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PowerPoint® Lecture Slide Presentation by Vince Austin
Human Anatomy & Physiology
FIFTH EDITION
Elaine N. Marieb
Chapter 19
The Cardiovascular
System: The Heart
Part A
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Heart Anatomy
• Approximately the size of your fist
• Location
• Superior surface of diaphragm
• Left of the midline
• Anterior to the vertebral column, posterior to the
sternum
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Heart Anatomy
Figure 19.1
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4
5
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Heart Covering
• Pericardial physiology
• Protects and anchors heart
• Prevents overfilling
Figure 19.2
9
Heart Covering
• Pericardial anatomy
• Fibrous pericardium
• Serous pericardium (separated by pericardial cavity)
• Epicardium (visceral layer)
Figure 19.2
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Heart Wall
• Epicardium – visceral layer of the serous
pericardium
• Myocardium – cardiac muscle layer forming the bulk
of the heart
• Fibrous skeleton of the heart – crisscrossing,
interlacing layer of connective tissue
• Endocardium – endothelial layer of the inner
myocardial surface
11
External Heart: Major Vessels of the Heart
(Anterior View)
• Returning blood to the heart
• Superior and inferior venae cavae
• Right and left pulmonary veins
• Conveying blood away from the heart
• Pulmonary trunk, which splits into right and left
pulmonary arteries
• Ascending aorta (three branches) – brachiocephalic,
left common carotid, and subclavian arteries
12
External Heart: Vessels that Supply/Drain the
Heart (Anterior View)
• Arteries – right and left coronary (in atrioventricular
groove), marginal, circumflex, and anterior
interventricular
• Veins – small cardiac vein, anterior cardiac vein, and
great cardiac vein
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External Heart: Anterior View
Figure 19.4b
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External Heart: Major Vessels of the Heart
(Posterior View)
• Returning blood to the heart
• Right and left pulmonary veins
• Superior and inferior venae cavae
• Conveying blood away from the heart
• Aorta
• Right and left pulmonary arteries
17
External Heart: Vessels that Supply/Drain the
Heart (Posterior View)
• Arteries – right coronary artery (in atrioventricular
groove) and the posterior interventricular artery (in
interventricular groove)
• Veins – great cardiac vein, posterior vein to left
ventricle, coronary sinus, and middle cardiac vein
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External Heart: Posterior View
Figure 19.4d
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Gross Anatomy of Heart: Frontal Section
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Gross Anatomy of Heart: Frontal Section
Figure 19.4e
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Atria of the Heart
• Atria are the receiving chambers of the heart
• Each atrium has a protruding auricle
• Pectinate muscles mark atrial walls
• Blood enters right atria from superior and inferior
venae cavae and coronary sinus
• Blood enters left atria from pulmonary veins
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Ventricles of the Heart
• Ventricles are the discharging chambers of the heart
• Papillary muscles and trabeculae carneae muscles
mark ventricular walls
• Right ventricle pumps blood into the pulmonary trunk
• Left ventricle pumps blood into the aorta
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PowerPoint® Lecture Slide Presentation by Vince Austin
Human Anatomy & Physiology
FIFTH EDITION
Elaine N. Marieb
Chapter 19
The Cardiovascular
System: The Heart
Part B
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Pathway of Blood through the Heart and Lungs
Figure 19.5
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Coronary Circulation
Figure 19.7a
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Coronary Circulation
Figure 19.7b
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Heart Valves
• Heart valves insure unidirectional blood flow through the
heart
• Atrioventricular (AV) valves lie between the atria and the
ventricles
• Also called the Tricuspid and Bicuspid (Mitral) valves
• AV valves prevent backflow into the atria when ventricles
contract
• Chordae tendineae anchor AV valves to papillary muscles
• Papillary muscles pre-tense the chordae prior to
ventricular contraction
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Heart Valves
Figure 19.9
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Heart Valves
• Aortic semilunar valve lies between the left ventricle
and the aorta
• Pulmonary semilunar valve lies between the right
ventricle and pulmonary trunk
• Semilunar valves prevent backflow of blood into the
ventricles
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Heart Valves
Figure 19.10
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PowerPoint® Lecture Slide Presentation by Vince Austin
Human Anatomy & Physiology
FIFTH EDITION
Elaine N. Marieb
Chapter 19
The Cardiovascular
System: The Heart
Histology & Microanatomy
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Microscopic Heart Muscle Anatomy
• Cardiac muscle is striated, short, fat, branched, and
interconnected
