USMLE Step 1Cardiovascular physiologyEP 06 of 16

The Frank-Starling curve: preload, inotropy and heart failure

The Frank-Starling curve plots stroke volume against preload. Filling moves the heart along one curve; inotropy and heart failure shift the curve itself.

4:44 video
3 min read
3 sources
Published 8 Nov 2026

Video lesson · 4:44 · Watch on YouTubeSeries: Pressure–Volume Loops & Cardiac Physiology · @medservatory

Chapters (7)

By the end of this lesson

Explain the length-tension basis of the Frank-Starling relationship and how inotropy and heart failure shift the curve.

The short version

Stretch lengthens sarcomeres, and part of the reason for the greater force is higher troponin C calcium sensitivity, so more filling means more force and more stroke volume.
A change in preload moves the heart along one Frank-Starling curve; it does not shift the curve.
More inotropy shifts the curve up and to the left; less inotropy or systolic heart failure shifts it down.
A failing ventricle compensates by filling more, moving right along its lower curve, at the cost of congestion and oedema.

The Frank-Starling curve: stroke volume against preload

Give two hearts the same extra filling and they respond very differently. In the lesson's teaching model, a healthy heart's stroke volume climbs from about 70 to about 85 mL when its filling pressure rises from 10 to 15 mm Hg. A failing heart given the same push goes only from about 40 to about 44 mL. The Frank-Starling curve explains both results.

The curve plots stroke volume against preload, the stretch on the ventricular muscle just before it contracts.^[1]^[3] In practice, preload is read as end-diastolic volume (EDV) or end-diastolic pressure (EDP).^[1]^[3]

Frank and Starling found that the more the heart is filled, the harder it contracts and the more it ejects.^[1]^[2] That is how a healthy ventricle matches its output to whatever venous return delivers.^[1]^[2]

Same stretch, different reward (illustrative model values)

Healthy: 70 → 85 mL, a gain of 15 mL for a 5 mm Hg rise in filling pressure
Failing: 40 → 44 mL, a gain of only 4 mL for the same rise
Same stretch, very different reward

Why stretch raises force: length-dependent activation

Filling stretches each muscle cell, and stretch lengthens its sarcomeres. A longer sarcomere generates more force.^[1]

Part of the reason is that stretch makes troponin C more sensitive to calcium, so the same calcium signal switches on more cross-bridges.^[1]^[2] This is length-dependent activation: more stretch, more force, at the same calcium level.

Moving along the Frank-Starling curve versus shifting it

Inotropy is a change in force at the same fibre length, regulated mainly by sympathetic nerves.^[1] Increase it, as in exercise, and the whole curve shifts up and to the left, so stroke volume is higher at any given filling.^[1] Decrease inotropy and the curve shifts down, so stroke volume is lower at any given filling.^[1]

What moves the heart along the curve, and what shifts it
Change	What happens	Effect on stroke volume
Preload rises or falls	Move along the same curve	Rises or falls with filling
Inotropy increases (for example, exercise)	Curve shifts up and to the left	Higher at any given filling
Inotropy decreases	Curve shifts down	Lower at any given filling
Afterload increases	Curve shifts down and to the right	Lower at any given filling

Heart failure on the Frank-Starling curve: a lower curve

In systolic heart failure, the muscle has lost intrinsic inotropy.^[1] The curve shifts downward and its slope falls, so the same stretch buys much less stroke volume.^[1]

The ventricle compensates by filling more, and its end-diastolic pressure rises.^[1] That moves the heart to the right along its new, lower curve and wins back some stroke volume. The cost is that pressure backs up, and congestion and oedema follow.^[1]

Inotropy is lostThe curve shifts down and its slope falls.
The ventricle fills moreEnd-diastolic pressure rises, moving the heart right along the lower curve.
Some stroke volume is regained, at a costMoving right along the lower curve wins back some stroke volume, but pressure backs up behind the ventricle, and congestion and oedema follow.

Practice question

Original · USMLE style

Your turnQB-MS-S1-CARD-006-01

A 24-year-old healthy man volunteers for a research study and has a left ventricular catheter in place. When his legs are passively raised, left ventricular end-diastolic pressure rises from 8 mm Hg to 12 mm Hg and stroke volume rises from 62 mL to 74 mL. Heart rate, systemic vascular resistance and plasma catecholamine concentrations do not change.

Common questions

What is the Frank-Starling curve?

It plots stroke volume against ventricular preload. The more the heart is filled, the harder it contracts and the more it ejects.

Why does more filling increase stroke volume?

Filling stretches the muscle cells and lengthens their sarcomeres, which generate more force. Part of the reason is that longer sarcomeres have a higher troponin C calcium sensitivity (length-dependent activation).

What is the difference between moving along the curve and shifting it?

A change in preload moves the heart along one curve. A change in inotropy shifts the curve itself: up and to the left with more inotropy, down with less.

How does systolic heart failure change the Frank-Starling curve?

Loss of intrinsic inotropy shifts the curve downward with a lower slope, so the same stretch buys much less stroke volume.

How does a failing ventricle compensate?

