Physiologic and Behavioral Adaptations of the Newborn

Chapter 22

Physiologic and Behavioral Adaptations of the Newborn

Kathryn R. Alden

The neonatal period includes the time from birth through day 28 of life. During this time the neonate must make many physiologic and behavioral adaptations to extrauterine life. Physiologic adjustment tasks are those that involve: (1) establishing and maintaining respirations; (2) adjusting to circulatory changes; (3) regulating temperature; (4) ingesting, retaining, and digesting nutrients; (5) eliminating waste; and (6) regulating weight. Behavioral tasks include: (1) establishing a regulated behavioral tempo independent of the mother, which involves self-regulating arousal, self-monitoring changes in state, and patterning sleep; (2) processing, storing, and organizing multiple stimuli; and (3) establishing a relationship with caregivers and the environment. The term infant usually makes these adjustments with little or no difficulty.

Transition to Extrauterine Life

The major adaptations associated with transition from intrauterine to extrauterine life occur during the first 6 to 8 hours after birth. The predictable series of events during transition are mediated by the sympathetic nervous system and result in changes that involve heart rate, respirations, temperature, and gastrointestinal function. This transition period represents a time of vulnerability for the neonate and warrants careful observation by nurses. To detect disorders in adaptation soon after birth, nurses must be aware of normal features of the transition period.

In their classic work on newborn adaptation to extrauterine life, Desmond, Rudolph, and Phitaksphraiwan (1966) proposed three stages of newborn transition. The stages are still considered valid today.

The first stage of the transition period lasts up to 30 minutes after birth and is called the first period of reactivity. The newborn’s heart rate increases rapidly to 160 to 180 beats/min but gradually falls after 30 minutes or so to a baseline rate of 100 to 120 beats/min. Respirations are irregular, with a rate between 60 and 80 breaths/min. Fine crackles can be present on auscultation. Audible grunting, nasal flaring, and retractions of the chest also can be present; but these should cease within the first hour of birth. The infant is alert and may have spontaneous startles, tremors, crying, and head movement from side to side. Bowel sounds are audible, and meconium may be passed.

After the first period of reactivity the newborn either sleeps or has a marked decrease in motor activity. This period of decreased responsiveness lasts from 60 to 100 minutes. During this time the infant is pink, and respirations are rapid and shallow (up to 60 breaths/min) but unlabored. Bowel sounds are audible, and peristaltic waves may be noted over the rounded abdomen.

The second period of reactivity occurs roughly between 2 and 8 hours after birth and lasts from 10 minutes to several hours. Brief periods of tachycardia and tachypnea occur, associated with increased muscle tone, changes in skin color, and mucus production. Meconium is commonly passed at this time. Most healthy newborns experience this transition, regardless of gestational age or type of birth; extremely and very preterm infants do not because of physiologic immaturity.

Physiologic Adjustments

Respiratory System

As the infant emerges from the intrauterine environment and the umbilical cord is severed, profound adaptations are necessary for survival. The most critical of these adaptations is the establishment of effective respirations. Most newborns breathe spontaneously after birth and are able to maintain adequate oxygenation. Preterm infants often encounter respiratory difficulties related to immaturity of the lungs.

Initiation of Breathing

During intrauterine life oxygenation of the fetus occurs through transplacental gas exchange. However, at birth the lungs must be established as the site of gas exchange. In utero fetal blood was shunted away from the lungs, but when birth occurs the pulmonary vasculature must be fully perfused for this purpose. Clamping the umbilical cord causes a rise in blood pressure (BP), which increases circulation and lung perfusion.

It has been recognized that there is no single trigger for newborn respiratory function. The initiation of respirations in the neonate is the result of a combination of chemical, mechanical, thermal, and sensory factors.

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.

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.

TABLE 22-1

Characteristics of the Respiratory System of the Neonate

Immature alveoli; decreased size and number of alveoli Risk of respiratory insufficiency and pulmonary problems
Thicker alveolar wall; decreased alveolar surface area Less efficient gas transport and exchange
Continued development of alveoli until childhood Possible opportunity to reduce effects of discrete lung injury
Decreased lung elastic tissue and recoil Decreased lung compliance requiring higher pressures and more work to expand; increased risk of atelectasis
Reduced diaphragm movement and maximal force potential Less effective respiratory movement; difficulty generating negative intrathoracic pressures; risk of atelectasis
Tendency to nose breathe; altered position of larynx and epiglottis Enhanced ability to synchronize swallowing and breathing; risk of airway obstruction; possibly more difficult to intubate
Small compliant airway passages with higher airway resistance; immature reflexes Risk of airway obstruction and apnea
Increased pulmonary vascular resistance with sensitive pulmonary arterioles Risk of ductal shunting and hypoxemia with events such as hypoxia, acidosis, hypothermia, hypoglycemia, and hypercarbia
Increased oxygen consumption Increased respiratory rate and work of breathing; risk of hypoxia
Increased intrapulmonary right-left shunting Increased risk of atelectasis with wasted ventilation; lower Pco2
Immaturity of pulmonary surfactant system in immature infants Increased risk of atelectasis and respiratory distress syndrome; increased work of breathing
Immature respiratory control Irregular respirations with periodic breathing; risk of apnea; inability to rapidly alter depth of respirations

Pco2, Partial pressure of carbon dioxide.

