Why COPD Exacerbation Is Examined
COPD is the third most common cause of death in the UK and acute exacerbations account for over 100,000 emergency admissions per year. OSCEs examine it as an acute deterioration station (the patient's oxygen saturations are falling), a prescribing station (write the drug chart), and a communication station (explaining the diagnosis or NIV to the patient). The key distinguishing feature from other breathlessness stations is controlled oxygen and the type 2 respiratory failure context.
⚠️ Red Flag
High-flow oxygen in COPD is dangerous. Some COPD patients with chronic hypercapnia have a blunted central chemoreceptor response to CO2 and rely partly on hypoxic drive. Unrestricted oxygen abolishes this drive, causing hypoventilation, rising CO2, and potentially fatal respiratory acidosis. Target SpO2 88-92% in all known or suspected COPD patients.
Background — Understanding COPD
- Irreversible airflow obstruction (FEV1/FVC below 0.7 post-bronchodilator)
- Usually caused by smoking (90%)
- GOLD staging based on FEV1 % predicted:
- GOLD 1: FEV1 80% or above — mild
- GOLD 2: FEV1 50-79% — moderate
- GOLD 3: FEV1 30-49% — severe
- GOLD 4: FEV1 below 30% — very severe
Recognising an Acute Exacerbation
Definition: Acute worsening of respiratory symptoms beyond normal day-to-day variation requiring a change in treatment.
Cardinal symptoms (Anthonisen criteria):
- Increased breathlessness
- Increased sputum volume
- Increased sputum purulence
Signs of severe exacerbation:
- SpO2 below 92% on air (or below 88% on target O2)
- RR above 25/min
- HR above 110 bpm
- Accessory muscle use (sternocleidomastoid, scalene)
- Paradoxical abdominal movement (diaphragmatic fatigue)
- Cyanosis, confusion, drowsiness (hypercapnic encephalopathy)
- Speaking in single words or unable to speak
Investigations
| Investigation | What you are looking for |
|---|---|
| ABG | Type 2 respiratory failure (raised PaCO2 above 6.0 kPa + acidosis pH below 7.35); assess compensation |
| Spirometry / peak flow | Baseline and comparison with best known values |
| CXR | Hyperinflation, pneumothorax (important complication), new consolidation (pneumonia as precipitant) |
| FBC | Polycythaemia (chronic hypoxia), raised WCC (infection) |
| U&E | Electrolyte disturbance (hypokalaemia from nebulisers), renal function before steroids/NSAIDs |
| Sputum MC&S | Common organisms: Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae |
| Blood cultures | If fever or systemic sepsis signs |
| ECG | Right heart strain (cor pulmonale), arrhythmia |
Immediate Management
1. Controlled Oxygen
- Start at 24-28% via Venturi mask (not a non-rebreathe mask)
- Target SpO2 88-92%
- Recheck ABG after 30-60 minutes on oxygen
- If SpO2 above 92% — reduce O2 to keep within target range
2. Bronchodilators (Back-to-Back Nebulisers)
| Drug | Dose | Route |
|---|---|---|
| Salbutamol (SABA) | 2.5-5 mg | Nebulised — driven by air (not oxygen, to avoid hyperoxia) |
| Ipratropium bromide (SAMA) | 500 micrograms | Nebulised — combined with salbutamol |
| Frequency | Every 4-6 hours | Titrated to response |
⚠️ Red Flag
Nebulisers in COPD must be driven by air, not oxygen. Driving nebulisers with 8-10 L/min oxygen as in the cardiac ward protocol causes dangerously high inspired oxygen concentrations. Use a compressed air supply or clarify the driving gas with nursing staff.
