Chapter 17 Review Notes PDF

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CHAPTER 17 REVIEW NEWBORN TRANSITIONING Newborn beginning the work of physiologically and behaviorally adapting to the new environment, 1 st 24 hours can be most precarious NEONATAL PERIOD : 1st 28 days of life, most dramatic and rapid physiologic changes in humans, after birth newborn = exposed to whole new world of sounds, colors, smells and sensations PHYSIOLOGIC TRANSITIONING Adaptation from intrauterine to extrauterine environment = complex and difficult, immediately after birth, respiratory gas exchange, along with circulatory modifications must occur to sustain extrauterine life ▪ During this time as newborns strive to attain homeostasis, they also experience complex changes in major organ systems ▪ Most dramatic & extreme extrauterine transitions occur in 4 interdependent areas: Respiratory, Circulatory, Thermoregulation, and their ability to stabilize their blood glucose levels (all 4 need successful transitions for the newborn to adapt to extrauterine life) usually takes place 1st 6-10hrs, but some adapt can take weeks CARDIOVASCULAR ADAPTATIONS When in utero the heart relies on certain unique structures to assist in providing adequate perfusion of vital body parts, Umbilical vein – carried oxygenated blood from placenta to fetus, Ductus Venosus – allowed maj of umbilical vein blood to bypass liver & merge with blood moving through vena cava, bringing it to heart sooner. Foramen Ovale – allows more than ½ blood entering R atrium to cross immed to the left atrium, bypassing pulmonary circulation, Ductus Arteriosis – connects pulmonary artery to aorta, allows bypassing of pulmonary circuit - only a small portion of blood passes through pulmonary circuit for main purpose of perfusion of the structure, rather than for oxygenation. FETUS DEPENDS ON PLACENTA - At birth the circulatory system must switch from fetal newborn circulation & from placental pulmonary gas exchange SUCCESSFUL TRANSITION NEEDS : increased pulmonary blood flow, removal of placenta, closure of intracardiac (foramen ovale and shunts (venosus, arteriosis) ; these changes are needed to = the R ventricular output with that of the left The physical forces of the contractions of labor & birth, mild asphyxia, increased intracranial pressure as a result of cord compression & uterine contractions, & the cold stress experiences immediately after birth lead to an increased release of catecholamines that = critical for changes in transition into extrauterine life

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Increase epinephrine and norepinephrine stimulate increased CO, contractility, surfactant release and promotion of pulmonary fluid clearance FETAL TO NEONATAL CIRCULATION CHANGES Changes in circulation immediately after birth as the fetus separates from the placenta, when the umbilical cord = clamped, 1st breath is taken & lungs begin to function. (as a result, systemic vascular resistance increases and blood return to the heart by the inferior vena cava decreases, concurrently with these changes, there = rapid decrease in pulmonary vasc resistance and an increase in pulmonary blood flow Foramen Ovale – functionally closes with a decrease in pulmonary vasc resistance decrease in R side heart pressures (before birth foramen ovale allowed most of oxygenated blood entering the R atrium from inferior vena cava to pass L atrium of heart - with the newborn’s 1st breath, air pushes into lungs (triggers increase in pulmonary blood flow & pulmonary venous return to the L side of heart (pressure L atrium becomes higher than R atrium, increased L atrial pressure causes foramen ovale to close (allowing output from the R ventricle to flow entirely into lungs) “closure of that shunt oxygenated = now separated from non-oxygenated (permanent closure = several weeks) Increase in systemic pressure, after clamping cord increased L sided heart pressures Ductus arteriosis, Venosus, umbilibal vessels that were vital in fetal life are no longer needed, over months these fetal vessels form nonfunctional ligaments