SSM Heart - Aina Aqilah

MM 10208 STRUCTURE, FUNCTION & METABOLISM OF HUMAN BODY I
Special Study Module
HEART
NAME :
MATRIC NUMBER :
LECTURER’S NAME :
Aina Aqilah Binti Ahmad Zaki
BM21110064
Prof Dr. Zainal Arifin Bin Mustapha

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1.0 AUTOBIOGRAPHY
My name is Aina aqilah Binti Ahmad Zaki. I was born on 3rd July 2002 at Hospital Kota Tinggi
and grew up at Johor Bahru, Johor. I am the second child among my five siblings. My father
works as a banker and my mother works as a primary school teacher. I received my secondary
school education at MRSM Johor Bahru and further my studies in foundation in science at UITM
Dengkil. Being a doctor was a childhood dream of mine and successfully entering the medical
program is like a step closer to my dream.
I would say I have been a very decisive person since a young age, I always know what I want
regardless of other people's opinions. I choose to be a doctor at the age of 5, always asking my
parents for doctors’ related toys. As I grew up, my ambition to be a doctor stayed the same but
I have upgraded by picking my choice of specialization in anesthesia at 12. I have early
exposure to the hospital settings as my father was a diabetic patient and had to go for
appointments regularly. So, I have always been awed by the healthcare workers in the hospital
and respected them as their main goal was to help the patient and alleviate their pain. I know
early on, I would follow their footsteps and face the obstacles along the way.
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You might be wondering why a doctor? Any healthcare professional helps the patient
and
works in a hospital too. Well, in my family circle, there is not a single doctor. However, 70% of
my family members and relatives had diabetes and I might be at risk of getting it as well.
Thus, I felt responsible to choose medicine as a career so that I could provide medical advice to
instill awareness and reduce the number of diabetic patients among my family members. Why
anesthesia? Well, first of all my father always jokes that anesthesiologists only put people to
sleep but through a bit of my research, I learned that anesthesiologists do a whole lot more and
contribute to the patient's well-being pre-operation, during operation and postoperative. I want
to learn more about it thus choosing it as my future career.
I chose heart as my study subject because my grandfather died due to cardiac arrest. He was
just getting discharged after being hospitalized due to his diabetes. But, suddenly he was in
cardiac arrest. I am very sad because I could not do anything, thus I wanted to learn more
about the heart and find the answers to my unsolved questions. Therefore, I am very grateful
to be admitted into UMS Bachelor of Medicine and will strive further in my pathway to be a safe
and good doctor.
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TABLE OF CONTENTS
CONTENT
page
1.0 AUTOBIOGRAPHY 2-3
2.0 INTRODUCTION 5-6
3.0 ACKNOWLEDGEMENT 7
4.0 GENERAL INTRODUCTION TO THE HEART
4.1 HISTOLOGY OF HEART
- Conducting system of the heart
5.0 ANATOMY OF HEART
8
9-12
13-17
- Heart Chambers
- Development of the heart
6.0 PHYSIOLOGY OF HEART
19-23
- Cardiac Cycle and its correlations with ECG
- Stroke Volume
- Cardiac Output
7.0 HEART COMPLICATIONS
- Coronary artery disease (CAD)
- Symptoms
- Risk factors
- Diagnosis
8.0 TREATMENT
23-30
31-34
- Coronary Bypass Graft
- Coronary Angioplasty
- Artificial Cardiac Pacemaker
- Drugs
9.0 CONCLUSION 35
10.0 REFERENCES 36
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2.0 INTRODUCTION
The heart is a muscular organ about the size of a fist, located just behind and slightly left of the
breastbone. The heart pumps blood through the network of arteries and veins called the
cardiovascular system. The heart has four chambers, the right atrium receives blood from the
veins and pumps it to the right ventricle. The right ventricle receives blood from the right atrium
and pumps it to the lungs, where it is loaded with oxygen. The left atrium receives oxygenated
blood from the lungs and pumps it to the left ventricle. The left ventricle (the strongest
chamber) pumps oxygen-rich blood to the rest of the body. The left ventricle’s vigorous
contractions create our blood pressure. The coronary arteries run along the surface of the heart
and provide oxygen-rich blood to the heart muscle. A web of nerve tissue also runs through the
heart, conducting the complex signals that govern contraction and relaxation. Surrounding the
heart is a sac called the pericardium.
