Physiology of pulmonary edema !
- Mechanism
- Exam priority: medium
When lung capillaries leak more fluid than the lymphatics can drain, the air sacs flood and oxygen can't get in.
Updated 2026-11-01
Also called: Cardiogenic pulmonary edema, Permeability edema
See it in 3D: Left atrium · Pulmonary veins · Thoracic duct
What it is
In healthy lung, capillary pressure is low and the interstitium is at negative pressure, so little fluid filters and lymphatics remove it. Edema appears when filtration outruns that drainage: through high capillary pressure (left heart failure, mitral stenosis or regurgitation) or through leaky capillaries that let protein out (ARDS, sepsis). The interstitium fills first, then the alveoli, and oxygenation falls because of shunt.
How it works, step by step
- Normally capillary pressure (≈7 mmHg) and negative interstitial pressure leave a small, continuous filtration.
- Pulmonary lymphatics remove that fluid and can raise their flow several-fold if filtration grows.
- If the left atrium does not empty well, pressure backs up into the pulmonary veins and capillaries.
- Filtration exceeds lymphatic capacity: fluid collects around bronchioles and vessels (interstitial edema).
- The interstitium saturates and fluid breaks into the alveoli; surfactant is diluted and alveoli collapse.
- Blood passes flooded alveoli without picking up oxygen: shunt and hypoxemia that responds poorly to O₂.
Starling forces along a capillary
Arteriolar NFP +14 mmHgVenular NFP +6 mmHgFiltration 10.0Reabsorption 0.0Net filtration 10.0 a.u. (lymph capacity 7.5)
Heart failure: high venous pressure raises Pc along the whole capillary; there is almost no reabsorption and filtration outruns the lymph (peripheral edema in right-sided failure, pulmonary edema in left-sided).
Edema: net filtration (10.0 a.u.) is more than the lymph can return (7.5 a.u.), so fluid collects in the interstitium.
Tap a force (Pc, πc, Pif, πif), the lymph or the net pressure value.
- Filtration (fluid out)
- Absorption (fluid in)
- Net filtration pressure
- Normal net pressure
- Lymphatic (returns the excess)
- Edema
Two kinds of pulmonary edema
| Feature | Cardiogenic | Permeability (ARDS) |
|---|---|---|
| Main cause | High capillary pressure | Damage to the alveolar–capillary membrane |
| Fluid protein | Low | High |
| Wedge pressure | High (>18 mmHg) | Normal |
| Examples | Infarction, mitral valve disease, volume overload | Sepsis, pneumonia, aspiration, trauma |
Clinical notes
- Orthopnea and paroxysmal nocturnal dyspnea: lying down returns more blood to the chest and raises pulmonary capillary pressure.
- Diuretics and vasodilators help cardiogenic edema by lowering capillary pressure; in ARDS the problem is the leak, not the pressure.
- Nursing: bibasal crackles, pink frothy sputum and saturation that drops when the patient lies flat.
Test yourself
Think of the answer, then tap the question to see it.
Why is cardiogenic edema fluid low in protein and ARDS fluid high in protein?
In cardiogenic edema the membrane is intact and pressure only pushes more water; in ARDS the damaged membrane lets plasma proteins through.
Why does a patient with chronic mitral stenosis tolerate atrial pressures that would cause acute edema in someone else?
The pulmonary lymphatics have gradually dilated and greatly increased their drainage capacity, widening the safety margin.
Why does hypoxemia from alveolar edema respond poorly to supplemental oxygen?
It is shunt: blood passes fluid-filled alveoli that never receive the inspired O₂, so raising FiO₂ barely reaches it.
Why does dyspnea worsen on lying down in left heart failure?
Lying flat increases venous return to the chest; the left ventricle cannot handle it, pulmonary capillary pressure rises and filtration increases.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- Starling forces at the capillary
- How edema forms
- Heart failure physiology
- How the lymphatic system works
- The pulmonary circulation and hypoxic vasoconstriction
- Surface tension, surfactant and Laplace's law
Related conditions
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: 20.5 Circulatory Pathways (OpenStax (Rice University), 2022); Heart Failure (Congestive Heart Failure) (StatPearls (NCBI Bookshelf), 2026); Acute Respiratory Distress Syndrome (StatPearls (NCBI Bookshelf), 2026); Mitral Regurgitation (StatPearls (NCBI Bookshelf), 2026); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 39). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).
Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake
Representative model, for educational purposes only.