Fetal and Neonatal Physiology
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Transcript of Fetal and Neonatal Physiology
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Fetal and Neonatal Physiology
新光醫院 小兒科
穆淑琪醫師
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Definitions
Preterm* Infant < 37 wks GA
Extremely LBW < 1000g
SGA > 37 wks, < 2.5 kg
Newborn < 24 h
Neonate < 1 month
Infant < 1 year
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Classification Significance Preterm Infants
Not yet matured Incomplete but normal IUG Prone to IRDS, IVH, PDA, apnea, ROP, hypothermia
Small for Gestational Age Matured but prone to certain conditions
IUGR for varied reasons Prone to hypoglycemia, infection, pneumonia, seizures
(not apnea)
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NEONATAL PHYSIOLOGY
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The Respiratory System
Airway Differences
Obligate nasal breather
Easy airway obstruction
Anatomic differences co
mplicate ETT intubation
Straight blade, uncuffed E
TT preferred
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缺氧窒息缺氧窒息 (Asphyxia)(Asphyxia) 的生理變化的生理變化 : : 胎兒之肺臟胎兒之肺臟 (Lung)(Lung) 及血液循環及血液循環Fetus
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胎兒之肺臟及血液循環胎兒之肺臟及血液循環Fetus
Diminished Blood Flow Through Fetal LungsDiminished Blood Flow Through Fetal Lungs
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出生時的轉變
肺泡之肺液吸收
臍靜脈及臍動脈收縮
肺血管擴張
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肺液的吸收 生產前開始減少 有效的初始呼吸可以促進吸收 減緩吸收
出生時不呼吸 淺而無效的呼吸
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BirthBirth
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Decreased Pulmonary PerfusionDecreased Pulmonary Perfusion
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缺氧窒息 (Asphyxia) 新生兒因活動力不佳,而不能建立有效之呼吸,缺氧狀態可能接續進行而導致缺氧窒息。
缺氧窒息的定義 : 不斷加重的缺氧、二氧化碳堆積及酸血症 (acidosis) 。
缺氧窒息進行到某個程度會造成永久性腦部傷害或死亡。
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缺氧窒息 初始反應
肺部、腸、胃、腎臟、肌肉及皮膚的血流量均減少,所保存的血主要用來供應心臟及腦部。
後期反應 當窒息持續時,心肌也受傷害,心輸出
量減少,到重要器官之血流量也減少。
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干擾轉變的因素
呼吸不足,呼吸道阻塞。
失血過多、心臟收縮力不佳、或缺
氧造成心搏緩慢
肺血管持續收縮。
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Chronological Development of Organs, Systems, and Body form-I
ORGAN CHRONOLOGY OF DEVELOPMENT
Bronchial apparatus and pharyngeal pouches4th week--ridges and grooves appear
over the future neck region
Thyroid gland 4th week--endoderm appears o
ver the floor of the pharynx
Tongue 4th week--primordia appear in
the of the pharynx
Face End of 4th week--primordia ap
pear
Palate Begins in the 5th week
Upper respiratory system 4th week--laryngotracheal g
roove appears
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Chronological Development of Organs, Systems, and
Body form-II ORGAN CHRONOLOGY OF DEVELOPMENT
Kidneys,urinary bladder,urethra 5th week,
permanent adult kidney begins to develop Adrenal glands 5th week,primordia of adre
nal glands develop Conads,genital ducts,external genitalia 5th week,
gonadal ridges form Heart 3rd week,development of t
he heart begins Atria 5th week,
the atria are formed Ventricles 5th week,the ventri
cles form
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ORGAN CHRONOLOGY OF VELOPMENT
Fetal circulation 3rd week,embryonic blood vessels develop
Brain and spinal cord End of 4th week,primary vesicles form and walls of the neural tube thicken to form the spinal core
Pituitary 6th week,connection of Rathke’s with oral cavity disappears
Limbs End of 4th week,limb buds appear Skull 7th week,paired cartilages begin t
o fuse to form the cranium
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Apnea Absence of respirations for 20 sec, causin
g cyanosis and bradycardia
At-risk neonates
Preterm and ex-preterm infants to 50 wks P
CA
Risk is ~60% at 42 wks PCA, <1% 54 wks
PCA
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Apnea: Primary ApneaApnea: Primary Apnea缺氧窒息缺氧窒息 (Asphyxia)(Asphyxia) 的生理變化 的生理變化 : : 呼吸暫停呼吸暫停 (Apnea)(Apnea)
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Apnea : Secondary ApneaApnea : Secondary Apnea缺氧窒息缺氧窒息 (Asphyxia)(Asphyxia) 的生理變化 的生理變化 : : 呼吸暫停呼吸暫停 (Apnea)(Apnea)
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The Respiratory System
Thorax and Lungs Increased O2 consumption (6 ml/kg/min)
Due to high BMR (+100%) Prone to cyanosis
Lung volumes vs. age – no change RR is increased
Diaphragmatic breathing Susceptible to abdominal distension
Fatigable – preterm infants
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The Cardiovascular System
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The Cardiovascular System
Myocardium Unable to SV by contractility
CO is primarily rate-controlled
Non-compliant ventricles
CHF
Bradycardia implies hypotension
High vagal tone at birth
