Fundamentals of Anatomy &

Physiology
Eleventh Edition

Chapter 20

The Heart

Lecture Presentation by
Deborah A. Hutchinson
Seattle University

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Learning outcomes 1
1. Describe the major functions of each component of the
cardiovascular system (blood, heart, vessels).
2. Identify and describe the function of major anatomical landmarks
of the heart.
3. Compare and contrast the structure and function of atrioventricular
and semilunar valves.
4. Describe the layers of the pericardium and their functions.

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20.1 Anatomy of the Heart (1 of 12)
• Pulmonary circuit
– Carries blood to and from gas exchange surfaces of
lungs
• Systemic circuit
– Carries blood to and from the rest of the body
• Each circuit begins and ends at the heart
– Blood travels through these circuits in sequence
– Arteries, Carry blood away from heart
– Veins, Return blood to heart
– Capillaries (exchange vessels)
▪Exchange dissolved gases, nutrients, and wastes
between blood and surrounding tissues
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Figure 20.1 An Overview of the
Cardiovascular System

Driven by the pumping of the heart, blood flows through the pulmonary and systemic circuits
in sequence. Each circuit begins and ends at the heart and contains arteries, capillaries, and
veins.
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20.1 Anatomy of the Heart (2 of 12)
• Four chambers of the heart
– Right atrium
▪Receives blood from systemic circuit
– Right ventricle
▪Pumps blood into pulmonary circuit
– Left atrium
▪Receives blood from pulmonary circuit
– Left ventricle
▪Pumps blood into systemic circuit

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20.1 Anatomy of the Heart (3 of 12)
• Heart
– Great vessels connect at base (superior)
– Pointed tip is apex (inferior)
– Sits between two pleural cavities in mediastinum

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Figure 20.2a The Location of the Heart
in the Thoracic Cavity

An anterior view of the chest, showing the position of the heart and major blood vessels
relative to the ribs, lungs, and diaphragm. ATLAS: Plates 47a,b

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20.1 Anatomy of the Heart (4 of 12)
• Pericardium
– Surrounds heart
– Outer fibrous pericardium
– Inner serous pericardium
▪Outer parietal layer and an Inner visceral layer
(epicardium)
– Pericardial cavity
▪Between parietal and visceral layers
▪Contains pericardial fluid
• Pericarditis – inflammation of the pericardium may be fatal.

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Figure 20.2b The Location of the Heart
in the Thoracic Cavity

A superior view of the organs in the mediastinum; portions of the lungs have been removed
to reveal blood vessels and airways. The heart is located in the anterior part of the
mediastinum, immediately posterior to the sternum. ATLAS: Plates 47a,b

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Figure 20.2c The Location of the Heart
in the Thoracic Cavity

The relationship between the heart and the pericardial cavity; compare with the fist-and-
balloon example. ATLAS: Plates 47a,b

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20.1 Anatomy of the Heart (5 of 12)
• Superficial Anatomy – models and heart dissection. See also lab manual 17A
page 462

• Identify the following external structures

• Coronary sulcus Anterior interventricular sulcus

• posterior interventricular sulcus Superior vena cava
• Right atrium Right ventricle
• Left atrium Left ventricle
• Ascending aorta Descending aorta
• Pulmonary trunk Pulmonary veins

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Figure 20.3b The Position and
Superficial Anatomy of the Heart

Major anatomical features on the anterior surface.

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Figure 20.3d The Position and
Superficial Anatomy of the Heart

Major anatomical features 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 (6 of 12)
• Heart wall consists of three distinct layers
– Visceral layer of serous pericardium (epicardium)
▪Covers surface of heart
▪Covered by parietal layer of serous pericardium
– Myocardium
▪Cardiac muscle tissue
– Endocardium
▪Covers inner surfaces of heart
▪Simple squamous epithelium and areolar tissue

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Figure 20.4a The Heart Wall

A diagrammatic section through the hear wall, showing the relative positions of the
myocardium, pericardium, and endocardium. The proportions are not to scale; the thickness
of the myodardial wall has been greatly reduced.

