Key Facts

Non-invasive ventilation (NIV) provides ventilatory support through a mask interface, avoiding the need for intubation. BiPAP (with separate inspiratory and expiratory pressures) augments ventilation and is used for hypercapnic failure. CPAP (single constant pressure) splints airways open and improves oxygenation.

Epidemiology

NIV use has increased dramatically over the past two decades. The 2017 UK National COPD Audit showed that ~14% of COPD admissions received NIV. Appropriate use of NIV reduces intubation rates and improves outcomes. However, audit data also shows significant variation in quality: only 43% of NIV episodes met BTS quality standards for setup and monitoring.

Aetiology

Conditions requiring BiPAP:

• Acute exacerbation of COPD with acidotic hypercapnia (commonest indication)
• Acute hypercapnic failure in neuromuscular disease, chest wall deformity, obesity hypoventilation
• Decompensated OSA with hypercapnia

Conditions requiring CPAP:

• Acute cardiogenic pulmonary oedema (reduces preload and afterload, improves oxygenation)
• Obstructive sleep apnoea
• Post-extubation support

Pathophysiology

BiPAP: IPAP augments tidal volume during inspiration, reducing the work of breathing and improving alveolar ventilation → lowers PaCO₂. EPAP maintains alveolar recruitment, prevents atelectasis, and counterbalances intrinsic PEEP (auto-PEEP) in COPD. The net effect is improved gas exchange with reduced respiratory muscle work.

CPAP: delivers a single positive pressure throughout the respiratory cycle. This recruits collapsed alveoli (improving V/Q matching and oxygenation), reduces preload (beneficial in pulmonary oedema), and splints the upper airway (treating OSA).

Indications for Acute NIV (BiPAP)

• COPD with acute hypercapnic respiratory failure: pH 7.25-7.35, PaCO₂ >6 kPa despite maximal medical therapy (nebulised bronchodilators, controlled O₂, steroids)
• Other causes of acute hypercapnic failure (neuromuscular, chest wall, OHS)

Indications for CPAP

• Acute cardiogenic pulmonary oedema not responding to IV diuretics/nitrates
• Type 1 respiratory failure (HFNO may be preferred in some settings)

Signs of NIV Failure

• pH not improving (or worsening) after 1-2 hours of NIV
• Worsening respiratory distress, rising respiratory rate
• Falling GCS, inability to tolerate mask
• Worsening hypoxaemia despite adequate FiO₂

Red Flags

• pH <7.25 at presentation (consider early intubation discussion)
• pH <7.15 (NIV unlikely to succeed — intubation usually required)
• GCS <8 or inability to protect airway
• Haemodynamic instability
• Respiratory arrest

Bedside

• ABG: essential before starting and at 1-2 hours after — pH, PaCO₂, PaO₂, HCO₃⁻
• SpO₂: continuous monitoring during NIV
• Respiratory rate: should reduce with effective NIV
• Mask fit assessment: minimise leak
• GCS: level of consciousness

Bloods

• FBC, U&Es, CRP: underlying cause assessment
• BNP: if cardiac cause suspected
• Venous blood gas: can screen for hypercapnia if ABG delayed

Imaging

• CXR: exclude pneumothorax (contraindication), identify underlying cause
• Portable echo: if cardiogenic pulmonary oedema vs COPD uncertain

Special Tests

• Serial ABG: at 1 hour, 4 hours, and as clinically indicated — to assess NIV response
• Tidal volume/minute ventilation: measured on NIV ventilator if available
• Sleep study: for ongoing domiciliary NIV assessment

Non-pharmacological

• Setup: full face mask (oronasal) is standard for acute NIV; nasal mask if not tolerated
• Starting pressures: IPAP 12-15 cmH₂O, EPAP 4-5 cmH₂O
• Titration: increase IPAP by 2-5 cmH₂O increments (max ~25-30 cmH₂O) targeting improved pH and PaCO₂
• Supplemental O₂: entrain via NIV circuit to target SpO₂ 88-92% (COPD)
• Monitoring: continuous SpO₂, ABG at 1 hour then 4 hours; respiratory rate, comfort, mask leak
• Duration: aim for continuous use initially; wean gradually as pH normalises
• Ceiling of care discussion: escalation plan (intubation if NIV fails?) should be documented before starting

Pharmacological

• Concurrent medical therapy: nebulised salbutamol 5 mg + ipratropium 500 mcg, prednisolone 30 mg OD (or hydrocortisone 200 mg IV), antibiotics if infective exacerbation
• CPAP for pulmonary oedema: combined with IV furosemide 40-80 mg, GTN infusion 1-10 mg/hr

Surgical/Interventional

• Invasive ventilation (intubation): if NIV fails — defined as pH not improving after 1-2 hours, worsening clinical state, or pH <7.15
• Tracheostomy: for prolonged ventilatory weaning or chronic NIV dependence

Referral Criteria

• ICU/HDU referral if pH <7.25 or failing NIV
• Home ventilation service referral if persistent hypercapnia after acute episode or chronic ventilatory failure
• Sleep service referral if OSA identified
• Palliative care discussion if NIV is ceiling of treatment and not improving

NIV for acute COPD exacerbations reduces intubation rate (RR 0.41), mortality (NNT ~10), and length of stay. In-hospital mortality for COPD patients receiving NIV is 12-15%. NIV failure (requiring intubation or death) occurs in approximately 15-20%. Predictors of failure: pH <7.25 after 1-2 hours, high APACHE II score, excessive secretions, poor mask tolerance. Domiciliary NIV for chronic hypercapnic COPD reduces readmission and improves quality of life (HOT-HMV trial).

NIV Setup Checklist

Key Trials and Guidelines