Preload, afterload and contractility !
- Concept
- Exam priority: medium
How much each beat pumps depends on how full the heart is, how hard it must push, and how strong the muscle is.
Updated 2026-11-01
Also called: Inotropy, Determinants of stroke volume
See it in 3D: Left ventricle
What it is
Stroke volume has three determinants. Preload is the stretch of the ventricle at the end of filling; afterload is the load the ventricle must overcome to eject; contractility is the strength of contraction at a given preload and afterload. Each can be changed by physiology, disease and drugs, and each shifts the pressure–volume loop in its own way.
Left-ventricular pressure–volume loop
EDV 120 mLESV 65 mLSV 55 mLEF 46%ESP 139 mmHg
↑ Afterload
↑ Afterload (e.g. hypertension): the Ea line is steeper and the aortic valve opens at a higher pressure; the loop gets taller and narrower: ESV rises and SV falls.
Tap a corner of the loop (MC, AO, AC, MO) to see the valve event.
- Current loop
- Normal loop
- ESPVR (contractility, Ees)
- EDPVR (passive filling)
- Ea (arterial afterload)
- Stroke volume (SV)
Equations
- σ
- wall stress
- P
- intraventricular pressure
- r
- chamber radius
- h
- wall thickness
A dilated ventricle (large r) faces more afterload at the same pressure; a thick wall faces less.
The three determinants side by side
| Determinant | Best index | Raised by | Lowered by |
|---|---|---|---|
| Preload | End-diastolic volume | Fluids, venoconstriction, lying down | Bleeding, diuretics, venodilators, standing |
| Afterload | Wall stress in systole ≈ aortic pressure | Hypertension, aortic stenosis, vasoconstriction | Arterial vasodilators, low SVR (sepsis) |
| Contractility | Slope of end-systolic P–V line (ESPVR) | Sympathetic β1, Ca²⁺, digoxin | Ischemia, acidosis, beta blockers, heart failure |
Clinical notes
- Afterload reduction (ACE inhibitors, vasodilators) increases forward stroke volume in failing ventricles and in mitral regurgitation.
- In aortic stenosis the afterload sits at the valve, so lowering SVR does not relieve the ventricle and can drop pressure dangerously.
Test yourself
Think of the answer, then tap the question to see it.
Why does a dilated ventricle face higher afterload than a normal one at the same arterial pressure?
By the law of LaPlace, wall stress rises with chamber radius; a larger radius means more stress per unit of wall for the same pressure.
Which determinant does a venodilator mainly change, and how does stroke volume respond in a healthy heart?
Preload falls because blood pools in the veins; on the steep part of the Starling curve, stroke volume falls.
How does concentric hypertrophy help, and what does it cost?
A thicker wall lowers wall stress (afterload) at high pressure, but the stiff chamber fills poorly, raising diastolic pressure (diastolic dysfunction).
Why is digoxin called a positive inotrope?
By inhibiting the Na⁺/K⁺ pump it raises intracellular Na⁺, slows Ca²⁺ removal by the Na⁺/Ca²⁺ exchanger, and increases SR Ca²⁺ stores, so contraction is stronger.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- The Frank–Starling mechanism
- The ventricular pressure–volume loop
- Cardiac output and what sets it
- Heart failure physiology
- Cardiac excitation–contraction coupling
Related conditions
In Pharmacology
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: 19.4 Cardiac Physiology (OpenStax (Rice University), 2022); Heart Failure (Congestive Heart Failure) (StatPearls (NCBI Bookshelf), 2025); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 9). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).
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Representative model, for educational purposes only.