FrankStarlingprinsippet

The Frank-Starling prinsippet, also known as the Frank-Starling mekanismen, describes the relationship between ventricular end-diastolic volume and the stroke volume (or cardiac output). Within physiological limits, increasing venous return and ventricular filling raises the stroke volume, helping to balance the output of the heart’s two ventricles.

Mechanism: The force of cardiac contraction rises with stretch of the cardiac muscle fibers. As the end-diastolic volume increases, sarcomeres lengthen toward an optimal length, enhancing cross-bridge formation and calcium sensitivity. This length–tension relationship leads to a stronger contraction and a larger stroke volume. Beyond an upper limit, excessive stretch reduces contractile efficiency, and the gain in stroke volume diminishes.

Clinical and physiological relevance: The principle explains how the heart adapts to changes in venous return during activities such as exercise or hemorrhage. It underpins interpretations of preload and contractility in echocardiography and invasive hemodynamics. In heart disease, particularly systolic dysfunction, the relationship can be altered; markedly elevated filling pressures may not produce proportional increases in stroke volume and can be detrimental.

History: The concept is named for Otto Frank and Ernst Starling, who described the link between ventricular filling and contraction in the early 20th century. The principle remains a foundational concept in cardiovascular physiology and is used to understand normal and pathological heart function.