Starling Forces

Describe the essential features of the micro-circulation including fluid exchange (Starling forces) and control mechanisms present in the pre- and post-capillary sphincters

Interstitial fluid is an ultrafiltrate of plasma, with the net filtration pressure determined by the net effect of opposing hydrostatic and oncotic pressures:

$NFP = P_{Capillary \ Hydrostatic} - P_{Interstitial \ Hydrostatic} - (P_{Capillary \ Oncotic} - P_{Interstitial \ Oncotic})$

These four variables are known as Starling's forces.

Actual fluid movement is (of course) more complicated. Hydrostatic pressure falls along the capillary, and movement of solute and water are affected by other factors. Some of these are described by the:

• Reflection coefficient (σ)
  This describes the fact that a small amount of protein leaks from the capillary, slightly increasing interstitial oncotic pressure and slightly decreasing capillary oncotic pressure. It is dependent on the interstitial protein content, and has a value between 0 and 1.

• Filtration coefficient (Kf)
  Encompasses membrane permeability (to water) and membrane surface area. Varies between tissues:

The Starling Equation becomes:

$Net \ Fluid \ Movement = K_f(P_{CH} - P_{IH} - \theta(P_{CO} - P_{IO})$

Typical Values for Pressures (mmHg)

Organ-Specific Values

In the glomerulus:

• Reflection coefficient is close to 1 due to the impermeability of the glomerulus to protein
• Kf is high due to both high permeability and a large surface area.
• Hydrostatic pressure is high
• Glomerular oncotic pressure is essentially 0

In the liver:

• Reflection coefficient is close to 0 in hepatic sinusoids as they are very permeable to protein

In the lungs:

• Reflection coefficient of ~0.5 in the lungs due to significant leak of protein
  • Protein leak decreases as interstitial oncotic pressure rises, limiting further oedema formation
• The oncotic pressure gradient is small, and favours reabsorption
• Hydrostatic pressure gradient is small, but favours extravasation of fluid
  • Interstitial hydrostatic pressure becomes more negative closer to the hilum, drawing fluid into the pulmonary lymphatics

Causes of Oedema

Oedema can be localised or generalised, and in both cases caused by:

• Increased Filtration Pressure
  Occurs when capillary hydrostatic pressure exceeds interstitial hydrostatic pressure. Causes:
  • Increased Venous pressure
    This includes an increase in CVP:
    • CCF
    • TR
    • Increased venoconstriction
    • Increased MSFP
  • Impaired venous return
    • Obstruction
    • Respiratory muscle pump
    • Skeletal muscle pump
  • Positioning

• Decreased Oncotic Pressure Gradient
  • Decreased plasma protein
    • Hepatic failure
    • Critical Illness
  • Increased interstitial oncotic pressure
    • Mannitol/starch extravasation

• Increased capillary permeability

  • Inflammatory proteins
    • Substance P
    • Histamine
    • Kinins

• Inadequate Lymph Flow

References

1. Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong's Review of Medical Physiology. 24th Ed. McGraw Hill. 2012.
2. Brandis, K. Starling's Hypothesis. Anaesthesia MCQ.
3. ANZCA August/September 2001