Chapter 20:
The Cardiovascular System:
The Heart
Copyright 2009, John Wiley & Sons, Inc.
Anatomy of the Heart
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Located in the mediastinum – anatomical region
extending from the sternum to the vertebral column,
the first rib and between the lungs
Apex at tip of left ventricle
Base is posterior surface
Anterior surface deep to sternum and ribs
Inferior surface between apex and right border
Right border faces right lung
Left border (pulmonary border) faces left lung
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Pericardium
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Membrane surrounding and protecting the heart
Confines while still allowing free movement
2 main parts
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Fibrous pericardium – tough, inelastic, dense irregular
connective tissue – prevents overstretching, protection,
anchorage
Serous pericardium – thinner, more delicate membrane
– double layer (parietal layer fused to fibrous
pericardium, visceral layer also called epicardium)
Pericardial fluid reduces friction – secreted into
pericardial cavity
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Pericardium and Heart Wall
Copyright 2009, John Wiley & Sons, Inc.
Layers of the Heart Wall
1. Epicardium (external layer)
 Visceral layer of serous pericardium
 Smooth, slippery texture to outermost surface
Myocardium
2.
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95% of heart is cardiac muscle
Endocardium (inner layer)
3.
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Smooth lining for chambers of heart, valves and
continuous with lining of large blood vessels
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Chambers of the Heart
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2 atria – receiving chambers
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Auricles increase capacity
2 ventricles – pumping chambers
Sulci – grooves
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Contain coronary blood vessels
Coronary sulcus
Anterior interventricular sulcus
Posterior interventricular sulcus
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Structure of the Heart
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Right Atrium
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Receives blood from
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Interatrial septum has fossa ovalis
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Superior vena cava
Inferior vena cava
Coronary sinus
Remnant of foramen ovale
Blood passes through tricuspid valve (right
atrioventricular valve) into right ventricle
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Right Ventricle
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Forms anterior surface of heart
Trabeculae carneae – ridges formed by raised
bundles of cardiac muscle fiber
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Part of conduction system of the heart
Tricuspid valve connected to chordae tendinae
connected to papillary muscles
Interventricular septum
Blood leaves through pulmonary valve (pulmonary
semilunar valve) into pulmonary trunk and then
right and left pulmonary arteries
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Internal Anatomy of the Heart
Copyright 2009, John Wiley & Sons, Inc.
Left Atrium
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About the same thickness as right atrium
Receives blood from the lungs through pulmonary
veins
Passes through bicuspid/ mitral/ left
atrioventricular valve into left ventricle
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Left Ventricle
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Thickest chamber of the heart
Forms apex
Chordae tendinae attached to papillary muscles
Blood passes through aortic valve (aortic
semilunar valve) into ascending aorta
Some blood flows into coronary arteries,
remainder to body
During fetal life ductus arteriosus shunts blood
from pulmonary trunk to aorta (lung bypass)
closes after birth with remnant called ligamentum
arteriosum
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Myocardial thickness
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Thin-walled atria deliver blood under less
pressure to ventricles
Right ventricle pumps blood to lungs
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Left ventricle pumps blood to body
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Shorter distance, lower pressure, less resistance
Longer distance, higher pressure, more resistance
Left ventricle works harder to maintain same rate
of blood flow as right ventricle
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Fibrous skeleton
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Dense connective tissue that forms a structural foundation,
point of insertion for muscle bundles, and electrical
insulator between atria and ventricles
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Heart Valves and Circulation of Blood
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Atrioventricular valves
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Tricuspid and bicuspid valves
Atria contracts/ ventricle relaxed
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AV valve opens, cusps project into ventricle
In ventricle, papillary muscles are relaxed and chordae
tendinae slack
Atria relaxed/ ventricle contracts
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Pressure drives cusps upward until edges meet and
close opening
Papillary muscles contract tightening chordae tendinae
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Prevents regurgitation
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Semilunar valves
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Aortic and pulmonary valves
Valves open when pressure in ventricle exceeds
pressure in arteries
As ventricles relax, some backflow permitted but
blood fills valve cusps closing them tightly
No valves guarding entrance to atria
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As atria contracts, compresses and closes
opening
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Systemic and pulmonary circulation - 2 circuits in
series
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Systemic circuit
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Left side of heart
Receives blood from lungs
Ejects blood into aorta
Systemic arteries, arterioles
Gas and nutrient exchange in systemic capillaries
Systemic venules and veins lead back to right atrium
Pulmonary circuit
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Right side of heart
Receives blood from systemic circulation
Ejects blood into pulmonary trunk then pulmonary arteries
Gas exchange in pulmonary capillaries
Pulmonary veins takes blood to left atrium
Copyright 2009, John Wiley & Sons, Inc.
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Coronary circulation
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Myocardium has its own network of blood vessels
Coronary arteries branch from ascending aorta
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Anastomoses provide alternate routes or collateral
circuits
Allows heart muscle to receive sufficient oxygen even if
an artery is partially blocked
Coronary capillaries
Coronary veins
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Collects in coronary sinus
Empties into right atrium
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Coronary Circulation
Copyright 2009, John Wiley & Sons, Inc.