According to the Department of Statistics Malaysia dated 2020, heart disease is the leading
cause of death in Malaysia. Ischaemic heart diseases remained as the principal causes of death,
15.0 per cent of the 109,164 medically certified deaths in 2019 and the condition affects all
genders as well as all racial and ethnic groups. Heart disease refers to any condition affecting
the heart. There are many types, some of which are preventable. Examples of heart disease are
myocardial infarction (heart attack), coronary artery disease, endocarditis, cardiomyopathy and
cardiac arrest. The common heart disease symptoms include chest pain, shortness of breath
and fainting.
Cardiology is a branch of medicine that deals with the disorders of the heart as well as some
parts of the circulatory system. The field includes medical diagnosis and treatment of congenital
heart defects, coronary artery disease, heart failure, valvular heart disease and
electrophysiology. Meanwhile, a cardiothoracic surgeon is a medical doctor who specializes in
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surgical procedures of the heart, lungs, esophagus, and other organs in the chest.
Cardiothoracic anesthesiology is a subspeciality of the medical practice of anesthesiology,
devoted to the preoperative, intraoperative, and postoperative care of adult and pediatric
patients undergoing cardiothoracic surgery and related invasive procedures. Example figures
famously known as experienced cardiothoracic anesthesiology are Dr. William New and Dr.
Leander Lee. These figures had contributed greatly to the field of sciences especially in
medicine, Dr. William had invented the current modern pulse oximeter thus helping the current
healthcare professionals in treating patients better.
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3.0 ACKNOWLEDGEMENT
The success and final outcome of this special study module (SSM) required countless hours of
researching and reading on the knowledge of the heart. I would like to express my heartfelt
gratitude to Prof. Dr. Zainal Arifin who gave me his guidance and the opportunity to explore and
understand the anatomy and physiology of the heart.
Special thanks to the immense resources that are easily accessible throughout the research
given by our faculty of medicine and health sciences. It gives us plenty of time and space to
skim through all the heart related books and gather more new information.
Last but not least, I would also like to thank all of my friends for their continuous support and
the direct or indirect help given throughout the research process.
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4.0 GENERAL INTRODUCTION TO THE HEART
The heart is located in the mediastinum, about two-thirds of its mass is to the left of the
midline. It is shaped like a cone lying on its side. Its apex is the pointed, inferior part; its base is
the broad, superior part.
The pericardium is a membrane that surrounds and protects the heart. It is made up of two
layers: an outside fibrous layer and an inner serous pericardium with a parietal and visceral
layer. The pericardial cavity is a possible area between the parietal and visceral layers of the
serous pericardium, filled with a few millilitres of lubricating pericardial fluid that decreases
friction between the two membranes. Epicardium, myocardium, and endocardium are the three
layers that make up the heart's wall. The epicardium is made up of mesothelium and connective
tissue, whereas the myocardium is made up of cardiac muscle tissue, and the endocardium is
made up of blood vessels. Endothelium and connective tissue make up the endothelium.
Two upper chambers, the right and left atria, and two inferior chambers, the right and left
ventricles, make up the heart chambers. The auricles, the coronary sulcus between the atria
and ventricles,the anterior and posterior sulci between the ventricles on the anterior side, and
the anterior and posterior sulci between the ventricles on the posterior side and the heart's
anterior and posterior surfaces, respectively are all external elements of the heart.
The right atrium receives blood from the superior vena cava, inferior vena cava, and coronary
sinus. It is separated internally from the left atrium by the interatrial septum, which contains the
fossa ovalis. Blood exits the right atrium through the tricuspid valve. The right ventricle receives
blood from the right atrium. The left ventricle is separated internally by the interventricular
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septum, it pumps blood through the pulmonary valve into the pulmonary trunk. From the
pulmonary veins, oxygenated blood enters the left atrium and leaves through the bicuspid
(mitral) valve. The left ventricle pumps oxygenated blood into the aorta through the aortic
valve. The thickness of the myocardium in each of the four chambers varies depending on the
function of the chamber. The left ventricle has the thickest wall since it has the most work.
The heart's fibrous skeleton is a dense connective tissue that surrounds and supports the heart
valves.
4.1 HISTOLOGY OF HEART
Cardiac muscle in the four chambers of the heart wall contracts rhythmically, pumping the
blood through the circulatory system. As stated before, the walls of all four heart chambers
consist of three major layers: the internal endocardium, the middle myocardium and the
external epicardium.
A thin inner layer of endothelium and supporting connective tissue, a middle myoelastic layer
of smooth muscle fibres and connective tissue, and a deep layer of connective tissue called the
subendocardial layer that merges with the myocardium make up the endocardium. The
subendocardial layer also contains branches of the heart's impulse-conducting system, which
are made up of modified cardiac muscle fibres.
