Cardiac Pressure-Volume Loops
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Direct answer
Plotting left ventricular pressure against volume across one cardiac cycle draws a rectangle-ish loop: filling raises volume from an end-systolic 40-50 mL to an end-diastolic 120 mL at near-zero pressure, isovolumic contraction climbs to about 80 mmHg where the aortic valve opens, ejection empties to end-systolic volume, and isovolumic relaxation falls to left atrial pressure. Loop width is the stroke volume (70 mL) and width over end-diastolic volume is the ejection fraction (about 60 per cent). The line joining end-systolic points at different loads — the ESPVR, slope Emax — is the load-independent index of contractility: catecholamines rotate it upward, cardiac failure flattens it.
What you must remember
- Corner values: EDV 120 mL, ESV 40-50 mL, stroke volume 70 mL, EF 60-65 per cent, peak LV pressure about 120 mmHg, LVEDP 5-8 mmHg.
- ESPVR (Emax): the end-systolic pressure-volume relation; its slope is contractility, immune to preload and afterload changes that confound ejection fraction and dP/dt.
- EDPVR: the passive filling curve of the ventricle, steep at high volumes — the graphical face of diastolic stiffness and of preload.
- Preload effect: raising EDV widens the loop along the same ESPVR (Frank-Starling), increasing stroke volume until the curve flattens.
- Afterload effect: raising resistance produces a higher end-systolic pressure and a narrower loop — less ejection, higher residual volume, which then feeds back as increased preload.
- Contractility effect: steeper ESPVR with smaller ESV at the same preload — a wider loop purely from inotropy; digoxin and adrenaline do this graphically.
- Pressure-volume area (PVA): the loop area plus the potential-energy triangle between loop and ESPVR; PVA correlates linearly with myocardial oxygen consumption — the quantitative basis of unloading therapy in heart failure.
- Valve lesions reshape the loop: mitral regurgitation abolishes true isovolumic contraction (blood escapes backwards), aortic regurgitation abolishes isovolumic relaxation and shifts the whole loop rightward.
Drawing four loops in words
Take the normal loop as reference and sketch disease. Aortic stenosis: peak systolic pressure soars to 200 mmHg or more, systolic ejection is slow, stroke volume preserved until late — a tall, narrow, pressure-dominated loop whose large PVA predicts the angina of aortic stenosis even with normal coronaries. Aortic regurgitation: the aortic valve never truly closes, so isovolumic relaxation vanishes and filling arrives from both atrium and aorta — the loop shifts right (EDV 200-plus mL), stroke volume is huge yet effective forward output small. Mitral regurgitation: during "isovolumic" contraction the regurgitant jet escapes to the left atrium, so pressure rise is blunted — no isovolumic phase, a shortened ejection, and the left atrial v wave climbs on the pressure trace. Volume loading (mitral stenosis with tachycardia aside): pure preload move — the loop slides right along an unchanged ESPVR, stroke volume up, contractility untouched. One drawing, four lesions, and each loop explains its own murmur timing.
High-yield viva angles
Examiners probe why ESPVR beats ejection fraction as a contractility index: EF is load-dependent — a failing ventricle can show a respectable EF when afterload drops, and a normal ventricle a poor one when afterload spikes — whereas Emax stays put across preload and afterload changes, changing only with inotropy. The second angle is PVA and oxygen: because PVA tracks myocardial oxygen consumption, interventions that shrink pressure and volume (diuretics, vasodilators) reduce the PVA and hence the oxygen bill — the physiological rationale for afterload reduction in aortic regurgitation and heart failure. Third, expect the question "which phase disappears in mitral regurgitation?" — isovolumic contraction, because the ventricle is never a closed chamber in systole.
Frequently asked questions
What does the slope of the ESPVR represent?
End-systolic pressure-volume relation slope (Emax) is the load-independent measure of myocardial contractility — steepened by inotropes, flattened by failure.
State the normal volumes framing the loop.
End-diastolic volume about 120 mL, end-systolic volume 40-50 mL, giving a stroke volume of 70 mL and an ejection fraction near 60 per cent.
How does increased afterload change the loop?
End-systolic pressure rises, ejection stops earlier, stroke volume falls and end-systolic volume increases, with the narrowed loop subsequently refilled by increased preload.
Why is the pressure-volume area clinically important?
The PVA — external stroke work plus potential energy — correlates linearly with myocardial oxygen consumption, quantifying why pressure loads cost the heart more than volume loads.
Which valve lesion abolishes isovolumic contraction, and why?
Mitral regurgitation: with an incompetent mitral valve, blood escapes to the left atrium as soon as ventricular pressure exceeds atrial pressure, so the ventricle never contracts as a closed chamber.