CV Physiology | Frank-Starling Mechanism
The Frank-Starling relationship characterizes the effect of preload, often meaning there is a difference in contractility for any given preload. The Frank-Starling relationship is based on the link between the initial length of myocardial fibers and the force generated by contraction. Looking for online definition of Frank-Starling relationship in the Medical Dictionary? Frank-Starling relationship explanation free. What is Frank-Starling.
Increases in preload stretch the ventricular myocytes to a length closer to the optimum value leading to an increase in active tension. It is unclear exactly how changes in sarcomere length alter the strength of contraction.
It was initially thought that changing the length of sarcomeres influences the overlap between thick and thin filaments causing different amounts of cross-bridge cycling. Further studies debate these findings by showing that the amount of active tension generated could be changed while the number of cross-bridges remained constant.
Frank–Starling law - Wikipedia
Decades of research have led to evidence supporting several mechanisms operating simultaneously. Increasing sarcomere length leads to increased affinity of troponin for calcium which facilitates the interaction of actin and myosin. Stretching the myocytes leads to decreased interfilament lattice spacing which brings actin and myosin closer together.
Stretch causes titin to reduce lattice space and change cross-bridge orientation. Calcium binding to troponin induces conformational changes in the troponin-tropomyosin complex allowing stretch-dependent activation. Stretching induces cooperativity in which initial cross-bridge formation potentiates further binding leading to increased active tension for any given calcium concentration. Clinical Significance The Frank-Starling relationship describes how the left ventricle responds to increased preload under normal conditions.
Figure 2 demonstrates this in a graphical representation. This is represented by moving along various points on the green curve and appears similar to the length-tension relationship image 1. Changes in contractility cause the normal curve to shift up or down meaning there is a difference in contractility for any given preload.Cardiology - Cardiac Output
Of note, there is a plateau of the Frank-Starling relationship at higher amounts of preload. This might be due to increases in sarcomere length that exceed the optimal value leading to decreases in affinity of calcium for troponin.
As a result, there is very little stretching to produce the length dependent activation observed in the Frank-Starling relationship.
Physiology, Frank Starling Law - StatPearls - NCBI Bookshelf
The Frank-Starling relationship is essential in understanding the underlying pathophysiology of heart failure. Heart failure is divided into diastolic and systolic dysfunction. Diastolic heart failure frequently occurs when the left ventricle has difficulty filling due to changes induced by chronic pressure overload as in hypertension or aortic stenosis.
Concentric hypertrophy is an adaptation to the increased wall tension leading to the formation of new sarcomeres in parallel. This causes an increase in wall thickness and a decrease in internal chamber size. Venous Return and Stroke Volume In the late19th century, Otto Frank found using isolated frog hearts that the strength of ventricular contraction was increased when the ventricle was stretched prior to contraction. This observation was extended by the elegant studies of Ernest Starling and colleagues in the early 20th century who found that increasing venous return to the heart see figurewhich increased the filling pressure left ventricular end-diatolic pressure; LVEDP in the figure of the ventricle, led to increased stroke volume SV.
Conversely, decreasing venous return decreased stroke volume. This cardiac response to changes in venous return and ventricular filling pressure is intrinsic to the heart and does not depend on extrinsic neurohumoral mechanisms although such mechanisms can modify the intrinsic cardiac response.
In honor of these two early pioneers, the ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return is called the Frank-Starling mechanism or Starling's Law of the heart. There is no single Frank-Starling curve on which the ventricle operates. Instead, there is a family of curves, each of which is defined by the afterload and inotropic state of the heart. In the figure showing multiple curves, the red dashed curve represents a "normal" ventricular Frank-Starling curve.
Increasing afterload or decreasing inotropy shifts the curve down and to the right. Decreasing afterload and increasing inotropy shifts the curve up and to the left.
At a given state of ventricular inotropy and afterload, the ventricle responds to changes in venous return and ventricular filling based on the unique curve for those conditions. To summarize, changes in venous return cause the ventricle to move up or down along a single Frank-Starling curve; however, the slope of that curve is defined by the existing conditions of afterload and inotropy.
Frank-Starling curves show how changes in ventricular preload lead to changes in stroke volume. This type of graphical representation, however, does not show how changes in venous return affect end-diastolic and end-systolic volumes. In order to do this, it is necessary to describe ventricular function in terms of pressure-volume diagrams.
When venous return is increased, there is increased filling of the ventricle along its passive pressure curve leading to an increase in end-diastolic volume see Figure. If the ventricle now contracts at this increased preload, and the afterload and inotropy are held constant, the ventricle empties to the same end-systolic volume, thereby increasing its stroke volume, which is defined as end-diastolic minus end-systolic volume.