1. ARDS
Atef Kamel

2. Outline
 Define ARDS and describe the pathological
process
 Know causes of ARDS, and differential diagnosis
 Understand specific challenges in mechanical
ventilation of patients with ARDS
 Understand treatment strategies and evidence
behind

3. ARDS
Severe lung injury characterized by non-
cardiogenic pulmonary
edema, decreased lung
compliance, refractory hypoxemia
Definition
 Acute onset (<2 weeks)
 Bilateral infiltrates on chest x ray
 PCWP ≤18mmHg
 Acute lung injury if PaO2/FiO2 ≤300
 ARDS if PaO2/FiO2 ≤200

4. Most common causes ARDS
Pneumonia (34%)
Sepsis (27%)
Aspiration (15%)
Trauma (11%)
 Pulmonary contusion
 Multiple fractures

5. Causes cont.

6. Risk factors for ARDS
 Preexisting lung disease
 Chronic alcohol use
 Low serum pH
 Sepsis
40% of patients with sepsis
develop ARDS

7. Differential diagnosis
Pulmonary edema from left heart failure
Diffuse alveolar hemorrhage
Lupus pneumonitis
Drug-induced pulmonary edema and
pneumonitis
Acute major pulmonary embolus
Sarcoidosis
Interstitial pulmonary fibrosis

8. Excluding other diagnoses
 Echo
 Central venous catheter
 Bronchoscopy with bronchoalveolar
lavage (to evaluate for
hemorrhage, etc)
 Chest CT

9. Pathogenesis

10. Pathophysiology
 Diffuse alveolar damage
 Lung capillary damage
 Inflammation/pulm edema
 Resulting severe hypoxemia and decreased
lung compliance

11. Phases of ARDS
 Acute - exudative, inflammatory
(0 - 3 days)
 Subacute - proliferative
(4 - 10 days)
 Chronic - fibrosing alveolitis
( > 10 days)

12. Phases of ARDS

13. Exudative phase (Acute Phase)
 Alveolar-capillary barrier is formed by
microvascular endothelium and alveolar
epithelium
 Under normal conditions epithelial barrier is
much less permeable than endothelium
 Epithelium is made up of type I and II cells
 Type I cells are injured easily and Type II cells
are more resistant

14. Exudative Phase
In ALI/ARDS – damage to either one
occurs resulting in increased permeability
of the barrier
influx of protein-rich edema fluid into the
alveolar space
Injury of Type I cells results loss of
epithelial integrity and fluid extravasation
(edema)
Injury of Type II cells then impairs the
removal of the edema fluid (loss of
surfactant)

15. Exudative Phase

16. Proliferative Phase
 With intervention (mechanical ventilation)
there is clearance of alveolar fluid
 Soluble proteins are removed by diffusion
between alveolar epithelial cells
 Insoluble proteins are removed by
endocytosis and transcytosis through
epithelial cells and phagocytosis through
macrophages

17. Proliferative Phase
 Type II cells begin to differentiate into Type I
cells and reepithelialize denuded alveolar
epithelium
 Further epithelialization leads to increased
alveolar clearance

18. Proliferative phase

19. ARDS - Outcomes
Most studies - mortality 40% to 60%;
similar for children/adults
Death is usually due to sepsis/MODS
rather than primary respiratory

20. Management of ARDS
Treat underlying illness
 Sepsis, etc
Nutrition
Supportive care
DVT prophylaxis
GI prophylaxis
Medications

21. Fluid management
“Dry lungs are happy lungs”
Conservative fluids:
 Improved oxygenation
 More ventilator-free days
 More days outside ICU
 No increase in shock or dialysis
 No mortality effects

22. Pulmonary support
KEYS
 Low tidal volumes – 6-8mL/kg ideal
body weight
 Maintain plateau (end-inspiratory)
pressures <30cm H20
 Permissive hypercapnia and
acidosis
Decreased mortality by 22%

23. Positive End-Expiratory Pressure
(PEEP)
Titrate PEEP to decrease FiO2
 Goal sat 88% with FiO2 <60%
Minimize oxygen toxicity
 PEEP can improve lung recruitment and
decrease end-expiratory alveolar
collapse (and therefore right-to-left
shunt)
 Can also decrease venous return, cause
hemodynamic compromise, worsen
pulmonary edema

24. Other Ideas in Ventilator
Management
 Prone positioning
 May be beneficial in certain subgroup, but
complications including pressure sores
 RCT of 304 patients showed no mortality benefit
 High-frequency oscillatory ventilation
 In RCT, improved oxygenation initially, but
results not sustained after 24 hours, no
mortality benefit
 ECMO
 RCT of 40 adults showed no benefit

25. Complications of mechanical
ventilation
Mechanical ventilation causes:
 Overdistention of lungs (volutrauma)
 Further damaging epithelium
 Increased fluid leak, indistinguishable from
ARDS damage
 Barotrauma
 Rupture alveolar membranes
 Pneuomothorax, pneumomediastinum
 Sheer stress
 Opening/closing alveoli
 Inflammatory reaction, cytokine release
Oxygen toxicity
 Free radical formation

26. Drug therapy
 Agents studied:
 Corticosteroids
 Ketoconazole
 Inhaled nitric oxide
 Surfactant
 No benefit demonstrated