COPD

Definition

A common, preventable and treatable disease characterised by persistent, usually progressive airflow limitation that is not fully reversible, associated with a chronic inflammatory response of the airways and lung to noxious particles or gases (chiefly tobacco smoke).

The COPD-X framework

C	Confirm diagnosis and assess severity
O	Optimise function
P	Prevent deterioration
D	Develop a plan of care (self-management)
X	Manage eXacerbations

C — Confirm diagnosis

Who to suspect

Consider COPD in anyone >35 years old with breathlessness, chronic cough, or sputum production, particularly current or ex-smokers. A history of ≥20 pack-years, progressive exertional dyspnoea and a productive cough in a lifelong smoker is the classic presentation, but COPD cannot be diagnosed reliably on history and examination alone — spirometry is required.

Causes/risk factors: cigarette smoking (the dominant cause; clinically significant COPD develops in ~25% of smokers), biomass/smoke exposure, occupational dusts and fumes (cadmium, silica), alpha-1 antitrypsin deficiency, chronic bronchial hyperresponsiveness/longstanding asthma, and childhood factors affecting lung development.

Symptoms and signs

• Breathlessness (initially exertional, insidiously progressive), chronic cough, sputum production, chest tightness, wheeze, airway irritability.
• Fatigue, anorexia and weight loss occur with more advanced disease.
• Signs are often absent early: later findings include tachypnoea, reduced chest expansion, hyperinflation, hyper-resonant percussion, diminished breath sounds ± wheeze, and signs of respiratory failure or cor pulmonale.

Spirometry

Perform pre- and post-bronchodilator spirometry. COPD is confirmed by persistent airflow limitation:

Post-bronchodilator FEV1/FVC < 0.7

Severity is then graded by % predicted FEV1:

Severity	% predicted FEV1	Typical symptoms
Mild	60–80%	Few symptoms; breathless on moderate exertion; recurrent chest infections
Moderate	40–59%	Breathless on level ground; increasing limitation of daily activities; cough/sputum; exacerbations needing steroids/antibiotics
Severe	<40%	Breathless on minimal exertion; daily activities severely curtailed; regular sputum production; frequent exacerbations

Overdiagnosis and underdiagnosis are both well-documented problems. Interpret borderline results cautiously, particularly in patients >65 (risk of overdiagnosis) or <45 (risk of underdiagnosis), or in those without a smoking or occupational-exposure history — a BOLD-cohort analysis found that a large proportion of people carrying a COPD label do not have obstructive spirometry, while many symptomatic patients with obstructive spirometry remain undiagnosed in primary care. If a bronchodilator response >400 mL FEV1 is seen, consider asthma or asthma-COPD overlap rather than pure COPD (see below).

Further investigations

Used to exclude alternative/coexisting diagnoses and assess comorbidity, not to diagnose COPD itself:

• Chest X-ray — usually to exclude lung cancer or other pathology; may be normal in COPD.
• FBC/UEC — identify anaemia or polycythaemia.
• ECG/echo — assess for cor pulmonale, cardiac comorbidity.
• Arterial blood gas — in advanced disease (↑PaCO2, ↓PaO2) and for long-term oxygen therapy (LTOT) assessment.
• DLCO (diffusing capacity for carbon monoxide) — reduced in COPD/emphysema but normal in asthma; useful where the diagnosis is unclear.
• Consider alpha-1 antitrypsin level in early-onset disease (<40 years) or a family history suggestive of the deficiency.

O — Optimise function

Non-pharmacological therapy

• Smoking cessation is the single most effective intervention — offer brief intervention at every visit; combination nicotine replacement (patch + short-acting form) or varenicline are more effective than either nicotine replacement alone.
• Pulmonary rehabilitation — offer to all patients with exertional dyspnoea (including soon after a hospitalised exacerbation, and to those who have stopped being active); a structured multidisciplinary program of exercise training, education (including breathing technique) and behaviour change. Reduces hospitalisation, improves exercise capacity and quality of life, and is cost-effective.
• Nutrition review, physical activity, and management of comorbidities.

Pharmacotherapy — current stepwise approach (COPD-X Handbook)

Reliever therapy: SABA (salbutamol) or SAMA (ipratropium) as needed — short-term symptomatic relief only, does not alter the rate of lung-function decline, exacerbations, or survival. SABA is generally preferred first-line (better side-effect profile); ipratropium is second-line (anticholinergic side effects) though may have marginally better efficacy in some patients. A combination of both can be used if response to either alone is inadequate.

