Approach to dyspnoea

At a glance

• Dyspnoea is the subjective experience of breathing discomfort. It doesn't match oxygen saturation well: patients can be very breathless with normal SpO2 (PE, anaemia, acidosis) or comfortable with chronic hypoxaemia.
• In acute breathlessness, exclude the immediate threats first, using ABCDE assessment, oximetry, ECG, CXR and a blood gas.
• In chronic breathlessness (over 4 to 8 weeks), heart and lung disease cause most cases. Many patients have more than one cause, so look for all contributors: obesity, anaemia, deconditioning and dysfunctional breathing.
• A staged work-up of CXR, ECG, spirometry, FBC and NT-proBNP sorts most patients, followed by echo, full lung function with DLCO, and CT where the first round doesn't explain the symptom.

Causes

Acute (minutes to days)

System	Causes
Airway	Anaphylaxis, foreign body, angioedema, acute asthma, COPD exacerbation
Lung and pleura	Pneumonia, pneumothorax, large effusion, ARDS, aspiration
Pulmonary vascular	Pulmonary embolism
Cardiac	Acute pulmonary oedema, ACS, arrhythmia, tamponade, acute valve failure
Metabolic	Diabetic ketoacidosis, lactic acidosis, salicylate toxicity, sepsis
Neuromuscular	Guillain-Barré syndrome, myasthenic crisis (see respiratory failure)
Other	Severe anaemia, panic and hyperventilation (a diagnosis of exclusion)

Chronic (weeks to months)

Group	Common causes	Clues
Airways	COPD, asthma	Smoking, wheeze, variability
Parenchyma	ILD, bronchiectasis	Fine crackles, clubbing, low DLCO
Pleura and chest wall	Effusion, kyphoscoliosis, obesity	Dullness, restriction with normal DLCO
Pulmonary vascular	Pulmonary hypertension, CTEPH	Loud P2, syncope on exertion, isolated low DLCO
Cardiac	HFrEF, HFpEF, valve disease, AF	Orthopnoea, PND, oedema, murmur
Neuromuscular	Motor neurone disease, diaphragm weakness	Orthopnoea, weak cough, supine fall in FVC
Systemic	Anaemia, thyroid disease, metabolic acidosis (CKD)	Pallor, low bicarbonate
Deconditioning and dysfunctional breathing	Inactivity, breathing pattern disorder	Normal tests, sighing, tingling

• HFpEF is underdiagnosed in older, obese, hypertensive women. Echo and natriuretic peptides are the starting point (see heart failure).
• In Aboriginal and Torres Strait Islander and Māori patients, think of rheumatic mitral stenosis and bronchiectasis at younger ages.

Focused history

• Tempo: sudden (pneumothorax, PE, arrhythmia), hours to days (pneumonia, pulmonary oedema, asthma), months (ILD, heart failure, pulmonary hypertension).
• Severity: use the mMRC scale (0 breathless only with strenuous exercise, 4 too breathless to leave the house). It matches the COPD assessment.
• Position:
  • Orthopnoea: heart failure, bilateral diaphragm weakness, large effusion, ascites
  • Paroxysmal nocturnal dyspnoea: heart failure; nocturnal asthma can mimic it
  • Platypnoea (worse upright): hepatopulmonary syndrome, intracardiac shunt
  • Trepopnoea (worse lying on one side): unilateral lung or pleural disease
  • Breathlessness on immersion in water or on bending: diaphragm weakness
• Associated features: chest pain, palpitations, exertional syncope (pulmonary hypertension, aortic stenosis), wheeze, cough and sputum, haemoptysis, leg swelling, weight change.
• Exposures and history: smoking, occupation (asbestos, silica, coal, engineered stone), birds, previous VTE, malignancy, connective tissue disease, radiotherapy.
• Drugs:
  • Lung toxicity: amiodarone, methotrexate, nitrofurantoin, bleomycin, checkpoint inhibitors
  • Bronchospasm: non-selective beta-blockers
  • Fluid retention: NSAIDs, pioglitazone, dihydropyridines (oedema only)
  • Dyspnoea as a direct effect: ticagrelor
• Breathing pattern disorder: air hunger with inability to take a satisfying breath, sighing, perioral tingling, normal tests. The Nijmegen questionnaire helps screen.

Focused examination

• Respiratory rate, SpO2 at rest and on exertion (desaturation on walking points to ILD or pulmonary vascular disease).
• Ability to speak in sentences, accessory muscle use, paradoxical abdominal movement (diaphragm weakness).
• Clubbing, cyanosis, pallor, lymphadenopathy, sclerodactyly or other connective tissue disease signs.
• JVP, displaced apex, murmurs, loud P2, right ventricular heave, peripheral oedema.
• Chest: wheeze, fine crackles, signs of effusion, hyperinflation.
• BMI and neck circumference.

