Medservatory
USMLE Step 1Cardiovascular physiologyEP 03 of 16

Afterload on the pressure-volume loop

Afterload on the pressure-volume loop is a line, not a number. Pivot it and the end-systolic point slides along a fixed ESPVR: higher afterload means a taller, narrower loop and less blood out.

  • 4:49 video
  • 3 min read
  • 5 sources
  • Published 24 Oct 2026
Video lesson · 4:49 · Watch on YouTubeSeries: Pressure–Volume Loops & Cardiac Physiology · @medservatory
Chapters (10)
By the end of this lesson

Predict how increased and decreased afterload change the aortic opening pressure, end-systolic volume (ESV) and stroke volume on the pressure–volume loop.

The short version

  1. Afterload is the load the ventricle has to overcome to eject blood; at the level of the wall it is wall stress, not simply blood pressure.
  2. On the pressure–volume loop, afterload is drawn as the arterial elastance (Ea) line, from the end-diastolic volume on the volume axis to the end-systolic corner; Ea = end-systolic pressure ÷ stroke volume.
  3. Ejection ends where the Ea line meets the ESPVR.
  4. Raising afterload (preload and contractility fixed) makes the loop taller and narrower: the aortic valve opens at a higher pressure, ESV rises and stroke volume falls.
  5. Afterload slides the end-systolic point along a fixed ESPVR; in the idealised model the ESPVR itself does not move.

What afterload is, and why it is not just blood pressure

Picture two hearts filled to exactly the same volume, with the same muscle. One pumps into clamped-down, high-resistance arteries; the other pumps into arteries relaxed by a vasodilator. The first ejects less blood. The difference is afterload, and the pressure-volume loop shows exactly how afterload changes the end-systolic volume and the stroke volume.

Afterload is the load the ventricle has to overcome to eject blood.[4] At the level of the ventricular wall, it is wall stress, which rises with ventricular pressure and chamber radius and falls with wall thickness.[1][4]

Wall stress (concept)
σ ∝ (P × r) / h

σ = wall stress; P = ventricular pressure; r = chamber radius; h = wall thickness. A proportionality, related to the law of Laplace.

At the bedside, afterload is usually estimated from arterial pressure, and resistance in the arteries (systemic vascular resistance) is a big driver of that pressure.[1][4]

Afterload on the pressure-volume loop: the Ea line

On the loop, afterload is drawn as a line. Start on the volume axis at the end-diastolic volume (EDV) and draw a straight line up to the end-systolic corner (the top left corner of the loop). The steepness of that line (its slope, taken as a positive number) is the arterial elastance, Ea: end-systolic pressure divided by stroke volume.[2]

Arterial elastance
Ea = Pes / SV

Pes = end-systolic pressure (mm Hg); SV = stroke volume (mL). The line runs from (EDV, 0) to the end-systolic point.

Ea is set mostly by peripheral resistance and heart rate.[2]

Here is the key picture: the end of ejection sits where the Ea line meets the ESPVR (the end-systolic pressure–volume relationship, the line that the loop's top left corner lies on, introduced with preload). Change the Ea line and you change where that meeting point falls.[2][3]

Raising afterload: a taller, narrower loop

The lesson's starting loop, from a simplified teaching model: EDV 120 mL, ESV 50 mL, stroke volume 70 mL.[5] Now raise afterload, holding preload and contractility constant.

  1. The aortic valve opens laterThe ventricle has to build more pressure before the aortic valve opens, so isovolumetric contraction lasts longer and the loop gets taller.[1]
  2. The Ea line gets steeperIt pivots on the end-diastolic volume, so it meets the ESPVR higher up and further to the right.[2][3]
  3. Less blood leavesESV rises, and stroke volume and ejection fraction fall.[1][4]
Worked example (teaching model)
  1. Baseline: SV = 120 − 50 = 70 mL; EF = 70 / 120 ≈ 58%
  2. Higher afterload: ESV rises from 50 to about 65 mL
  3. SV = 120 − 65 = 55 mL
  4. EF = 55 / 120 ≈ 46%

Taller and narrower: more pressure, less blood out.[1][3]

