Role of non-invasive ventilation in respiratory disorders, including COPD, motor neurone disease, and obesity hypoventilation
What NIV is
Positive pressure ventilation delivered through a mask rather than an endotracheal tube.
Modes
| Mode | Delivers | Use |
|---|---|---|
| CPAP | One continuous pressure. Not a ventilator - no inspiratory support, does not augment tidal volume | OSA, cardiogenic pulmonary oedema, type 1 failure with recruitable lung |
| BiPAP (bi-level) | IPAP + EPAP; the difference = pressure support = tidal volume | Type 2 (hypercapnic) failure |
| AVAPS / volume-assured | Bi-level with an automatically adjusted pressure to hit a target tidal volume | Obesity hypoventilation, neuromuscular |
| HFNO | High-flow humidified nasal oxygen; small PEEP effect, dead-space washout | Type 1 failure, post-extubation, comfort/palliation |
- inc IPAP -> dec PaCO2 (bigger tidal volume)
- inc EPAP -> inc oxygenation (recruitment, offsets intrinsic PEEP, splints upper airway)
The two physiological jobs
- Type 2 failure - unload the respiratory muscles, augment alveolar ventilation -> dec PaCO2
- Type 1 failure / pulmonary oedema - recruit alveoli, dec shunt, and dec preload and LV transmural pressure
Evidence
- NIV vs invasive ventilation in acute respiratory failure: dec mortality, dec intubation (~20% absolute reduction), dec nosocomial infection and antibiotic use, shorter ICU stay
- In acute COPD exacerbation (Cochrane): dec mortality, dec need for intubation, dec treatment failure and complications, rapid improvement in pH, PaCO2 and respiratory rate within the first hour, shorter length of stay
- Number needed to treat in COPD exacerbation: ~5 to prevent one intubation, ~8-10 to prevent one death
- OHS: >70% also have OSA
Why it works in hypercapnic failure
- Respiratory muscle fatigue + inc load (hyperinflation, intrinsic PEEP) -> dec alveolar ventilation -> inc PaCO2 -> respiratory acidosis
- IPAP-EPAP difference augments tidal volume -> inc alveolar ventilation -> dec PaCO2
- EPAP offsets intrinsic PEEP (auto-PEEP) -> dec the inspiratory threshold load the patient must overcome to trigger a breath
- -> respiratory muscles rest, pH corrects, drive normalises
Why it works in cardiogenic pulmonary oedema
- inc intrathoracic pressure
- -> dec venous return -> dec preload
- -> dec LV transmural pressure -> dec afterload
- -> inc LV performance, inc cardiac output (in the congested ventricle)
- Alveolar recruitment -> restores FRC -> dec right-to-left intrapulmonary shunt -> inc oxygenation
- dec work of breathing (which can consume 20-30% of cardiac output in severe oedema)
- This is why CPAP works within minutes, before any diuresis
Why it fails
- Mask leak, intolerance, agitation
- Excessive secretions, bulbar weakness -> cannot protect the airway
- Very high minute ventilation requirement, severe acidosis with no improvement at 1-2 h
- Patient-ventilator asynchrony
Acute - when to start
- ABG is the decision-making test: type 2 respiratory failure with respiratory acidosis (pH <7.35 with PaCO2 >45 mmHg) persisting after initial medical therapy and controlled oxygen
- Do not wait for pH to fall further - earlier is better
- Reassess ABG at 1 hour - improvement in pH and PaCO2 is the key prognostic marker
Chronic - detecting nocturnal hypoventilation
- Nocturnal hypoventilation = rise in CO2 >10 mmHg from wakefulness to sleep
- Measured by paired evening and morning ABGs and/or transcutaneous CO2
- Screening triggers: morning headache, unrefreshing sleep, daytime somnolence, awake HCO3- raised (a metabolic clue to chronic CO2 retention), SpO2 <88% for >5 min overnight
- Neuromuscular disease: fall in FVC (supine and erect - a >20% supine drop = diaphragm weakness), MIP/SNIP (see respiratory muscle testing)
- Sleep study with CO2 monitoring; simple oximetry alone under-detects hypoventilation
Acute hypercapnic respiratory failure in COPD - the strongest indication
A. Acute hypercapnic respiratory failure in COPD - the strongest indication
- Bi-level NIV is the recommended initial management for acute hypercapnic respiratory failure with respiratory acidosis, *even at pH 7.20-7.25, provided the patient is alert and cooperative*
- Ward-based or HDU delivery where staffing allows; escalate location with lower pH
- Typical start: IPAP 12-15, EPAP 4-5 cmH2O, titrate IPAP up in 2-5 cmH2O steps to a target tidal volume and falling PaCO2
- Controlled oxygen: target SpO2 88-92%
- Concurrent medical therapy is not optional - bronchodilators, corticosteroid, antibiotics if indicated
- Escalate to invasive ventilation if: no improvement at 1-2 h, deteriorating consciousness, cannot protect the airway, haemodynamic instability, intolerance
- *Make and document a ceiling-of-care decision before starting* - is NIV a bridge, or the ceiling?
