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Chapter 20
THE CARDIOVASCULAR SYSTEM: THE HEART
Lecture Outline
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INTRODUCTION
• The cardiovascular system consists of the blood, heart, and
blood vessels.
• The heart is the pump that circulates the blood through an
estimated 60,000 miles of blood vessels.
• The study of the normal heart and diseases associated with
it is known as cardiology.
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Chapter 20
The Cardiovascular System: The Heart
• Heart pumps over 1
million gallons per year.
• Over 60,000 miles of
blood vessels
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ANATOMY OF
THE HEART
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ANATOMY OF THE HEART
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Location of the heart
• The heart is situated between the lungs in the mediastinum
with about two-thirds of its mass to the left of the midline
(Figure 20.1).
• Because the heart lies between two rigid structures, the
vertebral column and the sternum, external compression on
the chest can be used to force blood out of the heart and
into the circulation. (Clinical Application)
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Heart Location
• Heart is located in the mediastinum
– area from the sternum to the vertebral column and
between the lungs
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Heart Orientation
•
•
•
•
•
•
Apex - directed anteriorly, inferiorly and to the left
Base - directed posteriorly, superiorly and to the right
Anterior surface - deep to the sternum and ribs
Inferior surface - rests on the diaphragm
Right border - faces right lung
Left border (pulmonary border) - faces left lung
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Heart Orientation
• Heart has 2 surfaces: anterior and inferior,
borders: right and left
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Surface Projection of the Heart
• Superior right point at the superior border of the 3rd right costal cartilage
• Superior left point at the inferior border of the 2nd left costal cartilage 3cm
to the left of midline
• Inferior left point at the 5th intercostal space, 9 cm from the midline
• Inferior right point at superior border of the 6th right costal cartilage, 3 cm
from the midline
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Pericardium
• The heart is enclosed and held in place by the pericardium.
– The pericardium consists of an outer fibrous pericardium
and an inner serous pericardium (epicardium. (Figure
20.2a).
• The serous pericardium is composed of a parietal layer and
a visceral layer.
– Between the parietal and visceral layers of the serous
pericardium is the pericardial cavity, a potential space
filled with pericardial fluid that reduces friction between
the two membranes.
– An inflammation of the pericardium is known as
pericarditis. Associated bleeding into the pericardial
cavity compresses the heart (cardiac tamponade) and is
potentially lethal (Clinical Application).
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Pericardium
• Fibrous pericardium
– dense irregular CT
– protects and anchors the
heart, prevents
overstretching
• Serous pericardium
– thin delicate membrane
– contains
• parietal layer-outer
layer
• pericardial cavity with
pericardial fluid
• visceral layer
(epicardium)
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Layers of the Heart Wall
• The wall of the heart has three layers: epicardium,
myocardium, and endocardium (Figure 20.2a).
• The epicardium consists of mesothelium and connective
tissue, the myocardium is composed of cardiac muscle, and
the endocardium consists of endothelium and connective
tissue (Figure 20.2c).
• Myocarditis is an inflammation of the myocardium.
• Endocarditis in an inflammation of the endocardium. It
usually involves the heart valves.
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Layers of Heart Wall
• Epicardium
– visceral layer of
serous pericardium
• Myocardium
– cardiac muscle layer
is the bulk of the heart
• Endocardium
– chamber lining &
valves
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Muscle Bundles of the Myocardium
• Cardiac muscle fibers swirl diagonally around the heart in
interlacing bundles
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Chambers and Sulci of the Heart (Figure 20.3).
