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© 2012 Pearson Education, Inc.
PowerPoint® Lecture Presentations prepared byJason LaPresLone Star College—North Harris
20The Heart
© 2012 Pearson Education, Inc.
An Introduction to the Cardiovascular System
• Learning Outcomes
• 20-1 Describe the anatomy of the heart, including vascular supply and pericardium structure,
and trace the flow of blood through the heart, identifying the major blood vessels,
chambers, and heart valves.
• 20-2 Explain the events of an action potential in cardiac muscle, indicate the importance of calcium ions to the contractile
process, describe the conducting system of the heart, and identify the electrical events associated with a normal electrocardiogram.
© 2012 Pearson Education, Inc.
An Introduction to the Cardiovascular System
• Learning Outcomes
• 20-3 Explain the events of the cardiac cycle, including atrial and ventricular systole and
diastole, and relate the heart sounds to specific events in the cycle.
• 20-4 Define cardiac output, describe the factors that influence heart rate and stroke volume,
and explain how adjustments in stroke volume and cardiac output are coordinated at different levels of physical activity.
© 2012 Pearson Education, Inc.
An Introduction to the Cardiovascular System
• The Pulmonary Circuit
• Carries blood to and from gas exchange surfaces of
lungs
• The Systemic Circuit
• Carries blood to and from the body
• Blood alternates between pulmonary circuit and
systemic circuit
© 2012 Pearson Education, Inc.
An Introduction to the Cardiovascular System
• Three Types of Blood Vessels
1. Arteries
• Carry blood away from heart
2. Veins
• Carry blood to heart
3. Capillaries
• Networks between arteries and veins
© 2012 Pearson Education, Inc.
An Introduction to the Cardiovascular System
• Capillaries
• Also called exchange vessels
• Exchange materials between blood and tissues
• Materials include dissolved gases, nutrients, waste
products
© 2012 Pearson Education, Inc.
Figure 20-1 An Overview of the Cardiovascular System
PULMONARY CIRCUIT SYSTEMIC CIRCUIT
Pulmonary arteries
Pulmonary veins Systemic veins
Systemic arteries
Capillariesin lungs
Rightatrium
Rightventricle
Capillariesin trunk
and lowerlimbs
Capillariesin head,neck, upperlimbs
Leftatrium
Leftventricle
© 2012 Pearson Education, Inc.
An Introduction to the Cardiovascular System
• Four Chambers of the Heart
1. Right atrium
• Collects blood from systemic circuit
2. Right ventricle
• Pumps blood to pulmonary circuit
3. Left atrium
• Collects blood from pulmonary circuit
4. Left ventricle
• Pumps blood to systemic circuit
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Heart
• Great veins and arteries at the base
• Pointed tip is apex
• Surrounded by pericardial sac
• Sits between two pleural cavities in the mediastinum
© 2012 Pearson Education, Inc.
Figure 20-2a The Location of the Heart in the Thoracic Cavity
Trachea
First rib (cut)
Base of heart
Right lung
Diaphragm
Thyroid gland
Left lung
Apex of heart
Parietal pericardium(cut)
An anterior view of the chest, showing the position of the heart andmajor blood vessels relative to the ribs, lungs, and diaphragm.
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Pericardium
• Double lining of the pericardial cavity
• Visceral pericardium
• Inner layer of pericardium
• Parietal pericardium
• Outer layer
• Forms inner layer of pericardial sac
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Pericardium
• Pericardial cavity
• Is between parietal and visceral layers
• Contains pericardial fluid
• Pericardial sac
• Fibrous tissue
• Surrounds and stabilizes heart
© 2012 Pearson Education, Inc.
Figure 20-2b The Location of the Heart in the Thoracic Cavity
Right ventricle
Aorticarch
Posterior mediastinum
Aorta (arch segment removed)
Left pulmonary artery
Left pulmonary vein
Pulmonary trunk
Left ventricle
Epicardium
Pericardial sac
Anterior mediastinum
Pericardial cavity
Right atrium
Left atrium
Right pulmonary artery
Right pulmonary vein
Superior vena cava
Esophagus
Right pleural cavity
Bronchus of lung
Rightlung Left
lung
Left pleural cavity
A superior view of the organs in the mediastinum; portions of the lungs havebeen removed to reveal blood vessels and airways. The heart is situated in the anterior part of the mediastinum, immediately posterior to the sternum.
© 2012 Pearson Education, Inc.
Figure 20-2c The Location of the Heart in the Thoracic Cavity
Wrist (correspondsto base of heart)
Inner wall (correspondsto epicardium)
Air space (correspondsto pericardial cavity)
Outer wall (correspondsto parietal pericardium)
Balloon
Cut edge ofparietal pericardium
Fibrous tissue ofpericardial sac
Parietal pericardium
Areolar tissueMesothelium
Cut edge of epicardium
Apex of heart
Base of heart
Fibrousattachment
to diaphragm
The relationship between the heart and the pericardial cavity; compare with the fist-and-balloon example.
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Superficial Anatomy of the Heart
• Atria
• Thin-walled
• Expandable outer auricle (atrial appendage)
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Superficial Anatomy of the Heart
• Sulci
• Coronary sulcus divides atria and ventricles
• Anterior interventricular sulcus and posterior
interventricular sulcus
• Separate left and right ventricles
• Contain blood vessels of cardiac muscle
© 2012 Pearson Education, Inc.
Figure 20-3a The Superficial Anatomy of the HeartLeft commoncarotid artery
Brachiocephalictrunk
Ascendingaorta
Superiorvena cava
Auricleof rightatrium
Fat andvessels incoronary
sulcus
Left subclavian artery
Arch of aorta
Ligamentumarteriosum
Descendingaorta
Left pulmonaryartery
Pulmonarytrunk
Auricle ofleft atrium
Fat and vesselsin anteriorinterventricularsulcus
LEFTVENTRICLE
RIGHTVENTRICLE
RIGHTATRIUM
Major anatomical features on the anterior surface.
© 2012 Pearson Education, Inc.
Figure 20-3a The Superficial Anatomy of the Heart
Ascendingaorta
Parietalpericardium
Superiorvena cava
Auricle ofright atrium
RIGHT ATRIUM
Right coronaryartery
Coronary sulcus
RIGHT VENTRICLE
Marginal branchof right coronary artery
Auricle ofleft atrium
Pulmonarytrunk
Fibrouspericardium
Parietal pericardiumfused to diaphragm
Anteriorinterventricular
sulcus
LEFTVENTRICLE
Major anatomical features on the anterior surface.
© 2012 Pearson Education, Inc.