Ductus arteriosis – b/w aorta & pulmonary artery, protected lungs against circulatory overload by shunting blood R L into descending aorta (bypassing pulmonary circulation) its patency during fetal life promoted by continual production of prostaglandin (E2), becomes closed within the first few hours of birth, oxygen = most important in its closure, (depends on high oxygen content of aortic blood that results from aeration of lungs at birth) @ birth pulm vasc resistance decreases allowing pulm blood flow to increase and oxygen exchange to occur in the lungs (2ndry to increase in PO2 coincident with 1 st breath & umbilibal cord clamping) Ductus Venosus – shunted blood from L umbilibcal to inferior vena cava, closes within a few days, as a result of activation of the liver (activated liver takes over placenta function) , becomes a ligament The 2 umbilical arteries and one vein begin to constrict @ birth , also turn into ligaments, successful closure of 3 shunts creates neonatal circulation where deoxygenated blood returns to heart through inferior and superior vena cava, deox enters R atrium then R vent and travels through pulm artery to pulm vasc bed, oxygenated returns through pulm veins into L atrium, L ventricle and through aorta to the system HEART RATE Minutes after birth HR = 110-160bpm, shortly after begins to decrease to an avg of 120-130, newbie = highly dependent on HR for maintaining CO & BP, BP = usually highest after birth & reaches plateau 2

within a week after birth, cardiac defects may be identified in nursery by a thorough physical assessment * Transient cardiac murmurs may be heard during neonatal period as a result of the changing of cardiovasc system @ birth * Fluctuations in HR & BP tend to follow changes in newborns behavioral state, Increased activity = increased HR & BP (wakeful, movement, cry), Compromised newborn demonstrates less physiologic variability overall, Tachycardia may be found with: Vol depletion, cardioresp disease, drug withdraw, hyperthyrpid, Bradycardia : apnea, hypoxia BLOOD VOLUME Depends on amount of blood transferred from placenta @ birth, usually = 80-85mL/kg of body wt in term baby. Vol may vary 25-40% depending when clamping occurs, (early before 30-40sec) or (late after 3 min) changes circulatory dynamics during transition ▪ Studies indicate benefits from DELAYED CORD CLAMPING – improving newborns cardiopulmonary adapt, prevent iron deficient anemia in full term w/o increases hypervolemia, improve oxygen trans, increase RBC flow ▪ Delayed clamping shows many benefits : 30% increase in blood vol (term), 50% increase (preterm) , improve systolic BP, increase cerebral oxygen index, high hemoglobin levels @ 2448hrs of age ▪ Cord blood is aka “natures 1st stem cell transplant” b/c possesses regenerative properties and can grow into different types of cells in body ▪ Infants who cords are clamped early are: twice as likely to be iron deficient @ 3-6MO BLOOD COMPONENTS Fetus has more RBC than an adult, have a greater affinity for oxygen @ lower oxygen pressure than adult RBC, larger in size (each cell can carry more oxygen), after born RBC count gradually increases and size decreases (b/c cells now live in an environment with much higher PO2) Newborns RBC life 8100days compared to 120 in adults - Hemoglobin initially declines as a result of a decrease in neonatal RBC mass (physiologic anemia of infancy), Leukocytosis (elevated WBC) present as result of birth trauma soon after born, platelet count & aggregation same as adult Normal Ranges : Hemoglobin – 16-18, Hematocrit- 46-68%, Platelets- 150-350,000, RBC- 4.5-7.0, WBC10-30,000 RESPIRATORY SYSTEM ADAPTATIONS Aeration of lungs, est of pulmonary gas exchange, changing the fetal circulation into adult type) ▪ LUNG AERATION : leads to est of functional residual capacity, allowing pulm gas exchange to start ▪ 1st breath (gasp) generates increase in transpulm pressure results � diaphragmatic descent ▪ Hypercapnia, hypoxia & acidosis (resulting from normal labor) = stimulus for initiating respirations 3

