CHAPTER 16 Blood
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- blo ...
CHAPTER 16 BloodSTUDENT LEARNING OBJECTIVESAt the completion
1. CHAPTER 16 Blood
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
5. 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)?
6. 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
7. 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.
8. 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
9. 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
10. 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
11. 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
12. 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
13. 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
14. 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
15. 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
16. 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
17. 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
18. 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
19. 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
20. 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 i njured
vessel. This may occur as a result of any one of several body
defense mechanisms. One of these mechanisms is formation of a
21. 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.
22. 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
23. 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
24. 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
25. 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 -
26. 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%
27. 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
28. 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
29. 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 bl eeding
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
30. 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
31. 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
32. 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?
33. •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, whi ch 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
34. 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.
35. 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
36. 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
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. 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
37. 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
38. 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
39. 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
40. 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
41. 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
42. 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.
43. 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)
48. (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
49. 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
50. 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
51. 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
52. 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
53. 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
54. 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
55. 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
56. 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 call ed
the aortic valve.
When the pulmonary and aortic semilunar valves are closed (see
57. 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
58. 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
![CHAPTER 16 Blood
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](https://image.slidesharecdn.com/chapter16bloodstudentlearningobjectivesatthecompletion-220921043637-4011ce11/85/CHAPTER-16-BloodSTUDENT-LEARNING-OBJECTIVESAt-the-completion-1-320.jpg)
![(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-](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)