Download Right ventricle - Anatomy and Physiology

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
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Figure 20-1 An Overview of the Cardiovascular System.
PULMONARY CIRCUIT
Pulmonary arteries
Pulmonary veins
Capillaries
in lungs
Right
atrium
Right
ventricle
Capillaries
in trunk
and lower
limbs
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SYSTEMIC CIRCUIT
Systemic arteries
Systemic veins
Capillaries
in head,
neck, upper
limbs
Left
atrium
Left
ventricle
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
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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
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Figure 20-2a The Location of the Heart in the Thoracic Cavity.
Trachea
First rib (cut)
Thyroid
gland
Base of
heart
Right lung
Left lung
Parietal
pericardium
(cut)
Apex of
heart
Diaphragm
a An anterior view of the chest, showing the
position of the heart and major blood vessels
relative to the ribs, lungs, and diaphragm.
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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
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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
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Figure 20-2c The Location of the Heart in the Thoracic Cavity.
Base of
heart
Cut edge of
parietal pericardium
Fibrous tissue of
pericardial sac
Wrist (corresponds
to base of heart)
Inner wall (corresponds
to epicardium)
Parietal pericardium
Areolar tissue
Mesothelium
Fibrous
attachment to
diaphragm
Air space (corresponds
to pericardial cavity)
Cut edge of epicardium
Outer wall (corresponds
to parietal pericardium)
Apex of heart
Balloon
c The relationship between the heart and the pericardial cavity; compare with the fist-and-balloon example.
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Figure 20-3a The Position and Superficial Anatomy of the Heart.
Base of heart
1
2
3
4
5
6
7
8
9
10
1
Ribs
2
3
4
5
6
7
8
9
10
a Heart position relative to the rib cage.
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Apex of
heart
Figure 20-3b The Position and Superficial Anatomy of the Heart.
Left subclavian artery
Left common
carotid artery
Arch of aorta
Ligamentum
arteriosum
Brachiocephalic
trunk
Descending
aorta
Ascending
aorta
Left pulmonary
artery
Superior
vena cava
Auricle
of right
atrium
Pulmonary
trunk
Right
atrium
Auricle of
left atrium
Right
ventricle
Fat and
vessels in
coronary
sulcus
Fat and vessels
in anterior
interventricular
sulcus
Left
ventricle
b Major anatomical features on the anterior surface.
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Figure 20-3d The Position and Superficial Anatomy of the Heart.
Arch of aorta
Left pulmonary artery
Right pulmonary
artery
Left pulmonary veins
Fat and vessels
in coronary
sulcus
Superior
vena cava
Left
atrium
Coronary
sinus
Right
atrium
Left
ventricle
Right
ventricle
Right
pulmonary
veins
(superior
and inferior)
Inferior
vena cava
Fat and vessels in posterior
interventricular sulcus
d Major landmarks on the posterior surface. Coronary
arteries (which supply the heart itself) are shown in
red; coronary veins are shown in blue.
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20-1 Anatomy of the Heart
• The Heart Wall
1. Epicardium
2. Myocardium
3. Endocardium
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20-1 Anatomy of the Heart
• Epicardium (Outer Layer)
• Visceral pericardium
• Covers the heart
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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
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Figure 20-4a The Heart Wall.
Myocardium
(cardiac muscle tissue)
Cardiac muscle cells
Connective tissues
Pericardial
cavity
Parietal
pericardium
Dense fibrous layer
Areolar tissue
Mesothelium
Artery
Vein
Endocardium
Endothelium
Areolar tissue
Epicardium
(visceral
pericardium)
Mesothelium
Areolar tissue
a A diagrammatic section through the heart
wall, showing the relative positions of the
epicardium, myocardium, and endocardium.
The proportions are not to scale; the
thickness of the myocardial wall has been
greatly reduced.
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Figure 20-4b The Heart Wall.
Atrial
musculature
Ventricular
musculature
b Cardiac muscle tissue
forms concentric layers that
wrap around the atria or spiral
within the walls of the ventricles.
