Chapter 19

Lecture PowerPoint

The Circulatory
System: The Heart

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 Overview of the
Cardiovascular System

• Expected Learning Outcomes

– Define and distinguish between the pulmonary and
systemic circuits.
– Describe the general location, size, and shape of the
heart.
– Describe the pericardial sac that encloses the heart.

2-2
 Overview of the
Cardiovascular System
• Cardiovascular system
– Heart and blood vessels

• Circulatory system
– Heart, blood vessels, and the blood

19-3
The Pulmonary and Systemic Circuits

• Major divisions of circulatory system

– Pulmonary circuit: right side of heart
• Carries blood to lungs for gas exchange and
back to heart
– Systemic circuit: left side of heart
• Supplies oxygenated blood to all tissues of
the body and returns it to the heart

19-4
The Pulmonary and Systemic Circuits
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CO2 O2

• Left side of heart

– Fully oxygenated blood
arrives from lungs via
Pulmonary circuit pulmonary veins
O2-poor,
– Blood sent to all organs of
CO2-rich O2-rich,
blood CO2-poor
blood the body via aorta

Systemic circuit
• Right side of heart
– Lesser oxygenated blood
CO2 O2 arrives from inferior and
superior venae cavae
– Blood sent to lungs via
pulmonary trunk
Figure 19.1 19-5
 Position, Size, and Shape
of the Heart
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• Heart located in
mediastinum, between
lungs Aorta
Pulmonary
Superior trunk
• Base—wide, superior vena cava
Right lung Base of
heart
portion of heart, blood Parietal
vessels attach here pleura (cut)
Pericardial

• Apex—inferior end, tilts to sac (cut) Apex

of heart

the left, tapers to point (c)

Diaphragm

• 3.5 in. wide at base,

5 in. from base to apex, Figure 19.2c
and 2.5 in. anterior to
posterior; weighs 10
ounces
19-6
 Position, Size, and Shape
of the Heart
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Sternum
Posterior
3rd rib
Lungs

Thoracic Pericardial
Diaphragm
vertebra cavity

Left
Right ventricle
ventricle

Interventricular
(a) septum
Sternum

(b) Anterior

Figure 19.2a,b
19-7
 Gross Anatomy of the Heart

• Expected Learning Outcomes

– Describe the three layers of the heart wall.
– Identify the four chambers of the heart.
– Identify the surface features of the heart and correlate
them with its internal four-chambered anatomy.
– Identify the four valves of the heart.
– Trace the flow of blood through the four chambers and
valves of the heart and adjacent blood vessels.
– Describe the arteries that nourish the myocardium and
the veins that drain it.

19-8
 The Heart Wall
• Pericardium—double-walled sac (pericardial sac)
that encloses the heart
– Allows heart to beat without friction, provides room
to expand, yet resists excessive expansion
– Anchored to diaphragm inferiorly and sternum
anteriorly

• Parietal pericardium—outer wall of sac

– Superficial fibrous layer of connective tissue
– Deep, thin serous layer

19-9
 The Heart Wall

• Visceral pericardium (epicardium)—heart

covering
– Serous lining of sac turns inward at base of heart
to cover the heart surface

• Pericardial cavity—space inside the pericardial

sac filled with 5 to 30 mL of pericardial fluid

• Pericarditis—inflammation of the membranes

– Painful friction rub with each heartbeat
19-10
Pericardium and Heart Wall
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Pericardial
cavity
Pericardial
sac:
Fibrous
layer
Serous
layer
Epicardium

Myocardium

Endocardium
Epicardium

Pericardial sac

Figure 19.3
19-11
 Human Cadaver Heart
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Fat in interventricular
sulcus

Left ventricle

Right ventricle

Anterior interventricular
artery

(a) Anterior view, external anatomy

Superior vena cava

Base of heart

Inferior vena cava

Right atrium
Interatrial septum

Left atrium
Opening of coronary sinus

Right AV valve
Left AV valve
Trabeculae carneae

Coronary blood vessels Right ventricle

Tendinous cords
Papillary muscles
Left ventricle
Endocardium Epicardial fat

Myocardium
Interventricular septum
Epicardium
Apex of heart
Figure 19.4a,b
(b) Posterior view, internal anatomy

© The McGraw-Hill Companies, Inc.

19-12
 The Heart Wall
• Epicardium (visceral pericardium)
– Serous membrane covering heart
– Adipose in thick layer in some places
– Coronary blood vessels travel through this layer

• Endocardium
– Smooth inner lining of heart and blood vessels
– Covers the valve surfaces and is continuous with
endothelium of blood vessels

19-13
 The Heart Wall
• Myocardium
– Layer of cardiac muscle proportional to work load
• Muscle spirals around heart which produces wringing
motion
– Fibrous skeleton of the heart: framework of
collagenous and elastic fibers
• Provides structural support and attachment for cardiac
muscle and anchor for valve tissue
• Electrical insulation between atria and ventricles; important
in timing and coordination of contractile activity

19-14
 The Chambers
• Four chambers
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– Right and left atria

• Two superior chambers Aorta

• Receive blood returning Right pulmonary

artery

Superior vena cava

Left pulmonary artery

Pulmonary trunk

to heart Right pulmonary

veins
Interatrial
Left pulmonary veins

Pulmonary valve
septum Left atrium

• Auricles (seen on Right atrium

Fossa ovalis
Aortic valve
Left AV (bicuspid)
valve
Pectinate muscles

surface) enlarge
Left ventricle
Right AV
(tricuspid) valve
Papillary muscle
Interventricular septum

chamber
Tendinous cords
Endocardium
Trabeculae carneae
Myocardium
Right ventricle
Inferior vena cava Epicardium

– Right and left ventricles

• Two inferior chambers Figure 19.7
• Pump blood into arteries

19-15
 The Chambers
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Aortic arch
Ligamentum
• Atrioventricular sulcus
arteriosum

Superior vena cava

Ascending
aorta
—separates atria and
Left pulmonary
artery
ventricles
Branches of the
right pulmonary
artery Pulmonary trunk

Right pulmonary
veins
Left pulmonary
veins
• Interventricular sulcus
Left auricle —overlies the
Right auricle
interventricular septum
Right atrium

Coronary sulcus
that divides the right
Right ventricle
Anterior
interventricular
sulcus
ventricle from the left
Inferior vena cava
Left ventricle

