S.

NO OBJECTIVES TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA

ACTIVITY ACTIVITY TION

MYOCARDIAL INFARCTION
Introduction:
1. Introduction of 2min. Black Discussing Listening
The heart muscle must have adequate blood supply to
Myocardial board. and and writing.
contract properly. The coronary arteries carry oxygen to
infraction. explaining.
the myocardium. When coronary arteries are narrowed or
blocked the area of heart muscle supplied by that artery
becomes ischemic and injured which gives rise to various
disease conditions.

2. Define 2min. Definition: OHP Teacher Listening What do

myocardial Myocardial infarction is leading cause of sudden death in explaining and writing. you mean
infraction. men and women. It is caused by an obstruction in a with the help by
coronary artery resulting in necrosis to the tissues supplied of OHP. myocardial
by the artery. The obstruction is usually due infraction
atherosclerotic plaque, a thrombus or an embolism. The on?
area most affected is left ventricle.
- According to Brunner& Suddarth’s
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
3. Enlist the risk 2min. Risk factors: Leaflet. Teacher Listening Knowing
factors of enumerates and writing. the various
myocardial the risk risk factors
Non-modifiable risk factors:
infarction. factors of mi of MI.
• Family history.
on leaflet.
• Increasing age.
• Race.
• Male gender.

Modifiable risk factors:

• Blood lipid level abnormalities.
• Diabetes mellitus.
• Hypertension.
• Physical inactivity.
• Obesity.
• Cigarette smoking.
• Alcohol consumption.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
4. Describe the 2min. Pathophysiology: Chart Teacher Listening ? Did you
pathophysiology explains and writing. understand
In an MI, an area of myocardium is permanently
Of MI in detail. pathophysiolo the
destroyed. MI is usually caused by reduced blood flow in a
gy by using pathophysi
coronary artery due to rupture of atherosclerotic plaque
chart & ology of
and subsequent occlusion of artery by the thrombus. Other
explaining. myocardial
causes of mi are vasospasm of coronary artery, decreased
infarction?
oxygen supply, and increased demand for oxygen. In each
case a profound imbalance exists between myocardial
supply and demand. The area of infarction develops over
minutes to hour. As the cells are deprived of oxygen,
ischemia develops and cellular injury occurs and lack of
oxygen results in infarction.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
5. Enumerate the 2min. Clinical manifestations: Pamphlet. Teacher Listening Did you
clinical enumerates and writing. understand
Cardiovascular:
manifestations the clinical the clinical
• Chest pain or discomfort.
of MI. manifestations manifestati
• Increased blood pressure.
by using ons of MI?
• Pulse deficit.
pamphlet.
• St segment and t wave changes.

Respiratory:
• Hotness of breath.
• Dyspnea.
• Tachypnea.
• Crackles.
• Pulmonary edema.

Gastrointestinal:
• Nausea and vomiting.

Genitourinary:
• Decreased urinary output indicates cardiogenic
shock.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
Skin:
• Cool.
• Clammy.
• Diaphoretic and pale appearance due to
sympathetic stimulation may indicate cardiogenic
shock.

Neurologic:
• Anxiety.
• Restlessness.
• Light headache.

Psychological:
• Fear with feeling of impending doom.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
6. Discuss the 2min. Assessment and diagnostic findings: Blackboard Teacher Asking What are
assessment and discusses the doubts. the
The diagnosis of mi is based on the presenting symptoms
Diagnostic Diagnostic diagnostics
and laboratory test results. The prognosis depends on the
findings of MI. techniques measures
severity of coronary artery obstruction and extent of
with the help used to
myocardial damage. Physical examination is always
of black board diagnose
conducted but the examination alone does not confirm the
and lecture MI?
diagnosis.
cum
discussion.
Patient’s history:
The patient’s history has two parts: the description of the
presenting symptoms and the history of previous illness
and family history of heart disease. Previous history also
includes the risk factors for heart disease.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
Electrocardiogram:
The ECG provides the information that assist in
diagnosing acute mi. It should be obtained within 10
minutes from the time the patient reports the pain or
arrives the emergency department. By monitoring ECG
changes over time, the location, evolution and resolution
of an MI can be identified and monitored. The classic
ECG changes are t wave inversion, ST segment elevation
and development of abnormal q wave. during recovery
from mi the ST segment often is the first ECG indicator to
return to normal.