• Connective tissue endomysium acts as both tendon
and insertion
• Intercalated discs anchor cardiac cells together and
allow free passage of ions
• Heart muscle behaves as a functional syncytium
39
Cardiac Muscle Contraction
• Heart muscle:
• Is stimulated by nerves and self-excitable (automaticity
or autorhythmicity)
• Contracts as a unit (functional syncytium)
• Has a long (250 ms) absolute refractory period
compared to skeletal’s (~ 5ms)
• Cardiac muscle contraction is similar to skeletal muscle
contraction (sliding filament theory)
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Cardiac Muscle Cells:
• Autorhythmic
• Myocardial Characteristics:
• Intercalated discs
•
Desmosomes
•
Gap Junctions
• Fast signals
• Cell to cell
• Many mitochondria
• Large T tubes
Figure 14-10: Cardiac muscle
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Cardiac Muscle Cells:
Figure 14-10: Cardiac muscle
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Microscopic Heart Muscle Anatomy
Figure 19.11b
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Cardiac Muscle
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Ions
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Heart Physiology: Intrinsic Conduction System
• Autorhythmic cells:
• Initiate action potentials
• Have unstable resting potentials called pacemaker
potentials
• Use calcium influx (rather than sodium) for rising
phase of the action potential
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PowerPoint® Lecture Slide Presentation by Vince Austin
Human Anatomy & Physiology
FIFTH EDITION
Elaine N. Marieb
Chapter 19
The Cardiovascular
System: The Heart
Electrophysiology
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Purkinje fibers 40X
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* Purkinje fibers 100X
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PowerPoint® Lecture Slide Presentation by Vince Austin
Human Anatomy & Physiology
FIFTH EDITION
Elaine N. Marieb
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Heart Physiology: Intrinsic Conduction System
Figure 19.13
55
Heart Physiology: Sequence of Excitation
• Sinoatrial (SA) node generates impulses about 75
times/minute
• Atrioventricular (AV) node delays the impulse
approximately 0.1 second
• Impulse passes from atria to ventricles via the
atrioventricular bundle (bundle of His)
56
Heart Physiology: Sequence of Excitation
• AV bundle splits into two pathways in the
interventricular septum (bundle branches)
• Bundle branches carry the impulse toward the apex
of the heart
• Purkinje fibers carry the impulse to the heart apex
and ventricular walls
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Heart Physiology: Sequence of Excitation
Figure 19.14a
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Electrocardiography
• Electrical activity is recorded by electrocardiogram
(ECG or EKG)
• P wave corresponds to depolarization of SA node
• QRS complex corresponds to ventricular
depolarization
• T wave corresponds to ventricular repolarization
• Atrial repolarization record is masked by the larger
QRS complex
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Electrocardiography
Figure 19.16
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Extrinsic Innervation of the Heart
• Heart is stimulated
by the sympathetic
cardioacceleratory
center
• Heart is inhibited by
the parasympathetic
cardioinhibitory
center
Figure 19.15
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Cardiac Cycle
• Cardiac cycle refers to all events associated with
blood flow through the heart
• Systole – contraction of heart muscle
• Diastole – relaxation of heart muscle
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Phases of the Cardiac Cycle
• Ventricular filling – mid-to-late diastole
• Heart blood pressure is low as blood enters atria and
flows into ventricles
• AV valves are open then atrial systole occurs
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Phases of the Cardiac Cycle
• Ventricular systole
• Atria relax
• Rising ventricular pressure results in closing of AV
valves
• Isovolumetric contraction phase
• Ventricular ejection phase opens semilunar valves
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Phases of the Cardiac Cycle
• Isovolumetric relaxation – early diastole
• Ventricles relax
• Backflow of blood in aorta and pulmonary trunk
closes semilunar valves
• Dicrotic notch – brief rise in aortic pressure caused
by backflow of blood rebounding off semilunar
valves
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Phases of the Cardiac Cycle
Figure 19.19a
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Phases of the Cardiac Cycle
Figure 19.19b
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Heart Sounds
• Heart sounds (lubdup) are associated
with closing of
heart valves
Figure 19.20
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Cardiac Output (CO) and Reserve
• CO is the amount of blood pumped by each ventricle
in one minute
• CO is the product of heart rate (HR) and stroke
volume (SV)
• HR is the number of heart beats per minute
• SV is the amount of blood pumped out by a ventricle
with each beat
• Cardiac reserve is the difference between resting and
maximal CO
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Cardiac Output: Example
• CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
