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PowerPoint® Lecture Slides
prepared by Vince Austin,
Bluegrass Technical
and Community College
CHAPTER
Elaine N. Marieb
Katja Hoehn
18
PART B
Human
Anatomy
& Physiology
SEVENTH EDITION
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
The
Cardiovascular
System: The
Heart
Cardiac Muscle Contraction (Review)

Heart muscle:

Is stimulated by nerves and is self-excitable
(automaticity)


Contracts as a unit or not at all


Even if all nerves in the heart were severed, the
heart would beat on its own
cells have gap junctions that allow ion passage
from one cell to another
Has a long (250 ms) absolute refractory period

Prevents tetany
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Heart Physiology: Intrinsic Conduction
System

Autorhythmic cells:

Located in SA node, AV node, AV bundle, rt. and
lf. bundle branches, Purkinje fibers

Initiate action potentials

Have unstable resting potentials called pacemaker
potentials which set the rhythm of the heart beat

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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Cardiac Membrane Potential
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Figure 18.12
Extrinsic Innervation of the Heart

Heart is stimulated by
the sympathetic
cardioacceleratory
center (increases rate
and force of heartbeat)

Heart is inhibited by
the parasympathetic
cardioinhibitory center
(slows the heart)
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 18.15
Location and Function of Cardiac Centers

Both are located in the medulla oblongata

Cardioacceleratory center sends impulses to the
SNS neurons in the spinal cord (T1-T5 level)


SNS neurons (sympathetic cardiac nerve) innervate
the SA node, AV node, heart muscle, and coronary
arteries
Cardioinhibitory center sends impulses to the PNS
neurons in the medulla

Sends inhibitory impulses to the heart via the vagus
nerve
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
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
PLAY
InterActive Physiology ®:
Intrinsic Conduction System, pages 3–6
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Electrocardiography
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 18.16
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
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 18.17
Heart Excitation Related to ECG
Ventricular excitation
complete
Purkinje
fibers
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 18.17
Heart Excitation Related to ECG
SA node generates impulse;
atrial excitation begins
SA node
Impulse delayed
at AV node
AV node
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Impulse passes to
heart apex; ventricular
excitation begins
Bundle
branches
Ventricular excitation
complete
Purkinje
fibers
Figure 18.17
ECG Tracings – see p. 697 in textbook
More P waves than QRS waves
NORMAL
Junctional rhythm – SA node
nonfunctional; P waves absent;
AV node becomes pacemaker
(40-60 bpm)
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2nd degree heart block –some P
waves not passing through AV node
Ventricular fibrillation –
acute heart attack
Figure 18.18
Cardiac Cycle

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
PLAY
InterActive Physiology ®: Cardiac Cycle, pages 3–18
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 18.20
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
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
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
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
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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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
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Extrinsic Factors Influencing Stroke Volume

Agents/factors that decrease contractility include:


Acidosis (increased acid (H+) in plasma)

Respiratory acidosis caused by build up of CO2
(hyperventilation, emphysema, pneumonia)

Metabolic acidosis caused by a)high intake of
acidic foods or b)kidneys inability to flush out
acid foods high in protein or sugar
Calcium channel blockers
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Regulation of Heart Rate: Autonomic Nervous
System

Sympathetic nervous system (SNS) stimulation is
activated by stress, anxiety, excitement, or exercise
release of epinephrine (adrenaline)

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
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Chemical Regulation of the Heart

The hormones epinephrine (adrenaline) and
thyroxine increase heart rate; acetylcholine (Ach)
decreases HR

Intra- and extracellular ion concentrations,
especially Ca++ and K+ , must be maintained for
normal heart function
PLAY
InterActive Physiology ®: Cardiac Output, pages 3–9
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
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

The most important factor that stretches cardiac
muscle is venous return (the amount of blood
returning to the heart)

Slow heartbeat and exercise increase venous return
to the heart, increasing SV

Blood loss and extremely rapid heartbeat decrease
SV
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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
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
See p. 703
in textbook
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Figure 18.23
Congestive Heart Failure (CHF)

Congestive heart failure (CHF) is caused by:

Coronary atherosclerosis (buildup of waxy plaque
on the inner lining of arteries – reducing their
elasticity)

Persistent high blood pressure

Multiple myocardial infarcts (heart attacks)

Dilated cardiomyopathy (DCM)- (enlarged heart
due to overworking of a weakened heart)
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Developmental Aspects of the Heart
Day 22 – heart begins to beat with child’s own blood
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Figure 18.24
Developmental Aspects of the Heart

Fetal heart structures (shunts) that bypass pulmonary
circulation (fetal lungs are fluid-filled and
nonfunctional)


Foramen ovale connects the two atria – closes
when baby takes it first breath
Ductus arteriosus connects pulmonary trunk and
the aorta – starts closing 10-15 hrs. after birth;
totally closed 10-21 days after birth
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Developmental (cont)

Ductus venosus

shunts about half of the blood flow of the umbilical
vein directly to the inferior vena cava

allows oxygenated blood from the placenta to
bypass the liver.

Closes shortly after birth when umbilical cord is
cut

All 3 shunts play a critical role in preferentially
shunting oxygenated blood to the fetal brain
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings