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USMLE Step 1Cardiovascular physiologyEP 04 of 16

Contractility on the pressure-volume loop: the ESPVR explained

Contractility on the pressure-volume loop shows up as the slope of the ESPVR. More contractility steepens it, so ejection runs to a smaller volume; less contractility flattens it.

  • 5:17 video
  • 3 min read
  • 5 sources
  • Published 24 Oct 2026
Video lesson · 5:17 · Watch on YouTubeSeries: Pressure–Volume Loops & Cardiac Physiology · @medservatory
Chapters (12)
By the end of this lesson

Explain how a change in contractility rotates the end-systolic pressure–volume relationship (ESPVR) and predict the effect on end-systolic volume (ESV), stroke volume and ejection fraction.

The short version

  1. Contractility is the muscle's built-in ability to generate force at a given preload and afterload; stroke volume and ejection fraction also depend on load.
  2. The ESPVR is the highest pressure the ventricle can generate at each volume for a given contractile state; its slope, end-systolic elastance (Ees), is a relatively load-independent index of contractility.
  3. More contractility steepens the ESPVR: ESV falls, stroke volume and ejection fraction rise, and, at the same arterial load, end-systolic pressure is a little higher.
  4. Less contractility flattens the ESPVR: ESV rises, and stroke volume and ejection fraction fall.
  5. Preload moves along the curves, afterload slides along the ESPVR, and contractility rotates it.

Contractility is not stroke volume

Take two hearts with the same filling and the same arteries. One is flooded with sympathetic drive; the other has been weakened by ischaemia. In the lesson's teaching model, the first ejects about 80 mL per beat and the second only about 50 mL. Nothing about the load changed, so the difference is contractility, and on the pressure-volume loop contractility has its own signature: the ESPVR.[1][3]

Contractility is the muscle's built-in ability to generate force at a given preload and afterload.[5] Stroke volume and ejection fraction move with load as well, as the preload and afterload lessons showed, so they are not pure markers of the muscle. We need a marker that is much less sensitive to load.[2][5]

The ESPVR on the pressure-volume loop: a wall the loop runs into

That marker is the ESPVR, the end-systolic pressure–volume relationship. Think of it as a wall that the loop's top left corner runs into. For a given contractile state, it is the highest pressure the ventricle can generate at each volume.[1]

  1. Reduce filling brieflyFor example, by occluding the inferior vena cava.[1]
  2. Record several shrinking loopsEach loop ejects from a smaller end-diastolic volume.[1]
  3. Join the top left cornersThey line up on a roughly straight line: the ESPVR. Its slope is the end-systolic elastance, Ees.[1][2][3]
ESPVR (linear teaching form)
Pes = Ees × (ESV − V0)

Pes = end-systolic pressure; Ees = slope (end-systolic elastance, mm Hg/mL); V0 = volume-axis intercept. The relation is approximately linear in the physiological range.[2][3]

Why Ees tracks contractility: Suga, Sagawa and Shoukas (1973)

In 1973, Suga, Sagawa and Shoukas showed in dog hearts that this peak elastance stayed the same when they changed preload or afterload, but rose with epinephrine.[4]

So Ees is treated as a relatively load-independent index of contractility. The word relatively matters: it is less load-sensitive than stroke volume or ejection fraction, not perfectly load-independent.[2][3]

Increasing contractility: a steeper ESPVR

The starting loop: end-diastolic volume (EDV) 120 mL, ESV 50 mL, stroke volume 70 mL. Now increase contractility, with a sympathetic surge or a positive inotrope like dobutamine.[3]

The ESPVR gets steeper, swinging up and to the left, while its volume intercept barely moves. Keep filling and the arterial load the same, and ejection now carries on to a smaller volume. The end-systolic pressure is a little higher too.[1][2]

Worked example (teaching model)
  1. Baseline: SV = 120 − 50 = 70 mL; EF = 70 / 120 ≈ 58%
  2. More contractility: ESV falls to about 40 mL
  3. SV = 120 − 40 = 80 mL
  4. EF = 80 / 120 ≈ 67%

Decreasing contractility: a flatter ESPVR

Now reduce contractility, as with ischaemia or a beta-blocker.[3] The ESPVR flattens, and the loop's top left corner hits the wall sooner.[1]

In the model, ESV rises to about 70 mL, stroke volume falls to about 50 mL (120 − 70), and ejection fraction falls to about 42% (50 / 120). The direction of each change is from[1]; the values are illustrative.

