USMLE Step 1Cardiovascular physiologyEP 02 of 16

Preload on the pressure-volume loop: EDV, stroke volume and the EDPVR

Give fluid or lose blood, and the same heart draws a different loop. See how preload slides one corner of the pressure-volume loop, and why the other side barely moves.

5:04 video
3 min read
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Published 23 Oct 2026

Video lesson · 5:04 · Watch on YouTubeSeries: Pressure–Volume Loops & Cardiac Physiology · @medservatory

Chapters (9)

By the end of this lesson

Predict how increased and decreased preload change the end-diastolic volume, the stroke volume and the shape of the pressure–volume loop.

The short version

Preload is the stretch on the ventricle just before it contracts, and it is estimated by the end-diastolic volume (EDV).
Preload moves the bottom right corner of the pressure-volume loop along the EDPVR: up and right with more filling, down and left with less.
With afterload and contractility held constant, more preload widens the loop to the right and raises stroke volume, while end-systolic volume changes little.
Ejection fraction changes in the same direction as stroke volume, but proportionally less.
IV fluid raises preload; blood loss and venodilation lower it.

What preload means on the pressure-volume loop

Recall that the left-ventricular pressure-volume loop runs anticlockwise, filling along the bottom and ejecting across the top.^[3]^[1] Preload on the pressure-volume loop is the stretch on the ventricle just before it contracts, and we estimate it with the end-diastolic volume (EDV): the bottom right corner of the loop.^[6]^[8]

Picture the same heart on two very different afternoons. In one, it is given a fast bolus of intravenous fluid. In the other, it is losing blood. Same muscle, same heart. What moves on its loop is the filling.

Two boundary lines: EDPVR and ESPVR

Two boundary lines frame every loop.

EDPVR (end-diastolic pressure–volume relationship): the filling limb at the bottom of the loop sits on this curve. It describes the relaxed ventricle: put more volume in, and the pressure rises along the curve. It is a curve, not a straight line.^[1]^[4]^[3]
ESPVR (end-systolic pressure–volume relationship): the top left corner, the end-systolic point, sits on this line. It is the most pressure the ventricle can generate at each volume, for its current contractility. The loop cannot cross it.^[1]^[4]

The rule: change filling only

To see the effect of preload on its own, change filling and hold afterload and contractility constant.^[1]^[5]

The starting loop: EDV about 120 mL, end-systolic volume (ESV) about 50 mL, stroke volume 70 mL.^[2]

Holding the other two constant matters because each one moves a different part of the loop. Preload moves the end-diastolic corner along the EDPVR. Afterload and contractility act on the end-systolic side; they are the next lessons.

Increased preload on the PV loop: IV fluid

Give the fluid. More blood returns to the heart, so the ventricle fills further. The bottom right corner slides up and to the right along the EDPVR. In the model, EDV rises to 150 mL, and end-diastolic pressure rises with it.^[5]^[1]

The extra stretch makes the muscle contract more forcefully: the Frank–Starling mechanism.^[6]^[1] With afterload and contractility unchanged, the ventricle empties down to about the same ESV, around 50 mL. So the loop gets wider, to the right, and in the model stroke volume rises from 70 to 100 mL.^[1]

Ejection fraction with more preload

Baseline: EF = 70 / 120 ≈ 58%
More preload: EF = 100 / 150 ≈ 67%
EF rises, but proportionally less than stroke volume

Decreased preload: blood loss and venodilation

Run it the other way. With blood loss, venous return falls and the ventricle fills less. The bottom right corner slides down and to the left along the same curve. In the model, EDV falls to 100 mL, ESV stays near 50 mL, and stroke volume drops to 50 mL. The loop gets narrower from the right, and ejection fraction dips to about 50% (50 / 100).^[5]^[1]

Preload in the teaching model (afterload and contractility fixed)
Loop	EDV	ESV	Stroke volume	Ejection fraction
Baseline	120 mL	≈ 50 mL	70 mL	≈ 58%
More preload (IV fluid)	150 mL	≈ 50 mL	100 mL	≈ 67%
Less preload (blood loss)	100 mL	≈ 50 mL	50 mL	50%

Overlay the three loops and they share the same left side. The less-preload loop sits inside the baseline loop, which sits inside the more-preload loop. All three filling limbs lie on the same EDPVR, and all three end-systolic points sit at the same place on the ESPVR. Only the right side, the end-diastolic corner, has moved.

