What are the types of respiratory failure?

Types of Respiratory Failure

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

Type 1 Respiratory Failure (Hypoxemic)

Definition and Diagnostic Criteria:

• Characterized by low oxygen levels (PaO₂ <8 kPa or 60 mmHg) with normal or low carbon dioxide levels (PaCO₂ typically ≤6 kPa or 45 mmHg) 1
• Represents failure to maintain adequate oxygenation despite normal or increased ventilatory effort 2

Pathophysiological Mechanisms:

• Ventilation-perfusion (V/Q) mismatch is the primary mechanism, where blood flows through poorly ventilated lung regions preventing adequate oxygenation 3, 1
• Intrapulmonary shunting occurs when blood bypasses ventilated alveoli entirely, flowing through completely unventilated or fluid-filled lung units—this does not respond to supplemental oxygen 3
• Diffusion impairment results from thickened alveolar-capillary membranes limiting oxygen transfer 3
• Alveolar hypoventilation can also contribute to hypoxemia 2

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) 2
• Pneumonia and community-acquired infections 2, 3
• Pulmonary edema, which fills alveoli with fluid creating shunt physiology and severe V/Q mismatch 2
• Pulmonary embolism causing V/Q mismatch through increased dead space ventilation 2
• Sepsis-related respiratory dysfunction, ranging from subclinical changes to full ARDS 2

Management Approach:

• Target oxygen saturation of 94-98% in most patients 4
• High-flow nasal oxygen (HFNO) may reduce intubation rates compared to conventional oxygen therapy, with significant mortality reduction (ARD -15.8%) 2
• For severe cases with refractory hypoxemia, invasive mechanical ventilation with lung-protective strategies (tidal volume 6 mL/kg predicted body weight, plateau pressure <30 cm H₂O) 2

Type 2 Respiratory Failure (Hypercapnic)

Definition and Diagnostic Criteria:

• Characterized by elevated carbon dioxide (PaCO₂ >6 kPa or 45 mmHg) with concurrent low oxygen levels (PaO₂ <8 kPa or 60 mmHg) 1
• Represents failure of the ventilatory pump function 2
• Normal range for carbon dioxide is 4.6-6.1 kPa (34-46 mmHg) 2

Pathophysiological Mechanisms:

• Alveolar hypoventilation is the fundamental mechanism, where minute ventilation is insufficient relative to CO₂ production 3, 1
• Increased airway resistance and dynamic hyperinflation with intrinsic PEEP (PEEPi) contribute significantly during acute respiratory failure 2
• Inspiratory muscle dysfunction plays a role in chronic hypercapnia, with increased mechanical workload raising energy consumption 2
• V/Q abnormalities worsen during acute exacerbations 2

Common Clinical Causes:

• COPD exacerbations account for the majority of Type 2 failures 2
• Neuromuscular disorders (ALS, muscular dystrophy, myasthenia gravis) causing progressive ventilatory pump failure 2
• Chest wall deformities (scoliosis, thoracoplasty) 2
• Obesity hypoventilation syndrome combining restrictive mechanics with central drive abnormalities 2

Management Approach:

• Target oxygen saturation of 88-92% to avoid worsening hypercapnia 4, 2, 1
• Non-invasive ventilation (NIV) should be initiated when pH <7.35 and PaCO₂ >6.0 kPa (45 mmHg) after optimal medical therapy, reducing mortality and intubation rates 2, 1
• Blood gases should be repeated at 30-60 minutes to check for rising PCO₂ or falling pH 4
• Adjunctive therapy includes systemic corticosteroids, bronchodilators, and antibiotics when bacterial infection is suspected in COPD exacerbations 2

Additional Classifications

Acute vs. Chronic Respiratory Failure:

• Acute respiratory failure is characterized by sudden onset with rapid deterioration of arterial blood gases 2
• Chronic respiratory failure develops gradually over time, often involving compensatory mechanisms such as renal bicarbonate retention 2
• Acute-on-chronic respiratory failure presents unique challenges due to altered baseline physiology 2

Critical Clinical Pitfalls to Avoid

For Type 2 Respiratory Failure:

• Administering high-flow oxygen without monitoring CO₂ can precipitate CO₂ narcosis and respiratory arrest—controlled oxygen with target saturation 88-92% is mandatory 3, 1
• Sudden cessation of supplementary oxygen therapy can cause life-threatening rebound hypoxaemia with rapid fall in oxygen saturations below the starting level 4
• Delaying NIV initiation when pH <7.35 and PaCO₂ >6.0 kPa misses the therapeutic window 2

For Type 1 Respiratory Failure:

• Standard chest radiographs are poor predictors of oxygenation defect severity or clinical outcome, and classic ARDS findings may be asymmetric, patchy, or focal 3
• Clinical recognition of hypoxemia is unreliable—continuous pulse oximetry is essential 3
• Delayed intubation in patients with ARDS or pneumonia who fail to improve on HFNO within 1 hour should be avoided, as NIV failure is an independent risk factor for mortality 2

NIV Contraindications:

• Impaired consciousness, severe hypoxemia, or copious respiratory secretions are contraindications to NIV 2
• Failure to improve PaCO₂ and pH after 4-6 hours of NIV indicates treatment failure and need for intubation 2