• Four chambers
– 2 upper atria
– 2 lower ventricles
• Sulci - grooves on surface of heart containing
coronary blood vessels and fat
– coronary sulcus
• encircles heart and marks the boundary
between the atria and the ventricles
– anterior interventricular sulcus
• marks the boundary between the ventricles
anteriorly
– posterior interventricular sulcus
• marks the boundary between the ventricles
posteriorly
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Chambers and Sulci
Anterior View
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Chambers and Sulci
Posterior View
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Right
Atrium
• Receives blood from 3 sources
– superior vena cava, inferior vena cava and coronary sinus
• Interatrial septum partitions the atria
• Fossa ovalis is a remnant of the fetal foramen ovale
• Tricuspid valve
– Blood flows through into right ventricle
– has three cusps composed of dense CT covered by endocardium
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Right Ventricle
•
•
•
•
•
Forms most of anterior surface of heart
Papillary muscles are cone shaped trabeculae carneae (raised bundles of cardiac
muscle)
Chordae tendineae: cords between valve cusps and papillary muscles
Interventricular septum: partitions ventricles
Pulmonary semilunar valve: blood flows into pulmonary trunk
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Left Atrium
• Forms most of the base of the heart
• Receives blood from lungs - 4 pulmonary veins (2 right + 2 left)
• Bicuspid valve: blood passes through into left ventricle
– has two cusps
– to remember names of this valve, try the pneumonic LAMB
• Left Atrioventricular, Mitral, or Bicuspid valve
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Left Ventricle
• Forms the apex of heart
• Chordae tendineae anchor bicuspid valve to papillary muscles (also
has trabeculae carneae like right ventricle)
• Aortic semilunar valve:
– blood passes through valve into the ascending aorta
– just above valve are the openings to the coronary arteries
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Myocardial Thickness and Function
• The thickness of the myocardium of the four chambers
varies according to the function of each chamber.
– The atria walls are thin because they deliver blood to the
ventricles.
– The ventricle walls are thicker because they pump blood
greater distances (Figure 20.4a).
– The right ventricle walls are thinner than the left because
they pump blood into the lungs, which are nearby and
offer very little resistance to blood flow.
– The left ventricle walls are thicker because they pump
blood through the body where the resistance to blood
flow is greater.
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Myocardial
Thickness and
Function
• Thickness of myocardium varies according to the function of the chamber
• Atria are thin walled, deliver blood to adjacent ventricles
• Ventricle walls are much thicker and stronger
– right ventricle supplies blood to the lungs (little flow resistance)
– left ventricle wall is the thickest to supply systemic circulation
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Thickness of Cardiac Walls
Myocardium of left ventricle is much thicker than the right.
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HEART VALVES AND CIRCULATION OF BLOOD
• Valves open and close in response to pressure changes as
the heart contracts and relaxes.
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Fibrous Skeleton of Heart
• (Figure 20.5). Dense CT rings surround the valves of the heart,
fuse and merge with the interventricular septum
– Support structure for heart valves
– Insertion point for cardiac muscle bundles
– Electrical insulator between atria and ventricles
• prevents direct propagation of AP’s to ventricles
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Atrioventricular Valves Open
• A-V valves open and allow blood to flow from atria into
ventricles when ventricular pressure is lower than atrial
pressure
– occurs when ventricles are relaxed, chordae tendineae are
slack and papillary muscles are relaxed
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Atrioventricular Valves Close
• A-V valves close preventing backflow of blood into atria
– occurs when ventricles contract, pushing valve cusps
closed, chordae tendinae are pulled taut and papillary
muscles contract to pull cords and prevent cusps from
everting
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Semilunar Valves
• SL valves open with ventricular contraction
– allow blood to flow into pulmonary trunk and aorta
• SL valves close with ventricular relaxation
– prevents blood from returning to ventricles, blood fills valve
cusps, tightly closing the SL valves
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Heart valve disorders
• Stenosis is a narrowing of a heart valve which restricts
blood flow.
• Insufficiency or incompetence is a failure of a valve to close
completely.
• Stenosed valves may be repaired by balloon valvuloplasty,
surgical repair, or valve replacement.
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Valve Function Review
Which side is anterior surface?
What are the ventricles doing?
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Valve Function Review
Atria contract, blood fills
ventricles through A-V
valves
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Ventricles contract, blood
pumped into aorta and
pulmonary trunk through
SL valves
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Blood Circulation
• Two closed circuits, the systemic and pulmonic
• Systemic circulation
– left side of heart pumps blood through body
– left ventricle pumps oxygenated blood into aorta
– aorta branches into many arteries that travel to organs
– arteries branch into many arterioles in tissue
– arterioles branch into thin-walled capillaries for exchange
of gases and nutrients
– deoxygenated blood begins its return in venules
– venules merge into veins and return to right atrium
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Blood Circulation (cont.)