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Figure 20.4b The Heart Wall

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 (7 of 12)
• Internal Anatomy and Organization – models and heart dissection. Page 462

• Identify the following internal structures

• Interatrial septum Interventricular septum

• Atrioventricular (AV) valves Semilunar valves
(bicuspid, tricuspid) (pulmonary, aortic)
• Coronary sinus Fossa ovalis
• Pectinate muscles chordae tendineae
• Trabeculae carneae Papillary muscles

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20.1 Anatomy of the Heart (8 of 12)
• Connective tissues of the heart
– Physically support cardiac muscle fibers, blood vessels, and nerves
of myocardium
– Distribute forces of contraction
– Add strength and prevent overexpansion of heart
– Provide elasticity that helps return heart to original size and shape
after contraction
• Cardiac skeleton
– Four dense bands of tough elastic tissue
▪Encircle heart valves and bases of pulmonary trunk and aorta
▪Stabilize positions of heart valves and ventricular muscle cells
▪Electrically insulate ventricular cells from atrial cells

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Figure 20.5a The Sectional Anatomy
of the Heart (1 of 2)

A diagrammatic frontal section through the heart, showing anatomical features and the path
of blood flow (marked by arrows) through the atria, ventricles, and associated vessels.

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Figure 20.5b The Sectional Anatomy
of the Heart

Papillary muscles and chordae tendineae support the mitral valve and tricuspid valve.

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Figure 20.5c The Sectional Anatomy
of the Heart

Anterior view of a frontally sectioned heart showing internal features and valves.

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20.1 Anatomy of the Heart (9 of 12)
• Compared to left ventricle, the right ventricle
– Holds and pumps the same amount of blood
– Has thinner walls
– Develops less pressure
– Is more pouch-shaped than round

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Figure 20.6a Structural Differences
between the Left and Right Ventricles

A diagrammatic sectional view through the heart, showing the relative thicknesses of the two
ventricular walls. Note the pouchlike shape of the right ventricle and the greater thickness of
the left ventricular muscle. ATLAS: Plate 45d

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Figure 20.6b Structural Differences
between the Left and Right Ventricles

Diagrammatic views of the ventricles just before a contractions (dilated) and just after a
contraction (contracted). ATLAS: Plate 45d

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20.1 Anatomy of the Heart (10 of 12)
• Heart valves
– Prevent backflow of blood
• Atrioventricular (A V) valves
– When ventricles contract,
▪Blood pressure closes valves
▪Papillary muscles contract and tense chordae
tendineae prevents valves from entering atria.
• Semilunar valves
– no muscular support, the cusps support like a tripod.
• Valvular heart disease (VH D)
▪Deterioration of valve function
▪May develop after carditis or rheumatic fever
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Figure 20.7a Valves of the Heart and
Blood Flow (Part 1 of 2)

When the ventricles are relaxed, the tricuspid and mitral valves are open and the aortic and
pulmonary valves are closed. The chordae tendineae are loose, and the papillary muscles
are relaxed.
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Figure 20.7a Valves of the Heart and
Blood Flow (Part 2 of 2)

When the ventricles are relaxed, the tricuspid and mitral valves are open and the aortic and
pulmonary valves are closed. The chordae tendineae are loose, and the papillary muscles
are relaxed.
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Figure 20.7b Valves of the Heart and
Blood Flow (Part 1 of 2)

When the ventricles are contracting, the tricuspid and mitral valves are closed and the aortic
and pulmonary valves are open. In the frontal section, note the attachment of the mitral valve
to the chordae tendineae and the papillary muscles.
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Figure 20.7b Valves of the Heart and
Blood Flow (Part 2 of 2)

When the ventricles are contracting, the tricuspid and mitral valves are closed and the aortic
and pulmonary valves are open. In the frontal section, note the attachment of the mitral valve
to the chordae tendineae and the papillary muscles.
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Learning outcomes 2
• Identify the right and left coronary arteries and their
branches, the cardiac veins, and the coronary sinus and
describe blood flow to and from the heart wall.

