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Chapter
15
1
ANATOMY
OF THE
HEART
2
ANATOMY OF THE HEART
3
Size of Heart
 Size
 12 - 14 cm x 8 - 9 cm
x6
 Weight,
 M – 280 to 340 g
 F – 230 to 280 g
 The heart continues to
increase in weight and size
up to an advanced period of
life
 This increase is more
marked in men than in
women.
4
Size of Heart
• The wall of the right
ventricle is thinner than
that of the left, the
proportion between them
being as 1 to 3; it is
thickest at the base, and
gradually becomes thinner
toward the apex. The
cavity equals in size that
of the left ventricle, and is
capable of containing
about 85 c.c.
5
Size of Heart
• The left ventricle is longer and
more conical in shape than the
right, and on transverse section
its concavity presents an oval or
nearly circular outline. It forms
a small part of the sternocostal
surface and a considerable part
of the diaphragmatic surface of
the heart; it also forms the apex
of the heart. Its walls are about
three times as thick as those of
the right ventricle.
6
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.
7
Thickness of Cardiac Walls
Myocardium of left ventricle is much thicker than the right.
8
Location of Heart
• posterior to sternum
• medial to lungs
• anterior to vertebral column
• base lies beneath 2nd rib
• apex at 5th intercostal space
• lies upon diaphragm
9
Coverings of Heart
10
Wall of the Heart
11
Wall of the Heart
12
Heart Chambers
Right Atrium
• receives blood from
• inferior vena cava
• superior vena cava
• coronary sinus
Right Ventricle
• receives blood from
right atrium
Left Atrium
• receives blood from
pulmonary veins
Left Ventricle
• receives blood from
left atrium
13
Chambers and Sulci
Anterior View
14
Chambers and Sulci
Posterior View
15
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
16
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 trunk17
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
18
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
19
Heart Valves
20
Coronal Sections of Heart
21
Heart Valves
Tricuspid Valve
Pulmonary and Aortic Valve
22
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
23
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
24
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
25
valve cusps, tightly closing the SL valves
Valve Function Review
Atria contract, blood fills
ventricles through A-V
valves
Ventricles contract, blood
pumped into aorta and
pulmonary trunk through
26
SL valves
Skeleton of Heart
• fibrous rings to which the heart valves are attached
27
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
28
Path of Blood
Through the Heart
29
Path of Blood
Through the Heart
30
Blood Supply to Heart
31
Blood Supply to Heart
32
Heart Actions
Atrial Systole/Ventricular Diastole
Atrial Diastole/Ventricular Systole
33
Cardiac Cycle
Atrial Systole/Ventricular Diastole
• blood flows passively into ventricles
• remaining 30% of blood pushed into ventricles
• A-V valves open/semilunar valves close
• ventricles relaxed
• ventricular pressure increases
34
Cardiac Cycle
Ventricular Systole/Atrial diastole
• A-V valves close
• chordae tendinae prevent cusps of valves from
bulging too far into atria
• atria relaxed
• blood flows into atria
• ventricular pressure increases and opens semilunar
valves
• blood flows into pulmonary trunk and aorta
35
Heart Sounds
Lubb
• first heart sound
• occurs during ventricular systole
• A-V valves closing
Dupp
• second heart sound
• occurs during ventricular diastole
• pulmonary and aortic semilunar valves closing
Murmur – abnormal heart sound
36
Heart Sounds
37
Cardiac Muscle Fibers
Cardiac muscle fibers form a functional
syncytium
• group of cells that function as a unit
• atrial syncytium
• ventricular syncytium
38
Cardiac Conduction System
39
Cardiac Conduction System
40
Muscle Fibers in
Ventricular Walls
41
Muscle Bundles of the Myocardium
• Cardiac muscle fibers swirl diagonally around the
heart in interlacing bundles
42
Electrocardiogram
• recording of electrical changes that occur in the myocardium
• used to assess heart’s ability to conduct impulses
P wave – atrial depolarization
QRS wave – ventricular depolarization
T wave – ventricular repolarization
43
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.
44
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
45
– ventricular repolarization
46
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)
47
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.
48
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.
49
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
50
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
51
Regulation of Cardiac Cycle
Autonomic nerve impulses alter the
activities of the S-A and A-V nodes
52
Regulation of Cardiac Cycle
Additional Factors that Influence HR
• physical exercise
• body temperature
• concentration of various ions
• potassium
• calcium
• parasympathetic impulses decrease heart action
• sympathetic impulses increase heart action
• cardiac center regulates autonomic impulses to the heart
53
CARDIAC OUTPUT
• 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.
54
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
55
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
56
Stroke Volume and Heart Rate
57
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.
58
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.
59
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.
60
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.
61
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
62
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
63
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 10190 mg/dl.
• Among the therapies used to reduce blood
cholesterol level are exercise, diet, and drugs.
