Guyton and Hall Textbook of Medical Physiology, 12th Ed

CHAPTER 15

Vascular Distensibility and Functions of the Arterial and Venous Systems

Vascular Distensibility

image A valuable characteristic of the vascular system is that all blood vessels are distensible. The distensible nature of the arteries allows them to accommodate the pulsatile output of the heart and to average out the pressure pulsations. This provides smooth, continuous flow of blood through the very small blood vessels of the tissues.

The most distensible by far of all the vessels are the veins. Even slight increases in venous pressure cause the veins to store 0.5 to 1.0 liter of extra blood. Therefore, the veins provide a reservoir function for storing large quantities of extra blood that can be called into use whenever required elsewhere in the circulation.

Units of Vascular Distensibility

Vascular distensibility normally is expressed as the fractional increase in volume for each millimeter of mercury rise in pressure, in accordance with the following formula:image

That is, if 1 mm Hg causes a vessel that originally contained 10 millimeters of blood to increase its volume by 1 milliliter, the distensibility would be 0.1 per mm Hg, or 10 percent per mm Hg.

Difference in Distensibility of the Arteries and the Veins

Anatomically, the walls of the arteries are far stronger than those of the veins. Consequently, the veins, on average, are about eight times more distensible than the arteries. That is, a given increase in pressure causes about eight times as much increase in blood in a vein as in an artery of comparable size.

In the pulmonary circulation, the pulmonary vein distensibilities are similar to those of the systemic circulation. But the pulmonary arteries normally operate under pressures about one sixth of those in the systemic arterial system, and their distensibilities are correspondingly greater, about six times the distensibility of systemic arteries.

Vascular Compliance (or Vascular Capacitance)

In hemodynamic studies, it usually is much more important to know the total quantity of blood that can be stored in a given portion of the circulation for each mm Hg pressure rise than to know the distensibilities of the individual vessels. This value is called the compliance or capacitance of the respective vascular bed; that is,image

Compliance and distensibility are quite different. A highly distensible vessel that has a slight volume may have far less compliance than a much less distensible vessel that has a large volume because compliance is equal to distensibility times volume.

The compliance of a systemic vein is about 24 times that of its corresponding artery because it is about 8 times as distensible and it has a volume about 3 times as great (8 × 3 = 24).

Volume-Pressure Curves of the Arterial and Venous Circulations

A convenient method for expressing the relation of pressure to volume in a vessel or in any portion of the circulation is to use the so-called volume-pressure curve. The red and blue solid curves in Figure 15-1represent, respectively, the volume-pressure curves of the normal systemic arterial system and venous system, showing that when the arterial system of the average adult person (including all the large arteries, small arteries, and arterioles) is filled with about 700 milliliters of blood, the mean arterial pressure is 100 mm Hg, but when it is filled with only 400 milliliters of blood, the pressure falls to zero.

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Figure 15-1 “Volume-pressure curves” of the systemic arterial and venous systems, showing the effects of stimulation or inhibition of the sympathetic nerves to the circulatory system.

In the entire systemic venous system, the volume normally ranges from 2000 to 3500 milliliters, and a change of several hundred millimeters in this volume is required to change the venous pressure only 3 to 5 mm Hg. This mainly explains why as much as one half liter of blood can be transfused into a healthy person in only a few minutes without greatly altering function of the circulation.

Effect of Sympathetic Stimulation or Sympathetic Inhibition on the Volume-Pressure Relations of the Arterial and Venous Systems

Also shown in Figure 15-1 are the effects of exciting or inhibiting the vascular sympathetic nerves on the volume-pressure curves. It is evident that increase in vascular smooth muscle tone caused by sympathetic stimulation increases the pressure at each volume of the arteries or veins, whereas sympathetic inhibition decreases the pressure at each volume. Control of the vessels in this manner by the sympathetics is a valuable means for diminishing the dimensions of one segment of the circulation, thus transferring blood to other segments. For instance, an increase in vascular tone throughout the systemic circulation often causes large volumes of blood to shift into the heart, which is one of the principal methods that the body uses to increase heart pumping.

