DYNAMICS OF BLOOD FLOW
The blood vessels are a closed system of conduits that carry blood from the heart to the tissues and back to the heart. Some of the interstitial fluid enters the lymphatics and passes via these vessels to the vascular system. Blood flows through the vessels primarily because of the forward motion imparted to it by the pumping of the heart, although in the case of the systemic circulation, diastolic recoil of the walls of the arteries, compression of the veins by skeletal muscles during exercise, and the negative pressure in the thorax during inspiration also move the blood forward. The resistance to flow depends to a minor degree upon the viscosity of the blood but mostly upon the diameter of the vessels, principally the arterioles. The blood flow to each tissue is regulated by local chemical and general neural and humoral mechanisms that dilate or constrict the vessels of the tissue. All of the blood flows through the lungs, but the systemic circulation is made up of numerous different circuits in parallel, an arrangement that permits wide variations in regional blood flow without changing total systemic flow.
This chapter is concerned with the general principles that apply to all parts of the circulation and with pressure and flow in the systemic circulation.
Arteries & Arterioles
The walls of all arteries are made up of an outer layer of connective tissue, the adventitia; a middle layer of smooth muscle, the media; and an inner layer, the intima, made up of the endothelium and underlying connective tissue. The walls of the aorta and other arteries of large diameter contain a relatively large amount of elastic tissue, primarily located in the inner and external elastic laminas. They are stretched during systole and recoil on the blood during diastole. The walls of the arterioles contain less elastic tissue but much more smooth muscle. The muscle is innervated by noradrenergic nerve fibers, which are constrictor in function, and in some instances by cholinergic fibers, which dilate the vessels. The arterioles are the major site of the resistance to blood flow, and small changes in their caliber cause large changes in the total peripheral resistance.
Capillaries The arterioles divide into smaller muscle-walled vessels, sometimes called metarterioles, and these in turn feed into capillaries. In some of the vascular beds that have been studied in detail, a metarteriole is connected directly with a venule by a capillary thoroughfare vessel, and the true capillaries are an anastomosing network of side branches of this thoroughfare vessel. The openings of the true capillaries are surrounded on the upstream side by minute smooth muscle precapillary sphincters. It is unsettled whether the metarterioles are innervated, and it appears that the precapillary sphincters are not. However, they can of course respond to local or circulating vasoconstrictor substances. The true capillaries are about 5 um in diameter at the arterial end and 9 um in diameter at the venous end. When the sphincters are dilated, the diameter of the capillaries is just sufficient to permit red blood cells to squeeze through in “single file.” As they pass through the capillaries, the red cells become thimble- or parachute-shaped, with the flow pushing the center ahead of the edges. This configuration appears to be due simply to the pressure in the center of the vessel whether or not the edges of the red blood cell are in contact with the capillary walls.
The total area of all the capillary walls in the body exceeds
Capillaries and postcapillary venules have pericytes outside the endothelial cells. These cells have long processes that wrap around the vessels. They are contractile and release a wide variety of vasoactive agents. They also synthesize and release constituents of the basement membrane and extracellular matrix. One of their physiologic functions appears to be regulation of flow through the junctions between endothelial cells, particularly in the presence of inflammation. They are closely related to the mesangial cells in the renal glomeruli.
Lymphatics The lymphatics drain from the lungs and from the rest of the body tissues via a system of vessels that coalesce and eventually enter the right and left subclavian veins at their junctions with the respective internal jugular veins. The lymph vessels contain valves and regularly traverse lymph nodes along their course. The ultrastructure of the small lymph vessels differs from that of the capillaries in several details: There are no visible fenestrations in the lymphatic endothelium; there is very little if any basal lamina under the endothelium; and the junctions between endothelial cells are open, with no tight intercellular connections.
