Frank–Starling law

The Frank-Starling mechanism allows the cardiac output to be synchronized with the venous return, arterial blood supply and humoral length,[2] without depending upon external regulation to make alterations.

[5][6][7] As striated muscle is stretched, active tension is created by altering the overlap of thick and thin filaments.

[13] Finally, there is thought to be a decrease in the spacing between thick and thin filaments, when a cardiac muscle is stretched, allowing an increased number of cross-bridges to form.

Therefore the force (pressure) generated by the cardiac muscle fibres is related to the end-diastolic volume of the left and right ventricles as determined by complexities of the force-sarcomere length relationship.

In order to relate the work of the heart to skeletal muscle mechanics, Frank observed changes in diastolic pressure with varying volumes of the frog ventricle.

His data was analyzed on a pressure-volume diagram, which resulted in his description of peak isovolumic pressure and its effects on ventricular volume.

[5] More than 30 years before the development of the sliding filament model of muscle contraction and the understanding of the relationship between active tension and sarcomere length, Starling hypothesized in 1914, "the mechanical energy set free in the passage from the resting to the active state is a function of the length of the fiber."

Starling's data and associated diagrams, provided evidence that the length of the muscle fibers, and resulting tension, altered the systolic pressure.

Cardiac function curve . In diagrams illustrating the Frank–Starling law of the heart , the y-axis often describes the stroke volume , stroke work , or cardiac output . The x-axis often describes end-diastolic volume , right atrial pressure , or pulmonary capillary wedge pressure . The three curves illustrate that shifts along the same line indicate a change in preload , while shifts from one line to another indicate a change in afterload or contractility . A blood volume increase would cause a shift along the line to the right, which increases left ventricular end diastolic volume (x axis), and therefore also increases stroke volume (y axis).