Apex of heart • Sulci contain coronary

(a) Anterior view

arteries
Figure 19.5a
19-16
 The Chambers
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Aorta

Left pulmonary
artery Superior
vena cava
Right pulmonary
Left pulmonary artery
veins
Right pulmonary
veins
Left atrium
Coronary sulcus

Right atrium
Coronary sinus

Inferior vena cava

Fat
Posterior
Left ventricle interventricular
sulcus
Apex of heart Figure 19.5b
Right ventricle

(b) Posterior view 19-17

 The Chambers
• Interatrial septum
– Wall that separates atria

• Pectinate muscles
– Internal ridges of myocardium in right atrium and both
auricles

• Interventricular septum
– Muscular wall that separates ventricles

• Trabeculae carneae
19-18
– Internal ridges in both ventricles
 The Chambers
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Aorta

Right pulmonary Left pulmonary artery

artery

Superior vena cava Pulmonary trunk

Right pulmonary Left pulmonary veins

veins
Pulmonary valve
Interatrial
septum Left atrium
Right atrium Aortic valve
Fossa ovalis Left AV (bicuspid) valve
Pectinate muscles
Left ventricle
Right AV
(tricuspid) valve
Papillary muscle
Interventricular septum
Tendinous cords
Endocardium
Trabeculae carneae
Myocardium
Right ventricle
Epicardium
Inferior vena cava

Figure 19.7
19-19
 The Valves
• Valves ensure a one-way flow of blood through
the heart
• Atrioventricular (AV) valves—control blood flow
between atria and ventricles
– Right AV valve has three cusps (tricuspid valve)
– Left AV valve has two cusps (mitral or bicuspid
valve)
– Chordae tendineae: cords connect AV valves to
papillary muscles on floor of ventricles
• Prevent AV valves from flipping inside out or bulging into
the atria when the ventricles contract

19-20
 The Valves

• Semilunar valves—control flow into great

arteries; open and close because of blood flow
and pressure
– Pulmonary semilunar valve: in opening between
right ventricle and pulmonary trunk
– Aortic semilunar valve: in opening between left
ventricle and aorta

19-21
 The Valves
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Left AV
(bicuspid) valve

Right AV
(tricuspid) valve

Fibrous
skeleton
Openings to
coronary arteries

Aortic
valve

Pulmonary
valve
Figure 19.8a

(a) 19-22
The Valves: Endoscopic View
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

(b)
© Manfred Kage/Peter Arnold, Inc.

Figure 19.8b 19-23

 The Valves
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Tendinous
cords

Papillary
muscle

Figure 19.8c
(c) 19-24
© The McGraw-Hill Companies, Inc.
 Blood Flow Through the Chambers
• Ventricles relax
– Pressure drops inside the ventricles
– Semilunar valves close as blood attempts to back up
into the ventricles from the vessels
– AV valves open
– Blood flows from atria to ventricles

19-25
 Blood Flow Through the Chambers

• Ventricles contract
– AV valves close as blood attempts to back up into the
atria
– Pressure rises inside of the ventricles
– Semilunar valves open and blood flows into great
vessels

19-26
 Blood Flow Through the Chambers
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10
1 Blood enters right atrium from superior
and inferior venae cavae.

2 Blood in right atrium flows through right

Aorta
Left pulmonary AV valve into right ventricle.
11 artery
3 Contraction of right ventricle forces
5 5 pulmonary valve open.

9 4 Blood flows through pulmonary valve

Pulmonary trunk
Superior into pulmonary trunk.
vena cava 4
6 Left pulmonary 5 Blood is distributed by right and left
veins pulmonary arteries to the lungs, where it
Right 6
pulmonary unloads CO2 and loads O2.
1 Left atrium
veins
Aortic valve 6 Blood returns from lungs via pulmonary
7 veins to left atrium.
3
Left AV
Right (bicuspid) valve 7 Blood in left atrium flows through left AV
8 valve into left ventricle.
atrium
2 Left ventricle 8 Contraction of left ventricle (simultaneous with
Right AV step 3 ) forces aortic valve open.
(tricuspid) valve
9 Blood flows through aortic valve into
Right
ascending aorta.
ventricle
Inferior 10 Blood in aorta is distributed to every organ in
11
vena cava the body, where it unloads O2 and loads CO2.

11 Blood returns to heart via venae cavae.

Figure 19.9
• Blood pathway travels from the right atrium through the body and
19-27
 The Coronary Circulation

• 5% of blood pumped by heart is pumped to the

heart itself through the coronary circulation to
sustain its strenuous workload
– 250 mL of blood per minute
– Needs abundant O2 and nutrients

19-28
 Arterial Supply

• Left coronary artery (LCA) branches off the

ascending aorta
– Anterior interventricular branch
• Supplies blood to both ventricles and anterior two-
thirds of the interventricular septum

– Circumflex branch
• Passes around left side of heart in coronary sulcus
• Gives off left marginal branch and then ends on
the posterior side of the heart
• Supplies left atrium and posterior wall of left
ventricle 19-29
 Arterial Supply

• Right coronary artery (RCA) branches off the

ascending aorta
– Supplies right atrium and sinoatrial node (pacemaker)

– Right marginal branch

• Supplies lateral aspect of right atrium and ventricle

– Posterior interventricular branch

• Supplies posterior walls of ventricles

19-30
 Arterial Supply
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Ligamentum
Aortic arch
arteriosum

Ascending
Superior vena cava aorta

Left pulmonary
artery
Branches of the
right pulmonary Pulmonary trunk
artery
Left pulmonary
Right pulmonary
veins
veins

Left auricle

Right auricle

Right atrium

Coronary sulcus
Anterior
Right ventricle interventricular
sulcus
Inferior vena cava Figure 19.5a
Left ventricle

Apex of heart 19-31

(a) Anterior view
 Arterial Supply
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Aorta

Left pulmonary
artery Superior
vena cava

Right pulmonary
Left pulmonary artery
veins
Right pulmonary
veins
Left atrium
Coronary sulcus

Right atrium
Coronary sinus

Inferior vena cava

Fat
Posterior
Left ventricle interventricular
sulcus
Apex of heart

Right ventricle

(b) Posterior view

Figure 19.5b 19-32
 Arterial Supply

• Myocardial infarction (MI)—heart attack

– Interruption of blood supply to the heart from a blood
clot or fatty deposit (atheroma) can cause death of
cardiac cells within minutes
– Some protection from MI is provided by arterial
anastomoses which provides an alternative route of
blood flow (collateral circulation) within the
myocardium

