chapter 19 lecture animation outline the circulatory system: the heart
TRANSCRIPT
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Chapter 19Lecture Animation Outline
The Circulatory System: The Heart
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Introduction
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• Chinese, Egyptian, Greek, Roman scholars– “The heart is a pump for filling vessels with blood”
• Thirteenth-century physician—Ibn an-Nafis– Described the role of the coronary blood vessels in
nourishing the heart
• Sixteen-century—Vesalius– Greatly improved knowledge of cardiovascular anatomy,
the study of the heart, and treatment of its disorders—cardiology
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Introduction
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Cont.• Twentieth century
– Discovery of nitroglycerin, improves coronary circulation; digitalis, abnormal heart rhythms; coronary bypass, valve replacement, among others
• Cardiology is one of today’s most dramatic attention-getting fields in medicine!
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Overview of the Cardiovascular System
• Expected Learning Outcomes– Define and distinguish between the pulmonary and
systemic circuits.– Describe the general location, size, and shape of the
heart.– Describe the pericardial sac that encloses the heart.
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Overview of the Cardiovascular System
• Cardiovascular system – Heart and blood vessels
• Circulatory system – Heart, blood vessels, and the blood
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The Pulmonary and Systemic Circuits
• Major divisions of circulatory system– Pulmonary circuit: right side of heart
• Carries blood to lungs for gas exchange and back to heart
– Systemic circuit: left side of heart• Supplies oxygenated blood to all tissues of
the body and returns it to the heart
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The Pulmonary and Systemic Circuits
• Left side of heart– Fully oxygenated blood
arrives from lungs via pulmonary veins
– Blood sent to all organs of the body via aorta
• Right side of heart– Lesser oxygenated blood
arrives from inferior and superior venae cavae
– Blood sent to lungs via pulmonary trunk
Figure 19.1
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Systemic circuit
Pulmonary circuit
O2-poor,CO2-richblood
O2CO2
O2-rich,CO2-poorblood
CO2 O2
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Position, Size, and Shape of the Heart
• Heart located in mediastinum, between lungs
• Base—wide, superior portion of heart, blood vessels attach here
• Apex—inferior end, tilts to the left, tapers to point
• 3.5 in. wide at base, 5 in. from base to apex, and 2.5 in. anterior to posterior; weighs 10 ounces
Figure 19.2c
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
(c)
Right lung
Aorta
Diaphragm
Superiorvena cava
Parietalpleura (cut)
Pericardialsac (cut)
Pulmonarytrunk
Base ofheart
Apexof heart
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Position, Size, and Shape of the Heart
Figure 19.2a,b
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Posterior
Anterior
Lungs
Sternum
Sternum
(a)
(b)
3rd rib
DiaphragmThoracicvertebra
Rightventricle
Pericardialcavity
Leftventricle
Interventricularseptum
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Gross Anatomy of the Heart
• Expected Learning Outcomes– Describe the three layers of the heart wall.– Identify the four chambers of the heart.– Identify the surface features of the heart and correlate
them with its internal four-chambered anatomy.– Identify the four valves of the heart.– Trace the flow of blood through the four chambers and
valves of the heart and adjacent blood vessels.– Describe the arteries that nourish the myocardium and
the veins that drain it.
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The Heart Wall
• Pericardium—double-walled sac (pericardial sac) that encloses the heart– Allows heart to beat without friction, provides room
to expand, yet resists excessive expansion
– Anchored to diaphragm inferiorly and sternum anteriorly
• Parietal pericardium—outer wall of sac– Superficial fibrous layer of connective tissue
– Deep, thin serous layer
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The Heart Wall
• Visceral pericardium (epicardium)—heart covering– Serous lining of sac turns inward at base of heart
to cover the heart surface
• Pericardial cavity—space inside the pericardial sac filled with 5 to 30 mL of pericardial fluid
• Pericarditis—inflammation of the membranes– Painful friction rub with each heartbeat
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Pericardium and Heart Wall
Figure 19.3
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Pericardial sac
Epicardium
Myocardium
Endocardium
Epicardium
Pericardial cavityPericardialsac:
Fibrouslayer
Serouslayer
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Human Cadaver Heart
Figure 19.4a,b
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Superior vena cava
Interatrial septum
Inferior vena cava
Base of heart
Apex of heart
Right atrium
Opening of coronary sinus
Right ventricle
Epicardial fat
Interventricular septum
Left atrium
Left ventricle
Endocardium
Myocardium
Epicardium
Papillary muscles
Right ventricle
Left ventricle
Fat in interventricularsulcus
Anterior interventricularartery
(a) Anterior view, external anatomy
Right AV valve
(b) Posterior view, internal anatomy
Left AV valve
Tendinous cords
Trabeculae carneae
Coronary blood vessels
© The McGraw-Hill Companies, Inc.
