Explore Heart mechanics

Diastolic properties

Compare a compliant and a stiff ventricle at the same volume and show how relaxation changes filling.

Experiment: Normal adult at rest · unchanged from its starting state

Key measurements

— mL

baseline not set

— mmHg

baseline not set

— mmHg

baseline not set

— mL

baseline not set

Inspect beats and technical detailsbeat selection, transient versus settled, timings

Position within the beat0.000 s

Early beats after a change are transient: the circulation is still re-balancing. A beat is called settled when three consecutive windows agree within the tolerance. Playback speed only moves the cursor over the finished simulation; it never changes the heart rate.

Compare scenariosbaseline, snapshots, axes, export

Baseline

No baseline is set.

Comparison snapshots

Keep up to three snapshots of states you want to compare with the baseline and the current state.

How comparisons are drawn

Side-by-side loops instead of an overlay Identical axes for every loop (turn off and each plot rescales to its own data)

Pressure–volume loop options

Show the ESPVR and EDPVR reference lines Shade stroke work Show the arterial elastance (Ea) line Show the right heart instead of the left

Export

Try it

Set values directly

LV passive stiffness (k)1/mL ×10⁻³

How this works

Exponent of the EDPVR P = P₀(e^{k(V−V₀)} − 1). Higher k = steeper diastolic pressure rise with volume.

Changes: chambers.lv.kp

LV relaxation durationms

How this works

Time for active elastance to decay to zero after peak. Longer = slower (impaired) active relaxation.

Changes: chambers.lv.tRelax

Changes so farundo, redo, restart

No changes yet. Every change is recorded here so the experiment can be reproduced.

More controlsevery control, exact values

Rhythm and timing9 controls

Heart ratebpm

How this works

Sets the sinus RR interval. Systolic durations shorten with rate as √(RR/RR₇₀).

Changes: rhythm.heartRate

AV delayms

How this works

Interval from atrial to ventricular activation onset.

Changes: rhythm.avDelay

PVC every N beats (0 = none)beats

How this works

A premature ventricular beat at the coupling interval, the next P blocked (compensatory pause), then a potentiated beat.

Changes: rhythm.pvcEveryN

PVC coupling interval× RR

How this works

Prematurity of the PVC as a fraction of the sinus RR interval.

Changes: rhythm.pvcCoupling

Post-extrasystolic potentiationfraction

How this works

Fractional Ees increase on the beat after the compensatory pause (force–interval relation).

Changes: rhythm.potentiation

RR irregularity (AF when atrial contraction off)CV

How this works

Coefficient of variation of a seeded log-normal RR distribution.

Changes: rhythm.irregularity

Atrial contraction (0 off = AF, 1 on)

How this works

Organised atrial contraction; off removes the a wave and the atrial kick.

Changes: rhythm.atrialContraction

AV dissociation (0 off, 1 on)

How this works

Atria beat at the atrial rate, ventricles at the heart rate, independently (cannon a waves when they coincide).

Changes: rhythm.avDissociation

Atrial rate (dissociated)bpm

How this works

Atrial clock rate used only under AV dissociation.

Changes: rhythm.atrialRate

Left ventricle4 controls

LV contractility (Ees)mmHg/mL

How this works

End-systolic elastance: slope of the ESPVR. Raises end-systolic pressure for a given volume.

Changes: chambers.lv.ees

LV relaxation durationms

How this works

Time for active elastance to decay to zero after peak. Longer = slower (impaired) active relaxation.

Changes: chambers.lv.tRelax

LV passive stiffness (k)1/mL ×10⁻³

How this works

Exponent of the EDPVR P = P₀(e^{k(V−V₀)} − 1). Higher k = steeper diastolic pressure rise with volume.

Changes: chambers.lv.kp

LA passive stiffness (k)1/mL ×10⁻³

How this works

EDPVR exponent of the left atrium: a stiff (acute) atrium produces a larger v wave for the same regurgitant volume.

Changes: chambers.la.kp

Right ventricle3 controls

RV contractility (Ees)mmHg/mL

How this works

RV end-systolic elastance.

Changes: chambers.rv.ees

Ventricular interaction gainfraction

How this works

Fraction of one ventricle's transmural pressure felt by the other through the septum (teaching approximation).

Changes: interaction.gain

RV passive stiffness (k)1/mL ×10⁻³

How this works

EDPVR exponent of the right ventricle.

Changes: chambers.rv.kp

Volume and venous tone3 controls

Circulating volumemL

How this works

Total blood volume. Changes enter or leave the systemic venous compartment (explicit external input).

Changes: totalBloodVolume

Venous unstressed volumemL

How this works

Venous tone. Venoconstriction lowers unstressed volume, converting it to stressed volume and raising mean systemic filling pressure.

Changes: vessels.sv.v0

Oxygen consumption (VO₂)mL/min

How this works

Whole-body oxygen consumption for the Fick teaching model (exercise raises it).

Changes: oxygen.oxygenConsumption

Systemic load2 controls

Systemic arteriolar resistancemmHg·s/mL

How this works

Resistance between systemic arteries and veins (the model SVR).

