NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.
Young DB. Control of Cardiac Output. San Rafael (CA): Morgan & Claypool Life Sciences; 2010.
Life began in the primordial ocean, the primitive cells surrounded by a nearly infinite aqueous medium supplying the needs for the single-celled inhabitants. As the complexity of life forms increased, cells could not be in contact with the exterior bathing medium, and consequently, a means to circulate the interior medium between the exterior and the cells on the interior was a necessary feature of even the first complex organisms. In man and other mammals, the means of circulation has become extremely complex, allowing for the development of tissues with large metabolic demands all located within a few microns of capillaries perfused with blood replete with oxygen and the cells’ metabolic substrates. The heart must pump blood through many kilometers of vascular channels so that exchange can occur between plasma and extracellular fluid across hundreds of square meters of capillary surface area.
In healthy individuals, cardiac output can increase from 5 to approximately 20 L/min. At rest, man’s cardiac output is approximately 5 L/min for a 70-kg person or, stated differently, the cardiac index of a healthy man with a surface area of 1.7 m2 is approximately 3 L/min/m2 of body surface. Cardiac output varies in approximate proportion to lean body mass. Normal blood volume is about equal to the amount of blood pumped from the heart each minute, and consequently, extensive exchange and mixing between the extracellular fluid and the plasma can be maintained. In healthy individuals, cardiac output can increase at least 3-fold to between 15 and 20 L/min. Such an increase can occur in response to maximal metabolic demand by large working muscles during extremely vigorous exercise, as would occur if one was running to escape mortal danger or competing in an especially intense sporting event. An average person can improve maximal cardiac output with training, but only by about 10–20%. However, world-class athletes can achieve maximal rates approaching 40 L/min; the apparent incongruity is probably due to a genetically determined greater than normal heart size along with the intensive long-term training undertaken by exceptionally able competitors. A person’s cardiac output is maximal in the early 20s and tends to decline later in life. The changes throughout life are probably secondary to changes in the body’s metabolic rate, unless the heart is severely weakened by disease.
In healthy individuals, metabolic rate and cardiac output are closely correlated. This was noted by Guyton and associates [1], who compiled previously published oxygen consumption and cardiac output data obtained from subjects working at rates spanning an order of magnitude. Figure 1.1 illustrates the parallel increases in cardiac output and oxygen consumption over the wide range of metabolic demand, both in sedentary individuals and in trained athletes.
![FIGURE 1.1. Correlation between maximum oxygen consumption and maximum cardiac output in trained athletes and untrained subjects. From reference [2].](/books/NBK54473/bin/fig1.1.gif)
FIGURE 1.1
Correlation between maximum oxygen consumption and maximum cardiac output in trained athletes and untrained subjects. From reference [2].
The close relationship between the variables is evident from these data, and it can be observed in response to other conditions in which metabolic rate changes. During digestion of a meal, the increased metabolic activity of the liver and gastrointestinal organs is associated with as much as a 25% elevation in cardiac output; during sleep, cardiac output decreases by about 25%, and in response to anxiety, elevation of metabolic rate driven by the sympathetic nervous system measurably raises cardiac output. During cold exposure, the muscle metabolic activity of shivering raises cardiac output, while in response to elevation of body temperature, cardiac output also increases to provide increased blood flow to the skin for thermoregulatory purposes. The interrelationship between cardiac output and oxygen consumption is apparent in both trained athletes and untrained individuals and in subjects before and after aerobic conditioning [2].
In two prominent organs, metabolic demand may not be the only factor associated with demand for blood flow. The two kidneys each receive about 10% of resting cardiac output, more than what is required to meet the metabolic requirements of their tissues. Instead, renal blood flow is maintained at a higher level to supply sufficient flow to the glomeruli to filter and excrete the metabolic waste products of the whole body. Skin blood flow also varies in a manner that is largely independent of its metabolic needs. The overriding determinant of flow to the skin is the body temperature. Blood flow to the body surface allows heat loss from the body, which may be desirable or undesirable, depending on the circumstance. When core body temperature is well below normal, or more precisely below the set point of the negative feedback control system that regulates body temperature, skin blood flow may be reduced to a few hundred millilitres per minute and in localized regions to near zero for intermittent periods. Conversely, when core temperature is several degrees above the normal level, skin blood flow can rise as high as 6 L/min.
1.1. Functional Characteristics of the Vascular System
The anatomy and basic function of the vascular system are probably well known by anyone interested in this topic. However, briefly reviewing some of the more subtle aspects of the functional characteristics will be helpful in appreciating the remainder of the presentation.
Ohm’s law can be applied to the study of cardiac output regulation. Although Ohm’s law was originally formulated to describe the flow of electric current, it can also be usefully adapted to the study of blood flow:
where “flow” is the flow of blood through a system of tubes, “change in pressure” is the difference in pressure measured at the beginning and end of the system, and “resistance” is the impediment to flow encountered by the blood moving through the system. For the systemic circulation, the flow is equal to the pressure in root of the aorta minus the right atrial pressure divided by the systemic resistance. Pulmonary flow is calculated from the pressure difference between the pulmonary artery and the left atrium divided by pulmonary resistance. The resistances of the two circulations are the sum of all resistances throughout the systems, values that cannot be measured but can be calculated if systemic flow (cardiac output) and the differences in pressure are known.
