The Frank–Starling mechanism !

Mechanism
Exam priority: high

The more the heart is filled, the harder it squeezes, so it pumps out whatever blood comes back to it.

Updated 2026-11-01

Also called: Starling's law of the heart, Heterometric autoregulation

See it in 3D: Left ventricle · Right ventricle

What it is

Within physiological limits, a ventricle that is stretched more in diastole contracts more strongly in the next systole. This intrinsic property matches the output of the heart to venous return beat by beat, and keeps the outputs of the right and left ventricles equal over time.

Key facts

Starling curve: x axis = preload (EDV, or atrial / wedge pressure), y axis = stroke volume or cardiac output.
Sympathetic stimulation and inotropes shift the curve up and left; heart failure, negative inotropes and acidosis shift it down.
In the clinic, a fluid challenge tests where a patient is on the curve: responders are on the steep part.

How it works, step by step

More venous return fills the ventricle more in diastole (higher EDV).
Myocytes stretch toward the length where actin and myosin overlap best.
Stretch increases the Ca²⁺ sensitivity of troponin and narrows the gap between filaments.
More cross-bridges form at the same Ca²⁺ level, so force rises.
The ventricle ejects more (higher stroke volume) and ends near its usual end-systolic volume.
Beyond the plateau, extra filling only raises diastolic pressure: congestion and edema without more output.

Left-ventricular pressure–volume loop

EDV 150 mLESV 62 mLSV 88 mLEF 59%ESP 132 mmHg

↑ Preload

↑ Preload (more end-diastolic volume, e.g. fluids): the loop stretches to the right and SV rises by Frank–Starling with the same contractility. ESV changes little.

Tap a corner of the loop (MC, AO, AC, MO) to see the valve event.

Current loop
Normal loop
ESPVR (contractility, Ees)
EDPVR (passive filling)
Ea (arterial afterload)
Stroke volume (SV)

Raise preload and see stroke volume grow while the end-systolic point stays on the same line.

Clinical notes

Hypovolemia puts the heart on the low, steep part of the curve: fluid raises output.
In decompensated heart failure diuretics move the patient left along a flat curve: less congestion with little loss of output.

Test yourself

Think of the answer, then tap the question to see it.

What is the cellular basis of the Frank–Starling mechanism?

Stretch brings sarcomeres closer to optimal length and increases myofilament Ca²⁺ sensitivity, so more cross-bridges form at the same Ca²⁺ level.

How does the Frank–Starling mechanism keep left and right ventricular outputs equal?

If one ventricle pumps more, the other receives more venous return a few beats later, stretches more and raises its output to match.

On a Starling curve, how do you tell a change in preload from a change in contractility?

Preload moves the point along the same curve; contractility shifts the whole curve up (more) or down (less).

Why does giving more fluid to a patient with severe heart failure often worsen breathlessness without raising output?

The patient is on the flat part of a depressed curve: more volume raises filling pressures and pulmonary congestion but adds little stroke volume.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

← All of physiology

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 19.4 Cardiac Physiology (OpenStax (Rice University), 2022); Heart Failure (Congestive Heart Failure) (StatPearls (NCBI Bookshelf), 2025); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 9). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.