Changes: vessels.sa.r

Arterial compliancemL/mmHg

How this works

Systemic arterial compliance; lower compliance widens pulse pressure.

Changes: vessels.sa.c

Pulmonary load2 controls

Pulmonary arteriolar resistancemmHg·s/mL

How this works

Resistance between pulmonary arteries and veins (the model PVR).

Changes: vessels.pa.r

Pulmonary arterial compliancemL/mmHg

How this works

Compliance of the pulmonary arterial compartment; lower compliance raises PA pulse pressure.

Changes: vessels.pa.c

Valves6 controls

Aortic valve areacm²

How this works

Effective orifice area; gradient rises with flow² / area². Not a clinical severity grade.

Changes: valves.av.eoa

Aortic regurgitant orificecm²

How this works

Regurgitant orifice area for the aortic valve. 0 = competent. Not a clinical severity grade.

Changes: valves.av.regurgitantArea

Mitral valve areacm²

How this works

Effective orifice area of the mitral valve.

Changes: valves.mv.eoa

Mitral regurgitant orificecm²

How this works

Regurgitant orifice area for the mitral valve. 0 = competent.

Changes: valves.mv.regurgitantArea

Tricuspid regurgitant orificecm²

How this works

Regurgitant orifice area for the tricuspid valve. 0 = competent.

Changes: valves.tv.regurgitantArea

Tricuspid valve areacm²

How this works

Effective orifice area of the tricuspid valve.

Changes: valves.tv.eoa

Thorax and respiration4 controls

Mean intrathoracic pressuremmHg

How this works

External pressure on all intrathoracic compartments (chambers, pulmonary vessels). Transmural = chamber − Pth.

Changes: respiration.meanPth

Respiratory pressure swingmmHg

How this works

Peak-to-trough swing of intrathoracic pressure each breath (0 = respiration off). Spontaneous: inspiration lowers Pth; positive pressure: inspiration raises it.

Changes: respiration.pthSwing

Respiratory rate/min

How this works

Breaths per minute for the sinusoidal pleural pressure model.

Changes: respiration.rate

Ventilation mode (0 spontaneous, 1 positive pressure)

How this works

Sign of the inspiratory pleural pressure change: negative for spontaneous breathing, positive for mechanical ventilation.

Changes: respiration.mode

Pericardium5 controls

Pericardial constraint (0 off, 1 on)

How this works

Enables the exponential pericardial pressure acting on all four chambers.

Changes: pericardium.enabled

Pericardial effusionmL

How this works

Fluid occupying the pericardial sac shifts the heart onto the steep part of the pericardial pressure–volume relation (tamponade). Drainage reduces it.

Changes: pericardium.effusion

Pericardial stiffness (φ)mL

How this works

Volume constant of the exponential pericardial relation; smaller φ = stiffer sac (constriction).

Changes: pericardium.phi

Pericardial volume threshold (V0)mL

How this works

Total heart volume (plus effusion) at which pericardial pressure equals the scale constant.

Changes: pericardium.v0

Pleural pressure transmission to chambersfraction

How this works

Fraction of intrathoracic pressure swing transmitted to the chambers; a constricting pericardium shields the heart (dissociation of intrathoracic and intracardiac pressures).

Changes: pericardium.transmission

Dynamic outflow obstruction2 controls

Dynamic LVOT obstruction (0 off, 1 on)

How this works

Enables a volume-dependent outflow orifice in series with the aortic valve (HOCM).

Changes: lvot.enabled

LVOT obstruction onset volumemL

How this works

LV volume below which the outflow area halves; higher values obstruct earlier in ejection.

Changes: lvot.vCrit

Baroreflex (explicit option)3 controls

Baroreflex (0 off, 1 on)

How this works

Explicit first-order baroreflex: MAP error drives heart rate, Ees, arteriolar resistance and venous tone with the stated time constant.

Changes: reflex.enabled

Baroreflex MAP set pointmmHg

How this works

Target mean arterial pressure of the reflex controller.

Changes: reflex.setpoint

Baroreflex time constantbeats

How this works

Beats over which the reflex approaches its target (modelled timescale, visible by design).

Changes: reflex.tauBeats

Intra-aortic balloon pump5 controls

IABP (0 off, 1 on)

How this works

Intra-aortic balloon: its volume is added to the arterial compartment during diastole (inflation at predicted aortic valve closure, deflation just before the next ejection).

Changes: devices.iabp.enabled

Balloon volumemL

How this works

Displaced volume of the balloon; larger balloons augment more and lower the assisted end-diastolic pressure more.

Changes: devices.iabp.balloonVolume

Assist ratio 1:nbeats

How this works

Augment every n-th beat (1:1, 1:2, 1:3); weaning compares assisted with unassisted beats.

Changes: devices.iabp.ratio

Inflation timing (− early, + late)ms

How this works

Offset of inflation from the predicted aortic valve closure (dicrotic notch). Early inflation loads the ejecting ventricle; late inflation wastes augmentation.

