Psychology Chapter 18 Homework Fibrosis Cardiac Muscle May Occur The Nodes

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CHAPTER
18
The Cardiovascular System:
The Heart
Objectives
Heart Anatomy
1. Describe the size, shape, location, and orientation of the heart in the thorax.
2. Name the coverings of the heart.
3. Describe the structure and function of each of the three layers of the heart wall.
Cardiac Muscle Fibers
8. Describe the structural and functional properties of cardiac muscle, and explain how it
differs from skeletal muscle.
Heart Physiology
10. Name the components of the conduction system of the heart, and trace the conduction
pathway.
11. Draw a diagram of a normal electrocardiogram tracing. Name the individual waves and
intervals, and indicate what each represents.
Developmental Aspects of the Heart
17. Describe the development of the heart, and indicate how the fetal heart differs from the
adult heart.
18. Provide examples of age-related changes in heart function.
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Suggested Lecture Outline
I. The Pulmonary and Systemic Circuits (p. 659; Fig. 18.1)
A. The right side of the heart receives oxygen-poor blood returning from body tissues and
pumps it to the lungs to release CO2 and pick up O2 (p. 659; Fig. 18.1).
II. Heart Anatomy (pp. 659–671; Figs. 18.2–18.11)
A. Size, Location, and Orientation (p. 659; Fig. 18.2)
1. The heart is the size of a fist and weighs 250–300 grams.
B. Coverings of the Heart (pp. 660–661; Fig. 18.3)
1. The heart is enclosed in a double-walled sac called the pericardium.
a. The superficial pericardium is the fibrous pericardium that protects the heart,
anchors it to surrounding structures, and prevents the heart from overfilling.
2. Between the visceral and parietal layers is the pericardial cavity, containing a film of
serous fluid that lubricates their movement against each other.
C. Layers of the Heart Wall (pp. 661–662; Figs. 18.3–18.4)
1. The epicardium is the visceral pericardium of the serous pericardium.
2. The myocardium is composed mainly of cardiac muscle and forms the bulk of the
heart.
3. The endocardium lines the chambers of the heart and is continuous with the endothe-
lial linings of the vascular system.
D. Chambers and Associated Great Vessels (p. 662; Fig. 18.5)
1. There are partitions that separate the heart longitudinally: the interatrial septum
divides the atria, and between the ventricles lies the interventricular septum.
2. The right and left atria are the receiving chambers of the heart and only minimally
contract to propel blood into the ventricles.
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E. Heart Valves (pp. 662–668; Figs. 18.5–18.8)
1. There are two atrioventricular (AV) valves between each atrial-ventricular junction:
the tricuspid valve in the right and the mitral valve in the left.
2. Aortic and pulmonary semilunar (SL) valves are located at the base of the arteries
exiting the heart and prevent backflow of blood into the ventricles.
3. There are no valves at the entrances of the vena cavae or pulmonary veins, because the
intertia of blood and the collapse of the atria during contraction minimizes backflow
into these vessels.
F. Pathway of Blood Through the Heart (p. 668; Figs. 18.9–18.10)
1. The right side of the heart pumps blood into the pulmonary circuit; the left side of the
heart pumps blood into the systemic circuit.
2. Equal volumes of blood are pumped to the pulmonary and systemic circuits at the
same time, but the two sides have different workloads.
G. Coronary Circulation (pp. 668–671; Fig. 18.11)
1. The heart receives no nourishment from the blood as it passes through the chamber, so
a series of vessels, the coronary circulation, exist to supply blood to the heart itself.
a. The left coronary artery gives rise to the anterior interventricular artery and the
circumflex artery, which supply blood to the left ventricle and atrium.
the coronary sinus.
2. In a myocardial infarction, there is prolonged coronary blockage that leads to cell
death.
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III. Cardiac Muscle Fibers (pp. 671–674; Figs. 18.12–18.13)
A. Microscopic Anatomy (p. 671; Fig. 18.12)
1. Cardiac muscle is striated and contraction occurs via the sliding filament mechanism.
2. The cells are short, fat, and branched, and each cardiac muscle fiber has one or two
large, pale, centrally located nuclei.