Sympathetic control of vascular capacitance is also highly important during hemorrhage. Enhancement of sympathetic tone, especially to the veins, reduces the vessel sizes enough that the circulation continues to operate almost normally even when as much as 25 percent of the total blood volume has been lost.

Delayed Compliance (Stress-Relaxation) of Vessels

The term “delayed compliance” means that a vessel exposed to increased volume at first exhibits a large increase in pressure, but progressive delayed stretching of smooth muscle in the vessel wall allows the pressure to return back toward normal over a period of minutes to hours. This effect is shown in Figure 15-2. In this figure, the pressure is recorded in a small segment of a vein that is occluded at both ends. An extra volume of blood is suddenly injected until the pressure rises from 5 to 12 mm Hg. Even though none of the blood is removed after it is injected, the pressure begins to decrease immediately and approaches about 9 mm Hg after several minutes. In other words, the volume of blood injected causes immediate elastic distention of the vein, but then the smooth muscle fibers of the vein begin to “creep” to longer lengths, and their tensions correspondingly decrease. This effect is a characteristic of all smooth muscle tissue and is called stress-relaxation, which was explained in Chapter 8.

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Figure 15-2 Effect on the intravascular pressure of injecting a volume of blood into a venous segment and later removing the excess blood, demonstrating the principle of delayed compliance.

Delayed compliance is a valuable mechanism by which the circulation can accommodate extra blood when necessary, such as after too large a transfusion. Delayed compliance in the reverse direction is one of the ways in which the circulation automatically adjusts itself over a period of minutes or hours to diminished blood volume after serious hemorrhage.

Arterial Pressure Pulsations

With each beat of the heart a new surge of blood fills the arteries. Were it not for distensibility of the arterial system, all of this new blood would have to flow through the peripheral blood vessels almost instantaneously, only during cardiac systole, and no flow would occur during diastole. However, the compliance of the arterial tree normally reduces the pressure pulsations to almost no pulsations by the time the blood reaches the capillaries; therefore, tissue blood flow is mainly continuous with very little pulsation.

A typical record of the pressure pulsations at the root of the aorta is shown in Figure 15-3. In the healthy young adult, the pressure at the top of each pulse, called the systolic pressure, is about 120 mm Hg. At the lowest point of each pulse, called the diastolic pressure, it is about 80 mm Hg. The difference between these two pressures, about 40 mm Hg, is called the pulse pressure.

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Figure 15-3 Pressure pulse contour in the ascending aorta.

Two major factors affect the pulse pressure: (1) the stroke volume output of the heart and (2) the compliance (total distensibility) of the arterial tree. A third, less important factor, is the character of ejection from the heart during systole.

In general, the greater the stroke volume output, the greater the amount of blood that must be accommodated in the arterial tree with each heartbeat, and, therefore, the greater the pressure rise and fall during systole and diastole, thus causing a greater pulse pressure. Conversely, the less the compliance of the arterial system, the greater the rise in pressure for a given stroke volume of blood pumped into the arteries. For instance, as demonstrated by the middle top curves in Figure 15-4, the pulse pressure in old age sometimes rises to as much as twice normal, because the arteries have become hardened with arteriosclerosis and therefore are relatively noncompliant.

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Figure 15-4 Aortic pressure pulse contours in arteriosclerosis, aortic stenosis, patent ductus arteriosus, and aortic regurgitation.

In effect, pulse pressure is determined approximately by the ratio of stroke volume output to compliance of the arterial tree. Any condition of the circulation that affects either of these two factors also affects the pulse pressure:

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Abnormal Pressure Pulse Contours

Some conditions of the circulation also cause abnormal contours of the pressure pulse wave in addition to altering the pulse pressure. Especially distinctive among these are aortic stenosis, patent ductus arteriosus, and aortic regurgitation, each of which is shown in Figure 15-4.