Arteriovenous Anastomoses In the fingers, palms, and ear lobes of humans and the paws, ears, and other tissues of some animals, there are short channels that connect arterioles to venules, bypassing the capillaries. These arteriovenous (A-V) anastomoses, or shunts, have thick, muscular walls and are abundantly innervated, presumably by vasoconstrictor nerve fibers.
Venules & Veins The walls of the venules are only slightly thicker than those of the capillaries. The walls of the veins are also thin and easily distended. They contain relatively little smooth muscle, but considerable venoconstriction is produced by activity in the noradrenergic nerves to the veins and by circulating vasoconstrictors such as endothelins. Anyone who has had trouble making venipunctures has observed the marked local venospasm produced in superficial forearm veins by injury. Variations in venous tone are important in circulatory adjustments.
The intima of the limb veins is folded at intervals to form venous valves that prevent retrograde flow. The way these valves function was first demonstrated by William Harvey in the 17th century. There are no valves in the very small veins, the great veins, or the veins from the brain and viscera.
Endothelium Located between the circulating blood and the media and adventitia of the blood vessels, the endothelial cells constitute a large and important organ. They respond to flow changes, stretch, a variety of circulating substances, and inflammatory mediators. They secrete growth regulators and vasoactive substances
Vascular Smooth Muscle The smooth muscle in blood vessel walls has been one of the most-studied forms of visceral smooth muscle because of its importance in the regulation of blood pressure and hypertension. The membranes of the muscle cells contain various types of K+, Ca2+, and Cl– channels. However, vascular smooth muscle also undergoes the prolonged contractions that determine vascular tone. These may be due in part to the latch-bridge mechanism, but other factors also play a role.
Vascular smooth muscle cells provide an interesting example of the way high and low cytosolic Ca2+ can have different and even opposite effects. In these cells, influx of Ca2+ via voltage-gated Ca2+ channels produces a diffuse increase in cytosolic Ca2+ that initiates contraction. However, the Ca2+ influx also initiates Ca2+ release from the sarcoplasmic reticulum via ryanodine receptors, and the high local Ca2+ concentration produced by these Ca2+ sparks increases the activity of Ca2+-activated K+ channels in the cell membrane. These are also known as big K or BK channels because K+ flows through them at a high rate. The increased K+ efflux increases the membrane potential, shutting off voltage-gated Ca2+ channels and producing relaxation. The site of action of the Ca2+ sparks is the β1-subunit of the BK channel, and mice in which this subunit is knocked out develop increased vascular tone and blood pressure. Obviously, therefore, the sensitivity of the β1 subunit to Ca2+ sparks plays an important role in the control of vascular tone.
Angiogenesis When tissues grow, blood vessels must proliferate if the tissue is to maintain a normal blood supply. Therefore, angiogenesis, the formation of new blood vessels, is important during fetal life and growth to adulthood. It is also important in adulthood for processes such as wound-healing, formation of the corpus luteum after ovulation, and formation of new endometrium after menstruation. Abnormally, it is important in tumor growth; if tumors do not develop a blood supply, they do not grow. During embryonic development, a network of leaky capillaries is formed in tissues from angioblasts: this process is sometimes called vasculogenesis. Vessels then branch off of nearby vessels, hook up with the capillaries, and provide them with smooth muscle, which brings about their maturation. Angiogenesis in adults is presumably similar.
Many factors are involved in angiogenesis. A key compound is the protein growth factor vascular endothelial growth factor (VEGF). This factor exists in multiple isoforms, and there are at least three VEGF receptors, two of which are known to be tyrosine kinases. VEGF appears to be primarily responsible for vasculogenesis, whereas the budding of vessels which connect to the immature capillary network is regulated by other as yet unidentified factors.
Some of the VEGF isoforms and some of its receptors seem to be concerned primarily with the formation of lymphatic vessels (lymphangiogenesis) rather than blood vessels. Most of the vascular growth factors act on all tissues. However, a VEGF produced by endocrine glands and acting only on the blood vessels of these glands has recently been described. The actions of VEGF and the other factors are complex, and there is much still to be learned about the factors involved in angiogenesis and the way they work together to regulate blood and lymph vessel formation in living animals.
