University of Perpetual Help System DALTA

Alabang Zapote Rd. Pamplona, Las Pinas City

COLLEGE OF NURSING
BSN III-A Group 3 Batch 2010 - 2011

A Case Study on
Non ST Elevation
Myocardial
Infarction
Submitted By: Galauran, ChristinaGarcia; Edgar
Raymond; Gatela, Leizl; Gozun, Bianca Marie;
Ibanez, Levilyn; Kho, Krista Ann; Lucido, Justin
Joseph; Mapanao, Jamie Therese; Padua, Ma.
Mercedita; Perez, Sherrylyn; Pinlac, Sheila; Ragas,
Allen Rey
Submitted To: Mrs. Zenaida Vinagrera RN

A Case Study on Non ST Elevation Myocardial Infarction

INTRODUCTION
Everything in the world today is in constant change. The present era is far different from what
our ancestors were used to. There are several innovations and todays technology creates a new
and modern culture far beyond what we have before. This transformation is accompanied by
changes in how we live our lives thus, making us more susceptible to diseases brought about by
our lifestyle. One of these diseases is Myocardial Infarction.
This is a case of Patient BAY from Las Pinas City. He was admitted at the UPHDMC JONELTA with a diagnosis of Non ST Elevation Myocardial Infarction: Killips I: Pneumonia in
the elderly to be considered aspiration pneumonia UGIB.
Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart
attack is the interruption of blood supply to a part of the heart, causing heart cells to die. This is
most commonly due to blockage of a coronary artery following the rupture of a atherosclerotic
plaque, which is an unstable collection of fatty acids and white blood cells in the wall of
an artery. The resulting ischemia due to restriction in blood supply and oxygen shortage, if left
untreated for a sufficient period of time, can cause damage or death (infarction) of heart muscle
tissue.

Classical symptoms of acute myocardial infarction include sudden chest pain (typically radiating
to the left arm or left side of the neck), shortness of breath, nausea, vomiting, palpitations,
sweating, and anxiety.

Clinically, a myocardial infarction can be further sub classified into a ST elevation MI (STEMI)
versus a non-ST elevation MI (non-STEMI) based on ECG changes.
In a NSTEMI, the blood clot only partly occludes the artery, and as a result only a portion of the
heart muscle being supplied by the affected artery dies. In contrast to the more severe form of
heart attack (the STEMI), the NSTEMI does not produce characteristic elevation in the "ST
segment" portion of the ECG. (ST segment elevation indicates that a relatively large amount of
heart muscle damage is occurring, because the coronary artery is totally blocked). This means
that in a NSTEMI, the artery is only partially blocked. A common problem when a patient has
an acute coronary syndrome without ST segment elevation is deciding whether an actual heart
attack is occurring or instead whether the patient is simply having unstable angina.
Measuring cardiac enzymes, which reflect heart muscle damage, is an important tool in making
this distinction.

A Case Study on Non ST Elevation Myocardial Infarction

The Killip classification is a system used in individuals with an acute myocardial infarction or
heart attack, in order to risk stratifies them. Individuals with a low Killip class are less likely to
die within the first 30 days after their myocardial infarction than individuals with a high Killip
class.
Patients were ranked by Killip class in the following way:

Killip class I Includes individuals with no clinical signs of heart failure.

Killip class II Includes individuals with rales or crackles in the lungs, an S3, and elevated
jugular venous pressure.
Killip class III Describes individuals with frank acute pulmonary edema.
Killip class IV Describes individuals in cardiogenic shock or hypotension (measured
as systolic blood pressure lower than 90 mmHg), and evidence of
peripheral vasoconstriction (oliguria, cyanosis or sweating).

The Killip-Kimball classification has played a fundamental role in classic cardiology, having
been used as stratifying criteria for many other studies. Worsening Killip class had been found to
be independently associated with increasing mortality in several studies.
Killip class 1 and no evidence of hypotension or bradycardia, in patients presenting with acute
coronary syndrome, should be considered for immediate IV beta blockade.

The prognosis post myocardial infarction varies greatly, depending on a person's health, the
extent of the heart damage and the treatment given. Prognosis is significantly worsened if
mechanical complications such as papillary muscle or myocardial free wall rupture
occur. Morbidity and mortality from myocardial infarction has improved over the years due to
better treatment.

A Case Study on Non ST Elevation Myocardial Infarction

NAME:

B.A.Y

AGE:

81 y/o

DATE OF BIRTH:
GENDER:

Female

ADDRESS:

Almanza, Uno, Las Pias City

DATE OF
ADMISSION:
TIME OF
ADMISSION:

December 2, 2010
1:17 am

DIAGNOSIS:

NSTEMI-Killips 1, Pneumonia in the elderly, T/C Aspiration

Pneumonia, UGIB

CHIEF
COMPLAINT:

DOB

HOSPITAL:

UPHDMC
PATIENTS PROFILE

NURSING HEALTH HISTORY

BIOGRAPHIC DATA

A Case Study on Non ST Elevation Myocardial Infarction

Patient B is an 81 year old female, currently residing at B4 L15 Gen. Malvar St. Soldier Hills 2
Almanza Uno, Las Pias City. She is a Roman Catholic and married to her husband. She is
blessed with 3 boys and 2 girls. Hospitals are her usual source of medical care, especially the
UPHDMC.
CHIEF COMPLAINT OR REASON FOR VISIT
The patient was admitted at the University of Perpetual Help Medical Center last December 2,
2010 with the chief complaint of difficulty of breathing.
HISTORY OF PRESENT ILLNESS
Few hours PTA, the pt. was apparently well until she experienced sudden onset of DOB with no
other associated Sx such as cough, fever, and vomiting. Pt. was brought to ER was subsequently
admitted.
PAST MEDICAL HISTORY
The pt. was diagnosed with DM and HPN last 2000 but it did not make her hospitalized. On the
same year, pt. was admitted because of UGIB. Her daughter said that she does not have any
allergies may it be on food or medicines. She never had any accidents (major or minor).
FAMILY HISTORY OF ILLNESS
The clients niece claimed that hypertension, heart disease and diabetes mellitus runs to their
family.
FAMILY GENOGRAM
Grandfather

Grandmother*

Grand-mother
Grandfa
(hyper-tensive)*

(heart disease) *

ther

Father
(hypertensive)
*

Mother
(hypertensive)

Brother
(diabetic)*

Grandfather
(hypertensive)*

Sister
(heart
disease)

Patient

Sister

Legend:
- boy
-girl
* - deceased
GORDONS FUNCTIONAL HEALTH PATTERNS
HEALTH PERCEPTION AND HEALTH MANAGEMENT

Brother
(hypertensive)

A Case Study on Non ST Elevation Myocardial Infarction

According to her daughter, the pt. keeps herself healthy by eating leafy vegetables especially
now that she is in her older age. She restricts herself on eating fatty foods and those that contain
sodium- liberal amount is allowed. She complies with the doctors drug prescription and takes
them on time.
NUTRITIONAL-METABOLIC PATTERN
According to her daughter, the pt. has good appetite when she is not yet confined. He eats three
meals a day in the required quantity. He was advised to limit fatty and sodium-containing foods.
In contrary to being hospitalized by the pt., she has now a diet of 1200kcal/day with liberal salt
divided by 3 EF, 400cc, Peptamen 5 scoops in 200cc of water through OF. The patient was able
to comply with the intended diet by the physician and she is also taking her prescribed medicine.
*In patients 24 hour recall, basically it is being supplemented by OF.
ELIMINATION PATTERN
Her daughter claimed that the patient urinates and defecates without discomfort before
hospitalization and that the patient has no history of urinal disorders. Today, the patient has an
IFC. Her urine is yellowish and no foul odor. She does not defecate everyday but her stool is in
semi-formed and yellowish in color. OLIGURIC. The pt. urinated 4 hours prior to assessment
and defecated last night. She does not use any laxatives or diuretics. There are significant effects
illness and hospitalization offer to him with regards to his elimination pattern.
ACTIVITY-EXERCISE PATTERN
The daughter of the pt. verbalized that because of aging, she can no longer do the activities of
daily living and exercise. She cannot give full force into activities that requires effort and large
body movement.
SLEEP-REST PATTERN
The pt. normally sleeps at around 8:00pm and wakes up at 6:00am the next day. She normally
has an average of ten hours of sleep but relative said that the pt. frequently urinates at night
normal at aging process. As a result of hospitalization and illness, the pt. keeps on sleeping but
easily wakes when there is procedure to be done to the patient.
COGNITIVE-PERCEPTUAL PATTERN
According to the pts. daughter since her mother is aging, there are already sensory deviations.
There are also memory lapses. The pt. is also noted to easily recognized pain (high pain
threshold) and cannot easily tolerate the pain being subjected (moderate pain tolerance).
SELF-PERCEPTION AND SELF-CONCEPT PATTERN
Even before hospitalized, the daughter of the pt. claimed that her mother has low self-esteem
provided that she is sick and immobile even at home. She thinks she is not healthy inside and
out.
ROLE-RELATIONSHIP PATTERN
The patients daughter verbalized that the patient is a loving mother and wife to her family. She
was able to provide the needs of her children and family back when the pt. is still strong and can
be able to work for them. According to patients daughter, the patient was a helpful person. She

A Case Study on Non ST Elevation Myocardial Infarction

always helps those in need especially her family. As an effect of illness, the pt. can no longer take
charge of the family. Decisions came from her children.
SEXUALLY-REPRODUCTIVE PATTERN
Can no longer be associated to the pt.
COPING AND STRESS TOLERANCE PATTERN
According to her daughter, the stressor to the pt. is when he feels DOB almost every time. The
only way she can cope and be able to manage it is when she consult a physician. Also,
restrictions to diet makes the pt. irritable so as a coping mechanism she just think of the bad
effects of those when she did not follow the order.
VALUE-BELIEF PATTERN
The patient is Roman Catholic in religion. According to patients daughter, before, the patient
always attends the mass every Sunday, and gives offerings to the church. She also verbalized that
the patient was active in church activities back in time.
PHYSICAL ASSESSMENT
GENERAL APPEARANCE
The client has thin body built. She is uncoordinated and is restricted in terms of movement due to
her present condition. She looks clean and neat. She is aphasic in her communication and has
stiffening movements in some of her body parts. There are signs of distress present in the clients
face.
VITAL SIGNS
Using the axillary route, the clients temperature is noted to be 36.8C. Blood pressure (taken in
moderate high back rest position position) is 100/70 mmHg. The pulse rate is 76 bpm, and
respiratory rate is 22 cpm..
SKIN
The clients skin is brownish, uniform in color, dry and scaling. There is no presence of edema,
no rash, no suspicious nevi, no petechiae or ecchymoses.. Severe bedsores have started to appear
in the clients lower extremities: grade 3 bedsores in her sacral area. Skin springs back to
previous state when pinched and has senile skin turgor. The nails have a convex curvature and
the nail plates angle is 160. Rough texture of the nail bed and is pallor in color. Intact epidermis
in the surrounding tissues and the capillary refill is less than 4 seconds.
HEAD
The clients head is normocephalic with smooth skull contour. There are no masses or nodules
present. Her hair is evenly distributed, and is thin, silky and resilient. No scalp lesions or flakings
are noted. Facial features are symmetrical. Symmetry of the clients facial movements is not
determined due to her unresponsiveness.
EYES
The clients eyebrows are evenly distributed and are symmetrically aligned. Her eyelashes are
also equally distributed and are curled slightly outwards. Eyelids close symmetrically and skin

