ARDS

Objectives
Definition

Etiology

Clinical Course

Pathophysiology

Pulmonary mechanics

Treatment / Ventilatory support

•Acute respiratory distress syndrome (ARDS) represents an acute lung injury
characterized by pulmonary edema and alveolar collapse secondary to the disruption
of the alveolar-capillary membrane and surfactant dysfunction.

•
•An alternative objective scoring system used in the clinical setting of ARDS is the
oxygenation index (OI)

•OI = Mean airway pressure x FiO2 / PaO2 x 100

• Paw is the mean airway pressure, FiO2 is the fraction of inspired oxygen, and PaO2
is the arterial oxygen tension
Risk Factors

Direct causes Indirect Causes

• Pneumonia • Sepsis
• Aspiration • Closed head injury
• Multiple trauma
• Chest trauma
• Transfusion reactions
• Smoke inhalation • Hemorrhagic shock.
Clinical Course
• Respiratory failure results in the failure of maintaining compensatory mechanism to
preserve gas exchange

• Tissue oxygen delivery can be impaired, resulting in anaerobic metabolism and lactic
acid formation

• Ventilation can be inadequate resulting in hypercapnia and worsening acidosis

• In patients with ARDS, impairment of oxygenation is an early finding, whereas

impairment of ventilation occurs much later in the disease process
Infants and young children are particularly prone to developing respiratory distress
and failure because of the following:

• Smaller caliber of airways resulting in a greater resistance to air flow

• Increased chest wall compliance, which can cause paradoxical breathing and restrict
lung capacitance as a result of chest wall retractions as may occur with forceful
inspiratory effort

• Greater propensity for rapid fatigue of the respiratory muscles and the diaphragm
Stages of ARDS

First stage – direct/Indirect Second stage-Latent period Third stage- ARF

Injury • Early signs of pulmonary injury • Rapid onset of respiratory failure
• mild tachypnea • Hyperventilation with hypocarbia • Hypoxemia refractory to
• Dyspnea • Respiratory alkalosis supplemental oxygen
• Normal radiographic findings • CXR – fine reticular pattern • Diffuse pulmonary edema
• Intrapulmonary shunting
• CXR :bilateral areas of
consolidation with air
bronchograms that reflect alveolar
filling and atelectasis
Insult ( direct /indirect)

Activation of inflammatory mediators( serotonin and histamine)

Damage to alveolar capillary membrane

Increased permeability of alveolar capillary membrane

Influx of protein rich edema fluid and inflammatory cells into air filled spaces,
dysfunction of surfactant and loss of lung tissue
Pathology/Pathophysiology
Exudative stage
• Development of diffuse injury to the alveolar-capillary membrane

• Influx of inflammatory cells and mediators destroy type I pneumocytes

• Sloughing of these cells and subsequent formation of a protein-rich hyaline membrane on

the denuded basement membrane

• Barrier dysfunction and formation of microthrombi within vasculature

• Disruption of both the epithelial and endothelial surfaces of the alveolar-capillary membrane
significantly increases permeability and results in flooding of the alveoli with proteinaceous
fluid.
Proliferative stage:

•Occurs after 1 to 3 weeks after initiation of injury

•Proliferation of type II pneumocytes to replace type I cells on the denuded basement membrane and
begin to replace surfactant
• Inflammatory cells continue to be recruited to phagocytose hyaline membrane
and debris
• Fibroblasts proliferate to convert hemorrhagic exudates into cellular granulation tissue

• The ability of the lung to recover depends on the presence of functional epithelium to clear the
alveolar fluid and the body’s ability to attenuate the inflammatory process

• If the lung injury and inflammation persists, it can progress to fibrotic stage
Fibrotic Stage :

• Presents as early as 5 to 7 days after the onset of disease

• Histologically- alveolar space becomes filled with mesenchymal cells, and lung
tissue is replaced by collagenous tissue

• Angiogenesis and obliteration of small precapillary vessels and an increase in the

medial thickness of intracinar pulmonary arteries

Reduces the available area for efficient gas exchange and it can progress to
respiratory failure, requiring prolonged mechanical ventilation.
Diagnosis
•Complete patient history

•On physical examination : abnormal breath sounds( crackles, B/L wheezing)

• ABG

•CXR

•Bronchoalveolar lavage

Other tests:

•Chest CT

•Echocardiogram
Pulmonary Mechanics

Hysteresis of P-V loop suggests that higher

tanspulmonary pressures are required during
inspiration than expiration.
-Lower inflection point. It reflects
the pressure point at which alveoli begin to open
and is
located above functional residual capacity
Recruitment maneuver were used with
appropriate PEEP to maintain the patency during
expiration
 Treatment/Ventilatory Support

Prone position
ventilation
Management of a patient with acute respiratory distress syndrome:

•Airway

•Breathing

•Circulation

The goal in the treatment of ARDS is to treat the underlying disease, achieve
adequate tissue oxygenation, and avoid complications
Positive End-Expiratory Pressure:

•PEEP helps maintain alveolar patency and restore functional residual capacity. Target
an arterial oxygen saturation (SaO2) of 85% or greater at an acceptable FiO2 of 0.60
or less

• A PEEP level of 10 to 15 cm H2O, or even higher, may be required to achieve

adequate oxygenation but increase in PEEP level can further increase intrathoracic
pressure and cause reduction in cardiac output( compensated by providing ionotropic
support)
Low Tidal Volume Ventilation

•The mortality rate was 31 % in the low tidal volume group and 39.8% (p $ 0.007) in
the higher tidal volume group

•Low tidal volume ventilation maintains the plateau pressure less than 26cmH2O
results in low lung injury
Gas Exchange Goals:

•Acceptable arterial oxygen saturation target remains controversial, ventilatory strategies

should aim to provide adequate tissue and organ oxygenation while minimizing oxygen
toxicity and ventilator-induced lung injury.

Permissive Hypercapnia:

•Reducing the tidal volume may decrease minute ventilation and result in hypercapnia.

•Respiratory acidosis with pH greater than approximately 7.20

• Not recommended for those patients with intracranial pathology

Adjunct Therapy
•Prone position: Improvement in ventilation /perfusion and chest mechanics

•Corticosteroids

• Inhaled nitric oxide

• Surfactant replacement therapy

•ECMO : Extra corporeal membrane oxygenation

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