Cardiac Output, Venous Return, and Their Regulation PDF

CHAPTER 20 UNIT IV Cardiac Output, Venous Return, and Their Reg...

CHAPTER 20 UNIT IV Cardiac Output, Venous Return, and Their Regulation Cardiac output is the quantity of blood pumped into the Effect of Age on Cardiac Output. Figure 20-1 shows aorta each minute by the heart. This is also the quantity of the cardiac output, expressed as cardiac index, at differ- blood that flows through the circulation. Because cardiac ent ages. The cardiac index rises rapidly to a level greater output is the sum of the blood flow to all the tissues of the than 4 L/min/m2 at age 10 years and declines to about 2.4 body, it is one of the most important factors to consider in L/min/m2 at age 80 years. We explain later in this chapter relation to function of the cardiovascular system. that the cardiac output is regulated throughout life almost Venous return is equally important because it is the directly in proportion to overall metabolic activity. There- quantity of blood flowing from the veins into the right fore, the declining cardiac index is indicative of declining atrium each minute. The venous return and the cardiac activity and/or declining muscle mass with age. output must equal each other except for a few heartbeats when blood is temporarily stored in or removed from the CONTROL OF CARDIAC OUTPUT BY heart and lungs. VENOUS RETURN—FRANK-STARLING MECHANISM OF THE HEART NORMAL VALUES FOR CARDIAC Although heart function is obviously crucial in determin- OUTPUT AT REST AND DURING ing cardiac output, the various factors of the peripheral ACTIVITY circulation that affect flow of blood into the heart from Cardiac output varies widely with the level of activity of the veins, called venous return, are normally the primary the body. The following factors, among others, directly controllers of cardiac output. affect cardiac output: (1) the basic level of body metabo- The main reason why peripheral factors are usually so lism; (2) whether the person is exercising; (3) the person’s important in controlling cardiac output is that the heart age; and (4) the size of the body. has a built-in mechanism that normally allows it to pump For young healthy men, resting cardiac output averages automatically the amount of blood that flows from the about 5.6 L/min. For women, this value is about 4.9 L/min. veins into the right atrium. This mechanism, called the When one considers the factor of age as well—because Frank-Starling law of the heart, was discussed in Chapter with increasing age, body activity and mass of some tis- 9. Basically, this law states that when increased quanti- sues (e.g., skeletal muscle) diminish—the average cardiac ties of blood flow into the heart, the increased volume output for the resting adult, in round numbers, is often of blood stretches the walls of the heart chambers. As a stated to be about 5 L/min. However, cardiac output var- result of the stretch, the cardiac muscle contracts with ies considerably among healthy men and women depend- increased force, and this action ejects the extra blood that ing on muscle mass, adiposity, physical activity, and other has entered from the systemic circulation. Therefore, the factors that influence metabolic rate and nutritional needs blood that flows into the heart is automatically pumped of the tissues. without delay into the aorta and flows again through the circulation. Cardiac Index Another important factor, discussed in Chapters 10 and 18, is that stretching the heart causes an increased heart rate. Experiments have shown that the cardiac output increases approximately in proportion to the surface area of the body. Stretch of the sinus node in the wall of the right atrium has Therefore, cardiac output is frequently stated in terms of a direct effect on the rhythmicity of the node to increase the the cardiac index, which is the cardiac output per square heart rate as much as 10% to 15%. In addition, the stretched meter of body surface area. The average person who weighs right atrium initiates a nervous reflex called the Bainbridge 70 kilograms has a body surface area of about 1.7 square reflex, passing first to the vasomotor center of the brain and meters, which means that the normal average cardiac index then back to the heart by way of the sympathetic nerves and for adults is about 3 L/min/m2 of body surface area. vagi, which also increases the heart rate. 245 UNIT IV The Circulation Cardiac output = Total tissue blood flow 4 4 Cardiac index (L/min/m2) 3 3 Right heart Lungs Left heart 2 2 14% Brain 4% Heart 1 1 Venous Cardiac return Splanchnic 27% output (vena cava) circulation (aorta) 0 0 22% Kidneys (years) 0 10 20 30 40 50 60 70 80 Age 