Pulmonology

Question 1

Describe the classical phases of ARDS pathogenesis

Answer 1

1. Injury
2. Exudative – alveolar capillary membrane disruption with inflammatory cell infiltrate and high protein exudate to form hyaline membranes
3. Proliferative – proliferation of abnormal Type II alveoli cells and inflammatory cells
4. Fibrotic – infiltration with fibroblasts which replace alveoli and alveolar ducts with fibrosis
5. Resolution – slow and incomplete repair and restoration of architecture

Source

Question 2

List conditions which commonly predispose to ARDS

Answer 2

• Direct
  
  • pneumonia (46%)
  • aspiration of gastric contents (29%)
  • lung contusion (34%)
  • fat embolism
  • near drowning
  • inhalational injury
  • reperfusion injury
• Indirect
  
  • non-pulmonary sepsis (25%)
  • multiple trauma (41%)
  • massive transfusion (34%)
  • pancreatitits (25%)
  • cardiopulmonary bypass

Question 3

What is the Berlin Definition of ARDS

Answer 3

1. acute (<1 week)
2. bilateral opacities consistent with pulmonary edema must be present (on plain x ray or CT)
3. PaO₂/FiO₂ ratio <300mmHg (minimum of 5 cmH₂0 PEEP)
4. must not be fully explained by cardiac failure or fluid overload, in the physician’s best estimation using available information — an “objective assessment“ (e.g. echocardiogram) should be performed in most cases if there is no clear cause such as trauma or sepsis

Source: doi:10.1001/jama.2012.5669

Question 4

What is the mortality of ARDS based on severity of PF ratio?

Answer 4

• Mild (200-300)
  
  • 27%
• Moderate (100-200)
  
  • 32%
• Severe (<100)
  
  • 45%

Question 5

Describe the clinical effects of ARDS

Answer 5

1. Hypoxaemia
   
   • V/Q mismatch
   • impaired hypoxic pulmonary vasoconstriction
2. Reduced ventillatory capacity (due to increased alveolar dead space)
3. Decreased compliance
   
   • increased dependent densities (surfactant dysfunction)
   • collapse/consolidation
4. Pulmonary hypertension
   
   • vasoconstriction
   • microthrombi
   • fibrosis
   • PEEP

Source

Question 6

Management approach to ARDS

Answer 6

1. Diagnose and treat cause
2. Protective lung ventillation
   
   • PaO2 55-80 or SaO2 88-95%
   • P_plat ≤ 30
   • pH 7.30-7.45
   • I:E ≤ 1
3. Strategies for refractory hypoxia
   
   • prone posture (severe ARDS)
   • recruitment manouvres (controversial)
   • inhaled NO
   • inhaled prostacycline
   • ECMO

Question 7

What is the positive predictive value of generally accepted ARDS criteria?

Answer 7

50%

Source: de Hemptinne, et al. (2009)

Question 8

What is the rationale for protective lung ventillation in ARDS?

Answer 8

• low tidal volume ventilation reduces ventilator-associated lung injury (VALI)
  
  • volutrauma (hyperinflation and shearing injury)
  • barotrauma (alveolar rupture and pneumothorax)
  • biotrauma (release of inflammatory mediators)
• hypercapnia may also have directly beneficial effects in ARDS
• clear evidence for benefit in ARDS in animals and humans

Question 9

What are the four targets for the ARDSnet lung protective ventillation strategy?

Answer 9

1. Tidal volume 6mL/kg (predicted body weight)
2. Plateau pressure ≤ 30mmH₂O
3. pH 7.3 to 7.45 (permissive hypercapnia)
4. I:E ratio ≤ 1

Source

Question 10

What are the three pathophysiological processes in ventillator-associated lung injury (VALI)?

Answer 10

1. volutrauma (hyperinflation and shearing injury)
2. barotrauma (alveolar rupture and sequelae)
3. biotrauma (release of inflammatory mediators)

Question 11

Causes of pulmonary fibrosis

Answer 11

Upper lobe:

• Silicosis/ Sarcoidosis
• Coal worker pneumonconiosis
• Ankylosing spondylitis
• Radiation

Lower lobe:

• Systemic sclerosis
• Cyptogenic fibrosing alveolitis
• Asbetosis
• Rheumatoid arthritis

Source