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In order to fulfill its role the vascular system of blood vessels must:
Types of Blood Vessels There are three main types of blood vessels:
The vascular system is composed of arteries, arterioles, capillaries, venules and veins. The structure of the vessels in the different parts of the vascular system varies and the differences relate directly to the function of each type of vessel. The walls of all the blood vessels, except the capillaries which are only one cell thick, have the same basic components but the proportion of the components varies with function. Layers of Blood VesselsAll blood vessels (except capillaries as mentioned above) are composed of three layers surrounding a central blood carrying canal (known as the lumen). The three layers vary in prominence in different vessel types. These layers are known as tunica (latin for tunic or cloak).
The tunica adventitia is the outer layer of blood vessels. It is composed largely of collagen, but smooth muscle cells may be present, particularly in veins. The tunica adventitia is often the most prominent layer in the walls of veins. Within the tunica adventitia of vessels with thick walls (such as large arteries and veins) are small blood vessels which send penetrating branches into the media to supply it with blood. These are known as the vasa vasorum which literally means vessels oif the vessels. Vasa vasorum are not seen in thinner vessels.They obtain their oxygen by diffusion from the red blood cells in the lumen. The adventitia also carries autonomic nerves which innervate the smooth muscle of the media and some lymphatic vessels that drain off excess interstitial fluid. The tunica media is the middle layer in a blood vessel wall and is composed predominantly of smooth muscle reinforced by organised layers of elastic tissue which form elastic laminae. The tunica media is particularly prominent in arteries, being relatively indistinct in veins and virtually non-existent in very small vessels. The tunica media also contains autonomic nerves. In vessels which are close to the heart, receiving the full thrust of the systolic pressure wave, elastic tissue is very well developed, hence the term elastic arteries. In muscular arteries and arterioles the prominent elastic lamina just below the tunica intima is termed the internal elastic lamina. The tunica intima is composed of a lining layer of highly specialised multifunctional flattened epithelial cells termed endothelium. This sits on a basal lamina; beneath this is a very thin layer of fibrocollagenous support tissue. It is continuous with the endocardial lining of the heart and is the only layer that is present in all blood vessels. In all types of blood vessels the endothelium of the tunica intima is highly specialised with endocrine, exocrine, cell adhesion, clotting and transport functions. The endothelium is composed of flattened cells. In routine histological sections the cytoplasm of most endothelial cells is barely visible and only the small flattened nuclei are seen. Ultrastructurally, each cell can be seen to be anchored to an underlying basal lamina; individual cells are anchored together by adhesion junctions, including prominent tight junctions which prevent diffusion between cells. A prominent feature of endothelial cells is the presence of many pinocytotic vesicles which are involved in the process of transport of substances from one side of the cell to the other. In small blood vessels of the nervous system the endothelial cells express transport proteins which are responsible for active transport of all substances, for example glucose, into the brain. Endothelial cells are able to sense changes in blood pressure, oxygen tension and blood flow by as yet unknown mechanisms. In response to changes in local conditions they respond by secreting substances which have powerful effects on the tone of vascular smooth muscle. Endothelial cells are also important in the control of blood coagulation. Under normal circumstances the endothelial surface prevents blood clotting and allows smooth flowing of the blood. The endothelium can adapt rapidly to changes in its environment. Under certain circumstances, especially in response to adverse stimuli such as wounds, infections or irritation (e.g. insect sting), the endothelium may become activated and change its function. The endothelium may become activated by cytokines and develop specialisation for emigration of lymphoid cells. The endothelial cells become cuboidal in shape and express surface adhesion molecules which facilitate lymphocyte adhesion and migration. This type of endothelium is normally seen in the specialised venules in the lymph node paracortex (high endothelial venules). Endothelium may become activated by cytokines and express cell adhesion molecules for neutrophils. This normally occurs after any form of tissue damage and allows neutrophils to migrate into local tissues in the process of acute inflammation. The substance P-selectin, a cell adhesion molecule, is stored in special vesicles (Weibel-Palade bodies) inside the endothelium. With appropriate