4. Cells are connected to each other at intercalated discs, containing desmosomes for
structural strength, and gap junctions that allow electrical current to travel from cell to
cell.
B. Mechanism and Events of Contraction (pp. 671–673; Fig. 18.13)
1. Some cardiac muscle cells are self-excitable and initiate their own depolarization, as
well as depolarizing the rest of the heart.
3. The heart’s absolute refractory period is longer than a skeletal muscle’s, preventing
tetanic contractions.
4. Although the basic contraction mechanism is the same between cardiac and skeletal
muscle cells, the events that trigger contraction differ, with roughly 20% of the Ca++
involved entering the cell from the extracellular space.
5. The mechanism of stimulation of cardiac muscle contraction is as follows:
a. When cardiac muscle cells are stimulated, voltage gated Na+ channels allow Na+ to
C. Energy Requirements (pp. 673–674)
1. Cardiac muscle has more mitochondria than skeletal muscle, indicating reliance on
exclusively aerobic respiration for its energy demands.
supply is available, including lactic acid.
IV. Heart Physiology (pp. 674–685; Figs. 18.14–18.23)
A. Electrical Events (pp. 674–678; Figs. 18.14–18.19)
1. The heart does not depend on the nervous system to provide stimulation; it relies on
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2. The cardiac pacemaker cells have an unstable resting potential and produce
pacemaker potentials that continuously depolarize, initiating the action potentials that
are conducted throughout the heart.
3. Impulses pass through the cardiac pacemaker cells in the following order: sinoatrial
node, atrioventricular node, atrioventricular bundle, right and left bundle branches,
and the subendocardial conducting network.
a. The sinoatrial node is located in the right atrium and is the primary pacemaker for
the heart.
4. The autonomic nervous system modifies the heartbeat through cardiac centers in the
medulla oblongata:
5. An electrocardiograph monitors and amplifies the electrical signals of the heart and
records it as an electrocardiogram (ECG).
a. A typical ECG has three deflections: a P wave, indicating depolarization of the
atria; a QRS complex, resulting from ventricular contraction; and a T wave, caused
by ventricular repolarization.
B. Heart Sounds (pp. 678–679; Fig. 18.20)
1. Normal
a. The first heart sound, lub, corresponds to closure of the AV valves, and occurs
2. Abnormal
a. Heart murmurs are extraneous heart sounds due to turbulent backflow of blood
through a valve that does not close tightly.
C. Mechanical Events: The Cardiac Cycle (pp. 679–681; Fig. 18.21)
1. Systole is the contractile phase of the cardiac cycle and diastole is the relaxation phase
of the cardiac cycle.
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b. The atria contract during the end of ventricular diastole, propelling the final volume
D. Cardiac Output (pp. 681–685; Figs. 18.22–18.23)
1. Cardiac output is defined as the amount of blood pumped out of a ventricle per beat
and is calculated as the product of stroke volume and heart rate.
a. Stroke volume is the volume of blood pumped out of a ventricle per beat, and
2. Regulation of Stroke Volume
a. Stroke volume represents the difference between the end diastolic volume (EDV),
the amount of blood that collects in the ventricle during diastole, and end systolic
volume (ESV), the volume of blood that remains in the ventricle after contraction is
3. Regulation of Heart Rate
a. Sympathetic stimulation of pacemaker cells increases heart rate and contractility by
increasing Ca++ movement into the cell.
b. Parasympathetic inhibition of cardiac pacemaker cells decreases heart rate by
increasing membrane permeability to K+.
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V. Developmental Aspects of the Heart (pp. 685–687; Figs. 18.24–18.25)
A. Before Birth (pp. 685–686; Figs. 18.24–18.25)
2. The foramen ovale is an opening in the interatrial septum that allows blood returning
to the pulmonary circuit to be directed into the atrium of the systemic circuit.