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20-1 Anatomy of the Heart
• Internal Anatomy and Organization
• Interatrial septum separates atria
• Interventricular septum separates ventricles
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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
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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
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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
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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
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Figure 20-6a The Sectional Anatomy of the Heart.
Left common carotid artery
Left subclavian artery
Brachiocephalic
trunk
Superior
vena cava
Ligamentum arteriosum
Pulmonary trunk
Aortic arch
Pulmonary valve
Right
pulmonary
arteries
Left pulmonary
arteries
Ascending aorta
Fossa ovalis
Opening of
coronary sinus
Right atrium
Pectinate muscles
Left
atrium
Left pulmonary
veins
Interatrial septum
Aortic valve
Cusp of left AV
(mitral) valve
Conus arteriosus
Left ventricle
Cusp of right AV
(tricuspid) valve
Chordae tendineae
Papillary muscles
Right ventricle
Interventricular
septum
Trabeculae
carneae
Inferior vena cava
Moderator band
Descending aorta
a A diagrammatic frontal section through the heart, showing
major landmarks and the path of blood flow (marked by
arrows) through the atria, ventricles, and associated vessels.
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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
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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
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Figure 20-6b The Sectional Anatomy of the Heart.
Chordae tendineae
Papillary muscles
b The papillary muscles and chordae
tendineae support the right AV (tricuspid)
valve. The photograph was taken from
inside the right ventricle, looking toward
a light shining from the right atrium.
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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
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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
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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
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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
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Figure 20-6c The Sectional Anatomy of the Heart.
Left subclavian artery
Left common carotid artery
Brachiocephalic trunk
Superior vena cava
Ascending aorta
Pulmonary
trunk
Cusp of
pulmonary valve
Auricle of left atrium
Right atrium
Cusp of left AV
(bicuspid) valve
Chordae tendineae
Cusps of right AV
(tricuspid) valve
Papillary muscles
Left ventricle
Trabeculae carneae
Right ventricle
c Anterior view of a frontally sectioned
heart showing internal features and valves.
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Interventricular
septum
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
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Figure 20-7a Structural Differences between the Left and Right Ventricles.
Posterior
interventricular
sulcus
Left
ventricle
Right
ventricle
Fat in anterior
interventricular sulcus
a
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A diagrammatic sectional view through
the heart, showing the relative thicknesses
of the two ventricles. Notice the pouchlike
shape of the right ventricle and the greater
thickness of the left ventricle.
Figure 20-7b Structural Differences between the Left and Right Ventricles.
Right
ventricle
Left
ventricle
Dilated
Contracted
b Diagrammatic views of the
ventricles just before a
contraction (dilated) and just
after a contraction (contracted).
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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
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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
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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
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Figure 20-8a Valves of the Heart (Part 1 of 2).
Transverse Sections, Superior View,
Atria and Vessels Removed
POSTERIOR
Cardiac
skeleton
Relaxed ventricles
RIGHT
VENTRICLE
Left AV (bicuspid)
valve (open)
LEFT
VENTRICLE
Right AV
(tricuspid)
valve (open)
Aortic valve
(closed)
ANTERIOR
a
Aortic valve closed
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Pulmonary
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.
Figure 20-8a Valves of the Heart (Part 2 of 2).
Frontal Sections through Left Atrium and Ventricle
Pulmonary
veins
Relaxed ventricles
LEFT
ATRIUM
Left AV (bicuspid)
valve (open)
Aortic valve
(closed)
Chordae
tendineae (loose)
Papillary muscles
(relaxed)
LEFT VENTRICLE
(relaxed and filling
with blood)
a
© 2015 Pearson Education, Inc.
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.
Figure 20-8b Valves of the Heart (Part 1 of 2).
Contracting ventricles
Right AV
(tricuspid) valve
(closed)
RIGHT
VENTRICLE
Cardiac
skeleton
Left AV
(bicuspid) valve
(closed)
LEFT
VENTRICLE
Aortic valve
(open)
Pulmonary
valve (open)
b When the ventricles are contracting,
Aortic valve open
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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.
Contracting ventricles
Figure 20-8b Valves of the Heart (Part 2 of 2).