64
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
65
Blood Vessels
• arteries
• carry blood away from ventricles of heart
• arterioles
• receive blood from arteries
• carry blood to capillaries
• capillaries
• sites of exchange of substances between
blood and body cells
• venules
• receive blood from capillaries
• veins
• carry blood toward ventricle of heart
66
Arteries and Arterioles
Artery
• thick strong wall
• endothelial lining
• middle layer of smooth
muscle and elastic tissue
• outer layer of
connective tissue
• carries blood under
relatively high pressure
Arterioles
• thinner wall than
artery
• endothelial lining
• some smooth muscle
tissue
• small amount of
connective tissue
• helps control blood
flow into a capillary
67
Walls of Artery and Vein
68
Arteriole
• smallest arterioles only have a few smooth muscle fibers
• capillaries lack muscle fibers
69
Capillaries
• smallest diameter blood vessels
• extensions of inner lining of arterioles
• walls are endothelium only
• semipermeable
• sinusoids – leaky capillaries
70
Regulation of Capillary
Blood Flow
Precapillary
sphincters
• may close a
capillary
• respond to
needs of the cells
• low oxygen and
nutrients cause
sphincter to
relax
71
Exchange in the Capillaries
• water and other substances leave capillaries because of net outward pressure
at the capillaries’ arteriolar ends
• water enters capillaries’ venular ends because of a net inward pressure
•substances move in and out along the length of the capillaries according to
their respective concentration gradients
72
Venules and Veins
Venule
• thinner wall than arteriole
• less smooth muscle and elastic tissue than arteriole
Vein
• thinner wall than artery
• three layers to wall but middle layer is poorly developed
• some have flaplike valves
• carries blood under relatively low pressure
• serves as blood reservoir
73
Venous Valves
74
Characteristics of Blood Vessels
75
Blood Volumes in Vessels
76
Arterial Blood Pressure
Blood Pressure – force the blood exerts against the
inner walls of the blood vessels
Arterial Blood Pressure
• rises when ventricles contract
• falls when ventricles relax
• systolic pressure – maximum pressure
• diastolic pressure – minimum pressure
77
Pulse
• alternate expanding and recoiling of the arterial wall
that can be felt
78
Factors That Influence
Arterial Blood Pressure
79
Regulation of Cardiac Cycle
Autonomic nerve impulses alter the
activities of the S-A and A-V nodes
80
Control of Blood Pressure
If blood pressure rises, baroreceptors initiate the
cardioinhibitory reflex, which lowers the blood pressure
81
Control of Blood Pressure
Dilating arterioles helps regulate blood pressure
82
Venous Blood Flow
• not a direct result of heart
action
• dependent on
• skeletal muscle
contraction
• breathing
• venoconstriction
83
Central Venous Pressure
• pressure in the right atrium
• factors that influence it alter flow of blood into
the right atrium
• affects pressure within the peripheral veins
• weakly beating heart increases central venous
pressure
• increase in central venous pressure causes blood
to back up into peripheral vein
84
Pulmonary Circuit
• consists of vessels that carry blood from the heart to the lungs
and back to the heart
85
Blood Flow Through Alveoli
• cells of alveolar wall are tightly joined together
• the high osmotic pressure of the interstitial fluid draws
water out of them
86
Systemic Circuit
• composed of vessels that lead from the heart to
all body parts (except the lungs) and back to the
heart
• includes the aorta and its branches
• includes the system of veins that return blood to
the right atrium
87
Life-Span Changes
• cholesterol deposition in blood vessels
• heart enlargement
• death of cardiac muscle cells
• increase in fibrous connective tissue of the heart
• increase in adipose tissue of the heart
• increase in blood pressure
• decrease in resting heart rate
88
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
89
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.
90
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).
91
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
92
By-pass Graft
93
Percutaneous
Transluminal
Coronary
Angioplasty
Stent
94
• Update on Digoxin Therapy in Congestive Heart
Failure
• SHOWKAT A. HAJI, M.D., and ASSAD MOVAHED,
M.D.
– East Carolina University School of Medicine,
Greenville, North Carolina
95
Digoxin and Other Medications
for Congestive Heart Failure
• ACE inhibitors, beta blockers and
spironolactone have been shown to improve
survival in patients with heart failure.
• Consequently, the role of digoxin in the
treatment of heart failure remains secondary
96
TABLE 4
Digoxin (Lanoxin) Therapy in
Congestive Heart Failure
1. Digoxin has been shown to improve morbidity
without any benefit on mortality.
2. Digoxin may act by decreasing sympathetic
activity.
3. Digoxin may not be effective in patients who
have normal left ventricular systolic function.
4. The benefits of digoxin therapy are greatest in
patients with severe heart failure, an enlarged
heart and a third heart sound gallop.
97
TABLE 4
Digoxin (Lanoxin) Therapy in
Congestive Heart Failure
5. Digoxin may be used in patients with mild to
moderate heart failure if they do not respond
to an angiotensin-converting enzyme inhibitor
or a beta blocker.
6. Low dosages of digoxin can be effective.
7. Renal function and possible drug interactions
must be considered in deciding on an
appropriate dosage of digoxin.
8. In general, digoxin therapy should be avoided
in the acute phase after myocardial infarction
98
Digoxin and Other Medications
for Congestive Heart Failure
• In the absence of a survival benefit, the goal of digoxin
therapy is to improve quality of life by reducing symptoms
and preventing hospitalizations
• Digoxin should be used routinely, in conjunction with
diuretics, ACE
inhibitors,
beta
blockers
and
spironolactone,
• In all patients with severe congestive heart failure and
reduced systolic function.
• It also should be added to the therapy of patients with mild
to moderate congestive heart failure if they have not
responded adequately to an ACE inhibitor or a beta
blocker.
99