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20.1 Anatomy of the Heart (11 of 12)
• Coronary circulation
– Supplies blood to muscle tissue of heart
– Coronary arteries
▪Originate at aortic sinuses
▪Elevated blood pressure and elastic rebound of
aorta maintain blood flow through coronary arteries
• The Cardiac Veins
– Drain blood from tissue and return to circulation via
coronary sinus.

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Figure 20.8a The Coronary Circulation

Coronary vessels supplying and draining the anterior surface of the heart. ATLAS: Plates
45b,c
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Figure 20.8b The Coronary Circulation

Coronary vessels supplying and draining the posterior surface of the heart. ATLAS: Plates
45b,c
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Figure 20.8c The Coronary Circulation

A posterior view of the heart; the vessels have been injected with colored latex (liquid
rubber). ATLAS: Plates 45b,c
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Structures to identify on models/dissection
3

• Identify the following cardiac vessels page 462

 Right coronary artery Great cardiac vein
 Marginal arteries Anterior cardiac veins
 Circumflex artery posterior cardiac veins
 Posterior interventricular artery middle cardiac vein
 Anterior interventricular artery small cardiac vein
 Ascending aorta superior vena cava
 Arch of aorta Inferior vena cava
 R&L pulmonary arteries R&L pulmonary veins

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20.1 Anatomy of the Heart (12 of 12)
• Coronary artery disease (CA D)
– 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 reduces cardiac
performance
• Coronary ischemia
– Reduced circulatory supply from partial or complete
blockage of coronary arteries

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Figure 20.9 Heart Disease and Heart
Attacks (Part 1 of 4)

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Figure 20.9 Heart Disease and Heart
Attacks (Part 2 of 4)

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Figure 20.9 Heart Disease and Heart
Attacks (Part 3 of 4)

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Learning outcomes 4
• Describe the blood flow through the heart naming each structure
blood passes through and classifying each as containing either
oxygenated or deoxygenated blood.

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Figure 20-1 An Overview of the Cardiovascular System

PULMONARY CIRCUIT SYSTEMIC CIRCUIT

Pulmonary arteries Systemic arteries
Pulmonary veins Systemic veins

Capillaries
in head,
neck, upper
Capillaries limbs
in lungs
Right Left
atrium atrium

Right Left
ventricle ventricle

Capillaries
in trunk
and lower
limbs
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ICA - circulation
• Complete lab activity 17B on page 470 of your lab manual.

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Learning outcomes 5
• Describe the physiology of cardiac muscle contraction including ion
movement.
• List the parts of the conduction system, and explain how the system
functions.
• Describe the role of the autonomic nervous system.
• Identify the waveforms in a normal EKG and what each represents.
• Discuss the phases of the cardiac cycle.
• Relate the electrical events represented on the EKG to the normal
events of the cardiac cycle.

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20.2 The Conducting System (1 of 13)
• Heartbeat
– A single cardiac contraction
– All heart chambers contract in series
▪ First the atria
▪ Then the ventricles
• Two types of cardiac muscle cells
– Autorhythmic cells
▪Control and coordinate heartbeat
– Contractile cells
▪Produce contractions that propel blood

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20.2 The Conducting System (2 of 13)
• Conducting system - video
– Consists of specialized cardiac muscle cells
▪Initiate and distribute electrical impulses that
stimulate contraction
– Autorhythmicity
▪Cardiac muscle tissue contracts without neural or
hormonal stimulation

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20.2 The Conducting System (3 of 13)
• Components of the conducting system
– Pacemaker cells found in
▪Sinoatrial (S A) node—in wall of right atrium
▪Atrioventricular (A V) node—at junction between
atria and ventricles
– Conducting cells found in
▪Internodal pathways of atria
▪Atrioventricular (A V) bundle, bundle branches,
and Purkinje fibers of ventricles

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20.2 The Conducting System (4 of 13)
• Pacemaker potential
– Gradual depolarization of pacemaker cells
▪Do not have a stable resting membrane potential
• Rate of spontaneous depolarization
– S A node: 60–100 action potentials per minute
– A V node: 40–60 action potentials per minute
• S A node depolarizes first
– Establishing sinus rhythm
• Parasympathetic stimulation slows heart rate

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Figure 20.10a The Conducting System
of the Heart and the Pacemaker
Potential

Components of the conducting system.

