BPTBuddy

Red flags

Acute severe dyspnoea with hypoxia, silent chest, or exhaustion in known asthma/COPD - impending respiratory failure, do not wait for gas exchange to look bad on paper
Sudden dyspnoea + pleuritic pain + tachycardia - PE (see chest pain (respiratory))
Acute cardiac causes (pulmonary oedema, tamponade, massive PE) - see breathlessness (cardiology) for that framework; a respiratory-sounding presentation does not exclude a cardiac driver
Stridor - upper airway obstruction, an airway emergency distinct from lower airway/parenchymal causes
Rapidly progressive dyspnoea over days in a previously well patient - consider rapidly progressive ILD, pneumonia, or an evolving pleural effusion

Airway disease

Asthma - variable airflow obstruction, wheeze, reversible, often episodic/triggered
COPD - fixed/progressive airflow obstruction, smoking history, exertional and progressive

Parenchymal disease

Interstitial lung disease - progressive exertional dyspnoea, dry cough, fine "velcro" crackles, restrictive pattern
Pneumonia - acute, fever, focal signs

Pulmonary vascular

PE (acute), chronic thromboembolic pulmonary hypertension (progressive, often missed after an initial PE)
Pulmonary arterial hypertension - progressive exertional dyspnoea, loud P2, signs of RHF in later disease

Pleural/chest wall

Pleural effusion - dull to percussion, reduced breath sounds, may be malignant/infective/cardiac in origin
Neuromuscular/chest wall disease - orthopnoea, weak cough, see other sleep-disordered breathing for the nocturnal hypoventilation angle

Non-respiratory (always keep on the list)

Cardiac causes - see breathlessness (cardiology)
Anaemia, metabolic acidosis (compensatory tachypnoea), anxiety/hyperventilation, obesity/deconditioning

MRC/mMRC dyspnoea scale - grades functional impact, useful for both diagnosis discussion and monitoring trajectory
Onset (acute vs chronic progressive), pattern (episodic/variable vs fixed/progressive), triggers (allergen, exercise, cold air - asthma)
Smoking history (pack-years) - COPD; occupational/environmental exposure history - ILD, occupational asthma
Associated cough/sputum/wheeze/haemoptysis, orthopnoea/PND (cardiac overlap)
Prior PE/VTE history - chronic thromboembolic pulmonary hypertension risk

Respiratory rate, SpO2, accessory muscle use, ability to speak in full sentences (severity marker)
Wheeze (asthma/COPD), fine bibasal "velcro" crackles (ILD - distinct from the coarser crackles of pulmonary oedema/pneumonia), reduced breath sounds/dullness (effusion)
Clubbing - ILD, bronchiectasis, malignancy (not COPD alone - clubbing in a COPD patient should prompt a search for coexisting lung cancer or bronchiectasis)
Signs of pulmonary hypertension/RHF - loud P2, raised JVP, peripheral oedema
Cardiac examination to exclude a cardiac contributor - see breathlessness (cardiology)

First-line for chronic/undifferentiated dyspnoea

Spirometry - obstructive (asthma/COPD) vs restrictive (ILD, chest wall/neuromuscular) pattern, the key branch point
CXR - hyperinflation (COPD), reticular/ground-glass changes (ILD), effusion, mass
FBE (anaemia, polycythaemia), BNP/NT-proBNP if cardiac contribution uncertain

Directed further testing by pattern

Obstructive pattern: bronchodilator reversibility testing, consider bronchial provocation if spirometry normal but asthma still suspected
Restrictive pattern: HRCT chest - defines ILD pattern (UIP vs NSIP vs other), guides need for further work-up (autoimmune serology, occupational history)
Isolated reduced DLCO with preserved spirometry - consider pulmonary vascular disease (PAH, CTEPH) or early ILD - echocardiogram +/- V/Q scan
Echocardiogram - if cardiac cause or pulmonary hypertension suspected

Direct management to the confirmed diagnosis (see individual disease notes for detail)

Asthma/COPD - bronchodilators, inhaled corticosteroids per guideline-directed stepwise therapy, pulmonary rehabilitation for COPD
ILD - antifibrotic therapy for progressive fibrosing patterns, immunosuppression for inflammatory/autoimmune-associated ILD, oxygen if hypoxic
Pulmonary hypertension/CTEPH - specialist pulmonary vascular unit referral; CTEPH is a rare but important "don't miss" as it may be surgically curable (pulmonary endarterectomy) unlike other forms of PH
Pleural effusion - drain and treat per underlying cause (see malignant effusions for the oncology-specific approach)

Symptomatic/palliative dyspnoea management (any advanced cause)

Opioids - the best-evidenced symptomatic treatment for refractory breathlessness in advanced disease, used at low dose, distinct from their use for pain
Handheld fan directed at the face, breathing techniques/pulmonary rehabilitation, anxiety management (breathlessness and anxiety amplify each other)
Oxygen only if hypoxic - does not relieve breathlessness in a normoxic patient and should not be used reflexively for symptom control alone

Attributing new clubbing in a COPD patient to the COPD itself rather than investigating for coexisting lung cancer/bronchiectasis
Missing chronic thromboembolic pulmonary hypertension in a patient with persistent dyspnoea after a treated PE - it needs specific screening (echo, V/Q), not just reassurance that the PE was treated
Prescribing supplemental oxygen for symptomatic relief of breathlessness in a patient who is not hypoxic
Assuming fine bibasal crackles are pulmonary oedema without considering ILD, especially in a patient without cardiac risk factors or with a normal BNP
Stopping at spirometry when it is normal but dyspnoea persists - isolated DLCO reduction or a cardiac/vascular cause may still be present

1. Spirometry sorts the majority into two buckets

"Obstructive versus restrictive on spirometry tells me almost immediately whether I'm chasing airway disease or parenchymal/chest wall disease."

2. Opioids for breathlessness aren't just for pain

"In advanced disease, low-dose opioids are the best-evidenced symptomatic treatment for refractory dyspnoea, separate from any analgesic use."

8 of 8 sections written · drafted 2026-09-14