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.
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.
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.
Key medicines
Intravenous loop diureticStart promptly for acute heart failure with congestion, selecting dose from prior diuretic exposure, renal function and the current local protocol.
Intravenous nitrate for selected patientsUse a titrated monitored infusion only for a defined indication such as severe hypertension, ischaemia or acute regurgitation and adequate blood pressure.