Cardiac Muscle Tissue and the Cardiac
Conduction System
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Histology
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Shorter and less circular than skeletal muscle fibers
Branching gives “stair-step” appearance
Usually one centrally located nucleus
Ends of fibers connected by intercalated discs
Discs contain desmosomes (hold fibers together) and gap
junctions (allow action potential conduction from one fiber
to the next)
Mitochondria are larger and more numerous than skeletal
muscle
Same arrangement of actin and myosin
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Autorhythmic Fibers
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Specialized cardiac muscle fibers
Self-excitable
Repeatedly generate action potentials that
trigger heart contractions
2 important functions
1. Act as pacemaker
2. Form conduction system
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Conduction system
1. Begins in sinoatrial (SA) node in right atrial wall
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Propagates through atria via gap junctions
Atria contact
2. Reaches atrioventricular (AV) node in interatrial septum
3. Enters atrioventricular (AV) bundle (Bundle of His)
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Only site where action potentials can conduct from atria to
ventricles due to fibrous skeleton
4. Enters right and left bundle branches which extends
through interventricular septum toward apex
5. Finally, large diameter Purkinje fibers conduct action
potential to remainder of ventricular myocardium
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Ventricles contract
Copyright 2009, John Wiley & Sons, Inc.
Frontal plane
Left atrium
Right
Right atrium
atrium
1 SINOATRIAL (SA) NODE
2 ATRIOVENTRICULAR
(AV) NODE
3 ATRIOVENTRICULAR (AV)
BUNDLE (BUNDLE OF HIS)
Left ventricle
4 RIGHT AND LEFT
BUNDLE BRANCHES
Right
Right ventricle
ventricle
5 PURKINJE FIBERS
Anterior view of frontal section
Conduction System
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SA node acts as natural pacemaker
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Faster than other autorhythmic fibers
Initiates 100 times per second
Nerve impulses from autonomic nervous
system (ANS) and hormones modify timing
and strength of each heartbeat
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Do not establish fundamental rhythm
Copyright 2009, John Wiley & Sons, Inc.
Action Potentials and Contraction
Action potential initiated by SA node spreads out
to excite “working” fibers called contractile fibers
1. Depolarization
2. Plateau
3. Repolarization
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Copyright 2009, John Wiley & Sons, Inc.
Action Potentials and Contraction
1. Depolarization – contractile fibers have stable
resting membrane potential
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Voltage-gated fast Na+ channels open – Na+ flows in
Then deactivate and Na+ inflow decreases
2. Plateau – period of maintained depolarization
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Due in part to opening of voltage-gated slow Ca2+
channels – Ca2+ moves from interstitial fluid into cytosol
Ultimately triggers contraction
Depolarization sustained due to voltage-gated K+
channels balancing Ca2+ inflow with K+ outflow
Copyright 2009, John Wiley & Sons, Inc.
Action Potentials and Contraction
3. Repolarization – recovery of resting membrane potential
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Resembles that in other excitable cells
Additional voltage-gated K+ channels open
Outflow K+ of restores negative resting membrane potential
Calcium channels closing
Refractory period – time interval during which
second contraction cannot be triggered
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Lasts longer than contraction itself
Tetanus (maintained contraction) cannot occur
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Blood flow would cease
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Action Potential in a ventricular contractile
fiber
Copyright 2009, John Wiley & Sons, Inc.
+ 20
2+
22 Plateau (maintained depolarization) due to Ca inflow
2+
when voltage-gated slow Ca channels open and
K+ outflow when some K+ channels open
0
–20
Membrane
potential (mV)
–40
– 60
33 Repolarization due to closure
of Ca2+ channels and K+ outflow
when additional voltage-gated
K+ channels open
11 Rapid depolarization due to
Na+ inflow when voltage-gated
fast Na+ channels open
– 80
–100
0.3 sec
Depolarization
Refractory period
Contraction
Repolarization
Electrocardiogram
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ECG or EKG
Composite record of
action potentials
produced by all the
heart muscle fibers
Compare tracings
from different leads
with one another and
with normal records
3 recognizable
waves
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P, QRS, and T
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Correlation of ECG Waves and Systole
Systole – contraction/ diastole – relaxation
1. Cardiac action potential arises in SA node
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P wave appears
2. Atrial contraction/ atrial systole
3. Action potential enters AV bundle and out over ventricles
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QRS complex
Masks atrial repolarization
4. Contraction of ventricles/ ventricular systole
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Begins shortly after QRS complex appears and continues
during S-T segment
5. Repolarization of ventricular fibers
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T wave
6. Ventricular relaxation/ diastole
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1 Depolarization of atrial
contractile fibers
produces P wave
6
diastole
6 Ventricular
(relaxation)
P
Action potential
in SA node
0
2 Atrial systole
(contraction)
0.2
Seconds
P
P
0
0.2
0.4
0.6
0.8
Seconds
5 Repolarization
of
5
ventricular contractile
fibers produces T
wave
0
0.2
Seconds
3 Depolarization of
ventricular contractile
fibers produces QRS
complex
T
P
0
0.2
0.4
Seconds
R
0.6
4 Ventricular
systole
(contraction)
P
Q
0
P
0
0.2
0.4
Seconds
S
0.2
0.4
Seconds
Cardiac Cycle
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All events associated with one heartbeat
Systole and diastole of atria and ventricles
In each cycle, atria and ventricles alternately
contract and relax
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During atrial systole, ventricles are relaxed
During ventricle systole, atria are relaxed
Forces blood from higher pressure to lower pressure
During relaxation period, both atria and ventricles
are relaxed
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The faster the heart beats, the shorter the relaxation period
Systole and diastole lengths shorten slightly
Copyright 2009, John Wiley & Sons, Inc.
