Dyspnoea (Shortness of Breath)

Pathophysiology and Aetiology

Dyspnoea results from complex interactions between physiological (respiratory and cardiovascular) and psychological (anxiety) mechanisms. Common underlying causes can be classified by system:

Respiratory Causes

• Asthma (acute exacerbation, poorly controlled chronic asthma)

• Chronic Obstructive Pulmonary Disease (COPD) (exacerbation)

• Pneumonia (bacterial, viral, atypical)

• Pulmonary Embolism (PE)

• Pneumothorax

• Interstitial lung disease

• Upper airway obstruction (e.g. anaphylaxis, epiglottitis, foreign body)

Cardiac Causes

• Heart failure (acute decompensation or chronic)

• Ischaemic heart disease (unstable angina, myocardial infarction)

• Arrhythmias (e.g. atrial fibrillation, supraventricular tachycardias)

• Valvular heart disease (e.g. aortic stenosis)

• Pericardial disease (tamponade, constrictive pericarditis)

Others

• Anaemia (may present with exertional dyspnoea)

• Metabolic acidosis (e.g. diabetic ketoacidosis)

• Anxiety and panic disorders (hyperventilation syndrome)

• Thyroid disorders (e.g. hyperthyroidism, which can precipitate atrial fibrillation or cause generalised hypermetabolic state)

History and Examination

History

• Onset and duration: acute (minutes to hours), subacute (days to weeks), or chronic (weeks to months).

• Nature of dyspnoea: exertional vs. rest, nocturnal episodes (e.g. paroxysmal nocturnal dyspnoea in heart failure), positional changes (orthopnoea).

• Associated symptoms:

  • Chest pain (could indicate PE, ACS, or pleurisy).

  • Wheeze, cough, sputum (suggestive of asthma, COPD, infection).

  • Fever, chills (infection).

  • Leg swelling or calf pain (DVT leading to PE).

  • Palpitations or light-headedness (arrhythmia).

• Past medical history:

  • Cardiac or respiratory disease (e.g. COPD, asthma, heart failure).

  • Recent surgery or immobilisation (risk for thromboembolism).

  • Medications (e.g. beta-blockers, ACE inhibitors).

• Social history:

  • Smoking status, occupational exposures, or inhaled irritants.

  • Recent travel (risk for DVT/PE if long-haul flights).

Physical Examination

• Vital signs: respiratory rate, oxygen saturation (SpO₂), heart rate, blood pressure, temperature.

  • Tachypnoea (>20 breaths/min) often indicates significant cardiorespiratory compromise.

  • Hypoxia (SpO₂ <94% in healthy adults; <88–92% for COPD target range) warrants urgent assessment.

• General appearance: can the patient speak in full sentences? Are they using accessory muscles? Are there signs of cyanosis?

• Cardiorespiratory exam:

  • Auscultation for wheezes, crackles, decreased breath sounds.

  • Percussion note changes (hyper-resonance in pneumothorax, dullness in consolidation or effusion).

  • Heart sounds (murmurs, gallops suggesting heart failure).

• Peripheral signs: oedema, raised JVP (heart failure), calf tenderness (possible DVT).

Immediate Assessment and Red Flags

Identify life-threatening causes of acute dyspnoea:

1. Pulmonary Embolism: sudden onset breathlessness, pleuritic chest pain, risk factors (recent surgery, immobility).

2. Pneumothorax: especially tension pneumothorax (tracheal deviation, hypotension).

3. Acute Severe Asthma: inability to speak, silent chest, exhaustion.

4. Anaphylaxis: urticaria, angio-oedema, hypotension.

5. Acute Pulmonary Oedema: frothy sputum, acute onset, high respiratory distress.

6. Acute Coronary Syndrome or arrhythmias causing cardiogenic shock.

Immediate oxygen therapy (except in certain COPD patients where target SpO₂ is typically 88–92%), urgent imaging (chest X-ray) and further investigations (ECG, blood gas analysis) may be needed.

Investigations

The choice of investigations depends on the clinical scenario, guided by the most likely differential diagnoses:

1. Chest X-ray (CXR)

   • Essential initial investigation for most causes of acute or chronic dyspnoea. Identifies pneumonia, pulmonary oedema, pleural effusion, pneumothorax, interstitial patterns, or mass lesions.