Flow, Pressure, & Resistance Blood always flows, of course, from areas of high pressure to areas of low pressure, except in certain situations when momentum transiently sustains flow. The relationship between mean flow, mean pressure, and resistance in the blood vessels is analogous in a general way to the relationship between the current, electromotive force, and resistance in an electrical circuit expressed in Ohm’s law.
Flow in any portion of the vascular system is equal to the effective perfusion pressure in that portion divided by the resistance. The effective perfusion pressure is the mean intraluminal pressure at the arterial end minus the mean pressure at the venous end. The units of resistance (pressure divided by flow) are dyne·s/cm5. To avoid dealing with such complex units, resistance in the cardiovascular system is sometimes expressed in R units, which are obtained by dividing pressure in mm Hg by flow in mL/s. Thus, for example, when the mean aortic pressure is
Methods for Measuring Blood Flow Blood flow can be measured by cannulating a blood vessel, but this has obvious limitations. Various devices have been developed to measure flow in a blood vessel without opening it. Electromagnetic flow meters depend on the principle that a voltage is generated in a conductor moving through a magnetic field and that the magnitude of the voltage is proportionate to the speed of movement. Since blood is a conductor, a magnet is placed around the vessel, and the voltage, which is proportionate to the volume flow, is measured with an appropriately placed electrode on the surface of the vessel. Blood flow velocity can be measured with Doppler flow meters. Ultrasonic waves are sent into a vessel diagonally from one crystal, and the waves reflected from the red and white blood cells are picked up by a second, downstream crystal. The frequency of the reflected waves is higher by an amount that is proportionate to the rate of flow toward the second crystal because of the Doppler effect.
Indirect methods for measuring the blood flow of various organs in humans include adaptations of the Fick and indicator dilution techniques. One example is the use of the Kety N2O method for measuring cerebral blood flow. Another is determination of the renal blood flow by measuring the clearance of para-aminohippuric acid. A considerable amount of data on blood flow in the extremities has been obtained by plethysmography. The forearm, for example, is sealed in a watertight chamber (plethysmograph). Changes in the volume of the forearm, reflecting changes in the amount of blood and interstitial fluid it contains, displace the water, and this displacement is measured with a volume recorder. When the venous drainage of the forearm is occluded, the rate of increase in the volume of the forearm is a function of the arterial blood flow (venous occlusion plethysmography).
Applicability of Physical Principles to Flow in Blood Vessels Physical principles and equations that are applicable to the description of the behavior of perfect fluids in rigid tubes have often been used indiscriminately to explain the behavior of blood in blood vessels. Blood vessels are not rigid tubes, and the blood is not a perfect fluid but a two-phase system of liquid and cells. Therefore, the behavior of the circulation deviates, sometimes mark-edly, from that predicted by these principles. However, the physical principles are of value when used as an aid to understanding what goes on in the body rather than as an end in themselves or as a test of the memorizing ability of students.
Laminar Flow The flow of blood in straight blood vessels, like the flow of liquids iarrow rigid tubes, is normally laminar (streamline). Within the blood vessels, an infinitely thin layer of blood in contact with the wall of the vessel does not move. The next layer within the vessel has a low velocity, the next a higher velocity, and so forth, velocity being greatest in the center of the stream. Laminar flow occurs at velocities up to a certain critical velocity. At or above this velocity, flow is turbulent. Streamline flow is silent, but turbulent flow creates sounds.
The probability of turbulence is also related to the diameter of the vessel and the viscosity of the blood. This probability can be expressed by the ratio of inertial to viscous forces. Laminar flow is disturbed at branching of arteries, but normally not to the point that turbulence is produced. Constriction of an artery increases the velocity of blood flow through the constriction, producing turbulence, and consequently sound, beyond the constriction. Examples are bruits heard over arteries constricted by atherosclerotic plaques and the sounds of Korotkoff heard when measuring blood pressure.
