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PV Loop Simulator

Interactive Pressure-Volume Loop Education
Ees ⓘEnd-Systolic Elastance (Contractility)
Slope of the ESPVR line. Reflects intrinsic LV contractility independent of loading conditions. Higher = stronger contraction.
2.5 mmHg/mL
Rs ⓘSystemic Vascular Resistance
Resistance of the systemic bed between the arterial and venous compartments. 1.07 mmHg·s/mL is 17.8 Wood units, about 1,430 dyn·s/cm⁵ with RAP as the downstream pressure. Arterial elastance Ea is no longer a slider: it emerges from Rs, heart rate and arterial compliance and is read out in the panel.
1.07 mmHg·s/mL
Vs ⓘStressed Blood Volume
The blood that distends the circulation above its unstressed volume, roughly 15 to 30 percent of total blood volume. Fluids raise it; venodilators and diuretics lower it. End-diastolic volume is no longer a slider: it emerges where venous return meets the EDPVR and is read out in the panel.
810 mL
B ⓘChamber Stiffness (Diastolic)
Exponent of the EDPVR curve. Higher = stiffer ventricle = steeper diastolic pressure rise. Elevated in HFpEF, concentric LVH, constriction.
0.025 mL-1
HR ⓘHeart Rate
Sets cycle length. The engine runs the beat: a faster rate shortens diastole so filling falls short, and raises Ea (about Rs × HR/60), so cardiac output rises less than in proportion to rate and falls again at high rates.
70 bpm
V0 ⓘUnstressed Volume
Volume-axis intercept of the ESPVR. The theoretical LV volume at zero pressure. Shifts the entire PV loop left or right. Increased in DCM/eccentric remodeling.
10 mL
Inotropes
Vasopressors
Vasodilators
Negative Inotrope
Volume
Heart Failure
Shock
Valve Disease
Mixed Valve
Remodeling
Pericardial
Counterpulsation
Transvalvular Pump
Extracorporeal
Combination
EDV— mL
SV— mL
EF— %
CO— L/min
Ao— mmHg
MAP— mmHg
ESP— mmHg
EDP— mmHg
PCWP— mmHg
RAP— mmHg
Ea— mmHg/mL
Ea/Ees—
SW— mmHg·mL
About the Pressure-Volume Loop Simulator

The closed-loop model behind the loop

This simulator runs a closed-loop circulation to steady state and draws the beat it settles on. The left ventricle is a time-varying elastance chamber: its pressure at any instant is the passive EDPVR pressure plus an activation fraction of the distance to the ESPVR, the Suga-Sagawa end-systolic line of slope Ees through the unstressed volume V0. It ejects through a Gorlin orifice into a Windkessel arterial compartment, which drains through the systemic resistance into a venous reservoir; a right-heart function curve returns that blood to a pulmonary reservoir from which the ventricle fills through the mitral orifice. Six sliders set Ees, systemic resistance, stressed blood volume, the chamber stiffness constant B, heart rate and V0. Everything else emerges: end-diastolic volume from venous return meeting the EDPVR, arterial elastance Ea from resistance, rate and arterial compliance, pulse pressure from stroke volume meeting arterial compliance. The integration uses a fixed 0.2 ms step, and the beat shown is the one after five beat-to-beat measures stop changing.

Hemodynamic readouts and ventriculo-arterial coupling

Each change updates end-diastolic volume, stroke volume, ejection fraction, cardiac output, aortic systolic and diastolic pressure, mean arterial pressure, end-systolic and end-diastolic pressure, a wedge-pressure proxy (the mean pressure of the pulmonary reservoir), a right atrial pressure proxy, stroke work as the loop area, arterial elastance and the Ea/Ees coupling ratio. Every printed number is computed from the printed operands: stroke volume is the printed EDV minus the printed ESV, ejection fraction the printed stroke volume over the printed EDV, cardiac output the printed forward stroke volume times the printed rate, Ea the printed end-systolic pressure over the printed stroke volume. Readouts are flagged against the tool's bands: ejection fraction normal from 55 to 70 percent, cardiac output from 4.0 to 8.0 L/min, wedge proxy up to 12, mean pressure from 65 to 110, and coupling normal from 0.5 to 1.3 and borderline up to 1.5. Heart rate acts through the beat itself: a faster rate shortens diastole so filling falls short and raises Ea, so cardiac output rises less than in proportion to rate and falls again at high rates. When the model is outside the range in which its numbers mean anything, for example when a pump keeps the aortic valve closed, the panel says so in a sentence instead of colouring a value.

