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CASE STUDY
MYOCARDIAL INFARCTION
Presented to:
PRESENTED BY:
Cuevas, Deanne M.
Group 5
BSN IV-B
2010
CHAPTER I
A. OBJECTIVES
After providing care to the client and conducting a careful and thorough study
of the client’s condition, the student will be able to gain knowledge, develop skills
and enhance attitude in rendering quality nursing care in actual situation to the
patient with diagnosis of MYOCARDIAL INFARCTION.
The world today is far different from what our ancestors were used to. Today,
several innovations and technology emerges creating a new and modern culture far
beyond what we know before. This change is accompanied by changes in lifestyle and
living of people thus, making us more susceptible to illness brought by our lifestyle. One
of these diseases is Myocardial Infarction.
Furthermore, the term myocardial infarction has major psychological and legal
implications for the individual and society. It is an indicator of one of the leading health
problems in the world, and it is an outcome measure in clinical trials and observational
studies. With these perspectives, myocardial infarction may be defined from a number of
different clinical, electrocardiographic, biochemical, imaging, and pathological
characteristics.
CHAPTER II
The term "myocardial infarction" focuses on the heart muscle, which is called the
myocardium, and the changes that occur in it due to the sudden deprivation of
circulating blood. This is usually caused by arteriosclerosis with narrowing of the
coronary arteries, the culminating event being a thrombosis (clot). The main change is
death (necrosis) of myocardial tissue.
The word "infarction" comes from the Latin "infarcire" meaning "to plug up or
cram." It refers to the clogging of the artery, which is frequently initiated by cholesterol
piling up on the inner wall of the blood vessels that distribute blood to the heart muscle.
The following prevalence estimates are for people age 18 and older from a survey in
2005:
• Among whites only, 12.0% have heart disease, 6.6% have CHD, 21.0% have
hypertension and 2.3% have had a stroke.
• Among blacks, 10.2% have heart disease, 6.2% have CHD, 31.2% have
hypertension and 3.4% have had a stroke.
• Among Hispanics or Latinos, 8.3% have heart disease, 5.9% have CHD, 20.3%
have hypertension and 2.2% have had a stroke.
• Among Asians, 6.7% have heart disease, 3.8% have CHD, 19.4% have
hypertension and 2.0% have had a stroke.
• Among Native Hawaiians or other Pacific Islanders, 22.4% have hypertension
(other prevalence estimates considered unreliable).
Other risk factors for STEMI mirror those for coronary artery disease (CAD) and
include diabetes mellitus, cerebrovascular disease manifested by stroke or transient
ischemic attack, peripheral arterial disease, aortic atherosclerosis and aneurysm, age
(male ≥45 years old, female ≥55 years old), family history of premature CAD (MI or
sudden death before age 55 in a first-degree male relative or before age 65 in a first-
degree female relative), tobacco abuse, hypertension and hyperlipidemia.
The mortality among patients who suffer STEMI has progressively declined in
recent years. From 1975 to 1997, one observational study reported that the in-hospital
mortality decreased from 24% to 14%. In the Global Registry of Acute Coronary Events
(GRACE), a multinational cohort study that includes 16,814 patients with STEMI were
enrolled and followed up in 113 hospitals in 14 countries between 1999 and 2006, in-
hospital mortality declined from 8.4% in 1999 to 4.6% in 2005.
The reason for this decline in mortality is likely multifactorial and includes, but is
certainly not limited to, decline in symptom onset-to-presentation time, more widespread
use of primary PCI, improvements in time to reperfusion (door-to-needle and door-to-
balloon times and improved medical therapy, including increases in the use of evidence-
based therapies such as aspirin beta blockers, clopidogrel, statins and angiotension
converting enzyme inhibitors or angiotensin receptor blockers.
Frequency
United States
International
Mortality/Morbidity
One third of patients who experience STEMI die within 24 hours of the onset of
ischemia, and many of the survivors experience significant morbidity. For many
patients, the first manifestation of coronary artery disease is sudden death likely from
malignant ventricular dysrhythmia.
Sex
A male predilection exists in persons aged 40-70 years. Evidence exists that
women more often have MIs without atypical symptoms. The atypical presentation in
women might explain the sometimes delayed diagnosis of MIs in women.
In persons older than 70 years, no sex predilection exists.
Age
CLINICAL
History
The history is critical in making the diagnosis of MI and sometimes may provide
the only clues that lead to the diagnosis in the initial phases of the patient presentation.
Physical Examination
• Patients with ongoing symptoms usually lie quietly in bed and appear pale and
diaphoretic.
• Hypertension may precipitate MI, or it may reflect elevated catecholamine levels
due to anxiety, pain, or exogenous sympathomimetics.
• Hypotension may indicate ventricular dysfunction due to ischemia. Hypotension
in the setting of MI usually indicates a large infarct secondary to either decreased
global cardiac contractility or a right ventricular infarct.
• Acute valvular dysfunction may be present. Valvular dysfunction usually results
from infarction that involves the papillary muscle. Mitral regurgitation due to
papillary muscle ischemia or necrosis may be present.
• Rales may represent congestive heart failure.
• Neck vein distention may represent pump failure. With right ventricular failure,
cannon jugular venous a waves may be noted.