In humans, the critical velocity is sometimes exceeded in the ascending aorta at the peak of systolic ejection, but it is usually exceeded only when an artery is constricted. Turbulence occurs more frequently in anemia because the viscosity of the blood is lower. This may be the explanation of the systolic murmurs that are common in anemia.
Shear Stress & Gene Activation Flowing blood creates a force on the endothelium that is parallel to the long axis of the vessel. This shear stress (γ) is proportionate to viscosity (η) times the shear rate (dy/dr), which is the rate at which the axial velocity increases from the vessel wall toward the lumen.
Change in shear stress and other physical variables such as cyclic strain and stretch produce marked changes in the expression of genes in the endothelial cells that are related to cardiovascular function. The receptors are probably integrins attached to the cytoskeleton of the cells. The second messengers are IP3, DAG, and components of the MAP kinase pathways, and the genes that are activated are those that produce growth factors, integrins, and related molecules. Over 15 endothelial cell genes have been shown to be activated by various physical forces.
Average Velocity When considering flow in a system of tubes, it is important to distinguish between velocity, which is displacement per unit time (eg, cm/s), and flow, which is volume per unit time (eg, cm3/s). Velocity is proportionate to flow (Q) divided by the area of the conduit (A). Therefore, Q = A, and if flow stays constant, velocity increases in direct proportion to any decrease in A.
The average velocity of fluid movement at any point in a system of tubes in parallel is inversely proportionate to the total cross-sectional area at that point. Therefore, the average velocity of the blood is high in the aorta, declines steadily in the smaller vessels, and is lowest in the capillaries, which have 1000 times the total cross-sectional area of the aorta. The average velocity of blood flow increases again as the blood enters the veins and is relatively high in the vena cava, although not so high as in the aorta. Clinically, the velocity of the circulation can be measured by injecting a bile salt preparation into an arm vein and timing the first appearance of the bitter taste it produces. The average normal arm-to-tongue circulation time is 15 seconds.
Poiseuille-Hagen Formula The relation between the flow in a long narrow tube, the viscosity of the fluid, and the radius of the tube is expressed mathematically in the Poiseuille-Hagen formula.
Since flow varies directly and resistance inversely with the fourth power of the radius, blood flow and resistance in vivo are markedly affected by small changes in the caliber of the vessels. Thus, for example, flow through a vessel is doubled by an increase of only 19% in its radius; and when the radius is doubled, resistance is reduced to 6% of its previous value. This is why organ blood flow is so effectively regulated by small changes in the caliber of the arterioles and why variations in arteriolar diameter have such a pronounced effect on systemic arterial pressure.
Viscosity & Resistance The resistance to blood flow is determined not only by the radius of the blood vessels (vascular hindrance) but also by the viscosity of the blood. Plasma is about 1.8 times as viscous as water, whereas whole blood is 3-4 times as viscous as water. Thus viscosity depends for the most part on the hematocrit, ie, the percentage of the volume of blood occupied by red blood cells. The effect of viscosity in vivo deviates from that predicted by the Poiseuille-Hagen formula. In large vessels, increases in hematocrit cause appreciable increases in viscosity. However, in vessels smaller than 100 um in diameter, ie, in arterioles, capillaries, and venules, the viscosity change per unit change in hematocrit is much less than it is in large-bore vessels. This is due to a difference in the nature of flow through the small vessels. Therefore, the net change in viscosity per unit change in hematocrit is considerably smaller in the body than it is in vitro. This is why hematocrit changes have relatively little effect on the peripheral resistance except when the changes are large. In severe polycythemia, the increase in resistance does increase the work of the heart. Conversely, in anemia, peripheral resistance is decreased, in part because of the decline in viscosity. Of course, the decrease in hemoglobin decreases the O2-carrying ability of the blood, but the improved blood flow due to the decrease in viscosity partially compensates for this.