Aorta
Aortic sinus
Aortic valve
(open)
LEFT
ATRIUM
Left AV (bicuspid)
valve (closed)
Chordae tendineae
(tense)
Papillary muscles
(contracted)
Left ventricle
(contracted)
b 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.
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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
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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
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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
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Figure 20-9a The Coronary Circulation.
Aortic
arch
Ascending
aorta
Right
coronary
artery
Left coronary
artery
Pulmonary
trunk
Circumflex
artery
Anterior
interventricular
artery
Atrial
arteries
Great
cardiac
vein
Anterior
cardiac
veins
Small
cardiac vein
Marginal
artery
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a Coronary vessels supplying
and draining the anterior
surface of the heart.
Figure 20-9b The Coronary Circulation.
Coronary sinus
Circumflex artery
Great cardiac vein
Marginal artery
Posterior
interventricular
artery
Posterior
cardiac
vein
Small
cardiac
vein
Left
ventricle
Right
coronary
artery
Middle cardiac vein
Marginal artery
b Coronary vessels supplying and draining
the posterior surface of the heart.
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Figure 20-9c The Coronary Circulation.
Auricle of
left atrium
Left pulmonary
veins
Left pulmonary
artery
Right
pulmonary
artery
Circumflex
artery
Superior
vena cava
Great cardiac
vein
Marginal
artery
Right
pulmonary
veins
Posterior
cardiac vein
Left atrium
Right atrium
Inferior
vena cava
Coronary sinus
Middle cardiac vein
Right ventricle
Posterior interventricular artery
c A posterior view of the heart; the vessels have
been injected with colored latex (liquid rubber).
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Figure 20-10 Heart Disease and Heart Attacks (Part 2 of 4).
Narrowing of Artery
Normal Artery
Tunica
externa
Lipid deposit
of plaque
Tunica
media
Cross section
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Cross section
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
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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
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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
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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)
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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
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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
© 2015 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
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20-1 Anatomy of the Heart
• Heart Disease – Coronary Artery Disease
• Treatment of CAD and myocardial infarction
• About 25 percent of MI patients die before
obtaining medical assistance
• 65 percent 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)
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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
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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
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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
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20-1 Anatomy of the Heart
• Heart Disease – Coronary Artery Disease
• Treatment of CAD and myocardial infarction
• Coronary artery bypass graft (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
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Figure 20-10 Heart Disease and Heart Attacks (Part 1 of 4).
Normal Heart
A color-enhanced digital
subtraction angiography (DSA)
scan of a normal heart.
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Figure 20-10 Heart Disease and Heart Attacks (Part 3 of 4).
Occluded
Coronary
Artery
Damaged
Heart
Muscle
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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 atria
• 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
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Figure 20-11a The Conducting System of the Heart.
Sinoatrial
(SA) node
Internodal
pathways
Atrioventricular
(AV) node
AV bundle
Bundle
branches
Purkinje
fibers
a Components of the
conducting system.
© 2015 Pearson Education, Inc.
Figure 20-11b The Conducting System of the Heart.
+20 mV
0 mV
−20 mV
Threshold
−40 mV
−60 mV
Prepotential
0
0.8
Time (sec)
1.6
b Changes in the membrane potential of a pacemaker
cell in the SA node that is establishing a heart rate
of 72 beats per minute. Note the presence of a
prepotential, a gradual spontaneous depolarization.
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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 (Part 1 of 5).
1
SA node activity and
atrial activation begin.
Time = 0
© 2015 Pearson Education, Inc.
SA
node
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
© 2015 Pearson Education, Inc.
Figure 20-12 Impulse Conduction through the Heart (Part 2 of 5).
2
Stimulus spreads across the
atrial surfaces and reaches
the AV node.
AV
node
Elapsed time = 50 msec
© 2015 Pearson Education, Inc.
Figure 20-12 Impulse Conduction through the Heart (Part 3 of 5).
3
There is a 100-msec delay
at the AV node. Atrial
contraction begins.