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The myocardium, the thickest layer, is primarily made up of cardiac muscle fibres that spiral
around each heart chamber. Because blood must be pumped through the systemic and
pulmonary circulations with great force, the myocardium in the ventricles, particularly the left, is
significantly thicker than in the atrial walls.
The epicardium is a basic squamous mesothelium with blood vessels and nerves that is
supported by a layer of loose connective tissue.
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The visceral layer of the pericardium, the membrane that surrounds the heart, is known as the
epicardium. The epicardium is reflected back as the parietal layer lining the pericardium where
the large vessels enter and exit the heart. During heartbeats, adipose tissue deposits in the
epicardium cushion underlying structures, while lubricating fluid produced by both layers of
serous mesothelial cells prevents friction inside the pericardium. Other structures vital to the
heart's overall function of transporting blood are found within these primary layers. The cardiac
skeleton's dense fibrous connective tissue is found in the interventricular and interatrial septa,
surrounds all heart valves, and extends into the valve cusps and chordae tendineae to which
they are linked. Other functions performed by these thick irregular connective tissue regions are
anchoring and supporting the heart valves, providing strong insertion sites for cardiac muscle
and providing electrical insulation between the atria and ventricles, which aids in the
coordination of the heartbeat.
Conducting system of the heart
Between the subendocardial layer and adjacent myocardium, the impulse conducting system
of the heart made by cardiac muscle tissue that generates and propagates depolarization waves
spreads throughout the myocardium to stimulate contractions. It consists of two nodes in the
right atrium: the sinoatrial (SA) node or pacemaker and also atrioventricular (AV) node followed
by the AV bundle or His and the subendocardial conducting network. SA node is located in the
right atrial wall near the superior vena cava and has small size, fewer myofibrils and intercalated
disks compared to other muscle fibers. The impulse received by the cell will travel along the
myocardial fibers of both atria and stimulate contraction. As it reaches the AV node, it
stimulates the depolarization of the cell thus forming the AV bundle which passes through the
opening in the cardiac skeleton and into the interventricular septum and bifurcate into the wall
of each ventricle.
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At the apex of the heart, the AV bundle branches off into a network of myofibers called
Purkinje fibers. They trigger contraction waves through both ventricles simultaneously.
Parasympathetic and sympathetic neural components innervate the heart. For example,
stimulation in parasympathetic division (vagus nerve) will slow our heartbeat whereas
stimulation in sympathetic nerves accelerates the activity of pacemakers. Angina pectoris is a
condition where partially occluded coronary arteries cause oxygen deprivation and make us feel
discomfort.
Other than that, compared to skeletal muscle fibers, cardiac muscle fibers are shorter and
less circular in the transverse section. It also exhibits branching thus giving each cardiac muscle
fiber a “ stair-step” appearance. A typical cardiac muscle fiber is 50–100 μm long with a
diameter of about 14 μm. They usually present with one centrally located nucleus but some
have two nuclei. Cardiac muscle fibers are connected by intercalated discs, an irregular
transverse thickening of the sarcolemma. It contains desmosomes, which holds the fibers
together and gap junction which allows muscle action potentials to conduct between its fibers
and allow the entire myocardium of atria or ventricles to contract as a single unit.
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5.0 ANATOMY OF HEART
The heart is irregularly conical in shape, and is placed obliquely in the middle of the
mediastinum. The right border is formed entirely by the right atrium, the left border partly by
the auricular appendage of the left atrium but mainly by the left ventricle, and the inferior
border chiefly by the right ventricle but also by the lower part of the right atrium and the apex
of the left ventricle. The bulk of the anterior surface is formed by the right ventricle, which is
separated from the right atrium by the vertical atrioventricular groove, and from the left
ventricle by the anterior interventricular groove. The inferior
surface consists of the right and
left ventricles separated by the posterior interventricular groove and the portion of the right
atrium that receives the inferior vena cava. The base, or posterior surface, is quadrilateral in
shape and is formed mainly by the left atrium with the openings of the pulmonary veins and, to
a lesser extent, by the right atrium.
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Heart Chambers
The right atrium receives the superior vena cava in its upper and posterior part, the inferior
vena cava and coronary sinus in its lower part, and the anterior cardiac vein (draining much of
the front of the heart) anteriorly. Running more or less vertically downwards between the venae
cavae is a distinct ridge, the crista terminalis (indicated on the outer surface of the atrium by a
shallow groove the sulcus terminalis). This ridge separates the smooth walled posterior part of
the atrium, derived from the sinus venosus, from the rough-walled anterior portion, which is
prolonged into the auricular appendage and which is derived from the fetal atrium. The
openings of the inferior vena cava and the coronary sinus are guarded by rudimentary valves;
that of the inferior vena cava being continuous with the annulus ovalis around the shallow
depression on the atrial septum, the fossa ovalis, which marks the site of the fetal foramen
ovale.
