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Starling's Law or the Frank-Starling Law of the heart.
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) and vice-versa.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.
stroke volume, end-diastolic volume, and contraction strength
Frank-Starling's law of the heart states that the stroke volume of the heart increases in response to an increase in the volume of blood received by the heart during diastole. This relationship helps to maintain cardiac output and ensure adequate blood flow to meet the body's demands.
Frank Starling's law of the heart refers to a length-tension relationship of cardiac muscle cells. As ventricles fill with blood, the extra blood causes a stretch of the muscle cells known as end diastolic volume. The greater the stretch, within limits, the greater the contractile force, and therefore the greater the ability to eject blood from the ventricles (end systolic volume) to the great vessels, pulmonary trunk or aorta.
Due to starling law,
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Stroke volume is regulated by the degree of stretch in the heart before it contracts, the forcefulness of contraction of individual ventricular muscle fibers, and the pressure required to eject blood from the ventricles. The first factor is governed by the Frank-Starling law of the heart which states that the more the heart is stretched as it fills during diastole, the greater the force of contraction during systole. The second factor can contribute to the regulation of stroke volume if different stimulants such as epinephrine and noepinephrine are present or can be inhibited if K+ levels are increased, for example. The third factor can be of significance if required pressure is higher than normal which causes the valves to open later than normal therefore causing stroke volume to decrease and, therefore, more blood remains in the ventricles at the end of systole.
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