The Frank-Starling mechanism explains how end diastolic volume (EDV) and pressure (EDP) (both of which determine preload) is related to stroke volume. This relationship is demonstrated by the green line in the figure, where an increasing venous return and therefore filling pressure, will result in increased stroke volume. This occurs because increased preload causes myocyte stretching. The stretching of the muscle fibers increases the contractile force of the cardiac muscle. This mechanism enables the heart to eject the additional venous return, thereby increasing stroke volume.
Stroke volume can also be influenced by intrinsic contractility (inotropic force of contraction) and/or afterload. Intrinsic contractility increases, for example, with increased sympathetic activation or under the influence of drugs such as digitalis. Afterload increases when aortic pressure or systemic vascular resistance is increased. Hence, the Frank-Starling curve shifts depending on the afterload and inotropic state of the heart.
Shifting along the line:
- decreased blood volume/venous return causes a shift along the line to the left, decreasing stroke volume
- increased blood volume/venous return causes a shift along the line to the right, increasing stroke volume
Shifting of the line:
- increased afterload/decreased contractility shifts the line down, decreasing stroke volume
- decreased afterload/increased contractility shifts the line up, increasing stroke volume