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. While the above diagram shows only one line, a classic Frank-Starling often shows three separate lines, each roughly the same shape, one on top of each other, to illustrate that shifts on the same line indicate a change in preload, while shifts from one line to another indicate a change in afterload or contractility.

The Frank-Starling law of the heart (also known as Starling's law or the Frank-Starling mechanism) states that the greater the volume of blood entering the heart during diastole (end-diastolic volume), the greater the volume of blood ejected during systolic contraction (stroke volume).

This allows the cardiac output to be synchronized with the venous return, arterial blood supply and humeral length^[1] without depending upon external regulation to make alterations.

[edit] Physiology

As the heart fills with more blood than usual, the force of the muscular contractions will increase.^[2] This is a result of an increase in the load experienced by each muscle fibre due to the extraneous blood entering the heart. The stretching of the muscle fibres increases the affinity of troponin C for calcium, causing a greater number of cross-bridges to form within the muscle fibres; this increases the contractile force of the cardiac muscle. The force that any single muscle fiber generates is proportional to the initial sarcomere length (known as preload), and the stretch on the individual fibers is related to the end-diastolic volume of the ventricle.

In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometers, a length which is rarely exceeded in the normal heart. Initial lengths larger or smaller than this optimal value will decrease the force the muscle can achieve. For larger sarcomere lengths, this is the result of less overlap of the thin and thick filaments; for smaller sarcomere lengths, the cause is the decreased sensitivity for calcium by the myofilaments.

Stroke Volume = End diastolic volume (preload volume) - End systolic volume (afterload volume)

[edit] Clinical examples

[edit] Shifting along the line

• A blood volume increase would cause a shift along the line to the right, increasing stroke volume.

This can be seen most dramatically in the case of premature ventricular contraction. The premature ventricular contraction causes early emptying of the left ventricle (LV) into the aorta. Since the next ventricular contraction will come at its regular time, the filling time for the LV increases, causing an increased LV end-diastolic volume. Because of the Frank-Starling law, the next ventricular contraction will be more forceful, causing the ejection of the larger than normal volume of blood, and bringing the LV end-systolic volume back to baseline.

For example, during vasoconstriction the end diastolic volume (EDV) will increase due to an increase in TPR (total peripheral resistance) (increased TPR causes a decrease in the stroke volume^{[citation needed]} which means that more blood will be left in the ventricle upon contraction - an increased end systolic volume (ESV). ESV + normal venous return will increase the end diastolic volume). Increased EDV causes the stretching of the venticular myocardial cells which in turn use more force when contracting. Cardiac output will then increase according to the Frank-Starling graph. (The above is true of healthy myocardium. In the failing heart, the more the myocardium is dilated, the weaker it can pump, as it then reverts to Laplace's law.)

• By contrast, pericardial effusion would result in a shift along the line to the left, decreasing stroke volume.

[edit] History

The law was named after the two physiologists, Otto Frank and Ernest Starling who first described it.^[3]

Long before the development of the sliding filament hypothesis and our understanding that active tension depends on the sarcomere's length, in 1914 Ernest Starling hypothesized that "the mechanical energy set free in the passage from the resting to the active state is a function of the length of the fiber." Therefore, the initial length of myocardial fibers determines the work done during the cardiac cycle.

[edit] See also

• Starling equation

[edit] References

[edit] External links

• 1355808810 at GPnotebook
• "New Concepts in the Control of Muscle Contraction" by Gerry A Smith PhD (Cantab)