A quote from Starling (1896)

"... there must be a balance between the hydrostatic pressure of the blood in the capillaries and the osmotic attraction of the blood for the surrounding fluids. "

" ... and whereas capillary pressure determines transudation, the osmotic pressure of the proteids of the serum determines absorption."

**Starling’s hypothesis** states that the fluid movement due to filtration across the wall of a capillary is dependent
on the balance between the hydrostatic pressure gradient and the oncotic pressure gradient across the capillary.

The four Starling’s forces are:

- hydrostatic pressure in the capillary (Pc)
- hydrostatic pressure in the interstitium (Pi)
- oncotic pressure in the capillary (pc )
- oncotic pressure in the interstitium (pi )

The balance of these forces allows calculation of the net driving pressure for filtration.

**Net Driving Pressure = [ ( Pc - Pi ) - ( pc - pi ) ]**

Net fluid flux is proportional to this net driving pressure. In order to derive an equation to measure this fluid flux several additional factors need to be considered:

- the reflection coefficient
- the filtration coefficient (Kf )

An additional point to note here is that the capillary hydrostatic pressure falls along the capillary from the arteriolar to the venous end and the driving pressure will decrease (& typically becomes negative) along the length of the capillary. The other Starling forces remain constant along the capillary.

The reflection coefficient can be thought of as a correction factor which is applied to the measured oncotic pressure gradient across the capillary wall. Consider the following:

The small leakage of proteins across the capillary membrane has two important effects:

- the interstitial fluid oncotic pressure is higher then it would otherwise be.
- not all of the protein present is effective in retaining water so the effective capillary oncotic pressure is lower than the measured oncotic pressure (in the same way that there is a difference between osmolality and tonicity).

Both these effects decrease the oncotic pressure gradient. The interstitial oncotic pressure is accounted for as its value is included in the calculation of the gradient.

The reflection coefficient is used to correct the magnitude of the measured gradient to take account of the ‘effective oncotic pressure’. It can have a value from 0 to 1. For example, CSF & the glomerular filtrate have very low protein concentrations and the reflection coefficient for protein in these capillaries is close to 1. Proteins cross the walls of the hepatic sinusoids relatively easily and the protein concentration of hepatic lymph is very high. The reflection coefficient for protein in the sinusoids is low. The reflection coefficient in the pulmonary capillaries is intermediate in value: about 0.5.

The net fluid flux (due to filtration) across the capillary wall is proportional to the net driving pressure. The filtration coefficient (Kf) is the constant of proportionality in the flux equation which is known as the Starling’s equation.

The **filtration coefficient** consists of two components as the net fluid flux is dependent on:

- the area of the capillary walls where the transfer occurs
- the permeability of the capillary wall to water. (This permeability factor is usually considered in terms of the ‘hydraulic conductivity’ of the wall.)

The filtration coefficient is the product of these two components: **Kf = Area x Hydraulic conductivity**

A ‘leaky’ capillary (eg due to histamine) would have a high filtration coefficient. The glomerular capillaries are naturally very leaky as this is necessary for their function; they have a high filtration coefficient.

Typical values of Starling Forces in Systemic Capillaries (mmHg) | ||

Arteriolar end of capillary |
Venous end of capillary | |

Capillary hydrostatic pressure | 25 | 10 |

Interstitial hydrostatic pressure | -6 | -6 |

Capillary oncotic pressure | 25 | 25 |

Interstitial oncotic pressure | 5 | 5 |

The net driving pressure is outward at the arteriolar end and inward at the venous end of the capillary. This change in net driving pressure is due to the decrease in the capillary hydrostatic pressure along the length of the capillary.

The values quoted in various sources vary but most authors ‘adjust’ the values to ensure the net gradients are in the appropriate direction they wish to show. The method (used in some sources) of just summing the various forces takes no account of the reflection coefficient. The values for hydrostatic pressure are not fixed and vary quite widely in different tissues and indeed within the same tissue. Contraction of precapillary sphincters and/or arterioles can drop the capillary hydrostatic pressure quite low and the capillary will close.

When first measured by Landis in 1930 in a capillary loop in a finger held at heart level, the hydrostatic pressures found were 32 mmHg at the arteriolar end and 12 mmHg at the venous end. The later discovery of negative values for interstitial hydrostatic pressure by Guyton did upset the status quo a bit.

The Starling equation cannot be used quantitatively in clinical work. To actually use the Starling equation clinically requires measurement of six unknowns. This is simply not possible and this limits the usefulness of the equation in patient care. It can be used in a general way to explain observations (eg to explain generalised oedema as due to hypoalbuminaemia).

The microcirculations of the kidney, the lung and the brain are special cases in the use of the Starling equation and are considered in the next three sections.