STUDENT LEARNING OBJECTIVES
At the completion of this chapter, you should be able to do the following:
1.Summarize the basic functions of blood.
2.Describe the components of blood and discuss their functions.
3.List the formed elements of blood and discuss their functions.
4.Discuss the origin and significance of sickle cell anemia in the world.
5.Outline the formation of erythrocytes, leukocytes, and thrombocytes from the stem cell hemocytoblast.
6.Discuss how blood doping could be dangerous.
7.List the different leukocytes and describe their functions.
8.Describe in detail the ABO blood group system and discuss its significance.
9.Discuss the physiological significance of the Rh system.
10.List the major components of blood plasma.
11.Outline the basic mechanism of blood clotting.
LANGUAGE OF SCIENCE AND MEDICINE
Before reading the chapter, say each of these terms out loud. This will help you avoid stumbling over them as you read.
agglutinate
(ah-GLOO-tin-ayt) [agglutin- glue, -ate process]
agranulocyte
(ah-GRAN-yoo-loh-syte) [a- without, -gran- grain, -ul- little, -cyte cell]
anemia
(ah-NEE-mee-ah) [an- without, -emia blood condition]
anticoagulant drug
(an-tee-koh-AG-yoo-lant) [anti- against, -coagul- curdle, -ant agent]
antigen
(AN-tih-jen) [anti- against, -gen produce]
antigen A
(AN-tih-jen) [anti- against, -gen produce]
antigen B
(AN-tih-jen) [anti- against, -gen produce]
antiplatelet drug
(an-tee-PLAYT-let) [anti- against, -plate- flat, -let small]
basophil
(BAY-soh-fil) [bas- foundation, -phil love]
blood boosting
blood doping
blood serum
(SEER-um) [serum watery fluid] pl., sera (SEER-ah)
blood type
[tupos- impression]
B lymphocyte
(B LIM-foh-syte) [B bursa-equivalent tissue, lympho- the lymph, -cyte cell]
coagulation
(koh-ag-yoo-LAY-shun) [coagul- curdle, -ation process]
complete blood cell count
(CBC)
coumarin
(KOO-mar-in) [coumarou- tonka bean tree]
diapedesis
(dye-ah-peh-DEE-sis) [dia- apart or through, -pedesis oozing]
differential white blood cell (WBC) count
(dif-er-EN-shal)
electrolyte
(eh-LEK-troh-lyte) [electro- electricity, -lyt- loosening]
eosinophil
(ee-oh-SIN-oh-fil) [eosin- reddish color, -phil love]
erythroblastosis fetalis
(eh-rith-roh-blas-TOH-sis feh-TAL-is) [erythro- red, -blast- bud, -osis condition]
erythrocyte
(eh-RITH-roh-syte) [erythro- red, -cyte cell]
erythropoiesis
(eh-rith-roh-poy-EE-sis) [erythro- red, -poiesis making]
erythropoietin (EPO)
(eh-rith-roh-POY-eh-tin) [erythro- red, -poiet- make, -in substance]
extrinsic pathway
(eks-TRIN-sik PATH-way) [extr- outside, -sic beside]
fibrinolysis
(fye-brin-OL-ih-sis) [fibr- fiber, -lysis loosening]
formed element
(EL-em-ent)
globin
(GLOH-bin) [glob- ball, -in substance]
granulocyte
(GRAN-yoo-loh-syte) [gran- grain, -ul- little, -cyte cell]
hematocrit
(hee-MAT-oh-krit) [hemato- blood, -crit separate]
hemocytoblast
(hee-moh-SYE-toh-blast) [hemo- blood, -cyto- cell, -blast embryonic state of development]
hemoglobin
(hee-moh-GLOH-bin) [hem- blood, -globus ball]
hemolysis
(hee-MAHL-ih-sis) [hemo- blood, -lysis loosening]
hemostasis
(hee-moh-STAY-sis) [hemo- blood, -stasis standing]
heparin
(HEP-ah-rin) [hepar- liver, -in substance]
intrinsic pathway
(in-TRIN-sik) [intr- within, -sic beside]
leukocyte
(LOO-koh-syte) [leuko- white, -cyte cell]
leukocytosis
(loo-koh-sye-TOH-sis) [leuko- white, -cyt- cell, -osis condition]
leukopenia
(loo-koh-PEE-nee-ah) [leuko- white, -penia lack]
lymphocyte
(LIM-foh-syte) [lymph- water (lymphatic system), -cyte cell]
monocyte
(MON-oh-syte) [mono- single, -cyte cell]
myeloid tissue
(MY-eh-loyd TISH-yoo) [myel- marrow, -oid like, tissue- fabric]
neutrophil
(NOO-troh-fil) [neuter- neither, -phil love]
nonelectrolyte
(non-ee-LEK-troh-lyte) [non- not, -electro- electricity, -lyt- loosening]
physiological polycythemia
(fiz-ee-oh-LOJ-ih-kal pol-ee-sye-THEE-mee-ah) [physi- nature, -o- combining form, -log- words (study of), -y activity, poly- many, -cyt- cell, -emia blood condition]
plasma
(PLAZ-mah) [plasma substance]
plasminogen
(plaz-MIN-oh-jen) [plasm- substance (plasma), -in- substance, -gen produce]
platelet
(PLAYT-let) [plate- flat, -let small]
platelet plug
(PLAYT-let) [plate- flat, -let small]
prothrombin
(pro-THROM-bin) [pro- first, -thromb- clot, -in substance]
Rh antigen
(R-H AN-tih-jen) [Rh Rhesus (monkey), anti- against, -gen produce]
streptokinase
(strep-toh-KIN-ayz) [strepto- twisted, -kin- motion, -ase enzyme]
thrombopoiesis
(throm-boh-poy-EE-sis) [thromb- clot, -poiesis making]
thrombosis
(throm-BOH-sis) [thromb- clot, -osis condition]
T lymphocyte
(LIM-foh-syte) [T thymus gland, lymph- water (lymphatic system), -cyte cell]
transfusion reaction
(tranz-FYOO-zhun ree-AK-shun) [trans- across, -fus- pour, -sion process, re- again, -action action]
whole blood volume
DUNCAN was slicing a bagel to put in the toaster. When the microwave beeped, he glanced in that direction, taking his eyes off the bagel. In that split second, the knife slipped and cut deeply into his finger. Immediately blood started spurting out of the damaged blood vessels. Duncan grabbed a towel and wrapped it tightly around the cut while holding his hand above his heart.
We've all done something similar by not paying attention, but did you ever wonder about all the complex physical and physiological processes that take place immediately after we cut ourselves? In this chapter, as you follow Duncan's story, you'll find out what really happens.
Now that you have read this chapter, try to answer these questions about Duncan's cut from the Introductory Story.
1. What is the main component of the blood coming out of Duncan's finger?
a. Erythrocytes
b. Leukocytes
c. Plasma
d. Thrombocytes
Because of the damage to his blood vessels, Duncan's body will immediately start the blood clotting process.
2. What's the first step in hemostasis (stopping bleeding)?
a. Vascular spasm
b. Platelet plug
c. Coagulation
d. Leukocytic plug
3. What is the last step in clot formation?
a. Fibrinogen converted to fibrin
b. Prothrombin converted to thrombin
c. Profibrin converted to fibrin
d. Collagen fibers trap RBCs
4. If Duncan were missing factor VIII, what condition would he have?
a. Thrombocytopenia
b. Pernicious anemia
c. Polycythemia
d. Hemophilia
To solve a case study, you may have to refer to the glossary or index, other chapters in this textbook, A&P Connect, Mechanisms of Disease, and other resources.
You have undoubtedly seen blood, but have you ever wondered about its properties? Blood is a wonderfully fluid transport medium that serves as a pickup and delivery system that services the entire body. For example, it picks up food and oxygen from the digestive and respiratory systems and delivers these vital elements to the cells throughout the body. At the same time it picks up wastes from cells for delivery to excretory organs. But blood does more than this. It also transports hormones, enzymes, buffers, and other important biochemicals. Finally, the flow of blood is vital to temperature regulation in our bodies. Blood exhibits a physical property called specific heat, which allows it to absorb heat energy while at the same time resisting significant temperature change. This property permits blood temperature to remain relatively constant and within very narrow limits even when burdened with a signifcant heat load. Because of its high specific heat, blood can efficiently absorb and then safely transfer large amounts of heat energy from metabolism to the body's surface where it is dissipated by evaporation, convection, and radiation to the environment (see box on p. 127 for a review of this process).
BLOOD COMPOSITION
First and foremost, blood is a liquid connective tissue consisting not only of fluid plasma, but also of cells. Plasma is the third major fluid in our bodies (the other two are the interstitial fluids and intracellular fluids). Our blood volume is often expressed as a percentage of our total body weight. However, the measurement of the plasma and formed elements is typically expressed as a percentage of the whole blood volume. Using this method, whole blood is equal to about 8% of total body weight. Plasma accounts for 55% and formed elements such as various blood cells account for 45% of the total volume (Figure 16-1).
Blood Volume
Males have about 5 to 6 liters of blood circulating in their bodies and females have about 4 to 5 liters. In addition to gender differences, blood volume varies with age and body composition. A unit of blood (about 0.5 liter or 1 pint)
FIGURE 16-1 Composition of whole blood. Approximate values for the components of blood in a normal adult.
is the amount collected from blood donors for blood transfusion. One unit is equal to about 10% of the total blood volume for an average adult. There are several methods of measuring blood volume. Regardless of which method is used, it is important to have an accurate measurement in case blood volume must be replaced for a variety of conditions, including hemorrhage and shock.
One of the most important variables influencing blood volume is the amount of body fat. Blood volume per kilogram of body weight varies inversely with the amount of excess body fat. This means that leaner people have more blood per kilogram of body weight than obese people. Because females typically have somewhat more body fat than males (per kilogram of weight), they have slightly lower blood volumes.
FORMED ELEMENTS OF BLOOD
As you can see from Figure 16-1, blood consists of about 55% plasma and 45% of a variety of formed elements. These include erythrocytes (red blood cells or RBCs), thrombocytes (platelets), and leukocytes (white blood cells or WBCs). The leukocytes are further broken down into granular leukocytes, whose cytoplasm appears granular, and nongranular leukocytes, whose cytoplasm lacks granular components (Table 16-1).
In Figure 16-2, A, you see the results of centrifuging whole blood (spinning a vial at a high rate of speed). The lighter
FIGURE 16-2 Hematocrit tubes showing normal blood, anemia, and polycythemia. Note the buffy coat located between the packed RBCs and the plasma. A, A normal percentage of red blood cells. B, Anemia (a low percentage of red blood cells). C, Polycythemia (a high percentage of red blood cells).
plasma remains at the top, and the middle-weight leukocytes and platelets form a so-called buffy coat in the middle. Erythrocytes are heavier and concentrate at the bottom of the test tube. The volume of packed red blood cells at the bottom of the test tube is called the hematocrit.
TABLE 16-1 Classes of Blood Cells
CELL TYPE
DESCRIPTION
FUNCTION
LIFE SPAN
Red Blood Cells
Erythrocyte
7 microns (μm) in diameter; concave disk shape; entire cell stains pale pink; no nucleus
Transportation of respiratory gases (O2 and some CO2)
105-120 days
Granular White Blood Cells
Neutrophil
12-1 5 μm in diameter; spherical shape; multilobed nucleus; small, pink–purple–staining cytoplasmic granules
Cellular defense–phagocytosis of small pathogenic microorganisms such as bacteria
Hours to 3 days
Basophil
11-14 (μm in diameter; spherical shape; generally two-lobed nucleus; large purple-staining cytoplasmic granules
Secretes heparin (anticoagulant) and histamine important in the inflammatory response)
Hours to 3 days
Eosinophil
10-12 μm in diameter; spherical shape; generally two-lobed nucleus; large, orange–red-staining cytoplasmic granule
Cellular defense-phagocytosis of large pathogenic microorganisms, such as protozoa and parasites; releases anti-inflammatory substances in allergic reactions
10-12 days
Nongranular White Blood Cells
Lymphocyte
6-9 μm in diameter; spherical shape; round (single-lobed) nucleus; small lymphocytes have scant cytoplasm
Humoral defense–secretes antibodies; involved in immune system response and regulation
Days to years
Monocyte
12-17 μm in diameter; spherical shape; nucleus generally kidney bean or horseshoe shaped with convoluted surface; ample cytoplasm often “steel blue” in color
Capable of migrating out ofthe blood to entertissue spaces as a macrophage–an aggressive phagocytic cell capable of ingesting bacteria, cellular debris, and cancerous cells
Months
Platelets
Thrombocyte
2-5 μm in diameter; irregularly shaped fragments; cytoplasm contains very small, pink-staining granules
Releases clot-activating substances and helps in formation of actual blood clot by forming platelet “plugs”
7-10 days
Average hematocrits vary but are normally around 45% for men and 42% for women. Conditions that result in decreased RBC numbers (Figure 16-2, B) are anemias. A reduced hematocrit number characterizes these disorders. However, healthy individuals living and working in high altitudes may have elevated RBC numbers and hematocrit values—a condition called physiological polycythemia (Figure 16-2, C).
Note that leukocytes and platelets make up less than 1% of blood volume.
1. What is the fluid portion of whole blood?
2. What constitutes the formed elements of whole blood?
3. What factors might influence blood volume?
4. What are the average component percentages of a normal hematocrit?
Red Blood Cells (Erythrocytes)
A normal, mature erythrocyte (RBC) is only about 7.5 μm in diameter. Amazingly, more than 1,500 of them can fit side by side in a 1-cm space. Before the cell reaches maturity in the bone marrow, it loses its nucleus. Unlike other cells, it also loses its ribosomes, mitochondria, and other organelles. In their place, nearly 35% of its volume is filled with hemoglobin, the protein responsible for transporting oxygen in the blood.
As you can see in Figure 16-3, erythrocytes are shaped like tiny biconcave disks. The microscopic depression on each flat surface of the cell creates a cell with a thin center and thicker edges. This unique shape gives an erythrocyte a very large surface area relative to its volume. RBCs can passively change their shapes as they are forced through capillaries under pressure. This ability is vital to the survival of RBCs, which are under almost constant mechanical stress and strain as they rush through the capillaries of our bodies. Their shape also allows faster blood flow throughout the circulatory system.
RBCs are the most numerous of all the formed elements of blood. In men, RBC counts average about 5.5 million per
FIGURE 16-3 Erythrocytes. Color-enhanced scanning electron micrograph shows normal erythrocytes. Note the biconcave shape.
cubic millimeter (mm3) of blood. In contrast, women have about 4.8 million/mm3.
Function of Red Blood Cells
RBCs play a critical role in the transport of oxygen and carbon dioxide in the body (this topic is discussed more fully in Chapter 18).
Altogether, the total surface area of all the RBCs in an adult is equivalent to an area larger than a football field. This is an enormous area for the efficient exchange of the respiratory gases between the RBCs (via their hemoglobin) and the interstitial fluid that bathes our body cells. (This is yet another excellent example of the relationship between form and function.)
Hemoglobin
Within each RBC are an estimated 200 to 300 million molecules of hemoglobin. Hemoglobin molecules are composed of four protein chains, each called a globin. Every globin molecule is bound to a heme group, each of which contains one atom of iron. This means that each hemoglobin molecule contains four iron atoms. Because of this arrangement, one hemoglobin molecule chemically bonds with four oxygen molecules to form oxyhemoglobin. This is a reversible reaction. Hemoglobin can also combine with carbon dioxide to form carbaminohemoglobin (also reversible). However, in this reaction, it is the globins, not the heme groups, that allow carbon dioxide to bond.
As we've seen, a man's blood usually contains more RBCs (and thus more hemoglobin) than a woman's blood. This is because higher levels of testosterone in men tend to stimulate erythrocyte production and cause an increase in RBC numbers. Normally, a man has 14 to 16 grams of hemoglobin for every 100 milliliters of blood in his system. An adult male who has a hemoglobin content of less than 10 g/100 ml of blood is diagnosed as having anemia (literally, a lack of blood). The term anemia is also used to describe a low RBC count. Anemias are classified according to the size and hemoglobin content of RBCs. Box 16-1 describes a specific type of anemia—sickle cell anemia—that is caused by the production of an abnormal type of hemoglobin due to a genetic error.
Formation of Red Blood Cells
The term erythropoiesis describes the entire process of RBC formation. Erythrocytes begin their maturation process in the red bone marrow from nucleated hematopoietic stem cells called hemocytoblasts (Figure 16-4). These adult stem cells have the ability to maintain a constant population of newly differentiating cells of a specific type. Note, however, that adult stem cells are not the same as embryonic stem cells (see Chapter 26), which are involved in embryonic and fetal development. Adult blood-forming stem cells divide by mitosis. Some of the daughter cells remain as undifferentiated adult stem cells. Others continue to develop into erythrocytes. You can follow this transformation in Figure 16-4.
FIGURE 16-4 Formation of blood cells. The hematopoietic stem cell, called the hemocytoblast, serves as the original stem cell from which all formed elements of the blood are derived. Note that all five precursor cells, which ultimately produce the different components of the formed elements, are derived from the hemocytoblast.
The entire maturation process requires about 4 days, after which the maturing cells lose their nuclei and become reticulocytes. Once released into the circulating blood, reticulocytes mature into erythrocytes in about a day. You should note in Figure 16-4 that overall cell size decreases as development proceeds from the stem cells to the mature erythrocytes.
