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Normal Newborn: Processes of Adaptation Ch 19

Terms in this set (81)

During fetal life, the alveoli produce fetal lung fluid that expands the alveoli and is essential for normal development of the lungs
Some of the fluid empties from the lungs into the amniotic fluid
The fluid is cont produced at a rate of 4-5 ml/kg/hr
As fetus nears term, the amt of fetal lung fluid produced decreases in prep for birth, when the fluid must be cleared for the infant to breathe air.
Absorption of lung fluid begins during early labor and by the time of birth only 35% of the original amt remains

During labor, the fluid begins to move into the interstitial spaces where it is absorbed
Absorption is accelerated by secretion of fetal epinephrine and corticosterioids, but may be delayed by cesarean birth without labor
Ther emoval of the fluid helps reduce pulmonary resistance to blood flow that is present before birth and enhances the advent of air breathing

Surfactant, a slippery, detergent-like combo of lipoproteins, is detectable by 24-25 weeks of gestation
Surfactant lines the inside of the alveoli and reduces surface tension within alveoli, allowing the alveoli to remain partially open when the infant begins to breathe at birth
Without surfactant, the alveoli collapse as the infant exhales
The alveoli must be re-expanded with each breath, greatly increasing the work of breathing and possibly resulting in atelectasis.
By 34-36 weeks of gestation sufficient surfactant is usually produced to prevent respiratory distress syndrome

Surfactant secretion increases during labor and immediately after birth to enhance the transition from fetal to neonatal life

Steroids given to a woman in preterm labor help increase surfactant production and speed maturation of the lungs
The fetus with intraauterine growth restriction (IUGR) or stressed by conditions such as maternal HTN, heroin addiction, preeclampsia, or infection; placental insufficiency, or premature rupture of membranes greater than 48 hours may also have accelerated lung maturation.
Infants of mothers with diabetes have slower lung maturation
At birth, the shunts close and the pulm vessels dilate
These changes occur in response to increases in blood oxygen and shifts in pressure within the heart, pulmonary, and systemic circulations, as well as clamping of the umbilical cord
The alterations necessary for transition from fetal to neonatal circulation occur simultaneously within the first few minutes

As the newborn takes the first breaths at birth, the rise in oxygen concentration causes the ductus arteriosus to constrict, preventing entry of blood from the pulmonary artery
The pulmonary blood vessels respond to the increased oxygenation by dilating
At the same time, fetal lung fluid shifts into the interstitial spaces and is removed by blood and lymph vessels
These changes decrease pulmonary vascular resistance by 80% and allow the vessels to expand to hold the suddenly increased blood flow from the pulmonary artery

At birth, pressures between the right and left sides of the heart are reversed. The sudden dilation of the vessels of the lungs allows blood to enter freely from the right ventricle and decreases pressure in the right side of the heart.
Clamping of the umbilical cord closes the ductus venosus and further decreases pressure in the right side of the heart.
Increased blood flow from the pulmonary veins into the left atrium causes pressure in the left side of the heart to build
Systemic resistance increases as blood flow to the placenta ends with clamping of the cord, and this also elevates pressure in the left heart.
The foramen ovale's flap valve closes when the pressure in the left atrium is higher than that in the right atrium.
This change forces the blood from the right atrium into the right ventricle and pulmonary artery.
Because the ductus arteriosus is lso closing, the blood continues into the lungs for oxygenation and returns to the left atrium through the pulmonary veins
Blood from the left atrium enters the left ventricle and leaves through the aorta to circulate to the rest of the body.
Thus blood flow through the heart and lungs changes from fetal to neonatal circulation and is similar to that in the normal adult

Conditions such as asphyxia and persistent pulmonary HTN however, may reverse the pressures in the heart and cause the foramen ovale to re-open
The ductus ateriosus closes gradually as oxygenation improves and prostaglandins, which helped keep it open, are metabolized.
Until closure is complete, a small amt of blood may shunt through the ductus arteriosus from the aorta to the pulm artery, a reverse of flow during fetal life.
This sequence occurs because pressure in the aorta has become higher than that in the pulm artery
A murmur may be heard as a result of blood flow through the partially open vessel

Low levels of oxygen in the blood may cause the ductus arteriosus to dilate and the pulm vessels to constrict, increasing resistance to blood flow to the lungs
The result may be opening of the foramen ovale to allow a right-to-left shunt of blood and flow from the pulmonary artery through the ductus arteriosus and into the aorta.
A patent ductus arteriosus may occur in the infant who experiences asphyxia at birth, becomes hypoxic, or is preterm
Heat is lost in 4 ways
1. Evaporation: air drying of the skin that results in cooling. Drying the infant, esp the head, as quickly as possible helps prevent loss of heat by evaporation. Insensible water loss from the skin and respiratory tract increases heat loss from evaporation.

2. Conduction: Movement of heat away from the body occurs when newborns have direct contact with objects that are cooler than their skin. Placing infants on cold surfaces or touching them with cool objects causes this type of heat loss. The reverse is also true: Contact with warm objects increases body heat by conduction. Warming objects that will touch the infant or placing the unclothed infant against the mother's skin helps prevent conductive heat loss.