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The Heart Wall
• Epicardium (visceral pericardium)– Serous membrane covering heart
– Adipose in thick layer in some places
– Coronary blood vessels travel through this layer
• Endocardium – Smooth inner lining of heart and blood vessels
– Covers the valve surfaces and is continuous with endothelium of blood vessels
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The Heart Wall
• Myocardium– Layer of cardiac muscle proportional to work load
• Muscle spirals around heart which produces wringing motion
– Fibrous skeleton of the heart: framework of collagenous and elastic fibers
• Provides structural support and attachment for cardiac muscle and anchor for valve tissue
• Electrical insulation between atria and ventricles; important in timing and coordination of contractile activity
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The Chambers
• Four chambers– Right and left atria
• Two superior chambers• Receive blood returning
to heart• Auricles (seen on
surface) enlarge chamber
– Right and left ventricles • Two inferior chambers• Pump blood into arteries
Figure 19.7
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Pulmonary trunk
Left pulmonary artery
Left pulmonary veins
Left atriumAortic valve
Left ventricle
Inferior vena cava
Right ventricle
Right atrium
Superior vena cava
Aorta
Pectinate muscles
Pulmonary valve
Papillary muscle
Interventricular septum
Endocardium
Myocardium
Epicardium
Fossa ovalis
Right pulmonaryartery
Right pulmonaryveins
Interatrialseptum
Right AV(tricuspid) valve
Left AV (bicuspid) valve
Tendinous cords
Trabeculae carneae
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The Chambers
• Atrioventricular sulcus—separates atria and ventricles
• Interventricular sulcus—overlies the interventricular septum that divides the right ventricle from the left
• Sulci contain coronary arteries
Figure 19.5a
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Pulmonary trunk
Left auricle
Apex of heart
Inferior vena cava
Right ventricle
Right atrium
Superior vena cava
Aortic arch
Coronary sulcus
Right auricle
Left ventricle
Branches of theright pulmonaryartery
Right pulmonaryveins
Ligamentumarteriosum
Ascendingaorta
Left pulmonaryartery
Left pulmonaryveins
Anteriorinterventricularsulcus
(a) Anterior view
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The Chambers
Figure 19.5b
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Left atrium
Left ventricle
Apex of heart
Right ventricle
Right atrium
Aorta
(b) Posterior view
Fat
Inferior vena cava
Coronary sulcus
Coronary sinus
Left pulmonaryartery
Left pulmonaryveins
Superiorvena cava
Right pulmonaryartery
Right pulmonaryveins
Posteriorinterventricularsulcus
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The Chambers
• Interatrial septum– Wall that separates atria
• Pectinate muscles– Internal ridges of myocardium in right atrium and both
auricles
• Interventricular septum– Muscular wall that separates ventricles
• Trabeculae carneae– Internal ridges in both ventricles
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The Chambers
Figure 19.7
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Pulmonary trunk
Left pulmonary artery
Left pulmonary veins
Left atriumAortic valve
Left ventricle
Inferior vena cava
Right ventricle
Right atrium
Superior vena cava
Aorta
Pectinate muscles
Pulmonary valve
Papillary muscle
Interventricular septum
Endocardium
Myocardium
Epicardium
Fossa ovalis
Right pulmonaryartery
Right pulmonaryveins
Interatrialseptum
Right AV(tricuspid) valve
Left AV (bicuspid) valve
Tendinous cords
Trabeculae carneae
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The Valves
• Valves ensure a one-way flow of blood through the heart
• Atrioventricular (AV) valves—control blood flow between atria and ventricles– Right AV valve has three cusps (tricuspid valve)– Left AV valve has two cusps (mitral or bicuspid
valve)– Chordae tendineae: cords connect AV valves to
papillary muscles on floor of ventricles• Prevent AV valves from flipping inside out or bulging into
the atria when the ventricles contract
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The Valves
• Semilunar valves—control flow into great arteries; open and close because of blood flow and pressure– Pulmonary semilunar valve: in opening between
right ventricle and pulmonary trunk– Aortic semilunar valve: in opening between left
ventricle and aorta
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The Valves
Figure 19.8a
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
(a)
Right AV(tricuspid) valve
FibrousskeletonOpenings tocoronary arteries
Aorticvalve
Pulmonaryvalve
Left AV(bicuspid) valve
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The Valves: Endoscopic View
Figure 19.8b
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
(b)© Manfred Kage/Peter Arnold, Inc.
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The Valves
Figure 19.8c
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
© The McGraw-Hill Companies, Inc. (c)
Tendinouscords
Papillarymuscle
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Blood Flow Through the Chambers
• Ventricles relax– Pressure drops inside the ventricles– Semilunar valves close as blood attempts to back up
into the ventricles from the vessels– AV valves open– Blood flows from atria to ventricles
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Blood Flow Through the Chambers
• Ventricles contract– AV valves close as blood attempts to back up into the
atria– Pressure rises inside of the ventricles– Semilunar valves open and blood flows into great
vessels
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Blood Flow Through the Chambers
Figure 19.9
• Blood pathway travels from the right atrium through the body and back to the starting point
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
3
6
4
55
2
1
7
8
9
Aorta
Pulmonary trunk
Aortic valve
Left atrium
Left ventricle
6
2
3
4
5
6
7
8
9
10
1
Blood returns to heart via venae cavae.
Superiorvena cava
Rightpulmonaryveins
Rightatrium
Right AV(tricuspid) valve
Rightventricle
Inferiorvena cava
11
11
10
Left AV(bicuspid) valve
Left pulmonaryveins
Left pulmonaryartery
Blood enters right atrium from superiorand inferior venae cavae.
Blood in right atrium flows through rightAV valve into right ventricle.
Contraction of right ventricle forcespulmonary valve open.
Blood is distributed by right and leftpulmonary arteries to the lungs, where itunloads CO2 and loads O2.
Blood returns from lungs via pulmonaryveins to left atrium.
Blood in left atrium flows through left AVvalve into left ventricle.
Contraction of left ventricle (simultaneous withstep 3 ) forces aortic valve open.
Blood flows through aortic valve intoascending aorta.
Blood in aorta is distributed to every organ inthe body, where it unloads O2 and loads CO2.
11
Blood flows through pulmonary valveinto pulmonary trunk.