Erythrocytes are formed and destroyed at a breathtaking rate. Normally, every day of our adult lives, more than 200 billion RBCs are formed to replace an equal number destroyed during that brief time. The number of RBCs remains relatively constant because efficient mechanisms maintain homeostasis. However, the rate of RBC production soon speeds up if blood oxygen levels in the tissues decline. Low oxygen level in the blood increases the secretion of a glycoprotein hormone called erythropoietin or EPO. If oxygen levels decrease, the kidneys release increasing amounts of erythropoietin. In turn, this stimulates bone marrow to accelerate its production of red blood cells. As more red blood cells increase the oxygen levels of the cells, a negative feedback system causes less erythropoietin to be produced. As a result, the production of RBCs falls back to normal. Figure 16-5 shows you how this negative feedback system works. Box 16-2 explores the controversial topic of “blood doping” sometimes used by athletes to enhance their performance.
BOX 16-1 FYI
Sickle Cell Anemia
Sickle cell anemia is a severe, sometimes fatal, hereditary disease characterized by an abnormal type of hemoglobin. A person who inherits only one defective gene develops a form of the disease called sickle cell trait. In these cases, red blood cells contain a small proportion of a hemoglobin type that is less soluble than normal. This abnormal hemoglobin forms solid crystals when the blood oxygen level is low, causing distortion and fragility of the red blood cell. If two defective genes are inherited (one from each parent), more of the defective hemoglobin is produced, and the distortion of red blood cells becomes even more severe. In the United States, about 1 in every 500 African-American and 1 in every 1,000 Hispanic newborns are affected each year. In these individuals, the distorted red blood cell walls can be damaged by drastic changes in shape. Red blood cells damaged in this way tend to stick to vessel walls. If a blood vessel in the brain is affected, a stroke may occur because of the decrease in blood flow velocity or the complete blockage of blood flow.
Stroke is one of the most devastating problems associated with sickle cell anemia in children and will affect about 10% of the 2,500 youngsters who have the disease in the United States. Studies have shown that frequent blood transfusions in addition to standard care can dramatically reduce the risk of stroke in many children suffering from sickle cell anemia. The illustration shows the characteristic shape of a red cell containing the abnormal hemoglobin.
Sickle cell anemia.
FIGURE 16-5 Erythropoiesis. In response to decreased blood oxygen, the kidneys release erythropoietin (EPO). This stimulates erythrocyte production in the red bone marrow.
BOX 16-2 Sports & Fitness
Blood Doping
Reports that some Olympic and other elite athletes use transfusions of their own blood to improve performance have surfaced repeatedly in the past several decades. The practice—called blood doping or blood boosting—is intended to increase oxygen delivery to muscles. A few weeks before competition, blood is drawn from the athlete and the red blood cells (RBCs) are separated and frozen. Just before competition, the RBCs are thawed and injected. Theoretically, infused RBCs and elevation of hemoglobin levels after transfusion should increase oxygen consumption and muscle performance during exercise. In practice, however, the advantage appears to be minimal. All blood transfusions carry some risk, and unnecessary or questionably indicated transfusions are medically and ethically unacceptable.
In addition to blood transfusions, injection of substances that increase RBC levels in an attempt to improve athletic performance has also been condemned by leading authorities in the area of sports medicine and by athletic organizations around the world. “Doping” with either the naturally occurring hormone erythropoietin (EPO) or with synthetic drugs that have similar biological effects—such as Epogen and Procrit—can result in devastating medical outcomes. For example, EPO abuse can produce dangerously high blood pressure that may lead to a heart attack or stroke.
Destruction of Red Blood Cells
The life span of RBCs circulating in the bloodstream averages between 105 and 120 days. They often break apart, or fragment, in the capillaries as they age. Macrophage cells in the lining of the blood vessels, especially those in the liver and spleen, phagocytose (ingest and destroy) the aged, abnormal, or fragmented RBCs. This process results in the breakdown of hemoglobin. As a result, amino acids, iron, and the pigment bilirubin are released into the bloodstream. Iron is returned to the bone marrow for use in the synthesis of new hemoglobin. Bilirubin is transported to the liver, where it is excreted as part of bile. Amino acids, released from the globin part of the hemoglobin, are reused by the body for energy or for the synthesis of new proteins.
For the RBC homeostatic mechanism to succeed in maintaining a normal number of RBCs, the bone marrow must function properly. To do this, the blood must supply it with the proper building components and catalysts with which to create new RBCs. In addition, the gastric mucosa of the stomach must provide intrinsic factor and perhaps other undiscovered factors necessary for the absorption of vitamin B12. This vitamin is vital to the formation of new erythrocytes.
5. What are the components of hemoglobin?
6. How many molecules of hemoglobin are in the average RBC?
7. Trace the formation of a mature erythrocyte from its stem cell precursor.
8. Explain the negative feedback loop that controls erythropoiesis.
White Blood Cells (Leukocytes)
There are five basic types of white blood cells, or leukocytes. They are classified according to the presence or absence of granules as well as the staining characteristics of their cytoplasm. Granulocytes include the three types of WBCs that have granules in their cytoplasm. They are named according to their cytoplasmic staining properties: basophils, neutrophils, and eosinophils. There are two types of agranulocytes (WBCs without cytoplasmic granules): lymphocytes and monocytes.
As a group, the leukocytes appear brightly colored in stained preparations. In addition, they all have nuclei and are generally larger than RBCs. Before continuing with the following discussion of each type, please look at Table 16-1 and briefly familiarize yourself with each cell type, its description, and function.
Granulocytes
Neutrophils
The cytoplasmic granules of neutrophils (Figure 16-6) stain a light purple with neutral dyes. The granules in these cells are small and numerous. They tend to give the cytoplasm a coarse appearance. The cytoplasmic granules contain powerful lysosomes that allow them to destroy most bacterial cells.
Neutrophils make up about 65% of the WBC count in a normal blood sample. They are highly mobile, active phagocytic cells that can migrate out of blood vessels and enter into the tissue spaces. This process is called diapedesis. It is vital to the body's fight against invading bacteria. It works like this: Bacterial infections produce an inflammatory response. In this process, damaged cells of the body release chemicals that attract neutrophils and other phagocytic WBCs to the infection site. The swelling, pain, and heat from the infection site are indications that the battle is underway.
FIGURE 16-6 Neutrophil.
FIGURE 16-7 Eosinophil.
Eosinophils
Eosinophils (Figure 16-7) contain many large cytoplasmic granules that stain orange with acid dyes such as eosin. Their nuclei generally have just two lobes. Eosinophils equal about 2% to 5% of circulating WBCs. They are abundant in the linings of the respiratory and digestive tracts. Eosinophils can ingest inflammatory chemicals and proteins associated with antigen-antibody reaction complexes. Perhaps their most important functions involve protection against infections caused by parasitic worms. They are also involved in allergic reactions, as we shall see in Chapter 19.
Basophils
Basophils (Figure 16-8) have few, but relatively large, cytoplasmic granules that stain dark purple with basic dyes. The cytoplasmic granules of basophils contain histamine (an inflammatory chemical) and heparin (an anticoagulant). Basophils have indistinct, S-shaped nuclei. They are the least numerous of the WBCs, numbering only 0.5% to 1% of the total leukocyte count. Like neutrophils, basophils are both mobile and capable of diapedesis.
FIGURE 16-8 Basophil.
Agranulocytes
Lymphocytes
Lymphocytes (Figure 16-9) are the smallest of the leukocytes, averaging only about 6 to 9 μm in diameter. They have large, spherical nuclei surrounded by a small amount of cytoplasm that stains a pale blue. After neutrophils, lymphocytes are the most numerous WBCs. They account for about 25% of all the leukocytes in our bodies.
There are two general types of lymphocytes: T lymphocytes and B lymphocytes. Both forms have important roles in our immunity. T lymphocytes function by directly attacking an infected or cancerous cell. B lymphocytes, in contrast, produce antibodies against specific antigens.
FIGURE 16-9 Lymphocyte.
Monocytes
Monocytes (Figure 16-10) are the largest of the leukocytes. They have dark, kidney bean–shaped nuclei surrounded by large quantities of distinctive blue-gray cytoplasm. Monocytes are mobile and highly phagocytic: They can engulf large bacterial organisms and virus-infected cells.
FIGURE 16-10 Monocyte.
BOX 16-3 Diagnostic Study
Complete Blood Cell Count
One of the most useful and frequently performed clinical blood tests is called the complete blood cell count or simply the CBC. The CBC is a collection of tests whose results, when interpreted as a whole, can yield an enormous amount of information regarding a person's health. Standard red blood cell, white blood cell, and thrombocyte counts, the differential white blood cell count, hematocrit, hemoglobin content, and other characteristics of the formed elements are usually included in this battery of tests.
White Blood Cell Numbers
Compared to erythrocytes, leukocytes are relatively rare. One cubic millimeter of normal blood usually contains only about 5,000 to 9,000 leukocytes. As we've seen, there are different percentages of each type. These numbers have clinical significance because they may change drastically under abnormal conditions such as infections or specific blood cancers. In acute appendicitis, for example, the percentage of neutrophils increases dramatically. So does the total WBC count. In fact, these characteristic changes may be deciding points for surgery to remove the infected organ.
An overall decrease in the number of WBCs is called leukopenia. An increase in the number of WBCs is leukocytosis. The number of each type of white blood cell can be determined by a differential white blood cell (WBC) count. In this special count (Table 16-2), the proportion of each type of white blood cell is reported as a percentage of the total WBC count. Because all disorders do not affect each type of WBC the same way, the differential WBC count is a valuable diagnostic tool. For example, some parasite infestations do not cause an increase in the total WBC count. However, they often do cause an increase in the proportion of eosinophils. Why? Because this type of WBC specializes in fighting large parasites such as parasitic nematode “worms.” Table 16-2 presents a differential count of the major white blood cell types in the blood of an average person.
Formation of White Blood Cells
Hematopoietic stem cells serve as the precursors not only of erythrocytes, but also of leukocytes and platelets. Refer to Figure 16-4 again and follow the formation and maturation of the various leukocytes from the precursor hematopoietic stem cells (hemocytoblasts). Like erythrocytes, neutrophils, eosinophils, basophils, and a few lymphocytes and monocytes originate in red bone marrow (myeloid tissue). However, note that most lymphocytes and monocytes are derived from hematopoietic adult stem cells in lymphatic tissue. So although many lymphocytes are found in bone marrow, most are formed in lymphatic tissue and later carried to the bone marrow by the bloodstream.
TABLE 16-2 Differential Count of White Blood Cells
DIFFERENTIAL COUNT*
CLASS
NORMAL RANGE (%)
TYPI CAL VALU E (%)†
Neutrophils
65–75
65
Lymphocytes (large and small)
20–25
25
Monocytes
0–3
6
Eosinophils
0–2
3
Basophils
½–1
1
TOTAL
100
100
* In any differential count the sum of the percentages of the different kinds of WBCs must, of course, total 100%.
† This mnemonic phrase may help you remember percent values in decreasing order: “Never Let Monkeys Eat Bananas.”
Myeloid tissue and lymphatic tissue together constitute the hematopoietic, or blood cell–forming, tissues of the body. Red bone marrow is myeloid tissue that actually produces (red) blood cells. Yellow marrow is yellow because it stores a large amount of fat. Yellow marrow remains yellow except during times of disease, when it can become active and red in color because it also produces red blood cells.
Platelets (Thrombocytes)
Platelets or thrombocytes are really tiny fragments of cells (see Table 16-1). They are nearly colorless bodies that appear as irregular spindles or oval disks about 2 to 4 μm in diameter. Their functions are varied and have to do with clotting: cell aggregation, adhesiveness, and agglutination. It's difficult to see them in a slide presentation because, as soon as blood is drawn, the platelets adhere to each other and to every surface they contact. This phenomenon makes them assume many irregular forms.
A range of 150,000 to 400,000 platelets/mm3 is considered normal for adults, but newborns often show reduced numbers. Unlike erythrocytes, there are no differences between the sexes in platelet count.
Function of Platelets
Platelets play vital roles in hemostasis and coagulation. Hemostasis refers to the stoppage of blood flow from an injured vessel. This may occur as a result of any one of several body defense mechanisms. One of these mechanisms is formation of a platelet plug, which temporarily reduces or stops blood flow. Formation of a platelet plug is usually followed by coagulation, which forms a more solid clot.
Within 1 to 5 seconds after injury to a blood capillary, a platelet plug is formed when platelets adhere to the damaged wall of the vessel. This plug helps stop the flow of blood into the tissues. The formation of the plug generally follows vascular spasms caused by the constriction of smooth muscle fibers in the wall of the damaged blood vessel, which also helps reduce blood flow.
When platelets encounter collagen in damaged vessel walls and surrounding tissue, they become sticky platelets. These sticky platelets then bind to underlying tissues and each other, forming the plug. In addition, sticky platelets secrete several biochemicals, including adenosine diphosphate (ADP), thromboxane (a local hormone), and a fatty acid (arachidonic acid). When these chemicals are released, they affect both local blood flow (by vasoconstriction) and platelet aggregation at the site of injury. If the injury is extensive, the blood-clotting mechanism (coagulation) is also activated.
Platelet plugs are also vital in controlling so-called microhemorrhages, which may involve a break in a single capillary. Failure to stop hemorrhage from minor but numerous and widespread capillary breaks can result in life-threatening internal blood loss. In certain types of peripheral vascular disease, platelet plugs may also be involved in creating blockage in small vessels, including arterioles.
Formation and Life Span of Platelets
Thrombopoiesis is the formation of platelets (see Figure 16-4). Mature megakaryocytes are huge cells that often have a bizarre shape. The abundant cytoplasm is blue to pink in color and contains a variable number of very fine granules. Between 2,000 and 3,000 platelets are created when the irregular cytoplasmic membrane surrounding the mature megakaryocyte ruptures. The resulting platelets have a plasma membrane but no nucleus. Platelets have a short life span of about 7 days.
BLOOD TYPES (BLOOD GROUPS)
The term blood type refers to the types of biochemical markers or antigens present on the plasma membranes of erythrocytes. (You can find a complete discussion of the concept of antigens and their associated antibodies in Chapter 19.) For example, there are blood antigens A and B in the ABO system. There is also a group of six Rh antigens. To date, researchers have isolated nearly two dozen additional blood antigens that vary from person to person. This variability is important because our immune system may “attack” donated blood cells (from a transfusion) if they have antigens different than our own. As you may know, antigens A, B, and Rh are the most important blood antigens as far as transfusions and newborn survival are concerned. The other blood antigens are less important clinically but may still cause occasional problems with transfusions.
Why do different people have different antigens on their RBCs? We don't have a complete answer to that question. However, a good working hypothesis is that their presence or absence may give some biological advantage to groups of people living under different environmental conditions. For example, an antigen called Duffy (after the patient in whom it was first discovered) is often missing in populations that have lived with the threat of malaria for many generations. The Duffy antigen is used by the malaria parasite to enter RBCs. So, its absence protects a person against developing malaria. This is because the parasite cannot “identify” its host red blood cells and, therefore, it cannot reproduce itself in the body.
FIGURE 16-11 ABO blood types. Note that antigens characteristic of each blood type are bound to the surface of RBCs. The antibodies of each blood type are found in the plasma and exhibit unique structural features. This permits agglutination to occur if exposure to the appropriate antigen occurs.
The term agglutinin is often used to describe the antibodies dissolved in plasma that react with specific blood group antigens, or agglutinogens. When they combine and react, they cause RBCs to clump together or agglutinate. When a blood transfusion is given, great care must be taken to prevent a mixture of agglutinogens (antigens) and agglutinins (antibodies) from agglutinating. This is especially true with the ABO and Rh blood groups. If the wrong blood types are mixed together during a blood transfusion, a transfusion reaction may take place. As the different blood types agglutinate, blood clots form that block blood vessels and cause serious problems in the body. Clinical laboratory tests, called blood typing and crossmatching, ensure the proper identification of blood group antigens and antibodies in both donor and recipient blood.
A&P CONNECT
Blood transfusions are an important therapeutic tool. Learn more about blood transfusions, blood banking, and even artificial blood in Blood Transfusions online at A&P Connect.
FIGURE 16-12 Agglutination. A, When mixing of donor and recipient blood of the same type (A) occurs, there is no agglutination because only type B antibodies are present. B, If type A donor blood is mixed with type B recipient blood, agglutination will occur because of the presence of type A antibodies in the type B recipient blood.
The ABO System
Every person's blood belongs to one of the four ABO blood types (groups). These blood types are named according to the antigen present on the membranes of the RBCs:
1.Type A—antigen A on RBCs
2.Type B—antigen B on RBCs
3.Type AB—both antigen A and B on RBCs
4.Type O—neither antigen A nor B on RBCs
Blood plasma may or may not contain antibodies (agglutinins) that can react with RBC antigen A or antigen B. An important principle related to this is that plasma never contains antibodies against the antigens present on its own red blood cells. If it did, the antibody would react with the antigen and destroy the RBCs by agglutination. However, plasma does contain antibodies against antigen A or antigen B if they are not present on its RBCs.
With this in mind, we can deduce the following: In type A blood, antigen A is present on its RBCs. Therefore, its plasma contains no anti-A antibodies but does contain anti-B antibodies. Similarly, in type B blood, antigen B is present on its RBCs. Therefore, its plasma contains no anti-B antibodies
FIGURE 16-13 Results of (crossmatching) different combinations (types) of donor and recipient blood. The left columns show the antigen and antibody characteristics that define the recipient's blood type, and the top row shows the donor's blood type. Crossmatching identifies either a compatible combination of donor-recipient blood (no agglutination) or an incompatible combination (agglutinated blood). Photo inset shows drops of blood showing appearance of agglutinated and nonagglutinated red blood cells.
but does contain anti-A antibodies (Figure 16-11). Before going on, re-read the last two paragraphs to make sure you have an understanding of antigen and antibody.