15% Muscle Figure 20-1. Cardiac index for a person—cardiac output per square (inactive) meter of surface area—at different ages. (Modified from Guyton AC, Jones CE, Coleman TG: Circulatory Physiology: Cardiac Output and Its 18% Skin, other Regulation, 2nd ed. Philadelphia: WB Saunders, 1973.) tissues Figure 20-2. Cardiac output is equal to venous return and is the sum Under most normal unstressed conditions, the cardiac of tissue and organ blood flows. Except when the heart is severely output is controlled mainly by peripheral factors that weakened and unable to pump the venous return adequately, cardiac determine venous return. However, as we discuss later output (total tissue blood flow) is determined mainly by the metabolic in the chapter, if the returning blood does become more needs of the tissues and organs of the body. than the heart can pump, then the heart becomes the lim- iting factor that determines cardiac output. Cardiac output 35 Oxygen consumption (L/min) and cardiac index Cardiac Output Is the Sum of All Tissue Cardiac output (L/min) 30 Oxygen Cardiac index (L/min/m2) Blood Flows—Tissue Metabolism 15 consumption 4 25 Regulates Most Local Blood Flow 20 3 The venous return to the heart is the sum of all the local 10 15 blood flow through all the individual tissue segments of 2 the peripheral circulation (Figure 20-2). Therefore, it fol- 5 10 1 lows that cardiac output regulation is normally the sum of 5 all the local blood flow regulations. 0 0 0 The mechanisms of local blood flow regulation were 0 400 800 1200 1600 discussed in Chapter 17. In most tissues, blood flow Work output during exercise (kg-m/min) increases mainly in proportion to each tissue’s metab- Figure 20-3. Effect of increasing levels of exercise to increase car- olism. For example, local blood flow almost always diac output (red solid line) and oxygen consumption (blue dashed increases when tissue oxygen consumption increases; this line). (Modified from Guyton AC, Jones CE, Coleman TG: Circulatory effect is demonstrated in Figure 20-3 for different lev- Physiology: Cardiac Output and Its Regulation, 2nd ed. Philadelphia: WB Saunders, 1973.) els of exercise. Note that at each increasing level of work output during exercise, oxygen consumption and cardiac output increase in parallel to each other. output control: Under many conditions, the long-term To summarize, cardiac output is usually determined cardiac output level varies reciprocally with changes in by the sum of all the various factors throughout the body total peripheral vascular resistance as long as the arterial that control local blood flow. All the local blood flows pressure is unchanged. Note in Figure 20-4 that when summate to form the venous return, and the heart auto- the total peripheral resistance is exactly normal (at the matically pumps this returning blood back into the arter- 100% mark in the figure), the cardiac output is also nor- ies to flow around the system again. mal. Then, when the total peripheral resistance increases above normal, the cardiac output falls; conversely, when Cardiac Output Varies Inversely With Total Peripheral the total peripheral resistance decreases, the cardiac out- Resistance When Arterial Pressure Is Unchanged. Fig- put increases. One can easily understand this phenom- ure 20-3 is the same as Figure 19-5. It is repeated here enon by reconsidering one of the forms of Ohm’s law, as to illustrate an extremely important principle in cardiac expressed in Chapter 14: 246  Chapter 20 Cardiac Output, Venous Return, and Their Regulation Removal of both arms and legs 25 Beriberi Hyperthyroidism AV shunts Pulmonary disease Paget’s disease 20 Arterial pressure or cardiac output 200 Hypereffective Cardiac output (L/min) Hypothyroidism UNIT IV Ca 15 Normal 150 ia rd (% of normal) c Normal Anemia 100 10 out put Hypoeffective 50 5 0 0 40 60 80 100 120 140 160 −4 0 +4 +8 Total peripheral resistance Right atrial pressure (mm Hg) (% of normal) Figure 20-5. Cardiac output curves for the normal heart and for Figure 20-4. Chronic effect of different levels of total peripheral hypoeffective and hypereffective hearts. (Modified from Guyton AC, resistance on cardiac output, showing a reciprocal relationship be- Jones CE, Coleman TG: Circulatory Physiology: Cardiac Output and Its tween total peripheral resistance and cardiac output. AV, Atrioven- Regulation, 2nd ed. Philadelphia: WB Saunders, 1973.) tricular. (Modified from Guyton AC: Arterial Pressure and Hyperten- sion. Philadelphia: WB Saunders, 1980.) Nervous Excitation Can Increase Heart Pumping. Arterial pressure In Chapter 9, we saw that a combination of sympathet- Cardiac output = Total peripheral resistance ic stimulation and