• Blood flow to the heart muscle during ventricular

contraction is slowed, unlike the rest of the body
19-33
 Arterial Supply

• Three reasons
– Contraction of the myocardium compresses the
coronary arteries and obstructs blood flow
– Opening of the aortic valve flap during ventricular
systole covers the openings to the coronary arteries
blocking blood flow into them
– During ventricular diastole, blood in the aorta surges
back toward the heart and into the openings of the
coronary arteries
• Blood flow to the myocardium increases during
ventricular relaxation

19-34
 Angina and Heart Attack

• Angina pectoris—chest pain from partial

obstruction of coronary blood flow
– Pain caused by ischemia of cardiac muscle
– Obstruction partially blocks blood flow
– Myocardium shifts to anaerobic fermentation,
producing lactic acid and thus stimulating pain

19-35
 Angina and Heart Attack
• Myocardial infarction—sudden death of a patch
of myocardium resulting from long-term
obstruction of coronary circulation
– Atheroma (blood clot or fatty deposit) often obstructs
coronary arteries
– Cardiac muscle downstream of the blockage dies
– Heavy pressure or squeezing pain radiating into the left
arm
– Some painless heart attacks may disrupt electrical
conduction pathways, leading to fibrillation and cardiac
arrest
• Silent heart attacks occur in diabetics and the elderly
– MI responsible for about half of all deaths in the United
States
19-36
 Venous Drainage

• 5% to 10% drains directly into heart chambers—

right atrium and right ventricle—by way of the
thebesian veins

• The rest returns to right atrium by the following

routes:
– Great cardiac vein
• Travels alongside anterior interventricular artery
• Collects blood from anterior portion of heart
• Empties into coronary sinus

19-37
 Venous Drainage
• The rest returns to right atrium by the following
routes (cont.):
– Middle cardiac vein (posterior interventricular)
• Found in posterior sulcus
• Collects blood from posterior portion of heart
• Drains into coronary sinus
– Left marginal vein
• Empties into coronary sinus
• Coronary sinus
– Large transverse vein in coronary sulcus on posterior
side of heart
– Collects blood and empties into right atrium
19-38
 Cardiac Muscle and the
Cardiac Conduction System
• Expected Learning Outcomes
– Describe the unique structural and metabolic
characteristics of cardiac muscle.
– Explain the nature and functional significance of the
intercellular junctions between cardiac muscle cells.
– Describe the heart’s pacemaker and internal electrical
conduction system.
– Describe the nerve supply to the heart and explain its
role.

19-39
 Structure of Cardiac Muscle
• Cardiocytes—striated, short, thick, branched cells,
one central nucleus surrounded by light-staining
mass of glycogen

• Intercalated discs—join cardiocytes end to end

– Interdigitating folds: folds interlock with each other,
and increase surface area of contact

19-40
 Structure of Cardiac Muscle

Cont.
– Mechanical junctions tightly join cardiocytes
• Fascia adherens—broad band in which the actin of the
thin myofilaments is anchored to the plasma membrane
– Each cell is linked to the next via transmembrane proteins
• Desmosomes—weldlike mechanical junctions between
cells
– Prevents cardiocytes from being pulled apart

19-41
 Structure of Cardiac Muscle
• Electrical junctions (gap junctions) allow ions to
flow between cells; can stimulate neighbors
– Entire myocardium of either two atria or two ventricles acts
like single, unified cell

• Repair of damage of cardiac muscle is almost

entirely by fibrosis (scarring)

19-42
Structure of Cardiac Muscle
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Striations

Nucleus

Intercalated discs

(a)

Striated myofibril Glycogen Nucleus Mitochondria Intercalated discs

(b)

Intercellular space

Desmosomes

Gap junctions

Figure 19.11a–c

(c)
a: © Ed Reschke
19-43
 Metabolism of Cardiac Muscle
• Cardiac muscle depends almost exclusively on
aerobic respiration used to make ATP
– Rich in myoglobin and glycogen
– Huge mitochondria: fill 25% of cell

• Adaptable to organic fuels used

– Fatty acids (60%); glucose (35%); ketones, lactic acid, and
amino acids (5%)
– More vulnerable to oxygen deficiency than lack of a specific
fuel

• Fatigue resistant because it makes little use of

anaerobic fermentation or oxygen debt mechanisms
– Does not fatigue for a lifetime
19-44
 The Conduction System
• Coordinates the heartbeat
– Composed of an internal pacemaker and nervelike
conduction pathways through myocardium

• Generates and conducts rhythmic electrical

signals in the following order:
– Sinoatrial (SA) node: modified cardiocytes
• Pacemaker initiates each heartbeat and determines
heart rate
• Pacemaker in right atrium near base of superior vena
cava
– Signals spread throughout atria

19-45
 The Conduction System
Cont.
– Atrioventricular (AV) node
• Located near the right AV valve at lower end of interatrial
septum
• Electrical gateway to the ventricles
• Fibrous skeleton—insulator prevents currents from getting to
ventricles from any other route

– Atrioventricular (AV) bundle (bundle of His)

• Bundle forks into right and left bundle branches
• Branches pass through interventricular septum toward apex

– Purkinje fibers
• Nervelike processes spread throughout ventricular myocardium
• Signal passes from cell to cell through gap junctions
19-46
 Structure of Cardiac Muscle
• Cardiocytes—striated, short, thick, branched cells,
one central nucleus surrounded by light-staining mass
of glycogen
• Intercalated discs—join cardiocytes end to end
– Interdigitating folds: folds interlock with each other,
and increase surface area of contact
– Mechanical junctions tightly join cardiocytes
• Fascia adherens—broad band in which the actin of the
thin myofilaments is anchored to the plasma membrane
– Each cell is linked to the next via transmembrane proteins
• Desmosomes—weldlike mechanical junctions between
cells
– Prevents cardiocytes from being pulled apart
19-47
 Structure of Cardiac Muscle
Cont.
– Mechanical junctions tightly join cardiocytes
• Fascia adherens—broad band in which the actin of the
thin myofilaments is anchored to the plasma membrane
– Each cell is linked to the next via transmembrane
proteins

• Desmosomes—weldlike mechanical junctions between

cells
– Prevents cardiocytes from being pulled apart

19-48
 The Conduction System
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1 SA node fires.

