by, Sowmya.M Narayana college of nursing nellore

1. Seminar on coronary artery disease
Submitted to: submitted by:

2. Mrs.asst.pro.padma,m.sc(n) m.sowmya
Dept.of msn 1 st yr m.sc (n)
Ncon ncon
Nellore nellore
Name of the institution : Narayana college of nursing
Programme : M.sc nursing
Year : 1 st M.Sc nursing
Subject : Medical and surgical nursing- I
Topic : pulmonary tuberculosis
Date : 25.3.19 time : 2-4pm
Venue : IInd floor , NCON
No. of. students : 4
Previous knowledge of the students: students have knowledge on anatomy and physiology of
Cardiovascular system during 1st year B.sc (N)
Method of teaching : lecture cum discussion & brcks method
A.V. aids : definition (roller board), etiology, risk factors (Hand outs),
Pathophysiology (chart) clinical manifestations (leaflet), diagnostic evalution ( OHP),
management (PPT)
Name of the evalutor : Mrs.PADMA, M.sc (N)
Assistent prof, Dept of MSN
Name of the student teacher : m.sowmya , M.sc(N) 1st year
General objectives:
The students will be able to gain in depth knowledge regarding coronary artery disease,develop
desirable attitude and skills to provide comprehensive nursing care in patient with CAD in all
health care settings.
Specific objectives:
At the end of the class , students will be able to
 define CAD.
 know the CAD.
 enlist the risk factors of CAD.
 illustrate the pathophysiology of CAD.

3.  enlist the clinical manifestation of CAD
 enumarate diagnostic findings of CAD
 brief out the medical management of CAD
 list out the alternative medicine for CAD
 identify the complications of CAD
 discuss the nursing management of CAD
 describe the life style modification of CAD
 know the research activities related to CAD
 verbalize in improving communication skills through group discussion
SEMINAR ON CORONARY ARTERY DISEASE
ANATOMY & PHYSIOLOGY:
 The heart is a muscular organ about the size of a closed fist that functions as
the body’s circulatory pump.
 It takes in deoxygenated blood through the veins and delivers it to the lungs
for oxygenation before pumping it into the various arteries (which provide
oxygen and nutrients to body tissues by transporting the blood throughout
the body).
 The heart is located in the thoracic cavity medial to the lungs and posterior
to the sternum.
 The heart itself is made up of 4 chambers, 2 atria and 2 ventricles.
 De-oxygenated blood returns to the right side of the heart via the venous
circulation.
 It is pumped into the right ventricle and then to the lungs where carbon
dioxide is released and oxygen is absorbed.
 The oxygenated blood then travels back to the left side of the heart into the
left atria, then into the left ventricle from where it is pumped into the aorta
and arterial circulation.

4.  The pressure created in the arteries by the contraction of the left ventricle is
the systolic blood pressure.
 Once the left ventricle has fully contracted it begins to relax and refill with
blood from the left atria.
 The pressure in the arteries falls whilst the ventricle refills. This is the
diastolic blood pressure.
 The atrio-ventricular septum completely separates the 2 sides of the heart.
 Unless there is a septal defect, the 2 sides of the heart never directly
communicate. Blood travels from right side to left side via the lungs only.
 However the chambers themselves work together .
 The 2 atria contractsimultaneously, and the 2 ventricles contract
simultaneously.
Coronary artery disease (CAD):
Defenitions:
It is also known as ischemic heart disease (IHD), involves the reduction of
blood flow to the heart muscle due to build up of plaque in the arteries of the heart.
It is the most common of the cardiovascular diseases.
Types include stable angina, unstable angina, myocardial infarction, and
sudden cardiac death.
A/C LEWIS
Impedance or blockage of one or more arteries that supply blood to the heart,
usually due to the atherosclerosis resulting in dysfunction of the heart.
A/C JOYCE & M.BLOCK

