CASE ANALYSIS:

Myocardial Infarction
 LEARNING OBJECTIVES:
This case presentation should enable the students to:

 Discuss incidence of Myocardial Infarction

 Elaborate risk factors of Myocardial infarction
 Explain Pathophysiology of Myocardial Infarction
 Enlist the clinical features and complications of Myocardial Infarction
 Explain diagnostic procedures of Myocardial Infarction
 Describe collaborative management of Myocardial Infarction
 Gain adequate knowledge about MI and will be able to apply in the clinical setting for improvement
in quality care
INTRODUCTION
• Myocardial infarction (MI) (colloquially known as a heart attack) results from interruption of
myocardial blood flow and resultant ischemia and is a leading cause of death worldwide.

• MI is mainly due to underlying coronary artery disease. When the coronary artery is occluded,

the myocardium is deprived of oxygen. Prolonged deprivation of oxygen supply to the
myocardium can lead to myocardial cell death and necrosis.

• Myocardial infarction is the end result of either acute or chronic myocardial ischemia. Myocardial
ischemia differs slightly from myocardial hypoxia in that ischemia results in a stasis of waste
products of cellular metabolism in addition to a lack of oxygen delivery, leading to cellular
damage above and beyond that from hypoxemia.
• Myocardial infarction is a pathologic diagnosis and, depending on whether
it is acute or chronic, is characterized by loss of normal cardiac myocyte structure
(i.e., myocytolysis, coagulative necrosis, inflammatory cell infiltration, and fibrosis).
Myocardial infarction has a host of causes and is a leading cause of cardiovascular
disease and death in humans.
PATIENT DATA AND
BRIEF HISTORY
• A 66-year-old man sought medical care at the hospital due to severe
chest pain lasting for 24 hours. The patient was aware of being
hypertensive and was a smoker. Without any prior symptom, he started
to have severe chest pain and sought emergency medical care after about
24 hours, due to pain persistence.
• At physical examination he had a heart rate of 90 bpm and blood
pressure of 110/70 mmHg. Lung examination showed no alterations.
Heart assessment showed a systolic murmur in the lower left sternal
border and mitral area.
• The initial electrocardiogram showed HR of 100 bpm, sinus rhythm, 1st-
degree atrioventricular block (PR 240 ms), low-voltage QRS complexes
in the frontal plane, QRS complex electrical alternans and extensive
ongoing anterior wall infarction (QS V1 to V6, ST elevation in the same
leads and QS in the inferior wall, II, III and aVF)
 BRIEF
HISTORY
Client Profile:
- A 66-year-old man sought medical care at the hospital due to severe chest pain lasting for 24
hours. The patient was aware of being hypertensive and was a smoker. Without any prior
symptom, he started to have severe chest pain and sought emergency medical care after about 24
hours, due to pain persistence.
- Dull; ill looking
- Smoker ( 20 sticks per day, for 35 years)
- Alcoholic
Treatment and Medication:
- The patient is currently taking ACE Inhibitor Drugs to lower the blood pressure and reduces stress
of the heart.
Past Surgery:
- No significant history of surgery
Past Illness/ Hospitalization:
- The patient was hospitalized 2 months ago with the same complaints.
Drug Allergies:
- Not known
Developmental history
- Family member stated that the patient is hypertensive for 1 year and suffered chest pain 2 months ago.

Health perception/ Health Management Pattern:

- Upon arrival, the patient is dull and ill looking and showed a heart rate of 90bpm and a blood pressure of
110/70 mmHg
- ECG: low QRS voltage in the frontal plane, electrically inactive lower wall area and anterior myocardial
infarction with increased ST elevation, still with positive T waves, "hyperacute phase of myocardial
infaction"
Nutritional – Metabolic
• Height- 5’3
• Weight- 54kg.
• Usual eating pattern – mixed diet 2-3x a day
• Food allergy: Not known
Bowel and Bladder: Normal
Sleeping Pattern: Disturbed because of chest pain
Activity/ Exercise Pattern: The patient has no regular exercise
 ANATOMY
and
PATHOPHYSIOLOGY
ANATOMY OF THE HEART
 Functions of the heart:
• Managing blood supply. 
• Producing blood pressure. 
• Securing one-way blood flow. 
• Transmitting blood.
 Heart Structure and Functions
• Weight. Approximately the size of a person’s fist, the hollow, cone-
shaped heart weighs less than a pound.
• Mediastinum. Snugly enclosed within the inferior mediastinum, the medial
cavity of the thorax, the heart is flanked on each side by the lungs.
• Apex. It’s more pointed apex is directed toward the left hip and rests on
the diaphragm, approximately at the level of the fifth intercostal space.
 Cont.
• Base. Its broad posterosuperior aspect, or base, from which the great vessels
of the body emerge, points toward the right shoulder and lies beneath the
second rib.
• Pericardium. The heart is enclosed in a double-walled sac called the
pericardium and is the outermost layer of the heart.
• Fibrous pericardium. The loosely fitting superficial part of this sac is referred
to as the fibrous pericardium, which helps protect the heart and anchors it to
surrounding structures such as the diaphragm and sternum.
• Serous pericardium. Deep to the fibrous pericardium is the slippery, two-layer
serous pericardium, where its parietal layer lines the interior of the fibrous
pericardium.
 Layers of the Heart
• The heart muscle has three layers and they are as follows:
• Epicardium. 
• Myocardium. 
• Endocardium.
 Chambers of the Heart
• The heart has four hollow chambers, or cavities: two
atria and two ventricles.
• Receiving chambers.
• Discharging chambers. 
• Septum. 
 Heart Valves
• The heart is equipped with four valves, which allow blood to flow
in only one direction through the heart chambers. 
• Atrioventricular valves. 
• Bicuspid valves..
• Tricuspid valve. 
• Semilunar valve. 
 Cardiac Circulation Vessels
• Although the heart chambers are bathed with blood almost
continuously, the blood contained in the heart does not nourish
the myocardium.
• Coronary arteries. 
• Cardiac veins.
 Blood Vessels
• Blood circulates inside the blood vessels, which form a closed
transport system, the so-called vascular system.
• Arteries.
• Arterioles. 
• Veins. 
 Physiology of the Heart
• As the heart beats or contracts, the blood makes
continuous round trips- into and out of the heart,
through the rest of the body, and then back to the
heart- only to be sent out again.
 Conduction System of the Heart
• The conduction system occurs systematically through:
• SA node.
• Atrial myocardium.
•  Atrioventricular node.
•  AV bundle.
•  Bundle branches and Purkinje fibers.
Pathophysiology of Myocardial
Infarction
Manifestation
and
Rationale
•pressure or tightness in the chest
•pain in the chest, back, jaw, and other areas of the upper body that lasts
more than a few minutes or that goes away and comes back
•shortness of breath
•sweating
•nausea
•vomiting
•anxiety
•a cough
•dizziness
• a fast heart rate
Symptoms of a heart attack in men
• standard chest pain/pressure that feels like “an elephant” is sitting on your
chest, with a squeezing sensation that may come and go or remain constant
and intense
• upper body pain or discomfort, including arms, left shoulder, back, neck, jaw,
or stomach
• rapid or irregular heartbeat
• stomach discomfort that feels like indigestion
• shortness of breath, which may leave you feeling like you can’t get enough air,
even when you’re resting
• dizziness or feeling like you’re going to pass out
• breaking out in a cold sweat
 Symptoms of a heart attack in
women
• unusual fatigue lasting for several days or sudden severe fatigue
• sleep disturbances
• anxiety
• lightheadedness
• shortness of breath
• indigestion or gas-like pain
• upper back, shoulder, or throat pain
• jaw pain or pain that spreads up to your jaw
• pressure or pain in the center of your chest, which may spread to your arm
 What causes acute myocardial
infarction?
• Your heart is the main organ in your cardiovascular system, which also
includes different types of blood vessels. Some of the most important vessels
are the arteries. Nex is the coronary arteries take oxygen rich blood specifically
to your heart muscle. When these arteries become blocked or narrowed due
to a buildup of plaque, the blood flow to your heart can decrease significantly
or stop completely. 
 Bad cholesterol
• Bad cholesterol, also called low-density lipoprotein (LDL), is one of the leading
causes of a blockage in the arteries. Cholesterol is a colorless substance that’s
found in the food you eat. Your body also makes it naturally.
 Saturated fats
• Saturated fats may also contribute to the buildup of plaque in the coronary
arteries. Saturated fats are found mostly in meat and dairy products, including
beef, butter, and cheese. These fats may lead to an arterial blockage by
increasing the amount of bad cholesterol in your blood system and reducing
the amount of good cholesterol.
 Trans fat
• another type of fat that contributes to clogged arteries is trans fat, or
hydrogenated fat. Trans fat is usually artificially produced and can be found in
a variety of processed foods. Trans fat is typically listed on food labels as
hydrogenated oil or partially hydrogenated oil
 How is acute myocardial infarction
diagnosed?
• To determine whether you’ve had a heart attack, your doctor will listen to your heart to check for
irregularities in your heartbeat. They may measure your blood pressure as well. Your doctor will
also run a number of different tests if they suspect that you’ve had a heart attack. An
electrocardiogram (EKG) may be done to measure your heart’s electrical activity. Blood tests can
also be used to check for proteins that are associated with heart damage, such as troponin.
• Other diagnostic tests include:

•a stress test to see how your heart responds to certain situations, such as exercise
•an angiogram with coronary catheterization to look for areas of blockage in your arteries
• an echocardiogram to help identify areas of your heart that aren’t working properly
DIAGNOSTIC
EVALUATION
 How is acute myocardial infarction
diagnosed?
• To determine whether you’ve had a heart attack, your doctor will listen to your heart to check for
irregularities in your heartbeat. They may measure your blood pressure as well. Your doctor will
also run a number of different tests if they suspect that you’ve had a heart attack. An
electrocardiogram (EKG) may be done to measure your heart’s electrical activity. Blood tests can
also be used to check for proteins that are associated with heart damage, such as troponin.
•
Other diagnostic tests include:
• a stress test 
• an angiogram 
• an echocardiogram
NORMAL ECG FINDINGS
Hyperacute Anterior STEMI:

There are hyperacute T-waves in V2-6 (most marked in V2 and V3) with loss of R wave height.
Normal sinus rhythm with 1st degree AV block
There are premature atrial complexes (beat 4 on the rhythm strip) and multifocal ventricular ectopy
(PVCs of two different types), indicating an “irritable” myocardium at risk of ventricular fibrillation
An ECG of the same patient taken around 40-50 minutes later:

There is progressive ST elevation and Q wave formation in V2-5

ST elevation is now also present in I and aVL
There is some reciprocal ST depression in lead III
INTERVENTION AND
TREATMENT
 How is acute myocardial infarction treated?

Medications

Medications to treat a heart attack might include:

• Aspirin
• Thrombolytics
• Antiplatelet agents
• Pain relievers
• Nitroglycerin
• Beta blockers
• ACE inhibitors
 Surgical and other procedures
 Coronary angioplasty and stenting 
• In this procedure, also known as percutaneous coronary intervention (PCI), doctors guide a long,
thin tube (catheter) through an artery in your groin or wrist to a blocked artery in your heart. If
you've had a heart attack, this procedure is often done immediately after a cardiac
catheterization, a procedure used to find blockages.
• The catheter has a special balloon that, once in position, is briefly inflated to open a blocked
coronary artery. A metal mesh stent almost always is inserted into the artery to keep it open long
term, restoring blood flow to the heart. Usually, you get a stent coated with a slow-releasing
medication to help keep your artery open.

Coronary artery bypass surgery
• In some cases, doctors perform emergency bypass surgery at the time of a heart attack. If
possible, however, you might have bypass surgery after your heart has had time — about three to
seven days — to recover from your heart attack.
• Bypass surgery involves sewing veins or arteries in place beyond a blocked or narrowed coronary
artery, allowing blood flow to the heart to bypass the narrowed section.
• You'll likely remain in the hospital for several days after blood flow to your heart is restored and
your condition is stable.
PHARMACOLOGICAL INTERVENTION
• Several large-scale trials have firmly established the
effectiveness of thrombolytic therapy, beta blockers, and
aspirin in the treatment of AMI. The critical issues include
reducing myocardial oxygen demand and restoring
adequate blood supply to the ischemic regions of the
myocardium.
 MEDICATIONS:

• Aspirin 
• Thrombolytics (Ex: Alteplase)
• Antiplatelet Drugs (Ex: GP IIb/IIIa glycoprotein receptor blockers (abciximab,
tirofiban, eptifibatide), acetylsalicylic acid)
• Nitroglycerin 
• Beta-blockers (Ex: Atenolol)
• ACE inhibitors (Ex: captopril)
• Pain relievers (Ex: analgesics)
 SURGICAL
INTERVENTION
• The goal of surgical reperfusion during the first hours of acute
evolving myocardial infarction is to limit the extent of the
infarction. This should be reflected by improved ventricular
function and low mortality. Over the past 10 years, 440 patients
with transmural myocardial infarction and 261 patients with
nontransmural myocardial infarction underwent coronary artery
bypass graft surgery within 24 hours of peak symptoms.
Drug study
• Medications: 
A number of medications are used in treating myocardial infarctio. They
include:

Vasodiltors: vasodilator drugs relax the smooth muscle in blood vessels, which
causes the vessels to dilate. 
• -  nitrodilators-  angiotensin converting enzyme inhibitors (ACE inhibitors)-  
angiotensin receptor blockers (ARBs)
• Cardiac Depressant drugs: Cardioinhibitory drugs depress cardiac function by
decreasing heart rate (chronotropy), myocardial contractility (inotropy), or
both, which decreases cardiac output and arterial pressure. These cardiac
changes reduce the work of the heart and myocardial oxygen consumption. 
Cont.
 beta-blockers
• Anti-thrombotics (prevent thrombus formation)
-  anticoagulant
-  anti-platelet drugs
• Thrombolytics (dissolve clots - i.e., "clot busters")
-  plasminogen activators
• Analgesics (reduce pain)
-  morphine

Antiplatelet agents have a strong mortality benefit. There is an increased risk of

bleeding in cases of emergency coronary artery bypass graft (CABG). Early
administration of aspirin in patients with acute myocardial infarction has been
shown to reduce cardiac mortality rate. 
 Drug Name  Indication Side/Adverse Effects Nursing Consideration

Generic Name:  • Mild to moderate pain The patient might have the Nursing Responsibilities:
Aspirin • Fever following side/adverse effects:  • Check and verify with
Brand Name:  • Inflammatory conditions Acute aspirin doctor’s order and Kardex.
Bayer Buffered Aspirin —rheumatic fever, toxicity: Respiratory alkalosis, • Observe rights in medication
Classification:  rheumatoid arthritis, hyperpnea, tachypnea,  administration such as giving
Antiplatelet Agents osteoarthritis hemorrhage, excitement, the right drug to the right
(Anti-thrombotics)  • Reduction of risk of confusion, asterixis, pulmonary patient using the right route
Dosage: recurrent TIAs or stroke in edema, seizures, tetany, and at the right time.
81 – 325 mg; chew males with history of TIA metabolic acidosis, fever, coma, • Assess skin color and
nonenteric- due to fibrin platelet CV collapse, renal and presence of lesions as this
coated tablet  emboli respiratory failure (dose related, may indicate hepatotoxicity,
Frequency:  • Reduction of risk of death 20–25 g in adults, 4 g in allergy, bleeding, and other
81-325 mg PO qDay or nonfatal MI in patients children) complications.
indefinitely (preferred with history of infarction Aspirin • Give drug with food or after
dose)  or unstable angina intolerance: Exacerbation of meal if GI upset occurs.
Route:  pectoris bronchospasm, rhinitis (with • Continue monitoring clotting
Orally • MI prophylaxis nasal polyps, asthma, rhinitis) factors, bleeding time, liver
• Unlabeled use: GI: Nausea, dyspepsia, and renal function tests for
Prophylaxis against heartburn, epigastric long-term drug therapy.
cataract formation with discomfort, anorexia, • Monitor vital signs.
long-term use hepatotoxicity
Hematologic: Occult blood
Drug Name Indication Side/Adverse Effects
The patient might have the
following side/adverse effects:
Hypersensitivity: Anaphylactoi
d reactions to anaphylactic
shock
Salicylism: Dizziness, tinnitus,
difficulty hearing, nausea,
vomiting, diarrhea, mental
confusion, lassitude (dose
related)
Nursing Consideration
Client and Family Teaching:
Provide a room environment
conducive for resting such as
raise side rails up to ensure
patient’s safety.
Encourage client to increase
oral fluid intake to facilitate
excretion of drug.
Instruct client to report bloody
stools, rapid or difficult
breathing, and confusion.
Emphasize with the client to
avoid or limit intake of highly-
seasoned and oily food such as
bacon and canned goods as
these can increase the risk of
developing heartburn and
nauseous feeling.
In case of nausea and vomiting,
instruct client to eat crackers
and have carbonated drink
before rising in the morning.
PROGNOSIS
Myocardial infarctions (heart attacks) are a serious event: approximately 25% of
patients die from the initial event – that is, they may die before reaching hospital, or in the first
day or so. Of the rest, 25% will die within the next two years, usually due to recurrent MI or
complications. About 50% of the initial survivors are alive after 10 years. The prognosis is better
for younger patients with less concurrent medical problems.

