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Hemodynamics

A simple view of the hemodynamics of systemic arterial pressure is based around mean arterial pressure (MAP) and pulse pressure. Most influences on blood pressure can be understood in terms of their effect on cardiac output, systemic vascular resistance, or arterial stiffness (the inverse of arterial compliance). Cardiac output is the product of stroke volume and heart rate. Stroke volume is influenced by 1) the end-diastolic volume or filling pressure of the ventricle acting via the Frank–Starling mechanism —this is influenced by blood volume; 2) cardiac contractility; and 3) afterload, the impedance to blood flow presented by the circulation. In the short-term, the greater the blood volume, the higher the cardiac output. This has been proposed as an explanation of the relationship between high dietary salt intake and increased blood pressure; however, responses to increased dietary sodium intake vary between individuals and are highly dependent on autonomic nervous system responses and the renin–angiotensin system, changes in plasma osmolarity may also be important. In the longer-term the relationship between volume and blood pressure is more complex. In simple terms, systemic vascular resistance is mainly determined by the caliber of small arteries and arterioles. The resistance attributable to a blood vessel depends on its radius as described by the Hagen-Poiseuille's equation (resistance∝1/radius). Hence, the smaller the radius, the higher the resistance. Other physical factors that affect resistance include: vessel length (the longer the vessel, the higher the resistance), blood viscosity (the higher the viscosity, the higher the resistance) and the number of vessels, particularly the smaller numerous, arterioles and capillaries. The presence of a severe arterial stenosis increases resistance to flow, however this increase in resistance rarely increases systemic blood pressure because its contribution to total systemic resistance is small, although it may profoundly decrease downstream flow. Substances called vasoconstrictors reduce the caliber of blood vessels, thereby increasing blood pressure. Vasodilators (such as nitroglycerin) increase the caliber of blood vessels, thereby decreasing arterial pressure. In the longer term a process termed remodeling also contributes to changing the caliber of small blood vessels and influencing resistance and reactivity to vasoactive agents. Reductions in capillary density, termed capillary rarefaction, may also contribute to increased resistance in some circumstances.

In practice, each individual's autonomic nervous system and other systems regulating blood pressure, notably the kidney, respond to and regulate all these factors so that, although the above issues are important, they rarely act in isolation and the actual arterial pressure response of a given individual can vary widely in the short and long term.