▪ Inspiration of air & expansion of lungs allow for increase in Tidal Vol SURFACTANT – surface tension lipoprotein, newborns lungs that prevent alveolar collapse @ end of expiration & loss of lung vol, lines alveoli to enhance aeration of gas-free lungs (reducing surface tension & lowering pressure req to open alveoli) NORMAL LUNG FUNCTION DEPENDS ON SURFACTANT !!! (permits decrease in surface tension @ end of expiration to prevent atelectasis) and increase surface tension when inhaling to help elastic recoil on inspiration) ONE OF MOST CRUCIAL ADAPT OF BABY = ADJUSTING FROM FLUID FILLED ENV TO A GASEOUS EXTRAUTERINE ENV, in fetal life lungs are filled with amniotic fluid, during & after birth the fluid needs to be removed & replaced with air (passing birth canal allows compression which expels some fluid, pulmonary capillaries & lymphatics remove remaining fluid * if the fluid = removed to slow/incomplete (decreased thoracic squeezing @ birth or diminished resp efort transient TACHYPNEA (resp rate above 60bpm) occurs. Ex: (c-sect, sedation in newborns) research shows the need of thoracic compression (c-sect does not get the squeezing vaginal birth does) LUNGS Before newborn’s lungs can maintain resp function, following events must occur : - Initiation of respiratory movement, Expansion of lungs, Est functional residual capacity (ability to retain some air in lungs on expiration), Increased pulmonary blood flow, Redistribution of CO ▪ Initial breathing = probably the result of a reflex by pressure changes, noise, light, temp changes, touching, compression of fetal chest during birthing process, high carbon dioxide & low oxygen concentrations of the newborn’s blood, Central chemoreceptors stimulated by hypoxia & hypercapnia further increase respiratory drive RESPIRATIONS After respirations are est in the newborn, (shallow, irregular, ranging from 30-60bpm) with short periods of apnea (less than 15 sec) RESP RATE varies accord to activity Resp Distress : cyanosis, tachypnea, expiratory grunting, sternal retraction, nasal flaring RESP SHOULD NOT BE LABORED, CHEST MOVEMENTS SHOULD BE SYMMETRIC, Periodic Breathing: can occur, which = cessation of breathing that lasts 5-10seconds w/o changes in color or HR (can happen 1st few days of life) BODY TEMP REGULATION One of the most important elements in a newborn’s survival = obtaining stable body temp to promote optimal transition to extrauterine life (AVG temp 97.9-99.7) NEWBORNS LOSE HEAT EASILY AFTER BIRTH (skin to skin = rec initially to maintain body temp & should be 1 st line measure for hypothermia) ▪ THERMOREGULATION : maintaining balance b/w heat loss & heat production in order to maintain body’s core temp, newborns tolerate a narrower range of environmental temperatures and are extremely vulnerable to under heating & overheating

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HEAT LOSS : have several characteristics predisposing to heat loss : Think skin with blood vessels close to the surface, lack of shivering ability to produce heat until 3 MO old, limited stores of metabolic substrates (glucose, glycogen, fat), limited use of voluntary muscle activity or movement to produce heat, large body surface area relative body wt, lack of subq fat, little ability to conserve heat by changing posture, no ability to adjust their own clothing or blankets to achieve warmth, inability to communicate that they are too cold or too warm - every newborn struggles to maintain body temp from moment of birth, when the wet body = exposed to much cooler environment, amniotic fluid covering newborn cools as it evaporates temp may decrease 3-5 degrees, TRANSFER OF HEAT DEPENDS ON temp of env, air speed, water vapor, pressure or humidity there are 4 mechanisms 1. CONDUCTION : involves transfer of heat from one object to another when the 2 objects are in DIRECT contact with each other, refers to heat fluctuation b/w newborns body surface when in contact with other SOLID surfaces, (cold mattress, scale, circumcision restraining board, conduction heat loss can also happen when touching a newborn with cold hands, or when baby has contact with colder object such