In aortic valve stenosis, the diameter of the aortic valve opening is reduced significantly, and the aortic pressure pulse is decreased significantly because of diminished blood flow outward through the stenotic valve.

In patent ductus arteriosus, one half or more of the blood pumped into the aorta by the left ventricle flows immediately backward through the wide-open ductus into the pulmonary artery and lung blood vessels, thus allowing the diastolic pressure to fall very low before the next heartbeat.

In aortic regurgitation, the aortic valve is absent or will not close completely. Therefore, after each heartbeat, the blood that has just been pumped into the aorta flows immediately backward into the left ventricle. As a result, the aortic pressure can fall all the way to zero between heartbeats. Also, there is no incisura in the aortic pulse contour because there is no aortic valve to close.

Transmission of Pressure Pulses to the Peripheral Arteries

When the heart ejects blood into the aorta during systole, at first only the proximal portion of the aorta becomes distended because the inertia of the blood prevents sudden blood movement all the way to the periphery. However, the rising pressure in the proximal aorta rapidly overcomes this inertia, and the wave front of distention spreads farther and farther along the aorta, as shown in Figure 15-5. This is called transmission of the pressure pulse in the arteries.

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Figure 15-5 Progressive stages in transmission of the pressure pulse along the aorta.

The velocity of pressure pulse transmission in the normal aorta is 3 to 5 m/sec; in the large arterial branches, 7 to 10 m/sec; and in the small arteries, 15 to 35 m/sec. In general, the greater the compliance of each vascular segment, the slower the velocity, which explains the slow transmission in the aorta and the much faster transmission in the much less compliant small distal arteries. In the aorta, the velocity of transmission of the pressure pulse is 15 or more times the velocity of blood flow because the pressure pulse is simply a moving wave of pressure that involves little forward total movement of blood volume.

Damping of the Pressure Pulses in the Smaller Arteries, Arterioles, and Capillaries

Figure 15-6 shows typical changes in the contours of the pressure pulse as the pulse travels into the peripheral vessels. Note especially in the three lower curves that the intensity of pulsation becomes progressively less in the smaller arteries, the arterioles, and, especially, the capillaries. In fact, only when the aortic pulsations are extremely large or the arterioles are greatly dilated can pulsations be observed in the capillaries.

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Figure 15-6 Changes in the pulse pressure contour as the pulse wave travels toward the smaller vessels.

This progressive diminution of the pulsations in the periphery is called damping of the pressure pulses. The cause of this is twofold: (1) resistance to blood movement in the vessels and (2) compliance of the vessels. The resistance damps the pulsations because a small amount of blood must flow forward at the pulse wave front to distend the next segment of the vessel; the greater the resistance, the more difficult it is for this to occur. The compliance damps the pulsations because the more compliant a vessel, the greater the quantity of blood required at the pulse wave front to cause an increase in pressure. Therefore, the degree of damping is almost directly proportional to the product of resistance times compliance.

Clinical Methods for Measuring Systolic and Diastolic Pressures

It is not reasonable to use pressure recorders that require needle insertion into an artery for making routine arterial pressure measurements in human patients, although these are used on occasion when special studies are necessary. Instead, the clinician determines systolic and diastolic pressures by indirect means, usually by the auscultatory method.

Auscultatory Method

Figure 15-7 shows the auscultatory method for determining systolic and diastolic arterial pressures. A stethoscope is placed over the antecubital artery and a blood pressure cuff is inflated around the upper arm. As long as the cuff continues to compress the arm with too little pressure to close the brachial artery, no sounds are heard from the antecubital artery with the stethoscope. However, when the cuff pressure is great enough to close the artery during part of the arterial pressure cycle, a sound then is heard with each pulsation. These sounds are called Korotkoff sounds, named after Nikolai Korotkoff, a Russian physician who described them in 1905.

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Figure 15-7 Auscultatory method for measuring systolic and diastolic arterial pressures.

The Korotkoff sounds are believed to be caused mainly by blood jetting through the partly occluded vessel and by vibrations of the vessel wall. The jet causes turbulence in the vessel beyond the cuff, and this sets up the vibrations heard through the stethoscope.

