Fetal-newborn transition Flashcards
Requirements for cardiorespiratory transition
structural maturity of lung replacement of fetal lung fluid --> air adequate pulmonary surfactant onset of breathing incrase in pulmonary blood flow
Embryonic maturity of lung
less than 5 weeks
trachea and bronchi
evidence of 5 lobes
Pseudoglandular lung
5-16 wks
airway branching x 15 generations
cuboidal cell lining
Canalicular lung
16-25 wks
airways enlarge
thinned epithelium
capillary development
Saccular lung
24-36 wks
basement membranes fuse –> future blood-gas barrier
type II cells –> surfactant
Alveolar lung
36 weeks to 2-8 years
capillaries bulge into terminal sacs
formation of septae, crests
increasing surface area
Immature lung histology
canalicular
thick blood-gas barrier
small area for gas exchange
poorly vascularized
Mature lung histology
thin blood-gas barrier
large area for gas exchange
highly vascular
In utero lung fluid
ultrafiltrate of pulmonary capillary blood
actively secrete (Cl ion transport)
250-300 ml/day
essential for fetal respiration and maintenance of FRC
Lung fluid in transition
fluid secretions slows in late pregnancy
absorption begins in labour (active transport of Na ions)
vaginal squeeze forces fluid out of lungs (not extremely significant)
cleared by capillaries and lymphatics postnatally
aided by lung distension driving fluid into interstitium
Transient tachypnea of the newborn
Retained fetal lung fluid increased central vascular markings hyperaeration evidence of interstitial/pleural fluid prominent interlobar fissures flat diaphragm - hyperinflated lungs
Embryonic maturity of lung
less than 5 weeks
5 lobules
trachea and bronchi
Canalicular lung
16-25 wks
airways enlarge
thinned epithelium
capillary development
Saccular lung
24-36 wks
basement membranes fuse –> future blood-gas barrier
type II cells –> surfactant
Fetal channels
umbilical vein ductus venosus foramen ovale ductus arteriosus umbilical arteries
Breathing after birth
Onset
Reduction in pulmonary vascular resistance: crying
increased lung blood flow
increased pO2 in blood
increased blood to the LA
functional closure of foramen ovale due to LA pressure> RA
Cord clamped - increased SVR, close umbilical vessels
closed DA: usually 24-48h in term infants
Mature lung histology
thin blood-gas barrier
large area for gas exchange
highly vascular
In utero lung fluid
ultrafiltrate of pulmonary capillary blood
actively secrete (Cl ion transport)
250-300 ml/day
essential for fetal respiration and maintenance of FRC
Lung fluid in transition
fluid secretions slows in late pregnancy
absorption begins in labour (active transport of Na ions)
vaginal squeeze forces fluid out of lungs (not extremely significant)
cleared by capillaries and lymphatics postnatally
aided by lung distension driving fluid into interstitium
Cord clamping time
Effects on infant from delayed (1-2 min) cord clamping
Higher Hb at 24-48 h
Reduced Fe deficiency at 3-6 mo
increase in phototherapy for neonatal jaundice (more blood, more jaundice)
Preterm infants: reduction in rates of interventricular hemorrhage
Transient tachypnea of the newborn
Retained fetal lung fluid increased central vascular markings hyperaeration evidence of interstitial/pleural fluid prominent interlobar fissures flat diaphragm - hyperinflated lungs
Surfactant production
by alveolar type II cell
stored in Lamellar body, secreted and then adsorped to alveolar space
Surfactant composition
70-80% phospholipids
10% proteins - apoproteins AD immunity, BC hydrophobic membrane proteins that increase the rate at which surfactant spreads over surface
10% neutral lipids - cholesterol
Respiratory distress syndrome
preterm infant
tachypnea, retractions, grunting, cyanosis
hypoxia
hypercapnia
Fetal breathing movements
rhythmic contarctions of diaphragm associated with movement of small volumes of fluid in fetal airway
1-60 min episodes
increase after each maternal meal
circadian rhythm, increasing at night
related to maternal melatonin concentration
inhibited by acute, severe hypoxia, sedatives, alcohol, PGE2