parasympathetic inhibition does two things to increase the pumping effectiveness of the heart: Thus, any time the long-term level of total peripheral (1) it greatly increases the heart rate—sometimes, in resistance changes (but no other functions of the circula- young people, from the normal level of 72 beats/min up to tion change), the cardiac output changes quantitatively in 180 to 200 beats/min—and (2) it increases the strength of exactly the opposite direction. heart contraction (called increased contractility) to twice its normal strength. Combining these two effects, maxi- Limits for the Cardiac Output mal nervous excitation of the heart can raise the plateau There are definite limits to the amount of blood that the level of the cardiac output curve to almost twice the pla- heart can pump, which can be expressed quantitatively in teau of the normal curve, as shown by the 25-L/min level the form of cardiac output curves. of the uppermost curve in Figure 20-5. Figure 20-5 demonstrates the normal cardiac output curve, showing the cardiac output per minute at each level Heart Hypertrophy Can Increase Pumping Effectiveness. of right atrial pressure. This is one type of cardiac func- A long-term increased workload, but not so much excess tion curve, which was discussed in Chapter 9. Note that load that it damages the heart, causes the heart muscle to the plateau level of this normal cardiac output curve is increase in mass and contractile strength in the same way about 13 L/min, 2.5 times the normal cardiac output of that heavy exercise causes skeletal muscles to hypertrophy. about 5 L/min. This means that the normal human heart, For example, the hearts of marathon runners may be in- functioning without any special stimulation, can pump a creased in mass by 50% to 75%. This factor increases the venous return up to about 2.5 times the normal venous plateau level of the cardiac output curve, sometimes 60% to return before the heart becomes a limiting factor in the 100%, and therefore allows the heart to pump much greater control of cardiac output. than the usual amounts of cardiac output. Shown in Figure 20-5 are several other cardiac output When one combines nervous excitation of the heart and curves for hearts that are not pumping normally. The upper- hypertrophy, as occurs in marathon runners, the total effect most curves are for hypereffective hearts that are pumping can allow the heart to pump as much 30 to 40 L/min, about better than normal. The lowermost curves are for hypoeffec- 2.5 times the level that can be achieved in the average person. tive hearts that are pumping at levels below normal. This increased level of pumping is one of the most important factors in determining the runner’s running time. Factors That Cause a Hypereffective Heart Two general types of factors that can make the heart a Factors That Cause a Hypoeffective Heart stronger pump than normal are nervous stimulation and Any factor that decreases the heart’s ability to pump hypertrophy of the heart muscle. blood causes hypoeffectivity. Some of the factors that 247 UNIT IV The Circulation can decrease the heart’s ability to pump blood are the Chapter 18, is essential to achieve high cardiac outputs following: when the peripheral tissues dilate their blood vessels to
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IZQPYJB However, the nervous system immediately compensates. The same brain activity that sends motor signals to the muscles sends simultaneous signals into the autonomic NERVOUS SYSTEM REGULATION OF nervous centers of the brain to excite circulatory activity, CARDIAC OUTPUT causing large vein constriction, increased heart rate, and Importance of Nervous System For Maintaining Ar- increased contractility of the heart. All these changes act- terial Pressure When Peripheral Blood Vessels Are ing together increase the arterial pressure above normal, Dilated and Venous Return and Cardiac Output In- which in turn forces still more blood flow through the ac- crease. Figure 20-6 shows an important difference in tive muscles. cardiac output control with and without a functioning In summary, when local tissue blood vessels dilate and autonomic nervous system. The solid curves demon- increase venous return and cardiac output above normal, strate the effect in the normal dog of intense dilation of the nervous system plays a key role in preventing the arte- the peripheral blood vessels caused by administering the rial pressure from falling to disastrously low levels. During drug dinitrophenol, which increased the metabolism of exercise, the nervous system goes even further, providing virtually all tissues of the body about fourfold. With nerv- additional signals to raise the arterial pressure above nor- ous control mechanisms intact, dilating all the peripheral mal, which serves to increase the cardiac output an extra blood vessels caused almost no change in arterial pressure 30% to 100%. but increased the cardiac output almost fourfold. How- ever, after autonomic control of the nervous system was Pathologically High or Low Cardiac Outputs blocked, vasodilation of the blood vessels with dinitro-.VMUJQMF
