Seeley−Stephens−Tate:
Anatomy and Physiology,
Sixth Edition
IV. Regulations and
Maintenance
20. Cardiovascular System:
The Heart
© The McGraw−Hill
Companies, 2004
Approximately370 years ago, it was
established thatthe heart’s pumping
action isessential to maintain the con-
tinuouscirculation of blood throughout
the body. Our current understanding of
the detailed function ofthis amazing pump,
its regulation, and modern treatments for
heartdisease is, in comparison, very recent.
The heartis actuallytwo pumps in one. The right side
ofthe heart receivesblood from the body and pumps blood through the pulmonary
(pu
˘lmo¯-na¯r-e¯) circulation,which carriesblood to the lungs and returns it to the left
side of the heart. In the lungs, carbon dioxide diffusesfrom the blood into the
lungs, and oxygen diffusesfrom the lungsinto the blood. The left side of the heart
pumpsblood through the systemic circulation, which delivers oxygen and nutri-
entsto all remaining tissues of the body. From those tissues carbon dioxide and
other waste productsare carried back to the rightside of the heart (figure 20.1).
The heartof a healthy 70 kg person pumps approximately 7200 L(approx-
imately1900 gallons) of blood each dayat a rate of 5 L/min. For most people, the
heartcontinues to pump for more than 75 years. During periods ofvigorous exer-
cise, the amountof blood pumped per minute increases severalfold. The life of
the individualis in danger if the heart loses its ability to pump blood for even a
few minutes. Cardiology(kar-de¯-olo¯-je¯ ) is a medical specialty concerned with
the diagnosisand treatment of heart disease.
Thischapter describes the functionsof the heart (668), size, shape, and lo-
cation of the heart(668), the anatomy of the heart (670), the route of blood flow
through the heart(677), and its histology (679) and electrical properties(681).
The cardiac cycle (685), mean arterial blood pressure (692), regulation of the
heart (693), and the heart and homeostasis (696) are described. The chapter
endswith the effects of aging on the heart (699).
Cardiovascular
System
The Heart
Colorized SEM of Purkinje fibersof the heart.
CHAPTER
20
Part 4 Regulationsand Maintenance
Seeley−Stephens−Tate:
Anatomy and Physiology,
Sixth Edition
IV. Regulations and
Maintenance
20. Cardiovascular System:
The Heart
© The McGraw−Hill
Companies, 2004
Functions of the Heart
Objective
■ Explain the functions of the heart
The functions ofthe heart include:
1. Generating blood pressure.Contractions of the heart
generate blood pressure,which is responsible for blood
movement through the blood vessels.
2. Routing blood.The heart separ ates the pulmonary and
systemic circulations and ensures better oxygenation of
blood flowing to tissues.
3. Ensuring one-way blood flow.The valves of the heart ensure
a one-way flow ofblood though the heart and blood vessels.
4. Regulating blood supply.Changes in the rate and force of
contraction match blood delivery to the changing metabolic
needs ofthe tissues, such as during rest, exercise, and
changes in body position.
1. List four major functions of the heart.
Part4 Regulationsand Maintenance668
Size, Shape, and Location
of the Heart
Objective
■ Describe the size, shape, and location of the heart.
The adult heart is shaped like a blunt cone and is approxi-
mately the size of a closed fist. The blunt, rounded point of the
cone is the apex;and the larger, flat part at the opposite end of the
cone is thebase.
The heart is located in the thoracic cavity between the
lungs. The heart, trachea, esophagus, and associated structures
form a midline partition, the mediastinum (mede¯-as-tı¯nu˘m;
see figure 1.14).
It’s important for clinical reasons to know the location of
the heart in the thoracic cavity.Positioning a stethoscope to hear
the heart sounds and positioning electrodes to record an electro-
cardiogram (e¯-lek-tro¯-karde¯-o¯-gram; ECG or EKG) from chest
leads depend on this knowledge. Effective cardiopulmonary
resuscitation (karde¯-o¯-pu˘lmo-na¯r-e¯ re¯-su˘si-ta¯-shu˘n;CPR)
Figure 20.1
Systemicand Pulmonary Circulation
The rightside of the heart receives deoxygenated blood (blue) from the bodyand pumps it to the lungs through the pulmonary circulation. The left side of the heart
receivesoxygenated blood (red) from the lungs and pumps it to the body through the systemic circulation to deliver oxygen to the tissues. After passing through the
tissues, deoxygenated blood isreturned to the rightside of the heart.
Tissue
capillaries
Circulation to
tissues of head
Circulation to
tissues of
lower body
Systemic
circulation
(to body)
Pulmonary
circulation
(to lungs)
Lung
Lung
capillaries
Right side of heart
Left side
of heart
Tissue
capillaries
CO
2
CO
2
O
2
O
2
CO
2
O
2
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Anatomy and Physiology,
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IV. Regulations and
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20. Cardiovascular System:
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© The McGraw−Hill
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Chapter 20 Cardiovascular System: The Heart 669
also depends on a reasonable knowledge of the position and
shape of the heart. The heart lies obliquely in the mediastinum,
with its base directed posteriorly and slightly superiorly and the
apex directed anteriorly and slightly inferiorly.The apex is also
directed to the left so that approximately two-thirds ofthe heart’s
mass lies to the left of the midline of the sternum (figure 20.2).
The base ofthe hear t is located deep to the sternum and extends
to the second intercostal space.The apex is approximately 9 cen-
timeters (cm) to the left of the sternum and is deep to the fifth
intercostal space.
2. Give the approximate size and shape of the heart. Where is
itlocated?
CardiopulmonaryResuscitation (CPR)
In casesin which the heart suddenly stops beating, CPR can save lives.
CPR involvesrhythmic compression of the chest combined with artificial
ventilation ofthe lungs. Applying pressure to the sternum compresses
the chestwall, which also compresses the heart and causesit to pump
blood. In manycases, CPR can provide an adequate blood supply to the
heartwall and brain until emergency medical assistance arrives.
Figure 20.2
Location ofthe Heart in the Thorax
(a) The heartlies deep and slightly to the left of the sternum. The base of the heart, located deep to the sternum, extendsto the second intercostal space, and the
apexof the heart is in the fifth intercostal space, approximately9 cm to the left of the midline.
Superior vena cava
Right lung
Right atrium
Right ventricle
Rib
Visceral pleura
Diaphragm
Aortic arch
Pulmonary trunk
Left atrium
Left lung
Left ventricle
Apex of heart
Visceral pericardium
Parietal pericardium
Larynx
Trachea
Pleural cavity
Parietal pleura
Fibrous pericardium
Pericardial cavity
Left lung
Visceral pleura
Pleural cavity
Parietal pleura
(a)
Seeley−Stephens−Tate:
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Anatomy of the Heart
Objectives
■ Describe the structure and function of the pericardium.
■ Describe the histology of the three major layers of the
heart.
■ Describe the external and internal anatomy of the heart.
Pericardium
The pericardium (per-i-karde¯-u˘ m), or pericardial sac, is a
double-layered closed sac that surrounds the heart (figure 20.3).
It consists ofa tough, fibrous connective tissue outer layer called
the fibrous pericardium and a thin, transparent inner layer of
simple squamous epithelium called the serous pericardium.The
fibrous pericardium prevents overdistention ofthe heart and an-
chors it within the mediastinum. Superiorly,the fibrous peri-
cardium is continuous with the connective tissue coverings ofthe
great vessels, and inferiorly it is attached to the surface of the
diaphragm.
The part of the serous pericardium lining the fibrous peri-
cardium is the parietal pericardium, and that part covering the
heart surface is the visceral pericardium,or epicardium (see figure
20.3).The parietal and visceral portions of the serous pericardium
are continuous with each other where the great vessels enter or
leave the heart. The pericardial cavity,between the visceral and
parietal pericardia,is filled with a thin layer of serous pericardial
fluid, which helps reduce friction as the heart moves within the
pericardial sac.
Part4 Regulationsand Maintenance670
Pericarditisand Cardiac Tamponade
Pericarditis(peri-kar-dı¯tis) isan inflammation ofthe serous
pericardium. The cause isfrequently unknown, but it can resultfrom
infection, diseasesof connective tissue, or damage due to radiation
treatmentfor cancer. It can be extremely painful, with sensationsof pain
referred to the backand chest, which can be confused with the pain ofa
myocardialinfarction (heart attack). Pericarditiscan result in a small
amountof fluid accumulation within the pericardial sac.
Cardiactamponade (tam-po˘-na¯d) isa potentially fatal condition
in which a large volume offluid or blood accumulatesin the pericardial
sac. The fluid compressesthe heart from the outside. Although the heart
isa powerful muscle, it relaxes passively. When itis compressed by fluid
within the pericardialsac, it cannot dilate when the cardiac muscle
relaxes. Consequently, itcannotfill with blood during relaxation, which
makesit impossible for it to pump blood. Cardiactamponade can cause
a person to die quicklyunless the fluid is removed. Causesof cardiac
tamponade include rupture ofthe heart wall following a myocardial
infarction, rupture ofblood vessels in the pericardium after a malignant
tumor invadesthe area, damage to the pericardium resulting from
radiation therapy, and trauma (e.g., a trafficaccident).
HeartWall
The heart wall is composed of three layers of tissue: the epi-
cardium,the myocardium, and the endocardium (figure 20.4).The
epicardium(ep-i-karde¯-u˘m) is a thin serous membrane that con-
stitutes the smooth outer surface ofthe heart. The epicardium and
Figure 20.2
(continued)
(b) Crosssection of the thorax showing the position of the heart in the mediastinum and itsrelationship to other structures.
Esophagus
Right pleural cavity
Right pulmonary artery
Right pulmonary vein
Superior vena cava
Ascending aorta
Right atrium
Right ventricle
Descending aorta
Tissue of mediastinum
Bronchus of lung
Left pulmonary artery
Left pleural cavity
Parietal pleura
Visceral pleura
Left pulmonary vein
Pulmonary trunk
Left atrium
Left ventricle
Pericardial cavity
Visceral pericardium
Parietal pericardium
Fibrous pericardium
(b)
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20. Cardiovascular System:
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Chapter 20 Cardiovascular System: The Heart 671
Figure 20.3
Heartin the Pericardium
The heartis located in the pericardium, which consistsof an outer fibrous pericardium and an inner serous pericardium. The serous pericardium has two parts: the
parietalpericardium lines the fibrous pericardium, and the visceralpericardium (epicardium) covers the surface of the heart. The pericardial cavity, between the
parietaland visceral pericardium, isfilled with a small amount of pericardial fluid.
Fibrous pericardium
Parietal pericardium
Visceral pericardium
(or epicardium)
Pericardial cavity
filled with pericardial
fluid
Serous pericardium
Pericardium
Figure 20.4
HeartWall
Partof the wall of the heart has been removed to show its structure. The enlarged section illustratesthe epicardium, the myocardium, and the endocardium.
Simple squamous
epithelium
Loose connective
tissue and fat
Epicardium
(visceral
pericardium)
Myocardium
Endocardium
Trabeculae
carneae
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the visceral pericardium are two names for the same structure.The
serous pericardium is called the epicardium when considered a
part of the heart and the visceral pericardium when considered a
part of the pericardium. The thick middle layer of the heart, the
myocardium (mı¯-o¯-karde¯-u˘ m), is composed of cardiac muscle
cells and is responsible for the ability ofthe hear t to contract.The
smooth inner surface of the heart chambers is the endocardium
(en-do¯ -karde¯-u˘ m),which consists of simple squamous epithe-
lium over a layer ofconnective tissue. The smooth inner surface al-
lows blood to move easily through the heart.The heart valves result
from a fold in the endocardium,thus making a double layer of en-
docardium with connective tissue in between.
The interior surfaces ofthe atria are mainly flat, but the inte-
rior ofboth auricles and a part of the right atrial wall contain mus-
cular ridges called musculi pectinati (pekti-nahte˘; hair comb).
The musculi pectinati of the right atrium are separated from the
larger,smooth portions of the atrial wall by a ridge called the crista
terminalis(krista˘termi-nalis; terminal crest). The interior walls
ofthe ventricles contain larger muscular ridges and columns called
trabeculae(tra˘-beku¯-le¯;beams) carneae (karne¯-e¯; flesh).
ExternalAnatomy and Coronary Circulation
The heart consists of four chambers: two atria (a¯tre¯-a˘; entrance
chamber) and two ventricles(ventri-klz; belly). The thin-walled
atria form the superior and posterior parts of the heart, and the
thick-walled ventricles form the anterior and inferior portions
Part4 Regulationsand Maintenance672
(figure 20.5). Flaplike auricles (awri-klz; ears) are extensions of
the atria that can be seen anteriorly between each atrium and ven-
tricle. The entire atrium used to be called the auricle, and some
medical personnel still refer to it as such.
Several large veins carry blood to the heart. The superior
vena cava (ve¯ na˘ka¯va˘ ) and the inferior vena cava carry blood
from the body to the right atrium, and four pulmonary veins
carry blood from the lungs to the left atrium. In addition, the
smaller coronary sinus carries blood from the walls ofthe hear t to
the right atrium.
Two arteries,the aorta and the pulmonary trunk, exit the
heart. The aorta carries blood from the left ventricle to the body,
and the pulmonary trunk carries blood from the right ventricle to
the lungs.
A large coronary (ko¯ro-na¯r-e¯; circling like a crown) sulcus
(soolku˘ s; ditch) runs obliquely around the heart, separating the
atria from the ventricles.Two more sulci extend inferiorly from the
coronary sulcus,indicating the division between the right and left
ventricles.The anterior interventr icular sulcus, or groove,is on
the anterior surface ofthe heart, and the posterior inter ventricu-
lar sulcus,or groove, is on the posterior surface of the heart. In a
healthy,intact heart the sulci are covered by fat, and only after this
fat is removed can the actual sulci be seen.
The major arteries supplying blood to the tissue of the heart
lie within the coronary sulcus and interventricular sulci on the sur-
face of the heart. The right and left coronary ar teries exit the
Figure 20.5
Surface ofthe Heart
(a) View ofthe anterior (sternocostal) surface.
Aortic arch
Superior vena cava
Coronary sulcus
Pulmonary trunk
Left pulmonary artery
Branches of left
pulmonary artery
Left pulmonary veins
Left atrium
Great cardiac vein
Left ventricle
Anterior interventricular artery
Branches of right
pulmonary artery
Right pulmonary veins
Right atrium
Right coronary artery
Right ventricle
Inferior vena cava
(a)
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Chapter 20 Cardiovascular System: The Heart 673
aorta just above the point where the aorta leaves the heart and lie
within the coronary sulcus (figure 20.6a).The r ight coronary ar-
tery is usually smaller than the left one, and it doesn’t supply as
much ofthe heart w ith blood.
A major branch of the left coronary artery,called the ante-
rior interventricular artery, or the left anterior descending ar-
tery,extends inferiorly in the anterior interventricular sulcus and
supplies blood to most of the anterior part of the heart. The left
marginal artery branches from the left coronary artery to supply
blood to the lateral wall of the left ventricle. The circumflex
(serku˘ m-fleks) artery branches from the left coronary artery and
extends around to the posterior side of the heart in the coronary
sulcus.Its branches supply blood to much of the posterior wall of
the heart.
The right coronary artery lies within the coronary sulcus and
extends from the aorta around to the posterior part ofthe hear t.A
Figure 20.5
(continued)
(b) Photograph ofthe anterior surface. (c) View ofthe posterior (base) and inferior (diaphragmatic) surfaces of the heart.
Aorta
Pericardium
(reflected laterally)
Pulmonary trunk
Anterior interventricular artery
Great cardiac vein
Left ventricle
Superior
vena cava
Right atrium
Right coronary
artery
Right ventricle
Small
cardiac vein
Right
marginal
artery
(b)
Superior vena cava
Right pulmonary artery
Right pulmonary veins
Right atrium
Inferior vena cava
Right coronary artery
Small cardiac vein
Posterior interventricular artery
Right ventricle
Aorta
Great cardiac vein
Left atrium
Left pulmonary veins
Left pulmonary artery
Apex
Middle cardiac vein
Left ventricle
Coronary sinus
(c)
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larger branch ofthe right coronary artery, called the right marginal
artery,and other branches supply blood to the lateral wall of the
right ventricle. A branch of the right coronary artery called the
posterior interventricular artery lies in the posterior interven-
tricular sulcus and supplies blood to the posterior and inferior part
ofthe heart.
PREDICT
Predictthe effect on the heart if blood flow through a coronary artery,
such asthe anterior interventricular artery, is restricted or completely
blocked.
Most ofthe myocardium receives blood from more than one
arterial branch.Furthermore, there are many anastamoses, or direct
connections,between the arterial branches. The anastamoses are ei-
ther between branches ofa given arter y or between branches of dif-
ferent arteries. In the event that one artery is blocked, the areas
primarily supplied by that artery may still receive some blood
through other arterial branches and through anastamoses with other
branches.Aerobic exercise tends to increase the density of blood ves-
sels supplying blood to the myocardium and the number and extent
ofthe anastamoses increase. Consequently,aerobic exercise increases
the chance that a person will survive the blockage ofa small coronary
artery.Blockage of larger coronary blood vessels still have the poten-
tial to permanently damage large areas ofthe heart wall.
Part4 Regulationsand Maintenance674
The major vein draining the tissue on the left side ofthe heart
is the great cardiac vein,and a small cardiac vein drains the r ight
margin of the heart (figure 20.6b).These veins converge toward the
posterior part of the coronary sulcus and empty into a large venous
cavity called the coronary sinus, which in turn empties into the
right atrium. A number of smaller veins empty into the cardiac
veins,into the coronary sinus, or directly into the right atrium.
Blood flow through the coronary blood vessels is not contin-
uous.When the cardiac muscle contracts, blood vessels in the wall
of the heart are compressed and blood does not readily flow
through them.When the cardiac muscle is relaxing, the blood ves-
sels are not compressed and blood flow through the coronary
blood vessels resumes.
Heart Chambers and Valves
Rightand Left Atria
The right atrium has three major openings: the openings from
the superior vena cava and the inferior vena cava receive blood
from the body,and the opening of the coronary sinus receives
blood from the heart itself(figure 20.7). The left atrium has four
relatively uniform openings that receive the four pulmonary
veins from the lungs.The two atria are separated from each other
by the interatrial septum. A slight oval depression, the fossa
ovalis(fosa˘ o¯-valis),on the right side of the septum marks the
Pulmonary
trunk
Left coronary
artery
Left atrium
Aortic arch
Left ventricle
Aortic arch
Left
ventricle
Great
cardiac
vein
Coronary
sinus
Posterior vein
of left ventricle
Left atrium
Pulmonary
trunk
Superior
vena cava
Right
atrium
Right ventricle
Small
cardiac
vein
Middle
cardiac vein
Into
right
atrium
Superior
vena cava
Aortic
semilunar
valve
Right
atrium
Right
coronary
artery
Posterior
interventricular
artery
Right
marginal
artery
Right ventricle
Anterior
interventricular
artery
Left marginal
artery
Circumflex
artery
Figure 20.6
CoronaryCirculation
(a) Arteriessupplying blood to the heart. The arteries of the anterior surface are seen directly and are darker in color; the arteriesof the posterior surface are seen
through the heartand are lighter in color. (b) Veinsdraining blood from the heart. The veins of the anterior surface are seen directly and are darker in color; the
veinsof the posterior surface are seen through the heart and are lighter in color.
(a)
(b)
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Chapter 20 Cardiovascular System: The Heart 675
former location of the foramen ovale (o¯-vale¯ ),an opening be-
tween the right and left atria in the embryo and the fetus (see
chapter 29).
