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USMLE Step 1Cardiovascular physiologyEP 07 of 16

Aortic stenosis vs mitral regurgitation on the pressure-volume loop

Aortic stenosis is pressure overload: a tall, narrow loop. Mitral regurgitation is volume overload: a wide loop shifted right, with no true isovolumetric sides. Read height first, then width.

  • 5:41 video
  • 3 min read
  • 7 sources
  • Published 9 Nov 2026
Video lesson · 5:41 · Watch on YouTubeSeries: Pressure–Volume Loops & Cardiac Physiology · @medservatory
Chapters (7)
By the end of this lesson

Predict how aortic stenosis (pressure overload) and mitral regurgitation (volume overload) each reshape the left-ventricular pressure–volume loop: height, width, position and the isovolumetric sides.

The short version

  1. Read any loop with two questions: how wide is it (stroke volume), and how tall is it (the pressure the ventricle must make)?
  2. Aortic stenosis is pressure overload: a large gradient across the valve makes the loop tall and narrow, with a higher end-systolic volume.
  3. Mitral regurgitation is volume overload: afterload falls, preload rises, and the loop is wide and shifted right with no true isovolumetric phases.
  4. In mitral regurgitation the wide loop overstates forward flow, because part of the ejected volume leaks back into the left atrium.
  5. Look at the height first, then the width, then the vertical sides.

Same heartbeat, two pressures

A 71-year-old man faints climbing the stairs. A catheter reads 220 mm Hg inside his left ventricle but only 130 mm Hg in his aorta. Same heartbeat, two pressures: where did 90 mm Hg go?

This lesson compares aortic stenosis vs mitral regurgitation on the pressure-volume loop. The two lesions sit at opposite ends: one overloads the ventricle with pressure, the other with volume.[1][2][5][7]

The normal pressure-volume loop: width and height

The normal loop has four corners and two vertical sides. On the vertical sides both valves are shut, so volume cannot change: isovolumetric contraction, then isovolumetric relaxation.[1][6]

In the lesson's teaching model, end-diastolic volume (EDV) is 120 mL and end-systolic volume (ESV) is 50 mL, so stroke volume is 70 mL. Peak pressure is about 120 mm Hg. The values are illustrative, not patient data.

Aortic stenosis on the pressure-volume loop: tall and narrow

In aortic stenosis the valve opening is narrow, so ejection meets high resistance and a large pressure gradient develops across the valve.[1][5]

The ventricle has to push harder just to open the way, so the loop gets taller. In the model, peak ventricular pressure is 200 mm Hg while the aorta only reaches 120 mm Hg. Wall stress, which is afterload, goes up, and the ventricle empties less.[1][6][7]

  • End-systolic volume rises, here from 50 to 60 mL.[1]
  • End-diastolic volume usually falls a little, here from 120 to 110 mL.[1]
  • Stroke volume falls from 70 to 50 mL: a loop that is tall and narrow.[1][6]

Over time the wall thickens, which brings wall stress back toward normal. This is concentric hypertrophy.[1][7]

Mitral regurgitation on the pressure-volume loop: wide and shifted right

In mitral regurgitation the leak goes the other way. The mitral valve does not seal, so during systole blood escapes into the left atrium. That atrium is a low-pressure chamber, so the ventricle meets less resistance and afterload is reduced.[2][6][7]

There is no true isovolumetric contraction, because volume starts leaving the ventricle at once. There is no true isovolumetric relaxation either, as the valve is already open to the atrium.[2][6]

The leaked blood returns to the left atrium, so left atrial volume and pressure rise during ventricular systole. The next beat then starts with more filling: preload goes up.[2][6]

  • End-diastolic volume moves right, here to 150 mL, while end-systolic volume stays near 50 mL.[2]
  • The loop is wide: the ventricle seems to eject 100 mL.[2][6]
  • Over years and decades the ventricle dilates and its compliance increases.[2][7]

Why the wide mitral regurgitation loop overstates forward flow

The width of the loop is the volume that leaves the ventricle. In mitral regurgitation not all of it goes the right way. The apparent stroke volume is increased, but the effective, forward stroke volume is reduced, because only a portion is forward flow.[2][6]