Lowering afterload with an arterial dilator

Now lower afterload with an arterial dilator. The aortic valve opens at a lower pressure, the Ea line flattens, and it meets the ESPVR lower and further left.[1][2]

In the model, ESV falls to about 40 mL, stroke volume rises to about 80 mL, and ejection fraction to about 67%.[1][4][5]

Afterload changes at a fixed EDV of 120 mL (teaching model; illustrative values)
LoopEa lineESVStroke volumeEjection fraction
Baseline—50 mL70 mL≈ 58%
↑ AfterloadSteeper≈ 65 mL≈ 55 mL≈ 46%
↓ Afterload (arterial dilator)Flatter≈ 40 mL≈ 80 mL≈ 67%

Afterload vs preload vs contractility on the loop

Because the ESPVR stays fixed, afterload changes are easy to separate from the other two moves on the loop:

  • Preload changes move the right side of the loop: the end-diastolic volume shifts.[4]
  • Afterload changes keep the end-diastolic volume and slide the end-systolic point along the same ESPVR.[3]
  • More contractility steepens the ESPVR, giving a smaller ESV and, with the same Ea line, a higher end-systolic pressure.[1][2]

The real-body footnote: afterload in heart failure

In a real body, the blood left behind after a beat adds to the next filling. So when afterload rises and ESV grows, end-diastolic volume creeps up and partly rescues stroke volume.[1]

In a healthy heart, that keeps the change in stroke volume fairly small. In a failing heart, afterload matters much more, which is why arterial dilators can raise cardiac output in heart failure.[1]

Practice question

Original · USMLE style
Your turnQB-MS-S1-CARD-003-01

A 58-year-old man with heart failure with reduced ejection fraction is admitted with worsening dyspnoea. His pulse is 92/min and blood pressure is 148/94 mm Hg. He is given intravenous hydralazine, an arterial dilator. Assume that left ventricular preload and contractility do not change.

Which of the following changes in this patient's left ventricular pressure–volume loop is most likely shortly after the dose?
Pick one option. Your answers stay on this device.

Common questions

What is afterload?

Afterload is the load the ventricle has to overcome to eject blood. At the level of the wall it is wall stress, which rises with ventricular pressure and chamber radius and falls with wall thickness.

Is afterload the same as blood pressure?

No. Arterial pressure is the usual bedside estimate of afterload, and arterial resistance is a big driver of it, but afterload itself is the load against ejection.

How is afterload shown on a pressure-volume loop?

As the arterial elastance (Ea) line, drawn from the end-diastolic volume on the volume axis to the end-systolic corner. Its slope is end-systolic pressure divided by stroke volume, and ejection ends where it meets the ESPVR.

Does afterload change the ESPVR?

No. With preload and contractility held constant, afterload slides the end-systolic point along the same ESPVR; changing the ESPVR itself is contractility.

Why does increased afterload decrease stroke volume?

The ventricle must build more pressure before the aortic valve opens, and the steeper Ea line meets the ESPVR higher and further right, so more blood is left behind: ESV rises and stroke volume falls.

Transcript

Read the full narration, by chapter624 words

0:00Two hearts, same filling

Two hearts, filled to exactly the same volume. One is pumping into clamped-down, high-resistance arteries. The other is pumping into arteries relaxed by a vasodilator. Same filling, same muscle. So why does one eject less blood? By the end of this lesson, you'll predict how afterload changes the aortic opening pressure, the end-systolic volume and the stroke volume on the pressure–volume loop.

0:26Recap: the ESPVR, and the afterload trap

Last time, preload moved the right side of the loop. The top left corner stayed on a line called the ESPVR. First, a common trap: afterload is not simply blood pressure.

0:40What afterload is: wall stress

Afterload is the load the ventricle has to overcome to eject blood. At the level of the wall, it's wall stress, which rises with ventricular pressure and chamber radius, and falls with wall thickness. Arterial pressure is the usual bedside estimate, and resistance in the arteries is a big driver of it.