Rightand Left Ventricles
The atria open into the ventricles through atrioventricular canals
(see figure 20.7). Each ventricle has one large, superiorly placed
outflow route near the midline of the heart. The right ventricle
opens into the pulmonary trunk,and the left ventricle opens into
the aorta.The two ventricles are separated from each other by the
interventricular septum,which has a thick muscular part toward
the apex and a thin membranous part toward the atria.
AtrioventricularValves
An atrioventricular valve is in each atrioventricular canal and is
composed ofcusps, or flaps. These valves allow blood to flow from
the atria into the ventricles but prevent blood from flowing back
into the atria.The atrioventricular valve between the right atrium
and the right ventricle has three cusps and is therefore called the
tricuspid (trı¯-ku˘spid) valve. The atrioventricular valve between
the left atrium and left ventricle has two cusps and is therefore
called the bicuspid (bı¯-ku˘spid),or mitral (mı¯tra˘l; resembling a
bishop’s miter,a two-pointed hat),valve.
Each ventricle contains cone-shaped muscular pillars called
papillary (papi-la¯r-e¯; nipple, or pimple-shaped) muscles. These
muscles are attached by thin,strong connective tissue strings called
chordae tendineae(ko¯rde¯tendi-ne¯-e¯;heart str ings) to the cusps
ofthe atrioventricular valves (see figure 20.7 and figure 20.8a). The
papillary muscles contract when the ventricles contract and pre-
vent the valves from opening into the atria by pulling on the chor-
dae tendineae attached to the valve cusps.Blood flowing from the
atrium into the ventricle pushes the valve open into the ventricle,
but,when the ventricle contracts, blood pushes the valve back to-
ward the atrium. The atrioventricular canal is closed as the valve
cusps meet (figure 20.9).
SemilunarValves
Within the aorta and pulmonary trunk are aortic and pulmonary
semilunar (sem-e¯-loona˘r; half-moon-shaped) valves. Each valve
consists ofthree pocketlike semilunar cusps, the free inner borders
of which meet in the center of the artery to block blood flow (see
figures 20.7 and 20.8b).Blood flowing out of the ventricles pushes
against each valve,forcing it open, but when blood flows back from
the aorta or pulmonary trunk toward the ventricles, it enters the
pockets ofthe cusps, causing them to meet in the center of the aorta
or pulmonary trunk, thus closing them and keeping blood from
flowing back into the ventricles (see figure 20.9).
Figure 20.7
InternalAnatomy of the Heart
The heartis cut in a frontal plane to show the internal anatomy.
Aortic arch
Pulmonary trunk
Left pulmonary artery
Branches of right
pulmonary artery
Left pulmonary veins
Left atrium
Right atrium
Left ventricle
Right ventricle
Left atrioventricular
canal
Right atrioventricular canal
Bicuspid (mitral) valve
Chordae tendineae
Papillary muscles
Papillary muscles
Interventricular septum
Superior vena cava
Inferior vena cava
Pulmonary
semilunar valve
Tricuspid valve
Aortic semilunar valve
Coronary sinus
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3. What is the pericardium? Name its parts and their functions.
4. Describe the three layers of the heart, and state their
functions. Name the muscularridges found on the interior
of the auricles. Name the ridgesand columns found on the
interiorwalls of the ventricles.
5. Name the major blood vessels that enter and leave the
heart. Which chambersof the heart do they enter or exit? Is
blood flowthrough the coronary vessels continuous?
Part4 Regulationsand Maintenance676
6. What structure separates the atria from each other? What
structure separatesthe ventricles from each other?
7. Name the valves that separate the right atrium from the
rightventricle and the left atrium from the left ventricle.
Whatare the functions of the papillary muscles and the
chordae tendineae?
8. Name the valves found in the aorta and pulmonary
trunk.
Pulmonary
trunk
Trabeculae on
interventricular
septum
Chordae
tendineae
Papillary
muscles
Superior
vena cava
Ascending
aorta
Right atrium
Anterior cusp
of tricuspid valve
Inferior vena cava
Pulmonary
trunk
Superior vena cava
Ascending aorta
Pulmonary
semilunar valve
Opening of left
coronary artery
Bicuspid valve
Left atrium (cut open)
Opening of
right coronary
artery
Aortic semilunar valve
Right atrium
Figure 20.8
HeartValves
(a) View ofthe tricuspid valve, the chordae tendineae, and the papillary muscles. (b) A superior view ofthe heart valves. Note the three cusps of each semilunar
valve meeting to preventthe backflow of blood.
(a) (b)
Pulmonary veins
Aortic semilunar
valve (closed)
Aorta
Left atrium
Bicuspid valve
(open)
Chordae tendineae
(tension low)
Papillary muscle
(relaxed)
Cardiac muscle
(relaxed)
Left ventricle
(dilated)
Pulmonary veins
Aortic semilunar
valve (open)
Left atrium
Bicuspid valve
(closed)
Chordae tendineae
(tension high)
Papillary muscle
(contracted)
Cardiac muscle
(contracted)
Left ventricle
(contracted)
Aorta
(a) When the bicuspid valve is open, the cusps of the valve are pushed by
blood into the ventricle. Papillary muscles are relaxed and tension on
the chordae tendineae is low. Blood flows from the left atrium into the
left ventricle. When the aortic semilunar valve is closed, the cusps of
the valve overlap as they are pushed by the blood in the aorta toward
the ventricle. There is no blood flow from the aorta into the ventricle.
(b) When the bicuspid valve is closed, the cusps of the valves overlap as
they are pushed by the blood toward the left atrium. There is no blood
flow from the ventricle into the atrium. Papillary muscles are contracted
and tension on the chordae tendineae is increased. When the aortic
semilunar valve is open, the cusps of the valve are pushed by the
blood toward the aorta. Blood then flows from the left ventricle
into the aorta.
Figure 20.9
Function ofthe Heart Valves
(a) Valve positionswhen blood isflowing into the left ventricle. (b) Valve positions when blood is flowing out of the left ventricle.
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Clinical Focus Angina, Infarctions, and Treatmentof Blocked CoronaryArteries
Angina pectoris (anji-na˘ , an-jı¯na˘ pekto¯-
ris) ispain that results from a reduction in
blood supplyto cardiac muscle. The pain is
temporaryand, if blood flow is restored, lit-
tle permanent change or damage results.
Angina pectoris is characterized bychest
discomfort deep to the sternum, often de-
scribed as heaviness, pressure, or moder-
ately severe pain. It is often mistaken for
indigestion. The pain can also be referred to
the neck, lower jaw, leftarm, and left shoul-
der (see chapter 14, p. 477).
Most often, angina pectoris results
from narrowed and hardened coronaryar-
terial walls. The reduced blood flow re-
sults in a reduced supply of oxygen to
cardiac muscle cells. As a consequence,
the limited anaerobic metabolism of car-
diac muscle results in a buildup of lactic
acid and reduced pH in affected areasof
the heart. Pain receptorsare stimulated by
the lacticacid. The pain is predictably as-
sociated with exercise because the in-
creased pumping activity of the heart
requires more oxygen, and the narrowed
blood vessels cannot supply it. Rest and
drugs like nitroglycerin frequentlyrelieve
angina pectoris. Nitroglycerin dilates the
blood vessels, including the coronary ar-
teries. Consequently, the drug increases
the oxygen supplyto cardiac muscle and
reduces the workload of the heart. Be-
cause peripheral arteries are dilated, the
hearthas to pump blood against a smaller
pressure, and the need for oxygen de-
creases. The heartalso pumps less blood
because blood tendsto remain in the di-
lated blood vessels and lessblood is re-
turned to the heart.
Myocardial infarction (mı¯-o¯-karde¯-a˘l
in-farkshu˘ n) results from a prolonged lack
ofblood flow to a par tof the cardiac mus-
cle, resulting in a lackof oxygen and ulti-
matelycellular death. Myocardialinfarctions
varywith the amount of cardiac muscle and
the partof the heart that is affected. If blood
supply to cardiac muscle is reestablished
within 20 minutes, no permanent damage
occurs. Ifthe lackof oxygen lasts longer, cell
death results. Within 30–60 secondsafter
blockage ofa coronary blood vessel, how-
ever, functional changesare obvious. The
electrical properties of the cardiac muscle
are altered, and the ability of the heart to
function properlyis lost. The most common
cause ofmyocardial infarction is thrombus
formation that blocks a coronary artery.
Coronary arteries narrowed byatheroscle-
rotic (ather-o¯-skler-otik)lesions provide
one of the conditions that increase the
chances of myocardialinfarction. Athero-
sclerotic lesions partially blockblood ves-
sels, resulting in turbulentblood flow, and
the surfacesof the lesions are rough. These
changesincrease the probability of throm-
busformation.
Angioplasty (anje¯-o¯-plas-te¯) is a
processwhereby a smallballoon is threaded
through the aorta and into a coronary ar-
tery. After the balloon hasentered the par-
tiallyoccluded coronary artery, it is inflated,
thereby flattening the atherosclerotic de-
positsagainst the vessel walls and opening
the occluded blood vessel. Thistechnique
improvesthe function of cardiac muscle in
patients suffering from an inadequate
blood flow to the cardiac muscle through
the coronaryarteries. Some controversy ex-
istsabout its effectiveness. At least in some
patients, dilation of the coronary arteries
can be reversed within a few weeks or
months and blood clots can form in coro-
naryar teriesfollowing angioplasty. To help
preventfuture blockage, a metal-mesh tube
called a stentis inserted into the vessel. Al-
though the stent isbetter able to hold the
vessel open, it too can eventuallybecome
blocked. Smallrotating blades and lasers
are also used to remove lesionsfrom coro-
naryvessels.
Acoronar y bypass is a surgical proce-
dure that relieves the effects of obstruc-
tionsin the coronary arteries. The technique
involves taking healthysegments of blood
vessels from other parts of the patient’s
body and using them to bypass obstruc-
tionsin the coronary arteries. The technique
iscommon for those who suffer from severe
occlusion in specific parts of coronary
arteries.
Special enzymes are used to break
down blood clots thatform in the coronary
arteries and cause heartattacks. The major
enzymes used are streptokinase(strep-to¯-
kı¯na¯s),tissue plasminogen(plaz-mino¯-jen)
activator (t-PA), or, sometimes, urokinase
(u¯r-o¯-kı¯na¯s). These enzymesfunction to acti-
vate plasminogen, which isan inactive form
ofan enzyme in the body that breaks down
the fibrin ofclots. The strategy is to adminis-
ter these drugsto people suffering from myo-
cardial infarctions as soon as possible
following the onsetof symptoms. Removalof
the occlusions produced byclots reestab-
lishesblood flow to the cardiac muscle and
reduces the amountof cardiac muscle per-
manentlydamaged by the occlusion.
Chapter 20 Cardiovascular System: The Heart 677
Route of Blood Flow
Through the Heart
Objective
■ Describe the flow of blood through the heart.
Blood flow through the heart is depicted in figure 20.10.Even
though it’s more convenient to discuss blood flow through the heart
one side at a time,it’s important to understand that both atria con-
tract at about the same time and both ventricles contract at about
the same time.This concept is particularly important when consid-
ering electrical activity,pressure changes, and heart sounds.
Blood enters the right atrium from the systemic circulation,
which returns blood from all the tissues of the body.Blood flows
from an area of higher pressure in the systemic circulation to the
right atrium,which has a lower pressure. Most of the blood in the
right atrium then passes into the right ventricle as the ventricle re-
laxes following the previous contraction. The right atrium then
contracts,and most of the blood remaining in the atrium is pushed
into the ventricle to complete right ventricular filling.
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Part4 Regulationsand Maintenance678
Superior
vena cava
Inferior
vena cava
Papillary muscles
Tricuspid valve
Right atrium
Pulmonary semilunar
valve
Pulmonary
arteries
Pulmonary arteries
Pulmonary veins
Left atrium
Bicuspid valve
Interventricular septum
Left ventricle
Right ventricle
Pulmonary trunk
Aortic arch
Aortic semilunar
valve
Superior and
inferior vena
cava
Right
atrium
Body tissues
(systemic
circulation)
Aorta
Left
ventricle
Left
atrium
Pulmonary
veins
Aortic
semilunar
valves
Tricuspid
valve
Bicuspid
valve
Right
ventricle
Pulmonary
trunk
Pulmonary
arteries
Lung tissue
(pulmonary
circulation)
Pulmonary
semilunar
valves
Figure 20.10
Blood Flow Through the Heart
(a) Frontalsection of the heart revealing the four chambers and the direction ofblood flow through the heart. (b) Diagram listing in order the structures through
which blood flowsin the systemic and pulmonary circulations. The heartvalves are indicated by circles: deoxygenated blood (blue); oxygenated blood (red).
(a)
(b)
Contraction of the right ventricle pushes blood against the
tricuspid valve,forcing it closed, and against the pulmonary semi-
lunar valve,forcing it open, thus allowing blood to enter the pul-
monary trunk.
The pulmonary trunk branches to form the pulmonary
arteries(see figure 20.5), which carry blood to the lungs, where
carbon dioxide is released and oxygen is picked up (see chapters
21 and 23). Blood returning from the lungs enters the left
atrium through the four pulmonary veins. The blood passing
from the left atrium to the left ventricle opens the bicuspid
valve,and contraction of the left atrium completes left ventric-
ular filling.
Contraction of the left ventricle pushes blood against the bi-
cuspid valve,closing it, and against the aortic semilunar valve, open-
ing it and allowing blood to enter the aorta.Blood flowing through
the aorta is distributed to all parts of the body except to the parts of
the lungs supplied by the pulmonary blood vessels (see chapter 23).
9. Starting at the venae cavae and ending at the aorta,
describe the flowof blood through the heart.
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Chapter 20 Cardiovascular System: The Heart 679
Histology
Objectives
■ List the characteristics of cardiac muscle.
■ Describe the conducting system of the heart.
Heart Skeleton
Thehear t skeleton consists of a plate of fibrous connective tissue
between the atria and ventricles.This connective tissue plate forms
fibrous rings around the atrioventricular and semilunar valves
and provides a solid support for them (figure 20.11).The fibrous
connective tissue plate also serves as electrical insulation between
the atria and the ventricles and provides a rigid site for attachment
ofthe cardiac muscles.
CardiacMuscle
Cardiac muscle cells are elongated, branching cells that contain
one or occasionally two centrally located nuclei. Cardiac muscle
cells contain actin and myosin myofilaments organized to form
sarcomeres,which join end to end to form myofibrils (see chapter 4).
The actin and myosin myofilaments are responsible for muscle
contraction,and their organization gives cardiac muscle a striated
(banded) appearance. The striations are less regularly arranged
and less numerous than in skeletal muscle (figure 20.12).
Cardiac muscle has a smooth sarcoplasmic reticulum,but
it is neither as regularly arranged nor as abundant as in skeletal
muscle fibers, and no dilated cisternae are present,as occurs in
skeletal muscle.The sarcoplasmic reticulum comes into close as-
sociation at various points with membranes of transverse
tubules (T tubules).Also, the T tubules of cardiac muscle are less
abundant than in skeletal muscle and they are found near the Z
disks of the sarcomeres instead of where the actin and myosin
overlaps as in skeletal muscle.The loose association between the
sarcoplasmic reticulum and the T tubules is partly responsible for
the slow onset of contraction and the prolonged contraction
phase in cardiac muscle. Depolarizations of the cardiac muscle
plasma membrane are not carried from the surface of the cell to
the sarcoplasmic reticulum as efficiently as they are in skeletal
Figure 20.11
Skeleton ofthe Heart
The skeleton ofthe heart consists of fibrous connective tissue ringsthat
surround the heartvalves and separate the atria from the ventricles. Cardiac
muscle attachesto the fibrous connective tissue. The muscle fibersare
arranged so thatwhen the ventricles contract a wringing motion isproduced
and the distance between the apexand base of the heart shortens.
Pulmonary semilunar valve
Aortic
semilunar valve
Tricuspid
valve
Cardiac muscle
of the right
ventricle
Cardiac muscle
of the left ventricle
Skeleton of the heart
including fibrous rings
around valves
Bicuspid
valve
Mitochondrion
Myofibril
Sarcomere
Sarcoplasmic
reticulum
T tubule
Connective tissue
Sarcolemma
Branching
muscle fibers
Nucleus of cardiac
muscle cell
Striations
Intercalated disks
LM 400x
Figure 20.12
Histologyof the Heart
(a) Heartmuscle demonstrating the structure and arrangement of the individual muscle fibers. (b) Photomicrograph of heart muscle.
(a)
(b)
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muscles,and calcium must diffuse a greater distance from the sar-
coplasmic reticulum to the actin myofilaments.In addition,a sub-
stantial number of Ca
2
enter the cardiac muscle cells from the
extracellular fluid.
Adenosine triphosphate (ATP) provides the energy for cardiac
muscle contraction, and, as in other tissues,ATP production de-
pends on oxygen availability.Cardiac muscle, however, cannot de-
velop a large oxygen debt,a characteristic that is consistent with the
function ofthe heart. Development of a large oxygen debt would re-
sult in muscular fatigue and cessation ofcardiac muscle contraction.
Cardiac muscle cells are rich in mitochondria,which perform oxida-
tive metabolism at a rate rapid enough to sustain normal myocardial
energy requirements. The extensive capillary network provides an
adequate oxygen supply to the cardiac muscle cells.
PREDICT
Under resting conditions, mostATP produced in cardiacmuscle is
derived from the metabolism offatty acids. During periods of heavy
exercise, however, cardiacmuscle cellsuse lactic acid as an energy
source. Explain whythis arrangement isan advantage.
Cardiac muscle cells are organized in spiral bundles or
sheets. The cells are bound end to end and laterally to adjacent
cells by specialized cell–cell contacts called intercalated (in-
terka˘-la¯-ted) disks (see figure 20.12).The membranes of the in-
tercalated disks have folds,and the adjacent cells fit together,thus
greatly increasing contact between them. Specialized plasma
membrane structures called desmosomes (dezmo¯-so¯mz) hold
the cells together,and g ap junctions function as areas of low
electric resistance between the cells,allowing action potentials to
pass from one cell to adjacent cells (see figure 4.3).Electrically,
the cardiac muscle cells behave as a single unit,and the highly co-
ordinated contractions of the heart depend on this functional
characteristic.
Part4 Regulationsand Maintenance680
Conducting System
The conducting system of the heart, which relays electric action
potentials through the heart, consists of modified cardiac muscle
cells that form two nodes (meaning a knot or lump) and a conduct-
ingbundle (figure 20.13). The two nodes are contained within the
walls ofthe right atrium and are named according to their position
in the atrium.The sinoatrial (SA) node is medial to the opening of
the superior vena cava,and the atrioventricular (AV) node is me-
dial to the right atrioventricular valve.The AV node gives rise to a
conducting bundle ofthe heart, the atrioventricular bundle. This
bundle passes through a small opening in the fibrous skeleton to
reach the interventricular septum, where it divides to form the
rightand left bundle branches, which extend beneath the endo-
cardium on either side ofthe interventricular septum to the apices
ofthe rig ht and left ventricles,respectively.
The inferior terminal branches of the bundle branches are
called Purkinje (per-kinje¯) fibers,which are large-diameter car-
diac muscle fibers.The y have fewer myofibrils than most cardiac
muscle cells and don’t contract as forcefully.Intercalated disks are
well developed between the Purkinje fibers and contain numerous
gap junctions.As a result of these structural modifications, action
potentials travel along the Purkinje fibers much more rapidly than
through other cardiac muscle tissue.
Cardiac muscle cells have the capacity to generate sponta-
neous action potentials,but cells of the SA node do so at a greater
frequency.As a result, the SA node is called the pacemaker of the
heart. Thus, the heart contracts spontaneously and rhythmically.