Figure 20-3b The Superficial Anatomy of the Heart Arch of aorta
Right pulmonaryartery
Superiorvena cava
Rightpulmonaryveins (superiorand inferior)
Inferiorvena cava
Fat and vessels in posteriorinterventricular sulcus
RIGHTVENTRICLE
LEFTVENTRICLE
RIGHTATRIUM
LEFTATRIUM
Left pulmonary artery
Left pulmonary veins
Fat and vessels incoronary sulcus
Coronarysinus
Major landmarks on the posterior surface. Coronaryarteries (which supply the heart itself) are shown inred; coronary veins are shown in blue.
© 2012 Pearson Education, Inc.
Figure 20-3c The Superficial Anatomy of the Heart
Base of heart
Apex ofheart
Ribs
Heart position relative to the rib cage.
1
2
3
4
5
6
7
89
10
1
2
3
4
5
6
7
8910
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Heart Wall
1. Epicardium
2. Myocardium
3. Endocardium
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Epicardium (Outer Layer)
• Visceral pericardium
• Covers the heart
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Myocardium (Middle Layer)
• Muscular wall of the heart
• Concentric layers of cardiac muscle tissue
• Atrial myocardium wraps around great vessels
• Two divisions of ventricular myocardium
• Endocardium (Inner Layer)
• Simple squamous epithelium
© 2012 Pearson Education, Inc.
Figure 20-4a The Heart Wall
Mesothelium
Endocardium
Areolar tissue
Endothelium
Mesothelium
Dense fibrous layer
Parietal pericardium
Pericardial cavity
Areolar tissue
Areolar tissue
Connective tissues
Cardiac muscle cells
Myocardium(cardiac muscle tissue)
Epicardium(visceral pericardium)
© 2012 Pearson Education, Inc.
Figure 20-4b The Heart Wall
Atrialmusculature
Cardiac muscle tissueforms concentric layersthat wrap around theatria or spiral within thewalls of the ventricles.
Ventricularmusculature
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Cardiac Muscle Tissue
• Intercalated discs
• Interconnect cardiac muscle cells
• Secured by desmosomes
• Linked by gap junctions
• Convey force of contraction
• Propagate action potentials
© 2012 Pearson Education, Inc.
Figure 20-5a Cardiac Muscle Cells
Cardiac muscle cells
Nucleus
Cardiac musclecell (sectioned)
Bundles ofmyofibrils
Cardiac muscle cell
Mitochondria
Intercalateddisc (sectioned)
Intercalated discs
© 2012 Pearson Education, Inc.
Figure 20-5b Cardiac Muscle Cells
Intercalated disc
Gap junction
Opposing plasmamembranes
Desmosomes
Structure of an intercalated disc
© 2012 Pearson Education, Inc.
Figure 20-5c Cardiac Muscle Cells
Intercalated discs
Cardiac muscle tissue
Cardiac muscle tissue LM 575
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Characteristics of Cardiac Muscle Cells
1. Small size
2. Single, central nucleus
3. Branching interconnections between cells
4. Intercalated discs
© 2012 Pearson Education, Inc.
Table 20-1 Structural and Functional Differences between Cardiac Muscle Cells and Skeletal Muscle Fibers
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Internal Anatomy and Organization
• Interatrial septum separates atria
• Interventricular septum separates ventricles
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Internal Anatomy and Organization
• Atrioventricular (AV) valves
• Connect right atrium to right ventricle and left
atrium to left ventricle
• Are folds of fibrous tissue that extend into
openings between atria and ventricles
• Permit blood flow in one direction
• From atria to ventricles
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Right Atrium
• Superior vena cava
• Receives blood from head, neck, upper limbs, and chest
• Inferior vena cava
• Receives blood from trunk, viscera, and lower limbs
• Coronary sinus
• Cardiac veins return blood to coronary sinus
• Coronary sinus opens into right atrium
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Right Atrium
• Foramen ovale
• Before birth, is an opening through interatrial septum
• Connects the two atria
• Seals off at birth, forming fossa ovalis
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Right Atrium
• Pectinate muscles
• Contain prominent muscular ridges
• On anterior atrial wall and inner surfaces of right
auricle
© 2012 Pearson Education, Inc.
Figure 20-6a The Sectional Anatomy of the Heart
Descending aorta
Left common carotid artery
Left subclavian artery
Ligamentum arteriosum
Pulmonary trunk
Pulmonary valve
Left pulmonaryarteries
Left pulmonaryveins
Interatrial septumAortic valve
Cusp of left AV(mitral) valve
LEFT VENTRICLE
Interventricularseptum
Trabeculaecarneae
Moderator band
Aortic arch
LEFTATRIUM
Brachiocephalictrunk
Superiorvena cava
Rightpulmonary
arteries
Ascending aorta
Fossa ovalis
Opening ofcoronary sinus
RIGHT ATRIUM
Pectinate muscles
Conus arteriosus
Cusp of right AV(tricuspid) valve
Chordae tendineae
Papillary muscles
RIGHT VENTRICLE
Inferior vena cava
© 2012 Pearson Education, Inc.
Figure 20-6c The Sectional Anatomy of the Heart
A frontal section, anterior view.
Inferior vena cava
RIGHT VENTRICLE
Papillary muscles
Cusps of right AV(tricuspid) valve
Pectinate muscles
RIGHT ATRIUM
Fossa ovalis
Ascending aorta
Cusp of left AV(bicuspid) valve
Interventricularseptum
LEFT VENTRICLE
Chordae tendineae
Left coronary arterybranches (red)and great cardiacvein (blue)
Cusp of aortic valve
Coronary sinus
Trabeculae carneae
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Right Ventricle
• Free edges attach to chordae tendineae from
papillary muscles of ventricle
• Prevent valve from opening backward
• Right atrioventricular (AV) valve
• Also called tricuspid valve
• Opening from right atrium to right ventricle
• Has three cusps
• Prevents backflow
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Right Ventricle
• Trabeculae carneae
• Muscular ridges on internal surface of right (and left)
ventricle
• Includes moderator band
• Ridge contains part of conducting system
• Coordinates contractions of cardiac muscle cells
© 2012 Pearson Education, Inc.
Figure 20-6b The Sectional Anatomy of the Heart
The papillary muscles and chordaetendinae supporting the right AV(tricuspid) valve. The photographwas taken from inside the rightventricle, looking toward a lightshining from the right atrium.
