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, characterized by PaO₂ <8 kPa (60 mmHg) with normal or low PaCO₂, and Type 2 (hypercapnic) respiratory failure, defined by PaO₂ <8 kPa and PaCO₂ >6 kPa (45 mmHg) with pH <7.35. 1, 2

Type 1 Respiratory Failure (Hypoxemic)

Definition and Gas Exchange Abnormalities:

• Characterized by failure to maintain adequate oxygenation with PaO₂ <8 kPa (60 mmHg) or SpO₂ <88%, while PaCO₂ remains normal or low 1, 3
• Results from impaired oxygen transfer across the alveolar-capillary membrane despite normal or increased ventilatory effort 2

Underlying Pathophysiological Mechanisms:

• Ventilation-perfusion (V/Q) mismatch: Blood flows to poorly ventilated alveoli, the most common mechanism 2, 3
• Intrapulmonary shunt: Blood bypasses ventilated alveoli entirely (right-to-left shunt) 2, 4
• Diffusion impairment: Thickened alveolar-capillary membrane prevents adequate oxygen transfer 2, 3
• Alveolar hypoventilation: Reduced minute ventilation relative to metabolic demands 2, 4

Common Clinical Scenarios:

• Acute respiratory distress syndrome (ARDS), which is further classified by severity: mild (PaO₂/FiO₂ 200-300 mmHg), moderate (100-200 mmHg), or severe (≤100 mmHg) 2
• Pneumonia causing alveolar consolidation and V/Q mismatch 2
• Cardiogenic pulmonary edema with alveolar flooding 1, 2

Key Management Principle:

• Type 1 failure typically responds to supplemental oxygen therapy, though severe cases may require high-flow nasal oxygen (HFNO) or mechanical ventilation 2

Type 2 Respiratory Failure (Hypercapnic)

Definition and Gas Exchange Abnormalities:

• Defined by elevated PaCO₂ >6 kPa (45 mmHg) with pH <7.35, indicating respiratory acidosis, often accompanied by hypoxemia 1, 3
• Represents failure of the ventilatory pump to eliminate carbon dioxide adequately 2, 5

Underlying Pathophysiological Mechanisms:

• Alveolar hypoventilation: Minute ventilation insufficient relative to CO₂ production, the primary mechanism 2, 6
• Increased airway resistance and dynamic hyperinflation: Particularly in COPD, leading to intrinsic PEEP (PEEPi) that increases work of breathing 2, 6
• Inspiratory muscle dysfunction: Respiratory muscles unable to maintain adequate ventilation due to fatigue or weakness 2, 6
• Increased dead space ventilation: Wasted ventilation to non-perfused alveoli 5

Common Clinical Scenarios:

• COPD exacerbations, the most frequent cause of acute hypercapnic respiratory failure 1, 6
• Neuromuscular disorders (e.g., Duchenne muscular dystrophy, myasthenia gravis) causing respiratory muscle weakness 1, 2
• Chest wall deformities (scoliosis, thoracoplasty) restricting lung expansion 1, 2
• Obesity hypoventilation syndrome (OHS) 6
• Decompensated obstructive sleep apnea 1

Critical Management Principle:

• Non-invasive ventilation (NIV) is first-line treatment when pH <7.35 and PaCO₂ >6 kPa after optimal medical therapy, particularly in COPD exacerbations 1, 2
• Controlled oxygen therapy targeting SpO₂ 88-92% is essential to avoid worsening hypercapnia and CO₂ narcosis 2

Additional Classification Considerations

Temporal Classification:

• Acute respiratory failure: Sudden onset with rapid deterioration of arterial blood gases over hours to days 2, 7
• Chronic respiratory failure: Gradual development over weeks to months with compensatory mechanisms (e.g., renal bicarbonate retention) 2
• Acute-on-chronic respiratory failure: Acute decompensation superimposed on chronic baseline respiratory insufficiency, presenting unique management challenges 2, 7

Critical Diagnostic Approach

Essential Diagnostic Steps:

• Arterial blood gas analysis is critical for definitive diagnosis and classification, measuring PaO₂, PaCO₂, and pH 1, 3
• Pulse oximetry (SpO₂) provides continuous monitoring but cannot detect hypercapnia 3
• Repeat arterial blood gas measurement after initial medical treatment and supplemental oxygen is essential, as many patients improve rapidly without requiring NIV 1

Common Pitfall to Avoid:

• Administering high-flow oxygen without monitoring CO₂ levels in suspected Type 2 failure can precipitate CO₂ narcosis and respiratory arrest 2
• Low threshold for measuring arterial blood gases in patients with neuromuscular diseases, chest wall deformity, obesity, or acute confusional states who may have respiratory failure without significant breathlessness 1