MYOCARDIAL
INFARCTION
ASHLEY ANN CAPANGPANGAN
COLYN CATURAN
AGENDA
01 02 03
Introduction ETIOLOGY DIAGNOSTIC TEST
04 05 06
CLINICAL MEDICAL/PHARMACOLOG NURSING
MANIFESTATION/ IC /SURGICALTREATMENT MANAGEMENT
SIGNS &
SYMPTOMS
INTRODUCTION
Myocardial infarction (MI), commonly
referred to as a heart attack, is a
critical cardiovascular event
characterized by the ischemic death
of myocardial tissue due to an abrupt
cessation or significant reduction of
blood supply to a portion of the heart
muscle. This condition represents an
acute manifestation of coronary
artery disease and is a leading cause
of morbidity and mortality worldwide.
ETIOLOGY
The primary cause of myocardial infarction is coronary artery disease (CAD),
which involves the narrowing or blockage of coronary arteries supplying
blood to the heart muscle. The most common pathophysiological mechanism
is:
Atherosclerosis and Plaque Rupture: The most frequent mechanism
causing MI, plaques have large lipid cores and thin fibrous caps prone to
rupture.
Coronary Artery Thrombosis: Triggered by plaque rupture and platelet
aggregation.
Coronary Artery Spasm: A less common cause involving transient
constriction of coronary arteries; can be induced by substances such as
cocaine or emotional stress.
Risk Factors
Non-modifiable: Age, male gender, family history of premature coronary
artery disease.
Modifiable: Hypertension, smoking, diabetes mellitus, obesity,
dyslipidemia, physical inactivity, unhealthy diet, and excessive alcohol
consumption.
Approximately 90% of MIs result from thrombus formation on an
atherosclerotic plaque. The vulnerable plaques usually have a large lipid core
and thin fibrous cap prone to rupture.
DIAGNOSTIC TESTS
1. Electrocardiogram (ECG or EKG):
Records the heart's electrical activity.
Detects characteristic changes such as ST-segment elevation (STEMI) or non-ST-segment elevation
(NSTEMI).
Usually performed immediately upon suspicion of MI.
2. Blood Tests (Cardiac Biomarkers):
Troponin (most specific and sensitive marker for myocardial injury).
Creatine Kinase-MB (CK-MB) (less commonly used now).
Elevated levels indicate myocardial cell death.
3. Coronary Angiography:
Imaging test to visualize blockages in coronary arteries.
Helps guide interventions like angioplasty or stenting.
4. Echocardiogram (Heart Ultrasound):
Assesses heart muscle function and wall-motion abnormalities caused by ischemia.
5. Additional Tests:
Cardiac MRI or CT scan for detailed heart imaging.
Exercise stress tests for assessing coronary artery function post-acute phase.
CLINICAL MANEFESTATIONS/
SIGNS AND SYMPTOMS
Crushing, severe, and persistent chest pain (substernal).
Pain may radiate to the left arm, jaw, neck, or shoulder blades.
Often described as heavy, squeezing, or tight.
Levine’s Sign – patient clutches chest with a clenched fist.
Shortness of breath.
Nausea and vomiting.
Fatigue.
Feeling of impending doom.
MEDICAL/PHARMACOLOGIC/
SURGICAL TREATMENT
PHARMACOLOGIC
Analgesic- Morphine Sulfate, Lidocaine or Nitroglycerine
are adminestered intravenously.
Thrombolytic Therapy- Streptokinase, Urokinase, tPA
(Tissue Plasminogen Activator)
After administer anticoagulant and antiplatelet
Other medications -Beta-Adrenergic Blockers
SURGICAL
Percutaneous Transluminal Coronary Angioplasty (PTCA)
NURSING MANAGEMENT
Promoting oxygenation and tissue perfusion
Instruct patient to avoid overfatigue.
Stop activity immediately if chest pain, dyspnea, lightheadedness, or
faintness occurs.
Administer oxygen via nasal cannula for 24–48 hours or longer if symptoms
persist
Position in semi-Fowler’s for better lung expansion and gas exchange.
Promoting adequate cardiac output
Monitor ECG for dysrhythmias.
Check vital signs regularly.
Observe effects of daily activity on cardiac status.
Assess pulse rate and rhythm.
NURSING MANAGEMENT
Promote comfort
Relive pain. Administer pain reliever as ordered
Bed Rest -to decrese oxygen demand
Promote low calorie, low cholesterol, low sodium diet.
Assist with range-of-motion exercises.
Provide emotional support, and help reduce stress and anxiety
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