AV
bundle
Bundle
branches
Elapsed time = 150 msec
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
Figure 20-12 Impulse Conduction through the Heart (Part 4 of 5).
4
The impulse travels along the
interventricular septum within
the AV bundle and the bundle
branches to the Purkinje fibers
and, by the moderator band,
to the papillary muscles of the
right ventricle.
Moderator
band
Elapsed time = 175 msec
© 2015 Pearson Education, Inc.
20-2 The Conducting System
• Purkinje Fibers
• Distribute impulse through ventricles (Step 5)
• Atrial contraction is completed
• Ventricular contraction begins
© 2015 Pearson Education, Inc.
Figure 20-12 Impulse Conduction through the Heart (Part 5 of 5).
5
The impulse is distributed by
Purkinje fibers and relayed
throughout the ventricular
myocardium. Atrial contraction
is completed, and ventricular
contraction begins.
Elapsed time = 225 msec
© 2015 Pearson Education, Inc.
Purkinje fibers
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
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
20-2 The Conducting System
• Features of an ECG
• P wave
• Atria depolarize
• QRS complex
• Ventricles depolarize
• T wave
• Ventricles repolarize
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
Figure 20-13a An Electrocardiogram.
a Electrode placement for
recording a standard ECG.
© 2015 Pearson Education, Inc.
Figure 20-13b An Electrocardiogram.
800 msec
+1
R
P wave
(atria
depolarize)
R
T wave
(ventricles
repolarize)
P–R segment
S–T
segment
+0.5
0
Q S
P–R
interval
S–T
interval
Q–T
interval
b
Millivolts
QRS interval
(ventricles depolarize)
−0.5
An ECG printout is a strip of graph paper containing a record of the electrical events
monitored by the electrodes. The placement of electrodes on the body surface affects
the size and shape of the waves recorded. The example is a normal ECG; the enlarged
section indicates the major components of the ECG and the measurements most often
taken during clinical analysis.
© 2015 Pearson Education, Inc.
Figure 20-14 Cardiac Arrhythmias (Part 1 of 2).
Premature Atrial Contractions (PACs)
P
P
P
Paroxysmal Atrial Tachycardia (PAR)
P
P
P
Atrial Fibrillation (AF)
© 2015 Pearson Education, Inc.
P
P
P
Premature atrial contractions (PACs)
often occur in healthy individuals. In a PAC,
the normal atrial rhythm is momentarily
interrupted by a “surprise” atrial contraction.
Stress, caffeine, and various drugs may
increase the incidence of PACs, presumably
by increasing the permeabilities of the SA
pacemakers. The impulse spreads along the
conduction pathway, and a normal ventricular
contraction follows the atrial beat.
In paroxysmal (par-ok-SIZ-mal) atrial
tachycardia, or PAT, a premature atrial
contraction triggers a flurry of atrial activity.
The ventricles are still able to keep pace, and the
heart rate jumps to about 180 beats per minute.
During atrial fibrillation (fib-ri-LĀ-shun), the
impulses move over the atrial surface at rates
of perhaps 500 beats per minute. The atrial wall
quivers instead of producing an organized
contraction. The ventricular rate cannot follow
the atrial rate and may remain within normal
limits. Even though the atria are now
nonfunctional, their contribution to ventricular
end-diastolic volume (the maximum amount of
blood the ventricles can hold at the end of atrial
contraction) is so small that the condition may
go unnoticed in older individuals.
Figure 20-14 Cardiac Arrhythmias (Part 2 of 2).
Premature Ventricular Contractions (PVCs)
P
T
P
T
P
Ventricular Tachycardia (VT)
P
Ventricular Fibrillation (VF)
© 2015 Pearson Education, Inc.
T
Premature ventricular contractions (PVCs)
occur when a Purkinje cell or ventricular
myocardial cell depolarizes to threshold and
triggers a premature contraction. Single PVCs
are common and not dangerous. The cell
Ventricular tachycardia is defined as four or
more PVCs without intervening normal beats. It
is also known as VT or V-tach. Multiple PVCs
and VT may indicate that serious cardiac
problems exist.