In determining blood pressure by the auscultatory method, the pressure in the cuff is first elevated well above arterial systolic pressure. As long as this cuff pressure is higher than systolic pressure, the brachial artery remains collapsed so that no blood jets into the lower artery during any part of the pressure cycle. Therefore, no Korotkoff sounds are heard in the lower artery. But then the cuff pressure gradually is reduced. Just as soon as the pressure in the cuff falls below systolic pressure (point B, Figure 15-7), blood begins to slip through the artery beneath the cuff during the peak of systolic pressure, and one begins to hear tapping sounds from the antecubital artery in synchrony with the heartbeat. As soon as these sounds begin to be heard, the pressure level indicated by the manometer connected to the cuff is about equal to the systolic pressure.

As the pressure in the cuff is lowered still more, the Korotkoff sounds change in quality, having less of the tapping quality and more of a rhythmical and harsher quality. Then, finally, when the pressure in the cuff falls near diastolic pressure, the sounds suddenly change to a muffled quality (point C, Figure 15-7). One notes the manometer pressure when the Korotkoff sounds change to the muffled quality and this pressure is about equal to the diastolic pressure, although it slightly overestimates the diastolic pressure determined by direct intra-arterial catheter. As the cuff pressure falls a few mm Hg further, the artery no longer closes during diastole, which means that the basic factor causing the sounds (the jetting of blood through a squeezed artery) is no longer present. Therefore, the sounds disappear entirely. Many clinicians believe that the pressure at which the Korotkoff sounds completely disappear should be used as the diastolic pressure, except in situations in which the disappearance of sounds cannot reliably be determined because sounds are audible even after complete deflation of the cuff. For example, in patients with arteriovenous fistulas for hemodialysis or with aortic insufficiency, Korotkoff sounds may be heard after complete deflation of the cuff.

The auscultatory method for determining systolic and diastolic pressures is not entirely accurate, but it usually gives values within 10 percent of those determined by direct catheter measurement from inside the arteries.

Normal Arterial Pressures as Measured by the Auscultatory Method

Figure 15-8 shows the approximate normal systolic and diastolic arterial pressures at different ages. The progressive increase in pressure with age results from the effects of aging on the blood pressure control mechanisms. We shall see in Chapter 19 that the kidneys are primarily responsible for this long-term regulation of arterial pressure; and it is well known that the kidneys exhibit definitive changes with age, especially after the age of 50 years.

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Figure 15-8 Changes in systolic, diastolic, and mean arterial pressures with age. The shaded areas show the approximate normal ranges.

A slight extra increase in systolic pressure usually occurs beyond the age of 60 years. This results from decreasing distensibility, or “hardening,” of the arteries, which is often a result of atherosclerosis. The final effect is a higher systolic pressure with considerable increase in pulse pressure, as previously explained.

Mean Arterial Pressure

The mean arterial pressure is the average of the arterial pressures measured millisecond by millisecond over a period of time. It is not equal to the average of systolic and diastolic pressure because at normal heart rates, a greater fraction of the cardiac cycle is spent in diastole than is systole; thus, the arterial pressure remains nearer to diastolic pressure than to systolic pressure during the greater part of the cardiac cycle. The mean arterial pressure is therefore determined about 60 percent by the diastolic pressure and 40 percent by the systolic pressure. Note in Figure 15-8 that the mean pressure (solid green line) at all ages is nearer to the diastolic pressure than to the systolic pressure. However, at very high heart rates diastole comprises a smaller fraction of the cardiac cycle and the mean arterial pressure is more closely approximated as the average of systolic and diastolic pressures.

Veins and Their Functions

For years, the veins were considered to be nothing more than passageways for flow of blood to the heart, but it is now apparent that they perform other special functions that are necessary for operation of the circulation. Especially important, they are capable of constricting and enlarging and thereby storing either small or large quantities of blood and making this blood available when it is required by the remainder of the circulation. The peripheral veins can also propel blood forward by means of a so-called venous pump, and they even help to regulate cardiac output, an exceedingly important function that is described in detail in Chapter 20.

