Human Anatomy and Physiology

Eleventh Edition

Chapter 18 Part A
The Cardiovascular
System

PowerPoint® Lectures Slides prepared by Karen Dunbar Kareiva, Ivy Tech Community College

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18.1 Heart Anatomy

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The Pulmonary and Systemic Circuits (1 of 2)
• Heart is a transport system consisting of two side-by-side pumps
– Right side receives oxygen-poor blood from tissues
 Pumps blood to lungs to get rid of CO2, pick up O2, via pulmonary circuit
– Left side receives oxygenated blood from lungs
 Pumps blood to body tissues via systemic circuit

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The Pulmonary and Systemic Circuits (2 of 2)
• Receiving chambers of heart
– Right atrium
 Receives blood returning from systemic circuit
– Left atrium
 Receives blood returning from pulmonary circuit

• Pumping chambers of heart

– Right ventricle
 Pumps blood through pulmonary circuit
– Left ventricle
 Pumps blood through systemic circuit

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 The Systemic and
Pulmonary Circuits

Figure 18.1 The systemic and pulmonary circuits.

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Size, Location, and Orientation of Heart
(1 of 2)
• Approximately the size of a fist
– Weighs less than 1 pound

• Location
– In mediastinum between second rib and fifth intercostal space
– On superior surface of diaphragm
– Two-thirds of heart to left of midsternal line
– Anterior to vertebral column, posterior to sternum

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 Location of the Heart in the Mediastinum
(1 of 4)

Figure 18.2a Location of the heart in the mediastinum.

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 Location of the Heart in the Mediastinum
(2 of 4)

Figure 18.2b Location of the heart in the mediastinum.

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Size, Location, and Orientation of Heart
(2 of 2)
• Base (posterior surface) leans toward right shoulder

• Apex points toward left hip

• Apical impulse palpated between fifth and sixth ribs, just below left nipple

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 Location of the Heart in the Mediastinum
(3 of 4)

Figure 18.2a Location of the heart in the mediastinum.

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 Location of the Heart in the Mediastinum
(4 of 4)

Figure 18.2b Location of the heart in the mediastinum.

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Coverings of the Heart
• Pericardium: double-walled sac that surrounds heart; made up of two layers
– Superficial fibrous pericardium: functions to protect, anchor heart to surrounding
structures, and prevent overfilling
– Deep two-layered serous pericardium
 Parietal layer lines internal surface of fibrous pericardium
 Visceral layer (epicardium) on external surface of heart
 Two layers separated by fluid-filled pericardial cavity (decreases friction)

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 The Layers of the Pericardium and of the Heart Wall (1

Figure 18.3 The layers of the pericardium and of the heart wall.

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Clinical – Homeostatic Imbalance 18.1
• Pericarditis
– Inflammation of pericardium
– Roughens membrane surfaces, causing pericardial friction rub (creaking sound)
heard with stethoscope
– Cardiac tamponade
 Excess fluid that leaks into pericardial space
 Can compress heart’s pumping ability
 Treatment: fluid is drawn out of cavity (usually with syringe)

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Layers of the Heart Wall (1 of 2)
• Three layers of heart wall
– Epicardium: visceral layer of serous pericardium
– Myocardium: circular or spiral bundles of contractile cardiac muscle cells
 Cardiac skeleton: crisscrossing, interlacing layer of connective tissue
– Anchors cardiac muscle fibers
– Supports great vessels and valves
– Limits spread of action potentials to specific paths

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The Circular and Spiral Arrangement of
Cardiac Muscle Bundles in the Myocardium
of the Heart

Figure 18.4 The circular and spiral arrangement of cardiac muscle bundles in the
myocardium of the heart.

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Layers of the Heart Wall (2 of 2)
– Endocardium: innermost layer; is continuous with endothelial lining of blood
vessels
 Lines heart chambers and covers cardiac skeleton of valves

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 The Layers of the Pericardium and of the Heart Wall (2

Figure 18.3 The layers of the pericardium and of the heart wall.

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Chambers and Associated Great Vessels
(1 of 6)
• Internal features
– Four chambers
 Two superior atria
 Two inferior ventricles
– Interatrial septum: separates atria
 Fossa ovalis: remnant of foramen ovale of fetal heart
– Interventricular septum: separates ventricles

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 Gross Anatomy of the Heart (1 of 9)

Figure 18.5e Gross anatomy of the heart.

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Chambers and Associated Great Vessels
(2 of 6)
• Surface features
– Coronary sulcus (atrioventricular groove)
 Encircles junction of atria and ventricles
– Anterior interventricular sulcus
 Anterior position of interventricular septum
– Posterior interventricular sulcus
 Landmark on posteroinferior surface

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 Gross Anatomy of the Heart (2 of 9)

Figure 18.5b Gross anatomy of the heart.

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 Gross Anatomy of the Heart (3 of 9)

Figure 18.5d Gross anatomy of the heart.

