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CHAPTER
Elaine N. Marieb
Katja Hoehn
18
PART A
Human
Anatomy
& Physiology
SEVENTH EDITION
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
The
Cardiovascular
System: The
Heart
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
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Heart Anatomy
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Figure 18.1
Pericardial Layers of the Heart
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Figure 18.2
Cardiac Muscle Bundles
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Figure 18.3
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
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Figure 18.5
Coronary Circulation

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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Heart Valves
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Figure 18.8c, d
Atrioventricular Valve Function
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Figure 18.9
Semilunar Valve Function
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Figure 18.10
Microscopic Anatomy of Heart Muscle

Cardiac muscle is striated, short, fat, branched, and
interconnected

The connective tissue endomysium acts as both
tendon and insertion

Intercalated discs anchor cardiac cells together and
allow free passage of ions

Heart muscle behaves as a functional syncytium
InterActive Physiology ®:
Anatomy Review: The Heart, pages 3–7
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Microscopic Anatomy of Cardiac Muscle
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Figure 18.11
Cardiac Muscle Contraction


Heart muscle:

Is stimulated by nerves and is self-excitable
(automaticity)

Contracts as a unit

Has a long (250 ms) absolute refractory period
Cardiac muscle contraction is similar to skeletal
muscle contraction
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Heart Physiology: Intrinsic Conduction
System

Autorhythmic cells:

Initiate action potentials

Have unstable resting potentials called pacemaker
potentials

Use calcium influx (rather than sodium) for rising
phase of the action potential
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Pacemaker and Action Potentials of the Heart
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Figure 18.13
Cardiac Membrane Potential
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Figure 18.12
Cardiac Intrinsic Conduction
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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)
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Heart Physiology: Sequence of Excitation

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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Heart Excitation Related to ECG
SA node generates impulse;
atrial excitation begins
SA node
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Figure 18.17
Heart Excitation Related to ECG
Impulse delayed
at AV node
AV node
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Figure 18.17
Heart Excitation Related to ECG
Impulse passes to
heart apex; ventricular
excitation begins
Bundle
branches
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Figure 18.17
Heart Excitation Related to ECG
Ventricular excitation
complete
Purkinje
fibers
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Figure 18.17
Heart Excitation Related to ECG
SA node generates impulse;
atrial excitation begins
SA node
Impulse delayed
at AV node
AV node
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Impulse passes to
heart apex; ventricular
excitation begins
Bundle
branches
Ventricular excitation
complete
Purkinje
fibers
Figure 18.17
Electrocardiography
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Figure 18.16

Heart Murmurs
Abnormal heart sounds produced by abnormal patterns of
blood flow in the heart.

Defective heart valves:


Mitral stenosis:


Valves become damaged by antibodies made in response to an
infection, or congenital defects.
Mitral valve becomes thickened and calcified.

Impairs blood flow from left atrium to left ventricle.

Accumulation of blood in left ventricle may cause
pulmonary HTN.
Incompetent valves:

Damage to papillary muscles.

Valves do not close properly.
Murmurs produced as blood regurgitates through valve
flaps.
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
Heart Murmurs

Septal defects:


Usually congenital.

Holes in septum
between the left and
right sides of the
heart.

May occur either in
interatrial or
interventricular
septum.
Blood passes from left to
right.
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Electrocardiogram (ECG/EKG)

The body is a good conductor of electricity.


Tissue fluids have a high [ions] that move in response
to potential differences.
Electrocardiogram:

Measure of the electrical activity of the heart per unit
time.


Potential differences generated by heart are
conducted to body surface where they can be
recorded on electrodes on the skin.
Does NOT measure the flow of blood through the
heart.
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Ischemic Heart Disease

Ischemia:

Oxygen supply to tissue is
deficient.



Increased [lactic acid]
produced by anaerobic
respiration.
Angina pectoris:


Most common cause is
atherosclerosis of
coronary arteries.
Substernal pain.
Myocardial infarction (MI):

Changes in T segment of
ECG.

Increased CPK and LDH.
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Arrhythmias Detected on ECG

Arrhythmias:


Abnormal heart rhythms.
Flutter:

Extremely rapid rates of
excitation and contraction of
atria or ventricles.


Atrial flutter degenerates into
atrial fibrillation.
Fibrillation:

Contractions of different groups
of myocardial cells at different
times.

