By

Rashid Hussain
Lecturer Nursing
Objectives:
 At the end of this presentation student will be able
to:
 Define MI
 Discuss Pathophysiology of MI
 Identify causes of MI
 Identify types of MI
 Identify Signs & Symptoms of MI
 Explain diagnostic test and management of MI
Acute Myocardial
Infarction
 Definition
• Acute MI known as a heart
attack, coronary occlusion
which is characterized by the
formation of localized necrotic
areas with the myocardium.
• Acute myocardial infarction
(MI) is defined as death or
necrosis of myocardial cells.

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MI
 Is the rapid development of
myocardial necrosis caused
by a critical imbalance
between oxygen supply and
demand of the myocardium.
This usually results from
plaque rupture with
thrombus formation in a
coronary vessel, resulting in
an acute reduction of blood
supply to a portion of the
myocardium.

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Pathophysiology
 Arteriosclerotic plaques gradually narrow the
coronary arteries, but it is a rupture of the
plaque and subsequent platelet aggregation
and thrombosis that occludes the artery.

 Blood flow to the heart muscles of affected

area decreases which leads to ischemia. Due
to ischemia lactic acid is produced which
make injury to the muscle.

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Cont….
 Prolong unrelieved ischemia causes irreversible
damage to the myocardium
 Cardiac cells can withstand ischemia for about 20

minutes before cellular death occurs

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Pathogenesis of AMI

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Mechanisms of Myocardial Damage
 The severity of an MI is dependent on three factors:
 The level of the occlusion in the coronary artery,
 The length of time of the occlusion.
 The presence or absence of collateral circulation .

 The death of myocardial cells first occurs in the area of

myocardium that most distal to the arterial blood supply, that
is, the endocardium. As the duration of the occlusion
increases, the area of myocardial cell death enlarges

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 Causes
• MI is usually caused by reduced blood flow in a coronary artery
due to atherosclerosis and occlusion of an artery by an embolus or
thrombus.

•
Other causes of MI include:
vasospasm (sudden constriction or narrowing) of a coronary artery

• decreased oxygen supply ( e.g., from acute blood loss, anemia or

low blood pressure)

• increased demand for oxygen (e.g, from a rapid heart rate,

thyrotoxicosis, or ingestion of cocaine)

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Risk factors
Tobacco smoking
Hypercholesterolemia
Diabetes (with or without insulin resistance)
High blood pressure
Obesity
Stress Occupations with high stress index are known to have
susceptibility for atherosclerosis.
Socioeconomic factors

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 Types of MI
• Myocardial infarction can be categorized on the basis of
anatomic, morphologic, and diagnostic clinical information.
• From an anatomic or morphologic standpoint, the two types of
MI are
– Transmural (Q wave MI
– Nontransmural(Non Q wave MI)

• A more common clinical diagnostic classification scheme is also

based on ECG findings
– ST elevation MI (STEMI)
– Non ST elevation MI (NSTEMI)
Collectively all types of MI is termed as Acute Coronary
Syndrome (ACS)

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STEMI & NSTEMI
 The distinction between an ST-elevation MI and a non-ST-
elevation MI also does not distinguish a Transmural from a
non-transmural MI. The presence of Q waves or ST segment
elevation is associated with higher early mortality and
morbidity.

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Types of MI

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Measuring ST Elevation

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Color Codes of ECG Leads

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Main Coronary Arteries

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Signs & Symptoms
 Acute MI may have unique presentations
in individual patients. The degree of
symptoms ranges from none at all to
sudden cardiac death. An asymptomatic
MI is not necessarily less severe than a
symptomatic event; but patients who
experience asymptomatic MI's are more
likely to be diabetic.

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Sign & Symptoms (Cont…)
• Chest pain described as a pressure sensation,
fullness, or squeezing in the midportion of the
thorax
• Radiation of chest pain into the jaw/teeth,
shoulder, arm, and/or back
• Associated Dyspnea or shortness of breath
• Associated epigastric discomfort with or
without nausea and vomiting
• Associated diaphoresis or sweating
• Syncope or near-syncope without other cause

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Diagnosis
• Electrocardiography:
• The first test is the ECG, which may
demonstrate that a MI is in progress or has
already occurred.
• Echocardiography
• An echocardiogram may be performed in
order to compare areas of the left ventricle that
are contracting normally with those that are
not.

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 Blood Tests (Cardiac Enzymes)
 Blood tests can be performed to detect evidence of myocardial
cell death. Living heart cells contain certain enzymes and
proteins (e.g., Creatinine phosphokinase, troponin, and
myoglobin) within cell membranes associated with specialized
cellular functions such as contraction

 When a heart muscle dies, cellular membranes lose integrity

and intracellular enzymes and proteins slowly leak into the
bloodstream. These enzymes and proteins can be detected by a
blood sample analysis. The concentration of enzymes in a
blood sample, and more importantly, the changes in
concentration found in samples taken over time, correlates
with the amount of heart muscle that has died

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Acute MI

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Cardiac enzymes

1. Creatinine Kinase and its isoenzymes.

There are three CK isoenzymes: CK-MM ( skeletal muscle),
CK-MB (heart muscle), CK-BB ( brain tissue).
CK-MB is the cardiac-specific, found mainly in cardiac
cells and only rises when there has been damage. It is the
most specific index for diagnosis of MI. The level started to
increase a few hours and peaks within 24 hours of an MI. if
the areas is damaged , it peaks earlier.