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Chambers and Associated Great Vessels
(3 of 6)
• Atria: the receiving chambers
– Small, thin-walled chambers; contribute little to propulsion of blood
– Auricles: appendages that increase atrial volume
– Right atrium: receives deoxygenated blood from body
 Anterior portion is smooth-walled
 Posterior portion contains ridges formed by pectinate muscles
 Posterior and anterior regions are separated by crista terminalis

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Chambers and Associated Great Vessels
(4 of 6)
• Atria: the receiving chambers (cont.)
– Three veins empty into right atrium:
 Superior vena cava: returns blood from body regions above the diaphragm
 Inferior vena cava: returns blood from body regions below the diaphragm
 Coronary sinus: returns blood from coronary veins
– Left atrium: receives oxygenated blood from lungs
 Pectinate muscles found only in auricles
 Four pulmonary veins return blood from lungs

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 Gross Anatomy of the Heart (4 of 9)

Figure 18.5e Gross anatomy of the heart.

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Chambers and Associated Great Vessels
(5 of 6)
• Ventricles: the discharging chambers
– Make up most of the volume of heart
– Right ventricle: most of anterior surface
– Left ventricle: posteroinferior surface
– Trabeculae carneae: irregular ridges of muscle on ventricular walls
– Papillary muscles: project into ventricular cavity
 Anchor chordae tendineae that are attached to heart valves

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Chambers and Associated Great Vessels
(6 of 6)
• Ventricles: the discharging chambers (cont.)
– Thicker walls than atria
– Actual pumps of heart
– Right ventricle
 Pumps blood into pulmonary trunk
– Left ventricle
 Pumps blood into aorta (largest artery in body)

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 Gross Anatomy of the Heart (5 of 9)

Figure 18.5e Gross anatomy of the heart.

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 Gross Anatomy of the Heart (6 of 9)

Figure 18.5c Gross anatomy of the heart.

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 Gross Anatomy of the Heart (7 of 9)

Figure 18.5f Gross anatomy of the heart.

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Animation – Rotating Heart Sectioned

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Rotating Heart Sectioned

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 Gross Anatomy of the Heart (8 of 9)

Figure 18.5a Gross anatomy of the heart.

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Animation – Rotating Heart

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Rotating Heart

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18.2 Heart Valves (1 of 2)
• Ensure unidirectional blood flow through heart

• Open and close in response to pressure changes

• Two major types of valves

– Atrioventricular valves located between atria and ventricles
– Semilunar valves located between ventricles and major arteries

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18.2 Heart Valves (2 of 2)
• No valves are found between major veins and atria; not a problem because:
– Inertia of incoming blood prevents backflow
– Heart contractions compress venous openings

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 Heart Valves (1 of 3)

Figure 18.6a, b Heart valves.

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Atrioventricular (AV) Valves
• Two atrioventricular (AV) valves prevent backflow into atria when ventricles contract
– Tricuspid valve (right AV valve): made up of three cusps and lies between right
atria and ventricle
– Mitral valve (left AV valve, bicuspid valve): made up of two cusps and lies between
left atria and ventricle
– Chordae tendineae: anchor cusps of AV valves to papillary muscles that function
to:
 Hold valve flaps in closed position
 Prevent flaps from everting back into atria

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 Heart Valves (2 of 3)

Figure 18.6c, d Heart valves.

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 The Function of the Atrioventricular (AV) Valves (1 of 2)

Figure 18.7a The function of the atrioventricular (AV) valves.

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 The Function of the Atrioventricular (AV)
Valves (2 of 2)

Figure 18.7b The function of the atrioventricular (AV) valves.

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 Heart Valves (3 of 3)

Figure 18.6a Heart valves.

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Semilunar (SL) Valves
• Two semilunar (SL) valves prevent backflow from major arteries back into ventricles
– Open and close in response to pressure changes
– Each valve consists of three cusps that roughly resemble a half moon
– Pulmonary semilunar valve: located between right ventricle and pulmonary trunk
– Aortic semilunar valve: located between left ventricle and aorta

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 The Function of the Semilunar (SL) Valves
(1 of 2)

Figure 18.8a The function of the semilunar (SL) valves.

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 The Function of the Semilunar (SL) Valves
(2 of 2)

Figure 18.8b The function of the semilunar (SL) valves.

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Clinical – Homeostatic Imbalance 18.2
• Two conditions severely weaken heart:
– Incompetent valve
 Blood backflows so heart repumps same blood over and over
– Valvular stenosis
 Stiff flaps that constrict opening
 Heart needs to exert more force to pump blood

• Defective valve can be replaced with mechanical, animal, or cadaver valve

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18.3 Pathway of Blood Through Heart (1 of 3)
• Right side of the heart
– Superior vena cava (SVC), inferior vena cava (IVC), and coronary sinus →
– Right atrium →
– Tricuspid valve →
– Right ventricle →
– Pulmonary semilunar valve →
– Pulmonary trunk →
– Pulmonary arteries →
– Lungs

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18.3 Pathway of Blood Through Heart (2 of 3)
• Left side of the heart
– Four pulmonary veins →
– Left atrium →
– Mitral valve →
– Left ventricle →
– Aortic semilunar valve →
– Aorta →
– Systemic circulation

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Figure Animation: Blood Flow Through the
Heart

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 The Heart is a Double Pump, Each Side
Supplying its Own Circuit (1 of 3)

FOCUS FIGURE 18.1 Blood Flow through the Heart

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 The Heart is a Double Pump, Each Side
Supplying its Own Circuit (2 of 3)

FOCUS FIGURE 18.1 Blood Flow through the Heart

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 The Heart is a Double Pump, Each Side Supplying its O
Circuit (3 of 3)

FOCUS FIGURE 18.1 Blood Flow through the Heart

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18.3 Pathway of Blood Through Heart (3 of 3)
• Equal volumes of blood are pumped to pulmonary and systemic circuits

• Pulmonary circuit is short, low-pressure circulation

• Systemic circuit is long, high-friction circulation

• Anatomy of ventricles reflects differences

– Left ventricle walls are 3× thicker than right
 Pumps with greater pressure

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Anatomical Differences Between the Right and Left
Ventricles

Figure 18.9 Anatomical differences between the right and left ventricles.