Ventricular fibrillation (VF) is
responsible for the condition known as
cardiac arrest. VF is rapidly fatal,
because the ventricles quiver and
stop pumping blood.
responsible is called an ectopic pacemaker.
The frequency of PVCs can be increased by
exposure to epinephrine, to other stimulatory
drugs, or to ionic changes that depolarize
cardiac muscle plasma membranes.
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
© 2015 Pearson Education, Inc.
Figure 20-15a The Action Potentials in Skeletal and Cardiac Muscle.
1
Rapid Depolarization
2
Cause: Na+ entry
Duration: 3–5 msec
Ends with: Closure of
voltage-gated fast
sodium channels
3
The Plateau
Cause: Ca2+ entry
Duration: ∼175 msec
Ends with: Closure
of slow calcium
channels
Repolarization
Cause: K+ loss
Duration: 75 msec
Ends with: Closure
of slow potassium
channels
+30
2
0
1
mV
3
Absolute refractory
−90
Relative
refractory
period
KEY
period
0
Stimulus
100
200
Time (msec)
a Events in an action potential in a ventricular
muscle cell.
© 2015 Pearson Education, Inc.
300
Absolute refractory
period
Relative refractory
period
Figure 20-15b The Action Potentials in Skeletal and Cardiac Muscle.
+30
Skeletal
muscle
Action
potential
0
Cardiac
muscle
+30
0
Action potential
mV
mV
−90
−85
Tension
Tension
Contraction
0
100
200
Contraction
300
0
Time (msec)
b Action potentials and twitch contractions in a
skeletal muscle (above) and cardiac muscle (below).
The shaded areas indicate the durations of the
absolute (blue) and relative (beige) refractory periods.
© 2015 Pearson Education, Inc.
100
200
300
Time (msec)
KEY
Absolute refractory
period
Relative refractory
period
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
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
20-2 The Conducting System
• The Role of Calcium Ions in Cardiac Contractions
1. 20 percent 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)
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
20-3 The Cardiac Cycle
• Two Phases of the Cardiac Cycle
• Within any one chamber
1. Systole (contraction)
2. Diastole (relaxation)
© 2015 Pearson Education, Inc.
Figure 20-16 Phases of the Cardiac Cycle.
Start
a Atrial systole begins:
Atrial contraction forces a small amount
of additional blood into relaxed ventricles.
b Atrial systole
ends, atrial
diastole begins
0
800
msec
msec
f Ventricular
100
msec
Cardiac
cycle
c Ventricular systole—
diastole—late:
All chambers are relaxed.
Ventricles fill passively.
370
msec
first phase: Ventricular
contraction pushes AV
valves closed but does
not create enough
pressure to open
semilunar valves.
d Ventricular systole—
e Ventricular diastole—early:
As ventricles relax, pressure in
ventricles drops; blood flows back
against cusps of semilunar valves
and forces them closed. Blood
flows into the relaxed atria.
© 2015 Pearson Education, Inc.
second phase: As
ventricular pressure rises
and exceeds pressure
in the arteries, the
semilunar valves
open and blood
is ejected.
Figure 20-16a Phases of the Cardiac Cycle.
Start
a
Atrial systole begins:
Atrial contraction forces a small amount
of additional blood into relaxed ventricles.
0
800
msec
msec
Cardiac
cycle
© 2015 Pearson Education, Inc.
100
msec
Figure 20-16b Phases of the Cardiac Cycle.
b Atrial systole
ends, atrial
diastole begins
100
msec
Cardiac
cycle
© 2015 Pearson Education, Inc.
Figure 20-16c Phases of the Cardiac Cycle.
Cardiac
cycle
© 2015 Pearson Education, Inc.
c Ventricular systole—
first phase: Ventricular
contraction pushes AV
valves closed but does
not create enough
pressure to open
semilunar valves.
Figure 20-16d Phases of the Cardiac Cycle.
d Ventricular systole—
Cardiac
cycle
370
msec
© 2015 Pearson Education, Inc.
second phase: As
ventricular pressure rises
and exceeds pressure
in the arteries, the
semilunar valves
open and blood
is ejected.
