Physiologic Adaptation to Extrauterine Life

Question 1

Factors of Pulmonary Adaptation

Answer 1

1. Lung growth and development
2. Physiologic maturation (surfactant, lung fluid absorption, importance of functional residual capacity)
3. Respiratory drive
4. Importance of lung inflation to cardiovascular transition

Question 2

Canalicular Phase

Answer 2

• 17-27 weeks
• Delineation of pulmonary acinus
• Type II cells begin to differentiate, capillary network begins

Question 3

Saccular Phase

Answer 3

• 26-36 weeks

- Thinning of interstitial space, closer association of endothelial and Type I cells

Question 4

Alveolar Phase

Answer 4

• 36 wk to 3 yrs
• Presence of true alveoli
• Lengthening and sprouting of capillary network

Question 5

Limit of viability of a fetus

Answer 5

approx 22-24 weeks, dev of acinus

Question 6

Role of surfactant

Answer 6

• Lowers surface tension
• Prevents alveolar collapse at end expiration
• Decreases work of breathing and improves compliance
• Aids host defense

Question 7

Where is surfactant made, stored and secreted?

Answer 7

Made in Type II alveolar cells
Stored as lamellar bodies
Secreted as tubular myelin into the alveolar space

Question 8

What mechanism prevents collapse of alveoli?

Answer 8

The surfactant has a hydrophilic head and hydrophobic tail, which when closely packed cause mutual repulsion and opposes collapse

Question 9

> 20 cm H20 opening pressure

Answer 9

Surfactant-deficient lungs; collapse to empty at end of expiration

Question 10

Importance of FRC

Answer 10

Normal FRC = best for easy breathing

Low FRC = underinflated balloon, hard to get started. Resembles surfactant deficiency (lung under-inflation). Takes more pressure generated. Atelectasis

High FRC = emphysema = lungs overdistended, gets hard for air to enter for any change in pressure.

Question 11

Hyaline Membrane Disease (HMD)

Answer 11

• Found in premature or delayed maturity babies
• Increased work of breathing (retractions, grunting - give themselves PEEP, and flaring)
• Cyanosis in room air
• CXR with diffuse microatelectasis in a reticulogranular pattern

Question 12

Treatment of surfactant deficiency

Answer 12

• Oxygen
• CPAP
• Intubation and mechanical ventilation
• Surfactant replacement

Question 13

Which cell type secretes fluid from lung?

Answer 13

Epithelial cells, driven by active Cl- secretion

Absorption driven by Na+ absorption

Question 14

Factors clearing fetal lung fluid

Answer 14

Maturity:
- amiloride-sensitive ENaC channels increase in late gestation due to fetal production of cortisol

Labor:

• increased transpulmonary pressure from uterine contractions
• burst of cortisol and catecholamines

Lung inflation:

• distal airways are either collapsed or filled with fluid prior to first breath.
• Air-liquid interface moves distally with each inspiration
• Step-wise increase in lung aeration and FRC

Question 15

What happens to babies from elective repeat C-section

Answer 15

More likely to get respiratory distress because they have more lung fluid at birth.

Question 16

Transient tachypnea of the newborn (TTN)

Answer 16

• If air space not maintained well-inflated, fluid can re-enter air spaces.
• Get respiratory distress
• From rapid labor, no labor, or maternal B-blockers (no response to catecholamines), or ineffective initial lung inflations

Question 17

Types of failure to breathe

Answer 17

Primary apnea = stimulation easily initiates cry

Secondary apnea = requires rescue with positive pressure ventilation to establish lung inflation

Neuromuscular impairment = hypotonia from maternal sedation, analgesia, MgSO4 during labor, or primary NM problems

Question 18

What happens when a fetus asphyxiates? What risk is there with this?

Answer 18

The fetus will gasp, which can move liquid into the fetal lung. This can sometimes cause meconium aspiration.

Question 19

Distinguish fetal apnea how?

Answer 19

Primary: HR and BP maintained, stimulation is effective - gasping causes decline

Secondary: HR and BP fall quickly, requires positive pressure ventilation

We always assume it’s secondary apnea!

Question 20

APGAR measured when?

Answer 20

Assigned at 1 and 5 minutes, and then every 5 minutes until 20 min or the score > 7

Question 21

Predictive value of APGAR?

Answer 21

Does NOT predict long-term outcome, but

Question 22

Why is lung inflation the key to cardiovascular transition?

Answer 22

• decreases PVR, increases PBF
• Increased PaO2 leads to constriction of ductus arteriosius
• Increased PBF increases left atrial volume and closes foramen ovale flap

Question 23

Abnormal cardiovascular transition = Persistent Pulmonary HTN of the Newborn (PPHN)

Answer 23

• PVR remains elevated (SVR fails to increase)
• Blood continues to flow R to L across foramen ovale
• Ductus remains open and blood bypasses the lungs

Result: insufficient pulmonary blood flow, severe hypoxemia

Problem: no placenta for gas exchange

Question 24

How will a PPHN baby look?

Answer 24

Pre-ductal blood = well oxygenated (R arm will be pink)

Post-ductal blood = mixed oxygenation (pale baby.. L arm sometimes will be included)

Question 25

3 main categories of PPHN

Answer 25

1. Abnormally constricted pulmonary vessels - reversible
2. Remodeled pulmonary vascular tree - not as easily reversible
3. Hypoplastic pulmonary vascular tree - not completely reversible

Question 26

Normal transitional vitals and exam signs

Answer 26

Respirations:

• Tachypnea for first hour
• Periodic breathing in first days
• Normal rate is 40-60

HR:

• 150-180 bpm, decreasing to 110-140 bpm within first hr of life
• HR may lower during sleep but should increase when touched

BP: 60-90/30-60 mmHg

Question 27

Glucose homeostasis

Answer 27

IDM: hypoglycemic because of mom’s insulin

IUGR: no fat/glycogen stores so hypoglycemia occurs

Premature: same as IUGR

Sign: Jittery!

Question 28

Diagnosis of neonatal hypoglycemia

Answer 28

Blood sugar