what are the 10 physiologic changes in neonate?


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Neonatal Physiology and Anesthetic Concerns

Anthony M. Fernandez, M.D.
Instructor, Department of Anesthesiology, Yale University School of Medicine.

Introduction
The neonatal period is defined as the first 28 days of life. As the neonate adapts to life after birth numerous physiologic changes occur. Thus, the anesthesiologist must understand the anesthetic implications associated with such changes. The following is a discussion of the pertinent aspects regarding physiologic conditions specifically related to the first 28 days of life.

Neurologic Physiology
It is during the last trimester of pregnancy that rapid maturation of the central nervous system occurs. Normal newborns show various primitive reflexes, which include the moro response and grasp reflex. Such milestones of development are useful indicators of mental development.

ANESTHETIC REQUIREMENTS: Full term neonates require lower concentrations of volatile anesthetics than do infants. This low requirement may be related to the immaturity of the central nervous system. The immature blood brain barrier may contribute to the increased sensitivity of the neonate to the effects of barbiturates and opioids. The neonatal response to neuromuscular blockers is affected by immaturity of the neuromuscular junction and the increased extracellular fluid associated with this sub-population. Therefore, initial dosing of non-depolarizers is similar to that of adults. The dosage of succinylcholine, however, is increased to as much as twice the adult dosage.

THERMOREGULATION: With regards to thermoregulation, shivering is virtually absent in the neonate and does not appear until 3 months of age. Therefore, nonshivering thermogenesis provided by brown fat metabolism contributes to euthermia in the neonate. Brown fat is present in the neck, between the scapulae, around the internal mammary arteries and around the kidneys and adrenals. When the neonate experiences a cold environment, norepinephrine release is increased which in turn stimulates brown fat metabolism by the breakdown of triglycerides. This action increases cardiac output through the brown fat tissue, thus warming the blood.

Cardiovascular Physiology
TRANSITION TO EXTRAUTERINE LIFE: Circulatory changes occur immediately at birth when the fetus is separated from the placenta and the lungs begin to function. This causes an acute increase in systemic vascular resistance and also a reduction in the return of inferior vena cava blood to the heart. Concurrent with these changes is a rapid decrease in pulmonary vascular resistance and an increase in pulmonary blood flow. The foramen ovale, ductus arteriosus, ductus venosus and umbilical vessels are no longer needed. The foramen ovale normally closes functionally at birth when left atrial pressure increases and right atrial pressure decreases. Permanent closure occurs in several months; however, in 15-20% of adults a patent foramen ovale may exist. The ductus arteriosus becomes functionally closed within the first 10-15 hours after birth. This process depends primarily on systemic arterial PO2 and is reversible with PGE1 and hypoxemia. Anatomic closure of the ductus arteriosus occurs within 4-6 weeks. The ductus venosus closes soon after birth and becomes the ligamentum venosum; it does not seem to be sensitive to varying levels of PO2, PCO2, or pH and its regulation postnatally is not well understood. The umbilical veins become the ligamentum teres. The umbilical artery becomes the medial umbilical ligaments and the superior vesical arteries, which supply the urinary bladder.

NEONATAL CARDIAC FUNCTION: During the first 10 minutes after birth, the average range of heart rate is 120-200 beats per minute (bpm); thereafter, the average is 120-130 bpm. Tachycardia may be found with volume depletion, cardiorespiratory disease, drug withdrawal and hyperthyroidism. Bradycardia is often associated with apnea and is often seen with hypoxia. The neonate is highly dependent on heart rate for maintenance of cardiac output and blood pressure. The vasoconstrictive response of the neonate to hemorrhage or volume depletion is less that that of an adult; hypotension that accompanies administration of a volatile anesthetic is most likely due to decreased intravascular fluid volume or anesthetic overdose, or both.

Respiratory Physiology
FIRST BREATH OF LIFE: The first breath is a gasp that generates a transpulmonary pressure of up to 80 cm of water and is the result of diaphragmatic descent. This overcomes the surface forces that develop as the air/fluid interface reaches the small airways, and overcomes tissue resistance. The chest wall of a neonate is floppy because of its high cartilage content and poorly developed musculature, rendering the ineffectiveness of accessory muscles to breathing.

FUNCTIONAL RESIDUAL CAPACITY (FRC): The FRC is smaller than that of the adult as a result of less compliant lungs and the more compliant chest wall. This reduced FRC leads to more rapid inductions with inhaled anesthetics as well as more rapid desaturation.

TYPE I MUSCLE FIBERS: The neonate is more prone to respiratory muscle fatigue due to the low content of type I muscle fibers. Type I fibers confer fatigue resistance. Airway compliance in neonates is twice that of adults and contributes to their potential for collapse with exhalation and inhalation.