• Pulmonary circulation
– right side of heart pumps deoxygenated blood to lungs
– right ventricle pumps blood to pulmonary trunk
– pulmonary trunk branches into pulmonary arteries
– pulmonary arteries carry blood to lungs for exchange of
gases
– oxygenated blood returns to heart in pulmonary veins
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Blood Circulation
• Blood flow
– blue = deoxygenated
– red = oxygenated
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Coronary Circulation
• The flow of blood through the many vessels that flow through the
myocardium of the heart is called the coronary (cardiac) circulation; it
delivers oxygenated blood and nutrients to and removes carbon dioxide
and wastes from the myocardium (Figure 20.8b).
• When blockage of a coronary artery deprives the heart muscle of
oxygen, reperfusion may damage the tissue further. This damage is due
to free radicals. Drugs that lessen reperfusion damage after a heart
attack are being developed .
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Coronary Circulation
• Coronary circulation is blood supply to the heart
• Heart as a very active muscle needs lots of O2
• When the heart relaxes high pressure of blood in aorta
pushes blood into coronary vessels
• Many anastomoses
– connections between arteries supplying blood to the
same region, provide alternate routes if one artery
becomes occluded
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Coronary Arteries
• Branches off aorta above aortic
semilunar valve
• Left coronary artery
– circumflex branch
• in coronary sulcus,
supplies left atrium and left
ventricle
– anterior interventricular art.
• supplies both ventricles
• Right coronary artery
– marginal branch
• in coronary sulcus,
supplies right ventricle
– posterior interventricular art.
• supplies both ventricles
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Coronary Veins
• Collects wastes from cardiac muscle
• Drains into a large sinus on posterior surface of heart called the coronary
sinus
• Coronary sinus empties into right atrium
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CARDIAC MUSCLE AND THE CARDIAC
CONDUCTION SYSTEM
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Histology of Cardiac Muscle
• Compared to skeletal muscle fibers, cardiac muscle fibers
are shorter in length, larger in diameter, and squarish rather
than circular in transverse section (Figure 20.9).
• They also exhibit branching (Table 4.4B).
• Fibers within the networks are connected by intercalated
discs, which consist of desmosomes and gap junctions
• Cardiac muscles have the same arrangement of actin and
myosin, and the same bands, zones, and Z discs as skeletal
muscles.
• They do have less sarcoplasmic reticulum than skeletal
muscles and require Ca+2 from extracellular fluid for
contraction.
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Cardiac Muscle Histology
• Branching, intercalated discs with gap junctions, involuntary, striated,
single central nucleus per cell
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Cardiac Myofibril
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Conduction System of Heart
Coordinates contraction of heart muscle.
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Myocardial ischemia and infarction
• Reduced blood flow through coronary arteris may cause
ischemia. Ischemia cuases hypoxia and may weaken the
myocardial cells. Ischemia is often manifested through
angina pectoris.
– A complete obstruction of flow in a coronary artery may
cause myocardial infarction (heart attack).
– Tissue distal to the obstruction dies and is replaced by
scar tissur.
– Treatment may involve injection of thrombolytic agents,
coronary angioplasty, or coronary artery bypass grafts.
• While it was long thought that cardiac muscle lacked stem
cells, recent studies five evidence for replacement of heart
cells. It appears that stem cells in the blood can migrate to
the heart and differentiate into myocardial cells.
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Autorhythmic Cells: The Conduction System
• Cardiac muscle cells are autorhythmic cells because they
are self-excitable. They repeatedly generate spontaneous
action potentials that then trigger heart contractions.
• These cells act as a pacemaker to set the rhythm for the
entire heart.
• They form the conduction system, the route for propagating
action potential through the heart muscle.
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Conduction System of Heart
Coordinates contraction of heart muscle.
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Conduction
• Components of this system are the sinoartrial (SA) node
(pacemaker), atrioventricular (AV) node, atrioventricular
bundle (bundle of His), right and left bundle branches, and
the conduction myofibers (Purkinje fibers) (Figure 20.10)
• Signals from the autonomic nervous system and hormones,
such as epinephrine, do modify the heartbeat (in terms of
rate and strength of contraction), but they do not establish
the fundamental rhythm.