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Coronary Circulation (1 of 6)
• Coronary circulation
– Functional blood supply to heart muscle itself
– Shortest circulation in body
– Delivered when heart is relaxed
– Left ventricle receives most of coronary blood supply

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Coronary Circulation (2 of 6)
• Coronary arteries
– Both left and right coronary arteries arise from base of aorta and supply arterial
blood to heart
– Both encircle heart in coronary sulcus
– Branching of coronary arteries varies among individuals
– Arteries contain many anastomoses (junctions)
 Provide additional routes for blood delivery
 Cannot compensate for coronary artery occlusion
– Heart receives 1/20th of body’s blood supply

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Coronary Circulation (3 of 6)
• Coronary arteries (cont.)
– Left coronary artery supplies interventricular septum, anterior ventricular walls,
left atrium, and posterior wall of left ventricle; has two branches:
 Anterior interventricular artery
 Circumflex artery
– Right coronary artery supplies right atrium and most of right ventricle; has two
branches:
 Right marginal artery
 Posterior interventricular artery

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 Coronary Circulation (4 of 6)

Figure 18.10a Coronary circulation.

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Coronary Circulation (5 of 6)
• Coronary veins
– Cardiac veins collect blood from capillary beds
– Coronary sinus empties into right atrium; formed by merging cardiac veins
 Great cardiac vein of anterior interventricular sulcus
 Middle cardiac vein in posterior interventricular sulcus
 Small cardiac vein from inferior margin
– Several anterior cardiac veins empty directly into right atrium anteriorly

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 Coronary Circulation (6 of 6)

Figure 18.10b Coronary circulation.

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 Gross Anatomy of the Heart (9 of 9)

Figure 18.5d Gross anatomy of the heart.

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Clinical – Homeostatic Imbalance 18.3
• Angina pectoris
– Thoracic pain caused by fleeting deficiency in blood delivery to myocardium
– Cells are weakened

• Myocardial infarction (heart attack)

– Prolonged coronary blockage
– Areas of cell death are repaired with noncontractile scar tissue

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18.4 Cardiac Muscle Fibers

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Microscopic Anatomy (1 of 3)
• Cardiac muscle cells: striated, short, branched, fat, interconnected
– One central nucleus (at most, 2 nuclei)
– Contain numerous large mitochondria (25–35% of cell volume) that afford
resistance to fatigue
– Rest of volume composed of sarcomeres
 Z discs, A bands, and I bands all present
– T tubules are wider, but less numerous
 Enter cell only once at Z disc
– SR simpler than in skeletal muscle; no triads

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Microscopic Anatomy (2 of 3)
• Intercalated discs are connecting junctions between cardiac cells that contain:
– Desmosomes: hold cells together; prevent cells from separating during contraction
– Gap junctions: allow ions to pass from cell to cell; electrically couple adjacent cells
 Allows heart to be a functional syncytium, a single coordinated unit

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Microscopic Anatomy (3 of 3)
• Intercellular space between cells has connective tissue matrix (endomysium)
– Contains numerous capillaries
– Connects cardiac muscle to cardiac skeleton, giving cells something to pull against

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 Microscopic Anatomy of Cardiac Muscle
(1 of 2)

Figure 18.11a Microscopic anatomy of cardiac muscle.

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 Microscopic Anatomy of Cardiac Muscle
(2 of 2)

Figure 18.11b Microscopic anatomy of cardiac muscle.

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How Does the Physiology of Skeletal and
Cardiac Muscle Differ? (1 of 5)
• Similarities with skeletal muscle
– Muscle contraction is preceded by depolarizing action potential
– Depolarization wave travels down T tubules; causes sarcoplasmic reticulum (SR)
to release Ca2+
– Excitation-contraction coupling occurs
 Ca2+ binds troponin causing filaments to slide

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How Does the Physiology of Skeletal and
Cardiac Muscle Differ? (2 of 5)
• Differences between cardiac and skeletal muscle
– Some cardiac muscle cells are self-excitable
 Two kinds of myocytes
– Contractile cells: responsible for contraction
– Pacemaker cells: noncontractile cells that spontaneously depolarize
• Initiate depolarization of entire heart
• Do not need nervous system stimulation, in contrast to skeletal
muscle fibers

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How Does the Physiology of Skeletal and
Cardiac Muscle Differ? (3 of 5)
– Heart contracts as a unit
 All cardiomyocytes contract as unit (functional syncytium), or none contract
 Contraction of all cardiac myocytes ensures effective pumping action
 Skeletal muscles contract independently
– Influx of Ca2+ from extracellular fluid triggers Ca2+ release from SR
 Depolarization opens slow Ca2+ channels in sarcolemma, allowing Ca2+ to
enter cell
 Extracellular Ca2+ then causes SR to release its intracellular Ca2+
 Skeletal muscles do not use extracellular Ca2+