A Case Study on Non ST Elevation Myocardial Infarction

intact with no redness, swelling, flaking, discharge, or discoloration noted. Infrequent blinking of
the client is observed. Bulbar conjunctiva is transparent while palpebral conjunctiva is shiny,
smooth, and pale in color. Sclera is white with no lesions present. Present cataract in her left eye
is noted. There is no edema or tenderness over clients lacrimal glands. Cornea is transparent and
smooth. Peripheral vision, extraocular movement and visual acuity are not assessed due to
clients condition.
EARS
The auricle is uniform in color with the skin and noted without deformity, lesions, scaling, or
tenderness. Auricles are mobile, firm and are symmetrically aligned with the outer canthus of the
eye. Bilateral auditory canals contain dry cerumen, grayish-tan in color. Hearing acuity is not
assessed to due to clients unresponsiveness.
NOSE
The external structure is symmetric and is uniform in color. Presence of Nasogastric tube is
noted. Nasal septum is in the midline. Frontal and maxillary sinuses are not tender. No epistaxis.
PHARYNX
The clients pharynx is not examined due to her inability to open her mouth.
MOUTH
The patients Lips are pale pinkish in color, cracked and symmetrical. Have no dentures already.
Poor swallowing and gag reflex was noted. Other parts of the patients mouth werent able to
assess due to patient condition.
NECK
Neck muscles are equal in size. Client has limited range of motion (ROM) and unequal muscle
strength. Her movements are noted to be stiff due to his prolonged physical immobility. Lymph
nodes are not palpable. Trachea is in midline of the neck, weak pulsations with thrusting feature
on both carotid arteries. His jugular veins are not palpable. No JVD. Thyroid glands are not
palpable.
CHEST AND LUNGS
The patients chest is symmetrical. No retractions. Difficulty in breathing was noted. Exerts
effort and has slightly irregular breathing pattern. (+) crackles @ left lung.
HEART
The patient has adynamic precordium. Irregular rate is noted with regular rhythm.

ABDOMEN
The patients skin integrity is uniform in color. The abdomen is flat, symmetric and there is no
evidence of enlargement of spleen or liver. No organomeagaly or masses. Normoactive sounds
were heard upon auscultation.

A Case Study on Non ST Elevation Myocardial Infarction

GENITO-URINARY SYSTEM
Client has a present IFC- intrafoley catheter. And has a grade 3 bed sore at sacral area. Genitourinary Reproductive assessment is limited due to clients condition
BACK AND EXTREMITIES
Atrophy in clients muscle size due to prolonged physical immobility. Muscle strength is
unequal. Muscle tone is noted to be atonic. No tenderness and swelling present. There is limited
range of motion in one or more joints. Upper extremities and lower extremities have limited
ROM.
Clinical Findings, Significant Signs and Symptoms
General
: Not in respiratory distress
Skin
: Senile skin turgor, afebrile to touch
HEENT
: Anicteric sclera, pink palpebral conjuctive, (-) CLAD
Chest / Lungs : Symmetrical Chest expansion, no retraction, (+) crackles @ Left lung tidy
Heart
: Adynamic precordium, irregular rate, regular rhythm.
Abdomen
: Flat, normoactive bowel sounds, non-tender
Extremities : Full and equal puses, no edema, no cyanosis, (+) scaling of bilateral upper and
lower extremities.