From Blackburn S: Maternal, fetal, and neonatal physiology: a clinical perspective, ed 4, St Louis, 2013, Saunders.

Signs of Respiratory Distress

Signs of respiratory distress can include nasal flaring, intercostal or subcostal retractions (in-drawing of tissue between the ribs or below the rib cage), or grunting with respirations. Suprasternal or subclavicular retractions with stridor or gasping most often represent an upper airway obstruction. Seesaw or paradoxical respirations (exaggerated rise in abdomen with respiration as the chest falls) instead of abdominal respirations are abnormal and should be reported. A respiratory rate of less than 30 or greater than 60 breaths/min with the infant at rest must be evaluated. The respiratory rate of the infant can be slowed, depressed, or absent as a result of the effects of analgesics or anesthetics administered to the mother during labor and birth. Apneic episodes can be related to several events (rapid increase in body temperature, hypothermia, hypoglycemia, or sepsis) that require thorough evaluation. Tachypnea can result from inadequate clearance of lung fluid, or it can be an indication of newborn respiratory distress syndrome (RDS).

Changes in the infant’s color can indicate respiratory distress. Acrocyanosis, the bluish discoloration of hands and feet, is a normal finding in the first 24 hours after birth. Transient periods of duskiness while crying are not uncommon immediately after birth; however, central cyanosis is abnormal and signifies hypoxemia. With central cyanosis the lips and mucous membranes are bluish. It can be the result of inadequate delivery of oxygen to the alveoli, poor perfusion of the lungs that inhibits gas exchange, or cardiac dysfunction. Because central cyanosis is a late sign of distress, newborns usually have significant hypoxemia when cyanosis appears (Askin, 2009).

Infants who experience mild TTNB often have signs of respiratory distress during the first 1 to 2 hours after birth as they transition to extrauterine life. Tachypnea with rates up to 100 breaths/min can be present along with intermittent grunting, nasal flaring, and mild retractions. Supplemental oxygen may be needed.

In neonates with more serious respiratory problems, symptoms of distress are more pronounced and tend to last beyond the first 2 hours after birth. Respiratory rates can exceed 120 breaths/min. Moderate-to-severe retractions, grunting, pallor, and central cyanosis can occur. The respiratory symptoms can be accompanied by hypotension, temperature instability, hypoglycemia, acidosis, and signs of cardiac problems. Common respiratory complications affecting neonates include RDS, meconium aspiration, pneumonia, and persistent pulmonary hypertension of the newborn (PPHN) (Askin, 2009) (see Chapter 25.)

Cardiovascular System

The cardiovascular system changes significantly after birth. The infant’s first breaths, combined with increased alveolar capillary distention, inflate the lungs and reduce pulmonary vascular resistance to pulmonary blood flow from the pulmonary arteries. Pulmonary artery pressure drops, and pressure in the right atrium declines. Increased pulmonary blood flow from the left side of the heart increases pressure in the left atrium, which causes a functional closure of the foramen ovale. During the first few days of life crying may temporarily reverse the flow through the foramen ovale and lead to mild cyanosis.

In utero fetal Po2 is 20 to 30 mm Hg. After birth, when the Po2 level in the arterial blood approximates 50 mm Hg, the ductus arteriosus constricts in response to increased oxygenation. Circulating hormone prostaglandin E (PGE2) levels also have an important role in closure of the ductus arteriosus. In term infants it functionally closes within the first hours after birth; permanent closure usually occurs within 3 to 4 weeks, and the ductus arteriosus becomes a ligament. The ductus arteriosus can open in response to low oxygen levels in association with hypoxia, asphyxia, or prematurity. With auscultation of the chest a patent ductus arteriosus can be detected as a heart murmur.

The umbilical vein and arteries constrict rapidly within the first 2 minutes after birth. It is thought that this is related to exposure of the cord to the cooler extrauterine environment and to increased oxygenation as the infant begins to breathe. With the clamping and severing of the cord, the umbilical arteries, the umbilical vein, and the ductus venosus are functionally closed; they are converted into ligaments within 2 to 3 months. The hypogastric arteries also occlude and become ligaments. Table 22-2 summarizes the cardiovascular changes at birth.