R
T
P
(a) ECG
1
4
8
Q
Atrial depolarization
2
Begin atrial systole
3
End (ventricular) diastolic volume
4
Ventricular depolarization
5
Isovolumetric contraction
6
Begin ventricular ejection
7
End (ventricular) systolic volume
8
Begin ventricular repolarization
9
Isovolumetric relaxation
S
0.1
sec
Atrial
systole
0.3 sec
Ventricular
systole
120
0.4 sec
Relaxation
period
9
Dicrotic wave
100
Aortic
pressure
5
80
6
(b) Pressure
(mmHg)
1
Left
ventricular
pressure
60
40
Left atrial
pressure
10
20
2
0
(c) Heart sounds
S1
S2
S3
S4
3 End (ventricular) diastolic volume
130
10 Ventricular filling
Stroke
volume
(d) Volume in
ventricle (mL)
60
7
0
(e) Phases of the
cardiac cycle
Atrial
contraction
Isovolumetric
contraction
Ventricular
ejection
Isovolumetric
relaxation
Ventricular
filling
Atrial
contraction
Heart Sounds
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Auscultation
Sound of heartbeat comes
primarily from blood
turbulence caused by
closing of heart valves
4 heart sounds in each
cardiac cycle – only 2 loud
enough to be heard
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Lubb – AV valves close
Dupp – SL valves close
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Cardiac Output
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CO = volume of blood ejected from left (or right)
ventricle into aorta (or pulmonary trunk) each minute
CO = stroke volume (SV) x heart rate (HR)
In typical resting male
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5.25L/min = 70mL/beat x 75 beats/min
Entire blood volume flows through pulmonary and
systemic circuits each minute
Cardiac reserve – difference between maximum CO
and CO at rest
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Average cardiac reserve 4-5 times resting value
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Regulation of stroke volume
3 factors ensure left and right ventricles pump
equal volumes of blood
1. Preload
2. Contractility
3. Afterload
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Preload
Degree of stretch on the heart before it contracts
Greater preload increases the force of
contraction
Frank-Starling law of the heart – the more the
heart fills with blood during diastole, the greater
the force of contraction during systole
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Preload proportional to end-diastolic volume (EDV)
2 factors determine EDV
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1.
2.
Duration of ventricular diastole
Venous return – volume of blood returning to right
ventricle
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Contractility
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Strength of contraction at any given preload
Positive inotropic agents increase contractility
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Often promote Ca2+ inflow during cardiac action potential
Increases stroke volume
Epinephrine, norepinephrine, digitalis
Negative inotropic agents decrease contractility
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Anoxia, acidosis, some anesthetics, and increased K+ in
interstitial fluid
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Afterload
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Pressure that must be overcome before a
semilunar valve can open
Increase in afterload causes stroke volume to
decrease
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Blood remains in ventricle at the end of systole
Hypertension and atherosclerosis increase
afterload
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Regulation of Heart Beat
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Cardiac output depends on heart rate and stroke
volume
Adjustments in heart rate important in short-term
control of cardiac output and blood pressure
Autonomic nervous system and epinephrine/
norepinephrine most important
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Autonomic regulation
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Originates in cardiovascular center of medulla oblongata
Increases or decreases frequency of nerve impulses in
both sympathetic and parasympathetic branches of ANS
Noreprinephrine has 2 separate effects
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In SA and AV node speeds rate of spontaneous depolarization
In contractile fibers enhances Ca2+ entry increasing
contractility
Parasympathetic nerves release acetylcholine which
decreases heart rate by slowing rate of spontaneous
depolarization
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Nervous System Control of the Heart
Copyright 2009, John Wiley & Sons, Inc.
Chemical regulation of heart rate
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Hormones
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Epinephrine and norepinephrine increase heart rate and
contractility
Thyroid hormones also increase heart rate and
contractility
Cations
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Ionic imbalance can compromise pumping effectiveness
Relative concentration of K+, Ca2+ and Na+ important
Copyright 2009, John Wiley & Sons, Inc.
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End of Chapter 20
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