Regulating Stroke Volume
There are three primary mechanisms that regulate EDV and ESV, and therefore SV.
1- Preload:-Changes in preload affect the SV through the Frank-Starling mechanism.
Briefly, an increase in venous return to the heart increases the filled volume (EDV) of the ventricle, which stretches the muscle fibers thereby increasing their preload. This leads to an increase in the force of ventricular contraction and enables the heart to eject the additional blood that was returned to it.
Therefore, an increase in EDV results in an increase in SV. Conversely, a decrease in venous return and EDV leads to a decrease in SV by this mechanism.
2- Afterload:-Afterload is related to the pressure that the ventricle must generate in order to eject blood into the aorta. Changes in afterload affect the ability of the ventricle to eject blood and thereby alter ESV and SV.
For example, an increase in afterload (e.g., increased aortic pressure) decreases SV, and causes ESV to increase.
Conversely, a decrease in afterload augments SV and decreases ESV.
3- Inotropy:-Changes in ventricular inotropy (contractility) alter the rate of ventricular pressure development, thereby affecting ESV and SV.
For example, an increase in inotropy (e.g., produced by sympathetic activation of the heart) increases SV and decreases ESV.
Conversely, a decrease in inotropy (e.g., heart failure) reduces SV and increases ESV.