2. Electrocardiogram (ECG)

   • Helps detect arrhythmias, signs of ischaemia, or right heart strain (in acute PE).

3. Pulse Oximetry and Arterial Blood Gas (ABG)

   • Pulse oximetry is a quick, non-invasive method to assess oxygen saturation.

   • ABG may be necessary if the oximetry is unreliable or if acid-base status requires evaluation (e.g. suspected DKA, severe asthma).

4. Full Blood Count (FBC)

   • Anaemia can contribute to exertional dyspnoea. Leucocytosis may indicate infection.

5. Biochemistry

   • Electrolytes, renal function, and liver function can be relevant, especially in chronic conditions or when starting diuretic therapy.

   • BNP or NT-proBNP if heart failure is suspected.

6. D-dimer

   • Used with validated risk scores (e.g. Wells score) to rule out pulmonary embolism in a low-probability setting.

   • A positive D-dimer is non-specific; proceed to imaging (CT pulmonary angiogram) if PE is still suspected.

7. Spirometry

   • In subacute or chronic dyspnoea, spirometry can diagnose or monitor COPD, asthma, restrictive lung disease.

8. Imaging

   • CT Pulmonary Angiogram (CTPA) is the gold standard for diagnosing PE.

   • High-resolution CT (HRCT) can be used to investigate interstitial lung disease.

   • Echocardiogram for suspected heart failure or valvular disease.

Management Principles

Tailor management based on the underlying cause, patient comorbidities, and severity of presentation:

Respiratory Causes

• Asthma/COPD

  • Ensure optimal inhaler technique and adherence to prevent exacerbations.

  • Oral corticosteroids for acute exacerbations.

  • Bronchodilators (short-acting and long-acting).

  • Consider antibiotics if a bacterial infection is suspected in a COPD exacerbation.

  • Oxygen therapy: aim for target SpO₂ of 88–92% in COPD to avoid CO₂ retention.

• Pneumonia

  • Empirical antibiotics guided by guidelines (e.g. Therapeutic Guidelines).

  • Supportive measures: fluids, antipyretics, oxygen if hypoxic.

  • Hospital admission if moderate-severe pneumonia or significant comorbidity.

• Pulmonary Embolism

  • Anticoagulation (low molecular weight heparin or direct oral anticoagulants).

  • Risk stratification (e.g. simplified PESI or Hestia criteria) to determine outpatient vs. inpatient treatment.

• Pneumothorax

  • Immediate needle decompression if tension pneumothorax.

  • Otherwise, chest tube insertion or observation depending on size, symptoms, and underlying lung disease.

Cardiac Causes

• Heart Failure

  • Address acute decompensation with diuretics (e.g. IV furosemide) for pulmonary oedema.

  • Chronic management with ACE inhibitors/ARBs, beta-blockers, and diuretics.

  • Control exacerbating factors (arrhythmias, ischaemia, infection).

• Coronary Artery Disease / ACS

  • MONA-B (Morphine, Oxygen [if hypoxic], Nitrates, Aspirin, Beta-blocker) as indicated.

  • Urgent cardiology input if ST-elevation MI or ongoing ischaemia.

• Arrhythmias

  • Rate control or rhythm control for tachyarrhythmias such as AF.

  • Consider anticoagulation if indicated (CHA₂DS₂-VASc score).

Other Causes

• Anaemia

  • Investigate for iron deficiency, B12/folate deficiency, chronic disease.

  • Correct underlying cause.

• Anxiety / Panic Disorder

  • Evaluate for organic pathology first.

  • Cognitive Behavioural Therapy, relaxation techniques, sometimes pharmacotherapy (SSRIs).

• Metabolic Causes

  • Manage underlying cause (e.g. insulin and fluids in DKA).

Chronic Dyspnoea: Ongoing Management and Follow-up

• Multidisciplinary care is often required (e.g. physiotherapy, chronic disease management nurses, respiratory or cardiac specialists).

• Optimise comorbidities: blood pressure control, glycaemic management, smoking cessation.

• Pulmonary rehabilitation for COPD or chronic respiratory disease.

• Home oxygen assessment if chronic hypoxaemia in advanced cardiorespiratory disease.

• Advance care planning in end-stage diseases (e.g. palliative approach where appropriate).