as metal scale, using a warm clothed blanket or diaper to cover any cold surface helps prevent heat loss, as well as skin-skin contact 2. CONVECTION : flow of heat from body surface to cooler surrounding air or to air circulating over a body surface, ex: cool breeze that flows over newborn, (keep newborn out of direct cool drafts: open doors, windows, fans, air conditioners) use clothing or blankets , transport in a warmed isolette, rather than carrying him or her 3. EVAPORATION : loss of heat when liquid = converted to vapor, may be insensible (from skin and respiration) or sensible (from sweating), insensible loss occurs, but the indiv Is not aware, sensible is objective and can be noticed. It depends on air speed and absolute humidity of air, EX: when born baby = covered In amniotic fluid, fluid evaporates in air � heat loss, heat loss by evap also occurs when bathing baby; drying newborns after birth with warmed blankets & placing a cap will prevent heat loss by evap, promptly changing wet linens, cloths, diapers can also reduce this & prevent chilling 4. RADIATION : involves loss of body heat to cooler, solid surfaces that are in proximity but not in direct contact with baby, amount of heat loss depends on size of cold surface area, surface temp of body, and temp of reveiving surface area, EX: baby = placed in single-wall isolette next to a cold window, heat loss from radiation occurs (baby will be cold even tho in warmed isolette) ; Keep cribs & isolettes away from outside walls, cold windows, air conditioners, use radiant warmers for transporting newborns when performing procedures that may expose newborn to cooler env OVERHEATING Newborn = also prone to overheating, Limited insulation & limited sweating ability can predispose any newborn to overheating, Control of body temp happens by Negative feedback system creates balance b/w heat prod, gain & heat loss. Primary heat regulator = @ hypothalamus & CNS. (immaturity of CNS makes it hard to create & maintain this balance) why they can overheat easily 5

“isolette that’s too warm or left close to sunny window can hyperthermia”Although heat production can increase in response to cool env, basal metabolic rate & resultant heat produced cannot be reduced, OVERHEATING : increases fluid loss, resp rate, metabolic rate THERMOREGULATION Newborns have decreased ability to reg body temp, producing heat through non-shivering thermogenesis, thermoreg = balance b/w heat loss & heat prod related to newborns rate of metab and oxygen consumption. Newborn attempts to conserve heat by: inc metab rate, muscular activity (moving), increasing peripheral vasoconstriction, assuming fetal position ▪ NEUTRAL THERMAL ENV : body temp = maintained w/o increase in metabolic rate or oxygen use, rates of oxygen consumption & metab are minimal, internal body temp = maintained b/c of thermal balance (promotes growth & stability) conserves energy for bodily func, minimizes heat energy & water loss b/c babies have a hard time maintaining heat through shivering they need higher environmental temp to maintain a neutral thermal environment. (if environ temp decreases baby responds by consuming more oxygen, resp rate increases, metabolic rate increases as a response) ▪ Primary method of heat production = nonshivering thermogenesis : Brown fat (adipose) oxidized in resp to cold exposure, brown fat = special fat found ONLY IN NEWBORNS, able to convert chem energy directly into heat when activated by sympathetic NS, produced during 3 rd trimester, disappears 3-5weeks after birth, (vital for thermogenesis), - BROWN COLOR FROM: Fat’s rich supply of blood vessels & nerve endings, FOUND: b/w scapulae, axillae, nape of neck, mediastinum, areas surrounding kidneys & adrenal glands (makes up 6% of term body wt) - WHEN BABY = COLD, NOREPINEPHRINE RELEASED STIM BROWN FAT METAB by breaking down triglycerides, CO INCREASES, INCREASING BLOOD FLOW TO BROWN TISSUE ▪ COLD STRESS : excessive heat loss req newborn to use compensatory mechanisms (nonshiver, tachypnea) to maintain core body temp, consequences of cold stress can be severe, as temp