Physiologic adaptations of the newborn

Question 1

Stages of lung development

Answer 1

Canalicular
Saccular
Alveolar

Question 2

Lung development - Canalicular Phase

Answer 2

16-26 weeks

Differentiation of Type II pneumocytes, development of capillary network

Question 3

Lung development - Saccular phase

Answer 3

26-36 weeks

Thinning of gas exchange surface
Closer association of capillaries with air spaces

Question 4

Lung development - Alveolar Phase

Answer 4

36 weeks - 3+ years

Development of mature alveoli

Question 5

Lung inflation

Answer 5

With first breaths, there is a step-wise movement of the air-fluid interface distally within the airways

Establishes lung volume and FRC

Question 6

Respiratory drive

Answer 6

At birth, onset of regular, consistent respirations occurs in response to sensory stimulation (cold, light, touch, noise, normal mild asphyxia / hypercarbia)

Question 7

Apnea

Answer 7

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

Question 8

Physiologic limit of viability

Answer 8

~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

Question 9

Surfactant

Answer 9

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

Question 10

Surfactant deficiency

Answer 10

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

Question 11

Lung fluid absorption

Answer 11

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

Question 12

How is lung inflation related to circulatory changes in the newborn?

Answer 12

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

Question 13

Fetal circulation

Answer 13

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

Question 14

What factors contribute to closure of the foramen ovale?

Answer 14

1. Increased venous return to the LA from the lungs after birth
2. Vasoconstriction in response to cold stress increasing vasoconstriction and causing elevated LA > RA pressure

Question 15

How do prostaglandins regulate the ductus arteriosus?

Answer 15

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

Question 16

Persistent Pulmonary Hypertension in the newborn (PPHN)

Answer 16

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

Question 17

PPHN - Causes

Answer 17

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

Question 18

Presentation of PPHN

Answer 18

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

Question 19

PPHN - 3 categories

Answer 19

1. “Reactive” - abnormally constricted pulmonary vessels due to parenchymal lung disease, sepsis, acidosis; usually reversible
2. Abnormal pulmonary vascular musculature, i.e. antenatal closure of the DA due to maternal NSAID use; not easily reversed
3. Hypoplastic pulmonary vasculature - i.e. pulmonary hypoplasia due to oligohydramnios; not completely reversible

Question 20

Factors that contribute to increased PVR

Answer 20

Low pO2 / High pCO2 
Low pH (Acidosis)

Question 21

Factors that contribute to decreased PVR

Answer 21

Alveolar distension (lung ventilation) 
High pO2 / Low pCO2 
High pH 
NO
Prostacyclin

Question 22

How is post-natal insulin secretion affected in infants of diabetic mothers?

Answer 22

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

Question 23

How are glucose concentrations maintained in the immediate post-natal period?

Answer 23

Mobilization of hepatic glycogen stores followed by gluconeogenesis from protein and fat

Question 24

Why are IUGR / pre-term infants at higher risk for hypoglycemia

Answer 24

Decreased hepatic glycogen stores

Decreased protein / fat stores for gluconeogenesis

Question 25

Neonatal glycemia - Diagnosis

Answer 25

Blood glucose < 45 + symptoms (jittery / tremulous, irritable, lethargic, apnea, seizures)

Blood glucose < 35-40 without symptoms

B

Question 26

Neonatal hypoglycemia - Treatment

Answer 26

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)

Question 27

Neonatal respirations

Answer 27

Normal rate is 40-60/min - easy, without retractions

Tachypnea is > 60 / min

Question 28

Neonatal heart rate

Answer 28

Initially 150-180 bpm

100-120 bpm after 30-60 minutes

Question 29

Neonatal BP

Answer 29

60 - 90 / 30 - 60

Question 30

Apgar scores

Answer 30

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)