2. Myoglobin. Myoglobin is a heme protein that helps to

transport oxygen. Myoglobin is also found in the cardiac and
skeletal muscles. The myoglobin level starts to rise within 1 to
3 hours and peaks within 12 hours after the onset of
symptoms. It is not a specific indicator of acute MI; however,
it can be an excellent parameter of ruling out an acute MI.

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3. Troponin
• Troponin, a protein found in myocardium, regulates the
myocardial contractile process. There are three isomers of
troponin (C, I, T). Because of the smaller size of the protein
and the increased specificity of troponin I and T for cardiac
muscle, these tests are used more frequently to identify
myocardial injury. The increase in the level of troponin in
the serum starts and peaks at approximately the same time
as CK-MB. However, it remains elevated for a longer
period often up to 3 weeks, and therefore cannot be used to
identify subsequent extension or expansion of an MI.

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Medications
 Thrombolytic: Streptokinase
Purpose: to dissolve the thrombus in a coronary artery,
allowing blood to flow through the coronary artery again
(reperfusion), minimizing the size of infarction and preserving
ventricular function.

 Analgesics: Morphine Sulfate

Purpose: reduce pain and anxiety. It produces preload, which
decreases the workload of the heart. It also relaxes bronchiole
to enhance oxygenation

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Antiplatelet Agents:
Aspirin in a dose of at least 160 mg and up to 325 mg should
be administered immediately on recognition of MI signs and
symptoms and continued daily indefinitely. Other Antiplatelet
agents—including clopidogrel, ticlopidine, and dipyridamole-
have not been shown in any large-scale trial to be superior to
aspirin in MI.
 Supplemental Oxygen:

There are no published studies demonstrating that oxygen

therapy reduces mortality or morbidity of a MI.

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• Triglyceride Nitrates (GTN) They produce vasodilatation,
and cardiac muscle relaxation, thus decrease oxygen demand.
They decrease the cardiac muscle damage. Angesid is given
sublingual. Isoket is given IV. Some also given tropically as
skin patches.
• Beta-blockers:
Beta-blocker therapy is recommended within 12 hours of MI
symptoms and is continued indefinitely. Treatment with a
beta-blocker reduces MI mortality

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Common Beta blockers and their dose
Beta-1-blocker Dosing
Metoprolol 25-200 mg every 12 hours
Atenolol 25-200 mg every 24 hours
Esmolol 50-300 mcg/kg/minute intravenously
Betaxolol 5-20 mg every 24 hours
Bisoprolol 5-20 mg every 24 hours
Acebutolol 200-600 mg every 12 hours

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 Low-molecular-weight Heparin (LMWH)
LMWH can be administered to MI patients not treated with
fibrinolytic therapy that have no contra-indication to heparin.

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• Angiotensin-Converting Enzymes Inhibitors (ACE-I)
Purpose: prevent conversion of angiotensin I to II. In the
absence of angio-II, the blood pressure decreases and the
kidneys excrete sodium and fluid, decreasing the oxygen
demand of the heart.

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 Percutaneous Coronary Intervention (PCI)
PCI may be used to open the occluded coronary artery in an
acute MI and promotes reperfusion to the area that has been
deprived of oxygen. Because the duration of oxygen
deprivation is directly related to the number of cells that die,
the time from the patient’s arrival in the emergency
department to the time PCI is performed should be less than
60 minutes.

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Post MI Management
• Cardiac Stress Testing:
Cardiac stress testing post-MI has established value in risk
stratification and assessment of functional capacity
• Lipid Management:
Post-MI patients with HDL-cholesterol levels < 35 mg/dL on
a Step II diet are recommended to participate in a regular
exercise program and on drug therapy designed to increase
HDL-cholesterol levels.Recent data indicate the all MI
patients should be on statin therapy, regardless of lipid levels
or diet
• Long-term Medications:
Most oral medications instituted in the hospital at the time of
MI will be continued long-term. Therapy with aspirin and
beta-blockade is continued indefinitely in all patients. ACEI
is continued indefinitely in patients with congestive heart
failure, left ventricular dysfunction (ejection fraction < 0.40),
hypertension, or diabetes. A lipid-lowering agent, specifically
a statin, in addition to dietary modification is continued
indefinitely
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 Implantable Cardiac Defibrillators:
Automatic Implantable Cardiac Defibrillators (AICD) in
patients post-MI has reduced 31% mortality risk in Mi
Patient.
 Cardiac Rehabilitation:
is a medically supervised program that helps improve the
health and well-being of people who have heart problems.
Rehab programs include exercise training, education on heart
healthy living, and counseling to reduce stress and help you
return to an active life.

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Nursing Management

Nursing Diagnosis:
 Risk for decreased tissue perfusion R/L decreased cardiac out

put.
 High risk for injury R/L anticoagulant therapy.

 Knowledge deficit

 Ineffective coping

 Anxiety

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Nursing interventions
• Assess Chest pain using COLDERRA , and other s/s for MI.
• Maintain large bore I/V line
• MONA (Morphine, Oxygen, Nitrates, Aspirin) and ECG in
Emergency
• Draw blood for cardiac enzyme
• Develop a trusting and caring relationship to reduce anxiety
• Relieving pain and other signs and symptoms of ischemia
• Oxygen administration. Flow rate of 2-4L/min
• Vital signs and record accordingly
• Physical bed rest with backrest elevated
• Ensuring a quiet environment, prevent interruptions that disturb rest
• Monitor potential complications

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Reference
 Source: Smeltzer, Suzanne, et al. Brunner and Suddarth’s
Textbook of Medical Surgical Nursing, 10th edition. USA:
Lippincott Williams and Wilkins. 2004. P276

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