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The Coronary Circulation
• 5% of blood pumped by heart is pumped to the heart itself through the coronary circulation to sustain its strenuous workload– 250 mL of blood per minute
– Needs abundant O2 and nutrients
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Arterial Supply
• Left coronary artery (LCA) branches off the ascending aorta– Anterior interventricular branch (left ant
descending)• Supplies blood to both ventricles and anterior two-
thirds of the interventricular septum
– Circumflex branch• Passes around left side of heart in coronary sulcus
• Gives off left marginal branch and then ends on the posterior side of the heart
• Supplies left atrium and posterior wall of left ventricle
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Arterial Supply
• Right coronary artery (RCA) branches off the ascending aorta– Supplies right atrium and sinoatrial node (pacemaker)
– Right marginal branch • Supplies lateral aspect of right atrium and ventricle
– Posterior interventricular branch• Supplies posterior walls of ventricles
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Arterial Supply
Figure 19.5a
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Pulmonary trunk
Left auricle
Apex of heart
Inferior vena cava
Right ventricle
Right atrium
Superior vena cava
Aortic arch
Coronary sulcus
Right auricle
Left ventricle
Branches of theright pulmonaryartery
Right pulmonaryveins
Ligamentumarteriosum
Ascendingaorta
Left pulmonaryartery
Left pulmonaryveins
Anteriorinterventricularsulcus
(a) Anterior view
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Arterial Supply
Figure 19.5b
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Left atrium
Left ventricle
Apex of heart
Right ventricle
Right atrium
Aorta
(b) Posterior view
Fat
Inferior vena cava
Coronary sulcus
Coronary sinus
Left pulmonaryartery
Left pulmonaryveins
Superiorvena cava
Right pulmonaryartery
Right pulmonaryveins
Posteriorinterventricularsulcus
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Arterial Supply
• Myocardial infarction (MI)—heart attack– Interruption of blood supply to the heart from a blood
clot or fatty deposit (atheroma) can cause death of cardiac cells within minutes
– Some protection from MI is provided by arterial anastomoses which provides an alternative route of blood flow (collateral circulation) within the myocardium
• Blood flow to the heart muscle during ventricular contraction is slowed, unlike the rest of the body
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Arterial Supply
• Three reasons– Contraction of the myocardium compresses the
coronary arteries and obstructs blood flow– Opening of the aortic valve flap during ventricular
systole covers the openings to the coronary arteries blocking blood flow into them
– During ventricular diastole, blood in the aorta surges back toward the heart and into the openings of the coronary arteries
• Blood flow to the myocardium increases during ventricular relaxation
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Angina and Heart Attack
• Angina pectoris—chest pain from partial obstruction of coronary blood flow – Pain caused by ischemia of cardiac muscle– Obstruction partially blocks blood flow
– Myocardium shifts to anaerobic fermentation, producing lactic acid and thus stimulating pain
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Angina and Heart Attack
• Myocardial infarction—sudden death of a patch of myocardium resulting from long-term obstruction of coronary circulation– Atheroma (blood clot or fatty deposit) often obstructs
coronary arteries– Cardiac muscle downstream of the blockage dies– Heavy pressure or squeezing pain radiating into the left
arm– Some painless heart attacks may disrupt electrical
conduction pathways, leading to fibrillation and cardiac arrest
• Silent heart attacks occur in diabetics and the elderly– MI responsible for about half of all deaths in the United
States
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Venous Drainage
• 5% to 10% drains directly into heart chambers—right atrium and right ventricle—by way of the thebesian veins
• The rest returns to right atrium by the following routes:– Great cardiac vein
• Travels alongside anterior interventricular artery• Collects blood from anterior portion of heart• Empties into coronary sinus
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Venous Drainage
• The rest returns to right atrium by the following routes (cont.):– Middle cardiac vein (posterior interventricular)
• Found in posterior sulcus• Collects blood from posterior portion of heart• Drains into coronary sinus
– Left marginal vein • Empties into coronary sinus
• Coronary sinus – Large transverse vein in coronary sulcus on posterior
side of heart
– Collects blood and empties into right atrium
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Cardiac Muscle and the Cardiac Conduction System
• Expected Learning Outcomes– Describe the unique structural and metabolic
characteristics of cardiac muscle.– Explain the nature and functional significance of the
intercellular junctions between cardiac muscle cells.– Describe the heart’s pacemaker and internal electrical
conduction system.– Describe the nerve supply to the heart and explain its
role.
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Structure of Cardiac Muscle
• Cardiocytes—striated, short, thick, branched cells, one central nucleus surrounded by light-staining mass of glycogen
• Intercalated discs—join cardiocytes end to end– Interdigitating folds: folds interlock with each other,
and increase surface area of contact
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Structure of Cardiac Muscle
Cont.– Mechanical junctions tightly join cardiocytes
• Fascia adherens—broad band in which the actin of the thin myofilaments is anchored to the plasma membrane
– Each cell is linked to the next via transmembrane proteins
• Desmosomes—weldlike mechanical junctions between cells
– Prevents cardiocytes from being pulled apart
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Structure of Cardiac Muscle
• Electrical junctions (gap junctions) allow ions to flow between cells; can stimulate neighbors– Entire myocardium of either two atria or two ventricles acts
like single, unified cell
• Repair of damage of cardiac muscle is almost entirely by fibrosis (scarring)
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Structure of Cardiac Muscle
Figure 19.11a–c
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Gap junctions
Desmosomes
Intercellular space
Mitochondria Intercalated discsGlycogen NucleusStriated myofibril
(c)
(b)
Striations
Nucleus
Intercalated discs
(a)
a: © Ed Reschke
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Metabolism of Cardiac Muscle
• Cardiac muscle depends almost exclusively on aerobic respiration used to make ATP– Rich in myoglobin and glycogen– Huge mitochondria: fill 25% of cell
• Adaptable to organic fuels used – Fatty acids (60%); glucose (35%); ketones, lactic acid, and
amino acids (5%)– More vulnerable to oxygen deficiency than lack of a specific
fuel
• Fatigue resistant because it makes little use of anaerobic fermentation or oxygen debt mechanisms– Does not fatigue for a lifetime
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The Conduction System
• Coordinates the heartbeat – Composed of an internal pacemaker and nervelike
conduction pathways through myocardium
• Generates and conducts rhythmic electrical signals in the following order:– Sinoatrial (SA) node: modified cardiocytes
• Pacemaker initiates each heartbeat and determines heart rate
• Pacemaker in right atrium near base of superior vena cava
– Signals spread throughout atria
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The Conduction System
Cont.– Atrioventricular (AV) node
• Located near the right AV valve at lower end of interatrial septum
• Electrical gateway to the ventricles• Fibrous skeleton—insulator prevents currents from getting to
ventricles from any other route
– Atrioventricular (AV) bundle (bundle of His)• Bundle forks into right and left bundle branches• Branches pass through interventricular septum toward apex
– Purkinje fibers • Nervelike processes spread throughout ventricular myocardium• Signal passes from cell to cell through gap junctions
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Structure of Cardiac Muscle
• Cardiocytes—striated, short, thick, branched cells, one central nucleus surrounded by light-staining mass of glycogen
• Intercalated discs—join cardiocytes end to end– Interdigitating folds: folds interlock with each other,
and increase surface area of contact– Mechanical junctions tightly join cardiocytes
• Fascia adherens—broad band in which the actin of the thin myofilaments is anchored to the plasma membrane
– Each cell is linked to the next via transmembrane proteins
• Desmosomes—weldlike mechanical junctions between cells
– Prevents cardiocytes from being pulled apart
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Structure of Cardiac Muscle
Cont.– Mechanical junctions tightly join cardiocytes
• Fascia adherens—broad band in which the actin of the thin myofilaments is anchored to the plasma membrane
– Each cell is linked to the next via transmembrane proteins
• Desmosomes—weldlike mechanical junctions between cells
– Prevents cardiocytes from being pulled apart
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The Conduction System
Figure 19.12
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
2
3
4
5
1
1
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4 5
2Right atrium
Purkinje fibers
Sinoatrial node(pacemaker)
Atrioventricularnode
Atrioventricularbundle
SA node fires.