2 Excitation spreads through

Right atrium 1 2 atrial myocardium.
Sinoatrial node
(pacemaker) Left 3 AV node fires.
atrium
2
Purkinje
Atrioventricular 3 fibers 4 Excitation spreads down AV
node bundle.
Bundle
Atrioventricular branches 5 Purkinje fibers distribute
bundle 4 excitation through
5
ventricular myocardium.

Purkinje fibers

Figure 19.12 19-49

 Nerve Supply to the Heart

• Sympathetic nerves (raise heart rate)

– Sympathetic pathway to the heart originates in the
lower cervical to upper thoracic segments of the
spinal cord
– Continues to adjacent sympathetic chain ganglia
– Some pass through cardiac plexus in mediastinum

19-50
 Nerve Supply to the Heart
Cont.
– Some pass through cardiac plexus in mediastinum
– Continue as cardiac nerves to the heart
– Fibers terminate in SA and AV nodes, in atrial and
ventricular myocardium, as well as the aorta,
pulmonary trunk, and coronary arteries
• Increase heart rate and contraction strength
• Dilates coronary arteries to increase myocardial blood
flow

19-51
 Nerve Supply to the Heart

• Parasympathetic nerves (slows heart rate)

– Pathway begins with nuclei of the vagus nerves in
the medulla oblongata
– Extend to cardiac plexus and continue to the heart by
way of the cardiac nerves
– Fibers of right vagus nerve lead to the SA node
– Fibers of left vagus nerve lead to the AV node
– Little or no vagal stimulation of the myocardium
• Parasympathetic stimulation reduces the heart rate

19-52
Electrical and Contractile Activity
of the Heart
• Expected Learning Outcomes
– Explain why the SA node fires spontaneously and
rhythmically.
– Explain how the SA node excites the myocardium.
– Describe the unusual action potentials of cardiac
muscle and relate them to the contractile behavior of
the heart.
– Interpret a normal electrocardiogram.

19-53
Electrical and Contractile Activity
of the Heart

• Cycle of events in heart—special names

– Systole: atrial or ventricular contraction
– Diastole: atrial or ventricular relaxation

19-54
 The Cardiac Rhythm

• Sinus rhythm—normal heartbeat triggered by

the SA node
– Set by SA node at 60 to 100 bpm
– Adult at rest is 70 to 80 bpm (vagal tone)

• Ectopic focus—another part of heart fires before

the SA node
– Caused by hypoxia, electrolyte imbalance, or caffeine,
nicotine, and other drugs

19-55
 The Cardiac Rhythm
• Spontaneous firing from some part of heart; not the SA
node
– Ectopic foci: region of spontaneous firing
• Nodal rhythm—if SA node is damaged, heart rate is set
by AV node, 40 to 50 bpm
• Intrinsic ventricular rhythm—if both SA and AV nodes
are not functioning, rate set at 20 to 40 bpm
– Requires pacemaker to sustain life

• Arrhythmia—any abnormal cardiac rhythm

– Failure of conduction system to transmit signals (heart
block)
• Bundle branch block
• Total heart block (damage to AV node)
19-56
 Cardiac Arrhythmias

• Atrial flutter—ectopic foci in atria

– Atrial fibrillation
– Atria beat 200 to 400 times per minute

• Premature ventricular contractions (PVCs)

– Caused by stimulants, stress, or lack of sleep

19-57
 Cardiac Arrhythmias
• Ventricular fibrillation
– Serious arrhythmia caused by electrical signals
reaching different regions at widely different times
• Heart cannot pump blood and no coronary perfusion

– Kills quickly if not stopped

• Defibrillation—strong electrical shock whose intent is to
depolarize the entire myocardium, stop the fibrillation, and
reset SA nodes to sinus rhythm

19-58
 Pacemaker Physiology

• SA node does not have a stable resting

membrane potential
– Starts at −60 mV and drifts upward from a slow
inflow of Na+
• Gradual depolarization is called pacemaker
potential
– Slow inflow of Na+ without compensating outflow of K+

19-59
 Pacemaker Physiology
Cont.
– When it reaches threshold of −40 mV, voltage-
gated fast Ca2+ and Na+ channels open
• Faster depolarization occurs peaking at 0 mV
• K+ channels then open and K+ leaves the cell
– Causing repolarization
– Once K+ channels close, pacemaker potential starts
over

19-60
 Pacemaker Physiology

• Each depolarization of the SA node sets off

one heartbeat
– At rest, fires every 0.8 second or 75 bpm

• SA node is the system’s pacemaker

19-61
 Pacemaker Physiology
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

+10

0
Membrane potential (mV)

–10 Fast K+
Fast
outflow Action
Ca2+–Na+
–20 inflow potential

–30 Threshold

–40

–50 Pacemaker
potential
–60 Slow Na+
inflow
–70

0 .4 .8 1.2 1.6
Time (sec)
Figure 19.13
19-62
Impulse Conduction to the Myocardium

• Signal from SA node stimulates two atria to

contract almost simultaneously
– Reaches AV node in 50 ms

• Signal slows down through AV node

– Thin cardiocytes have fewer gap junctions
– Delays signal 100 ms which allows the ventricles to
fill

19-63
Impulse Conduction to the Myocardium

• Signals travel very quickly through AV bundle and

Purkinje fibers
– Entire ventricular myocardium depolarizes and contracts
in near unison
• Papillary muscles contract an instant earlier than the rest,
tightening slack in chordae tendineae

• Ventricular systole progresses up from the apex of

the heart
– Spiral arrangement of cardiocytes twists ventricles
slightly; like someone wringing out a towel
19-64
Electrical Behavior of the Myocardium
• Cardiocytes have stable resting potential of −90 mV
• Depolarize only when stimulated
– Depolarization phase (very brief)
• Stimulus opens voltage-regulated Na+ gates (Na+ rushes in),
membrane depolarizes rapidly
• Action potential peaks at +30 mV
• Na+ gates close quickly

– Plateau phase lasts 200 to 250 ms, sustains contraction

for expulsion of blood from heart
• Ca2+ channels are slow to close and SR is slow to remove Ca2+
from the cytosol

19-65
Electrical Behavior of the Myocardium

• Depolarize only when stimulated (cont.)

