11: Pulmonary Edema & ARDS

Question 1

Define pulmonary edema

Answer 1

increase in amount of **extravascular lung water (EVLW) **(interstitium and alveolar space).

Question 2

Cause of pulmonary edema

Answer 2

Most often due to osmosis of fluid from lumen of pulmonary capillary. Rarely due to lymphatic obstruction.

Question 3

Starling Equation

Answer 3

Flow = K_f (ΔP - Δπ)

K<sub>f</sub> = membrane characteristics
ΔP = hydrostatic pressure gradient
Δπ = oncotic pressure gradient

Question 4

Ways to ↑EVLW

Answer 4

↑pulmonary capillary pressure: “hydrostatic” pulmonary edema

↑permeability of alveolar capillary membrane: “permeability” pulmonary edema

Question 5

Pulmonary edema of unclear mechanistic cause

Answer 5

• Upper airway obstruction (negative pressure) pulmonary edema
• High-altitude pulmonary edema
• Neurogenic pulmonary edema
• Re-expansion pulmonary edema
• Pulmonary embolism

Question 6

Causes of hydrostatic pulmonary edema

Answer 6

• ↑LA pressure
  
  • LV dysfunction
  • Mitral dz
  • Volume overload
• Pulmonary venous HTN

Question 7

Causes of permeability pulmonary edema

Answer 7

• Direct lung insult
  
  • Pneumonia
  • Aspiration
  • Trauma
• Indirect lung insult
  
  • Sepsis
  • Trauma (non-pulmonary)

ALL CAUSE ARDS

Question 8

Clinical (“Berlin”) definition of ARDS

Answer 8

• Acute onset (< 7 days, most within 72 hours)
• Bilateral pulmonary infiltrates on CXR or CT consistent with PA
• No alternative explanation (e.g., heart failure)
• Moderate to severe gas exchange impairment while receiving mechanical ventilation with a PEEP > or = 5cm H2O:

(PaO2 / FiO2) < 300

Question 9

ARDS Severity Grading

Answer 9

• Mild: PaO2:FiO2 ratio < 300
• Moderate: PaO2:FiO2 ratio < 200
• Severe: PaO2:FiO2 ratio < 100

Question 10

ARDS risk factors

Answer 10

• EtOH abuse
• Poor nutritional status
• Advanced age
• Obesity
• Cirrhosis

Question 11

ARDS pathophysiology

Answer 11

• Alveolar flooding: ↑permeability alveolar-capillary barrier, endothelia & epithelial injury, surfactant depletion
• Inflammatory injury: TNFalpha, IL1, IL6
• Coagulation abnormalities

Question 12

ARDS clinical course

Answer 12

• Exudative stage:
  
  • ​Refractory hypoxemia
  • Intrapulmonary shunt
  • ↓compliance
  • Edema & hyaline membranes
• Proliferative stage:
  
  • ↑dead space & V_E
  • Pulmonary HTN
  • Type II pneumocyte hyperplasia
• Resolution:
  
  • Fibrin deposition & fibroblast proliferation

Question 13

ARDS gross pathology

Answer 13

Diffuse alveolar damage; firm and airless, heavy and “beefy”

Question 14

ARDS histopathology

Answer 14

• Diffuse alveolar damage stages:
  
  • Earliest/exudative: edema + hyaline membranes (mixtures of cellular debris and fibrin; peak at 2-3 days)
  • Fibroproliferative: type II pneumocyte hyperplasia
  • Organization/fibroproliferative: interstitium with fibroblastic proliferation

Question 15

Management of ARDS

Answer 15

• Treat underlying cause
• Low tidal volume venilation
  
  • Otherwise risk ventilator-associated lung injury (VALI)
  • Administer lung protective ventilation: 6cc/kg body weight
• PEEP (improve gas exchange)
• Fluid management (keep dry)
• Salvage ventilatory strategies for severe ARDS
  
  • **Extracorporeal Membrane Oxygenation (ECMO) **- “heart-lung machine”

Question 16

Cause of death with ARDS

Answer 16

• Early ARDS: underlying illness/injury
• Late ARDS: multi-organ failure

Small % die from hypoxemia

Question 17

Other complications of ARDS

Answer 17

• Barotrauma (pop lung –> subQ emphysema)
• Nosocomial infx
• DVT
• ICU-acquired weakness
• Poor nutrition
• Catheter-related infx
• GI bleeding (stress ulceration)
• Long-term:
  
  • Neurocog deficits
  • Neuropsych changes
  • Neuromusc weakness
  • ↓QOL