Excitation spreads throughatrial myocardium.
AV node fires.
Excitation spreads down AVbundle.
Purkinje fibers distributeexcitation throughventricular myocardium.
Leftatrium
Purkinjefibers
Bundlebranches
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Please note that due to differing operating systems, some animations will not appear until the presentation is viewed in Presentation Mode (Slide Show view). You may see blank slides in the “Normal” or “Slide Sorter” views. All animations will appear after viewing in Presentation Mode and playing each animation. Most animations will require the latest version of the Flash Player, which is available at http://get.adobe.com/flashplayer.
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Nerve Supply to the Heart
• Sympathetic nerves (raise heart rate) – Sympathetic pathway to the heart originates in the
lower cervical to upper thoracic segments of the spinal cord
– Continues to adjacent sympathetic chain ganglia– Some pass through cardiac plexus in mediastinum
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Nerve Supply to the Heart
Cont.– Some pass through cardiac plexus in mediastinum– Continue as cardiac nerves to the heart– Fibers terminate in SA and AV nodes, in atrial and
ventricular myocardium, as well as the aorta, pulmonary trunk, and coronary arteries
• Increase heart rate and contraction strength
• Dilates coronary arteries to increase myocardial blood flow
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Nerve Supply to the Heart
• Parasympathetic nerves (slows heart rate)– Pathway begins with nuclei of the vagus nerves in
the medulla oblongata– Extend to cardiac plexus and continue to the heart by
way of the cardiac nerves– Fibers of right vagus nerve lead to the SA node– Fibers of left vagus nerve lead to the AV node– Little or no vagal stimulation of the myocardium
• Parasympathetic stimulation reduces the heart rate
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Electrical and Contractile Activity of the Heart
• Expected Learning Outcomes– Explain why the SA node fires spontaneously and
rhythmically.– Explain how the SA node excites the myocardium.– Describe the unusual action potentials of cardiac
muscle and relate them to the contractile behavior of the heart.
– Interpret a normal electrocardiogram.
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Electrical and Contractile Activity of the Heart
• Cycle of events in heart—special names
– Systole: atrial or ventricular contraction
– Diastole: atrial or ventricular relaxation
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The Cardiac Rhythm
• Sinus rhythm—normal heartbeat triggered by the SA node– Set by SA node at 60 to 100 bpm– Adult at rest is 70 to 80 bpm (vagal tone)
• Ectopic focus—another part of heart fires before the SA node– Caused by hypoxia, electrolyte imbalance, or caffeine,
nicotine, and other drugs
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The Cardiac Rhythm
• Spontaneous firing from some part of heart; not the SA node– Ectopic foci: region of spontaneous firing
• Nodal rhythm—if SA node is damaged, heart rate is set by AV node, 40 to 50 bpm
• Intrinsic ventricular rhythm—if both SA and AV nodes are not functioning, rate set at 20 to 40 bpm
– Requires pacemaker to sustain life
• Arrhythmia—any abnormal cardiac rhythm– Failure of conduction system to transmit signals (heart
block)• Bundle branch block• Total heart block (damage to AV node)
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Cardiac Arrhythmias
• Atrial flutter—ectopic foci in atria– Atrial fibrillation– Atria beat 200 to 400 times per minute
• Premature ventricular contractions (PVCs)– Caused by stimulants, stress, or lack of sleep
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Cardiac Arrhythmias
• Ventricular fibrillation– Serious arrhythmia caused by electrical signals
reaching different regions at widely different times• Heart cannot pump blood and no coronary perfusion
– Kills quickly if not stopped• Defibrillation—strong electrical shock whose intent is to
depolarize the entire myocardium, stop the fibrillation, and reset SA nodes to sinus rhythm
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Pacemaker Physiology
• SA node does not have a stable resting membrane potential– Starts at −60 mV and drifts upward from a slow
inflow of Na+
• Gradual depolarization is called pacemaker potential
– Slow inflow of Na+ without compensating outflow of K+
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Pacemaker Physiology
Cont.– When it reaches threshold of −40 mV, voltage-
gated fast Ca2+ and Na+ channels open• Faster depolarization occurs peaking at 0 mV• K+ channels then open and K+ leaves the cell
– Causing repolarization– Once K+ channels close, pacemaker potential starts
over
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Pacemaker Physiology
• Each depolarization of the SA node sets off one heartbeat – At rest, fires every 0.8 second or 75 bpm
• SA node is the system’s pacemaker
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Pacemaker Physiology
Figure 19.13
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
+10
0
–10
–20
–30
–40
–50
–60
–70
0 .8.4 1.2 1.6
Mem
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Threshold
Fast K+
outflow Actionpotential
Slow Na+
inflow
Pacemakerpotential
Time (sec)
FastCa2+–Na+
inflow
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Impulse Conduction to the Myocardium
• Signal from SA node stimulates two atria to contract almost simultaneously– Reaches AV node in 50 ms
• Signal slows down through AV node – Thin cardiocytes have fewer gap junctions– Delays signal 100 ms which allows the ventricles to
fill
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Impulse Conduction to the Myocardium
• Signals travel very quickly through AV bundle and Purkinje fibers– Entire ventricular myocardium depolarizes and contracts
in near unison• Papillary muscles contract an instant earlier than the rest,
tightening slack in chordae tendineae
• Ventricular systole progresses up from the apex of the heart– Spiral arrangement of cardiocytes twists ventricles
slightly; like someone wringing out a towel
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Electrical Behavior of the Myocardium
• Cardiocytes have stable resting potential of −90 mV• Depolarize only when stimulated
– Depolarization phase (very brief) • Stimulus opens voltage-regulated Na+ gates (Na+ rushes in),
membrane depolarizes rapidly• Action potential peaks at +30 mV • Na+ gates close quickly
– Plateau phase lasts 200 to 250 ms, sustains contraction for expulsion of blood from heart
• Ca2+ channels are slow to close and SR is slow to remove Ca2+ from the cytosol
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Electrical Behavior of the Myocardium
• Depolarize only when stimulated (cont.)– Repolarization phase: Ca2+ channels close, K+
channels open, rapid diffusion of K+ out of cell returns it to resting potential
• Has a long absolute refractory period of 250 ms compared to 1 to 2 ms in skeletal muscle– Prevents wave summation and tetanus which would
stop the pumping action of the heart
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Electrical Behavior of the Myocardium
1. Na+ gates open
2. Rapid depolarization
3. Na+ gates close
4. Slow Ca2+ channels open
5. Ca2+ channels close, K+ channels open (repolarization)
Figure 19.14
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
0 .15 .30
Plateau1
2
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Mem
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+20
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–40
–60
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Voltage-gated Na+ channels open.
Na+ inflow depolarizes the membraneand triggers the opening of still more Na+
channels, creating a positive feedbackcycle and a rapidly rising membrane voltage.
Na+ channels close when the celldepolarizes, and the voltage peaks atnearly +30 mV.
Ca2+ entering through slow Ca2+
channels prolongs depolarization ofmembrane, creating a plateau. Plateau fallsslightly because of some K+ leakage, but mostK+ channels remain closed until end ofplateau.
Ca2+ channels close and Ca2+ is transportedout of cell. K+ channels open, and rapid K+
outflow returns membrane to its restingpotential.
Time (sec)
Myocardialcontraction
Actionpotential
Absoluterefractory
period
Myocardialrelaxation
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The Electrocardiogram
• Electrocardiogram (ECG or EKG)– Composite of all
action potentials of nodal and myocardial cells detected, amplified and recorded by electrodes on arms, legs, and chest
Figure 19.15
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
0.8 second
+1
0
–1
Mil
livo
lts
T wave
QRS interval
R R
QS
P wave
PRinterval
QTinterval
PQsegment
STsegment
Ventriclescontract
Atriacontract
Atriacontract
Ventriclescontract
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The Electrocardiogram
• P wave– SA node fires, atria depolarize and contract– Atrial systole begins 100 ms after SA signal
• QRS complex– Ventricular depolarization– Complex shape of spike due to different thickness
and shape of the two ventricles
• ST segment—ventricular systole – Plateau in myocardial action potential
• T wave– Ventricular repolarization and relaxation
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The Electrocardiogram
Figure 19.15
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
0.8 second
+1
0
–1
Mil
liv
olt
s
T wave
QRS interval
R R
QS
P wave
PRinterval
QTinterval
PQsegment
STsegment
Ventriclescontract
Atriacontract
Atriacontract
Ventriclescontract
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1. Atrial depolarization begins
2. Atrial depolarization complete (atria contracted)
3. Ventricles begin to depolarize at apex; atria repolarize (atria relaxed)
4. Ventricular depolarization complete (ventricles contracted)
5. Ventricles begin to repolarize at apex
6. Ventricular repolarization complete (ventricles relaxed)
The Electrocardiogram
Figure 19.16
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
5
6
1 4
2
T
SQ
R
P
T
SQ
R
P
SQ
R
P
Q
R
P
P
P
3
KeyWave ofdepolarizationWave ofrepolarization
Atria begin depolarizing.
Atrial depolarization complete.
Ventricular depolarization complete.
Ventricular repolarization begins at apexand progresses superiorly.
Ventricular repolarization complete; heartis ready for the next cycle.
Ventricular depolarization begins at apexand progresses superiorly as atria repolarize.
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ECGs: Normal and Abnormal
• Abnormalities in conduction pathways
• Myocardial infarction
• Heart enlargement
• Electrolyte and hormone imbalances
Figure 19.17a,b
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
(a) Sinus rhythm (normal)
(b) Nodal rhythm—no SA node activity
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Blood Flow, Heart Sounds, and the Cardiac Cycle
• Expected Learning Outcomes– Explain why blood pressure is expressed in millimeters of
mercury.– Describe how changes in blood pressure operate the
heart valves.– Explain what causes the sounds of the heartbeat.– Describe in detail one complete cycle of heart contraction
and relaxation.– Relate the events of the cardiac cycle to the volume of
blood entering and leaving the heart.
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Blood Flow, Heart Sounds, and the Cardiac Cycle
• Cardiac cycle—one complete contraction and relaxation of all four chambers of the heart
• Atrial systole (contraction) occurs while ventricles are in diastole (relaxation)
• Atrial diastole occurs while ventricles in systole • Quiescent period— all four chambers relaxed at same
time• Questions to consider: How does pressure affect blood
flow? How are heart sounds produced?
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Principles of Pressure and Flow• Two main variables govern fluid
movement– Pressure causes a fluid to flow
(fluid dynamics)• Pressure gradient—pressure difference
between two points• Measured in mm Hg
with a manometer orsphygmomanometer
– Resistance opposes fluid flow• Great vessels have positive blood
pressure• Ventricular pressure must rise above
this resistance for blood to flow into great vessels
Figure 19.18
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
1
2
3 Air flows in
1
2
3 Air flows out
P1
P2<P1
P1
P2
P2
Pressure gradient
Pressure gradient
(b)
(a)
Volumeincreases
Pressuredecreases
P2>P1
Volumedecreases
Pressureincreases
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Pressure Gradients and Flow
• Fluid flows only if it is subjected to more pressure at one point than another which creates a pressure gradient– Fluid flows down its pressure gradient from high
pressure to low pressure
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Pressure Gradients and Flow
• Events occurring on left side of heart– When ventricle relaxes and expands, its internal
pressure falls– If bicuspid valve is open, blood flows into left ventricle– When ventricle contracts, internal pressure rises– AV valves close and the aortic valve is pushed open
and blood flows into aorta from left ventricle
• Opening and closing of valves are governed by these pressure changes– AV valves limp when ventricles relaxed– Semilunar valves under pressure from blood in vessels
when ventricles relaxed
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Aorta
Semilunar valves open
Atrioventricular valves closed
Semilunar valves closed
Atrium
(b)
Atrioventricular valves open
(a)
Pulmonaryartery
Semilunarvalve
Atrioventricularvalve
Ventricle
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Operation of the Heart Valves
Figure 19.19
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
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Valvular Insufficiency Disorders
• Valvular insufficiency (incompetence)—any failure of a valve to prevent reflux (regurgitation), the backward flow of blood– Valvular stenosis: cusps are stiffened and opening is
constricted by scar tissue• Result of rheumatic fever, autoimmune attack on the mitral and
aortic valves• Heart overworks and may become enlarged• Heart murmur—abnormal heart sound produced by
regurgitation of blood through incompetent valves
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Valvular Insufficiency Disorders
Cont.
– Mitral valve prolapse: insufficiency in which one or both mitral valve cusps bulge into atria during ventricular contraction
• Hereditary in 1 out of 40 people• May cause chest pain and shortness of breath
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Heart Sounds
• Auscultation—listening to sounds made by body
• First heart sound (S1), louder and longer “lubb,”
occurs with closure of AV valves, turbulence in the bloodstream, and movements of the heart wall
• Second heart sound (S2), softer and sharper “dupp,”
occurs with closure of semilunar valves, turbulence in the bloodstream, and movements of the heart wall
• S3—rarely heard in people over 30
• Exact cause of each sound is not known with certainty
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Phases of the Cardiac Cycle
• Ventricular filling• Isovolumetric contraction• Ventricular ejection• Isovolumetric relaxation• All the events in the cardiac cycle are completed
in less than 1 second!
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Phases of the Cardiac Cycle
• Ventricular filling– During diastole, ventricles expand– Their pressure drops below that of the atria– AV valves open and blood flows into the ventricles
• Ventricular filling occurs in three phases– Rapid ventricular filling: first one-third
• Blood enters very quickly
– Diastasis: second one-third• Marked by slower filling• P wave occurs at the end of diastasis
– Atrial systole: final one-third• Atria contract
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Phases of the Cardiac Cycle
• End-diastolic volume (EDV)—amount of blood contained in each ventricle at end of ventricular filling (130 mL)
• Isovolumetric contraction– Atria repolarize and relax– Remain in diastole for the rest of the cardiac cycle– Ventricles depolarize, create the QRS complex, and
begin to contract
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Phases of the Cardiac Cycle
• AV valves close as ventricular blood surges back against the cusps
• Heart sound S1 occurs at the beginning of this phase
• “Isovolumetric” because even though the ventricles contract, they do not eject blood– Because pressure in the aorta (80 mm Hg) and in the
pulmonary trunk (10 mm Hg) is still greater than in the ventricles
• Cariocytes exert force, but with all four valves closed, the blood cannot go anywhere
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Phases of the Cardiac Cycle
• Ventricular ejection of blood begins when the ventricular pressure exceeds arterial pressure and forces semilunar valves open– Pressure peaks in left ventricle at about 120 mm Hg
and 25 mm Hg in the right
• Blood spurts out of each ventricle rapidly at first—rapid ejection
• Then more slowly under reduced pressure—reduced ejection
• Ventricular ejections last about 200 to 250 ms– Corresponds to the plateau phase of the cardiac
action potential
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Phases of the Cardiac Cycle
• Ventricular ejection (cont.)• T wave occurs late in this phase• Stroke volume (SV) of about 70 mL of blood is
ejected of the 130 mL in each ventricle– Ejection fraction of about 54%– As high as 90% in vigorous exercise
• End-systolic volume (ESV)—the 60 mL of blood left behind
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Phases of the Cardiac Cycle
• Isovolumetric relaxation is early ventricular diastole– When T wave ends and ventricles begin to expand
• Elastic recoil and expansion would cause pressure to drop rapidly and suck blood into the ventricles– Blood from the aorta and pulmonary trunk briefly flows
backward– Filling the semilunar valves and closing the cusps– Creates a slight pressure rebound that appears as the
dicrotic notch of the aortic pressure curve
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Phases of the Cardiac Cycle
• Isovolumetric relaxation (cont.)– Heart sound S2 occurs as blood rebounds from the
closed semilunar valves and the ventricle expands– “Isovolumetric” because semilunar valves are closed
and AV valves have not yet opened• Ventricles are therefore taking in no blood
– When AV valves open, ventricular filling begins again
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Please note that due to differing operating systems, some animations will not appear until the presentation is viewed in Presentation Mode (Slide Show view). You may see blank slides in the “Normal” or “Slide Sorter” views. All animations will appear after viewing in Presentation Mode and playing each animation. Most animations will require the latest version of the Flash Player, which is available at http://get.adobe.com/flashplayer.
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Phases of the Cardiac Cycle
• In a resting person– Atrial systole lasts about 0.1 second– Ventricular systole lasts about 0.3 second– Quiescent period, when all four chambers are in
diastole, 0.4 second
• Total duration of the cardiac cycle is therefore 0.8 second in a heart beating 75 bpm
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Events of the Cardiac Cycle
• Ventricular filling
• Isovolumetric contraction
• Ventricular ejection
• Isovolumetric relaxation
Figure 19.20
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
ECG
Pre
ssu
re (
mm
Hg
)
120
60
90
120
100
80
60
40
20
0
SystoleDiastole Diastole
0 .2 .4 .6 .8 .2 .4
End-systolic volume
Q
R
S
P
S1
TP
Q
R
S
S2 S3 S3
1a 1b 1c 3
S1
2 1a 1b 1c 24
S2
Ventricular filling
Ven
tric
ula
rv
olu
me
(mL
)
Heart sounds
Phase ofcardiac cycle
Aorticpressure
Leftventricularpressure
Left atrialpressure
Aorticvalveopens
Aortic valvecloses(dicrotic notch)
AVvalvecloses
AVvalveopens
End-diastolicvolume
Time (sec)
1a Rapid filling1b Diastasis
1c Atrial systole 2Isovolumetriccontraction
3Ventricularejection
4Isovolumetricrelaxation
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Overview of Volume Changes
End-systolic volume (ESV) 60 mL
Passively added to ventricle
during atrial diastole +30 mL
Added by atrial systole +40 mL
Total: End-diastolic volume (EDV) 130 mL
Stroke volume (SV) ejected
by ventricular systole −70 mL
Leaves: End-systolic volume (ESV) 60 mL
Both ventricles must eject same amount of blood
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Overview of Volume Changes
Figure 19.21a
• If the left ventricle pumps less blood than the right, the blood pressure backs up into the lungs and causes pulmonary edema
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Pressure backs up.