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Figure 20.10b The Conducting System
of the Heart and the Pacemaker
Potential

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 pacemaker potential, a gradual spontaneous
depolarization.
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Figure 20.11 Impulse Conduction
through the Heart and Accompanying
EC G Tracings (Part 1 of 5)

The EC G tracings are explained in the next section and in Figure 20.12 on page 706. After
reading about the electrocardiogram, come back to this figure to integrate the electrical
activity of the heart and atrial and ventricular contractions.
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Figure 20.11 Impulse Conduction
through the Heart and Accompanying
EC G Tracings (Part 2 of 5)

The EC G tracings are explained in the next section and in Figure 20.12 on page 706. After
reading about the electrocardiogram, come back to this figure to integrate the electrical
activity of the heart and atrial and ventricular contractions.
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Figure 20.11 Impulse Conduction
through the Heart and Accompanying
EC G Tracings (Part 3 of 5)

The EC G tracings are explained in the next section and in Figure 20.12 on page 706. After
reading about the electrocardiogram, come back to this figure to integrate the electrical
activity of the heart and atrial and ventricular contractions.
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Figure 20.11 Impulse Conduction
through the Heart and Accompanying
EC G Tracings (Part 4 of 5)

The EC G tracings are explained in the next section and in Figure 20.12 on page 706. After
reading about the electrocardiogram, come back to this figure to integrate the electrical
activity of the heart and atrial and ventricular contractions.
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Figure 20.11 Impulse Conduction
through the Heart and Accompanying
EC G Tracings (Part 5 of 5)

The EC G tracings are explained in the next section and in Figure 20.12 on page 706. After
reading about the electrocardiogram, come back to this figure to integrate the electrical
activity of the heart and atrial and ventricular contractions.
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20.2 The Conducting System (5 of 13)
• Disturbances in heart rhythm
– Bradycardia—abnormally slow heart rate
– Tachycardia—abnormally fast heart rate
– Ectopic pacemaker
▪Abnormal cells generate high rate of action
potentials
▪Bypasses conducting system
▪Disrupts timing of ventricular contractions

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20.2 The Conducting System (6 of 13)
• Electrocardiogram (EC G or EK G)
– A recording of electrical events in the heart
– Obtained by placing electrodes at specific locations on
body surface
– Abnormal patterns are used to diagnose damage

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20.2 The Conducting System (7 of 13)
• Features of an EC G
– P wave
▪Depolarization of atria
– Q R S complex
▪Depolarization of ventricles
▪Ventricles begin contracting shortly after R wave
– T wave
▪Repolarization of ventricles

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20.2 The Conducting System (8 of 13)
• Time intervals between EC G waves
– P–R interval
▪From start of atrial depolarization
▪To start of Q R S complex
– Q–T interval
▪Time required for ventricles to undergo a single
cycle of depolarization and repolarization

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Figure 20.12a An Electrocardiogram
(EC G)

Electrode placement for recording a standard EC G.

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Figure 20.12b An Electrocardiogram
(EC G)

An EC G 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 EC G; the enlarged section
indicates the major components of the EC G and the measurements most often taken during
clinical analysis.
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Figure 20.13 Cardiac Arrhythmias (Part
1 of 2)

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Figure 20.13 Cardiac Arrhythmias
(Part 2 of 2)

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ICA - ECG
• Complete lab exercise 17D part 1 the ECG page 475

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20.2 The Conducting System (9 of 13)
• Cardiac contractile cells
– Form bulk of atrial and ventricular walls
– Receive stimulus from Purkinje fibers
– Resting membrane potential
▪Of ventricular cell is about –90 mV
▪Of atrial cell is about –80 mV
• Intercalated discs
– Interconnect cardiac contractile cells
– Transfer force of contraction from cell to cell
– Propagate action potentials

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Figure 20.14a Cardiac Contractile
Cells

Cardiac contractile cells

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Figure 20.14b Cardiac Contractile
Cells

Structure of an intercalated disc

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Figure 20.14c Cardiac Contractile
Cells

Cardiac muscle tissue

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20.2 The Conducting System (10 of 13)
• Characteristics of cardiac contractile cells
– Small size
– Single, central nucleus
– Branching interconnections between cells
– Intercalated discs

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20.2 The Conducting System (11 of 13)

• Influx of Na depolarizes cell

• At +20mV Na+ channels close, Ca+ and K+ channels open
• Ca+ enters cell, K+ leaves cell = membrane potential does
not change (plateau)
• Increase of Ca+ inside cell causes SR to release additional
Ca+
• Ca+ binds troponin, moves tropomyosin from myosin
binding sites on actin. Power stroke.