stimulation, these vesicles dock with the endothelial cell membrane. P-selectin is then available on the cell surface for neutrophil adhesion. Endothelium is normally locally impermeable to substances in the blood. Under the effects of certain factors, for example histamine, endothelial cells lose attachment to each other and retract. This allows fluid and proteins to diffuse out into the local tissues causing tissue swelling termed oedema. This reorganisation of cell-cell junctions is rapid and reversible and takes place in the space of a few minutes. ArteriesThe systemic arterial circulation is an extensive high-pressure system. The structure of its vessels reflects the high pressures to which they are subjected. The output of the left ventricle of the heart is carried in large diameter vessels with a high component of elastic tissue in their walls which smoothes the systolic pressure wave. These are called the large elastic arteries (i.e. the aorta and its large branches such as the carotid, subclavian and renal arteries). Moving away from the heart these large elastic arteries branch off into smaller vessels in which the artery walls become proportionately more muscular. Elastic Arteries Elastic arteries are the largest arteries and receive the main output of the left ventricle: thus they are subjected to the high systolic pressures of 120-160 mmHg. These large vessels are adapted to smooth out the surges in blood flow, since blood is impelled through them only during the systolic phase of the cardiac cycle. The elastic tissue in their walls provides the resilience to smooth out the pressure wave. The intima of large elastic arteries is composed of endothelium with a thin layer of underlying fibrocollagenous tissue. Elastic arteries have a thick, highly developed media of which elastic fibres are the main component. These are gathered together in sheets arranged in concentric layers throughout the thickness of the media. In thelargest artery, the aorta, there are often 50 or more layers. The elastic fibres are arranged so that they run in bands around the circumference (circumferentially) rather than along the length of the artery (longitudinally) in order to counteract the tendency for the vessel to over distend during systole. When the heart contracts and forces blood into the aorta, the elastic fibres are stretched and, as a result the aorta distends. At the end of the left ventricular contraction, the force generated by the heart diminishes and so the force stretching the fibres is removed. As a result of this they tend to return to their starting size. The effect of this recoil is to maintain the pressure head and thus force the blood pumped out of the left ventricle away from the heart and into the systemic vascular system. This occurs as a result of the conversion of potential energy created by the distension of the elastic wall of the aorta into kinetic energy which continues to move blood away from the heart even in the diastolic phase. Return of the elastic fibres from their stretched to unstretched state during diastole maintains a diastolic pressure within the aorta and large arteries of about 60-80 mmHg. It is this mechanism which helps to smooth out the explosive expulsion of blood from the left ventricle into a steady flow throughout the arterial system. Interposed between the elastic layers are smooth muscle cells and some collagen. The adventitia of the large vessels carries vasa vasorum and nerves. Muscular Arteries Muscular arteries have a media composed almost entirely of smooth muscle. The large elastic arteries gradually merge into muscular arteries by losing most of their medial elastic sheets, usually leaving only two layers, an internal elastic lamina and an external elastic lamina at the junction of the media with the intima and adventitia, respectively. Although the walls of muscular arteries are distensible to a certain extent, as they become smaller and smaller with each successive branching the amount of elastic tissue decreases whilst the muscular component proportionately increases. In a muscular artery the media is composed almost entirely of smooth muscle. These arteries are therefore highly contractile, their degree of contraction or relaxation being controlled by the autonomic nervous system as well as by endothelium-derived vasoactive substances. A few fine elastic fibres are scattered among the smooth muscle cells, but are not organised into sheets. These are most numerous in the large muscular arteries, which are a direct continuation of the distal end of the elastic arteries. Muscular arteries vary in size from about 1 cm in diameter close to their origin at the elastic arteries, to about 0.5 mm in diameter. In the larger arteries there may be 30 or more layers of smooth muscle cells, whereas in the smallest peripheral arteries, there are only 2 or 3 layers. The smooth muscle cells are usually arranged circumferentially at right angles to the long axis of the vessel. The internal elastic lamina is commonly a distinct prominent layer, but the external elastic lamina is less well defined, and is often incomplete. ArteriolesArterioles are the