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The Cardiovascular System: The Heart
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Heart Anatomy
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 18.1
Heart: Anatomy

Approximately the size of your fist

Location


Superior surface of diaphragm

Left of the midline

Anterior to the vertebral column, posterior to the sternum
Pericardium – a double-walled sac around the heart composed of:

A superficial fibrous pericardium

A deep two-layer serous pericardium

The parietal layer lines the internal surface of the fibrous
pericardium

The visceral layer or epicardium lines the surface of the heart

They are separated by the fluid-filled pericardial cavity
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Pericardial Layers of the Heart
The pericardium:
Protects and anchors the heart
Prevents overfilling of the heart with blood
Allows for the heart to work in a relatively friction-free environment
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Heart Wall




Epicardium – visceral layer
of the serous pericardium
Myocardium – cardiac
muscle layer forming the
bulk of the heart
Fibrous skeleton of the heart
– crisscrossing, interlacing
layer of connective tissue
Endocardium – endothelial
layer of the inner
myocardial surface
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Four chambers


Two atria

Separated internally by the interatrial septum

Coronary sulcus (atrioventricular groove)
encircles the junction of the atria and ventricles

Auricles increase atrial volume
Two ventricles

Separated by the interventricular septum

Anterior and posterior interventricular sulci mark
the position of the septum externally
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Brachiocephalic
trunk
Superior
vena cava
Left common
carotid artery
Left
subclavian artery
Aortic arch
Right
pulmonary artery
Ligamentum
arteriosum
Left pulmonary artery
Ascending
aorta
Pulmonary trunk
Right
pulmonary veins
Right atrium
Right coronary
artery (in coronary
sulcus)
Anterior
cardiac vein
Right ventricle
Marginal artery
Small cardiac vein
Inferior
vena cava
(b)
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Left pulmonary veins
Left atrium
Auricle
Circumflex
artery
Left coronary
artery (in coronary
sulcus)
Left ventricle
Great cardiac vein
Anterior
interventricular artery
(in anterior
interventricular sulcus)
Apex
Figure 18.4b
Atria: The
Receiving
Chambers



Walls are ridged by pectinate
muscles
Ventricles: The
Discharging
Chambers

Walls are ridged by trabeculae
carneae

Papillary muscles project into the
ventricular cavities

Vessel leaving the right ventricle
Vessels entering right atrium

Superior vena cava

Inferior vena cava

Coronary sinus

Vessels entering left atrium

Right and left pulmonary
veins
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
Pulmonary trunk
Vessel leaving the left ventricle

Aorta
External Heart: Major Vessels of the Heart
(Anterior View)


Vessels returning blood to the heart include:

Superior and inferior venae cavae

Right and left pulmonary veins
Vessels conveying blood away from the heart:




Pulmonary trunk, which splits into right and left pulmonary
arteries
Ascending aorta (three branches) – brachiocephalic, left common
carotid, and subclavian arteries
Arteries – right and left coronary (in atrioventricular groove), marginal,
circumflex, and anterior interventricular arteries
Veins – small cardiac, anterior cardiac, and great cardiac veins
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External Heart: Major Vessels of the Heart
(Posterior View)


Vessels returning blood to the heart include:

Right and left pulmonary veins

Superior and inferior venae cavae
Vessels conveying blood away from the heart
include:

Aorta

Right and left pulmonary arteries
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External Heart: Vessels that Supply/Drain the
Heart (Posterior View)


Arteries – right coronary artery (in atrioventricular
groove) and the posterior interventricular artery (in
interventricular groove)
Veins – great cardiac vein, posterior vein to left
ventricle, coronary sinus, and middle cardiac vein
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Aorta
Left
pulmonary artery
Left
pulmonary veins
Auricle
of left atrium
Left atrium
Superior
vena cava
Right
pulmonary artery
Right
pulmonary veins
Right atrium
Great cardiac vein
Inferior
vena cava
Posterior vein
of left ventricle
Right coronary
artery (in coronary
sulcus)
Coronary sinus
Apex
Posterior
interventricular artery
(in posterior
interventricular sulcus)
Middle cardiac vein
(d)
Right ventricle
Left ventricle
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Figure 18.4d
Aorta
Superior vena cava
Right
pulmonary artery
Pulmonary trunk
Right atrium
Right
pulmonary veins
Fossa
ovalis
Pectinate
muscles
Tricuspid
valve
Right ventricle
Chordae
tendineae
Trabeculae
carneae
Inferior
vena cava
(e)
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Left
pulmonary artery
Left atrium
Left
pulmonary veins
Mitral
(bicuspid) valve
Aortic
valve
Pulmonary
valve
Left ventricle
Papillary
muscle
Interventricular
septum
Myocardium
Visceral
pericardium
Endocardium
Figure 18.4e
Atria of the Heart