Once action potentials are produced,they spread from the SA node
to adjacent cardiac muscle fibers ofthe at rium.Preferential path-
ways conduct action potentials from the SA node to the AV node at
a greater velocity than they are transmitted in the remainder ofthe
atrial muscle fibers, although such pathways cannot be distin-
guished structurally from the remainder ofthe atr ium.
Left atrium
Left ventricle
Apex
Atrioventricular
(AV) bundle
Atrioventricular
(AV) node
Sinoatrial
(SA) node
1. Action potentials originate in the sinoatrial (SA)
node and travel across the wall of the atrium (
arrows
)
from the SA node to the atrioventricular (AV) node.
2. Action potentials pass through the AV node and
along the atrioventricular (AV) bundle, which extends
from the AV node, through the fibrous skeleton, into
the interventricular septum.
3. The AV bundle divides into right and left bundle branches,
and action potentials descend to the apex of each ventricle
along the bundle branches.
4. Action potentials are carried by the Purkinje fibers
from the bundle branches to the ventricular walls.
Left and right
bundle branches
Purkinje
fibers
1
2
4
3
ProcessFigure 20.13
Conducting System ofthe Heart
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Chapter 20 Cardiovascular System: The Heart 681
When the heart beats under resting conditions, approxi-
mately 0.04 second is required for action potentials to travel from
the SA node to the AV node.Within the AV node,action potentials
are propagated slowly compared to the remainder ofthe conduct-
ing system.As a consequence, a delay occurs of 0.11 second from
the time action potentials reach the AV node until they pass to the
AV bundle.The total delay of0.15 second allows completion of the
atrial contraction before ventricular contraction begins.
After action potentials pass from the AV node to the highly
specialized conducting bundles, the velocity of conduction in-
creases dramatically.The action potentials pass through the left
and right bundle branches and through the individual Purkinje
fibers that penetrate into the myocardium ofthe ventricles (see fig-
ure 20.13).
Because of the arrangement of the conducting system, the
first part of the myocardium that is stimulated is the inner wall of
the ventricles near the apex.Thus ventricular contraction begins at
the apex and progresses throughout the ventricles. Once stimu-
lated, the spiral arrangement of muscle layers in the wall of the
heart results in a wringing action that proceeds from the apex to-
ward the base of the heart. During the process, the distance be-
tween the apex and the base ofthe heart decreases.
10. Describe and list the functions of the skeleton of the heart.
11. Describe the similarities and differences between cardiac
muscle and skeletal muscle.
12. Why does cardiac muscle have a slow onset of contraction
and a prolonged contraction?
13. What substances do cardiac muscle cells use as an energy
source? Do cardiacmuscle cells develop an oxygen debt?
14. What anatomic features are responsible for the ability of
cardiacmuscle cells to contract asa unit?
15. List the parts of the conducting system of the heart. Explain
howthe conducting system coordinates contraction of the
atria and ventricles. Explain whyPurkinje fibers conduct
action potentialsmore rapidly than other cardiac muscle
cells.
PREDICT
Explain whyit’s more efficient for contraction of the ventricles to
begin atthe apex of the heart than at the base.
Electrical Properties
Objectives
■ Describe action potentials in cardiac muscle cells.
■ Define the term autorhythmic, and explain how the SA node
functionsas the pacemaker.
■ Explain the features of an electrocardiogram and the events
thatthose features represent.
Cardiac muscle cells, like other electrically excitable cells
such as neurons and skeletal muscle fibers, have a resting
membrane potential (RMP).The RMP depends on a low perme-
ability of the plasma membrane to Na
and Ca
2
and a higher
permeability to K
. When neurons, skeletal muscle cells,and
cardiac muscle cells are depolarized to their threshold level,action
potentials result (see chapter 11).
Action Potentials
Like action potentials in skeletal muscle,those in cardiac muscle
exhibit depolarization followed by repolarization of the RMP.Al-
terations in membrane channels are responsible for the changes in
the permeability of the plasma membrane that produce the action
potentials. Action potentials in cardiac muscle last longer than
those in skeletal muscle,and the membrane channels differ from
those in skeletal muscle.In contrast to action potentials in skeletal
muscle,which take less than 2 milliseconds (ms) to complete, ac-
tion potentials in cardiac muscle take approximately 200–500 ms
to complete.
In cardiac muscle,the action potential consists of a rapid de-
polarization phase, followed by rapid,but par tial,early repolar-
ization. Then a prolonged period of slow repolarization occurs,
called the plateau phase.At the end of the plateau, a more rapid fi-
nal repolarization phasetakes place, during which the membrane
potential returns to its resting level (figure 20.14).
Membrane channels,called voltage-gated Na
ⴙ
channels,or
sodium fast channels(or fast channels), open bringing about the
depolarization phase of the action potential. As the voltage-gated
Na
channels open,Na
diffuses into the cell,causing rapid depo-
larization until the cell is depolarized to approximately 20 milli-
volts (mV).
The voltage change occurring during depolarization affects
other ion channels in the plasma membrane.Several different types
ofvoltage-gated K
ⴙ
channelsexist, each of which opens and closes
at different membrane potentials, causing changes in membrane
permeability to K
. For example, at rest,the movement of K
through open voltage-gated K
channels is primarily responsible
for establishing the resting membrane potential in cardiac muscle
cells. Depolarization causes these voltage-gated K
channels to
close,thereby decreasing membrane permeability to K
.Depolar-
ization also causes voltage-gated Ca
2ⴙ
,or calcium slow channels
(or slow channels) to begin to open. Compared to sodium fast
channels,the calcium slow channels open and close slowly.
Repolarization is the result ofchanges in membrane perme-
ability to Na
,K
,and Ca
2
.Early repolarization occurs when the
voltage-gated Na
channels close and a small number of voltage-
gated K
channels open. Na
movement into the cell stops,and
K
move out ofthe cell. The plateau phase occurs as voltage-gated
Ca
2
channels continue to open,and the movement of Ca
2
into
the cell counteracts the potential change produced by the move-
ment ofK
out ofthe cell. The plateau phase ends and final repo-
larization begins as the voltage-gated Ca
2
channels close and
many more voltage-gated K
channels open.Thus Ca
2
stops dif-
fusing into the cell,and the tendency for K
to diffuse out of the
cell increases.These permeability changes cause the membrane po-
tential to return to its resting level.
Action potentials in cardiac muscle are conducted from cell
to cell, whereas action potentials in skeletal muscle fibers are
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Repolarization
phase
–85
12
0
Depolarization
phase
(mV)
Time (ms)
Permeability changes during an action potential in
skeletal muscle:
1. Depolarization phase
• Voltage-gated Na
+
channels open.
• Voltage-gated K
+
channels begin to open.
2. Repolarization phase
• Voltage-gated Na
+
channels close.
• Voltage-gated K
+
channels continue to open.
• Voltage-gated K
+
channels close at the end of
repolarization and return the membrane potential
to its resting value.
Permeability changes during an action potential in
cardiac muscle:
1. Depolarization phase
• Voltage-gated Na
+
channels open.
• Voltage-gated K
+
channels close.
• Voltage-gated Ca
2+
channels begin to open.
2. Early repolarization and plateau phases
• Voltage-gated Na
+
channels close.
• Some voltage-gated K
+
channels open, causing
early repolarization.
• Voltage-gated Ca
2+
channels are open, producing
the plateau by slowing further repolarization.
3. Final repolarization phase
• Voltage-gated Ca
2+
channels close.
• Many voltage-gated K
+
channels open.
Final
repolarization
phase
Early
repolarization
phase
Plateau
phase
Depolarization
phase
(mV)
12
Time (ms)
500
–85
0
1
1
2
2
3
Figure 20.14
Comparison ofAction Potentials in Skeletal and CardiacMuscle
(a) An action potentialin skeletal muscle consists ofdepolarization and repolarization phases. (b) An action potential in cardiac muscle consists of depolarization,
earlyrepolarization, plateau, and final repolarization phases. Cardiacmuscle does not repolarize as rapidly as skeletal muscle (indicated by the breakin the curve)
because ofthe plateau phase.
(a)
(b)
conducted along the length of a single muscle fiber,but not from
fiber to fiber.Also,the rate of action potential propagation is slower
in cardiac muscle than in skeletal muscle because cardiac muscle
cells are smaller in diameter and much shorter than skeletal muscle
fibers.Although the gap junctions of intercalated disks allow trans-
fer ofaction potentials between cardiac muscle cells, they do slow the
rate ofaction potential conduction between the cardiac muscle cells.
Autorhythmicityof Cardiac Muscle
The heart is said to be autorhythmic (awto¯-rithmik) because it
stimulates itself(auto) to contract at regular intervals (rhythmic).If
the heart is removed from the body and maintained under physio-
logic conditions with the proper nutrients and temperature,it will
continue to beat autorhythmically for a long time.
In the SA node, pacemaker cells generate action potentials
spontaneously and at regular intervals. These action potentials
spread through the conducting system ofthe heart to other cardiac
muscle cells,causing voltage-gated Na
channels to open.As a result,
action potentials are produced and the cardiac muscle cells contract.
The generation of action potentials in the SA node results
when a spontaneously developing local potential, called the
prepotential, reaches threshold (figure 20.15). Changes in ion
movement into and out of the pacemaker cells cause the prepo-
tential.Na
cause depolarization by moving into the cells through
specialized non-gated Na
channels.A decreasing permeability to
K
also causes depolarization as fewer K
move out of the cells.
As a result of the depolarization, voltage-gated Ca
2
channels
open,and the movement of Ca
2
into the pacemaker cells causes
further depolarization.When the prepotential reaches threshold,
many voltage-gated Ca
2
channels open. Unlike other cardiac
muscle cells, the movement of Ca
2
into the pacemaker cells is
primarily responsible for the depolarization phase of the action
potential.Repolarization occurs, as in other cardiac muscle cells,
when the voltage-gated Ca
2
channels close and the voltage-gated
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Chapter 20 Cardiovascular System: The Heart 683
Permeability changes in pacemaker cells:
1. Prepotential
• A small number of Na
+
channels are open.
• Voltage-gated K
+
channels that opened in the
repolarization phase of the previous action potential
are closing.
• Voltage-gated Ca
2+
channels begin to open.
2. Depolarization phase
• Voltage-gated Ca
2+
channels are open.
• Voltage-gated K
+
channels are closed.
3. Repolarization phase
• Voltage-gated Ca
2+
channels close.
• Voltage-gated K
+
channels open.
Time (ms)
3001
0
60
Threshold
Depolarization
phase
Repolarization
phase
Prepotential
(mV)
32
1
Figure 20.15
SA Node Action Potential
The production ofaction potentials by the SA node is responsible for the autorhythmicityof the heart.
K
channels open.After the RMP is reestablished, production of
another prepotential starts the generation of the next action po-
tential.
Drugsthat Block Calcium Channels
Variouschemical agentslike manganese ions (Mn
2
) and verapamil
(ver-apa˘-mil) blockvoltage-gated Ca
2
channels. Voltage-gated Ca
2
channel-blocking agentsprevent the movementof Ca
2
through voltage-
gated Ca
2
channelsinto the cell and, for that reason, are called calcium
channelblockers.Some calcium channel blockers are widely used
clinicallyin the treatment of various cardiacdisorders, including
tachycardia and certain arrhythmias. Calcium channelblockersslow the
developmentof the prepotential and thus reduce the heart rate. If action
potentialsarise prematurely within the SA node or other areasof the heart,
calcium channelblockersreduce that tendency. Calcium channel blockers
also reduce the amountof work performed by the heart because less
calcium enterscardiac muscle cellsto activate the contractile mechanism.
On the other hand, epinephrine and norepinephrine increase the heart
rate and itsforce of contraction by opening voltage-gated Ca
2
channels.
Although most cardiac muscle cells respond to action poten-
tials produced by the SA node, some cardiac muscle cells in the
conducting system can generate spontaneous action potentials.
Normally,the SA node controls the rhythm of the heart because its
pacemaker cells generate action potentials at a faster rate than
other potential pacemaker cells to produce a heart rate of 70–80
beats per minute (bpm).An ectopic focus (ek-topik fo¯ku˘s; pl.,
foci,fo¯sı¯) is any part of the heart other than the SA node that gen-
erates a heartbeat. For example,if the SA node doesn’t function
properly,the part of the heart to produce action potentials at the
next highest frequency is the AV node,which produces a heart rate
of40–60 bpm. Another cause of an ectopic focus is blockage of the
conducting pathways between the SA node and other parts ofthe
heart.For example, if action potentials do not pass through the AV
node,an ectopic focus can develop in an AV bundle, resulting in a
heart rate of 30 bpm.
Ectopic foci can also appear when the rate ofaction potential
generation in the ectopic focus becomes enhanced.For example,
when cells are injured their plasma membranes become more per-
meable,resulting in depolarization. These injured cells can be the
source ofectopic action potentials.
PREDICT
Predictthe consequences for the pumping effectiveness of the heart if
numerousectopic foci in the ventricles produce action potentials at
the same time.
Refractory Period ofCardiac Muscle
Cardiac muscle,like skeletal muscle, has refractory (re¯-frakto¯r-e¯)
periodsassociated with its action potentials. During the absolute
refractory period, the cardiac muscle cell is completely insensitive
to further stimulation,and during the relative refractory p eriod
the cell exhibits reduced sensitivity to additional stimulation.Be-
cause the plateau phase of the action potential in cardiac muscle
delays repolarization to the RMP,the refractory period is pro-
longed.The long refractory period ensures that, after contraction,
relaxation is nearly complete before another action potential can
be initiated,thus preventing tetanic contractions in cardiac muscle.
PREDICT
Predictthe consequences if cardiac muscle could undergo tetanic
contraction.
Electrocardiogram
The conduction ofaction potentials through the myocardium dur-
ing the cardiac cycle produces electric currents that can be meas-
ured at the surface ofthe body. Electrodes placed on the surface of
the body and attached to an appropriate recording device can
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Table 20.1
Conditions Symptoms Possible Causes
Abnormal Heart Rhythms
Tachycardia Heart rate in excess of 100 bpm Elevated body temperature; excessive
sympathetic stimulation; toxic conditions
Paroxysmal atrial tachycardia Sudden increase in heart rate to 95–150 bpm Excessive sympathetic stimulation; abnormally
for a few seconds or even for several hours; elevated permeability of slow channels
P wave precedes every QRS complex; P wave
inverted and superimposed on T wave
Ventricular tachycardia Frequently causes fibrillation Often associated with damage to AV node or
ventricular muscle
Abnormal Rhythms Resulting from Ectopic Action Potentials
Atrial flutter 300 P waves/min; 125 QRS complexes/min Ectopic action potentials in the atria
resulting in two or three P waves (atrial
contraction) for evry QRS complex
(ventricular contraction)
Atrial fibrillation No P waves; normal QRS complexes; irregular Ectopic action potentials in the atria
timing; ventricles constantly stimulated by
atria; reduced pumping effectiveness and
filling time
Ventricular fibrillation No QRS complexes; no rhythmic contraction of Ectopic action potentials in the ventricles
the myocardium; many patches of
asynchronously contracting ventricular
muscle
Bradycardia Heart rate less than 60 bpm Elevated stroke volume in athletes; excessive
vagal stimulation; carotid sinus syndrome
Sinus Arrhythmia Heart rate varies 5% during respiratory cycle Cause not always known; occasionally caused
and up to 30% during deep respiration by ischemia or inflammation or associated
with cardiac failure
SA Node Block Cessation of P wave; new low heart rate due to Ischemia; tissue damage due to infarction;
AV node acting as pacemaker; normal QRS causes unknown
complex and T wave
AV Node Block
First-degree PR interval greater than 0.2 second Inflammation of AV bundle
Second-degree PR interval 0.25–0.45 second; some P waves trigger Excessive vagal stimulation
QRS complexes and others do not; 2:1, 3:1,
and 3:2 P wave/QRS complex ratios may occur
Complete heart block P wave dissociated from QRS complex; atrial Ischemia of AV nodal fibers or compression of
rhythm approximately 100 bpm; ventricular AV bundle
rhythm less than 40 bpm
Premature Atrial Contractions Occasional shortened ntervals between one Excessive smoking; lack of sleep; too much
contraction and the succeeding contraction; caffeine; alcoholism
frequently occurs in healthy people
P wave superimposed on QRS complex
Premature Ventricular Prolonged QRS complex; exaggerated voltage Ectopic foci in ventricles; lack of sleep; too
Contractions (PVCs) because only one ventricle may depolarize; much caffeine, irritability; occasionally occurs
inverted T wave; increased probability of with coronary thrombosis
fibrillation
Major Cardiac Arrhythmias
Abbreviations:SA sinoatrial; AV atrioventricular.
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Chapter 20 Cardiovascular System: The Heart 685
detect small voltage changes resulting from action potentials in the
cardiac muscle.The electrodes detect a summation of all the action
potentials that are transmitted through the heart at a given time.
Electrodes do not detect individual action potentials. The sum-
mated record of the cardiac action potentials is an electrocardio-
gram (ECG or EKG).
The ECG is not a direct measurement of mechanical events
in the heart, and neither the force of contraction nor blood
pressure can be determined from it.Each deflection in the ECG
record,however, indicates an electrical event within the heart and
correlates with a subsequent mechanical event.Consequently, it’s
an extremely valuable diagnostic tool in identifying a number of
cardiac abnormalities (table 20.1),par ticularly because it is pain-
less, easy to record,and noninvasive (meaning that it doesn’t re-
quire surgical procedures). Abnormal heart rates or rhythms,
abnormal conduction pathways,hyp ertrophy or atrophy ofpor-
tions of the heart, and the approximate location of damaged car-
diac muscle can be determined from analysis ofan ECG.
The normal ECG consists ofa P wave, a QRS complex, and a
T wave (figure 20.16).The P wave, which is the result of action
potentials that cause depolarization ofthe at rial myocardium,sig-
nals the onset ofatrial contraction. The QRS complex is composed
ofthree individual waves: the Q, R, and S waves. The QRS complex
results from ventricular depolarization and signals the onset of
ventricular contraction. The T wave represents repolarization of
the ventricles and precedes ventricular relaxation.A wave repre-
senting repolarization ofthe atria cannot be seen because it occurs
during the QRS complex.
The time between the beginning of the P wave and the be-
ginning of the QRS complex is the PQ interval, commonly called
the PR interval because the Q wave is often very small.During the
PR interval,which lasts approximately 0.16 second, the atria con-
tract and begin to relax.The ventricles beg in to depolarize at the
end ofthe PR interval. The QT interval extends from the beginning
of the QRS complex to the end of the T wave,lasts approximately
0.36 second, and represents the approximate length of time re-
quired for the ventricles to contract and begin to relax.
Alterationsin the Electrocardiogram
Elongation ofthe PR interval can result from (1) a delay in action
potentialconduction through the atrial muscle because of damage, such
asthat caused by ischemia (is-ke¯me¯-a˘ ), which isthe obstruction of the
blood supplyto the walls of the heart, (2) a delay of action potential
conduction through atrialmuscle because of a dilated atrium, or (3) a
delayof action potential conduction through the AV node and bundle
because ofischemia, compression, or necrosisof the AV node or bundle.
These conditionsresult in slow conduction of action potentials through
the bundle branches. An unusuallylong QT interval reflects the abnormal
conduction ofaction potentials through the ventricles, which can result
from myocardialinfarctions or from an abnormally enlarged leftor right
ventricle.
Examplesof alteration in the form of the electrocardiogram due to
cardiacabnormalities are illustrated in figure 20.17. Examples include
complete heartblock, premature ventricular contraction, bundle branch
block, atrialfibrillation, and ventricular fibrillation.
16. For cardiac muscle action potentials, describe ion
movementduring the depolarization, early repolarization,
plateau, and final repolarization phases. Whations are
associated with fastchannels and slow channels?
17. Why is cardiac muscle referred to as autorhythmic? What
are ectopicfoci?
