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Acute dyspnoea

Acute dyspnoea is the sudden or rapidly progressive sensation of difficult, laboured or uncomfortable breathing, developing over minutes to days (under 4 weeks, usually under 48 hours). It is a symptom, not a sign. The patient reports it, while observers record respiratory rate, effort and oxygen saturation.

It signals a threat to airway, breathing or circulation until proved otherwise. The first duty is stabilisation, not diagnosis.

Clinical relevance. Acute dyspnoea accounts for up to 5% of emergency attendances. It carries high mortality when due to pulmonary embolism, acute coronary syndrome, acute heart failure, pneumonia, tension pneumothorax, anaphylaxis or exacerbation of asthma and chronic obstructive pulmonary disease. Multiple causes coexist in older patients. Early use of bedside ultrasound, natriuretic peptide and gas analysis changes the diagnosis in many.

Classification.

  • By cause group:
    • airway (obstruction, anaphylaxis, aspiration)
    • lung (asthma, chronic obstructive pulmonary disease, pneumonia, pneumothorax, effusion, pulmonary oedema, pulmonary embolism, acute respiratory distress syndrome, interstitial exacerbation)
    • cardiac (acute heart failure, ischaemia, arrhythmia, valve failure, tamponade, myocarditis)
    • metabolic and haematological (acidosis, anaemia, sepsis, thyrotoxicosis, carbon monoxide poisoning)
    • neuromuscular and chest wall (Guillain-Barre syndrome, myasthenic crisis, rib fractures, flail chest)
    • psychogenic (panic, hyperventilation)
  • By severity: mild (speaks in sentences), moderate (speaks in phrases), severe (speaks in words, accessory muscles, saturation under 92%), life threatening (exhaustion, silent chest, cyanosis, confusion, bradycardia, hypotension).
  • By pattern: sudden onset (pneumothorax, pulmonary embolism, foreign body, arrhythmia, anaphylaxis), hours to days (pneumonia, heart failure, asthma, chronic obstructive pulmonary disease), orthopnoea and paroxysmal nocturnal dyspnoea (heart failure), platypnoea (right to left shunt).

Mechanism. Dyspnoea arises from increased respiratory drive (hypoxia, hypercapnia, acidosis), increased mechanical load (obstruction, stiff lungs or chest wall), and weakness of respiratory muscles. Afferent signals from chemoreceptors, lung receptors and chest wall mismatch with central motor command.

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