What are the phases of the pressure-volume loop?

Traced counterclockwise, the left ventricular loop has four phases: filling with the mitral valve open, isovolumetric contraction with all valves closed, ejection with the aortic valve open, and isovolumetric relaxation with all valves closed. The FIRE acronym (Fill, Isovolumetric contraction, Release, Ease off) keeps the order. Mitral closure (S1) starts isovolumetric contraction at end-diastolic volume, and aortic closure (S2) starts isovolumetric relaxation at end-systolic volume.

How does increased afterload change the pressure-volume loop?

The ventricle must build more pressure before the aortic valve opens, so the loop gets taller, and slower ejection leaves a larger end-systolic volume, so the loop gets narrower. Stroke volume and ejection fraction fall. In the intact body, the extra residual blood raises the next end-diastolic volume, and the Frank-Starling mechanism partly restores stroke volume.

How do preload and contractility change the pressure-volume loop?

Increased preload raises end-diastolic volume and moves the right wall of the loop to the right; with afterload and contractility constant, end-systolic volume stays the same, so stroke volume rises. Increased contractility steepens the end-systolic pressure-volume relationship and lowers end-systolic volume, moving the left wall to the left and raising stroke volume and ejection fraction. Decreased contractility does the opposite.

What does aortic stenosis look like on a pressure-volume loop?

Aortic stenosis makes the loop tall and narrow. Peak left ventricular pressure is very high because of the gradient across the narrowed valve, end-systolic volume rises and stroke volume falls. Over time, concentric hypertrophy stiffens the ventricle, so end-diastolic pressure is high while end-diastolic volume is normal or low, and ejection fraction stays near normal until late.

Which valve lesions remove the isovolumetric phases of the PV loop?

The regurgitant lesions do. In mitral regurgitation, blood leaks into the left atrium whenever ventricular pressure exceeds atrial pressure, so volume falls during both phases that should be isovolumetric. In aortic regurgitation, blood flows back from the aorta as soon as the ventricle starts to relax and keeps flowing until ejection begins, so neither phase is truly isovolumetric. Stenotic lesions keep both vertical walls straight.

What does the area inside a pressure-volume loop represent?

The area inside the loop is the stroke work done by the ventricle in one beat. The width of the loop is the stroke volume, end-diastolic volume minus end-systolic volume. Ejection fraction is stroke volume divided by end-diastolic volume, about 58% for a typical resting ventricle with an end-diastolic volume of about 120 mL and a stroke volume of about 70 mL.

Pressure-Volume Loop Mnemonic: Preload, Afterload & Valves

A left ventricular pressure-volume (PV) loop plots LV pressure (y-axis) against LV volume (x-axis) for one heartbeat and runs counterclockwise through four phases: Fill, Isovolumetric contraction, Release (ejection) and Ease off (isovolumetric relaxation), or FIRE. Its corners are the four valve events: the mitral valve closes at end-diastolic volume (EDV, bottom right, S1), the aortic valve opens, the aortic valve closes at end-systolic volume (ESV, top left, S2) and the mitral valve opens. Loop width is stroke volume (EDV − ESV), the area inside is stroke work, and EF = SV/EDV. Preload moves the right wall (EDV), afterload and contractility move the left wall (ESV), and regurgitant valves bend the straight isovolumetric walls.

The FIRE acronym, decoded

Start at the bottom-left corner, where the mitral valve opens, and trace the loop counterclockwise:

Letter	Phase	Edge of the loop	Valves	LV volume	LV pressure	Starts when
F	Fill (diastole)	Bottom edge, moving right	Mitral open, aortic closed	Rises from ESV to EDV	Dips briefly as relaxation finishes, then creeps up along the passive filling curve (EDPVR)	Mitral valve opens: LV pressure falls below LA pressure
I	Isovolumetric contraction	Right wall, straight up	All closed	Constant at EDV	Rises steeply	Mitral valve closes (S1): LV pressure exceeds LA pressure
R	Release (ejection)	Top edge, moving left	Aortic open, mitral closed	Falls from EDV to ESV	Rises to peak systolic, then falls	Aortic valve opens: LV pressure exceeds aortic diastolic pressure
E	Ease off (isovolumetric relaxation)	Left wall, straight down	All closed	Constant at ESV	Falls steeply	Aortic valve closes (S2)

Corner check: "Ma'am, C-O-C-O." Start at the bottom-right corner and go counterclockwise: Mitral Closes, Aortic Opens, Aortic Closes, Mitral Opens. The two closures are the two heart sounds and the two volumes you need: S1 sits at EDV and S2 sits at ESV. Healthy valves open silently. The same four events laid out on a time axis are in the Wiggers diagram cheat sheet.