3. The ductus arteriosus is a vessel extending between the pulmonary trunk and the aortic
arch that allows blood in the pulmonary trunk to be shunted to the aorta.
B. Heart Function Throughout Life (pp. 686–687)
1. Regular exercise causes the heart to enlarge and become more powerful and efficient.
2. Sclerosis and thickening of the valve flaps occurs over time, in response to constant
pressure of the blood against the valve flaps.
vessels.
Cross References
Additional information on topics covered in Chapter 18 can be found in the chapters listed below.
1. Chapter 1: Ventral body cavity; mediastinum
2. Chapter 3: Cell junctions
3. Chapter 4: Serous membranes; cardiac muscle; squamous epithelium; collagen
4. Chapter 9: Sliding filament mechanisms
5. Chapter 11: Membrane potential
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Lecture Hints
1. Point out that the visceral layer of the pericardium (epicardium) is the same as the
outermost layer of the heart wall.
2. Display a single diagram of both pericardium and heart wall so that students get an
overall perspective of construction.
5. Describe the construction differences between the atrioventricular valves and the
semilunar valves, and why the construction of each type of valve works best in its
location. Stress that the valves are not rigid structures, but flimsy.
6. Compare ion movement, depolarization, and repolarization in cardiac muscle to that of
7. Emphasize that the pacemaker cells are cardiac muscle cells, just modified so that they
produce pacemaker potentials.
8. Clearly distinguish between the basic rate set by the conduction system of the heart and
9. Emphasize that the ECG is the measurement of the total electrical activity of the heart at
11. Note that while the ventricles have both a passive and active phase to filling, the atria
only fill passively.
13. Clearly differentiate between preload as a function of mechanical stretch and contrac-
tility as a function of strength of stimulation of contraction.
Activities/Demonstrations
1. Audiovisual materials are listed in the Multimedia in the Classroom and Lab section of
this Instructor Guide (p. 387).
2. Play a recording of normal and abnormal heart sounds to accompany your presentation of
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3. Record the heart rates of student volunteers as they stand quietly and run in place for a
few minutes. Using a standard stroke volume, calculate the change in cardiac output.
Critical Thinking/Discussion Topics
1. Discuss the signs of impending heart attack.
2. Compare the significance of ventricular fibrillation as opposed to atrial fibrillation.
3. Discuss the role of cardiac muscle in ejecting blood from the ventricles as opposed to
ejecting blood from the atria.
Library Research Topics
1. Research the role of antihypertensive drugs on the action of the heart.
2. Study the alternatives to coronary bypass operations.
3. Investigate the known effects of street drugs on heart activity.
4. Research the effect of smoking on the heart and its function.
5. Examine the criteria used for heart transplants and their success rate.
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226 INSTRUCTOR GUIDE FOR HUMAN ANATOMY & PHYSIOLOGY, 9e Copyright © 2013 Pearson Education, Inc.
List of Figures and Tables
All of the figures in the main text are available in JPEG format, PPT, and labeled & unlabeled
format on the Instructor Resource DVD. All of the figures and tables will also be available in
Transparency Acetate format. For more information, go to www.pearsonhighered.com/educator.
Figure 18.1 The systemic and pulmonary circuits.
Figure 18.5 Gross anatomy of the heart.
Figure 18.6 Heart valves.
Figure 18.7 The atrioventricular (AV) valves.
Figure 18.8 The semilunar (SL) valves.
Figure 18.9 Blood Flow Through the Heart.
Figure 18.10 Anatomical differences between the right and left ventricles.
one heartbeat.
Figure 18.16 Autonomic innervation of the heart.
Figure 18.17 An electrocardiogram (ECG) tracing.
Figure 18.18 The sequence of depolarization and repolarization of the heart related to
the deflection waves of an ECG tracing.
Figure 18.19 Normal and abnormal ECG tracings.
Figure 18.20 Areas of the thoracic surface where the sounds of individual valves can
best be detected.
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Answers to End-of-Chapter Questions
Multiple-Choice and Matching Question answers appear in Appendix H of the main text.