Forward flow in the teaching model
  1. Loop width: 150 − 50 = 100 mL
  2. Forward flow into the aorta: 60 mL
  3. Leaked backwards into the left atrium: 100 − 60 = 40 mL

Pressure overload vs volume overload: side by side

Teaching-model values; chronic, compensated disease
FeatureAortic stenosisMitral regurgitation
Type of loadPressure overloadVolume overload
Loop shapeTaller, narrowerWider, shifted right
AfterloadIncreased: high resistance, large gradientReduced: ejection into the low-pressure left atrium
End-diastolic volumeUsually falls a little (120 → 110 mL)Increased (to 150 mL)
End-systolic volumeRises (50 → 60 mL)Stays near 50 mL
Vertical sidesPresent[1][6]No true isovolumetric phases
Chronic changeWall thickens (concentric hypertrophy)Ventricle dilates; compliance increases
  1. Height firstA tall loop means the ventricle is working against pressure.
  2. Then widthA wide loop means volume, but ask how much of it went forward.
  3. Then the vertical sidesIf they are missing, think a regurgitant valve; here, with the leak into the left atrium, mitral regurgitation.

Practice question

Original · USMLE style
Your turnQB-MS-S1-CARD-008-01

A 59-year-old woman undergoes cardiac catheterisation for progressive breathlessness. Left-ventricular volumes and pressures are recorded:

Results
End-diastolic volume190 mL
End-systolic volume74 mL
Peak left-ventricular pressure110 mm Hg
Aortic systolic pressure108 mm Hg
Cardiac output4.5 L/min
Heart rate70/min
Left atrial pressurelarge rise during ventricular systole
Which of the following is the most likely cause of these findings?
Pick one option. Your answers stay on this device.

Common questions

How does aortic stenosis change the pressure-volume loop?

The loop gets taller and narrower. Peak ventricular pressure rises because of the gradient across the valve, end-systolic volume rises and stroke volume falls.[1]

How does mitral regurgitation change the pressure-volume loop?

The loop becomes wide and shifts right, with no true isovolumetric contraction or relaxation. Afterload is reduced and preload is increased.[2][6]

What is the difference between pressure overload and volume overload?

Pressure overload (aortic stenosis) gives higher left-ventricular pressure and an abbreviated stroke volume. Volume overload (mitral regurgitation) shifts end-diastolic volume to the right and increases the loop width.[7]

Why does the mitral regurgitation loop overstate stroke volume?

The width of the loop includes the volume that leaks back into the left atrium. Only part of the ejected volume is forward flow into the aorta.[2][6]

Why is there no isovolumetric phase in mitral regurgitation?

Volume starts leaving the ventricle at once, into the left atrium, and the mitral valve is already open to the atrium during relaxation.[2][6]

Transcript

Read the full narration, by chapter685 words

0:00Same heartbeat, two pressures

A 71-year-old man faints climbing the stairs. A catheter reads 220 millimetres of mercury inside his left ventricle, but only 130 in his aorta. Same heartbeat, two pressures. Where did 90 go? Today: how aortic stenosis and mitral regurgitation each reshape the pressure-volume loop.

0:22The normal loop: width and height

Quick reset on the normal loop. It has four corners, and two vertical sides. On those vertical sides, both valves are shut, so the volume cannot change: isovolumetric contraction, then isovolumetric relaxation. In our model, end-diastolic volume is 120 mL, end-systolic volume 50, so stroke volume is 70. Peak pressure is about 120 millimetres of mercury. Two questions read any loop. How wide is it, which is stroke volume? How tall is it, which is the pressure the ventricle must make? Now break the valves. First, aortic stenosis.

1:04Aortic stenosis: tall and narrow

The valve opening is narrow, so ejection meets high resistance. That creates a large pressure gradient across the valve during ejection. The ventricle must push harder just to open the way, so the loop gets taller. Say peak ventricular pressure 200, while the aorta only reaches 120. Wall stress, which is afterload, goes up, and the ventricle empties less. End-systolic volume rises, here to 60. End-diastolic volume usually falls a little, here to 110. So stroke volume falls to 50: a loop that is tall and narrow. Over time the wall thickens, which brings wall stress back toward normal. Aortic stenosis is pressure overload: tall and narrow. Second, mitral regurgitation.