Long-acting bronchodilators (LAMA/LABA): provide symptomatic relief, improve exercise capacity, and — unlike short-acting agents — reduce the frequency and severity of exacerbations and improve quality of life. If starting a LAMA, cease regular SAMA. Available as LAMA monotherapy, LABA monotherapy, or fixed-dose LAMA/LABA combination inhalers (e.g. tiotropium/ olodaterol, umeclidinium/vilanterol, indacaterol/glycopyrronium, aclidinium/formoterol).

Triple therapy (ICS/LABA/LAMA): reserved for the exacerbation-history criterion above. Rinse the mouth after ICS use (reduces oral candidiasis and systemic absorption) and use a spacer with a pMDI. ICS use carries an increased risk of pneumonia in COPD, which must be weighed against the exacerbation-reduction benefit — hence ICS is never used as monotherapy and is reserved for those who meet the exacerbation criteria above.

Assessment interval: there’s no single fixed timeframe for judging a step-up — symptoms/dyspnoea can usually be assessed at around 6 weeks, but exacerbation frequency and quality-of-life change may take 6 months or longer to become apparent.

P — Prevent deterioration

• Smoking cessation — the single most important intervention to slow disease progression; anxiety/depression are associated with higher smoking rates and lower quit success, so treat these in parallel.
• Vaccination — offer and keep up to date: annual influenza, pneumococcal, and COVID-19 vaccination for everyone with COPD, per the current Australian Immunisation Handbook (specific dosing/interval schedules are set there rather than being fixed in the COPD-X guideline — check the current Handbook rather than relying on a fixed interval).
• Reduce exacerbations — the strongest predictor of a future exacerbation is a past exacerbation in the last 12 months; frequent exacerbations drive faster FEV1 decline, worse health status and higher mortality. Optimise pharmacotherapy and use a written action plan to treat exacerbations early.
• Long-term oxygen therapy (LTOT) — survival benefit in patients with persistent resting hypoxaemia. Eligibility (confirmed by arterial blood gas): PaO2 <55 mmHg (roughly SpO2 <88%) at rest on air, or PaO2 ≤59 mmHg with evidence of polycythaemia, pulmonary hypertension, or right heart failure. Must be worn >18 hours/day for benefit. Current smoking is an absolute contraindication (fire risk). Refer to a specialist service for LTOT assessment if resting SpO2 is below 90%.
• Manage comorbidities — cardiovascular disease (cardioselective beta-blockers are generally safe in COPD and shouldn’t be withheld — up-titrate gradually), anxiety/depression (CBT ± medication), osteoporosis (COPD patients have lower bone density and higher fracture risk — manage per standard osteoporosis guidelines), diabetes (worsened by high-dose ICS; limit oral-steroid courses and monitor glucose more closely), and pulmonary hypertension/cor pulmonale (consider with ankle oedema, raised JVP, palpable parasternal heave, loud P2 — vasodilators are not generally effective in COPD-associated pulmonary hypertension).
• Consider referral for surgical options in selected patients: bullectomy, lung volume reduction surgery, lung transplantation.

D — Develop a plan of care

• GP Management Plan / Team Care Arrangement, engaging practice nurses, physiotherapists, dietitians, exercise physiologists and pharmacists (e.g. Home Medicines Review) as needed.
• Written COPD Action Plan — a self-management plan the patient (and carers) use to recognise a flare-up early and know what action to take (increase reliever use → start prednisolone/antibiotics per pre-agreed regimen → when to call for urgent review). Lung Foundation Australia provides a standard template. Review it annually and after every exacerbation.
• Address psychological impact and initiate advanced care planning where appropriate — accurately judging approaching end-of-life in COPD is acknowledged to be difficult, so this conversation should start earlier than it might in some other progressive diseases.
• Refer to a respiratory physiotherapist for airway clearance technique training if there is chronic cough with ongoing sputum production/clearance difficulty.

Indications for respiratory referral

Reason	Purpose
Diagnostic uncertainty / exclusion of asthma	Confirm diagnosis, optimise treatment
Haemoptysis	Urgent exclusion of malignancy
Rapid functional decline	Optimise management
Persistent symptoms despite treatment	Optimise management, exclude other conditions
Frequent chest infections (>1/year)	Assess for bronchiectasis
New-onset ankle oedema	Assess for cor pulmonale
SpO2 <92% (or <90% for LTOT assessment specifically) when stable	Assess for oxygen therapy
Bullous disease on imaging	Assess for bullectomy
Onset <40 years	Confirm diagnosis, exclude alpha-1 antitrypsin deficiency
Daytime sleepiness/snoring	Assess for sleep-disordered breathing
Dyspnoea with chest tightness, anxiety, dizziness	Consider dysfunctional breathing
Severe disease	Consider transplant/lung-volume-reduction assessment

X — Manage eXacerbations

Definition: an acute (minutes-to-hours) worsening of the patient’s baseline dyspnoea, cough and/or sputum, beyond normal day-to-day variation, that may warrant a change in regular medication or hospital admission. Exacerbations cluster in time — a recent exacerbation is the strongest predictor of a future one — and frequency increases as disease severity worsens. Delay ≥24 hours in presenting/starting treatment roughly doubles the chance of hospitalisation, so early recognition and treatment matters.

