthermia, or sepsis. Persistent bradycardia (less than 100 beats/min) can be a sign of a congenital heart block or hypoxemia.

The newborn’s skin color can reflect cardiovascular problems. Pallor in the immediate post birth period is often symptomatic of underlying problems such as anemia or marked peripheral vasoconstriction as a result of intrapartum asphyxia or sepsis. Any prolonged cyanosis other than in the hands or feet can indicate respiratory and/or cardiac problems. The presence of jaundice can indicate ABO or Rh factor incompatibility problems (see Chapter 25).

Congenital heart defects are the most common type of congenital malformations (see Chapter 36). Although the more serious defects such as tetralogy of Fallot are likely to have clinical manifestations such as cyanosis, dyspnea, and hypoxia, others such as small ventricular septal defects can be asymptomatic. The prenatal history can provide information regarding risk factors for congenital heart defects so the nurse knows to be more alert for symptoms. Maternal illness such as rubella, metabolic disease such as diabetes, and drug ingestion are associated with an increased risk of cardiac defects.

Red Blood Cells and Hemoglobin

Because fetal circulation is less efficient at oxygen exchange than the lungs, the fetus needs additional RBCs for transport of oxygen in utero. Therefore at birth the average levels of RBCs, hemoglobin, and hematocrit are higher than those in the adult; these levels fall slowly over the first month. At birth the RBC count ranges from 4.6 to 5.2 million/mm³ (Blackburn, 2013). The term newborn can have a hemoglobin concentration of 13.7 to 20.1 g/dL at birth, decreasing gradually to 12 to 20 g/dL during the first 2 weeks (Pagana and Pagana, 2009). Hematocrit levels at birth range from 51% to 56%, increase slightly in the first few hours or days as fluid shifts from intravascular to interstitial spaces (Blackburn, 2013), and by 8 weeks are between 39% and 59% (Pagana and Pagana, 2009). Polycythemia (central venous hematocrit greater than 65%) can occur in term and preterm infants as a result of delayed cord clamping, maternal hypertension or diabetes, or intrauterine growth restriction.

The source of the sample is a significant factor in levels of RBCs, hemoglobin, and hematocrit because capillary blood yields higher values than venous blood. The timing of blood sampling is also significant; the slight rise in RBCs after birth is followed by a substantial drop. At birth the infant’s blood contains an average of 70% fetal hemoglobin; however, because of the shorter life span of the cells containing fetal hemoglobin, the percentage falls to 55% by 5 weeks and to 5% by 20 weeks. Iron stores generally are sufficient to sustain normal RBC production for 4 to 5 months in the term infant, at which time a transient physiologic anemia can occur.

Leukocytes

Leukocytosis, with a white blood cell (WBC) count of approximately 18,000/mm³ (range 9000 to 30,000/mm³), is normal at birth (Pagana and Pagana, 2009). The number of WBCs increases to 23,000 to 24,000/mm³ during the first day after birth. The initial high WBC count of the newborn decreases rapidly, and a stable level of 12,000/mm³ is normally maintained during the neonatal period. Serious infection is not tolerated well by the newborn; leukocytes are slow to recognize foreign protein and localize and fight infection early in life. Sepsis may be accompanied by a concomitant rise in neutrophils; however, some infants initially may be seen with clinical signs of sepsis without a significant elevation in WBCs. In addition, events other than infection (i.e., prolonged crying, maternal hypertension, asymptomatic hypoglycemia, hemolytic disease, meconium aspiration syndrome, labor induction with oxytocin, surgery, difficult labor, high altitude, and maternal fever) can cause neutrophilia in the newborn.

Platelets

Platelet count ranges between 150,000 and 300,000/mm³ and is essentially the same in newborns as in adults (Pagana and Pagana, 2009). The levels of factors II, VII, IX, and X found in the liver decrease during the first few days of life because the newborn cannot synthesize vitamin K. However, bleeding tendencies in the newborn are rare; and, unless the vitamin K deficiency is great, clotting is sufficient to prevent hemorrhage.