Venous Pressures—Right Atrial Pressure (Central Venous Pressure) and Peripheral Venous Pressures

To understand the various functions of the veins, it is first necessary to know something about pressure in the veins and what determines the pressure.

Blood from all the systemic veins flows into the right atrium of the heart; therefore, the pressure in the right atrium is called the central venous pressure.

Right atrial pressure is regulated by a balance between (1) the ability of the heart to pump blood out of the right atrium and ventricle into the lungs and (2) the tendency for blood to flow from the peripheral veins into the right atrium. If the right heart is pumping strongly, the right atrial pressure decreases. Conversely, weakness of the heart elevates the right atrial pressure. Also, any effect that causes rapid inflow of blood into the right atrium from the peripheral veins elevates the right atrial pressure. Some of the factors that can increase this venous return (and thereby increase the right atrial pressure) are (1) increased blood volume, (2) increased large vessel tone throughout the body with resultant increased peripheral venous pressures, and (3) dilatation of the arterioles, which decreases the peripheral resistance and allows rapid flow of blood from the arteries into the veins.

The same factors that regulate right atrial pressure also contribute to regulation of cardiac output because the amount of blood pumped by the heart depends on both the ability of the heart to pump and the tendency for blood to flow into the heart from the peripheral vessels. Therefore, we will discuss regulation of right atrial pressure in much more depth in Chapter 20 in connection with regulation of cardiac output.

The normal right atrial pressure is about 0 mm Hg, which is equal to the atmospheric pressure around the body. It can increase to 20 to 30 mm Hg under very abnormal conditions, such as (1) serious heart failure or (2) after massive transfusion of blood, which greatly increases the total blood volume and causes excessive quantities of blood to attempt to flow into the heart from the peripheral vessels.

The lower limit to the right atrial pressure is usually about −3 to −5 mm Hg below atmospheric pressure. This is also the pressure in the chest cavity that surrounds the heart. The right atrial pressure approaches these low values when the heart pumps with exceptional vigor or when blood flow into the heart from the peripheral vessels is greatly depressed, such as after severe hemorrhage.

Venous Resistance and Peripheral Venous Pressure

Large veins have so little resistance to blood flow when they are distended that the resistance then is almost zero and is of almost no importance. However, as shown in Figure 15-9, most of the large veins that enter the thorax are compressed at many points by the surrounding tissues so that blood flow is impeded at these points. For instance, the veins from the arms are compressed by their sharp angulations over the first rib. Also, the pressure in the neck veins often falls so low that the atmospheric pressure on the outside of the neck causes these veins to collapse. Finally, veins coursing through the abdomen are often compressed by different organs and by the intra-abdominal pressure, so they usually are at least partially collapsed to an ovoid or slitlike state. For these reasons, the large veins do usually offer some resistance to blood flow, and because of this, the pressure in the more peripheral small veins in a person lying down is usually +4 to +6 mm Hg greater than the right atrial pressure.

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Figure 15-9 Compression points that tend to collapse the veins entering the thorax.

Effect of High Right Atrial Pressure on Peripheral Venous Pressure

When the right atrial pressure rises above its normal value of 0 mm Hg, blood begins to back up in the large veins. This enlarges the veins, and even the collapse points in the veins open up when the right atrial pressure rises above +4 to +6 mm Hg. Then, as the right atrial pressure rises still further, the additional increase causes a corresponding rise in peripheral venous pressure in the limbs and elsewhere. Because the heart must be weakened to cause a rise in right atrial pressure as high as +4 to +6 mm Hg, one often finds that the peripheral venous pressure is not noticeably elevated even in the early stages of heart failure.

