Respiratory Adaptations at Birth

Question 1

PULMONARY DEVELOPMENT:
How does the Trachea form?

What’s the 1ST stage of its development? When does it take place? What occurs?

What’s the 2ND stage of its development? When does it take place? What occurs?
→ What occurs in Week 22?
→ What occurs in Week 24?

What’s the 3RD stage of its development? When does it take place? What occurs?
→ What causes Capillaries to form alongside?

What’s the 4TH stage of its development? When does it take place? What occurs?

Answer 1

• • Forms to the Right of the Gut tube (Foregut) - Joint by Oesophagotracheal ridge
  • Rotation of Gut tube moves Trachea Anterior to Gut tube
• PSEUDOGLANDULAR (5-16 weeks) - Branching up to Terminal Bronchioles
• CANALICULAR (17-26 weeks) - Division into Respiratory Bronchioles
  → Week 22 - Appearance of Type 1 and 2 Pneumocytes
  → Week 24 - Saccule development, Angiogenesis, Lamellar body formation (stores Pulmonary Surfactant)
• SACULLAR (27 - Term) - Division into Alveolar ducts, which then become Terminal sacs
  → VEGF
• ALVEOLAR (Post Term) - Mature Alveoli with a well-developed epithelial-endothelial association

Question 2

STRUCTURAL PATHOLOGY:
What’s the effect a pathology begins BEFORE 16 weeks?

What’s the effect if a pathology begins AFTER 16 weeks?

What pathologies can cause Extrinsic restriction of the lung?

What pathologies can cause Intrinsic restriction of the lung?

Answer 2

• Branching irreversibly affected; may lead to a PERMANENT REDUCTION in the number of Alveoli
• Reduction in number of Alveoli
• Congenital Diaphragmatic Hernia (CDH), Effusions, Thoracic/Vertebral abnormality
• Lung cysts, Malnutrition (Vit A deficiency), Smoking

Question 3

LUNG FLUID:
How much of it is in the lung at Mid-gestation compared to at Term?

How does its composition compare with Plasma?

What is its function?

Secretion:
What occurs here?

How does it signal growth?

Absorption:
What occurs here?
→ How does this change when Newborn is exposed to Oxygen?

How is affected during Labour and Delivery?

Pathology:
What is Oligohydramnios? What causes it?

What can cause Foetal Breathing Abnormalities?
Why’s it important for the Foetus to keep breathing?

What can happen when a baby is delivered with labour, for example in an Elective C-section?

Answer 3

• 4-6ml/kg Mid-gestation, 20ml/kg at Term
• Similar to Plasma, except it has Lower Protein and Bicarbonate, Higher K and Cl
• Lung growth, but not Branching

• Secondary active transport of Cl from Interstitium to lumen; Passive transport of Na and H2O
• Liquid production causes a Positive pressure of 1cmH2O

• Active transport of Na on luminal membranes
  → Increases Na transport
• Adrenaline is released = ↓Secretion and ↑Resorption

• ↓Amniotic Fluid - due to Early rupture of membranes, Kidney abnormalities
• Neuromuscular disorders, CDH
  → Foetal breathing slows lung fluid loss – Maintains expansion
• TTN (Transient Tachypnoea Newborn)

Question 4

PULMONARY SURFACTANT:
What produces it? Where’s it stored?

What’s the role of Alveolar cells with it?

What regulates its release?

What’s its function?

What does it produce when Compressed? What does this do?

What are its components?

What’s involved in the maturation of surfactants?

What pathologies can occur here?

Answer 4

• • Produced by Type 2 Pneumocytes
  • Stored in Lamellar Bodies
• Absorbed, Degraded and Recycled by Alveolar cells
• Negative feedback - β-receptors on Type 2 Pneumocytes (↑during gestation)
• • Reduces Breathing work - PREVENTS ATELECSTASIS (Lung collapse)
  • Forms a Solid monolayer to reduce Surface tension
• Tubular Myelin, which, when compressed, transforms from a Gel to a Liquid Crystal phase = ↓↓↓Surface tension (near 0)
• Phospholipids, Neutral lipids, Proteins (SP-A, SP-B, SP-C, SP-D)
  o 80% Phosphatidylcholine, 10% Phosphatidylglycerol
• • Glucocorticoids - ↑Surfactant production at end of gestation, Stimulates β2-receptor gene expression = ↑Surfactant production
  • THs - T4 increases surfactant production, T3 crosses placenta, TRH increases Phospholipids
  • Insulin - Delays maturation of Type 2 Pneumocytes, ↓Prostaglandin production
  o Hyperglycaemia delays lung maturation
• • Prematurity
  o Unstable monolayer, which buckles on expiration
  o Leaky capillary membranes lead to Fibrin deposition, Hyaline membrane formation and ↑Surface tension
  • Surfactant Protein Deficiencies
  o SP-B - Causes reduced Prostaglandin = no secretion of normal surfactant = RDS (Lethal)
  o SP-C - Interstitial Lung disease

Question 5

EVENTS AT BIRTH:
What changes occur in the lung?

What’s the function of the central chemoreceptor?

What does Hypoxia in a foetus lead to?

Where is the Respiratory centre located?

Why do Premature babies have Apnoea?

What breathing change is seen in a cold baby?
→ How is this treated?

What neurological adaptations occur to allow the baby to survive Labour and Delivery?
→ What type of respiration does it use more?
→ What’s its main energy source during that time?

Answer 5

• Cessation of Lung fluid production and Foetal breathing
  o Air replaces Lung fluid within minutes
  o Rapid fall in airway resistance
  o Slower increase in Compliance over 24 hours
• Detects hypoxia
• Redirection of blood flow to vital organs
• Ventrolateral brainstem
• They have an Underdeveloped Respiratory centre, so respond like a Foetus
• No initial hyperventilation
  → IV Caffeine
• Fewer synapses and Reduced oxygen requirements
  → Anaerobic respiration
  → KETONE BODIES