Short Answer Essay Questions
11. The pericardium has two layers, a fibrous and a serous layer. The outer fibrous layer is a
fibrous connective tissue that protects the heart and anchors it to surrounding structures.
12. The path from the right atrium to the left atrium is as follows: right atrium, right ventri-
13. a. When the ventricles begin to relax following contraction, blood flows back toward the
ventricles, getting caught in the semilunar valves. During this time, the coronary
arteries are actively delivering blood to the myocardium. During ventricular contraction,
the coronary vessels are compressed and ineffective in blood delivery. (pp. 667, 670)
14. A longer refractory period of cardiac muscle is desirable because it prevents the heart
from going into prolonged or tetanic contractions, which would stop its pumping action.
(p. 673)
15. a. The elements of the intrinsic conduction system of the heart, beginning with the
pacemaker, are: the SA node or pacemaker, AV node, AV bundle, right and left
16. See Figure 18.17. The P wave results from impulse conduction from the SA node
through the atria during atrial depolarization. The QRS complex results from ventricular
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17. The cardiac cycle includes all events associated with the flow of blood through the
heart during one complete heartbeat. One cycle includes a period of ventricular filling
18. Cardiac output is the amount of blood pumped out by the left ventricle in one minute. It
19. The Frank-Starling law explains that the critical factor controlling stroke volume is the
20. a. In a fetus, the common function of the foramen ovale and the ductus arteriosus is to
allow blood to bypass the pulmonary circulation, and move directly into the systemic
circulation.
Critical Thinking and Clinical Application Questions
1. Cardiac tamponade is compression of the heart due to accumulation of blood or inflam-
matory fluid in the pericardial sac. Such compression reduces the ability of the heart to
beat and act as an effective pump, leading to inadequate blood delivery (which results in
ischemia and cyanosis) and ultimately cardiogenic shock. (p. 661)
2. a. To auscultate the aortic valve, place the stethoscope over the second intercostal space
at the right sternal margin. To auscultate the mitral valve, place the stethoscope over
the heart apex, in the fifth intercostal space in line with the middle of the clavicle.
3. Failure of the left ventricle (which pumps blood to the body) can result in chest pain due
to dying or dead ischemic cardiac cells; pale, cold skin due to lack of circulation of blood
4. Oxygen-deficient blood returning from the systemic circulation to the right heart will
5. Gabriel, being a user of an injectable drug, probably was infected by a bacteria-
contaminated (“dirty”) needle used to administer heroin. (p. 690)
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6. The synonyms are as follows:
a. atrioventricular groove: coronary sulcus
b. tricuspid valve: right AV valve
c. bicuspid valve: left AV or mitral valve
d. atrioventricular bundle: bundle of His. (pp. 662–667, 675)
Suggested Readings
Anversa, P., and B. Nadal-Ginard. “Myocyte Renewal and Ventricular Remodelling.”
Nature 415 (6868) (Jan. 2002): 240–243.
Balakumar, P., and N. K. Sharma. “Healing the Diabetic Heart: Does Myocardial Precondi-
tioning Work?” Cellular Signalling 24 (1) (Jan. 2012): 53–59.
7 (12) (Dec. 2001): 1277–1278.
Harder, B. “Vitamin Void.” Science News 161 (7) (Feb. 2002): 161.
Hoffman-Kim, Diane. “Tissue Engineering: Heart Valves.” Science and Medicine
8 (March/April 2002): 62–64.
Isner, J. M. “Myocardial Gene Therapy.” Nature 415 (6868) (Jan. 2002): 234–239.
Malagò, R., et al. “Coronary Artery Anatomy and Variants.” Pediatric Radiology 41 (12)
(Dec. 2011): 1505–1515.
Marban, E. “Cardiac Channelopathies.” Nature 415 (6868) (Jan. 2002): 213–218.
Towbin, J. A., and N. E. Bowles. “The Failing Heart.” Nature 415 (6868) (Jan. 2002):
227–233.
Vane, John R. “Back to an Aspirin a Day?” Science 296 (5567) (April 2002): 474–475.

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