1
2
3
(a) Pulmonary edema
32
1
Right ventricularoutput exceeds leftventricular output.
Fluid accumulates inpulmonary tissue.
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Overview of Volume Changes
Figure 19.21b
• If the right ventricle pumps less blood than the left, pressure backs up in the systemic circulation and causes systemic edema
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Pressure backs up.
1
2
3
(b) Systemic edema
12
3
Left ventricularoutput exceeds rightventricular output.
Fluid accumulates insystemic tissue.
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Overview of Volume Changes
• Congestive heart failure (CHF)—results from the failure of either ventricle to eject blood effectively– Usually due to a heart weakened by myocardial
infarction, chronic hypertension, valvular insufficiency, or congenital defects in heart structure
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Overview of Volume Changes
• Left ventricular failure—blood backs up into the lungs causing pulmonary edema– Shortness of breath or sense of suffocation
• Right ventricular failure—blood backs up in the vena cava causing systemic or generalized edema– Enlargement of the liver, ascites (pooling of fluid in
abdominal cavity), distension of jugular veins, swelling of the fingers, ankles, and feet
• Eventually leads to total heart failure
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Cardiac Output
• Expected Learning Outcomes– Define cardiac output and explain its importance.– Identify the factors that govern cardiac output.– Discuss some of the nervous and chemical factors that
alter heart rate, stroke volume, and cardiac output.– Explain how the right and left ventricles achieve balanced
output.– Describe some effects of exercise on cardiac output.
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Cardiac Output
• Cardiac output (CO)—the amount ejected by ventricle in 1 minute
• Cardiac output = heart rate x stroke volume– About 4 to 6 L/min at rest– A RBC leaving the left ventricle will arrive back at the
left ventricle in about 1 minute– Vigorous exercise increases CO to 21 L/min for a fit
person and up to 35 L/min for a world-class athlete
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Cardiac Output
Cont.
• Cardiac reserve—the difference between a person’s maximum and resting CO– Increases with fitness, decreases with disease
• To keep cardiac output constant as we increase in age, the heart rate increases as the stroke volume decreases
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Heart Rate
• Pulse—surge of pressure produced by each heart beat that can be felt by palpating a superficial artery with the fingertips– Infants have HR of 120 bpm or more– Young adult females average 72 to 80 bpm– Young adult males average 64 to 72 bpm– Heart rate rises again in the elderly
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Heart Rate
• Tachycardia—resting adult heart rate above 100 bpm– Stress, anxiety, drugs, heart disease, or fever– Loss of blood or damage to myocardium
• Bradycardia—resting adult heart rate of less than 60 bpm– In sleep, low body temperature, and endurance-trained
athletes
• Positive chronotropic agents—factors that raise the heart rate
• Negative chronotropic agents—factors that lower heart rate
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Chronotropic Effects of the Autonomic Nervous System
• Autonomic nervous system does not initiate the heartbeat, it modulates rhythm and force
• Cardiac centers in the reticular formation of the medulla oblongata initiate autonomic output to the heart
• Cardiostimulatory effect—some neurons of the cardiac center transmit signals to the heart by way of sympathetic pathways
• Cardioinhibitory effect—others transmit parasympathetic signals by way of the vagus nerve
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Chronotropic Effects of the Autonomic Nervous System
• Sympathetic postganglionic fibers are adrenergic– They release norepinephrine– Bind to β-adrenergic fibers in the heart– Activate cAMP second-messenger system in
cardiocytes and nodal cells– Lead to opening of Ca2+ channels in plasma
membrane
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Chronotropic Effects of the Autonomic Nervous System
• Sympathetic postganglionic fibers are adrenergic (cont.)– Increased Ca2+ inflow accelerated depolarization of SA
node– cAMP accelerates the uptake of Ca2+ by the
sarcoplasmic reticulum allowing the cardiocytes to relax more quickly
– By accelerating both contraction and relaxation, norepinephrine and cAMP increase the heart rate as high as 230 bpm
– Diastole becomes too brief for adequate filling– Both stroke volume and cardiac output are reduced
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Chronotropic Effects of the Autonomic Nervous System
• Parasympathetic vagus nerves have cholinergic, inhibitory effects on the SA and AV nodes– Acetylcholine (ACh) binds to muscarinic receptors– Opens K+ gates in the nodal cells– As K+ leaves the cells, they become hyperpolarized
and fire less frequently– Heart slows down– Parasympathetics work on the heart faster than
sympathetics• Parasympathetics do not need a second-messenger
system
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Chronotropic Effects of the Autonomic Nervous System
• Without influence from the cardiac centers, the heart has an intrinsic “natural” firing rate of 100 bpm
• Vagal tone—holds down this heart rate to 70 to 80 bpm at rest– Steady background firing rate of the vagus nerves
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Chronotropic Effects of the Autonomic Nervous System
• Cardiac centers in the medulla receive input from many sources and integrate it into the “decision” to speed or slow the heart
• Higher brain centers affect heart rate– Cerebral cortex, limbic system, hypothalamus
• Sensory or emotional stimuli
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Chronotropic Effects of the Autonomic Nervous System
• Medulla also receives input from muscles, joints, arteries, and brainstem– Proprioceptors in the muscles and joints
• Inform cardiac center about changes in activity, HR increases before metabolic demands of muscle arise
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Chronotropic Effects of the Autonomic Nervous System
Cont.– Baroreceptors signal cardiac center
• Pressure sensors in aorta and internal carotid arteries
• Blood pressure decreases, signal rate drops, cardiac center increases heart rate
• If blood pressure increases, signal rate rises, cardiac center decreases heart rate
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Chronotropic Effects of the Autonomic Nervous System
• Medulla also receives input from muscles, joints, arteries, and brainstem (cont.)– Chemoreceptors
• In aortic arch, carotid arteries, and medulla oblongata • Sensitive to blood pH, CO2 and O2 levels• More important in respiratory control than cardiac control
– If CO2 accumulates in blood or CSF (hypercapnia), reacts with water and causes increase in H+ levels