Chordae tendineae
Papillary muscles
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Pulmonary Circuit
• Conus arteriosus (superior end of right ventricle)
leads to pulmonary trunk
• Pulmonary trunk divides into left and right
pulmonary arteries
• Blood flows from right ventricle to pulmonary trunk
through pulmonary valve
• Pulmonary valve has three semilunar cusps
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Left Atrium
• Blood gathers into left and right pulmonary veins
• Pulmonary veins deliver to left atrium
• Blood from left atrium passes to left ventricle through
left atrioventricular (AV) valve
• A two-cusped bicuspid valve or mitral valve
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Left Ventricle
• Holds same volume as right ventricle
• Is larger; muscle is thicker and more powerful
• Similar internally to right ventricle but does not have
moderator band
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Left Ventricle
• Systemic circulation
• Blood leaves left ventricle through aortic valve
into ascending aorta
• Ascending aorta turns (aortic arch) and becomes
descending aorta
© 2012 Pearson Education, Inc.
Figure 20-6c The Sectional Anatomy of the Heart
A frontal section, anterior view.
Inferior vena cava
RIGHT VENTRICLE
Papillary muscles
Cusps of right AV(tricuspid) valve
Pectinate muscles
RIGHT ATRIUM
Fossa ovalis
Ascending aorta
Cusp of left AV(bicuspid) valve
Interventricularseptum
LEFT VENTRICLE
Chordae tendineae
Left coronary arterybranches (red)and great cardiacvein (blue)
Cusp of aortic valve
Coronary sinus
Trabeculae carneae
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Structural Differences between the Left and
Right Ventricles
• Right ventricle wall is thinner, develops less pressure
than left ventricle
• Right ventricle is pouch-shaped, left ventricle is round
ANIMATION The Heart: Heart Anatomy
© 2012 Pearson Education, Inc.
Figure 20-7a Structural Differences between the Left and Right Ventricles
Left ventricle
Rightventricle
Posteriorinterventricular sulcus
Fat in anteriorinterventricular sulcus
A diagrammatic sectional view through the heart,showing the relative thicknesses of the two ventricles.Notice the pouchlike shape of the right ventricle andthe greater thickness of the left ventricle.
© 2012 Pearson Education, Inc.
Figure 20-7b Structural Differences between the Left and Right Ventricles
Dilated Contracted
Diagrammatic views of the ventricles justbefore a contraction (dilated) and just after acontraction (contracted).
Left ventricle
Rightventricle
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Heart Valves
• Two pairs of one-way valves prevent backflow
during contraction
• Atrioventricular (AV) valves
• Between atria and ventricles
• Blood pressure closes valve cusps during ventricular
contraction
• Papillary muscles tense chordae tendineae to prevent
valves from swinging into atria
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Heart Valves
• Semilunar valves
• Pulmonary and aortic tricuspid valves
• Prevent backflow from pulmonary trunk and aorta
into ventricles
• Have no muscular support
• Three cusps support like tripod
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Aortic Sinuses
• At base of ascending aorta
• Sacs that prevent valve cusps from sticking to
aorta
• Origin of right and left coronary arteries
ANIMATION The Heart: Valves
© 2012 Pearson Education, Inc.
Figure 20-8a Valves of the Heart
Rel
axe
d v
entr
icle
s
Right AV(tricuspid)
valve (open)
Transverse Sections, Superior View,Atria and Vessels Removed
POSTERIOR
RIGHTVENTRICLE
Cardiacskeleton
Left AV (bicuspid)valve (open)
LEFTVENTRICLE
Aortic valve(closed)
Pulmonaryvalve (closed)ANTERIOR
Aortic valve closed
When the ventricles are relaxed, the AV valves are open and the semilunar valves are closed. The chordae tendineae are loose, and the papillary muscles are relaxed.
© 2012 Pearson Education, Inc.
Figure 20-8a Valves of the Heart
Aortic valve(closed)
LEFTATRIUM
Left AV (bicuspid)valve (open)
Chordaetendineae (loose)
Papillary muscles(relaxed)
LEFT VENTRICLE(relaxed and fillingwith blood)
Pulmonaryveins
Frontal Sections through Left Atrium and Ventricle
Rel
axe
d v
entr
icle
s
© 2012 Pearson Education, Inc.
Figure 20-8b Valves of the Heart
Co
ntr
acti
ng
ven
tric
les
Aortic valve open
RIGHTVENTRICLE
Right AV(tricuspid) valve
(closed)
Cardiacskeleton
Left AV(bicuspid) valve
(closed)LEFTVENTRICLE
Aortic valve(open)
Pulmonaryvalve (open)
When the ventricles are contracting, the AV valves are closed and the semilunar valves are open. In the frontal section notice the attachment of the left AV valve to the chordae tendineae and papillary muscles.
© 2012 Pearson Education, Inc.
Figure 20-8b Valves of the Heart
Co
ntr
acti
ng
ven
tric
les
Aorta
Aortic sinus
LEFTATRIUM
Aortic valve(open)
Left AV (bicuspid)valve (closed)
Chordae tendineae(tense)
Papillary muscles(contracted)
Left ventricle(contracted)
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Connective Tissues and the Cardiac Skeleton
• Connective Tissue Fibers
1. Physically support cardiac muscle fibers
2. Distribute forces of contraction
3. Add strength and prevent overexpansion of heart
4. Provide elasticity that helps return heart to original
size and shape after contraction
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Cardiac Skeleton
• Four bands around heart valves and bases of
pulmonary trunk and aorta
• Stabilize valves
• Electrically insulate ventricular cells from atrial cells
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Blood Supply to the Heart
• = Coronary circulation
• Supplies blood to muscle tissue of heart
• Coronary arteries and cardiac veins
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Coronary Arteries
• Left and right
• Originate at aortic sinuses
• High blood pressure, elastic rebound forces blood
through coronary arteries between contractions
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20-1 Anatomy of the Heart
• Right Coronary Artery
• Supplies blood to:
• Right atrium
• Portions of both ventricles
• Cells of sinoatrial (SA) and atrioventricular nodes
• Marginal arteries (surface of right ventricle)
• Posterior interventricular artery
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20-1 Anatomy of the Heart
• Left Coronary Artery
• Supplies blood to:
• Left ventricle
• Left atrium
• Interventricular septum
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20-1 Anatomy of the Heart
• Two Main Branches of Left Coronary Artery
1. Circumflex artery
2. Anterior interventricular artery
• Arterial Anastomoses
• Interconnect anterior and posterior interventricular
arteries
• Stabilize blood supply to cardiac muscle
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• The Cardiac Veins
• Great cardiac vein
• Drains blood from area of anterior interventricular artery into
coronary sinus
• Anterior cardiac veins
• Empty into right atrium
• Posterior cardiac vein, middle cardiac vein, and
small cardiac vein
• Empty into great cardiac vein or coronary sinus
© 2012 Pearson Education, Inc.