18. How does the depolarization of pacemaker cells differ from
the depolarization of othercardiac muscle cells? What is
the prepotential?
19. Whydoes cardiac muscle have a prolonged refractoryperiod?
Whatis the advantage of a prolonged refractory period?
20. What does an ECG measure? Name the waves produced by
an ECG, and state whatevents occur during each wave.
Cardiac Cycle
Objectives
■ Describe the five events of the cardiac cycle that occur
during ventricularsystole and ventricular diastole.
■ Explain the bases of the major heart sounds.
■ Describe the aortic pressure curve.
The heart is actually two separate pumps that work together,
one in the right halfand the other in the left half of the heart.Each
pump consists of a primer pump—the atrium—and a power
pump—the ventricle.Both atrial primer pumps complete the fill-
ing ofthe ventricles with blood, and both ventricular power pumps
Figure 20.16
Electrocardiogram
The major wavesand intervals of an electrocardiogram are labeled. Each thin
horizontalline on the ECG recording represents 1 mV, and each thin vertical
line represents0.04 second.
QRS complex
(mV)
PR interval QT interval
Time (seconds)
R
P
T
Q
S
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produce the major force that causes blood to flow through the pul-
monary and systemic arteries.The term cardiac cycle refers to the
repetitive pumping process that begins with the onset of cardiac
muscle contraction and ends with the beginning of the next con-
traction (figures 20.18 and 20.19). Pressure changes produced
within the heart chambers as a result ofcardiac muscle contraction
are responsible for blood movement because blood moves from ar-
eas ofhigher pressure to areas of lower pressure.
The duration ofthe cardiac cycle varies considerably among
humans and also during an individual’s lifetime.It can be as short
as 0.25–0.3 second in a newborn infant or as long as 1 or more
Part4 Regulationsand Maintenance686
seconds in a well-trained athlete. The normal cardiac cycle of
0.7–0.8 second depends on the capability ofcardiac muscle to con-
tract and on the functional integrity of the conducting system.
The term systole(sisto¯-le¯) means to contract, and diastole
(dı¯-asto¯-le¯) means to dilate.Atrial systole is contraction of the
atrial myocardium, and atrial diastole is relaxation of the atrial
myocardium.Similarly, ventricular systole is contraction of the
ventricular myocardium,and ventricular diastole is relaxation of
the ventricular myocardium.When the terms systole and diastole
are used without reference to specific chambers, however,they
mean ventricular systole or diastole.
Before considering the details of the cardiac cycle, an
overview of the main events is helpful. Just before systole begins,
the atria and ventricles are relaxed, the ventricles are filled with
blood,the semilunar valves are closed, and the AV valves are open.
As systole begins,contraction of the ventricles increases ventricu-
lar pressures,causing blood to flow toward the atria and close the
AV valves.As contraction proceeds,ventricular pressures continue
to rise,but no blood flows from the ventricles because all the valves
are closed. This brief interval is called the period of isovolumic
(ı¯so¯-vol-u¯mik)contraction because the volume of blood in the
ventricles does not change,even though the ventricles are contract-
ing (see figure 20.18 1).As the ventricles continue to contract, ven-
tricular pressures become greater than the pressures in the
pulmonary trunk and aorta.As a result, during the period of ejec-
tion,the semilunar valves are pushed open and blood flows from
the ventricles into those arteries (see figure 20.182).
As diastole begins,the ventricles relax and ventricular pres-
sures decrease below the pressures in the pulmonary trunk and
aorta.Consequently, blood begins to flow back toward the ventri-
cles,causing the semilunar valves to close (see figure 20.18 3). With
closure of the semilunar valves,all the heart valves are closed and
no blood flows into the relaxing ventricles during the period of
isovolumic relaxation.
Throughout ventricular systole and the period of isovolu-
mic relaxation,the atria relax and blood flows into them from the
veins.As the ventricles continue to relax, ventricular pressures be-
come lower than atrial pressures,the AV valves open, and blood
flows from the atria into the relaxed ventricles (see figure 20.184).
At rest,most ventricular filling is a passive process resulting from
the greater pressure of blood in the veins and atria than in the
completely relaxed ventricles.Completion of ventricular filling is
an active process resulting from increased atrial pressure pro-
duced by contraction ofthe at ria (see figure 20.185 ). During ex-
ercise,atrial contraction is more important for ventricular filling
because, as heart rate increases, less time is available for passive
ventricular filling.
EventsOccurring During
Ventricular Systole
Figure 20.19 displays the main events of the cardiac cycle in
graphic form and should be examined from top to bottom for
each period ofthe cardiac cycle. The ECG indicates the electrical
events that cause contraction and relaxation ofthe atria and ven-
tricles. The pressure graph shows the pressure changes within
the left atrium,left ventricle, and aorta resulting from atrial and
Figure 20.17
Examplesof Alterations in the
Electrocardiogram
Complete heart block (P waves and QRS complexes are not coordinated)
Premature ventricular contraction (PVC) (no P waves precede PVC's)
Bundle branch block
Atrial fibrillation (no clear P waves and rapid QRS complexes)
Ventricular fibrillation (no P, QRS, or T waves)
P P P P P P P P P P
PVC PVC
Prolonged QRS complexes
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Chapter 20 Cardiovascular System: The Heart 687
Semilunar
valves closed
AV valves
closed
Semilunar
valves opened
AV valves
closed
1.
Systole: Period of isovolumic contraction.
Ventricular
contraction causes the AV valves to close, which is the
beginning of ventricular systole. The semilunar valves
were closed in the previous diastole and remain closed
during this period.
2.
Systole: Period of ejection.
Continued ventricular
contraction pushes blood out of the ventricles,
causing the semilunar valves to open.
3.
Diastole: Period of isovolumic relaxation.
Blood
flowing back toward the relaxed ventricles causes
the semilunar valves to close, which is the beginning
of ventricular diastole. Note that the AV valves
closed, also.
4.
Diastole: Passive ventricular filling
.The AV valves open
and blood flows into the relaxed ventricles, accounting for
most of the ventricular filling.
5.
Diastole: Active ventricular filling
.The atria contract and
complete ventricular filling.
Semilunar
valves closed
AV valves
closed
Semilunar
valves closed
AV valves
opened
Semilunar
valves closed
AV valves
opened
Figure 20.18
The CardiacCycle
The cardiaccycle is a repeating series of
contraction and relaxation thatmoves blood
through the heart. See figure 20.19 and
table 20.2 for additionaldetails and
explanations. (AV atrioventricular)
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Q
S
R
T T
Time periods:
120
100
80
55
90
125
60
40
20
0
(mV)Pressure (mm Hg)Left ventricular
volume (mL)
"Sound" frequency
(cycles/second)
First
heart
sound
Second
heart
sound
First
heart
sound
Second
heart
sound
Third
heart
sound
P
Q
S
R
P
Systole SystoleDiastole
AV valves
close
End-diastolic
volume
AV valves
open
Semilunar
valves
open
Semilunar
valves
close
Period of
isovolumic
contraction
Period of
isovolumic
relaxation
Passive
ventricular
filling
Active
ventricular
filling
Period of
ejection
AV valves
close
Diastolic
pressure
Semilunar
valves open
End-diastolic
volume
End-systolic
volume
End-systolic
volume
AV valves
open
Semilunar
valves
close
Systolic
pressure
Dicrotic
notch
Systole Diastole
Figure 20.19
EventsOccurring During the Cardiac Cycle
The cardiaccycle is divided into five periods (see top of figure). Within these periods, four graphsare presented. From top to bottom, the electrocardiograph;
pressure changesfor the left atrium (blue line), left ventricle (blackline), and aorta (red line); left ventricular volume curve; and heart sounds are illustrated. See
table 20.2 for explanationsof events during each period and figure 20.18 for illustrationsof the valves and blood flow movement.
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ventricular contraction and relaxation. Although pressure
changes in the right side of the heart are not shown, they are
similar to those in the left side, only lower.The volume graph
presents the changes in left ventricular volume as blood flows
into and out of the left ventricle as a result of the pressure
changes.The sound graph records the closing of valves caused by
blood flow. See also figure 20.18 for illustrations of the valves
and blood flow and table 20.2 for a summary of the events oc-
curring during each period.
Period of IsovolumicContraction
Completion of the QRS complex initiates contraction of the ven-
tricles.Ventricular pressure rapidly increases, resulting in closure
ofthe AV valves. During the previous ventricular diastole,the ven-
tricles were filled with 120–130 mL of blood, which is called the
end-diastolic volume.Ventricular volume doesn’t change during
the period of isovolumic contraction because all the heart valves
are closed at this time.
PREDICT
Isthe cardiac muscle contracting isotonically or isometricallyduring
the period ofisovolumic contraction?
Period of Ejection
As soon as ventricular pressures exceed the pressures in the aorta
and pulmonary trunk, the semilunar valves open. The aortic
semilunar valve opens at approximately 80 millimeters ofmercury
(mm Hg) ventricular pressure,whereas the pulmonary semilunar
valve opens at approximately 8 mm Hg.Although the pressures are
different,both valves open at nearly the same time.
As blood flows from the ventricles during the period ofejec-
tion, the left ventricular pressure continues to climb to approxi-
mately 120 mm Hg,and the right ventricular pressure increases to
approximately 25 mm Hg. The larger left ventricular pressure
causes blood to flow throughout the body (systemic circulation),
whereas the lower right ventricle pressure causes blood to flow
through the lungs (pulmonary circuit). Even though the pressure
generated by the left ventricle is much higher than that ofthe right
ventricle,the amount of blood pumped by each is almost the same.
PREDICT
Which ventricle hasthe thickestwall? Why is it important for each
ventricle to pump approximatelythe same volume of blood?
During the first part of ejection, blood flows rapidly out of
the ventricles. Toward the end ofejection, very little blood flow
occurs, which causes the ventricular pressure to decrease despite
continued ventricular contraction.At the end of ejection, the vol-
ume has decreased to 50–60 mL,which is called the end-systolic
volume.
EventsOccurring During Ventricular Diastole
Period of IsovolumicRelaxation
Completion ofthe T wave results in ventricular repolarization and
relaxation. The already decreasing ventricular pressure falls very
rapidly as the ventricles suddenly relax. When the ventricular
pressures fall below the pressures in the aorta and pulmonary
trunk,the recoil of the elastic ar terial walls,which were stretched
during the period ofe jection,forces the blood to flow back toward
the ventricles,thereby closing the semilunar valves.Ventricular vol-
ume doesn’t change during the period ofisovolumic relaxation be-
cause all the heart valves are closed at this time.
Passive VentricularFilling
During ventricular systole and the period of isovolumic relax-
ation, the relaxed atria fills with blood. As ventricular pressure
drops below atrial pressure,the atrioventricular valves open and
allow blood to flow from the atria into the ventricles.Blood flows
from the area ofhigher pressure in the veins and atria toward the
area of lower pressure in the relaxed ventricles.Most ventricular
filling occurs during the first one-third of ventricular diastole.At
the end of passive ventricular filling, the ventricles are approxi-
mately 70% filled.
PREDICT
Fibrillation isabnormal, rapid contractions ofdifferent parts of the
heartthat prevent the heart muscle from contracting as a single unit.
Explain whyatrial fibrillation does not immediately cause death, but
ventricular fibrillation does.
Active VentricularFilling
Depolarization of the SA node generates action potentials that
spread over the atria,producing the P wave and stimulating both
atria to contract (atrial systole).The atria contract dur ing the last
one-third ofventricular diastole and complete ventricular filling.
Under most conditions,the atria function primarily as reser-
voirs, and the ventricles can pump sufficient blood to maintain
homeostasis even ifthe atria do not contract at all. During exercise,
however,the heart pumps 300%–400% more blood than during
resting conditions.It is under these conditions that the pumping
action of the atria becomes important in maintaining the pump-
ingefficiency of the hear t.
HeartSounds
Distinct sounds are heard when a stethoscope is used to listen to
the heart (figures 20.19 and 20.20).The first heart sound is a low-
pitched sound,often described as a “lubb”sound. It’s caused by vi-
bration ofthe atrioventricular valves and surrounding fluid as the
valves close at the beginning of ventricular systole. The second
heart sound is a higher-pitched sound often described as a
“dupp”sound.It results from closure of the aortic and pulmonar y
semilunar valves,at the beginning of ventricular diastole. Systole
is,therefore, approximately the time between the first and second
heart sounds. Diastole,which lasts somewhat longer, is approxi-
mately the time between the second heart sound and the next first
heart sound.
Occasionally,a third heart sound, caused by blood flow-
ing in a turbulent fashion into the ventricles, can be detected
near the end of the first one-third of diastole. The third heart
sound is normal, although faint, and is detected most easily in
thin,young people.
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Table 20.2
Ventricular Systole
Summary of the Events of the Cardiac Cycle
Time Period
Condition of Valves
ECG
Atrial Pressure Graph
Ventricular Pressure Graph
Aortic Pressure Graph
Volume Graph
Sound Graph
Period of Isovolumic Contraction
The ventricles begin to contract, but ventricular
volume doesn't change.
Semilunar valves closed; AV valves closed (see
figure 20.18a).
The QRS complex is completed and the ventricles are
depolarized. As a result, the ventricles begin to
contract.
Atrial repolarization is masked by the QRS complex.
The atria are relaxed (atrial diastole).
Atrial pressure decreases in the relaxed atria. When
atrial pressure is less than venous pressure, blood
flows into the atria.
Atrial pressure increases briefly as the contracting
ventricles push blood back toward the atria.
Ventricular contraction causes an increase in
ventricular pressure, which causes blood to flow
toward the atria, closing the AV valves.
Ventricular pressure increases rapidly.
Just before the semilunar valves open, pressure in the
aorta decreases to its lowest value, called the
diastolic pressure (approximately 80 mm Hg).
During the period of isovolumic contraction,
ventricular volume doesn't change because the
semilunar and AV valves are closed.
Blood flowing from the ventricles toward the atria
closes the AV valves. Vibrations of the valves and
the turbulent flow of blood produce the first
heart sound, which marks the beginning of
ventricular systole.
Period of Ejection
The ventricles continue to contract and blood is
pumped out of the ventricles.
Semilunar valves opened; AV valves closed (see
figure 20.18b).
TheT wave results from ventricular repolarization.
Atrial pressure increases gradually as blood flows
from the veins into the relaxed atria.
Ventricular pressure becomes greater than pressure
in the aorta as the ventricles continue to
contract. The semilunar valves are pushed open
as blood flows out of the ventricles.
Ventricular pressure peaks as the ventricles contract
maximally; then pressure decreases as blood flow
out of the ventricles decreases.
As ventricular contraction forces blood into the
aorta, pressure in the aorta increases to its
highest value, called the systolic pressure
(approximately 120 mm Hg).
After the semilunar valves open, blood volume
decreases as blood flows out of the ventricles
during the period of ejection.
The amount of blood left in a ventricle at the end of
the period of ejection is called the end-systolic
volume.
Aortic Pressure Curve
The elastic walls of the aorta are stretched as blood is ejected into
the aorta from the left ventricle. Aortic pressure remains slightly
below ventricular pressure during this period of ejection.As ven-
tricular pressure drops below that in the aorta,blood flows back to-
ward the ventricle because of the elastic recoil of the aorta.
Consequently, the aortic semilunar valve closes, and pressure
within the aorta increases slightly, producing a dicrotic (dı¯-
krotik)notch in the aortic pressure curve (see figure 20.19).The
term dicrotic means double-beating; when increased pressure
caused by recoil is large,a double pulse can be felt. The dicrotic
notch is also called an incisura(insı¯-soora˘; a cutting into). Aor-
tic pressure then gradually falls throughout the rest of ventricular
diastole as blood flows through the peripheral vessels.By the time
aortic pressure has fallen to approximately 80 mm Hg,the ventri-
cles again contract,forcing blood once more into the aorta.
Blood pressure measurements performed for clinical pur-
poses reflect the pressure changes that occur in the aorta rather
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than in the left ventricle (see chapter 21).The blood pressure in the
aorta fluctuates between systolic pressure,which is about 120 mm
Hg,and diastolic pressure, which is about 80 mm Hg for the aver-
age young adult at rest.
21. Define systole and diastole.
22. List the five periods of the cardiac cycle, and state whether
the AV and semilunarvalves are open or closed during each
period.
23. Define isovolumic. When does most ventricular filling
occur?
24. Define end-diastolic volume and end-systolic volume.
25. What produces the first heart sound, the second heart
sound, and the third heartsound?
26. Explain the production in the aorta of systolic pressure,
diastolicpressure, and the dicrotic notch, or incisura.
Ventricular Diastole
Period of Isovolumic Relaxation
The ventricles relax, but ventricular volume
doesn't change.
Semilunar valves closed; AV valves closed
(see figure 20.18c).
The T wave is completed and the ventricles
are repolarized. The ventricles relax.
Atrial pressure continues to increase
gradually as blood flows from the veins
into the relaxed atria.
Elastic recoil of the aorta pushes blood back
toward the heart, causing the semilunar
valves to close.
After closure of the semilunar valves, the
pressure in the relaxing ventricles rapidly
decreases.
After the semilunar valves close, elastic
recoil of the aorta causes a slight
increase in aortic pressure, producing the
dicrotic notch, or incisura.
During the period of isovolumic
relaxation, ventricular volume doesn't
change because the semilunar and AV
valves are closed.
Blood flowing from the ventricles toward
the aorta and pulmonary trunk closes
the semilunar valves. Vibrations of the
valves and the turbulent flow of blood
produce the second heart sound, which
marks the beginning of ventricular
diastole.
Passive Ventricular Filling
Blood flows into the ventricles because blood
pressure is higher in the veins and atria than
in the relaxed ventricles.
Semilunar valves closed; AV valves opened
(see figure 20.18d).
TheP wave is produced when the SA node
generates action potentials and a wave of
depolarization begins to propagate across
the atria.
After the AV valves open, atrial pressure
decreases as blood flows out of the atria
into the relaxed ventricles.
No significant change occurs in ventricular
pressure during this time period.
Aortic pressure gradually decreases as blood
runs out of the aorta into other systemic
blood vessels.
After the AV valves open, blood flows from the
atria and veins into the ventricles because of
pressure differences. Most ventricular filling
occurs during the first one-third of diastole.
Little ventricular filling occurs during the
middle one-third of diastole.
Sometimes the turbulent flow of blood into the
ventricles produces a third heart sound.
Active Ventricular Filling
Contraction of the atria pumps blood into
the ventricles.
Semilunar valves closed; AV valves opened
(see figure 20.18e).
The P wave is completed and the atria are
stimulated to contract. Action
potentials are delayed in the AV node
for 0.11 second, allowing time for the
atria to contract.
TheQRS complex begins as action
potentials are propagated from the AV
node to the ventricles.
Atrial contraction (systole) causes an
increase in atrial pressure, and blood is
forced to flow from the atria into the
ventricles.
Atrial contraction (systole) and the
movement of blood into the ventricles
cause a slight increase in ventricular
pressure.
Aortic pressure gradually decreases as
blood runs out of the aorta into other
systemic blood vessels.
Atrial contraction (systole) completes
ventricular filling during the last
one-third of diastole.
The amount of blood in a ventricle at the
end of ventricular diastole is called the
end-diastolic volume.
Abbreviation:AV atrioventricular.
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Clinical Focus AbnormalHeart Sounds
Heart sounds provide important informa-
tion to cliniciansabout the normal function
of the heart and assist in diagnosing car-
diacabnormalities. Abnormal heart sounds
are called murmurs(mermerz), and certain
murmurs are important indicators of spe-
cificcardiac abnormalities. For example, an
incompetentvalve leaks significantly. After
an incompetent valve closes, blood flows
through it but in a reverse direction. The
movementof blood in a direction opposite
to normal results in turbulence, which
causesa gurgling or swishing sound imme-
diatelyaf ter the valve closes. An incompe-
tenttricuspid valve or bicuspid valve makes
a swish sound immediately after the first
heartsound, and the first heart sound may
be muffled. An incompetent aortic or pul-
monary semilunar valve resultsin a swish
sound immediately after the second heart
sound.
