01Purpose and principlesWhat the treatment does and how it fits into care.
Bilevel NIV uses a higher inspiratory pressure (IPAP) and lower expiratory pressure (EPAP). Their difference drives ventilatory assistance; EPAP helps recruit alveoli and overcome intrinsic PEEP.
The evidence is strongest for acute acidotic COPD exacerbation. NIV may also help obesity hypoventilation and chest-wall/neuromuscular disease, often at earlier thresholds with specialist input.
A mask and machine do not constitute safe NIV. Success depends on patient selection, explanation, fit, secretion management, rapid titration, close nursing observation and a pre-agreed failure response.
Severe acidosis does not automatically prohibit a trial where intubation capability is available, but it increases failure risk and should trigger critical-care involvement rather than prolonged ward-only NIV.
Key points
- For acute COPD, consider NIV when pH remains below 7.35 with PaCO2 above 6.5 kPa and tachypnoea after about 1 hour of optimal medical treatment.
- NICE calls NIV the treatment of choice for persistent hypercapnic ventilatory failure during a COPD exacerbation despite optimal medical therapy.
- Start acute NIV within 60 minutes of the qualifying blood-gas result and, for patients presenting with AHRF, within 120 minutes of hospital arrival where possible.
- Before starting, treat reversible factors and document diagnosis, target SpO2, interface/settings, monitoring location, escalation to intubation and what to do if NIV fails.
- Typical initial bilevel settings are IPAP 10–15 cmH2O and EPAP 4–5 cmH2O, with a backup rate around 12–16/min; titrate IPAP over 10–30 minutes toward 20–30 as needed and tolerated.
- Increase pressure support (IPAP minus EPAP) to improve tidal volume and lower PaCO2; increase EPAP/FiO2 for persistent hypoxaemia while preserving adequate pressure support.
- Repeat ABG about 1 hour after starting and after material setting changes, then around 4 hours; improving pH, PaCO2, respiratory rate and distress indicates response.
- Continuous SpO2 and cardiac monitoring are expected early; trained staff, an appropriate NIV area and rapid access to blood gases are treatment requirements, not extras.
- An undrained pneumothorax, fixed upper-airway obstruction, major facial injury/burn or inability to protect the airway makes NIV unsafe or impossible until the problem is corrected.
- NIV is not routine for acute asthma or isolated hypoxaemic pneumonia; these groups need early critical-care assessment because failure can be abrupt.
02Indications, selection and cautionsWho may benefit, who needs urgent treatment and important alternatives.
Persistent pH below 7.35 and PaCO2 above 6.5 kPa with tachypnoea after controlled oxygen, bronchodilators, steroids and cause treatment.
Hypercapnia, rapid shallow breathing, vital-capacity decline or weak cough may justify NIV before severe acidosis; bulbar dysfunction and secretion load increase failure risk.
Respiratory arrest, inability to protect airway, worsening consciousness, severe haemodynamic instability, refractory hypoxaemia or rapidly worsening acidosis.
Large mask leak, wrong circuit/exhalation port, poor synchrony, insufficient IPAP, blocked secretions or an untreated pneumothorax can mimic biological failure.
Less distress and respiratory rate, improving pH and falling PaCO2 within 1–2 hours support continuation; improvement in saturation alone is insufficient.
03Assessment before treatmentTests and checks that guide safe selection.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Pre-NIV ABGFirst step - Why
- Confirm acute hypercapnic failure and establish severity.
- Interpretation and limitations
- In COPD, pH below 7.35 with PaCO2 above 6.5 kPa after initial therapy supports NIV; pH below about 7.25 carries higher failure risk and warrants critical-care review.
- 02
Chest X-ray or thoracic imaging - Why
- Identify pneumonia, oedema, pneumothorax, effusion or another cause.
- Interpretation and limitations
- Drain a pneumothorax before NIV where clinically possible; do not delay emergency decompression for imaging.
- 03
ABG at about 1 hour and 4 hours - Why
- Measure response and detect failure.
- Interpretation and limitations
- Rising pH and falling PaCO2 are favourable. Persistent pH below 7.25, respiratory rate above 25 or new confusion despite optimised NIV needs immediate senior/critical-care review.
- 04
Continuous SpO2 and ECG - Why
- Detect hypoxaemia and arrhythmia during a high-risk treatment.
- Interpretation and limitations
- Maintain prescribed target, usually 88–92% in hypercapnic failure; sudden desaturation prompts patient, circuit, mask, secretion and pneumothorax checks.
- 05
FBC, U&E, CRP/cultures and ECG - Why
- Find infection, anaemia, electrolyte triggers and cardiac disease.
- Interpretation and limitations
- Treat the precipitant; NIV cannot compensate for uncorrected sepsis, severe hypokalaemia or uncontrolled arrhythmia.
- 06
Interface/circuit and synchrony assessment - Why
- Ensure prescribed pressures reach the patient.
- Interpretation and limitations
- Check exhalation port, intentional versus excessive leak, trigger, rise time and cycling; escalate technical problems to a competent NIV practitioner.
04Treatment approachPreparation, options, escalation and aftercare.
01PrepareOne-hour optimisation and decisionFirst stepSuspected COPD-related acute hypercapnic respiratory failure.+
- 1Give controlled oxygen to 88–92%, nebulised bronchodilators, systemic steroid and antibiotics when indicated; stop/reverse respiratory depressants and manage secretions.
- 2Obtain/repeat ABG after initial treatment. If pH remains below 7.35 with PaCO2 above 6.5 kPa and tachypnoea, decide on NIV promptly.