5. Coronary artery disease is the buildup of fatty material in the walls of coronary
arteries causing decreased blood supply to the heart muscle resulting in
dysfunction of the heart.
A/C BRUNNER&SIDDARTH
Incidence:
In 2017, CAD affected 110 million people and resulted in 8.9 million deaths.
It makes up 15.6% of all deaths, making it the most common cause of death
globally.
Th e number of cases of CAD for a given age also decreased between 2010 and
2018.In the United States in 2010, about 20% of those over 65 had CAD, while it
was present in 7% of those 45 to 64, and 1.3% of those 18 to 45; rates were higher
among men than women of a given age.
Registrar general of india reported that CAD led to 17% of total deaths and 26%
of adult deaths in 2016.
Risk factors
Coronary artery disease has a number of well determined risk factors.
These include:
Modifiable risk factors
Non modifiable risk factors
Modifiable risk factors:
 smoking
 lack of exercise
 obesity
 high blood cholesterol,
 poor diet
 depression
 excessive alcohol.

6. Non modifiable risk factors
 high blood pressure
 diabetes,
 genetics
 Positive family history ( first degree relative with cardiovascular disease at age 55 or less
for males at age 65 or less for female
 Age ( more than 45 yrs. for men, more than 55 yrs for women)
 Gender ( occurs 3 times more often in men than in women)
 Race: higher incidence in Africans Americans than in Caucasian.

Smoking, just one cigarette per day about doubles the risk of CAD.
 Lack of exercise has been linked to 7–12% of cases.
 Exposure to the herbicide Agent Orange may increase risk.
 Rheumatologic diseases such as rheumatoid arthritis, systemic lupus
erythematosus, psoriasis, and psoriatic arthritis are independent risk factors
as well.
 Job stress appears to play a minor role accounting for about 3% of cases. In
one study, women who were free of stress from work life saw an increase in
the diameter of their blood vessels, leading to decreased progression of
atherosclerosis.
 In contrast, women who had high levels of work-related stress experienced
a decrease in the diameter of their blood vessels and significantly increased
disease progression. Having a type A behavior pattern, a group of
personality characteristics including time urgency, competitiveness,
hostility, and impatience, is linked to an increased risk of coronary disease.
Blood fats:
 High blood cholesterol (specifically, serum LDL concentrations).
 HDL (high density lipoprotein) has a protective effect over development of
coronary artery disease.
 High blood triglycerides may play a role.
 High levels of lipoprotein(a), a compound formed when LDL cholesterol
combines with a protein known as apolipoprotein(a).
 Dietary cholesterol does not appear to have a significant effect on blood
cholesterol and thus recommendations about its consumption may not be
needed.

7.  Saturated fat is still a concern.
Genetics:
The heritability of coronary artery disease has been estimated between 40% and
60%. Genome-wide association studies have identified around 60 genetic
susceptibility loci for coronary artery disease.
Other
 Endometriosis in women under the age of 40.
 Depression and hostility appear to be risks.
 The number of categories of adverse childhood experiences (psychological,
physical, or sexual abuse; violence against mother; or living with household
members who were substance abusers, mentally ill, suicidal, or incarcerated)
showed a graded correlation with the presence of adult diseases including
coronary artery (ischemic heart) disease.
 Hemostatic factors: High levels of fibrinogen and coagulation factor VII are
associated with an increased risk of CAD.
 Low hemoglobin.
 In the Asian population, the b fibrinogen gene G-455A polymorphism was
associated with the risk of CAD.
Pathophysiology:

8. Micrograph of a coronary artery with the most common form of coronary artery
disease (atherosclerosis) and marked luminal narrowing. Masson's trichrome.
Illustration depicting coronary artery disease
pathophysiology
Limitation of blood flow to the heart causes ischemia (cell starvation secondary to
a lack of oxygen) of the heart's muscle cells.
The heart's muscle cells may die from lack of oxygen and this is called a
myocardial infarction (commonly referred to as a heart attack).

