Acute Respiratory Distress Syndrome — ARDS
Pathophysiology & Risk Factors
A lung or systemic insult injures the alveolar-capillary membrane, flooding alveoli with protein-rich fluid and destroying surfactant. Alveoli collapse, blood shunts past non-functioning units, and the result is refractory hypoxemia in stiff, non-compliant lungs.
ARDS pathophysiology
- Lung or systemic insultsepsis, aspiration, pneumonia, trauma
- Alveolar-capillary membrane injuryinflammation + surfactant loss
- Non-cardiogenic pulmonary edemaprotein-rich fluid floods alveoli
- Alveolar collapse + intrapulmonary shuntblood bypasses gas exchange
- Refractory hypoxemia + stiff lungsnot corrected by supplemental O2
Signs & Symptoms
Diagnostics & Labs
ARDS vs cardiogenic pulmonary edema
ARDS
- Mechanism
- Membrane injury / shunting
- PCWP
- <=18 mmHg
- BNP
- Normal
- Response to FiO2
- Refractory
- Infiltrates
- Bilateral diffuse
Cardiogenic edema
- Mechanism
- Elevated cardiac pressures
- PCWP
- > 18 mmHg
- BNP
- Elevated
- Response to FiO2
- Improves
- Infiltrates
- Bilateral, with cardiac signs
Interventions & Priorities
Treatments & Medications
Patient Teaching
Complications
Clinical Pearl
ARDS = refractory hypoxemia + bilateral white-out with a normal heart; rescue it with low-tidal-volume PEEP and prone positioning.