smallest branches of the arterial tree. Arterioles vary in diameter ranging from 30 mm (0.03 mm) to 400 mm (0.4 mm). Any artery smaller than 0.5mm in diameter is considered to be an arteriole. The intima of an arteriole is composed of endothelial cells lying on a basement membrane with an underlying fine internal elastic lamina in the larger arterioles. The arteriolar media is composed of one or two layers of smooth muscle cells. As the arterioles get smaller, the continuous layers of smooth musclebecome progressively discontinuous. In the smallest arterioles, the endothelial cells have basal processes whichpierce the basement membrane and make junctional contacts with the smooth muscle cells. The adventitia of arterioles is insignificant. The arterioles offer considerable resistance to blood flow because of their very small radius, and are the major site of resistance to flow in the vascular tree. Thus the total peripheral resistance, that is the total resistance to blood flow, is mainly determined by the radius of the arterioles. This area of high resistance to blood flow serves several functions: first, together with the elastic arteries, it converts the pulsatile ejection of blood from the heart into a steady flow through the capillaries; second, if no resistance were present and a high pressure persisted into the capillaries, there would be a considerable loss of blood volume into the tissue by transudation of fluid across the capillary wall. The pulmonary circulation is a low pressure circulation partly to prevent this happening; if pulmonary pressures increase for some pathological reason, pulmonary oedema may develop. The arterioles are also important in determining the blood supply to different tissues and regions. There are specialised regions near the junction between the terminal (smallest) arterioles and the capillaries known as pre capillary sphincters, which consist of a few smooth muscle cells arranged circularly. If the sphincters are relaxed and the lumen patent, the capillary beds distal to the sphincter are open and perfused. If the sphincters are partially constricted, blood flow to the capillaries will be reduced, and if fully contracted, no blood will flow through. In active muscle, for instance, many more capillaries are patent due to relaxation of the sphincters and thus blood flow is increased; this has the effect of greatly increasing the surface area available for exchange of substances and at the same time reduces the distance across which substances have to diffuse to reach the cells. The mechanisms that control the arteriolar radius and pre capillary sphincters will be considered in detail later. Altering the radius is the normal mechanism for controlling the resistance and altering blood flow, and both the sympathetic nervous system and local factors are involved. The microvasculature starts at the level of the arterioles. It is composed of small diameter blood vessels with partly permeable thin walls that permit the transfer of some blood components to the tissues and vice versa. The structure of the microvasculature varies in different tissues in order to meet specific functional requirements. Some tissues have a much more abundant network of capillaries than others. For example dense connective tissue has a poor capillary network when compared to cardiac tissue or that of the kidneys and liver. Most of this exchange between blood and tissues occurs in the extensive capillary network, the smallest arterioles (metarterioles) emptying into the capillary system. The capillary networks drain into the first components of the venous system, the venules. CapillariesCapillaries are specialized for diffusion of substances across their wall. Capillaries are the smallest vessels of the blood circulatory system and form a complex inter linking network. Capillaries have the thinnest walls of all blood vessels and are the major site of gaseous exchange, permitting the transfer of oxygen from blood to tissues, and carbon dioxide from the tissues to the blood. Fluids containing large molecules pass across the capillary walls in both directions. The capillary wall is composed of endothelial cells, a basement membrane, and occasional scattered contractile cells called pericytes. The capillaries form a dense network of narrow, short tubes; they can be as little as 3-4 mm in diameter (i.e. half the diameter of red blood cells), and up to 30-40 mm (these large blood spaces are usually known as sinusoids). On average, capillaries have a diameter of 6-8 mm and are approximately 750 mm long. The total number of capillaries in the body has been estimated to be of the order of 40,000-50,000 million. In the resting state, probably only about 25% of the capillary beds are patent. For exchange of substances to be efficient, it is necessary to have short distances for substances to diffuse, a large surface area (the total cross-sectional area of all the capillaries is about 700 times larger than that of the aorta), and a slow steady flow of blood, about 0.3-0.5 mm/s (the flow velocity is about 700 times lower in the capillaries than in the aorta because of the narrower vessels). This