A Case Study on Non ST Elevation Myocardial Infarction

A. ANATOMY & PHYSIOLOGY

SIZE, FORM AND LOCATION OF THE HEART
The adult heart is shaped like a blunt cone and is approximately the size of a closed fist. It is
larger in physically active adults than in less active but otherwise healthy adults, and it generally
decreases in size after approximately age 65, especially in those who are not physically active.
APEX- blunt, rounded point of the cone
BASE- larger, flat part at the opposite end of the cone
The heart is located at in the thoracic cavity between the two pleural cavities, which surround the
lungs. The heart lies obliquely in the mediastinum, with its base directed posteriorly and slightly
superiorly and the apex directed anteriorly and slightly inferiorly. The apex is also directed to the
left so that approximately two-thirds of the hearts mass lies to the left of the midline of the
sternum. The base of the heart is located deep to the sternum and extends to the level of the
second intercostal space. The apex is located deep to the left fifth intercostal space,
approximately 7-9cm. to the left of the sternum near the midclavicular line, which is
perpendicular line that extends down from the middle of the clavicle.
ANATOMY OF THE HEART
The heart is the muscular organ of the circulatory system that constantly pumps blood throughout
the body. Approximately the size of a clenched fist, the heart is composed of cardiac muscle
tissue that is very strong and able to contract and relax rhythmically throughout a person's
lifetime.
The heart has four separate compartments or chambers:
ATRIUM - upper chamber on each side of the heart
-receives and collects the blood coming to the heart.
-atrium then delivers blood to the ventricle
VENTRICLE- powerful lower chamber
-pumps blood away from the heart through powerful, rhythmic
contractions.
The human heart is actually two pumps in one. The right side receives oxygen-poor blood from
the various regions of the body and delivers it to the lungs. In the lungs, oxygen is absorbed in

A Case Study on Non ST Elevation Myocardial Infarction

the blood. The left side of the heart receives the oxygen-rich blood from the lungs and delivers it
to the rest of the body.
a) Coronary Arteries- network of blood vessels that carry oxygen- and nutrient-rich blood to
the cardiac muscle tissue.

The blood leaving the left ventricle exits through the aorta, the bodys main artery. Two coronary
arteries, referred to as the "left" and "right" coronary arteries, emerge from the beginning of the
aorta, near the top of the heart.
left main coronary- initial segment of the left coronary artery
-approximately the width of a soda straw and is less
than an inch long.
-branches into two slightly smaller arteries: the left
anterior descending coronary artery and the left
circumflex coronary artery.
The left anterior descending coronary artery is embedded in the surface of the front side of the
heart.
The left circumflex coronary artery circles around the left side of the heart and is embedded in
the surface of the back of the heart.
Just like branches on a tree, the coronary arteries branch into progressively smaller vessels. The
larger vessels travel along the surface of the heart; however, the smaller branches penetrate the
heart muscle. The smallest branches, called capillaries, are so narrow that the red blood cells
must travel in single file. In the capillaries, the red blood cells provide oxygen and nutrients to
the cardiac muscle tissue and bond with carbon dioxide and other metabolic waste products,
taking them away from the heart for disposal through the lungs, kidneys and liver.
When cholesterol plaque accumulates to the point of blocking the flow of blood through a
coronary artery, the cardiac muscle tissue fed by the coronary artery beyond the point of the
blockage is deprived of oxygen and nutrients. This area of cardiac muscle tissue ceases to
function properly. The condition when a coronary artery becomes blocked causing damage to the
cardiac muscle tissue it serves is called a myocardial infarction or heart attack.
b) Superior Vena Cava- one of the two main veins bringing de-oxygenated blood from the
body to the heart. Veins from the head and upper body feed into the superior vena cava,
which empties into the right atrium of the heart.
c) Inferior Vena Cava- one of the two main veins bringing de-oxygenated blood from the
body to the heart. Veins from the legs and lower torso feed into the inferior vena cava,
which empties into the right atrium of the heart.
d) Aorta- largest single blood vessel in the body. It is approximately the diameter of your
thumb. This vessel carries oxygen-rich blood from the left ventricle to the various parts of
the body.
e) Pulmonary Artery- vessel transporting de-oxygenated blood from the right ventricle to
the lungs. A common misconception is that all arteries carry oxygen-rich blood. It is more
appropriate to classify arteries as vessels carrying blood away from the heart.

A Case Study on Non ST Elevation Myocardial Infarction

f) Pulmonary Vein- vessel transporting oxygen-rich blood from the lungs to the left atrium.
A common misconception is that all veins carry de-oxygenated blood. It is more
appropriate to classify veins as vessels carrying blood to the heart.
g) Right Atrium- receives de-oxygenated blood from the body through the superior vena
cava (head and upper body) and inferior vena cava (legs and lower torso).
h) Right Ventricle- receives de-oxygenated blood as the right atrium contracts.
i) Left Atrium- receives oxygenated blood from the lungs through the pulmonary vein.
j) Left Ventricle- receives oxygenated blood as the left atrium contracts.
k) Papillary Muscles- attach to the lower portion of the interior wall of the ventricles. They
connect to the chordae tendineae, which attach to the tricuspid valve in the right ventricle
and the mitral valve in the left ventricle. The contraction of the papillary muscles opens
these valves. When the papillary muscles relax, the valves close.
l) Chordae Tendineae- are tendons linking the papillary muscles to the tricuspid valve in the
right ventricle and the mitral valve in the left ventricle. As the papillary muscles contract
and relax, the chordae tendineae transmit the resulting increase and decrease in tension to
the respective valves, causing them to open and close. The chordae tendineae are stringlike in appearance and are sometimes referred to as "heart strings."
m) Tricuspid Valve- separates the right atrium from the right ventricle. It opens to allow the
de-oxygenated blood collected in the right atrium to flow into the right ventricle. It closes
as the right ventricle contracts, preventing blood from returning to the right atrium;
thereby, forcing it to exit through the pulmonary valve into the pulmonary artery.
n) Mitral Value- the left atrium from the left ventricle. It opens to allow the oxygenated
blood collected in the left atrium to flow into the left ventricle. It closes as the left
ventricle contracts, preventing blood from returning to the left atrium; thereby, forcing it
to exit through the aortic valve into the aorta.
o) Pulmonary Valve- separates the right ventricle from the pulmonary artery. As the
ventricles contract, it opens to allow the de-oxygenated blood collected in the right
ventricle to flow to the lungs. It closes as the ventricles relax, preventing blood from
returning to the heart.
p) Aortic Valve- separates the left ventricle from the aorta. As the ventricles contract, it
opens to allow the oxygenated blood collected in the left ventricle to flow throughout the
body. It closes as the ventricles relax, preventing blood from returning to the heart.
q) Heart Wall
The heart wall is divided into three layers:

Epicardium- describes the outer layer of heart tissue (from Greek; epi- outer, cardium
heart). When considered as a part of the pericardium, it is the inner layer, or visceral
pericardium.Its largest constituent is connective tissue and functions as a protective layer.
The visceral pericardium apparently produces the pericardial fluid, which lubricates
motion between the inner and outer layers of the pericardium.During ventricular
contraction, the wave of depolarization moves from endocardial to epicardial surface.

Myocardium- muscular middle layer of the wall of the heart. Composed of spontaneously
contracting cardiac muscle fibers which allow the heart to contract. Stimulates heart

A Case Study on Non ST Elevation Myocardial Infarction

contractions to pump blood from the ventricles and relaxes the heart to allow the artria to
receive blood. The walls of the heart are largely made from myocardium, which is a
special kind of muscle tissue. This muscle is so constructed that it is able to perform the
60 to 70 contractions which the healthy adult human heart undergoes every minute. It is
the muscular tissue responsible for the contraction of the heart

B.

Endocardium- innermost layer of tissue that lines the chambers of the heart. Its cells are
embryologically and biologically similar to the endothelial cells that line blood vessels.

OVERVIEW OF THE DISEASE

Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart
attack, is the interruption of blood supply to part of the heart, causing some heart cells to die.
This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of
a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (fatty acids) and
white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia
(restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time,
can cause damage or death (infarction) of heart muscle tissue (myocardium).

Classification
There are two basic types of acute myocardial infarction:

Transmural: associated with atherosclerosis involving major coronary artery. It can be

subclassified into anterior, posterior, or inferior. Transmural infarcts extend through the
whole thickness of the heart muscle and are usually a result of complete occlusion of the
area's blood supply.
Subendocardial: involves small area in the subendocardial wall of the left ventricle,
ventricular septum, or papillary muscles. Subendocardial infarcts are thought to be a
result of locally decreased blood supply, possibly from a narrowing of the coronary
arteries. The subendocardial area is farthest from the heart's blood supply and is more
susceptible to this type of pathology.

Clinically, myocardial infarction is further subclassified into ST elevation MI versus non ST

elevation MI based on ECG changes.

Signs and Symptoms

A Case Study on Non ST Elevation Myocardial Infarction

Not all people who have heart attacks experience the same symptoms or experience them to the
same degree. Many heart attacks aren't as dramatic as the ones you've seen on TV. Some people
have no symptoms at all. Still, the more signs and symptoms you have, the greater the likelihood
that you may be having a heart attack.

Common heart attack symptoms include:

Pressure, a feeling of fullness or a squeezing pain in the center of your chest that lasts for
more than a few minutes
Pain extending beyond your chest to your shoulder, arm, back, or even to your teeth and
jaw
Increasing episodes of chest pain
Prolonged pain in the upper abdomen
Shortness of breath
Sweating
Impending sense of doom
Fainting
Nausea and vomiting

Additional, or different, heart attack symptoms in women may include:

Abdominal pain or heartburn
Clammy skin
Lightheadedness or dizziness
Unusual or unexplained fatigue
Causes

A heart attack occurs when one or more of the arteries supplying your heart with oxygen-rich
blood (coronary arteries) become blocked. Over time, a coronary artery can become narrowed
from the buildup of cholesterol. This buildup collectively known as plaques in arteries
throughout the body is called atherosclerosis.

During a heart attack, one of these plaques can rupture and a blood clot forms on the site of the
rupture. If the clot is large enough, it can block the flow of blood through the artery. When your
coronary arteries have narrowed due to atherosclerosis, the condition is known as coronary artery
disease. Coronary artery disease is the major underlying cause of heart attacks.

A Case Study on Non ST Elevation Myocardial Infarction

An uncommon cause of a heart attack is a spasm of a coronary artery that shuts down blood flow
to part of the heart muscle.

A heart attack is the end of a process that typically evolves over several hours. With each passing
minute, more heart tissue is deprived of blood and deteriorates or dies. However, if blood flow
can be restored in time, damage to the heart can be limited or prevented.