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How Does the Physiology of Skeletal and
Cardiac Muscle Differ? (4 of 5)
– Tetanic contractions cannot occur in cardiac muscles
 Cardiac muscle fibers have longer absolute refractory period than skeletal
muscle fibers
– Absolute refractory period is almost as long as contraction itself
– Prevents tetanic contractions
– Allows heart to relax and fill as needed to be an efficient pump

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How Does the Physiology of Skeletal and
Cardiac Muscle Differ? (5 of 5)
– The heart relies almost exclusively on aerobic respiration
 Cardiac muscle has more mitochondria than skeletal muscle so has greater
dependence on oxygen
– Cannot function without oxygen
 Skeletal muscle can go through fermentation when oxygen not present
 Both types of tissues can use other fuel sources
– Cardiac is more adaptable to other fuels, including lactic acid, but must
have oxygen

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Table 18.1 Key Differences between Skeletal and Cardiac
Muscle

Table 18.1 Key Differences between Skeletal and Cardiac Muscle

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Human Anatomy and Physiology
Eleventh Edition

Chapter 18 Part B
The Cardiovascular
System

PowerPoint® Lectures Slides prepared by Karen Dunbar Kareiva, Ivy Tech Community College

Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved
18.5 Electrical Events of the Heart
• Heart depolarizes and contracts without nervous system stimulation, although
rhythm can be altered by autonomic nervous system

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Setting the Basic Rhythm: The Intrinsic
Conduction System (1 of 3)
• Coordinated heartbeat is a function of:
– Presence of gap junctions
– Intrinsic cardiac conduction system
 Network of noncontractile (autorhythmic) cells
 Initiate and distribute impulses to coordinate depolarization and
contraction of heart

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Setting the Basic Rhythm: The Intrinsic
Conduction System (2 of 3)
• Action potential initiation by pacemaker cells
– Cardiac pacemaker cells have unstable resting membrane potentials called
pacemaker potentials or prepotentials
– Three parts of action potential
1. Pacemaker potential: K+ channels are closed, but slow Na+ channels are
open, causing interior to become more positive

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Setting the Basic Rhythm: The Intrinsic
Conduction System (3 of 3)
• Action potential initiation by pacemaker cells (cont.)
2. Depolarization: Ca2+ channels open (around 40 mV), allowing huge influx
of Ca2+, leading to rising phase of action potential
3. Repolarization: K+ channels open, allowing efflux of K+, and cell becomes
more negative

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 Pacemaker and Action Potentials of
Typical Cardiac Pacemaker Cells (1 of 3)

Figure 18.12 Pacemaker and action potentials of typical cardiac pacemaker cells.

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 Pacemaker and Action Potentials of
Typical Cardiac Pacemaker Cells (2 of 3)

Figure 18.12 Pacemaker and action potentials of typical cardiac pacemaker cells.

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 Pacemaker and Action Potentials of
Typical Cardiac Pacemaker Cells (3 of 3)

Figure 18.12 Pacemaker and action potentials of typical cardiac pacemaker cells.

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Setting the Basic Rhythm: The Intrinsic
Conduction System (4 of 8)
• Sequence of excitation
– Cardiac pacemaker cells pass impulses, in following order, across heart in
~0.22 seconds
1. Sinoatrial node →
2. Atrioventricular node →
3. Atrioventricular bundle →
4. Right and left bundle branches →
5. Subendocardial conducting network (Purkinje fibers)

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Setting the Basic Rhythm: The Intrinsic
Conduction System (5 of 8)
1. Sinoatrial (SA) node
– Pacemaker of heart in right atrial wall
 Depolarizes faster than rest of myocardium
– Generates impulses about 75×/minute (sinus rhythm)
 Inherent rate of 100×/minute tempered by extrinsic factors
– Impulse spreads across atria, and to AV node

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Setting the Basic Rhythm: The Intrinsic
Conduction System (6 of 8)
2. Atrioventricular (AV) node
– In inferior interatrial septum
– Delays impulses approximately 0.1 second
 Because fibers are smaller in diameter, have fewer gap junctions
 Allows atrial contraction prior to ventricular contraction
– Inherent rate of 50×/minute in absence of SA node input

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Setting the Basic Rhythm: The Intrinsic
Conduction System (7 of 8)
3. Atrioventricular (AV) bundle (bundle of His)
– In superior interventricular septum
– Only electrical connection between atria and ventricles
 Atria and ventricles not connected via gap junctions

4. Right and left bundle branches

– Two pathways in interventricular septum
– Carry impulses toward apex of heart

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Setting the Basic Rhythm: The Intrinsic
Conduction System (8 of 8)
5. Subendocardial conducting network
 Also referred to as Purkinje fibers
– Complete pathway through interventricular septum into apex and ventricular walls
– More elaborate on left side of heart
– AV bundle and subendocardial conducting network depolarize 30/minute in
absence of AV node input
– Ventricular contraction immediately follows from apex toward atria
– Process from initiation at SA node to complete contraction takes ~0.22 seconds

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IP2: Pathway of Depolarization

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IP2: Pathway of Depolarization

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 Intrinsic Cardiac Conduction System and Action
Potential Succession During one Heartbeat (1 of 4)

Figure 18.13 The intrinsic cardiac conduction system.