The pulmonary valve admits three fingers and bears three flaplike cusps (medial, anterior and
inferior) These are attached by their base to the fibrous ring of the tricuspid orifice. A muscular
ridge, the infundibular ventricular crest, lies between the atrioventricular and pulmonary orifices
and divides the 'inflow' and 'outflow' tracts of the ventricle. The moderator band is a muscular
bundle crossing the ventricular cavity from the interventricular septum to the anterior wall.
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The left ventricle is the part of the heart that communicates with the left atrium by way of the
mitral valve, which is large enough to admit two fingers. It possesses a large anterior and
smaller posterior cusp attached to papillary muscles by chordae tendineae. With the exception
of the fibrous vestibule immediately below the aortic orifice, the wall of the left ventricularle is
marked by thick trabeculae carneae. The mouths of the right and left coronary arteries are seen
in the anterior and left posterior sinus, respectively.
The anaesthetist's view of the chambers of the heart is increasingly important as part of the
treatment for a range of conditions, such as coronary artery bypass grafting and heart surgery.
The increasing use of transoesophageal echocardiography (TECAD) has led to an increase in the
number of successful cardiac procedures being carried out.
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Development of the heart
The heart begins its development from a group of mesodermal cells called the cardiogenic
area during the third week after fertilization.
During day 19 and 20, the sinus venosus develops into part of the right atrium (posterior
wall), coronary sinus, and sinoatrial (SA) node. Then at day 21, the primitive atrium develops
into part of the right atrium (anterior wall), right auricle, part of the left atrium (anterior wall),
and the left auricle. On day 22, the primitive ventricle gives rise to the left ventricle. Day 23 and
24, the bulbus cordis develops into the right ventricle. Finally on day 28, the truncus arteriosus
gives rise to the ascending aorta and pulmonary trunk.
The primitive heart starts to contract on day 23, as the primitive heart tube elongates.
Because the bulbus cordis and primitive ventricle grow more rapidly than other parts of the tube
and because the atrial and venous ends of the tube are confined by the pericardium, the tube
begins to loop and fold. At first, the primitive heart tube assumes a U-shape; later it becomes
S-shaped. As a result of these movements, which are completed by day 28, the primitive atria
and ventricles of the future heart are reoriented to assume their final adult positions. The
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remainder of heart development consists of remodeling of the chambers and the formation of
septa and valves to form a four-chambered heart.
On about day 28, thickenings of mesoderm of the inner
lining of the heart wall, called endocardial cushions,
appear. They grow toward each other, fuse, and divide the
single atrioventricular canal (region between atria and
ventricles) into smaller, separate left and right
atrioventricular canals. Also, the interatrial septum begins
its growth toward the fused endocardial cushions.
Ultimately, the interatrial septum and endocardial cushions
unite and an opening in the septum, the foramen ovale,
develops. The interatrial septum divides the atrial region into a right atrium and a left atrium.
Before birth, the foramen ovale allows most blood entering the right atrium to pass into the left
atrium. After birth, it normally closes so that the interatrial septum is a complete partition. The
remnant of the foramen ovale is the fossa ovalis. Formation of the interventricular septum
partitions the ventricular region into a right ventricle and
a left ventricle. Partitioning of the atrioventricular canal,
atrial region, and ventricular region is basically complete
by the end of the fifth week. The atrioventricular valves
form between the fifth and eighth weeks. The semilunar
valves form between the fifth and ninth weeks.
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6.0 PHYSIOLOGY OF HEART
Cardiac Cycle and its correlations with ECG
The cardiac cycle refers to the complete sequence of events that occur in the heart, from the
beginning of one heart beat to the beginning of the next. The cardiac cycle consists of two
phases:
The diastolic phase, during which the ventricles fill with blood. Diastole consists of four stages:
– isovolumetric relaxation
– rapid ventricular filling
– slow ventricular filling
– atrial contraction.
The systolic phase, during which the ventricles contract and eject blood into the aorta and
pulmonary artery. Systole consists of two stages:
– isovolumetric contraction
– ejection.
Traditionally, the cardiac cycle is described from late diastole, when the atria and ventricles are
relaxed and the AV valves are open:
●
Slow ventricular filling.