Figure 20-9a Coronary Circulation
Aorticarch
Ascendingaorta
Right coronaryartery
Atrial arteries
Anteriorcardiac veins
Smallcardiac vein
Marginalartery
Left coronaryartery
Pulmonarytrunk
Circumflexartery
Anteriorinterventricularartery
Greatcardiacvein
Coronary vessels supplyingand draining the anteriorsurface of the heart.
© 2012 Pearson Education, Inc.
Figure 20-9b Coronary Circulation
Coronary sinusCircumflex artery
Great cardiac vein
Marginal artery
Posteriorinterventricular
artery
Posteriorcardiac
vein
Leftventricle
Middle cardiac vein Marginal artery
Right coronaryartery
Small cardiacvein
Coronary vessels supplying and drainingthe posterior surface of the heart.
© 2012 Pearson Education, Inc.
Figure 20-9c Coronary Circulation
Posterior interventricular artery
Posteriorcardiac vein
Marginal artery
Great cardiac vein
Circumflex artery
Auricle ofleft atrium
Left pulmonaryveins
Left pulmonaryartery
Right pulmonaryartery
Superiorvena cava
Right pulmonaryveins
Left atrium
Right atrium
Inferior vena cava
Coronary sinus
Middle cardiac vein
Right ventricle
A posterior view of the heart; the vessels have beeninjected with colored latex (liquid rubber).
© 2012 Pearson Education, Inc.
Figure 20-10 Heart Disease and Heart Attacks
Narrowing of Artery
Lipid depositof plaque
Cross-section
Tunicaexterna
Tunicamedia
Cross-section
Normal Artery
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Heart Disease - Coronary Artery Disease
• Coronary artery disease (CAD)
• Areas of partial or complete blockage of coronary circulation
• Cardiac muscle cells need a constant supply of oxygen and nutrients
• Reduction in blood flow to heart muscle produces a corresponding reduction in cardiac performance
• Reduced circulatory supply, coronary ischemia, results from partial or complete blockage of coronary arteries
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Heart Disease - Coronary Artery Disease
• Usual cause is formation of a fatty deposit, or atherosclerotic plaque, in the wall of a coronary vessel
• The plaque, or an associated thrombus (clot), then narrows the passageway and reduces blood flow
• Spasms in smooth muscles of vessel wall can further decrease or stop blood flow
• One of the first symptoms of CAD is commonly angina pectoris
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Heart Disease - Coronary Artery Disease
• Angina Pectoris
• In its most common form, a temporary ischemia develops when the workload of the heart increases
• Although the individual may feel comfortable at rest, exertion or emotional stress can produce a sensation of pressure, chest constriction, and pain that may radiate from the sternal area to the arms, back, and neck
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Heart Disease - Coronary Artery Disease
• Myocardial infarction (MI), or heart attack
• Part of the coronary circulation becomes blocked, and cardiac muscle cells die from lack of oxygen
• The death of affected tissue creates a nonfunctional area known as an infarct
• Heart attacks most commonly result from severe coronary artery disease (CAD)
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Heart Disease - Coronary Artery Disease• Myocardial infarction (MI), or heart attack
• Consequences depend on the site and nature of the circulatory blockage
• If it occurs near the start of one of the coronary arteries:
• The damage will be widespread and the heart may stop beating
• If the blockage involves one of the smaller arterial branches:
• The individual may survive the immediate crisis but may have many complications such as reduced contractility and cardiac arrhythmias
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Heart Disease - Coronary Artery Disease
• Myocardial infarction (MI), or heart attack
• A crisis often develops as a result of thrombus formation at a plaque (the most common cause of an MI), a condition called coronary thrombosis
• A vessel already narrowed by plaque formation may also become blocked by a sudden spasm in the smooth muscles of the vascular wall
• Individuals having an MI experience intense pain, similar to that felt in angina, but persisting even at rest
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Heart Disease - Coronary Artery Disease• Myocardial infarction (MI), or heart attack
• Pain does not always accompany a heart attack, therefore, the condition may go undiagnosed and may not be treated before a fatal MI occurs
• A myocardial infarction can usually be diagnosed with an ECG and blood studies
• Damaged myocardial cells release enzymes into the circulation, and these elevated enzymes can be measured in diagnostic blood tests
• The enzymes include:
• Cardiac troponin T,
• Cardiac troponin I,
• A special form of creatinine phosphokinase, CK-MB
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Heart Disease - Coronary Artery Disease
• Treatment of CAD and Myocardial Infarction
• About 25% of MI patients die before obtaining medical
assistance
• 65% of MI deaths among those under age 50 occur
within an hour after the initial infarction
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20-1 Anatomy of the Heart
• Heart Disease - Coronary Artery Disease
• Treatment of CAD and Myocardial Infarction
• Risk Factor Modification
• Stop smoking
• High blood pressure treatment
• Dietary modification to lower cholesterol and
promote weight loss
• Stress reduction
• Increased physical activity (where appropriate)
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Heart Disease - Coronary Artery Disease
• Treatment of CAD and Myocardial Infarction
• Drug Treatment
• Drugs that reduce coagulation and therefore the risk of thrombosis, such as aspirin and coumadin
• Drugs that block sympathetic stimulation (propranolol or metoprolol)
• Drugs that cause vasodilation, such as nitroglycerin
• Drugs that block calcium movement into the cardiac and vascular smooth muscle cells (calcium channel blockers)
• In a myocardial infarction, drugs to relieve pain, fibrinolytic agents to help dissolve clots, and oxygen
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Heart Disease - Coronary Artery Disease
• Treatment of CAD and Myocardial Infarction
• Noninvasive Surgery
• Atherectomy
• Blockage by a single, soft plaque may be reduced with the aid of a long, slender catheter inserted into a coronary artery to the plaque
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Heart Disease - Coronary Artery Disease
• Treatment of CAD and Myocardial Infarction
• Noninvasive Surgery
• Balloon angioplasty
• The tip of the catheter contains an inflatable balloon
• Once in position, the balloon is inflated, pressing the plaque against the vessel walls
• Because plaques commonly redevelop after angioplasty, a fine tubular wire mesh called a stent may be inserted into the vessel, holding it open
© 2012 Pearson Education, Inc.
20-1 Anatomy of the Heart
• Heart Disease - Coronary Artery Disease
• Treatment of CAD and Myocardial Infarction
• Coronary Artery Bypass Surgery (CABG)
• In a coronary artery bypass graft, a small section is removed from either a small artery or a peripheral vein and is used to create a detour around the obstructed portion of a coronary artery
• As many as four coronary arteries can be rerouted this way during a single operation
• The procedures are named according to the number of vessels repaired, so we speak of single, double, triple, or quadruple coronary bypasses
© 2012 Pearson Education, Inc.