Now look at Figure 16-12, A. You can see that type A blood donated to a type A recipient does not cause an agglutination transfusion reaction. This is because the type B antibodies in the recipient do not combine with the type A antigens in the donated blood. However, type A blood donated to a type B recipient causes an agglutination transfusion reaction. This is because the type A antibodies in the recipient combine with the type A antigens in the donated blood (Figure 16-12, B). Figure 16-13 shows you the results of different combinations of donor and recipient blood.
Because type O blood does not contain either antigen A or B, it has often been called the universal donor. This is not quite true because the recipient's blood may contain agglutinins other than anti-A or anti-B antibodies. This is why the recipient's and the donor's blood—even if it is type O—should be crossmatched to check for agglutination. In contrast, universal recipient (type AB) blood contains neither anti-A nor anti-B antibodies. For this reason, it cannot agglutinate type A or type B donor red blood cells. However, other agglutinins may be present in this so-called universal recipient blood and may clump unidentified antigens in the donor's blood. Again, as with type O blood, crossmatching tests should be conducted to make sure there is no agglutination due to other agglutinins.
As you can see from the examples above, improperly typed and crossmatched blood given during a blood transfusion can cause a transfusion reaction in the recipient. As the host antibodies attack the donor RBCs, the RBCs are broken apart in a process called hemolysis. Hemoglobin is released into the bloodstream, which may overload the kidneys and cause their failure and death. Signs of this type of transfusion reaction include fever, difficulty breathing, and pink urine.
9. Name the granulocytic and agranulocytic leukocytes.
10. List the normal percentages of the different types of WBCs found in a differential count.
11. What is the ABO blood group system?
12. Identify the antigens and antibodies (if any) associated with the ABO blood groups.
The Rh System
The term Rh-positive blood means that an Rh antigen is present on the blood's RBCs. In contrast, Rh-negative blood does not have Rh antigens present on its red blood cells. We should note here that blood does not normally contain anti-Rh antibodies. However, anti-Rh antibodies can appear in the blood of an Rh-negative person if Rh-positive RBCs have at one time in the past entered the bloodstream. One way this can happen is by giving an Rh-negative person a transfusion of Rh-positive blood. In a short time, the person's immune system makes anti-Rh antibodies, and these remain in the blood.
The other way in which Rh-positive RBCs can enter the bloodstream of an Rh-negative individual can happen
FIGURE 16-14 Erythroblastosis fetalis. A, Rh-positive blood cells enter the mother's bloodstream during delivery of an Rh-positive baby. If not treated, the mother's body will produce anti-Rh antibodies. B, A later pregnancy involving an Rh-negative baby is normal because there are no Rh antigens in the baby's blood. C, A later pregnancy involving an Rh-positive baby may result in erythroblastosis fetalis. Anti-Rh antibodies enter the baby's blood supply and cause agglutination of RBCs with the Rh antigen.
to a woman during pregnancy. Herein lies the danger for a baby born to an Rh-negative mother and an Rh-positive father: If the offspring inherits the Rh-positive trait from the father, the Rh factor on the offspring's RBCs may stimulate the mother's body to form anti-Rh antibodies. Then, if the mother carries another Rh-positive fetus in a future pregnancy, the fetus may develop a disease called erythroblastosis fetalis. This is a serious hemolytic condition caused by the mother's anti-Rh antibodies reacting with the offspring's Rh-positive cells (Figure 16-14). All Rh-negative mothers who carry an Rh-positive baby should be treated with a protein marketed under the name RhoGAM. This product stops the mother's body from forming anti-Rh antibodies and thus prevents the possibility of harm to the next Rh-positive offspring she may have.
TABLE 16-3 Blood Typing
BLOOD TYPE (ABO, RH)
ANTIGENS PRESENT*
ANTIBODIES PRESENT*
PERCENTAGE OF GENERAL POPULATION
O,+
Rh
A, B
35%
O, −†
None
A, B, Rh?
7%
A, +
A, Rh
B
35%
A, −
A
B, Rh?
7%
B, +
B, Rh
A
8%
B, −
B
A, Rh?
2%
AB, +‡
A, B, Rh
None
4%
AB, −
A, B
Rh?
2%
From Pagana KD, Pagana TJ: Mosby's Manual of Diagnostic and Laboratory Tests, ed 4. St. Louis: Mosby, 2010.
* Anti-Rh antibodies may be present, depending on exposure to Rh antigens.
† Universal donor.
‡ Universal recipient.
Table 16-3 summarizes for you the ABO and Rh blood types, including the frequency of each in the general population. Of course, the frequency of these and other blood types may be different within a family or ethnic group based on regional differences in human populations.
BLOOD PLASMA
Plasma is the liquid part of the blood. That is, plasma is whole blood without the formed elements (see again Figures 16-1 and 16-2). Plasma is prepared by spinning whole blood down in a centrifuge at a high rate of speed. The end result is a clear, straw-colored fluid—blood plasma—lying above the cell layer in the test tube.
Plasma consists of 90% water and 10% solutes. Normally, about 6% to 8% of the solutes consist of proteins. These proteins include some clotting factors, gamma globulins (important in treating weakened immune systems), and albumin (a blood volume expander). Other solutes present in much smaller amounts include glucose, amino acids, and lipids, as well as urea, uric acid, creatinine, and lactic acid; oxygen and carbon dioxide; and hormones and enzymes.
Blood solutes are classified as electrolytes (molecules that ionize in solution, such as proteins and inorganic salts) or nonelectrolytes (molecules that do not ionize, such as glucose and lipids).
The proteins in blood plasma consist of three main kinds of compounds: albumins, globulins, and clotting proteins (principally fibrinogen). A total of approximately 6 to 8 grams of proteins occupy a blood plasma volume of 100 ml. Albumins constitute about 55% of this total, globulins about 38%, and fibrinogen about 7%.
Plasma proteins are critically important substances. For example, fibrinogen and a clotting protein named prothrombin are vital to our blood-clotting mechanism. Globulins function as essential components of the immunity mechanism. Many modified globulins, called gamma globulins, serve important roles as circulating antibodies (see Chapter 19). All plasma proteins contribute to the maintenance of normal (1) blood viscosity, (2) blood osmotic pressure, and (3) blood volume. As you might surmise, therefore, plasma proteins play an essential part in maintaining normal circulation.
Synthesis of most plasma proteins occurs in our liver cells. These cells form many of the plasma proteins—except some of the gamma globulin antibodies synthesized by plasma cells (recall that plasma cells are a type of lymphocyte). Cancer of plasma cells, called multiple myeloma, results in the production of an abnormal myeloma antibody. These gamma globulin antibodies cause a number of very serious disease symptoms.
BLOOD CLOTTING (COAGULATION)
The coagulation of blood seals ruptured vessels to stop bleeding in a process called hemostasis, as we have seen. A secondary function of coagulation is to prevent bacteria from invading our tissues. Somehow, our bodies must know when to coagulate. After all, coagulation of blood when it is not necessary can lead to blood clots and blockage of vessels. Such random clotting would deprive our tissues from life-sustaining oxygen. Such abnormal clotting is a frequent cause of heart attacks and strokes.
Although we have an abundance of information about the process of blood clotting, we are still shy of a complete understanding. Our best efforts to summarize what we know are presented for you in Figure 16-15.
Over a century ago, researchers determined that there are four essential components critical to coagulation: (1) prothrombin, (2) thrombin, (3) fibrinogen, and (4) fibrin. However, many coagulation factors and their functions have been discovered in recent decades. Here we divide the basic process into an extrinsic clotting pathway and intrinsic clotting pathway.
As you read through the following paragraphs, please refer to Figure 16-15. Notice that there are two pathways in the process of blood clotting. In both pathways, a series of chemical reactions called a clotting cascade precedes the formation of prothrombin activator.
In the extrinsic pathway, chemicals are released from damaged tissue outside the blood that ultimately results in the formation of prothrombin activator.
In contrast, the intrinsic pathway involves a series of reactions that begin with factors normally present in, or intrinsic to, the blood. For example, damage to the endothelial lining of blood vessels exposes collagen fibers. In turn, exposure of these fibers triggers the activation of a number of coagulation factors in the plasma. Sticky platelets participate in the intrinsic pathway, ultimately inducing the production of prothrombin activator.
Regardless of the pathway involved, after prothrombin activator is produced, a clot will form. Thrombin accelerates conversion of the soluble plasma protein fibrinogen to insoluble fibrin. Then formation of fibrin strands forms a fibrin clot. Fibrin appears in blood as fine tangled threads. As blood flows through the fibrin mesh, its formed elements are caught in the mesh. Because most of the cells are RBCs, clotted blood has a red color. The pale yellowish liquid left after a clot forms is blood serum. This serum is different from plasma because it has lost its clotting elements.
The overall reactions of clotting can be summarized as follows:
Liver cells synthesize both prothrombin and fibrinogen, as they do almost all other plasma proteins. For the liver to synthesize prothrombin at a normal rate, blood must contain an adequate amount of vitamin K. This vitamin is absorbed into the blood from the intestine. Some foods contain vitamin K, but it is also synthesized in the intestine by certain bacteria (not present for a time in newborn infants). Because vitamin K is fat soluble, its absorption requires bile (from the liver). Therefore, if the bile ducts become obstructed and bile cannot enter the intestine, a vitamin K deficiency develops. As a result, the liver cannot produce prothrombin at its normal rate, and the blood's prothrombin concentration soon falls below its normal level. A prothrombin deficiency gives rise to a bleeding tendency. As a preoperative safeguard, therefore, surgical patients with jaundice caused by
FIGURE 16-15 Blood-clotting mechanism. A, The complex clotting mechanism can be summarized into three basic steps: (1) release of clotting factors from both injured tissue cells and sticky platelets at the injury site (which forms a temporary platelet plug); (2) a series of chemical reactions that eventually result in the formation of thrombin; and (3) formation of fibrin and trapping of blood cells to form a clot. B, Photo inset is a colorized electron micrograph showing RBCs and platelets (blue) entrapped in a fibrin (yellow) mesh during clot formation.
obstruction of the bile ducts are generally given some kind of vitamin K preparation.
Conditions that Oppose Clotting
There are several conditions that oppose clot formation in intact vessels to prevent abnormal, unnecessary clots from forming. The most important of these anti-clotting mechanisms is the perfectly smooth surface of the interior of the vessel created by the endothelial lining. Platelets cannot adhere to this lining and therefore do not activate and release platelet factors into the blood.
Additional deterrents to clotting are antithrombins, which inactivate thrombin. In this manner, antithrombins prevent thrombin from converting fibrinogen to fibrin. Heparin, a natural constituent of blood, acts as an antithrombin. It was first discovered in the liver (heparin means “liver substance”), but other organs also contain heparin. Injections of heparin are used to prevent abnormal clots from forming in vessels.
Coumarin compounds impair the liver's use of vitamin K and slow its synthesis of prothrombin and clotting factors. Indirectly, therefore, coumarin compounds retard coagulation. Citrates keep donor blood from clotting before transfusion. Aspirin and other drugs, such as clopidogrel (Plavix) or cilostazol (Pletal), that inhibit platelet aggregation, also inhibit coagulation (Box 16-4).
BOX 16-4 Health Matters
Anticoagulant and Antiplatelet Drug Treatments
If an individual is at risk for abnormal clot formation, selecting a so-called targeted or rational drug treatment plan may depend on the location in the vascular system in which the clots may form. Research has shown that abnormal clots in veins consist mainly of fibrin and red blood cells, whereas in arteries they consist mainly of platelet aggregates. This information provides a theoretical basis for selecting different types of drug treatment for conditions caused by either venous or arterial clots.
For example, anticoagulant drugs such as heparin and warfarin (Coumadin) should be more effective in prevention of venous thrombi. However, drugs that decrease the tendency for platelets to become sticky and form aggregates (antiplatelet drugs) should be more effective in preventing arterial thrombi.
A number of antiplatelet drugs, such as cilostazol (Pletal) and ticlopidine (Ticlid), exert effects by inhibiting an enzyme called phosphodiesterase, which is involved in platelet aggregation activity. Another popular antiplatelet drug, clopidogrel (Plavix), is used to prevent arterial clots that may cause a heart attack or stroke.
BOX 16-5 Health Matters
Clinical Methods of Hastening Clotting
One way of treating excessive bleeding is to speed up the blood-clotting mechanism. This can be accomplished by increasing any of the substances essential for clotting, for example:
•By applying a rough surface such as gauze or by gently squeezing the tissues around a cut vessel. Each procedure causes more platelets to activate and release more platelet factors. This in turn accelerates the first of the clotting reactions.
•By applying purified thrombin (in the form of sprays or impregnated gelatin sponges that can be left in a wound). Which stage of the clotting mechanism do you think this treatment should accelerate?
•By applying fibrin foam, films, and similar applications.
Another useful strategy for speeding up the blood-clotting mechanism is the application of cold, which causes vasoconstriction and slows blood flow.
Conditions that Hasten Clotting
Two conditions especially favor clot formation: (1) a rough spot in the endothelial lining of a blood vessel and (2) abnormally slow blood flow.
Atherosclerosis, for example, is associated with an increase tendency toward thrombosis (clot formation). This is because plaques of accumulated cholesterol lipid material in the endothelial lining of arteries form rough spots. Body immobility may also lead to thrombosis because blood flow slows down as movements decrease. (This explains why physicians insist that bed patients must either move or be moved frequently, cruel as this may sound.)
Once started, a clot tends to grow. Platelets enmeshed in the fibrin threads activate, releasing more clotting factors, which in turns causes more clotting. Clot-hastening substances have proved valuable for speeding up this process. We discuss these methods more fully for you in Box 16-5.
Clot Dissolution
Blood clots are dissolved by the physiological process of fibrinolysis. Fibrinolysis occurs slowly, eventually dissolving the clot as the underlying vessel wall repairs itself. Blood clotting occurs continuously and simultaneously with clot dissolution (fibrinolysis). Normal blood contains an inactive plasma protein called plasminogen that can be activated by several substances released from damaged cells. These converting substances include thrombin, clotting factors, tissue plasminogen activator (t-PA), and lysosomal enzymes. Plasminogen hydrolyzes (breaks down) fibrin strands and dissolves the clot.
In today's clinical practice, several different kinds of proteins are used to dissolve blood clots that can cause an acute medical crisis. These are enzymes that generate plasmin when injected into patients. Streptokinase (SK) is a plasminogen-activating factor made by certain bacteria. This factor and recombinant t-PA can be used to dissolve clots in the large arteries of the heart. As you may have heard, blockage of these vital arteries can produce a myocardial infarction or heart attack (for further information, see Chapter 18). In addition, t-PA is a promising drug for the early treatment of strokes caused by a blood clot in a cerebrovascular accident (CVA). If given within the first 6 hours after a clot forms in a cerebral vessel, it can often improve blood flow and greatly reduce the serious aftereffects of this type of stroke.
You may find it interesting that streptococcal bacteria produce blood-dissolving factors such as SK. Recall that a secondary function of blood clotting is to trap bacteria that attempt to enter our tissues. To make their attack more effective, many bacteria such as Streptococcus (strep), Staphylococcus (staph), Escherichia coli (E. coli), and others, release anti-clotting agents to overcome our defenses. Such agents often activate plasminogen and thus disrupt formation of the initial blood clot. In contrast, other bacterial agents bind fibrinogen instead, which disrupts normal clotting as well.
13. What is the significance of the Rh system in pregnancy?
14. Briefly outline the process of clotting.
The BIG Picture
Throughout this book we've stressed the importance of homeostasis and the homeostatic processes that maintain the stability of the internal environment of our bodies. It makes sense that the fluids feeding and bathing our cells must also be kept stable. This is especially true of the blood plasma fluid. It is the blood plasma that transports substances, and even heat energy, around the entire body so that all our tissues are intimately linked together. This, of course, means that substances such as nutrients, wastes, dissolved gases, water, antibodies, and hormones can be transported between almost any two points in the body.
As we've seen, however, blood tissue is not just plasma. It contains the formed elements—blood cells and platelets. The RBCs permit the efficient transport of gaseous oxygen and carbon dioxide. WBCs are vital components of our defense mechanisms. Their presence in blood ensures that they are available to all parts of the body, all of the time, to fight cancer, resist infectious agents, and clean up injured tissues. Platelets provide mechanisms for preventing loss of the fluid that constitutes our internal environment.
All organs and organ systems of the body rely on blood to perform their functions. It's a two-way street. In fact, no organ or organ system can maintain the proper levels of nutrients, dissolved gases, or water without direct or indirect help from the blood. The list is long. For example, the respiratory system excretes carbon dioxide from the blood and picks up oxygen for the entire body via the bloodstream. Likewise, organs of the digestive system pick up nutrients, remove some toxins, and dispose of old blood cells through the flow of blood. The endocrine system regulates the production of blood cells and water content of the plasma. Besides removing toxic wastes such as urea, the urinary system has a vital role in maintaining homeostasis of plasma water concentration and pH.
Of course, blood is useless unless it continually and rapidly flows throughout the entire body. It must transport, defend, and maintain balance for us to survive. The following chapters will show you how blood circulation takes place and how the physiology of the circulatory system is maintained. We will then end our tour of transportation and defense with a thorough review of the lymphatic and immune systems.
