Increased cardiac output is due to increased heart rate or stroke volume, or both. Increased stroke volume is due to increased force of contraction. This can be accomplished by optimizing myofilament overlap (initial sarcomere length) or improving the strength of contraction (contractility).
The Frank-Starling mechanism ensures that increased venous return increases end-diastolic volume (EDV), which then increases the stetch of the cardiac muscle cells and the strength of contraction, according to the length-tension relationship for muscle cells. This results in an increase in stroke volume that matches the increase in EDV. This stretching of the ventricles prior to contraction that generates more forceful emptying is called preload.
Myocardial contractility is how forceful the cardiac muscle contracts. It depends on available Ca. Positive inotropy is an increase in contractility (due to catecholamines) at a given initial stretch of the myocardium. It is often in response to an increase in afterload. Afterload is the load against which the left ventricle must pump (that is arterial blood pressure). Long-term increases in afterload will cause thickening (hypertrophy) of the ventricular wall.
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