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ARDS and Ventilation Strategy — Complete Answer (15 Marks)

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1. DEFINITION

• Increased alveolo-capillary permeability → non-cardiogenic pulmonary edema
• Decreased lung compliance (increased lung elastance)
• Severe hypoxemia with increased venous admixture and dead space

(ARDS: Definition, Phenotyping and Respiratory Support Strategies, p. 2)

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2. BERLIN DEFINITION (2012) — Diagnostic Criteria

Severity Classification (Berlin)

Key point for exams: PEEP ≥ 5 cmH₂O is MANDATORY at time of diagnosis; patients NOT on positive pressure ventilation technically cannot be classified as ARDS by Berlin criteria.

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3. ETIOLOGY

Direct (Pulmonary) Causes

• Pneumonia (bacterial, viral — including COVID-19)
• Aspiration of gastric contents
• Pulmonary contusion
• Inhalation injury
• Near-drowning

Indirect (Extrapulmonary) Causes

• Sepsis (most common overall cause — ~40%)
• Severe trauma with shock
• Pancreatitis
• Burns
• Massive blood transfusion / TRALI
• Drug overdose (heroin, aspirin)

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4. PATHOPHYSIOLOGY

Phase 1: Exudative (Day 1–7)

• Activation of alveolar macrophages and neutrophils
• Release of cytokines (IL-1, IL-6, IL-8, TNF-α)
• Damage to Type I pneumocytes → loss of alveolar epithelial barrier
• Damage to capillary endothelium → protein-rich fluid floods alveoli
• Hyaline membrane formation — pathognomonic
• Surfactant depletion → alveolar collapse

Phase 2: Proliferative (Day 7–21)

• Type II pneumocyte proliferation (attempt at repair)
• Fibroblast activation → early fibrosis
• Resolution of edema begins
• Clinical improvement or progression to fibrosis

Phase 3: Fibrotic (>21 days)

• Irreversible fibrosis in some patients
• Obliteration of alveolar architecture
• Increased dead space → CO₂ retention
• Predisposition to barotrauma

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5. CLINICAL FEATURES

• Onset: Within 12–48 hours of precipitating event
• Dyspnea at rest, rapidly progressive
• Tachypnea, accessory muscle use
• Hypoxemia — refractory to supplemental O₂ (hallmark)
• Diffuse crackles on auscultation
• CXR: Bilateral alveolar infiltrates ("white-out" lungs)
• No clinical evidence of left heart failure (PCWP < 18 mmHg)

Chest X-Ray / CT Findings in ARDS

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6. VENTILATION STRATEGY IN ARDS ⭐ (Most Important for MD Exam)

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A. LUNG-PROTECTIVE VENTILATION (ARDSNet Protocol)

Tidal Volume (Vt)

• Target: 6 mL/kg Predicted Body Weight (PBW)
• Can reduce to 4 mL/kg PBW if plateau pressure remains > 30 cmH₂O
• AVOID: Vt > 6 mL/kg + Plateau > 30 cmH₂O
• Very low Vt may cause patient-ventilator dyssynchrony

Predicted Body Weight (PBW) Calculation

• Males: 50 + 2.3 × [height(in) − 60]
• Females: 45.5 + 2.3 × [height(in) − 60]

Plateau Pressure

• Target: ≤ 30 cmH₂O (measured during inspiratory hold, patient must be passive)
• In patients with high chest wall compliance (obesity, ascites), higher plateau pressures may be tolerated as transpulmonary pressure remains low

Driving Pressure (DP)

• DP = Plateau Pressure − PEEP
• Target: < 12–15 cmH₂O (strong predictor of mortality)
• Recent evidence suggests DP may be a better titration target than Vt alone
• (Surviving Sepsis Campaign 2021, p. 34)

PEEP (Positive End-Expiratory Pressure)

• Minimum 5 cmH₂O (required for Berlin diagnosis)
• Higher PEEP strategy for moderate-severe ARDS (PaO₂/FiO₂ < 200)
• Titrated using ARDSNet PEEP/FiO₂ tables or by esophageal manometry

Respiratory Rate (RR)

• Increase RR up to 35 breaths/min to compensate for low Vt
• Maintain acceptable minute ventilation

FiO₂

• Target PaO₂: 55–80 mmHg (SpO₂: 88–95%)
• Avoid hyperoxia (FiO₂ > 0.6 for prolonged periods is toxic)

pH / Permissive Hypercapnia

• Accept pH ≥ 7.20 (permissive hypercapnia)
• If pH < 7.20: increase RR → consider sodium bicarbonate → increase Vt as last resort
• Contraindicated in raised ICP, severe pulmonary hypertension, right heart failure