Cycle of LIFE
The moment you are born, your body must quickly destroy all the erythrocytes containing fetal hemoglobin and replace them with erythrocytes containing adult hemoglobin. Fortunately, your body is capable of this tremendous feat! Your body destroys over 2.5 million erythrocytes every second. Once you reach adulthood, this is just a tiny fraction of your body's estimated 25 trillion cells. Incredibly, new erythrocytes take only 4 days to develop from stem cells in the bone marrow to mature erythrocytes.
However, because they lack a nucleus and organelles for cellular repair, erythrocytes live for only about 120 days. Damaged and aged blood cells are continually removed from the circulatory system by macrophages in our lymph nodes, spleen, and liver and replaced with newer cells from red bone marrow This process continues throughout our life span.
As we age, the amount of fat in the bone marrow increases, reducing the volume of blood-forming cells. Ordinarily this is not a problem, but under stress caused by disease, the body may require additional erythrocytes, leukocytes, and thrombocytes. When the body cannot meet the additional demand for higher production of erythrocytes, for example, anemia often results.
MECHANISMS OF DISEASE
There are numerous disorders of the formed elements of the blood. These include red blood cell disorders such as anemias, and white blood cell disorders that range from abnormally low or high white blood cell counts to a variety of cancers called leukemias and myelomas. There are also clotting disorders and serious inherited disorders such as sickle cell anemia. Many of these disorders are very difficult to treat.
Find out more about these blood tissue diseases online at Mechanisms of Disease: Blood.
CHAPTER SUMMARY
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INTRODUCTION
A. Blood is a fluid transport medium that serves as a pickup and delivery system throughout the body
B. Blood also transports hormones, enzymes, buffers, and other important biochemicals
C. Flow of blood is vital to temperature regulation in our bodies
BLOOD COMPOSITION
A. Blood is a liquid connective tissue consisting not only of fluid plasma, but also of cells (formed elements)
1. Plasma—third major fluid in our bodies; accounts for 55% of total volume (Figure 16-1)
2. Formed elements—blood cells; accounts for 45% of total volume
B. Blood volume—males have about 5 to 6 liters of blood circulating in their bodies; females have about 4 to 5 liters
1. Blood volume varies with age and body composition
FORMED ELEMENTS OF BLOOD
A. Formed elements include:
1. Erythrocytes—red blood cells (RBCs)
2. Thrombocytes—platelets
3. Leukocytes—white blood cells (WBCs)
B. Red blood cells (erythrocytes)
1. Erythrocytes—shaped like tiny biconcave disks; before the cell reaches maturity in the bone marrow, it extrudes its nucleus (Figure 16-3)
a. Loses its ribosomes, mitochondria, and other organelles
b. Primary component is hemoglobin
c. RBCs are the most numerous of all the formed elements of blood
2. Function of red blood cells—play a critical role in the transport of oxygen and carbon dioxide in the body
3. Hemoglobin—within each RBC are an estimated 200 to 300 million molecules of hemoglobin
a. Composed of four protein (globin) chains with each attached to a heme group
b. One hemoglobin molecule chemically bonds with four oxygen molecules to form oxyhemoglobin
c. Hemoglobin can also combine with carbon dioxide to form carbaminohemoglobin
d. Males' blood usually contains more hemoglobin than that of females
e. Anemia—low RBC count (Box 16-1)
4. Formation of red blood cells (erythropoiesis)
a. Erythrocytes begin their maturation process in the red bone marrow from hematopoietic stem cells called hemocytoblasts
b. Adult blood-forming stem cells divide by mitosis
c. Some of the daughter cells remain as undifferentiated adult stem cells; others continue to develop into erythrocytes (Figure 16-4)
d. Every day of our adult lives, more than 200 billion RBCs are formed to replace an equal number destroyed
e. Homeostatic mechanisms operate to balance the number of cells formed against the number destroyed (Figure 16-5)
5. Destruction of red blood cells—life span of RBCs circulating in the bloodstream averages between 105 and 120 days
a. Macrophage cells phagocytose the aged, abnormal, or fragmented RBCs
(1) This process results in the breakdown of hemoglobin; iron, bilirubin, and amino acids are released
C. White blood cells (leukocytes)
1. Five basic types of white blood cells—classified according to the presence or absence of granules as well as the staining characteristics of their cytoplasm (Table 16-1)
2. Granulocytes—include the three WBCs that have large granules in their cytoplasm
a. Neutrophils—make up about 65% of the WBC count in a normal blood sample (Figure 16-6)
(1) Highly mobile and active phagocytic cells; can migrate out of blood vessels and enter into the tissue spaces (diapedesis)
b. Eosinophils—account for about 2% to 5% of circulating WBCs (Figure 16-7)
(1) Abundant in the linings of the respiratory and digestive tracts
(2) Can ingest inflammatory chemicals and proteins associated with antigen-antibody reaction complexes
(3) Their most important functions involve protection against infections caused by parasitic worms; also involved in allergic reactions
c. Basophils—least numerous of the WBCs, numbering only 0.5% to 1% of the total leukocyte count (Figure 16-8)
(1) Contain histamine and heparin
(2) Mobile and capable of diapedesis
3. Agranulocytes
a. Lymphocytes—account for about 25% of all the leukocytes in our bodies (Figure 16-9)
(1) Two general types of lymphocytes: T lymphocytes and B lymphocytes
b. Monocytes—largest of the leukocytes (Figure 16-10)
(1) Mobile and highly phagocytic
4. White blood cell numbers—one cubic millimeter of normal blood usually contains only about 5,000 to 9,000 leukocytes
a. These numbers have clinical significance because they may change drastically under abnormal conditions (Box 16-3)
5. Formation of white blood cells—granulocytes and agranulocytes mature from the hematopoietic stem cells (Figure 16-4)
a. Neutrophils, eosinophils, basophils, and a few lymphocytes and monocytes originate in red bone marrow
b. Most lymphocytes and monocytes are derived from hematopoietic adult stem cells in lymphatic tissue
c. Myeloid tissue and lymphatic tissue together constitute the hematopoietic tissues of the body
D. Platelets (thrombocytes)—really tiny shards of cells; nearly colorless bodies that appear as irregular spindles or oval disks about 2 to 4 μm in diameter (Table 16-1)
1. A range of 150,000 to 400,000 platelets/mm3 is considered normal for adults; newborns often show reduced numbers
2. Functions are varied and have to do with clotting: cell aggregation, adhesiveness, and agglutination
3. Function of platelets—play vital roles in hemostasis and coagulation
a. Hemostasis—stoppage of blood flow from an injured vessel
b. Platelet plug—helps stop the flow of blood into the tissues
(1) Formed when platelets adhere to the damaged wall of the vessel
(2) Formation of the plug generally follows vascular spasms of smooth muscle fibers in the wall of the damaged blood vessel; helps reduce blood flow
c. When platelets encounter collagen in damaged vessel walls and surrounding tissue, they become sticky platelets
(1) Sticky platelets then form the plug
(2) Sticky platelets secrete several biochemicals that affect local blood flow
d. If the injury is extensive, the coagulation mechanism is also activated
4. Formation and life span of platelets—thrombopoiesis is the formation of platelets
a. Between 2,000 and 3,000 platelets are created when the cytoplasmic membrane of huge mature megakaryocytes rupture
b. Platelets have a short life span of about 7 days
BLOOD TYPES (BLOOD GROUPS)
A. Blood type—refers to the types of biochemical markers or antigens present on the plasma membranes of erythrocytes
1. A, B, and Rh are the most important blood antigens as far as transfusions and newborn survival are concerned
2. Agglutinin—the antibodies dissolved in plasma that react with specific blood group antigens or agglutinogens
a. When they combine and react, they cause RBCs to clump together or agglutinate
B. The ABO system—every person's blood belongs to one of the four ABO blood types (Table 16-3)
1. Blood types are named according to the antigen present on the membranes of the RBCs
a. Type A—antigen A on RBCs
b. Type B—antigen B on RBCs
c. Type AB—both antigen A and B on RBCs
d. Type O—neither antigen A nor B on RBCs
2. Universal donor—type O; does not contain either antigen A or B
3. Universal recipient—type AB; contains neither anti-A nor anti-B antibodies
C. The Rh system (Figure 16-14)
1. Rh positive—Rh antigen is present on its RBCs
2. Rh negative—RBCs have no Rh antigen present
3. Blood does not normally contain anti-Rh antibodies; anti-Rh antibodies can appear in the blood of an Rh-negative person if it has come in contact with Rh-positive RBCs
BLOOD PLASMA
A. Plasma—liquid part of the blood; consists of 90% water and 10% solutes (Figure 16-2)
B. Solutes—6% to 8% of the solutes consist of proteins; three main compounds:
1. Albumins
2. Globulins
3. Clotting proteins (fibrinogen)
C. Plasma proteins contribute to the maintenance of normal blood viscosity, blood osmotic pressure, and blood volume
BLOOD CLOTTING (COAGULATION)
A. Coagulation of blood plugs ruptured vessels to stop bleeding and prevents bacteria from invading our tissues
B. Four essential components critical to coagulation (Figure 16-15):
1. Prothrombin
2. Thrombin
3. Fibrinogen
4. Fibrin
C. Two basic processes of coagulation
1. Extrinsic clotting pathway—chemicals are released from damaged tissue outside the blood that ultimately results in the formation of prothrombin activator
2. Intrinsic clotting pathway—involves a series of reactions that begin with factors normally present in, or intrinsic to, the blood
a. After prothrombin activator is produced, a clot will form
b. Thrombin accelerates conversion of the soluble plasma protein fibrinogen to insoluble fibrin
c. Polymerization of fibrin strands forms a fibrin clot
D. Conditions that oppose clotting
1. Perfectly smooth surface of the interior of a blood vessel
2. Antithrombins—prevent thrombin from converting fibrinogen to fibrin; example: heparin
E. Conditions that hasten clotting
1. Abnormally slow blood flow
F. Clot dissolution—clots are dissolved by the physiological process of fibrinolysis
1. Plasminogen—hydrolyzes fibrin strands and dissolves the clot
2. Streptokinase (SK)—plasminogen-activating factor made by certain streptococci bacteria; used to dissolve clots in the large arteries of the heart
CHAPTER 17 Anatomy of the Cardiovascular System
STUDENT LEARNING OBJECTIVES
At the completion of this chapter, you should be able to do the following:
1.Describe the position of the heart and its coverings.
2.Outline the major chambers and valves of the heart and give their functions.
3.Trace a drop of blood as it travels through the heart.
4.Discuss the role and operation of the coronary arteries and veins.
5.Compare the physical properties of arteries, veins, and capillaries.
6.Compare systemic circulation with pulmonary circulation.
7.List the major arteries and veins servicing the thoracic and abdominal regions.
8.List the major arteries and veins servicing the head and neck regions.
9.List the major arteries and veins servicing the arms and legs.
10.Discuss the significance of the hepatic portal system.
11.Outline the basic plan of fetal circulation.
12.Describe the changes in fetal circulation that take place at birth.
LANGUAGE OF SCIENCE AND MEDICINE
Before reading the chapter, say each of these terms out loud. This will help you avoid stumbling over them as you read.
abdominal aorta (ab-DOM-ih-nal ay-OR-tah)
[abdomin- belly, -al relating to, aort- lifted, -a thing] pl., aortae or aortas (ay-OR-tee, ay-OR-tahz)
angiography (an-jee-AH-graf-ee)
[angi- vessel, -graph- draw, -y process]
aorta (ay-OR-tah)
[aort- lifted, -a thing] pl., aortae or aortas (ay-OR-tee, ay-OR-tahz)
aortic aneurysm (ay-OR-tik AN-yoo-riz-em)
[aort- lifted, -ic relating to, aneurysm widening]
aortic arch (ay-OR-tik)
[aort- lifted, -ic relating to]
arterial anastomosis (ar-TEER-ee-al ah-nas-toh-MOH-sis)
[arteria- vessel, -al relating to, ana- anew, -stomo- mouth, -osis condition] pl., anastomoses (ah-nas-toh-MOH-seez)
arteriole (ar-TEER-ee-ohl)
[arteri- vessel, -ole little]
artery (AR-ter-ee)
[arteri- vessel]
ascending aorta (ah-SEND-ing ay-OR-tah)
[ascend- climb, aort- lifted, -a thing] pl., aortae or aortas (ay-OR-tee, ay-OR-tahz)
ascites (a-SYT-eez)
[acites baglike]
atherosclerosis (ath-er-oh-skleh-ROH-sis)
[athero- gruel, -scler- hardening, -osis condition]
atrioventricular (AV) valve (ay-tree-oh-ven-TRIK-yoo-lar)
[atrio- entrance courtyard, -ventr- belly, -icul- little, -ar relating to]
atrium (AY-tree-um)
[atrium entrance courtyard] pl., atria (AY-tree-ah)
autorhythmic (aw-toh-RITH-mic)
[auto- self, -rhythm- rhythm, -ic relating to]
avascular (ah-VAS-kyoo-lar)
[a- without, -vas- vessel, -ula- little, -ar relating to]
axillary vein (AK-sih-lair-ee)
[axilla wing, -ary relating to]
bicuspid valve (bye-KUS-pid)
[bi- double, -cusp- point, -id characterized by]
brachial vein (BRAY-kee-al)
[brachi- arm, -al relating to]
brachiocephalic artery (brayk-ee-oh-seh-FAL-ik AR-ter-ee)
[brachi- arm, -cephal- head, -ic relating to, arteri- vessel]
brachiocephalic vein (brayk-ee-oh-seh-FAL-ik)
[brachi- arm, -cephal- head, -ic relating to]
capacitance (kah-PASS-ih-tens)
[capacit- space or volume, -ance state]
capillary (KAP-ih-lair-ee)
[capill- hair, -ary relating to]
cardiovascular system (kar-dee-oh-VAS-kyoo-lar SIS-tem)
[cardi- heart, -vas- vessel, -cul- little, -ar relating to]
chordae tendineae (KOR-dee ten-DIN-ee-ee)
[chorda string or cord, tendinea pulled tight] sing., chorda tendinea (KOR-dah ten-DIN-ee-ah)
collateral circulation (koh-LAT-er-al ser-kyoo-LAY-shun)
[co- together, -later- side, -al relating to, circulat- go around, -tion process]
common carotid artery (kah-ROT-id AR-ter-ee)
[caro- heavy sleep, -id relating to, arteri- vessel]
conduction system of the heart (kon-DUK-shen SIS-tem)
[conduct- lead, -tion process, system organized whole]
coronary artery (KOHR-oh-nair-ee AR-ter-ee)
[corona- crown, -ary relating to, arteri- vessel]
coronary sinus (KOR-oh-nair-ee SYE-nus)
[corona- crown, -ary relating to, sinus- hollow]
cusp (kusp)
[cusp point]
descending aorta (ay-OR-tah)
[aort- lifted, -a thing] pl., aortae or aortas (ay-OR-tee, ay-OR-tahz)
ductus arteriosus (DUK-tus ar-teer-ee-OH-sus)
[ductus duct, arteri- vessel, -osus relating to]
ductus venosus (DUK-tus veh-NO-sus)
[ductus duct, ven- vein, -osus relating to]
elastic artery (eh-LAS-tik AR-ter-ee)
[elast- drive or beat out, -ic relating to, arteri- vessel]
endocardium (en-doh-KAR-dee-um)
[endo- within, -cardi- heart, -um thing]
epicardium (ep-ih-KAR-dee-um)
[epi- on or upon, -cardi- heart, -um thing]
external iliac vein (eks-TER-nal IL-ee-ak)
[extern- outside, -al relating to, ilium flank]
external jugular vein (eks-TER-nal JUG-yoo-lar)
[extern- outside, -al relating to, jugul- neck, -ar relating to]
femoral vein (FEM-or-al)
[femor- thigh, -al relating to]
fetal alcohol syndrome (FAS) (FEE-tal AL-koh-hol SIN-drohm)
[fet- offspring, -al relating to, syn- together, -drome running or (race) course]
fibrous pericardium (FYE-brus pair-ih-KAR-dee-um)
[fibr- fiber, -ous relating to, peri- around, -cardi- heart, -um thing]
foramen ovale (foh-RAY-men oh-VAL-ee)
[foramen opening, ovale egg shaped] pl., foramina ovales (foh-RAM-ih-nah oh-VAL-eez)
glycogen (GLYE-koh-jen)
[glyco- sweet, -gen produce]
great saphenous vein (sah-FEE-nus)
[saphen- manifest, -ous relating to]
heart
hepatic portal vein (heh-PAT-ik POR-tal)
[hepa- liver, -ic relating to, port- doorway, -al relating to]
inferior vena cava (in-FEER-ee-or VEE-nah KAY-vah)
[infer- lower, -or quality, vena vein, cava hollow] pl., venae cavae (VEE-nee KAY-vee)
internal jugular vein (in-TER-nal JUG-yoo-lar)
[intern- inside, -al relating to, jugul- neck, -ar relating to]
ischemic (is-KEE-mik)
[ischem- hold back, -ic relating to]
metarteriole (met-ar-TEER-ee-ohl)
[meta- change or exchange, arteri- vessel, -ole little]
microcirculation (my-kroh-ser-kyoo-LAY-shun)
[micro- small, circulat- go around, -tion process]
mitral valve (MY-tral)
[mitr- bishop's hat, -al relating to]
muscular artery (MUSS-kyoo-lar AR-ter-ee)
[mus- mouse, -cul- little, -ar relating to, arteri- vessel]
myocardial infarction (MI) (my-oh-KAR-dee-al in-FARK-shun)
[myo- muscle, -cardi- heart, -al relating to, in- in, -farc- stuff -tion- process]
myocardium (my-oh-KAR-dee-um)
[myo- muscle, -cardi- heart, -um thing] pl., myocardia (my-oh-KAR-dee-ah)
papillary muscle (PAP-ih-lair-ee MUSS-el)
[papilla- nipple, -ary relating to, mus- mouse, -cle small]
pericardial fluid (pair-ih-KAR-dee-al FLOO-id)
[peri- around, -cardi- heart, -al relating to, fluid flow]
pericardial space (pair-ih-KAR-dee-al)
[peri- around, -cardi- heart, -al relating to]
pericardium (pair-ih-KAR-dee-um)
[peri- around, -cardi- heart, -um thing] pl., pericardia (pair-ih-KAR-dee-ah)
placenta (plah-SEN-tah)
[placenta flat cake] pl., placentae or placentas (plah-SEN-tee, plah-SEN-tahz)
popliteal vein (pop-lih-TEE-al)
[poplit- back of knee, -al relating to]
portal system (POR-tal SIS-tem)
[port- doorway, -al relating to]
precapillary sphincter (pree-KAP-ih-lair-ee SFINGK-ter)
[pre- before, -capill- hair, -ary relating to]
pulmonary circulation (PUL-moh-nair-ee ser- kyoo-LAY-shun)
[pulmon- lung, -ary relating to, circulat- go around, -tion process]
semilunar (SL) valve (sem-ih-LOO-nar)
[semi- half, -luna moon]
septum (SEP-tum)
[septum fence] pl., septa (SEP-tah)
serous pericardium (SEER-us pair-ih-KAR-dee-um)
[sero- watery fluid, -ous relating to, peri- around, -cardi- heart, -um thing] pl., pericardia (pair-ih-KAR-dee-ah)
subclavian artery (sub-KLAY-vee-an AR-ter-ee)
[sub- below, -clavi- key (clavicle bone), -ula little, arteri- vessel]
subclavian vein (sub-KLAY-vee-an)
[sub- below, -clavi- key (clavicle bone), -an relating to]
superior vena cava (soo-PEER-ee-or VEE-nah KAY-vah)
[super- over or above, -or quality, vena vein, cava hollow] pl., venae cavae (VEE-nee KAY-vee)
systemic circulation (sis-TEM-ik ser-kyoo-LAY-shun)
[system- organized whole, -ic relating to, circulat- go around, -tion process]
thoracic aorta (tho-RASS-ik ay-OR-tah)
[thorac- chest, -ic relating to, aort- lifted, -a thing] pl., aortae or aortas (ay-OR-tee, ay-OR-tahz)
thoroughfare channel (THUR-oh-fair CHAN-el)
[thoroughfare main road, chanel- groove]
tricuspid valve (try-KUS-pid)
[tri- three, -cusp- point, -id characterized by]
true capillary (KAP-ih-lair-ee)
[capill- hair, -ary relating to]
tunica externa (TOO-nih-kah ex-TER-nah)
[tunica tunic or coat, extern- outside] pl., tunicae externae (TOO-nih-kee ex-TER-nee)
tunica intima (TOO-nih-kah IN-tih-mah)
[tunica tunic or coat, intima innermost] pl., tunicae intimae (TOO-nih-kee IN-tih-mee)
tunica media (TOO-nih-kah MEE-dee-ah)
[tunica tunic or coat, media middle] pl., tunicae mediae (TOO-nih-kee MEE-dee-ee)
umbilical artery (um-BIL-ih-kul AR-ter-ee)
[umbilic- navel, -al relating to, arteri- vessel]
umbilical cord (um-BIL-ih-kul)
[umbilic- navel, -al relating to]
umbilical vein (um-BIL-ih-kul)
[umbilic- navel, -al relating to]
vascular anastomosis (VAS-kyoo-lar ah-nas-toh-MOH-sis)
[vas- vessel, -ular relating to, ana- anew, -stomo- mouth, -osis condition] pl., anatomoses (ah-nas-toh-MOH-seez)
vein
venous anastomosis (VEE-nus ah-nas-toh-MOH-sis)
[ven- vein, -ous relating to, ana- anew, -stomo- mouth, -osis condition] pl., anastomoses (ah-nas-toh-MOH-seez)
ventricle (VEN-trih-kul)
[ventr- belly, -icle little]
venule (VEN-yool)
[ven- vein, -ule little]
KYLE (45 years old) finally gave in to his wife's insistence and stopped by his local health clinic. After all, it was in the same building where he was working on a construction job. He had been having some minor chest pain for a couple of days. But, he'd been telling himself the pain was just sore muscles caused by his recent weight lifting. Kyle was expecting the receptionist to make an appointment for him. However, as he described his symptoms (chest pain, some sweating, slight nausea), she interrupted him and called over her shoulder to the nurse. As soon as the nurse was made aware of his symptoms, Kyle was rushed into an exam room, where his heart rate and blood pressure were checked and the electrical activity of his heart was measured (by performing an ECG).