Acute MI still carries a high mortality rate, with most deaths occurring prior to arrival to
the hospital. At least 5%-10% of survivors die within the first 12 months after the MI, and close
to 50% need hospitalization within the same year. The overall prognosis depends on the extent
of muscle damage. Good outcomes are seen in patients who undergo early perfusion-
thrombolytic therapy within 30 minutes of arrival or PCI within 90 minutes). In addition,
outcomes are good if the ejection fraction is preserved and the patient is started in aspirin,
beta-blockers, and ACE inhibitors.
 Factors that negatively affect prognosis
include:
• Diabetes
• Advanced age
• Prior MI, peripheral vascular disease (PVD), or stroke
• Delayed reperfusion
• Diminished ejection fraction (the strongest predictor)
• Presence of congestive heart failure (CHF)
• Elevated C-reactive protein and BNP levels
• Depression
Acute myocardial infarction, reperfusion type. In this case, the infarct is diffusely
hemorrhagic. There is a rupture track through the center of this posterior left ventricular
transmural infarct. The mechanism of death was hemopericardium
Acute anterior myocardial infarction
Acute myocardial infarction. At 3
days, there is a zone of yellow necrosis surrounded by darker hyperemic borders. The arrows
point to a transmural infarct in the posterior wall of the left ventricle, in this short axis slice
through the left and right ventricular chambers.
Acute myocardial infarction, reperfusion type
Healing myocardial infarction, lateral left
Early healed myocardial infarction
Healed myocardial infarction, anterior left ventricle
NURSING CARE PLAN
 ASSESSMENT DIAGNOSIS PLANNING NTERVENTION AND NTERVENTION AND
RATIONALE RATIONALE
Subjective data: Acute pain related to At the end of 8hr the Monitor and document At the end of 8hr the
Chest Pain tissue ischemia(coronary client will: characteristic of pain, client was able to:
Shortness of Breath artery occlusion) Verbalize relief/control of noting verbal reports, Verbalize relief/control of
Fatigue chest pain within nonverbal cues (moaning, chest pain within
Palpitations appropriate time frame crying, grimacing, appropriate time frame
Weakness for administered restlessness, diaphoresis, for administered
Dizziness medications. clutching of chest) and BP medications.
Light-headedness Antianginals: nitroglycerin or heart rate changes. Display reduced tension,
Objective data: (Nitro-Bid, Nitrostat, Variation of appearance relaxed manner, ease of
Diaphoresis Nitro-Dur), isosorbide and behavior of patients movement.
Syncope  dinitrate (Isordil), in pain may present a Demonstrate use of
Dysrhythmias mononitrate (Imdur), challenge in assessment. relaxation techniques.
Aspirin Most patients with an
acute MI appear ill,
distracted, and focused on
pain. Verbal history and
deeper investigation of
precipitating factors
should be postponed until
pain is relieved.
Respirations may be
increased as a result of
pain and associated 
anxiety; release of stress-
induced catecholamines
increases heart rate and
BP.
ASSESSMENT DIAGNOSIS PLANNING INTERVENTION AND EVALUATION
RATIONALE

