The Frank-Starling Law of the heart predicts the relationship between changes in end diastolic volume, i.e., preload, and stroke volume.
As left ventricular end-diastolic volume increases, so, too, does stroke volume.
This is because the volume of blood in the ventricle determines the degree of myofibril stretch; In turn, the degree of myofibril stretch, aka, the tension on the myofibril, determines the mechanical force produced by the myofibril during contraction.
And, as we know, the force of contraction determines how much blood is ejected from the ventricle.
Changes in contractility shift the Stroke Volume – End Diastolic Volume curve to the Right or Left.
Positive inotropic agents:
The sympathetic nervous system
Adrenergic agonists
Cardiac glycosides (such as digoxin)
Angiotensin II
Reduced sodium levels
Increased heart rate
Several these agents act by increasing the
intracellular calcium concentration; in their presence, stroke volume is increased at any given end diastolic volume.
Negative inotropic agents:
The parasympathetic nervous system
Beta blockers
Reduced intracellular calcium (and, therefore, calcium channel blockers)
Some antiarrhythmics
High sodium concentrations
Reduced heart rate
Thus, in the presences of these agents, stroke volume is decreased at any given end diastolic volume.