Raise in stroke volume:
The rise in the stroke volume during the preload can be seen during the fast filling of blood in ventricles at a particular time. This also increases due to the increase in the venous returns. Hence, this leads to an increase in end-diastolic volume with a rise in the stroke volume. During contractility, an increase in the stimulation and functioning of the sympathetic nerve occurs, the hormones like epinephrine and norepinephrine activate intracellular calcium ions to increase at a very high level and the level of glucagon and thyroid hormone increases. This leads to a decrease in the end-systolic volume but simultaneously an increase in the stroke volume. Whereas, during the afterload, the resistance of the vascular system increases, and damage of the semilunar valve is managed. This increases the end-systolic volume but eventually, the stroke volume decreases.
Lower stroke volume:
The stroke volume reduces due to many factors. Factors that affect during the preload are, decrease in the thyroid hormone, higher or lower quantity of potassium ions, the hypoxia condition, that is, insufficient supply of the oxygen through the blood circulation, the abnormality in the pH maintenance, lower or higher sodium ions in the blood, diminish in the calcium ions, decrease in the body temperature, the involvement of drugs in the body that causes the blockage of the calcium channels. This eventually leads to a decrease in end-diastolic volume and a significant decrease in the stroke volume. During contractility, the increase in functioning and stimulation of the parasympathetic nerve, balance the supply of oxygen or condition of hypoxia, situations are maintained like hyperkalemia and acetylcholine quantity increases. This results in an increase in the end-systolic volume and a gradual decrease in the stroke volume. During the afterload, the resistance of the vascular system decreases which results in a decrease in end-systolic volume and a significant increase in the stroke volume.
The method used in Frank-Starling law:
There is an experiment used to explain the frank-starling law of the heart. This experiment used an example of a frogâ€™s heart having one atrium one ventricle. This experimental model is attached to an artificially built systemic circuit. The artificial model has three main sections of
1. An arterial section that manages the low capacitance of the high pressure of the blood,
2. A venous section that manages the low pressure or high capacitance of the blood, and
3. The peripheral section provides resistance to the variable peripheries.
The stroke volume, flow of blood in ventricles, and pressure exerted by the flow of blood are managed by the preload and afterload of the artificially arranged circulation system. The height of the venous reservoir is regulated by the preload, whereas, afterload is influenced by the section of flow resistance of vessels. There are two valves present in the artificial systemic circuit model, named output and input. When the heart contracts and increases the flow of blood, the blood flow becomes unidirectional due to the presence of output and input valves. The arterial section of the high-pressure section, cause the dependency of pressure on the afterload. This concludes that pressure depends on the output of cardiac valves and resistant flow variable. On the other hand, the venous section or the low-pressure section results in the dependency of pressure on the preload. This provides the level of the blood in the venous reservoir.
Clinical example of Frank-starling law:
Premature ventricular contraction:
In the premature ventricular contractions, the aorta gets filled with the blood of the left ventricle by completely emptying them. This premature contraction occurs early for emptying the ventricles. As the successive ventricle contraction will occur on its regular time, thus early contraction of the left ventricle will cause the excessive filling of the left ventricle gradually. This significantly increases the end-diastolic volume of the left ventricle. In this situation the Frank-Starling mechanism causes a strong forceful contraction in the left ventricle to push the extra filled blood in the aorta to maintain the end-systolic volume of the left ventricle.
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