9. It leads to damage, death, and eventual scarring of the heart muscle without
regrowth of heart muscle cells.
Chronic high-grade narrowing of the coronary arteries can induce transient
ischemia which leads to the induction of a ventricular arrhythmia, which may
terminate into a dangerous heart rhythm known as ventricular fibrillation, which
often leads to death.
 Typically, coronary artery disease occurs when part of the smooth, elastic
lining inside a coronary artery (the arteries that supply blood to the heart
muscle) develops atherosclerosis.
 With atherosclerosis, the artery's lining becomes hardened, stiffened, and
accumulates deposits of calcium, fatty lipids, and abnormal inflammatory
cells – to form a plaque.
 Calcium phosphate (hydroxyapatite) deposits in the muscular layer of the
blood vessels appear to play a significant role in stiffening the arteries and
inducing the early phase of coronary arteriosclerosis.
 This can be seen in a so-called metastatic mechanism of calciphylaxis as it
occurs in chronic kidney disease and hemodialysis (Rainer Liedtke 2008)
 Although these people suffer from a kidney dysfunction, almost fifty percent
of them die due to coronary artery disease.
 Plaques can be thought of as large "pimples" that protrude into the channel
of an artery, causing a partial obstruction to blood flow. People with
coronary artery disease might have just one or two plaques, or might have
dozens distributed throughout their coronary arteries.
 A more severe form is chronic total occlusion (CTO) when a coronary artery
is completely obstructed for more than 3 months.
Developmental Stages.
CAD is a progressive disease that develops over many years. When it becomes
symptomatic, the disease process is usually well advanced. The stages of
development in atherosclerosis are (1) fatty streak, (2) fibrous plaque, and (3)
complicated lesion.

10. Fatty Streak.
 Fatty streaks, the earliest lesions of atherosclerosis, are characterized by
lipid-filled smooth muscle cells.

As streaks of fat develop within the smooth muscle cells, a yellow tinge
appears.
 Fatty streaks can be seen in the coronary arteries by age 15 and involve an
increasing amount of surface area as one ages.
 Treatment that lowers LDL cholesterol may reverse this process .
Fibrous Plaque.
 The fibrous plaque stage is the beginning of progressive changes in the
endothelium of the arterial wall.
 These changes can appear in the coronary arteries by age 30 and increase
with age.
 Normally the endothelium repairs itself immediately.
 This does not happen in the individual with CAD. LDLs and growth factors
from platelets stimulate smooth muscle proliferation and thickening of the
arterial wall.
 Once endothelial injury has taken place, lipoproteins (carrier proteins within
the bloodstream) transport cholesterol and other lipids into the arterial
intima. Collagen covers the fatty streak and forms a fibrous plaque with a
grayish or whitish appearance.
 These plaques can form on one portion of the artery or in a circular fashion
involving the entire lumen.
 The borders can be smooth or irregular with rough, jagged edges.
 The result is a narrowing of the vessel lumen and a reduction in blood flow
to the distal tissues.
Complicated Lesion.
 The final stage in the development of the atherosclerotic lesion is the most
dangerous.
 As the fibrous plaque grows, continued inflammation can result in plaque
instability, ulceration, and rupture.
 Once the integrity of the artery’s inner wall is compromised, platelets
accumulate in large numbers, leading to a thrombus.
 The thrombus may adhere to the wall of the artery, leading to further
narrowing or total occlusion of the artery.
 Activation of the exposed platelets causes expression of glycoprotein Ilb/IIIa
receptors that bind fibrinogen.

11.  This, in turn, leads to further platelet aggregation and adhesion, further
enlarging the thrombus. At this stage the plaque is referred to as a
complicated lesion
Collateral Circulation.
 Normally some arterial anastomoses or connections, termed collateral
circulation, exist within the coronary circulation.
 Two factors contribute to the growth and extent of collateral circulation: (1)
the inherited predisposition to develop new blood vessels (angiogenesis) and
(2) the presence of chronic ischemia.
 When a plaque occludes the normal flow of blood through a coronary artery
and the resulting ischemia is chronic, increased collateral circulation
develops
 When occlusion of the coronary arteries occurs slowly over a long period,
there is a greater chance of adequate collateral circulation developing, and
the myocardium may still receive an adequate amount of blood and oxygen.
-
A, Open, functioning coronary artery. B, Partial coronary artery closure with
collateral circulation being established. C, Total coronary artery occlusion with
collateral circulation bypassing the occlusion to supply blood to the myocardium.
However, with rapid-onset CAD (e.g., familial hypercholesterolemia) or
coronary spasm, time is inadequate for collateral development. Consequently, a
diminished blood flow results in a more severe ischemia or infarction.

