Myocardial infarction, also known as a heart attack, refers to necrosis of heart muscle tissue caused by prolonged ischemia. It is usually caused by a coronary thrombosis that blocks blood supply to the heart. Symptoms include chest pain that may radiate to the arms, shoulders, or jaw. Diagnosis involves ECG changes, elevated cardiac enzymes, and imaging tests. Treatment focuses on restoring blood flow through thrombolysis or angioplasty while managing pain, heart failure risk, and arrhythmias with medications.

1. 1
MYOCARDIAL INFARCTION
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2. MYOCARDIAL INFARCTION
 MI refers to a dynamic process by which one
or more regions of the heart experience a
severe and prolonged decrease in oxygen
supply due to insufficient coronary blood flow;
subsequently, necrosis or “death” to the
myocardial tissue occurs.
 The onset of the MI process may be sudden or
gradual, and the progression takes
approximately 3 to 6 hours.
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3. Pathophysiology and Etiology
 1. Acute coronary thrombosis (partial or
total) associated with 90% of MIs.
 2. Other etiologic factors include
• Coronary artery spasm.
• Coronary artery embolism.
• Anemia
• Severe exertion or stress on the heart .
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4. Degrees of damage
Different degrees of damage occur to the heart muscle.
 a. Zone of necrosis— death to the heart muscle
caused by extensive and complete oxygen
deprivation; irreversible damage
 b. Zone of injury —region of the heart muscle
surrounding the area of necrosis; inflamed and
injured, but still viable if adequate oxygenation can be
restored.
 c. Zone of ischemia — region of the heart muscle
surrounding the area of injury, which is ischemic and
viable; not endangered unless extension of the
infarction occurs 47/23/2020

5. Degrees of damage
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6. Classification of MI
 A. STEMI— ST-segment elevations are seen on
ECG. The area of necrosis may or may not occur
through the entire wall of heart muscle.
 B. NSTEMI— no ST-segment elevations can be
seen on ECG. ST depressions may be noted as well
as positive cardiac markers, T-wave inversions.
 Area of necrosis may or may not occur through the
entire myocardium.
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7. Clinical Manifestations
1. Chest pain
• a. Severe, diffuse, sub sternal pain; may be described
as crushing, squeezing, or dull
• b. Not relieved by rest or sublingual nitrate but
requires opioids(morphine).
• c. Radiate to the arms , shoulders, neck, back, or jaw
• d. Continues for more than 15 minutes
• e. May produce anxiety and fear.
• f. Some patients exhibit no complaints of pain.
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8. Clinical Manifestations
 2. Diaphoresis, cool clammy skin, facial pallor
 3. Hypertension or hypotension
 4. Bradycardia or tachycardia
 6. Palpitations, severe anxiety, dyspnea
 7. Disorientation, confusion, restlessness
 8. Nausea, vomiting, hiccups
 9.Atypical symptoms: epigastric or abdominal
distress (usually diabetics and elderly ).
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9. Diagnostic Evaluation
 ECG Changes
• Generally occur within 2 to 12 hours, but may take
72 to 96 hours.
• a. ST-segment depression and T-wave inversion
indicate a pattern of ischemia.
• b. ST elevation indicates an injury pattern.
• c. Q waves indicate tissue necrosis and are
permanent.
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10. Diagnostic Evaluation
 Cardiac Markers
A rise in a cardiac marker confirms cardiac cell death
 Troponin (positive in STEMI)
• Troponin I <10 ng/L
 CK-MB (isoenzyme found in the heart muscle).
Reference Values
• Males: <6.7 ng/mL
• Females: <3.8 ng/mL
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11. cont
■■ Cardiac enzymes released with cardiac muscle injury:
☐ Myoglobin – Earliest marker of injury to cardiac or skeletal
muscle. Levels no longer evident
after 24 hr.
☐Creatine kinase-MB – Peaks around 24 hr after onset of
chest pain. Levels no longer evident after 3 days.
☐Troponin I or T – Any positive value indicates damage to
cardiac tissue and should be reported.
Troponin I – Levels no longer evident after 7 days.
Troponin T – Levels no longer evident after 14 to 21 days.
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12. Diagnostic Evaluation
 Chest X .RAY
 Elevated CRP and lipoprotein .
 Abnormal coagulation studies .
 Elevated white blood cell (WBC) count
 Radionuclide imaging allows recognition of
areas of decreased perfusion.
 Echocardiography
 Cardiac magnetic resonance imaging (MRI)
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13. Management
The aime of Therapy is :
 Reversing ischemia to preserve cardiac
muscle function.
 Reduce the infarct size and prevent death.
 Provide early restoration of coronary blood
flow.
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14. Pharmacologic Therapy
 MONA—the immediate pharmacologic interventions
used to treat MI.
• 1. M (Morphine) given I.V. Used to treat chest pain.
• 2. O (Oxygen)—via nasal cannula or face mask.
• 3. N (Nitrates)—given sublingually or I.V.
• 4. A (Aspirin)—immediate dosing by mouth is
recommended to halt platelet aggregation
 Beta-adrenergic blockers atenolol
 Angiotensin-converting enzyme inhibitors (captopril
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15.  Thrombolytic agents (Indicated in ST-elevation)
• Such as tissue plasma activator (Activase)
• Streptokinase and reteplase and alteplase
• Act by Reestablish blood flow in coronary vessels
by dissolving thrombus.
• Administered I.V. or I.C. under monitoring .
 Anti-arrhythmics, such as amiodarone (decrease
the ventricular irritability that occurs after MI.
 Anticoagulant low-molecular-weight heparin
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16. Contraindications to Thrombolytic
Therapy
Absolute contraindications include:
- Recent head trauma or caranial tumor
- Previous hemorrhagic shock
- Stroke or cerebro-vascular events 1 year old
- Active internal bleeding
- Major surgery within two weeks
Relative contraindications include:
Active peptic ulcer, diabetic retinopathy, pregnancy,
uncontrolled HTN