part of the circulatory system is often referred to as the microvasculature. The structure of the microvasculature is modified in different tissues to meet specific functional requirements. Different tissues have varying abundance of capillaries, e.g. dense connective tissue has a poor capillary network as compared to cardiac muscle. Electron microscopy has shown that the nature of the endothelium is not the same in all parts of the circulation. Three different kinds of capillary walls have been identified, and the terms continuous, fenestrated and discontinuous are used to describe them, according to the size of the intercellular gaps or pores present in each. Another modification in the structure of the microvasculature in tissues is the presence of arteriovenous shunts or arteriovenous anastomoses. These are direct connections between the arterial and venous systems that bypass the capillary beds. If these shunts are patent, blood can flow rapidly through the vessels, but does not serve any nutritive purpose. These short connecting vessels have strongly developed muscular control and are under sympathetic nervous control. They are found in many tissues and organs. In the skin, for example, they enable cutaneous blood flow to be increased to allow dissipation of heat from the body surfaces when exercising or in high environmental temperatures. The capillary network, whatever its form, drains into a series of vessels of increasing diameter to form venules and veins. VeinsThe venous system acts as a collecting system, returning blood from the capillary networks to the heart passively down a pressure gradient. The capillaries merge to form venules, which in turn unite to form larger, but fewer, veins which amalgamate finally into the venae cavae. The walls of veins consist of the same three layers as arteries, but the elastic muscle components are much less prominent; the walls in general are thinner and more distensible than those of arteries. The vessels have a relatively large diameter (the vena cava is 2-3 cm in diameter) and thus offer low resistance to blood flow. Some veins, especially in the arms and legs, have internal folds of the endothelial lining that function as valves and allow blood to flow in one direction only, towards the heart. These valves can be damaged if over stretched by high venous pressures for long periods, for example during pregnancy or in people who stand for extended periods; the valves become incompetent, lose their function, and varicose veins develop. As a result of this, oedema and varicose ulcers can develop. A major part of the blood volume, approximately 60%, is contained within the venous system and for this reason veins are sometimes referred to as capacity vessels. The capacity of the venous system can be modified by altering the lumen size of the muscular venules and veins; the changes are mediated by altering the venomotor tone, that is, the degree of contraction of the smooth muscle in the tunica media. Venomotor tone is mainly under the control of the sympathetic nervous system. Changes in the venomotor tone can increase or decrease the capacity of the venous circulation and therefore can partially compensate for variations in the effective circulating blood volume. Venous blood flow occurs along relatively small pressure gradients and even small variations in resistance and vessel radius affect the return flow. The effect of gravity retards venous return: when upright, as the veins are distensible and due to the hydrostatic pressure of a column of blood in the veins below the level of the heart, blood tends to collect or pool in the feet and legs. When vertical, the leg veins take on a circular form which has a greater capacity; when horizontal the veins take on an elliptical shape with a lower capacity. Increased venomotor tone, reducing the diameter and hence capacity of the veins, helps to reduce venous pooling. Venous pooling is a useful term but it suggests stagnation which does not occur; venous pooling simply indicates that the veins accommodate a greater volume of blood. One can see the effect of gravity on the veins in the neck: when sitting or standing the neck veins above a level 5-10 cm higher than the heart are not prominent, but when lying down the veins distend. This is due to the fact that, in contrast to venous return from the feet, blood from the head returns to the heart aided by gravity when upright. However, the blood supply to the head has to overcome the effect of gravity; failure of this phenomenon can be observed when someone stands up too quickly after bending down and feels dizzy due to a temporary reduction in the effective pressure head delivering blood to the brain. It is vital that an adequate venous return to the heart is maintained at all times because the cardiac output depends on the venous return - in most instances the cardiac output equals the venous return. Thus, if the venous return falls, cardiac output and blood pressure may also drop. Several mechanisms exist to help maintain the venous return at all times. Increasing the venomotor tone is an important mechanism as it decreases the capacity