Echocardiogram:
The echocardiogram is used to evaluate ventricular
function.
It may be used to assist in diagnosing an MI especially
when ECG is non diagnostic.
The echocardiogram can detect hypokinetic and akinetic
wall motion and can determine the ejection fraction.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION

Laboratory tests:
Creatinine kinase and its isoenzymes:
Ck-mb is the cardiac-specific isoenzyme, found in cardiac
cells. Elevated ck-mb assessed by mass assay is an
indicator of acute mi. Its level begins to rise within a few
hours and peaks within 24 hours of an MI.
Myoglobin:
Myoglobin is heme protein helps transport oxygen. It is
found in cardiac cells and skeletal muscle. It starts to
increase within 1-3 hours and peaks within 12 hours after
onset of symptoms.
Troponin:
It is a protein found in the myocardium regulates the
contractile process. There are three isomers of troponin c, i
and t. Troponin and t are specific for cardiac muscles and
these tests are currently recognized as reliable and critical
markers of myocardial injury. An increased level of
troponins in serum can be detected within few hours
during acute mi. It remains elevated for a long period often
as long as 3 weeks and can be used to detect recent
myocardial damage.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
7. Enlist the 3min. Complications: Flash cards. Teacher Listening What are
complications of discusses the and writing. the
• Acute pulmonary edema.
MI. complications complicatio
• Heart failure.
with the help ns of MI?
• Cardiogenic shock.
of black board
• Dysrhythmias.
and lecture
• Pericardial effusion.
cum
• Myocardial rupture.
discussion.

Teacher
8. Explain the 3min. Management: PPT describes the Listening What can
management of • Medical management management and writing. be the
the patient with • Surgical management. with the help medical
MI. • Dietary management of PPT. manageme
• Nursing management. nt of the
• Other management. patient
with mi?
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION

Medical management:
It focuses on reducing the workload of heart,
Relieving pain, improving tissue perfusion, preventing
complications and further tissue damage. Immediately
after mi a client is admitted to a coronary unit. The client
heart rate is continuously monitored for dysrhythmias. The
client’s vital signs are monitored by arterial line for
hemodynamic monitoring or noninvasive B.P monitoring
system.
Pharmacological therapy:
• The patient with mi is given aspire.
• Nitroglycerin.
• Morphine.
• Betablockers.

Thrombolytics:
These medications are administered I/V, can be given
directly into coronary artery in cardiac catheterization lab
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
Analgesics:
• The analgesics of choice for acute mi is morphine
sulphate administered in I/V boluses to decrease
pain and anxiety.
• It decreases the preload and afterload thus
decreasing the workload of heart.
• It also relaxes the bronchioles to enhance the
oxygenation.
• The cardiovascular response to morphine is
monitored closely, particularly B.P which can
decrease and respiratory rate can be depressed.