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20.2 The Conducting System (12 of 13)
• Ca channels slowly close, K+ channels stay open
• Membrane repolarizes, Ca2+ pumped out of cell and into SR.
• Na/K pump restores resting membrane potential.
• Note LONG refractory period where cell cannot respond to a second
stimulus
• Prevents wave summation and tetany
• https://youtu.be/DMOelVeSQ1w?si=YPQ3Tz2z5cBSNQzT

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Figure 20.15a Action Potentials in
Cardiac Contractile Cells and Skeletal
Muscle Fibers

Events in an action potential in a ventricular contractile cell.

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Figure 20.15b Action Potentials in
Cardiac Contractile Cells and Skeletal
Muscle Fibers
Action Potentials in Cardiac Contractile Cells and Skeletal
Muscle Fibers.

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20.2 The Conducting System (13 of 13)
• Calcium
– 20% of required calcium ions from extracellular space.
– This triggers release from sarcoplasmic reticulum (SR)
– Heart very sensitive to variations in plasma Ca2+ concentrations
• Energy for contraction
– Cardiomyocytes use aerobic respiration to generate ATP
– Uses fatty acid not glucose
– High O2 requirement, stable blood supply, backup O2 stored in
myoglobin in cells

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ICA - contraction
• What ions move into the cell to depolarize?
• What maintains the plateau?
• Why do Ca ions trigger contraction?
• Draw and label depolarization of cardiomyocyte showing all ion flow
• Why is it important that heart cells do not enter tetany?

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20.3 The Cardiac Cycle (1 of 9)
Learning Outcomes:
• Relate the opening and closing of the specific heart valves
to each phase of the cardiac cycle.
• Relate the heart sounds to the cardiac cycle.

• Cardiac cycle
– From start of one heartbeat to beginning of next
– Includes alternating periods of contraction and
relaxation
• Phases of the cardiac cycle within each chamber
– Systole (contraction)
– Diastole (relaxation)
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Figure 20.16 Phases of the Cardiac
Cycle

Thin black arrows indicate blood flow, green arrows indicate contractions, and the red-hued
areas indicate which heart chambers are in systole.
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Figure 20.16a Phases of the Cardiac
Cycle

Atrial systole begins: Atrial contraction forces a small amount of additional blood into
relaxed ventricles.
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Figure 20.16b Phases of the Cardiac
Cycle

Atrial systole ends, atrial diastole begins

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Figure 20.16c Phases of the Cardiac
Cycle

Ventricular systole—first phase: Ventricular contraction exerts enough pressure on the blood
to close AV valves but not enough to open semilunar valves.
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Figure 20.16d Phases of the Cardiac
Cycle

Ventricular systole—second phase: As ventricular pressure rises and exceeds pressure in

the arteries, the semilunar valves open and blood is ejected.
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Figure 20.16e Phases of the Cardiac
Cycle

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.

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Figure 20.16f Phases of the Cardiac
Cycle

Ventricular diastole—late: All chambers are relaxed. Ventricles fill passively.

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20.3 The Cardiac Cycle (2 of 9)
• Blood pressure in each chamber
– Rises during systole
– Falls during diastole
• Blood flows from an area of higher pressure to one of lower
pressure
– Controlled by timing of contractions
– Directed by one-way valves
• At 75 beats per minute (bpm) cardiac cycle lasts about
800msec
– When heart rate increases all phases of cardiac cycle
shorten, particularly diastole.