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 Intrinsic Cardiac Conduction System and Action
Potential Succession During one Heartbeat (2 of 4)

Figure 18.13 The intrinsic cardiac conduction system.

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 Intrinsic Cardiac Conduction System and Action
Potential Succession During one Heartbeat (3 of 4)

Figure 18.13 The intrinsic cardiac conduction system.

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 Intrinsic Cardiac Conduction System and Action
Potential Succession During one Heartbeat (4 of 4)

Figure 18.13 The intrinsic cardiac conduction system.

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Clinical – Homeostatic Imbalance 18.4
(1 of 3)
• Defects in intrinsic conduction system may cause:
– Arrhythmias: irregular heart rhythms
– Uncoordinated atrial and ventricular contractions
– Fibrillation: rapid, irregular contractions
 Heart becomes useless for pumping blood, causing circulation to cease;
may result in brain death
 Treatment: defibrillation interrupts chaotic twitching, giving heart “clean
slate” to start regular, normal depolarizations

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Clinical – Homeostatic Imbalance 18.4
(2 of 3)
• Defective SA node may cause ectopic focus, an abnormal pacemaker that takes
over pacing
– If AV node takes over, it sets junctional rhythm at 40–60 beats/min
– Extrasystole (premature contraction): ectopic focus of small region of heart
that triggers impulse before SA node can, causing delay in next impulse
 Heart has longer time to fill, so next contraction is felt as thud as larger
volume of blood is being pushed out
 Can be from excessive caffeine or nicotine

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Clinical – Homeostatic Imbalance 18.4
(3 of 3)
• To reach ventricles, impulse must pass through AV node

• If AV node is defective, may cause a heart block

– Few impulses (partial block) or no impulses (total block) reach ventricles
– Ventricles beat at their own intrinsic rate
 Too slow to maintain adequate circulation
– Treatment: artificial pacemaker, which recouples atria and ventricles

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Modifying the Basic Rhthym: Extrinsic
Innervation of the Heart
• Heartbeat modified by ANS via cardiac centers in medulla oblongata
– Cardioacceleratory center: sends signals through sympathetic trunk to
increase both rate and force
 Stimulates SA and AV nodes, heart muscle, and coronary arteries
– Cardioinhibitory center: parasympathetic signals via vagus nerve to
decrease rate
 Inhibits SA and AV nodes via vagus nerves

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 Autonomic Innervation of the Heart

Figure 18.14 Autonomic innervation of the heart.

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Action Potentials of Contractile Cardiac
Muscle Cells (1 of 3)
• Contractile muscle fibers make up bulk of heart and are responsible for pumping
action
– Different from skeletal muscle contraction; cardiac muscle action potentials
have plateau

• Steps involved in AP:

1. Depolarization opens fast voltage-gated Na+ channels; Na+ enters cell
 Positive feedback influx of Na+ causes rising phase of AP (from 90 mV to
+30 mV)

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Action Potentials of Contractile Cardiac
Muscle Cells (2 of 3)
2. Depolarization by Na+ also opens slow Ca2+ channels
 At +30 mV, Na+ channels close, but slow Ca2+ channels remain open,
prolonging depolarization
– Seen as a plateau
3. After about 200 ms, slow Ca2+ channels are closed, and voltage-gated K+
channels are open
 Rapid efflux of K+ repolarizes cell to RMP
 Ca2+ is pumped both back into SR and out of cell into extracellular space

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Action Potentials of Contractile Cardiac
Muscle Cells (3 of 3)
• Difference between contractile muscle fiber and skeletal muscle fiber contractions
– AP in skeletal muscle lasts 1–2 ms; in cardiac muscle it lasts 200 ms
– Contraction in skeletal muscle lasts 15–100 ms; in cardiac contraction lasts
over 200 ms

• Benefit of longer AP and contraction:

– Sustained contraction ensures efficient ejection of blood
– Longer refractory period prevents tetanic contractions

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 The Action Potential of Contractile Cardiac
Muscle Cells (1 of 3)

Figure 18.15 The action potential of contractile cardiac muscle cells.

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 The Action Potential of Contractile Cardiac
Muscle Cells (2 of 3)

Figure 18.15 The action potential of contractile cardiac muscle cells.

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 The Action Potential of Contractile Cardiac Muscle Ce
of 3)

Figure 18.15 The action potential of contractile cardiac muscle cells.

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Electrocardiography (1 of 2)
• Electrocardiograph can detect electrical currents generated by heart

• Electrocardiogram (ECG or EKG) is a graphic recording of electrical activity

– Composite of all action potentials at given time; not a tracing of a single AP
– Electrodes are placed at various points on body to measure voltage differences
 12 lead ECG is most typical

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Electrocardiography (2 of 2)
• Main features:
– P wave: depolarization of SA node and atria
– QRS complex: ventricular depolarization and atrial repolarization
– T wave: ventricular repolarization
– P-R interval: beginning of atrial excitation to beginning of ventricular excitation
– S-T segment: entire ventricular myocardium depolarized
– Q-T interval: beginning of ventricular depolarization through ventricular
repolarization

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 The Electrocardiogram (ECG) (1 of 2)

Figure 18.16a The electrocardiogram (ECG).

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 The Electrocardiogram (ECG) (2 of 2)

Figure 18.16b The electrocardiogram (ECG).