– Repolarization phase: Ca2+ channels close, K+
channels open, rapid diffusion of K+ out of cell returns it
to resting potential

• Has a long absolute refractory period of 250 ms

compared to 1 to 2 ms in skeletal muscle
– Prevents wave summation and tetanus which would
stop the pumping action of the heart

19-66
Electrical Behavior of the Myocardium
1. Na+ gates open Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

3 1 Voltage-gated Na+ channels open.

2. Rapid
Plateau

+20 2 Na+ inflow depolarizes the membrane

4
and triggers the opening of still more Na+
channels, creating a positive feedback

depolarization 0 Action
potential
5
cycle and a rapidly rising membrane voltage.

3 Na+ channels close when the cell

Membrane potential (mV)

depolarizes, and the voltage peaks at

3. Na gates close
Myocardial nearly +30 mV.
+ –20
relaxation

4 Ca2+ entering through slow Ca2+

–40 2 channels prolongs depolarization of
Myocardial membrane, creating a plateau. Plateau falls
contraction slightly because of some K+ leakage, but most

4. Slow Ca2+ channels –60 Absolute

refractory
K+ channels remain closed until end of
plateau.

open
period
5 Ca2+ channels close and Ca2+ is transported
–80 1 out of cell. K+ channels open, and rapid K+
outflow returns membrane to its resting
potential.

5. Ca2+ channels 0 .15

Time (sec)
.30

close, K+ channels Figure 19.14

open
(repolarization)
19-67
 The Electrocardiogram
• Electrocardiogram
(ECG or EKG)
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

0.8 second

– Composite of all
action potentials of
R R
nodal and
+1 myocardial cells
PQ
segment
ST
segment detected, amplified
Millivolts

T wave
and recorded by
P wave

0
PR
interval
Q
S electrodes on arms,
QT
interval
QRS interval legs, and chest
–1

Atria Ventricles Atria Ventricles

contract contract contract contract

Figure 19.15
19-68
 The Electrocardiogram
• P wave
– SA node fires, atria depolarize and contract
– Atrial systole begins 100 ms after SA signal

• QRS complex
– Ventricular depolarization
– Complex shape of spike due to different thickness
and shape of the two ventricles

• ST segment—ventricular systole
– Plateau in myocardial action potential

• T wave
19-69
– Ventricular repolarization and relaxation
 The Electrocardiogram
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

0.8 second

R R

+1

PQ ST
segment segment
Millivolts

P wave T wave

PR Q
interval S
QT
interval
QRS interval

–1

Atria Ventricles Atria Ventricles

contract contract contract contract

Figure 19.15 19-70

 The Electrocardiogram
1. Atrial depolarization Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

begins Key
Wave of
depolarization
R
Wave of

2. Atrial depolarization repolarization

P P

complete (atria Q
S

contracted)
1 Atria begin depolarizing. 4 Ventricular depolarization complete.

3. Ventricles begin to
depolarize at apex; atria R

repolarize (atria relaxed) P P

Q
T

4. Ventricular depolarization 2 Atrial depolarization complete. 5 Ventricular repolarization begins at apex

complete (ventricles and progresses superiorly.

contracted) R R

5. Ventricles begin to
P P T

Q Q

repolarize at apex
S

3 Ventricular depolarization begins at apex 6 Ventricular repolarization complete; heart

and progresses superiorly as atria repolarize. is ready for the next cycle.

6. Ventricular repolarization
complete (ventricles
relaxed) Figure 19.16
19-71
 ECGs: Normal and Abnormal
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

• Abnormalities in
conduction pathways

(a) Sinus rhythm (normal)

• Myocardial infarction

• Heart enlargement

• Electrolyte and
(b) Nodal rhythm—no SA node activity
hormone imbalances
Figure 19.17a,b
19-72
 Blood Flow, Heart Sounds,
and the Cardiac Cycle
• Expected Learning Outcomes
– Explain why blood pressure is expressed in millimeters of
mercury.
– Describe how changes in blood pressure operate the
heart valves.
– Explain what causes the sounds of the heartbeat.
– Describe in detail one complete cycle of heart contraction
and relaxation.
– Relate the events of the cardiac cycle to the volume of
blood entering and leaving the heart.

19-73
 Blood Flow, Heart Sounds,
and the Cardiac Cycle

• Cardiac cycle—one complete contraction and relaxation

of all four chambers of the heart
• Atrial systole (contraction) occurs while ventricles are in
diastole (relaxation)
• Atrial diastole occurs while ventricles in systole
• Quiescent period— all four chambers relaxed at same
time
• Questions to consider: How does pressure affect blood
flow? How are heart sounds produced?

19-74
 Principles of Pressure and Flow
• Two main variables govern fluid
movement Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

– Pressure causes a fluid to flow

(fluid dynamics) 1 Volume
increases

• Pressure gradient—pressure difference 2 Pressure

decreases

3 Air flows in

between two points

P1
P2>P1
Pressure gradient
P2

• Measured in mm Hg (a)

with a manometer or
sphygmomanometer
1 Volume
decreases

2 Pressure
increases

3 Air flows out

P1

– Resistance opposes fluid flow P2

P2<P1

Pressure gradient

(b)

• Great vessels have positive blood

pressure
Figure 19.18
• Ventricular pressure must rise above
this resistance for blood to flow into
19-75
great vessels
 Pressure Gradients and Flow

• Fluid flows only if it is subjected to more

pressure at one point than another which
creates a pressure gradient
– Fluid flows down its pressure gradient from high
pressure to low pressure

19-76
 Pressure Gradients and Flow
• Events occurring on left side of heart
– When ventricle relaxes and expands, its internal
pressure falls
– If bicuspid valve is open, blood flows into left ventricle
– When ventricle contracts, internal pressure rises
– AV valves close and the aortic valve is pushed open
and blood flows into aorta from left ventricle

• Opening and closing of valves are governed by

these pressure changes
– AV valves limp when ventricles relaxed
– Semilunar valves under pressure from blood in vessels
when ventricles relaxed
19-77
Operation of the Heart Valves
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Atrium

Atrioventricular
valve

Ventricle

Atrioventricular valves open Atrioventricular valves closed

(a)

Aorta
Figure 19.19
Pulmonary
artery

Semilunar
valve

19-78
Semilunar valves open Semilunar valves closed
(b)
 Valvular Insufficiency Disorders

• Valvular insufficiency (incompetence)—any

failure of a valve to prevent reflux (regurgitation),
the backward flow of blood
– Valvular stenosis: cusps are stiffened and opening is
constricted by scar tissue
• Result of rheumatic fever, autoimmune attack on the mitral and
aortic valves
• Heart overworks and may become enlarged
• Heart murmur—abnormal heart sound produced by
regurgitation of blood through incompetent valves

19-79
 Valvular Insufficiency Disorders
Cont.

