Synopsis
Stabilise acute pulmonary oedema, distinguish raised hydrostatic pressure from permeability injury using bedside physiology and targeted tests, and treat the mechanism rather than the radiograph alone.
- Cardiogenic oedema results mainly from raised pulmonary capillary hydrostatic pressure; non-cardiogenic oedema reflects increased alveolar–capillary permeability, as in ARDS.
- Orthopnoea, raised JVP, peripheral oedema, ischaemia, hypertension, new murmur or known ventricular disease support cardiogenic physiology, but overlap is common.
- Sepsis, aspiration, pancreatitis, transfusion, trauma or inhalational injury with bilateral opacities and no dominant left-heart failure suggests non-cardiogenic injury.
- Chest radiography can show bat-wing shadowing, septal lines, cardiomegaly or effusions in cardiogenic oedema; ARDS more often has diffuse opacities without cardiomegaly, but no sign is definitive.
- Lung ultrasound confirms interstitial fluid through B-lines but cannot alone establish its cause. Add focused cardiac ultrasound, IVC context and the clinical story.
- Natriuretic peptides support heart-failure assessment but rise with age, renal dysfunction, right-heart strain and critical illness; low values are more useful for reducing likelihood than high values are for proving cause.
- Give intravenous loop diuretic promptly in acute heart failure with congestion and monitor renal function, weight and urine output. Do not use diuresis reflexively in permeability oedema with shock.
- NICE advises against routine nitrates, opiates or non-invasive ventilation for every acute-heart-failure patient. Use NIV for severe dyspnoea with acidaemia or failure of initial treatment, and nitrates only in selected circumstances.
- Non-cardiogenic oedema management centres on source control, lung-protective support and a conservative fluid strategy after shock has resolved.
- Repeated reassessment matters because mixed cardiogenic and inflammatory oedema is common, especially in older people with sepsis and cardiac disease.
Key red flags
Acute orthopnoea, widespread crackles, raised JVP, oedema, cool or hypertensive physiology, cardiomegaly, effusions and a compatible cardiac trigger make hydrostatic oedema likely.
Abrupt severe distress with hypertension may follow acute ischaemia, rapid arrhythmia, renal-artery disease or acute mitral/aortic valve dysfunction; little peripheral oedema may be present.
A recognised inflammatory insult, bilateral opacities, hypoxaemia disproportionate to congestion and no dominant left-heart failure suggests ARDS or another permeability process.
Sepsis, renal disease, transfusion or major surgery can combine ventricular dysfunction, fluid loading and inflammatory capillary leak; discordant findings should prompt a mixed model rather than forced categorisation.
Bilateral pneumonia, diffuse alveolar haemorrhage, lymphangitic cancer, acute eosinophilic pneumonia and severe interstitial-lung-disease exacerbation can resemble oedema radiographically.
Hypotension, cool peripheries, confusion, oliguria and elevated lactate with pulmonary congestion indicate low output; standard diuretic or vasodilator treatment alone may worsen perfusion.
Investigation priorities
Quantify immediate respiratory and circulatory failure and identify hypercapnia, acidosis or lactate elevation.
Management branches
Acute respiratory distress with bilateral crackles or pulmonary opacities.
- Sit upright if tolerated, attach monitoring, obtain IV access, prescribe oxygen to target and call senior help while assessing airway, breathing and circulation.
- Use CPAP or NIV when severe dyspnoea with acidaemia persists or initial treatment fails, with immediate intubation planning if consciousness, shock or work of breathing worsens.
- Obtain ECG, portable chest radiograph, blood gas, renal profile, troponin and focused ultrasound without delaying treatment.
- Identify a trigger: ACS, arrhythmia, hypertensive emergency, valve catastrophe, infection, aspiration, transfusion, renal failure or toxin.