3. Atelectasis, Pulmonary Edema, ARDS - Cox

Cards (46)

  • **cardiogenic is most associated with bilateral pulmonary edema (bat wing on x-ray)
  • What disease?
    • diminished lung volume
    • imperfect expansion
    • alveolar collapse or incomplete expansion of alveoli 

    Atelectasis
  • Atelectasis will cause?
    1. decrease lung volume 2nd to collapse
    2. impair ventilation
    3. V/Q mismatch
    4. intrapulmonary R->L shunt (wasted perfusion)
  • Atelectasis cause what type of shunt?
    intrapulmonary R to L shunting - wasted perfusion
  • Atelectasis classification:
    • obstructive - resorptive
    • cicatrisation - scarring
    • passive - disrupted visceral-parietal pleura - extrapulmonary
    • compressive - mass effect - extra/intra pulmonary
    • adhesive - surfactant deficiency
  • Atelectasis will cause VQ mismatch?
    • alveolar collapse
    • perfusion without ventilation
    • intrapulmonary R to L blood shunting
  • what is the most common type of Atelectasis?
    Resorptive (AKA Obstructive) - complete airway obstruction
  • What is atelectasis?
    diminish lung volume
  • resorptive or obstructive - Atelectasis is due to?
    • occur from large to small airways
    • no alveoli airflow
    • residual alveolar air will be absorbed by blood causing alveolar collapse
  • What will resorptive (obstructive) Atelectasis eventually lead to?
    block will lead to no airflow causing residual air to be absorbed by blood causing alveolar collapse
    • no air pressure to maintain alveolar patency
  • Cicatrisation atelectasis (scarring) is a result of?
    1. parenchymal scarring
    2. reduced compliance
    3. decrease lung expansion
  • Classic example of Cicatrisation atelectasis (scarring) is? 

    tuberculosis - Granulomatous disease
  • Relaxation or passive atelectasis is due to?
    1. Extrapulmonary defect
    2. Loss of contact between parietal and visceral pleurae
    3. lung passively ‘relaxes
    4. Passive elastic lung recoil reduces lung volume
  • passive atelectasis from reduced motion altering pleural pressure
    1. Loss of pleural space negative pressure
    2. lung no longer held against chest wall
    3. lung “relax"
    4. Decrease volume
  • Compression atelectasis is?
    mechanical compression due to mass effect space occupying defect
  • Compression atelectasis - extrapulmonary
    • pleural effusion
    • hemothorax
    • pneumothorax
    • chest wall lesion
  • Compression atelectasis - intrapulmonary
    • space occupying lesion - like cancer and cystic disease
  • Adhesive atelectasis is due to?
    Surfactant deficiency
  • Adhesive atelectasis will cause
    • Global lung collapse
    • Massive VQ mismatch (perfusion without ventilation)
  • Adhesive atelectasis will cause in what disease?
    Neonatal Respiratory Distress Syndrome (NRDS)
  • Neonatal Respiratory Distress Syndrome (NRDS) is?
    • fluid filled alveoli - hyaline membranes
    • worsen condition will lead to leaked plasma protein and necrotic cellular debris
  • Neonatal Respiratory Distress Syndrome vs. ARDS?
    • NRDS - no inflammatory changes
  • Adhesive atelectasis pathogenesis
    1. decrease surfactant
    2. increase alveolar surface tension
    3. collapse
  • What can cause impair synthesis or loss of surfactant?
    • drug induced
    • premature - 24-37 weeks
    • c-section
  • How does c-section cause decrease in surfactant?
    1. decrease stress
    2. decrease cortisol
    3. decrease surfactant
  • surfactant synthesis increases with?
    thyroxine and cortisol
  • pulmonary edema - pathogenesis
    • elevated pulmonary capillary hydrostatic pressure
    • cardiogenic (congestive heart failure)
    • vascular endothelial cell or alveolar epithelial cell permeability increase
    • sepsis
    • oncotic pressure gradient decreases
    • hypoalbuminemia
    • lymphatic drainage impaired
    • physical obstruction lymph system
  • Stage 1 of pulmonary edema pathogenesis
    • elevated vessel pressure causing
    • distention and opening small pulmonary capillaries
    • gas exchange is not impaired
  • Stage 2 - pulmonary edema - pathogenesis
    • fluid and protein shift into lung interstitial space from pulmonary capillaries
    • initially fluid collects in compliant interstitial compartment
    • initial increase in lymphatic outflow --> overwhelm lymphatic drainage capacity
  • stage 2 - pulmonary edema what happens to gas exchange?
    compromise gas exchange causing mild hypoxemia
  • Stage 3 - pulmonary edema pathogenesis
    • fluid crosses alveolar epithelium into alveoli --> alveolar edema
    • impaired gas exchange --> decrease O2 saturation (hypoxemia)
    • VQ mismatch
  • Stage 4 - pulmonary edema pathogenesis
    • lung volume decreases --> decrease respiratory volumes
    • decrease compliance due to surfactant loss
    • severely impaired diffusing capacity --> R to L shunting (wasted perfusion)
  • pulmonary edema can cause impaired diffusing capacity?
    R to L shunting (wasting perfusion)
  • what can you see in chronic pulmonary edema?
    siderophage - hemosiderin-laden macrophages ("heart failure cells")
  • How does siderophage develop in pulmonary edema?
    1. chronic congestion causes thin walled alveolar capillaries to leak
    2. RBC are phagocytized by macrophages
    3. Heme degraded within macrophages
    4. intracellular hemosiderin deposits
  • Noncardiogenic pulmonary edema (NPE) is due to
    altered capillary permeability
  • Acute Respiratory Distress Syndrome (ARDS) can lead to?
    rapid progressive hypoxia
  • Acute respiratory distress syndrome (ARDS) is due to?
    alveolar/endothelial injury caused by direct pulmonary injury or systemic insults
  • Acute Respiratory Distress Syndrome (ARDS) - criteria
    • timing - acute: < 1 week or 12-48 hr after insult
    • acute severe hypoxemia - PaO2/FiO2: < 300 mmHg
    • bilateral infiltrates on CXR
  • ARDS is associated with diffuse alveolar damage (DAD)
    • manifested by injury to alveolar and endothelial cells
    • causing
    • pulmonary edema
    • hyaline membrane formation - composed of necrotic cells, surfactant and proteins