Blood pressure factors affecting

Catalyst circulation is like blood circulation to the human body. Without proper catalyst circulation, the unit is dead. Troubleshooting circulation problems requires a good understanding of the pressure balance around the reactor-regenerator circuit and the factors affecting catalyst fluidization. The fundamentals of fluidization and catalyst circulation are discussed in Chapter 5. 

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

An effective HE or cost-effectiveness analysis is designed to answer certain questions, such as Is the treatment effective What will it cost and How do the gains compare with the costs By combining answers to all of these questions, the technique helps decision makers weigh the factors, compare alternative treatments, and decide which treatments are most appropriate for specific situations. Typically, one chooses the option with the least cost per unit of measure gained the results are represented by the ratio of cost to effectiveness (C E). With this type of analysis, called a cost-effectiveness analysis (CEA), various disease end points that are affected by therapy (risk markers, disease severity, death) can be assessed by corresponding indexes of therapeutic outcome (mmHg blood pressure reduction, hospitalizations averted, life years saved, respectively). It is beyond the scope of this chapter to elaborate further on principles of cost-effectiveness analyses. A number of references are available for this purpose [11-13]. 

Antidiuretic hormone promotes the reabsorption of water from the tubules of the kidney, or antidiuresis. Specifically, it acts on the collecting ducts and increases the number of water channels, which increases the diffusion coefficient for water. This results in the body s conservation of water and the production of a low volume of concentrated urine. The reabsorbed water affects plasma osmolarity and blood volume. This effect of ADH on the kidney occurs at relatively low concentrations. At higher concentrations, ADH causes constriction of arterioles, which serves to increase blood pressure. Antidiuretic hormone secretion is regulated by several factors ... 

Sodium is freely filtered at the glomerulus. Therefore, any factor that affects GFR will also affect sodium filtration. As discussed previously, GFR is directly related to RBF. In turn, RBF is determined by blood pressure and the resistance of the afferent arteriole (RBF = AP/R). For example, an increase in blood pressure or a decrease in resistance of the afferent arteriole will increase RBF, GFR, and, consequently, filtration of sodium. The amount of sodium reabsorbed from the tubules is physiologically regulated, primarily by aldosterone and, to a lesser extent, by ANP. Aldosterone promotes reabsorption and ANP inhibits it. The alterations in sodium filtration and sodium reabsorption in response to decreased plasma volume are illustrated in Figure 19.6. 

It is discussed in Chapter 18, Section F, and in Section 7 of this chapter. Also affecting blood pressure is the potent vasorelaxant atrial natriuretic factor. This 28-residue peptide, which is discussed in Box 22-D, is produced by the cardiac atria and stimulates the excretion of Na+ and of water by the kidneys.184 It also promotes hydrolysis of lipids within human adipocytes.185... 

Merely because a substance depresses blood pressure does not make it a true antihypertensive substance. The level of blood pressure is the resultant of several factors the viscosity of the blood, the cardiac output, the volume of circulating blood, and the state of the arterial and arteriolar bed, which determines the peripheral resistance to blood flow, other factors being equal. This discussion has indicated that peripheral resistance through arteriolar constriction may be affected by renal blood flow and the production of circulating pressor agents. Therefore, a definition of a true antihypertensive substance is necessary, in order that we be not misled by depressor substances which lower blood pressure at a detriment to the body s economy. 

Physiologically, hypertension may be defined as an elevation of blood pressure above the normal limits of variability. There are at least five basic factors involved in the maintenance of blood pressure. Aberrations of any one or a combination of these factors could produce an elevation affecting principally systolic or diastolic pressure, or influencing both more or less equally. These factors include peripheral resistance, elasticity of the arteries, cardiac output (heart rate and stroke volume), blood volume, and viscosity of the blood. The central nervous system, the endocrine glands, and the kidney must exert their influence on blood pressure through the above factors. 

Sodium and salt intake remain controversial as risk factors for hypertension. While it s true that some individuals are particularly sensitive to sodium, whether from the salt shaker or from sodium-based ingredients in processed and fast foods, not everyone responds to sodium equally. As we ll see, sodium is but one of many minerals, or electrolytes, that affect blood pressure. Increasing your intake of the others may be as important as, or more important than, decreasing your intake of sodium, other than for people who are proven to be sodium sensitive. 

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