Pouseuille’s law is an extension of Ohm’s law that is more useful in studying the cardiovascular system:
where π is the mathematical constant (3.14159), “change in pressure” is the difference in pressure at the beginning and end of a tube or vessel, “radius” is that of the tube, “viscosity” is that of the fluid or blood, and “length” is that of the tube. Significantly, flow is proportional to the fourth power of the radius; therefore, doubling the radius of a vessel will cause a 16-fold increase in flow.
Mean blood pressure in the systemic circulation normally ranges from 100 mm Hg in the root of the aorta to approximately 0 mm Hg in the right atrium. Arterial pressure is much higher in the systemic circulation than in the pulmonary circuit, averaging approximately 100 mm Hg versus approximately 20 mm Hg in the pulmonary circulation. The majority of the reduction in pressure in the systemic side occurs in the arterioles due to the high resistance of these small vessels. Table 1.1 lists the total cross-sectional areas and pressures in the vessel types of the systemic circulation.
Table 1.1
Cross-sectional areas and pressures of blood vessels.
The total blood volume is approximately 7% of the body weight and is distributed throughout the segments of the circulatory system as indicated in Table 1.2. Noteworthy is the large percentage of blood present on the venous side of the system.
Table 1.2
Distribution of blood volume throughout the vascular system (%)
| Heart | 7 | |
| Pulmonary circulation | 9 | |
| Arteries | 13 | |
| Arterioles and capillaries | 7 | |
| Veins, venules, and venous sinuses | 64 |
The capacity of a segment of the circulation to contain blood at a given pressure level is termed capacitance or compliance:
The thin-walled veins are more distensible than the thicker walled arteries, and the veins contain more blood. Consequently, the veins’ capacitance is much greater (18 times greater) than that of the arteries [3].
Mean systemic pressure refers to the pressure measured anywhere in the systemic vascular system immediately after the cessation of circulation when all pressures have equalized. Actual measurement of this pressure is difficult because several seconds are required for the pressures through the system to equalize after the heart has stopped, and within approximately 7 s, activation of sympathetic nervous system reflexes begins to constrict the blood vessels. However, the pressure can be determined from experiments designed to minimize artifacts, which Guyton and coworkers performed in an extensive series of studies beginning in 1954 [4]. Interestingly, their initial publication of this work included venous and arterial pressure measurements recorded on a kymograph. The mean value that they obtained in anesthetized dogs was 7.0 mm Hg. Mean circulatory pressure is the pressure measured anywhere in the vascular system, including the pulmonary circulation, when the heart has stopped and arterial and venous pressures have equalized. They found that, in the anesthetized dog, the pressure averages 6.9 mm Hg. Mean pulmonary pressure can be determined similarly, and it averages a few millimeters of mercury less than mean systemic pressure.
1.2. Local Tissue Autoregulation of Blood Flow and Its Importance in Determining Cardiac Output
Cardiac output is distributed throughout the organs and tissues of the body, generally according to metabolic demand. In most conditions, the metabolic need for oxygen is the dominant factor affecting a tissue’s blood flow resistance. Each gram of tissue has the capability to control the flow of blood through its microcirculation by altering the resistance of the small arteries and arterioles supplying its capillary network. The physiology of the microcirculation is an important and fascinating discipline, but it lies beyond the scope of this presentation. Another volume of this series fully presents the topic. For our purposes, it is sufficient to state that, while a variety of factors are capable of affecting microcirculatory resistance, the oxygen concentration of the local extracellular fluid has the greatest long-term effect.
Tissue blood flow is regulated by a local feedback control system. When the metabolic activity of a region of tissue increases, its utilization of oxygen increases, thus increasing the rate of removal of oxygen from the local extracellular fluid below the rate of delivery from the blood in the capillaries. Consequently, oxygen concentration in the extracellular fluid declines. Local mechanisms sensitive to extracellular fluid oxygen concentration respond with actions that cause vasodilation of the arterioles supplying the capillaries in that region of the tissue. With the subsequent reduction in resistance, blood flow to the capillaries increases and oxygen delivery rises, allowing the rate of oxygen diffusion into the extracellular fluid to increase. The process continues until the rate of entry of oxygen returns the extracellular fluid oxygen concentration close to the desired level or set point concentration. This negative feedback control system regulates tissue blood flow throughout the body, acting within seconds to maintain oxygen concentration near the set point level in response to changing metabolic demand. The control system is referred to as the short-term tissue autoregulatory mechanism. A related long-term system also operates over periods of days and weeks; in response to prolonged reductions in tissue oxygen concentration, growth of additional capillaries and other microcirculatory vessels takes place, stimulated by mechanisms of the long-term autoregulatory system. The increased capillary density provides a long-term increase in oxygen delivery to the tissue.
1.3. Summary
Cardiac output is equal to the summated blood flow throughout all tissues of the body. Therefore, the factors that control local tissue blood flow strongly affect the regulation of cardiac output. Consequently, the requirement of the body’s tissues for oxygen is a prominent determinant of cardiac output. The mechanisms linking the concepts in these three sentences comprise most of what is contained in the remainder of this presentation.
- Introduction - Control of Cardiac OutputIntroduction - Control of Cardiac Output
Your browsing activity is empty.
Activity recording is turned off.
See more...