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IP2: Electrocardiogram (ECGs)

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The Sequence of Depolarization and
Repolarization of the Heart Related to the
Deflection Waves of an ECG Tracing (1 of 6)

Figure 18.17 The sequence of depolarization and repolarization of the heart related to
the ECG waves.
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The Sequence of Depolarization and
Repolarization of the Heart Related to the
Deflection Waves of an ECG Tracing (2 of 6)

Figure 18.17 The sequence of depolarization and repolarization of the heart related to
the ECG waves.
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The Sequence of Depolarization and
Repolarization of the Heart Related to the
Deflection Waves of an ECG Tracing (3 of 6)

Figure 18.17 The sequence of depolarization and repolarization of the heart related to
the ECG waves.
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The Sequence of Depolarization and
Repolarization of the Heart Related to the
Deflection Waves of an ECG Tracing (4 of 6)

Figure 18.17 The sequence of depolarization and repolarization of the heart related to
the ECG waves.
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The Sequence of Depolarization and
Repolarization of the Heart Related to the
Deflection Waves of an ECG Tracing (5 of 6)

Figure 18.17 The sequence of depolarization and repolarization of the heart related to
the ECG waves.
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The Sequence of Depolarization and
Repolarization of the Heart Related to the
Deflection Waves of an ECG Tracing (6 of 6)

Figure 18.17 The sequence of depolarization and repolarization of the heart related to
the ECG waves.
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Clinical – Homeostatic Imbalance 18.5
(1 of 2)
• Changes in patterns or timing of ECG may reveal diseased or damaged heart, or
problems with heart’s conduction system

• Problems that can be detected:

– Enlarged R waves may indicate enlarged ventricles
– Elevated or depressed S-T segment indicates cardiac ischemia

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Clinical – Homeostatic Imbalance 18.5
(2 of 2)
• Problems that can be detected: (cont.)
– Prolonged Q-T interval reveals a repolarization abnormality that increases risk
of ventricular arrhythmias

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Normal and Abnormal ECG Tracings (1 of 4)

Figure 18.18a Normal and abnormal ECG tracings.

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Normal and Abnormal ECG Tracings (2 of 4)

Figure 18.18b Normal and abnormal ECG tracings.

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 Normal and Abnormal ECG Tracings (3 of 4)

Figure 18.18c Normal and abnormal ECG tracings.

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 Normal and Abnormal ECG Tracings (4 of 4)

Figure 18.18d Normal and abnormal ECG tracings.

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18.6 Mechanical Events of Heart (1 of 5)
• Systole: period of heart contraction
• Diastole: period of heart relaxation
• Cardiac cycle: blood flow through heart during one complete heartbeat
– Atrial systole and diastole are followed by ventricular systole and diastole
– Cycle represents series of pressure and blood volume changes
– Mechanical events follow electrical events seen on ECG
• Three phases of the cardiac cycle (following left side, starting with total relaxation)

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18.6 Mechanical Events of Heart (2 of 5)
1. Ventricular filling: mid-to-late diastole
 Pressure is low; 80% of blood passively flows from atria through open AV
valves into ventricles from atria (SL valves closed)
 Atrial depolarization triggers atrial systole (P wave), atria contract, pushing
remaining 20% of blood into ventricle
– End diastolic volume (EDV): volume of blood in each ventricle at
end of ventricular diastole
 Depolarization spreads to ventricles (QRS wave)
 Atria finish contracting and return to diastole while ventricles begin systole

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18.6 Mechanical Events of Heart (3 of 5)
2. Isovolumetric contraction
 Atria relax; ventricles begin to contract
 Rising ventricular pressure causes closing of AV valves
 Isovolumetric contraction phase is split-second period when ventricles are
completely closed (all valves closed), volume remains constant, ventricles
continue to contract
 When ventricular pressure exceeds pressure in large arteries, SL valves
are forced open
– Pressure in aorta reaches about 120 mm Hg

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18.6 Mechanical Events of Heart (4 of 5)
3. Isovolumetric relaxation: early diastole
 Following ventricular repolarization (T wave), ventricles relax
 End systolic volume (ESV): volume of blood remaining in each ventricle
after systole
 Ventricular pressure drops causing backflow of blood from aorta and
pulmonary trunk that triggers closing of SL valves
 Ventricles are completely closed chambers momentarily
– Referred to as isovolumetric relaxation phase

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18.6 Mechanical Events of Heart (5 of 5)
 Closure of aortic valve raises aortic pressure as backflow rebounds off
closed valve cusps
– Referred to as dicrotic notch
 Atria continue to fill during ventricular systole and when atrial pressure
exceeds ventricular pressure, AV valves open; cycle begins again
 Heart beats around 75 times per minute
 Cardiac cycle lasts about 0.8 seconds
– Atrial systole lasts about 0.1 seconds
– Ventricular systole lasts about 0.3 seconds
– Quiescent period is total heart relaxation that lasts about 0.4 seconds

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 The Cardiac Cycle (1 of 2)

FOCUS FIGURE 18.2 The Cardiac Cycle

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 The Cardiac Cycle (2 of 2)

FOCUS FIGURE 18.2 The Cardiac Cycle

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IP2: Events of the Cardiac Cycle

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Heart Sounds (1 of 2)
• Two sounds (lub-dup) associated with closing of heart valves
– First sound is closing of AV valves at beginning of ventricular systole
– Second sound is closing of SL valves at beginning of ventricular diastole
– Pause between lub-dups indicates heart relaxation