Figure 20-10 Heart Disease and Heart Attacks
Normal Heart
Advanced Coronary Artery DiseaseA color-enhanced DSA scan showing advancedcoronary artery disease. Blood flow to the ven-tricular myocardium is severely restricted.
A color-enhanced digital subtractionangiography (DSA) scan of a normalheart.
© 2012 Pearson Education, Inc.
Figure 20-10 Heart Disease and Heart Attacks
OccludedCoronaryArtery
DamagedHeartMuscle
© 2012 Pearson Education, Inc.
20-2 The Conducting System
• Heartbeat
• A single contraction of the heart
• The entire heart contracts in series
• First the atria
• Then the ventricles
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20-2 The Conducting System
• Cardiac Physiology
• Two Types of Cardiac Muscle Cells
1. Conducting system
• Controls and coordinates heartbeat
2. Contractile cells
• Produce contractions that propel blood
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20-2 The Conducting System
• The Cardiac Cycle
• Begins with action potential at SA node
• Transmitted through conducting system
• Produces action potentials in cardiac muscle cells
(contractile cells)
• Electrocardiogram (ECG or EKG)
• Electrical events in the cardiac cycle can be recorded
on an electrocardiogram
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20-2 The Conducting System
• The Conducting System
• A system of specialized cardiac muscle cells
• Initiates and distributes electrical impulses that
stimulate contraction
• Automaticity
• Cardiac muscle tissue contracts automatically
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20-2 The Conducting System
• Structures of the Conducting System
• Sinoatrial (SA) node - wall of right atrium
• Atrioventricular (AV) node - junction between atria
and ventricles
• Conducting cells - throughout myocardium
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20-2 The Conducting System
• Conducting Cells
• Interconnect SA and AV nodes
• Distribute stimulus through myocardium
• In the atrium
• Internodal pathways
• In the ventricles
• AV bundle and the bundle branches
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20-2 The Conducting System
• Prepotential
• Also called pacemaker potential
• Resting potential of conducting cells
• Gradually depolarizes toward threshold
• SA node depolarizes first, establishing heart rate
ANIMATION The Heart: Conduction System
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Figure 20-11a The Conducting System of the Heart
AV bundle
Components of the conductingsystem
Purkinjefibers
Bundlebranches
Atrioventricular(AV) node
Internodalpathways
Sinoatrial(SA) node
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Figure 20-11b The Conducting System of the Heart
Changes in the membrane potential of a pacemakercell in the SA node that is establishing a heart rate of72 beats per minute. Note the presence of a prepotential, a gradual spontaneous depolarization.
Time (sec)
Prepotential(spontaneous depolarization)
Threshold
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20-2 The Conducting System
• Heart Rate
• SA node generates 80–100 action potentials per
minute
• Parasympathetic stimulation slows heart rate
• AV node generates 40–60 action potentials per
minute
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20-2 The Conducting System
• The Sinoatrial (SA) Node
• In posterior wall of right atrium
• Contains pacemaker cells
• Connected to AV node by internodal pathways
• Begins atrial activation (Step 1)
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Figure 20-12 Impulse Conduction through the Heart (Step 1)
Time = 0
SAnode
SA node activityand atrialactivation begin.
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20-2 The Conducting System
• The Atrioventricular (AV) Node
• In floor of right atrium
• Receives impulse from SA node (Step 2)
• Delays impulse (Step 3)
• Atrial contraction begins
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Figure 20-12 Impulse Conduction through the Heart (Step 2)
Elapsed time = 50 msec
AVnode
Stimulus spreads acrossthe atrial surfaces andreaches the AV node.
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Figure 20-12 Impulse Conduction through the Heart (Step 3)
Elapsed time = 150 msec
Bundlebranches
AVbundle
There is a 100-msec delayat the AV node. Atrialcontraction begins.
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20-2 The Conducting System
• The AV Bundle
• In the septum
• Carries impulse to left and right bundle branches
• Which conduct to Purkinje fibers (Step 4)
• And to the moderator band
• Which conducts to papillary muscles
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Figure 20-12 Impulse Conduction through the Heart (Step 4)
Elapsed time = 175 msecModerator
band
The impulse travels alongthe interventricular septumwithin the AV bundle andthe bundle branches to thePurkinje fibers and, via themoderator band, to thepapillary muscles of theright ventricle.
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20-2 The Conducting System
• Purkinje Fibers
• Distribute impulse through ventricles (Step 5)
• Atrial contraction is completed
• Ventricular contraction begins
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Figure 20-12 Impulse Conduction through the Heart (Step 5)
Elapsed time = 225 msecPurkinje
fibers
The impulse is distributedby Purkinje fibers andrelayed throughout theventricular myocardium.Atrial contraction iscompleted, and ventricularcontraction begins.
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20-2 The Conducting System
• Abnormal Pacemaker Function
• Bradycardia - abnormally slow heart rate
• Tachycardia - abnormally fast heart rate
• Ectopic pacemaker
• Abnormal cells
• Generate high rate of action potentials
• Bypass conducting system
• Disrupt ventricular contractions
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20-2 The Conducting System
• The Electrocardiogram (ECG or EKG)
• A recording of electrical events in the heart
• Obtained by electrodes at specific body locations
• Abnormal patterns diagnose damage
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20-2 The Conducting System
• Features of an ECG
• P wave
• Atria depolarize
• QRS complex
• Ventricles depolarize
• T wave
• Ventricles repolarize
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20-2 The Conducting System
• Time Intervals between ECG Waves
• P–R interval
• From start of atrial depolarization
• To start of QRS complex
• Q–T interval
• From ventricular depolarization
• To ventricular repolarization
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Figure 20-13a An Electrocardiogram
Electrode placement forrecording a standard ECG.