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Conduction System of Heart
• Autorhythmic Cells
– Cells fire spontaneously, act as pacemaker and form
conduction system for the heart
• SA node
– cluster of cells in wall of Rt. Atria
– begins heart activity that spreads to both atria
– excitation spreads to AV node
• AV node
– in atrial septum, transmits signal to bundle of His
• AV bundle of His
– the connection between atria and ventricles
– divides into bundle branches & purkinje fibers, large
diameter fibers that conduct signals quickly
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Rhythm of Conduction System
• SA node fires spontaneously 90-100 times per minute
• AV node fires at 40-50 times per minute
• If both nodes are suppressed fibers in ventricles by
themselves fire only 20-40 times per minute
• Artificial pacemaker needed if pace is too slow
• Extra beats forming at other sites are called ectopic
pacemakers
– caffeine & nicotine increase activity
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Timing of Atrial &
Ventricular Excitation
• SA node setting pace since is the fastest
• In 50 msec excitation spreads through both atria and down to
AV node
• 100 msec delay at AV node due to smaller diameter fibersallows atria to fully contract filling ventricles before ventricles
contract
• In 50 msec excitation spreads through both ventricles
simultaneously
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Abnormal Conduction
• Sick sinus syndrome describes an abnormally functioning
SA node that initiates irregular heart beats.
• When abnormal pacing of the heart develops, heart rhythm
can be restored by implanting an artificail pacemaker, a
device that sends out small, regular currents to stimulate
myocardial contraction..
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Action potential and contraction of contractile fibers
• An impulse in a ventricular contractile fiber is characterized
by rapid depolarization, plateau, and repolarization (Figure
20.11).
• The refractory period of a cardiac muscle fiber (the time
interval when a second contraction cannot be triggered) is
longer than the contraction itself (Figure 20.11). Therefore
tetanus cannot occur in myocardial cells.
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Conduction System of the Heart
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Physiology of Contraction
• Depolarization, plateau, repolarization
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Depolarization & Repolarization
• Depolarization
– Cardiac cell resting membrane potential is -90mv
– excitation spreads through gap junctions
– fast Na+ channels open for rapid depolarization
• Plateau phase
– 250 msec (only 1msec in neuron)
– slow Ca+2 channels open, let Ca +2 enter from outside cell and from
storage in sarcoplasmic reticulum, while K+ channels close
– Ca +2 binds to troponin to allow for actin-myosin cross-bridge formation
& tension development
• Repolarization
– Ca+2 channels close and K+ channels open & -90mv is restored as
potassium leaves the cell
• Refractory period
– very long so heart can fill
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Action Potential in Cardiac Muscle
Changes in cell membrane permeability.
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ATP production in cardiac muscle
• Cardiac muscle relies on aerobic cellular respiration for ATP
production.
• Cardiac muscle also produces some ATP from creatine
phosphate
• The presence of creatine kinase (CK) in the blood indicates
injury of cardiac muscle usually caused by a myocardial
infarction.
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Electrocardiogram
• Impulse conduction through the heart generates electrical
currents that can be detected at the surface of the body. A
recording of the electrical changes that accompany each
cardiac cycle (heartbeat) is called an electrocardiogram
(ECG or EKG).
• The ECG helps to determine if the conduction pathway is
abnormal, if the heart is enlarged, and if certain regions are
damaged.
• Figure 20.12 shows a typical ECG.
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Electrocardiogram---ECG or EKG
• EKG
– Action potentials of all active cells
can be detected and recorded
• P wave
– atrial depolarization
• P to Q interval
– conduction time from atrial to
ventricular excitation
• QRS complex
– ventricular depolarization
• T wave
– ventricular repolarization
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ECG
• In a typical Lead II record, three clearly visible waves
accompany each heartbeat It consists of:.
• P wave (atrial depolarization - spread of impulse from SA
node over atria)
• QRS complex (ventricular depolarization - spread of impulse
through ventricles)
• T wave (ventricular repolarization).
• Correlation of ECG waves with atrial and ventricular systole
(Figure 20.13)
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ECG
• As atrial fibers depolarize, the P wave appears.
• After the P wave begins, the atria contract (atrial systole).
Action potential slows at the AV node giving the atria time to
contract.
• The action potential moves rapidly through the bundle
branches, Purkinje fibers, and the ventricular myocardium
producing the QRS complex.
• Ventricular contraction after the QRS comples and
continues through the ST segment.
• Repolarization of the ventricles produces the T wave.
• Both atria and ventricles repolarize and the P wave appears.
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THE CARDIAC CYCLE
• A cardiac cycle consists of the systole (contraction) and
diastole (relaxation) of both atria, rapidly followed by the
systole and diastole of both ventricles.