“What's going on?” Kyle asked the doctor a few minutes later. The physician replied, “Based on your symptoms, we think you may have some blockage in your coronary arteries. We'd like to do an angiogram to see what's going on.”
Perhaps you already have an idea what may be taking place in Kyle's body, but certainly you'll know after reading this chapter exactly why the nurse and physician acted immediately.
With the knowledge you have gained from reading this chapter, see if you can answer these questions about Kyle from the Introductory Story.
1. The doctor suspects the potential blockage is in what part of Kyle's body?
a. His brain
b. His liver
c. His neck
d. His heart
“Let's take him over to the Cath Lab,” the physician ordered. Kyle said, “I've heard of a cath lab, but I'm not sure what that means.” “Cardiac catheterization lab,” clarified the nurse. “We're going to insert a small tube…” She kept talking, but Kyle couldn't concentrate on her words. He was suddenly feeling a little anxious. He signed the consent form without really reading it.
In the lab, Kyle changed into a hospital gown as instructed; next he was asked to lie on the table. A nurse began cleaning a spot on his thigh in preparation for inserting a catheter. Kyle was confused—why were they cleaning his leg when it seemed like his heart was the problem?
2. Into which artery will the catheter be inserted?
a. Brachial
b. Popliteal
c. Femoral
d. Tibial
3. From this artery, the catheter will be moved toward the heart through which path?
a. External iliac artery, abdominal aorta, descending aorta, aortic arch, ascending aorta
b. Internal iliac artery, abdominal aorta, ascending aorta, aortic arch, descending aorta
c. Abdominal aorta, descending aorta, aortic arch, ascending aorta
d. Popliteal artery, external iliac artery, abdominal aorta, thoracic aorta, aortic arch
After some dye was injected, the screen monitor showed that Kyle's right coronary artery was partially blocked. The surgeon inserted a balloon through the catheter, which was then inflated to press against the sides of the artery and enlarge its diameter. Next she inserted a metal stent to keep the artery open.
4. The coronary arteries supply oxygen and nutrients for cardiac muscle contraction. The myocardium of which heart chamber receives the most abundant blood supply from the coronary arteries?
a. Left atrium
b. Left ventricle
c. Right atrium
d. Right ventricle
To solve a case study, you may have to refer to the glossary or index, other chapters in this textbook, A&P Connect, Mechanisms of Disease, and other resources.
The cardiovascular system, or circulatory system, consists of a muscular heart and a closed system of vessels (arteries, veins, and capillaries). As the name suggests, blood within the circulatory system is pumped by the heart through a closed circuit of vessels.
As in the adult, survival of the developing embryo also depends on the circulation of blood to maintain homeostasis. In response to this need, the cardiovascular system develops early and reaches a functional state long before any other major organ system. Incredible as it seems, the heart begins to beat regularly early in the fourth week after fertilization.
HEART
Location, Shape, and Size of the Heart
The human heart is a four-chambered muscular organ, shaped and sized roughly like a person's closed fist. It lies in the mediastinum, or middle region of the thorax, just behind the body of the sternum.
You can see the anatomical position of the heart in the thoracic cavity in Figure 17-1, A. The lower border of the heart, forming the apex, lies on the diaphragm. The apex points to the left. To count the apical beat, a physician places a stethoscope directly over the apex, in the space between the fifth and sixth ribs.
At birth, the heart is wide and appears large in proportion to the diameter of the chest cavity. In infants, the heart is 1/130 of the total body weight
FIGURE 17-1 Location of the heart. A, Heart in mediastinum showing relationship to lungs and other anterior thoracic structures. B, Detail of heart with pericardial sac opened.
compared with about 1/300 in the adult. Between puberty and 25 years of age, the heart attains its adult shape and weight—about 310 grams in the average male and 225 grams in the average female. We've illustrated the external details of the heart and great vessels for you in Figures 17-1, B and 17-2. Take a moment to review those before continuing.
Coverings of the Heart
An outer sac, the pericardium, encloses your heart, as you can see in Figure 17-1, B. The loosely fitting outer layer of this sac is the fibrous pericardium. This layer is made of tough, white fibrous tissue and protects the heart and also anchors it to surrounding structures. It also prevents the heart from overfilling with blood. The fibrous pericardium is lined with a smooth, moist serous membrane—the parietal layer of the serous pericardium (Figure 17-3). The same kind of serous membrane directly covers the entire surface of the heart, so we call it the visceral layer of the serous pericardium, or the epicardium. The epicardium is an integral part of the heart wall. (It is important to note that the two layers of the serous pericardium are continuous: At the superior margin of the heart, the parietal layer attaches to the large arteries leaving the heart, and then turns inferiorly and continues over the external heart surfaces as the visceral layer.)
FIGURE 17-2 The heart and great vessels. A, Anterior view. B, Posterior view.
Look again at Figure 17-1, B. Note that the fibrous part of the pericardial sac attaches to the large blood vessels emerging from the top of the heart, but does not attach to the heart itself. Thus, the sac fits loosely around the heart, with a slight space between the visceral layer that adheres to the heart wall and the parietal layer that adheres to the inside of the fibrous sac. The space in between these two layers is called the pericardial space and contains 10 to 15 ml of pericardial fluid (see Figure 17-3). This fluid lubricates the space between the parietal layer of the pericardium and the visceral layer forming the (serous) epicardium.
The fibrous pericardial sac with its smooth, well-lubricated lining provides protection against friction as the heart beats.
Structures of the Heart
Wall of the Heart
Epicardium
The outer layer of the heart wall is called the epicardium, as we've just seen. The epicardium is actually the visceral layer of the serous pericardium already described. In other words, the same structure has two different names: epicardium and serous pericardium.
Myocardium
A thick, contractile, middle layer comprises the bulk of the heart wall. This myocardium is composed largely of cardiac muscle (take a moment to review the structure of cardiac muscle in Chapter 6, page 106). Because
FIGURE 17-3 Wall of the heart. The cutout section of the heart wall shows the outer fibrous pericardium and the parietal and visceral layers of the serous pericardium (with the pericardial space between them). A layer of fatty connective tissue is located between the visceral layer of the serous pericardium (epicardium) and the myocardium. Note that the endocardium covers beamlike projections of myocardial muscle tissue, called trabeculae carneae.
intercalated disks join adjacent cells of the heart (Table 6-5, page 106), large areas of cardiac muscle are electrically coupled into a single functioning unit. This allows your heart to conduct action potentials quickly, thereby ensuring that the chambers contract rhythmically, with great force, rather than as a flutter from a group of disconnected cells.
Unfortunately, myocardial damage can occur in a myocardial infarction (MI) or “heart attack.”
Endocardium
The lining of the interior of the myocardial wall is a delicate layer called the endocardium. The endocardium is made of endothelial tissue, or endothelium. Endothelium lines the heart and continues to line all the vessels of the cardiovascular system. Note in Figure 17-3 that the endocardium covers branched projections of myocardial tissue. These muscular projections are called trabeculae carneae (“fleshy beams”). They help to add force to the inward contraction of the heart wall.
Inward folds or pockets formed by the endocardium also make up the flaps or cusps of the major valves that regulate the flow of blood through the chambers of the heart.
FIGURE 17-4 Interior of the heart. This illustration shows the heart as it would appear if it were cut along a frontal plane and opened like a book. The front portion of the heart lies to your right; the back portion of the heart lies to your left. (Note that each portion has a separate anatomical rosette to facilitate orientation.) The four chambers of the heart—two atria and two ventricles—are easily seen. AV, Atrioventricular; SL, semilunar.
A&P CONNECT
How does a heart attack develop? Take a tour through an illustrated description of the process of an MI in Heart Attack! online at A&P Connect.
1. Describe the position of the heart in anatomical terms.
2. Describe the shape of the heart.
3. What are the major coverings of the heart?
4. What is the primary function of each heart covering?
Chambers of the Heart
The interior of the heart is divided into four cavities, or heart chambers (Figure 17-4). The two upper chambers are called atria (singular, atrium). The two lower chambers are called ventricles. An extension of the heart wall, the septum, separates the left chambers from the right chambers.
The two atria are separated into left and right chambers by the interatrial septum. These chambers receive blood from veins—large blood vessels that return blood to the heart from the entire body. Figure 17-5 shows you how the atria alternately relax to receive blood and then contract to push the blood into the ventricles below. The atria are not very muscular because not much force is needed to deliver the blood to the chambers below. Thus, the muscular walls of the atria are not very thick. Return to Figure 17-2 for a moment. Notice that the auricle (meaning “little ear”) is only the visible earlike flap protruding from each atrium. For this reason, you should not use auricle and atria as synonyms.
Like the atria above them, the two ventricles are also separated into left and right chambers. This very muscular separation is called the interventricular septum. Because the ventricles receive blood from the atria and pump blood out
FIGURE 17-5 Chambers and valves of the heart. A, During atrial contraction, cardiac muscle in the atrial wall contracts, forcing blood through the atrioventricular (AV) valves and into the ventricles. Bottom illustration shows superior view of all four valves, with semilunar (SL) valves closed and AV valves open. B, During ventricular contraction that follows, the AV valves close and the blood is forced out of the ventricles through the SL valves and into the arteries. Bottom illustration shows superior view of SL valves open and AV valves closed.
of the heart into the arteries, the ventricles are really the primary “pumping chambers” of the heart. Because more force is required to pump blood from the ventricles than from the atria, the myocardium of the ventricles is quite thick.
The pumping action of the heart chambers is summarized for you in Figure 17-5. We describe it in much greater detail in Chapter 18.
Valves of the Heart
The heart valves are tough, fibrous structures that permit the flow of blood in one direction only. There are four valves that are vital to the normal functioning of the heart (Figures 17-5 and 17-6). Two of the valves, the atrioventricular (AV) valves, service the openings between the atria and the ventricles. The AV valves have pointed flaps called cusps and for this reason are called cuspid valves. The other two heart valves, the semilunar (SL) valves, are located (1) where the pulmonary artery joins the right ventricle (pulmonary valve) and (2) where the aorta joins the left ventricle (aortic valve). Notice that the valves are named simply for the areas of the heart they service, so you can memorize them by position alone.
Atrioventricular Valves
A strong, fibrous ring encircles and anchors the right atrioventricular (AV) valve within the myocardium. This valve, which regulates the flow of blood from the right atrium into the right ventricle, consists of three cusps of endocardium. The free edge of each flap is anchored to the papillary muscles of the right ventricle by several tendinous cords called chordae tendineae. In a way, these cords are the true “heartstrings” of our hearts.
FIGURE 17-6 Skeleton of the heart. This posterior view shows part of the ventricular myocardium with the heart valves still attached. The rim of each heart valve is supported by a fibrous structure (the skeleton of the heart) that encircles all four valves.
Because the right AV valve has three cusps, it is also called the tricuspid valve. The valve that regulates the left AV opening is similar in structure to the right AV valve, except that it has only two flaps. For this reason we call it the bicuspid valve. More commonly, it is called the mitral valve because it resembles the hat (miter) worn by bishops. The construction of both AV valves allows blood to flow from the atria into the ventricles but prevents it from flowing backward. When the ventricles relax, blood flows through the AV valves from the atria above simply by pushing the flimsy valve cusps aside.
Ventricular contraction, however, forces the blood in the ventricles hard against the valve flaps, closing the valves. Under normal conditions, this prevents blood from leaking back into the atria. The harder the ventricular myocardium contracts, the more strongly it pushes against the AV valves—and the more strongly the papillary muscles hold the AV valves shut. This mechanism thus prevents backflow, no matter how strongly the heart ventricles contract.
Semilunar Valves
The semilunar (SL) valves consist of pocketlike flaps that extend inward from the lining of the pulmonary artery and the aorta. If you were facing a person and looking at a frontal section of his or her heart, you would see that each semilunar valve looks very much like a “half-moon,” after which these valves are named. The semilunar valve at the entrance of the pulmonary artery (pulmonary trunk) is called the pulmonary valve. The semilunar valve at the entrance of the aorta is called the aortic valve.
When the pulmonary and aortic semilunar valves are closed (see Figure 17-5, A), blood fills the spaces between the flaps of the valve and the vessel wall. This makes each flap look like a tiny, filled bucket. When the next ventricular contraction takes place, the blood flowing into the aorta and pulmonary artery pushes the flaps flat against the vessel walls and opens the valves (see Figure 17-5, B). Closure of the semilunar valves prevents the flow of blood backward into the ventricles and ensures that the blood rushes forward.
You should note that the atrioventricular valves prevent blood from flowing back up into the atria from the ventricles. Likewise, the semilunar valves prevent it from flowing back down into the ventricles from the aorta and pulmonary arteries.