12. Signs and symptoms
Chest pain that occurs regularly with activity, after eating, or at other predictable
times is termed stable angina and is associated with narrowings of the arteries of
the heart.
 Angina that changes in intensity, character or frequency is termed unstable.
Unstable angina may precede myocardial infarction. In adults who go to the
emergency department with an unclear cause of pain, about 30% have pain
due to coronary artery disease.
In addition to angina, CAD may cause the following symptoms:
The following symptoms can be signs of either angina or the onset of a heart attack
caused by underlying CAD:
 shortness of breath
 sweating
 dizziness
 nausea
 rapid heartbeat
 palpitations — the feeling that your heart is pounding hard and rapidly and is
fluttering or skipping beats
 pain, discomfort, pressure, tightness, numbness, or burning sensation in your
chest, arms, shoulders, back, upper abdomen, or jaw
 weakness or fatigue
 nausea or vomiting
 indigestion or heartburn
 sweating or clammy skin
 fast heart rate or irregular heart rhythm
 anxiety or a general feeling of being unwell
Diagnosis

For symptomatic people, stress echocardiography can be used to make a
diagnosis for obstructive coronary artery disease.

13.  The use of echocardiography, stress cardiac imaging, and/or advanced non-
invasive imaging is not recommended on individuals who are exhibiting no
symptoms and are otherwise at low risk for developing coronary disease.
 The diagnosis of "Cardiac Syndrome X" – the rare coronary artery disease
that is more common in women, as mentioned, is a diagnosis of exclusion.
Therefore, usually the same tests are used as in any person with the suspected of
having coronary artery disease:
 Baseline electrocardiography (ECG)
 Exercise ECG – Stress test
 Exercise radioisotope test (nuclear stress test, myocardial scintigraphy)
 Echocardiography (including stress echocardiography)
 Coronary angiography
 Intravascular ultrasound
 Magnetic resonance imaging (MRI)
The diagnosis of coronary disease underlying particular symptoms depends largely
on the nature of the symptoms. The first investigation is an electrocardiogram
(ECG/EKG), both for "stable" angina and acute coronary syndrome.
An X-ray of the chest and blood tests may be performed.
Stable angina
In "stable" angina, chest pain with typical features occurring at predictable levels
of exertion, various forms of cardiac stress tests may be used to induce both
symptoms and detect changes by way of electrocardiography (using an ECG),
echocardiography (using ultrasound of the heart) or scintigraphy (using uptake of
radionuclide by the heart muscle).
If part of the heart seems to receive an insufficient blood supply, coronary
angiography may be used to identify stenosis of the coronary arteries and
suitability for angioplasty or bypass surgery.
Stable coronary artery disease (SCAD) is also often called stable ischemic
heart disease (SIHD).
A 2015 monograph explains that "Regardless of the nomenclature, stable
angina is the chief manifestation of SIHD or SCAD."

