The Frank-Starling law of the heart (also known as Starling`s law or Frank-Starling mechanism) states that the more blood is filled with the ventricle during diastole (final diastolic volume), the greater the volume of blood expelled during the resulting systolic contraction (stroke volume). This relationship lasts up to a certain volume, but beyond this volume, there is a decrease in contractility. This decrease in contractility is called the “case of the starling curve”. This is the mechanism by which the left ventricle initially expands and increases contractility to accommodate chronic aortic insufficiency, but eventually fails when it becomes too large and “falls off Starling`s curve.” Starling has experimented on intact mammalian hearts, for example: dogs to understand why fluctuations in blood pressure, heart rate and temperature do not affect relatively constant cardiac output. [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 that “the mechanical energy released during the transition from resting to active state is a function of fiber length.” Starling used a volume-pressure diagram to create a length-stress diagram from his data. Starling`s data and associated graphs provided evidence that muscle fiber length and resulting tension altered systolic pressure. [28] According to the Frank-Starling mechanism, the left ventricle increases its contractile strength and thus the volume of stroke in response to an increased preload (2,4). Changes in afterload or inotropy move the curve up or down. In heart failure, the Frank-Starling curve is shifted downward and flattened due to reduced inotropia, so greater venous reflux and therefore preload are required to increase stroke volume. Clinical evidence of myocardial dysfunction during hypovolemic shock is scarce.46,56,162 Nevertheless, it is conceivable that severe hypotension reduces the balance between oxygen supply and cardiac needs, as many patients with hypovolemic shock may be elderly and have coronary artery disease, impairing coronary vasodilation. In a patient with systolic heart failure with reduced ejection fraction and resulting pulmonary congestion, treatment with a diuretic such as furosemide or hydrochlorothiazide or a pure venous vasodilator such as nitrates reduces preload without significantly altering stroke volume. Indeed, the Frank-Starling curve is almost horizontal at a higher preload in a patient whose curve is shifted downwards due to systolic contractile dysfunction. However, excessive diuresis or venous vasodilation can lead to an unwanted decrease in stroke volume, leading to hypotension.

More than a century ago, two physiologists, Otto Frank and Ernest Starling, discovered that when the heart is filled with more blood during diastole, it contracts more and pumps more blood during systole. So they invented the Frank Starling law to explain this relationship. Frank-Starling`s law states that the force or tension developed in a muscle fiber depends on the extent to which the fiber is stretched. In a clinical situation, when increased amounts of blood flow to the heart (increased preload), the walls of the heart expand. The heart muscle then contracts with increased force and empties the dilated cavities within limits with the increase in stroke volume. There is an optimal sarcomere length and therefore an optimal fiber length, from which the strongest contraction occurs. The left ventricle normally functions at a final diastolic LV volume with less than optimal fiber lengths. The clinical implication of this is that stroke volume increases with increasing preload until the optimal length of myocardial fibers is reached. A further increase in preload leads to a reduction in displacement. Pentoxifylline may improve endothelial and myocardial function.164 Myocardial edema and compression of capillaries, resulting in impaired oxygen diffusion and extraction, may also contribute to decreased regional coronary blood flow, regional myocardial ischemia, and decreased myocardial function in hemorrhagic animals.128,132,141,161 Hypovolemic shock may induce decreased ventricular compliance left.159 Myocardial dysfunction after decreased adherence (diastolic dysfunction) may be particularly pronounced during resuscitation due to hypovolemic shock.157,159 Post-ischemic insufficiency (“anesthesia”) may also play a role, at least temporarily, during resuscitation. It was believed that the increase in heart mass during postnatal development and in response to a hemodynamic challenge was entirely due to hypertrophic growth of individual cardiomyocytes.

However, proliferative cardiomyocytes were identified in the embryonic heart, and pre-existing cardiomyocytes retained the ability to re-enter the cell cycle for a short time after birth. During cardiac maturation, the majority of cardiomyocytes withdraw from the cell cycle and the number of dinucleated/multinucleated postmitotic terminal cells increases. Nevertheless, a modest population of cyclic cardiomyocytes persists during postnatal development, contributing to the increase in heart mass. After ischemic injury, the percentage of cyclic cardiomyocytes is further increased and detected mainly in the peri-infarction/infarct region. Although the adult heart appears to retain a limited degree of cardiac regeneration, wound healing is the predominant physiological response after myocardial infarction (MI).