Viscosity is also affected by the composition of the plasma and the resistance of the cells to deformation. Clinically significant increases in viscosity are seen in diseases in which plasma proteins such as the immunoglobulins are markedly elevated and in diseases such as hereditary spherocytosis, in which the red blood cells are abnormally rigid.
Critical Closing Pressure In rigid tubes the relation between pressure and flow of homogeneous fluids is linear, but in thin-walled blood vessels in vivo it is not. When the pressure in a small blood vessel is reduced, a point is reached at which there is no flow of blood even though the pressure is not zero. The vessels are surrounded by tissues that exert a small but definite pressure on the vessels, and when the intraluminal pressure falls below the tissue pressure, the vessels collapse. In inactive tissues, for example, the pressure in many capillaries is low because the precapillary sphincters and metarterioles are constricted, and many of these capillaries are collapsed. The pressure at which flow ceases is called the critical closing pressure.
Law of Laplace It is perhaps surprising that structures as thin-walled and delicate as the capillaries are not more prone to rupture. The principal reason for their relative invulnerability is their small diameter. The protective effect of small size in this case is an example of the operation of the law of Laplace, an important physical principle with several other applications in physiology. This law states that tension in the wall of a cylinder (T) is equal to the product of the transmural pressure (P) and the radius (r) divided by the wall thickness (w).
The transmural pressure is the pressure inside the cylinder minus the pressure outside the cylinder, but since tissue pressure in the body is low, it can generally be ignored and P equated to the pressure inside the viscus. In a thin-walled viscus, w is very small and it too can be ignored, but it becomes a significant factor in vessels such as arteries. Therefore, in a thin-walled viscus, P = T divided by the two principal radii of curvature of the viscus.
Consequently, the smaller the radius of a blood vessel, the lower the tension in the wall necessary to balance the distending pressure. In the human aorta, for example, the tension at normal pressures is about 170,000 dynes/cm, and in the vena cava it is about 21,000 dynes/cm; but in the capillaries, it is approximately 16 dynes/cm. The law of Laplace also makes clear a disadvantage faced by dilated hearts. When the radius of a cardiac chamber is increased, a greater tension must be developed in the myocardium to produce any given pressure; consequently, a dilated heart must do more work than a nondilated heart. In the lungs, the radii of curvature of the alveoli become smaller during expiration, and these structures would tend to collapse because of the pull of surface tension if the tension were not reduced by the surface-tension-lowering agent, surfactant. Another example of the operation of this law is seen in the urinary bladder.
Resistance & Capacitance Vessels When a segment of the vena cava or another large distensible vein is filled with blood, the pressure does not rise rapidly until large volumes of fluid are injected. In vivo, the veins are an important blood reservoir. Normally they are partially collapsed and oval in cross section. A large amount of blood can be added to the venous system before the veins become distended to the point where further increments in volume produce a large rise in venous pressure. The veins are therefore called capacitance vessels. The small arteries and arterioles are referred to as resistance vessels because they are the principal site of the peripheral resistance (see below).
At rest, at least 50% of the circulating blood volume is in the systemic veins. Twelve percent is in the heart cavities, and 18% is in the low-pressure pulmonary circulation. Only 2% is in the aorta, 8% in the arteries, 1% in the arterioles, and 5% in the capillaries. When extra blood is administered by transfusion, less than 1% of it is distributed in the arterial system (the “high-pressure system”), and all the rest is found in the systemic veins, pulmonary circulation, and heart chambers other than the left ventricle (the “low-pressure system”).
ARTERIAL & ARTERIOLAR CIRCULATION
The general relationships in the pulmonary circulation are similar, but the pressure in the pulmonary artery is 25/10 mm Hg or less.
