# Cardiac Pressure-Volume Loops

> Cardiac pressure-volume loops in MBBS Physiology: EDV, ESV, stroke volume, ESPVR contractility, preload-afterload effects and PVA oxygen demand.

- Canonical URL: https://prepelephant.com/topics/mbbs/physiology/cardiac-pressure-volume-loops
- Exam / course: MBBS · Subject: Physiology
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-02
- Last updated: 2026-10-02
- How to cite: "Cardiac Pressure-Volume Loops", PrepElephant, https://prepelephant.com/topics/mbbs/physiology/cardiac-pressure-volume-loops

## 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.