Reading the numbers off the loop

$SV = EDV - ESV \qquad EF = \frac{SV}{EDV} \qquad CO = SV \times HR$

Textbook resting LV (Klabunde): ESV about 50 mL and SV about 70 mL, so EDV is about 120 mL and $EF = 70/120 \approx 58\%$ . OpenStax puts the normal EF at about 55–70%.
Width = stroke volume; area = stroke work. A wider loop ejects more; a bigger loop does more work per beat.
ESPVR (end-systolic pressure-volume relationship): the line through the top-left corner. Its slope reflects contractility, and the loop can never cross it. It is relatively load-independent, which is why it is used to separate a contractility change from a loading change.
EDPVR (end-diastolic pressure-volume relationship): the passive filling curve under the bottom edge. Its slope is the reciprocal of compliance: steeper in a stiff, hypertrophied ventricle (higher filling pressure at any volume) and flatter in a chronically dilated one (dilated cardiomyopathy, chronic regurgitation).

Preload, afterload and contractility: which wall moves

PRE-load is the volume present before contraction, so it moves the right wall (EDV). AFTER-load and contractility decide where ejection stops, so they move the left wall (ESV).

Change (example)	EDV	ESV	SV	EF	What the loop does
↑ Preload (IV fluid bolus, more venous return)	↑	Unchanged*	↑	Slightly ↑	Right wall moves right: wider
↓ Preload (hemorrhage, dehydration)	↓	Unchanged*	↓	↓	Right wall moves left: narrower
↑ Afterload (higher aortic pressure, e.g., arteriolar vasoconstriction)	Unchanged at first, then ↑	↑	↓	↓	Aortic valve opens at a higher pressure: taller; left wall moves right: narrower
↓ Afterload (arterial dilator such as hydralazine)	Unchanged at first, then slightly ↓	↓	↑	↑	Shorter and wider to the left
↑ Contractility (sympathetic stimulation, dobutamine)	Slightly ↓	↓	↑	↑	ESPVR steeper and shifted left; left wall moves left
↓ Contractility (acute ischemia, systolic heart failure)	↑ (compensatory, smaller than the ESV rise)	↑↑	↓	↓	ESPVR flatter; loop shifts right and narrows

*With afterload and contractility held constant. In Klabunde's example, raising preload increases SV from 75 to 100 mL and EF from 60% to 67%, and lowering it drops SV to 50 mL and EF to 50%, while ESV stays put.

Afterload and contractility both move ESV. Afterload slides the end-systolic corner along the same ESPVR; contractility changes the ESPVR slope. Steeper line = inotropy.
The variables interact in a real body. Higher afterload leaves more blood behind (↑ ESV); that residual volume raises the next EDV, and the Frank-Starling mechanism partly restores SV. So in a normal heart a change in aortic pressure changes SV relatively little, but a failing ventricle already at maximal EDV loses a lot of SV, which is why arterial dilators help in heart failure.
Exercise combines a modest rise in EDV (more venous return) with a large rise in contractility, so ESV falls and SV and EF rise. How venous return and cardiac output meet is covered in the venous return curve guide.

Valve lesions: four loop shapes

Stenosis keeps the walls straight; regurgitation bends them. Aortic stenosis stands tall, mitral stenosis shrinks, aortic regurgitation balloons to the right, and mitral regurgitation loses both vertical walls.

Lesion (chronic)	Loop shape	EDV	ESV	Loop width (total SV)	Peak LV pressure	Isovolumetric walls
Aortic stenosis	Tall and narrow	Normal, often ↓ as hypertrophy stiffens the LV (end-diastolic pressure high)	↑	↓	↑↑ (gradient across the valve)	Straight
Aortic regurgitation	Very wide, shifted right	↑↑ (fills from the aorta and the LA; dilated LV)	Slightly ↑ (large ↑ once the LV fails)	↑↑	↑	No true isovolumetric relaxation (volume rises as soon as the valve should close) or contraction (aortic backflow continues until ejection)
Mitral regurgitation	Wide, both vertical walls sloped	↑ (high LA pressure, dilated LV)	Normal to ↑ as the LV dilates, ↑↑ once it fails (↓ only in acute MR, when the LV suddenly empties into a low-pressure LA)	↑, but forward SV ↓	Not raised	Neither: blood leaks into the LA whenever LV pressure exceeds LA pressure, before the aortic valve opens and after it closes
Mitral stenosis	Small, shifted left	↓ (impaired filling)	Slightly ↓	↓	Normal or ↓	Straight; the high pressure is in the LA, not the LV