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phenol (dashed curves) then caused a profound fall in ar- cardiac outputs. Some of the more important of these ab- terial pressure to about one-half normal, and the cardiac normal cardiac outputs are shown in Figure 20-7. output increased only 1.6-fold instead of fourfold. Thus, maintenance of a normal arterial pressure by High Cardiac Output Caused by Reduced Total the nervous system reflexes, by mechanisms explained in Peripheral Resistance The left side of Figure 20-7 identifies conditions that cause With nervous control abnormally high cardiac outputs. One of the distinguish- Without nervous control ing features of these conditions is that they all result from 6 chronically reduced total peripheral resistance None of Cardiac output Dinitrophenol 5 them result from excessive excitation of the heart itself, (L/min) 4 which we will explain subsequently. Let us consider some 3 of the conditions that can decrease the peripheral resist- 2 ance and at the same time increase the cardiac output to 0 above normal. 1. Beriberi. This disease is caused by insufficient quantity Arterial pressure 100 of the vitamin thiamine (vitamin B1) in the diet. Lack (mm Hg) 75 of this vitamin causes diminished ability of the tis- sues to use some cellular nutrients, and the local tissue 50 blood flow control mechanisms in turn cause marked 0 compensatory peripheral vasodilation. Sometimes the 0 10 20 30 total peripheral resistance decreases to as little as half- Minutes normal. Consequently, the long-term levels of venous Figure 20-6. Experiment in a dog to demonstrate the importance return and cardiac output also may increase to twice the of nervous maintenance of the arterial pressure as a prerequisite for normal value. cardiac output control. Note that with pressure control, the meta- 2. Arteriovenous (AV) fistula (shunt). Earlier, we pointed out bolic stimulant dinitrophenol increased cardiac output greatly; with- that whenever a fistula (also called an AV shunt) occurs out pressure control, the arterial pressure fell, and the cardiac output between a major artery and major vein, large amounts increased very little. (Drawn from experiments by Dr. M. Banet.) 248  Chapter 20 Cardiac Output, Venous Return, and Their Regulation of blood flow directly from the artery into the vein. This (4) cardiac tamponade; and (5) cardiac metabolic derange- also greatly decreases the total peripheral resistance and, ments. The effects of several of these conditions are shown likewise, increases the venous return and cardiac output. on the right in Figure 20-7, demonstrating the low cardiac 3. Hyperthyroidism. In hyperthyroidism, the metabolism outputs that result. of most tissues of the body becomes greatly increased. When the cardiac output falls so low that the tissues Oxygen usage increases, and vasodilator products are throughout the body begin to suffer nutritional deficiency, UNIT IV released from the tissues. Therefore, total peripheral the condition is called cardiac shock. This condition is dis- resistance decreases markedly because of local tissue cussed in Chapter 22 in relationship to cardiac failure. blood flow control reactions throughout the body; con- Decreased Cardiac Output Caused by Noncardiac sequently, venous return and cardiac output often in- Peripheral Factors—Decreased Venous Return. Anything crease to 40% to 80% above normal. that interferes with venous return also can lead to decreased 4. Anemia. In anemia, two peripheral effects greatly de- cardiac output. Some of these factors are as follows: crease total peripheral resistance. One of these effects 1. Decreased blood volume. The most common noncardiac is reduced viscosity of the blood, resulting from the peripheral factor that leads to decreased cardiac output decreased concentration of red blood cells. The other is decreased blood volume, often from hemorrhage. effect is diminished delivery of oxygen to the tissues, Loss of blood may decrease the filling of the vascular which causes local vasodilation. As a consequence, car- system to such a low level that there is not enough blood diac output increases greatly. in the peripheral vessels to create peripheral vascular Any other factor that decreases total