• CO = 5250 ml/min (5.25 L/min)
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Regulation of Stroke Volume
• SV = end diastolic volume (EDV) minus end systolic
volume (ESV)
• SV = EDV-ESV
• EDV = amount of blood collected in a ventricle
during diastole
• ESV = amount of blood remaining in a ventricle after
contraction
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Factors Affecting Stroke Volume
• Preload – amount ventricles are stretched by
contained blood
• Contractility – cardiac cell contractile force due to
factors other than EDV
• Afterload – back pressure exerted by blood in the
large arteries leaving the heart
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Frank-Starling Law of the Heart
• Preload, or degree of stretch, of cardiac muscle cells
before they contract is the critical factor controlling
stroke volume
• Slow heartbeat and exercise increase venous return to
the heart, increasing SV
• Blood loss and extremely rapid heartbeat decrease
SV
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Preload and Afterload
Figure 19.21
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PowerPoint® Lecture Slide Presentation by Vince Austin
Human Anatomy & Physiology
FIFTH EDITION
Elaine N. Marieb
Chapter 19
The Cardiovascular
System: The Heart
Part D
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Extrinsic Factors Influencing Stroke Volume
• Contractility is the increase in contractile strength,
independent of stretch and EDV
• Increase in contractility comes from:
• Increased sympathetic stimuli
• Certain hormones
• Ca2+ and some drugs
• Agents/factors that decrease contractility include:
• Acidosis
• Increased extracellular potassium
• Calcium channel blockers
81
Contractility and Norepinephrine
• Sympathetic
stimulation releases
norepinephrine and
initiates a cyclic AMP
second-messenger
system
Figure 19.22
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Regulation of Heart Rate: Autonomic Nervous
System
• Sympathetic nervous system (SNS) stimulation is
activated by stress, anxiety, excitement, or exercise
(FIGHT or FLIGHT)
• Parasympathetic nervous system (PNS) stimulation is
mediated by acetylcholine and opposes the SNS
(HOUSEKEEPING & MAINTENANCE)
• PNS dominates the autonomic stimulation, slowing
heart rate and causing vagal tone
83
Extrinsic Innervation of the Heart
• Heart is stimulated
by the sympathetic
cardioacceleratory
center
• Heart is inhibited by
the parasympathetic
cardioinhibitory
center
Figure 19.15
84
Chemical Regulation of the Heart
• The hormones epinephrine and thyroxine increase
heart rate
• Intra- and extracellular ion concentrations must be
maintained for normal heart function
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Factors Involved in Regulation of Cardiac Output
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Factors Involved in Regulation of Cardiac Output
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Factors Involved in Regulation of Cardiac Output
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Factors Involved in Regulation of Cardiac Output
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Factors Involved in Regulation of Cardiac Output
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Developmental Aspects of the Heart
• Embryonic heart chambers
• Sinus venous
• Atrium
• Ventricle
• Bulbus cordis
Figure 19.24
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Developmental Aspects of the Heart
• Fetal heart structures that bypass pulmonary
circulation
• Foramen ovale connects the two atria
• Ductus arteriosus connects pulmonary trunk and the
aorta
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Normal Heart Sound
Mitral valve prolapse
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PowerPoint® Lecture Slide Presentation by Vince Austin
Human Anatomy & Physiology
FIFTH EDITION
Elaine N. Marieb
Chapter 19
Pathologies
Part D
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Endocarditis-symptoms
• Fever
• Paleness
• Chills
• Persistent cough
• Weakness
• Swelling in your feet,
legs or abdomen
• Fatigue
• Aching joints and
muscles
• Night sweats
• Shortness of breath
• Unexplained weight
loss
• Blood in your urine
• A new heart murmur
• Tenderness in your
spleen
98
Endocarditis
• Endocarditis occurs when germs enter your bloodstream, travel
to your heart and lodge on abnormal heart valves or damaged
heart tissue. Bacteria are the cause of most cases, but fungi,
viruses or other microorganisms also may be responsible.
• Sometimes the culprit is one of many common bacteria that live
in your mouth, upper respiratory tract or other parts of your body.
In other cases, the offending organism may gain entry to your
bloodstream through:
• Certain dental or medical procedures.
• An infection or other medical condition..
• Catheters or needles..
• Common activities..
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Endocarditis
• Typically, your immune system destroys bacteria that
make it into your bloodstream. Even if bacteria reach
your heart, they may pass through without causing an
infection.
• Most people who develop endocarditis have a
diseased or damaged heart valve — an ideal spot for
bacteria to settle. This damaged tissue in the
endocardium provides bacteria with the roughened
surface they need to attach and multiply.