Skeleton of the Heart
Figure 17-6 shows you the fibrous structure that we often call the skeleton of the heart. This skeleton consists of a set of connected rings that serve as a semirigid support for the heart valves (on the inside of the rings). It also serves as sites for the attachment of cardiac muscle of the myocardium (on the outside of the rings). The skeleton of the heart also serves as an electrical barrier between the myocardium of the atria and the myocardium of the ventricles. This arrangement allows the ventricles to contract separately from the atria, ensuring the effective pumping of the blood.
Flow of Blood Through the Heart
Try tracing the path of blood flow with your finger, using Figure 17-5 as your guide.
Beginning with the right atrium, blood flows through the right AV (tricuspid) valve into the right ventricle. From the right ventricle, blood then flows through the pulmonary semilunar valve into the first portion of the pulmonary artery, the pulmonary trunk. The pulmonary trunk branches to form the left and right pulmonary arteries. These arteries conduct blood with carbon dioxide to the gas exchange tissues of the lungs. Here they will dispose of the carbon dioxide and pick up oxygen.
Blood flows from the lungs via the pulmonary veins back to the heart. (Note that these veins are carrying blood that is oxygenated from its journey through the lungs.) Oxygenated blood from the pulmonary veins flows into the left atrium of the heart. From the left atrium, blood flows through the left atrioventricular (mitral) valve into the left ventricle. From the left ventricle, blood then flows through the aortic semilunar valve into the aorta. Branches of the aorta then supply all the tissues of the body except the gas exchange tissues of the lungs.
Blood leaving the head and neck is deoxygenated and empties into the superior vena cava. Deoxygenated blood from the lower body empties into the inferior vena cava. Both of these large vessels then conduct blood into the right atrium, bringing us back to our beginning point.
FIGURE 17-7 Coronary arteries. A, Diagram showing the major coronary arteries (anterior view). B, The unusual placement of the coronary artery opening behind the leaflets of the aortic valve allows the coronary arteries to fill during ventricular relaxation.
Blood Supply of the Heart Tissue
Coronary Arteries
Myocardial cells receive blood via the right and left coronary arteries (Figure 17-7, A). The openings from the aorta into these vitally important vessels lie behind the flaps of the aortic semilunar valve. As a result, they are the first branches off the aorta and supply the heart muscle first. Ordinarily, arteries that branch from the aorta fill during ventricular contraction when the great force of ventricular pressure pushes blood into the arteries. However, the coronary arteries are squeezed during ventricular contraction and cannot fill during this time (Figure 17-7, B). Because the coronary artery openings are located behind the flaps of the aortic valve, blood flow is largely prevented from entering these openings during ventricular contraction. This is because, when the blood rushes out of the ventricle, the valve flaps are compressed flat against the wall of the aorta and cover the openings to the coronaries. When the ventricle relaxes, however, the coronary arteries expand somewhat, and blood flow is diverted into their openings as the aortic valve closes. This allows the coronary arteries to fill. Both right and left coronary arteries have two main branches, as shown in Figure 17-7.
More than 500,000 Americans die every year from coronary disease and another 3,500,000 suffer some degree of incapacitation. Knowledge about the distribution of coronary artery branches therefore has great practical importance. Here are some principles related to the heart's own blood supply that you should know:
1.Both ventricles receive their blood supply from branches of the right and left coronary arteries.
BOX 17-1Diagnostic Study
Angiography
A special type of radiography called angiography is often used to visualize arteries. A radiopaque dye—a substance that cannot be penetrated by x rays—is injected into an artery to better visualize vessels that would otherwise be invisible in a radiograph. This dye is often called contrast medium.
Sometimes the dye is released through a long, thin tube called a catheter—a procedure called catheterization. The catheter can be pushed through arteries until its tip is in just the right location to release the dye. As the dye begins to circulate, an angiogram (radiograph) will show the outline of the arteries as clearly as if they were made of bone or other dense material (see figure).
Coronary arteriogram. This angiogram of the coronary arteries shows a narrowing (arrow) of the channel in the anterior ventricular (left anterior descending) artery of the heart.
2.Each atrium, in contrast, receives blood only from a small branch of the corresponding coronary artery.
3.The most abundant blood supply goes to the myocardium of the left ventricle. This makes sense because the left ventricle does the most work and thus needs the most oxygen and nutrients delivered to it.
Another important fact concerning the heart's own blood supply is this: Only a few connections, or anastomoses, exist between the larger branches of the coronary arteries. Anastomoses provide circulation “detours” so that arterial blood can still supply its target tissues even if the main circulation routes become obstructed. In short, they provide what we call collateral circulation to a body part. This explains why the scarcity of anastomoses between larger coronary arteries can be such a threat to life.
Let's look at a real life example: If a blood clot plugs one of the larger coronary artery branches (as it frequently does in coronary thrombosis or embolism), too little or possibly no blood at all can reach some of the heart muscle cells. As a result, these tissues become ischemic—they are deprived of oxygen. Myocardial infarction (MI)—the death of ischemic heart muscle cells—soon results.
Although few anastomoses exist between the larger coronary arteries, many anastomoses exist between the very small arteries of the heart. Given time, new anastomoses between the very small coronary arteries develop and provide some collateral circulation to ischemic areas. Currently, several surgical procedures are used to aid this process. In Box 17-1, we show you a special type of radiography called angiography—a method of visualizing the state of the coronary arteries.
Cardiac Veins
After blood has passed through the capillary networks in the myocardium, most of it enters a series of cardiac veins before draining into the right atrium. It does so through a common venous channel called the coronary sinus. However, several small veins from the right ventricle drain directly into the right atrium. As a rule, the cardiac veins (Figure 17-8) follow a pattern that closely parallels that of the coronary arteries.
Nerve Supply of the Heart
The myocardium is autorhythmic, which means that it creates its own internal rhythm for contraction and relaxation even without external nervous control. In fact, the heart has a system of myocardial fibers specialized for rapid electrical conduction. This pathway starts at the top of the heart and extends to the bottom of the heart. The myocardial system that generates and conducts action potentials is called the conduction system of the heart. In this system, both sympathetic fibers and parasympathetic fibers (from branches of
FIGURE 17-8 Coronary veins. Diagram showing the major veins of the coronary circulation (anterior view). Vessels near the anterior surface are more darkly colored than vessels of the posterior surface (seen through the heart).
the vagus nerve) combine to form cardiac plexuses located close to the arch of the aorta.
From the cardiac plexuses, fibers follow the right and left coronary arteries to enter the heart. Here most of the fibers terminate in the sinoatrial (SA) node. This structure is found near the junction of the superior vena cava and the right atrial wall. The SA node is part of the heart's own conduction system (see Figure 18-1, page 406). The SA node is the heart's pacemaker—a function we will look at more closely in Chapter 18.
5. Briefly describe the general structure and function of coronary circulation.
6. Why is a full understanding of the coronary circulation so critical to understanding major types of heart disease?
7. Describe, in general, the conduction system of the heart.
8. What is a myocardial infarction?
BLOOD VESSELS
There are nearly 100,000 km (60,000 miles) of vessels carrying blood through your body right now! As you may know, arteries conduct blood away from the heart, capillaries conduct blood through tissues, and veins conduct blood back to the heart. At this point we'll examine these vessels in more detail (Figure 17-9).
Arteries
There are several types of arteries in the cardiovascular system.
Elastic arteries are the largest and include the aorta and some of its major branches. These huge arteries can stretch without injury. This allows them to accommodate the surge of blood forced into them when the heart ventricles contract and then recoil when the ventricles relax.
Muscular arteries, in contrast, carry blood farther away from the heart to specific organs and areas of the body. They are smaller in diameter than elastic arteries, and the muscular layer in their walls is proportionately thicker. Because of this, these arteries also have thicker muscular walls than similarly sized veins. Examples include brachial (arm), femoral (thigh), and gastric (stomach) arteries.
Arterioles are the smallest arteries. They are not named individually, as are the larger arteries, but as a group of arterioles. They are critically important in regulating blood flow throughout the body. They function by variable contraction of the smooth muscle in their walls. This in turn increases resistance to blood flow and helps regulate blood pressure. Their regulatory action also determines the quantity of
FIGURE 17-9 Structure of blood vessels. The tunica externa of the vein is color-coded blue and the artery red.
blood that enters a particular organ. For this reason they are sometimes called resistance vessels.
Metarterioles are short connecting vessels that connect true arterioles with the proximal ends of between 20 and 100 capillaries (Figure 17-10). Special “regulatory valves” encircle the proximal ends of metarterioles. These are actually smooth muscle cells called precapillary sphincters. These valves contract and relax, thereby regulating blood flow into specific capillaries and networks as they do so. The distal end of a metarteriole lacks precapillary sphincters and is called a thoroughfare channel. It is possible for blood passing directly through a metarteriole into a thoroughfare channel to bypass the intervening capillary bed.
As you will see shortly, all arteries except the pulmonary artery and its branches carry oxygenated blood after birth.
Capillaries
Capillaries are the microscopic vessels that carry blood from arterioles to small veins called venules. Blood flow through the arterioles, capillary beds, and venules is called microcirculation (see Figure 17-10). Transfer of nutrients and other vital substances between blood and tissue cells occurs at or very near a capillary, particularly within the capillary beds. This is why we often call capillaries the primary exchange vessels of the cardiovascular system. So vital is this function to our bodies that no cell is far removed from a capillary.
FIGURE 17-10 Microcirculation. Control of blood flow through a capillary network is regulated by the contraction of precapillary sphincters surrounding arterioles and metarterioles. A, Sphincters are relaxed, permitting blood flow to enter the capillary bed. B, With sphincters contracted, blood flows from the metarteriole directly into the thoroughfare channel, bypassing the capillary bed.
Although capillaries are small in size, it is estimated that our bodies carry more than 1 billion of them! However, they are not uniformly distributed. Some body tissues, such as those of the liver or cardiac muscle, or tissues with high metabolic rates, have many more of them. Therefore they require large numbers of capillary vessels to service them. Other tissues, such as cartilage and some types of epithelium, are avascular and lack capillary networks altogether.
True capillaries receive blood flowing out of metarterioles or other small arterioles. Precapillary sphincters regulate the volume of inflowing blood and its rate of passage through a true capillary. If the sphincter is “open,” blood flows into the capillary. If the sphincter is closed, or partially so, blood flow into the capillary bed decreases significantly (see Figure 17-10).
Veins
After passing through the complex capillary networks of our bodies, blood from several capillaries flows into the distal end of the metarteriole, the thoroughfare channel, or directly enters the first of a series of venous vessels that will eventually return blood to the heart.
The first venous structures are small-diameter vessels called venules. Initially, these tiny veins have very narrow lumens and porous, thin walls. As in capillaries, fluid can be exchanged between blood in the smallest venules and the tissue spaces. Their walls consist of little more than endothelial cells, and a few muscle cells.
The blood in the venules enters progressively larger venous channels—the veins. The names of veins correspond to their arterial counterparts. For example, there is a subclavian artery and a subclavian vein. The veins become larger as they approach the heart. As they increase in size, structural changes take place in the walls of the larger veins to accommodate and regulate the increasing blood volume. Veins do this with virtually no increase in blood pressure. This is because veins can stretch and increase their capacity—we say they have capacitance. For this reason they are called capacitance vessels. This feature permits veins to serve as reservoirs for blood as well as conduits for blood's passage back to the heart. Veins also have one-way valves that keep blood moving toward the heart and prevent potential backflow.
Structure of Blood Vessels
Four types of tissue “fabrics” make up a typical vessel wall: (1) a lining of endothelial cells, (2) collagen fibers, (3) elastic fibers, and (4) smooth muscle cells (see Figure 17-9).
Endothelial Cells
The endothelial cells that line the entire vascular system perform a number of different functions, depending on their location. First, they provide a smooth surface, reducing friction that creates turbulent blood flow. A smooth surface also inhibits coagulation and thus reduces clot formation. Some capillary vessels have intercellular clefts in their endothelium. These clefts vary in size and number and greatly influence the diffusion and movement of substances or cells into and out of the circulating blood.
In veins, the endothelium also forms valves that help maintain the one-way flow of blood. The capillaries are composed only of endothelium.
Fibers
Collagen fibers in the vascular wall are woven together much like the reinforcing strands found in the wall of a tire or hose. They function largely to strengthen the wall and keep the lumen of the vessel open.
Elastic fibers are secreted into the extracellular matrix and form a rubberlike network. In your largest arteries, elastic fibers are organized into nearly circular patterns, and allow for recoil after distention from blood flow. This elasticity plays a vital role in maintaining passive tension in the vessels of our cardiovascular system.
Smooth muscle fibers are found in the walls of the entire vascular system except in capillaries. They are most numerous in elastic and muscular arteries. Smooth muscle exerts active tension in these vessels when they contract.
Layers of Blood Vessels
The walls of arteries and veins consist of three separate layers: (1) tunica externa, (2) tunica media, and (3) tunica intima. As the names suggest, these layers are arranged from the outside of the vessel to the interior of the vessel. As blood vessels decrease in diameter, the relative thickness of their walls also decreases. There are also differences in the thickness of the layers, depending on the vessel's function in the body (see Figure 17-9).
Tunica Externa: The Outer Layer
The outermost layer is the tunica externa (external coat). It is composed of strong, flexible fibrous connective tissue. It functions to prevent tearing of the vessels walls during body movements. Collagen fibers extend outward from this layer to connect to nearby structures. The fibers anchor the vessel and help to keep the lumen open.
Tunica Media: The Middle Layer
The middle layer, the tunica media, is made of a layer of smooth muscle tissue sandwiched together with a layer of elastic connective tissue. The encircling smooth muscles of the tunica media permit changes in the blood vessel diameter. The tunica media is innervated by autonomic nerves and is supplied with its own blood circulation. As a rule, arteries have a thicker layer of smooth muscles than do veins.
Tunica Intima: The Inner Layer
The innermost layer of a blood vessel is the tunica intima (inside coat). The tunica intima is made of endothelium that is continuous with the endothelium that lines the heart. As such, it has a basement membrane to support it. Elastic arteries also have an internal elastic membrane that helps to accommodate changes in vessel diameter.
9. Discuss the flow of blood through an artery, a capillary, and a vein.
10. How do elastic arteries differ from muscular arteries?
11. What is the difference between capacitance vessels and resistance vessels?
12. What are the major layers of arteries, veins, and capillaries?
MAJOR BLOOD VESSELS
The complexity of our cardiovascular system is amazing. It is simply not possible in an essentials text to name and describe all the blood vessels of your body. For this reason, we have concentrated our efforts on the major components.
General Circulatory Routes
Our enclosed systemic circulation route conducts blood from the heart through blood vessels to all parts of the body (except the tissues of the lungs), and then back to the heart. Refer to Figure 17-11 as we continue our discussion.
The left ventricle pumps blood into the ascending aorta. From here it flows into arteries that carry the blood into the various tissues and organs of the body. (Notice that blood moves from arteries to arterioles to capillaries as we progress.) Here the vital two-way exchange of substances occurs between the blood and cells. Blood then flows out of each organ by way of venules. These enlarge into veins that drain ultimately into the inferior or superior vena cava. The two enormous veins return the venous blood to the right atrium to complete the systemic circulation. It's almost a complete circuit, but not quite, because we don't reach our original starting point, the left ventricle.
This is where the pulmonary circulation route takes over. The venous blood from the right atrium is pumped to the right ventricle and then out the pulmonary trunk and its arteries to the lungs. Here, exchange of gases between blood and air takes place, converting deoxygenated blood to oxygenated blood. This oxygenated blood then flows on through lung venules into four pulmonary veins and returns to the left atrium of the heart. From the left atrium, it enters the left ventricle to be pumped again through the systemic circulation.
In a simplified circuit, blood passes through only one capillary network. However, there are several important exceptions to this general rule. In a portal system, blood flowing through the systemic circulation passes through two consecutive capillary beds rather than one. For example, notice in Figure 17-11 that blood coming from the digestive organs passes through a second capillary network in the liver before return to the heart. We will discuss this hepatic portal system in more detail later in this chapter.
There is a second exception to our general systemic circulation pattern. This involves vascular anastomosis, a direct connection or merger of blood vessels to one another. In vascular anastomoses, blood moves from veins to other veins or arteries to other arteries without passing through a capillary network. For example, arterial anastomoses involve the merger of one artery directly into another artery. Venous anastomoses often produce a direct connection between different veins.
FIGURE 17-11 Circulatory routes. The pulmonary circulation routes blood flow to and from the gas-exchange tissues of the lungs. The systemic circulation, on the other hand, routes blood flow to and from the oxygen-consuming tissues of the body.
Systemic Circulation
The systemic circulatory route includes the majority of the body's vessels. Please consult the figures and tables as you read through the following discussion. At this point, it is more important to understand the “big picture” rather than memorizing the content of any table.
Systemic Arteries
As you learn the names of the main arteries, keep in mind that the entire vascular tree is complex, but beyond the scope of this book. Most arteries ultimately diverge into capillaries. These end-arteries are vital to all of our organs. For example, permanent blindness results when the central artery of the retina, an end-artery, is blocked. Thus, blockage of end-arteries almost always has some negative effect. As we've seen, our bodies also have a number of vital arterial anastomoses. Their incidence increases as distance from the heart increases. Examples of arterial anastomoses are the palmar and plantar arches and the cerebral arterial circle (circle of Willis) at the base of the brain (see Figure 17-15).