of the venous system and so aids venous return. After a long period of bed rest when the body is not constantly being exposed to the force of gravity and the veins do not have to compensate, venomotor tone is reduced, and this method of reducing the effect of gravity is temporarily less efficient. This should be remembered when helping someone to get up after a period of bed rest. It is essential to move slowly and steadily and to support the person in case he or she becomes dizzy and faint. Venous return is also assisted by two systems sometimes referred to as the skeletal muscle pump and respiratory pump. Contraction of the skeletal muscles, especially in the limbs, squeezes the veins and this pushes blood in the extremities towards the heart; back flow is prevented by the presence of numerous valves. There are also many communicating channels which allow emptying of blood from the superficial limb veins into the deep veins when rhythmic muscular contractions occur. Consequently, every time a person moves his or her legs or tenses the muscles, a certain amount of blood is pushed towards the heart. The more frequent and powerful such rhythmic contractions are, the more efficient their action. (Sustained continuous muscle contractions, unlike rhythmic contractions, impede blood flow due to the veins being continuously 'blocked'.) The muscle pump mechanism is an efficient system: the venous pressure in the feet of someone walking is of the order of 25 mmHg (3.3kPa), whereas in the feet of an individual standing absolutely still it is of the order of 90 mmHg (12kPa). So when an individual stands still for long periods of time, the muscle pump cannot operate and venous return is decreased. This can result in people fainting due to an inadequate cerebral blood flow. e.g. soldiers fainting on parade, people fainting in operating theatres after standing still for long periods. Thus it is advisable to contract the muscles of the legs and buttocks voluntarily to aid venous return if standing still for long periods. Respiration produces cyclical variations in intra pleural and intra thoracic pressure. With each inspiration, the pressure is lowered with the thorax and hence also within the right atrium of the heart; this increases the pressure gradient and aids blood flow back to the heart. Simultaneously, the descent of the diaphragm into the abdomen raises the intra-abdominal pressure and increases the gradient to the thorax, again favoring venous return. With expiration, the pressure gradients are reversed and blood tends to flow in the opposite direction; fortunately this tendency is prevented by the valves in the medium sized veins. Thus venous return is maintained by changes in veno-motor tone, altering the capacity of the venous system, and by the skeletal muscle and respiratory pumps. Obviously it is also necessary to maintain an adequate circulating blood volume. If the blood volume is depleted for some reason, e.g. dehydration or hemorrhage, in the short term veno-constriction and vasoconstriction in the body's blood reservoirs, such as the skin, liver, lungs and spleen, can increase the effective circulating blood volume. However, the blood volume must be restored eventually by fluid replacement. The pressures in the central regions of the venous system directly reflect the blood volume; thus central venous pressure (CVP), or right atrial pressure, is a good indicator of blood volume, unlike arterial pressures which are regulated and controlled by reflexes. Basic Principles of Fluid DynamicsBefore discussing blood pressure, it is necessary to consider briefly some of the properties of fluids and the principles that govern the flow of fluids through vessels. All fluids (when in a confined space) exert a pressure. The term hydrostatic pressure refers to the force that a liquid exerts against the walls of its container. The pressure that blood exerts in the vascular system is known as blood pressure. Pressure varies with the height of the liquid column and this can be observed in the veins of a person standing up. The venous pressures in the feet are considerably greater than in the head (this is, of course, related to the effect of gravity). The effect of density on hydrostatic pressure is shown by the fact that 1 mm of mercury (mm Hg) exerts the same pressure as 13 mm of water (mm H2O) because mercury is more than 13 times as heavy as water for an equal volume. If pressure is exerted on a confined fluid, the pressure will be transmitted equally in all directions - this is known as Pascal's principle. If there is a weak point in the container's wall and the pressure exerted is great enough, the container wall may burst. This is what happens when an aneurysm bursts. When an individual is hypertensive, the blood vessels harden or undergo sclerotic changes (arteriosclerosis) to prevent the vessels bursting with the elevated blood pressure. The distensibility of the container also influences the hydrostatic pressure that develops: if the container is distensible, the pressure in the fluid is less than in a rigid container. Flow of Fluids The flow of a fluid through a vessel is determined