Physiologic adaptations of the newborn Flashcards
Stages of lung development
Canalicular
Saccular
Alveolar
Lung development - Canalicular Phase
16-26 weeks
Differentiation of Type II pneumocytes, development of capillary network
Lung development - Saccular phase
26-36 weeks
Thinning of gas exchange surface
Closer association of capillaries with air spaces
Lung development - Alveolar Phase
36 weeks - 3+ years
Development of mature alveoli
Lung inflation
With first breaths, there is a step-wise movement of the air-fluid interface distally within the airways
Establishes lung volume and FRC
Respiratory drive
At birth, onset of regular, consistent respirations occurs in response to sensory stimulation (cold, light, touch, noise, normal mild asphyxia / hypercarbia)
Apnea
Primary - stimulation easily initiates cry followed by gasping and regular respirations; HR and BP remain stable
Secondary - requires positive pressure ventilation to establish lung inflation and initiate regular respirations; HR and BP fall quickly and death occurs without rescue ventilation
Physiologic limit of viability
~23 weeks
Prior to this point, anatomic requirements for pulmonary gas exchange are not present; primarily there is too great a distance between developing capillaries and rudimentary air spaces
Surfactant
Phospholipid-protein complex (90% lipid / 10% protein); produced by type II cells and extruded into air space by exocytosis
Formation of an amphipathic mono-layer at the air-fluid interface lowers surface tension within air spaces, preventing alveolar collapse at end expiration
Maintains FRC
Surfactant deficiency
History: Premature birth
Causes diffuse microatelectasis with very poor compliance (poorly expanded airspaces)
Presents as increased work of breathing (retractions, nasal flaring, cyanosis); CXR shows diffuse microatelectasis (“ground glass” appearance)
Treated with oxygen, CPAP / PEEP, intubation/mechanical ventilation, and surfactant replacement via endotracheal tube
Lung fluid absorption
Labor signals a switch from active Cl- secretion (in utero) to active Na+ absorption via ENaC channels
ENaC channels are expressed late in gestation; expression can be induced by glucocorticoids
How is lung inflation related to circulatory changes in the newborn?
Lung inflation and aeration causes increased alveolar O2 and decreased pulmonary vascular resistance, which increases pulmonary blood flow and leads to increased arterial pO2
Increased arterial pO2 signals closure of the ductus arteriosis, and increased venous return to the LA from the lungs triggers closure of the foramen ovale
Fetal circulation
Oxygenated blood returns from the placenta via the placental vein and empties into the RA through the ductus venosus
Pulmonary vascular resistance is high due to active pulmonary vasoconstriction; only 10% of CO flows through pulmonary vasculature
Blood is shunted from RA to LA via the foramen ovale, and from pulmonary artery to aorta through the ductus arteriosus
What factors contribute to closure of the foramen ovale?
- Increased venous return to the LA from the lungs after birth
- Vasoconstriction in response to cold stress increasing vasoconstriction and causing elevated LA > RA pressure
How do prostaglandins regulate the ductus arteriosus?
PGE1 maintains the ductus arteriosus patent
Decreased PGE1 after birth causes constriction of the ductus arteriosus near the time of birth; anatomic closure occurs over days-weeks
Persistent Pulmonary Hypertension in the newborn (PPHN)
Occurs because of persistently increased pulmonary vascular resistance and/or decreased systemic vascular resistance (hypotension, shock) allowsing R > L shunting via the foramen ovale and ductus arteriosus
PPHN - Causes
Lung diseases with inadequate lung inflation - failure to initiate decrease in PVR
Chronic intrauterine hypoxemia causing vascular remodeling of pulmonary vessels with inability to dilate after birth
Acidosis, sepsis, or shock causing systemic hypotension
Presentation of PPHN
R > L shunting across the ductus arteriosus causes higher O2 saturation in the R arm (pre-ductal) vs. the leg (post-ductal)
R > L shunting across the FO does not cause differential saturation
PPHN - 3 categories
- “Reactive” - abnormally constricted pulmonary vessels due to parenchymal lung disease, sepsis, acidosis; usually reversible
- Abnormal pulmonary vascular musculature, i.e. antenatal closure of the DA due to maternal NSAID use; not easily reversed
- Hypoplastic pulmonary vasculature - i.e. pulmonary hypoplasia due to oligohydramnios; not completely reversible
Factors that contribute to increased PVR
Low pO2 / High pCO2 Low pH (Acidosis)
Factors that contribute to decreased PVR
Alveolar distension (lung ventilation) High pO2 / Low pCO2 High pH NO Prostacyclin
How is post-natal insulin secretion affected in infants of diabetic mothers?
Chronic exposure to high levels of glucose in the maternal serum causes islet cell hyperplasia in the fetal pancreas; after birth, insulin secretion does not fall at the same rate as glucose exposure and so infants of diabetic mothers are at increased risk of neonatal hypoglycemia
How are glucose concentrations maintained in the immediate post-natal period?
Mobilization of hepatic glycogen stores followed by gluconeogenesis from protein and fat
Why are IUGR / pre-term infants at higher risk for hypoglycemia
Decreased hepatic glycogen stores
Decreased protein / fat stores for gluconeogenesis
Neonatal glycemia - Diagnosis
Blood glucose < 45 + symptoms (jittery / tremulous, irritable, lethargic, apnea, seizures)
Blood glucose < 35-40 without symptoms
B
Neonatal hypoglycemia - Treatment
Feed - if infant is able and willing
IV glucose if not able to feed, if not improved after feeding, or for life-threatening symptoms (apnea, seizures)
Neonatal respirations
Normal rate is 40-60/min - easy, without retractions
Tachypnea is > 60 / min
Neonatal heart rate
Initially 150-180 bpm
100-120 bpm after 30-60 minutes
Neonatal BP
60 - 90 / 30 - 60
Apgar scores
0 - 2 points assigned to each of 5 categories: for a maximum of 10 points; assigned at 1 and 5 minutes, then every 5 minutes until > 6 scores are recorded or infant leaves delivery room
Heart Rate (> 100) Respirations (Regular, crying) Tone (Active motion) Response to suction (Cough, sneeze, or cry) Color (Pink)