TABLE 22-2

Cardiovascular Changes at Birth

Primary Changes
Pulmonary circulation: High pulmonary vascular resistance, increased pressure in right ventricle and pulmonary arteries Low pulmonary vascular resistance; decreased pressure in right atrium, ventricle, and pulmonary arteries Expansion of collapsed fetal lung with air
Systemic circulation: Low pressures in left atrium, ventricle, and aorta High systemic vascular resistance; increased pressure in left atrium, ventricle, and aorta Loss of placental blood flow
Secondary Changes
Umbilical arteries: Patent, carrying of blood from hypogastric arteries to placenta Functionally closed at birth; obliteration by fibrous proliferation possibly taking 2 to 3 months, distal portions becoming lateral vesicoumbilical ligaments, proximal portions remaining open as superior vesicle arteries Closure preceding that of umbilical vein, probably accomplished by smooth muscle contraction in response to thermal and mechanical stimuli and alteration in oxygen tension
Mechanically severed with cord at birth
Umbilical vein: Patent, carrying of blood from placenta to ductus venosus and liver Closed; becoming ligamentum teres hepatis after obliteration Closure shortly after umbilical arteries; hence blood from placenta possibly entering neonate for short period after birth
Mechanically severed with cord at birth
Ductus venosus: Patent, connection of umbilical vein to inferior vena cava Closed; becoming ligamentum venosum after obliteration Loss of blood flow from umbilical vein
Ductus arteriosus: Patent, shunting of blood from pulmonary artery to descending aorta Functionally closed almost immediately after birth; anatomic obliteration of lumen by fibrous proliferation requiring 1 to 3 months, becoming ligamentum arteriosum Increased oxygen content of blood in ductus arteriosus creating vasospasm of its muscular wall
High systemic resistance increasing aortic pressure; low pulmonary resistance reducing pulmonary arterial pressure
Foramen ovale: Formation of a valve opening that allows blood to flow directly to left atrium (shunting of blood from right to left atrium) Functionally closed at birth; constant apposition gradually leading to fusion and permanent closure within a few months or years in majority of persons Increased pressure in left atrium and decreased pressure in right atrium, causing closure of valve over foramen


Data from Blackburn S: Maternal, fetal, and neonatal physiology: a clinical perspective, ed 4, St Louis, 2013, Saunders.

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.

Hematopoietic System

The hematopoietic system of the newborn exhibits certain variations from that of the adult. Levels of RBCs and leukocytes differ, but platelets levels are relatively the same.

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.


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.


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.

Thermogenic System

Next to establishing respirations and adequate circulation, heat regulation is most critical to the newborn’s survival. During the first 12 hours after birth the neonate attempts to achieve thermal balance in adjusting to the extrauterine environmental temperature. Thermoregulation is the maintenance of balance between heat loss and heat production. Newborns attempt to stabilize their core body temperatures within a narrow range. Hypothermia from excessive heat loss is a common and dangerous problem.

Anatomic and physiologic characteristics of neonates place them at risk for heat loss. Newborns have a thin layer of subcutaneous fat. The blood vessels are close to the surface of the skin. Changes in environmental temperature alter the temperature of the blood, thereby influencing temperature regulation centers in the hypothalamus. Newborns have larger body surface–to–body weight (mass) ratios than do children and adults (Blackburn, 2013).

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:

1. Convection is the flow of heat from the body surface to cooler ambient air. Because of heat loss by convection, the ambient temperature in the nursery is kept at approximately 24° C (75.2° F), and newborns in open bassinets are wrapped to protect them from the cold. A cap may be worn to decrease heat loss from the infant’s head.

2. Radiation is the loss of heat from the body surface to a cooler solid surface not in direct contact but in relative proximity. To prevent this type of loss, cribs and examining tables are placed away from outside windows, and care is taken to avoid direct air drafts.

3. Evaporation is the loss of heat that occurs when a liquid is converted to a vapor. In the newborn heat loss by evaporation occurs as a result of vaporization of moisture from the skin. This heat loss is intensified by failing to dry the newborn directly after birth or by drying the infant too slowly after a bath. The less mature the newborn, the more severe the evaporative heat loss. Evaporative heat loss, as a component of insensible water loss, is the most significant cause of heat loss in the first few days of life.

4. Conduction is the loss of heat from the body surface to cooler surfaces in direct contact. When admitted to the nursery, the newborn is placed in a warmed crib to minimize heat loss. The scales used for weighing the newborn should have a protective cover to minimize conductive heat loss.

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).


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.


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).

Renal System

At term the kidneys occupy a large portion of the posterior abdominal wall. The bladder lies close to the anterior abdominal wall and is both an abdominal and a pelvic organ. In the newborn almost all palpable masses in the abdomen are renal in origin.