by the pressure difference between the two ends of the vessel and also the resistance to flow. Pressure Difference For any fluid to flow along a vessel there must be a pressure difference otherwise the fluid will not move. In the cardiovascular system the 'pressure head' or force is generated by the pumping of the heart and there is a continuous drop in pressure from the left ventricle of the heart to the tissues and also from the tissues back to the right atrium of the heart. Without this drop in blood pressure, no blood would flow around the circulatory system. Resistance to Flow Resistance is a measure of the ease with which a fluid will flow through a tube: the easier it is, the less the resistance to flow, and vice versa. In the circulatory system the resistance is usually described as the vascular resistance; as it mainly originates in the peripheral blood vessels, it is also known simply as the peripheral resistance. Resistance is essentially a measure of the friction between the molecules of the fluid, and between the tube wall and the fluid. The resistance depends on the viscosity of the fluid and the radius and length of the tube. Radius of The Blood Vessel The smaller the radius of a vessel, the greater is the resistance to the movement of particles; this increased resistance results from a greater probability of the particles of the fluid colliding with the vessel wall. When a particle collides with the wall, some of the particle's kinetic energy (energy of movement) is lost on impact, resulting in the slowing of the particle. Thus, in a smaller diameter vessel, there will be a greater number of collisions and a reduction in the energy content and speed of the particles moving through the vessel. This results in a decrease in the hydrostatic pressure. Small alterations in the size of the radius of the blood vessels, particularly of the more peripheral vessels, can greatly influence the flow of blood. Atheromatous changes in the walls of large and medium-sized arteries cause narrowing of the lumen of the vessels and result in an increased vascular resistance. Blood Vessel Length The longer the tube, the greater the resistance to the flow of liquid through it. A longer vessel will require a greater pressure to force a given volume of liquid through it than will a shorter vessel. However, the length of the blood vessels in the body is not altered significantly and the overall length is kept to a minimum because of the parallel circuits in the systemic circulation. Fluid Viscosity Viscosity is a measure of the intermolecular or internal friction within a fluid or, in other words, of the tendency of a liquid to resist flow. The rate of flow varies inversely with the viscosity: the greater the viscosity of a fluid, the greater is the force required to move that liquid. Thus, changes in blood viscosity affect flow. Normally the viscosity of blood remains fairly constant, but in polycythaemia, in which there is an increased red cell content, the viscosity of the blood can be considerably increased and the blood flow reduced. Severe dehydration, where there is a loss of plasma, can also lead to increased viscosity. Cooling of the blood similarly increases its viscosity. The nature of the lining of the tube or vessel also influences the way fluids flow. If the lining of the blood vessel is smooth, the fluid will flow evenly; this is known as streamline or laminar flow. However, if the lining is rough or uneven or the fluid flows irregularly, turbulent flow is set up. Laminar flow is characteristic of most parts of the vascular system and is silent, whereas turbulent flow can be heard, e.g. during blood pressure measurements with a sphygmomanometer. It is sometimes necessary to measure blood flow in patients and it is usual simply to measure the quantity of blood that passes a given point in the circulation over a given period of time. One method used in the clinical situation is by means of an ultrasonic flowmeter applied to the surface of the skin over a blood vessel. This makes use of the Doppler effect (a shift in the frequency of the ultrasonic waves when they are reflected off the moving blood cells). It is a useful and non-invasive method of assessing the condition of the peripheral arteries, in peripheral vascular disease or after vascular surgery for example. Blood PressureBlood pressure refers to the pressure of blood on the walls of the blood vessels of the body. It is a fundamental principle of Physics that all fluids when held in a container exert a pressure upon the container walls. This pressure is a hydrostatic pressure. Blood is no exception to this physical principle and therefore blood pressure is a hydrostatic pressure. Each blood vessel has it's own blood pressure value, arterial blood pressure, capillary blood pressure, venous blood pressure, left atrial blood pressure, right ventricular blood pressure etc. The pressure in the systemic blood vessels falls continuously from the aorta until the blood re-enters the heart in the right atrium. Blood pressure in the pulmonary system is considerably lower than that of the systemic system but there is still a