Ace inhibitors:
Ace inhibitors prevent the conversion of gitonin.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
Antidysrhythmic agents:
Three dysrhythmias may occur following an MI are:
• Ventricular fibrillation, bradycardias, tachycardias.
• Ventricular fibrillation is treated with
defibrillation. Atropine and if needed a temporary
pacemaker may be inserted for bradycardias.
• Two tachycardias that may occur are atrial
fibrillation and ventricular tachycardia.
• Atrial tachycardias is treated with digoxin or
amiodarone. Ventricular tachycardias is treated
with lidocaine or cardioversion.
• If the dysrhythmias are continuous then
magnesium sulphate can be given.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
Medical treatment guidelines for acute
myocardial infarction:
• Use rapid transit to the hospital obtain 12-lead
ECG to read within 10 minutes.
• Obtain laboratory blood specimens of cardiac
biomarkers, including troponins.
• Obtain other diagnostics to clarify diagnosis.
• Begin routine medical interventions:
o Supplemental oxygen.
o Nitroglycerin.
o Morphine.
o Aspirin 162-325mg.
o Beta blockers.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
Emergent percutaneous coronary intervention:
• The patient in whom an acute mi is suspected may
be referred for an immediate PCI.PCI may be used
to open the occluded coronary artery in an acute mi
and promote reperfusion.
• To the area that has been deprived of oxygen.
Superior outcomes have been reported with the use
of PCI treats the underlying atherosclerotic lesions.
• Because the duration of oxygen deprivation is
directly related to number of cells that die, the time
from the patient’s arrival in the emergency
department to time PCI is performed should be less
than 60 minutes.
• This is frequently referred door to balloon time.
• Cardiac catheterization lab and staff must be
available if an emergent PCI is performed within
short time.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
Surgical management:
• Acute evolving myocardial infraction less than six
hours from onset,
In patients in whom PTCA or streptokinase,
depending on the coronary anatomy,
Has been unsuccessful, in single vessel disease,
CABG is preferable to SK/PTCA therapy unless a
very major "culprit" lesion can be identified with
certainty.
• Post-infraction angina hours to days after a
transmural myocardial infarction unyielding to
maximal medical therapy and in patients with a
coronary artery obstruction not amenable to PTCA.
• Occlusion of coronary artery during PTCA causing
hemodynamic obstruction. And threatened
myocardium subtended by the obstructed coronary
artery.
• Balloon dependent patients in cardiogenic shock
without mechanical defects who have adequate
residual left ventricular function as determined by
regional wall motion studies.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
• Ventricular septal defect secondary to myocardial
infraction unless there is terminal organ damage.
• Mitral valve replacement with or without coronary
bypass for acute papillary muscle rupture.
• Semi emergent cardiac transplantation, either with
or without a mechanical bridge to transplant in
young individuals (less than 50 years) who have
suffered massive destruction
Of left ventricular myocardium by an acute
coronary occlusion with or with recurring
ventricular tachyarrhythmias. Ejection fraction in
this clinical category is always under 0.20 and
usually under 0.15.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
Dietary management:
➢ The prospect for dietary management of the
coronary disease problem lies primarily in the
ability of dietary measures to lower these
lipoprotein Levels.
➢ Animal fat contains some factor (or factors) which
provokes elevation in the serum level of S,"0-12
and S" 12-20 lipoproteins.
➢ No valid evidence exists that any I protective
factor is present in vegetable oils which will lower
S,"012 or," 12-20 lipoprotein levels. Dietary
carbohydrate intake is ai prime factor in controlling
the serum level of the S," 20 100 and S," 100400
lipoprotein classes. Restriction of dietary
carbohydrate can provoke mar ked falls in the
serum level of these lipoproteins.
➢ The effect of caloric restriction and weight
reduction can be largely explained on the basis of
the alteration in animal fat intake and carbohydrate
intake in such diets.
➢ The serum cholesterol measurement can be a
dangerously misleading guide in evaluation of the
effect of diet upon the serum lipids.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
Nursing management:
Elaborate the nursing management of the patient with mi
in detail the nursing priorities are
1. To relieve pain, anxiety.
2. To reduce myocardial workload.
3. To prevent and assist in treatment of life-
threatening dysrhythmias.
4. To promote selfcare.

Nursing diagnosis, intervention and rationale

Pain related to tissue ischemia secondary.to coronary
occlusion manifested by complaints of chest pain, facial
grimacing.
➢ Intervention: Obtain full description of pain from
patient including location, intensity, duration,
quality and radiation.
Rationale: pain is a subjective symptom and must
be described by the patient.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
➢ Intervention: provide calm and quiet environment
and other comfort measures.
Rationale: decreases external stimuli may
aggravate anxiety.
➢ Intervention: administer supplementary oxygen.
Rationale: increases the oxygen supply to
myocardium there by relieving discomfort.
Anxiety/ fear related to change in health and
socioeconomic status manifested by hypertension,
restlessness, uncertainty etc.
➢ Intervention: note presence of hostility
withdrawal or denial.
Rationale: ongoing anxiety may present
manifested by depression.
➢ Intervention: encourage patient to communicate
with one another, sharing questions.
Rationale: sharing information may relieve
tension of unexpressed worries.
➢ Intervention: answer all questions honestly.
Rationale: to win the confidence of the patient.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
Altered tissue perfusion related to reduction of blood flow
due to vasoconstriction manifested by thromboembolic
formation.
➢ Intervention: inspect for cyanosis, cold and
clammy skin.
Rationale: systemic vasoconstriction resulting
from decreased cardiac output may be evidenced
by decreased skin prefusion.
➢ Intervention: assess for homan’s sign,
Rationale: indicator for deep vein thrombosis.
➢ Interventions: monitor laboratory details e.g.:
ABG’S, BUN indicators of organ perfusion.
Prepare the patient for thromboembolic therapy.
Rationale: to dissolve the clot and to restore
perfusion of myocardium.
S.NO SPECIFIC TIME CONTENT AV AIDS TEACHING LEARNIG EVALUA
OBJECTIVES ACTIVITY ACTIVITY TION
Excess fluid volume related to increased sodium and water
retention manifested by dependent edema.
➢ Intervention: measure intake output to detect
whether there is decrease in output.
Rationale: decreased cardiac output results in
impaired kidney perfusion.na/h2o retention.

Other nursing management:

• Provide semi fowler’s positions to promote chest
expansions and comfort.
• Oxygen administration to treat tissue hypoxia.
• Check vital signs every15 minutes watch for PVC
[premature ventricular contraction].
• ECG.
• Assess the L.O.C. morphine is the drug of choice
to relieve chest pain.
• strict I/O chart.
• Bed rest.
• Sedation and hypnotism.