1:57Mitral regurgitation: wide and shifted right

Now the leak goes the other way. The mitral valve does not seal, so during systole blood escapes into the left atrium. That atrium is a low-pressure chamber, so the ventricle meets less resistance. Afterload is reduced. There is no true isovolumetric contraction, because volume starts leaving the ventricle at once. And no true isovolumetric relaxation either, as the valve is already open to the atrium. The leaked blood comes back to the left atrium, so left atrial pressure rises during systole. The next beat then starts with more filling: preload goes up. End-diastolic volume moves right, say 150, while end-systolic volume stays near 50. The loop is wide: the ventricle seems to eject 100 mL. But the forward flow into the aorta is lower, only 60, because 40 mL leaked backwards. Over years and decades the ventricle dilates, and its compliance increases. Mitral regurgitation is volume overload: wide, shifted right, no vertical sides. Side by side.

3:11Side by side: height, width, vertical sides

Aortic stenosis: the loop gets taller, narrower, and the ventricle works against pressure. Mitral regurgitation: the loop gets wider and shifts right, and the ventricle works against volume. Look at the height first, then the width, then the vertical sides.

3:30Practice question

Your turn. A 59-year-old woman has a cardiac catheterisation for breathlessness. End-diastolic volume is 190 mL, end-systolic volume 74. Peak left ventricular pressure is 110, and aortic systolic pressure 108 millimetres of mercury. Cardiac output is 4.5 litres per minute at 70 bpm. The left atrial pressure tracing shows a large rise during ventricular systole. Which valve lesion is most likely? A, aortic regurgitation. B, aortic stenosis. C, increased contractility from dobutamine. D, mitral regurgitation. E, mitral stenosis. Pause here and decide. A is out: aortic regurgitation fills the ventricle from the aorta, and raises the peak pressure, and there is no atrial rise in systole. B is out: aortic stenosis gives a tall, narrow loop with a big gradient, but here peak ventricular and aortic pressures are almost equal. C is out: dobutamine would send nearly the whole stroke volume forward, and would not raise atrial pressure in systole. E is out: mitral stenosis lowers end-diastolic volume, but ours is high. So the answer is D. The loop is wide, 116 mL, yet forward flow is only about 64, so about 52 mL went backwards into the left atrium.

5:10Recap and next lesson

Three things to keep. One: aortic stenosis is pressure overload. The loop is tall and narrow, with higher end-systolic volume. Two: mitral regurgitation is volume overload. The loop is wide and shifted right, with no true isovolumetric phases. Three: in mitral regurgitation the wide loop overstates forward flow. Next up: cardiac output and the Fick principle.

Sources

Numbers in the text, e.g. [1], point here
  1. Klabunde RE. Cardiovascular Physiology Concepts: Aortic Valve Stenosis (hd009b). cvphysiology.com/heart-disease/hd009b
  2. Klabunde RE. Mitral Valve Regurgitation (hd009c). cvphysiology.com/heart-disease/hd009c
  3. Klabunde RE. Mitral Valve Stenosis (hd009a). cvphysiology.com/heart-disease/hd009a
  4. Klabunde RE. Aortic Valve Regurgitation (hd009d). cvphysiology.com/heart-disease/hd009d
  5. Klabunde RE. Valvular Heart Disease overview (hd003). cvphysiology.com/heart-disease/hd003
  6. LITFL. Pressure-Volume Relationships (Part One). partone.litfl.com/pressure-volume_relationships.html
  7. Pitoulis FG, Terracciano CM. Heart plasticity in response to pressure- and volume-overload. Front Physiol 2020. pmc.ncbi.nlm.nih.gov/articles/PMC7031419

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. All video diagrams (pressure-volume loops, valve and chamber sketches, charts, cards and handwriting) are original and drawn in code; no third-party artwork is used in the video. Thumbnail heart illustration: Servier Medical Art (smart.servier.com), CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/), adapted (recoloured, outlined). Previous: Frank-Starling curve (MS-S1-CARD-006) · Next: Cardiac Output and the Fick Principle (MS-S1-CARD-007)

Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-CARD-008.

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

In this series

Playlist on YouTube
← Previous · EP 06The Frank-Starling curve: preload, inotropy and heart failure
  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