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Physiologic Basis for the Management of Acute
Respiratory Disorders in the Newborn
Marc Collin, MD18 November 2003
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Developmental Anatomy
• Alveoli-developed by 25th week -increase in # until 8 yr. -from 20 to 300 million -surface area: 2.8 m2 @ birth 32 m2 @ 8 yr.
75 m2 @ adulthood -diameter: 150- 300 um(NB-Adult)
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Developmental Anatomy
• Airways- cartilaginous - relatively weak in infancy - dynamic compression - bronchiolitis (RSV)
- RAD - crying!
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Developmental Anatomy
– airways enlarge in diameter/length– distal airways lag in first 5 yr.– high peripheral resistance in infancy
– Resistance = 1/R4
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Pulmonary Physiology
• Compliance = Change in Volume Change in Pressure
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Static Lung Volumes
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Mechanics of Infant v. Adult Lung
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Pulmonary Physiology
• Alveoli at birth• fluid-filled v. air-filled v. air-liquid interface
• pressures up to 80 cm H2O @ birth
• alveolar rupture
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Pressure-Volume Curves after Air v. Liquid Lung Expansion
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Pulmonary Physiology
LaPlace relationship:
P = 2T/R
P= distending pressure
T= wall tension
R= radius (alveolar)
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Pressure-Volume Curves of First 3 Breaths
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Developmental Biochemistry of Alveoli
• History: Avery & Mead-1959 - RDS secondary to surfactant deficiency - Treatment: CPAP
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Surfactant
• Phospholipids - phosphatidylcholine
- phosphatidylglycerol
• Surfactant proteins - A, B, C
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Surfactant Components
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Surfactant
• Type II alveolar epithelial cells-responsible for synthesis,
storage, secretion, and reuptake
• Lamellar bodies -intracellular storage form of surfactant -secreted via exocytosis -forms tubular myelin in extracellular space
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Surfactant and Type II Cells
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Surfactant
• Inactivation by: - alveolar-capillary leak - pulmonary edema - hemorrhage (hemoglobin) - alveolar cell injury - meconium
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Surfactant
• Recycling - spent forms taken up/reused by Type II cells. - process facilitated by SP-A, B, and C - half-life = 3.5 days
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RDS
• US incidence: 30,000/yr.
• Inversely related to gestational age
• Onset-shortly after birth
• Signs-grunting, flaring,retracting
• Duration-1 week
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RDS
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RDS
• Progressive atelectasis
• V/Q mismatch
• Decreased FRC
• Impaired ventilation (weak respiratory m’s, compliant chest wall)
• Increased PVR due to hypoxia, acidosis
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RDS
• Right to left shunting leading to further hypoxemia
• Left to right shunting leading to pulmonary edema
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Exogenous Surfactants
• Replacement therapy/Fujiwara, Japan, 1980
• Human (from C/S)
• Artificial (Exosurf)
• Bovine (Survanta)
• Calf (Infasurf)
• Pig (Curosurf)
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Compliance Before and After Surfactant
Before surfactant
After surfactant
VOLUME
PRESSURE
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Air Leaks
• Pulmonary interstitial emphysema (PIE)
• Pneumomediastinum
• Pneumothorax
• Pneumopericardium
• Pneumoperitoneum
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Subtle left pneumothorax
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Left pneumothorax now more obvious
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Left pneumothorax?
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pneumothorax
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Transillumination of left pneumothorax
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pneumomediastinum
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Pneumopericardium (note air under heart)
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Air Leaks
• initiating factor: PIE (alveolar rupture into perivascular and peribronchial spaces)
• dissection into mediastinum
• further dissection into pleural, pericardial space
• rupture from surface blebs
• direct lung rupture-VERY rare
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Air Leak Risk Factors
• RDS: 12-26%
• MAS/other aspirations
• Spontaneous
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Air Leak Management
• early recognition (esp. in preterms)
• nitrogen wash-out (term/near-term)
• needle aspiration v. tube thoracotomy
• limit barotrauma
• HFOV
• positioning
• selective ET intubation
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Meconium Aspiration Syndrome (MAS)
• GI secretions, cellular debris, bile, pancreatic juice, mucus, lanugo hairs, vernix; blood.
• incidence: ~15% (30% @ >42 wks)
• cause v. result of ‘asphyxia’
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MAS
• Asphyxia intestinal ischemia
anal sphincter relaxation
meconium passage
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MAS
• Asphyxia fetal gasping
enhanced meconium entry into respiratory tract
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MAS-Presentation
• Respiratory distress
- tachypnea
- prolonged expiratory phase - hypoxemia
• Increased A-P diameter (‘barrel’ chest)
• Pulmonary hypertension
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MAS-Radiographic Findings
• coarse alveolar infiltrates
• consolidation/hyperaeration
• pleural effusion (30%)
• pneumothorax/pneumomediastinum
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Meconium aspiration syndrome
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Meconium aspiration syndrome
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MAS-Pathophysiology
• Acute small airway obstruction -increased expiratory resistance -increased FRC -regional atelectasis -V/Q mismatching
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MAS-Pathophysiology
• Surfactant inactivation -decreased compliance -hypoxia
• Pulmonary hypertension
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MAS-Treatment
• Intubation/tracheal suction @ delivery
• Saline lavage?
• Surfactant therapy
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MAS-Ventilatory Support
• CPAP/PEEP (be careful)
• Air leak due to ball-valve phenomenon
• Decreased I/E ratio (more E time)
• Hyperventilation (CMV)
• HFOV
• iNO
• ECMO
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Persistent Pulmonary Hypertension of the Newborn
(PPHN)
• Etiology: Primary v. Secondary
• Failure of transition from high to low PVR after birth
• PFO and PDA rightleft shunting
• Intrapulmonary shunting, esp. w/ pulmonary parenchymal disease
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PPHN
• PVR decreases secondary to:
• -mechanical distention of pulmonary vascular bed
• improved oxygenation of pulmonary vascular bed
• prostacyclin and NO production
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PPHN
• Remodeling of pulmonary vascular musculature
• Normally, fully muscularized preacinar arteries extend to terminal bronchiolar level.
• Muscularization begins to decrease w/in days, complete w/in months.
• Regression process delayed by hypoxia
• Chronic hypoxia stimulates further muscularization
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PPHN
• Differential Diagnosis:
- Primary (chronic hypoxia) - Parenchymal disease (MAS, pneumonia, RDS, hemorrhage) - Cyanotic heart disease (TGV, critical PS, HLHS, severe coarctation) - Pulmonary hypoplasia (Potter’s S., Oligohydramnios, CDH, CCAM)
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Congenital cystic adenomatoid malformation
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Congenital diaphragmatic hernia
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Thoracic hypoplasia
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Hypoplastic right lung
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Hypoplastic lungs
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PPHN-Treatment/Medical
• Intravascular volume
• Correct metabolic acidosis
• Pressors (be careful!)
• Sedation (for lability) v. paralysis
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PPHN-Treatment/Respiratory
• induction of respiratory alkalosis
• pressure support/barotrauma risk depending on etiology (compliance)
• very labile….SLOW wean (maintain relative HYPERoxia, if possible)
• iNO
• ECMO