Contractility changes at a fixed EDV of 120 mL and the same arterial load (teaching model: linear ESPVR, V0 = 10 mL; illustrative values)
LoopESPVRESVStroke volumeEjection fraction
Baseline—50 mL70 mL≈ 58%
↑ ContractilitySteeper≈ 40 mL≈ 80 mL≈ 67%
↓ ContractilityFlatter≈ 70 mL≈ 50 mL≈ 42%

Preload vs afterload vs contractility on the pressure-volume loop

Put the three moves side by side and each one has its own geometry:

What each change does to the loop
ChangeWhat movesESPVR
PreloadThe bottom right corner moves along the end-diastolic curveUnchanged
AfterloadThe arterial elastance (Ea) line (a measure of afterload, from the afterload lesson) pivots; the top left corner slides along the ESPVRUnchanged
ContractilityThe ESPVR itself rotatesSteeper or flatter

Practice question

Original · USMLE style
Your turnQB-MS-S1-CARD-004-01

A 64-year-old man in the cardiac intensive care unit has a left ventricular conductance catheter in place for a research protocol. He receives a continuous intravenous infusion of one drug. Heart rate does not change. Compared with the recording before the infusion:

Results
End-diastolic volume120 mL before · 120 mL during infusion
End-systolic volume50 mL before · 40 mL during infusion
End-systolic pressure100 mm Hg before · 115 mm Hg during infusion
Which of the following drugs was most likely infused?
Pick one option. Your answers stay on this device.

Common questions

What is contractility?

Contractility is the heart muscle's built-in ability to generate force at a given preload and afterload.

What is the ESPVR?

The end-systolic pressure–volume relationship: for a given contractile state, the highest pressure the ventricle can generate at each volume. It is found by briefly reducing filling, for example by occluding the inferior vena cava, and joining the top left corners of the shrinking loops.

What is end-systolic elastance (Ees)?

Ees is the slope of the ESPVR. It is treated as a relatively load-independent index of contractility: it rises when contractility increases and falls when it decreases.

Is ejection fraction a measure of contractility?

Not a pure one. Stroke volume and ejection fraction depend on preload and afterload as well as contractility, which is why the slope of the ESPVR is used as the less load-sensitive marker.

What does decreased contractility do to the pressure-volume loop?

The ESPVR flattens, so the top left corner hits it sooner: end-systolic volume rises, and stroke volume and ejection fraction fall. Ischaemia and beta-blockers are examples.

Transcript

Read the full narration, by chapter653 words

0:00Same load, two different hearts

Same filling, same arteries, two very different hearts. One is flooded with sympathetic drive. The other has been weakened by ischaemia. In our model, the first ejects about 80 mL per beat, and the second only about 50. Nothing about the load changed. So what did? By the end of this lesson, you'll explain how contractility rotates the end-systolic pressure–volume relationship, and predict what happens to end-systolic volume, stroke volume and ejection fraction.

0:33The trap: contractility ≠ stroke volume

First, the trap: contractility is not the same thing as stroke volume. Contractility is the muscle's built-in ability to generate force at a given preload and afterload. Stroke volume also depends on preload and afterload, as the last two lessons showed. So we need a marker of the muscle that's much less sensitive to load.

0:56The ESPVR: a wall the loop runs into

That marker is the ESPVR, the end-systolic pressure–volume relationship. Think of it as a wall that the loop's top left corner runs into. For a given contractile state, it's the highest pressure the ventricle can generate at each volume.

1:13How the ESPVR is found (IVC occlusion, Ees)

To find it, you briefly reduce filling, for example by occluding the inferior vena cava, and record several shrinking loops. Their top left corners line up on a roughly straight line. Its slope is called end-systolic elastance, Ees.

1:30Suga, Sagawa & Shoukas 1973: load independence

In 1973, Suga, Sagawa and Shoukas showed in dog hearts that this peak elastance stayed the same when they changed preload or afterload, but rose with epinephrine. So Ees is treated as a relatively load-independent index of contractility.

1:49The starting loop

Our starting loop: end-diastolic volume 120 mL, end-systolic volume 50, stroke volume 70.

1:59Increasing contractility

Now increase contractility, with a sympathetic surge or a positive inotrope like dobutamine. The ESPVR gets steeper, swinging up and to the left, while its volume intercept barely moves. Keep filling and the arterial load the same, and ejection now carries on to a smaller volume. In our model, end-systolic volume falls to about 40, stroke volume rises to about 80, and ejection fraction from about 58 to about 67 percent. The end-systolic pressure is a little higher too.

2:34Decreasing contractility

Now reduce contractility, as with ischaemia or a beta-blocker. The ESPVR flattens, and the loop's top left corner hits the wall sooner. End-systolic volume rises to about 70, stroke volume falls to about 50, and ejection fraction to about 42%. In a real body, filling shifts a little too: slightly less with stronger contraction, slightly more with weaker contraction.

3:02Preload vs afterload vs contractility

Now put all three side by side. Preload moves the bottom right corner along the end-diastolic curve. Afterload pivots the arterial elastance line, sliding the top left corner along a fixed ESPVR. Contractility rotates the ESPVR itself.