• Third heart sound (S3) may be present.
• A fourth heart sound is a common finding in patients with poor ventricular
compliance that is due to preexisting heart disease or hypertension.
• Dysrhythmias may present as an irregular heartbeat or pulse.
• Low-grade fever is not uncommon.
Causes
Killip Classification
The study was a case series with unblinded, unobjective outcomes, not adjusted
for confounding factors, nor validated in an independent set of patients. The setting was
the coronary care unit of a university hospital in the USA.
250 patients were included in the study (aged 28 to 94; mean 64, 72% male) with
a myocardial infarction. Patients with a cardiac arrest prior to admission were excluded.
Conclusions
The numbers below were accurate in 1967. Nowadays, they have diminished by
30 to 50% in every class.
• Killip class I: 81/250 patients; 32% (27–38%). Mortality rate was found to be at
6%.
• Killip class II: 96/250 patients; 38% (32–44%). Mortality rate was found to be at
17%.
• Killip class III: 26/250 patients; 10% (6.6–14%). Mortality rate was found to be at
38%.
• Killip class IV: 47/250 patients; 19% (14–24%). Mortality rate was found to be at
81%.
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
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
heart’s 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.
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 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 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 body’s 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.
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.
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.
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 string-like 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
• 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.
Classification
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.
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 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.
• 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.
• 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.
• 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.
• 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.
• 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.
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:
• 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, life-threatening leakage problems.
Treatment
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.
• Pain relievers. If your chest pain or associated pain is great, you may receive a
pain reliever, such as morphine, to reduce your discomfort.
• 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.
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
A. GENERAL DATA
Age/Sex : 64 y/o
Occupation : none
Two months prior the admission the patient felt chest pain. He ignored the pain
thinking that it will be gone later on. One week prior to admission, the patient felt chest
pain that is severe. The pain scale is 8. It is now radiating to his left arm. He also
experienced difficulty of breathing. Thus, his family decided to bring him to the hospital
in Sariaya, Quezon. The doctor assessed the patient and was referred to the Quezon
Medical Center.
C. FAMILY HEALTH HISTORY
E. PSYCHOSOCIAL HISTORY
Lorenzo Mendoza is fond of eating fatty foods, drinking alcohol and smoking.
Due to his age he also found exercising difficult and very tiring.
The patient’s daughter said his father doesn’t have a regular bowel movement.
He seldom defecates. Whenever his daughter offers him fruits to help him defecate
regularly, he’s just eating a small amount of those and just enjoys himself doing vices
and watching television shows.
During an ordinary day he usually hangs out with his friends, do some chat and
later that day, drinks alcohol or smokes. When he felt that there is something wrong in
his body and there is already pain in his chest, his routine changed and decided to
eliminate his vices eventually.
F. PHYSICAL EXAMINATION
I. General Survey
Skin
• The skin is pale and slightly warm to touch. He has a fair skin turgor.
Hair
• The patient has evenly distributed black and white and thick hair.
Nails
• The nails are pale with capillary refill of 2-3 seconds. It has convex
curvature and with hard texture. It has intact epidermis. He has long and
uncut nails.
IV. HEENT
Head
Eyes
• Eyebrows are evenly distributed, symmetrically aligned and with good eye
movement.
• The patient has slightly pinkish conjuctiva. No edema and redness over
• The pupils are equally reactive to light accommodation and corneal reflex
Ears
• The auricle’s color is same as facial skin with symmetrical in size and
shape. It is inline to the outer canthus of the eyes and recoils after it is
folded.
• Cerumen noted on both ears.
Nose
discharges noted.
Mouth
• The patient has slightly pale lips which is soft and dry texture.
V. Neck
• The chest is symmetric with skin intact and has uniform temperature.
• There is clear breath sounds heard on both lung fields upon auscultation.
VII. Heart
• The patient has slightly normal rhythm and heart rate is within the normal
range.
VIII. Abdomen
• The patient has soft abdomen upon palpation with no scars noted.
• The patient has limited range of motion. Large blister noted at left foot.
Dra. Luce as his admitting physician ordered for TPR monitoring every shift. He
was hooked with IVF of PNSS 1L x KVO. He was also ordered to have diet as tolerated.
The following medications were also ordered: Tramadol 50 mg amp IVP q8 PRN for
chest pain and Captopril 250mg 1 tab SL q6 if BP is 140/90mmHG. Exams like ECG,
CK-MB, and Prothrombin time were also instructed to be done.
On December 3, 2009 the doctor read the ECG result which revealed that there
is a poor R-wave progression V1-V3, lateral wall ischemia and LVA by voltage criteria.
On December 4, 2009 the result of CK-MB is 142 and was interpreted by Dra.
Luce. Same IVF was ordered.
On December 5, 2009 Clopidogrel 75mg 4 tabs now then OD, Clexane 0.4 SQ
BID, Imidapril 10mg 1 tab OD, Diazepam 5mg 1 tab BID and Aspilet 80mg 1 tab OD
were ordered.
On December 6, 2009 same IVF was ordered and also Tramadol was given due
to severe chest pain.
On December 8, 2009 his ECG result was followed up, if vital signs are normal
and there is no further complication, possible discharge for the next 2 days.