Atria are the receiving chambers of the heart

Each atrium has a protruding auricle

Pectinate muscles mark atrial walls

Blood enters right atria from superior and inferior
venae cavae and coronary sinus

Blood enters left atria from pulmonary veins
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Ventricles of the Heart

Ventricles are the discharging chambers of the
heart

Papillary muscles and trabeculae carneae muscles
mark ventricular walls

Right ventricle pumps blood into the pulmonary
trunk

Left ventricle pumps blood into the aorta
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Right and Left Ventricles
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Figure 18.6
Pathway of Blood Through the Heart and
Lungs


Right atrium  tricuspid valve  right ventricle
Right ventricle  pulmonary semilunar valve 
pulmonary arteries  lungs

Lungs  pulmonary veins  left atrium

Left atrium  bicuspid valve  left ventricle

Left ventricle  aortic semilunar valve  aorta

Aorta  systemic circulation
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Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 18.5
Coronary Circulation: Arterial Supply
Coronary
circulation is the
functional blood
supply to the
heart muscle
itself
Collateral routes
ensure blood
delivery to heart
even if major
vessels are
occluded
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Coronary Circulation: Venous Supply
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Homeostatic Imbalances


Angina pectoris

Thoracic pain caused by a fleeting deficiency in
blood delivery to the myocardium

Cells are weakened
Myocardial infarction (heart attack)

Prolonged coronary blockage

Areas of cell death are repaired with
noncontractile scar tissue
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Heart Valves

Heart valves ensure unidirectional blood flow
through the heart

Atrioventricular (AV) valves lie between the atria
and the ventricles

AV valves prevent backflow into the atria when
ventricles contract

Chordae tendineae anchor AV valves to papillary
muscles
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Heart Valves

Aortic semilunar valve lies between the left
ventricle and the aorta

Pulmonary semilunar valve lies between the right
ventricle and pulmonary trunk

Semilunar valves prevent backflow of blood into
the ventricles
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Heart Valves
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Figure 18.8a, b
Heart Valves
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Figure 18.8c, d
Atrioventricular Valve Function
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Figure 18.9
Semilunar Valve Function
Review of the Heart Circuit
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Figure 18.10
Cardiac Intrinsic Conduction
Heart Function
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Figure 18.14a
Microscopic Anatomy of Cardiac Muscle

Cardiac muscle cells are striated, short, fat,
branched, and interconnected

Connective tissue matrix (endomysium) connects
to the fibrous skeleton

T tubules are wide but less numerous; SR is
simpler than in skeletal muscle

Numerous large mitochondria (25–35% of cell
volume)
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Cardiac Muscle Contraction

Depolarization of the heart is rhythmic and spontaneous

About 1% of cardiac cells have automaticity— (are self-excitable)

Gap junctions ensure the heart contracts as a unit

Long absolute refractory period (250 ms)

Depolarization opens voltage-gated fast Na+ channels in the sarcolemma

Reversal of membrane potential from –90 mV to +30 mV

Depolarization wave in T tubules causes the SR to release Ca2+

Depolarization wave also opens slow Ca2+ channels in the sarcolemma

Ca2+ surge prolongs the depolarization phase (plateau)

Ca2+ influx triggers opening of Ca2+-sensitive channels in the SR, which liberates bursts
of Ca2+

E-C coupling occurs as Ca2+ binds to troponin and sliding of the filaments begins

Duration of the AP and the contractile phase is much greater in cardiac muscle than in
skeletal muscle
Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated
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2006 Pearson Education, Inc., publishing as Benjamin Cummings
K+ ©channels

1 Depolarization is
2
Tension
development
(contraction)
3
1
Absolute
refractory
period
Time (ms)
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Tension (g)
Membrane potential (mV)
Action
potential
Plateau
due to Na+ influx through
fast voltage-gated Na+
channels. A positive
feedback cycle rapidly
opens many Na+
channels, reversing the
membrane potential.
Channel inactivation ends
this phase.
2 Plateau phase is
due to Ca2+ influx through
slow Ca2+ channels. This
keeps the cell depolarized
because few K+ channels
are open.
3 Repolarization is
due to Ca2+ channels
inactivating and K+
channels opening. This
allows K+ efflux, which
brings the membrane
potential back to its
resting voltage.
Figure 18.12
Heart Physiology: Intrinsic Conduction System

A network of noncontractile (autorhythmic) cells that
initiate and distribute impulses to coordinate the
depolarization and contraction of the heart

Initiate action potentials

Have unstable resting potentials called pacemaker
potentials

Use calcium influx (rather than sodium) for rising
phase of the action potential

Repolarization results from inactivation of Ca2+
channels and opening of voltage-gated K+ channels
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Pacemaker and Action Potentials of the Heart
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Figure 18.13
Cardiac Membrane Potential: Cardiomyocytes
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Figure 18.12
Superior vena cava
Right atrium
1 The sinoatrial (SA)
node (pacemaker)
generates impulses.
Internodal pathway
2 The impulses
pause (0.1 s) at the
atrioventricular
(AV) node.
3 The atrioventricular
(AV) bundle
connects the atria
to the ventricles.
4 The bundle branches
conduct the impulses
through the
interventricular septum.
5 The Purkinje fibers
Left atrium
Purkinje
fibers
Interventricular
septum
depolarize the contractile
cells of both ventricles.
(a) Anatomy of the intrinsic conduction system showing the
sequence of electrical excitation
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Figure 18.14a
Heart Physiology: Sequence of Excitation

Sinoatrial (SA) node generates impulses about 75
times/minute

Atrioventricular (AV) node delays the impulse approximately
0.1 second

Impulse passes from atria to ventricles via the
atrioventricular bundle (bundle of His)

AV bundle splits into two pathways in the interventricular
septum (bundle branches)

Bundle branches carry the impulse toward the apex of
the heart

Purkinje fibers carry the impulse to the heart apex and
ventricular walls
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Homeostatic Imbalances
Defects in the intrinsic conduction system may result in
1.
Arrhythmias: irregular heart rhythms
2.
Uncoordinated atrial and ventricular contractions
3.
Fibrillation: rapid, irregular contractions; useless for pumping blood
4.
Defective SA node may result in Ectopic focus: abnormal pacemaker
takes over
5.
If AV node takes over, there will be a junctional rhythm (40–60 bpm)
6.
Defective AV node may result in

Partial or total heart block

Few or no impulses from SA node reach the ventricles
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The vagus nerve
(parasympathetic)
decreases heart rate.
Dorsal motor nucleus of vagus
Cardioinhibitory center
Medulla oblongata
Cardioacceleratory
center
Sympathetic trunk ganglion
Thoracic spinal cord
Sympathetic trunk
Sympathetic cardiac
nerves increase heart rate
and force of contraction.
AV node
SA node
Parasympathetic fibers
Sympathetic fibers
Interneurons
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Figure 18.15
Electrocardiography

Electrocardiogram (ECG or EKG): a composite
of all the action potentials generated by nodal
and contractile cells at a given time

Three waves
1.
P wave: depolarization of SA node
2.
QRS complex: ventricular depolarization
3.
T wave: ventricular repolarization
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QRS complex
Sinoatrial
node
Atrial
depolarization
Ventricular
depolarization
Ventricular
repolarization
Atrioventricular
node
P-Q
Interval
S-T
Segment
Q-T
Interval
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Figure 18.16
SA node
Depolarization
R
Repolarization
R
T
P
S
1 Atrial depolarization, initiated
by the SA node, causes the
P wave.
R
AV node
T
P
Q
Q
S
4 Ventricular depolarization
is complete.
R
T
P
T
P
Q
S
2 With atrial depolarization
complete, the impulse is
delayed at the AV node.
R
Q
S
5 Ventricular repolarization
begins at apex, causing the
T wave.
R
T
P
T
P
Q
S
3 Ventricular depolarization
begins at apex, causing the
QRS complex. Atrial
repolarization occurs.
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Q
S
6 Ventricular repolarization
is complete.
Figure 18.17
Electrocardiography
 Electrical activity is recorded by electrocardiogram
(ECG)

P wave corresponds to depolarization of SA node

QRS complex corresponds to ventricular
depolarization

T wave corresponds to ventricular repolarization

Atrial repolarization record is masked by the larger
QRS complex
Cardiac conduction system and its relationship with ECG
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(a) Normal sinus rhythm.
(b) Junctional rhythm. The SA
node is nonfunctional, P waves
are absent, and heart is paced by
the AV node at 40 - 60 beats/min.
(c) Second-degree heart block. (d) Ventricular fibrillation. These
chaotic, grossly irregular ECG
Some P waves are not conducted
deflections are seen in acute
through the AV node; hence more
heart attack and electrical shock.
P than QRS waves are seen. In
this tracing, the ratio of P waves
to QRS waves is mostly 2:1.
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Figure 18.18
Heart Sounds
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Figure 18.19
Heart Sounds