– Mitral valve prolapse: insufficiency in which one or both

mitral valve cusps bulge into atria during ventricular
contraction
• Hereditary in 1 out of 40 people
• May cause chest pain and shortness of breath

19-80
 Heart Sounds
• Auscultation—listening to sounds made by body

• First heart sound (S1), louder and longer “lubb,”

occurs with closure of AV valves, turbulence in the
bloodstream, and movements of the heart wall
• Second heart sound (S2), softer and sharper “dupp,”
occurs with closure of semilunar valves, turbulence in
the bloodstream, and movements of the heart wall
• S3—rarely heard in people over 30

• Exact cause of each sound is not known with

certainty 19-81
 Phases of the Cardiac Cycle

• Ventricular filling
• Isovolumetric contraction
• Ventricular ejection
• Isovolumetric relaxation
• All the events in the cardiac cycle are completed
in less than 1 second!

19-82
 Phases of the Cardiac Cycle
• Ventricular filling
– During diastole, ventricles expand
– Their pressure drops below that of the atria
– AV valves open and blood flows into the ventricles
• Ventricular filling occurs in three phases
– Rapid ventricular filling: first one-third
• Blood enters very quickly
– Diastasis: second one-third
• Marked by slower filling
• P wave occurs at the end of diastasis
– Atrial systole: final one-third
• Atria contract

19-83
 Phases of the Cardiac Cycle

• End-diastolic volume (EDV)—amount of blood

contained in each ventricle at end of ventricular
filling (130 mL)
• Isovolumetric contraction
– Atria repolarize and relax
– Remain in diastole for the rest of the cardiac cycle
– Ventricles depolarize, create the QRS complex, and
begin to contract

19-84
 Phases of the Cardiac Cycle

• AV valves close as ventricular blood surges back

against the cusps
• Heart sound S1 occurs at the beginning of this
phase
• “Isovolumetric” because even though the ventricles
contract, they do not eject blood
– Because pressure in the aorta (80 mm Hg) and in the
pulmonary trunk (10 mm Hg) is still greater than in the
ventricles
• Cariocytes exert force, but with all four valves
closed, the blood cannot go anywhere

19-85
 Phases of the Cardiac Cycle
• Ventricular ejection of blood begins when the
ventricular pressure exceeds arterial pressure and
forces semilunar valves open
– Pressure peaks in left ventricle at about 120 mm Hg
and 25 mm Hg in the right
• Blood spurts out of each ventricle rapidly at first—
rapid ejection
• Then more slowly under reduced pressure—
reduced ejection
• Ventricular ejections last about 200 to 250 ms
– Corresponds to the plateau phase of the cardiac
action potential
19-86
 Phases of the Cardiac Cycle

• Ventricular ejection (cont.)

• T wave occurs late in this phase
• Stroke volume (SV) of about 70 mL of blood is
ejected of the 130 mL in each ventricle
– Ejection fraction of about 54%
– As high as 90% in vigorous exercise
• End-systolic volume (ESV)—the 60 mL of blood
left behind

19-87
 Phases of the Cardiac Cycle
• Isovolumetric relaxation is early ventricular
diastole
– When T wave ends and ventricles begin to expand

• Elastic recoil and expansion would cause pressure

to drop rapidly and suck blood into the ventricles
– Blood from the aorta and pulmonary trunk briefly flows
backward
– Filling the semilunar valves and closing the cusps
– Creates a slight pressure rebound that appears as the
dicrotic notch of the aortic pressure curve

19-88
 Phases of the Cardiac Cycle
• Isovolumetric relaxation (cont.)
– Heart sound S2 occurs as blood rebounds from the
closed semilunar valves and the ventricle expands
– “Isovolumetric” because semilunar valves are closed
and AV valves have not yet opened
• Ventricles are therefore taking in no blood
– When AV valves open, ventricular filling begins again

19-89
 Phases of the Cardiac Cycle
• In a resting person
– Atrial systole lasts about 0.1 second
– Ventricular systole lasts about 0.3 second
– Quiescent period, when all four chambers are in
diastole, 0.4 second

• Total duration of the cardiac cycle is therefore

0.8 second in a heart beating 75 bpm

19-90
 Events of the Cardiac Cycle
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Diastole Systole Diastole

120 Aortic

100
pressure
• Ventricular filling
Pressure (mm Hg)

80 Aortic
Aortic valve
valve
Left closes
60 opens
ventricular (dicrotic notch)
pressure
AV
40 AV
valve
Left atrial

• Isovolumetric
closes valve
20 pressure opens
0

contraction
120 End-diastolic
volume (mL)

volume
Ventricular

90

60 End-systolic volume
R R
T
P P
ECG
Q
S
Q
S
• Ventricular ejection
Heart
sounds
S2 S3 S1 S2 S3 S1

Phase of
cardiac cycle
1a 1b 1c 2 3 4 1a 1b 1c 2 • Isovolumetric
0 .2 .4 .6 .8 .2 .4

Ventricular filling
Time (sec)

2 3 4
relaxation
1a Rapid filling 1c Atrial systole Isovolumetric Ventricular Isovolumetric
1b Diastasis contraction ejection relaxation

19-91
Figure 19.20
 Overview of Volume Changes
End-systolic volume (ESV) 60 mL
Passively added to ventricle
during atrial diastole +30 mL
Added by atrial systole +40 mL
Total: End-diastolic volume (EDV) 130 mL
Stroke volume (SV) ejected
by ventricular systole −70 mL
Leaves: End-systolic volume (ESV) 60 mL
Both ventricles must eject same amount of blood

19-92
 Overview of Volume Changes
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

1 Right ventricular
output exceeds left
ventricular output. • If the left ventricle
2 Pressure backs up.

3 Fluid accumulates in
pumps less blood
pulmonary tissue. 1 than the right, the
blood pressure
backs up into the
2
3 lungs and causes
pulmonary edema