Drugs and interventions

Fifteen agents are grouped as inotropes (dobutamine, milrinone, isoproterenol, low- and high-dose dopamine), vasopressors (phenylephrine, norepinephrine), vasodilators (nitroprusside, nitroglycerin, phentolamine, an ACE inhibitor and a dihydropyridine calcium channel blocker), metoprolol as a negative inotrope, and volume as fluids or diuretics. Each is a set of shifts on the engine's parameters, contractility, systemic resistance, stressed volume, stiffness, rate and right-heart gain, so phenylephrine raises resistance alone and the loop narrows and tilts while mean pressure rises, and nitroglycerin, mainly a venodilator, lowers stressed volume so preload and wedge pressure fall. When agents stack, contractility and right-heart gain multiply and resistance, volume, stiffness and rate add, and the transition between states is eased over 400 milliseconds with a fresh steady state each frame.

Disease states

Eighteen presets set the engine's parameters at once; drugs then stack on top. Heart failure covers HFrEF, HFpEF and dilated cardiomyopathy; shock, cardiogenic shock at SCAI stage C/D, warm septic shock and hypovolemic shock; remodeling, concentric and eccentric LVH; pericardial disease, constrictive pericarditis and tamponade. Valve disease is expressed as orifices: aortic stenosis as an aortic valve area of 0.9 square centimetres, which produces a mean gradient above the 40 mmHg severe threshold of the 2020 ACC/AHA valvular guideline; mitral stenosis as a mitral valve area of 1.2, which raises wedge pressure while the ventricle's own diastolic pressure stays low; aortic and mitral regurgitation as effective regurgitant orifices of 0.35 and 0.45 square centimetres, above the ASE 2017 severe thresholds of 0.3 and 0.4. Regurgitant loops lose their vertical limbs because the flow itself does: mitral regurgitation empties the ventricle before the aortic valve opens, aortic regurgitation refills it before the mitral valve opens. Mixed lesions AS+AR, AS+MR, MS+MR and MS+AS combine the orifices, and MS+AS shows low-flow, low-gradient aortic stenosis because the restricted inflow lowers the flow that generates the gradient.

Mechanical circulatory support

Five configurations layer onto any disease and drug combination, each as a flow or a volume rather than a hand-set effect. The intra-aortic balloon pump displaces 40 millilitres into the arterial compartment during diastole and withdraws it at the onset of systole, so diastolic augmentation and systolic unloading appear in the aortic pressure. Impella CP and Impella 5.0 are transvalvular pumps of 3.5 and 5 litres per minute whose flow falls as the pressure head rises; they draw from the ventricle in every phase, which is what triangularizes the loop and lowers wedge pressure, and on a failing ventricle the 5.0 may keep the aortic valve closed. VA-ECMO drains the venous reservoir at 4 litres per minute and returns it to the arteries, raising the afterload a failing ventricle must open the aortic valve against; bronchial return keeps filling that ventricle, so its end-diastolic pressure rises. That is the ECMO paradox, and here it emerges from the circuit rather than being asserted. ECPELLA adds an Impella to ECMO, draining the ventricle that ECMO would distend.

Comparing loops and worked cases

A ghost loop is stored automatically before the first drug, disease or device is chosen, so each new loop is drawn against its own baseline; snapshots can also be taken manually. Toggles hide the ESPVR, EDPVR and Ea lines, the phase labels and the animated tracing; the tracing takes 60/HR seconds per revolution and dwells in each phase for that phase's real share of the cycle, and it does not run for a visitor whose system asks for reduced motion. The phase-label toggle also carries markers for mitral and aortic valve opening and closing, and renames any limb no longer isovolumic. Three worked examples load full scenarios, one of them cardiogenic shock supported with an Impella CP and dobutamine.