Stenosed (steno¯zd) valves have an
abnormally narrow opening and also pro-
duce abnormal heart sounds. Blood flows
through stenosed valvesin a very turbulent
fashion and producesa rushing sound be-
fore the valve closes. A stenosed atrioven-
tricular valve, therefore, resultsin a rushing
sound immediately before the first heart
sound, and a stenosed semilunar valve re-
sultsin a rushing sound immediately before
the second heartsound.
Inflammation of the heart valves, re-
sulting from conditions like rheumatic
fever, can cause valvesto become either
incompetentor stenosed. In addition, myo-
cardial infarctions that make papillary
musclesnonfunctional can cause bicuspid
or tricuspid valvesto be incompetent.
Mean Arterial Blood Pressure
Objective
■ Describe the factors that determine mean arterial pressure.
Blood pressure is responsible for blood movement and,
therefore,is critical to the maintenance of homeostasis in the body.
Blood flows from areas ofhigher to areas of lower pressure. For ex-
ample,during one cardiac cycle, blood flows from the higher pres-
sure in the aorta toward the lower pressure in the relaxed left
ventricle.
Mean arterial pressure (MAP)is the average blood pressure
between systolic and diastolic pressure in the aorta. It’s propor-
tional to cardiac output (CO)times peripheral resistance (PR).
Cardiac output, or minute volume, is the amount of blood
pumped by the heart per minute,and peripher al resistance is the
total resistance against which blood must be pumped.
MAP CO PR
Changes in cardiac output and peripheral resistance (figure
20.21) can alter mean arterial pressure.Cardiac output is discussed
in this chapter,and peripheral resistance is explained in chapter 21.
Cardiac output is equal to heart rate times stroke volume.
Heart rate (HR) is the number of times the heart beats (contracts)
per minute. Stroke volume (SV), which is the volume of blood
pumped during each heartbeat (cardiac cycle), is equal to end-
diastolic volume minus end-systolic volume.During diastole, blood
flows from the atria into the ventricles,and end-diastolic volume nor-
mally increases to approximately 125 mL.After the ventricles partially
empty during systole,end-systolic volume decreases to approximately
55 mL.The stroke volume is therefore equal to 70 mL (12555).
To better understand stroke volume,imagine that you’re
rinsing out a sponge under a running water faucet. As you relax
your hand,the sponge fills with water; as your fingers contract, wa-
ter is squeezed out of the sponge; and,after you have squeezed it,
some water is left in the sponge.In this analogy, the amount of wa-
ter you squeeze out ofthe sponge (stroke volume) is the difference
between the amount ofwater in the sponge when your hand is re-
laxed (end-diastolic volume) and the amount that is left in the
sponge after you squeeze it (end-systolic volume).
Stroke volume can be increased by increasing end-diastolic
volume or by decreasing end-systolic volume (see figure 20.21).
During exercise,end-diastolic volume increases because of an in-
crease in venous return,which is the amount of blood returning
to the heart from the peripheral circulation. End-systolic volume
decreases because the heart contracts more forcefully.For example,
stroke volume could increase from a resting value of70 mL to an
Figure 20.20
Location ofthe Heart Valves in the Thorax
Surface markingsof the heart in the male. The positionsof the four heart
valvesare indicated by blue ellipses, and the sites where the sounds of the
valvesare best heard with the stethoscope are indicated by pink circles.
Bicuspid
valve
Tricuspid
valve
Pulmonary
semilunar valve
Outline of
heart
Aortic
semilunar valve
Part4 Regulationsand Maintenance692
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Chapter 20 Cardiovascular System: The Heart 693
exercising value of 115 mL by increasing end-diastolic volume to
145 mL and decreasing end-systolic volume to 30 mL.
Under resting conditions,the heart rate is approximately 72
bpm,and the stroke volume is approximately 70 mL/beat,although
these values can vary considerably from person to person.The car-
diac output is therefore
CO HR SV
72 bpm 70 mL/beat
5040 mL/min (approximately 5 L/min)
During exercise,heart rate can increase to 190 bpm, and the
stroke volume can increase to 115 mL.Consequently, cardiac out-
put is
CO 190 bpm 115 mL/beat
21,850 mL/min (approximately 22 L/min)
The difference between cardiac output when a person is at rest
and maximum cardiac output is called cardiac reserve.The greater
a person’s cardiac reserve,the greater his or her capacity for doing
exercise.Lack of exercise and cardiovascular diseases can reduce car-
diac reserve and affect a person’s quality oflife. Exercise training can
greatly increase cardiac reserve by increasing cardiac output.In well-
trained athletes,stroke volume during exercise can increase to over
200 mL/beat,resulting in cardiac outputs of 40 L/min or more.
27. Define mean arterial pressure, cardiac output, and
peripheral resistance. Explain the role of mean arterial
pressure in causing blood flow.
28. Define stroke volume, and state two ways to increase stroke
volume.
29. What is cardiac reserve? How can exercise training
influence cardiacreserve?
Regulation of the Heart
Objectives
■ Describe intrinsic regulation of the heart.
■ Describe the mechanisms involved in extrinsic regulation of
the heart.
To maintain homeostasis,the amount of blood pumped by
the heart must vary dramatically. For example,dur ing exercise
cardiac output can increase several times over resting values.Ei-
ther intrinsic or extrinsic regulatory mechanisms control cardiac
output. Intrinsic regulation results from the normal functional
characteristics of the heart and does not depend on either neural
or hormonal regulation.It functions when the heart is in place in
the body or is removed and maintained outside the body under
proper conditions. On the other hand, extrinsic regulation
Decreased blood pressure, decreased blood
pH, increased blood carbon dioxide, decreased
blood oxygen, exercise, and emotions.
Increased sympathetic stimulation
Decreased parasympathetic stimulation
Increased epinephrine and norepinephrine
secretion
Increased blood volume, exercise,
changing from a standing to a lying
down position
Increased venous return increases
end-diastolic volume and preload
Increased force
of contraction
decreases end-
systolic volume
Increased force of contraction
(Starling's law of the heart)
ejects increased end-diastolic
volume
See chapter 21 for the regulation
of blood vessels
Increased vasoconstriction
Increased heart rate Increased cardiac output Increased stroke volume Increased peripheral resistance
Increased mean arterial pressure
Figure 20.21
FactorsAffecting Mean Arterial Pressure
Mean arterialpressure is regulated by controlling cardiac output and peripheralresistance.
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involves neural and hormonal control.Neural regulation of the
heart results from sympathetic and parasympathetic reflexes,and
the major hormonal regulation comes from epinephrine and nor-
epinephrine secreted from the adrenal medulla.
IntrinsicRegulation
The amount ofblood that flows into the right atrium from the veins
during diastole is called the venous return. As venous return in-
creases,end-diastolic volume increases (see figure 20.21). A greater
end-diastolic volume increases the stretch of the ventricular walls.
The extent to which the ventricular walls are stretched is sometimes
called the preload.An increased preload causes an increase in cardiac
output,and a decreased preload causes a decrease in cardiac output.
Cardiac muscle exhibits a length-versus-tension relationship
similar to that of skeletal muscle. Skeletal muscle, however,is
stretched to nearly its optimal length before contraction,whereas
cardiac muscle fibers are not stretched to the point at which they
contract with a maximal force (see chapter 9).An increased pre-
load,therefore, causes the cardiac muscle fibers to contract with a
greater force and produce a greater stroke volume.This relation-
ship between preload and stroke volume is commonly referred to
asStarling’s law of the heart, which describes the relationship be-
tween changes in the pumping effectiveness of the heart and
changes in preload (see figure 20.21).Venous return can decrease
to a value as low as 2 L/min or increase to as much as 24 L/min,
which has a major effect on the preload.
Afterload is the pressure the contracting ventricles must
produce to overcome the pressure in the aorta and move blood
into the aorta.Although the pumping effectiveness of the heart is
greatly influenced by relatively small changes in the preload,it is
very insensitive to large changes in afterload.Aortic blood pressure
must increase to more than 170 mm Hg before it hampers the abil-
ity ofthe ventricles to pump blood.
During physical exercise,blood vessels in exercising skeletal
muscles dilate and allow increased flow ofblood through the vessels.
The increased blood flow increases oxygen and nutrient delivery to
the exercising muscles.In addition, skeletal muscle contractions re-
peatedly compress veins and cause an increased rate ofblood flow
from the skeletal muscles toward the heart.As blood rapidly flows
through skeletal muscles and back to the heart,venous return to the
heart increases,resulting in an increased preload. The increased pre-
load causes an increased force ofcardiac muscle contraction, which
increases stroke volume.The increase in stroke volume results in in-
creased cardiac output,and the volume of blood flowing to the exer-
cising muscles increases.When a person rests, venous return to the
heart decreases because arteries in the skeletal muscles constrict and
because muscular contractions no longer repeatedly compress the
veins.As a result blood flow through skeletal muscles decreases, and
there is a decrease in preload and cardiac output.
ExtrinsicRegulation
The heart is innervated by both parasympathetic and sympa-
thetic nerve fibers (figure 20.22).They influence the pumping ac-
tion of the heart by affecting both heart rate and stroke volume.
Part4 Regulationsand Maintenance694
The influence ofparasympathetic stimulation on the heart is much
less than that ofsympathetic stimulation. Sympathetic stimulation
can increase cardiac output by 50%–100% over resting values,
whereas parasympathetic stimulation can cause only a 10%–20%
decrease.
Extrinsic regulation of the heart functions to keep blood
pressure, blood oxygen levels,blood carbon dioxide levels, and
blood pH within their normal ranges of values. For example, if
blood pressure suddenly decreases, extrinsic mechanisms detect
the decrease and initiate responses that increase cardiac output to
bring blood pressure back to its normal range.
ParasympatheticControl
Parasympathetic nerve fibers are carried to the heart through the
vagus nerves.Preganglionic fibers of the vagus ner ve extend from
the brainstem to terminal ganglia within the wall of the heart, and
postganglionic fibers extend from the ganglia to the SA node,AV
node,coronary vessels, and atrial myocardium.
Parasympathetic stimulation has an inhibitory influence on
the heart, primarily by decreasing the heart rate. During resting
conditions, continuous parasympathetic stimulation inhibits the
heart to a small degree.An increase in heart rate during exercise re-
sults,in part, from decreased parasympathetic stimulation. Strong
parasympathetic stimulation can decrease the heart rate 20–30
bpm but it has little effect on stroke volume.In fact, if venous re-
turn remains constant while the heart is inhibited by parasympa-
thetic stimulation,stroke volume actually can increase. The longer
time between heartbeats allows the heart to fill to a greater capac-
ity,resulting in an increased preload, which increases stroke vol-
ume because ofStarling’s law of the heart.
Acetylcholine, the neurotransmitter produced by postgan-
glionic parasympathetic neurons, binds to ligand-gated channels
that cause cardiac plasma membranes to become more permeable
to K
.As a consequence, the membrane hyperpolarizes. Heart rate
decreases because the hyperpolarized membrane takes longer to
depolarize and cause an action potential.
SympatheticControl
Sympathetic nerve fibers originate in the thoracic region of the
spinal cord as preganglionic neurons. These neurons synapse
with postganglionic neurons of the inferior cervical and upper
thoracic sympathetic chain ganglia, which project to the heart
as cardiac nerves (see figure 20.22 and chapter 16). The post-
ganglionic sympathetic nerve fibers innervate the SA and AV
nodes, the coronary vessels, and the atrial and ventricular
myocardium.
Sympathetic stimulation increases both the heart rate and
the force ofmuscular contraction. In response to strong sympa-
thetic stimulation, the heart rate can increase to 250 or,occa-
sionally, 300 bpm. Stronger contractions also can increase
stroke volume. The increased force of contraction resulting
from sympathetic stimulation causes a lower end-systolic vol-
ume in the heart;therefore, the heart empties to a greater extent
(see figure 20.21).
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Chapter 20 Cardiovascular System: The Heart 695
PREDICT
Whateffect does sympathetic stimulation have on stroke volume ifthe
venousreturn remains constant? Sympatheticstimulation of the heart
also resultsin dilation of the coronary blood vessels. Explain the
functionaladvantage of that effect.
Limitations exist, however,to the relationship between in-
creased heart rate and cardiac output.If the heart rate becomes too
fast,diastole is not long enough to allow complete ventricular fill-
ing,end-diastolic volume decreases, and stroke volume actually de-
creases.In addition, if heart rate increases beyond a critical level,
the strength ofcontraction decreases, probably as a result of the ac-
cumulation ofmetabolites in cardiac muscle cells. The limit of the
heart’s ability to increase the volume ofblood pumped is 170–250
bpm in response to intense sympathetic stimulation.
Sympathetic stimulation of the ventricular myocardium
plays a significant role in regulation ofits contraction force during
resting conditions.Sympathetic stimulation maintains the strength
of ventricular contraction at a level approximately 20% greater
than it would be with no sympathetic stimulation.
Norepinephrine, the postganglionic sympathetic neuro-
transmitter,increases the rate and degree of cardiac muscle depo-
larization so that both the frequency and amplitude of the action
potentials are increased.The effect of norepinephrine on the heart
involves the association between norepinephrine and cell surface
-adrenergic receptors.This combination causes a G protein–me-
diated synthesis and accumulation of cAMP in the cytoplasm of
cardiac muscle cells.Cyclic AMP increases the permeability of the
plasma membrane to Ca
2
, primarily by opening calcium slow
channels in the plasma membrane.
Hormonal Control
Epinephrine and norepinephrine released from the adrenal
medulla can markedly influence the pumping effectiveness ofthe
heart.Epinephrine has essentially the same effect on cardiac mus-
cle as norepinephrine and,therefore, increases the rate and force of
heart contractions (see figure 20.21).The secretion of epinephrine
and norepinephrine from the adrenal medulla is controlled by
sympathetic stimulation of the medulla and occurs in response to
increased physical activity, emotional excitement, or stressful
conditions.Many stimuli that increase sympathetic stimulation of
the heart also increase release of epinephrine and norepinephrine
from the adrenal gland (see chapter 18). Epinephrine and
Sensory nerve
fibers
Baroreceptors
in wall of internal
carotid artery
Baroreceptors
in aorta
Carotid body
chemoreceptors
SA node
Heart
Circulation
Epinephrine and norepinephrine
Adrenal medulla
Sympathetic
nerve fibers to
adrenal gland
Sensory
nerve
fibers
P
a
r
a
s
y
m
p
a
t
h
e
t
i
c
n
e
r
v
e
f
i
b
e
r
s
S
y
m
p
a
t
h
e
t
i
c
n
e
r
v
e
f
i
b
e
r
s
Cardioregulatory center and
chemoreceptors in medulla oblongata
Sensory (
green
) neurons carry
action potentials from baroreceptors
to the cardioregulatory center.
Chemoreceptors in the medulla
oblongata influence the
cardioregulatory center.
The cardioregulatory center controls
the frequency of action potentials in
the parasympathetic (
red
) neurons
extending to the heart. The
parasympathetic neurons decrease
the heart rate.
The cardioregulatory center controls
the frequency of action potential in
the sympathetic (
blue
) neurons
extending to the heart. The
sympathetic neurons increase the
heart rate and the stroke volume.
The cardioregulatory center
influences the frequency of action
potentials in the sympathetic (
blue
)
neurons extending to the adrenal
medulla. The sympathetic neurons
increase the secretion of epinephrine
and some norepinephrine into the
general circulation. Epinephrine and
norepinephrine increase the heart
rate and stroke volume.
1.
2.
3.
4.
1
2
3
4
ProcessFigure 20.22
Baroreceptor and Chemoreceptor Reflexes
Sensory(green) nerves carry action potentials from sensory receptors to the medulla oblongata. Sympathetic (blue) and parasympathetic (red) nerves exit the
spinalcord or medulla oblongata and extend to the heart to regulate its function. Epinephrine and norepinephrine from the adrenalgland also help regulate the
heart’saction. (SA sinoatrial)
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norepinephrine are transported in the blood through the vessels of
the heart to the cardiac muscle cells,where they bind to -adrener-
gic receptors and stimulate cAMP synthesis.Epinephrine takes a
longer time to act on the heart than sympathetic stimulation does,
but the effect lasts longer.
30. Define the term venous return, and explain how it affects
preload. Howdoes preload affect cardiac output? State
Starling’slaw of the heart.
31. Define the term afterload, and describe its effect on the
pumping effectivenessof the heart.
32. What part of the brain regulates the heart? Describe the
autonomicnerve supply to the heart.
33. What effect do parasympathetic stimulation and
sympatheticstimulation have on heart rate, force of
contraction, and stroke volume?
34. What neurotransmitters are released by the
parasympatheticand sympathetic postganglionic neurons
of the heart? Whateffects do they have on membrane
permeabilityand excitablity?
35. Name the two main hormones that affect the heart. Where
are theyproduced, what causes theirrelease, and what
effectsdo they have on the heart?
Heart and Homeostasis
Objective
■ Describe the major factors that help maintain homeostasis
byregulating heart activity.
The pumping efficiency ofthe hear t plays an important role
in the maintenance ofhomeostasis. Blood pressure in the systemic
vessels must be maintained at a level which is high enough to
achieve nutrient and waste product exchange across the walls of
the capillaries that meets metabolic demands. The activity of the
heart must be regulated because the metabolic activities ofthe tis-
sues change under such conditions as exercise and rest.
Effectof Blood Pressure
Baroreceptor (baro¯-re¯-septer, baro¯-re¯-septo¯r)reflexes detect
changes in blood pressure and result in changes in heart rate and in
the force ofcontraction. The sensory receptors of the baroreceptor
reflexes are stretch receptors.They are in the walls of certain large
arteries,such as the internal carotid arteries and the aorta, and they
function to measure blood pressure (see figure 20.22). The
anatomy ofthese sensory structures and their afferent pathways are
described in chapter 21.
Afferent neurons project primarily through the glossopha-
ryngeal (cranial nerve IX) and vagus (cranial nerve X) nerves from
the baroreceptors to an area in the medulla oblongata called the
cardioregulatory center,where sensory action potentials are inte-
grated (see figure 20.22). The part of the cardioregulatory center
that functions to increase heart rate is called the cardioaccelera-
tory center, and the part that functions to decrease heart rate is
called the cardioinhibitory center.Efferent action potentials then
are sent from the cardioregulatory center to the heart through both
Part4 Regulationsand Maintenance696
the sympathetic and parasympathetic divisions of the autonomic
nervous system.
Increased blood pressure within the internal carotid arteries
and aorta causes their walls to stretch,thereby stimulating an in-
crease in action potential frequency in the baroreceptors (figure
20.23).At normal blood pressures (80–120 mm Hg), afferent ac-
tion potentials are sent from the baroreceptors to the medulla ob-
longata at a relatively constant frequency.When blood pressure
increases,the arterial walls are stretched further, and the afferent
action potential frequency increases. When blood pressure de-
creases,the ar terial walls are stretched to a lesser extent,and the
afferent action potential frequency decreases.In response to in-
creased blood pressure,the baroreceptor reflexes decrease sympa-
thetic stimulation and increase parasympathetic stimulation of
the heart, causing the heart rate to decrease. Decreased blood
pressure causes decreased parasympathetic and increased sympa-
thetic stimulation ofthe heart, resulting in an increased heart rate
and force ofcontraction. Withdrawal of parasympathetic stimula-
tion is primarily responsible for increases in heart rate up to ap-
proximately 100 bpm. Larger increases in heart rate,especial ly
during exercise,result from sympathetic stimulation. The barore-
ceptor reflexes are homeostatic because they keep the blood pres-
sure within a narrow range of values, which is adequate to
maintain blood flow to the tissues.