PNS mature (not SNS)
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The Cardiovascular System
Pulmonary Vasculature
Reactive, thick muscularis layer
Acidosis, hypercarbia, hypoxemi
a, stress
Stressors may cause acute CHF
Acidosis results and worsens
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Fetal Cardiovascular System
UV →RA (FO) → AO
SVC→PA→(DA)→AO
Ductus Arteriosus (DA)
Foramen Ovale (FO) Umbilical Arteries and
Veins
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Perinatal Cardiorespiratory physiology
Fetal lungs 24 days -arises from the foregut 26-28 weeks -terminal airways developed 30-32 weeks -final surface active material
(SAM) developed Plasma ultrafiltrate is a normal part of the
lungs Every day IU (intrauterine) 50-150 ml/kg/day
of plasma is produced Plasma is swallowed in the gut and excreted
by kidneys
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Perinatal Cardiorespiratory physiology Plasma ultrafiltrate (2) 2/3 is expelled during vaginal delivery 1/3 is removed capillaries, lymphatics, breathing If fluid is retained into lungs causes TTBN (transient tachypnea of newborn)
Causes: Small infants Preterm infants Rapidly born Cesarean section born babies
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Perinatal Cardiorespiratory physiology
Stimulate DepressMild acidosis Severe acidosisHypercarbia CNS damage
Hypoxia HypoxiaPain DrugsCold Magnesium
Touch AlcoholNoise Opiods
Umbilical cord clamping Barbiturates
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Perinatal Cardiorespiratory physiology
Normal breathing - 30/min at 90 sec of age (reminder)
Normal breathing - 40-60/min at few minutes of age:
Removal of increased CO2 produced High metabolic rate Helps maintain FRC
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Perinatal Cardiorespiratory physiology Circulation of the fetus: RV ~ 2/3 CO LV ~ 1/3 CO
Foramen ovale Ductus arteriosus
Blood is coming from placenta - high O2
content 95% of the blood coming from placenta
goes to LA through foramen ovale
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Perinatal Cardiorespiratory physiology
Circulation of the newborn: PVR is due to pulmonary expansion, breath
ing, pH, and O2 tension If neonate is born by CS - PAP’s and P
VR PVR is :
Hypoxia Acidosis Hypovolemia Hypoventilation Atelectasis Cold
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Perinatal Cardiorespiratory physiology Changes in circulation of the newborn: PVR - pulmonary blood flow Right/left shunting will be decreased LA pressures are , and seal foramen ovale Ductus arteriosus closes (10-14 days) in response
to O2 Ach Parasympathetic nerve stimulation PG
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Asphyxia PaO2
PCO2
pH
Uteroplacental blood flow
Maternal or Fetal disease (cause)
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Asphyxia
Intrauterine asphyxia: PaO2 decreases from 25-40 to 5 mmHg Anaerobic metabolism occurs pH drops < 7.0 : respiratory and metabolic acidosis Lactate is accumulating in the body Redistribution of blood flow in the body CO starting normal is now decreasing Because of high doses of opioids in the blood fetus may
survive severe hypoxia (may reduce total O2
consumption)
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Development and maturation of the cardiopulmonary systemThe Fetal Circulation
Four unique shunts
Placenta
Ductus Venosus
Foramen Ovale
Ductus Arteriosus
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Cardiopulmonary Adjustments at Birth-I
Loss of the placental circulation
Newborn breathe on its own
Mild hypoxia
Mild hypercapnia
Tactile stimuli trigger the first breath
Cold skin
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Respiratory Distress Syndrome
Etiology-Surfactant deficiency during disease
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Factors precipitating to HMD
High risk:
Prematurity
Asphyxia
IDM ( Infant of Diabetic
Mother )
Maternal hemorrhage
C/S
Multiple births
Male >female
Low risk:
IUGR
Maternal hypertension
Steroids
Placental insufficiency
Heroin addictive
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Synthesis of surfactant
Maturation of alveolar type II cells and the subsequent
synthesis of surfactant
--started since 24 wks’ gestation
--complete by 32 wks’ gestation
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Pathophysiology
Reduce lung compliance
Reduce FRC
Poor lung distensibility
Poor alveolar stability
Right-to-left shunt
Reduce effective pulmonary blood flow
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Clinical signs
Onset near the time of birth
Retraction and tachypnea
Expiratory grunting
Cyanosis
Systemic hypotension
Characteristic chest radiography
Course lasts 3-5 days