• Pressure and volume changes during the cardiac cycle
• During a cardiac cycle atria and ventricles alternately
contract and relax forcing blood from areas of high pressure
to areas of lower pressure.
• Figure 20.14 shows the relation between the ECG and
changes in atrial pressure, ventricular pressure, aortic
pressure, and ventricular volume during the cardia cycle.
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One Cardiac Cycle - Vocabulary
• At 75 beats/min, one cycle requires 0.8 sec.
– systole (contraction) and diastole (relaxation) of both atria, plus the
systole and diastole of both ventricles
• End diastolic volume (EDV)
– volume in ventricle at end of diastole, about 130ml
• End systolic volume (ESV)
– volume in ventricle at end of systole, about 60ml
• Stroke volume (SV)
– the volume ejected per beat from each ventricle, about 70ml
– SV = EDV - ESV
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Phases of Cardiac Cycle
• Isovolumetric relaxation
– brief period when volume in ventricles does not change--as ventricles
relax, pressure drops and AV valves open
• Ventricular filling
– rapid ventricular filling:as blood flows from full atria
– diastasis: as blood flows from atria in smaller volume
– atrial systole pushes final 20-25 ml blood into ventricle
• Ventricular systole
– ventricular systole
– isovolumetric contraction
• brief period, AV valves close before SL valves open
– ventricular ejection: as SL valves open and blood is ejected
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Cardiac Cycle
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Atrial systole/ventricular diastole
• The atria contract, increasing pressure forces the AV valves to open.
– The amount of blood in the ventricle at the end of diastole is the End
Diastolic Volume (EDV)
• Ventricular systole/atrial diastole
– Ventricles contract and increasing pressure forces the AV valves to
close.
– AV and SL valves are all closed (isovolumetric contraction).
– Pressure continues to rise opening the SL valves leading to
ventricular ejection.
– The amount of blood in the left ventrical at the end of systole is End
Systolic Volume (ESV). Stroke volume (SV) is the volume of blood
ejected from the left ventricle SV = EDV-ESV.
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Relaxation period
• Both atria and ventricles are relaxed. Pressure in the
ventricles fall and the SL valves close. Brief time all four
valves are closed is the isovolumetric relaxation. Pressure
in the ventricles continues to fall, the AV valves open, and
ventricular filling begins.
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Ventricular Pressures
• Blood pressure in aorta is 120mm Hg
• Blood pressure in pulmonary trunk is 30mm Hg
• Differences in ventricle wall thickness allows heart to push the
same amount of blood with more force from the left ventricle
• The volume of blood ejected from each ventricle is 70ml
(stroke volume)
• Why do both stroke volumes need to be same?
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Auscultation
• The act of listening to sounds within the body is called
auscultation, and it is usually done with a stethoscope. The
sound of a heartbeat comes primarily from the turbulence in
blood flow caused by the closure of the valves, not from the
contraction of the heart muscle (Figure 20.15).
• The first heart sound (lubb) is created by blood turbulence
associated with the closing of the atrioventricular valves
soon after ventricular systole begins.
• The second heart sound (dupp) represents the closing of
the semilunar valves close to the end of the ventricular
systole.
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Heart Sounds
Where to listen on chest wall for heart sounds.
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Murmurs
• A heart murmur is an abnormal sound that consists of a flow
noise that is heard before, between, or after the lubb-dupp
or that may mask the normal sounds entirely.
• Some murmurs are caused by turbulent blood flow around
valves due to abnormal anatomy or increased volume of
flow.
• Not all murmurs are abnormal or symptomatic, but most
indicate a valve disorder.
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CARDIAC OUTPUT
• Since the body’s need for oxygen varies with the level of
activity, the heart’s ability to discharge oxygen-carrying
blood must also be variable. Body cells need specific
amounts of blood each minute to maintain health and life.
• Cardiac output (CO) is the volume of blood ejected from the
left ventricle (or the right ventricle) into the aorta (or
pulmonary trunk) each minute.
– Cardiac output equals the stroke volume, the volume of
blood ejected by the ventricle with each contraction,
multiplied by the heart rate, the number of beats per
minute. CO = SV X HR
• Cardiac reserve is the ratio between the maximum cardiac
output a person can achieve and the cardiac output at rest.