17. Non Pharmacologic Therapy
 Percutaneous Coronary Interventions
• Including percutaneous transluminal coronary
angioplasty, coronary stenting, and atherectomy.
• Should be performed within 30 minutes of initial
diagnosis of MI.
 Surgical Revascularization
• Emergency CABG surgery can be performed
within 6 hours of evolving infarction.
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18. Myocardial Infarction vs Stable Angina
Myocardial Infarction
 Causes: Complete blockage of
blood supply to heart muscle.
 Occurrence of pain:
Happen at anytime
 Symptoms: Chest pain with
damage to the heart. crushing.
 Outcome May be fatal
 Relieving Factors : not
relieved by rest or nitro.
 Duration : Chest pain usually
more than 15 minutes
 Cardiac marker : Present
Stable Angina
 Decrease in blood supply to
heart
 Occurs on physical activity or
due to emotional stress
 Chest pain with no damage
to the heart. Pressure
 Usually not fatal
 Relieved by rest or nitro
 Chest pain for less than 15
minutes.
 Not present
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19. Complications
 Dysrhythmias
 Sudden cardiac death
 Heart failure
 Reinfarction
 Cardiac rupture
 Thromboemboli
 Ventricular aneurysm
 Pericarditis (2 to 3 days after MI)
 Dissection of coronary arteries during angioplasty
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20. Nursing Assessment
 1. Ask patient to describe anginal attacks. Type
,onset ,duration ,location ,radiation ,relief by
increased by ,associated symptoms .
 2. Obtain a baseline 12-lead ECG.
 3. Assess patient’s and family’s knowledge of
disease.
 4. Identify patient’s and family’s level of anxiety
 5. Gather information about the patient’s cardiac
risk factors.
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21.  6. Evaluate patient’s for conditions such as
diabetes, heart failure, previous (MI), or
COPD.
 7. Identify factors that may contribute to
noncompliance with prescribed drug
therapy.
 8. Review laboratory test
 9. Discuss with patient current activity
levels.
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22. Nursing Diagnoses
 Acute Pain related to an imbalance in oxygen
supply and demand.
 Decreased Cardiac Output related to reduced
preload, afterload, contractility, and heart rate
secondary to hemodynamic effects of drug therapy.
 Anxiety related to chest pain, uncertain
prognosis, and threatening environment.
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23. Nursing Interventions
Relieving Pain
1. Determine intensity of patient’s angina.
2. Position patient for comfort; Fowler’s position
3. Administer oxygen if prescribed.
4. Take vital signs every 5 to 10 minutes until angina
pain subsides.
5. Obtain a 12-lead ECG as directed.
6. Administer antianginal drugs as prescribed.
7. Monitor for relief of pain, and note duration of
anginal
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24.  8. Monitor for progression of stable angina to
unstable angina
 9. Determine level of activity that precipitated
anginal episode.
 10. Identify specific activities patient may engage
in that are below the level at which anginal pain
occurs.
 11. Reinforce the importance of notifying
nursing staff when angina pain is experienced.
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25. Maintaining Cardiac Output
 Carefully monitor the patient’s response to drug
therapy.
 Recheck vital signs as indicated by onset of action of
drug and at time of drug’s peak effect.
 Note patient complaints of headache (especially with
use of nitrates)
 Continuous ECG monitoring or obtain 12- lead
ECG.
 Evaluate for development of heart failure
 Monitor laboratory tests as cardiac markers.
 Be sure to remove previous nitrate patch(prevents
hypotension
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26. Decreasing Anxiety
 Rule out physiologic causes for increasing or new
onset anxiety before administering sedatives.
 Assess patient for signs of hypoperfusion,
auscultate heart and lung sounds,
 Obtain a rhythm strip, and administer oxygen as
prescribed.
 Explain to patient and family the reasons for
hospitalization, diagnostic tests, and therapies
administered.
 Answer patient’s questions with concise
explanations
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27. Instruct about Appropriate Use of
Medications and Adverse Effects
 Carry nitroglycerin at all times.
 Place nitroglycerin under the tongue at first
sign of chest pain .
 Stop all effort or activity; sit, and take
nitroglycerin tablet—relief should be
obtained in a few minutes.
 Repeat dosage in 5 minutes for total of
three tablets if relief is not obtained.
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28.  Keep a record of the number of tablets taken
to evaluate change in anginal pattern.
 Take nitroglycerin prophylactically to avoid
pain known to occur with certain activities.
 Instruct patient on administration of
transdermal nitroglycerin patches
 Ensure that patient has enough medication
until next follow- up appointment
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29. PATIENT TEACHING
 • Identify the patient’s priorities, provide
adequate
 education about heart-healthy living, and
facilitate the
 patient’s involvement in a cardiac rehabilitation
 program.
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30. CONT
• Work with the patient to develop a plan to meet
specific needs to enhance compliance
• Provide home care referral if warranted.
• Assist the patient with scheduling and keeping
follow-up appointments and with adhering to the
prescribed cardiac rehabilitation regimen.
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31. CONT
 Provide reminders about follow-up monitoring,
including periodic laboratory testing and ECGs,
as well as general health screening.
 Monitor the patient’s adherence to dietary
restrictions and to prescribed medications.
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32. CONT
 • If the patient is receiving home oxygen, ensure
that the patient is using the oxygen as prescribed
and that appropriate home safety measures are
maintained.
 • If the patient has evidence of heart failure
secondary to an MI, appropriate home care
guidelines for the patient with heart failure are
followed.
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33. Any question
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