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Function of surfactant
Stabilize the lung during deflation
Prevent high surface tension pulmonary edema
Protect the lung against epithelial and endothelial
injury
Provide a defense against infection
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Homodynamics of surfactant treatment in RDS
Immediate effect ( up to 10 min after instillation)
- related to the mode of administration
- transient obstruction of the large
airways with fluid
PaCO2↑
cerebral vasodilatation with CBF↑
- PaCO2↑
pulmonary vasoconstriction
reduction in L to R ductal flow
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Cardiopulmonary Adjustments at Birth-II
Closure of placental circulation-
increase systemic vascular resistance Opening of pulmonary circulation
decrease pulmonary vascular resistance Closure of the ductus venosus within the first three hours of
life
forces portal blood to perfuse the liver Left atrial pressure > right atrial pressure
causing the foramen ovale to close
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Closure of the ductus arteriosus completes the separation between pulmonary and systemic circulation
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Renal System and Fluids
Total Body Water 80% in newborns Diuresis (lower fluid requirements)
First 5 days Hypovolemia
Acidosis, tachycardia, hypotension Hypervolemia
CHF
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Renal System and Fluids Renal Function
GFR increases rapidly for first 3 mos
Tubular function increases over 12 mos
Poor tolerance for over / under hydration
Age Max UOsm
Newborn 525
15-30 d 950
12 m 1200 (adult)
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Blood Function Fetal Hemoglobin
High affinity for O2 at lo
w tensions 80% at 25 mmHg
Persists until age 3 mos replaced by adult Hgb
Birth Hgb ~ 17 g/dl
maintains O2 delivery
despite high affinity
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Temperature Homeostasis
Challenges Larger surface-to-volume ratio Lack of significant fat stores
Adaptations Non-shivering thermogenesis Activity, crying
Consequences Acidosis, apnea, hypotension
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PREMATURE INFANTS
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Preterm Respiratory Function
Higher incidence of airway obstruction Respiratory control is underdeveloped
Increased WOB, O2 consumption Muscle fiber immaturity Compliant chest wall
Intubation recommended over mask ventilation
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Bronchopulmonary Dysplasia BPD
Persistent respiratory distress requiring O2
Sequela of chronic lung disease 10 – 15% of formerly intubated infants
High index of suspicion Present with
Increased: FRC, airway resistance, dead space, A-a gradient and reactive airways
Decreased: lung compliance Medicated with
Corticosteroids, diuretics
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Retinopathy of Prematurity Exact cause is not certain
Retinal artery vasoconstriction Retina ischemia, neovascularization, retinopa
thy Risk factors
prematurity, very low birth weights, mechanical ventilation, PaO2 > 80 mmHg, < 44 wks PCA
Evidence for FiO2 causing ROP under GA is lacking
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Retinopathy of Prematurity
Empirically keep SaO2 90 – 95%
Two pulse oximeter technique
Measure at a preductal site (ear, R finger)
Measures retinal perfusion Postductal sites
Effect of PDA reopening, shunt reversal
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Fetus assessment at birth: The Apgar Scoring Systema
SCORE SIGN 0 1 2
Heart rate Absent Less than 100/ min More than 100/ min Respiratory effort Absent Slow, irregular Good, crying
Color Blue, pale Body pink, extremities blue (acrocyanosis) Completely pink
Reflex irritability (response to insertion of a nasal catheter)
Absent Grimace Cough, sneeze
Muscle tone Limp Some flexion of extremities Active motion
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Neonatal Resuscitation Apgar Score Guides ResuscitationApgar Cause Treatment
8 – 10 Normal Birth Oropharyngeal suctioning, radiant warmer
5 – 7 Mild Asphyxia External stimulation, O2 to face. If inadequate response, start BVM
3 – 6 Moderate Asphyxia
Start BVM, if inadequate, intubate and analyze cord blood.
0 – 2 Severe Asphyxia
Immediate intubation ± external compressions ± epinephrine (gluc, bicarb?)
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Neonatal Physiology
Breast milk
Mobilize glucose and fatty acid soon after delivery
Easy to develop fluid and acid-base imbalance
high rates of fluid and turnover and acid production
Nonshivering thermogenesis in brown fat
keep the neonates warm
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