Note in Figures 17-12 and 17-13 that the aorta is the major artery that serves as the main trunk for the entire systemic arterial system. However, the different segments of the aorta are known by different names, much like the names of streets may change as you drive into a new neighborhood. The first few centimeters of the aorta conduct blood upward out of the left ventricle and are called the ascending aorta. As you've seen, the coronary arteries are branches of the ascending aorta (see Figure 17-7 and Table 17-1). The aorta then turns 180 degrees to the left, forming a curved segment called the aortic arch. Arterial blood is then conducted downward from
FIGURE 17-12 Principal arteries of the body.
the aortic arch through the descending aorta. In the thorax, the descending aorta is called the thoracic aorta; in the abdomen, it is called the abdominal aorta. Note from Figure 17-1, B, and Figure 17-12 that all systemic arteries clearly branch from the aorta, or one of its branches.
Look again at the figures; notice how the main branches from the aortic arch on the right differ from those on the left. The right side of the head and neck are supplied by the brachiocephalic artery, which branches to become the right subclavian artery, and the right common carotid artery. On the left, however, the left subclavian artery and the left common carotid artery branch directly from the arch of the aorta—without an intervening brachiocephalic artery.
FIGURE 17-13 Divisions and primary branches of the aorta (anterior view). The aorta is the main systemic artery, serving as a trunk from which other arteries branch. Blood is conducted from the heart first through the ascending aorta, then through the arch of the aorta, and then through the thoracic and abdominal segments of the descending aorta. Note the designation of visceral and parietal branches in the thoracic and abdominal aortic divisions. Table 17-1 lists branches of the aortic divisions to assist you in interpreting chapter illustrations of arterial vessels.
TABLE 17-1 Major Systemic Arteries
ARTERY*
REGION SUPPLIED
Ascending Aorta
Coronary arteries
Myocardium
Arch of Aorta
Brachiocephalic (Innominate)
Head, upper extremity
Right subclavian
Head, upper extremity
Right vertebral†
Spinal cord, brain
Right axillary (continuation of subclavian)
Shoulder, chest, axillary region
Right brachial (continuation of axillary)
Arm, hand
Right radial
Lower arm, hand (lateral)
Right ulnar
Lower arm, hand (medial)
Superficial and deep palmar arches (formed by anastomosis of branches of radial and ulnar)
Hand, fingers
Digital
Fingers
Right common carotid
Head, neck
Right internal carotid†
Brain, eye, forehead, nose
Right external carotid†
Thyroid, tongue, tonsils, ear, etc.
Left Subclavian
Head, upper extremity
Left vertebral †
Spinal cord, brain
Left axillary (continuation of subclavian)
Shoulder, chest, axillary region
Left brachial (continuation of axillary)
Arm, hand
Left radial
Lower arm, hand (lateral)
Left ulnar
Lower arm, hand (medial)
Superficial and deep palmar arches (formed by anastomosis of branches of radial and ulnar)
Hand, fingers
Digital
Fingers
Left Common Carotid
Head, neck
Left internal carotid †
Brain, eye, forehead, nose
Left external carotid †
Thyroid, tongue, tonsils, ear, etc.
Descending Thoracic Aorta
Visceral Branches
Thoracic viscera
Bronchial
Lungs, bronchi
Esophageal
Esophagus
Parietal Branches
Thoracic walls
Intercostal
Lateral thoracic walls (rib cage)
Superior phrenic
Superior surface of diaphragm
Descending Abdominal Aorta
Visceral Branches
Abdominal viscera
Celiac artery (trunk)
Abdominal viscera
Left gastric
Stomach, esophagus
Common hepatic
Liver
Splenic
Spleen, pancreas, stomach
Superior mesenteric
Pancreas, small intestine, colon
Inferior mesenteric
Descending colon, rectum
Suprarenal
Adrenal (suprarenal) gland
Renal
Kidney
Ovarian
Ovary, uterine tube, ureter
Testicular
Testis, ureter
Parietal Branches
Walls of abdomen
Inferior phrenic
Inferior surface of diaphragm, adrenal gland
Lumbar
Lumbar vertebrae, muscles of back
Median sacral
Lower vertebrae
Common Iliac (Formed by terminal branches of aorta)
Pelvis, lower extremity
External Iliac
Thigh, leg, foot
Femoral (continuation of external iliac)
Thigh, leg, foot
Popliteal (continuation of femoral)
Leg, foot
Anterior tibial
Leg, foot
Posterior tibial
Leg, foot
Plantar arch (formed by anastomosis of branches of anterior and posterior tibial arteries)
Foot, toes
Digital
Toes
Internal Iliac
Pelvis
Visceral Branches
Pelvic viscera
Middle rectal
Rectum
Vaginal
Vagina, uterus
Uterine
Uterus, vagina, uterine tube, ovary
Parietal Branches
Pelvic wall, external regions
Lateral sacral
Sacrum
Superior gluteal
Gluteal muscles
Obturator
Pubic region, hip joint, groin
Internal pudendal
Rectum, external genitals, floor of pelvis
Inferior gluteal
Lower gluteal region, coccyx, upper thigh
* Branches of each artery are indented below its name.
† See text and/or figures for branches of the artery.
FIGURE 17-14 Major arteries of the head and neck. See Figure 17-15 for arteries at the base of the brain.
Major Arteries of the Head and Neck
Figure 17-14 illustrates the major arteries of the head, neck, and face. Trace the branching of the arteries in the figure with your finger as you read through Table 17-1. Notice in this figure how the right and left vertebral arteries extend from their origin as branches of the subclavian arteries up the neck, through openings (foramina) in the transverse processes of the cervical vertebrae, through the foramen magnum, and into the cranial cavity.
Next, look at Figure 17-15 and look at the arteries servicing the base of the brain. Note how the vertebral arteries unite on the undersurface of the brainstem to form the basilar artery. This artery branches quickly into the right and left posterior cerebral arteries. The basilar artery also branches to the pons and cerebellum. The internal carotid arteries enter the cranial cavity in the midpart of the cranial floor. Here they are known as the anterior cerebral arteries. Small vessels, the communicating arteries, join the anterior and posterior cerebral arteries to form the cerebral arterial circle (circle of Willis) at the base of the brain. This is a fine example of arterial anastomosis.
Major Arteries of the Thorax and Abdomen
The aortic arch continues downward as the thoracic aorta, which begins at the level of the fifth thoracic vertebra and ends at the diaphragm. The abdominal aorta is a downward continuation of the thoracic portion above it. It extends from the diaphragm to the point where it divides into the right and left common iliac arteries at the fourth lumbar vertebra.
FIGURE 17-15 Arteries at the base of the brain. A, Diagram shows the cerebral arterial circle (circle of Willis) and related structures on the base of the brain. Note the arterial anastomoses. B, Origins of blood vessels that form the cerebral arterial circle.
Note in Figure 17-13 that this segment of the aorta lies just anterior to the vertebral bodies. As a result, a physician can feel the aortic pulse during deep palpation of the abdomen where this vessel is compressed against the underlying vertebrae. The presence of a pulsating swelling (a weak spot in the aorta)—an aortic aneurysm—is often diagnosed in this manner.
Major abdominal and pelvic branches of the abdominal aorta may also be described as parietal or visceral depending on the location of the organ or structures they service. You can see the branches of this segment of the aorta illustrated in Figure 17-13.
Major Arteries of the Extremities
Now, take a look back at Figure 17-12, which includes the arteries of the upper and lower extremity. Trace these arteries with your finger as you read through Table 17-1. Not every artery listed in the table appears in every illustration because of differences in view.
13. Compare the systemic circulation route with the pulmonary circulation route.
14. What is the significance of vascular anastomoses?
15. List the major arteries coming off the aortic arch.
16. What is the significance of blockage in an end-artery?
Systemic Veins
There are a number of facts to keep in mind as you read about the names and locations of the major veins presented in the following discussion. First, veins are really larger extensions of capillaries, just as capillaries are the extensions of arteries. Thus, veins are enlargements of venules.
Second, although all vessels vary considerably in location and branches—and whether or not they are even present—the veins are especially variable. For example, the median cubital vein in the forearm is absent in many individuals.
Third, many of the main arteries have corresponding veins bearing the same name that are located alongside or near the arteries. These veins, like the arteries, lie in deep, well-protected areas, often running close to the bones. One example is the femoral artery and the femoral vein, both located along the femur bone.
You should note that some veins—for example, the large veins of the cranial cavity—are called sinuses. This is because they are venous enlargements that collect blood as it exits a tissue.
Finally, veins anastomose with each other in the same way as arteries. In fact, the venous portion of the systemic circulation has even more anastomoses than does the arterial portion. These anastomoses provide collateral return blood flow in cases of venous obstruction.
The major veins are listed for you Table 17-2. As you read the following discussion, follow along with Figures 17-16 through 17-19. As with the arteries, you may find it easier to learn the names of the major veins and their anatomical relation to each other from the diagrams and tables presented here.
Veins of the Head and Neck
The deep veins of the head and neck lie mostly within the cranial cavity. These are mainly dural sinuses and other veins that drain into the internal jugular vein.
Note that the superficial veins of the head and neck drain into the right and left external jugular veins in the neck (Figure 17-17). These veins receive blood from small superficial veins of the face, scalp, and neck, and terminate in subclavian veins. Small veins connect veins of the scalp and face with blood sinuses of the cranial cavity. This is of clinical interest because this arrangement presents a possible avenue for infections to enter the cranial cavity.
Veins of the Upper Extremity
Deep veins of the upper extremity drain into the brachial vein, which in turn drains into the axillary vein. From there blood flows into the subclavian vein before joining the brachiocephalic vein—a major tributary of the superior vena cava. You can review the major veins of the upper extremity in Figure 17-16. You'll see that the tributaries of the superior vena cava are more symmetrical from left to right than the nearby branches of the aorta. Compare Figures 17-12 and 17-16 to verify this for yourself.
Veins of the Thorax
Several small veins—such as the bronchial vein, esophageal vein, and pericardial vein—return blood from thoracic organs directly into the superior vena cava. The superior vena cava lies to the right of the spinal column and extends from the inferior vena cava through the diaphragm to the terminal part of the superior vena cava (Figure 17-18).
Veins of the Abdomen
The abdominal tributaries are another example of the differences between the left and right portions of the systemic venous circulation. For example, Figure 17-18 shows that the left ovarian vein or testicular vein and left suprarenal vein usually drain into the left renal vein instead of into the inferior vena cava—as occurs on the right side. The return of blood from the abdominal digestive organs follows below.
Hepatic Portal Circulation
Veins from the spleen, stomach, pancreas, gallbladder, and intestines do not pour their blood directly into the inferior vena cava, as do the veins from other abdominal organs. Instead they send their blood to the liver by means of the hepatic portal vein. Here the blood mingles with the arterial blood in the capillaries. Eventually it is drained from the liver by the hepatic veins that join the inferior vena cava. Any arrangement in which venous
FIGURE 17-16 Principal veins of the body.
FIGURE 17-17 Major veins of the head and neck. Anterior view showing veins on the right side of the head and neck.
blood flows through a second capillary network before returning to the heart is called a portal circulatory system. Portal means “gateway,” and the liver acts as a gateway through which blood returning from the digestive tract must pass before it returns to the heart.
TABLE 17-2 Major Systemic Veins
VEIN*
REGION DRAINED
Superior Vena Cava
Head, neck, thorax, upper extremity
Brachiocephalic (Innominate)
Head, neck, upper extremity
Internal jugular (continuation of sigmoid sinus)
Brain
Lingual
Tongue, mouth
Superior thyroid
Thyroid, deep face
Facial
Superficial face
Sigmoid sinus (continuation of transverse sinus/direct tributary of internal jugular)
Brain, meninges, skull
Superior and inferior petrosal sinuses
Anterior brain, skull
Cavernous sinus
Anterior brain, skull
Ophthalmic veins
Eye, orbit
Transverse sinus (direct tributary of sigmoid sinus)
Brain, meninges, skull
Occipital sinus
Inferior, central region of cranial cavity
Straight sinus
Central region of brain, meninges
Inferior sagittal sinus
Central region of brain, meninges
Superior sagittal (longitudinal) sinus
Superior region of cranial cavity
External jugular
Superficial, posterior head, neck
Subclavian (continuation of axillary/direct tributary of brachiocephalic)
Axilla, lower extremity
Axillary (continuation of basilic direct tributary of subclavian)
Axilla, lower extremity
Cephalic
Lateral and lower arm, hand
Brachial
Deep arm
Radial
Deep lateral forearm
Ulnar
Deep medial forearm
Basilic (direct tributary of axillary)
Medial and lower arm, hand
Median cubital (basilic) (formed by anastomosis of cephalic and basilic)
Arm, hand
Deep and superficial palmarvenous arches (formed by anastomosis of cephalic and basilic)
Hand
Digital
Fingers
Azygos (anastomoses with right ascending lumbar)
Right posterior wall of thorax and abdomen, esophagus, bronchi, pericardium, mediastinum
Hemiazygos (anastomoses with left renal)
Left inferior posterior wall of thorax and abdomen, esophagus, mediastinum
Accessory hemiazygos
Left superior posterior wall of thorax
Inferior Vena Cava
Lower trunk and extremity
Phrenic
Diaphragm
Hepatic portal system
Upper abdominal viscera
Hepaticveins (continuations of liver venules and sinusoids and, ultimately, the hepatic portal vein)
Liver
Hepatic portal vein
Gastrointestinal organs, pancreas, spleen, gallbladder
Cystic
Gallbladder
Gastric
Stomach
Splenic
Spleen
Inferior mesenteric
Descending colon, rectum
Pancreatic
Pancreas
Superior mesenteric
Small intestine, most of colon
Castroepiploic
Stomach
Renal
Kidneys
Suprarenal
Adrenal (suprarenal) gland
Left ovarian
Left ovary
Left testicular
Left testis
Left ascending lumbar (anastomoses with hemiazygos)
Left lumbar region
Right ovarian
Right ovary
Right testicular
Right testis
Right ascending lumbar (anastomoses with azygos)
Right lumbar region
Common iliac (continuation of external iliac; common iliacs unite to form inferior vena cava)
Lower extremity
External iliac (continuation of femoral direct tributary of common iliac)
Thigh, leg, foot
Femoral (continuation of popliteal direct tributary of external iliac)
Thigh, leg, foot
Popliteal
Leg, foot
Posterior tibial
Deep posterior leg
Medial and lateral plantar
Sole of foot
Fibular (peroneal) (continuation of anterior tibial)
Lateral and anterior leg, foot
Anterior tibial
Anterior leg, foot
Dorsal veins of foot
Anterior (dorsal) foot, toes
Small (external, short)
Superficial posterior leg, lateral foot
Great (internal, long) saphenous
Superficial medial and anterior thigh, leg, foot
Dorsal veins of foot
Anterior (dorsal) foot, toes
Dorsal venous arch
Anterior (dorsal) foot, toes
Digital
Toes
Internal Iliac
Pelvic region
* Tributaries of each vein are identified below its name; deep veins are printed in dark blue, and superficial veins are printed in light blue.
There are several advantages to this “detour” from the digestive tract through the liver before returning the blood to the heart. Shortly after a meal, blood flowing through digestive organs begins absorbing glucose and other simple nutrients. The result is a tremendous increase in the blood glucose level. As the blood travels through the liver, however, excess glucose is removed and stored in liver cells as the polysaccharide glycogen. Thus blood returned to the heart carries only a moderate level of glucose. Many hours after food has yielded its nutrients, low-glucose blood coming from the digestive organs can pick up glucose released from the breakdown of glycogen stores. It's a simple solution to prevent the glucose from flooding the body immediately after digestion.
Yet another advantage of the hepatic portal system is that toxic molecules such as alcohol can be partially removed or detoxified before the blood is distributed to the remainder of the body. Figure 17-11 shows the basic layout of the hepatic portal system in relation to the overall pattern of circulation. Figure 17-19 shows the details of the veins involved in the hepatic portal circulation. In most of us, the hepatic portal vein is formed by the union of the splenic and superior mesenteric veins.
Sometimes the hepatic portal system or the venous return of blood from the liver is slowed or blocked (as sometimes happens in liver disease or heart disease). In such cases, venous drainage from most of the other abdominal organs may also be obstructed. The accompanying increase in capillary pressure in these organs may account for abdominal bloating or ascites.
Veins of the Lower Extremity
Deep veins of the lower leg drain from the anterior tibial vein, which continues as the fibular (peroneal) vein, and the posterior tibial vein. The fibular and posterior tibial veins join to form the popliteal vein. This vein runs behind the knee joint and continues up along the femur as the deep femoral vein. The femoral vein then continues as the external iliac vein, draining into the common iliac vein and from there into the inferior vena cava.
FIGURE 17-18 Inferior vena cava and its abdominopelvic tributaries. Anterior view of ventral body cavity with many of the viscera removed. Note the close anatomical relationship between the inferior vena cava and the descending aorta. Smaller veins of the thorax drain blood into the inferior vena cava or into the azygos vein—both are shown here.
Superficial veins of the lower extremity include the small saphenous vein, a tributary of the popliteal vein, and the great saphenous vein, which drains much of the superficial leg and foot. Saphenous means “apparent” and refers to the location of these veins near the surface of the skin.
Fetal Circulation
Basic Plan of Fetal Circulation
Of necessity, the circulation of blood before birth must be different from that after birth. This is because the fetus obtains oxygen and food from maternal blood and digestive
FIGURE 17-19 Hepatic portal circulation. In this unusual circulatory route, a vein is located between two capillary beds (see Figure 17-11). The hepatic portal vein collects blood from capillaries in visceral structures located in the abdomen and empties it into the liver. Hepatic veins return blood to the inferior vena cava.
organs. Let's look briefly at the structures of fetal circulation using Figure 17-20 as your visual guide.