Risk Factors
Certain factors contribute to the unwanted buildup of fatty deposits (atherosclerosis) that narrow
arteries throughout your body, including arteries to your heart. You can improve or eliminate
many of these risk factors to reduce your chances of having a first or second heart attack.
Heart attack risk factors include:
Age. Men who are 45 or older and women who are 55 or older are more likely to have a
heart attack than younger men and women.
Tobacco. Smoking and long-term exposure to secondhand smoke damage the interior
walls of arteries including arteries to your heart allowing deposits of cholesterol
and other substances to collect and slow blood flow. Smoking also increases the risk of
deadly blood clots forming and causing a heart attack.
Diabetes. Diabetes is the inability of your body to adequately produce or respond to
insulin properly. Insulin, a hormone secreted by your pancreas, allows your body to use
glucose, which is a form of sugar from foods. Diabetes can occur in childhood, but it
appears more often in middle age and among overweight people. Diabetes greatly
increases your risk of a heart attack.
High blood pressure. Over time, high blood pressure can damage arteries that feed your
heart by accelerating atherosclerosis. The risk of high blood pressure increases as you
age, but the main culprits for most people are eating a diet too high in salt and being
overweight. High blood pressure can also be an inherited problem.
High blood cholesterol or triglyceride levels. Cholesterol is a major part of the deposits
that can narrow arteries throughout your body, including those that supply your heart. A
high level of the wrong kind of cholesterol in your blood increases your risk of a heart
attack. Low-density lipoprotein (LDL) cholesterol (the "bad" cholesterol) is most likely
to narrow arteries. A high LDL level is undesirable and is often a result of a diet high in
saturated fats and cholesterol. A high level of triglycerides, a type of blood fat related to
your diet, also is undesirable. However, a high level of high-density lipoprotein (HDL)
cholesterol (the "good" cholesterol), which helps the body clean up excess cholesterol, is
desirable and lowers your risk of heart attack.

A Case Study on Non ST Elevation Myocardial Infarction

Family history of heart attack. If your siblings, parents or grandparents have had heart
attacks, you may be at risk, too. Your family may have a genetic condition that raises
unwanted blood cholesterol levels. High blood pressure also can run in families.
Lack of physical activity. An inactive lifestyle contributes to high blood cholesterol levels
and obesity. People who get regular aerobic exercise have better cardiovascular fitness,
which decreases their overall risk of heart attack. Exercise is also beneficial in lowering
high blood pressure.
Obesity. Obese people have a high proportion of body fat (a body mass index of 30 or
higher). Obesity raises the risk of heart disease because it's associated with high blood
cholesterol levels, high blood pressure and diabetes.
Stress. You may respond to stress in ways that can increase your risk of a heart attack. If
you're under stress, you may overeat or smoke from nervous tension. Too much stress, as
well as anger, can also raise your blood pressure.
Illegal drug use. Using stimulant drugs, such as cocaine or amphetamines, can trigger a
spasm of your heart muscle that causes a heart attack.

Test and Diagnosis

Electrocardiogram (ECG). This is the first test done to diagnose a heart attack. It's often
done while you are being asked questions about your symptoms. This test records the
electrical activity of your heart via electrodes attached to your skin. Impulses are
recorded as "waves" displayed on a monitor or printed on paper. Because injured heart
muscle doesn't conduct electrical impulses normally, the ECG may show that a heart
attack has occurred or is in progress.
Blood tests. Certain heart enzymes slowly leak out into your blood if your heart has been
damaged by a heart attack. Emergency room doctors will take samples of your blood to
test for the presence of these enzymes.
Additional Tests
Chest X-ray. An X-ray image of your chest allows your doctor to check the size and
shape of your heart and its blood vessels.
Echocardiogram. This test uses sound waves to produce an image of your heart. During
an echocardiogram, sound waves are directed at your heart from a transducer, a wand-like
device, held on your chest. The sound waves bounce off your heart and are reflected back
through your chest wall and processed electronically to provide video images of your
heart. An echocardiogram can help identify whether an area of your heart has been
damaged by a heart attack and isn't pumping normally or at peak capacity.
Nuclear scan. This test helps identify blood flow problems to your heart. Small amounts
of radioactive material are injected into your bloodstream. Special cameras can detect the
radioactive material as it flows through your heart and lungs. Areas of reduced blood
flow to the heart muscle through which less of the radioactive material flows
appear as dark spots on the scan.
Coronary catheterization (angiogram). This test can show if your coronary arteries are
narrowed or blocked. A liquid dye is injected into the arteries of your heart through a
long, thin tube (catheter) that's fed through an artery, usually in your leg, to the arteries in
your heart. As the dye fills your arteries, the arteries become visible on X-ray, revealing

A Case Study on Non ST Elevation Myocardial Infarction

areas of blockage. Additionally, while the catheter is in position, your doctor may treat
the blockage by performing an angioplasty, also known as coronary artery balloon
dilation, balloon angioplasty and percutaneous coronary intervention. Angioplasty uses
tiny balloons threaded through a blood vessel and into a coronary artery to widen the
blocked area. In most cases, a mesh tube (stent) is also placed inside the artery to hold it
open more widely and prevent re-narrowing in the future.
Exercise stress test. In the days or weeks following your heart attack, you may also
undergo a stress test. Stress tests measure how your heart and blood vessels respond to
exertion. You may walk on a treadmill or pedal a stationary bike while attached to an
ECG machine. Or you may receive a drug intravenously that stimulates your heart similar
to exercise.
Stress tests help doctors decide the best long-term treatment for you. If your doctor also
wants to see images of your heart while you're exercising, he or she may order a nuclear
stress test, which is similar to an exercise stress test, but uses an injected dye and special
imaging techniques.
Cardiac computerized tomography (CT) or magnetic resonance imaging (MRI). These
tests can be used to diagnose heart problems, including the extent of damage from heart
attacks. In a cardiac CT scan, you lie on a table inside a doughnut-shaped machine. An Xray tube inside the machine rotates around your body and collects images of your heart
and chest. In a cardiac MRI, you lie on a table inside a long tube-like machine that
produces a magnetic field. The magnetic field aligns atomic particles in some of your
cells. When radio waves are broadcast toward these aligned particles, they produce
signals that vary according to the type of tissue they are. The signals create images of
your heart.