Effect of Intra-abdominal Pressure on Venous Pressures of the Leg

The pressure in the abdominal cavity of a recumbent person normally averages about +6 mm Hg, but it can rise to +15 to +30 mm Hg as a result of pregnancy, large tumors, abdominal obesity, or excessive fluid (called “ascites”) in the abdominal cavity. When the intra-abdominal pressure does rise, the pressure in the veins of the legs must rise above the abdominal pressure before the abdominal veins will open and allow the blood to flow from the legs to the heart. Thus, if the intra-abdominal pressure is +20 mm Hg, the lowest possible pressure in the femoral veins is also about +20 mm Hg.

Effect of Gravitational Pressure on Venous Pressure

In any body of water that is exposed to air, the pressure at the surface of the water is equal to atmospheric pressure, but the pressure rises 1 mm Hg for each 13.6 millimeters of distance below the surface. This pressure results from the weight of the water and therefore is called gravitational pressure or hydrostatic pressure.

Gravitational pressure also occurs in the vascular system of the human being because of weight of the blood in the vessels, as shown in Figure 15-10. When a person is standing, the pressure in the right atrium remains about 0 mm Hg because the heart pumps into the arteries any excess blood that attempts to accumulate at this point. However, in an adult who is standing absolutely still, the pressure in the veins of the feet is about +90 mm Hg simply because of the gravitational weight of the blood in the veins between the heart and the feet. The venous pressures at other levels of the body are proportionately between 0 and 90 mm Hg.

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Figure 15-10 Effect of gravitational pressure on the venous pressures throughout the body in the standing person.

In the arm veins, the pressure at the level of the top rib is usually about +6 mm Hg because of compression of the subclavian vein as it passes over this rib. The gravitational pressure down the length of the arm then is determined by the distance below the level of this rib. Thus, if the gravitational difference between the level of the rib and the hand is +29 mm Hg, this gravitational pressure is added to the +6 mm Hg pressure caused by compression of the vein as it crosses the rib, making a total of +35 mm Hg pressure in the veins of the hand.

The neck veins of a person standing upright collapse almost completely all the way to the skull because of atmospheric pressure on the outside of the neck. This collapse causes the pressure in these veins to remain at zero along their entire extent. The reason for this is that any tendency for the pressure to rise above this level opens the veins and allows the pressure to fall back to zero because of flow of the blood. Conversely, any tendency for the neck vein pressure to fall below zero collapses the veins still more, which further increases their resistance and again returns the pressure back to zero.

The veins inside the skull, on the other hand, are in a noncollapsible chamber (the skull cavity) so that they cannot collapse. Consequently, negative pressure can exist in the dural sinuses of the head; in the standing position, the venous pressure in the sagittal sinus at the top of the brain is about −10 mm Hg because of the hydrostatic “suction” between the top of the skull and the base of the skull. Therefore, if the sagittal sinus is opened during surgery, air can be sucked immediately into the venous system; the air may even pass downward to cause air embolism in the heart, and death can ensue.

Effect of the Gravitational Factor on Arterial and Other Pressures

The gravitational factor also affects pressures in the peripheral arteries and capillaries, in addition to its effects in the veins. For instance, a standing person who has a mean arterial pressure of 100 mm Hg at the level of the heart has an arterial pressure in the feet of about 190 mm Hg. Therefore, when one states that the arterial pressure is 100 mm Hg, this generally means that this is the pressure at the gravitational level of the heart but not necessarily elsewhere in the arterial vessels.

Venous Valves and the “Venous Pump”: Their Effects on Venous Pressure

Were it not for valves in the veins, the gravitational pressure effect would cause the venous pressure in the feet always to be about +90 mm Hg in a standing adult. However, every time one moves the legs, one tightens the muscles and compresses the veins in or adjacent to the muscles, and this squeezes the blood out of the veins. But the valves in the veins, shown in Figure 15-11, are arranged so that the direction of venous blood flow can be only toward the heart. Consequently, every time a person moves the legs or even tenses the leg muscles, a certain amount of venous blood is propelled toward the heart. This pumping system is known as the “venous pump” or “muscle pump,” and it is efficient enough that under ordinary circumstances, the venous pressure in the feet of a walking adult remains less than +20 mm Hg.