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Figure 20-13b An Electrocardiogram
800 msec
SQ
QRS interval(ventricles depolarize)
Millivolts
R
P–R segmentT wave
(ventricles repolarize)
R
P wave(atria
depolarize)S–T
segment
S–Tinterval
Q–Tinterval
P–Rinterval
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Figure 20-14 Cardiac Arrhythmias
Premature Atrial Contractions (PACs)
Paroxysmal Atrial Tachycardia (PAT)
Atrial Fibrillation (AF)
PPP
PPPPPP
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Figure 20-14 Cardiac Arrhythmias
Premature Ventricular Contractions (PVCs)
Ventricular Tachycardia (VT)
Ventricular Fibrillation (VF)
PPP
P
TTT
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20-2 The Conducting System
• Contractile Cells
• Purkinje fibers distribute the stimulus to the contractile
cells, which make up most of the muscle cells in the
heart
• Resting Potential
• Of a ventricular cell about –90 mV
• Of an atrial cell about –80 mV
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Figure 20-15a The Action Potential in Skeletal and Cardiac Muscle
Rapid Depolarization The Plateau RepolarizationCause: Na+ entryDuration: 3–5 msecEnds with: Closure of voltage-gated fast sodium channels
Cause: Ca2+ entryDuration: ~175 msecEnds with: Closure of slow calcium channels
Cause: K+ lossDuration: 75 msecEnds with: Closure of slow potassium channels
Relativerefractoryperiod
Stimulus
Events in an action potential in a ventricular musclecell.
KEY
Absolute refractoryperiod
Relative refractoryperiod
Absolute refractoryperiod
Time (msec)
mV
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Figure 20-15b The Action Potential in Skeletal and Cardiac Muscle
mV
SKELETALMUSCLE
CARDIACMUSCLE
Action potentialmV
Contraction
Tension
Time (msec)
Time (msec)
ContractionTension
Actionpotential
KEY
Absolute refractoryperiod
Relative refractoryperiod
Action potentials and twitchcontractions in a skeletal muscle(above) and cardiac muscle (below).
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20-2 The Conducting System
• Refractory Period
• Absolute refractory period
• Long
• Cardiac muscle cells cannot respond
• Relative refractory period
• Short
• Response depends on degree of stimulus
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20-2 The Conducting System
• Timing of Refractory Periods
• Length of cardiac action potential in ventricular cell
• 250–300 msec
• 30 times longer than skeletal muscle fiber
• Long refractory period prevents summation and
tetany
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20-2 The Conducting System
• The Role of Calcium Ions in Cardiac
Contractions
• Contraction of a cardiac muscle cell
• Is produced by an increase in calcium ion
concentration around myofibrils
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20-2 The Conducting System
• The Role of Calcium Ions in Cardiac
Contractions
1. 20% of calcium ions required for a contraction
• Calcium ions enter plasma membrane during plateau
phase
2. Arrival of extracellular Ca2+
• Triggers release of calcium ion reserves from
sarcoplasmic reticulum (SR)
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20-2 The Conducting System
• The Role of Calcium Ions in Cardiac
Contractions
• As slow calcium channels close
• Intracellular Ca2+ is absorbed by the SR
• Or pumped out of cell
• Cardiac muscle tissue
• Very sensitive to extracellular Ca2+ concentrations
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20-2 The Conducting System
• The Energy for Cardiac Contractions
• Aerobic energy of heart
• From mitochondrial breakdown of fatty acids and
glucose
• Oxygen from circulating hemoglobin
• Cardiac muscles store oxygen in myoglobin
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20-3 The Cardiac Cycle
• The Cardiac Cycle
• Is the period between the start of one heartbeat
and the beginning of the next
• Includes both contraction and relaxation
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20-3 The Cardiac Cycle
• Two Phases of the Cardiac Cycle
• Within any one chamber
1. Systole (contraction)
2. Diastole (relaxation)
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Figure 20-16 Phases of the Cardiac Cycle
Cardiaccycle
370msec
100 msec
0msec800
msec
Start
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Figure 20-16a Phases of the Cardiac Cycle
Cardiaccycle
100 msec
0msec800
msec
Atrial systole begins:Atrial contraction forces a small amount ofadditional blood into relaxed ventricles.
Start
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Figure 20-16b Phases of the Cardiac Cycle
Cardiaccycle
100 msec
Atrial systole ends,atrial diastolebegins
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Figure 20-16c Phases of the Cardiac Cycle
Cardiaccycle
Ventricular systole—first phase: Ventricularcontraction pushes AVvalves closed but doesnot create enoughpressure to opensemilunar valves.
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Figure 20-16d Phases of the Cardiac Cycle
Cardiaccycle
370msec
Ventricular systole—second phase: Asventricular pressure risesand exceeds pressurein the arteries, thesemilunar valvesopen and bloodis ejected.
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Figure 20-16e Phases of the Cardiac Cycle
Cardiaccycle
370msec
Ventricular diastole—early:As ventricles relax, pressure inventricles drops; blood flows backagainst cusps of semilunar valvesand forces them closed. Bloodflows into the relaxed atria.
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Figure 20-16f Phases of the Cardiac Cycle
Cardiaccycle
Ventriculardiastole—late:All chambers arerelaxed.Ventricles fillpassively.
800msec
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20-3 The Cardiac Cycle
• Blood Pressure
• In any chamber
• Rises during systole
• Falls during diastole
• Blood flows from high to low pressure
• Controlled by timing of contractions
• Directed by one-way valves
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20-3 The Cardiac Cycle
• Cardiac Cycle and Heart Rate
• At 75 beats per minute (bpm)
• Cardiac cycle lasts about 800 msec
• When heart rate increases
• All phases of cardiac cycle shorten, particularly diastole
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20-3 The Cardiac Cycle
• Phases of the Cardiac Cycle
• Atrial systole
• Atrial diastole
• Ventricular systole
• Ventricular diastole
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20-3 The Cardiac Cycle
• Atrial Systole
1. Atrial systole
• Atrial contraction begins
• Right and left AV valves are open
2. Atria eject blood into ventricles
• Filling ventricles
3. Atrial systole ends
• AV valves close
• Ventricles contain maximum blood volume
• Known as end-diastolic volume (EDV)
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20-3 The Cardiac Cycle
• Ventricular Systole
4. Ventricles contract and build pressure
• AV valves close cause isovolumetric contraction
5. Ventricular ejection
• Ventricular pressure exceeds vessel pressure opening the
semilunar valves and allowing blood to leave the ventricle
• Amount of blood ejected is called the stroke volume (SV)
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20-3 The Cardiac Cycle
• Ventricular Systole
6. Ventricular pressure falls
• Semilunar valves close
• Ventricles contain end-systolic volume (ESV), about 40%
of end-diastolic volume
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Figure 20-17 Pressure and Volume Relationships in the Cardiac CycleATRIAL
SYSTOLEATRIAL
DIASTOLE
VENTRICULARDIASTOLE
VENTRICULARSYSTOLE
Strokevolume
End-diastolicvolume
Le
ftv
en
tric
ula
rv
olu
me
(m
L)
Pre
ss
ure
(mm
Hg
)
Aortic valveopens
Aorta
Leftventricle
Left atrium Left AVvalve closes AV valves open; passive ventricular
filling occurs.