peripheral resist- pressures high enough to push the blood back to the ance chronically also increases cardiac output if arterial heart. pressure does not decrease too much. 2. Acute venous dilation. Acute venous dilation results most often when the sympathetic nervous system sud- Low Cardiac Output denly becomes inactive. For example, fainting often Figure 20-7 shows at the far right several conditions that results from sudden loss of sympathetic nervous sys- cause abnormally low cardiac output. These conditions fall tem activity, which causes the peripheral capacitative into two categories: (1) abnormalities that decrease pump- vessels, especially the veins, to dilate markedly. This ing effectiveness of the heart; and (2) those that decrease dilation decreases the filling pressure of the vascular venous return. system because the blood volume can no longer create Decreased Cardiac Output Caused by Cardiac Factors. adequate pressure in the now flaccid peripheral blood Whenever the heart becomes severely damaged, regardless vessels. As a result, the blood pools in the vessels and of the cause, its limited level of pumping may fall below does not return to the heart as rapidly as normal. that needed for adequate blood flow to the tissues. Some 3. Obstruction of the large veins. On rare occasions, the large examples of this condition include the following: (1) severe veins leading into the heart become obstructed, and the coronary blood vessel blockage and consequent myocardial blood in the peripheral vessels cannot flow back into the infarction; (2) severe valvular heart disease; (3) myocarditis; heart. Consequently, the cardiac output falls markedly. 200 7 175 6 150 5 125 Cardiac output (% of control) Cardiac index 4 (L/min/m2) Control (young adults) 100 Average 45-year-old adult 3 Control (young adults) (308) Pulmonary disease (29) 75 Hyperthyroidism (29) Myocardial infarction (22) Mild valve disease (31) Severe valve disease (29) Paget’s disease (9) 2 Traumatic shock (4) Hypertension (47) 50 Pregnancy (46) AV shunts (33) Cardiac shock (7) Mild shock (4) Anemia (75) Anxiety (21) Beriberi (5) 1 25 0 0 Figure 20-7. Cardiac output in different pathological conditions. The numbers in parentheses indicate the number of patients studied in each condition. AV, Atrioventricular. (Modified from Guyton AC, Jones CE, Coleman TG: Circulatory Physiology: Cardiac Output and Its Regulation, 2nd ed. Philadelphia: WB Saunders, 1973.) 249 UNIT IV The Circulation 4. Decreased tissue mass, especially decreased skeletal shifts the entire cardiac output curve to the right by the muscle mass. With normal aging or with prolonged pe- same amount. This shift occurs because filling the car- riods of physical inactivity, a reduction in the size of the diac chambers with blood requires an extra 2 mm Hg skeletal muscles usually occurs. This reduction, in turn, of right atrial pressure to overcome the increased pres- decreases the total oxygen consumption and blood flow sure on the outside of the heart. Likewise, an increase in needs of the muscles, resulting in decreases in skeletal intrapleural pressure to +2 mm Hg requires a 6 mm Hg muscle blood flow and cardiac output. 5. Decreased metabolic rate of the tissues. If the tissue met- increase in right atrial pressure from the normal −4 mm abolic rate is reduced, as occurs in skeletal muscle dur- Hg, which shifts the entire cardiac output curve 6 mm ing prolonged bed rest, the oxygen consumption and Hg to the right. nutrition needs of the tissues will also be lower, which Some factors that can alter the external pressure on the decreases blood flow to the tissues, resulting in reduced heart and thereby shift the cardiac output curve are the cardiac output. Other conditions, such as hypothyroid- following: ism, may also reduce metabolic rate and therefore tissue 1. Cyclical changes of intrapleural pressure during res- blood flow and cardiac output. piration, which are about ±2 mm Hg during normal Regardless of the cause of low cardiac output, whether it breathing but can be as much as ±50 mm Hg during is a peripheral factor or a cardiac factor, if the cardiac out- strenuous breathing put ever falls below the level required for adequate nutrition 2. Breathing against a negative pressure, which shifts of the tissues, the person is said to experience circulatory shock. This condition can be lethal within a few minutes to the curve to a more negative right atrial pressure (to a few hours. Circulatory shock is such an important clinical the left). problem that it is discussed in detail in Chapter 24. 