Acute respiratory distress syndrome (ARDS) is a heterogeneous disease. It presents with a wide range of severity, varying degrees of hypoxemia and varying degrees of pulmonary mechanical impairment. Failure of hypoxemic vasoconstriction (Naeije and Brimioulle, 2001), alveolar collapse, low V/Q, vascular obstruction and shunt are likely present to varying degrees in any unselected cohort of patients.

Nevertheless, there is a common pathway of inflammation, then localized alveolar collapse leading to simultaneous over-distension (of the remaining “baby lung”) and need for recruitment (of the collapsed lung).

Diseases in which this pathologic sequence plays out are characterized clinically by hypoxemia and bilateral infiltrates, pathologically by diffuse alveolar damage and are optimally treated by a strategy that minimizes distending pressure and lung stretch.

COVID-19 is such a disease and on that basis, it is ARDS.

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