What are the types of respiratory failure?

Types of Respiratory Failure

Respiratory failure is classified into two main types: Type 1 (hypoxemic) respiratory failure, characterized by low oxygen with normal or low carbon dioxide, and Type 2 (hypercapnic) respiratory failure, characterized by elevated carbon dioxide often with concurrent hypoxemia. 1

Type 1 Respiratory Failure (Hypoxemic)

Definition and Diagnostic Criteria:

• Defined by PaO₂ <60 mmHg or SaO₂ <88% with normal or low PaCO₂ levels 2
• Represents failure to maintain adequate oxygenation despite normal or increased ventilatory effort 1

Pathophysiological Mechanisms:

• Ventilation-perfusion (V/Q) mismatch occurs when blood flows through poorly ventilated lung regions, preventing adequate oxygenation 3
• Intrapulmonary shunting develops when blood bypasses ventilated alveoli entirely through completely unventilated or fluid-filled lung units—this mechanism does not respond to supplemental oxygen 3
• Diffusion impairment results from thickened alveolar-capillary membranes limiting oxygen transfer 3
• Alveolar hypoventilation can contribute when minute ventilation is inadequate 1

Common Clinical Causes:

• Acute Respiratory Distress Syndrome (ARDS), classified by severity: mild (PaO₂/FiO₂ 200-300 mmHg), moderate (100-200 mmHg), or severe (≤100 mmHg) with mortality approximately 30-40% 1
• Pneumonia and community-acquired infections 1
• Pulmonary edema from increased pulmonary vascular permeability, increased hydrostatic pressures, or lowered oncotic pressure 1
• Pulmonary embolism causing V/Q mismatch through increased dead space ventilation 1

Type 2 Respiratory Failure (Hypercapnic)

Definition and Diagnostic Criteria:

• Defined by PaCO₂ ≥45 mmHg (>6.0 kPa) with pH <7.35 2, 1
• Represents failure of the ventilatory pump function 1
• Normal carbon dioxide range is 4.6-6.1 kPa (34-46 mmHg) 1

Pathophysiological Mechanisms:

• Alveolar hypoventilation is the fundamental mechanism where minute ventilation is insufficient relative to CO₂ production 3
• Increased work of breathing develops from increased airway resistance, dynamic hyperinflation with intrinsic PEEP (PEEPi), and inspiratory muscle dysfunction 1
• Inspiratory muscle dysfunction occurs from impaired muscle function with increased mechanical workload raising energy consumption 1
• V/Q abnormalities worsen during acute exacerbations 1

Common Clinical Causes:

• COPD exacerbations account for the majority of Type 2 failures, with flow-limited expiration and dynamic hyperinflation 1
• Obesity hypoventilation syndrome combining restrictive mechanics with central drive abnormalities 1
• Neuromuscular disorders (ALS, muscular dystrophy, myasthenia gravis) causing progressive ventilatory pump failure 1
• Chest wall deformities (scoliosis, thoracoplasty) 1
• Central nervous system depression 4

Additional Classifications

Temporal Classification:

• Acute respiratory failure is characterized by sudden onset with rapid deterioration of arterial blood gases 1
• Chronic respiratory failure develops gradually over time, often involving compensatory mechanisms such as renal bicarbonate retention 1
• Acute-on-chronic respiratory failure presents unique challenges due to altered baseline physiology 1, 5

Critical Clinical Pitfalls

Diagnostic Considerations:

• Standard chest radiographs are poor predictors of oxygenation defect severity, and classic ARDS findings may be asymmetric, patchy, or focal rather than diffuse 3
• Clinical recognition of hypoxemia is unreliable; continuous pulse oximetry is essential, though it may be unreliable with poor peripheral perfusion, carbon monoxide poisoning, or methemoglobinemia 3

Management Pitfalls:

• Administering high-flow oxygen without monitoring CO₂ can precipitate CO₂ narcosis and respiratory arrest in Type 2 respiratory failure—controlled oxygen with target saturation 88-92% is mandatory 1, 3
• Delaying NIV initiation when pH <7.35 and PaCO₂ >6.0 kPa misses the therapeutic window 1
• In Type 1 failure, delayed intubation in patients with ARDS or pneumonia who fail to improve on high-flow nasal oxygen within 1 hour should be avoided, as NIV failure is an independent risk factor for mortality 1