Beta-blockers: atenolol Obtain full description of

(Tenormin), pindolol(Visken), pain from patient including
propranolol (Inderal), nadolol location, intensity (using
(Corgard), metoprolol scale of 0–10), duration,
(Lopressor) characteristics (dull, crushing,
Analgesics: morphine, described as “like an
meperidine (Demerol) elephant in my chest”), and
  radiation. Assist patient to
  quantify pain by comparing it
Display reduced tension, to other experiences.
relaxed manner, ease of Pain is a subjective
movement. experience and must be
Demonstrate use of described by patient. Provides
relaxation techniques. baseline for comparison to
aid in determining
effectiveness of therapy,
resolution and progression of
problem.
Review history of previous 
angina, anginal equivalent, or
MI pain. Discuss family
history if pertinent
 Delay in reporting pain
hinders pain relief and may
require increased dosage of 
medication to achieve relief.
In addition, severe pain may
induce shock by stimulating
the
ASSESSMENT DIAGNOSIS PLANNING INTERVENTION AND EVALUATION
RATIONALE

sympathetic nervous system,
thereby creating further
damage and interfering with
diagnostics and relief of
pain.
Instruct patient to report
pain immediately. Provide
quiet environment, calm
activities, and comfort
measures. Approach patient
calmly and confidently. 
Decreases external stimuli,
which may aggravate
anxiety and cardiac strain,
limit coping abilities and
adjustment to current
situation.
Instruct patient to do 
relaxation techniques: deep
and slow breathing,
distraction behaviors,
visualization, guided
imagery. Assist as needed.
Helpful in decreasing
perception and response to
pain. Provides a sense of
having some control over
the situation, increase in
positive attitude.
RECOMMENDATIONS
• CLOPIDOGREL AND TICAGRELOR ARE RECOMMENDED FOR CONSERVATIVE
MEDICAL MANAGEMENT OF MI IN COMBINATION WITH ASPIRIN (162 TO 325
MG PER DAY) FOR UP TO 12 MONTHS. EARLY ADMINISTRATION OF
BETA BLOCKERS IS RECOMMENDED DURING HOSPITALIZATION AFTER AN MI.​

• Early administration of beta blockers is recommended during hospitalization

after an MI. These agents should be continued indefinitely in patients
without contraindications who have a left ventricular ejection fraction of 40%
or less.​

• Angiotensin receptor blockers are indicated in all patients who have had an
MI and are allergic to or cannot tolerate ACE inhibitors. Angiotensin
receptor blockers should not be used in combination with ACE inhibitors.​
• Statin therapy is recommended after an MI and should be continued
indefinitely in patients without contraindications.

• Before a patient who has had an MI is discharged from the hospital, the
physician should initiate counseling about diet and smoking cessation, and
should refer the patient for exercise-based cardiac rehabilitation​
 REFERENCES
• https://www.google.com/search?q=what+is+recommendation+of+
+myocardial+infarction&source=lmns&bih=648&biw=360&prmd=sinv&hl=en&sa=X&ved=2ahUKEwjrktSnp8rvAhWKz
4sBHUC1CBYQ_AUoAHoECAAQAw​
• Cardiovascular System Anatomy and Physiology: Study Guide for Nurses (nurseslabs.com)
• Myocardial Infarction: Nursing Care Management and Study Guide (nurseslabs.com)
• Case presentation on Myocardial Infarction (slideshare.net)
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4193075/
• https://www.healthline.com/health/acute-myocardial-infarction#diagnosis
• https://www.mayoclinic.org/diseases-conditions/heart-attack/diagnosis-treatment/drc-20373112
• REFERENCES:
• • https://www.healthline.com/health/acute-myocardial-infarction#diagnosis
• • https://www.mayoclinic.org/diseases-conditions/heart-attack/diagnosis-treatment/drc-20373112

• REFERENCES:
• https://pubmed.ncbi.nlm.nih.gov/10969622/#:~:text=Several%20large%2Dscale%20trials%20have,ischemic
%20regions%20of%20the%20myocardium.
THANK YOU!