pressure gradient from the blood leaving the right ventricle to the left atrium. In both systems it is essential to have a pressure gradient so that the blood will flow from the area of highest pressure to the area of lowest pressure thus maintaining the circulation. In nursing practice reference to blood pressure normally means systemic arterial blood pressure. The use of this as the basic measure is quite appropriate as it is this pressure that ensures an adequate blood flow to the tissues and vital organs. If the pressure falls too far blood flow is reduced, perfusion of the tissues is lowered and shock can occur. Fainting is an example of this, here blood flow to the brain is reduced and loss of consciousness is the result. There are several mechanisms which exist in order to maintain the blood pressure within normal limits. It is important that the correct blood pressure is maintained if the individual is to maintain a healthy status. As mentioned above low blood pressure leading to shock or fainting. Abnormal pressure in the blood capillaries can result in abnormal exchange of fluids to and from tissues which can result in conditions such as edema. Blood Pressure, Blood Flow & Vascular Resistance
As mentioned already, (in the pages on structure and function of blood vessels) the cardiovascular system is a closed system. As a result the total blood flow leaving and entering the heart (in normal health) will be the same. Thus blood flow is equivalent to the cardiac output. Pressure difference is the difference between the mean pressure in the aorta and the pressure in the vena cava just before the blood enters the heart (this latter value is almost zero). Since the blood pressure is essentially the same in the aorta and all large arteries, the pressure difference can be said to be equivalent to mean arterial pressure. Resistance to flow is the total resistance to blood flow. As the majority of the resistance is found in the peripheral vessels, especially the arterioles, it is often described as the total peripheral resistance. Thus we have the equation Blood Pressure = Cardiac Output (CO) x Total Peripheral Resistance (TPR)This is one of the fundamental equations of cardiovascular physiology. You can see from the equation that blood pressure can be maintained by altering cardiac output and/or total peripheral resistance. The cardiac output itself is changed by altering the heart rate and stroke volume. Arterial blood pressure fluctuates throughout the cardiac cycle. The contraction of the ventricles ejects blood into the pulmonary and systemic arteries during systole and this additional volume of blood distends the arteries and raises the arterial pressure. When the contraction ends, the stretched elastic arterial walls recoil passively and this continues to drive blood through the arterioles. As the blood leaves the arteries the pressure falls; the arterial pressure never falls to zero because the next ventricular contraction occurs whilst there is still an appreciable amount of blood within the arteries. Thus the pressure in the major arteries rises and falls as the heart contracts and relaxes. The maximum pressure occurs after ventricular systole and is known as the systolic pressure. When the blood pressure in the aorta exceeds that in the ventricle, the aortic valve closes; this accounts for the dicrotic notch. Once the aortic valve has closed, the blood pressure in the aorta and large arteries falls as blood flows through the arterioles and capillaries to the veins. The level to which the arterial pressure has fallen before the next ventricular systole, that is the minimum pressure, is known as the diastolic pressure. The systolic pressure is determined by the amount of blood being forced into the aorta and arteries with each ventricular contraction, i.e. the stroke volume, and also by the force of contraction. An increase in either will increase the systolic pressure. Similarly, if the arterial wall becomes stiffer, as happens in arteriosclerosis, the vessels are not able to distend with the increased blood volume and so the systolic pressure is increased. Diastolic pressure is also influenced by several factors. The diastolic pressure provides information on the degree of peripheral resistance: if there is increased arteriolar vasoconstriction, this will impede blood flowing out of the arterial system to the capillaries, and the diastolic pressure will rise. Conversely, if the peripheral resistance is reduced by vasodilation, more blood will flow out of the arterial system and thus diastolic pressure will fall. Drugs that modify the degree of arterial vasoconstriction and alter the peripheral resistance will obviously affect the diastolic pressure, and vasodilator drugs, for example hydralazine hydrochloride (Apresoline), minoxidil (Loniten), are sometimes used in the treatment of severe hypertension. The diastolic pressure also depends on the level of the systolic pressure, the elasticity of the arteries and the viscosity of the blood. Alterations in the heart rate will also affect diastolic pressure: with a slower heart rate, the diastolic pressure will be lower as there