4.2 Acute Respiratory Distress Syndrome (ARDS)

Acute Respiratory Distress Syndrome (ARDS)

Acute respiratory distress syndrome (ARDS) is diffuse inflammatory lung injury producing non-cardiogenic pulmonary edema, refractory hypoxemia, and stiff, low-compliance lungs. Injury to the alveolar-capillary membrane lets protein-rich fluid flood the alveoli, collapsing them and creating a large intrapulmonary shunt. The CCRN expects you to recognize ARDS by the Berlin definition, grade it by P/F ratio, and apply lung-protective ventilation.

The Berlin Definition (2012)

All four criteria must be met:

1. Timing -- onset within one week of a known clinical insult or new/worsening respiratory symptoms.
2. Chest imaging -- bilateral opacities not fully explained by effusions, lobar/lung collapse, or nodules.
3. Origin of edema -- respiratory failure not fully explained by cardiac failure or fluid overload; objective assessment (such as echocardiography) is used to exclude hydrostatic edema when no ARDS risk factor is present. A pulmonary artery wedge pressure (PAWP) <= 18 mmHg supports non-cardiogenic edema.
4. Oxygenation -- graded by the P/F ratio with PEEP or CPAP >= 5 cmH2O.

Worked example: a PaO2 of 70 on FiO2 0.70 gives a P/F of 100 -- severe ARDS. The leading risk factor is sepsis, followed by pneumonia, gastric aspiration, pancreatitis, massive transfusion (TRALI), and major trauma.

Phases of Lung Injury

ARDS evolves through an exudative phase (days 1-7: alveolar flooding, hyaline-membrane formation), a proliferative phase (days 7-21: type II pneumocyte proliferation and early repair), and, in some patients, a fibrotic phase (beyond 3 weeks) with lasting reduced compliance. Recognizing the timeline helps set realistic weaning expectations.

Lung-Protective Ventilation

The landmark ARDSNet strategy reduces ventilator-induced lung injury and mortality. Core targets:

• Tidal volume 6 mL/kg predicted body weight (PBW) -- calculated from height and sex, NOT actual weight -- limiting volutrauma to the small volume of aerated "baby lung."
• Plateau pressure <= 30 cmH2O -- reflects alveolar distending pressure; keep it low to prevent barotrauma.
• Permissive hypercapnia -- accept a rising PaCO2 and a pH as low as about 7.20-7.25 rather than raising tidal volume. Do not chase a normal CO2.
• PEEP titrated to oxygenation -- recruits collapsed alveoli, restores functional residual capacity, and reduces cyclic atelectrauma. Higher PEEP is generally used in moderate-to-severe disease.
• Conservative fluid management -- a dry-side strategy improves oxygenation and ventilator-free days once shock has resolved.

The oxygenation goal is a PaO2 of 55-80 mmHg or SpO2 88-95%, avoiding hyperoxia. Raising tidal volume to normalize CO2 pushes up plateau pressure and further injures the lung -- the single most common ARDS trap on the exam.

Prone Positioning

For moderate-to-severe ARDS (P/F < 150), early prone positioning for 12-16 hours per day reduces mortality (PROSEVA trial). Proning improves oxygenation by recruiting dependent dorsal lung regions that collapse when supine, improving V/Q matching, and relieving the compressive weight of the heart and abdomen on posterior lung. Nursing priorities: secure the endotracheal tube (accidental extubation is the feared complication), protect pressure points (face, chest, iliac crests) to prevent pressure injuries, and reposition the head and arms on a schedule. Contraindications include unstable spine, open abdomen, and severe hemodynamic instability.

Adjuncts and Rescue Therapies

• Neuromuscular blockade (e.g., cisatracurium) may be used briefly in early severe ARDS to abolish dyssynchrony and lower oxygen consumption -- always with deep sedation.
• Inhaled pulmonary vasodilators (nitric oxide, epoprostenol) transiently improve oxygenation and V/Q matching but have not reduced mortality; they are a bridge, not a cure.
• Venovenous ECMO (extracorporeal membrane oxygenation) is a rescue option for refractory hypoxemia despite optimized ventilation and proning.

Common traps: confusing ARDS with cardiogenic edema (ARDS has a normal PAWP and ejection fraction and does not resolve with diuresis alone); using 8-10 mL/kg tidal volumes; proning too late or for too few hours; and crediting nitric oxide with a survival benefit it does not have.

ARDS vs Cardiogenic Pulmonary Edema

Both flood the alveoli, but cause and treatment differ sharply. Cardiogenic edema comes from high hydrostatic pressure (left-heart failure) and responds to diuresis, afterload reduction, and inotropes; ARDS comes from increased capillary permeability and does not.

Monitoring and Complications

Watch for barotrauma (pneumothorax, subcutaneous emphysema) from high pressures, hemodynamic compromise when high PEEP reduces venous return, and ventilator-associated pneumonia during prolonged support. Trend the P/F ratio, plateau pressure, and driving pressure (plateau minus PEEP; keep below 15 cmH2O) to gauge response. Daily assessment of sedation and any neuromuscular blockade, nutrition, DVT and stress-ulcer prophylaxis, and early mobility once stable round out supportive care that shortens ICU stay. Criteria to consider venovenous ECMO include a P/F ratio below 80 or an uncompensated respiratory acidosis (pH < 7.25) despite optimized lung-protective settings and proning. Throughout, the guiding principle is to protect the aerated lung: minimize distending pressure, tolerate a modestly high CO2, and aggressively treat the underlying trigger -- most often sepsis.