Adaptation to Extrauterine Life Flashcards
What are four critical aspects or consequences of pulmonary adaptation?
Lung growth and development
Physiologic maturation
Respiratory drive
Relationship of lung inflation to cardiovascular transition
What are the phases of lung development?
Canalicular phase (17-27 weeks) Type II cells begin to differentiate, capillary network begins
Saccular phase (26-36 weeks) Thinning of interstitial space and association of endothelial and type I cells
Alveolar phase (36 weeks - 3 years) Presence of true alveoli
What are the three aspects of physiologic maturation?
Surfactant generation
Functional residual capacity
Lung fluid absorption
What is surfactant and where is it made?
Surfactant is a phospholipid-protein complex (90% lipid, 10% protein) which lowers surface tension and prevents alveolar collapse at end expiration. Also decreases work of breathing (improves compliance, DV/DP) and aids host defense.
Made in Type II alveolar cells, stored as lamellar bodies, and secreted as tubular myelin into the alveolar space
Molecules line up in the presence of surfactant proteins and phospholipids into a monolayer-multilayer film along the liquid-air interface
How does surfactant function and what is its overall physiologic action?
The surfactant molecules have a hydrophilic head and a hydrophobic tail which extends into the air space. When the air space collapses, the tails are densely packed, leading to mutual repulsion, opposing collapse.
Surfactant lowers the opening pressure, increases the maximal lung gas volume, and maintains gas volume on deflation (FRC- functional reserve capacity)
What is the term for surfactant deficiency?
Hyaline membrane disease
What is the importance of functional reserve capacity?
FRC leads to optimal compliance (compliance = ΔV/ΔP) in the lung. High or low FRC leads to diminished compliance (S-shaped compliance curve).
What are signs of surfactant deficiency/hyaline membrane disease?
Premature, or delayed maturity (e.g. Infant of Diabetic Mother)
Increased work of breathing
- Retractions (often marked due to soft chest wall)
- Grunting, flaring
Cyanosis in room air
Chest XR with diffuse microatelectasis (very poorly aerated)
- Reticulogranular pattern
- Air bronchograms
What is the treatment for HMD?
Oxygen
Improve lung inflation, establish FRC
- Continuous positive airway pressure (nasal CPAP)
- Intubation and mechanical ventilation
- Surfactant replacement
How is lung fluid absorbed?
Fluid is produced by the lung, egresses from trachea, forms amniotic fluid
Fluid is secreted by lung epithelial cells, driven by active Cl- secretion
At birth, reabsorption depends on Na+ absorption
Influence of Maturity:
- Presence and activity of amiloride-sensitive selective epithelial Na channels (ENaC) increase in late gestation, probably due to increased fetal production of cortisol
- Can be induced by exogenous glucocorticoids, and somewhat by catecholamines (stress of labor)
Labor: Increased transpulmonary pressure
- Uterine contractions squeeze fluid out at a greater rate than it is produced
- If no labor, more fluid remains to be removed after birth (e.g. elective C/S)
What is the pathophysiology of Transient Tachypnea of the Newborn?
Fluid moves from the air space to the interstitium quickly, then can take hours to be absorbed by vasculature and lymph. If air spaces are not maintained well-inflated, fluid can re-enter air spaces.
Result is respiratory distress: Retained fetal lung fluid, or Transient Tachypnea of the Newborn (TTN), may be brought on by:
- Rapid labor, no labor (elective C/S),
- maternal b-blockers (at least in theory)
- Ineffective initial lung inflations (premature, poor muscle tone, overly compliant chest wall)
What are the differences between fetal and neonatal breathing?
Fetal “breathing” is inconsistent, shallow, with no net movement of fluid in. Fetal gasping occurs with asphyxia, can result in movement of liquid into the fetal lung before birth (Example: Meconium aspiration)
At birth, onset of regular, consistent respirations due to:
- Sensory stimulation: cold, touch, light, noise
- Mild asphyxia and hypercarbia of normal labor
Three causes of failure to breath
Primary apnea
- Stimulation (drying, rubbing) easily initiates cry
Secondary apnea
- Requires rescue with positive pressure ventilation to establish lung inflation and begin regular respirations
Neuromuscular Impairment
- Hypotonia can be a reason not to breathe as well as a consequence of asphyxia (not breathing)
- Maternal sedation, analgesia, MgSO4 during labor
- Primary neuromuscular problems in newborn: such as myotonic dystrophy, congenital myopathies, spinal cord injury, spinal muscular atrophy
What is the difference between primary and secondary apnea?
Primary Apnea
- HR and BP relatively maintained
- Stimulation effective
- Followed by gasping for several minutes, HR and BP gradually decline
Secondary (terminal) Apnea
- HR and BP fall quickly
- Requires positive pressure ventilation to resolve
At birth, we assume it’s secondary apnea, and intervene quickly
What is the APGAR score and how is it assessed and used? (Not the specific criteria)
Rapid description of newborn condition at birth and response to resuscitation
0-2 points assigned for each of 5 categories: maximum 10, minimum 0 (dead)
Assigned at 1 and 5 minutes, then every 5 minutes until 20 min, or score is 7 or more
NOT used to determine need for resuscitation
Score does NOT predict long-term outcome, but score less than 3 at 10-15 minutes or more does correlate with increased population risk for poor outcome
Does not diagnose asphyxia (that is a biochemical diagnosis)
If score remains 0 at 10 minutes, may indicate time to stop
