Type II Respiratory Failure

Type II Respiratory Failure (Hypercapnic Respiratory Failure) 

Definition 

Type II respiratory failure is characterized by alveolar hypoventilation, resulting in: 
PaO₂ < 8KPa or 60 mmHg (hypoxemia) 
PaCO₂ > 6.7KPa or 50 mmHg (hypercapnia) 

Sometimes referred to as hypercapnic respiratory failure, because CO₂ retention is a hallmark. 

Pathophysiology 

Type II respiratory failure occurs when the respiratory system fails to remove CO₂ adequately.  

This can result from: 

Decreased ventilation due to respiratory muscle weakness or central drive failure. 
Increased dead space ventilation
Severe airway obstruction

Key mechanisms: 

Hypoventilation → CO₂ retention → respiratory acidosis. 
Chronic cases → renal compensation (HCO₃⁻ retention). 

Common physiological scenarios: 


 
Causes:
 
Mnemonic: “CHAMPS” 
C – CNS depression (drug overdose, head injury) 
H – Hypoventilation due to neuromuscular disease 
A – Airway obstruction (COPD, asthma, severe bronchitis) 
M – Mechanical chest wall problem (trauma, obesity) 
P – Pneumothorax, pleural effusion (severe restriction) 
S – Severe lung disease (advanced COPD, cystic fibrosis) 

Clinical Features:

General signs: 

Dyspnoea (often progressive (if chromic)) 
Tachypnoea (may be absent if fatigue develops) 
Confusion, drowsiness, or headache (due to CO₂ retention) 
Cyanosis (may be less prominent than in hypoxemic RF) 
Use of accessory muscles 

Severe or chronic hypercapnia: 
Flapping tremor (asterixis) 
Morning headaches (CO₂ buildup overnight) 
Papilledema in extreme cases 

Investigations 

Arterial Blood Gas (ABG) 

PaO₂ < 8KPa or 60 mmHg 
PaCO₂ > 6.7KPa or 50 mmHg 
pH: ↓ in acute, near-normal in chronic (renal compensation) 
HCO₃⁻: ↑ in chronic hypercapnia (renal compensation) 

Chest X-ray 
Evaluate lung pathology (COPD changes, consolidation, effusions) 

Pulmonary function tests (PFTs) 
Obstructive patterns in COPD/asthma 
Restrictive patterns in chest wall disease 

Other tests 
ECG, echocardiography (right heart strain in chronic cases) 
Sleep studies if obesity hypoventilation suspected 
 
Management 

1. Treat underlying cause: 
Bronchodilators for COPD/asthma 
Treat infections 
Adjust medications that depress respiration 
Address neuromuscular/chest wall disease 

2. Supportive oxygen therapy: 
Caution: In chronic CO₂ retainers (COPD), high-flow oxygen may worsen hypercapnia however in the acute phase give high flow oxygen in extremis and titrate down/support early with NIV 
Target SaO₂ 88–92% if indictaed by a medical professional (and documented)

3. Ventilatory support: 

Non-invasive ventilation (NIV) preferred for COPD exacerbations or obesity hypoventilation. 
Invasive mechanical ventilation if severe or NIV fails (note: can be difficult to wean from mechanical ventilation so ethical decision making essential). 

4. Monitoring: 
ABG monitoring for PaCO₂ trends 
Clinical signs of CO₂ retention or respiratory distress 

Key Points: 

Type II RF = hypercapnic → PaCO₂ > 6.7KPa or 50 mmHg 
Usually due to hypoventilation, not oxygen diffusion problems 
Chronic hypercapnia = body partially compensates via renal HCO₃⁻ retention → pH may be near normal 
Main danger: CO₂ narcosis (confusion, drowsiness, coma and apnoea) 
Management = treat cause + support ventilation, carefully titrate oxygen therapy 

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