1:01Afterload as a line: arterial elastance (Ea)

On the loop, we draw afterload as a line. Start on the volume axis at the end-diastolic volume, and draw a straight line up to the end-systolic corner. Its slope is called arterial elastance, Ea: end-systolic pressure divided by stroke volume. It's set mostly by peripheral resistance and heart rate. Here's the key picture: the end of ejection sits where the Ea line meets the ESPVR.

1:29The baseline loop

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

1:39Raising afterload

Now raise afterload, and hold preload and contractility constant. The ventricle has to build more pressure before the aortic valve opens, so isovolumetric contraction lasts longer, and the loop gets taller. The Ea line pivots on the end-diastolic volume and gets steeper. So it meets the ESPVR higher up and further to the right. In our model, end-systolic volume rises from 50 to about 65 mL. Stroke volume falls from 70 to about 55, and ejection fraction from about 58 to about 46%. Taller and narrower: more pressure, less blood out.

2:21Lowering afterload (arterial dilator)

Now lower afterload, with an arterial dilator. The aortic valve opens at a lower pressure, the Ea line flattens, and it meets the ESPVR lower and further left. End-systolic volume falls to about 40, stroke volume rises to about 80, and ejection fraction to about 67 percent. Notice what never moved: the ESPVR itself. Afterload slides the end-systolic point along it.

2:50The real-body footnote: heart failure

One real-body footnote. When more blood is left behind, it adds to the next filling, so end-diastolic volume creeps up and partly rescues stroke volume. In a healthy heart, that keeps the change in stroke volume fairly small. In a failing heart, afterload matters much more. That's why arterial dilators can raise cardiac output in heart failure.

3:16Practice question

Your turn. Pause if you want to work it out. A 58-year-old man with heart failure with reduced ejection fraction is given intravenous hydralazine, an arterial dilator. Assume preload and contractility don't change. Which change in his left ventricular pressure–volume loop is most likely? The answer is A: a lower end-systolic pressure, with a smaller end-systolic volume and a larger stroke volume. Hydralazine lowers arterial resistance, so the Ea line flattens and the end-systolic point slides down and left along the same ESPVR. B is the reverse, a rise in afterload, like a hypertensive emergency. C and E are changes in filling, so the end-diastolic volume moves, and we held preload fixed. D has a smaller end-systolic volume too, but at a higher pressure on a steeper ESPVR. That's more contractility, not less afterload.

4:19Recap

Quick recap. One: afterload is the load against ejection, wall stress at fibre level, shown on the loop by the Ea line. Two: more afterload means a taller, narrower loop, a bigger end-systolic volume and a smaller stroke volume. Three: afterload slides the end-systolic point along a fixed ESPVR. Next, we change the ESPVR itself. That's contractility.

Sources

Numbers in the text, e.g. [1], point here
  1. Klabunde RE. CV Physiology: Cardiac Afterload (cf008); Ventricular Pressure-Volume Relationship (cf024); Effects of Preload, Afterload and Inotropy on PV Loops (cf025); Interdependent Effects (cf026); Cardiac Inotropy (cf010). cvphysiology.com
  2. Bastos MB et al. Invasive left ventricle pressure–volume analysis: overview and practical clinical implications. Eur Heart J 2020;41(12):1286–1297. pmc.ncbi.nlm.nih.gov/articles/PMC7084193/
  3. 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
  4. StatPearls: Physiology, Stroke Volume (NBK547686); Physiology, Afterload Reduction (NBK493174); Physiology, Cardiac Preload (NBK541109). ncbi.nlm.nih.gov/books/
  5. Loop values come from a simplified teaching model and are illustrative, not patient data.

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. Thumbnail art: cardiac cycle illustration ("cardiac-cycle") by Servier via Bioicons (bioicons.com), CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/), adapted (cropped, recoloured). Illustrations: Servier Medical Art (smart.servier.com), CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/), adapted (recoloured, outlined): narrowed artery, dilated artery, sphygmomanometer, arteriole with smooth muscle. "heart-cros-section" 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).

Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-CARD-003.

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

In this series

Playlist on YouTube
← Previous · EP 02Preload on the pressure-volume loop: EDV, stroke volume and the EDPVR
  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