Fetal and Neonatal Physiology

Fetal and Neonatal Physiology

新光醫院小兒科

穆淑琪醫師

Definitions

Preterm* Infant < 37 wks GA

Extremely LBW < 1000g

SGA > 37 wks, < 2.5 kg

Newborn < 24 h

Neonate < 1 month

Infant < 1 year

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)

NEONATAL PHYSIOLOGY

The Respiratory System

Airway Differences

Obligate nasal breather

Easy airway obstruction

Anatomic differences co

mplicate ETT intubation

Straight blade, uncuffed E

TT preferred

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

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

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

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

BirthBirth

Decreased Pulmonary PerfusionDecreased Pulmonary Perfusion

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。

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。

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。

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

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

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

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

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)

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)

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

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)


Pulmonary Vasculature

Reactive, thick muscularis layer

Acidosis, hypercarbia, hypoxemi

a, stress

Stressors may cause acute CHF

Acidosis results and worsens

Fetal Cardiovascular System

UV →RA (FO) → AO

SVC→PA→(DA)→AO

Ductus Arteriosus (DA)

Foramen Ovale (FO) Umbilical Arteries and

Veins

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

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


Stimulate DepressMild acidosis Severe acidosisHypercarbia CNS damage

Hypoxia HypoxiaPain DrugsCold Magnesium

Touch AlcoholNoise Opiods

Umbilical cord clamping Barbiturates


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

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


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

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

Asphyxia PaO2

PCO2

pH

Uteroplacental blood flow

Maternal or Fetal disease (cause)

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)

Development and maturation of the cardiopulmonary systemThe Fetal Circulation

Four unique shunts

Placenta

Ductus Venosus

Foramen Ovale

Ductus Arteriosus

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

Respiratory Distress Syndrome

Etiology-Surfactant deficiency during disease

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

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

Pathophysiology

Reduce lung compliance

Reduce FRC

Poor lung distensibility

Poor alveolar stability

Right-to-left shunt

Reduce effective pulmonary blood flow

Clinical signs

Onset near the time of birth

Retraction and tachypnea

Expiratory grunting

Cyanosis

Systemic hypotension

Characteristic chest radiography

Course lasts 3-5 days

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

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

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

Closure of the ductus arteriosus completes the separation between pulmonary and systemic circulation

Renal System and Fluids

Total Body Water 80% in newborns Diuresis (lower fluid requirements)

First 5 days Hypovolemia

Acidosis, tachycardia, hypotension Hypervolemia

CHF

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)

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

Temperature Homeostasis

Challenges Larger surface-to-volume ratio Lack of significant fat stores

Adaptations Non-shivering thermogenesis Activity, crying

Consequences Acidosis, apnea, hypotension

PREMATURE INFANTS

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

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

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

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

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

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?)

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

Fetal and Neonatal Physiology

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