Figure 20-16e Phases of the Cardiac Cycle.
Cardiac
cycle
370
msec
e
© 2015 Pearson Education, Inc.
Ventricular diastole—early:
As ventricles relax, pressure in
ventricles drops; blood flows back
against cusps of semilunar valves
and forces them closed. Blood
flows into the relaxed atria.
Figure 20-16f Phases of the Cardiac Cycle.
800
msec
Cardiac
cycle
f Ventricular
diastole—late:
All chambers are relaxed.
Ventricles fill passively.
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
20-3 The Cardiac Cycle
• Phases of the Cardiac Cycle
•
•
•
•
Atrial systole
Atrial diastole
Ventricular systole
Ventricular diastole
© 2015 Pearson Education, Inc.
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)
© 2015 Pearson Education, Inc.
20-3 The Cardiac Cycle
• Ventricular Systole
4. Ventricles contract and build pressure
• AV valves close causing 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)
© 2015 Pearson Education, Inc.
20-3 The Cardiac Cycle
• Ventricular Systole
6. Ventricular pressure falls
• Semilunar valves close
• Ventricles contain end-systolic volume (ESV),
about 40 percent of end-diastolic volume
© 2015 Pearson Education, Inc.
Figure 20-17 Pressure and Volume Relationships in the Cardiac Cycle (Part 3 of 4).
ATRIAL
ATRIAL
DIASTOLE SYSTOLE
VENTRICULAR
DIASTOLE
ATRIAL DIASTOLE
VENTRICULAR
SYSTOLE
5
120
Aortic valve
opens
Aorta
90
Pressure
(mm Hg)
1 Atrial contraction begins.
2 Atria eject blood into ventricles.
3 Atrial systole ends; AV valves close.
60
Left
ventricle
4 Isovolumetric ventricular contraction.
4
5 Ventricular ejection occurs.
6 Semilunar valves close.
30
7 Isovolumetric relaxation occurs.
Left AV
valve closes
Left atrium
8 AV valves open; passive ventricular
filling occurs.
2
1
3
0
Left
ventricular
volume (mL)
130
3
End-diastolic
volume
2
1
Stroke
volume
50
0
100
200
300
Time (msec)
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
Figure 20-17 Pressure and Volume Relationships in the Cardiac Cycle (Part 4 of 4).
ATRIAL
SYSTOLE
ATRIAL DIASTOLE
VENTRICULAR
SYSTOLE
VENTRICULAR DIASTOLE
120
Aortic valve
closes
6
90
Pressure
(mm Hg)
Dicrotic
notch
1 Atrial contraction begins.
2 Atria eject blood into ventricles.
3 Atrial systole ends; AV valves close.
60
4 Isovolumetric ventricular contraction.
7
5 Ventricular ejection occurs.
6 Semilunar valves close.
7 Isovolumetric relaxation occurs.
Left AV
valve opens
30
8 AV valves open; passive ventricular
filling occurs.
8
0
Left
ventricular
volume (mL)
130
End-systolic
volume
6
50
300
400
Time (msec)
© 2015 Pearson Education, Inc.
500
600
700
800
20-3 The Cardiac Cycle
• Heart Sounds
• S1
• Loud sounds
• Produced by AV valves
• S2
• Loud sounds
• Produced by semilunar valves
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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
© 2015 Pearson Education, Inc.
Figure 20-18a Heart Sounds.
Sounds heard
Valve location
Aortic
valve
Valve location Pulmonary
Sounds heard valve
Sounds heard
Valve location
Left
AV
valve
Valve location
Sounds heard
Right
AV
valve
a Placements of a stethoscope for
listening to the different sounds
produced by individual valves
© 2015 Pearson Education, Inc.
Figure 20-18b Heart Sounds.
120
Semilunar
valves open
Semilunar
valves close
Pressure
(mm Hg)
90
60
Left
ventricle
Left
atrium
30
AV valves
close
AV valves
open
0
S1
S4
S2
S3
Heart sounds
“Lubb”
“Dupp”
b The relationship between heart sounds and key events in the
cardiac cycle
© 2015 Pearson Education, Inc.
