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KEY POINTS
Acute respiratory distress syndrome (ARDS) is a common critical illness that is diagnosed by a constellation of clinical findings, representing an end consequence of numerous different pathophysiological pathways.
The diagnosis of ARDS is often delayed or inaccurate, frustrating attempts to implement effective therapeutic and supportive care.
Therapeutics targeting ARDS pathogenesis have largely failed, likely due to the false homogenization of ARDS as a single disease state.
The major goals of mechanical ventilation in ARDS are to ensure adequate oxygenation and ventilation while minimizing ventilator-induced lung injury.
Lung-protective ventilation consists of lower-tidal volume (6 mL/kg PBW) and low-pressure (<30 cm H2O plateau pressure) ventilation.
Prone positioning in moderate-to-severe ARDS is underutilized, improves mortality, reduces VILI, and improves oxygenation.
Driving pressure may be a reasonable measure to personalize the tidal volume and pressure targets identified in larger randomized control trials to minimize VILI.
Corticosteroids decrease mortality in ARDS due to COVID-19.
Conservative fluid management strategies and minimization of sedative medications likely reduce the duration of mechanical ventilation for patients with ARDS.
Inhaled pulmonary vasodilators and extracorporeal membrane oxygenation are potential salvage therapies for patients with refractory hypoxemia.
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THE HISTORY OF ACUTE RESPIRATORY DISTRESS SYNDROME: AN EVOLVING DEFINITION
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For over 100 years, military medicine recognized a syndrome of acute respiratory failure occurring shortly after a traumatic injury or nontraumatic illness. Known as “posttraumatic massive pulmonary collapse” (World War I), “wet lung” (World War II), “shock lung” (Korean War), or “Da Nang lung” (Vietnam War), previously healthy combatants would develop pulmonary infiltrates and rapidly progressive respiratory failure after an inciting pulmonary or extrapulmonary insult.1,2
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This wartime syndrome was formally recognized by civilian medicine in 1967, when Ashbaugh and colleagues reported a case series of 12 patients who developed acute respiratory distress within 96 hours of a pulmonary or extrapulmonary insult.3 These insults were heterogeneous, ranging from polytrauma to viral pneumonia to acute pancreatitis. However, their pulmonary consequence was seemingly uniform: all 12 patients developed bilateral pulmonary infiltrates with progressive, severe hypoxemia that benefitted from positive airway pressure. Ashbaugh and colleagues termed this syndrome the “Adult Respiratory Distress Syndrome,”4 given its clinical and pathologic similarities to the infant respiratory distress syndrome. However, as one of the patients of the original report was only 11 years old, the syndrome quickly became regarded as the “Acute Respiratory Distress Syndrome,” or ARDS.5
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Over the 50 years since its first civilian description, ARDS is perhaps the most extensively studied critical illness,6 being deemed the “mother of intensive care.”7 Effective mechanistic and clinical investigation of this disease, however, was hampered by a lack of a clear clinical definition. As noted by Murray and colleagues in 19888:
How can you collect, much less compare, epidemiologic data and mortality figures when there is no uniformly accepted (and used) definition [of ARDS]? How can you study basic ...