Blood Groups

The infant’s blood group is determined genetically and established early in fetal life. However, during the neonatal period the strength of the agglutinogens present in the RBC membrane gradually increases. Cord blood samples may be used to identify the infant’s blood type and Rh status.

Heat Loss

The body temperature of newborn infants depends on the heat transfer between the infant and the external environment. Factors that influence heat loss to the environment include the temperature and humidity of the air, the flow and velocity of the air, and the temperature of surfaces in contact with and around the infant. The goal of care is to maintain a neutral thermal environment for the neonate in which heat balance is maintained. The neutral thermal environment is the ideal environmental temperature that allows the neonate to maintain a normal body temperature to minimize oxygen and glucose consumption. Heat loss in the newborn occurs by four modes:

Loss of heat must be controlled to protect the infant. Control of such modes of heat loss is the basis of caregiving policies and techniques. One method for promoting thermoregulation and maternal-newborn interaction is to place the naked newborn on the mother’s bare chest and cover both with a blanket (Fig. 22-1). This skin-to-skin contact reduces conductive and radiant heat loss and enhances newborn temperature control and maternal-infant interaction (Brown and Landers, 2011).

Thermogenesis

In response to cold the neonate attempts to generate heat (thermogenesis) by increasing muscle activity. Cold infants may cry and appear restless. Because of vasoconstriction the skin can feel cool to touch, and acrocyanosis can be present. There is an increase in cellular metabolic activity, primarily in the brain, heart, and liver; this also increases oxygen and glucose consumption.

In an effort to conserve heat, term newborns assume a position of flexion that helps guard against heat loss because it diminishes the amount of body surface exposed to the environment. Infants also can reduce the loss of internal heat through the body surface by constricting peripheral blood vessels.

Adults are able to produce heat through shivering; however, the shivering mechanism of heat production is rarely operable in the newborn unless there is prolonged cold exposure (Blackburn, 2013). Newborns produce heat through nonshivering thermogenesis. This is accomplished primarily by metabolism of brown fat, which is unique to the newborn; and secondarily by increased metabolic activity in the brain, heart, and liver. Brown fat is located in superficial deposits in the interscapular region and axillae and in deep deposits at the thoracic inlet, along the vertebral column, and around the kidneys. Brown fat has a richer vascular and nerve supply than ordinary fat. Heat produced by intense lipid metabolic activity in brown fat can warm the newborn by increasing heat production as much as 100%. Reserves of brown fat, usually present for several weeks after birth, are rapidly depleted with cold stress. The amount of brown fat reserve increases with the weeks of gestation. A full-term newborn has greater stores than a preterm infant.

Cold Stress

Cold stress imposes metabolic and physiologic demands on all infants, regardless of gestational age and condition. The respiratory rate increases in response to the increased need for oxygen. In the cold-stressed infant oxygen consumption and energy are diverted from maintaining normal brain and cardiac function and growth to thermogenesis for survival. If the infant cannot maintain an adequate oxygen tension, vasoconstriction follows and jeopardizes pulmonary perfusion. As a consequence the Po₂ is decreased, and the blood pH drops. These changes can prompt a transient respiratory distress or aggravate existing RDS. Moreover, decreased pulmonary perfusion and oxygen tension can maintain or reopen the right-to-left shunt across the ductus arteriosus.

The basal metabolic rate increases with cold stress. If cold stress is protracted, anaerobic glycolysis occurs, resulting in increased production of acids. Metabolic acidosis develops; and, if a defect in respiratory function is present, respiratory acidosis also develops (Fig. 22-2). Excessive fatty acids can displace the bilirubin from the albumin-binding sites and exacerbate hyperbilirubinemia.