The pressure within the atria is slightly higher than intraventricular pressure. The AV valves are
therefore open, allowing blood to flow slowly from atrium to ventricle.
●
Atrial contraction.
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– The pacemaker cells of the SA node spontaneously depolarize, generating an action potential.
The resulting electrical impulse is rapidly conducted throughout the atria, triggering atrial
contraction.
– When diastole is shortened during exercise, atrial contraction contributes up to 40% of
ventricular filling. At rest, the atrial 'kick' accounts for only 10% - 90% of the blood that flows
passively into the ventricle. As a result, during activity, much of the leftover atrial blood is
ejected back into the body through the AV valves.
– The pressure generated during atrial contraction is transmitted along the venae cavae and
pulmonary veins as they have no valves: atrial contraction is represented by a wave on the
atrial pressure waveform.
– The volume of blood within the ventricle at the end of atrial contraction is the end-diastolic
volume (EDV).
●
Isovolumetric contraction.
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The action potential continues through the AV node and is conducted throughout the ventricles
by the His–Purkinje system, represented on the ECG by the QRS complex. Initially, ventricular
contraction causes a rapid rise in intraventricular pressure:
– Once intraventricular pressure exceeds atrial pressure, the AV valves close, resulting in the
first heart sound, S 1 . The mitral valve normally closes slightly earlier than the tricuspid valve,
resulting in a ‘split’ S 1 .
– There is a period of time between the closure of the AV valves and the opening of the aortic
and pulmonary valves (semilunar valves) during which ventricular pressure rises without a
change in ventricular volume – this is isovolumetric contraction.
– The increased right ventricular pressure causes the tricuspid valve to bulge into the right
atrium during isovolumetric contraction - this corresponds to the c wave on the atrial pressure
waveform - and the mitral valve of the left ventricular valve to bulge into the left atrium.
●
Ejection.
Once ventricular pressure exceeds the pressure in the aorta and pulmonary artery, the
semilunar valves open and blood is ejected from the ventricles.
– The x descent on the atrial pressure waveform is caused by the right atrium's pressure falling
to zero as its length increases, and it is rapidly filling with blood. Right ventricular contraction
pulls the tricuspid valve downward, pushing the inner working area of the heart upward.
– Initially, the flow of blood through the semilunar valves is rapid; but as the ventricular
myocytes start to repolarize, the force of contraction wanes.
– As time passes, the ventricular pressure falls below that of the aorta and pulmonary artery,
causing the semilunar valves to close and producing the second heart sound, S 2 . The aortic
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valve typically closes slightly before the pulmonary valve. Inspiration, particularly in young
people, can amplify this difference, resulting in a 'physiological split S 2 '.
– Aortic valve closure is represented on the aortic pressure curve by the dicrotic notch, a
positive deflection caused by the elastic recoil of the aortic valve and the aorta.
– The volume of blood within the ventricle following valve closure is the end-systolic volume
(ESV).
●
Isovolumetric relaxation.
During late systole and isovolumetric relaxation, the ventricular ventricles close and their
pressure falls below that of the atria, or heart. The v wave of the atrial pressure waveform
corresponds to the gradual rise in atrial pressure caused by venous return from the lungs and
venae cavae.
●
Rapid ventricular filling.
During the early stages of cardiac surgery, diastole is a rapid increase in blood flow from the
atria to the ventricles, which are the inner chambers of the heart. The AV valves open when
atrial pressure exceeds ventricular pressure, allowing blood to flow into and out of the two
organ chambers. The descent of the atrial pressure waveform represents the fall in
intraventricular pressure.
Ventricular filling is normally silent, but an increased volume of atrial blood (for example, in
mitral regurgitation) flowing into a poorly compliant LV (as occurs after a myocardial infarction
or in dilated cardiomyopathy) causes ventricular wall reverberation and a third heart sound, S 3 .
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Stroke Volume (SV)
SV is the volume of blood ejected from the LV per heart beat. The volume of blood in the LV
prior to contraction is the left ventricular end-diastolic volume (LVEDV), and the volume of blood
remaining in the LV after contraction is the left ventricular end-systolic volume (LVESV). Thus:
SV = LVEDV - LVESV
Typical values for a 70 kg man are:
●
●
LVEDV of 120 mL.
LVESV of 50 mL.
So, SV = 70 mL
The ‘normal range’ for SV is 55–100 mL, though this depends on the size of the patient.
Cardiac output (CO)
The CO is the volume of blood ejected by the left or right ventricle per minute. It depends on
two factors: Heart rate (HR) and stroke volume (SV).
