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Physiologic Basis for the Management of Acute Respiratory Disorders in the Newborn. Marc Collin, MD. 18 November 2003. Developmental Anatomy.

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physiologic basis for the management of acute respiratory disorders in the newborn

Physiologic Basis for the Management of Acute Respiratory Disorders in the Newborn

Marc Collin, MD

18 November 2003

developmental anatomy
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)
developmental anatomy1
Developmental Anatomy
  • Airways- cartilaginous - relatively weak in infancy - dynamic compression - bronchiolitis (RSV) - RAD - crying!
developmental anatomy2
Developmental Anatomy
  • airways enlarge in diameter/length
  • distal airways lag in first 5 yr.
  • high peripheral resistance in infancy
  • Resistance = 1/R4
pulmonary physiology
Pulmonary Physiology
  • Compliance = Change in Volume Change in Pressure
pulmonary physiology1
Pulmonary Physiology
  • Alveoli at birth
      • fluid-filled v. air-filled v. air-liquid interface
      • pressures up to 80 cm H2O @ birth
      • alveolar rupture
pulmonary physiology2

Pulmonary Physiology

 LaPlace relationship:

P = 2T/R

P= distending pressure

T= wall tension

R= radius (alveolar)

developmental biochemistry of alveoli
Developmental Biochemistry of Alveoli
  • History: Avery & Mead-1959 - RDS secondary to surfactant deficiency - Treatment: CPAP
surfactant
Surfactant
  • Phospholipids - phosphatidylcholine - phosphatidylglycerol
  • Surfactant proteins - A, B, C
surfactant1
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
surfactant2
Surfactant
  • Inactivation by: - alveolar-capillary leak - pulmonary edema - hemorrhage (hemoglobin) - alveolar cell injury - meconium
surfactant3
Surfactant
  • Recycling - spent forms taken up/reused by Type II cells. - process facilitated by SP-A, B, and C - half-life = 3.5 days
slide22
RDS
  • US incidence: 30,000/yr.
  • Inversely related to gestational age
  • Onset-shortly after birth
  • Signs-grunting, flaring,retracting
  • Duration-1 week
slide24
RDS
  • Progressive atelectasis
  • V/Q mismatch
  • Decreased FRC
  • Impaired ventilation (weak respiratory m’s, compliant chest wall)
  • Increased PVR due to hypoxia, acidosis
slide25
RDS
  • Right to left shunting leading to further hypoxemia
  • Left to right shunting leading to pulmonary edema
exogenous surfactants
Exogenous Surfactants
  • Replacement therapy/Fujiwara, Japan, 1980
  • Human (from C/S)
  • Artificial (Exosurf)
  • Bovine (Survanta)
  • Calf (Infasurf)
  • Pig (Curosurf)
compliance before and after surfactant
Compliance Before and After Surfactant

VOLUME

Before surfactant

After surfactant

PRESSURE

air leaks
Air Leaks
  • Pulmonary interstitial emphysema (PIE)
  • Pneumomediastinum
  • Pneumothorax
  • Pneumopericardium
  • Pneumoperitoneum
air leaks1
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
air leak risk factors
Air Leak Risk Factors
  • RDS: 12-26%
  • MAS/other aspirations
  • Spontaneous
air leak management
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
meconium aspiration syndrome mas
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’
slide42
MAS
  • Asphyxia

 intestinal ischemia

 anal sphincter relaxation

 meconium passage

slide43
MAS
  • Asphyxia

 fetal gasping

 enhanced meconium entry into respiratory tract

mas presentation
MAS-Presentation
  • Respiratory distress

- tachypnea

- prolonged expiratory phase - hypoxemia

  • Increased A-P diameter (‘barrel’ chest)
  • Pulmonary hypertension
mas radiographic findings
MAS-Radiographic Findings
  • coarse alveolar infiltrates
  • consolidation/hyperaeration
  • pleural effusion (30%)
  • pneumothorax/pneumomediastinum
mas pathophysiology
MAS-Pathophysiology
  • Acute small airway obstruction -increased expiratory resistance -increased FRC -regional atelectasis -V/Q mismatching
mas pathophysiology1
MAS-Pathophysiology
  • Surfactant inactivation -decreased compliance -hypoxia
  • Pulmonary hypertension
mas treatment
MAS-Treatment
  • Intubation/tracheal suction @ delivery
  • Saline lavage?
  • Surfactant therapy
mas ventilatory support
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
persistent pulmonary hypertension of the newborn pphn
Persistent Pulmonary Hypertension of the Newborn (PPHN)
  • Etiology: Primary v. Secondary
  • Failure of transition from high to low PVR after birth
  • PFO and PDA rightleft shunting
  • Intrapulmonary shunting, esp. w/ pulmonary parenchymal disease
slide53
PPHN
  • PVR decreases secondary to:
  • -mechanical distention of pulmonary vascular bed
  • improved oxygenation of pulmonary vascular bed
  • prostacyclin and NO production
slide54
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
slide55
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)

pphn treatment medical
PPHN-Treatment/Medical
  • Intravascular volume
  • Correct metabolic acidosis
  • Pressors (be careful!)
  • Sedation (for lability) v. paralysis
pphn treatment respiratory
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