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20.3 The Cardiac Cycle (4 of 9)
• Phases of the cardiac cycle
– Atrial systole, contraction of atria blood moves into
ventricles
– Atrial diastole, atria relax, atria contain maximum blood
volume (end diastolic volume, EDV)
– Ventricular systole, contraction of ventricles, blood
moves through SL valves
– Ventricular diastole, ventricles relaxed but AV valves still
closed

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Figure 20.17 Pressure and Volume
Relationships in the Cardiac Cycle
(Part 3 of 4)

Major features of the cardiac cycle are shown for a heart rate of 75 bp m.
The circled numbers correspond to those in the associated box. For
further details, see the numbered list in the text pp. 713 – 715 .
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Figure 20.17 Pressure and Volume
Relationships in the Cardiac Cycle
(Part 4 of 4)

Major features of the cardiac cycle are shown for a heart rate of 75 bp m. The circled
numbers correspond to those in the associated box. For further details, see the numbered
list in the text (pp. 713–715).
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20.3 The Cardiac Cycle (9 of 9)
• Heart sounds
– Detected with a stethoscope
– S1 —Loud sound as A V valves close
– S2 —Loud sound as semilunar valves close
– S3 ,S4 —Soft sounds

▪ Blood flowing into ventricles and atrial contraction

– Heart murmur
▪ Sounds produced by regurgitation through valves

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Figure 20.18a Heart Sounds

Placements of a stethoscope for listening to the different sounds produced by individual

valves
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Figure 20.18b Heart Sounds

The relationship between heart sounds and key events in the cardiac cycle
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Heart sounds
• Using the stethoscopes complete auscultation of heart sounds 17D
part 2 from your lab manual page 478

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20.4 Cardiac Output (1 of 19)

• Learning Outcome: Define and calculate cardiac output.

▪Predict how changes in heart rate and/or stroke
volume will affect cardiac output.
• Cardiac output (C O)
– 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)

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Figure 20.19 Factors Affecting Cardiac
Output

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20.4 Cardiac Output (2 of 19)
• Stroke volume (S V)
– S V = ED V – ES V
– End-diastolic volume (ED V)
▪Amount of blood in each ventricle at end of
ventricular diastole
– End-systolic volume (ES V)
▪Amount of blood remaining in each ventricle at end
of ventricular systole
– Ejection fraction
▪Percentage of ED V ejected during contraction

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Figure 20.20 A Simple Model of Stroke
Volume (Part 1 of 4)

The stroke volume of the heart can be compared to the amount of water ejected from a
simple pump. The amount of water ejected varies with the amount of movement of the pump
handle.
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Figure 20.20 A Simple Model of Stroke
Volume (Part 2 of 4)

The stroke volume of the heart can be compared to the amount of water ejected from a
simple pump. The amount of water ejected varies with the amount of movement of the pump
handle.
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Figure 20.20 A Simple Model of Stroke
Volume (Part 3 of 4)

The stroke volume of the heart can be compared to the amount of water ejected from a
simple pump. The amount of water ejected varies with the amount of movement of the pump
handle.
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Figure 20.20 A Simple Model of Stroke
Volume (Part 4 of 4)

The stroke volume of the heart can be compared to the amount of water ejected from a
simple pump. The amount of water ejected varies with the amount of movement of the pump
handle.
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20.4 Cardiac Output (3 of 19)
• Factors affecting heart rate
– Autonomic activity
– Circulating hormones

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20.4 Cardiac Output (4 of 19)

• Autonomic innervation.
– Cardiac plexuses innervate heart
– Vagus nerves (N X) carry parasympathetic nerves to cardiac
plexus
• Cardiac center of medulla oblongata
monitors – blood pressure, arterial O2 and CO2 levels

• Adjusts cardiac activity.