Red flags

• Stridor, inability to complete sentences, silent chest, SpO2 under 92% on air
• Hypotension, raised JVP with clear lungs (PE, tamponade, right ventricular infarct)
• Exertional syncope or chest pain
• Drowsiness or confusion (hypercapnia)
• Haemoptysis or weight loss
• Rapid progression over weeks

Investigations

First line

Test	What it shows
Chest X-ray	Consolidation, effusion, pneumothorax, oedema, hyperinflation, interstitial change
ECG	Ischaemia, AF, right heart strain, low voltages (effusion)
FBC, electrolytes, renal function, glucose, TSH	Anaemia, acidosis, thyroid disease
Spirometry with bronchodilator	Obstruction, possible restriction
NT-proBNP or BNP	Rule-out of heart failure: NT-proBNP under 125 pg/mL (chronic) or under 300 pg/mL (acute)
Blood gas (acute or if hypoxaemic)	Type 1 or 2 respiratory failure, A-a gradient, metabolic acidosis

Second line

• Echocardiogram: LV function, valves, estimated pulmonary artery pressure. A tricuspid regurgitant velocity over 2.8 m/s suggests pulmonary hypertension.
• Full lung function: lung volumes and DLCO. A low DLCO with normal spirometry and volumes points to pulmonary vascular disease or early ILD.
• HRCT for suspected ILD or bronchiectasis.
• CTPA for suspected acute PE (after Wells score, PERC and age-adjusted D-dimer). V/Q scan when CTPA is unsuitable (pregnancy, contrast allergy, renal impairment) and to screen for CTEPH.
• Iron studies: iron deficiency worsens exercise tolerance in heart failure.

Third line

• Cardiopulmonary exercise testing (CPET) separates cardiac, ventilatory, pulmonary vascular, deconditioning and dysfunctional breathing limitation when everything else is normal.
• Six-minute walk test with oximetry for exertional desaturation and to track disease.
• Right heart catheterisation to confirm pulmonary hypertension: mean PA pressure over 20 mmHg (ESC/ERS 2022).
• Respiratory muscle tests (supine and erect FVC; a fall over 20% suggests diaphragm weakness), sleep study, or stress testing as indicated.

Pitfall: a normal resting SpO2 doesn't exclude PE or pulmonary hypertension. Walk the patient with an oximeter.

Management

Acute

• Treat the cause: bronchodilators, diuretics and nitrates, decompression, anticoagulation or reperfusion, antibiotics.
• Oxygen to target, not routinely: SpO2 92 to 96% for most adults, 88 to 92% for those at risk of hypercapnia (TSANZ 2022, matching respiratory failure).
• Escalate early to high-flow nasal oxygen, NIV or intubation as the cause dictates.

Chronic breathlessness

When breathlessness persists despite optimal treatment of the underlying disease, it becomes a target in its own right (sometimes called chronic breathlessness syndrome).

• Non-drug measures first:
  • Hand-held fan directed at the face (ERS 2024 suggests increased airflow)
  • Pulmonary rehabilitation in COPD, ILD, bronchiectasis and pulmonary hypertension
  • Breathing techniques, pacing, positioning, and help with anxiety (the Breathing, Thinking, Functioning model)
  • Weight loss, treatment of anaemia and iron deficiency
• Oxygen helps only with hypoxaemia. In non-hypoxaemic patients, palliative oxygen was no better than medical air (Abernethy 2010).
• Opioids: the Australian BEAMS trial found low-dose extended-release morphine didn't improve breathlessness in COPD. ERS 2024 makes a conditional recommendation against opioids for breathlessness in serious respiratory illness. Reserve low-dose oral morphine for advanced or palliative disease after non-drug measures, with laxatives and review. In Australia, Kapanol (sustained-release morphine 10 and 20 mg) was TGA-registered in 2019 for chronic breathlessness in palliative care (10 mg daily, up to 30 mg), after the cause is optimised and non-drug measures have failed.
• Benzodiazepines don't relieve breathlessness and add sedation and falls. Use only for anxiety at the end of life.
• Dysfunctional breathing: explanation and physiotherapy-led breathing retraining.

Special populations

• Pregnancy: mild breathlessness is physiological (progesterone drives ventilation, giving a PaCO2 of about 30 mmHg). New or severe breathlessness needs exclusion of PE, peripartum cardiomyopathy, mitral stenosis and asthma. V/Q or CTPA can both be used.
• Older people: multiple causes are the rule. Heart failure, AF, anaemia, COPD and deconditioning often coexist.
• Obesity: consider obesity hypoventilation syndrome (awake PaCO2 over 45 mmHg with BMI over 30) and OSA.

Pitfalls

• Attributing breathlessness to anxiety before excluding PE, pulmonary hypertension and arrhythmia.
• Accepting COPD as the explanation without spirometry, or missing coexisting heart failure in a known COPD patient.
• Missing diaphragm weakness: orthopnoea with clear lungs. Check supine FVC.
• Not checking DLCO: isolated reduction is the clue to pulmonary vascular disease.
• Starting home oxygen for breathlessness when the patient isn't hypoxaemic.
• Forgetting drug causes, especially ticagrelor, amiodarone and methotrexate.