Onset of breathing at birth
breathing becomes regular
mechanisms: sensory/chemical stimuli, removal of placental inhibitor peptide
Baby must overcome:
- viscosity of lung fluid
- resistance of lung tissue
- surface tension at air-liquid interface
Newborn thermal properties
Cooler environment
heat loss via conduction, convection, radiation, evaporation
Breathing after birth
Onset breathing
Reduction in pulmonary vascular resistance: crying
increased lung blood flow
increased pO2 in blood
increased blood to the LA
functional closure of foramen ovale due to LA pressure> RA
Cord clamped - increased SVR, close umbilical vessels
closed DA: usually 24-48h in term infants
Newborn arterial gases
pO2: 1 h 60 , 24 h 90 O2 sat: 1 h 90, 24 h 98 O2 content, 18 then 20 pCO2 35-45 pH 7.3-7.4transition
Time course of cardiorespiratory transition
Seconds: first breath, high transpulmonary pressure, not pink
Minutes: pink, regular breathing, pulmonary blood flow increases, absorption of lung fluid
Hours: rising pO2, FRC established, absorption of FLF, increasing lung compliance, RR40-60
Days: remodelling of pulmonary arteries, further increase in lung compliance
Pseudoglandular lung
5-16 wks
airway branching x 15 generations
cuboidal cell lining
Cord clamping time
Effects on infant from delayed (1-2 min) cord clamping
Higher Hb at 24-48 h
Reduced Fe deficiency at 3-6 mo
increase in phototherapy for neonatal jaundice (more blood, more jaundice)
Preterm infants: reduction in rates of interventricular hemorrhage
APGAR heart rate
0 absent
1 less than 100, almost always due to lung issues
> 100
APGAR respiratory effort
0 absent
1 slow, irregular
2 good, crying
APGAR muscle tone
0 limp
1 some flexion
2 active motion
Neonatal hypoglycemia
Glucose less than 2.6 mmol/L
APGAR colour
0 blue/pale
1 body pink, blue extremities
2 all pink
Fetus thermal properties
0.5C > mother
heat transfer via placenta
suppression of thermogenesis: dont waste energy on heat generation
Newborn thermal properties
Cooler environment
heat loss via conduction, convection, radiation, evaporation
Brown fat
mitochondria rich sympathetic stimulation: - hydrolysis of triglyceride - release of FA, glycerol - heat generated
Cold stress
36-36.5
Moderate hypothermia
32-36
severe hypothermia
less than 32 C
WHO warm chain
warm delivery room immediate drying skin to skin contact breastfeeding bathing and weighing postponed - recommended not to bathe during first 6 hours appropriate clothing and bedding mother and baby together warm transportation warm resuscitation training/awareness raising
Fetal metabolism
anabolism dominant
90-100kcal/kg/day
glucose, lactate, amino acids
glucose levels 70-80% maternal
RDS causes
1) surfactant deficiency
2) atelectasis –> V/Q mismatch, hypoventilation
3) hypoxemia + hypercarbia –> respiratory + metabolic acidosis
4) pulmonary vasoconstriction –> persistent fetal circulation
5) proteinaceous exudate
Symptomatic hypoglycemia
jitteriness, tremor, seizure, coma irritability, lethargy, stupor hypotonia, limpness apnea, cyanotic spells poor feeding hypothermia
TTN risks
precipitous delivery
mtaernal diabetes
maternal sedation
perinatal depression
Retractions at birth
- neonates with increased chest wall compliance/reduced lung compliance will have increased negative intrapleural P during inspiration
- worsening lung compliance before respiratory failure is apparent by blood gas abnormalities
Grunting at birth
vocal cords partially closed at end of expiration
generates positive end expiratory pressure (PEEP) to stent open small airways, increasing ventilated areas and improving V/Q ratio
Head Bobbing at birth
Contractions of SCM when accessory muscles in upper thorax are recruited indicating severe respiratory distress
DDx neonatal respiratory distress
TTN RDS meconium aspiration non-pulmonary - anemia, medication, pneumothorax - congenital heart disease, malformation - persistent pulmonary HTN
aCORN respiratory score
Scores 0,1,2
Respiratory rate: 40-60, 60-80, 80
O requirement none, 50
Retractions none, mild-mod, severe