Changes: devices.iabp.inflationDelayMs

Deflation timing (− early, + late)ms

How this works

Offset of deflation from 40 ms before the next ventricular activation. Late deflation raises the pressure the ventricle must open the valve against; early deflation loses the end-diastolic unloading.

Changes: devices.iabp.deflationDelayMs

Microaxial LV pump4 controls

Microaxial LV pump (0 off, 1 on)

How this works

Transvalvular pump moving blood from the LV to the systemic arteries; flow falls as the aorta–LV pressure head rises.

Changes: devices.impella.enabled

Pump speed (fraction of maximum)fraction

How this works

Speed scales zero-head flow linearly and zero-flow head with speed². Higher speed into an under-filled LV causes suction.

Changes: devices.impella.speed

Pump zero-head flow (device size)L/min

How this works

Placeholder device characteristic: 3.5 (CP-like), 5 (5.0-like), 5.5 (5.5-like) L/min at zero head and full speed. Not manufacturer data.

Changes: devices.impella.qMax

Pump suction volumemL

How this works

LV volume below which inflow to the pump collapses (suction alarm). A placeholder for cannula position and filling.

Changes: devices.impella.suctionVolume

VA-ECMO circuit2 controls

VA-ECMO (0 off, 1 on)

How this works

Peripheral veno-arterial circuit draining the RA and returning into the systemic arteries (retrograde arterial return raises LV afterload).

Changes: devices.ecmo.enabled

Circuit flowL/min

How this works

Set pump flow, reduced by a placeholder afterload sensitivity at high arterial pressure and by RA suction when the atrium empties.

Changes: devices.ecmo.flow

Intracardiac shunts2 controls

Atrial septal defect areacm²

How this works

Pressure-driven orifice between the left and right atria; direction follows the instantaneous atrial pressure difference.

Changes: devices.shunts.asdArea

Ventricular septal defect areacm²

How this works

Pressure-driven orifice between the ventricles; mostly systolic left-to-right flow unless RV pressure is high.

Changes: devices.shunts.vsdArea

Drug effectsqualitative multi-target mappings

Strength (qualitative, not a dose)

α1 > β1 agonist. α1 arteriolar constriction: vessels.sa.r ×1.6; α venoconstriction (recruits unstressed volume): vessels.sv.v0 -200; β1 inotropy (modest): chambers.lv.ees, chambers.rv.ees ×1.15

Each drug changes several targets at once. Strengths are qualitative mappings, not doses.

Load a different scenarioreplaces the experiment, with confirmation

Load a different scenario

Calibrated virtual phenotype

About this scenario

A resting adult with normal chamber function, competent valves, sinus rhythm at 70 bpm and no external constraint. Parameter values were chosen so that the closed-loop model reproduces textbook resting hemodynamics; they are a teaching approximation pending expert review, not population constants.

Checked by automated tests: closed-system volume conservation (<0.1% over 100 beats); timestep sensitivity (<1% change in core stable measurements at dt/2); seeded repeatability; resting pressures, volumes and flows within stated textbook ranges; directional response to fluid bolus and afterload increase.

quantitative compartment model · content review: proposed

Go deeper

Starting a lesson or case loads its own scenario; your experiment here is kept until you do.

Equations and model assumptions

Compare a compliant and a stiff ventricle at the same volume and show how relaxation changes filling.

Every number is computed from one closed-loop model; each measurement's definition is under “All measurements”.

Sources & model detailsreview status, testing, limitations

Sources

Content review

Teaching text and answer keys: Proposed. None of the 1 source claims behind it has been expert reviewed. Where a question has more than one defensible answer, more than one is accepted.

Simulation testing

Finding Hemo closed-loop lumped-parameter model: Quantitatively tested. Software, conservation and qualitative pattern tests pass. Not expert reviewed; normal ranges and phenotype parameter sets are proposed teaching values.
Scenario “Normal adult at rest” is checked for: closed-system volume conservation (<0.1% over 100 beats); timestep sensitivity (<1% change in core stable measurements at dt/2); seeded repeatability; resting pressures, volumes and flows within stated textbook ranges; directional response to fluid bolus and afterload increase.

Passing these tests means the equations are solved correctly and behave as stated. It does not mean the teaching statements, parameter values or answer keys have been expert reviewed.

Limitations that matter here

Volume is added to the systemic venous compartment at once (no infusion time).
No redistribution to interstitium; the whole bolus stays intravascular.
No reflex response unless reflexes are enabled.
Net intravascular volume falls linearly over 20 simulated beats; a real diuresis takes hours and is partly offset by refilling from the interstitium.
Distinct from direct intravascular fluid removal (ultrafiltration), which would be immediate.
Reflexes are off: no autonomic compensation follows a change (the optional baroreflex is not enabled).
Constant intrathoracic pressure -3 mmHg (respiratory swing disabled).

Technical details

Model: fh-closed-loop 0.4.0
App / content version: 0.5.0 / 0.5.0
Scenario id: normal-adult
Solver: rk4, dt 0.2 ms
Topic id: diastolic-function