Anaes · Applied cardiovascular & respiratory physiology

Cardiac cycle & pressure-volume loops

Also known as Cardiac cycle · Wiggers diagram · Pressure-volume loop · Frank-Starling mechanism · Preload afterload contractility · Stroke volume

The cardiac cycle is the repeating sequence of pressure and volume changes that ejects blood from the heart, and the left-ventricular pressure-volume loop is its clearest graphical summary. The framework rests on five exam-critical ideas: the cycle has the phases atrial systole, isovolumetric contraction, ejection, isovolumetric relaxation, and filling, with the mitral and aortic valves opening and closing in a fixed order (the first and second heart sounds); stroke volume is end-diastolic volume minus end-systolic volume, and ejection fraction is stroke volume over end-diastolic volume; stroke volume is set by three determinants — preload, afterload and contractility; preload operates through the Frank-Starling mechanism, in which greater diastolic stretch (longer sarcomeres, and the elastic titin filament) yields stronger systole; and the pressure-volume loop makes all three determinants visible at once — preload shifts the end-diastolic point along the EDPVR, afterload tilts the loop, and contractility steepens the ESPVR. Built on the titin-and-heart-function review (Granzier 2025), the length-dependent-activation review (Cazorla 2011), the cardiac electromechanical-modelling review (Trayanova 2011), the working-heart preparation review (Usai 2025), the positive-airway-pressure haemodynamics review (Di Cristo 2025), the heart-lung-interactions review (Hamahata 2023), the Wiggers-diagram construction activity (Silverthorn 2022), and the non-invasive PV-loop load-manipulation study (Pola 2026).

high8 referencesUpdated 26 July 20269 min readVerification in progress

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Red flags

Stroke volume equals end-diastolic volume minus end-systolic volume; ejection fraction is stroke volume over end-diastolic volume, normally around 55 to 70 percent — a falling ejection fraction signals systolic dysfunction and predicts perioperative risk.
Preload is ventricular end-diastolic volume (or wall stress), not central venous pressure alone — venous return determines preload, which is why positive-pressure ventilation and high intrathoracic pressure reduce venous return and lower stroke volume.
Afterload is the wall stress during ejection, clinically approximated by systemic vascular resistance and arterial pressure — vasopressors raise afterload and can lower stroke volume in the failing heart.
The Frank-Starling mechanism has a limit: once sarcomeres are at optimal length, further stretch does not increase force and the heart fails up — the flat upper part of the curve explains why volume loading beyond a point no longer helps.
Contractility (inotropy) is independent of preload and afterload and is read off the pressure-volume loop as the slope of the ESPVR — it is what inotropes increase and what negatively-inotropic anaesthetics and acidosis depress.

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Practise this topic8 MCQs with explanations

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ANZCAFRCAABAEDAICFCAIFCA_SA

Red flags

Stroke volume equals end-diastolic volume minus end-systolic volume; ejection fraction is stroke volume over end-diastolic volume, normally around 55 to 70 percent — a falling ejection fraction signals systolic dysfunction and predicts perioperative risk.
Preload is ventricular end-diastolic volume (or wall stress), not central venous pressure alone — venous return determines preload, which is why positive-pressure ventilation and high intrathoracic pressure reduce venous return and lower stroke volume.
Afterload is the wall stress during ejection, clinically approximated by systemic vascular resistance and arterial pressure — vasopressors raise afterload and can lower stroke volume in the failing heart.
The Frank-Starling mechanism has a limit: once sarcomeres are at optimal length, further stretch does not increase force and the heart fails up — the flat upper part of the curve explains why volume loading beyond a point no longer helps.
Contractility (inotropy) is independent of preload and afterload and is read off the pressure-volume loop as the slope of the ESPVR — it is what inotropes increase and what negatively-inotropic anaesthetics and acidosis depress.

The one-line answer

The cardiac cycle is the repeating sequence of pressure and volume changes that ejects blood from the heart, and the left-ventricular pressure–volume loop is its clearest graphical summary. Loop width equals stroke volume (SV equals EDV minus ESV); the ESPVR slope equals contractility; the EDPVR equals diastolic stiffness. Stroke volume is governed by three determinants — preload, afterload and contractility — and preload operates through the Frank–Starling mechanism. If you can draw a PV loop and move it correctly for each determinant, you can reason any haemodynamic stem. The Wiggers diagram is built from two core concepts — blood flow down pressure gradients and the structure-function relationship of heart valves producing one-way flow — and that construction transfers directly to reading the left-ventricular pressure-volume loop.^[7]^[8]

Meet the patient

A 68-year-old man with aortic stenosis and an ejection fraction of 55 percent becomes profoundly hypotensive during spinal anaesthesia for a hip fracture. His blood pressure was fine until the block reached T4, then the sympathetic block dropped his SVR, his preload fell from venodilation, and his stroke volume collapsed against the fixed outflow obstruction. The PV loop tells this story in geometry: a narrow rectangle that could not widen when preload fell. (Illustrative scenario — none of the cited studies enrolled spinal-anaesthesia patients.)^[8]

Hold one image: a rectangle on pressure–volume axes. Load manipulation moves it measurably: volume loading shifts end-diastolic and end-systolic volumes while vasodilation shrinks ventricular volumes, and each determinant — preload, afterload, contractility — moves a different corner. Master the rectangle and every haemodynamic intervention has a picture.^[7]^[8]

References8Show

[1]Granzier HL. Discovery of Titin and Its Role in Heart Function and Disease Circ Res, 2025.PMID 39745989
[2]Cazorla O, et al. Regional variation in myofilament length-dependent activation Pflugers Arch, 2011.PMID 21336586
[3]Trayanova NA, et al. Cardiac electromechanical models: from cell to organ Front Physiol, 2011.PMID 21886622
[4]Usai DS, et al. The isolated, perfused working heart preparation of the mouse-Advantages and pitfalls Acta Physiol (Oxf), 2025.PMID 40078031
[5]Di Cristo A, et al. Hemodynamic Effects of Positive Airway Pressure: A Cardiologist's Overview J Cardiovasc Dev Dis, 2025.PMID 40137095
[6]Hamahata N. Heart-Lung Interactions Semin Respir Crit Care Med, 2023.PMID 37541314
[7]Silverthorn DU. Constructing the Wiggers diagram using core concepts: a classroom activity Adv Physiol Educ, 2022.PMID 36201306
[8]Pola K, et al. Non-invasive pressure-volume loop analysis in left ventricular load manipulation Clin Physiol Funct Imaging, 2026.PMID 42439270