PaO₂:FiO₂ Ratio

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About this Calculator

Acute respiratory distress syndrome (ARDS) is classically described as noncardiogenic pulmonary edema, thought to be secondary to increased pulmonary capillary permeability. This process may occur for a number of reasons, both pulmonary and systemic in origin. Common causes of ARDS include pulmonary or systemic infection, trauma, burns, pancreatitis, near-drowning, transfusion, medication overdose, and toxic inhalations.

Treatment of ARDS is evolving, with several recent large-scale studies that have altered standard practice:

  • Low tidal volume ventilation (6mL/kg) improves absolute mortality 9% (ARDSNet, 2000)
  • Restrictive fluid management strategies (initiated after hemodynamic stabilization) increases ventilation-free and ICU-free days, but has no effect on 60-day mortality (ARDSNet, 2006)
  • High versus low levels of positive end-expiratory pressure (PEEP) has no effect on clinically relevant outcomes (Brower et al, 2004)
  • No benefit, but increased complication rates when pulmonary arterial catheters are used to guide treatment (ARDSNet, 2006)
  • Steroid therapy increases morbidity and possibly increases mortality, especially if initiated late (> 14 days) in ARDS course (Steinberg et al, 2006)


Herbert P Wiedemann et al.

Comparison of two fluid-management strategies in acute lung injury.

New England Journal of Medicine 2006 June 15, 354 (24): 2564-75

Brower RG, et al.

Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome.

New England Journal of Medicine 2004 July 22, 351 (4): 327-36

Arthur P Wheeler et al.

Pulmonary-artery versus central venous catheter to guide treatment of acute lung injury.

New England Journal of Medicine 2006 May 25, 354 (21): 2213-24

Steinberg KP et al.

Efficacy and safety of corticosteroids for persistent acute respiratory distress syndrome.

New England Journal of Medicine 2006 April 20, 354 (16): 1671-84

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