3. Positive-pressure breathing, which shifts the curve to the right 4. Opening the thoracic cage, which increases the in- trapleural pressure to 0 mm Hg and shifts the car- CARDIAC OUTPUT CURVES USED IN diac output curve to the right by 4 mm Hg QUANTITATIVE ANALYSIS OF CARDIAC 5. Cardiac tamponade, which means accumulation OUTPUT REGULATION of a large quantity of fluid in the pericardial cavity Our discussion of cardiac output regulation thus far around the heart with a resultant increase in exter- is adequate for understanding the factors that control nal cardiac pressure and shifting of the curve to the cardiac output in most simple conditions. However, to right understand cardiac output regulation in especially stress- Note in Figure 20-8 that cardiac tamponade shifts ful situations, such as the extremes of exercise, cardiac the upper parts of the curves farther to the right than failure, and circulatory shock, a more complex quantita- the lower parts because the external tamponade pressure tive analysis is presented in the following sections. rises to higher values as the chambers of the heart fill to To perform the more quantitative analysis, it is nec- increased volumes during high cardiac output. essary to distinguish separately the two primary factors concerned with cardiac output regulation: (1) the pump- Combinations of Different Patterns of Cardiac Output ing ability of the heart, as represented by cardiac output Curves. Figure 20-9 shows that the final cardiac output curves; and (2) the peripheral factors that affect flow curve can change as a result of simultaneous changes of blood from the veins into the heart, as represented in the following: (1) external cardiac pressure; and (2) by venous return curves. Then we can put these curves effectiveness of the heart as a pump. For example, the together in a quantitative way to show how they inter- act with each other to determine cardiac output, venous 15 return, and right atrial pressure at the same time. Hg m 4) g Cardiac output (L/min) Some of the cardiac output curves used to depict m Hg H =– e onad mm res.5 mm e amp 5 quantitative heart pumping effectiveness have already iac t r =– su Card = +2 –2 10 been shown in Figure 20-5. However, an additional set sure ure = ural p e ssur al pres of curves is required to show the effect on cardiac output press ap le l pre caused by changing external pressures on the outside of pleur l (intr 5 ural a the heart, as explained in the next section. leur Intra aple r ma rap Intr No Int Effect of External Pressure Outside the Heart on 0 Cardiac Output Curves. Figure 20-8 shows the effect –4 0 +4 +8 +12 of changes in external cardiac pressure on the cardiac Right atrial pressure (mm Hg) output curve. The normal external pressure is equal to Figure 20-8. Cardiac output curves at different levels of intrapleural the normal intrapleural pressure (the pressure in the pressure and different degrees of cardiac tamponade. (Modified from chest cavity), which is about −4 mm Hg. Note in the fig- Guyton AC, Jones CE, Coleman TG: Circulatory Physiology: Cardiac ure that a rise in intrapleural pressure, to −2 mm Hg, Output and Its Regulation, 2nd ed. Philadelphia: WB Saunders, 1973.) 250  Chapter 20 Cardiac Output, Venous Return, and Their Regulation Transitional Venous return (L/min) Hypereffective + increased intrapleural pressure Plateau zone 15 Mean Normal 5 Do systemic Cardiac output (L/min) wn slo filling pe pressure 10 UNIT IV 0 Hypoeffective + reduced –8 –4 0 +4 +8 5 intrapleural pressure Right atrial pressure (mm Hg) Figure 20-10. Normal venous return curve. The plateau is caused by collapse of the large veins entering the chest when the right atrial 0 pressure falls below atmospheric pressure. Note also that venous re- –4 0 +4 +8 +12 turn becomes zero when the right atrial pressure rises to equal the Right atrial pressure (mm Hg) mean systemic filling pressure. Figure 20-9. Combinations of two major patterns of cardiac output curves showing the effect of alterations in both extracardiac pressure and effectiveness of the heart as a pump. (Modified from Guyton AC, Normal Venous Return Curve Jones CE, Coleman TG: Circulatory Physiology: Cardiac Output and Its In the same way that the cardiac output curve relates Regulation, 2nd ed. Philadelphia: WB Saunders, 1973.) pumping of blood by the heart to right atrial pressure, the venous return curve relates venous return also to right combination of a hypereffective heart and increased in- atrial pressure—that is, the venous flow of blood into the trapleural pressure would lead to an increased maximum heart from the systemic circulation at different levels of level of cardiac output due to the increased pumping ca- right atrial pressure. pability of the heart, but the cardiac output curve would The curve in Figure 20-10 is the normal