The stroke volume of the heart increases in response to the rise in volume of blood filling the heart (end diastolic volume) when all other factors remain constant.
The increased volume of blood (preload) stretches the ventricular wall, causing the cardiac muscle to contract more forcefully. The stroke volume may also increase as a result of greater contractility of the cardiac muscle during exercise, independent of the end-diastolic volume.
Performance change with increase in preload and contractility
Suppose point A is normal functioning heart,
When preload is increased (e.g. on laying down), point A will move to point B. This increase in performance is entirely due to preload.
In response to increasing preload, a healthy heart will increase its contractility and shift point B to D. Therefore, increase in performance from point A to point D is combined effect of preload and contractility (e.g. exercise).
If contractility is independently increased (e.g. digoxin, dobutamine), it would shift the heart performance from point A to point C. Thus, point A to C is entirely due to increasing in contractility.
Effects of preload, afterload, contractility and heart rate on cardiac output*
When line shifts to left (upward), contractility increases and when line shift to right (downward) contractility decreases. Various positive inotropic drugs like digoxin, catecholamine and exercise will cause an increase in contractility.
Negative inotropic drugs (beta-blockers, calcium channel blockers), dilated cardiomyopathy and heart failure will cause a decrease in contractility.
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