CO = SV × HR
At rest, the typical SV is 70 mL, and HR is 75 bpm.
Typical resting CO is therefore 70×75 = 5.25 L/min, but CO may increase fivefold during
maximal exercise.
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7.0 HEART COMPLICATIONS
Coronary artery disease (CAD)
Coronary artery disease (CAD) is one of the leading causes of death. It has many causes, all of
which result in a reduced blood supply to the vital myocardial tissue.
Myocardial infarction
With sudden occlusion of a major artery by an embolus (plug), the region of myocardium
supplied by the occluded vessel becomes infarcted (rendered virtually bloodless) and undergoes
necrosis (pathological tissue death). The three most common sites of coronary artery occlusion
are:
●
●
●
Anterior IV (LAD) branch of the LCA
RCA
Circumflex branch of the LCA
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Coronary artery insufficiency caused by atherosclerosis is the most common cause of ischemic
heart disease. A myocardial infarction (MI) is a necrotic area of the myocardium. MI refers to an
area of the heart that has become infected, damaged, or partially collapsed as a result of stress
or infection.
Coronary atherosclerosis
The atherosclerotic process, characterized by lipid deposits in the intima (lining layer) of the
coronary arteries, begins during early adulthood and slowly results in stenosis of the lumina of
the arteries.
Insufficiency of blood supply to the heart (myocardial ischemia) may result in MI. As coronary
atherosclerosis progresses, the collateral channels connecting one coronary artery with the
other expand. Despite this compensatory mechanism, the myocardium may not receive enough
oxygen when the heart needs to perform increased amounts of work.
Also, when arteries become clogged, fatty material, cholesterol, cellular waste, and other
substances can accumulate in the endothelial cell lining of the artery, resulting in plaque
formation and blockages that deprive the heart of oxygen and cause a heart attack.
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Symptoms
When your coronary arteries narrow, they can't deliver enough oxygen-rich blood to your heart,
especially when it's working hard, as it does during exercise. Initially, the reduced blood flow
may not cause any symptoms. However, as plaque accumulates in your coronary arteries, you
may experience the following coronary artery disease signs and symptoms:
●
Chest pain (angina).
You may feel pressure or tightness in your chest, as if someone were standing on your chest.
This pain, called angina, is generally triggered by physical or emotional stress. Angina usually
goes away within minutes after stopping the stressful activity. In some people, especially
women, the pain may be brief or sharp and felt in the neck, arm or back.
●
Shortness of breath.
If your heart is unable to pump enough blood to meet your body's demands, you may
experience shortness of breath or extreme fatigue during physical activity.
●
Heart attack.
A completely blocked coronary artery will cause a heart attack. The classic signs and symptoms
of a heart attack include crushing pressure in your chest and pain in your shoulder or arm,
sometimes with shortness of breath and sweating. Women are somewhat more likely than men
to have less typical signs - such as neck or jaw pain - and may also have other symptoms such
as fatigue and nausea.
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Risk factors
●
Age.
Getting older increases your risk of damaged and narrowed arteries.
●
Sex.
Men are generally at greater risk of coronary artery disease. However, the risk for women
increases after menopause.
●
Family history.
A family history of heart disease can put you at an increased risk of developing coronary artery
disease. Your risk is highest if your father or a brother or sister was diagnosed with heart
disease before age 55 or if your mother or a sister developed it before age 65.
●
Smoking.
People who smoke are at a significantly higher risk of developing heart disease. Being a passive
smoker also raises a person's risk of coronary artery disease.
●
High blood pressure.
Uncontrolled high blood pressure can result in hardening and thickening of your arteries,
narrowing the channel through which blood can flow.
●
High blood cholesterol levels.
High cholesterol can be caused by a high level of low-density lipoprotein (LDL) cholesterol,
known as the "bad" cholesterol. It can also contribute to the development of atherosclerosis.
High levels of HDL cholesterol are better than low levels of LDL cholesterol.
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●
Diabetes.
Diabetes is associated with an increased risk of coronary artery disease. Type 2 diabetes and
coronary artery disease share similar risk factors, such as obesity and high blood pressure.
●
Overweight or obesity.
Excess weight typically worsens other risk factors.
●
Physical inactivity.
Lack of exercise also is associated with coronary artery disease and some of its risk factors, as
well.
●
High stress.
Unrelieved stress in your life may damage your arteries as well as worsen other risk factors for
coronary artery disease.
●
Unhealthy diet.
Eating too much food that has high amounts of saturated fat, trans fat, salt and sugar can
increase your risk of coronary artery disease.