Effectof pH, Carbon Dioxide, and Oxygen
Chemoreceptor(ke¯mo¯-re¯-septor) reflexes help regulate the ac-
tivity of the heart.Chemoreceptors sensitive to changes in pH and
carbon dioxide levels exist within the medulla oblongata.A drop in
pH and a rise in carbon dioxide decrease parasympathetic and in-
crease sympathetic stimulation of the heart, resulting in an in-
creased heart rate and force ofcontraction (figure 20.24).
The increased cardiac output causes greater blood flow
through the lungs, where carbon dioxide is eliminated from the
body.This helps bring the blood carbon dioxide level down to its
normal range ofvalues and helps to increase the blood pH.
Chemoreceptors primarily sensitive to blood oxygen levels
are found in the carotid and aortic bodies.These small structures
are located near large arteries close to the brain and heart, and
they monitor blood flowing to the brain and to the rest of the
body.A dramatic decrease in blood oxygen levels, such as during
asphyxiation,activates the carotid and aortic body chemorecep-
tor reflexes.In carefully controlled experiments, it’s possible to
isolate the effects of the carotid and aortic body chemoreceptor
reflexes from other reflexes,such as the medullary chemorecep-
tor reflexes.These experiments indicate that a decrease in blood
oxygen results in a decrease in heart rate and an increase in vaso-
constriction. The increased vasoconstriction causes blood pres-
sure to rise,which promotes blood delivery despite the decrease
in heart rate.The carotid and aortic body chemoreceptor reflexes
may protect the heart for a short time by slowing the heart and
thereby reducing its need for oxygen. The carotid and aortic
body chemoreceptor reflexes normally don’t function indepen-
dently of other regulatory mechanisms. When all regulatory
mechanisms function together, the effect of large, prolonged
Seeley−Stephens−Tate:
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Chapter 20 Cardiovascular System: The Heart 697
decreases in blood oxygen levels is to increase the heart rate.Low
blood oxygen levels result in increased stimulation ofrespiratory
movements (see chapter 23). Increased inflation of the lungs
stimulates stretch receptors in the lungs.Afferent action poten-
tials from these stretch receptors influence the cardioregulatory
center,which causes an increase in heart rate. The reduced oxy-
gen levels that exist at high altitudes can cause an increase in
heart rate even when blood carbon dioxide levels remain low.
The carotid and aortic body chemoreceptor reflexes are more im-
portant in the regulation of respiration (see chapter 23) and
blood vessel constriction (see chapter 21) than in the regulation
ofhear t rate.
Effectof Extracellular
Ion Concentration
Ions that affect cardiac muscle function are the same ions (potas-
sium,calcium, and sodium) that influence membrane potentials in
other electrically excitable tissues.Some differences do exist, how-
ever,between the response of cardiac muscle and that of nerve or
muscle tissue to these ions.For example, the extracellular levels of
Na
rarely deviate enough from the normal value to affect the
function ofcardiac muscle significantly.
Excess K
in cardiac tissue causes the heart rate and stroke
volume to decrease.A twofold increase in extracellular K
results in
Blood pressure
(normal range)
Blood pressure
decreases
Blood pressure
increases
Blood pressure
(normal range)
Blood pressure
homeostasis
is maintained
• Increased heart rate and stroke volume result
from the changed ANS stimulation of the heart.
• Increased heart rate and stroke volume result
from the increased release of epinephrine and
norepinephrine from the adrenal medulla.
The blood pressure decreases because of the
decreased cardiac output resulting from the
decreased heart rate and stroke volume.
• Decreased heart rate and stroke volume result
from the changed ANS stimulation of the
heart.
• Decreased heart rate and stroke volume result
from the decreased release of epinephrine
and norepinephrine from the adrenal medulla.
A sudden decrease in blood pressure is detected
by the baroreceptors in the internal carotid
arteries and aorta,
which affects the baroreceptor reflex.
The cardioregulatory center decreases
parasympathetic stimulation of the heart and
increases sympathetic stimulation of the heart
and adrenal medulla.
The blood pressure increases because of the
increased cardiac output resulting from the
increased heart rate and stroke volume.
A sudden increase in blood pressure is detected
by the baroreceptors in the internal carotid
arteries and aorta, which affect the baroreceptor
reflex.
The cardioregulatory center increases
parasympathetic stimulation of the heart and
decreases sympathetic stimulation of the heart
and adrenal medulla.
HomeostasisFigure 20.23
Baroreceptor Reflex
The baroreceptor reflexmaintains homeostasisin response to changes in blood pressure. (ANS autonomic nervous system)
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Part4 Regulationsand Maintenance698
Blood pH
(normal range)
Blood pH decreases
Blood pH increases
Blood pH
homeostasis
is maintained
• Increased heart rate and stroke volume result
from the changed ANS stimulation of the heart.
• Increased heart rate and stroke volume result
from the increased release of epinephrine and
norepinephrine from the adrenal medulla.
A decrease in blood pH (caused by an increase in
blood CO
2
) results from decreased blood flow to
the lungs. The decreased blood flow results from
the decreased cardiac output caused by
decreased heart rate and stroke volume.
• Decreased heart rate and stroke volume result
from the changed ANS stimulation of the heart.
• Decreased heart rate and stroke volume result
from the decreased release of epinephrine and
norepinephrine from the adrenal medulla.
A decrease in blood pH (often caused by an
increase in blood CO
2
) is detected by
chemoreceptors in the medulla oblongata, which
affects the chemoreceptor reflex.
The cardioregulatory center decreases
parasympathetic stimulation of the heart and
increases sympathetic stimulation of the heart
and adrenal medulla.
An increase in blood pH (caused by a decrease
in blood CO
2
) results from increased blood flow
to the lungs. The increased blood flow results
from the increased cardiac output caused by
increased heart rate and stroke volume.
An increase in blood pH (often caused by a
decrease in blood CO
2
) is detected by
chemoreceptors in the medulla oblongata, which
affects the chemoreceptor reflex.
The cardioregulatory center increases
parasympathetic stimulation of the heart and
decreases sympathetic
stimulation of the heart and adrenal medulla.
Blood pH
(normal range)
HomeostasisFigure 20.24
Chemoreceptor Reflex-pH
The chemoreceptor reflexmaintains homeostasisin response to changes in blood concentrations of CO
2
and H
. (ANS autonomic nervous system)
heart block, which is loss of the functional conduction of action
potentials through the conducting system of the heart. The excess
K
in the extracellular fluid causes partial depolarization of the
resting membrane potential,resulting in a decreased amplitude of
action potentials and a decreased rate at which action potentials are
conducted along muscle fibers.As the conduction rates decrease,
ectopic action potentials can occur.The reduced action potential
amplitude also results in less calcium entering the sarcoplasm ofthe
cell;thus the strength of cardiac muscle contraction decreases.
Although the extracellular concentration of K
normally is
small, a decrease in extracellular K
results in a decrease in the
heart rate because the resting membrane potential is hyperpolar-
ized;as a consequence, it takes longer for the membrane to depo-
larize to threshold. The force of contraction is not affected,
however.
An increase in the extracellular concentration of Ca
2
pro-
duces an increase in the force ofcardiac contraction because of a
greater influx ofCa
2
into the sarcoplasm during action potential
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Chapter 20 Cardiovascular System: The Heart 699
generation.Elevated plasma Ca
2
levels have an indirect effect on
heart rate because they reduce the frequency ofaction potentials in
nerve fibers,thus reducing sympathetic and parasympathetic stim-
ulation of the heart (see chapter 11). Generally, elevated blood
Ca
2
levels reduce the heart rate.
A low blood Ca
2
level increases the heart rate,although the
effect is imperceptible until blood Ca
2
levels are reduced to ap-
proximately one-tenth of their normal value.The reduced extra-
cellular Ca
2
levels cause Na
channels to open,which allows Na
to diffuse more readily into the cell,resulting in depolarization and
action potential generation.Reduced Ca
2
levels,however, usually
cause death as a result oftetany of skeletal muscles before they de-
crease enough to markedly influence the heart’s function.
Effectof Body Temperature
Under resting conditions, the temperature of cardiac muscle
normally doesn’t change dramatically in humans,althoug h al-
terations in temperature influence the heart rate.Small increases
in cardiac muscle temperature cause the heart rate to increase,
and decreases in temperature cause the heart rate to decrease.
For example, during exercise or fever,increased heart rate and
force of contraction accompany temperature increases,but the
heart rate decreases under conditions of hypothermia. During
heart surgery,the body temperature sometimes is reduced dra-
matically to slow the heart rate and other metabolic functions in
the body.
36. How does the nervous system detect and respond to (a) a
decrease in blood pressure, (b) an increase in carbon
dioxide levels, (c) a decrease in blood pH, and (d) a
decrease in blood oxygen levels?
37. Describe the baroreceptor reflex and the response of the
heartto an increase in venous return.
38. What effect does an increase or decrease in extracellular
potassium, calcium, and sodium ionshave on heart rate
and the force of contraction of the heart?
39. What effect does temperature have on heart rate?
Effects of Aging on the Heart
Objective
■ List the major age-related changes of the heart.
Aging results in gradual changes in the function ofthe heart,
which are minor under resting conditions, but become more
significant in response to exercise and when age-related diseases
develop.The mechanisms that regulate the heart effectively com-
pensate for most ofthe changes under resting conditions.
Hypertrophy of the left ventricle is a common age-related
change.This appears to result from a gradual increase in the pres-
sure in the aorta against which the left ventricle must pump blood
and a gradual increase in the stiffness ofcardiac muscle tissue. The
increased pressure in the aorta results from a gradual decrease in
arterial elasticity resulting in an increased stiffness ofthe aorta and
other large arteries.Myocardial cells accumulate lipid and collagen
fibers increase in cardiac tissue. These changes make the cardiac
muscle tissue stiffer and less compliant.The increased volume of
the left ventricle can sometimes result in an increase in left atrial
pressure and increased pulmonary capillary pressure. This can
cause pulmonary edema and a tendency for people to feel out of
breath when they exercise strenuously.
There is a gradual decrease in the maximum heart rate.This
can be roughly predicted by the following formula: Maximum
heart rate 220 age of the individual. There is an increase in
the rate at which ATP is broken down by cardiac muscle and a de-
crease in the rate of Ca
2
transport. There is a decrease in the
maximum rate at which cardiac muscle can carry out aerobic me-
tabolism.In addition, there is a decrease in the degree to which ep-
inephrine and norepinephrine can increase the heart rate. These
changes are consistent with longer contraction and relaxation
times for cardiac muscle and a decrease in the maximum heart
rate. Both the resting and maximum cardiac output slowly de-
crease as people age and, by 85 years of age, the cardiac output
may be decreased by 30%–60%.
Age-related changes in the connective tissue of the heart
valves occur.The connective tissue becomes less flexible and Ca
2
deposits increase. The result is an increased tendency for heart
valves to function abnormally.There is especially an increased ten-
dency for the aortic semilunar valve to become stenosed,but other
heart valves, such as the bicuspid valve, may become either
stenosed or incompetent.
Atrophy and replacement ofcells of the left bundle branch
and a decrease in the number of SA node cells alter the electrical
conduction system ofthe heart and lead to a higher rate of cardiac
arrhythmias in elderly people.
The enlarged and thickened cardiac muscle,especially in the
left ventricle,consumes more oxygen to pump the same amount of
blood pumped by a younger heart.This change is not significant
except if the coronary circulation is decreased by coronary artery
disease. However,the development of coronary artery disease is
age-related.Congestive heart disease is also age-related. Approxi-
mately 10% ofelderly people over 80 have congestive heart failure,
and a major contributing factor is coronary artery disease.Because
of the age-related changes in the heart, many elderly people are
limited in their ability to respond to emergencies,infections, blood
loss,or stress.
Exercise has many beneficial effects on the heart. Regular
aerobic exercise improves the functional capacity ofthe heart at all
ages, providing no conditions develop which cause the increased
workload ofthe heart to be harmful.
40. Explain how age-related changes affect the function of the
leftvetricle.
41. Describe the age-related changes in the heart rate.
42. Describe how increasing age affects the function of the
conduction system and the heartvalves.
43. Describe the effect of two age-related heart diseases on
functionsof the aging heart.
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Clinical Focus Conditionsand Diseases Affecting the Heart
Inflammation ofHeart Tissues
Endocarditis (endo¯-kar-dı¯tis) is inflamma-
tion ofthe endocardium. It affects the valves
more severely than other areasof the heart
and can lead to deposition of scar tissue,
causing valves to become stenosed or in-
competent.
Myocarditis(mı¯o¯-kar-dı¯tis) is inflam-
mation of the myocardium and can lead to
heartfailure.
Pericarditisis inflammation of the peri-
cardium. Pericarditiscan result from bacte-
rial or viralinfections and can be extremely
painful.
Rheumatic (roo-matik) heart disease
can result from a streptococcalinfection in
young people. Toxin produced bythe bacte-
ria can cause an immune reaction called
rheumatic fever about 2–4 weeks after the
infection. The immune reaction can cause in-
flammation ofthe endocardium, called rheu-
matic endocarditis. The inflamed valves,
especially the bicuspid valve, can become
stenosed or incompetent. The effective treat-
mentof streptococcal infections with antibi-
oticshas reduced the frequencyof rheumatic
heartdisease.
Reduced Blood Flow to Cardiac
Muscle
Coronaryheart dis ease reduces the amount of
blood thatthe coronary arteries are able to de-
liver to the myocardium. The reduction in blood
flow damagesthe myocardium. The degree of
damage dependson the size of the arteries in-
volved, whether occlusion (blockage) ispartial
or complete, and whether occlusion isgradual
or sudden. Asthe walls of the arteries thicken
and harden with age, the volume ofblood they
can supplyto the heart muscle declines, and
the ability of the heart to pump blood de-
creases. Inadequate blood flow to the heart
muscle can resultin angina pectoris, which isa
poorlylocalized sensation of pain in the region
ofthe chest, left arm, and left shoulder.
Degenerative changesin the artery wall
can cause the inside surface ofthe artery to
become roughened. The chance ofplatelet
aggregation increasesat the rough surface,
which increases the chance of coronary
thrombosis (throm-bo¯sis; formation of a
blood clotin a coronary vessel). Inadequate
blood flow can cause an infarct(infarkt), an
area of damaged cardiactissue. A heart at-
tackis often referred to as a coronary throm-
bosisor a myocardialinfarct. The outcome of
coronarythrombosis depends on the extent
ofthe damage to heart muscle caused by in-
adequate blood flow and whether other
blood vessels can supply enough blood to
maintain the heart’sfunction. Death can oc-
cur swiftlyif the infarct is large; if the infarct
issmall, the heart can continue to function.
In mostcases, scar tissue replaces damaged
cardiacmuscle in the area of the infarct.
People who survive infarctions often
lead fairly normal lives ifthey take precau-
tions. Mostcases call for moderate exercise,
adequate rest, a disciplined diet, and re-
duced stress.
CongenitalConditions Affecting the
Heart
Congenitalhear t disease is the result of ab-
normaldevelopment of the heart. The follow-
ing conditions are common congenital
defects.
Septal defect is a hole in a septum be-
tween the leftand right sides of the heart. The
hole maybe in the interatrial or interventricu-
lar septum. These defectsallow blood to flow
from one side ofthe heart to the other and, as
a consequence, greatlyreduce the pumping
effectivenessof the heart (see chapter 29).
Patent ductus arteriosus (du˘ktu˘sar-
te¯re¯-o¯-su˘s) results when a blood vessel
called the ductusarteriosus, which is pres-
entin the fetus, fails to close after birth. The
ductusar teriosus extendsbetween the pul-
monary trunkand the aorta. It allows blood
to pass from the pulmonary trunk to the
aorta, thusbypassing the lungs. This is nor-
mal before birth because the lungs are not
functioning (see chapter 29). Ifthe ductusar-
teriosusfails to close after birth, blood flows
in the opposite direction, from the aorta to
the pulmonary trunk. As a consequence,
blood flowsthrough the lungs under higher
pressure, causing damage to the lungs. In
addition, the amountof work required of the
leftventricle to maintain adequate systemic
blood pressure increases.
Stenosis(ste-no¯sis)ofa heart valve is a
narrowed opening through one of the heart
valves. In aorticor pulmonary valve stenosis,
the workload of the heart is increased be-
cause the ventricles must contract with a
much greater force to pump blood from the
ventricles. Stenosis of the bicuspid valve pre-
vents the flow of blood into the leftventricle,
causing blood to backup in the left atrium and
in the lungs, resulting in congestion of the
lungs. Stenosis of the tricuspid valve causes
blood to backup in the right atrium and sys-
temicveins, causing swelling in the periphery.
An incompetent heart valve is one that
leaks. Blood, therefore, flowsthrough the valve
when it’sclosed. The workload of the heart is in-
creased because incompetentvalves reduce the
pumping efficiencyof the heart. For example, an
incompetentaortic semilunar valve allows blood
to flow from the aorta into the leftventricle during
diastole. Thus, the leftventricle fillswith blood to
a greater degree than normal. The increased fill-
ing ofthe left ventricle results in a greater stroke
volume because ofStarling’s law of the heart.
The pressure produced bythe contracting ventri-
cle and the pressure in the aorta isgreater than
normalduring ventricular systole. The pressure in
the aorta, however, decreases very rapidly as
blood leaksinto the left ventricle during diastole.
An incompetent bicuspid valve allows
blood to flow backinto the left atrium from the
leftventricle during ventricular systole. This in-
creasesthe pressure in the left atrium and pul-
monary veins, which results in pulmonary
edema. Also, the stroke volume ofthe left ven-
tricle is reduced, which causesa decrease in
systemic blood pressure. Similarly, an incom-
petent tricuspid valve allows blood to flow
backinto the right atrium and systemic veins,
causing edema in the periphery.
Cyanosis(sı¯-a˘-no¯ sis) is a symptom of in-
adequate heart function in babies suffering
from congenital heart disease. The term blue
babyis sometimes used to refer to infants with
cyanosis. Low blood oxygen levelsin the periph-
eralblood vessels cause the skin to look blue.
HeartFailure
Heartfailure is the result of progressive weak-
ening ofthe heart muscle and the failure of the
heartto pump blood effectively. Hypertension
(high blood pressure) increases the afterload
on the heart, can produce significantenlarge-
mentof the heart, and can finally resultin heart
failure. Advanced age, malnutrition, chronic
infections, toxins, severe anemias, or hyper-
thyroidism can cause degeneration of the
heartmuscle, resulting in heart failure. Heredi-
tary factors can also be responsible for in-
creased susceptibilityto heart failure.
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HeartMedications
Digitalis (dij-i-talis, dij-i-talis) slows and
strengthens contractionsof the heart muscle.
Thisdrug is frequently given to people who suf-
fer from heart failure, although italso can be
used to treatatrial tachycardia.
Nitroglycerin (nı¯-tro¯ -gliser-in) causes di-
lation ofall of the veins and arteries, including
coronaryarteries, without an increase in heart
rate or stroke volume. When allblood vessels
dilate, a greater volume ofblood poolsin the di-
lated blood vessels, causing a decrease in the
venous return to the heart. The flow of blood
through coronary arteries also increases. The
reduced preload causes cardiacoutput to de-
crease, resulting in a decreased amountofwork
performed by the heart. Nitroglycerin is fre-
quently given to people who suffer from coro-
nary artery disease, which restricts coronary
blood flow. The decreased workperformed by
the heart reduces the amount of oxygen re-
quired by the cardiac muscle. Consequently,
the heartdoesn’t suffer from a lack of oxygen,
and angina pectorisdoesn’t develop.