S4
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
© 2015 Pearson Education, Inc.
Figure 20-19 A Simple Model of Stroke Volume.
Start
When the pump handle is
raised, pressure within
the cylinder decreases,
and water enters through
a one-way valve. This
corresponds to passive
filling during ventricular
diastole.
Filling
At the start of the pumping
cycle, the amount of water
in the cylinder corresponds
to the amount of blood in
a ventricle at the end of
ventricular diastole. This
amount is known as the enddiastolic volume (EDV).
Ventricular
diastole
End-systolic
volume
(ESV)
End-diastolic
volume (EDV)
Stroke
volume
Pumping
When the handle is depressed
as far as it will go, some water
will remain in the cylinder. That
amount corresponds to the
end-systolic volume (ESV)
remaining in the ventricle at the
end of ventricular systole. The
amount of water pumped out
corresponds to the stroke
volume of the heart; the stroke
volume is the difference
between the EDV and the ESV.
© 2015 Pearson Education, Inc.
Ventricular
systole
As the pump handle is
pushed down, water is
forced out of the cylinder.
This corresponds to the
period of ventricular ejection.
Figure 20-19 A Simple Model of Stroke Volume (Part 1 of 4).
Start
When the pump handle is
raised, pressure within
the cylinder decreases,
and water enters through
a one-way valve. This
corresponds to passive
filling during ventricular
diastole.
Filling
Ventricular
diastole
© 2015 Pearson Education, Inc.
Figure 20-19 A Simple Model of Stroke Volume (Part 2 of 4).
At the start of the pumping
cycle, the amount of water
in the cylinder corresponds
to the amount of blood in
a ventricle at the end of
ventricular diastole. This
amount is known as the enddiastolic volume (EDV).
End-diastolic
volume (EDV)
© 2015 Pearson Education, Inc.
Figure 20-19 A Simple Model of Stroke Volume (Part 3 of 4).
As the pump handle
is pushed down, water
is forced out of the
cylinder. This corresponds
to the period of ventricular
ejection.
Pumping
Ventricular
systole
© 2015 Pearson Education, Inc.
Figure 20-19 A Simple Model of Stroke Volume (Part 4 of 4).
End-systolic
volume
(ESV)
Stroke
volume
© 2015 Pearson Education, Inc.
When the handle is depressed
as far as it will go, some water
will remain in the cylinder. That
amount corresponds to the
end-systolic volume (ESV)
remaining in the ventricle at the
end of ventricular systole. The
amount of water pumped out
corresponds to the stroke
volume of the heart; the stroke
volume is the difference
between the EDV and the ESV.
20-4 Cardiodynamics
• Cardiac Output (CO)
• The volume pumped by left ventricle in one minute
• CO = HR  SV
• CO = cardiac output (mL/min)
• HR = heart rate (beats/min)
• SV = stroke volume (mL/beat)
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
Figure 20-20 Factors Affecting Cardiac Output.
Factors Affecting
Heart Rate (HR)
Autonomic
innervation
Hormones
HEART RATE (HR)
Factors Affecting
Stroke Volume (SV)
End-diastolic
volume
End-systolic
volume
STROKE VOLUME (SV) = EDV − ESV
CARDIAC OUTPUT (CO) = HR × SV
© 2015 Pearson Education, Inc.
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)
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
Figure 20-21 Autonomic Innervation of the Heart.
Cardioinhibitory
center
Vagal nucleus
Cardioacceleratory
center
Medulla
oblongata
Vagus (N X)
Spinal cord
Sympathetic
Sympathetic
preganglionic
fiber
Sympathetic ganglia
(cervical ganglia and
superior thoracic
ganglia [T1–T4])
Sympathetic
postganglionic fiber
Cardiac nerve
© 2015 Pearson Education, Inc.
Parasympathetic
Parasympathetic
preganglionic
fiber
Synapses in
cardiac plexus
Parasympathetic
postganglionic
fibers
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
© 2015 Pearson Education, Inc.