(a) Pulmonary edema

Figure 19.21a 19-93

 Overview of Volume Changes
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

1 Left ventricular
output exceeds right
ventricular output. • If the right ventricle
2 Pressure backs up.
3 Fluid accumulates in
pumps less blood than
systemic tissue.
the left, pressure
backs up in the
systemic circulation
and causes systemic
edema
2 1

(b) Systemic edema

3
Figure 19.21b
19-94
 Overview of Volume Changes

• Congestive heart failure (CHF)—results from

the failure of either ventricle to eject blood
effectively
– Usually due to a heart weakened by myocardial
infarction, chronic hypertension, valvular
insufficiency, or congenital defects in heart
structure

19-95
 Overview of Volume Changes
• Left ventricular failure—blood backs up into the
lungs causing pulmonary edema
– Shortness of breath or sense of suffocation
• Right ventricular failure—blood backs up in the
vena cava causing systemic or generalized
edema
– Enlargement of the liver, ascites (pooling of fluid in
abdominal cavity), distension of jugular veins, swelling
of the fingers, ankles, and feet
• Eventually leads to total heart failure

19-96
 Cardiac Output
• Expected Learning Outcomes
– Define cardiac output and explain its importance.
– Identify the factors that govern cardiac output.
– Discuss some of the nervous and chemical factors that
alter heart rate, stroke volume, and cardiac output.
– Explain how the right and left ventricles achieve balanced
output.
– Describe some effects of exercise on cardiac output.

19-97
 Cardiac Output
• Cardiac output (CO)—the amount ejected by
ventricle in 1 minute
• Cardiac output = heart rate x stroke volume
– About 4 to 6 L/min at rest
– A RBC leaving the left ventricle will arrive back at the
left ventricle in about 1 minute
– Vigorous exercise increases CO to 21 L/min for a fit
person and up to 35 L/min for a world-class athlete

19-98
 Cardiac Output

Cont.
• Cardiac reserve—the difference between a
person’s maximum and resting CO
– Increases with fitness, decreases with disease

• To keep cardiac output constant as we increase in

age, the heart rate increases as the stroke
volume decreases

19-99
 Heart Rate

• Pulse—surge of pressure produced by each

heart beat that can be felt by palpating a
superficial artery with the fingertips
– Infants have HR of 120 bpm or more
– Young adult females average 72 to 80 bpm
– Young adult males average 64 to 72 bpm
– Heart rate rises again in the elderly

19-100
 Heart Rate
• Tachycardia—resting adult heart rate above 100
bpm
– Stress, anxiety, drugs, heart disease, or fever
– Loss of blood or damage to myocardium
• Bradycardia—resting adult heart rate of less than
60 bpm
– In sleep, low body temperature, and endurance-trained
athletes
• Positive chronotropic agents—factors that raise
the heart rate
• Negative chronotropic agents—factors that
lower heart rate
19-101
 Chronotropic Effects of the
Autonomic Nervous System
• Autonomic nervous system does not initiate the
heartbeat, it modulates rhythm and force
• Cardiac centers in the reticular formation of
the medulla oblongata initiate autonomic output
to the heart
• Cardiostimulatory effect—some neurons of the
cardiac center transmit signals to the heart by way
of sympathetic pathways
• Cardioinhibitory effect—others transmit
parasympathetic signals by way of the vagus
nerve
19-102
 Chronotropic Effects of the
Autonomic Nervous System
• Sympathetic postganglionic fibers are
adrenergic
– They release norepinephrine
– Bind to β-adrenergic fibers in the heart
– Activate cAMP second-messenger system in
cardiocytes and nodal cells
– Lead to opening of Ca2+ channels in plasma
membrane

19-103
 Chronotropic Effects of the
Autonomic Nervous System
• Sympathetic postganglionic fibers are adrenergic
(cont.)
– Increased Ca2+ inflow accelerated depolarization of SA
node
– cAMP accelerates the uptake of Ca2+ by the
sarcoplasmic reticulum allowing the cardiocytes to
relax more quickly
– By accelerating both contraction and relaxation,
norepinephrine and cAMP increase the heart rate as high
as 230 bpm
– Diastole becomes too brief for adequate filling
– Both stroke volume and cardiac output are reduced

19-104
 Chronotropic Effects of the
Autonomic Nervous System

• Parasympathetic vagus nerves have

cholinergic, inhibitory effects on the SA and AV
nodes
– Acetylcholine (ACh) binds to muscarinic receptors
– Opens K+ gates in the nodal cells
– As K+ leaves the cells, they become hyperpolarized
and fire less frequently
– Heart slows down
– Parasympathetics work on the heart faster than
sympathetics
• Parasympathetics do not need a second-messenger
system
19-105
 Chronotropic Effects of the
Autonomic Nervous System

• Without influence from the cardiac centers, the

heart has an intrinsic “natural” firing rate of
100 bpm
• Vagal tone—holds down this heart rate to 70 to
80 bpm at rest
– Steady background firing rate of the vagus nerves

19-106
 Chronotropic Effects of the
Autonomic Nervous System
• Cardiac centers in the medulla receive input
from many sources and integrate it into the
“decision” to speed or slow the heart
• Higher brain centers affect heart rate
– Cerebral cortex, limbic system, hypothalamus
• Sensory or emotional stimuli

19-107
 Chronotropic Effects of the
Autonomic Nervous System
• Medulla also receives input from muscles, joints,
arteries, and brainstem
– Proprioceptors in the muscles and joints
• Inform cardiac center about changes in activity, HR
increases before metabolic demands of muscle arise

19-108
 Chronotropic Effects of the
Autonomic Nervous System

Cont.
– Baroreceptors signal cardiac center
• Pressure sensors in aorta and internal carotid arteries
• Blood pressure decreases, signal rate drops, cardiac
center increases heart rate
• If blood pressure increases, signal rate rises, cardiac
center decreases heart rate

19-109
 Chronotropic Effects of the
Autonomic Nervous System
• Medulla also receives input from muscles, joints,
arteries, and brainstem (cont.)
– Chemoreceptors
• In aortic arch, carotid arteries, and medulla oblongata
• Sensitive to blood pH, CO2 and O2 levels
• More important in respiratory control than cardiac control
– If CO2 accumulates in blood or CSF (hypercapnia), reacts
with water and causes increase in H+ levels
– H+ lowers the pH of the blood possibly creating acidosis (pH
< 7.35)

