Adaptation to extrauterine life

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At the end of pregnancy, the fetus must take the journey of childbirth to leave the reproductive mother. Upon its entry to the air-breathing world, the newborn must begin to adjust to life outside the uterus. This is true for all viviparous animals; this article discusses humans as the most-researched example.[ citation needed ]

Contents

The outside environment is a drastic change for the neonate, therefore the neonate must be assessed frequently and thoroughly. The Apgar scale is an assessment performed immediately following birth. It consists of the assessment of heart rate, respiratory effort, muscle tone, reflex irritability, and generalized skin color. Apgar scoring is performed one minute and five minutes after birth. Scoring ranges from 0 to 10, with 0 indicating severe neonatal distress and 10 indicating a smooth transition to extrauterine life. [1]

Newborns transitioning into extrauterine life will undergo periods of reactivity. These periods are divided into three stages. The first stage occurs in the first 30 minutes of life; during this stage the infant is alert and responsive with heart rate peaking at 160-180 beats per minute and then stabilizes to a baseline rate of 100-120 beats per minute. Crackles upon auscultation and irregular respirations are a normal finding. In the second stage, there is a decrease in responsiveness and motor activity which is often manifested as sleep. This period can last from 1–2 hours. The third stage marks the second period of reactivity. This period can occur anywhere in the first 2 to 8 hours after birth and lasts anywhere from 10 minutes to several hours. Tachycardia and tachypnea may be present during brief periods. Passing of meconium also occurs. [1]

Cardiac

Physiology: In utero, the placenta delivers oxygenated blood to the fetus through the umbilical vein. Upon delivery, the umbilical cord is cut. The cardiovascular system must now adapt. Blood CO2 rises because it is now not removed by the placenta. This is a powerful stimulus for the infant to start breathing. Breathing sharply increases O2 in the lungs, thus quickly reverting hypoxic pulmonary vasoconstriction that had held the pulmonary vascular resistance high during the uterine life. Lung ventilation also extends the so far convoluted, shrunk pulmonary vessels, also contributing to the quick and marked drop in the pulmonary vascular resistance. As a result, much higher proportion of the right ventricle output flows into the pulmonary vessels than into the systemic circulation through the ductus arteriosus. The detachment of the placenta causes an increase in systemic vascular resistance, which leads to an increase in pressure gradient from the left atrium. [2] The left atrium now has higher pressure than the right atrium causing the foramen ovale to close. Within the first 10 minutes of birth, blood begins to flow left-to-right through the ductus arteriosus. This causes a significant increase in output of the left ventricle and increase in stroke volume. Subsequently, calcium channel activity increases and potassium channel decreases furthering ductal constriction. Functional closure of the ductus arteriosus occurs within the first 24 hours, with permanent closure following within 4 weeks. Lastly cardiac output increases to nearly double what it was in utero. All of these cardiovascular system changes result in the adaptation from fetal circulation patterns to an adult circulation pattern. During this transition, some types of congenital heart disease that were not symptomatic in utero during fetal circulation will present with cyanosis or respiratory signs.

Changing the composition of hemoglobin before and after birth. Also identifies the types of cells and organs in which the gene expression (data on Wood W.G., (1976). Br. Med. Bull. 32, 282.) Postnatal genetics en.svg
Changing the composition of hemoglobin before and after birth. Also identifies the types of cells and organs in which the gene expression (data on Wood W.G., (1976). Br. Med. Bull. 32, 282.)

Manifestations: When the newborn cries, there is a reversal of blood flow through the foramen ovale which causes the newborn to appear mildly cyanotic in the first few days of life. The heart rate of the newborn should be between 110 and 160 beats per minute and it is common for the heart rate to be irregular in the first few hours following birth. The heart sounds will have a variation in pitch, duration, and intensity than that of an adult. Blood pressure readings should range from 60 to 80 mm Hg systolic and 40–50 mm Hg diastolic. Mean arterial pressure should be the same as the weeks of gestation at birth. Within the first hour after birth, there may be a drop of up to 15 mm Hg in the systolic blood pressure. [1]

Delayed cord clamping is defined as waiting more than 2 minutes to clamp the newborn's umbilical cord. This has been proven to be beneficial in improving hematocrit and iron while also decreasing anemia. These benefits can last up to 6 months for the newborn. [3]

Assessments/Interventions: Assessment and monitoring of vital signs and skin color are important in detecting cardiovascular issues in the infant. The apical pulse rate should be auscultated for one full minute when the newborn is calm or sleeping. Any irregular heart rate after the first few hours of life that is not related to crying or another outside factor should be monitored and evaluated. [1] Blood pressure will be taken with an appropriately sized cuff, preferably when the newborn is at rest. Consistent tachycardia should be evaluated for conditions such as anemia, hyperthermia, hypovolemia, and sepsis. Consistent bradycardia could be an indication of congenital heart block or hypoxemia. Pallor and central cyanosis (cyanosis in hands and feet is a common and normal finding) can also indicate cardiovascular issues. [1]