Hypoglycemia is another metabolic consequence of cold stress. The process of anaerobic glycolysis uses approximately 3 to 4 times the amount of blood glucose, thereby depleting existing stores. If the infant is sufficiently stressed and low glucose stores are not replaced, hypoglycemia, which can be asymptomatic in the newborn, can develop.

Hyperthermia

Although occurring less frequently than hypothermia, hyperthermia can occur and must be corrected. A body temperature greater than 37.5° C (99.5° F) is considered to be abnormally high and is typically caused by excess heat production related to sepsis or a decrease in heat loss. Hyperthermia can result from the inappropriate use of external heat sources such as radiant warmers, phototherapy, sunlight, increased environmental temperature, and the use of excessive clothing or blankets (Brown and Landers, 2011). The clinical appearance of the infant who is hyperthermic often indicates the causative mechanism. Infants who are overheated because of environmental factors such as being swaddled in too many blankets exhibit signs of heat-losing mechanisms: skin vessels dilate, skin appears flushed, hands and feet are warm to touch, and the infant assumes a posture of extension. The newborn who is hyperthermic because of sepsis appears stressed: vessels in the skin are constricted, color is pale, and hands and feet are cool. Hyperthermia develops more rapidly in a newborn than in an adult because of the relatively larger surface area of an infant. Sweat glands do not function well. Serious overheating of the newborn can cause cerebral damage from dehydration or even heat stroke and death (Brown and Landers, 2011).

Fluid and Electrolyte Balance

In the term neonate approximately 75% of body weight consists of total body water (extracellular and intracellular). A reduction in extracellular fluid occurs with diuresis during the first few days after birth. The weight loss experienced by most newborns during the first few days after birth is caused primarily by extracellular water loss (Dell, 2011).

The daily fluid requirement for neonates weighing more than 1500 g is 60 to 80 mL/kg during the first 2 days of life. From 3 to 7 days the requirement is 100 to 150 mL/kg/day; and from 8 to 30 days it is 120 to 180 mL/kg/day (Dell, 2011).

At birth the glomerular filtration rate (GFR) of a newborn is approximately 30% to 50% that of the adult. This results in a decreased ability to remove nitrogenous and other waste products from the blood. The GFR rapidly increases during the first month of life as a result of postnatal physiologic changes, including decreased renal vascular resistance, increased renal blood flow, and increased filtration pressure.

Sodium reabsorption is decreased as a result of a lowered sodium- or potassium-activated adenosine triphosphatase activity. The decreased ability to excrete excess sodium results in hypotonic urine compared with plasma, leading to a higher concentration of sodium, phosphates, chloride, and organic acids and a lower concentration of bicarbonate ions. The infant has a higher renal threshold for glucose than adults.

Bicarbonate concentration and buffering capacity are decreased. This can lead to acidosis and electrolyte imbalance.

Signs of Renal System Problems

The renal system has a wide range of functions. Dysfunction resulting from physiologic abnormalities can range from the lack of a steady stream of urine to gross anomalies such as hypospadias and exstrophy of the bladder, which can be identified easily at birth. Enlarged or cystic kidneys can be identified as masses during abdominal palpation. Some kidney anomalies also can be detected by ultrasound examination during pregnancy (see Chapter 25).

Digestion

The infant’s ability to digest carbohydrates, fats, and proteins is regulated by the presence of certain enzymes. Most of these enzymes are functional at birth except for pancreatic amylase and lipase. Amylase is produced by the salivary glands after approximately 3 months and by the pancreas at approximately 6 months of age. This enzyme is necessary to convert starch into maltose and occurs in high amounts in colostrum. The other exception is lipase, also secreted by the pancreas; it is necessary for the digestion of fat. Therefore the normal newborn is capable of digesting simple carbohydrates and proteins but has a limited ability to digest fats. Mammary lipase in human milk aids in digestion of fats by the neonate.

Lactase levels in newborns are higher than in older infants. This enzyme is necessary for digestion of lactose, the major carbohydrate in human milk and commercial infant formula.