# Cardiogenic Versus Non-Cardiogenic Pulmonary Oedema > Cardiogenic versus non-cardiogenic pulmonary oedema for NEET-PG Medicine: Starling forces, wedge pressure, chest X-ray clues, BNP and differing treatment. - Canonical URL: https://prepelephant.com/topics/neet-pg/medicine/pulmonary-oedema-cardiogenic-versus-non-cardiogenic - Exam / course: NEET-PG · Subject: Medicine - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-08 - Last updated: 2026-10-08 - Reference basis: Harrison's Principles of Internal Medicine; Murray and Nadel's Textbook of Respiratory Medicine; ESC Guidelines for Acute and Chronic Heart Failure - How to cite: "Cardiogenic Versus Non-Cardiogenic Pulmonary Oedema", PrepElephant, https://prepelephant.com/topics/neet-pg/medicine/pulmonary-oedema-cardiogenic-versus-non-cardiogenic ## Direct answer Cardiogenic versus non-cardiogenic pulmonary oedema separates raised hydrostatic pressure from injured alveolar membranes. Cardiogenic oedema, usually from left ventricular failure, shows a wedge pressure above about 18 mmHg and a low-protein fluid, whereas non-cardiogenic oedema from ARDS, transfusion reaction or organophosphate poisoning has a normal wedge pressure and protein-rich fluid. Diuretics and afterload reduction treat the first; lung-protective ventilation and removal of the cause treat the second. ## What you must remember - **Starling basis:** oedema follows when capillary hydrostatic pressure overwhelms oncotic and interstitial opposing forces, so raised left atrial pressure is the commonest cardiogenic driver. - **Wedge pressure:** a value above about 18 mmHg favours cardiogenic oedema, while a normal value with bilateral alveolar opacities points to permeability injury. - **Fluid protein ratio:** an oedema-fluid to plasma protein ratio above about 0.65 indicates permeability oedema, whereas cardiogenic fluid is a low-protein transudate. - **Chest radiograph:** cardiogenic oedema shows cardiomegaly, upper lobe diversion, Kerley B lines and effusions, whereas ARDS shows bilateral patchy opacities with a normal heart size. - **Natriuretic peptides:** raised BNP or NT-proBNP supports heart failure, and a normal value argues strongly against cardiogenic dyspnoea. - **Berlin definition:** ARDS needs onset within one week and bilateral opacities not explained by cardiac failure or fluid overload, graded by PaO2 to FiO2 ratio as mild (200 to 300), moderate (100 to 200) and severe (100 or less). - **Ventilation:** ARDS is managed with a tidal volume of 6 mL/kg predicted body weight and adequate PEEP, while cardiogenic oedema may respond to non-invasive ventilation. ## A bedside contrast in two breathless patients Consider a 58-year-old man with a previous anterior infarction who arrives breathless, with a raised jugular venous pressure, bibasal crackles and frothy sputum. His chest film shows a cardiothoracic ratio above 0.5, prominent upper lobe vessels, Kerley B lines and small effusions, and echocardiography reveals a dilated left ventricle with reduced function. Every axis points the same way: hydrostatic pressure is high, so treatment is sitting him up, oxygen to saturation, intravenous furosemide and a nitrate, with non-invasive ventilation if work of breathing stays high. Now a 30-year-old with sepsis from pneumonia develops bilateral alveolar opacities within a day, with a PaO2 to FiO2 ratio near 150. His heart looks normal on the film, echocardiography shows preserved function and the wedge pressure is normal. This is ARDS, and the same furosemide that relieved the first patient would reduce his circulating volume while doing nothing for damaged alveolar membranes. The team instead uses a conservative fluid strategy, low tidal volumes and source control. 1. **Check the wedge pressure:** Above about 18 mmHg favours cardiogenic oedema; normal with bilateral opacities points to permeability injury. 2. **Read the chest film:** Cardiomegaly, upper lobe diversion and Kerley B lines favour cardiogenic oedema; bilateral patchy opacities with a normal heart suggest ARDS. 3. **Look at the echocardiogram:** A dilated, poorly functioning left ventricle supports cardiogenic oedema. 4. **Choose treatment by mechanism:** Diuretics and afterload reduction treat hydrostatic oedema; lung-protective ventilation and removal of the cause treat permeability oedema. ## Where the exam tries to catch you Several traps mimic cardiogenic oedema. - **Trap:** Choosing furosemide for a stem with bilateral infiltrates and a normal heart. — **Correct:** Diuretics treat hydrostatic oedema and do not repair leaky membranes, so a normal heart with bilateral infiltrates points to ARDS and supportive care. - **Trap:** Treating negative pressure pulmonary oedema with diuresis. — **Correct:** It follows forceful inspiration against a closed glottis, so the obstruction must be removed. - **Trap:** Missing re-expansion oedema after drainage of a large pneumothorax. — **Correct:** It is a classic non-cardiogenic cause after rapid drainage. - **Trap:** Calling a transfusion reaction cardiogenic oedema. — **Correct:** Transfusion-related acute lung injury appears within about six hours of a plasma-rich transfusion and carries a normal wedge pressure. In Indian practice, organophosphate poisoning causes bronchorrhoea with non-cardiogenic oedema. High-altitude pulmonary oedema, driven by hypoxic pulmonary vasoconstriction, is treated by descent rather than dehydration. ## Frequently asked questions ### What wedge pressure separates cardiogenic from non-cardiogenic pulmonary oedema? A wedge pressure above about 18 mmHg favours cardiogenic pulmonary oedema. A normal wedge pressure with bilateral alveolar opacities points to a permeability cause such as ARDS, transfusion-related acute lung injury or negative pressure oedema. ### Which chest X-ray features favour cardiogenic pulmonary oedema over ARDS? Cardiomegaly, upper lobe blood diversion, Kerley B lines and bilateral pleural effusions favour cardiogenic pulmonary oedema. ARDS typically shows patchy or confluent alveolar opacities with a normal heart size and air bronchograms. ### Why does furosemide help cardiogenic pulmonary oedema but not ARDS? Furosemide reduces venous return and pulmonary capillary pressure, lowering the hydrostatic force that drives fluid into the alveoli. In ARDS the alveolar-capillary membrane itself is leaky, so removing fluid does not repair the permeability defect. ### What is negative pressure pulmonary oedema? Negative pressure pulmonary oedema develops after a strong inspiratory effort against a closed or obstructed upper airway, as in laryngospasm, airway obstruction or after extubation. The wedge pressure is normal, so treatment is relief of the obstruction with supportive ventilation.