4. RISK OF ARDS:
Increases in a patient with multiple predisposing clinical conditions
25% in patients with severe trauma, which increases to 56% if there is
associated sepsis
Other risk factors:
Alcohol-abuse disorder
Cigarette smoking
Obesity
5.
6.
7.
8. EXUDATIVE PHASE
Effects on lung function:
“Stiff lungs” → reduced lung compliance
Reduced diffusing capacity, shortness of breath, and hypoxemia
Intrapulmonary shunting results from alveolar microvascular occlusion.
Reduction of pulmonary arterial blood flow to the ventilated portions of the lung
Pulmonary dead space is increased, ultimately leading to hypercapnia in addition
to hypoxemia
9.
10. DIFFUSE ALVEOLAR DAMAGE WITH HYALINE MEMBRANES LINING THE ALVEOLAR SURFACES
(ARROW) CONSISTENT WITH ARDS.
11.
12. Severe oedema formation
Severe disruption of tight
junctions
Epithelial necrosis
Hyaline membrane formation
Absent sodium and chlorine
transport
Glycocalyx shedding
Increased chemokines and
adhesion molecules
RBCs in airspace
13. HOW THE CELLULAR AND MOLECULAR MECHANISMS OF ACUTE RESPIRATORY DISTRESS
SYNDROME LEAD TO THE CHARACTERISTIC PHYSIOLOGICAL AND CLINICAL FINDINGS
Physiological manifestation Clinical findings
Alveolar–capillary barrier injury with
interstitial and alveolar oedema
formation
Decreased lung compliance Increased work of breathing
Diffuse alveolar filling Ventilation perfusion mismatch and
shunt
Severe hypoxaemia with diffuse
bilateral radiographic opacities
Surfactant inactivation and
decreased production
End-expiratory alveolar collapse Favourable response to positive
end-expiratory pressure
Platelet and endothelial activation
with lung microvascular thrombosis,
and obstruction or destruction of the
lung vascular bed
Increased dead space ventilation
and pulmonary arterial hypertension
High minute ventilation,
hypercarbia, right heart failure
Leak of lung inflammatory
mediators into systemic circulation
Systemic inflammatory response
syndrome
Multi-organ dysfunction
15. DIAGNOSIS
Acute onset (within 1 week)
Diffuse bilateral infiltrates on chest X-ray
No evidence of left heart failure or fluid overload
Partial pressure of O2/fraction of inspired O2 (PaO2/FiO2) < 300 mm Hg:
Mild ARDS: 201–300 mm Hg
Moderate ARDS: 101–200 mm Hg
Severe ARDS: ≤ 100 mm Hg
Berlin diagnostic criteria of ARDS
16. LABORATORY TESTS
BNP levels < 100 pg/mL favors ARDS (higher levels neither confirm heart failure nor exclude ARDS).
Arterial blood gas (ABG):
Hypoxemia
Acute respiratory alkalosis
Alveolar-arterial (A-a) gradient widening:
A-a gradient measures the difference between alveolar oxygen concentration and arterial oxygen.
Calculated using the following factors: age, atmospheric pressure, FiO₂, arterial O₂ and CO₂ in blood gas
18. CT SCAN:
Not necessary, but gives more pulmonary details
ARDS: widespread patchy airspace opacities that
are more apparent in the dependent lung zones
ARDS excluded by the following findings:
Pericardial effusion
Cardiomegaly
Pleural effusion
Cavitation
19. LUNG ULTRASOUND/
B lines with smooth pleural morphology
are suggestive of cardiogenic
pulmonary edema.
B lines with uneven pleural line may
indicate ARDS.
20. ADDITIONAL TESTS
Right heart catheterization:
Not performed routinely
Helps in determining fluid status
Pulmonary-artery capillary wedge pressure:
Normal left ventricular (LV) function implies a non-cardiogenic cause.
High pulmonary-artery capillary wedge pressure (≥ 18 mm Hg) implies a cardiogenic cause.
Bronchoscopy:
If etiology is unclear
Specimens can be obtained for cytological and biochemical evaluation.
21. Non-pulmonary imaging in cases of trauma
(brain and spine imaging) or abdominal etiology, such
as peritonitis or pancreatitis (abdominal CT)
Lung biopsy:
Invasive and rarely needed
Performed if it will guide therapeutic management