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Figure 15-11 Venous valves of the leg.

If a person stands perfectly still, the venous pump does not work, and the venous pressures in the lower legs increase to the full gravitational value of 90 mm Hg in about 30 seconds. The pressures in the capillaries also increase greatly, causing fluid to leak from the circulatory system into the tissue spaces. As a result, the legs swell and the blood volume diminishes. Indeed, 10 to 20 percent of the blood volume can be lost from the circulatory system within the 15 to 30 minutes of standing absolutely still, as often occurs when a soldier is made to stand at rigid attention.

Venous Valve Incompetence Causes “Varicose” Veins

The valves of the venous system frequently become “incompetent” or sometimes even are destroyed. This is especially true when the veins have been overstretched by excess venous pressure lasting weeks or months, as occurs in pregnancy or when one stands most of the time. Stretching the veins increases their cross-sectional areas, but the leaflets of the valves do not increase in size. Therefore, the leaflets of the valves no longer close completely. When this develops, the pressure in the veins of the legs increases greatly because of failure of the venous pump; this further increases the sizes of the veins and finally destroys the function of the valves entirely. Thus, the person develops “varicose veins,” which are characterized by large, bulbous protrusions of the veins beneath the skin of the entire leg, particularly the lower leg.

Whenever people with varicose veins stand for more than a few minutes, the venous and capillary pressures become very high and leakage of fluid from the capillaries causes constant edema in the legs. The edema in turn prevents adequate diffusion of nutritional materials from the capillaries to the muscle and skin cells, so the muscles become painful and weak and the skin frequently becomes gangrenous and ulcerates. The best treatment for such a condition is continual elevation of the legs to a level at least as high as the heart. Tight binders on the legs also can be of considerable assistance in preventing the edema and its sequelae.

Clinical Estimation of Venous Pressure

The venous pressure often can be estimated by simply observing the degree of distention of the peripheral veins—especially of the neck veins. For instance, in the sitting position, the neck veins are never distended in the normal quietly resting person. However, when the right atrial pressure becomes increased to as much as +10 mm Hg, the lower veins of the neck begin to protrude; and at +15 mm Hg atrial pressure essentially all the veins in the neck become distended.

Direct Measurement of Venous Pressure and Right Atrial Pressure

Venous pressure can also be measured with ease by inserting a needle directly into a vein and connecting it to a pressure recorder. The only means by which right atrial pressure can be measured accurately is by inserting a catheter through the peripheral veins and into the right atrium. Pressures measured through such central venous catheters are used almost routinely in some types of hospitalized cardiac patients to provide constant assessment of heart pumping ability.

Pressure Reference Level for Measuring Venous and Other Circulatory Pressures

In discussions up to this point, we often have spoken of right atrial pressure as being 0 mm Hg and arterial pressure as being 100 mm Hg, but we have not stated the gravitational level in the circulatory system to which this pressure is referred. There is one point in the circulatory system at which gravitational pressure factors caused by changes in body position of a healthy person usually do not affect the pressure measurement by more than 1 to 2 mm Hg. This is at or near the level of the tricuspid valve, as shown by the crossed axes in Figure 15-12. Therefore, all circulatory pressure measurements discussed in this text are referred to this level, which is called the reference level for pressure measurement.

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Figure 15-12 Reference point for circulatory pressure measurement (located near the tricuspid valve).

The reason for lack of gravitational effects at the tricuspid valve is that the heart automatically prevents significant gravitational changes in pressure at this point in the following way:

If the pressure at the tricuspid valve rises slightly above normal, the right ventricle fills to a greater extent than usual, causing the heart to pump blood more rapidly and therefore to decrease the pressure at the tricuspid valve back toward the normal mean value. Conversely, if the pressure falls, the right ventricle fails to fill adequately, its pumping decreases, and blood dams up in the venous system until the pressure at the tricuspid level again rises to the normal value. In other words, the heart acts as a feedback regulator of pressure at the tricuspid valve.

