CorpusHuman Anatomy
CardiovascularPhysiological process

Capillary exchange (Starling forces)

Permutatio capillaris

Also known as: Starling forces, Starling equation, filtration and reabsorption, oncotic pressure

Fluid moves across capillary walls according to the balance between hydrostatic pressure and colloid osmotic (oncotic) pressure. Fluid is filtered out at the arteriolar end and partly reabsorbed at the venular end, and the lymphatics return the rest.

Overview

Capillary pressure≈30 (arteriolar) → 10 mmHg (venular)
Plasma oncotic pressure≈25–28 mmHg
Interstitial pressure≈ −3 mmHg (subcutaneous)
Net arteriolar / venular pressure≈ +13 / −7 mmHg

The Starling equation. Net fluid movement out of a capillary (Jv) equals Kf × [(Pc − Pi) − σ(πc − πi)].

Pc is capillary hydrostatic pressure and Pi is interstitial hydrostatic pressure. πc is plasma oncotic pressure, about 70–80% of which comes from albumin, and πi is interstitial oncotic pressure. Kf is the filtration coefficient, which reflects the permeability and surface area of the wall. σ is the reflection coefficient for proteins, close to 1 in most capillaries.

Typical systemic values (Guyton). Pc is about 30 mmHg at the arteriolar end and about 10 mmHg at the venular end. Pi is about −3 mmHg in loose subcutaneous tissue. πc is about 28 mmHg and πi about 8 mmHg.

The net outward pressure is therefore about +13 mmHg at the arteriolar end, so fluid filters out. At the venular end it is about −7 mmHg, so fluid is reabsorbed. On average there is a small excess of filtration. Across the whole body this excess, a few litres a day, is returned to the blood as lymph.

The revised Starling principle. More recent work shows that the endothelial glycocalyx makes the effective oncotic gradient act across the glycocalyx itself. In most steady-state tissues, sustained reabsorption at the venular end is small, and the lymphatics remove most of the filtrate.

Special capillary beds. In glomerular capillaries, Pc is about 50–60 mmHg, so filtration continues along their whole length. In pulmonary capillaries, Pc is low (about 7–10 mmHg), which keeps the alveoli dry. In the intestinal and peritubular capillaries, net reabsorption occurs.

Diffusion. For solutes, diffusion across the capillary wall moves far more material than bulk flow does.

Function

  • Distributes fluid between the plasma and interstitial compartments.
  • Delivers nutrients and removes wastes, together with diffusion.
  • Supplies the fluid that becomes lymph.

Clinical significance

Causes of oedema

There are four main causes of oedema.

Raised capillary hydrostatic pressure: heart failure, venous obstruction or DVT, fluid overload, or dihydropyridine calcium channel blockers (ankle swelling).

Reduced plasma oncotic pressure: low albumin in nephrotic syndrome, cirrhosis, malnutrition (kwashiorkor) or protein-losing enteropathy.

Increased permeability: inflammation, burns, sepsis or ARDS.

Lymphatic obstruction: filariasis, or removal or irradiation of lymph nodes. This produces non-pitting lymphoedema.

Pulmonary oedema

When left atrial and pulmonary capillary pressures rise above about 20–25 mmHg, filtration into the lungs exceeds what the lymphatics can remove. Fluid first collects in the interstitium and then floods the alveoli. Typical causes are left ventricular failure and mitral stenosis.

Compiled from standard anatomy and physiology references — see the Cardiovascular System sources. For education only; not medical advice.