What lowers preload in practice: blood loss, and veins that dilate and hold more blood. What raises it: intravenous fluid.^[5]^[6]^[7]

Exam trap: end-systolic volume barely moves

In a real body, more filling raises wall stress and arterial pressure a little, so ESV creeps up slightly. It changes little, not never.^[1]^[4]

Changes at the left side of the loop point elsewhere: a bigger ESV at a higher pressure is a rise in afterload, a smaller ESV at a lower pressure is a fall in afterload, and a steeper ESPVR means more contractility.^[1]^[6]

Practice question

Original · USMLE style

Your turnQB-MS-S1-CARD-002-01

A 61-year-old woman comes to the clinic because of substernal chest pressure that occurs when she climbs two flights of stairs and resolves with rest. Her pulse is 78/min and blood pressure is 122/80 mm Hg. She is given a sublingual nitroglycerin tablet. Assume that left ventricular contractility does not change.

Common questions

What is preload on a pressure-volume loop?

Preload is the stretch on the ventricle just before it contracts. It is estimated by the end-diastolic volume, the bottom right corner of the loop.

What happens to the PV loop when preload increases?

The bottom right corner slides up and right along the EDPVR, so the loop widens to the right and stroke volume rises. With afterload and contractility constant, end-systolic volume changes little.

Does end-systolic volume change with preload?

In the exam model it stays about the same. In a real body, more filling raises wall stress and arterial pressure a little, so it creeps up slightly.

What is the EDPVR?

The end-diastolic pressure–volume relationship: the curve the filling limb of the loop sits on. It describes the relaxed ventricle and is a curve, not a straight line.

Does ejection fraction change with preload?

Yes. EF moves the same way as stroke volume, but proportionally less. In the teaching model it goes from about 58% to about 67% with more preload, and to about 50% with less.

Transcript

Read the full narration, by chapter672 words

0:00Same heart, two afternoons

Same heart, two very different afternoons. In one, it's given a fast bolus of intravenous fluid. In the other, it's losing blood. Same muscle, same heart. So what moves on its pressure–volume loop? By the end of this lesson, you'll predict how more or less preload changes the end-diastolic volume, the stroke volume and the shape of the loop.

0:24Recap: the loop runs anticlockwise

Quick recap: the loop runs anticlockwise, filling along the bottom and ejecting across the top. Preload is the stretch on the ventricle just before it contracts, and we estimate it with the end-diastolic volume, EDV.

0:39Two boundary lines: EDPVR and ESPVR

Now add two boundary lines to the graph. The bottom of the loop, the filling limb, sits on a curve called the end-diastolic pressure–volume relationship, or EDPVR. It describes the relaxed ventricle: put more volume in, and the pressure rises along that curve. It's a curve, not a straight line. The top left corner, the end-systolic point, sits on a line called the end-systolic pressure–volume relationship, or ESPVR. That line is the most pressure the ventricle can generate at each volume, for its current contractility. The loop can't cross it.

1:18The rule: change filling only

So here's the rule for this lesson: we change filling, and hold afterload and contractility constant. Our starting loop: EDV about 120 mL, end-systolic volume about 50, stroke volume 70.