14. ECG:
 ECGs may be performed sequentially to identify "evolving changes"
(indicating ongoing damage to the heart muscle).
 Diagnosis is clear-cut if ECGs show elevation of the "ST segment", which in
the context of severe typical chest pain is strongly indicative of an acute
myocardial infarction (MI); this is termed a STEMI (ST-elevation MI) and is
treated as an emergency with either urgent coronary angiography and
percutaneous coronary intervention (angioplasty with or without stent
insertion) or with thrombolysis ("clot buster" medication), whichever is
available.
 In the absence of ST-segment elevation, heart damage is detected by cardiac
markers (blood tests that identify heart muscle damage).
 If there is evidence of damage (infarction), the chest pain is attributed to a
"non-ST elevation MI" (NSTEMI).
 If there is no evidence of damage, the term "unstable angina" is used. This
process usually necessitates hospital admission and close observation on a
coronary care unit for possible complications (such as cardiac arrhythmias –
irregularities in the heart rate).
 Depending on the risk assessment, stress testing or angiography may be used
to identify and treat coronary artery disease in patients who have had an
NSTEMI or unstable angina.
 There are various risk assessment systems for determining the risk of
coronary artery disease, with various emphasis on different variables above.
 A notable example is Framingham Score, used in the Framingham Heart
Study. It is mainly based on age, gender, diabetes, total cholesterol, HDL
cholesterol, tobacco smoking and systolic blood pressure.
Prevention:

Up to 90% of cardiovascular disease may be preventable if established risk
factors are avoided.
 Prevention involves adequate physical exercise, decreasing obesity, treating
high blood pressure, eating a healthy diet, decreasing cholesterol levels, and
stopping smoking.
 Medications and exercise are roughly equally effective. High levels of
physical activity reduce the risk of coronary artery disease by about 25%.
 Most guidelines recommend combining these preventive strategies. A 2015
Cochrane Review found some evidence that counselling and education in an
effort to bring about behavioral change might help in high risk groups.

15. However, there was insufficient evidence to show an effect on mortality or
actual cardiovascular events.
 In diabetes mellitus, there is little evidence that very tight blood sugar
control improves cardiac risk although improved sugar control appears to
decrease other problems such as kidney failure and blindness.
 The World Health Organization (WHO) recommends "low to moderate
alcohol intake" to reduce risk of coronary artery disease while high intake
increases the risk.
Diet:
 A diet high in fruits and vegetables decreases the risk of cardiovascular
disease and death.
 Vegetarians have a lower risk of heart disease, possibly due to their greater
consumption of fruits and vegetables.
 Evidence also suggests that the Mediterranean diet and a high fiber diet
lower the risk.
 The consumption of trans fat (commonly found in hydrogenated products
such as margarine) has been shown to cause a precursor to atherosclerosis
and increase the risk of coronary artery disease.
 Evidence does not support a beneficial role for omega-3 fatty acid
supplementation in preventing cardiovascular disease (including myocardial
infarction and sudden cardiac death).
 There is tentative evidence that intake of menaquinone (Vitamin K2), but not
phylloquinone (Vitamin K1), may reduce the risk of CAD mortality.
Secondary prevention:
Secondary prevention is preventing further sequelae of already established disease.
Effective lifestyle changes include:
 Weight control
 Smoking cessation
 Avoiding the consumption of trans fats (in partially hydrogenated oils)
 Decreasing psychosocial stress
 Exercise
Aerobic exercise, like walking, jogging, or swimming, can reduce the risk of
mortality from coronary artery disease.[

16. Aerobic exercise can help decrease blood pressure and the amount of blood
cholesterol (LDL) over time. It also increases HDL cholesterol which is considered
"good cholesterol".
Although exercise is beneficial, it is unclear whether doctors should spend
time counseling patients to exercise. The U.S. Preventive Services Task Force
found "insufficient evidence" to recommend that doctors counsel patients on
exercise but "it did not review the evidence for the effectiveness of physical
activity to reduce chronic disease, morbidity and mortality", only the effectiveness
of counseling itself. The American Heart Association, based on a non-systematic
review, recommends that doctors counsel patients on exercise.
Treatment
There are a number of treatment options for coronary artery disease:[88]
 Lifestyle changes
 Medical treatment – drugs (e.g., cholesterol lowering medications, beta-
blockers, nitroglycerin, calcium channel blockers, etc.);
 Coronary interventions as angioplasty and coronary stent;
 Coronary artery bypass grafting (CABG)
Medical management
 Statins, which reduce cholesterol, reduce the risk of coronary artery disease
 Nitroglycerin
 Calcium channel blockers and/or beta-blockers
 Antiplatelet drugs such as aspirin
 It is recommended that blood pressure typically be reduced to less than
140/90 mmHg.
 The diastolic blood pressure however should not be lower than 60 mmHg.]
Beta blockers are recommended first line for this use.
Aspirin:
In those with no previous history of heart disease, aspirin decreases the risk of
a myocardial infarction but does not change the overall risk of death.
It is thus only recommended in adults who are at increased risk for coronary
artery disease where increased risk is defined as "men older than 90 years of age,