19-110
 Chronotropic Effects of the
Autonomic Nervous System

Cont.
• Hypercapnia and acidosis stimulate the cardiac center to
increase heart rate
• Also respond to hypoxemia—oxygen deficiency in the
blood that usually slows down the heart

– Chemoreceptors (cont.)
• Chemoreflexes and baroreflexes—responses to
fluctuation in blood chemistry—are both negative
feedback loops

19-111
 Chronotropic Effects of Chemicals
• Chemicals affect heart rate as well as
neurotransmitters from cardiac nerves
– Blood-borne adrenal catecholamines (NE and
epinephrine) are potent cardiac stimulants

• Drugs that stimulate heart

– Nicotine stimulates catecholamine secretion
– Thyroid hormone increases number of adrenergic
receptors on heart so more responsive to sympathetic
stimulation
– Caffeine inhibits cAMP breakdown prolonging
adrenergic effect
19-112
 Chronotropic Effects of Chemicals
• Electrolytes
– K+ has greatest chronotropic effect
• Hyperkalemia—excess K+ in cardiocytes
– Myocardium less excitable, heart rate slows and
becomes irregular
• Hypokalemia—deficiency K+ in cardiocytes
– Cells hyperpolarized, require increased stimulation

– Calcium
• Hypercalcemia—excess of Ca2+
– Decreases heart rate and contraction strength
• Hypocalcemia—deficiency of Ca2+
– Increases heart rate and contraction strength

19-113
 Stroke Volume

• The other factor in cardiac output, besides heart

rate, is stroke volume (SV)
• Three variables govern stroke volume
– Preload
– Contractility
– Afterload

• Examples
– Increased preload or contractility increases stroke
volume
– Increased afterload decreases stroke volume 19-114
 Preload
• Preload—the amount of tension in ventricular
myocardium immediately before it begins to
contract
– Increased preload causes increased force of
contraction
– Exercise increases venous return and stretches
myocardium
– Cardiocytes generate more tension during
contraction
– Increased cardiac output matches increased
venous return
19-115
 Preload

• Frank–Starling law of the heart: SV  EDV

– Stroke volume is proportional to the end diastolic
volume
– Ventricles eject as much blood as they receive
– The more they are stretched, the harder they
contract

19-116
 Contractility
• Contractility refers to how hard the myocardium
contracts for a given preload

• Positive inotropic agents increase contractility

– Hypercalcemia can cause strong, prolonged
contractions and even cardiac arrest in systole
– Catecholamines increase calcium levels
– Glucagon stimulates cAMP production
– Digitalis raises intracellular calcium levels and
contraction strength

19-117
 Contractility
• Negative inotropic agents reduce contractility
– Hypocalcemia can cause weak, irregular
heartbeat and cardiac arrest in diastole
– Hyperkalemia reduces strength of myocardial
action potentials and the release of Ca2+ into the
sarcoplasm
– Vagus nerves have effect on atria but too few
nerves to ventricles for a significant effect

19-118
 Afterload

• Afterload—the blood pressure in the aorta and

pulmonary trunk immediately distal to the
semilunar valves
– Opposes the opening of these valves
– Limits stroke volume
• Hypertension increases afterload and opposes
ventricular ejection

19-119
 Afterload

• Anything that impedes arterial circulation can also

increase afterload
– Lung diseases that restrict pulmonary circulation
– Cor pulmonale: right ventricular failure due to
obstructed pulmonary circulation
• In emphysema, chronic bronchitis, and black lung disease

19-120
 Exercise and Cardiac Output
• Exercise makes the heart work harder and
increases cardiac output
• Proprioceptors signal cardiac center
– At beginning of exercise, signals from joints and
muscles reach the cardiac center of brain
– Sympathetic output from cardiac center increases
cardiac output

• Increased muscular activity increases venous

return
– Increases preload and ultimately cardiac output

19-121
 Exercise and Cardiac Output

• Increases in heart rate and stroke volume cause

an increase in cardiac output
• Exercise produces ventricular hypertrophy
– Increased stroke volume allows heart to beat more
slowly at rest
– Athletes with increased cardiac reserve can tolerate
more exertion than a sedentary person

19-122
 Coronary Artery Disease

• Coronary artery disease (CAD)—a constriction

of the coronary arteries
– Usually the result of atherosclerosis: an
accumulation of lipid deposits that degrade the arterial
wall and obstruct the lumen
– Endothelium damaged by hypertension, virus,
diabetes, or other causes

19-123
 Coronary Artery Disease
Cont.
– Monocytes penetrate walls of damaged vessels and
transform into macrophages
• Absorb cholesterol and fats to be called foam cells
– Look like fatty streak on vessel wall
– Can grow into atherosclerotic plaques (atheromas)

– Platelets adhere to damaged areas and secrete platelet-

derived growth factor
• Attracting immune cells and promoting mitosis of muscle
and fibroblasts, and the deposition of collagen

• Bulging mass grows to obstruct arterial lumen

19-124
 Coronary Artery Disease
• Causes angina pectoris, intermittent chest pain,
by obstructing 75% or more of the blood flow
• Immune cells of atheroma stimulate inflammation
– May rupture, resulting in traveling clots or fatty emboli

• Cause coronary artery spasms due to lack of

secretion of nitric oxide (vasodilator)
• Inflammation transforms atheroma into a
hardened complicated plaque called
arteriosclerosis

19-125
 Coronary Artery Disease

• Major risk factor for atherosclerosis is excess of

low-density lipoprotein (LDL) in the blood
combined with defective LDL receptors in the
arterial walls
– Protein-coated droplets of cholesterol, neutral fats, free
fatty acids, and phospholipids
• Most cells have LDL receptors that take up these
droplets from blood by receptor-mediated
endocytosis
– Dysfunctional receptors in arterial cells accumulate
excess cholesterol
19-126
 Coronary Artery Disease
• Unavoidable risk factors: heredity, aging, being
male
• Preventable risk factors: obesity, smoking, lack of
exercise, anxious personality, stress, aggression,
and diet
• Treatment
– Coronary bypass surgery
• Great saphenous vein
– Balloon angioplasty
– Laser angioplasty

19-127
19-128