Aortic stenosis keeps EF near normal until late. SV and EDV fall together, the pattern of heart failure with preserved EF. Late decompensation brings LV dilation, a falling EF and a misleadingly low valve gradient.
AR vs MR: both widen the loop to the right. AR adds a high peak systolic pressure and a wide pulse pressure; MR does not raise peak pressure, and part of every beat goes backward into the left atrium. A small ESV is the acute MR picture; chronic MR carries a normal or rising ESV.
Width is total stroke volume (EDV − ESV), not forward flow. In MR, the wide loop includes the regurgitant volume.
Murmurs, pulses and maneuvers for each lesion are in the heart murmurs USMLE table, and the two heart failure loops (↓ contractility vs a stiff ventricle) are compared in the HFrEF vs HFpEF mnemonic.

Practice question

A 74-year-old man has exertional chest pressure and has nearly fainted twice while climbing stairs. He has a harsh crescendo-decrescendo systolic murmur at the right upper sternal border radiating to both carotids, a weak and delayed carotid upstroke, and an S4. Echocardiography shows concentric left ventricular hypertrophy and an ejection fraction of 60%. Compared with a normal loop, which change in his left ventricular pressure-volume loop is most likely?

A. Taller, narrower loop with a higher peak systolic pressure, a larger end-systolic volume and a smaller stroke volume
B. Much wider loop shifted to the right, with a higher peak pressure and no true isovolumetric relaxation
C. Wider loop with sloped walls in place of both isovolumetric phases and no rise in peak pressure
D. Smaller loop shifted to the left, with a low end-diastolic volume and a normal or low peak pressure
E. Wider loop from a smaller end-systolic volume, with a steeper ESPVR

Answer: A. Exertional angina and near-syncope, a crescendo-decrescendo murmur radiating to the carotids and a weak, delayed carotid pulse (pulsus parvus et tardus) point to aortic stenosis. The LV must generate a very high pressure to force blood through the narrow valve (tall loop); the high afterload slows ejection, leaving a larger ESV and a smaller SV (narrow loop). Concentric hypertrophy steepens the EDPVR, so end-diastolic pressure is high even though EDV is normal or low, and EF stays near normal, as in this patient.

Why the others are wrong:

B: aortic regurgitation. Expect bounding pulses, a wide pulse pressure and an early diastolic decrescendo murmur, with a huge EDV.
C: mitral regurgitation. Expect a holosystolic apical murmur radiating to the axilla; the leak into the left atrium removes both isovolumetric phases.
D: mitral stenosis. Expect an opening snap and a diastolic rumble; the LV is underfilled, so the loop is small.
E: increased contractility (dobutamine, sympathetic stimulation) lowers ESV. Aortic stenosis raises it.

Exam traps

ESPVR vs EDPVR: the top-left line is contractility; the bottom curve is compliance. A stiff ventricle (hypertrophy, HFpEF) steepens the EDPVR, not the ESPVR.
An isolated preload change does not move ESV. If both corners move, something besides preload changed.
A taller loop has two classic causes. With high aortic pressure (hypertension), the aortic valve opens at a higher pressure; in aortic stenosis, peak LV pressure far exceeds aortic pressure because of the gradient across the valve.
A normal EF does not mean a normal loop. Aortic stenosis and other stiff-ventricle states keep EF near normal while SV falls.
Regurgitant lesions widen the loop because the width counts blood that leaks backward.

Key takeaways

FIRE, counterclockwise: Fill (mitral open), Isovolumetric contraction (all valves closed, starts at S1), Release (aortic open), Ease off (all valves closed, starts at S2).
Ma'am, C-O-C-O: mitral closes (S1, EDV), aortic opens, aortic closes (S2, ESV), mitral opens.
SV = EDV − ESV (width), EF = SV/EDV (about 55–70% normally), stroke work = area.
Preload moves the right wall; afterload and contractility move the left wall; only contractility changes the ESPVR slope.
Valve loops: AS tall and narrow; AR very wide with high peak pressure; MR wide with no isovolumetric walls; MS small and shifted left.