Grunting none, with stimulation, continuous at rest
Breath sounds on ausc: easily heard, decreased, barely heard
Prematurity: >34 w, 30-34, 8 severe
Pneumothorax Tx
small pneumothorax: often minimally symptomatic
conservative management if not underlying disease, not ventilated, minimal respiratory distress, no continuous leak
Ventilated: minimize pressures (may need to increase rate)
Observe signs of deterioration
Consider 100% Oxygen for nitrogen washout if smaller leaks
Needle aspiration
Chest tube of continuous leak
Dx of TTN
CXR: hyperinflation, hyperaeration, flat domes of diaphragm, vascular markings in lungs, prominent interlobular fissures
Tachypnea
Intercostal retractions, grunting, nasal flaring: difficulty breathing, low gas exchange
Hypoxia without hypercapnia
Cyanotic
Tx TTN
self-resolved in 1-3 d
respiratory support and monitoring
O2 requirements usually 4 h, further assessment
RDS causes
lack of surfactant production/release in alveoli
progressive collapse of terminal bronchiole/alveoli
increased surface tension in alveolus - increased effort for inflation
RDS prevalence/popn
preterm
male
prenatal depression
maternal diabetes
RDS prevention
antenatal corticosteroids to increase surfactant production
tocolytic agents potentially arrest preterm labour
TTN risks
precipitous delivery
mtaernal diabetes
maternal sedation
perinatal depression
RDS Dx
CXR: ground glass, loss of cardiac silhouette, small lung volume
may see atelectasis
histology: hyaline membranes and collapsed air spaces
tachypnea
intercostal retractions, grunting, nasal flaring, difficulty breathing, low gas exchange
hypoxia with hypercapnia
cyanotic
RDS Tx
artificial surfactant
varying needs of respiratory support and O2
respiratory distress will worsen if respiratory effort or support unable to prevent progressive lung collapse
fluid and metabolic management
Pneumothorax risks
aspiration
underlying lung disease
high venitlatory pressures
Pneumothorax prevalence/popn
primarily in babies with lung disease (aspiration syndromes and RDS) receiving respiratory support, like CPAP or ventilation
spontaneous pneumothorax can occur in 1-2% of health infants during initial spontaneous breaths
Pneumothorax Dx
present with acute increase in respiratory distress and O2 requirements
Tension pneumothorax may present with sudden onset of CV collapse
Pneumothorax Tx
small pneumothorax: often minimally symptomatic
conservative management if not underlying disease, not ventilated, minimal respiratory distress, no continuous leak
Ventilated: minimize pressures (may need to increase rate)
Observe signs of deterioration
Consider 100% Oxygen for nitrogen washout if smaller leaks
Needle aspiration
Chest tube of continuous leak
Meconium aspiration causes
stress during delivery
leads to obstruction of small airways and alveoli
Presents as pneumonitis, disrupts surfactant, mechanical disruption of airway
mechanical obstruction, chemical inflammation, surfactant inactivation
Prevalence/popn of meconium aspiration
more likely in cases of fetal distress/difficult labour
usually full term infants >34 w
in utero hypoxia, meconium stained amniotic fluid
Dx meconium aspiration
usually stained amniotic fluid
CXR: atelectasis, consolidation, hyperinflation of lungs/air trapping, spontaneous pneumothorax
audible grunting, severe retractions
may be accompanied by persistent pulmonary HTN of newborn
Tx meconium aspiration
severe cases are life-threatening respiratory ventilator support manage pulmonary HTN monitor for pneumothorax Abx may need surfactant administration
Congenital diaphragmatic hernia causes
developmental defect (bowel loops, liver, spleen) in chest cavity
Prevalence/popn of congenital diaphragmatic hernia
Unilateral: 1/2200 births
80% involve left hemidiaphragm
associated with lethal anomalies (16-22%)
Dx congenital diaphragmatic hernia
CXR: hypoplastic lungs and obvious defects
wide clinical presentation
Tx congenital diaphragmatic hernia
surgery
Sudden respiratory depression DDx
may occur in intubed baby DOPE dislodged obstruction pneumothorax equipment