Complications
Heart attack complications are often related to the damage done to the heart during a heart attack.
This damage can lead to the following conditions:
Abnormal heart rhythms (arrhythmias). If your heart muscle is damaged from a heart
attack, electrical "short circuits" can develop resulting in abnormal heart rhythms, some
of which can be serious, even fatal.
Heart failure. The amount of damaged tissue in your heart may be so great that the
remaining heart muscle can't do an adequate job of pumping blood out of your heart. This
decreases blood flow to tissues and organs throughout your body and may produce
shortness of breath, fatigue, and swelling in your ankles and feet. Heart failure may be a
temporary problem that goes away after your heart, which has been stunned by a heart
attack, recovers over a few days to weeks. However, it can also be a chronic condition
resulting from extensive and permanent damage to your heart following your heart attack.
Heart rupture. Areas of heart muscle weakened by a heart attack can rupture, leaving a
hole in part of the heart. This rupture is often fatal.
Valve problems. Heart valves damaged during a heart attack may develop severe, lifethreatening leakage problems.
Treatment

A Case Study on Non ST Elevation Myocardial Infarction

Medications
With each passing minute after a heart attack, more heart tissue loses oxygen and deteriorates or
dies. The main way to prevent heart damage is to restore blood flow quickly.
Medications given to treat a heart attack include:
Aspirin. You may be given aspirin by emergency medical personnel soon after they arrive
or as soon as you get to the hospital. Aspirin reduces blood clotting, thus helping
maintain blood flow through a narrowed artery.
Thrombolytics. These drugs, also called clotbusters, help dissolve a blood clot that's
blocking blood flow to your heart. The earlier you receive a thrombolytic drug following
a heart attack, the greater the chance you will survive and lessen the damage to your
heart.
Superaspirins. Doctors in the emergency room may give you other drugs that are
somewhat similar to aspirin to help prevent new clots from forming. These include
medications such as clopidogrel (Plavix) and others called platelet IIb/IIIa receptor
blockers.
Other blood-thinning medications. You'll likely be given other medications, such as
heparin, to make your blood less "sticky" and less likely to form more dangerous clots.
Heparin is given intravenously or by an injection under your skin and is usually used
during the first few days after a heart attack.
Pain relievers. If your chest pain or associated pain is great, you may receive a pain
reliever, such as morphine, to reduce your discomfort.
Nitroglycerin. This medication, used to treat chest pain (angina), temporarily opens
arterial blood vessels, improving blood flow to and from your heart.
Beta blockers. These medications help relax your heart muscle, slow your heartbeat and
decrease blood pressure making your heart's job easier. Beta blockers can limit the
amount of heart muscle damage and prevent future heart attacks.
Cholesterol-lowering medications. Examples include statins, niacin, fibrates and bile acid
sequestrants. These drugs help lower levels of unwanted blood cholesterol and may be
helpful if given soon after a heart attack to improve survival.
Surgical and Other Procedures
Coronary angioplasty and stenting. Emergency angioplasty opens blocked coronary
arteries, letting blood flow more freely to your heart. Doctors insert a long, thin tube
(catheter) that's passed through an artery, usually in your leg, to a blocked artery in your
heart. This catheter is equipped with a special balloon tip. Once in position, the balloon
tip is briefly inflated to open up a blocked coronary artery. At the same time, a metal
mesh stent may be inserted into the artery to keep it open long term, restoring blood flow
to the heart. Depending on your condition, your doctor may opt to place a stent coated
with a slow-releasing medication to help keep your artery open.
Coronary angioplasty is done at the same time as a coronary catheterization (angiogram),
a procedure that doctors do first to locate narrowed arteries to the heart. When getting an
angioplasty for heart attack treatment, the sooner the better to limit the damage to your
heart.

A Case Study on Non ST Elevation Myocardial Infarction

Coronary artery bypass surgery. In rare cases, doctors may perform emergency bypass
surgery at the time of a heart attack. Usually, your doctor may suggest that you have
bypass surgery after your heart has had time to recover from your heart attack. Bypass
surgery involves sewing veins or arteries in place at a site beyond a blocked or narrowed
coronary artery (bypassing the narrowed section), restoring blood flow to the heart.
Once blood flow to your heart is restored and your condition is stable following your
heart attack, you may be hospitalized for observation. Visitors are usually limited to
family members and close friends.