Figure 20-22a Autonomic Regulation of Pacemaker Function.
+20
Membrane
potential
(mV)
Normal (resting)
Spontaneous
depolarization
0
−30
Threshold
−60
Heart rate: 75 bpm
0.8
a
© 2015 Pearson Education, Inc.
1.6
2.4
Pacemaker cells have membrane potentials closer to
threshold than those of other cardiac muscle cells (–60 mV
versus –90 mV). Their plasma membranes undergo
spontaneous depolarization to threshold, producing
action potentials at a frequency determined by (1) the
membrane potential and (2) the rate of depolarization.
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
© 2015 Pearson Education, Inc.
Figure 20-22b Autonomic Regulation of Pacemaker Function.
+20
Membrane
potential
(mV)
Parasympathetic stimulation
0
−30
Threshold
Hyperpolarization
−60
Heart rate: 40 bpm
0.8
b
© 2015 Pearson Education, Inc.
Slower depolarization
1.6
2.4
Parasympathetic stimulation releases ACh, which
extends repolarization and decreases the rate of
spontaneous depolarization. The heart rate slows.
Figure 20-22c Autonomic Regulation of Pacemaker Function.
Sympathetic stimulation
+20
Membrane
potential
(mV)
0
−30
Threshold
−60
Reduced repolarization
Heart rate: 120 bpm
0.8
More rapid
depolarization
1.6
2.4
Time (sec)
c Sympathetic stimulation releases NE, which shortens
repolarization and accelerates the rate of spontaneous
depolarization. As a result, the heart rate increases.
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
20-4 Cardiodynamics
• Hormonal Effects on Heart Rate
• Increase heart rate (by sympathetic stimulation of
SA node)
• Epinephrine (E)
• Norepinephrine (NE)
• Thyroid hormone
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
20-4 Cardiodynamics
• Preload
• The degree of ventricular stretching during
ventricular diastole
• Directly proportional to EDV
• Affects ability of muscle cells to produce tension
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
20-4 Cardiodynamics
• End-Systolic Volume (ESV)
• Is the amount of blood that remains in the ventricle
at the end of ventricular systole
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
20-4 Cardiodynamics
• Contractility
• Is affected by:
• Autonomic activity
• Hormones
© 2015 Pearson Education, Inc.
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
© 2015 Pearson Education, Inc.
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.
Factors Affecting Stroke Volume (SV)
Venous return (VR)
VR = EDV
VR = EDV
Filling time (FT)
FT = EDV
FT = EDV
Increased by
sympathetic
stimulation
Decreased by
parasympathetic
stimulation
Contractility (Cont)
of muscle cells
Cont = ESV
Cont = ESV
Preload
End-diastolic
volume (EDV)
End-systolic
volume (ESV)
STROKE VOLUME (SV)
EDV =
EDV =
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SV
SV
ESV =
ESV =
SV
SV
Increased by E, NE,
glucagon,
thyroid hormones
Increased by
vasoconstriction
Decreased by
vasodilation
Afterload (AL)
AL = ESV
AL = ESV
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 outputs
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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 20-24a A Summary of the Factors Affecting Cardiac Output.
40
Maximum for
trained athletes
exercising at
peak levels
35
Cardiac output (L/min)
30
25
Normal range
of cardiac
output during
heavy exercise
20
15
10
5
Average resting
cardiac output
Heart failure
0
a
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Cardiac output varies widely
to meet metabolic demands
Figure 20-24b A Summary of the Factors Affecting Cardiac Output.
Factors affecting Factors affecting
heart rate (HR)
stroke volume (SV)
Skeletal Blood Changes in
muscle volume peripheral
activity
circulation
Atrial
reflex
Autonomic
innervation
Venous
return
Hormones
HEART RATE (HR)
Filling
time
Autonomic
innervation
Preload
Contractility
End-diastolic
volume
End-systolic
volume
b
Vasodilation
or
vasoconstriction
STROKE VOLUME (SV) = EDV − ESV
CARDIAC OUTPUT (CO) = HR × SV
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Hormones
Factors affecting cardiac output
Afterload