Heart sounds (lub-dup) are associated with closing of
heart valves

First sound occurs as AV valves close and signifies
beginning of systole

Second sound occurs when SL valves close at the
beginning of ventricular diastole
Cardiac cycle refers to all events associated with
blood flow through the heart

Systole – contraction of heart muscle

Diastole – relaxation of heart muscle
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Phases of the Cardiac Cycle

Ventricular filling – mid-to-late diastole

Heart blood pressure is low as blood enters atria
and flows into ventricles

AV valves are open, then atrial systole occurs
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Phases of the Cardiac Cycle

Ventricular systole

Atria relax

Rising ventricular pressure results in closing of AV
valves

Isovolumetric contraction phase

Ventricular ejection phase opens semilunar valves
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Phases of the Cardiac Cycle


Isovolumetric relaxation – early diastole

Ventricles relax

Backflow of blood in aorta and pulmonary trunk
closes semilunar valves
Dicrotic notch – brief rise in aortic pressure caused
by backflow of blood rebounding off semilunar
valves
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Figure 18.20
Cardiac Output (CO)

At rest

CO (ml/min) = HR (75 beats/min)  SV (70 ml/beat)
= 5.25 L/min

Maximal CO is 4–5 times resting CO in nonathletic people

Maximal CO may reach 35 L/min in trained athletes

Cardiac reserve: difference between resting and maximal
CO
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Regulation of Stroke Volume

SV = EDV – ESV

Three main factors affect SV

Preload

Contractility

Afterload
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Regulation of Stroke Volume

Preload: degree of stretch of cardiac muscle cells before
they contract (Frank-Starling law of the heart)

Cardiac muscle exhibits a length-tension relationship

At rest, cardiac muscle cells are shorter than optimal length

Slow heartbeat and exercise increase venous return

Increased venous return distends (stretches) the ventricles
and increases contraction force
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Regulation of Stroke Volume

Contractility: contractile strength at a given muscle length, independent
of muscle stretch and EDV

Positive inotropic agents increase contractility


Increased Ca2+ influx due to sympathetic stimulation

Hormones (thyroxine, glucagon, and epinephrine)
Negative inotropic agents decrease contractility

Acidosis

Increased extracellular K+

Calcium channel blockers

Afterload: pressure that must be overcome for ventricles to eject blood

Hypertension increases afterload, resulting in increased ESV and reduced SV
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Autonomic Nervous System Regulation

Sympathetic nervous system is activated by emotional or
physical stressors


Norepinephrine causes the pacemaker to fire more rapidly
(and at the same time increases contractility)
Parasympathetic nervous system opposes sympathetic effects

Acetylcholine hyperpolarizes pacemaker cells by opening K+
channels

The heart at rest exhibits vagal tone (parasympathetic)

Atrial (Bainbridge) reflex: a sympathetic reflex initiated by
increased venous return

Stretch of the atrial walls stimulates the SA node

Also stimulates atrial stretch receptors activating sympathetic
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Chemical Regulation of Heart Rate
Hormones
1.

Epinephrine from adrenal medulla enhances heart rate and contractility

Thyroxine increases heart rate and enhances the effects of
norepinephrine and epinephrine
Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be
maintained for normal heart function
2.
Other Factors that Influence Heart Rate

Age

Gender

Exercise

Body temperature
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Homeostatic Imbalances

Tachycardia: abnormally fast heart rate
(>100 bpm)


If persistent, may lead to fibrillation
Bradycardia: heart rate slower than 60 bpm

May result in grossly inadequate blood circulation

May be desirable result of endurance training
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Congestive Heart Failure (CHF)

Progressive condition where the CO is so low that
blood circulation is inadequate to meet tissue needs

Caused by

Coronary atherosclerosis

Persistent high blood pressure

Multiple myocardial infarcts

Dilated cardiomyopathy (DCM)
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Supplement

http://www.youtube.com/watch?v=D3ZDJgFDdk0

http://www.youtube.com/watch?v=H04d3rJCLCE&feature=related

http://www.youtube.com/watch?v=aWpuuNopsZI

http://www.youtube.com/watch?v=UsTorPkPDXE&feature=channel

http://www.youtube.com/watch?v=Lhl897Mz-h8&feature=related

http://www.youtube.com/watch?v=rguztY8aqpk&feature=related
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