17. Is the distribution of arteries and veins throughout the circulation completely symmetrical?
18. Do vein location and number vary from individual to individual?
19. What are the advantages of the hepatic portal system in the liver?
A&P CONNECT
A valuable skill is the ability to trace the flow of blood completely through the normal adult circulatory route. Check out How to Trace the Flow of Blood online at A&P Connect for some tips and a handy diagram of the route of blood flow through the body.
The two umbilical arteries are really temporary extensions of the internal iliac arteries. They carry fetal blood to the placenta, which is a structure created by both the fetus and the mother. It is attached to the uterine wall. Exchange of oxygen and other substances between maternal and fetal blood takes place in the placenta. However, note that no mixing of maternal and fetal blood occurs under normal conditions of pregnancy. The fetus is vulnerable, however, to many substances ingested or inhaled by the mother. Box 17-2 shows you how alcohol from the maternal blood can damage a developing fetus.
The umbilical vein returns oxygenated blood from the placenta. It enters the fetal body through the umbilicus and extends up to the underside of the liver. Here it gives off two or three branches to the liver, and then continues on as the ductus venosus. Two umbilical arteries and the umbilical vein together constitute the umbilical cord. These are shed after birth along with the placenta when the umbilical cord is cut.
The other three structures of fetal circulation are involved as ducts or detours of circulation. The ductus venosus is a continuation of the umbilical vein. It runs along the underside of the liver and drains into the inferior vena cava. Most of the blood returning from the placenta bypasses the liver because of this. Only a small amount of blood enters the liver via the branches from the umbilical vein into the liver.
The foramen ovale is an opening in the septum between the right and left atria. A valve at the opening of the inferior vena cava into the right atrium directs most of the blood through the foramen ovale into the left atrium so that it bypasses the fetal lungs. Thus, most of the blood does not flow into the lungs. This is because of another detour, the ductus arteriosus, a small vessel that connects the pulmonary artery with the descending thoracic aorta.
Changes in Circulation at Birth
Dramatic changes in the circulatory system must take place immediately upon the birth of a child. First and foremost, the six structures that serve fetal circulation are no longer needed.
As soon as the umbilical cord is cut, the two umbilical arteries, the placenta, and the umbilical vein obviously can no longer function. After the baby is born, the placenta is shed from the mother's body as the so-called afterbirth, along with the severed ends of the umbilical vessels still attached. The sections of these vessels that remain in the infant's body eventually become fibrous cords. These cords
FIGURE 17-20 Plan of fetal circulation. Before birth, the human circulatory system has several special features that adapt the body to life in the womb. These features (labeled in red type) include two umbilical arteries, one umbilical vein, ductus venosus, foramen ovale, ductus arteriosus, and umbilical cord.
remain throughout life. For example, the umbilical vein becomes the round ligament of the liver and the ductus venosus (no longer needed to bypass blood around the liver) eventually becomes the ligamentum venosum of the liver.
Beyond this, the foramen ovale normally becomes at least functionally closed soon after birth. This takes place when the baby takes his or her first breath and full circulation is established through the lungs. Complete structural closure, however, usually requires 9 months or more. Eventually, the foramen ovale becomes a small depression (fossa ovalis) in the wall of the right atrial septum. The ductus arteriosus contracts as soon as respiration is established. Eventually, it also turns into a fibrous cord, the ligamentum arteriosum.
20. Identify the six structures unique to fetal circulation.
21. What is the function of the placenta and the umbilical vessels?
22. What major changes occur in an infant's circulation at the time of birth?
BOX 17-2 Health Matters
Fetal Alcohol Syndrome
Consumption of alcohol by a woman during her pregnancy can have tragic effects on the developing fetus. Educational efforts to inform pregnant women about the dangers of alcohol continue to receive national attention. Even very limited consumption of alcohol during pregnancy poses significant hazards to the developing baby because alcohol can easily cross the placental barrier and enter the fetal bloodstream.
When alcohol enters the fetal blood, the potential result, called fetal alcohol syndrome (FAS), can cause serious congenital abnormalities such as “small head,” or microcephaly; low birth weight; cardiovascular defects; developmental disabilities such as physical and mental retardation; and even fetal death.
The photograph shows the small head, thinned upper lip, small eye openings (palpebral fissures), epicanthal folds, and receded upper jaw (retrognathia) typical of fetal alcohol syndrome.
Fetal alcohol syndrome.
The BIG Picture
In this chapter, you've observed the basic structural and functional anatomy of the heart, major arteries, and major veins. You've also examined the structure and function of arterioles, venules, and capillaries. In essence, we have described a widely distributed, interconnected network of transport vessels for blood.
You've seen how the components of our circulatory system are integrated to form a functioning, closed circulatory loop. Now, step back from this collection of facts for a moment and think about how each component of the heart works in this important system. Use your mind's eye to envision the entire system: Keep in mind the “big picture” of the circulatory system. What are the components? How are they integrated? What is the significance of a properly functioning circulatory system for the entire body? If you continue in this vein, you'll discover how putting the big picture together really aids in your understanding of this system.
Your understanding of the components of the circulatory system are very important to your understanding of the functional anatomy of the cardiovascular system in the next chapter. Chapter 18 will deal with issues that relate to the function of the cardiovascular system and its importance in maintaining the homeostatic mechanisms of our bodies.
Cycle of LIFE
As we've seen, the heart and blood vessels undergo profound anatomical changes during early fetal development. Then at birth, the abrupt switch from a placenta-dependent circulatory system to an independent circulatory system causes yet another set of profound anatomical changes. Throughout childhood, adolescence, and adulthood, the heart and blood vessels normally maintain their basic structure and function. The only apparent changes in these structures occur as a result of regular exercise. After rigorous exercise over prolonged periods, the myocardium thickens and the supply of blood vessels in skeletal muscle tissues increases.
As we pass through adulthood, especially later adulthood, various degenerative changes can occur in the heart and the blood vessels. For example, atherosclerosis (“hardening of the arteries”) can result in the blockage or weakening of critical arteries. Such blockage in the coronary arteries can cause a myocardial infarction. In the brain, such blockage can cause a stroke. Both can be life altering or life threatening. In addition, the heart valves and myocardial tissues often degenerate with age. They become hardened and more fibrous and lose some of their elasticity and regenerative capacity. They are thus less able to perform their functions properly. This, of course, reduces the heart's pumping efficiency and threatens homeostasis of our entire internal environment.
MECHANISMS OF DISEASE
There are numerous diseases of the heart and circulatory system, including disorders involving the pericardial lining, the heart valves, the pericardium, the arteries, and the veins. A number of these are congenital and apparent at birth, but many others develop as injury, disease, and age take their toll on our circulation system. The structural defects can often be remedied by surgery. However, many heart diseases require exercise, behavioral changes, and medications, which have proven to be effective tools.
Find out more about these cardiovascular disorders and diseases online at Mechanisms of Disease: Anatomy of the Cardiovascular System.
CHAPTER SUMMARY
To download an MP3 version of the chapter summary for use with your iPod or other portable media player, access the Audio Chapter Summaries online at http://evolve.elsevier.com.
Scan this summary after reading the chapter to help you reinforce the key concepts. Later, use the summary as a quick review before your class or before a test.
INTRODUCTION
A. Cardiovascular system (circulatory system)—consists of a muscular heart and a closed system of vessels
B. Cardiovascular system develops early and reaches a functional state long before any other major organ system
HEART
A. Location, shape and size of the heart (Figure 17-1)
1. Lies in the mediastinum just behind the body of the sternum
2. In infants, it is 1/130 of the total body weight; 1/300 in the adult
3. Between puberty and 25 years of age, the heart attains its adult shape and weight
B. Coverings of the heart
1. Pericardium—outer sac that encloses the heart
a. Fibrous pericardium—loosely fitting outer layer of this sac
b. Serous pericardium—smooth, moist serous membrane (parietal layer) that lines the fibrous pericardium; visceral layer (epicardium) directly covers the surface of the heart (Figure 17-3)
c. Pericardial space—space between the two layers; contains pericardial fluid
d. Pericardial sac provides protection against friction as the heart beats
C. Wall of the heart
1. Epicardium—outer layer of the heart wall; visceral layer of the serous pericardium
2. Myocardium—thick, contractile, middle layer; comprises the bulk of the heart wall
3. Endocardium—delicate layer lining the interior of the myocardial wall
D. Chambers of the heart—interior of the heart is divided into four cavities (chambers) (Figure 17-4)
1. Atria—two upper chambers
a. Separated into left and right chambers by the interatrial septum
b. Receive blood from veins
c. Muscular walls are not very thick
2. Ventricles—two lower chambers
a. Separated into left and right chambers by the interventricular septum
b. Receive blood from the atria and pump blood out of the heart into the arteries; “pumping chambers”
c. Myocardium is quite thick
E. Valves of the heart—four tough, fibrous structures that permit the flow of blood in one direction only and are vital to the normal functioning of the heart (Figures 17-5 and 17-6)
1. Atrioventricular (AV) valves—service the openings between the atria and the ventricles; have pointed flaps called cusps
a. AV valves allow blood to flow from the atria into the ventricles but prevents it from flowing backward
b. Right AV (tricuspid) valve—consists of three cusps of endocardium
(2) Free edge of each flap is anchored to the papillary muscles of the right ventricle by several tendinous cords (chordae tendineae)
c. Left AV (bicuspid/mitral) valve—two cusps of endocardium
2. Semilunar (SL) valves—located where the pulmonary artery joins the right ventricle (pulmonary valve) and where the aorta joins the left ventricle (aortic valve)
a. Pocketlike flaps that extend inward from the lining of the pulmonary artery and the aorta; look very much like a “half-moon” (Figure 17-5)
b. Pulmonary valve—semilunar valve at the entrance of the pulmonary artery
c. Aortic valve—semilunar valve at the entrance of the aorta
3. Skeleton of the heart (Figure 17-6)
a. Consists of a set of connected rings that serve as a semirigid support for the heart valves
b. Serves as sites for the attachment of cardiac muscle of the myocardium
c. Also serves as an electrical barrier between the myocardium of the atria and the myocardium of the ventricles
4. Flow of blood through the heart (Figure 17-5)
a. Beginning with the right atrium, blood flows through the right AV (tricuspid) valve into the right ventricle
b. From the right ventricle, blood then flows into the first portion of the pulmonary artery
c. Pulmonary arteries carry blood to the lungs for gas exchange
d. From the lungs, blood flows back through pulmonary veins into the left atrium of the heart
e. From the left atrium, blood flows into the left ventricle
f. From the left ventricle, blood then flows into the aorta
F. Blood supply of the heart tissue (Figures 17-7 and 17-8)
1. Coronary arteries (Figure 17-7, A)
a. First branches off the aorta and supplies the heart muscle first
b. Both right and left coronary arteries have two main branches
c. Both ventricles receive their blood supply from branches of the right and left coronary arteries
d. Each atrium receives blood only from a small branch of the corresponding coronary artery
e. The most abundant blood supply goes to the myocardium of the left ventricle
f. Few connections (anastomoses) exist between the larger branches of the coronary arteries
G. Nerve supply of the heart
1. Myocardium is autorhythmic—creates its own internal rhythm for contraction and relaxation even without external nervous control
2. Sympathetic fibers and parasympathetic fibers combine to form cardiac plexuses
a. From the cardiac plexuses, fibers follow the right and left coronary arteries to enter the heart
b. Most of the fibers terminate in the sinoatrial (SA) node
BLOOD VESSELS
A. Arteries—conduct blood away from the heart
1. Elastic arteries—largest; include the aorta and some of its major branches
a. Can stretch without injury
2. Muscular arteries—carry blood farther away from the heart to specific organs and areas of the body
a. Smaller in diameter than elastic arteries
b. Muscular layer in their walls is proportionately thicker
3. Arterioles—smallest arteries
a. Important in regulating blood flow throughout the body
4. Metarterioles—short connecting vessels; connect true arterioles with the proximal ends of between 20 and 100 capillaries (Figure 17-10)
a. Precapillary sphincters—regulating blood flow into specific capillaries and networks
B. Capillaries—conduct blood through tissues
1. Microscopic vessels
2. Carry blood from arterioles to small veins called venules; constitute microcirculation (Figure 17-10)
3. Primary exchange vessels of the cardiovascular system
4. Not uniformly distributed; body tissues with high metabolic rates have many more of them
5. True capillaries—receive blood flowing out of metarterioles or other small arterioles (Figure 17-10)
C. Veins—conduct blood back to the heart
1. Venules—first venous structures; very narrow lumens and porous, thin walls
2. Veins can stretch and increase their capacity; capacitance vessels
3. Venous sinus—large venous structure with very thin endothelial walls
D. Structure of blood vessels—four types of tissue “fabrics” make up a typical vessel wall
1. Endothelial cells
2. Collagen fibers
3. Elastic fibers
4. Smooth muscle cells
E. Endothelial cells—line the entire vascular system
1. Provide a smooth surface; reducing friction that creates turbulent blood flow
2. In capillaries, allows the efficient exchange of materials between the blood plasma and the interstitial fluid of the surrounding tissues
F. Fibers
1. Collagen fibers—reinforcing strands found in the vascular wall; strengthen the wall and keep the lumen of the vessel open
2. Elastic fibers—secreted into the extracellular matrix and form a rubberlike network; help maintain passive tension in the vessels of our cardiovascular system
3. Smooth muscle fibers—found in the walls of the entire vascular system except in capillaries; exert active tension in these vessels when they contract
G. Layers of blood vessels—walls of arteries and veins consist of three separate layers (Figure 17-9)
1. Tunica externa—outermost layer
a. Composed of strong, flexible fibrous connective tissue
b. Functions to prevent tearing of the vessel walls during body movements
2. Tunica media—middle layer
a. Made of a layer of smooth muscle tissue sandwiched together with a layer of elastic connective tissue
b. Arteries have a thicker layer of smooth muscles than do veins
3. Tunica intima—inner layer
a. Made of endothelium that is continuous with the endothelium that lines the heart
MAJOR BLOOD VESSELS
A. General circulatory routes
1. Systemic circulation—blood flow from the heart through blood vessels to all parts of the body (except the tissues of the lungs), and then back to the heart (Figure 17-11)
2. Pulmonary circulation—venous blood flow from the right atrium to the right ventricle and then out the pulmonary trunk and its arteries to the lungs
3. Portal system—blood flowing through the systemic circulation passes through two consecutive capillary beds rather than one (Figure 17-11)
4. Vascular anastomosis—direct connection or merger of blood vessels to one another
a. Arterial anastomosis—involves the merger of one artery directly into another artery
b. Venous anastomosis—produces a direct connection between different veins
B. Systemic circulation—includes the majority of the body's vessels
C. Systemic arteries (Table 17-1 and Figures 17-12 to 17-15)
1. End-arteries—arteries that diverge into capillaries
2. Aorta—major artery that serves as the main trunk for the entire systemic arterial system
3. Major arteries of the head and neck (Figures 17-14 and 17-15)
4. Major arteries of the thorax and abdomen (Figure 17-13)
5. Major arteries of the extremities (Figure 17-12)
D. Systemic veins (Table 17-2 and Figures 17-16 to 17-19)
1. Veins are really larger extensions of capillaries
2. Veins are especially variable
3. Many of the main arteries have corresponding veins bearing the same name that are located alongside or near the arteries
4. Large veins of the cranial cavity are called sinuses
5. Veins of the head and neck (Figure 17-17)
6. Veins of the upper extremity (Figure 17-2)
7. Veins of the thorax (Figure 17-18)
8. Veins of the abdomen (Figure 17-18)
9. Hepatic portal circulation (Figure 17-19)
a. Veins of the spleen, stomach, pancreas, gallbladder, and intestines send their blood to the liver by way of the hepatic portal vein
b. Blood travels through the liver and excess glucose is removed and stored in liver cells as glycogen
c. Toxic molecules such as alcohol can be partially removed or detoxified before the blood is distributed to the remainder of the body
10. Veins of the lower extremity
E. Fetal circulation—additional blood vessels in the fetus are needed to carry the fetal blood into close approximation with the maternal blood and then to return it to the fetal body
1. Structures that allow this to happen are two umbilical arteries, the umbilical vein, and the ductus venosus
2. Placenta—provides a place where there can be an interchange of gas, foods, and wastes between the fetal and maternal circulation
3. Three structures located within the fetus play a vital role in fetal circulation:
a. Ductus venous
b. Foramen ovale
c. Ductus arteriosus
4. Changes in circulation at birth
a. When umbilical cord is cut, the two umbilical arteries, the placenta, and the umbilical vein obviously can no longer function
b. Placenta is shed from the mother's body
c. Umbilical vein becomes the round ligament of the liver
d. Ductus venosus—becomes the ligamentum venosum of the liver
e. Foramen ovale normally becomes at least functionally closed soon after birth (fossa ovalis)
f. Ductus arteriosus contracts as soon as respiration is established; turns into a fibrous cord, the ligamentum arteriosum
REVIEW QUESTIONS
Write out the answers to these questions after reading the chapter and reviewing the Chapter Summary. If you simply think through the answer without writing it down, you won't retain much of your new learning.
1. Discuss the size, position, and location of the heart in the thoracic cavity.
2. Describe the pericardium, differentiating between the fibrous and serous portions.
3. Exactly where is pericardial fluid found? Explain its function.
4. Define the following terms: intercalated disks and autorhythmic.
5. Name and locate the chambers and valves of the heart.
6. Trace the flow of blood through the heart.
7. Describe the six unique structures necessary for fetal circulation.
8. Explain how the separation of oxygenated and deoxygenated blood occurs after birth.
9. Briefly define the following terms: aneurysm and atherosclerosis.
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