– H+ lowers the pH of the blood possibly creating acidosis (pH < 7.35)
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Chronotropic Effects of the Autonomic Nervous System
Cont.• Hypercapnia and acidosis stimulate the cardiac center to
increase heart rate• Also respond to hypoxemia—oxygen deficiency in the
blood that usually slows down the heart
– Chemoreceptors (cont.)• Chemoreflexes and baroreflexes—responses to
fluctuation in blood chemistry—are both negative feedback loops
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Chronotropic Effects of Chemicals
• Chemicals affect heart rate as well as neurotransmitters from cardiac nerves– Blood-borne adrenal catecholamines (NE and
epinephrine) are potent cardiac stimulants
• Drugs that stimulate heart– Nicotine stimulates catecholamine secretion– Thyroid hormone increases number of adrenergic
receptors on heart so more responsive to sympathetic stimulation
– Caffeine inhibits cAMP breakdown prolonging adrenergic effect
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• Electrolytes– K+ has greatest chronotropic effect
• Hyperkalemia—excess K+ in cardiocytes – Myocardium less excitable, heart rate slows and
becomes irregular
• Hypokalemia—deficiency K+ in cardiocytes– Cells hyperpolarized, require increased stimulation
– Calcium• Hypercalcemia—excess of Ca2+
– Decreases heart rate and contraction strength
• Hypocalcemia—deficiency of Ca2+
– Increases heart rate and contraction strength
Chronotropic Effects of Chemicals
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Stroke Volume
• The other factor in cardiac output, besides heart rate, is stroke volume (SV)
• Three variables govern stroke volume– Preload– Contractility– Afterload
• Examples– Increased preload or contractility increases stroke
volume– Increased afterload decreases stroke volume
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Preload
• Preload—the amount of tension in ventricular myocardium immediately before it begins to contract– Increased preload causes increased force of
contraction
– Exercise increases venous return and stretches myocardium
– Cardiocytes generate more tension during contraction
– Increased cardiac output matches increased venous return
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Preload
• Frank–Starling law of the heart: SV EDV– Stroke volume is proportional to the end diastolic
volume
– Ventricles eject as much blood as they receive
– The more they are stretched, the harder they contract
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Contractility
• Contractility refers to how hard the myocardium contracts for a given preload
• Positive inotropic agents increase contractility – Hypercalcemia can cause strong, prolonged
contractions and even cardiac arrest in systole
– Catecholamines increase calcium levels
– Glucagon stimulates cAMP production
– Digitalis raises intracellular calcium levels and contraction strength
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Contractility
• Negative inotropic agents reduce contractility– Hypocalcemia can cause weak, irregular
heartbeat and cardiac arrest in diastole
– Hyperkalemia reduces strength of myocardial action potentials and the release of Ca2+ into the sarcoplasm
– Vagus nerves have effect on atria but too few nerves to ventricles for a significant effect
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Afterload
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• Afterload—the blood pressure in the aorta and pulmonary trunk immediately distal to the semilunar valves– Opposes the opening of these valves– Limits stroke volume
• Hypertension increases afterload and opposes ventricular ejection
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Afterload
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• Anything that impedes arterial circulation can also increase afterload– Lung diseases that restrict pulmonary circulation– Cor pulmonale: right ventricular failure due to
obstructed pulmonary circulation• In emphysema, chronic bronchitis, and black lung disease
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Exercise and Cardiac Output
• Exercise makes the heart work harder and increases cardiac output
• Proprioceptors signal cardiac center– At beginning of exercise, signals from joints and
muscles reach the cardiac center of brain – Sympathetic output from cardiac center increases
cardiac output
• Increased muscular activity increases venous return– Increases preload and ultimately cardiac output
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Exercise and Cardiac Output
• Increases in heart rate and stroke volume cause an increase in cardiac output
• Exercise produces ventricular hypertrophy– Increased stroke volume allows heart to beat more
slowly at rest– Athletes with increased cardiac reserve can tolerate
more exertion than a sedentary person
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Coronary Artery Disease
• Coronary artery disease (CAD)—a constriction of the coronary arteries– Usually the result of atherosclerosis: an
accumulation of lipid deposits that degrade the arterial wall and obstruct the lumen
– Endothelium damaged by hypertension, virus, diabetes, or other causes
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Coronary Artery Disease
Cont.– Monocytes penetrate walls of damaged vessels and
transform into macrophages• Absorb cholesterol and fats to be called foam cells
– Look like fatty streak on vessel wall– Can grow into atherosclerotic plaques (atheromas)
– Platelets adhere to damaged areas and secrete platelet-derived growth factor
• Attracting immune cells and promoting mitosis of muscle and fibroblasts, and the deposition of collagen
• Bulging mass grows to obstruct arterial lumen
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Coronary Artery Disease
• Causes angina pectoris, intermittent chest pain, by obstructing 75% or more of the blood flow
• Immune cells of atheroma stimulate inflammation– May rupture, resulting in traveling clots or fatty emboli
• Cause coronary artery spasms due to lack of secretion of nitric oxide (vasodilator)
• Inflammation transforms atheroma into a hardened complicated plaque called arteriosclerosis
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Coronary Artery Disease
• Major risk factor for atherosclerosis is excess of low-density lipoprotein (LDL) in the blood combined with defective LDL receptors in the arterial walls– Protein-coated droplets of cholesterol, neutral fats, free
fatty acids, and phospholipids
• Most cells have LDL receptors that take up these droplets from blood by receptor-mediated endocytosis– Dysfunctional receptors in arterial cells accumulate
excess cholesterol
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Coronary Artery Disease
• Unavoidable risk factors: heredity, aging, being male
• Preventable risk factors: obesity, smoking, lack of exercise, anxious personality, stress, aggression, and diet
• Treatment– Coronary bypass surgery
• Great saphenous vein
– Balloon angioplasty
– Laser angioplasty