Physiologic Adaptation to Extrauterine Life Flashcards
Factors of Pulmonary Adaptation
- Lung growth and development
- Physiologic maturation (surfactant, lung fluid absorption, importance of functional residual capacity)
- Respiratory drive
- Importance of lung inflation to cardiovascular transition
Canalicular Phase
- 17-27 weeks
- Delineation of pulmonary acinus
- Type II cells begin to differentiate, capillary network begins
Saccular Phase
- 26-36 weeks
- Thinning of interstitial space, closer association of endothelial and Type I cells
Alveolar Phase
- 36 wk to 3 yrs
- Presence of true alveoli
- Lengthening and sprouting of capillary network
Limit of viability of a fetus
approx 22-24 weeks, dev of acinus
Role of surfactant
- Lowers surface tension
- Prevents alveolar collapse at end expiration
- Decreases work of breathing and improves compliance
- Aids host defense
Where is surfactant made, stored and secreted?
Made in Type II alveolar cells
Stored as lamellar bodies
Secreted as tubular myelin into the alveolar space
What mechanism prevents collapse of alveoli?
The surfactant has a hydrophilic head and hydrophobic tail, which when closely packed cause mutual repulsion and opposes collapse
> 20 cm H20 opening pressure
Surfactant-deficient lungs; collapse to empty at end of expiration
Importance of FRC
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.
Hyaline Membrane Disease (HMD)
- 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
Treatment of surfactant deficiency
- Oxygen
- CPAP
- Intubation and mechanical ventilation
- Surfactant replacement
Which cell type secretes fluid from lung?
Epithelial cells, driven by active Cl- secretion
Absorption driven by Na+ absorption
Factors clearing fetal lung fluid
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
What happens to babies from elective repeat C-section
More likely to get respiratory distress because they have more lung fluid at birth.
Transient tachypnea of the newborn (TTN)
- 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
Types of failure to breathe
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
What happens when a fetus asphyxiates? What risk is there with this?
The fetus will gasp, which can move liquid into the fetal lung. This can sometimes cause meconium aspiration.
Distinguish fetal apnea how?
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!
APGAR measured when?
Assigned at 1 and 5 minutes, and then every 5 minutes until 20 min or the score > 7
Predictive value of APGAR?
Does NOT predict long-term outcome, but
Why is lung inflation the key to cardiovascular transition?
- decreases PVR, increases PBF
- Increased PaO2 leads to constriction of ductus arteriosius
- Increased PBF increases left atrial volume and closes foramen ovale flap
Abnormal cardiovascular transition = Persistent Pulmonary HTN of the Newborn (PPHN)
- 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
How will a PPHN baby look?
Pre-ductal blood = well oxygenated (R arm will be pink)
Post-ductal blood = mixed oxygenation (pale baby.. L arm sometimes will be included)
3 main categories of PPHN
- Abnormally constricted pulmonary vessels - reversible
- Remodeled pulmonary vascular tree - not as easily reversible
- Hypoplastic pulmonary vascular tree - not completely reversible
Normal transitional vitals and exam signs
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
Glucose homeostasis
IDM: hypoglycemic because of mom’s insulin
IUGR: no fat/glycogen stores so hypoglycemia occurs
Premature: same as IUGR
Sign: Jittery!
Diagnosis of neonatal hypoglycemia
Blood sugar