3. Prednisolone
- 30-40 mg orally OD for 5 days
- Reduces treatment failure, length of stay, and relapse rate
- Consider IV hydrocortisone 100 mg QDS if unable to swallow
4. Antibiotics
- Prescribe if: purulent sputum (green/yellow), clinical signs of pneumonia, or systemic sepsis
- Amoxicillin 500 mg TDS for 5 days (first-line if no penicillin allergy)
- Alternatives: doxycycline 200 mg loading then 100 mg OD; clarithromycin 500 mg BD
- Antibiotic choice should follow local microbiology guidance
ABG Interpretation in COPD Exacerbation
| Pattern | Meaning | Action |
|---|---|---|
| Acidosis + raised PaCO2 + normal/low HCO3 | Acute type 2 respiratory failure (uncompensated) | Urgent NIV |
| Acidosis + raised PaCO2 + raised HCO3 | Acute-on-chronic type 2 failure (partially compensated) | NIV if pH below 7.35 |
| Normal pH + raised PaCO2 + raised HCO3 | Chronic hypercapnia (compensated) | Adjust O2 target; monitor closely |
| Hypoxaemia (pO2 below 8 kPa) without hypercapnia | Type 1 failure — not classic COPD | Consider pneumonia, PE, pneumothorax |
Non-Invasive Ventilation (NIV — BiPAP)
NICE indication for NIV in COPD:
Persistent acidotic hypercapnic respiratory failure despite 1 hour of maximal medical treatment:
- pH below 7.35
- PaCO2 above 6.0 kPa
| NIV parameter | Starting settings |
|---|---|
| IPAP (inspiratory pressure) | 10-15 cmH2O (titrate up to 20-30) |
| EPAP (expiratory pressure) | 4-5 cmH2O |
| Backup rate | 14-16 breaths/min |
| FiO2 | Titrate to SpO2 88-92% |
Recheck ABG after 1-2 hours. If not improving — escalate to ITU/intubation.
Discharge Planning
Before discharge ensure:
- SpO2 stable on air (or prescribed home oxygen) at target range
- Able to manage inhalers independently
- Complete prednisolone course and antibiotics dispensed
- Rescue pack prescribed (prednisolone + antibiotic) if 2 or more exacerbations/year
- Review inhalers and inhaler technique
- Pulmonary rehabilitation referral
- Spirometry on recovery (for GOLD staging)
- GP follow-up within 6 weeks
Frequently Asked Questions
"What is hypoxic drive and does it really matter in COPD?"
The hypoxic drive theory holds that some chronic hypercapnic COPD patients lose their sensitivity to CO2 as the primary respiratory stimulus and come to rely on hypoxaemia to drive breathing. While the hypoxic drive mechanism is more nuanced than classically taught, the clinical evidence is clear: unrestricted high-flow oxygen in COPD exacerbations is associated with increased mortality (the PRISM and Austin trials). The Haldane effect — oxygen displacing CO2 from haemoglobin in exchange for oxygen — also contributes to hypercapnia. Target SpO2 88-92% is the standard.
"What organisms most commonly cause infective COPD exacerbations?"
Haemophilus influenzae (most common bacterial pathogen, approximately 30%), Streptococcus pneumoniae (20%), Moraxella catarrhalis (10%), and Pseudomonas aeruginosa (in severe COPD with frequent exacerbations or recurrent hospital admissions — requires broader-spectrum antibiotic cover such as co-amoxiclav or ciprofloxacin). Respiratory viruses (rhinovirus, influenza, RSV, SARS-CoV-2) cause up to 50% of exacerbations.
"What is a rescue pack and who should have one?"
A rescue pack contains a course of prednisolone (usually 30 mg OD for 5 days) and an antibiotic (usually amoxicillin or doxycycline) for the patient to self-start at home at the first sign of an exacerbation. NICE recommends rescue packs for patients who have 2 or more exacerbations per year and are competent to self-manage. They significantly reduce hospitalisation rates and are associated with faster recovery. Patients need education on when and how to use the pack, and clear instructions to seek medical review if not improving in 48 hours.
"What is the role of long-term oxygen therapy (LTOT) in COPD?"
LTOT is indicated when PaO2 falls below 7.3 kPa (or below 8.0 kPa with polycythaemia, pulmonary hypertension, or peripheral oedema) on two occasions at least 3 weeks apart when clinically stable. It must be used for at least 15 hours per day (including sleep) to achieve survival benefit. The two RCTs that established its benefit (MRC and NOTT trials) showed it slows the progression of pulmonary hypertension and improves survival in hypoxaemic COPD. Ambulatory oxygen (for exercise) and palliative oxygen are separate prescriptions.
"What is pulmonary rehabilitation and who benefits?"
Pulmonary rehabilitation (PR) is a multidisciplinary programme combining supervised exercise training with education and self-management support, delivered over 6-8 weeks. It is one of the most effective interventions in COPD — improving exercise capacity, dyspnoea, quality of life, and reducing hospital readmissions. NICE recommends offering PR to all COPD patients with a Medical Research Council dyspnoea score of 3 or above (stops for breath after walking on level ground). It is also recommended post-exacerbation within 4 weeks of hospital discharge.
Related Posts
- Respiratory Examination OSCE — examining the COPD patient including barrel chest and wheeze
- ABG Interpretation OSCE — systematic arterial blood gas analysis in type 2 respiratory failure
- Acute Asthma Management OSCE — differentiating asthma from COPD exacerbation and comparing management