– Cardioacceleratory center controls sympathetic neurons
(increases heart rate)
– Cardioinhibitory center controls parasympathetic neurons
(slows heart rate)
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Figure 20.21 Autonomic Innervation of
the Heart

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20.4 Cardiac Output (5 of 19)
• Effects on pacemaker cells of S A node
– Membrane potentials of pacemaker cells
▪Are closer to threshold than those of cardiac
contractile cells
– Any factor that changes the rate of spontaneous
depolarization or the duration of repolarization
▪Will alter heart rate
▪By changing time required to reach threshold

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Figure 20.22a Autonomic Regulation
of Pacemaker Cell Function

Pacemaker cells have membrane potentials closer to threshold than those of cardiac
contractile cells ( 60 mV versus  90 mV). Their plasma membranes spontaneously
depolarize to threshold, producing action potentials at a frequency determined by (1) the
membrane potential and (2) the rate of depolarization.
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20.4 Cardiac Output (6 of 19)
• Effects on pacemaker cells of S A node
– AC h released by parasympathetic neurons
▪Decreases heart rate
– N E released by sympathetic neurons
▪Increases heart rate

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Figure 20.22b Autonomic Regulation
of Pacemaker Cell Function

Parasympathetic stimulation releases AC h, which extends repolarization and decreases the

rate of spontaneous depolarization. The hear rate slows.
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Figure 20.22c Autonomic Regulation
of Pacemaker Cell Function

Sympathetic stimulation releases N E, which shortens repolarization and accelerates the rate
of spontaneous depolarization. As a result, the heart rate increases.
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20.4 Cardiac Output (7 of 19)
• Bainbridge reflex (atrial reflex)
– increase in venous return triggers stretch receptors
which stimulate sympathetic activity and increase in
heart rate.
• Hormonal effects on heart rate
– Heart rate is increased by: epinephrine, norepinephrine
and thyroid hormone

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20.4 Cardiac Output (8 of 19)
• Factors affecting stroke volume
– Changes in ED V or ES V affect stroke volume
▪And thus cardiac output
– Two factors affect ED V
▪Filling time
–Duration of ventricular diastole
▪Venous return

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20.4 Cardiac Output (9 of 19)
• Effects of autonomic activity on contractility
– Sympathetic stimulation
▪NE released by cardiac nerves
▪E and N E released by adrenal medullae
▪Causes ventricles to contract with more force
▪Increases ejection fraction, decreases ES V
– Parasympathetic stimulation
▪AC h released by vagus nerves
▪Reduces force of cardiac contractions

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20.4 Cardiac Output (10 of 19)
• Hormones
– Many hormones affect heart contractility
– Pharmaceutical drugs mimic hormone actions
▪Stimulate or block alpha or beta receptors
▪Block calcium channels
• Afterload
– Increased by any factor that restricts blood flow
– As afterload increases, stroke volume decreases

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Figure 20.23 Factors Affecting Stroke
Volume

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20.4 Cardiac Output (11 of 19)
• Summary: the control of cardiac output
– Heart rate control factors
▪Autonomic nervous system
–Sympathetic and parasympathetic
▪Circulating hormones
▪Venous return and stretch receptors
– Stroke volume control factors
▪ED V—filling time and rate of venous return
▪ES V—preload, contractility, and afterload

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Figure 20.24 A Summary of the
Factors Affecting Cardiac Output

a) Cardiac output varies widely to meet metabolic demands

b) Factors affecting cardia output

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20.4 Cardiac Output (12 of 19)
• Cardiac reserve
– Difference between resting and maximal cardiac outputs
• 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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 Normal values
Measure Typical value Normal range
end-diastolic volume (EDV) 120 mL 65–240 mL
end-systolic volume (ESV) 50 mL 16–143 mL
stroke volume (SV) 70 mL 55–100 mL
ejection fraction (Ef) 58% 55–70%
heart rate (HR) 75 bpm 60–100 bpm
cardiac output (CO) 5.25 4.0–8.0 L/min

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Review – cardiac output (1 of 2)

• If veins contract (under sympathetic stimulation)

what factors change?
• What does this do to cardiac output?
• If heart rate increases how does output change?
• If ejection volume decreases how does output
change?

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Review cardiac output (2 of 2)

• If EDV = 120 and ESV = 50 for a heart rate of 70bpm

what is the CO?
• Given the same values of EDV and ESV if heart rate
is 120bpm what is CO?
• If EDV is 240 and ESV is 60, what is CO at 60bpm
and at 100bpm?
• Which (if any) of these values either abnormally low or
abnormally high?

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