Isovolumetric relaxation occurs.
Semilunar valves close.
Ventricular ejection occurs.
Isovolumetric ventricular contraction.
Atrial systole ends; AV valves close.
Atria eject blood into ventricles.
Atrial contraction begins.
ATRIAL DIASTOLE
Time (msec)
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20-3 The Cardiac Cycle
• Ventricular Diastole
7. Ventricular diastole
• Ventricular pressure is higher than atrial pressure
• All heart valves are closed
• Ventricles relax (isovolumetric relaxation)
8. Atrial pressure is higher than ventricular pressure
• AV valves open
• Passive atrial filling
• Passive ventricular filling
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Figure 20-17 Pressure and Volume Relationships in the Cardiac CycleATRIAL
SYSTOLEATRIAL DIASTOLE
VENTRICULARSYSTOLE
VENTRICULAR DIASTOLE
AV valves open; passive ventricularfilling occurs.
Isovolumetric relaxation occurs.
Semilunar valves close.
Ventricular ejection occurs.
Isovolumetric ventricular contraction.
Atrial systole ends; AV valves close.
Atria eject blood into ventricles.
Atrial contraction begins.
Time (msec)
End-systolicvolume
Aortic valvecloses
Dicroticnotch
Left AVvalve opens
Le
ftv
en
tric
ula
rv
olu
me
(m
L)
Pre
ss
ure
(mm
Hg
)
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20-3 The Cardiac Cycle
• Heart Sounds
• S1
• Loud sounds
• Produced by AV valves
• S2
• Loud sounds
• Produced by semilunar valves
ANIMATION The Heart: Cardiac Cycle
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20-3 The Cardiac Cycle
• S3, S4
• Soft sounds
• Blood flow into ventricles and atrial contraction
• Heart Murmur
• Sounds produced by regurgitation through valves
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Figure 20-18a Heart Sounds
Aorticvalve
Pulmonaryvalve
Valve locationSounds heard
LeftAVvalve
RightAVvalve
Placements of a stethoscope forlistening to the different soundsproduced by individual valves
Valve location
Sounds heard
Valve locationSounds heard
Valve locationSounds heard
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Figure 20-18b Heart Sounds
Semilunarvalves close
AV valvesopen
AV valvesclose
“Dubb”“Lubb”
The relationship between heart sounds and key events in thecardiac cycle
Heart sounds
Pre
ss
ure
(mm
Hg
)
Aorta
Semilunarvalves open
Leftventricle
Leftatrium
S1
S4S4
S2S3
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20-4 Cardiodynamics
• Cardiodynamics
• The movement and force generated by cardiac contractions
• End-diastolic volume (EDV)
• End-systolic volume (ESV)
• Stroke volume (SV)
• SV = EDV – ESV
• Ejection fraction
• The percentage of EDV represented by SV
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Figure 20-19 A Simple Model of Stroke Volume
Filling
Ventriculardiastole
End-diastolicvolume (EDV)
Pumping
Ventricularsystole
Strokevolume
End-systolicvolume(ESV)
Start
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Figure 20-19 A Simple Model of Stroke Volume
Filling
Ventriculardiastole
When the pump handle israised, pressure within thecylinder decreases, andwater enters through aone-way valve. This corresponds to passive filling during ventricular diastole.
Start
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Figure 20-19 A Simple Model of Stroke Volume
At the start of the pumpingcycle, the amount of water inthe cylinder corresponds to theamount of blood in a ventricleat the end of ventriculardiastole. This amount is knownas the end-diastolic volume(EDV).
End-diastolicvolume (EDV)
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Figure 20-19 A Simple Model of Stroke Volume
Pumping
As the pump handle ispushed down, water is forcedout of the cylinder. This cor-responds to the period ofventricular ejection.
Ventricularsystole
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Figure 20-19 A Simple Model of Stroke Volume
When the handle is depressed asfar as it will go, some water willremain in the cylinder. That amountcorresponds to the end-systolicvolume (ESV) remaining in theventricle at the end of ventricularsystole. The amount of waterpumped out corresponds to thestroke volume of the heart; thestroke volume is the differencebetween the EDV and the ESV.
Strokevolume
End-systolicvolume(ESV)
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20-4 Cardiodynamics
• Cardiac Output (CO)
• The volume pumped by left ventricle in 1 minute
• CO = HR SV
• CO = cardiac output (mL/min)
• HR = heart rate (beats/min)
• SV = stroke volume (mL/beat)
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20-4 Cardiodynamics
• Factors Affecting Cardiac Output
• Cardiac output
• Adjusted by changes in heart rate or stroke volume
• Heart rate
• Adjusted by autonomic nervous system or hormones
• Stroke volume
• Adjusted by changing EDV or ESV
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Figure 20-20 Factors Affecting Cardiac Output
End-systolicvolume
End-diastolicvolume
HormonesAutonomicinnervation
STROKE VOLUME (SV) = EDV – ESVHEART RATE (HR)
CARDIAC OUTPUT (CO) = HR SV
Factors AffectingHeart Rate (HR)
Factors AffectingStroke Volume (SV)
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20-4 Cardiodynamics
• Autonomic Innervation
• Cardiac plexuses innervate heart
• Vagus nerves (N X) carry parasympathetic
preganglionic fibers to small ganglia in cardiac plexus
• Cardiac centers of medulla oblongata
• Cardioacceleratory center controls sympathetic neurons
(increases heart rate)
• Cardioinhibitory center controls parasympathetic neurons
(slows heart rate)
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20-4 Cardiodynamics
• Autonomic Innervation
• Cardiac reflexes
• Cardiac centers monitor:
• Blood pressure (baroreceptors)
• Arterial oxygen and carbon dioxide levels (chemoreceptors)
• Cardiac centers adjust cardiac activity
• Autonomic tone
• Dual innervation maintains resting tone by releasing ACh and NE
• Fine adjustments meet needs of other systems
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Figure 20-21 Autonomic Innervation of the Heart
Cardioinhibitorycenter
Cardioacceleratorycenter
Vagal nucleus
Medullaoblongata
Vagus (N X)
Spinal cord
Parasympathetic
Parasympatheticpreganglionicfiber
Synapses incardiac plexus
Parasympatheticpostganglionicfibers
Cardiac nerve
Sympatheticpostganglionic fiber
Sympatheticpreganglionicfiber
Sympatheticganglia (cervicalganglia andsuperior thoracicganglia [T1–T4])
Sympathetic
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20-4 Cardiodynamics
• Effects on the SA Node
• Membrane potential of pacemaker cells
• Lower than other cardiac cells
• Rate of spontaneous depolarization depends on:
• Resting membrane potential
• Rate of depolarization
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Figure 20-22a Autonomic Regulation of Pacemaker Function
Prepotential(spontaneous
depolarization)
Normal (resting)
Membranepotential
(mV)
Threshold
Heart rate: 75 bpm
Pacemaker cells have membrane potentials closer to thresholdthan those of other cardiac muscle cells (–60 mV versus–90 mV). Their plasma membranes undergo spontaneousdepolarization to threshold, producing action potentials at afrequency determined by (1) the resting-membrane potentialand (2) the rate of depolarization.