When a person is lying on his or her back, the tricuspid valve is located at almost exactly 60 percent of the chest thickness in front of the back. This is the zero pressure reference level for a person lying down.

Blood Reservoir Function of the Veins

As pointed out in Chapter 14, more than 60 percent of all the blood in the circulatory system is usually in the veins. For this reason and also because the veins are so compliant, it is said that the venous system serves as a blood reservoir for the circulation.

When blood is lost from the body and the arterial pressure begins to fall, nervous signals are elicited from the carotid sinuses and other pressure-sensitive areas of the circulation, as discussed in Chapter 18. These in turn elicit nerve signals from the brain and spinal cord mainly through sympathetic nerves to the veins, causing them to constrict. This takes up much of the slack in the circulatory system caused by the lost blood. Indeed, even after as much as 20 percent of the total blood volume has been lost, the circulatory system often functions almost normally because of this variable reservoir function of the veins.

Specific Blood Reservoirs

Certain portions of the circulatory system are so extensive and/or so compliant that they are called “specific blood reservoirs.” These include (1) the spleen, which sometimes can decrease in size sufficiently to release as much as 100 milliliters of blood into other areas of the circulation; (2) the liver, the sinuses of which can release several hundred milliliters of blood into the remainder of the circulation; (3) the large abdominal veins, which can contribute as much as 300 milliliters; and (4) the venous plexus beneath the skin, which also can contribute several hundred milliliters. The heart and the lungs, although not parts of the systemic venous reservoir system, must also be considered blood reservoirs. The heart, for instance, shrinks during sympathetic stimulation and in this way can contribute some 50 to 100 milliliters of blood; the lungs can contribute another 100 to 200 milliliters when the pulmonary pressures decrease to low values.

The Spleen as a Reservoir for Storing Red Blood Cells

Figure 15-13 shows that the spleen has two separate areas for storing blood: the venous sinuses and the pulp. The sinuses can swell the same as any other part of the venous system and store whole blood.

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Figure 15-13 Functional structures of the spleen.

(Courtesy Dr. Don W. Fawcett, Montana.)

In the splenic pulp, the capillaries are so permeable that whole blood, including the red blood cells, oozes through the capillary walls into a trabecular mesh, forming the red pulp. The red cells are trapped by the trabeculae, while the plasma flows on into the venous sinuses and then into the general circulation. As a consequence, the red pulp of the spleen is a special reservoir that contains large quantities of concentrated red blood cells. These can then be expelled into the general circulation whenever the sympathetic nervous system becomes excited and causes the spleen and its vessels to contract. As much as 50 milliliters of concentrated red blood cells can be released into the circulation, raising the hematocrit 1 to 2 percent.

In other areas of the splenic pulp are islands of white blood cells, which collectively are called the white pulp. Here lymphoid cells are manufactured similar to those manufactured in the lymph nodes. They are part of the body’s immune system, described in Chapter 34.

Blood-Cleansing Function of the Spleen—Removal of Old Cells

Blood cells passing through the splenic pulp before entering the sinuses undergo thorough squeezing. Therefore, it is to be expected that fragile red blood cells would not withstand the trauma. For this reason, many of the red blood cells destroyed in the body have their final demise in the spleen. After the cells rupture, the released hemoglobin and the cell stroma are digested by the reticuloendothelial cells of the spleen, and the products of digestion are mainly reused by the body as nutrients, often for making new blood cells.

Reticuloendothelial Cells of the Spleen

The pulp of the spleen contains many large phagocytic reticuloendothelial cells, and the venous sinuses are lined with similar cells. These cells function as part of a cleansing system for the blood, acting in concert with a similar system of reticuloendothelial cells in the venous sinuses of the liver. When the blood is invaded by infectious agents, the reticuloendothelial cells of the spleen rapidly remove debris, bacteria, parasites, and so forth. Also, in many chronic infectious processes, the spleen enlarges in the same manner that lymph nodes enlarge and then performs its cleansing function even more avidly.

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