Preload: how full before the squeeze
Preload is the stretch on the ventricle wall right before it contracts — in practice, how full the chamber is at the end of filling, i.e. the end-diastolic volume. More blood returning to the heart (venous return) means more stretch, means more preload. Picture stretching a rubber band a little further before you let it fly.
Here is the beautiful part — the Frank–Starling mechanism: within limits, the more the heart muscle is stretched before it contracts, the harder it squeezes and the more it ejects. So a bigger preload automatically produces a bigger stroke volume, with no nerve signal or drug required. It is how the two ventricles keep their outputs perfectly matched beat to beat: if one receives a little extra blood, it stretches and ejects a little extra in turn.
Afterload: the resistance to pushing out
Afterload is the load the ventricle must push against to eject blood — chiefly the pressure in the aorta and the systemic vascular resistance downstream. The higher the afterload, the harder the ventricle works to open the aortic valve and the less it manages to eject, all else equal. This is why uncontrolled hypertension is such a burden: the heart fights a higher pressure on every single beat, year after year.
Contractility: the intrinsic strength of the squeeze
Contractility (also called inotropy) is the muscle's intrinsic vigour of contraction — how hard it squeezes at any given degree of stretch. Crucially, it is independent of preload: you can crank up contractility without changing how full the chamber is. Adrenaline does exactly this during exercise or stress, boosting stroke volume beyond what filling alone would give.
- Preload up → SV up (Frank–Starling: more stretch, harder squeeze).
- Afterload up → SV down (harder to push against, less ejected).
- Contractility up → SV up (stronger squeeze at the same filling — e.g. adrenaline).