Hydrostatic pressure pushes fluid out, oncotic pressure pulls it back
Mnemonic
“Hydrostatic pushes out, oncotic pulls in”, on both sides of the capillary wall:
Net filtration = Kf [ (Pc - Pi) - sigma (pi c - pi i) ]
- Pc - capillary hydrostatic pressure, pushing fluid out
- Pi - interstitial hydrostatic pressure
- pi c - capillary oncotic pressure, from albumin, pulling fluid in
- pi i - interstitial oncotic pressure
At the arteriolar end hydrostatic pressure dominates so fluid filters out; at the venular end oncotic pressure dominates so most is reabsorbed; the remainder returns as lymph.
Oedema therefore has four mechanisms, one per term: raised hydrostatic pressure (heart failure, venous obstruction), reduced oncotic pressure (hypoalbuminaemia from nephrotic syndrome, liver failure, malnutrition), increased permeability (sepsis, burns, inflammation) and lymphatic obstruction.
Expansion
Four forces:
- Capillary hydrostatic pressure - pushes fluid out; about 32 mmHg at the arteriolar end, 15 mmHg at the venular end
- Interstitial hydrostatic pressure - opposes filtration; near zero or slightly negative
- Capillary oncotic pressure - pulls fluid in; about 25 mmHg, mostly from albumin
- Interstitial oncotic pressure - pulls fluid out; about 5 mmHg
Classically, filtration occurs at the arteriolar end and reabsorption at the venular end, with the surplus (about 2 to 4 litres a day) returned by the lymphatics.
The revised model, incorporating the endothelial glycocalyx, holds that most capillaries filter along their whole length with little venular reabsorption, and that the lymphatics handle proportionately more. The oncotic gradient that matters is the one across the glycocalyx, not across the whole wall.