# Capillary Exchange and Starling Forces

> Capillary exchange and Starling forces in MBBS Physiology — hydrostatic and oncotic pressures, the Starling equation and clinical oedema reasoning.

- Canonical URL: https://prepelephant.com/topics/mbbs/physiology/capillary-exchange-starling-forces
- Exam / course: MBBS · Subject: Physiology
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-02
- Last updated: 2026-10-02
- How to cite: "Capillary Exchange and Starling Forces", PrepElephant, https://prepelephant.com/topics/mbbs/physiology/capillary-exchange-starling-forces

## Direct answer

Four pressures decide whether fluid leaves or enters a capillary: capillary hydrostatic pressure pushing out, interstitial fluid hydrostatic pressure opposing it, plasma colloid osmotic pressure pulling in, and interstitial fluid colloid osmotic pressure pulling out. In a typical skin or muscle capillary the net force is about +13 mmHg (filtration) at the arteriolar end and about −7 mmHg (absorption) at the venular end, with the small overall excess filtered being carted back by lymph — this is Starling's hypothesis of capillary exchange.

## What you must remember

- Starling equation: Jv = Kf [(Pc − Pi) − σ (πp − πi)], where Kf is hydraulic conductance (permeability) and σ is the reflection coefficient for protein (1 means protein cannot cross at all).
- Classic values in skin and muscle: Pc falls from about 30 mmHg at the arteriolar end to 10 mmHg at the venular end; Pi is about −3 mmHg; πp is 28 mmHg; πi is about 8 mmHg.
- Mean capillary pressure is roughly 17 mmHg; precapillary sphincter tone is the main lever on it.
- Capillary pressure is organ-specific: glomerular capillaries around 60 mmHg (designed to filter), pulmonary capillaries only about 7 mmHg (designed to stay dry).
- Liver sinusoids are discontinuous, so protein leaks freely and hepatic lymph carries nearly plasma-level protein; most systemic capillaries are continuous with σ close to 1 for albumin.
- Arteriolar constriction in haemorrhage lowers Pc along the capillary, tipping the balance to absorption — interstitial fluid enters the vessels as autotransfusion.
- Venous congestion raises Pc throughout the capillary length, abolishing the absorption end entirely — the physiology behind cardiac oedema.

## Two patients with swollen ankles

A 60-year-old with right heart failure and a 30-year-old with nephrotic syndrome both have pitting ankles, yet the equation is disturbed at opposite ends. In the cardiac patient, venous pressure is raised, so Pc of 30 and 10 mmHg becomes 35 and 20; run the numbers and even the venular end now filters, so fluid accumulates whenever the patient stands, which is why the swelling is dependent — ankles by evening, sacrum after a night supine.

In the nephrotic patient, Pc is normal but albumin loss drops πp from 28 towards 18 mmHg once serum albumin falls below about 2.5 g/dL. Now both ends of every capillary in the body filter, so the oedema is generalised and periorbital — the loose periorbital tissue shows it first after a night recumbent. The therapeutic logic also forks: the cardiac ankle needs venous pressure lowered (diuretics, afterload reduction), while the nephrotic face needs albumin replaced and the glomerular leak treated. One equation, two entirely different management plans — which is exactly why examiners keep asking Starling questions.

Note what the body does to compensate in both: lymph flow rises up to ten-fold and interstitial protein is washed down, which is why oedema takes time to develop and why Guyton assigns the interstitium a safety factor of roughly 17 mmHg before fluid appears.

## Viva traps around the four pressures

The most common single-mark loss is forgetting that interstitial hydrostatic pressure is negative (about −3 mmHg) because lymphatics suck and tissue solids press; candidates quote +3 and lose the filtering arithmetic. Second, σ is not permeability itself but the protein reflection coefficient — in the glomerulus σ for albumin is near 1 (why albuminuria means basement membrane disease), while in hepatic sinusoids it approaches 0. Third, never say colloid osmotic pressure is caused by sodium; it belongs to plasma protein, principally albumin, and only solutes that cannot cross the wall (effective osmoles) generate it.

## Frequently asked questions

### What are the four Starling forces?
Capillary hydrostatic pressure and interstitial fluid oncotic pressure favour filtration; plasma colloid osmotic pressure and interstitial fluid hydrostatic pressure favour reabsorption.

### Why is fluid reabsorbed at the venular end of a capillary?
Pc falls from about 30 to 10 mmHg along the capillary, so the outward hydrostatic force drops below the inward oncotic gradient of about 20 mmHg.

### Which capillaries in the body are the most permeable to protein?
Liver sinusoids and, to a lesser degree, glomerular and intestinal capillaries; discontinuous hepatic endothelium lets nearly all plasma protein through.

### Why does haemorrhage promote fluid absorption from the interstitium?
Sympathetic arteriolar constriction lowers capillary hydrostatic pressure, so the net Starling force swings inward and plasma volume is partially restored.

### What does the reflection coefficient sigma signify?
It expresses how completely a membrane restricts protein; a value of 1 means no protein crosses (ideal capillary) and 0 means free passage, as in liver sinusoids.