Velocity & Flow of Blood
Although the mean velocity of the blood in the proximal portion of the aorta is 40 cm/s, the flow is phasic, and velocity ranges from 120 cm/s during systole to a negative value at the time of the transient backflow before the aortic valve closes in diastole. In the distal portions of the aorta and in the large arteries, velocity is also greater in systole than it is in diastole. However, the vessels are elastic, and forward flow is continuous because of the recoil during diastole of the vessel walls that have been stretched during systole. This recoil effect is sometimes called the Windkessel effect, and the vessels are called Windkessel vessels; Windkessel is the German word for an elastic reservoir. Pulsatile flow appears, in some poorly understood way, to maintain optimal function of the tissues. If an organ is perfused with a pump that delivers a nonpulsatile flow, there is a gradual rise in vascular resistance, and tissue perfusion fails.
Arterial Pressure The pressure in the aorta and in the brachial and other large arteries in a young adult human rises to a peak value (systolic pressure) of about
The pressure falls very slightly in the large and medium-sized arteries because their resistance to flow is small, but it falls rapidly in the small arteries and arterioles, which are the main sites of the peripheral resistance against which the heart pumps. The mean pressure at the end of the arterioles is 30-
Effect of Gravity The pressure in any vessel below heart level is increased and that in any vessel above heart level is decreased by the effect of gravity. The magnitude of the gravitational effect—the product of the density of the blood, the acceleration due to gravity (980 cm/s/s), and the vertical distance above or below the heart—is
Methods of Measuring Blood Pressure If a cannula is inserted into an artery, the arterial pressure can be measured directly with a mercury manometer or a suitably calibrated strain gauge and an oscillograph arranged to write directly on a moving strip of paper. When an artery is tied off beyond the point at which the cannula is inserted, an end pressure is recorded. Flow in the artery is interrupted, and all the kinetic energy of flow is converted into pressure energy. If, alternatively, a T tube is inserted into a vessel and the pressure is measured in the side arm of the tube, the recorded side pressure under conditions where pressure drop due to resistance is negligible is lower than the end pressure by the kinetic energy of flow. This is because in a tube or a blood vessel the total energy—the sum of the kinetic energy of flow and the pressure energy—is constant (Bernoulli’s principle).
It is worth noting that the pressure drop in any segment of the arterial system is due both to resistance and to conversion of potential into kinetic energy. The pressure drop due to energy lost in overcoming resistance is irreversible, since the energy is dissipated as heat; but the pressure drop due to conversion of potential to kinetic energy as a vessel narrows is reversed when the vessel widens out again.
Bernoulli’s principle also has a significant application in pathophysiology. According to the principle, the greater the velocity of flow in a vessel, the lower the lateral pressure distending its walls. When a vessel is narrowed, the velocity of flow in the narrowed portion increases and the distending pressure decreases. Therefore, when a vessel is narrowed by a pathologic process such as an atherosclerotic plaque, the lateral pressure at the constriction is decreased and the narrowing tends to maintain itself.
Auscultatory Method The arterial blood pressure in humans is routinely measured by the auscultatory method. An inflatable cuff (Riva-Rocci cuff) attached to a mercury manometer (sphygmomanometer) is wrapped around the arm and a stethoscope is placed over the brachial artery at the elbow. The cuff is rapidly inflated until the pressure in it is well above the expected systolic pressure in the brachial artery. The artery is occluded by the cuff, and no sound is heard with the stethoscope. The pressure in the cuff is then lowered slowly. At the point at which systolic pressure in the artery just exceeds the cuff pressure, a spurt of blood passes through with each heartbeat and, synchronously with each beat, a tapping sound is heard below the cuff. The cuff pressure at which the sounds are first heard is the systolic pressure. As the cuff pressure is lowered further, the sounds become louder, then dull and muffled. Finally, in most individuals, they disappear. These are the sounds of Korotkoff. When direct and indirect blood pressure measurements are made simultaneously, the diastolic pressure in resting adults correlates best with the pressure at which the sound disappears. However, in adults after exercise and in children, the diastolic pressure correlates best with the pressure at which the sounds become muffled. This is also true in diseases such as hyperthyroidism and aortic insufficiency.
