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The heart is the central organ of the cardiovascular system. It is essential for carrying out the blood circulation process vital for maintaining normal homeostasis as per the bodys requirements. In this regard, it is essential to know the various functions of the cardiovascular system. The various mechanisms that regulate arterial blood pressure are those that may be instantly performing well and others that possess extended performance durations (Guyton and Hall, 2006). Here, the timing of an Electrocardiogram (ECG) depends on PTQ which is considered as a method to detect cardiac glycoside pharmacodynamics. The linear correlation between PTQ change and systolic time intervals influence arterial pressure which is regulated by local blood flow control and cardiac output control. The cardiac output is in turn regulated by altogether the blood flows of local tissues (Guyton and Hall, 2006). The mechanism proceeds with a high flow of blood through the tissues that leads to high venous return and good cardiac output.
This is because the heart pumps in an inherently regulated manner based on the Frank-Starling mechanism where certain neural involvement is believed to exist. Other mechanisms include Baroreceptor, Chemoreceptor, renal blood volume pressure control. Baroreceptor and chemoreceptor-mediated mechanisms are based on reflex actions that are neutrally, instantly, and long-acting (Guyton and Hall, 2006). A negative feedback action is always connected to this kind of mechanism. When there is high arterial blood pressure, the stimulation of these nerve endings leads to reduced activity of the sympathetic vasoconstrictor part of the vasomotor center and enhanced activity of the parasympathetic part of the vasomotor center (Guyton and Hall, 2006). Ventricular pressure may lead to blood flow to the atrium, A-Valve that is in agreement with the peak R wave of ECG, causing first hear sound. Subsequently, ventricular contraction, causes blood released out of arteries where the elastic nature of the artery could enable aorta and pulmonary circulation down the atrium and close the aortic valve, leading to the second heart sound.
This mechanism is essential in promoting the impulses to the vasomotor center and is essential for continuous and rapid monitoring of arterial blood pressure within a normal limit (Guyton and Hall, 2006). However, they are limited to long-term control actions. The chemoreceptor-mediated mechanism involves action during low levels of oxygen. It begins when there is a fall in arterial blood pressure which leads to decreased oxygen amount that finally causes stimulation of vasomotor center and a rise in arterial blood pressure (Guyton and Hall, 2006). The first and second Heart sounds could be subjected to analysis by Fourier transform enabled the digital spectrum analysis. This leads to assess the cardiac blood flow during conditions where cardiac blood flow is minimum which in turn requires the long term control of systemic arterial pressure: This involves the action of kidneys that exert long term control on arterial blood pressure by regulating extracellular fluid volume (Guyton and Hall, 2006).
This occurs when there is high arterial blood pressure that enables increased water to get filtered from the glomerular capillaries. This also lowers blood volume and raises urinary output through the action of the Frank-Starling mechanism (Guyton and Hall, 2006). The renin-angiotensin system of mechanism offers efficient renal excretion of Na+ and water leading to decreased vasoconstriction(Guyton and Hall, 2006). Rennin gets released due to a fall in arterial blood pressure and is responsible for the conversion of angiotensin II angiotensin I in the lungs(Guyton and Hall, 2006). Other mechanisms regulate arterial blood pressure more slowly as they depend on enhancing the volume of blood by lowering the output of urine (Guyton and Hall, 2006). These are the Central nervous system ischaemic response which is a potent control system that enhances arterial blood pressure when cerebral ischemia occurs due to inimical low arterial blood pressure (Guyton and Hall, 2006). Muscle (venous) pump which facilitates compression of the venous region by the nearby contraction of skeletal muscles that promotes venous return when the exercise gets initiated.
Abdominal compression reflex involves Baroreflex or chemoreflex mediated activation of abdominal skeletal muscles that exert a kind of compressing action on the large abdominal capacitance veins which promotes venous return. The speed of onset of mechanisms involved in the cardiovascular system has a beneficial role in the compensation of cardiac failure (Guyton and Hall, 2006). Whenever there is heart damage, there could be a low cardiac output (Guyton and Hall, 2006). This is counteracted by reflex mechanisms of baroreceptors and chemoreceptors that influence sympathetic stimulation and parasympathetic inhibition of the heart and blood vessels. Semi-chronic accumulation of fluid by the kidneys to enhance increased cardiac output through the Frank-Starling law of the heart and the Bainbridge reflex (Guyton and Hall, 2006).
References
Guyton GC and JE Hall. Textbook of Medical Physiology.11th ed. Philadelphia: Elsevier Saunders.. 2006.
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