What are the types of acute respiratory failure?

Types of Acute Respiratory Failure

Acute respiratory failure is classified into two main types: Type 1 (hypoxemic) respiratory failure, defined by PaO₂ <8 kPa (60 mmHg) with normal or low PaCO₂, and Type 2 (hypercapnic) respiratory failure, defined by PaO₂ <8 kPa (60 mmHg) AND PaCO₂ >6 kPa (45 mmHg). 1, 2

Type 1 Respiratory Failure (Hypoxemic)

Primary Characteristics:

• PaO₂ <8 kPa (60 mmHg) with normal or low PaCO₂ (typically ≤6 kPa or 45 mmHg) 2
• Represents failure of oxygenation despite adequate ventilatory effort 1
• The European Respiratory Society uses PaO₂ <8 kPa as the diagnostic threshold 2

Pathophysiological Mechanisms:

• Ventilation-perfusion (V/Q) mismatch is the primary mechanism 1, 2
• Right-to-left intrapulmonary shunting contributes to refractory hypoxemia 1
• Diffusion impairment across the alveolar-capillary membrane 1
• Alveolar hypoventilation in certain contexts 1

Common Clinical Scenarios:

• Acute respiratory distress syndrome (ARDS), classified as mild (PaO₂/FiO₂ 200-300 mmHg), moderate (100-200 mmHg), or severe (≤100 mmHg) 3, 1
• Pneumonia with bilateral infiltrates 1
• Cardiogenic or non-cardiogenic pulmonary edema 1

Management Approach:

• Oxygen therapy is typically effective as Type 1 failure generally responds to supplemental oxygen 1
• High-flow nasal oxygen (HFNO) may reduce intubation rates compared to conventional oxygen therapy, with mortality reduction (ARD -15.8%) 3, 1
• Target SpO₂ >94% in most cases 1

Type 2 Respiratory Failure (Hypercapnic)

Primary Characteristics:

• PaO₂ <8 kPa (60 mmHg) AND PaCO₂ >6 kPa (45 mmHg) 2
• Represents failure of the ventilatory pump to eliminate CO₂ 1, 2
• Often accompanied by respiratory acidosis (pH <7.35) 1

Pathophysiological Mechanisms:

• Alveolar hypoventilation is the primary mechanism, where minute ventilation is insufficient relative to CO₂ production 1, 2
• Increased airway resistance and dynamic hyperinflation with intrinsic PEEP (PEEPi) 1
• Inspiratory muscle dysfunction leading to inadequate ventilatory effort 1
• Increased mechanical workload with greater energy consumption by respiratory muscles 1

Common Clinical Scenarios:

• COPD exacerbations are the most frequent cause 1, 4
• Obesity hypoventilation syndrome (OHS) 4
• Neuromuscular disorders (e.g., Duchenne muscular dystrophy, myasthenia gravis) 1
• Chest wall deformities (scoliosis, thoracoplasty) 1

Management Approach:

• Controlled oxygen therapy with target saturation 88-92% to avoid worsening hypercapnia 1, 2
• Non-invasive ventilation (NIV) is first-line treatment when pH <7.35 and PaCO₂ >6 kPa after optimal medical therapy 1, 4
• The British Thoracic Society recommends NIV particularly when pH 7.25-7.35 in COPD exacerbations 1
• Ventilator settings require long expiration time and short inspiration time to avoid further hyperinflation 4

Additional Classifications

Temporal Classification:

• Acute respiratory failure develops suddenly with rapid deterioration of arterial blood gases 1
• Chronic respiratory failure develops gradually over time with compensatory mechanisms (e.g., renal bicarbonate retention) 1
• Acute-on-chronic respiratory failure presents unique challenges due to altered baseline physiology 1

ARDS Severity Classification (Subset of Type 1):

• Mild ARDS: PaO₂/FiO₂ 200-300 mmHg with minimum PEEP 5 cmH₂O 3
• Moderate ARDS: PaO₂/FiO₂ 100-200 mmHg 3
• Severe ARDS: PaO₂/FiO₂ ≤100 mmHg 3

Critical Diagnostic Considerations

Essential Monitoring:

• Arterial blood gas analysis is mandatory for proper classification of respiratory failure type 2
• The British Thoracic Society recommends ABG analysis as the gold standard 2
• Serial ABGs should be obtained to monitor treatment response, especially in Type 2 failure 2
• Continuous pulse oximetry and early warning scores (e.g., NEWS) for ongoing assessment 1

Key Clinical Pitfalls to Avoid

Type 2 Respiratory Failure Specific:

• Never administer high-flow oxygen without monitoring CO₂ levels, as this can precipitate CO₂ narcosis and respiratory arrest 1
• Delaying NIV initiation when pH <7.35 and PaCO₂ >6.0 kPa misses the therapeutic window 1
• Monitor arterial blood gases after 1-2 hours of NIV and again after 4-6 hours if initial improvement is minimal 1

Type 1 Respiratory Failure Specific:

• Recognize that standard oxygen therapy may fail in severe cases, requiring escalation to HFNO or mechanical ventilation 3
• In ARDS, use lung-protective ventilation with low tidal volumes (6 mL/kg predicted body weight) and plateau pressures <30 cmH₂O 1