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Age-Related Changes Affecting the Heart
• Sclerosis and thickening of valve flaps
• Decline in cardiac reserve
• Fibrosis of cardiac muscle
• Atherosclerosis
102
Homeostatic Imbalances
• Hypocalcemia – reduced ionic calcium depresses the
heart
• Hypercalcemia – dramatically increases heart
irritability and leads to spastic contractions
• Hypernatremia (Na ??!!)– blocks heart contraction by
inhibiting ionic calcium transport
• Hyperkalemia (K) – leads to heart block and cardiac
arrest
103
Homeostatic Imbalances
• Tachycardia – heart rate over 100 beats/min
• Bradycardia – heart rate less than 60 beats/min
• Pericarditis
• inflammation of the pericardium
• Reduces cardiac output
• Antibiotics, anti-inflammatory
104
Congestive Heart Failure (CHF)
• Congestive heart failure (CHF), caused by:
• Coronary atherosclerosis
• Increased blood pressure in aorta
• Successive myocardial infarcts
• Dilated cardiomyopathy (DCM)
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Cardiopathologies
• Congestive Heart Failure
• If RIGHT side fails, then peripheral congestion
because the blood can’t return from the body to the
right atrium causing edema in the extremities.
• Ultimately, since the failure of one side now strains
the effectiveness of the healthy side, the myocardium
weakens over time and a heart transplant is
inevitable.
• Temporary treatment is to lower blood volume,
reducing exertion, lowering BP
106
Cardiopathologies
Atherosclerosis (CAD)
• Blockage of coronary arteries from deposition of
LDL due to tissue insult of tunica interna.
• Stenosis relieved by balloon angioplasty, insertion
of stent, coronary by-pass.
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Illust.
110
Illust.
111
Illust.
Coronary Artery
Fatty Deposit
Stenosis
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Illust.
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Illust.
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Illust.
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Illust.
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Cardiopathologies
• Myocardial Infarction
• Ischemia (holding back blood) is due to a stenosis
caused by atheroschlosis. The pain, angina pectoris
is usually an indicator of a TIA (transient ischemic
attack)
• Necrosis (death) of myocardium due to ischemia
associated w/ the stenosis.
• Myocardia is amitotic and therefore will not repair
itself. Scar tissue instead.
• Seriousness depends on location/extent
• Treatment would include dealing w/ stenosis,
vasodilators, beta-blockers (reduce blood pressure),
heart transplant, LVAD.
120
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Cardiopathologies
• Valvular Stenosis
• Stiffening of valves constrict opening to next vessel.
• Increases cardiac workload
• Valve replacement if needed.
122
Cardiopathologies
• Arrhythmia
• Ectopic Signals (extrasystole)
• Damage to SA node, AV node, bundle branches
(need pacemaker, drugs)
• Ventricualar fibrillation is most extreme case of
extrasystole.
• Tachycardia – could lead to Vfib
• Bradycardia caused by many factors (faulty SA
node)
123
Cardiopathologies
• Congestive Heart Failure
• Chronic situation caused by atherosclerosis
myocardial infarcts, and/or high diastolic pressure.
• Results in hypertrophy of the myocardium which
reduces its effectiveness which then enhances
hypertrophy.
• If LEFT side fails, then Pulmonary Congestion
because the blood can’t flow back as fast to the heart
from the lungs causing edema and then suffocation.
124
Cardiopathologies
• Congenitial Defects
• Septal defects
• Patent ductus arteriosis
• Coarctation of aorta
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Cardiopathologies
• Age-related changes
• sclerosis of valve flaps
• Fibrosis of myocardium
• Atherosclerosis
• Reduction in cardiac output
129
Circulatory Shock
• Circulatory shock – any condition in which blood
vessels are inadequately filled and blood cannot
circulate normally
• Results in inadequate blood flow to meet tissue needs
• Three types include:
• Hypovolemic shock – results from large-scale blood
loss
• Vascular shock – poor circulation resulting from
extreme vasodilation
• Cardiogenic shock – the heart cannot sustain
adequate circulation
130
Alterations in Blood Pressure
• Hypotension – low BP in which systolic pressure is
below 100 mm Hg
• Hypertension – condition of sustained elevated
arterial pressure of 140/90 or higher
• Transient elevations are normal and can be caused by
fever, physical exertion, and emotional upset
• Chronic elevation is a major cause of heart failure,
vascular disease, renal failure, and stroke
(cerebrovascular accident)
131
Hypotension
• Orthostatic hypotension – temporary low BP and
dizziness when suddenly rising from a sitting or
reclining position
• Chronic hypotension – hint of poor nutrition and
warning sign for Addison’s disease
• Acute hypotension – important sign of circulatory
shock
• Threat to patients undergoing surgery and those in
intensive care units
132
Hypertension
• Primary or essential hypertension – risk factors in
primary hypertension include diet, obesity, age, race,
heredity, stress, and smoking
• Secondary hypertension – due to identifiable
disorders, including excessive renin secretion,
arteriosclerosis, and endocrine disorders
133
Aneurysm
• A weakening of the arteries and subsequent bursting
• Due to hypertension or arteriosclerosis
• Generally affect cerebral arteries, aorta, and renal
arteries
134
Cardiopathologies
135
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Capillary with red
blood cells.
SEM x5140
138