Common triggers: viral or bacterial respiratory infection (lower airways are frequently colonised by Haemophilus influenzae, Streptococcus pneumoniae and Moraxella catarrhalis — colonisation itself doesn’t always mean the exacerbation is infective), left ventricular failure, psychosocial stressors, air pollution. Consider pulmonary embolism in patients requiring hospitalisation for an exacerbation, especially if it doesn’t respond as expected.

Community-based treatment

• Inhaled bronchodilators: salbutamol 400–800 mcg (4–8 puffs) via MDI + spacer every 3–4 hours, titrated to response (a nebuliser is no more effective than MDI+spacer if technique is adequate).
• Oral corticosteroids: prednisolone 30–50 mg each morning for 5 days, then stop — tapering is not necessary for courses of this length.
• Antibiotics if there are clinical features of infection (increased sputum volume, increased sputum purulence, and/or fever): amoxicillin 500 mg TDS (or 1 g BD) or doxycycline 200 mg stat then 100 mg daily, for 5 days. Routine sputum culture is not recommended unless there is a poor treatment response or recurrent infections.

Indications for hospitalisation

Marked increase in symptom severity, plus any of: inadequate response to community management, inability to walk between rooms or eat/sleep because of symptoms, not coping at home even with home-care support, a high-risk comorbidity, altered mental state suggesting hypercapnia, worsening hypoxaemia/cor pulmonale, new arrhythmia, or SpO2 <92%.

Hospital-level treatment

• Oxygen: titrate to a target saturation of 88–92% — avoid high-flow oxygen because of the risk of hypoventilation/hypercapnia in CO2-retaining patients.
• Non-invasive ventilation (NIV): indicated for acute hypercapnic respiratory failure (e.g. PaCO2 >45 mmHg or pH <7.35) — reduces mortality, length of stay, and the need for intubation.
• Continue inhaled bronchodilators, oral corticosteroids and antibiotics as above; IV antibiotics are only needed for altered mental state, inability to swallow, or evidence of severe pneumonia.

Post-exacerbation / discharge care

Use a structured discharge checklist covering: reassessment of medication and inhaler technique (consider stepping up therapy, e.g. adding a second long-acting bronchodilator or reviewing the case for triple therapy per the criteria above), spirometry, updated COPD Action Plan, pulmonary rehabilitation referral, vaccination status, smoking cessation support, review of any persistent CXR abnormality at 4–6 weeks, osteoporosis risk, and reassessment of LTOT need at 4–6 weeks post-discharge. Comprehensive structured follow-up (ideally GP review within 7 days of discharge, with the hospital discharge summary reaching the primary care team within 24 hours) reduces readmissions compared with unstructured usual care.

Asthma–COPD overlap

Many COPD patients show some bronchodilator reversibility, which does not by itself indicate asthma. Some patients genuinely have overlapping asthma and COPD — these patients tend to have more symptoms, faster lung-function decline, and more frequent, more severe exacerbations. Refer for specialist assessment if there’s diagnostic uncertainty.

FEV1 response to bronchodilator on spirometry:

• >400 mL — consider asthma alone, or asthma/COPD overlap.
• 200–400 mL and ≥12% — consider asthma/COPD overlap.

Favours COPD: onset after 40, heavier smoking history, symptoms persisting despite several weeks/months of ICS, persistent (non-variable) airflow limitation.

Favours asthma: onset before 40, marked day-to-day variability, nocturnal/ early-morning symptom pattern, normal lung function between symptomatic episodes, prior asthma diagnosis, atopic family history, seasonal pattern, spontaneous symptom improvement.

Treatment of overlap: evidence is limited; avoid monotherapy with either ICS alone or a long-acting bronchodilator alone, given the risks of each as monotherapy in the respective single conditions.

Early detection — a genuine care gap

An AJGP viewpoint (Perret et al, 2023) highlights that COPD is substantially under-recognised before a first hospitalisation, despite people with undiagnosed COPD carrying a markedly increased risk of exacerbations, pneumonia and premature death even while asymptomatic. The authors propose using a validated risk-prediction questionnaire (PRECURSOR — “Predicting Your Patient’s Risk of Airway Obstruction”) to identify smokers/ex-smokers in their 40s worth referring proactively for spirometry, rather than relying solely on opportunistic case-finding once symptoms are already present — this is not yet standard practice but reflects where COPD case-finding is heading.