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B. MODE OF VENTILATION

• Volume-controlled AC (Assist Control) — most commonly used; ensures consistent Vt
• Pressure-controlled ventilation — used when precise Vt delivery is secondary to pressure limitation
• PRVC (Pressure-Regulated Volume Control) — combines benefits of both

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C. PRONE POSITIONING ⭐

• Recommended for severe ARDS (PaO₂/FiO₂ < 150) unresponsive to conventional ventilation
• Duration: ≥ 16 hours/day (PROSEVA trial — 28% relative mortality reduction)
• Mechanism:
  • Redistributes lung edema
  • Recruits dorsal (dependent) atelectatic alveoli
  • Improves V/Q matching
  • Reduces lung stress/strain
• Contraindications: spinal injury, open chest/abdomen, hemodynamic instability, raised ICP

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D. NEUROMUSCULAR BLOCKADE (NMB)

• Short-term NMB (cisatracurium for 48 hours) reduces mortality in moderate-severe ARDS
• Improves patient-ventilator synchrony
• Reduces O₂ consumption and cytokine release
• ACURASYS trial: benefit shown; ROSE trial: no benefit with lighter sedation baseline
• Current practice: consider NMB when dyssynchrony persists despite deep sedation

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E. RECRUITMENT MANEUVERS (RM)

• Transient increase in airway pressure to open collapsed alveoli
• Methods: sustained inflation (40 cmH₂O × 40 sec), incremental PEEP, sighs
• ART trial (2017): high-pressure RM + PEEP titration strategy increased mortality → NOT routinely recommended
• Use with caution in hemodynamically unstable patients

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F. HIGH-FREQUENCY OSCILLATORY VENTILATION (HFOV)

• Previously used for severe ARDS refractory to conventional LPV
• OSCILLATE and OSCAR trials (2013): HFOV showed increased mortality or no benefit
• Currently NOT recommended as routine strategy (may be used as rescue in select centers)

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G. EXTRACORPOREAL MEMBRANE OXYGENATION (ECMO)

• VV-ECMO (veno-venous) for severe ARDS refractory to all conventional strategies
• CESAR trial and EOLIA trial support its use in severe ARDS (PaO₂/FiO₂ < 80 on optimal settings)
• Allows "ultra-lung-protective ventilation" while ECMO handles gas exchange
• Requires specialized center, high resources

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H. OTHER ADJUNCT THERAPIES

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7. SUMMARY TABLE — VENTILATION TARGETS IN ARDS

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8. COMPLICATIONS OF ARDS

• Ventilator-induced lung injury (VILI): volutrauma, barotrauma, atelectrauma, biotrauma
• Pneumothorax / pneumomediastinum
• Ventilator-associated pneumonia (VAP)
• Multi-organ dysfunction syndrome (MODS)
• Post-ARDS fibrosis
• Neuromuscular weakness (ICU-acquired weakness)
• Cognitive impairment / PTSD (long-term)

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9. PROGNOSIS

• Overall mortality: 35–45% (varies with severity and etiology)
• Sepsis-related ARDS has the worst prognosis
• Survivors may have long-term pulmonary, neurocognitive, and psychological sequelae (Post-Intensive Care Syndrome)
• Lung function typically recovers within 6–12 months in survivors

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EXAM HIGH-YIELD POINTS 📌

1. Berlin 2012 replaced the American-European Consensus Conference (AECC) 1994 definition — no longer uses "ALI" terminology
2. PEEP ≥ 5 cmH₂O is mandatory for Berlin classification
3. ARDSNet trial (2000): 6 mL/kg Vt vs. 12 mL/kg → 22% relative mortality reduction
4. Driving pressure < 15 cmH₂O is the most predictive parameter of outcome
5. PROSEVA trial: prone ≥ 16 hrs → gold standard for severe ARDS
6. HFOV is harmful (OSCILLATE/OSCAR); ECMO is last resort
7. Conservative fluid strategy preferred (negative fluid balance when hemodynamically stable)
8. Permissive hypercapnia is accepted as long as pH ≥ 7.20
9. Avoid hyperoxia — target SpO₂ 88–95%, not 100%
10. Corticosteroids benefit in early/mid ARDS; NOT in late fibrotic phase

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