Ventilation and Oxygenation

Physiology: Upon birth, the newborn's lungs become the center for gas exchange. There are a variety of factors that influence newborn respiratory functions; these factors include chemical, mechanical, thermal, and sensory. Respirations begin when fetal aortic and carotid chemoreceptors are stimulated by the varying concentrations of oxygen and carbon dioxide. During vaginal birth, the newborn's chest is compressed by the birth canal. Upon delivery, negative pressure allows air into the lungs. The first cries of the infant allow for alveoli expansion and absorption of fetal lung fluid. Temperature changes and other sensory stimulation contributes to respiratory function as well.

Manifestations: Breathing patterns are often irregular and shallow. The infants respiration rate should be between 30 and 60 breaths per minute with preference for nasal breathing. Ribs expands horizontally. Breath sounds should be clear and equal in both lungs. Abdominal breathing is normal. Acrocyanosis is a normal finding. [1]

Assessments/Interventions: Suctioning of nasal and oral secretions promotes fluid clearance. Auscultation of lung sounds to assess for any abnormalities. Pulse oximetry is performed to determine oxygen saturation. Monitor signs of respiratory distress such as: nasal flaring, grunting, central cyanosis. [1]

Metabolic

Physiology: At birth, the newborn is cut off from the mother's glucose supply and will begin to rely on stored fat for energy. Glycogen stores are maximal at term. Within the first hour of life, blood glucose will typically reach its lowest point and then stabilize within 2 to 4 hours, hence breastfeeding is promoted immediately. In cases where feeding is delayed, the neonate can use lactate, free-fatty acids, and ketone bodies.

Manifestations: Normal blood glucose levels range from 40 to 50 mg/dl. [1] Rooting and sucking reflex should be present and the neonate will eat small amounts frequently. All vital signs should be within normal limits coinciding with the neonates presentation of calmness and satiation.

Assessments/Interventions: Monitor blood glucose level and encourage breastfeeding or formula feeding as early as possible. Lactation and breastfeeding education should be provided as appropriate.

Temperature regulation

Physiology: Newborns lack the ability of thermogenesis due to underdeveloped shivering mechanism. Body heat is lost through conduction, convection, and radiant heat. [1] Thermoregulation is achieved through several methods: the metabolism of brown fat and Kangaroo care, also known as skin to skin. "Brown fat" is specialized adipose tissue with a high concentration of mitochondria designed to rapidly oxidize fatty acids in order to generate metabolic heat.[ citation needed ] Skin to skin to care is the immediate placement of the neonate directly onto a caregiver's bare chest. This promotes thermoregulation of the neonate through heat generated from caregiver.

Manifestations: Normal temperature ranges from 97.7 to 100.0 °F (36.5 to 37.8 °C). Cold infants may cry or appear restless. The neonates' arms and legs maintain a fetal position, lessening their body surface area and reducing heat loss. [1]

Assessments/Interventions: Dry neonate immediately after birth and initiate skin-to-skin contact. Provide warm blankets and a hat. Utilize a radiant warmer if skin-to-skin is not appropriate. Frequently monitor axillary body temperature. Limit neonate's exposure during diaper changes and assessments.

See also

Related Research Articles

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Cyanosis is the change of body tissue color to a bluish-purple hue, as a result of decrease in the amount of oxygen bound to the hemoglobin in the red blood cells of the capillary bed. Cyanosis is apparent usually in the body tissues covered with thin skin, including the mucous membranes, lips, nail beds, and ear lobes. Some medications may cause discoloration such as medications containing amiodarone or silver. Furthermore, mongolian spots, large birthmarks, and the consumption of food products with blue or purple dyes can also result in the bluish skin tissue discoloration and may be mistaken for cyanosis. Appropriate physical examination and history taking is a crucial part to diagnose cyanosis. Management of cyanosis involves treating the main cause, as cyanosis isn’t a disease, it is a symptom.

<span class="mw-page-title-main">Patent ductus arteriosus</span> Condition wherein the ductus arteriosus fails to close after birth

Patent ductus arteriosus (PDA) is a medical condition in which the ductus arteriosus fails to close after birth: this allows a portion of oxygenated blood from the left heart to flow back to the lungs through the aorta, which has a higher blood pressure, to the pulmonary artery, which has a lower blood pressure. Symptoms are uncommon at birth and shortly thereafter, but later in the first year of life there is often the onset of an increased work of breathing and failure to gain weight at a normal rate. With time, an uncorrected PDA usually leads to pulmonary hypertension followed by right-sided heart failure.