venous be shifted to the right (to higher atrial pressures) because return curve. This curve shows that when heart pump- of the increased intrapleural pressure. Thus, by knowing ing capability becomes diminished and causes the right what is happening to the external pressure, and to the ca- atrial pressure to rise, the backward force of the rising pability of the heart as a pump, one can express the mo- atrial pressure on the veins of the systemic circulation mentary ability of the heart to pump blood by a single decreases venous return of blood to the heart. If all cardiac output curve. nervous circulatory reflexes are prevented from acting, venous return decreases to zero when the right atrial pressure rises to about +7 mm Hg. Such a slight rise in VENOUS RETURN CURVES right atrial pressure causes a drastic decrease in venous The entire systemic circulation must be considered before return because any increase in back pressure causes complete analysis of cardiac regulation can be achieved. blood to dam up in the systemic circulation instead of To analyze the function of the systemic circulation exper- returning to the heart. imentally, the heart and lungs were removed from the At the same time that the right atrial pressure is ris- circulation of an animal and replaced with a pump and ing and causing venous stasis, pumping by the heart also artificial oxygenator system. Then, different factors, such approaches zero because of decreasing venous return. as blood volume, vascular resistances, and central venous Both the arterial and venous pressures reach equilibrium pressure in the right atrium, were altered to determine when all flow in the systemic circulation ceases at a pres- how the systemic circulation operates in different circu- sure of 7 mm Hg, which, by definition, is the mean sys- latory states. From these studies, one finds the following temic filling pressure. three principal factors that affect venous return to the heart from the systemic circulation: Plateau in Venous Return Curve at Negative Atrial 1. Right atrial pressure, which exerts a backward force Pressures Caused by Collapse of the Large Veins. on the veins to impede flow of blood from the veins When the right atrial pressure falls below zero—that is, into the right atrium. below atmospheric pressure—any further increase in ve- 2. Degree of filling of the systemic circulation (meas- nous return almost ceases, and by the time the right atrial ured by the mean systemic filling pressure), which pressure has fallen to about −2 mm Hg, the venous return forces the systemic blood toward the heart (this is reaches a plateau. It remains at this plateau level, even the pressure measured everywhere in the systemic though the right atrial pressure falls to −20 mm Hg, −50 circulation when all flow of blood is stopped, dis- mm Hg or even further. This plateau is caused by collapse cussed in detail later). of the veins entering the chest. Negative pressure in the 3. Resistance to blood flow between the peripheral ves- right atrium sucks the walls of the veins together where sels and the right atrium. they enter the chest, which prevents any additional flow of These factors can all be expressed quantitatively by the blood from the peripheral veins. Consequently, even very venous return curve, as we explain in the next sections. negative pressures in the right atrium cannot increase 251 UNIT IV The Circulation venous return significantly above that which exists at a chambers of the heart. Therefore, the capacity of the sys- normal atrial pressure of 0 mm Hg. tem decreases so that at each level of blood volume, the mean circulatory filling pressure is increased. At normal Mean Circulatory Filling Pressure, Mean blood volume, maximal sympathetic stimulation increas- Systemic Filling Pressure—Effects on es the mean circulatory filling pressure from 7 mm Hg to Venous Return about twice that value or about 14 mm Hg. When heart pumping is stopped by shocking the heart Conversely, complete inhibition of the sympathetic with electricity to cause ventricular fibrillation or is nervous system relaxes both the blood vessels and heart, stopped in any other way, flow of blood everywhere in decreasing the mean circulatory filling pressure from the the circulation ceases a few seconds later. Without blood normal value of 7 mm Hg down to about 4 mm Hg. Note flow, the pressures everywhere in the circulation become in Figure 20-11 how steep the curves are, which means equal. This equilibrated pressure level is called the mean that even slight changes in blood volume or capacity of the circulatory filling pressure. system caused by various levels of sympathetic activity can have large effects on the mean circulatory filling pressure. Increased Blood Volume Raises Mean Circulatory Filling Pressure. The greater the volume of blood in the circula- Mean Systemic Filling Pressure and Relationship to tion, the greater is the mean circulatory filling pressure Mean Circulatory Filling Pressure. The mean systemic because extra blood volume stretches the walls of the filling pressure