SHUNTING: Venous admixture is elevated in neonates, estimated as high as 20 percent compared to just 5 percent in adults. This is the result of intrapulmonary anatomic shunting. The neonatal response to hypercapnia is not potentiated by hypoxia. On the contrary, hypoxia may depress the hypercapnic ventilatory response. Neonates and infants are obligate nose breathers, but up to 40 percent of term neonates can convert to oral breathing in the face of nasal obstruction. Dead space ventilation is similar to that of adults, however oxygen consumption is two to three times more, which can explain the increased minute ventilation.

AIRWAY: Of note is the anatomic considerations of the infant airway that include: narrow nares, small pharynx, large tongue, mobile, short stubby epiglottis, high (C3) anterior tapered larynx and angled vocal cords.

Gastrointestinal Physiology
At birth, the pH of the stomach contents is mildly acidic reflecting the pH of amniotic fluid. Normal neonates exhibit uncoordinated swallowing and regurgitation. Immaturity of the phayrngoesophageal sphincter and absence of lower esophageal peristaltic waves also contribute to the reflux of gastric contents. Upwards of 6 weeks are needed to reach adult levels of lower esophageal pressures. Persistent gastroesophageal reflux beyond 6 weeks is pathologic and is often accompanied by reactive airway disease.

Renal Physiology
At birth, glomerular filtration rate (GFR) is up to 30% of normal adult values but reaches 50% of normal adult values by the tenth day of life and full adult values by the first year of life. The low GFR affects the neonatal ability to excrete saline, water loads and drugs. Thus, adequate exogenous sodium and water must be supplied during the preoperative period. It must be appreciated, however, that because the neonate is likely to excrete a volume load slower than an adult, the possibility of fluid overload is increased.

Endocrine and Metabolic Issues
Neonates undergo a metabolic adjustment after birth with regard to glucose. It must be appreciated that they may not show symptoms in the face of hypoglycemia. Hyperglycemia occurs in the stressed neonate, for example during surgery. Therefore, infusion of glucose containing solutions must be judiciously monitored. Hyperbilirubinemia is an important consideration in the neonate. Bilirubin levels in the term neonate peak on the third day of life then gradually decline within four weeks. In the face of hyperbilirubinemia and prematurity, physiologic jaundice must be ruled out.

PHYSIOLOGIC JAUNDICE: Physiologic jaundice is found in 60% of term infants. In healthy full term neonates, physiologic jaundice causes no damage; however, in premature infants and newborns with severe systemic disease, the risk of developing bilirubin encephalopathy is increased.

Hematologic Concerns
Immediately at birth the neonatal blood volume is between 80-95 cc/kg, depending on time of cord clamping. Within four hours, there is volume contraction of as much as 25 percent. Normal hemoglobin range is between 14 gm/100 ml and 20 gm/100 ml. Heel sticks performed for lab studies may confer falsely elevated values of hemoglobin; therefore venipuncture is ideal. White blood count may be elevated to as much as 21,000 in the first 24 hours of life and by the first week decreased to 12,000. During the first week of life and for four years after, the lymphocyte is the predominant cell. Neonates are more susceptible to bacterial infection due to the immature leukocyte function.

NEONATAL POLYCYTHEMIA: 3-5% of full-term neonates are diagnosed with neonatal polycythemia with a hematocrit > 65%. This is associated with increased systemic and pulmonary vascular resistance as well as decreased cardiac output. Treatment usually entails exchange transfusion to prevent hyperviscosity syndrome.

HEMORRHAGIC DISEASE OF THE NEWBORN: Vitamin K factors are below adult levels in the neonate due to the immature liver where syntheses of such factors occur. All newborns should receive prophylactic vitamin K to prevent hemorrhagic disease of the newborn (HDN). HDN is a self-limited bleeding disorder resulting from a deficiency of the coagulation factors dependent on vitamin K. In most instances, hemorrhagic manifestations become evident on the second or third day of life. Melena, bleeding from the navel and hematuria are frequent signs. Intracranial hemorrhage is also possible and can result in death or severe central nervous system dysfunction.

References
Anesthesia and Co-Existing Disease. 3rd ed. Stoelting, RK., Dierdorf, SF. New York: Churchill Livingstone, 1993. pp.579-627.

Pediatric Anesthesia. 3rd ed. Gregory, G. New York: Churchill Livingstone, 1994. pp. 93-10.

Pediatric Cardiac Anesthesia. 2nd ed. Lake, C. Connecticut: Appleton and Lange, 1993. pp. 28-30.

A Practice of Anesthesia for Infants and Children. 2nd ed. Cote, C.; Ryan,J.; Todres, D.; Goudsouzian, N. Philadelphia, PA: WB Saunders Co. 1993. pp. 7-37.

Rudolph Pediatrics. 19th ed. Rudolph, AM. Connecticut: Appleton and Lange, 1991. pp.182-191.

Source(s):
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