What are the types of acute respiratory failure?

Acute Respiratory Failure Types

Primary Classification

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 with PaCO₂ >6 kPa (45 mmHg). 1, 2

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Type 1 Respiratory Failure (Hypoxemic)

Definition and Pathophysiology

• Characterized by failure to maintain adequate oxygenation with PaO₂ <8 kPa (60 mmHg) or SaO₂ <88% while PaCO₂ remains normal or low 1, 3
• Results from four primary pathophysiological mechanisms 2, 4:
  • Ventilation-perfusion (V/Q) mismatch - the most common mechanism 2
  • Intrapulmonary shunting - blood bypasses ventilated alveoli entirely, flowing through completely unventilated or fluid-filled lung units 2
  • Diffusion impairment - impaired gas exchange across alveolar-capillary membrane 2
  • Alveolar hypoventilation - reduced minute ventilation 2

Common Clinical Causes

• Acute Respiratory Distress Syndrome (ARDS) - bilateral pulmonary infiltrates with severe hypoxemia, classified by severity: mild (PaO₂/FiO₂ 200-300 mmHg), moderate (100-200 mmHg), or severe (≤100 mmHg) with mortality approximately 30-40% 2
• Pneumonia - community-acquired or nosocomial infections causing alveolar consolidation 2
• Cardiogenic pulmonary edema - fluid fills alveoli creating shunt physiology and severe V/Q mismatch 2
• Sepsis-related respiratory dysfunction - causes spectrum from subclinical changes to full ARDS with increased dead space ventilation and intrapulmonary shunting 2

Management Approach

• High-flow nasal oxygen (HFNO) may reduce intubation rates compared to conventional oxygen therapy with mortality reduction (ARD -15.8%) 2
• Target SpO₂ >94% in Type 1 failure 2
• NIV may be attempted in carefully selected cooperative patients with isolated respiratory failure, no major organ dysfunction, cardiac ischemia, or secretion clearance limitations, though NIV failure is an independent risk factor for mortality in Type 1 failure 2
• Predictors of NIV failure include higher severity score, older age, ARDS or pneumonia as etiology, or failure to improve after 1 hour 2
• Delayed intubation in patients who fail to improve on HFNO within 1 hour should be avoided 2
• When intubation is required, use lung-protective ventilation with tidal volume 6 mL/kg predicted body weight and plateau pressure <30 cm H₂O 2

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Type 2 Respiratory Failure (Hypercapnic)

Definition and Pathophysiology

• Defined by PaCO₂ >6 kPa (45 mmHg) with pH <7.35, representing failure of ventilatory pump function 1, 3
• Normal carbon dioxide range is 4.6-6.1 kPa (34-46 mmHg) 2
• Primary mechanism is alveolar hypoventilation where minute ventilation is insufficient relative to CO₂ production 2, 5
• Contributing factors include 2, 5:
  • Increased airway resistance with flow-limited expiration 2
  • Dynamic hyperinflation creating intrinsic PEEP (PEEPi) - an inspiratory threshold load 2
  • Inspiratory muscle dysfunction with increased mechanical workload and energy consumption 2
  • V/Q abnormalities that worsen during acute exacerbations 2

Common Clinical Causes

• COPD exacerbations - the most common cause 1, 2, 5
• Obesity hypoventilation syndrome (OHS) 5
• Neuromuscular disorders - Duchenne muscular dystrophy, myasthenia gravis 1, 2
• Chest wall deformities - scoliosis, thoracoplasty 1, 2
• Drug overdose - opioids, benzodiazepines 2

Management Approach

• Controlled oxygen therapy targeting saturation of 88-92% using 24-28% Venturi mask or 1-2 L/min via nasal cannula to avoid worsening hypercapnia 2, 6
• Critical pitfall: Administering high-flow oxygen without monitoring CO₂ can precipitate CO₂ narcosis and respiratory arrest 2
• Monitor CO₂ levels closely with arterial blood gas analysis or transcutaneous CO₂ measurement 2

Non-Invasive Ventilation (NIV) Indications

• Initiate NIV when pH <7.35 and PaCO₂ >6 kPa (45 mmHg) after optimal medical therapy 1, 2, 6
• Specific indications include 1, 2:
  • COPD with respiratory acidosis (pH 7.25-7.35) - reduces mortality and intubation rates 2
  • Hypercapnic respiratory failure from chest wall deformity or neuromuscular disease 1
  • Weaning from tracheal intubation 1
• Use bi-level positive pressure ventilation (BiPAP) with initial settings: IPAP 10-15 cmH₂O and EPAP 4-8 cmH₂O 2, 6
• Delaying NIV initiation when pH <7.35 and PaCO₂ >6.0 kPa misses the therapeutic window 2

NIV Contraindications

• Impaired consciousness 1, 2
• Severe hypoxemia 1
• Copious respiratory secretions 1, 2
• Inability to protect airway 2
• Hemodynamic instability 2

Monitoring and Escalation

• Obtain arterial blood gases within 1-2 hours of starting NIV to assess for improvement in pH and PaCO₂ 6
• Repeat blood gases after 30-60 minutes if earlier sample showed little improvement 2, 6
• Failure to improve PaCO₂ and pH after 4-6 hours of NIV indicates treatment failure and need for intubation 2
• Signs of NIV failure requiring escalation 2, 6:
  • Worsening acidosis (pH <7.25) unresponsive to NIV 2, 6
  • Deteriorating level of consciousness 2, 6
  • Rising respiratory rate 2
  • Inability to clear secretions 2, 6

Ventilator Settings for COPD

• Use longer expiratory time and shorter inspiratory time to avoid further hyperinflation and increase in intrinsic PEEP 2, 5
• High levels of pressure support (>15 cmH₂O) may be needed for prolonged periods (>24 hours) during NIV weaning 2

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Acute vs. Chronic Respiratory Failure

Temporal Classification

• Acute respiratory failure - sudden onset with rapid deterioration of arterial blood gases 2
• Chronic respiratory failure - develops gradually over time with compensatory mechanisms such as renal bicarbonate retention 2
• Acute-on-chronic respiratory failure - presents unique challenges due to altered baseline physiology with elevated bicarbonate indicating chronic hypercapnia with renal adaptation 2, 6

Recognition of Acute-on-Chronic Pattern

• Blood gas pattern shows acidotic pH despite elevated bicarbonate (e.g., pH 7.2, HCO₃ 36 mmol/L, PCO₂ 77 mmHg) 6
• The acidotic pH suggests compensatory increase in bicarbonate is insufficient to normalize pH, indicating acute worsening of chronic condition 6
• Critical caveat: Rapid correction of hypercapnia in chronic respiratory failure should be avoided as it may lead to metabolic alkalosis 6

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Key Clinical Pitfalls to Avoid

• Never administer high-flow oxygen without CO₂ monitoring in suspected Type 2 failure - can precipitate respiratory arrest 2
• Do not delay NIV when arterial blood gases show pH <7.35 and PaCO₂ >6.0 kPa after optimal medical therapy 2
• Avoid delayed intubation in ARDS or pneumonia patients who fail to improve on HFNO within 1 hour 2
• Standard chest radiographs are poor predictors of oxygenation defect severity - classic ARDS findings may be asymmetric, patchy, or focal 2
• Measure arterial blood gases in patients with neuromuscular diseases, chest wall deformity, obesity, or acute confusional states even without significant breathlessness - they may be in respiratory failure 1