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20-4 Cardiodynamics
• Effects on the SA Node
• Sympathetic and parasympathetic stimulation
• Greatest at SA node (heart rate)
• ACh (parasympathetic stimulation)
• Slows the heart
• NE (sympathetic stimulation)
• Speeds the heart
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Figure 20-22b Autonomic Regulation of Pacemaker Function
Parasympathetic stimulation releases ACh, whichextends repolarization and decreases the rate ofspontaneous depolarization. The heart rate slows.
Slower depolarization
Hyperpolarization
Parasympathetic stimulation
Heart rate: 40 bpm
Membranepotential
(mV)
Threshold
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Figure 20-22c Autonomic Regulation of Pacemaker Function
Sympathetic stimulation releases NE, which shortensrepolarization and accelerates the rate of spontaneousdepolarization. As a result, the heart rate increases.
Time (sec)
More rapiddepolarization
Reduced repolarization
Sympathetic stimulation
Heart rate: 120 bpm
Membranepotential
(mV)
Threshold
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20-4 Cardiodynamics
• Atrial Reflex
• Also called Bainbridge reflex
• Adjusts heart rate in response to venous return
• Stretch receptors in right atrium
• Trigger increase in heart rate
• Through increased sympathetic activity
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20-4 Cardiodynamics
• Hormonal Effects on Heart Rate
• Increase heart rate (by sympathetic stimulation of
SA node)
• Epinephrine (E)
• Norepinephrine (NE)
• Thyroid hormone
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20-4 Cardiodynamics
• Factors Affecting the Stroke Volume
• The EDV amount of blood a ventricle contains at the
end of diastole
• Filling time
• Duration of ventricular diastole
• Venous return
• Rate of blood flow during ventricular diastole
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20-4 Cardiodynamics
• Preload
• The degree of ventricular stretching during ventricular
diastole
• Directly proportional to EDV
• Affects ability of muscle cells to produce tension
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20-4 Cardiodynamics
• The EDV and Stroke Volume
• At rest
• EDV is low
• Myocardium stretches less
• Stroke volume is low
• With exercise
• EDV increases
• Myocardium stretches more
• Stroke volume increases
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20-4 Cardiodynamics
• The Frank–Starling Principle
• As EDV increases, stroke volume increases
• Physical Limits
• Ventricular expansion is limited by:
• Myocardial connective tissue
• The cardiac (fibrous) skeleton
• The pericardial sac
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20-4 Cardiodynamics
• End-Systolic Volume (ESV)
• Is the amount of blood that remains in the ventricle
at the end of ventricular systole
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20-4 Cardiodynamics
• Three Factors That Affect ESV
1. Preload
• Ventricular stretching during diastole
2. Contractility
• Force produced during contraction, at a given preload
3. Afterload
• Tension the ventricle produces to open the semilunar
valve and eject blood
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20-4 Cardiodynamics
• Contractility
• Is affected by:
• Autonomic activity
• Hormones
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20-4 Cardiodynamics
• Effects of Autonomic Activity on Contractility
• Sympathetic stimulation
• NE released by postganglionic fibers of cardiac nerves
• Epinephrine and NE released by adrenal medullae
• Causes ventricles to contract with more force
• Increases ejection fraction and decreases ESV
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20-4 Cardiodynamics
• Effects of Autonomic Activity on Contractility
• Parasympathetic activity
• Acetylcholine released by vagus nerves
• Reduces force of cardiac contractions
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20-4 Cardiodynamics
• Hormones
• Many hormones affect heart contraction
• Pharmaceutical drugs mimic hormone actions
• Stimulate or block beta receptors
• Affect calcium ions (e.g., calcium channel blockers)
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20-4 Cardiodynamics
• Afterload
• Is increased by any factor that restricts arterial
blood flow
• As afterload increases, stroke volume decreases
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Figure 20-23 Factors Affecting Stroke Volume
Preload
Factors Affecting Stroke Volume (SV)
Venous return (VR)VR = EDV FT = EDV
Filling time (FT) Increased bysympatheticstimulation
Decreased byparasympathetic
stimulation
Increased by E, NE,glucagon,
thyroid hormones
Contractility (Cont)of muscle cellsCont = ESV Increased by
vasoconstrictionDecreased byvasodilation
Afterload (AL)AL = ESVEnd-systolic
volume (ESV)End-diastolicvolume (EDV)
STROKE VOLUME (SV)ESV = SV
VR = EDV FT = EDV
Cont = ESV
AL = ESV
ESV = SVEDV = SVEDV = SV
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20-4 Cardiodynamics
• Summary: The Control of Cardiac Output
• Heart Rate Control Factors
• Autonomic nervous system
• Sympathetic and parasympathetic
• Circulating hormones
• Venous return and stretch receptors
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20-4 Cardiodynamics
• Summary: The Control of Cardiac Output
• Stroke Volume Control Factors
• EDV
• Filling time, and rate of venous return
• ESV
• Preload, contractility, afterload
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20-4 Cardiodynamics
• Cardiac Reserve
• The difference between resting and maximal
cardiac output
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20-4 Cardiodynamics
• The Heart and Cardiovascular System
• Cardiovascular regulation
• Ensures adequate circulation to body tissues
• Cardiovascular centers
• Control heart and peripheral blood vessels
• Cardiovascular system responds to:
• Changing activity patterns
• Circulatory emergencies
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Figure 20-24 A Summary of the Factors Affecting Cardiac Output
Hormones
Factors affecting heart fate (HR) Factors affecting stroke volume (SV)
CARDIAC OUTPUT (CO) = HR SV
STROKE VOLUME (SV) = EDV – ESVHEART RATE (HR)
AfterloadEnd-systolicvolume
End-diastolicvolume
Vasodilation orvasoconstriction
ContractilityPreload
HormonesAutonomicinnervation
Fillingtime
Venousreturn
Changes inperipheralcirculation
Bloodvolume
Skeletalmuscleactivity
Autonomicinnervation
Atrialreflex