It fills more, so end-diastolic pressure rises and the heart moves right along its lower curve, winning back some stroke volume at the cost of congestion and oedema.

Transcript

Read the full narration, by chapter637 words

0:00Two hearts, the same extra filling

Give two hearts the same extra filling, and watch what happens. In our model, a healthy heart's stroke volume climbs from about 70 to about 85 mL when its filling pressure rises from 10 to 15 mm Hg. A failing heart, given the very same push, only goes from about 40 to about 44. Same stretch, very different reward. Why? By the end of this lesson, you'll explain why filling raises stroke volume, and how inotropy and heart failure shift the Frank–Starling curve.

0:35The trap and the curve: preload, EDV and EDP

First, the trap: moving along the curve is not the same as shifting the curve. The curve plots stroke volume against preload, which is the stretch on the ventricular muscle just before it contracts. In practice, we read preload as end-diastolic volume or end-diastolic pressure. Frank and Starling found that the more the heart is filled, the harder it contracts, and the more it ejects. That is how a healthy ventricle matches its output to whatever venous return delivers.

1:07Why stretch raises force: length-dependent activation

Now the mechanism. Filling stretches each muscle cell, and stretch lengthens its sarcomeres. A longer sarcomere generates more force. Part of the reason is that stretch makes troponin C more sensitive to calcium, so the same calcium signal switches on more cross-bridges. That is length-dependent activation: more stretch, more force, at the same calcium level. Notice what changed: only the starting length. The muscle itself is the same.

1:39Preload slides you along; inotropy shifts the curve

So a change in preload moves the heart along one curve. Inotropy is different. It is a change in force at the same fibre length, regulated mainly by sympathetic nerves. Increase inotropy, as in exercise, and the whole curve shifts up and to the left. At any given filling, stroke volume is now higher. Decrease inotropy, and the curve shifts down. At any given filling, stroke volume is lower. Raising afterload also pushes the curve down and to the right.

2:14Heart failure: a lower curve and compensation

Now heart failure. In systolic failure, the muscle has lost intrinsic inotropy. That is a downward shift in the curve, with a lower slope, so the same stretch buys much less stroke volume. But the ventricle compensates by filling more, and end-diastolic pressure rises. That moves the heart to the right along its new, lower curve, and wins back some stroke volume. The cost is that the pressure backs up, and congestion and oedema follow. So remember two moves: preload slides you along the curve, and inotropy or failure shifts the curve.

2:53Practice question

Your turn. Pause if you want to work it out. A 24-year-old healthy man volunteers for a research study with a left ventricular catheter. When his legs are passively raised, left ventricular end-diastolic pressure rises from 8 to 12 mm Hg, and stroke volume rises from 62 to 74 mL. Heart rate, systemic vascular resistance and plasma catecholamines don't change. Which of the following best explains the rise in stroke volume? Let's strike the wrong ones first. A, increased sympathetic inotropy, would shift the curve, but catecholamines didn't change; here the heart moved along its curve. C, a fall in systemic vascular resistance, is ruled out, because resistance didn't change. D, a faster heart rate, is also ruled out, because the rate stayed the same. And E, a loss of intrinsic contractility, would lower stroke volume, not raise it. The answer is B. The leg raise increased filling, which stretched the sarcomeres, and longer sarcomeres are more sensitive to calcium, so force and stroke volume rose along the same curve.

4:11Recap and next lesson

Quick recap. One: stretch lengthens sarcomeres and raises calcium sensitivity, so more filling means more stroke volume. Two: more inotropy shifts the curve up and left; less inotropy or systolic failure shifts it down. Three: a failing heart compensates by moving right along a lower curve, at the cost of congestion. Next, we put the Frank-Starling curve to work on damaged valves, using pressure-volume loops.

Sources

Numbers in the text, e.g. [1], point here

Klabunde RE. Cardiovascular Physiology Concepts: Frank-Starling Mechanism (cf003); Cardiac Inotropy (cf010); Pathophysiology of Heart Failure (hf003). cvphysiology.com/cardiac-function/cf003 · cvphysiology.com/cardiac-function/cf010 · cvphysiology.com/heart-failure/hf003
Sequeira V, van der Velden J. Historical perspective on heart function: the Frank-Starling Law. Biophys Rev 2015;7(4):421-447. pmc.ncbi.nlm.nih.gov/articles/PMC5418489/
StatPearls: Physiology, Cardiac Preload (NBK541109). ncbi.nlm.nih.gov/books/NBK541109/

The practice question is original and its patient is synthetic. Every fact is checked against the sources above in independent accuracy reviews. Always follow your local guidelines and your own laboratory’s ranges.

Image credits. Illustrations: Servier Medical Art (smart.servier.com), CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/), adapted (recoloured, outlined): sarcomere and sarcoplasmic reticulum; systolic heart failure. 3D heart: "Anatomical Human Heart" by Nexal 3D (BlenderKit). Frank-Starling curves, sarcomere sketches, charts and all handwriting are drawn in code (original).

Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-CARD-006.

For exam study only, not medical advice. Read the medical disclaimer.

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