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Cardiac Output
• CO = SV x HR
– at 70ml stroke volume & 75 beat/min----5 and 1/4 liters/min
– entire blood supply passes through circulatory system every minute
• Cardiac reserve is maximum output/output at rest
– average is 4-5x while athlete’s is 7-8x
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Influences on Stroke Volume
• Preload (affect of stretching)
– Frank-Starling Law of Heart
– more muscle is stretched, greater force of contraction
– more blood more force of contraction results
• Contractility
– autonomic nerves, hormones, Ca+2 or K+ levels
• Afterload
– amount of pressure created by the blood in the way
– high blood pressure creates high afterload
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Stroke Volume and Heart Rate
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Preload: Effect of Stretching
• According to the Frank-Starling law of the heart, a greater
preload (stretch) on cardiac muscle fibers just before they
contract increases their force of contraction during systole.
– Preload is proportional to EDV.
– EDV is determined by length of ventricular diastole and
venous return.
• The Frank-Starling law of the heart equalizes the output of
the right and left ventricles and keeps the same volume of
blood flowing to both the systemic and pulmonary
circulations.
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Contractility
• Myocardial contractility, the strength of contraction at any
given preload, is affected by positive and negative inotropic
agents.
– Positive inotropic agents increase contractility
– Negative inotropic agents decrease contractility.
• For a constant preload, the stroke volume increases when
positive inotropic agents are present and decreases when
negative inotropic agents are present.
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Afterload
• The pressure that must be overcome before a semilunar
valve can open is the afterload.
• In congestive heart failure, blood begins to remain in the
ventricles increasing the preload and ultimately causing an
overstretching of the heart and less forceful contraction
– Left ventricular failure results in pulmonary edema
– Right ventricular failure results in peripheral edema.
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Regulation of Heart Rate
• Cardiac output depends on heart rate as well as stroke
volume. Changing heart rate is the body’s principal
mechanism of short-term control over cardiac output and
blood pressure. Several factors contribute to regulation of
heart rate.
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Regulation of Heart Rate
• Nervous control from the cardiovascular center in the
medulla
– Sympathetic impulses increase heart rate and force of
contraction
– parasympathetic impulses decrease heart rate.
– Baroreceptors (pressure receptors) detect change in BP
and send info to the cardiovascular center
• located in the arch of the aorta and carotid arteries
• Heart rate is also affected by hormones
– epinephrine, norepinephrine, thyroid hormones
– ions (Na+, K+, Ca2+)
– age, gender, physical fitness, and temperature
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Regulation of Heart Rate
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Autonomic regulation of the heart
• Nervous control of the cardiovascular system stems from
the cardiovascular center in the medulla oblongata (Figure
20.16).
• Proprioceptors, baroreceptors, and chemoreceptors monitor
factors that influence the heart rate.
• Sympathetic impulses increase heart rate and force of
contraction; parasympathetic impulses decrease heart rate.
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Chemical regulation of heart rate
• Heart rate affected by hormones (epinephrine,
norepinephrine, thyroid hormones).
• Cations (Na+, K+, Ca+2) also affect heart rate.
• Other factors such as age, gender, physical fitness, and
temperature also affect heart rate.
• Figure 20.16 summarizes the factors that can increase
stoke volume and heart rate to cause an increase in cardiac
output..
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Risk Factors for Heart Disease
• Risk factors in heart disease:
– high blood cholesterol level
– high blood pressure
– cigarette smoking
– obesity & lack of regular exercise.
• Other factors include:
– diabetes mellitus
– genetic predisposition
– male gender
– high blood levels of fibrinogen
– left ventricular hypertrophy
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Plasma Lipids and Heart Disease
• Risk factor for developing heart disease is high blood cholesterol level.
– promotes growth of fatty plaques
– Most lipids are transported as lipoproteins
• low-density lipoproteins (LDLs)
• high-density lipoproteins (HDLs)
• very low-density lipoproteins (VLDLs)
– HDLs remove excess cholesterol from circulation
– LDLs are associated with the formation of fatty plaques
– VLDLs contribute to increased fatty plaque formation
• There are two sources of cholesterol in the body:
– in foods we ingest & formed by liver
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Desirable Levels of Blood Cholesterol for Adults
• TC (total cholesterol) under 200 mg/dl
• LDL under 130 mg/dl
• HDL over 40 mg/dl
• Normally, triglycerides are in the range of 10-190 mg/dl.