Obesity can lead to type 2 diabetes and high blood pressure; high triglycerides can cause high
cholesterol; excess body fat around the waist can put you at risk for coronary artery disease.
When grouped together, certain risk factors make you even more likely to develop heart
disease. Metabolic syndrome is a cluster of conditions that includes high blood pressures, low
HDL cholesterol and extra body fat.
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Sometimes CAD develops without any classic risk factors. Researchers are studying other
possible risk factors, such as:
●
Sleep apnea.
This disorder causes you to stop and start breathing repeatedly while sleeping. Sudden drops in
blood oxygen levels caused by sleep apnea raise blood pressure and put strain on the
cardiovascular system, potentially leading to coronary artery disease.
●
High-sensitivity C-reactive protein (hs-CRP).
This protein appears in higher-than-normal levels when there's inflammation somewhere in your
body. High hs-CRP levels may be a risk factor for heart disease, especially if you have narrow
coronary arteries.
●
High triglycerides.
This is a type of fat (lipid) found in your bloodstream. High levels have been linked to an
increased risk of coronary artery disease, particularly in women.
●
Homocysteine.
Homocysteine is an amino acid your body uses to make protein and to build and maintain
tissue. But high levels of homocysteine may increase your risk of coronary artery disease.
●
Preeclampsia.
This condition that can develop in women during pregnancy causes high blood pressure and a
higher amount of protein in urine. It can lead to a higher risk of heart disease later in life.
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●
Alcohol use.
Heavy alcohol use can lead to heart muscle damage. It can also worsen other risk factors of
coronary artery disease.
●
Autoimmune diseases.
People who have conditions such as rheumatoid arthritis and lupus (and other inflammatory
conditions) have an increased risk of atherosclerosis.
Diagnosis
The doctor will inquire about your medical history, perform a physical examination, and
order routine blood tests. He or she may also recommend one or more diagnostic tests,
such as:
●
Electrocardiogram (ECG). An electrocardiogram records electrical signals
as they travel through your heart. An ECG can often reveal evidence of a
previous heart attack or one that's in progress.
●
Echocardiogram. An echocardiogram is a vital test to ensure that all parts
of the heart wall are contributing normally to your heart's pumping activity.
Parts that move weakly may have been damaged during a heart attack or
are receiving too little oxygen. This could be a sign of coronary artery
disease or other conditions.
●
Exercise stress test. If your signs and symptoms occur most often during
exercise, you may need to walk on a treadmill or ride a stationary bike
during an ECG. Sometimes, an echocardiogram is also done while you do
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these exercises - this is called a stress echo. In some cases, medication to
stimulate your heart may be used instead of exercise.
●
Nuclear stress test. Similar to the exercise stress test. The ECG is an
electrocardiogram, which measures blood flow to your heart muscle at rest
and during stress. In this test, a tracer is injected into your bloodstream, and
special cameras detect areas in your heart that receive less blood flow.
●
Cardiac catheterization and angiogram. During cardiac catheterization, a
doctor inserts a catheter into an artery or vein in your groin, neck or arm and
up to your heart. X-rays are used to guide the catheter to the correct
position; dye is injected to help show blood vessels clearly. If you have a
blockage that requires treatment, a balloon can be inflated to improve the
blood flow in your coronary arteries.
●
Cardiac CT scan. A CT scan of the heart can help your doctor see calcium
deposits in your arteries that can narrow the arteries. If a substantial amount
of calcium is discovered, coronary artery disease may be likely. A CT
coronary angiogram, in which you receive a contrast dye that is given by IV
during a CT scan, can produce detailed images of your heart arteries..
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8.0 TREATMENT
Coronary Bypass Graft
Patients with obstruction of their coronary circulation and severe angina may undergo a
coronary bypass graft operation. A segment of an artery or vein is connected to the ascending
aorta or to the proximal part of a coronary artery and then to the coronary artery distal to
the stenosis.
The great saphenous vein is commonly harvested for coronary bypass surgery because it,
●
●
●
Has a diameter equal to or greater than that of the coronary arteries,
can be easily dissected from the lower limb,
offers relatively lengthy portions with a minimum occurrence of valves or branching.
If a valved segment must be used, reversing the implanted vein segment can negate the effect
of the valve. The use of the radial artery in bypass surgery is becoming more common. To
increase flow distal to the obstruction, a coronary bypass graft shunts blood from the aorta to a
stenotic coronary artery. Simply put, it creates a path around the stenotic area (arterial
stenosis) or blockage (arterial atresia). The myocardium can also be revascularized surgically by
anastomosing an internal thoracic artery with a coronary artery.