1:34More preload: IV fluid

Now give the fluid. More blood returns to the heart, so the ventricle fills further. The bottom right corner slides up and to the right along the EDPVR. In our model, end-diastolic volume rises to 150 mL, and end-diastolic pressure rises with it. The extra stretch makes the muscle contract more forcefully. That's the Frank–Starling mechanism. With afterload and contractility unchanged, the ventricle empties down to about the same end-systolic volume, around 50. So the loop gets wider, to the right. Stroke volume rises from 70 to 100 mL. Ejection fraction rises too, from about 58 to about 67 percent, proportionally much less than stroke volume.

2:25Less preload: blood loss

Now run it the other way. With blood loss, venous return falls, and the ventricle fills less. The bottom right corner slides down and to the left along the same curve. In our model, EDV falls to 100, the end-systolic volume stays near 50, and stroke volume drops to 50 mL. The loop gets narrower from the right, and ejection fraction dips to about 50%.

2:51The trap: ESV barely moves

Here's the trap. More preload does not mean a bigger end-systolic volume. In the exam model, preload moves the right side of the loop. The left side barely moves. In a real body, more filling raises wall stress and arterial pressure a little, so end-systolic volume creeps up slightly. It changes little, not never. And remember what lowers preload in practice: blood loss, and veins that dilate and hold more blood.

3:22Practice question

Your turn. Pause if you want to work it out. A 61-year-old woman with exertional chest pain is given sublingual nitroglycerin. Assume contractility doesn't change. Which change in her left ventricular pressure–volume loop best shows the drug's main effect? The answer is E: a smaller end-diastolic volume and stroke volume, with end-systolic volume nearly unchanged. Nitroglycerin acts mainly on veins. Venodilation lowers venous return, so preload falls. That moves the bottom right corner down and left along the EDPVR, and the loop narrows from the right. A is the opposite: more preload, like a fluid bolus. B, a bigger end-systolic volume at a higher pressure, is a rise in afterload, and D, a smaller end-systolic volume at a lower pressure, is a fall in afterload. At usual doses, nitroglycerin's arterial effect is limited, so D isn't its main effect. And C needs a steeper ESPVR, which means more contractility, and we held that constant.

4:34High-yield recap

Quick recap. One: preload is estimated by end-diastolic volume, and it moves the bottom right corner along the EDPVR. Two: more preload widens the loop to the right and raises stroke volume, while end-systolic volume changes little. Three: fluid raises preload, and blood loss or venodilation lowers it. Next, we keep the filling the same and squeeze the outflow instead. That's afterload.

Sources

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

Klabunde RE. Ventricular Pressure-Volume Relationship (cf024); Effects of Preload, Afterload and Inotropy on Ventricular Pressure-Volume Loops (cf025); Interdependent Effects of Preload, Afterload and Inotropy (cf026). CV Physiology, rev. 11/04/2023. cvphysiology.com/cardiac-function/cf024 · cvphysiology.com/cardiac-function/cf025 · cvphysiology.com/cardiac-function/cf026
Klabunde RE. Cardiac Inotropy (cf010) and cardiac cycle phase pages (hd002a, hd002e). cvphysiology.com/cardiac-function/cf010 · cvphysiology.com/heart-disease/hd002a
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/
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
O'Keefe E, Singh P. Physiology, Cardiac Preload. StatPearls (NBK541109). ncbi.nlm.nih.gov/books/NBK541109/
Khalil B, Foster C, Launico MV. Physiology, Stroke Volume. StatPearls (NBK547686). ncbi.nlm.nih.gov/books/NBK547686/
LaCombe P, Tariq MA, Lappin SL. Physiology, Afterload Reduction. StatPearls (NBK493174). ncbi.nlm.nih.gov/books/NBK493174/
OpenStax. Anatomy and Physiology 2e, §19.4 Cardiac Physiology. openstax.org/books/anatomy-and-physiology-2e/pages/19-4-cardiac-physiology

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 (cropped, recoloured): sarcomere. "infusion-bag-blue", "vein" and "drug-tablet-1" 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, the schematic ventricle 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-002.

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

In this series

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