• Among the therapies used to reduce blood cholesterol level
are exercise, diet, and drugs.
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EXERCISE AND THE HEART
• A person’s cardiovascular fitness can be improved with regular exercise.
– Aerobic exercise (any activity that works large body muscles for at
least 20 minutes, preferably 3 – 5 times per week) increases cardiac
output and elevates metabolic rate.
– Several weeks of training results in maximal cardiac output and
oxygen delivery to tissues
– Regular exercise also decreases anxiety and depression, controls
weight, and increases fibrinolytic activity.
– Sustained exercise increases oxygen demand in muscles
• As a heart fails, a person’s mobility decreases. Heart transplants may
help such individuals. Other possibilities include cardiac assist devices
and surgical procedures. Table 20.1 describes several devices and
procedures.
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DEVELOPMENT OF THE HEART
• The heart develops from mesoderm before the end of the
third week of gestation.
• The endothelial tubes develop into the four-chambered
heart and great vessels of the heart (Figure 20.18).
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Developmental Anatomy of the Heart
• The heart develops from
mesoderm before the end
of the third week of
gestation.
• The tubes develop into
the four-chambered heart
and great vessels of the
heart.
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DISORDERS: HOMEOSTATIC IMBALANCES
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Clinical Problems
• MI = myocardial infarction
– death of area of heart muscle from lack of O2
– replaced with scar tissue
– results depend on size & location of damage
• Blood clot
– use clot dissolving drugs streptokinase or t-PA &
heparin
– balloon angioplasty
• Angina pectoris----heart pain from ischemia of
cardiac muscle
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CAD
• Coronary artery disease (CAD), or coronary heart disease
(CHD), is a condition in which the heart muscle receives an
inadequate amount of blood due to obstruction of its blood
supply. It is the leading cause of death in the United States
each year. The principal causes of obstruction include
atherosclerosis, coronary artery spasm, or a clot in a
coronary artery.
• Risk factors for development of CAD include high blood
cholesterol levels, high blood pressure, cigarette smoking,
obesity, diabetes, “type A” personality, and sedentary
lifestyle.
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CAD
• Atherosclerosis is a process in which smooth muscle cells
proliferate and fatty substances, especially cholesterol and
triglycerides (neutral fats), accumulate in the walls of the
medium-sized and large arteries in response to certain
stimuli, such as endothelial damage (Figure 20.18).
• Diagnosis of CAD includes such procedures as cardiac
catherization and cardiac angiography.
• Treatment options for CAD include drugs and coronary
artery bypass grafting (Figure 20.19).
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Coronary Artery Disease
• Heart muscle receiving
insufficient blood supply
– narrowing of vessels--atherosclerosis, artery
spasm or clot
– atherosclerosis--smooth
muscle & fatty deposits in
walls of arteries
• Treatment
– drugs, bypass graft,
angioplasty, stent
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By-pass Graft
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Percutaneous
Transluminal Coronary
Angioplasty
Stent
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Congenital Heart Defects
• A congenital defect is a defect that exists at birth, and
usually before birth.
• Congenital defects of the heart include coarctation of the
aorta, patent ductus arteriosus, septal defects (interatrial or
interventricular), valvular stenosis, and tetralogy of Fallot.
• Some congenital defects are not serious or remain
asymptomatic; others heal themselves.
• A few congenital defects are life threatening and must be
corrected surgically. Fortunately, surgical techniques are
highly refined for most of the defects listed.
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Arrythmia
• Arrhythmia (disrhythmia) is an irregularity in heart rhythm
resulting from a defect in the conduction system of the
heart.
• Categories are bradycardia, tachycardia, and fibrillation.
• Those that begin in the atria are supraventricular or atrial.
• Those that begin in the ventricle are ventricular.
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Congestive Heart Failure
• Congestive heart failure is a chronic or acute state that results when the
heart is not capable of supplying the oxygen demands of the body.
• Causes of CHF
– coronary artery disease, hypertension, MI, valve disorders, congenital
defects
• Left side heart failure
– less effective pump so more blood remains in ventricle
– heart is overstretched & even more blood remains
– blood backs up into lungs as pulmonary edema
– suffocation & lack of oxygen to the tissues
• Right side failure
– fluid builds up in tissues as peripheral edema
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end
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