3. Convection: Transfer of heat from the infant to cooler surrounding air occurs in convection. When infants are in incubators, the circulating warm ir helps keep them warm by convection. Providing a warm, draft-free environment avoids convective heat loss. "Draft, wind, open window"

4. Radiation: Transfer of heat to cooler objects that are not in direct contact with the infant. Infants in incubators transfer heat to the walls of the incubator. If the walls of the incubator are cold, the infant is cooled, even when the temperature of the air inside the incubator is warm. To combat this problem, incubators have double walls. Placing cribs and incubators away from windows and outside walls minimizes radiant heat loss. Newborns can gain heat by radiation, too. sing a radiant warmer transfers heat from the warmer to the cooler infant.
When adults are cold, they shiver, increasing muscle activity to produce heat
Shivering is not an important method of thermogenesis for newborns who rarely shiver except during prolonged exposure to low temperatures. Instead, they become restless and cry.
Their increased activity and flexion help generate some warmth and reduce heat loss from exposed surface areas of the body
Exposure to cool temperatures also results in peripheral vasoconstriction, decreasing flow of warm blood to the skin
This helps prevent heat loss from the skin and causes the skin to feel cool to the touch
Acrocyanosis (bluish discoloration of the hands and feet) may occur.
In addition, a drop in temp increases the metabolic rate as much as 200-300%, causing above-normal oxygen and glucose use.

The primary method of heat production in infants is nonshivering thermogenesis (NST), the metabolism of brown fat to produce heat
Newborns can increase heat production by 100% by using NST
Brown fat contains and abundant supply of blood vessels, which cause the brown color.
Brown fat is located primarily around the back of the neck; in the axillae; around the heart, kidney and adrenals; between the scapulae; and along the abdominal aorta

As brown fat is metabolized, it generates more heat than white subQ fat.
Blood passing through brown fat is warmed and carries heat to the rest of the body

NST begins when thermal receptors in the skin detect a skin temp of 35-36 C (95-96 F)
Thermal receptor stimulation is transmitted to the hypothalamic thermal center
As a result, norepinephrine is released in brown fat, initiating its metabolism
NST goes into effects even before a change occurs in core (interior) body temp, as measured with a rectal thermometer
Activating thermogenesis before core temp decreases allows the body to maintain internal heat at an even level.
Therefore, NST may begin in an infant when skin temp has been cooled, even though core measurements show normal readings
A decreased core temp will not occur until NST is no longer effective.

Some infants have adequate bornw fat stores. It is accumulated mainly during the 3rd trimester, so preterm infants may be born before adequate stores of brown fat have accumulated.
IUGR may deplete brown fat stores before birth.
Hypoxia, hypoglycemia, and acidosis may interfere with the infant's ability to use bornw fat to generate heat
These infants are not able to raise their body temperature if they are subjected to cold stressand may have serious complications
Throughout gestation, glucose is supplied to the fetus by the placenta.
During the third trimester, glucose is stored as glycogen primarily in the fetal liver and skeletal muscles for use after birth.
These stores are almost completely depleted within 12 hours after birth
They are used for energy during the stress of delivery and for breathing, heat production, movement against gravity, and activation of all the functions that the neonate must assume at birth.
Until newborns begin regular feedings and their intake is adequate to meet energy requirements, the glucose present in the body is used,
As the blood glucose level falls, stored glycogen in the liver is converted to glucose for use.
Although the brain can use alternative fuels such as ketones and fatty acids if necessary, glucose is the primary source of energy,
Glucose concentration in the blood commonly falls to the lowest levels by 60 to 90 minutes after birth but rises and stabilizes in 2 to 3 hours after birth

In the term infant, lucose levels should be 40-60 mg/dL on the first day and 50-90 mg/dL thereafter
There is no general consensus about the level of blood glucose that defines hypoglycemia, but a level below 40-45 mg/dL in the term infant is often used

Many newborns are at increased risk for hypoglycemia.
In the preterm, late preterm (34-36 wks gestation), and SGA infant, adequate stores of glycogen or even fat for metabolism may not have accumulated.
Stores may be used up before birth in the postterm infant because of poor intrauterine nourishment from a deteriorating placenta.
LGA infants and those with diabetic mothers may produce excessive insulin that consumes available glucose quickly.

Infants exposed to such stressors as asphyxia or infection may exhaust their stores of glycogen.
The cold-stressed infant may deplete glycogen to increase metabolsim and raise body temperature
When unconjugated bilirubin is released into the bloodstream, it attaches to binding sites on albumin in the plasma and is carried to the liver.
If an adequate number of albumin-binding sites are not available, bilirubin circulates as unbound or free unconjugated bilirubin
Bilirubin can be displaced from albumin by some medications.
Free fatty acids, acidosis, and infection also decrease albumin binding of bilirubin
It is the freem unbound unconjugated bilirubin that can move into the tissues and cross the blood-brain barrier.

When the albumin-bound bilirubin reaches the liver, it is changed to the conjugated form of bilirubin by the enzyme uridine diphosphate glucuronyl transferase (UDPGT)
Conjugated bilirubin is excreted into the bile and then into the duodenum
In the intestines, the normal flora act to reduce bilirubin to urobilinogen and stercoblin, which are excreted in the stools
Some urobilinogen is excreted by the kidneys.

A small percentage of conjugated bilirubin may be deconjugated, or converted back to unconjugated state, by the intestinal enzyme beta-glucuronidase.
This enzyme is important in fetal life because only unconjugated bilirubin can be cleared by the placenta for the conjugation by the mother's liver.
In the newborn, deconjugated bilirubin in the intestines in reabsorbed into the portal circulation and carried back to the liver, where it again undergoes the conjugation process.
The recirculation of bilirubin is called enterohepatic circuit and it creates additional work for the liver.
Blood tests for biliruibin measure total serum bilirubin (TSB) and direct (conjugated) bilirubin the serum.
TSB is a combination of indirect (unconjugated) and direct bilirubin.