Coordination of pumping
impossible.

Ventricular fibrillation is
life-threatening.
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Arrhythmias Detected on ECG

(continued)
Third-degree (complete)
AV nodal block:

None of the atrial
waves can pass
through the AV node.

Ventricles paced by
ectopic pacemaker.
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Extrinsic Innervation of the Heart

Heart is stimulated by
the sympathetic
cardioacceleratory
center

Heart is inhibited by
the parasympathetic
cardioinhibitory center
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Figure 18.15
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Figure 18.20
Cardiac Cycle
(continued)
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Correlation of ECG with Heart Sounds


First heart sound:

Produced immediately
after QRS wave.

Rise of intraventricular
pressure causes AV
valves to close.
Second heart sound:

Produced after T wave
begins.

Fall in intraventricular
pressure causes semilunar
valves to close.
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Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 18.20
Cardiac Output (CO) and Reserve

CO is the amount of blood pumped by each
ventricle in one minute

CO is the product of heart rate (HR) and stroke
volume (SV)

HR is the number of heart beats per minute

SV is the amount of blood pumped out by a
ventricle with each beat

Cardiac reserve is the difference between resting
and maximal CO
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Cardiac Output: Example

CO (ml/min) = HR (75 beats/min) x SV (70
ml/beat)

CO = 5250 ml/min (5.25 L/min)
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Regulation of Stroke Volume

SV = end diastolic volume (EDV) minus end
systolic volume (ESV)

EDV = amount of blood collected in a ventricle
during diastole

ESV = amount of blood remaining in a ventricle
after contraction
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Factors Affecting Stroke Volume



Preload – amount ventricles are stretched by
contained blood
Contractility – cardiac cell contractile force due to
factors other than EDV
Afterload – back pressure exerted by blood in the
large arteries leaving the heart
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Cardiac Output (CO)

Volume of blood
pumped/min. by each
ventricle.


CO = SV x HR


Pumping ability of the
heart is a function of
the beats/ min. and the
volume of blood
ejected per beat.
Total blood volume
averages about 5.5
liters.
Each ventricle pumps the
equivalent of the total
blood volume each min.
(resting conditions).
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Frank-Starling Law of the Heart

Preload, or degree of stretch, of cardiac muscle
cells before they contract is the critical factor
controlling stroke volume

Slow heartbeat and exercise increase venous return
to the heart, increasing SV

Blood loss and extremely rapid heartbeat decrease
SV
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Preload and Afterload
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Figure 18.21
Extrinsic Factors Influencing Stroke Volume

Contractility is the increase in contractile strength,
independent of stretch and EDV

Increase in contractility comes from:

Increased sympathetic stimuli

Certain hormones

Ca2+ and some drugs
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Extrinsic Factors Influencing Stroke Volume

Agents/factors that decrease contractility include:

Acidosis

Increased extracellular K+

Calcium channel blockers
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Regulation of Heart Rate

Positive chronotropic factors increase heart rate

Negative chronotropic factors decrease heart rate
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Circulatory Changes During Exercise
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(continued)
Regulation of Heart Rate: Autonomic Nervous
System

Sympathetic nervous system (SNS) stimulation is
activated by stress, anxiety, excitement, or exercise

Parasympathetic nervous system (PNS) stimulation
is mediated by acetylcholine and opposes the SNS

PNS dominates the autonomic stimulation, slowing
heart rate and causing vagal tone
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Atrial (Bainbridge) Reflex

Atrial (Bainbridge) reflex – a sympathetic reflex
initiated by increased blood in the atria

Causes stimulation of the SA node

Stimulates baroreceptors in the atria, causing
increased SNS stimulation
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Chemical Regulation of the Heart

The hormones epinephrine and thyroxine increase
heart rate

Intra- and extracellular ion concentrations must be
maintained for normal heart function
InterActive Physiology ®: Cardiac Output, pages 3–9
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Baroreceptor Reflex
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(continued)
Renin-Angiotension-Aldosterone System
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(continued)
Regulation by ADH

Released by posterior
pituitary when
osmoreceptors detect
an increase in plasma
osmolality.

Dehydration or
excess salt intake:

Produces sensation
of thirst.

Stimulates H20
reabsorption from
urine.
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