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inhibition the curve shifts downward and to the left. 10 Normal volume Venous return (L/min) 8 10 6 Psf = 3.5 Psf = 7 4 5 No Psf = 14 rm al 2 0 0 –4 0 +4 +8 +12 0 1000 2000 3000 4000 5000 6000 7000 Right atrial pressure (mm Hg) Volume (milliliters) Figure 20-12. Venous return curves showing the normal curve when Figure 20-11. Effect of changes in total blood volume on the mean the mean systemic filling pressure (Psf) is 7 mm Hg and the effect of circulatory filling pressure (volume-pressure curve for the entire circulatory altering the Psf to 3.5, 7, or 14 mm Hg. (Modified from Guyton AC, system). These curves also show the effects of strong sympathetic Jones CE, Coleman TG: Circulatory Physiology: Cardiac Output and Its stimulation and complete sympathetic inhibition. Regulation, 2nd ed. Philadelphia: WB Saunders, 1973.) 252  Chapter 20 Cardiac Output, Venous Return, and Their Regulation Expressing this another way, the greater the degree to 20 which the system is filled, the easier it is for blood to flow into the heart. The lesser the degree to which the system is filled, the more difficult it is for blood to flow into the heart. 15 Venous return (L/min) UNIT IV When Pressure Gradient for Venous Return Is Zero There Is No Venous Return. When the right atrial pres- TVSF
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2 ⫻ resis e tance proportionately, as can be seen by studying any of the ve- nous return curves in Figure 20-12. That is, the greater 0 the difference between the Psf and right atrial pressure, the –4 0 +4 +8 greater becomes the venous return. Therefore, the differ- Right atrial pressure (mm Hg) ence between these two pressures is called the pressure Figure 20-13. Venous return curves depicting the effect of altering gradient for venous return. the resistance to venous return. Psf, Mean systemic filling pressure. (Modified from Guyton AC, Jones CE, Coleman TG: Circulatory Physi- Resistance to Venous Return ology: Cardiac Output and Its Regulation, 2nd ed. Philadelphia: WB *O
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Saunders, 1973.) venous blood from the periphery toward the heart, there is also resistance to this venous flow of blood. This is called Effect of Resistance to Venous Return on the Venous the resistance to venous return
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systemic circulation. and resistance to venous return = 1.4 mm Hg/L/min of Therefore, one can predict the cardiac output and right blood flow. atrial pressure in the following way: 253 UNIT IV The Circulation Normal resistance heart and systemic circulation. Therefore, in the normal circulation, the right atrial pressure, cardiac output, and 15 2 ⫻ resistance 1/2 resistance venous return are all depicted by point A, called the equi- librium point, giving a normal value for cardiac output of Venous return (L/min) 1/3 resistance 5 L/min and a right atrial pressure of 0 mm Hg. 10 Effect of Increased Blood Volume on Cardiac Output. A sudden increase in blood volume of about 20% increas- es the cardiac output to about 2.5 to 3 times normal. An 5 Psf = 10.5 analysis of this effect is shown in Figure 20-15. Imme- Psf = 10 diately on infusing the large quantity of extra blood, the Psf = 2.3 JODSFBTFE
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Psf = 7 to 16 mm Hg, which shifts the venous return curve to 0 –4 0 +4 +8 +12 the right. At the same time, the increased blood volume Right atrial pressure (mm Hg) distends the blood vessels, reducing their resistance and Figure 20-14. Combinations of the major patterns of venous return thereby reducing the resistance to venous return, which curves showing the effects of simultaneous changes in the mean sys- rotates the curve upward. As a result of these two effects, temic filling pressure (Psf) and in resistance to venous return. (Modi- the venous return curve of Figure 20-15 is shifted to the fied from Guyton AC, Jones CE, Coleman TG: Circulatory Physiology: right. This new curve equates with the cardiac output Cardiac Output and Its Regulation, 2nd ed. Philadelphia: WB Saun- ders, 1973.) curve at point B, showing that the cardiac output and ve- nous return increase 2.5 to 3 times and that the right atrial pressure rises to about +8 mm Hg. Cardiac output and veno