Clinical meaning
ARDS is characterized by diffuse alveolar damage from pulmonary or extrapulmonary insults. The exudative phase (days 1-7) involves damage to the alveolar-capillary membrane: type I pneumocyte injury allows protein-rich edema fluid to flood alveoli, forming hyaline membranes. Neutrophil-mediated inflammation releases proteases and reactive oxygen species, amplifying damage. Surfactant dysfunction increases surface tension, promoting alveolar collapse. The result is bilateral pulmonary infiltrates, severe hypoxemia refractory to supplemental oxygen, and reduced lung compliance. Berlin criteria classify severity by PaO2/FiO2 ratio on PEEP >= 5: mild (200-300), moderate (100-200), severe (< 100). Lung-protective ventilation targeting low tidal volumes (6 mL/kg IBW) reduces ventilator-induced lung injury (VILI) from overdistention (volutrauma), cyclic opening/closing of atelectatic alveoli (atelectrauma), and biotrauma (cytokine release). The ARDS Network trial demonstrated a 22% mortality reduction with low Vt strategy.
Diagnosis & workup
Diagnostics & workup: - Berlin criteria: acute onset (within 1 week of insult), bilateral opacities on CXR/CT not fully explained by effusions/atelectasis, respiratory failure not fully explained by cardiac failure, PaO2/FiO2 ratio on PEEP >= 5 cmH2O - P/F ratio classification: mild 200-300, moderate 100-200, severe < 100 - ABG: severe hypoxemia, wide A-a gradient, respiratory acidosis (or alkalosis with compensation) - CXR: bilateral diffuse opacities (patchy or homogeneous, not cardiogenic pulmonary edema pattern) - CT chest: ground-glass opacities, consolidation, dependent atelectasis, may show underlying cause - Echocardiography: rule out cardiogenic pulmonary edema (normal LVEF, PCWP < 18 if PA catheter placed) - BNP/NT-proBNP: helps distinguish cardiogenic from non-cardiogenic pulmonary edema (low in ARDS) - Respiratory mechanics: reduced static compliance (< 40 mL/cmH2O), elevated plateau pressure