Beta-adrenergic-blocking agentsreduce
the rate and strength of cardiac muscle con-
tractions, thusreducing the heart’s demand for
oxygen. These blocking agentsbind to recep-
tors for norepinephrine and epinephrine and
prevent these substances from having their
normal effects. They are often used to treat
people who suffer from rapid heartrates, cer-
tain typesof arrhythmias, and hypertension.
Calcium channelblockersreduce the rate at
which Ca
2
diffuse into cardiacmuscle cells and
smooth muscle cells. Because the action poten-
tials that produce cardiacmuscle contractions
depend in parton the flow of Ca
2
into cardiac
muscle cells, calcium channelblockers can be
used to control the force ofhear tcontractions
and reduce arrhythmia, tachycardia, and hyper-
tension. Because entry of Ca
2
into smooth
muscle cellscauses contraction, calcium chan-
nel blockers cause dilation ofcoronary blood
vesselsand can be used to treat angina pectoris.
Antihypertensive (ante¯-hı¯-per-tensiv)
agents comprise several drugs used specifi-
callyto treat hypertension. These drugs reduce
blood pressure and, therefore, reduce the work
required bythe heart to pump blood. In addi-
tion, the reduction of blood pressure reduces
the risk of heart attacksand strokes. Drugs
used to treat hypertension include those that
reduce the activityof the sympathetic nervous
system, that dilate arteries and veins, that
increase urine production (diuretics), and
that blockthe conversion of angiotensino-
gen to angiotensin I.
Anticoagulants (ante¯-ko¯-agu¯-lantz)
preventclot formation in persons with dam-
age to heartvalves or blood vessels or in per-
sonswho have had a myocardial infarction.
Aspirin functionsas a weak anticoagulant.
Instrumentsand Selected
Procedures
An artificial pacemaker is an instrument
placed beneath the skin, equipped with an
electrode that extends to the heart. The in-
strumentprovides an electric stimulus to the
heartat a set frequency. Artificial pacemak-
ersare used in patients in whom the natural
pacemaker of the heart doesn’tproduce a
heart rate high enough to sustain normal
physical activity. Modern electronics has
made it possible to design artificial pace-
makers that can increase the heart rate
as increases in physical activity occur.
Pacemakers can also detectcardiac arrest,
extreme arrythmias, or fibrillation. In re-
sponse, strong stimulation of the heart by
the pacemaker mayrestore heart function.
A heart lung machine serves as a tem-
porary substitute for a patient’s heart and
lungs. Itoxygenates the blood, removes car-
bon dioxide, and pumps blood throughout
the body. Ithas made possible many surger-
ieson the heart and lungs.
Heart valve replacement or repairis a
surgical procedure performed on those who
have diseased valvesthat are so deformed
and scarred from conditionslike endocarditis
that the valves are severely incompetent or
stenosed. Substitute valvesmade of synthetic
materialslike plastic or Dacron are effective;
valvestransplanted from pigs are also used.
A heart transplant is a surgical proce-
dure made possible when the immune char-
acteristics of a donor and the recipientare
closelymatched (see chapter 22). The heart
ofa recently deceased donor is transplanted
to the recipient, and the diseased heart of
the recipient is removed. People who have
received hearttransplants must continue to
take drugs that suppresstheir immune re-
sponses for the rest of their lives. If they
don’t, their immune system will reject the
transplanted heart.
Anartificial heart is a mechanical pump
thatreplaces the heart. It is still experimental
and cannotbe viewed as a permanent substi-
tute for the heart. Ithas been used to keep a
patientalive until a donor heart can be found.
Cardiacassistance involves temporarily
implanting a mechanicaldevice that assists
the heartin pumping blood. In some cases,
the decreased workload on the heart pro-
vided bythe device appears to promote re-
coveryof failing hearts, and the device has
been successfully removed. In cardio-
myoplasty,a piece of a back muscle (latis-
simus dorsi) is wrapped around the heart
and stimulated to contractin synchrony with
the heart.
Prevention ofHeart Disease
Proper nutrition is important in reducing the
riskof heart disease (see chapter 25). A rec-
ommended dietis low in fats, especially satu-
rated fatsand cholesterol, and low in refined
sugar. Diets should be high in fiber, whole
grains, fruits, and vegetables. Totalfood intake
should be limited to avoid obesity, and
sodium chloride intake should be reduced.
Tobacco and excessive use ofalcohol
should be avoided. Smoking increasesthe
riskof heart disease at least 10-fold, and ex-
cessive use ofalcohol also substantially in-
creasesthe risk of heart disease.
Chronic stress, frequent emotional up-
sets, and a lackof physical exercise can in-
crease the risk of cardiovascular disease.
Remediesinclude relaxation techniques and
aerobicexercise programs involving gradual
increasesin duration and difficulty in activi-
ties, such aswalking, swimming, jogging, or
aerobicdancing.
Hypertension (hı¯per-tenshu˘n) is ab-
normallyhigh systemic blood pressure. It af-
fectsabout one-fifth of the U.S. population.
Regular blood pressure measurementsare
important because hypertension does not
produce obvioussymptoms. If hypertension
cannot be controlled bydiet and exercise,
it’simportant to treat the condition with pre-
scribed drugs. The cause ofhypertension in
the majorityof cases is unknown.
Some data suggest that taking an as-
pirin daily reduces the chance of a heart
attack. Aspirin inhibits the synthesis of
prostaglandinsin platelets, thereby helping
to preventclot formation.
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Mr. P was an overweight, out-of-shape executive who regularly
smoked and consumed food with a high fatcontent. He viewed hisjob
as frustrating because he wasfrequently confronted with stressful
deadlines. He had nothad a physicalexamination for several years, so
he wasnot aware that his blood pressure washigh. One evening, Mr. P
waswalking to his car after workwhen he began to feel chest pain that
radiated down hisleft arm. Shortly after the onset of pain, he felt out
of breath, developed marked pallor, became dizzy, and had to lie
down on the sidewalk. The pain in hischest and arm was poorly local-
ized, butintense, and he became anxious and then disoriented. Mr. P
lostconsciousness, although he did not stop breathing. After a short
delay, one of hiscoworkers noticed him and called for help. When
paramedicsarrived they determined that Mr. P’s blood pressure was
low and he exhibited arrhythmia and tachycardia. The paramedics
transmitted the electrocardiogram theytook to a physician by way of
their electronic communicationssystem, and they discussed Mr. P’s
symptomswith the physician who was atthe hospital. The paramedics
were directed to administer oxygen and medication to controlarrhyth-
mias and transporthim to the hospital. At the hospital, tissue plas-
minogen activator (t-PA) wasadministered, which improved blood
flow to the damaged area of the heart by activating plasminogen,
which dissolvesblood clots. Enzymes, like creatine phosphokinase,
increased in Mr. P’sblood over the next few days, which confirmed
thatdamage to cardiac muscle resulted from an infarction.
In the hospital, Mr. P began to experience shortnessof breath
because ofpulmonary edema, and after a few days in the hospital, he
developed pneumonia. He wastreated for pneumonia and gradually
improved over the nextfew weeks. An angiogram performed several
daysafter Mr. P’s infarction indicated that he had suffered damage to
a significantpart of the lateral wall of hisleft ventricle and that neither
angioplasty nor bypasssurgery were necessary, although Mr. P has
some seriousrestrictions to blood flow in his coronary arteries.
Background Information
Mr. P experienced a myocardialinfarction. A thrombosis in one of the
branchesof the left coronaryar tery reducesthe blood supply to the lat-
eralwall of the left ventricle, resulting in ischemia of the left ventricle
wall. Thatt-PA is effective in treating a heart attack is consistentwith
the conclusion thatthe infarction was caused by a thrombosis. An is-
chemic area of the heart wallis not able to contract normally and,
therefore, the pumping effectiveness of the heart is dramatically
reduced. The reduced pumping capacityof the heart is responsible for
the low blood pressure, which causesthe blood flow to the brain to de-
crease resulting in confusion, disorientation, and unconsciousness.
Low blood pressure, increasing blood carbon dioxide levels,
pain, and anxiousnessincrease sympathetic stimulation of the heart
and adrenalglands. Increased sympathetic stimulation of the adrenal
medulla resultsin release of epinephrine. Increased parasympathetic
stimulation ofthe heart results from pain sensations. In such cases,
the heart is periodically arrhythmicdue to the combined effects of
parasympathetic stimulation, epinephrine and norepinephrine from
the adrenalgland, and sympathetic stimulation. In addition, ectopic
beatsare produced by the ischemic areas of the leftventricle.
Pulmonary edema resultsfrom the increased pressure in the
pulmonaryveins because of the inability of the left ventricle to pump
blood. The edema allows bacteria to infect the lungs and cause
pneumonia.
Mr. P’sheart began to beat rhythmically in response to medica-
tion because the infarction did notdamage the conducting system of
the heart, which isan indication that the no permanent arrhythmias
developed. Permanentarrhythmias are indications of damage done to
cardiacmuscle specialized to conduct action potentials in the heart.
Analysis of the electrocardiogram, blood pressure measure-
ments, and the angiogram (figure A) indicate thatthe infarction, in this
case, waslocated on the left side of Mr. P’s heart. Mr. P exhibited sev-
eralcharacteristics that are correlated with an increased probabilityof
myocardial infarction: lackof physical exercise, being overweight,
smoking, and stress.
Mr. P’sphysician made it very clear to him that he was lucky to
have survived a myocardial infarction, and the physician recom-
mended a weight-lossprogram, a low-sodium and low-fat diet, and
thatMr. P should stop smoking. He explained that Mr. P would have
to take medication for high blood pressure ifhis blood pressure did
notdecrease in response to the recommended changes. After a pe-
riod ofrecovery, Mr. P’s physician recommended an aerobic exercise
program to him. He advised Mr. P to seekways to reduce the stress
associated with hisjob. His physician also recommended that Mr. P
regularlytake a small amountof aspirin. The aspirin was prescribed to
reduce the probability of thrombosis. Because aspirin inhibits
prostaglandin synthesis, itreduces the tendency for blood to clot. Mr.
P followed the doctor’srecommendations, and after several months,
he began to feelbetter than he had in years, and his blood pressure
wasnormal.
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Systems Pathology
MyocardialInfarction
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PREDICT
Severe ischemia in the wallof a ventricle can resultin the death of
cardiacmuscle cells. Inflammation around the necrotic tissue results,
and macrophagesinvade the necrotic tissue and phagocytize dead
cells. Atthe same time, blood vessels and connective tissue grow into
the necroticarea and begin to deposit connective tissue to replace the
necrotictissue. Assume that Mr. P had a myocardialinfarction and
wasrecovering. After about a week, however, hisblood pressure
suddenlydecreased to very low levels, and he died within a very short
time. Atautopsy, a large amount of blood wasfound in the pericardial
sac, and the wallof the left ventricle was ruptured. Explain.
Chapter 20 Cardiovascular System: The Heart 703
Occluded coronary
artery
Figure A
Angiogram
An angiogram (anje¯-o¯-gram) is a picture of a blood vessel. It is usually
obtained byplacing a catheter into a blood vessel and injecting a dye that
can be detected with x-rays. Note the occluded (blocked) coronaryblood
vesselin this angiogram, which has been computer-enhanced to show colors.
System Interactions
System Interaction
Effect of Myocardial Infarction on Other Systems
Integumentary Pallor of the skin resulted from intense constriction of peripheral blood vessels, including those in the skin.
Muscular Reduced skeletal muscle activity required for activities such as walking results from lack of blood flow to the brain and because
blood is shunted from blood vessels that supply skeletal muscles to those that supply the heart and brain.
Nervous Decreased bood flow to the brain, decreased blood pressure, and pain due to ischemia of heart muscle result in increased
sympathetic and decreased parasympathetic stimulation of the heart. Loss of consciousness occurs when the blood flow to
the brain decreases enough to result in too little oxygen to maintain normal brain function, especially in the reticular
activating system.
Endocrine When blood pressure decreases to low values, antidiuretic hormone (ADH) is released from the posterior pituitary gland and
renin, released from the kidney, activates the renin-angiotensinogen-aldosterone mechanism. ADH, secreted in large
amounts, and angiotensin II cause vasoconstriction of peripheral blood vessels. ADH and aldosterone act on the kidneys to
retain water and electrolytes. An increased blood volume increases venous return, which results in an increased stroke
volume of the heart and an increase in blood pressure unless damage to the heart is very severe.
Lymphatic or Immune White blood cells, including macrophages, move to the area of cardiac muscle damaged and phagocytize any dead cardiac
muscle cells.
Respiratory Decreased blood pressure results in a decreased blood flow to the lungs. The decrease in gas exchange results in increased
blood C0
2
levels, acidosis, and decreased blood 0
2
levels. Initially, respiration becomes deep and labored because of the
elevated C0
2
levels, decreased blood pH, and depressed 0
2
levels. If the blood 0
2
levels decrease too much, the person
loses consciousness. Pulmonary edema can result when the pumping effectiveness of the left ventricle is substantially
reduced.
Digestive Decreased blood flow to the digestive system to very low levels often results in increased nausea and vomiting.
Urinary Blood flow to the kidney decreases dramatically in response to sympathetic stimulation. If the kidney becomes ischemic,
damage to the kidney tubules can occur, resulting in acute renal failure. Acute renalfailure reduces urine production.
Increased blood urea nitrogen, increased blood levels of K
, and edema are indications that the kidneys cannot eliminate
waste products and excess water. If damage is not too great, the period of reduced urine production may last up to 3 weeks
and then the rate of urine production slowly returnsto normal as the kidney tubules heal.
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Part4 Regulationsand Maintenance704
Functionsof the Heart
(p. 668)
The heart produces the force that causes blood circulation.
Size, Shape, and Location ofthe Heart
(p. 668)
The heart is approximately the size of a closed fist and is shaped like a
blunt cone.It is in the mediastinum.
Anatomyof the Heart
(p. 670)
The heart consists oftwo atria and two ventricles.
Pericardium
1. The pericardium is a sac that surrounds the heart and consists of the
fibrous pericardium and the serous pericardium.
2. The fibrous pericardium helps hold the heart in place.
3. The serous pericardium reduces friction as the heart beats. It
consists ofthe following parts:
• The parietal pericardium lines the fibrous pericardium.
• The visceral pericardium lines the exterior surface of the heart.
• The pericardial cavity lies between the parietal and visceral
pericardium and is filled with pericardial fluid.
HeartWall
1. The heart wall has three layers:
• The outer epicardium (visceral pericardium) provides protection
against the friction ofrubbing organs.
• The middle myocardium is responsible for contraction.
• The inner endocardium reduces the friction resulting from blood’s
passing through the heart.
2. The inner surfaces of the atria are mainly smooth. The auricles have
raised areas called musculi pectinati.
3. The ventricles have ridges called trabeculae carneae.
ExternalAnatomy and Coronary Circulation
1. Each atrium has a flap called the auricle.
2. The coronary sulcus separates the atria from the ventricles. The
interventricular grooves separate the right and left ventricles.
3. The inferior and superior venae cavae and the coronary sinus enter
the right atrium.The four pulmonary veins enter the left atrium.
4. The pulmonary trunk exits the right ventricle, and the aorta exits
the left ventricle.
5. Coronary arteries branch off the aorta to supply the heart. Blood
returns from the heart tissues to the right atrium through the
coronary sinus and cardiac veins.
HeartChambers and Valves
1. The interatrial septum separates the atria from each other,and the
interventricular septum separates the ventricles.
2. The tricuspid valve separates the right atrium and ventricle. The
bicuspid valve separates the left atrium and ventricle.The chordae
tendineae attach the papillary muscles to the atrioventricular valves.
3. The semilunar valves separate the aorta and pulmonary trunk from
the ventricles.
Route ofBlood Flow Through the Heart
(p. 677)
1. Blood from the body flows through the right atrium into the right
ventricle and then to the lungs.
2. Blood returns from the lungs to the left atrium, enters the left
ventricle,and is pumped back to the body.
Histology
(p. 679)
HeartSkeleton
The fibrous heart skeleton supports the openings ofthe heart, electrically
insulates the atria from the ventricles,and provides a point of attachment
for heart muscle.
CardiacMuscle
1. Cardiac muscle cells are branched and have a centrally located
nucleus.Actin and myosin are organized to form sarcomeres.The
sarcoplasmic reticulum and T tubules are not as organized as in
skeletal muscle.
2. Cardiac muscle cells are joined by intercalated disks,which allow
action potentials to move from one cell to the next.Thus, cardiac
muscle cells function as a unit.
3. Cardiac muscle cells have a slow onset of contraction and a
prolonged contraction time caused by the length oftime required
for calcium to move to and from the myofibrils.
4. Cardiac muscle is well supplied with blood vessels that support
aerobic respiration.
5. Cardiac muscle aerobically uses glucose,fatt y acids,and lactic acid
to produce ATP for energy.Cardiac muscle does not develop a
significant oxygen debt.
Conducting System
1. The SA node and the AV node are in the right atrium.
2. The AV node is connected to the bundle branches in the
interventricular septum by the AV bundle.
3. The bundle branches give rise to Purkinje fibers,which supply the
ventricles.
4. The SA node initiates action potentials,which spread across the
atria and cause them to contract.
5. Action potentials are slowed in the AV node,allowing the atria to
contract and blood to move into the ventricles.Then, the action
potentials travel through the AV bundles and bundle branches to the
Purkinje fibers,causing the ventricles to contract, starting at the apex.
ElectricalProperties
(p. 681)
Action Potentials
1. After depolarization and partial repolarization, a plateau is reached,
during which the membrane potential only slowly repolarizes.
2. The movement of Na
through the voltage-gated Na
channels
causes depolarization.
3. During depolarization, voltage-gated K
channels close and voltage-
gated Ca
2
channels begin to open.
4. Early repolarization results from closure of the voltage-gated Na
channels and the opening ofsome voltage-gated K
channels.
5. The plateau exists because voltage-gated Ca
2
channels remain
open.
6. The rapid phase of repolarization results from closure of the
voltage-gated Ca
channels and the opening ofmany voltage-gated
K
channels.
Autorhythmicityof Cardiac Muscle
1. Cardiac pacemaker muscle cells are autorhythmic because of the
spontaneous development ofa prepotential.
2. The prepotential results from the movement of Na
and Ca
2
into
the pacemaker cells.
3. Ectopic foci are areas of the heart that regulate heart rate under
abnormal conditions.
SUMMARY
Seeley−Stephens−Tate:
Anatomy and Physiology,
Sixth Edition
IV. Regulations and
Maintenance
20. Cardiovascular System:
The Heart
© The McGraw−Hill
Companies, 2004
Chapter 20 Cardiovascular System: The Heart 705
RefractoryPeriod of Cardiac Muscle
Cardiac muscle has a prolonged depolarization and thus a prolonged re-
fractory period,which allows time for the cardiac muscle to relax before
the next action potential causes a contraction.
Electrocardiogram
1. The ECG records only the electrical activities of the heart.
• Depolarization of the atria produces the P wave.
• Depolarization of the ventricles produces the QRS complex.
Repolarization ofthe atria occurs during the QRS complex.
• Repolarization of the ventricles produces the T wave.
2. Based on the magnitude of the ECG waves and the time between
waves,ECGs can be used to diagnose heart abnormalities.
CardiacCycle
(p. 685)
1. The cardiac cycle is repetitive contraction and relaxation of the
heart chambers.
2. Blood moves through the circulatory system from areas of higher
pressure to areas oflower pressure. Contraction of the heart
produces the pressure.
3. The cardiac cycle is divided into five periods.
• Although the heart is contracting, during the period of isovolumic
contraction ventricular volume doesn’t change because all the
heart valves are closed.
• During the period of ejection, the semilunar valves open, and
blood is ejected from the heart.