3:21Practice question

Your turn. Pause if you want to work it out. A 64-year-old man in the cardiac intensive care unit receives a continuous intravenous infusion, and his heart rate doesn't change. His end-diastolic volume stays at 120 mL, but end-systolic volume falls from 50 to 40, and end-systolic pressure rises from about 100 to about 115 mm Hg. Which drug was most likely infused? The answer is D: dobutamine. A smaller end-systolic volume at a higher end-systolic pressure puts the new corner above the old ESPVR. Only a steeper ESPVR allows that, which means more contractility. C, hydralazine, also shrinks end-systolic volume, but by lowering afterload, so end-systolic pressure falls along the same line. B, phenylephrine, raises afterload, so end-systolic volume would rise, not fall. A, a saline bolus, would raise end-diastolic volume, which didn't change. And E, esmolol, is a beta-blocker, which would flatten the ESPVR and enlarge end-systolic volume.

4:38Recap

Quick recap. One: stroke volume and ejection fraction depend on load. The slope of the ESPVR is the relatively load-independent marker of contractility. Two: more contractility steepens the ESPVR, lowering end-systolic volume and raising stroke volume and ejection fraction. Three: preload moves along the curves, afterload slides along the ESPVR, and contractility rotates it.

5:08Next lesson

Next, we'll use these three moves to read heart failure on the loop: reduced versus preserved ejection fraction.

Sources

Numbers in the text, e.g. [1], point here
  1. Klabunde RE. CV Physiology: Ventricular Pressure-Volume Relationship (cf024); Effects of Preload, Afterload and Inotropy on Ventricular Pressure-Volume Loops (cf025); Interdependent Effects (cf026); Cardiac Inotropy (cf010); Ventricular Ejection Fraction (cf012). cvphysiology.com/cardiac-function/cf024 · cvphysiology.com/cardiac-function/cf025 · cvphysiology.com/cardiac-function/cf026 · cvphysiology.com/cardiac-function/cf010 · cvphysiology.com/cardiac-function/cf012
  2. Burkhoff D, Mirsky I, Suga H. Assessment of systolic and diastolic ventricular properties via pressure-volume analysis. Am J Physiol Heart Circ Physiol 2005;289(2). journals.physiology.org/doi/full/10.1152/ajpheart.00138.2005
  3. Bastos MB et al. Invasive left ventricle pressure–volume analysis. Eur Heart J 2020;41(12):1286–1297. pmc.ncbi.nlm.nih.gov/articles/PMC7084193/
  4. Suga H, Sagawa K, Shoukas AA. Circ Res 1973;32(3):314–322. ahajournals.org/doi/10.1161/01.RES.32.3.314
  5. StatPearls: Physiology, Stroke Volume (NBK547686) · Physiology, Cardiac Preload (NBK541109) · Physiology, Afterload Reduction (NBK493174) · Esmolol (NBK518965) ncbi.nlm.nih.gov/books/NBK547686/ · ncbi.nlm.nih.gov/books/NBK541109/ · ncbi.nlm.nih.gov/books/NBK493174/ · ncbi.nlm.nih.gov/books/NBK518965/

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): heart with anterolateral infarct, dog, cardiac catheterisation. "actin-myosin" by Servier via Bioicons (bioicons.com), CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/), adapted (recoloured, outlined). 3D heart: "Anatomical Human Heart" by Nexal 3D (BlenderKit). Pressure–volume loops, charts and all handwriting are drawn in code (original). The Suga 1973 study is cited, not reproduced. Previous: EP 03 · Afterload on the PV loop · Next: EP 09 · HFrEF vs HFpEF on the loop

Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-CARD-004.

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

In this series

Playlist on YouTube
← Previous · EP 03Afterload on the pressure-volume loop
  1. EP 01Pressure-volume loop explained: four phases, four valve events5:00
  2. EP 02Preload on the pressure-volume loop: EDV, stroke volume and the EDPVR5:04
  3. EP 03Afterload on the pressure-volume loop4:49
  4. EP 04Contractility on the pressure-volume loop: the ESPVR explained5:17
  5. EP 05Wiggers diagram explained: the cardiac cycle step by step5:30
  6. EP 06The Frank-Starling curve: preload, inotropy and heart failure4:44
  7. EP 07Aortic stenosis vs mitral regurgitation on the pressure-volume loop5:41
  8. EP 08Fick principle: how to calculate cardiac output5:07
  9. EP 09HFrEF vs HFpEF on the pressure-volume loop5:33
  10. EP 10Poiseuille's law and vascular resistance: why arterioles matter5:15
  11. EP 11Venous return and cardiac function curves: where they cross5:11
  12. EP 12The baroreceptor reflex: from stretch to vagal and sympathetic output5:17
  13. EP 13Myocardial oxygen supply and demand: why tachycardia causes ischaemia4:50
  14. EP 14Unstable angina vs NSTEMI vs STEMI: from plaque to ACS4:50
  15. EP 15Antianginal drugs: nitrates, beta blockers, calcium channel blockers4:56
  16. EP 16Complications of myocardial infarction, by timeline4:59