Acute Respiratory Distress Syndrome (ARDS)

The acute respiratory distress syndrome (ARDS) is an acute, diffuse inflammatory lung injury that causes increased pulmonary vascular permeability, non-cardiogenic pulmonary edema, and severe hypoxemia. It is a common form of acute hypoxemic respiratory failure in the intensive care unit, arising from direct lung insults such as pneumonia and aspiration or indirect insults such as sepsis and trauma.

Definition

ARDS is defined, under the Berlin Definition, as acute respiratory failure with bilateral opacities on chest imaging not fully explained by cardiac failure or fluid overload, occurring within one week of a known clinical insult, with hypoxemia graded as mild, moderate, or severe by the ratio of arterial oxygen tension to inspired oxygen fraction measured with a minimum level of positive end-expiratory pressure (Ranieri-2012-berlin).

Scope

This entry covers the definition and severity classification of ARDS, its pathophysiology, the epidemiology of the syndrome, and the principal evidence on supportive management, including lung-protective ventilation and prone positioning. It is a reference and educational topic within respiratory failure and mechanical ventilation and does not provide individualised clinical instructions.

Core questions

• What distinguishes ARDS from cardiogenic pulmonary edema?
• How is the severity of ARDS graded?
• Why does a lung-protective ventilation strategy improve survival in ARDS?
• Which supportive interventions have reduced mortality in severe ARDS?

Key concepts

• Diffuse alveolar damage
• Increased alveolar-capillary permeability
• Non-cardiogenic pulmonary edema
• Berlin Definition severity grading
• Baby lung concept
• Lung-protective (low tidal volume) ventilation
• Prone positioning

Mechanisms

ARDS begins with injury to the alveolar-capillary barrier, producing the exudative phase of diffuse alveolar damage: protein-rich edema floods the alveoli, surfactant function is lost, and hyaline membranes form, causing widespread alveolar collapse and shunt physiology with refractory hypoxemia. Because aerated lung volume is markedly reduced, the remaining functional lung behaves as a small "baby lung," so conventional tidal volumes can overdistend it; this rationale underlies lung-protective ventilation with low tidal volumes (Thompson-2017; ARDSnet-2000). A subsequent proliferative and sometimes fibrotic phase may follow. Prone positioning improves the homogeneity of lung aeration and ventilation-perfusion matching in severe disease (Guerin-2013).

Clinical relevance

ARDS is a leading cause of acute hypoxemic respiratory failure and of mechanical-ventilation use in the intensive care unit, and its recognition shapes how clinicians appraise ventilation evidence. This entry describes the syndrome and the evidence base; it is not a protocol for diagnosis or treatment of an individual patient.

Epidemiology

ARDS accounts for a substantial share of intensive care admissions and mechanically ventilated patients, with hospital mortality rising across the mild, moderate, and severe categories of the Berlin Definition; international surveys have noted that the syndrome is frequently under-recognised at the bedside (Ranieri-2012-berlin; Thompson-2017).

Evidence & guidelines

Randomised evidence established that ventilation with lower tidal volumes reduces mortality compared with traditional larger tidal volumes (ARDSnet-2000), and that prone positioning reduces mortality in severe ARDS (Guerin-2013). Professional-society guidelines synthesise these and related trials into graded recommendations on mechanical ventilation in ARDS (Fan-2017-guideline). This entry summarises the direction of that evidence without specifying individual settings.

History

ARDS was first described by Ashbaugh and colleagues in 1967 as acute respiratory distress in adults. Definitions evolved through the 1994 American-European Consensus Conference and were refined into the 2012 Berlin Definition, which standardised timing, imaging, oxygenation thresholds, and positive end-expiratory pressure criteria and replaced the older term acute lung injury (Ranieri-2012-berlin). Landmark trials in 2000 and 2013 transformed supportive care by establishing low tidal volumes and prone positioning, respectively (ARDSnet-2000; Guerin-2013).

Debates

How should ARDS be defined and subclassified?

The Berlin Definition improved on earlier criteria but remains a syndromic, physiology-based definition; debate continues over biological subphenotypes and whether they should refine the definition and guide therapy.

Key figures

• Arthur Slutsky
• V. Marco Ranieri
• B. Taylor Thompson
• Claude Guerin
• Luciano Gattinoni

Seminal works

• ardsnet-2000
• ranieri-2012-berlin
• guerin-2013

Frequently asked questions

How is ARDS different from heart failure causing pulmonary edema?

Both cause bilateral pulmonary edema and hypoxemia, but ARDS edema results from increased permeability of the inflamed alveolar-capillary barrier and, by definition, is not fully explained by cardiac failure or fluid overload, whereas cardiogenic edema results from raised hydrostatic pressure.

Why are lower tidal volumes used in ARDS?

Because the volume of aerated lung is greatly reduced, normal-sized breaths can overdistend the remaining functional lung; randomised evidence showed that ventilation with lower tidal volumes reduced mortality compared with traditional larger volumes.