At birth a small quantity (approximately 40 mL) of urine is usually present in the bladder of a full-term infant. Many newborns void at the time of birth, although this is easily missed and may not be recorded. During the first few days term infants generally excrete 15 to 60 mL/kg; output gradually increases over the first month (Blackburn, 2013). The frequency of voiding varies from 2 to 6 times per day during the first and second days of life and from 5 to 25 times during the subsequent 24 hours. Approximately six to eight voidings per day of pale, straw-colored urine indicate adequate fluid intake.

Full-term newborns have limited capacity to concentrate urine; therefore the specific gravity ranges from 1.001 to 1.020 (Pagana and Pagana, 2009). The ability to concentrate urine fully is attained by about 3 months of age. After the first voiding the infant’s urine may appear cloudy (because of mucus content) and have a much higher specific gravity. This decreases as fluid intake increases. Normal urine during early infancy is usually straw colored and almost odorless. Sometimes pink-tinged uric acid crystal stains or “brick dust” appear on the diaper; these stains are normal, although they can be misinterpreted as blood. Loss of fluid through urine, feces, lungs, increased metabolic rate, and limited fluid intake results in a 5% to 10% loss of the birth weight. This usually occurs over the first 3 to 5 days of life. If the mother is breastfeeding and her milk supply has not come in yet (which occurs by the third or fourth day after birth), the neonate is somewhat protected from dehydration by its increased extracellular fluid volume. The neonate should regain the birth weight within 10 to 14 days, depending on the feeding method (breast or bottle).

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.

Gastrointestinal System

The full-term newborn is capable of swallowing, digesting, metabolizing and absorbing proteins and simple carbohydrates and emulsifying fats. With the exception of pancreatic amylase, the characteristic enzymes and digestive juices are present even in low-birth-weight neonates.

In the adequately hydrated infant the mucous membrane of the mouth is moist and pink; the hard and soft palates are intact. The presence of moderate-to-large amounts of mucus is common in the first few hours after birth. Small whitish areas (Epstein pearls) may be found on the gum margins and at the juncture of the hard and soft palates. The cheeks are full because of well-developed sucking pads. These, like the labial tubercles (sucking calluses) on the upper lip, disappear around the age of 12 months when the sucking period is over.

Sucking is a reflex behavior that begins in utero as early as 15 to 16 weeks. Sucking behavior is influenced by neuromuscular maturity, maternal medications received during labor and birth, and the type of initial feeding. As early as 28 weeks some infants can coordinate sucking and swallowing while breastfeeding. Bottle-feeding infants may not coordinate sucking and swallowing until 32 to 34 weeks. A special mechanism present in healthy term newborns coordinates the breathing, sucking, and swallowing reflexes necessary for oral feeding. This is well developed in most infants by 37 weeks (Gardner and Lawrence, 2011). Sucking takes place in small bursts of 3 or 4 and up to 8 to 10 sucks at a time, with a brief pause between bursts. The infant is unable to move food from the lips to the pharynx; therefore placing the nipple (breast or bottle) well inside the baby’s mouth is necessary. Peristaltic activity in the esophagus is uncoordinated in the first few days of life. It quickly becomes a coordinated pattern in healthy full-term infants, and they swallow easily.

Teeth begin developing in utero, with enamel formation continuing until about 10 years of age. Tooth development is influenced by neonatal or infant illnesses and medications and by illnesses of or medications taken by the mother during pregnancy. The fluoride level in the water supply also influences tooth development. Occasionally an infant may be born with one or more teeth. These natal teeth have poorly formed roots and as they loosen place the infant at risk of aspiration. Therefore they are usually extracted.

Bacteria are not present in the infant’s gastrointestinal tract at birth. Soon after birth oral and anal orifices permit entrance of bacteria and air. Generally the highest bacterial concentration is found in the lower portion of the intestine, particularly in the large intestine. Normal colonic bacteria are established within the first week after birth; and normal intestinal flora help synthesize vitamin K, folate, and biotin. Bowel sounds can usually be heard shortly after birth.

The capacity of the newborn stomach varies widely, depending on the size of the infant, from less than 30 mL on day 1 to more than 90 mL on day 3. After birth the newborn stomach becomes increasingly more compliant and relaxed to accommodate larger volumes. Several factors such as time and volume of feedings or type and temperature of food may affect the emptying time. The cardiac sphincter and nervous control of the stomach are immature; thus some regurgitation may occur. Regurgitation during the first day or two of life can be decreased by avoiding overfeeding, and burping the infant and positioning him or her with the head slightly elevated.


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.

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Sep 16, 2016 | Posted by in NURSING | Comments Off on Physiologic and Behavioral Adaptations of the Newborn

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