• Although the heart is relaxing, during the period of isovolumic
relaxation,ventricular volume doesn’t change because all the heart
valves are closed.
• Passive ventricular filling results when blood flows from the higher
pressure in the veins and atria to the lower pressure in the relaxed
ventricles.
• Active ventricular filling results when the atria contract and pump
blood into the ventricles.
EventsOccurring During Ventricular Systole
1. Contraction of the ventricles closes the AV valves,opens the
semilunar valves,and ejects blood from the heart.
2. The volume of blood in a ventricle just before it contracts is the
end-diastolic volume.The volume of blood after contraction is the
end-systolic volume.
EventsOccurring During Ventricular Diastole
1. Relaxation of the ventricles results in closing of the semilunar
valves,opening of the AV valves,and the movement of blood into
the ventricles.
2. Most ventricular filling occurs when blood flows from the higher
pressure in the veins and atria to the lower pressure in the relaxed
ventricles.
3. Contraction of the atria completes ventricular filling.
HeartSounds
1. Closure of the atrioventricular valves produces the first heart sound.
2. Closure of the semilunar valves produces the second heart sound.
AorticPressure Curve
1. Contraction of the ventricles forces blood into the aorta, thus
producing the peak systolic pressure.
2. Blood pressure in the aorta falls to the diastolic level as blood flows
out ofthe aorta.
3. Elastic recoil of the aorta maintains pressure in the aorta and
produces the dicrotic notch.
Mean ArterialBlood Pressure
(p. 692)
1. Mean arterial pressure is the average blood pressure in the aorta.
Adequate blood pressure is necessary to ensure delivery ofblood to
the tissues.
2. Mean arterial pressure is proportional to cardiac output (amount of
blood pumped by the heart per minute) times peripheral resistance
(total resistance to blood flow through blood vessels).
3. Cardiac output is equal to stroke volume times heart rate.
4. Stroke volume,the amount of blood pumped by the heart per beat,
is equal to end-diastolic volume minus end-systolic volume.
• Venous return is the amount ofblood returning to the heart.
Increased venous return increases stroke volume by increasing
end-diastolic volume.
• Increased force of contraction increases stroke volume by
decreasing end-systolic volume.
5. Cardiac reserve is the difference between resting and exercising
cardiac output.
Regulation ofthe Heart
(p. 693)
IntrinsicRegulation
1. Venous return is the amount ofblood that returns to the heart
during each cardiac cycle.
2. Starling’s law ofthe hear t describes the relationship between preload
and the stroke volume ofthe heart. An increased preload causes the
cardiac muscle fibers to contract with a greater force and produce a
greater stroke volume.
ExtrinsicRegulation
1. The cardioregulatory center in the medulla oblongata regulates the
parasympathetic and sympathetic nervous control ofthe heart.
2. Parasympathetic control
• Parasympathetic stimulation is supplied by the vagus nerve.
• Parasympathetic stimulation decreases heart rate.
• Postganglionic neurons secrete acetylcholine,which increases
membrane permeability to K
,producing hyperpolarization of
the membrane.
3. Sympathetic control
• Sympathetic stimulation is supplied by the cardiac nerves.
• Sympathetic stimulation increases heart rate and the force of
contraction (stroke volume).
• Postganglionic neurons secrete norepinephrine,which increases
membrane permeability to Na
and Ca
2
and produces
depolarization ofthe membrane.
4. Epinephrine and norepinephrine are released into the blood from
the adrenal medulla as a result ofsympathetic stimulation.
• The effects of epinephrine and norepinephrine on the heart are
long lasting compared to those ofneural stimulation.
• Epinephrine and norepinephrine increase the rate and force of
heart contraction.
Heartand Homeostasis
(p. 696)
Effectof Blood Pressure
1. Baroreceptors monitor blood pressure.
2. In response to a decrease in blood pressure,the baroreceptor reflexes
increase sympathetic stimulation and decrease parasympathetic
stimulation ofthe heart, resulting in an increase in heart rate and
force ofcontraction.
Seeley−Stephens−Tate:
Anatomy and Physiology,
Sixth Edition
IV. Regulations and
Maintenance
20. Cardiovascular System:
The Heart
© The McGraw−Hill
Companies, 2004
Effectof pH, Carbon Dioxide, and Oxygen
1. Chemoreceptors monitor blood carbon dioxide,pH, and oxygen levels.
2. In response to increased carbon dioxide and decreased pH,
medullary chemoreceptor reflexes increase sympathetic stimulation
and decrease parasympathetic stimulation ofthe heart.
3. Carotid body chemoreceptor receptors stimulated by low oxygen
levels result in a decreased heart rate and vasoconstriction.
4. All regulatory mechanisms functioning together in response to low
blood pH,high blood carbon dioxide, and low blood oxygen levels
usually produce an increase in heart rate and vasoconstriction.
Decreased oxygen levels stimulate an increase in heart rate indirectly
by stimulating respiration,and the stretch of the lungs activates a
reflex that increases sympathetic stimulation ofthe heart.
Effectof Extracellular Ion Concentration
1. An increase or decrease in extracellular K
decreases heart rate.
2. Increased extracellular Ca
2
increase the force ofcontraction of the
heart and decrease the heart rate.Decreased Ca
2
levels produce the
opposite effect.
Part4 Regulationsand Maintenance706
Effectof Body Temperature
Heart rate increases when body temperature increases,and it decreases
when body temperature decreases.
Effectsof Aging on the Heart
(p. 699)
1. Aging results in gradual changes in the function of the heart which
are minor under resting conditions but are more significant during
exercise.
2. Hypertrophy of the left ventricle is a common age-related condition.
3. The maximum heart rate decreases and by age 85 the cardiac output
may be decreased by 30–60%.
4. There is an increased tendency for valves to function abnormally
and for arrhythmias to occur.
5. An increased oxygen consumption,required to pump the same
amount ofblood, makes age-related coronary artery disease more
severe.
6. Exercise improves the functional capacity of the heart at all ages.
1. The fibrous pericardium
a. is in contact with the heart.
b. is a serous membrane.
c. is also known as the epicardium.
d. forms the outer layer ofthe pericardial sac.
e. all of the above.
2. Which of these structures returns blood to the right atrium?
a. coronary sinus
b. inferior vena cava
c. superior vena cava
d. both b and c
e. all of the above
3. The valve located between the right atrium and the right ventricle is the
a. aortic semilunar valve.
b. pulmonary semilunar valve.
c. tricuspid valve.
d. bicuspid (mitral) valve.
4. The papillary muscles
a. are attached to chordae tendineae.
b. are found in the atria.
c. contract to close the foramen ovale.
d. are attached to the semilunar valves.
e. surround the openings of the coronary arteries.
5. Given these blood vessels:
1. aorta
2. inferior vena cava
3. pulmonary trunk
4. pulmonary vein
Choose the arrangement that lists the vessels in the order a red
blood cell would encounter them in going from the systemic veins
back to the systemic arteries.
a. 1,3,4,2
b. 2,3,4,1
c. 2,4,3,1
d. 3,2,1,4
e. 3,4,2,1
6. Which of these does not correctly describe the skeleton of the heart?
a. electrically insulates the atria from the ventricles
b. provides a rigid source of attachment for the cardiac muscle
c. functions to reinforce or support the valve openings
d. is composed mainly ofcartilage
7. The bulk of the heart wall is
a. epicardium.
b. pericardium.
c. myocardium.
d. endocardium.
e. exocardium.
8. Muscular ridges on the interior surface of the auricles are called
a. trabeculae carneae.
b. crista terminalis.
c. musculi pectinati.
d. endocardium.
e. papillary muscles.
9. Cardiac muscle has
a. sarcomeres.
b. a sarcoplasmic reticulum.
c. transverse tubules.
d. many mitochondria.
e. all of the above.
10. Action potentials pass from one cardiac muscle cell to another
a. through gap junctions.
b. by a special cardiac nervous system.
c. because of the large voltage of the action potentials.
d. because ofthe plateau phase of the action potentials.
e. by neurotransmitters.
11. During the transmission of action potentials through the
conducting system ofthe heart, there is a temporary delay at the
a. bundle branches.
b. Purkinje fibers.
c. AV node.
d. SA node.
e. AV bundle.
12. Given these structures of the conduction system of the heart:
1. atrioventricular bundle
2. AV node
3. bundle branches
4. Purkinje fibers
5. SA node
REVIEW AND COMPREHENSION
Seeley−Stephens−Tate:
Anatomy and Physiology,
Sixth Edition
IV. Regulations and
Maintenance
20. Cardiovascular System:
The Heart
© The McGraw−Hill
Companies, 2004
Chapter 20 Cardiovascular System: The Heart 707
Choose the arrangement that lists the structures in the order an
action potential passes through them.
a. 2,5,1,3,4
b. 2,5,3,1,4
c. 2,5,4,1,3
d. 5,2,1,3,4
e. 5,2,4,3,1
13. Purkinje fibers
a. are specialized cardiac muscle cells.
b. conduct impulses much more slowly than ordinary cardiac
muscle.
c. conduct action potentials through the atria.
d. connect between the SA node and the AV node.
e. ensure that ventricular contraction starts at the base of the heart.
14. T waves on an ECG represent
a. depolarization of the ventricles.
b. repolarization of the ventricles.
c. depolarization of the atria.
d. repolarization ofthe atr ia.
15. Which of these conditions observed in an electrocardiogram
suggests that the AV node is not conducting action potentials?
a. complete lack of the P wave
b. complete lack ofthe QRS complex
c. more QRS complexes than P waves
d. a prolonged PR interval
e. P waves and QRS complexes are not synchronized
16. The greatest amount of ventricular filling occurs during
a. the first one-third of diastole.
b. the middle one-third of diastole.
c. the last one-third of diastole.
d. ventricular systole.
17. While the semilunar valves are open during a normal cardiac cycle,
the pressure in the left ventricle is
a. greater than the pressure in the aorta.
b. less than the pressure in the aorta.
c. the same as the pressure in the left atrium.
d. less than the pressure in the left atrium.
18. The pressure within the left ventricle fluctuates between
a. 120 and 80 mm Hg.
b. 120 and 0 mm Hg.
c. 80 and 0 mm Hg.
d. 20 and 0 mm Hg.
19. Blood flows neither into nor out of the ventricles during
a. the period of isovolumic contraction.
b. the period of isovolumic relaxation.
c. diastole.
d. systole.
e. both a and b.
20. Stroke volume is the
a. amount of blood pumped by the heart per minute.
b. difference between end-diastolic and end-systolic volume.
c. difference between the amount of blood pumped at rest and that
pumped at maximum output.
d. amount ofblood pumped from the atria into the ventricles.
21. Cardiac output is defined as
a. blood pressure times peripheral resistance.
b. peripheral resistance times heart rate.
c. heart rate times stroke volume.
d. stroke volume times blood pressure.
e. blood pressure minus peripheral resistance.
22. Pressure in the aorta is at its lowest
a. at the time of the first heart sound.
b. at the time of the second heart sound.
c. just before the AV valves open.
d. just before the semilunar valves open.
23. Just after the dicrotic notch on the aortic pressure curve,
a. the pressure in the aorta is greater than the pressure in the left
ventricle.
b. the pressure in the left ventricle is greater than the pressure in the
aorta.
c. the pressure in the left atrium is greater than the pressure in the
left ventricle.
d. the pressure in the left atrium is greater than the pressure in the
aorta.
e. blood pressure in the aorta is 0 mm Hg.
24. The “lubb”sound (first heart sound) of the heart is caused by the
a. closing of the AV valves.
b. closing of the semilunar valves.
c. blood rushing out of the ventricles.
d. filling ofthe ventricles.
e. ventricular contraction.
25. Increased venous return results in
a. increased stroke volume.
b. increased cardiac output.
c. decreased heart rate.
d. both a and b.
26. Parasympathetic nerve fibers are found in the
nerves and release at the heart.
a. cardiac, acetylcholine
b. cardiac,norepinephrine
c. vagus, acetylcholine
d. vagus,norepinephrine
27. Increased parasympathetic stimulation of the heart
a. increases the force of ventricular contraction.
b. increases the rate ofdepolar ization in the SA node.
c. decreases the heart rate.
d. increases cardiac output.
28. Because of the baroreceptor reflex,when normal ar terial blood
pressure decreases
a. heart rate decreases.
b. stroke volume decreases.
c. the frequency of afferent action potentials from baroreceptors
decreases.
d. the cardioregulatory center stimulates parasympathetic neurons.
e. all of the above.
29. A decrease in blood pH and an increase in blood carbon dioxide
levels result in
a. increased heart rate.
b. increased stroke volume.
c. increased sympathetic stimulation of the heart.
d. increased cardiac output.
e. all of the above.
30. An increase in extracellular potassium levels could cause
a. an increase in stroke volume.
b. an increase in the force ofcontraction.
c. a decrease in heart rate.
d. both a and b.
Answers in Appendix F
Seeley−Stephens−Tate:
Anatomy and Physiology,
Sixth Edition
IV. Regulations and
Maintenance
20. Cardiovascular System:
The Heart
© The McGraw−Hill
Companies, 2004
Part4 Regulationsand Maintenance708
1. Explain why the walls of the ventricles are thicker than the walls of
the atria.
2. In most tissues, peak blood flow occurs during systole and decreases
during diastole.In heart tissue, however,the opposite is true, and
peak blood flow occurs during diastole.Explain why this difference
occurs.
3. A patient has tachycardia.Would you recommend a drug that
prolongs or shortens the plateau ofcardiac muscle cell action
potentials?
4. Endurance-trained athletes often have a decreased heart rate
compared to that ofa nonathlete when both are resting. Explain
why an endurance-trained athlete’s heart rate decreases rather than
increases.
5. A doctor lets you listen to a patient’s heart with a stethoscope at the
same time that you feel the patient’s pulse.Once in a while you hear
two heartbeats very close together,but you feel only one pulse beat.
Later,the doctor tells you that the patient has an ectopic focus in the
right atrium.Explain why you hear two heartbeats very close
together.The doctor also tells you that the patient exhibits a pulse
deficit (i.e.,the number of pulse beats felt is fewer than the number
ofheartbeats heard). Explain why a pulse deficit occurs.
6. Heart rate and cardiac output were measured in a group of
nonathletic students.After 2 months of aerobic exercise training,
their measurements were repeated.It was found that heart rate had
decreased,but cardiac output remained the same for many
activities.Explain these findings.
7. Explain why it’s sufficient to replace the ventricles,but not the atria,
in artificial heart transplantation.
8. During an experiment in a physiology laboratory,a student named
Cee Saw was placed on a table that could be tilted.The instructor
asked the students to predict what would happen to Cee Saw’s heart
rate ifthe table were tilted so that her head was lower than her feet.
Some students predicted an increase in heart rate,and others
claimed it would decrease.Can you explain why both predictions
might be true?
9. After Cee Saw is tilted so that her head is lower than her feet for a few
minutes,the regulatory mechanisms that control blood pressure
adjust so that the heart pumps sufficient blood to supply the needs of
her tissues.If she is then tilted so that her head is higher than her
feet,gravity causes blood to flow toward her feet, and the blood
pressure in the carotid sinus and aortic arch decreases.The decrease
in blood pressure is detected by the baroreceptors in these vessels and
activates baroreceptor reflexes.The result is increased sympathetic
and decreased parasympathetic stimulation ofthe heart and an
increase in the heart rate.The increased heart rate functions to
increase the blood pressure to its normal value.
10. A friend tells you that her son had an ECG and it revealed that he
has a slight heart murmur.Should you be convinced that he has a
heart murmur? Explain.
11. An experiment on a dog was performed in which the mean arterial
blood pressure was monitored before and after the common carotid
arteries were partially clamped (at time A).The results are graphed
below:
Explain the change in mean arterial blood pressure (hint:
baroreceptors are located in the internal carotid arteries,which are
superior to the site ofclamping of the common carotid arteries).
12. During hemorrhagic shock (caused by loss of blood) the blood
pressure may fall dramatically,although the heart rate is elevated.
Explain why the blood pressure falls despite the increase in heart rate.
Answers in Appendix G
Time (minutes)
Arterial pressure
(mm Hg)
A
CRITICAL THINKING
1. The heart tissues supplied by the artery lose their oxygen and
nutrient supply and die.This part of the heart (and possibly the
entire heart) stops functioning.If this condition develops rapidly,
it’s called a heart attack,or myocardial infarction.
2. The heart must continue to function under all conditions and
requires energy in the form ofATP.During heavy exercise, lactic
acid is produced in skeletal muscle as a by-product ofanaerobic
metabolism.The ability to use lactic acid provides the heart with an
additional energy source.
3. Contraction of the ventricles, beginning at the apex and moving
toward the base ofthe heart, forces blood out of the ventricles and
toward their outflow vessels—the aorta and pulmonary trunk.The
aorta and pulmonary trunks are located at the base ofthe hear t.
4. Ectopic foci cause various regions of the heart to contract at
different times.As a result, pumping effectiveness is reduced.
Cardiac muscle contraction is not coordinated,which interrupts the
cyclic filling and emptying ofthe ventricles.
5. If cardiac muscle could undergo tetanic contraction, it would
contract for a long time without relaxing.Its pumping action then
would stop because that action requires alternating contraction and
relaxation.
6. During isovolumic contraction, the volume of the ventricles does
not change because no blood leaves the ventricle.Therefore, the
pressure increases but the length ofthe cardiac muscle doesn’t
change significantly.Therefore, the contraction is isometric (see
chapter 9).
7. The left ventricle has the thickest wall. The pressure produced by the
left ventricle is much higher than the pressure produced by the right
ventricle,when the ventricles contract. It’s important for each
ventricle to pump the same amount ofblood because, with two
connected circulation loops,the blood flowing into one must equal
the blood flowing into the other so that one doesn’t become
overfilled with blood at the expense ofthe other. For example, if the
right ventricle pumps less blood than the left ventricle,blood must
accumulate in the systemic blood vessels.If the left ventricle pumps
less blood than the right ventricle,blood accumulates in the
pulmonary blood vessels.
ANSWERS TO PREDICT QUESTIONS
Seeley−Stephens−Tate:
Anatomy and Physiology,
Sixth Edition
IV. Regulations and
Maintenance
20. Cardiovascular System:
The Heart
© The McGraw−Hill
Companies, 2004
Chapter 20 Cardiovascular System: The Heart 709
8. Fibrillation makes cardiac muscle an ineffective pump.The
pumping action ofthe heart depends on coordinated contraction of
cardiac muscle.Fibrillation destroys the coordinated contractions
and results in the loss ofthe ability for cardiac muscle to function as
a pump.The ventricles are the primary pumping chambers of the
heart.Ventricular fibrillation results in death because of the inability
ofthe heart to pump blood. The atria function primarily as
reservoirs.Their pumping action is most important during exercise.
Therefore atrial fibrillation does not destroy the ability ofthe
ventricles to pump blood.
9. Sympathetic stimulation increases heart rate. If venous return
remains constant,stroke volume decreases as the number of beats per
minute increases.Dilation of the coronary arteries is important
because,as the heart does more work, the cardiac tissue requires more
energy and,therefore, a greater blood supply to carry more oxygen.
10. Rupture of the left ventricle, as experienced by Mr.P,is more likely
several days after a myocardial infarction.As the necrotic tissues are
removed by macrophages,the wall of the ventricle becomes thinner
and may bulge during systole.If the wall of the ventricle becomes
very thin before new connective tissue is deposited,it may rupture.
Ifthe left ventricle ruptures, blood flows from the left ventricle into
the pericardial sac.As blood fills the pericardial sac, it compresses
the ventricle from the outside.This is called cardiac tamponade
(tam-po˘-na¯d).Thus the ventricle is not able to fill with blood and
its pumping ability is eliminated.Death occurs quickly in response
to a ruptured wall ofthe left ventricle.
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