Prognosis
The prognosis for patients with myocardial infarction varies greatly, depending on the patient,
the condition itself and the given treatment. Using simple variables which are immediately
available in the emergency room, patients with a higher risk of adverse outcome can be
identified. For example, one study found that 0.4% of patients with a low risk profile had died
after 90 days, whereas the mortality rate in high risk patients was 21.1%.
Prevention
It's never too late to take steps to prevent a heart attack - even if you've already had one. Taking
medications can reduce your risk of a second heart attack and help your damaged heart function
better. Lifestyle factors also play a critical role in heart attack prevention and recovery.
Lifestyle Changes
In addition to medications, the same lifestyle changes that can help you recover from a heart
attack can also help prevent future heart attacks. These include:
Smoking cessation
Controlling certain conditions, such as high blood pressure, high cholesterol and
diabetes
Staying physically active
Eating healthy foods
Maintaining a healthy weight
Reducing and managing stress

Pathophysiology of Non - ST Elevation Myocardial Infarction

Coronary arteries supply the heart muscles with oxygen-rich blood
Deposition of cholesterol

A Case Study on Non ST Elevation Myocardial Infarction

Formation of plaque

Restricted blood flow due to atherosclerotic plaque in the arterial wall

If part of this plaque ruptures, platelets will come to the area

Blood clots or thrombus will be formed and will narrow the vessel further

When the thrombus breaks, it may cause embolism which may obstruct the blood
flow into the artery (Note: NSTEMI: The artery is partly occluded)

Myocardial cells become ischemic

Heart muscle will be damaged (Note: In a NSTEMI, the blood clot only partly
occludes the artery, and as a result only a portion of the heart muscle being
supplied by the affected artery dies.)

Symptom experiences (SOB, tightness in the chest, intense prolonged chest pain,
nausea, fainting and intense sweating, pain in the left shoulder, arm jaw and back)

Prioritization of the Problems

Ineffective airway clearance r/t retained
secretions 2 pneumonia in elderly
Risk for aspiration pneumonia r/t

According to Maslows hierarchy of

needs, we need first to solve the
physiologic needs like breathing,
human nutrition, water, homeostasis,

A Case Study on Non ST Elevation Myocardial Infarction

presence of NGT.

Impaired Skin Integrity r/t pressure

ulcer
secondary
to
prolonged
immobility and unrelieved pressure.
Ineffective cardiopulmonary tissue
perfusion r/t reduced coronary blood
flow from coronary thrombus and
atherosclerotic plaque
Risk for infection r/t pressure ulcer
secondary to prolonged immobility as
evidenced by bed sore on the sacral
area

sleep, excretion and sexual activity

before we can proceed to next level. We
need to clear first the airway for the
patient have an adequate supply of
oxygen needed.
Next to physiologic needs is safety and
security. We need to help the patient to
have safe physical environment to be
free from the threat of physical and
emotional harm.

A Case Study on Non ST Elevation Myocardial Infarction

Actual
Diagnoses

A Case Study on Non ST Elevation Myocardial Infarction

Potential
Diagnoses

Discharge Planning
Diet

With NGT: Advice the patient and the support system to comply with the diet regimen of
1200 kcal/day with liberal salt, 3EF 400cc, peptamin scoops in 200 cc water.
If the physician ordered to remove the NGT:
Determine the clients ability to chew, swallow and taste food. Evaluate teeth and
gums for poor oral health and note denture feet, as indicated. All factors that can
affect ingestion and/or digestion of nutrients.
Consult a nutritionist for appropriate diet regimen

Medications

A Case Study on Non ST Elevation Myocardial Infarction

Advise the client to continue the medication as prescribed by the physician.

Emphasize compliance and strict adherence to dosage and the time of intake of the
medicines to attain the desired therapeutic effects.
Make sure that the client and the support system understands the medication regimen, can
read the instructions, can open the container, and is prepared to adjust to postural
hypotensive effects of antihypertensive medications (change position slowly, use
supportive devices)
Explain the consequences of not strictly adhering to the drug regimen.
Instruct the patient not to alter doses of medications and emphasize the importance of
continuous medication.
Report immediately for any unusual symptoms.

Environment
Instruct the patient to maintain a clean environment conducive to health for immediate
recovery and maintenance of health.
Health teachings
Teach the patient and family how to measure blood pressure.
Advice the patient and support system to monitor vital signs.
Instruct the patient to consult first the physician or physical therapist to learn which
exercises are appropriate and how to do them.
Educate the patient range-of-motion exercises to help reduce stiffness and maintain or
increase proper joint movement and flexibility as well as improve overall circulation.

A Case Study on Non ST Elevation Myocardial Infarction

Drug Study

Reference and Bibliography

Books
Doenges, Marilyn E. , Moorhouse, Mary Frances and Murr, Alice C.. Nurse's Pocket Guide
11th edition: 2008
Karch, Amy M.. 2010 lippincott's nursing drug guide: 2010
Berman, Audrey, Snyder, Shirlee, kozier, Barbara, glenora erb. kozier & Erbs Fundamentals
of Nursing 8th edition: 2008

A Case Study on Non ST Elevation Myocardial Infarction

Marieb, Elaine N.. Essentials of Human Anatomy and Physiology seventh edition: 2004
Internet
http://www.medscape.com
http://www.discovernursing.com/
http://www.amsn.org/cgi-bin/WebObjects/AMSNMain.woa
http://books.google.com/books?
id=4SOA3rg5DK0C&pg=PA57&lpg=PA57&dq=breakthrough+seizure&as_brr=3&ie=ISO8859-1&output=html
http://www.supportiveoncology.net/journal/articles/0401009.pdf
http://www.medicinenet.com/hyperthermia/article.htm

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