decreases baby = less active, lethargic, weak, hypotonic, HIGHEST RISK WITHIN 1ST 12HRS, preterm = biggest risk (fewer fat stores, poor vasomotor resp, less insulation) - CAN LEAD TO : DEPLETED BROWN FAT, INC OXYGEN NEEDS, RESP DISTRESS, INC GLUCOSE HYPOGLYCEMIA, METAB ACIDOSIS, JAUNDICE, HYPOXIA, DECREASED SURFACTANT MINIMIZE EFFECTS OF COLD STRESS & MAINTAIN NTE, BY THE FOLLOWING INTERVENTIONS : - Prewarming blankets & hats to reduce heat loss by conduction - Keep infant transporter (warmed isolette) fully charged & heated at all times - Drying newborn completely after birth to prevent heat loss by evaporation - Encouraging skin to skin contact - Promote early breast feeding to provide fueling for nonshivering thermogenesis - Use heated & humidified oxygen - Use radiant warmers and double wall isolettes to prevent heat loss by radiation - Defer bath until newborn = medically stable, use radiant heat source while bathing

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- avoid placing skin temp probe over a bony area or one with brown fat, b/c it does not give an accurate assessment of whole body temp (most temp probes are placed over liver when baby = supine or side lying) ( all of those interventions help minimize the metabolic rate & oxygen consumption to conserve vital energy) HEPATIC SYSTEM FUNCTION Liver = essential in : synthesis, degradation, regulation of pathways involved in metabolism of carbs, proteins, lipids, trace elements & vitamins. At birth newborn liver slowly assumes function that placenta took care of prior, most enzymatic pathways are present but inactive @ birth (generally full active @ 3MO) ▪ Functions include : blood coag, iron storage, carb metab, conjugation of bilirubin ▪ Glycogen reserves prov energy & can become depleted if metab needs of newborn increase like with (cold or resp distress) IRON STORAGE As RBC destroyed after birth, iron = released & stored by LIVER until new RBC need to be made, newborn iron stores are determined by total body hemoglobin content & length of gestation (if moms iron intake was enough, sufficient iron has been stored in newborns liver) CARBOHYDRATE METAB Glucose = essential fuel for brain metab, when placenta = expelled maternal glucose supply is cut of, at 1st babys glucose declines (they have to learn to regulate their blood glucose concentration and adjust to an intermittent feeding sched usually term babys glucose = 70-80% maternal blood glucose ▪ Hypoglycemia = one of most freq problems encountered, maintaining glucose homeostasis is one of the important physiologic events during fetal-to-newborn transition (first 24-48hrs plasma glucose may be lower) ▪ Glucose = main source of energy many hours after birth, with increased energy needs the liver releases glucose from glycogen stores for 1st 24hrs BILIRUBIN CONJUGATION Liver = resp for conjugation of bilirubin, (yellow-orange bile pigment from breakdown of RBC) in the womb elimination of bilirubin in blood = handled by the placenta, the principal source of bilirubin in a newborn = hemolysis of RBCS (ERYTHROCYTES) , rbc die after 80days and the heme = converted to bilirubin, bilirubin = released in unconjugated form “indirect bilirubin” = fat sol. Newborns produce bilirubin 6-8mg/kg/day 2x amt in adult (declines to adult level in 10-14days) , pathways of liver are relatively immature & cannot conjugate bilirubin as quickly as needed ▪ Failure of liver cells to break down & excrete bilirubin can cause increased amt of bilirubin in blood � JAUNDICE (bilirubin = toxic & needs to be excreted out) to measure look @ conjugated & unconj ▪ When unconj bilirubin pigment = deposited in skin & mucous membranes as a result of increased bilirubin levels jaundice aka icterus dev. (yellowing skin, sclera & mucous membr) ▪ Visible jaundice occurs in > ½ healthy babys ▪ Elevated blood levels of bilirubin during 1st week can � BILIRUBIN ENCEPHALOPATHY : permanent brain damage 7

▪ Common risk factors to dev jaundice : fetal-maternal group incomp, prematurity, asphyxia at birth, insufficient milk intake, drugs (diazepam, oxytocin, erythro...