The sounds of Korotkoff are produced by turbulent flow in the brachial artery. The streamline flow in the unconstricted artery is silent, but when the artery is narrowed, the velocity of flow through the constriction exceeds the critical velocity and turbulent flow results. At cuff pressures just below the systolic pressure, flow through the artery occurs only at the peak of systole, and the intermittent turbulence produces a tapping sound. As long as the pressure in the cuff is above the diastolic pressure in the artery, flow is interrupted at least during part of diastole, and the intermittent sounds have a staccato quality. When the cuff pressure is near the arterial diastolic pressure, the vessel is still constricted, but the turbulent flow is continuous. Continuous sounds have a muffled rather than a staccato quality.
The auscultatory method is accurate when used properly, but a number of precautions must be observed. The cuff must be at heart level to obtain a pressure that is uninfluenced by gravity. The blood pressure in the thighs can be measured with the cuff around the thigh and the stethoscope over the popliteal artery, but there is more tissue between the cuff and the artery in the leg than there is in the arm, and some of the cuff pressure is dissipated. Therefore, pressures obtained by using the standard arm cuff are falsely high. The same thing is true when brachial arterial pressures are measured in individuals with obese arms, because the blanket of fat dissipates some of the cuff pressure. In both situations, accurate pressures can be obtained by using a cuff that is wider than the standard arm cuff. If the cuff is left inflated for some time, the discomfort may cause generalized reflex vasoconstriction, raising the blood pressure. It is always wise to compare the blood pressure in both arms when examining an individual for the first time. Persistent major differences between the pressure on the two sides indicate the presence of vascular obstruction. Automated machines employing the auscultatory or other methods are now routinely used for continuous monitoring of blood pressure in hospitals and in the home.
Palpation Method The systolic pressure can be determined by inflating an arm cuff and then letting the pressure fall and determining the pressure at which the radial pulse first becomes palpable. Because of the difficulty in determining exactly when the first beat is felt, pressures obtained by this palpation method are usually 2-
It is wise to form a habit of palpating the radial pulse while inflating the blood pressure cuff during measurement of the blood pressure by the auscultatory method. When the cuff pressure is lowered, the sounds of Korotkoff sometimes disappear at pressures well above diastolic pressure, then reappear at lower pressures (“auscultatory gap”). If the cuff is initially inflated until the radial pulse disappears, the examiner can be sure that the cuff pressure is above systolic pressure, and falsely low pressure values will be avoided.
Normal Arterial Blood Pressure The blood pressure in the brachial artery in young adults in the sitting or lying position at rest is approximately 120/70 mm Hg. Since the arterial pressure is the product of the cardiac output and the peripheral resistance, it is affected by conditions that affect either or both of these factors. Emotion increases the cardiac output and peripheral resis-tance, and about 20% of hypertensive patients have blood pressures that are higher in the doctor’s office than at home, going about their regular daily activities (“white coat hypertension”). Blood pressure normally falls up to 20 mg Hg during sleep. This fall is reduced or absent in hypertension. Consequently, normals are sometimes called “dippers” and hypertensives “nondippers.”
There is general agreement that blood pressure rises with advancing age, but there has been uncertainty about the magnitude of this rise because hypertension is a common disease and its incidence increases with advancing age. One way to mitigate the problem is to select groups of young people with various systolic blood pressures and follow them prospectively over a period of years. Four groups of individuals were followed: those with initial systolic blood pressures <
It is interesting that systolic and diastolic blood pressures are lower in young women than in young men until age 55-65, after which they become comparable. Since there is a positive correlation between blood pressure and the incidence of heart attacks and strokes (see below), the lower blood pressure before menopause in women may be one reason that, on average, they live longer than men.
