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    138 Colloid-Osmotic Pressure (COP)

    138 Colloid-Osmotic Pressure (COP)

    Colloid osmotic pressure: albumin, Starling forces, the revised Starling principle and causes of oedema.

    Colloid osmotic pressure (COP), also called oncotic pressure, is the osmotic pressure created by the proteins in blood plasma, mainly albumin. Because these large molecules pass through the capillary wall only with difficulty, they hold water inside the vessels. Fluid exchange across capillaries depends on the balance of forces described by Starling: the hydrostatic pressure in the capillary (about 36 mmHg at the arterial end, falling to about 15 mmHg at the venous end) pushes fluid out, while plasma COP (about 25 mmHg) holds it in. The revised Starling principle adds that the endothelial glycocalyx forms the true barrier and that, in most tissues, slight filtration predominates, with excess fluid returned by the lymphatics. When COP falls, fluid accumulates in the tissues as oedema.

    MicrocirculationAlbuminOedema
    Normal plasma COP≈ 25 mmHg
    Main contributoralbumin (about three quarters)
    Interstitial COPlower; limited effect on filtration
    Measured bymembrane oncometer
    Plasma colloid osmotic pressure: below about 15 mmHg very low with high oedema risk, about 15 to 20 low, about 20 to 30 normal, above 30 high Plasma colloid osmotic pressure (mmHg) Very low below ≈ 15 15 Low ≈ 15–20 20 Normal ≈ 20–30 30 High above 30
    Figure 1. Approximate plasma colloid osmotic pressure zones. Low COP, mostly from low albumin, favours oedema, especially when capillary pressure is raised.

    Measurement and estimation

    COP is measured directly with a membrane oncometer, which compares plasma with saline across a semi-permeable membrane. It can be estimated from total protein or albumin concentration, although the estimates are less accurate in critical illness. Albumin contributes about 75–80% of plasma COP because of its high concentration and negative charge.

    Clinical significance

    Low COP

    Low albumin from liver cirrhosis, nephrotic syndrome, protein-losing enteropathy, malnutrition, burns, sepsis and dilution by large volumes of crystalloid fluids. Results: oedema of the legs, ascites, pleural effusions and, together with raised pulmonary capillary pressure, pulmonary oedema.

    High COP

    Dehydration with concentrated plasma proteins, high globulins (myeloma, chronic inflammation), infusion of colloids. Fluid is drawn from the tissues into the vessels.

    Oedema develops when the balance shifts: raised capillary pressure (heart failure, venous obstruction), reduced COP, increased capillary permeability (inflammation, sepsis) or impaired lymphatic drainage.

    When to see a doctor

    New or worsening swelling of the legs, abdomen or face, breathlessness when lying down, or foamy urine need medical assessment, including albumin and kidney and liver tests.

    References

    1. Levick JR, Michel CC. Microvascular fluid exchange and the revised Starling principle. Cardiovasc Res. 2010;87(2):198–210. doi:10.1093/cvr/cvq062
    2. Woodcock TE, Woodcock TM. Revised Starling equation and the glycocalyx model of transvascular fluid exchange: an improved paradigm for prescribing intravenous fluid therapy. Br J Anaesth. 2012;108(3):384–394.

    This article is for general information and does not replace a consultation with a doctor. Measurements must be interpreted by a physician together with symptoms and other tests.

    Published on 26 April 2024