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Coronary Angioplasty
Surgery involves passing a catheter with an inflatable
balloon attached to its tip into the obstructed coronary
artery. When the catheter reaches the obstruction, the
balloon is inflated, flattening the atherosclerotic plaque
against the vessel's wall. The vessel is stretched to
increase the size of the lumen, thus improving blood flow.
After dilation of the vessel, an intravascular stent may be
introduced to maintain the dilation.
The stents are made
up of rigid or semi rigid tubular meshes which will collapse
when introduced and once in place, it expands or expands
with the balloon catheter to maintain luminal patency.
Intraluminal instruments with rotating blades and lasers have also been employed. Other cases
involved injection of thrombokinase to dissolve blood clot.
Artificial Cardiac Pacemaker
An artificial cardiac pacemaker (about the size of a pocket watch) is inserted subcutaneously in
some people who have a heart block. A pacemaker is made up of three parts: a pulse generator
or battery pack, a wire (lead), and an electrode. Pacemakers generate electrical impulses that
cause ventricular contractions to occur at a predetermined rate. An electrode with a catheter
attached is inserted into a vein, and its progression through the venous pathway is monitored
with a fluoroscope, a device that uses radio graphs to examine deep structures in real time (as
motion occurs). The electrode terminal is routed through the SVC to the right atrium and then
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through the tricuspid valve into the right ventricle. The electrode is securely attached to the
trabeculae carneae in the ventricular wall and is in contact with the endocardium.
Other than that, various drugs can be used to treat coronary artery disease, including:
●
Cholesterol-modifying medications.
These medications reduce (or modify) the primary material that deposits on the coronary
arteries. As a result, cholesterol levels — especially low-density lipoprotein (LDL, or the "bad"
cholesterol — decrease. Your doctor can choose from a range of medications, including statins
and other medications.
●
Aspirin.
Aspirin is a drug that can reduce the tendency of your blood to clot, which may help prevent
obstruction of your coronary arteries. But aspirin can be dangerous if you have a bleeding
disorder or if you're already taking another blood thinner, so ask your doctor before taking it.
●
Beta blockers.
These drugs slow your heart rate and decrease your blood pressure, which decreases your
heart's demand for oxygen. If you've had a heart attack, beta blockers reduce the risk of future
attacks.
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●
Calcium channel blockers.
These drugs may be used with beta blockers if beta blockers alone aren't effective or instead of
beta blockers if you're not able to take them. These drugs can help improve symptoms of chest
pain.
●
Ranolazine.
This medication may help people with chest pain (angina). It may be prescribed with a beta
blocker or instead of a beta blocker if you can't take it.
●
Nitroglycerin.
Nitroglycerin tablets, sprays and patches can control chest pain by temporarily dilating your
coronary arteries and reducing your heart's demand for blood.
●
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers
(ARBs).
These similar drugs decrease blood pressure and may help prevent progression of coronary
artery disease.
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9.0 CONCLUSION
Finally, the heart is a necessary organ for our bodies to function. The heart is constantly
working in our bodies, pumping blood and ensuring that oxygen is delivered to all parts of the
body. The most common disease in the world is atherosclerosis. We can, however, reduce our
risk of contracting this disease by adopting a healthier lifestyle. Furthermore, many advanced
medical technologies, such as electrocardiograms, bypass surgery, and angioplasty, can
effectively treat atherosclerosis.
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10.0 REFERENCES
Moore, K. L., Dalley, A. F., & R., A. A. M. (2014). Chapter 1: Thorax: Viscera Of Thoracic
Cavity. Clinically oriented anatomy. 7th ed, (pp 128 - 171). Wolters Kluwer Health/Lippincott
Williams & Wilkins.
Mescher, A. L. (2013). Chapter 11: Circulatory System. In Junqueira's basic histology:
Text and Atlas (pp. 216–232). essay, McGraw Hill Medical.
Ellis, H., & Feldman, S. (2004). Chapter 2: The Heart. In Anatomy for anaesthetists (pp.
75–86). essay, Blackwell.
Chambers, D., Huang, C. L.-H., & Matthews, G. (2015). Section 3: Cardiovascular
physiology: Chapter 27: Cardiac cycle. In Basic physiology for Anaesthetists (pp. 117–120).
essay, Cambridge University Press.
Mayo Foundation for Medical Education and Research. (2020, June 5). Coronary artery
disease. Mayo Clinic. Retrieved December 19, 2021, from
https://www.mayoclinic.org/diseases-conditions/coronary-artery-disease/symptoms-causes/syc-
20350613
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