The loop runs counter-clockwise through four phases. The width is stroke volume; the enclosed area is stroke work.
Three boundary lines define the space. ESPVR (top-left) is set by contractility. EDPVR (bottom) is set by passive stiffness. Ea (the diagonal) is the arterial load the ventricle ejects against.
Exercise recruits both preload (venous return) and contractility (β-adrenergic ESPVR steepening). Stroke volume and output climb together.
Note that Ea/Ees falls. Contractility rises faster than load, so coupling shifts toward the efficient end. This is contractile reserve.
Everything hinges on preload. Less filling → the loop starts further left on the EDPVR → smaller stroke volume by the Frank–Starling mechanism.
Because ESPVR (contractility) is unchanged, ejection fraction stays normal even as output falls. EF is a poor marker of volume status.
Inotropes act on the ESPVR slope. A steeper line means the same end-systolic pressure is reached at a much smaller volume. The ventricle empties more completely.
The result is a taller, wider loop with a low ESV. Efficiency improves, but at a real cost the loop does not show: myocardial oxygen demand rises.
Afterload is the diagonal Ea line. Steepen it and the loop must reach a higher pressure to eject. The aortic valve opens later, and the loop closes at a higher end-systolic volume.
Net effect: taller, narrower loop, lower stroke volume. The failing ventricle is far more afterload-sensitive than the normal one.
Drop the afterload and the ventricle empties more completely: lower ESV, larger SV. The loop widens and drops.
This is why afterload reduction helps the failing heart so much more than the normal one. A flat, weak ESPVR is very sensitive to afterload.
HFrEF is a contractility problem: the ESPVR flattens. The ventricle cannot generate pressure, so it dilates to keep stroke volume up. The loop shifts far to the right.
EDV rises but ESV rises more, so ejection fraction falls below 40%. Chronic eccentric remodelling makes the chamber more compliant, which is why filling pressure stays survivable despite the large volume.
HFpEF is a filling problem. The EDPVR is steep and shifted up, so end-diastolic pressure is high even though the chamber is small.
Systolic function (ESPVR) is intact, so ejection fraction stays ≥50%, which is exactly why the diagnosis is missed. The pathology lives on the bottom border of the loop, not the top.
Cardiogenic shock is HFrEF taken to the edge: a nearly flat ESPVR plus hypotension. Cardiac output and blood pressure fall together, and the loop collapses.
Ventriculo-arterial coupling is severely deranged. The ventricle can no longer match its load. This is the physiologic substrate where mechanical circulatory support is considered.
Restrictive cardiomyopathy is HFpEF's severe cousin: an extremely steep EDPVR in a small, non-compliant chamber. Filling stops abruptly at high pressure.
The loop is small and tall-floored. EF can look near-normal, masking a ventricle that physically cannot accept volume. This is the hallmark of infiltrative disease such as amyloid.
HCM gives a hyperdynamic, small-cavity loop: a steep ESPVR empties the ventricle almost completely (high EF), while a stiff EDPVR impairs filling.
The main clinical problem, dynamic LVOT obstruction, depends on flow, geometry and SAM, which a lumped single-chamber model cannot represent. Read this loop as the substrate, not the gradient.
Sustained hypertension is chronic afterload overload. The ventricle answers with concentric hypertrophy: thicker walls that generate high pressure but stiffen diastole.
Early on EF is preserved and the loop is simply tall. Over years the stiff EDPVR dominates and the picture converges on HFpEF.
AS is an outflow obstruction. The ventricle generates a much higher pressure than the aorta ever sees. The difference is the trans-valvular gradient.
Toggle Peak LV pressure and Aortic pressure lines: the gap between them is the gradient, and it is the whole disease. Chronic pressure overload drives concentric hypertrophy and a stiffer EDPVR.
In aortic regurgitation, blood leaks back into the ventricle during diastole. The loop loses its clean isovolumic relaxation. Volume keeps entering as pressure falls.
Chronic AR gives the heart time to dilate eccentrically, so it carries a huge total stroke volume at survivable filling pressure. The runoff back through the valve drops aortic diastolic pressure, widening the pulse pressure.
Acute AR is a different disease from the chronic form. The leak is just as severe, but the ventricle is normal-sized and stiff. It has had no time to dilate.
Unable to accommodate the regurgitant volume, end-diastolic pressure rises steeply. Clinically this can slam the mitral valve shut early and cause flash pulmonary oedema.
Mitral stenosis is unique here: the lesion sits upstream of the ventricle. The LV simply cannot fill, so the loop is small and shifted left with a reduced stroke volume.
Crucially, LV contractility and ejection fraction are preserved. The ventricle is normal, it is simply underfilled. The high pressure and the pathology are in the left atrium (↑LAP, ↑PCWP), which this LV-only loop cannot show.
In MR the ventricle has a low-pressure escape route into the left atrium. It starts ejecting as soon as LV pressure passes atrial pressure, so there is no true isovolumic contraction. The top-left corner of the loop is gone.
Because part of the ejection is backward, EF overstates real function: a \"normal\" EF of 65% may hide meaningful systolic impairment. Chronic MR dilates the ventricle eccentrically.
Acute MR is the emergency form: the leak hits a normal, non-compliant left atrium. Pressure has nowhere to go, so LA (and PCWP) pressure spikes with giant v-waves.
The ventricle is hyperdynamic and small, but forward output collapses. The picture is flash pulmonary oedema and cardiogenic shock, classically after papillary-muscle rupture in acute MI.
This is severe aortic stenosis just before valve replacement. The ventricle is generating a large gradient to force blood through a fixed orifice, with concentric hypertrophy behind it.
Switch to After TAVR to watch the intervention: the gradient collapses, afterload falls, and the loop widens as forward stroke volume recovers.
The valve is fixed. Peak LV pressure and aortic systolic pressure are reunited: the gradient is gone. The abrupt fall in afterload lets stroke volume rise.
Toggle back to Before TAVR to see the contrast. The concentric hypertrophy and stiff EDPVR take months to regress, so filling pressure improves more slowly than output.
Severe chronic MR just before surgery: dilated ventricle, wide loop, no isovolumic contraction, and a deceptively preserved EF.
Switch to After MV surgery. Restoring valve competence removes the backward escape. End-diastolic volume falls and true function is revealed, sometimes with a lower EF than before.
The valve is competent again. The top-left corner of the loop, isovolumic contraction, reappears, and the dilated ventricle shrinks toward normal.
Forward stroke volume improves, but EF may fall: without the low-pressure escape route, the ventricle's real contractile state shows through. That drop is expected, not a complication.
In LBBB, the ventricle contracts out of sequence. The septum fires early and the free wall late. Force is wasted stretching still-relaxed segments rather than ejecting, and functional MR appears.
The loop is wide, flat and inefficient. Switch to After CRT to resynchronise: biventricular pacing recovers coordinated contraction, effectively raising functional contractility without any drug.
Resynchronisation recoordinates the contraction. Functional contractility rises, functional MR falls, and the loop lifts and narrows. There is more stroke volume for less wasted work.
The acute benefit is immediate; reverse remodelling then shrinks the ventricle over 3–6 months. Compare with Before CRT to see both the height gain and the width reduction.