17. postmenopausal women, and younger persons with risk factors for coronary artery
disease (for example, hypertension, diabetes, or smoking) are at increased risk for
heart disease and may wish to consider aspirin therapy". More specifically, high-
risk persons are "those with a 5-year risk ≥ 3%".
Anti-platelet therapy
Clopidogrel plus aspirin (dual anti-platelet therapy ) reduces cardiovascular events
more than aspirin alone in those with a STEMI. In others at high risk but not
having an acute event the evidence is weak. Specifically, its use does not change
the risk of death in this group. In those who have had a stent more than 12 months
of clopidogrel plus aspirin does not affect the risk of death.
Surgical management:
Revascularization for acute coronary syndrome has a mortality benefit.[99]
Percutaneous revascularization for stable ischaemic heart disease does not appear
to have benefits over medical therapy alone.
In those with disease in more than one artery coronary artery bypass grafts
appear better than percutaneous coronary interventions.
Newer "anaortic" or no-touch off-pump coronary artery revascularization
techniques have shown reduced postoperative stroke rates comparable to
percutaneous coronary intervention. Hybrid coronary revascularization has also
been shown to be a safe and feasible procedure that may offer some advantages
over conventional CABG though it is more expensive.
Nursing management
Nursing Diagnosis :
Acute Pain related to heart tissue ischemia, or blockages in the coronary arteries.
Goal: The client is expected to be able to demonstrate a decrease in chest pain,
showed a decrease in pressure and how relaxation.
Interventions:
 Monitor and review the characteristics and location of pain.

18.  Monitor vital signs (blood pressure, pulse, respiration, consciousness).
 Instruct the patient to immediately report instances of chest pain.
 Create an atmosphere of calm and comfortable environment.
 Teach and encourage the patient to do relaxation techniques.
 Collaboration in: Giving oxygen and drugs
 Measure vital signs before and after treatment.
2. Nursing Diagnosis: Activity Intolerance related to imbalance between oxygen
supply and demand, and the presence of necrotic tissue in myocardial ischemia.
Goal : The client shows an increase in the ability to perform activities (blood
pressure, pulse, rhythm within normal limits) the absence of angina.
Interventions:
 Record the heart rhythm, blood pressure and pulse before, during and after
the activity.
 Instruct the patient to have more rest first.
 Instruct the patient not to "push" at the time of defecation.
 Explain to the patient about the stages of activity that may be performed by
the patient.
 Show to patients about physical signs that activity exceeds the limit.
3. Nursing Diagnosis :
Risk for Decreased Cardiac Output related to changes in the rate, rhythm,
cardiac conduction, decrease preload or increased SVR, miocardial infarction.
Goal : improve the cardiac output
Interventions:
 Perform blood pressure measurements (compare the two arms in a standing
position, sitting and lying down, if possible).
 Assess the quality of the pulse.

