ARDS

1. ARDS

2. ARDS DEFINATION
 ARDS is characterized by the acute onset of hypoxemia
and bilateral pulmonary infiltrates consistent with
pulmonary edema but without evidence of left heart
failure
Characterized by:
• - diffuse alveolar
• - capillary wall injury
• - increased alveolar- capillary permeability
• - noncardiogenic pulmonary edema
• - hyaline membrane formation, and atelectasis

3. PATHOPHYSIOLOGY
 The physiologic reaction of all body tissues sometimes results in pathologic
changes in the lung
 A systemic insults causes low tissue perfusion and cellular hypoxia
 Consequently, peripheral tissues are deprived of essential nutrients, and
intracellular metabolic derangements result
 Certain chemical factors such as prostaglandins, clotting factors, lysosomal
enzymes, activated complement, or histamine are released into the
systemic circulation
 Prostaglandin contribute to vasodilation, capillary permeability, pain and fever,
which accompany cell injury
 Changes in the vessel walls and disturbances in blood flow increase platelet
function, causing adhesiveness and aggregation

4. PATHOPHYSIOLOGY CONTINU..
 Lysosomal enzymes from neutrophils increase vascular permeability
and cause tissue damage
 Histamine is released from platelets, mast cell, and basophils and
cause arterial vasodilation and enhanced permeability of capillaries
and venules
 Neutrophils and other inflammatory mediators can thus gain access
to the lung parenchyma and carry on the inflammatory process
 The inflammation then produces the lung injury,
 Severe ventilation-perfusion mismatching occurs
 Alveolar collapse of the inflammatory infiltrate, blood fluid and
surfactant dysfunction

5. PATHOPHYSIOLOGY CONTI..
 The lung compliance becomes markedly decreased (stiff lung)
 The blood returning to the lung for gas exchange is pumped
through the nonventilated, nonfunctioning areas of the lung,
causing a shunt to develop
 The blood interfacing with nonfunctioning alveoli and gas
exchange is markedly impaired, resulting in severe refractory
hypoxemia

6. REVISION OF DEFINITION 1988
Four-Point Lung Injury Score:
 Level of PEEP
 PaO2 / FiO2 ratio
 Static lung compliance
 Degree of chest infiltrates

7. INICIATING/PREDOSPOSING FACTORS
 Aspiration of (Gastric Secretion, drowning, hydrocarbons)
 Hematologic disorders (disseminated intravascular coagulopathy
(DIC) , Massive transfusion of blood products, cardiopulmonary
bypass
 Prolonged inhalation of high concentration of oxygen, smoke, or
corrosive substances, Toxic Gases and Fumes
 Systemic Sepsis
 Drugs and poisons
 Shock (any cause)

8. INICIATING/PREDOSPOSING FACTORS
 Localized infection (Bacterial, Fungal, Viral Pneumonias),
 Trauma (Pulmonary contusion, Multiple Fracture, Head injury)
 Major surgery
 Metabolic disorders (Pancreatitis, Uremia)
 Urosepsis,
 Amniotic fluid embolism
 Long bone fracture
 Fat or air embolism

9. ETIOLOGY
Examples of common causes of ARDS include:
 Breathing vomit into the lungs (aspiration)
 Inhaling toxic chemicals
 Pneumonia
 Septic shock or sepsis
 Trauma

10. PHASES OF ARDS
1. Acute, Exudative Phase
 Rapid onset of respiratory failure after trigger
 Diffuse alveolar damage with inflammatory cell
infiltration
 hyaline membrane formation
 Capillary injury
 Protein-rich edema fluid in alveoli
 Disruption of alveolar epithelium

11. PHASES OF ARDS CONT..
2. Subacute, Proliferative Phase:
 Persistent hypoxemia
 Development of hypercarbia
 Fibrosing alveolitis
 Further decrease in pulmonary compliance
 Pulmonary hypertension

12. PHASES OF ARDS CONTI…
3. RESOLUTION OR RECOVERY PHASE
 Recovery phase
 Gradual resolution of hypoxemia
 Improved lung compliance
 Resolution of radiographic abnormalities

13. CLINICAL FEATURES OF ARDS
The Earliest Clinical signs of ARDS include:
 Tachypnea and progressive hypoxemia
 Within 24 hours, the chest x-ray begins to Reveal
Bilateral Pulmonary infiltrates
 Progression to mechanical ventilation often occurs in
the first 48 hours of the illness

14. MANAGEMENT OF ARDS
 Treat the underlying Cause
 Maintaining Tissue Oxygenation
 Drug Therapy
 Lung Protective Strategies
 Reducing Lung Water
 Specific Therapies

15. Maintaining Tissue Oxygenation
 Safest FiO2
 Optimal PEEP
 Inverse Ratio Ventilation
 Early Prone Position
 ECMO

16. Drug Therapy
 Antibiothetics
 Steroids
 Gastrokinetics
 Thromboprophylaxis
 Sedatives
 Analgesics
 Neuromuscular block Agent
 Nutrition

17. Lung Protective Strategies
 Lung protective Ventilation
 Low Tidal volume and High RR (Baby Lung
Ventilation)
 Lung Mechanics Monitoring (Peak Pressure,
Plateau Pressure, Driving Pressure,)
 Lung Compliance
 Permissive Hypercapnia

18. Reducing Lung Water
 The two measures that are advocated for reducing lung water are diuretics and
PEEP
 Unfortunately , neither measure is likely to be effective in ARDS (Few Studies)
 The application of PEEP does not reduce extra vascular lung water in ARDS
 The use of diuretics to minimize or reduce fluid overload seems a more reasonable
measure, but only when renal water excretion is impaired (otherwise the best way
to prevent fluid overload is to maintain an adequate cardiac output)
 Positive End-Expiratory Pressure In fact, high levels of PEEP can actually
increase lung water (Right Heart failure)
 This latter effect may be the result of alveolar overdistension, or may be the result
of PEEP-induced impairment of lymphatic drainage from the lungs

19. Specific Therapies
1) Surfactant: Aerosolized surfactant has proven effective in improving outcomes in the
neonatal form of respiratory distress syndrome, but it has not met with similar
success in adults with ARDS (Anzueto 1996).
2) Antioxidant: Neutrophil-mediated tissue injury may play an important role in the
pathogenesis of ARDS, it is no surprise that there is conciderable interest in the
possible role of antioxidants as a specific therapy for ARDS
3) Nitric oxide: Nitric Oxide can improve oxygenation and reduce pulmonary artery
pressures in ARDS, mortality is unchanged (Lunn 1995)
• Nitric oxide is a pulmonary vasodilator, which inhaled crosses the alveolar membrane
and acts locally on the pulmonary vasculature, dilating vessels and increasing blood
flow

20. Specific Therapies
4. Prone Position: Study shows that prone positioning significantly
improves oxygenation in about 65 of patients. This help in reduce the
percentage of inspired oxygen and positive end-expiratory pressure.
Prone therapy assists pts with ARDS by reducing the
ventilationperfusion mismatch
5. ECMO

21. SUMMARY
 ARDS Definition
 SIGN AND SYMPTOMS
 AIM OF MANAGEMENT
 OPTIMAL TISSUE OXYGENATION (At lowest possible FiO2 and Optimal Peep, Inverse Ration
Ventilation and Prone Position)
 LUNG PROTECTIVE VENTILATION (ARDs.net)
 Low Tidal and High RR
 Optimal PEEP
 Peak Pressure <45
 Plateau Pressure <30
 Driving Pressure < 15
 Permissive hypercapnia
 Ph >7.15
 PO2 > 55mmhg
 ECMO

22. THANK YOU