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Heart Sounds (2 of 2)
• Mitral valve closes slightly before tricuspid, and aortic closes slightly before
pulmonary valve
– Differences allow auscultation of each valve when stethoscope is placed in four
different regions

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Areas of the Thoracic Surface Where the
Sounds of Individual Valves are Heard
Most Clearly

Figure 18.19 Areas of the thoracic surface where the sounds of individual valves are
heard most clearly.
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Clinical – Homeostatic Imbalance 18.6
• Heart murmurs: abnormal heart sounds heard when blood hits obstructions

• Usually indicate valve problems

– Incompetent (or insufficient) valve: fails to close completely, allowing backflow of
blood
 Causes swishing sound as blood regurgitates backward from ventricle into atria
– Stenotic valve: fails to open completely, restricting blood flow through valve
 Causes high-pitched sound or clicking as blood is forced through narrow valve

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18.7 Regulation of Pumping (1 of 2)
• Cardiac output: amount of blood pumped out by each ventricle in 1 minute
– Equals heart rate (HR) times stroke volume (SV)
 Stroke volume: volume of blood pumped out by one ventricle with each beat
– Correlates with force of contraction

• At rest:
CO  ml / min   HR  75 beats / min   SV 70 ml / beat 
 5.25 L / min

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18.7 Regulation of Pumping (2 of 2)
• Maximal CO is 4–5 times resting CO in nonathletic people (20–25 L/min)
• Maximal CO may reach 35 L/min in trained athletes
• Cardiac reserve: difference between resting and maximal CO
• CO changes (increases/decreases) if either or both SV or HR is changed
• CO is affected by factors leading to:
– Regulation of stroke volume
– Regulation of heart rates

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IP2: Cardiac Output

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 Factors Involved in Determining Cardiac Output (1 of 2

Figure 18.20 Factors involved in determining cardiac output.

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Regulation of Stroke Volume (1 of 5)
• Mathematically: SV = EDV  ESV
– EDV is affected by length of ventricular diastole and venous pressure (~120
ml/beat)
– ESV is affected by arterial BP and force of ventricular contraction (~50 ml/beat)
– Normal SV = 120 ml  50 ml = 70 ml/beat

• Three main factors that affect SV:

– Preload
– Contractility
– Afterload

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Regulation of Stroke Volume (2 of 5)
• Preload: degree of stretch of heart muscle
– Preload: degree to which cardiac muscle cells are stretched just before they
contract
 Changes in preload cause changes in SV
– Affects EDV
– Relationship between preload and SV called Frank-Starling law of
the heart
– Cardiac muscle exhibits a length-tension relationship
 At rest, cardiac muscle cells are shorter than optimal length; leads to
dramatic increase in contractile force

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Regulation of Stroke Volume (3 of 5)
• Preload (cont.)
– Most important factor in preload stretching of cardiac muscle is venous return
—amount of blood returning to heart
 Slow heartbeat and exercise increase venous return
 Increased venous return distends (stretches) ventricles and increases
contraction force

Venous Return  EDV  SV  CO

Frank-Starling Law

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Regulation of Stroke Volume (4 of 5)
• Contractility
– Contractile strength at given muscle length
 Independent of muscle stretch and EDV
– Increased contractility lowers ESV; caused by:
 Sympathetic epinephrine release stimulates increased Ca2+ influx, leading to
more cross bridge formations
 Positive inotropic agents increase contractility
– Thyroxine, glucagon, epinephrine, digitalis, high extracellular Ca2+
– Decreased by negative inotropic agents
 Acidosis (excess H+), increased extracellular K+, calcium channel blockers

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Regulation of Stroke Volume (5 of 5)
• Afterload: back pressure exerted by arterial blood
– Afterload is pressure that ventricles must overcome to eject blood
 Back pressure from arterial blood pushing on SL valves is major pressure
– Aortic pressure is around 80 mm Hg
– Pulmonary trunk pressure is around 10 mm Hg
– Hypertension increases afterload, resulting in increased ESV and reduced SV

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Regulation of Heart Rate (1 of 7)
• If SV decreases as a result of decreased blood volume or weakened heart, CO can
be maintained by increasing HR and contractility
– Positive chronotropic factors increase heart rate
– Negative chronotropic factors decrease heart rate

• Heart rate can be regulated by:

– Autonomic nervous system
– Chemicals
– Other factors

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Regulation of Heart Rate (2 of 7)
• Autonomic nervous system regulation of heart rate
– Sympathetic nervous system can be activated by emotional or physical stressors
– Norepinephrine is released and binds to β1-adrenergic receptors on heart, causing:
 Pacemaker to fire more rapidly, increasing HR
– EDV decreased because of decreased fill time
 Increased contractility
– ESV decreased because of increased volume of ejected blood

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Regulation of Heart Rate (3 of 7)
• Autonomic nervous system regulation of heart rate (cont.)
– Because both EDV and ESV decrease, SV can remain unchanged
– Parasympathetic nervous system opposes sympathetic effects
 Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels,
which slows HR
 Has little to no effect on contractility

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Regulation of Heart Rate (4 of 7)
• Autonomic nervous system regulation of heart rate (cont.)
– Heart at rest exhibits vagal tone
 Parasympathetic is dominant influence on heart rate
 Decreases rate about 25 beats/min
 Cutting vagal nerve leads to HR of ~100

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Regulation of Heart Rate (5 of 7)
• Autonomic nervous system regulation of heart rate (cont.)
– When sympathetic is activated, parasympathetic is inhibited, and vice-versa
– Atrial (Bainbridge) reflex: sympathetic reflex initiated by increased venous
return, hence increased atrial filling
 Atrial walls are stretched with increased volume
 Stimulates SA node, which increases HR
 Also stimulates atrial stretch receptors that activate sympathetic reflexes

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 Factors Involved in Determining Cardiac
Output (2 of 2)

Figure 18.20 Factors involved in determining cardiac output.