Fetal distress, also known as non-reassuring fetal status, is a condition during pregnancy or labor in which the fetus shows signs of inadequate oxygenation. Due to its imprecision, the term "fetal distress" has fallen out of use in American obstetrics. The term "non-reassuring fetal status" has largely replaced it. It is characterized by changes in fetal movement, growth, heart rate, and presence of meconium stained fluid.

<span class="mw-page-title-main">Umbilical vein</span> Vein running from the placenta to the fetus

The umbilical vein is a vein present during fetal development that carries oxygenated blood from the placenta into the growing fetus. The umbilical vein provides convenient access to the central circulation of a neonate for restoration of blood volume and for administration of glucose and drugs.

dextro-Transposition of the great arteries Medical condition

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<span class="mw-page-title-main">Ductus arteriosus</span> Blood vessel connecting the pulmonary artery to the proximal descending aorta

The ductus arteriosus, also called the ductus Botalli, named after the Italian physiologist Leonardo Botallo, is a blood vessel in the developing fetus connecting the trunk of the pulmonary artery to the proximal descending aorta. It allows most of the blood from the right ventricle to bypass the fetus's fluid-filled non-functioning lungs. Upon closure at birth, it becomes the ligamentum arteriosum.

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Blue baby syndrome can refer to conditions that cause cyanosis, or blueness of the skin, in babies as a result of low oxygen levels in the blood. This term has traditionally been applied to cyanosis as a result of:.

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Hypoplastic left heart syndrome (HLHS) is a rare congenital heart defect in which the left side of the heart is severely underdeveloped and incapable of supporting the systemic circulation. It is estimated to account for 2-3% of all congenital heart disease. Early signs and symptoms include poor feeding, cyanosis, and diminished pulse in the extremities. The etiology is believed to be multifactorial resulting from a combination of genetic mutations and defects resulting in altered blood flow in the heart. Several structures can be affected including the left ventricle, aorta, aortic valve, or mitral valve all resulting in decreased systemic blood flow.

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Tricuspid atresia is a form of congenital heart disease whereby there is a complete absence of the tricuspid valve. Therefore, there is an absence of right atrioventricular connection. This leads to a hypoplastic (undersized) or absent right ventricle. This defect is contracted during prenatal development, when the heart does not finish developing. It causes the systemic circulation to be filled with relatively deoxygenated blood. The causes of tricuspid atresia are unknown.

<span class="mw-page-title-main">Fetal circulation</span> Circulatory system of fetuses

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<span class="mw-page-title-main">Intrauterine hypoxia</span> Medical condition when the fetus is deprived of sufficient oxygen

Intrauterine hypoxia occurs when the fetus is deprived of an adequate supply of oxygen. It may be due to a variety of reasons such as prolapse or occlusion of the umbilical cord, placental infarction, maternal diabetes and maternal smoking. Intrauterine growth restriction may cause or be the result of hypoxia. Intrauterine hypoxia can cause cellular damage that occurs within the central nervous system. This results in an increased mortality rate, including an increased risk of sudden infant death syndrome (SIDS). Oxygen deprivation in the fetus and neonate have been implicated as either a primary or as a contributing risk factor in numerous neurological and neuropsychiatric disorders such as epilepsy, attention deficit hyperactivity disorder, eating disorders and cerebral palsy.

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A fetus or foetus is the unborn offspring that develops from an animal embryo. Following embryonic development, the fetal stage of development takes place. In human prenatal development, fetal development begins from the ninth week after fertilization and continues until birth. Prenatal development is a continuum, with no clear defining feature distinguishing an embryo from a fetus. However, a fetus is characterized by the presence of all the major body organs, though they will not yet be fully developed and functional and some not yet situated in their final anatomical location.

<span class="mw-page-title-main">Pulmonary artery stenosis</span> Medical condition

Pulmonary artery stenosis (PAS) is a narrowing of the pulmonary artery. The pulmonary artery is a blood vessel moving blood from the right side of the heart to the lungs. This narrowing can be due to many causes, including infection during pregnancy, a congenital heart defect, a problem with blood clotting in childhood or early adulthood, or a genetic change.

<span class="mw-page-title-main">Neonatal resuscitation</span>

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References

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  3. Anderson, O (15 November 2011). "Effect of delayed versus early umbilical cord clamping on neonatal outcomes and iron status at 4 months: a randomised controlled trial". The BMJ. 343: d7157. doi:10.1136/bmj.d7157. PMC   3217058 . PMID   22089242.