Other acute indications
B. Other acute indications
- Cardiogenic pulmonary oedema - CPAP or bi-level; dec intubation, faster resolution (no clear mortality difference between CPAP and BiPAP)
- Acute hypoxaemic (type 1) respiratory failure - weaker evidence; HFNO is often preferred (FLORALI). Avoid delaying necessary intubation
- Prevention of post-extubation respiratory failure - in high-risk patients (COPD, hypercapnia, obesity, cardiac failure)
- Facilitating early extubation in COPD ("weaning to NIV")
- Immunocompromised patients with hypoxaemia - avoid intubation where possible
- Chest wall trauma, blunt chest injury
- Palliative - relief of dyspnoea where intubation is not appropriate
Chronic domiciliary NIV
C. Chronic domiciliary NIV
1. Obesity hypoventilation syndrome (OHS)
- Definition: BMI >=30 + awake PaCO2 >45 mmHg + no other cause of hypoventilation
- CPAP is first-line (since >70% have coexisting OSA), bi-level if CPAP fails to correct CO2 or there is severe hypoventilation
- Both are effective at improving PaCO2 in stable disease
- Weight loss is the definitive treatment - diet, exercise, pharmacotherapy (GLP-1/GIP), bariatric surgery
- Treat comorbid OSA, hypothyroidism, sedative use
2. Neuromuscular disease and chest wall disease
- The clearest survival and quality-of-life benefit of any chronic NIV indication
- Motor neurone disease: NIV improves survival (by months) and quality of life in patients without severe bulbar involvement
- In bulbar-predominant disease the survival benefit is attenuated and the aim is symptom and quality-of-life benefit; secretion management and mask tolerance are the limiting problems
- Start when: symptoms of hypoventilation, FVC <50% predicted (or <80% with symptoms), MIP <60 cmH2O, nocturnal SpO2 <88% for >5 min, or daytime PaCO2 >45 mmHg
- Add cough assist / mechanical insufflation-exsufflation when MEP <60 cmH2O or peak cough flow <270 L/min
- Kyphoscoliosis, post-polio, diaphragm paralysis - similar approach, often excellent long-term outcomes
3. COPD
- The most contested indication - practice varies worldwide
- Evidence supports high-intensity NIV targeted at lowering PaCO2 in selected patients with persistent hypercapnia (PaCO2 >53 mmHg) 2-4 weeks after an acute exacerbation - dec readmission and mortality (HOT-HMV, Köhnlein)
- Not indicated for stable COPD without significant chronic hypercapnia
Contraindications
D. Contraindications
- Absolute: cardiac or respiratory arrest, inability to protect the airway, facial trauma/burns/surgery, complete upper airway obstruction, undrained pneumothorax (relative - drain first)
- Relative: agitation/uncooperative, severe haemodynamic instability, copious secretions, vomiting, recent upper GI surgery, severe encephalopathy
Practical
E. Practical
- Full face mask usually for acute; nasal or pillows for chronic
- Humidification, pressure-area care to the nasal bridge
- Monitor: RR, tidal volume, leak, synchrony, conscious level, ABG at 1 h, 4 h and after any change
- Regular breaks for drinks, medications and nebulisers once stabilising
Associations
- OSA - coexists with OHS (>70%) and with COPD ("overlap syndrome" - worse nocturnal desaturation, higher pulmonary hypertension and mortality)
- Neuromuscular disease - MND/ALS, Duchenne muscular dystrophy, myotonic dystrophy, SMA, post-polio, high cervical cord injury, phrenic nerve palsy, myasthenia (crisis - NIV can avert intubation)
- Chest wall disease - kyphoscoliosis, thoracoplasty, severe obesity
- Cor pulmonale and pulmonary hypertension - a consequence of chronic nocturnal hypoventilation
- Bronchiectasis and CF - NIV as a bridge to transplant
- Long-term oxygen therapy - a separate decision, made on PaO2 <=55 mmHg (or <=59 with cor pulmonale/polycythaemia) when stable on optimal therapy; oxygen alone does not treat hypoventilation and can worsen it
Outcomes
- Acute COPD exacerbation with NIV: hospital survival ~80-90%; those who fail NIV and are not intubated have very high mortality
- Chronic NIV in neuromuscular disease: survival benefit measured in months to years, with substantial symptomatic benefit
- OHS: untreated mortality is high (~20-25% at 18 months in some series); treatment markedly improves this
Complications
- Mask-related: pressure ulceration of the nasal bridge, claustrophobia, conjunctivitis from leak
- Gastric distension and aspiration
- Dry mucosa, epistaxis
- Hypotension (inc intrathoracic pressure -> dec venous return) - especially in the preload-dependent or hypovolaemic patient
- Barotrauma / pneumothorax (uncommon)
- Delay in necessary intubation - the most dangerous complication
- Patient-ventilator asynchrony, sleep fragmentation
Follow-up in chronic NIV
- Download compliance and leak data; target >4 h/night
- Repeat morning ABG or transcutaneous CO2, overnight oximetry
- Re-titrate with disease progression; anticipate need for daytime use in neuromuscular decline
- Revisit goals of care as the disease progresses - NIV can become a life-prolonging therapy the patient did not intend
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