19.  Note the development of the S3 and S4.
 Auscultation of breath sounds.
 Stay with the patient at the time of the activity.
 Serve food that is easy to digest and reduce the consumption of kafeine.
 Collaboration in: serial ECG examination, chest radiographs, administering
medications anti dysrhythmias.
4. Nursing Diagnosis :
Risk for Impaired Tissue Perfusion related to decreased blood pressure,
hypovolemia.
Goal:
Improve the tissue perfusion
Interventions:
 Assess the changes in consciousness.
 Inspection of the pale, cyanosis, cold skin and peripheral pulse degradation.
 Assess the Homans sign (pain in calf on dorsoflextion), erythema, edema.
 Assess respiration (rhythm, and effort into breathing).
 Assess gastrointestinal function (bowel sounds, abdominal distention,
constipasi).
 Monitor intake and output.
 Collaboration in: Examination ABG, BUN, serum ceratinin and electrolyte.
5. Nursing Diagnosis: Risk for Excess Fluid Volume related to decreased organ
perfusion (renal), increased sodium retention, decreased plasma protein.
Goal : Reduce the amount of fluid in the body of the client after the treatment.
Interventions:
 Auscultation of breath flare (examine the crackless).
 Assess the jugular vein distension, increased occurrenceof edema.

20.  Measure intake and output (fluid balance).
 Assess the weight every day.
 Instruct the patient to consume a maximum of 2000 total liquids cc/24 hours.
 Serve a meal with a low-salt diet.
 Collaboration in the provision of diuretics.
THEORY APPLICATION
This theory has the potential to place comfort in the forefront of healthcare.
According to the model, comfort is an immediate desirable outcome of nursing
care.
The Theory of Comfort was developed when Katharine Kolcaba conducted a
concept analysis of comfort that examined literature from several disciplines,
including nursing, medicine, psychology, psychiatry, ergonomics, and English.
According to Kolcaba, comfort is the product of holistic nursing art.
Kolcaba described comfort existing in three forms: relief, ease, and
transcendence. If specific comfort needs of a patient are met, the patient
experiences comfort in the sense of relief.
Relief : Any symptomatic relief which is causing the discomfort of patient
Ease: Addresses comfort in a state of contentment. For example, the patient's
anxieties are calmed.
Transcendence: It is described as a state of comfort in which patients are able to
rise above their challenges.
The four contexts in which patient comfort can occur are:

21. o physical
o psychospiritual
o environmental
o sociocultural.
The Theory of Comfort considers patients to be individuals, families,
institutions, or communities in need of health care.
The environment is any aspect of the patient, family, or institutional
surroundings that can be manipulated by a nurse or loved one in order to enhance
comfort.
In the model, nursing is described as the process of assessing the
patient's comfort needs, developing and implementing appropriate nursing care
plans, and evaluating the patient's comfort after the care plans have been carried
out.
Comfortin
three forms
relief ease transcendence

22. ABSTRACT:
Coronary artery disease is the major cause of mortality and morbidity in Malaysia and
worldwide. This paper reviews all research and publications on coronary artery disease in Malaysia
published between 2000-2015. 508 papers were identified of which 146 papers were selected and
reviewed on the basis of their relevance. The epidemiology, etiology, risk factors, prevention,
assessment, treatment, and outcomes of coronary artery disease in the country are reviewed and
summarized. The clinical relevance of the studies done in the country are discussed along with
recommendations for future research.
Summary:
coronary artery disease is the one of the leading non communicable
disease which causing the increased morbidity of adult population. Risk
factors may be of two types modifiable and non modifiable risk factors.
Symptoms like chest pain, angina, giddiness, fatigue, palpitations. Treatment
may be of Statins, which reduce cholesterol, reduce the risk of coronary artery
disease, Nitroglycerin, Calcium channel blockers and/or beta-blockers,Antiplatelet
drugs such as aspirin
bibliography:
Text book reference:
1.A text book of medical surgical nursing by brunner and siddarth 7 th edition
page no: 1011-1021.
2.A text book of medical surgical nursing by joycee and m.block 5 th edition page
no: 992-1068.
3.A text book of medical surgical nursing by lewis 2 nd volume page no 886-991.
4. A text book of medical surgical nursing by B.T.Basavanthappa page no: 994-
998.
Journal reference:

23. 1. journal of coronary artery disease,2018 volume-1.
2. AHA journal on arteriosclerosis.
3. The American journal on coronary artery disease.
Net reference:
1. http://www.medline plus.org.
2. http://www.myoclinic.org.
3. http://www.medical newstoday.org.
4. http://www.heart.org.