Neonatal Transition Flashcards
Which 2 hormones prep baby for birth? (specific roles of ea)
1- CORTISOL
- Surfactant production (by type II cells) and alveolar development - Cardio development - Gluconeogenesis (liver) - Free water excretion by kidney - Modulates inflammation
2- CATECHOLAMINES
- Absorb fetal lung fluid (Na+ channels) - Surfactant secretion - Mobilize glycogen stores
5 Stages of Lung Development
1 - Embryonic (first 8 wks) esophagus and trachea separate; lung bud arises from foregut
2 - Pseudoglandular (5-17 wks) tracheal-bronchial tree and some branching
3 - Canalicular (16-27 wks) diff of type 1 v. type 2 cells; terminal and respiratory bronchioles form; lamellar bodies form w/ early surfactant
4 - Saccular (24 wks to term) sacs form (alveolar ducts) so gas exchange can occur but still working on making actual alveoli (very little reserve); inc surfactant formation
5 - Alveolar (36 wks on) alveoli present at 34 wks gestation; cont to inc SA
Fetal Lung Fluid
- Fetal lung filled w/ fluid during pregnancy (active Cl- transport into lumen) –> distention and growth
- Requires Na-K pump
- At birth … fluid reabsorbed (dep on Na+ channels) –> pulmonary vasculature –> lymphatics –> removed
- Requires Na-K pump and beta - adrenergic epinephrine stimulation
What can cause delayed lung fluid reabsorption?
- inc transvascular pressure
- inc vascular permeability (sepsis)
- damage to type II cells
- less # type II cells b/c premature
- hypoxia leading to dec Na-K pumps
- not active labor
Transient Tachypnea of Newborn
- slow activation of Na channels so delayed reabsorption of fluid (inc RR and mild cyanosis)
- but resolves w/in hrs to days w/ supportive O2
- In term babies typically
Causes of Surfactant Deficiency
- Inact by bacteria and meconium
- inhibition of secretion (acidosis, hypoxia) or
- genetic def in production or secretion,
- prematurity (immature type II cells)
RDS
- Resp Distress Syndrome (RDS)
- dec surfactant production b/c immature type II cells –> inc alveolar surface tension / poor compliance/ alveoli collapse at end of ea breath
- Present - ground glass on Xray, usually get better in 72-96 hrs
- Tx - corticosteroid b/f delivery then exogenous surfactant, ventilation, CPAP
Fetal Circulation
- Pulmonary - high resistance (b/c no exchange poss) so pulmonary artery pressures are very high; RV output bypasses lung
- Systemic and Placental Circ - low resistance; high flow
PARALLEL CIRCUIT
- Umbilical vein –> liver –> ductus venosus –> IVC –> thru foramen ovale –> L atrium –> L vent –> aorta –> brain/heart/upper body (PREFERENTIAL)
- SVC and IVC flow from lower body –> R atrium –> R ventricle –> PA –> ductus arteriosus –> descending aorta –> abdomen/ lower body / umbilical artery
4 Fetal Shunts
- Ductus venosus - b/n umbilical vein and inferior vena cava
- Foramen ovale - allows shunt from R atrium –> L atrium
- Ductus arteriosus - b/n aorta and pulmonary artery
- Placental shunt
How does circulation change at birth?
- Clamp cord which inc systemic resistance
- Expansion of lung –> higher O2 content –> dec pulmonary resistance
- Causes shunts to close
- Foramen ovale shuts when flow switches to L –> R
- Ductus arteriosus closes from combo of high oxygen content and no more prostaglandins
Persistent Pulm HTN
- when pulm resistance does not dec at birth which prevents fetal shunts from closing (foramen ovale and ductus arteriosus)
- Deoxy blood returning to R side cannot go to lungs; goes R –> L via foramen ovale (hypoxemia)
- Primary - vascular defect (abnormal pulmonary arteries) but lungs normally fine
- Secondary - lung parenchyma disease; hypercarbic is #1 problem
- Tx - ECMO
APGAR Score
- Taken at 1 min and 5 min; cont every 5 min until 20 min if score < 7
- 5 components = color, heart rate, reflexes, muscle tone, respiration (ea gets 0, 1 or 2)
Fetal Nutrient Stores
- Inc fat stores (esp brown fat) and glycogen stores in 3rd trimester
- Store proteins throughout
- Babies lose 10% wt in first 3 days (water content) then regain by 1 wk via nutrients
Causes and Tx of Neonatal Hypoglycemia
- Risk - premature or small gestational wt (less glycogen stores and may have poor feeding) or large gestational wt (exaggerated insulin in response to high maternal glucose in utero)
- Tx - feeding and IV glucose solutions
Jaundice (physio v pathological)
- Physio jaundice in majority of infants
- Pathological - worry about kernicterus / bilirubin encephalopathy (delayed Moro or arching reflexes; poor feeding, high-pitched cry, hypotonia, sz)
**Long term - sensorineural hearing loss; dev delay; cerebral palsy