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Regulation of Heart Rate (6 of 7)
• Chemical regulation of heart rate
– Hormones
 Epinephrine from adrenal medulla increases heart rate and contractility
 Thyroxine increases heart rate; enhances effects of norepinephrine and
epinephrine
– Ions
 Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained
for normal heart function
– Imbalances are very dangerous to heart

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Clinical – Homeostatic Imbalance 18.7
• Hypocalcemia: depresses heart

• Hypercalcemia: increases HR and contractility

• Hyperkalemia: alters electrical activity, which can lead to heart block and cardiac arrest

• Hypokalemia: results in feeble heartbeat; arrhythmias

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Regulation of Heart Rate (7 of 7)
• Other factors that influence heart rate
– Age
 Fetus has fastest HR; declines with age
– Gender
 Females have faster HR than males
– Exercise
 Increases HR
 Trained atheles can have slow HR
– Body temperature
 HR increases with increased body temperature

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Clinical – Homeostatic Imbalance 18.8
• Tachycardia: abnormally fast heart rate (>100 beats/min)
– If persistent, may lead to fibrillation

• Bradycardia: heart rate slower than 60 beats/min

– May result in grossly inadequate blood circulation in nonathletes
– May be desirable result of endurance training

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Homeostatic Imbalance of Cardiac Output
(1 of 3)
• Congestive heart failure (CHF)
– Progressive condition; CO is so low that blood circulation is inadequate to meet
tissue needs
– Reflects weakened myocardium caused by:
 Coronary atherosclerosis: clogged arteries caused by fat buildup; impairs
oxygen delivery to cardiac cells
– Heart becomes hypoxic, contracts inefficiently

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Homeostatic Imbalance of Cardiac Output
(2 of 3)
• Congestive heart failure (CHF) (cont.)
 Persistent high blood pressure: aortic pressure 90 mmHg causes
myocardium to exert more force
– Chronic increased ESV causes myocardium hypertrophy and weakness
 Multiple myocardial infarcts: heart becomes weak as contractile cells are
replaced with scar tissue
 Dilated cardiomyopathy (DCM): ventricles stretch and become flabby, and
myocardium deteriorates
– Drug toxicity or chronic inflammation may play a role

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Homeostatic Imbalance of Cardiac Output
(3 of 3)
• Congestive heart failure (CHF) (cont.)
– Either side of heart can be affected:
 Left-sided failure results in pulmonary congestion
– Blood backs up in lungs
 Right-sided failure results in peripheral congestion
– Blood pools in body organs, causing edema
– Failure of either side ultimately weakens other side
 Leads to decompensated, seriously weakened heart
 Treatment: removal of fluid, drugs to reduce afterload and increase contractility

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Developmental Aspects of the Heart (1 of 3)
• Human heart is derived from mesoderm

• Begins as two endothelial chambers that fuse to form single actively pumping chamber
by day 22

• Tube develops four bulges that represent earliest chambers

– Sinus venosus: gives rise to right atrium, coronary sinus, and SA node
– Atrium: becomes pectinate muscles of atria
– Ventricle: becomes left ventricle
– Bulbus cordis: gives rise to aorta, pulmonary trunk, and right ventricle

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 Development of the Human Heart

Figure 18.22 Development of the human heart.

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Developmental Aspects of the Heart (2 of 3)
• Heart tube contorts, and structural changes convert into a four-chambered heart by
day 35

• Two fetal heart structures bypass pulmonary circulation

– Foramen ovale: opening that connects atria
 Remnant is fossa ovalis in adult
– Ductus arteriosus connects pulmonary trunk to aorta
 Remnant: ligamentum arteriosum in adult
– Close at or shortly after birth

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Clinical – Homeostatic Imbalance 18.9
• Congenital heart defects are most common birth defects (40,000 per year)
– Corrected with surgery
– Most defects are one of two types:
 Mixing of oxygen-poor and oxygen-rich blood, as in septal defects, patent
ductus arteriosus
 Narrowed valves or vessels that cause increased workload on heart, as in
coarctation of aorta
– Tetralogy of Fallot
 Both types of disorders present

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 Three Examples of Congenital Heart
Defects

Figure 18.23 Three examples of congenital heart defects.

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Developmental Aspects of the Heart (3 of 3)
Age-Related Changes Affecting the Heart

• Regular exercise can keep heart healthy

• Age-related changes include:

– Sclerosis and thickening of valve flaps: lead to heart murmurs
– Decline in cardiac reserve: heart becomes less efficient
– Fibrosis of cardiac muscle: leads to stiffened heart, arrhythmias caused by
conduction system problems
– Atherosclerosis: may be averted by good diet

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Copyright

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