is a greater time for blood to flow out of the arteries, and vice versa. Blood Pressure ValuesBlood pressure values. There is no such value as a 'normal' blood pressure for the population as a whole; there is a usual or 'normal' value for any particular individual, but even that value varies from moment to moment under different circumstances and over longer periods of time. Many factors, both physiological and genetic, have an influence on blood pressure and thus it is not surprising that individuals have significantly different, but 'normal', blood pressure values. Therefore it is more appropriate to refer to a normal range of blood pressure than to a single value. Normal blood pressures are said to range from 100/60 mmHg to 150/90 mmHg. Parameters such as age, sex, and race influence blood pressure values. In Western societies, blood pressure values tend to increase with advancing age therefore a blood pressure which would be 'normal' for a 70 year old might be considered 'abnormal' for a 40 year old. This is not universal, for example South Pacific Islanders show little, if any, increase in mean blood pressure with increasing age . The elevation in blood pressure with age may be due either to genetic or environmental factors and is likely to be a result of arteriosclerosis. Men generally have higher blood pressures than women. Race also seems to influence blood pressure levels, e.g. in the USA Afro-Caribbean races tend to have higher blood pressures than whites. Most authorities agree that a resting diastolic pressure persistently exceeding 90 mmHg or 95 mmHg indicates hypertension, that is, a raised blood pressure; this is an arbitrary definition but proves to be useful for clinical practice. A persistently low blood pressure, hypo-tension, is relatively rare, although temporary or transient hypo-tension is more common, e.g. in hemorrhage or fainting. HypertensionOne of the reasons that clinicians are so concerned about the level of an individual's blood pressure is that there is a significantly increased mortality in those with untreated hypertension when compared with individuals with a 'normal' blood pressure (normotensive): a 35-year-old man with a diastolic pressure of 100 mmHg can expect a 16-year reduction in life expectancy. It has been estimated that nearly one-quarter of the adult population in the UK has an elevated blood pressure. Individuals who are hypertensive usually have few, if any, symptoms and often the hypertension is only diagnosed as part of a routine medical screening, for example for insurance purposes. The effects of a raised blood pressure are insidious and develop over many years: the heart has to increase in size (detectable on x-ray) and strength to overcome the increased resistance caused by the increased blood pressure. The arteries respond to the increased pressure by hypertrophy of the smooth muscle in their walls, so that they are able to withstand exposure to the higher pressures. Atherosclerosis formation is also potentiated. The blood vessels most commonly affected are the cerebral, coronary and renal vessels; cerebrovascular accidents (strokes) and myocardial infarctions are the commonest clinical manifestations, followed by renal disease. There has been much research and discussion into the causes of hypertension. In a few instances, hypertension is secondary to renal or endocrine disease, but in the majority of cases the cause of primary or essential hypertension is not fully understood. The aetiology of essential hypertension is almost certainly multifactorial and it is likely to prove to be a combination of genetic and environmental factors. Mechanisms that seem to be involved include some that affect the extracellular fluid volume and expand the circulating blood volume, e.g. excessive renin secretion and angiotensin production, increased sympathetic activity and excessive dietary salt intake, possibly associated with a low potassium intake. Some of the treatments prescribed for hypertension relate to these mechanisms, i.e. diuretics (e.g. a thiazide) to increase sodium and water loss; methyldopa, B-adrenoreceptor blocking drugs (e.g. propranolol), and relaxation techniques to reduce sympathetic activity; restriction of salt intake. One drug, captopril, inhibits angiotensin converting enzyme in the lungs and reduces the production of angiotensin II. Raised peripheral resistance is linked with hypertension and so drugs that produce vasodilation are useful. There are many risk factors associated with the development of hypertension, including obesity, high alcohol and salt intakes and some drugs (e.g. oral contraceptives, corticosteroids, monoamine oxidase inhibitors). There is also often a positive family history of hypertension: if both parents are hypertensive, there is a significantly greater risk that their children will also develop high blood pressure. If hypertension is diagnosed and effectively treated, usually by drug therapy, much of the cardiovascular-related disease can be prevented.
Adapted From Dr. John Ross - Faculty of Healthcare & Social Studies, University of Luton
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