- 3EscalationBefore the mask, document escalation/ceiling, treatment location, target SpO2, settings, ABG schedule and the clinician to call for failure.
02StartInitial bilevel prescriptionAppropriate patient has consented or assented and trained staff/equipment are ready.+
- 1Sit upright, explain the treatment and select the smallest comfortable full-face/oronasal interface with the correct circuit and exhalation port.
- 2Start S/T mode around IPAP 10–15 and EPAP 4–5 cmH2O with backup rate 12–16/min; entrain oxygen to the prescribed target.
- 3Over 10–30 minutes, increase IPAP in 2–5 cmH2O steps toward effective ventilation, commonly 20–30, while correcting leak and synchrony. Seek expert review before pressures beyond the service's protocol.
- 4Use as continuously as tolerated in the first hours/24 hours, with supervised breaks for hydration, medication, skin care and secretion clearance.
03ReassessOne-hour responseApproximately 1 hour after NIV begins or sooner if deterioration occurs.+
- 1Repeat ABG and review pH, PaCO2, PaO2, respiratory rate, consciousness, comfort, leak and tidal-volume/chest-movement trend.
- 2High PaCO2/low tidal volume: improve fit/synchrony and raise IPAP. Persistent hypoxaemia: check cause, raise FiO2 and/or EPAP while preserving pressure support.
- 3If pH/PaCO2 and distress improve, continue and repeat around 4 hours. If pH worsens, remains below about 7.25, RR stays above 25, confusion develops or oxygen target cannot be met, activate the intubation/critical-care plan.
04WeanAfter acidosis resolvespH and PaCO2 have improved, cause is controlled and work of breathing is falling.+
- 1Continue substantial NIV use during the first 24 hours, then lengthen daytime breaks while monitoring symptoms and gases.
- 2Reduce overnight support later, commonly over the next 48–72 hours, if the acute trigger resolves and gases remain stable.
- 3If hypercapnia, somnolence or repeated failure persists, seek specialist home-ventilation assessment rather than arranging unsupported discharge.
05Regimens, contraindications and interactionsTreatment details and the circumstances that modify them.
Salbutamol nebuliser
2.5 mg nebulised, increasing to 5 mg in severe bronchospasm and repeating according to response; use compressed air to drive in hypercapnia risk while oxygen is delivered separately to target.Tachycardia, tremor, hypokalaemia and lactate rise; review frequent dosing and cardiac rhythm.
Ipratropium bromide nebuliser
500 micrograms nebulised, commonly every 4–6 hours during a severe COPD exacerbation, alongside short-acting beta2 agonist.Dry mouth, urinary retention and acute angle-closure glaucoma if aerosol reaches the eyes; not a treatment for ventilatory failure itself.
Prednisolone
30 mg orally once daily for 5 days for a COPD exacerbation; use an equivalent parenteral corticosteroid only when oral treatment is not feasible.Hyperglycaemia, delirium, fluid retention and infection risk; record stop date.
Oxygen entrained into NIV
Titrate flow/FiO2 to SpO2 88–92% for acute hypercapnic respiratory failure unless an individual target is documented.Excess FiO2 can worsen hypercapnia; oxygen concentration varies with leak, circuit and pressure. Verify with blood gases, not SpO2 alone.
06Complications, monitoring and follow-upAdverse effects, response and longer-term review.
- Continuous SpO2 and ECG early, with frequent respiratory rate, effort, consciousness, BP, comfort, mask leak and skin checks.
- ABG approximately 1 hour after starting, around 4 hours and after significant setting/oxygen changes; act on failure rather than collecting gases passively.
- Ensure trained review is immediately available and a senior competent clinician reviews progress within 4 hours at the latest.
- Inspect nasal bridge/face, eyes, mouth and pressure areas; alternate interface or protective dressing without creating a large leak.
- Track fluid balance, secretions, cough and nutrition; coordinate supervised mask breaks and consider NG decompression when gastric distension/vomiting risk is important.
- Reassess the escalation decision whenever pH, consciousness or haemodynamics worsen; a 'not for intubation' decision still requires symptom and palliative planning if NIV fails.
07Special situationsVariants, exceptions and circumstances that change the usual approach.
Pressure support ventilates
IPAP minus EPAP is the assisting pressure. Raising both equally may improve recruitment but does not increase pressure support.
Early IPAP underdosing is common
Starting gently improves tolerance, but leaving IPAP at 10–12 despite persistent hypercapnia often fails to unload the patient; titrate with competent monitoring.
A mask leak is a clinical finding
It can reduce delivered support, disturb triggering, dry the eyes and falsely suggest treatment failure; troubleshoot before escalating pressures blindly.
The first hour predicts the pathway
Clinical and gas improvement supports continuation; worsening acidosis despite a technically sound trial should accelerate intubation decisions.
NIV has a location requirement
Mortality is high and failure can be rapid. A designated area, competent staff and point-of-care gases are part of the intervention.
08Common pitfallsFrequent interpretation and management errors.
- 01
Starting NIV before writing an escalation plan.
- 02
Using NIV for a patient who cannot protect the airway or has an undrained pneumothorax.
- 03
Leaving IPAP too low despite persistent hypercapnia and high work of breathing.
- 04
Judging success from improved SpO2 without checking pH and PaCO2.
- 05
Continuing a failing NIV trial for hours and delaying intubation.
- 06
Using routine sedatives to force tolerance without airway-capable monitoring and senior critical-care oversight.